PMID-sentid Pub_year Sent_text compound_name comp_offset prot_official_name organism prot_offset 24351824-0 2013 Cbl-b enhances sensitivity to 5-fluorouracil via EGFR- and mitochondria-mediated pathways in gastric cancer cells. Fluorouracil 30-44 epidermal growth factor receptor Homo sapiens 49-53 24336083-10 2013 Moreover, Patz1-ko MEFs show a decreased percentage of apoptotic cells, either spontaneous or induced by treatment with 5-fluorouracil (5FU), compared with wt controls, suggesting a pro-apoptotic role for PATZ1 in these cells. Fluorouracil 120-134 POZ (BTB) and AT hook containing zinc finger 1 Mus musculus 10-15 24336083-10 2013 Moreover, Patz1-ko MEFs show a decreased percentage of apoptotic cells, either spontaneous or induced by treatment with 5-fluorouracil (5FU), compared with wt controls, suggesting a pro-apoptotic role for PATZ1 in these cells. Fluorouracil 136-139 POZ (BTB) and AT hook containing zinc finger 1 Mus musculus 10-15 24336083-12 2013 Indeed, knockdown of PATZ1 in p53-null osteosarcoma cells upregulates BAX expression and decreases survival of 5FU-treated cells, then suggesting an anti-apoptotic role of PATZ1 in p53-null cancer cells. Fluorouracil 111-114 POZ (BTB) and AT hook containing zinc finger 1 Mus musculus 21-26 24351824-7 2013 These results suggest that Cbl-b enhances sensitivity to 5-FU via EGFR- and mitochondria-mediated pathways in gastric cancer cells. Fluorouracil 57-61 epidermal growth factor receptor Homo sapiens 66-70 23800895-0 2013 Associations between genetic polymorphisms of epidermal growth factor receptor (EGFR) and survival of colorectal cancer (CRC) patients treated with 5-fluorouracil-based chemotherapy. Fluorouracil 148-162 epidermal growth factor receptor Homo sapiens 46-78 24363520-10 2013 The up-regulation of Bax and down-regulation of Bcl-2 showed that the essential mechanism of apoptosis induced by SIN and 5-FU occurs via the mitochondrial pathway. Fluorouracil 122-126 BCL2 associated X, apoptosis regulator Homo sapiens 21-24 24363520-10 2013 The up-regulation of Bax and down-regulation of Bcl-2 showed that the essential mechanism of apoptosis induced by SIN and 5-FU occurs via the mitochondrial pathway. Fluorouracil 122-126 BCL2 apoptosis regulator Homo sapiens 48-53 23800895-0 2013 Associations between genetic polymorphisms of epidermal growth factor receptor (EGFR) and survival of colorectal cancer (CRC) patients treated with 5-fluorouracil-based chemotherapy. Fluorouracil 148-162 epidermal growth factor receptor Homo sapiens 80-84 23800895-1 2013 PURPOSE: This retrospective cohort study investigated the association between epidermal growth factor receptor (EGFR) polymorphisms and clinical outcomes in colorectal cancer (CRC) patients treated with 5-fluorouracil (5-FU)-based chemotherapy. Fluorouracil 203-217 epidermal growth factor receptor Homo sapiens 78-110 23800895-1 2013 PURPOSE: This retrospective cohort study investigated the association between epidermal growth factor receptor (EGFR) polymorphisms and clinical outcomes in colorectal cancer (CRC) patients treated with 5-fluorouracil (5-FU)-based chemotherapy. Fluorouracil 203-217 epidermal growth factor receptor Homo sapiens 112-116 23800895-8 2013 CONCLUSIONS: EGFR polymorphisms can serve as prognostic predictors for CRC patients receiving 5-FU-based chemotherapy. Fluorouracil 94-98 epidermal growth factor receptor Homo sapiens 13-17 24033642-6 2013 We found that PARP inhibition synergized with cisplatin, and the cells were highly sensitive, in a similar manner to the combination of cisplatin and 5-fluorouracil (5-FU). Fluorouracil 150-164 poly(ADP-ribose) polymerase 1 Homo sapiens 14-18 23508585-0 2013 PTK787/ZK222584 combined with interferon alpha and 5-fluorouracil synergistically inhibits VEGF signaling pathway in hepatocellular carcinoma. Fluorouracil 51-65 vascular endothelial growth factor A Homo sapiens 91-95 24018051-4 2013 Our study found that the expression of miR-27a was down-regulated in the multidrug-resistant hepatocellular carcinoma cell line BEL-7402/5-fluorouracil (BEL/5-FU) compared with its parental BEL-7402 cell line, while the MDR1/P-glycoprotein expression was elevated. Fluorouracil 137-151 microRNA 27a Homo sapiens 39-46 24018051-4 2013 Our study found that the expression of miR-27a was down-regulated in the multidrug-resistant hepatocellular carcinoma cell line BEL-7402/5-fluorouracil (BEL/5-FU) compared with its parental BEL-7402 cell line, while the MDR1/P-glycoprotein expression was elevated. Fluorouracil 137-151 ATP binding cassette subfamily B member 1 Homo sapiens 220-224 24018051-4 2013 Our study found that the expression of miR-27a was down-regulated in the multidrug-resistant hepatocellular carcinoma cell line BEL-7402/5-fluorouracil (BEL/5-FU) compared with its parental BEL-7402 cell line, while the MDR1/P-glycoprotein expression was elevated. Fluorouracil 137-151 ATP binding cassette subfamily B member 1 Homo sapiens 225-239 24018051-5 2013 Overexpression of miR-27a by transfecting with miR-27a mimics in the BEL/5-FU cells could reduce the MDR1/P-glycoprotein and beta-catenin expressions, enhance the sensitivity of these cells to 5-fluorouracil and 5-fluorouracil-induced apoptosis. Fluorouracil 193-207 microRNA 27a Homo sapiens 18-25 24018051-5 2013 Overexpression of miR-27a by transfecting with miR-27a mimics in the BEL/5-FU cells could reduce the MDR1/P-glycoprotein and beta-catenin expressions, enhance the sensitivity of these cells to 5-fluorouracil and 5-fluorouracil-induced apoptosis. Fluorouracil 193-207 microRNA 27a Homo sapiens 47-54 24219283-6 2013 Treatment of RCC cell lines with interferon alpha (IFN-alpha) increased thymidine phosphorylase levels and prior treatment of RCC cell lines with IFN-alpha followed by 5-FU or DFUR resulted in enhanced sensitivity of all cell lines to 5-FU and two of three cell lines to DFUR. Fluorouracil 235-239 interferon alpha 1 Homo sapiens 33-60 24219283-6 2013 Treatment of RCC cell lines with interferon alpha (IFN-alpha) increased thymidine phosphorylase levels and prior treatment of RCC cell lines with IFN-alpha followed by 5-FU or DFUR resulted in enhanced sensitivity of all cell lines to 5-FU and two of three cell lines to DFUR. Fluorouracil 235-239 interferon alpha 1 Homo sapiens 51-60 24219283-8 2013 In addition, our in vitro cytotoxicity results showed that RCC cell lines differed in their response to 5-FU and DFUR and prior treatment with IFN-alpha potentiated cytotoxic response to metabolites of capecitabine. Fluorouracil 104-108 interferon alpha 1 Homo sapiens 143-152 24018051-5 2013 Overexpression of miR-27a by transfecting with miR-27a mimics in the BEL/5-FU cells could reduce the MDR1/P-glycoprotein and beta-catenin expressions, enhance the sensitivity of these cells to 5-fluorouracil and 5-fluorouracil-induced apoptosis. Fluorouracil 212-226 microRNA 27a Homo sapiens 18-25 24018051-5 2013 Overexpression of miR-27a by transfecting with miR-27a mimics in the BEL/5-FU cells could reduce the MDR1/P-glycoprotein and beta-catenin expressions, enhance the sensitivity of these cells to 5-fluorouracil and 5-fluorouracil-induced apoptosis. Fluorouracil 212-226 microRNA 27a Homo sapiens 47-54 24033642-6 2013 We found that PARP inhibition synergized with cisplatin, and the cells were highly sensitive, in a similar manner to the combination of cisplatin and 5-fluorouracil (5-FU). Fluorouracil 166-170 poly(ADP-ribose) polymerase 1 Homo sapiens 14-18 25337561-11 2013 The expressions of occludin and claudin-1, not ZO-1 protein expressions in 200 mg/kg 5-FU treated animals were significantly reduced compared to those of the control group or 100 mg/kg 5-FU group. Fluorouracil 85-89 occludin Mus musculus 19-27 24036626-0 2013 Nanoassemblies containing a fluorouracil/zidovudine glyceryl prodrug with phospholipase A2-triggered drug release for cancer treatment. Fluorouracil 28-40 phospholipase A2 group IB Homo sapiens 74-90 23837948-0 2013 Selenocystine potentiates cancer cell apoptosis induced by 5-fluorouracil by triggering reactive oxygen species-mediated DNA damage and inactivation of the ERK pathway. Fluorouracil 59-73 mitogen-activated protein kinase 1 Homo sapiens 156-159 23837948-4 2013 This study demonstrates that SeC acts as an effective enhancer of 5-FU-induced apoptosis in A375 human melanoma cells through induction of mitochondria-mediated apoptosis with the involvement of DNA damage-mediated p53 phosphorylation and ERK inactivation. Fluorouracil 66-70 tumor protein p53 Homo sapiens 215-218 23837948-4 2013 This study demonstrates that SeC acts as an effective enhancer of 5-FU-induced apoptosis in A375 human melanoma cells through induction of mitochondria-mediated apoptosis with the involvement of DNA damage-mediated p53 phosphorylation and ERK inactivation. Fluorouracil 66-70 mitogen-activated protein kinase 1 Homo sapiens 239-242 23837948-6 2013 SeC and 5-FU in combination also triggered cell oxidative stress through regulation of the intracellular redox system and led to DNA damage and inactivation of ERK and AKT. Fluorouracil 8-12 mitogen-activated protein kinase 1 Homo sapiens 160-163 23837948-6 2013 SeC and 5-FU in combination also triggered cell oxidative stress through regulation of the intracellular redox system and led to DNA damage and inactivation of ERK and AKT. Fluorouracil 8-12 AKT serine/threonine kinase 1 Homo sapiens 168-171 24100731-6 2013 In this study, we investigated whether treatment of gastric cancer cells with shRNA targeting cyclin D1 (ShCCND1) or 5-FU, alone or in combination, influences the activation of phosphorylated AKT (pAKT) and pNFkappaB, which are markers that are increased in 5-FU chemoresistance. Fluorouracil 117-121 AKT serine/threonine kinase 1 Homo sapiens 192-195 25337561-12 2013 The expression of Nuclear factor-kappa B p65 (NF-kappaB p65) protein and TNF-alpha mRNA were significantly higher in 5-FU treated group compared to those of control group. Fluorouracil 117-121 tumor necrosis factor Mus musculus 73-82 23990352-0 2013 The effects of silencing of PI3K p85alpha on 5-FU-induced colorectal cancer cells apoptosis. Fluorouracil 45-49 phosphoinositide-3-kinase regulatory subunit 1 Homo sapiens 33-41 23990352-5 2013 Silencing of PI3K p85alpha in colorectal cancer cells increased disruption of mitochondrial membrane potential and enhanced 5-FU-induced apoptosis. Fluorouracil 124-128 phosphoinositide-3-kinase regulatory subunit 1 Homo sapiens 18-26 24100378-11 2013 The present results propose the possibility that PSK induces PBMCs to express IFN-alpha which inhibits DPD expression, and consequently augments the antitumor effect of 5-FU or 5"-DFUR. Fluorouracil 169-173 interferon alpha 1 Homo sapiens 78-87 24211581-10 2013 Moreover, we found that 5-aza-2"-deoxycytidine-mediated or enforced up-regulation of BNIP3 in DLD-1 cells results in KRas-dependent resistance to 5-Fluorouracil. Fluorouracil 146-160 BCL2 interacting protein 3 Homo sapiens 85-90 24095863-7 2013 Nicotine addition to Caco-2 and HCT-8, treated with 5-FU or CPT, decreased the cleavage of substrate of caspase 3 and 7, poly-ADP-ribose polymerase (PARP). Fluorouracil 52-56 poly(ADP-ribose) polymerase 1 Homo sapiens 121-147 24095863-7 2013 Nicotine addition to Caco-2 and HCT-8, treated with 5-FU or CPT, decreased the cleavage of substrate of caspase 3 and 7, poly-ADP-ribose polymerase (PARP). Fluorouracil 52-56 poly(ADP-ribose) polymerase 1 Homo sapiens 149-153 24312415-7 2013 In-vitro BCAA reduced the frequency of EpCAM-positive cells and improved sensitivity to the anti-proliferative effect of 5-FU. Fluorouracil 121-125 AT-rich interaction domain 4B Homo sapiens 9-13 24312415-8 2013 Combined 5-FU and BCAA provided better antitumor efficacy than 5-FU alone in the xenograft model. Fluorouracil 63-67 AT-rich interaction domain 4B Homo sapiens 18-22 24095863-8 2013 Moreover, P-ERK/ERK ratio was modified by nicotine addition to 5-FU and CPT treated cells in an opposite manner. Fluorouracil 63-67 mitogen-activated protein kinase 1 Homo sapiens 12-15 23982118-8 2013 The exploratory pharmacokinetic/pharmacogenetic study showed that CYP2A6 variants (*4, *7, *9) are associated with a lower metabolic ratio of S-1 (exposure ratio of 5-fluorouracil to tegafur). Fluorouracil 165-179 proteasome 26S subunit, non-ATPase 1 Homo sapiens 142-145 23952905-7 2013 Although acetylated TDG has reduced glycosylase activity towards T/G, 5-formylcytosine/G and 5-carboxylcytosine/G, it has a stronger activity towards a 5-fluorouracil/G substrate as compared with unmodified TDG. Fluorouracil 152-166 thymine DNA glycosylase Homo sapiens 20-23 23952905-10 2013 The physical and functional interactions between SIRT1 and TDG may mediate DNA repair, gene expression and FU (5-fluorouracil)-mediated cytotoxicity. Fluorouracil 111-125 thymine DNA glycosylase Homo sapiens 59-62 24244394-5 2013 We have previously reported that haploinsufficiency of PSF1 resulted in failure of acute proliferation of bone marrow hematopoietic stem cells (HSCs) during reconstitution of bone marrow ablated by 5-FU treatment. Fluorouracil 198-202 GINS complex subunit 1 (Psf1 homolog) Mus musculus 55-59 23954321-7 2013 Importantly, the combination treatment with RES and 5-FU induced a remarkably synergistic enhancement of growth inhibition and apoptosis through the additional suppression of the MAPK/Erk1/2 signaling pathway in colon cancer DLD-1 cells. Fluorouracil 52-56 mitogen-activated protein kinase 3 Homo sapiens 179-183 24221219-3 2013 Epidermal growth factor receptor (EGFR) inhibitors have proven to significantly prolong survival and have therefore become the first line treatment in recurrent and metastatic squamous cell carcinoma of the head and neck in addition to platinum and 5-FU treatment. Fluorouracil 249-253 epidermal growth factor receptor Homo sapiens 34-38 24013415-2 2013 Among these derivatives, compound 6 was more potent than positive control 5-fluorouracil (5-Fu) on QGY-7703 and SMMC-7721 cells with IC50 values of 6.27 muM, 7.50 muM and 15.56 muM, 14.55 muM, respectively. Fluorouracil 74-88 latexin Homo sapiens 153-156 24013415-2 2013 Among these derivatives, compound 6 was more potent than positive control 5-fluorouracil (5-Fu) on QGY-7703 and SMMC-7721 cells with IC50 values of 6.27 muM, 7.50 muM and 15.56 muM, 14.55 muM, respectively. Fluorouracil 74-88 latexin Homo sapiens 163-166 24013415-2 2013 Among these derivatives, compound 6 was more potent than positive control 5-fluorouracil (5-Fu) on QGY-7703 and SMMC-7721 cells with IC50 values of 6.27 muM, 7.50 muM and 15.56 muM, 14.55 muM, respectively. Fluorouracil 74-88 latexin Homo sapiens 163-166 24013415-2 2013 Among these derivatives, compound 6 was more potent than positive control 5-fluorouracil (5-Fu) on QGY-7703 and SMMC-7721 cells with IC50 values of 6.27 muM, 7.50 muM and 15.56 muM, 14.55 muM, respectively. Fluorouracil 74-88 latexin Homo sapiens 163-166 24013415-2 2013 Among these derivatives, compound 6 was more potent than positive control 5-fluorouracil (5-Fu) on QGY-7703 and SMMC-7721 cells with IC50 values of 6.27 muM, 7.50 muM and 15.56 muM, 14.55 muM, respectively. Fluorouracil 90-94 latexin Homo sapiens 153-156 24013415-2 2013 Among these derivatives, compound 6 was more potent than positive control 5-fluorouracil (5-Fu) on QGY-7703 and SMMC-7721 cells with IC50 values of 6.27 muM, 7.50 muM and 15.56 muM, 14.55 muM, respectively. Fluorouracil 90-94 latexin Homo sapiens 163-166 24013415-2 2013 Among these derivatives, compound 6 was more potent than positive control 5-fluorouracil (5-Fu) on QGY-7703 and SMMC-7721 cells with IC50 values of 6.27 muM, 7.50 muM and 15.56 muM, 14.55 muM, respectively. Fluorouracil 90-94 latexin Homo sapiens 163-166 24013415-2 2013 Among these derivatives, compound 6 was more potent than positive control 5-fluorouracil (5-Fu) on QGY-7703 and SMMC-7721 cells with IC50 values of 6.27 muM, 7.50 muM and 15.56 muM, 14.55 muM, respectively. Fluorouracil 90-94 latexin Homo sapiens 163-166 24008552-10 2013 A strong anti-tumorigenic effect of rAAV-FHL2-shRNA was shown in nude mice and this antitumor effect was enhanced when combined with 5-FU treatment. Fluorouracil 133-137 four and a half LIM domains 2 Mus musculus 41-45 23954321-7 2013 Importantly, the combination treatment with RES and 5-FU induced a remarkably synergistic enhancement of growth inhibition and apoptosis through the additional suppression of the MAPK/Erk1/2 signaling pathway in colon cancer DLD-1 cells. Fluorouracil 52-56 mitogen-activated protein kinase 3 Homo sapiens 184-190 24331695-11 2013 Moreover, sorafenib alone significantly inhibited the RAF/MEK/ERK and STAT3 pathways, with the fold-changes of p-C-RAF, p-ERK1/2 and p-STAT3 being 0.56 +/- 0.05, 0.54 +/- 0.02 and 0.36 +/- 0.02, respectively (all P less than 0.01); 5-FU alone produced no significant effects on these pathways. Fluorouracil 232-236 mitogen-activated protein kinase kinase 7 Homo sapiens 58-61 24331695-14 2013 Sorafenib-inhibited RAF/MEK/ERK and STAT3 signaling and cyclinD1 expression may have induced the observed G1phase arrest and S phase reduction, thereby reducing the cells" sensitivity to 5-FU. Fluorouracil 187-191 mitogen-activated protein kinase kinase 7 Homo sapiens 24-27 23939464-5 2013 Based on the linear relationship (R = -0.9994) between the ratiometric PL intensity (IQD2/IQD1) and the molar concentration of 5-FU (0-1 muM), a ratiometric PL sensor for 5-FU was achieved and displays a low limit of detection (20 nM). Fluorouracil 127-131 latexin Homo sapiens 137-140 24161202-6 2013 CpG-ODN or 5-FU could down-regulate the mRNA expression of Bcl-2 within HepG2 cells. Fluorouracil 11-15 BCL2 apoptosis regulator Homo sapiens 59-64 24104963-1 2013 BACKGROUND: Genomic rearrangements at the fragile site FRA1E may disrupt the dihydropyrimidine dehydrogenase gene (DPYD) which is involved in 5-fluorouracil (5-FU) catabolism. Fluorouracil 142-156 fragile site, aphidicolin type, common, fra(1)(p21.2) Homo sapiens 55-60 24104963-1 2013 BACKGROUND: Genomic rearrangements at the fragile site FRA1E may disrupt the dihydropyrimidine dehydrogenase gene (DPYD) which is involved in 5-fluorouracil (5-FU) catabolism. Fluorouracil 158-162 fragile site, aphidicolin type, common, fra(1)(p21.2) Homo sapiens 55-60 24131658-10 2013 Both in vitro and in vivo preliminary experiments indicated that BCH significantly suppressed growth of the tumor and yielded an additive therapeutic efficacy to gemcitabine and 5-FU. Fluorouracil 178-182 NK2 homeobox 1 Homo sapiens 65-68 23553437-6 2013 We show that specific blocking of IL-4 and IL-13-mediated STAT6 activation by either an IL-4-binding fusion protein APG598 or an IL-4R antagonist APG201 (R121D/Y124D) renders HL cells more prone to apoptotic killing by chemotherapeutic drugs such as Mitomycin C, 5-Fluorouracil, Etopside, Doxorubicin and Paclitaxel. Fluorouracil 263-277 interleukin 4 Homo sapiens 34-38 23553437-6 2013 We show that specific blocking of IL-4 and IL-13-mediated STAT6 activation by either an IL-4-binding fusion protein APG598 or an IL-4R antagonist APG201 (R121D/Y124D) renders HL cells more prone to apoptotic killing by chemotherapeutic drugs such as Mitomycin C, 5-Fluorouracil, Etopside, Doxorubicin and Paclitaxel. Fluorouracil 263-277 interleukin 13 Homo sapiens 43-48 23553437-6 2013 We show that specific blocking of IL-4 and IL-13-mediated STAT6 activation by either an IL-4-binding fusion protein APG598 or an IL-4R antagonist APG201 (R121D/Y124D) renders HL cells more prone to apoptotic killing by chemotherapeutic drugs such as Mitomycin C, 5-Fluorouracil, Etopside, Doxorubicin and Paclitaxel. Fluorouracil 263-277 interleukin 4 Homo sapiens 88-92 24228120-7 2013 The positive rate of Bcl-2 expression was 80%, and Bcl-2 expression was significantly associated with chemoresistance to 5-FU (r(s) = 0.265, P = 0.041), ADM (r(s) = 0.425, P = 0.001) and MMC (r(s) = 0.40, P = 0.002). Fluorouracil 121-125 BCL2 apoptosis regulator Homo sapiens 51-56 24151445-0 2013 TNF-alpha -857C>T genotype is predictive of clinical response after treatment with definitive 5-fluorouracil/cisplatin-based chemoradiotherapy in Japanese patients with esophageal squamous cell carcinoma. Fluorouracil 97-111 tumor necrosis factor Homo sapiens 0-9 24151445-6 2013 CONCLUSIONS: The TNF-alpha -857C>T genotype was found to be predictive of clinical response and was more likely to predict long-term survival in Japanese ESCC patients receiving definitive 5-FU/CDDP-based CRT. Fluorouracil 192-196 tumor necrosis factor Homo sapiens 17-26 24228095-9 2013 5-FU induced dramatic increase of serum endotoxin, D-lactate and D-Amino-Acid Oxidase (DAO) that were significantly reversed by Curcumin treatment. Fluorouracil 0-4 D-amino-acid oxidase Rattus norvegicus 65-85 24228120-9 2013 CONCLUSION: Overexpression of Bcl-2 may predict a loss of the efficacy of the chemotherapy drugs 5-FU, ADM and MMC in patients with gastric cancer. Fluorouracil 97-101 BCL2 apoptosis regulator Homo sapiens 30-35 24228095-9 2013 5-FU induced dramatic increase of serum endotoxin, D-lactate and D-Amino-Acid Oxidase (DAO) that were significantly reversed by Curcumin treatment. Fluorouracil 0-4 D-amino-acid oxidase Rattus norvegicus 87-90 25505563-0 2013 Enantioselectivity in the cytochrome P450-dependent conversion of tegafur to 5-fluorouracil in human liver microsomes. Fluorouracil 77-91 cytochrome P450 family 4 subfamily F member 3 Homo sapiens 26-41 24228095-14 2013 Curcumin also reduced the expression of pro-apoptotic Bax but stimulated anti-apoptotic Bcl-2 to attenuate 5-FU-induced apoptosis of intestinal epithelial cells. Fluorouracil 107-111 BCL2, apoptosis regulator Rattus norvegicus 88-93 24124598-6 2013 Down-regulation of ATP5J expression attenuated the ability of cell migration and increased the sensitivity to 5-fluorouracil (5-Fu) in cells of the DLD1 cell line. Fluorouracil 110-124 ATP synthase peripheral stalk subunit F6 Homo sapiens 19-24 24124598-6 2013 Down-regulation of ATP5J expression attenuated the ability of cell migration and increased the sensitivity to 5-fluorouracil (5-Fu) in cells of the DLD1 cell line. Fluorouracil 126-130 ATP synthase peripheral stalk subunit F6 Homo sapiens 19-24 24124598-7 2013 Inversely, up-regulation of ATP5J expression enhanced cell migration and decreased 5-Fu sensitivity, suggesting that the function of ATP5J in colorectal cancer might involve cell migration and 5-Fu sensitivity. Fluorouracil 83-87 ATP synthase peripheral stalk subunit F6 Homo sapiens 28-33 24124598-7 2013 Inversely, up-regulation of ATP5J expression enhanced cell migration and decreased 5-Fu sensitivity, suggesting that the function of ATP5J in colorectal cancer might involve cell migration and 5-Fu sensitivity. Fluorouracil 83-87 ATP synthase peripheral stalk subunit F6 Homo sapiens 133-138 24124598-7 2013 Inversely, up-regulation of ATP5J expression enhanced cell migration and decreased 5-Fu sensitivity, suggesting that the function of ATP5J in colorectal cancer might involve cell migration and 5-Fu sensitivity. Fluorouracil 193-197 ATP synthase peripheral stalk subunit F6 Homo sapiens 28-33 24124598-7 2013 Inversely, up-regulation of ATP5J expression enhanced cell migration and decreased 5-Fu sensitivity, suggesting that the function of ATP5J in colorectal cancer might involve cell migration and 5-Fu sensitivity. Fluorouracil 193-197 ATP synthase peripheral stalk subunit F6 Homo sapiens 133-138 23822592-2 2013 This meta-analysis was performed to determine whether the addition of monoclonal antibodies (mAbs) of epidermal growth factor receptor (EGFR) to oxaliplatin-based chemotherapy treatment improves efficacy in KRAS wild-type metastatic colorectal cancer (mCRC), and whether infusional 5-fluorouracil (5-FU) and oxaliplatin is a preferred combination for EGFR mAbs. Fluorouracil 282-296 epidermal growth factor receptor Homo sapiens 102-134 23822592-2 2013 This meta-analysis was performed to determine whether the addition of monoclonal antibodies (mAbs) of epidermal growth factor receptor (EGFR) to oxaliplatin-based chemotherapy treatment improves efficacy in KRAS wild-type metastatic colorectal cancer (mCRC), and whether infusional 5-fluorouracil (5-FU) and oxaliplatin is a preferred combination for EGFR mAbs. Fluorouracil 282-296 epidermal growth factor receptor Homo sapiens 136-140 23822592-2 2013 This meta-analysis was performed to determine whether the addition of monoclonal antibodies (mAbs) of epidermal growth factor receptor (EGFR) to oxaliplatin-based chemotherapy treatment improves efficacy in KRAS wild-type metastatic colorectal cancer (mCRC), and whether infusional 5-fluorouracil (5-FU) and oxaliplatin is a preferred combination for EGFR mAbs. Fluorouracil 298-302 epidermal growth factor receptor Homo sapiens 102-134 23822592-2 2013 This meta-analysis was performed to determine whether the addition of monoclonal antibodies (mAbs) of epidermal growth factor receptor (EGFR) to oxaliplatin-based chemotherapy treatment improves efficacy in KRAS wild-type metastatic colorectal cancer (mCRC), and whether infusional 5-fluorouracil (5-FU) and oxaliplatin is a preferred combination for EGFR mAbs. Fluorouracil 298-302 epidermal growth factor receptor Homo sapiens 136-140 23987469-4 2013 Moreover, FAAP-02 could obviously increase the thymus and spleen indices, the levels of serum Interleukin 2 (IL-2), Interleukin 6 (IL-6), Interleukin 12 (IL-12) and tumor necrosis factor-alpha (TNF-alpha), and the expression of CD4+ and CD8+ splenic T lymphocytes which were suppressed by the transplanted tumor or/and 5-fluorouracil (5-FU) in the mice. Fluorouracil 319-333 RNA 2',3'-cyclic phosphate and 5'-OH ligase Mus musculus 10-14 23987469-4 2013 Moreover, FAAP-02 could obviously increase the thymus and spleen indices, the levels of serum Interleukin 2 (IL-2), Interleukin 6 (IL-6), Interleukin 12 (IL-12) and tumor necrosis factor-alpha (TNF-alpha), and the expression of CD4+ and CD8+ splenic T lymphocytes which were suppressed by the transplanted tumor or/and 5-fluorouracil (5-FU) in the mice. Fluorouracil 335-339 RNA 2',3'-cyclic phosphate and 5'-OH ligase Mus musculus 10-14 24124598-0 2013 Over-expression of the ATP5J gene correlates with cell migration and 5-fluorouracil sensitivity in colorectal cancer. Fluorouracil 69-83 ATP synthase peripheral stalk subunit F6 Homo sapiens 23-28 25505563-1 2013 Tegafur (FT) is a prodrug of 5-fluorouracil (5-FU) used in cancer chemotherapy, and the bioactivation of FT to 5-FU is mainly catalyzed by cytochrome P450 (CYP) in hepatic microsomes. Fluorouracil 29-43 cytochrome P450 family 4 subfamily F member 3 Homo sapiens 139-154 25505563-1 2013 Tegafur (FT) is a prodrug of 5-fluorouracil (5-FU) used in cancer chemotherapy, and the bioactivation of FT to 5-FU is mainly catalyzed by cytochrome P450 (CYP) in hepatic microsomes. Fluorouracil 29-43 cytochrome P450 family 4 subfamily F member 3 Homo sapiens 156-159 25505563-1 2013 Tegafur (FT) is a prodrug of 5-fluorouracil (5-FU) used in cancer chemotherapy, and the bioactivation of FT to 5-FU is mainly catalyzed by cytochrome P450 (CYP) in hepatic microsomes. Fluorouracil 45-49 cytochrome P450 family 4 subfamily F member 3 Homo sapiens 139-154 25505563-1 2013 Tegafur (FT) is a prodrug of 5-fluorouracil (5-FU) used in cancer chemotherapy, and the bioactivation of FT to 5-FU is mainly catalyzed by cytochrome P450 (CYP) in hepatic microsomes. Fluorouracil 45-49 cytochrome P450 family 4 subfamily F member 3 Homo sapiens 156-159 25505563-1 2013 Tegafur (FT) is a prodrug of 5-fluorouracil (5-FU) used in cancer chemotherapy, and the bioactivation of FT to 5-FU is mainly catalyzed by cytochrome P450 (CYP) in hepatic microsomes. Fluorouracil 111-115 cytochrome P450 family 4 subfamily F member 3 Homo sapiens 139-154 25505563-1 2013 Tegafur (FT) is a prodrug of 5-fluorouracil (5-FU) used in cancer chemotherapy, and the bioactivation of FT to 5-FU is mainly catalyzed by cytochrome P450 (CYP) in hepatic microsomes. Fluorouracil 111-115 cytochrome P450 family 4 subfamily F member 3 Homo sapiens 156-159 24103265-7 2013 Compared with the control group, IC50; of shMRE11 group treated with DDP, MMC, ADM, 5-FU was reduced significantly as shown by MTT assay (P<0.05); qRT-PCR and Western blot analysis of MRP1 showed that its expression significantly decreased at the mRNA and protein levels (P<0.05). Fluorouracil 84-88 ATP binding cassette subfamily C member 1 Homo sapiens 187-191 23108402-0 2013 5-Fluorouracil signaling through a calcium-calmodulin-dependent pathway is required for p53 activation and apoptosis in colon carcinoma cells. Fluorouracil 0-14 tumor protein p53 Homo sapiens 88-91 23108402-3 2013 Current knowledge states that in certain cell types, 5-FU-induced stress is signaling through a p53-dependent induction of tumor necrosis factor-receptor oligomerization required for death-inducing signaling complex formation and caspase-8 activation. Fluorouracil 53-57 tumor protein p53 Homo sapiens 96-99 23108402-4 2013 Here we establish a role of calcium (Ca(2+)) as a messenger for p53 activation in response to 5-FU. Fluorouracil 94-98 tumor protein p53 Homo sapiens 64-67 23108402-7 2013 Moreover, ectopic expression of p53 S15A in HCT116 p53(-/-) cells confirmed the importance of a Ca(2+)-CaM-p53 axis in 5-FU-induced extrinsic apoptosis. Fluorouracil 119-123 tumor protein p53 Homo sapiens 32-35 23684481-6 2013 Results showed that the siRNA could downregulate Bcl-2 expression, which increased apoptosis and sensitivity of SGC-7901 cell to 5-Fluorouracil (P<0.05). Fluorouracil 129-143 BCL2 apoptosis regulator Homo sapiens 49-54 23963147-1 2013 BACKGROUND: S-1 is an oral fluoropyrimidine that mimics infusional 5-fluorouracil. Fluorouracil 67-81 proteasome 26S subunit, non-ATPase 1 Homo sapiens 12-15 24040364-0 2013 53BP1 sensitizes breast cancer cells to 5-fluorouracil. Fluorouracil 40-54 transformation related protein 53 binding protein 1 Mus musculus 0-5 24040364-3 2013 Here we aimed to reveal whether 53BP1 could sensitize breast cancer to 5-Fu. Fluorouracil 71-75 transformation related protein 53 binding protein 1 Mus musculus 32-37 24040364-4 2013 We found that ectopic expression of 53BP1 can significantly sensitize breast cancer cells to 5-Fu while knockdown of 53BP1 conferred the resistance. Fluorouracil 93-97 transformation related protein 53 binding protein 1 Mus musculus 36-41 24040364-6 2013 Furthermore, we demonstrated that 53BP1 regulated the sensitivity to 5-Fu through thymidylate synthase (TS) and dihydropyrimidine dehydrogenase (DPYD). Fluorouracil 69-73 transformation related protein 53 binding protein 1 Mus musculus 34-39 23684481-0 2013 Bcl-2 gene silence enhances the sensitivity toward 5-Fluorouracil in gastric adenocarcinoma cells. Fluorouracil 51-65 BCL2 apoptosis regulator Homo sapiens 0-5 23684481-2 2013 This study was to investigate whether downregulation of Bcl-2 expression by small interfering RNA (siRNA) against the Bcl-2 gene would enhance the apoptosis and sensitivity of gastric adenocarcinoma SGC-7901 cell to 5-Fluorouracil. Fluorouracil 216-230 BCL2 apoptosis regulator Homo sapiens 56-61 23684481-2 2013 This study was to investigate whether downregulation of Bcl-2 expression by small interfering RNA (siRNA) against the Bcl-2 gene would enhance the apoptosis and sensitivity of gastric adenocarcinoma SGC-7901 cell to 5-Fluorouracil. Fluorouracil 216-230 BCL2 apoptosis regulator Homo sapiens 118-123 23684481-7 2013 This study indicated that inhibition of Bcl-2 expression by siRNA would be useful a new useful protocol to increase the effect of 5-Fluorouracil on treatment of gastric adenocarcinoma, which may play an important role in developing novel therapeutic strategies in the future. Fluorouracil 130-144 BCL2 apoptosis regulator Homo sapiens 40-45 24069522-2 2013 METHODS: To apply this strategy to the treatment of HNSCC, we used a human NSC line expressing cytosine deaminase (HB1.F3-CD), an enzyme that converts 5-fluorocytosine (5-FC) into 5-fluorouracil (5-FU), an anticancer agent. Fluorouracil 180-194 histocompatibility minor HB-1 Homo sapiens 115-118 24047774-1 2013 S-1 is a novel oral anticancer agent consisting of tegafur, a prodrug of 5-fluorouracil, and 2 modulators. Fluorouracil 73-87 proteasome 26S subunit, non-ATPase 1 Homo sapiens 0-3 23997941-3 2013 Bevacizumab, a monoclonal antibody that targets the angiogenesis-driving ligand vascular endothelial growth factor A (VEGF-A), is the only anti-angiogenic agent approved in first-line therapy for metastatic colorectal cancer, where it can be used in combination with intravenous 5-fluorouracil-containing chemotherapy regimens. Fluorouracil 279-293 vascular endothelial growth factor A Homo sapiens 80-116 23997941-3 2013 Bevacizumab, a monoclonal antibody that targets the angiogenesis-driving ligand vascular endothelial growth factor A (VEGF-A), is the only anti-angiogenic agent approved in first-line therapy for metastatic colorectal cancer, where it can be used in combination with intravenous 5-fluorouracil-containing chemotherapy regimens. Fluorouracil 279-293 vascular endothelial growth factor A Homo sapiens 118-124 24069522-2 2013 METHODS: To apply this strategy to the treatment of HNSCC, we used a human NSC line expressing cytosine deaminase (HB1.F3-CD), an enzyme that converts 5-fluorocytosine (5-FC) into 5-fluorouracil (5-FU), an anticancer agent. Fluorouracil 196-200 histocompatibility minor HB-1 Homo sapiens 115-118 24649260-2 2013 The aim of this study was to determine the association between BCRP expression and 5-fluorouracil (5-FU) resistance in clinical breast cancer tissue specimens. Fluorouracil 83-97 ATP binding cassette subfamily G member 2 (Junior blood group) Homo sapiens 63-67 23810214-6 2013 By contrast, 5-fluorouracil induced G2 cell-cycle arrest and apoptosis that may be associated with p53 activation and p21 up-regulation. Fluorouracil 13-27 tumor protein p53 Homo sapiens 99-102 23810214-7 2013 The modulation of Col-1, VEGF, TGF-beta1 and MMP-2 expression by triamcinolone and 5-fluorouracil alone or their combination varied between individual cell lines; the trend is to promote a reduction in Col-1 and TGF-beta1 but up-regulation of MMP-2 expression. Fluorouracil 83-97 vascular endothelial growth factor A Homo sapiens 25-29 23810214-7 2013 The modulation of Col-1, VEGF, TGF-beta1 and MMP-2 expression by triamcinolone and 5-fluorouracil alone or their combination varied between individual cell lines; the trend is to promote a reduction in Col-1 and TGF-beta1 but up-regulation of MMP-2 expression. Fluorouracil 83-97 transforming growth factor beta 1 Homo sapiens 31-40 23810214-7 2013 The modulation of Col-1, VEGF, TGF-beta1 and MMP-2 expression by triamcinolone and 5-fluorouracil alone or their combination varied between individual cell lines; the trend is to promote a reduction in Col-1 and TGF-beta1 but up-regulation of MMP-2 expression. Fluorouracil 83-97 transforming growth factor beta 1 Homo sapiens 212-221 23456958-5 2013 The role of GRP78 in 5-FU sensitivity was examined in CRC cells using siRNA, drug inhibition and flow cytometry. Fluorouracil 21-25 heat shock protein family A (Hsp70) member 5 Homo sapiens 12-17 23456958-11 2013 In vitro, inhibition of GRP78 reduces apoptosis in response to 5-FU in p53 wild-type cells. Fluorouracil 63-67 heat shock protein family A (Hsp70) member 5 Homo sapiens 24-29 23456958-11 2013 In vitro, inhibition of GRP78 reduces apoptosis in response to 5-FU in p53 wild-type cells. Fluorouracil 63-67 tumor protein p53 Homo sapiens 71-74 24649260-2 2013 The aim of this study was to determine the association between BCRP expression and 5-fluorouracil (5-FU) resistance in clinical breast cancer tissue specimens. Fluorouracil 99-103 ATP binding cassette subfamily G member 2 (Junior blood group) Homo sapiens 63-67 24649260-4 2013 Chemosensitivity to 5-FU for BCRP-positive clinical breast cancer tissue specimens was colorimetrically assessed with the cytotoxicity assay through methyl thiazolyl tetrazolium (MTT) reduction. Fluorouracil 20-24 ATP binding cassette subfamily G member 2 (Junior blood group) Homo sapiens 29-33 24649260-8 2013 Our study results indicated that 5-FU resistance may be mediated by BCRP expression in clinical breast cancer tissue specimens, which may help optimize the design of breast cancer clinical chemotherapy schemes in BCRP-positive specimens. Fluorouracil 33-37 ATP binding cassette subfamily G member 2 (Junior blood group) Homo sapiens 68-72 24649260-8 2013 Our study results indicated that 5-FU resistance may be mediated by BCRP expression in clinical breast cancer tissue specimens, which may help optimize the design of breast cancer clinical chemotherapy schemes in BCRP-positive specimens. Fluorouracil 33-37 ATP binding cassette subfamily G member 2 (Junior blood group) Homo sapiens 213-217 23859016-0 2013 Enhanced 5-fluorouracil cytotoxicity in high COX-2 expressing hepatocellular carcinoma cells by wogonin via the PI3K/Akt pathway. Fluorouracil 9-23 mitochondrially encoded cytochrome c oxidase II Homo sapiens 45-50 23915286-11 2013 Furthermore, miR-433 increased inhibition of cell proliferation in HeLa cells treated with 5-FU at over 2.0 muM. Fluorouracil 91-95 latexin Homo sapiens 108-111 23760813-7 2013 However, other polymorphisms could account for 5-FU-induced toxicity, with the CHST1 rs9787901 and GSTM3 rs1799735 having the strongest association. Fluorouracil 47-51 carbohydrate sulfotransferase 1 Homo sapiens 79-84 24009080-6 2013 Furthermore, ectopic expression of c-Kit conferred resistance of colorectal cancer (CRC) cells to treatment with 5-fluorouracil (5-FU), whereas ectopic miR-34a sensitized the cells to 5-FU. Fluorouracil 113-127 KIT proto-oncogene, receptor tyrosine kinase Homo sapiens 35-40 24009080-6 2013 Furthermore, ectopic expression of c-Kit conferred resistance of colorectal cancer (CRC) cells to treatment with 5-fluorouracil (5-FU), whereas ectopic miR-34a sensitized the cells to 5-FU. Fluorouracil 129-133 KIT proto-oncogene, receptor tyrosine kinase Homo sapiens 35-40 23850691-6 2013 Ectopic expression of Ell3 in breast cancer cell lines induces proliferation and 5-FU resistance. Fluorouracil 81-85 elongation factor RNA polymerase II-like 3 Mus musculus 22-26 24156021-2 2013 Recently, it has been reported that S-1, a novel 5-FU-based agent has an effect on bladder cancer. Fluorouracil 49-53 proteasome 26S subunit, non-ATPase 1 Homo sapiens 36-39 23859016-0 2013 Enhanced 5-fluorouracil cytotoxicity in high COX-2 expressing hepatocellular carcinoma cells by wogonin via the PI3K/Akt pathway. Fluorouracil 9-23 AKT serine/threonine kinase 1 Homo sapiens 117-120 23784204-4 2013 We demonstrated that the constructed Bcl-2 siRNA vector effectively silenced Bcl-2 gene expression in the GBC-SD human gallbladder carcinoma cells, inhibited cell proliferation, induced cell apoptosis, increased chemotherapeutic sensitivity to 5-fluorouracil and inhibited tumor growth in vivo. Fluorouracil 244-258 BCL2 apoptosis regulator Homo sapiens 37-42 23755922-1 2013 PURPOSE: To investigate the prognostic value of epidermal growth factor receptor (EGFR) expression in pretreatment tumor biopsy specimens of patients with anal cancer treated with concurrent 5-fluorouracil and mitomycin C-based chemoradiation therapy (CRT). Fluorouracil 191-205 epidermal growth factor receptor Homo sapiens 48-80 23755922-1 2013 PURPOSE: To investigate the prognostic value of epidermal growth factor receptor (EGFR) expression in pretreatment tumor biopsy specimens of patients with anal cancer treated with concurrent 5-fluorouracil and mitomycin C-based chemoradiation therapy (CRT). Fluorouracil 191-205 epidermal growth factor receptor Homo sapiens 82-86 23708506-8 2013 Lapatinib in combination with 5-FU had more potent antitumor effects in the primary ESCC xenograft model, and markedly reduced the phosphorylation of EGFR and HER2, compared with lapatinib alone or in combination with oxaliplatin. Fluorouracil 30-34 epidermal growth factor receptor Homo sapiens 150-154 23708506-8 2013 Lapatinib in combination with 5-FU had more potent antitumor effects in the primary ESCC xenograft model, and markedly reduced the phosphorylation of EGFR and HER2, compared with lapatinib alone or in combination with oxaliplatin. Fluorouracil 30-34 erb-b2 receptor tyrosine kinase 2 Homo sapiens 159-163 23936455-10 2013 We observed that cells with complete loss of wild-type TP53 alleles ((-/-) or (-/mut)) were resistant to CRT following treatment with 5-fluorouracil and radiation. Fluorouracil 134-148 tumor protein p53 Homo sapiens 55-59 23553029-0 2013 Overexpression of ECRG4 enhances chemosensitivity to 5-fluorouracil in the human gastric cancer SGC-7901 cell line. Fluorouracil 53-67 ECRG4 augurin precursor Homo sapiens 18-23 23553029-6 2013 Compared with control cells, the growth inhibition rate of cells with ECRG4 overexpression was significantly increased when treated with 5-FU. Fluorouracil 137-141 ECRG4 augurin precursor Homo sapiens 70-75 23553029-8 2013 In conclusion, overexpression of ECRG4 enhanced the chemosensitivity of gastric cancer SGC-7901 cells to 5-FU through induction of apoptosis. Fluorouracil 105-109 ECRG4 augurin precursor Homo sapiens 33-38 23729362-8 2013 Cell death of 5-fluorouracil (5FU)-treated p53-null GSK3B-silenced colon carcinoma cells occurred via PARP1-dependent and AIF-mediated but RIP1-independent necroptosis. Fluorouracil 14-28 tumor protein p53 Homo sapiens 43-46 23729362-8 2013 Cell death of 5-fluorouracil (5FU)-treated p53-null GSK3B-silenced colon carcinoma cells occurred via PARP1-dependent and AIF-mediated but RIP1-independent necroptosis. Fluorouracil 14-28 poly(ADP-ribose) polymerase 1 Homo sapiens 102-107 23729362-8 2013 Cell death of 5-fluorouracil (5FU)-treated p53-null GSK3B-silenced colon carcinoma cells occurred via PARP1-dependent and AIF-mediated but RIP1-independent necroptosis. Fluorouracil 30-33 poly(ADP-ribose) polymerase 1 Homo sapiens 102-107 23729362-8 2013 Cell death of 5-fluorouracil (5FU)-treated p53-null GSK3B-silenced colon carcinoma cells occurred via PARP1-dependent and AIF-mediated but RIP1-independent necroptosis. Fluorouracil 30-33 tumor protein p53 Homo sapiens 43-46 23683592-2 2013 Compound 15 possessed remarkable broad-spectrum antitumor activity which almost sevenfold more active than the known drug 5-FU with GI50 values of 3.16 and 22.60 muM, respectively. Fluorouracil 122-126 latexin Homo sapiens 162-165 23525071-0 2013 Induction of pancreatic cancer cell apoptosis, invasion, migration, and enhancement of chemotherapy sensitivity of gemcitabine, 5-FU, and oxaliplatin by hnRNP A2/B1 siRNA. Fluorouracil 128-132 heterogeneous nuclear ribonucleoprotein A2/B1 Homo sapiens 153-164 23525071-8 2013 Inhibition of hnRNP A2/B1 expression significantly reduced the IC(50) of gemcitabine, 5-FU, and oxaliplatin (P<0.01). Fluorouracil 86-90 heterogeneous nuclear ribonucleoprotein A2/B1 Homo sapiens 14-25 23525071-9 2013 hnRNP A2/B1 siRNA combined with gemcitabine, 5-FU and oxaliplatin significantly increased (P<0.01) apoptosis of pancreatic cancer cell lines SW1990 and BxPC-3, increased the expression level of Bax mRNA, decreased Bcl-2 mRNA and MDR1 mRNA expression (P<0.01), and induced no change in p53, TRAIL, and Survivin mRNA expression in SW1990. Fluorouracil 45-49 heterogeneous nuclear ribonucleoprotein A2/B1 Homo sapiens 0-11 23525071-13 2013 Inhibition of hnRNP A2/B1 expression can induce apoptosis in pancreatic cancer cells and improve chemosensitivity to gemcitabine, 5-FU, and oxaliplatin. Fluorouracil 130-134 heterogeneous nuclear ribonucleoprotein A2/B1 Homo sapiens 14-25 23852891-8 2013 MATERIALS AND METHODS: The 5-FU sensitivity of GC cell lines SGC-7901, MKN-45, RF-48, N87, AGS, MKN-28, RF-1, MGC-803 were determined by MTT assays. Fluorouracil 27-31 mitochondrial translation release factor 1 Homo sapiens 104-108 23727578-3 2013 p53 activation by 5-fluorouracil significantly increased hGBP1 expression in wild-type p53 cells, but not in p53-null cells. Fluorouracil 18-32 tumor protein p53 Homo sapiens 0-3 23863744-5 2013 After 8 courses of adjuvant chemotherapy with modified 5-fluorouracil/Leucovorin/oxaliplatin(mFOLFOX6), carcinoembryonic antigen( CEA)decreased to a normal level, and positron emission tomography-computed tomography(PET-CT)showed no abnormal accumulation that suggested metastasis. Fluorouracil 55-69 CEA cell adhesion molecule 3 Homo sapiens 130-133 23814492-6 2013 OK-432-induced IL-10 and TGF-beta but not Th1 cytokines were significantly inhibited by 5-FU and/or X-ray. Fluorouracil 88-92 transforming growth factor beta 1 Homo sapiens 25-33 23619566-7 2013 Further investigation revealed that NK4 gene expression enhanced 5-FU-induced caspase-3 and caspase-9 activation, and that the apoptosis of cells was associated with modulation of expression of the Bcl-2 family members. Fluorouracil 65-69 caspase 3 Homo sapiens 78-87 23814490-7 2013 The sensitization to 5-fluorouracil (5-FU) treatment upon Pim-1 knockdown offers new possibilities for combinatorial treatment approaches. Fluorouracil 21-35 Pim-1 proto-oncogene, serine/threonine kinase Homo sapiens 58-63 23814490-7 2013 The sensitization to 5-fluorouracil (5-FU) treatment upon Pim-1 knockdown offers new possibilities for combinatorial treatment approaches. Fluorouracil 37-41 Pim-1 proto-oncogene, serine/threonine kinase Homo sapiens 58-63 23814490-8 2013 Importantly, this also antagonizes a 5-FU-triggered Pim-1 up-regulation, which is mediated by decreased levels of miR-15b, a microRNA we newly identify to regulate Pim-1. Fluorouracil 37-41 Pim-1 proto-oncogene, serine/threonine kinase Homo sapiens 52-57 23814490-8 2013 Importantly, this also antagonizes a 5-FU-triggered Pim-1 up-regulation, which is mediated by decreased levels of miR-15b, a microRNA we newly identify to regulate Pim-1. Fluorouracil 37-41 Pim-1 proto-oncogene, serine/threonine kinase Homo sapiens 164-169 23946796-7 2013 Functional assays demonstrated that HuR and FOXO1 expression levels were markedly enhanced upon 5-fluorouracil (5-FU) stimulation in MDA-MB-231 cells. Fluorouracil 96-110 forkhead box O1 Homo sapiens 44-49 23946796-7 2013 Functional assays demonstrated that HuR and FOXO1 expression levels were markedly enhanced upon 5-fluorouracil (5-FU) stimulation in MDA-MB-231 cells. Fluorouracil 112-116 forkhead box O1 Homo sapiens 44-49 23946796-8 2013 Knockdown of HuR apparently abrogated 5-FU-induced apoptosis detected by caspase-3 activities. Fluorouracil 38-42 caspase 3 Homo sapiens 73-82 23946796-9 2013 Furthermore, in HuR knockdown cells, additional overexpression of FOXO1 moderately recovered 5-FU-induced apoptosis, which verified that HuR-modulated apoptosis upon 5-FU treatment was partially mediated by its post-transcriptional regulation of FOXO1. Fluorouracil 93-97 forkhead box O1 Homo sapiens 66-71 23946796-9 2013 Furthermore, in HuR knockdown cells, additional overexpression of FOXO1 moderately recovered 5-FU-induced apoptosis, which verified that HuR-modulated apoptosis upon 5-FU treatment was partially mediated by its post-transcriptional regulation of FOXO1. Fluorouracil 93-97 forkhead box O1 Homo sapiens 246-251 23946796-9 2013 Furthermore, in HuR knockdown cells, additional overexpression of FOXO1 moderately recovered 5-FU-induced apoptosis, which verified that HuR-modulated apoptosis upon 5-FU treatment was partially mediated by its post-transcriptional regulation of FOXO1. Fluorouracil 166-170 forkhead box O1 Homo sapiens 66-71 23946796-9 2013 Furthermore, in HuR knockdown cells, additional overexpression of FOXO1 moderately recovered 5-FU-induced apoptosis, which verified that HuR-modulated apoptosis upon 5-FU treatment was partially mediated by its post-transcriptional regulation of FOXO1. Fluorouracil 166-170 forkhead box O1 Homo sapiens 246-251 23727578-3 2013 p53 activation by 5-fluorouracil significantly increased hGBP1 expression in wild-type p53 cells, but not in p53-null cells. Fluorouracil 18-32 tumor protein p53 Homo sapiens 87-90 23727578-3 2013 p53 activation by 5-fluorouracil significantly increased hGBP1 expression in wild-type p53 cells, but not in p53-null cells. Fluorouracil 18-32 tumor protein p53 Homo sapiens 87-90 23727578-4 2013 Knockdown of p53 expression remarkably impaired hGBP1 expression induced by 5-fluorouracil, type I interferon treatment, or influenza A virus infection. Fluorouracil 76-90 tumor protein p53 Homo sapiens 13-16 23749896-0 2013 Unexpected alteration of beta-catenin and c-KIT expression by 5-FU and docetaxel in p16-positive squamous cell carcinoma compared to HPV-negative HNSCC cells in vitro. Fluorouracil 62-66 KIT proto-oncogene, receptor tyrosine kinase Homo sapiens 42-47 23749896-0 2013 Unexpected alteration of beta-catenin and c-KIT expression by 5-FU and docetaxel in p16-positive squamous cell carcinoma compared to HPV-negative HNSCC cells in vitro. Fluorouracil 62-66 cyclin dependent kinase inhibitor 2A Homo sapiens 84-87 23749896-6 2013 The aim of this study is to investigate the expression patterns of c-KIT and beta-catenin in human papillomavirus-negative and p16-positive SCC and to evaluate the chemosensitivity of the tumour cells to the chemotherapeutical agents docetaxel and 5-fluorouracil (5-FU). Fluorouracil 248-262 KIT proto-oncogene, receptor tyrosine kinase Homo sapiens 67-72 23749896-6 2013 The aim of this study is to investigate the expression patterns of c-KIT and beta-catenin in human papillomavirus-negative and p16-positive SCC and to evaluate the chemosensitivity of the tumour cells to the chemotherapeutical agents docetaxel and 5-fluorouracil (5-FU). Fluorouracil 264-268 KIT proto-oncogene, receptor tyrosine kinase Homo sapiens 67-72 23749899-8 2013 Under treatment with low concentrations of 5-fluorouracil and cisplatin, all examined cell lines showed an increasing secretion of the cytokines IL-6 and G-CSF. Fluorouracil 43-57 interleukin 6 Homo sapiens 145-149 23438367-0 2013 Novel MEK inhibitor trametinib and other retinoblastoma gene (RB)-reactivating agents enhance efficacy of 5-fluorouracil on human colon cancer cells. Fluorouracil 106-120 mitogen-activated protein kinase kinase 7 Homo sapiens 6-9 23396606-0 2013 Genetic variability in the multidrug resistance associated protein-1 (ABCC1/MRP1) predicts hematological toxicity in breast cancer patients receiving (neo-)adjuvant chemotherapy with 5-fluorouracil, epirubicin and cyclophosphamide (FEC). Fluorouracil 183-197 ATP binding cassette subfamily C member 1 Homo sapiens 27-68 23396606-0 2013 Genetic variability in the multidrug resistance associated protein-1 (ABCC1/MRP1) predicts hematological toxicity in breast cancer patients receiving (neo-)adjuvant chemotherapy with 5-fluorouracil, epirubicin and cyclophosphamide (FEC). Fluorouracil 183-197 ATP binding cassette subfamily C member 1 Homo sapiens 70-75 23396606-0 2013 Genetic variability in the multidrug resistance associated protein-1 (ABCC1/MRP1) predicts hematological toxicity in breast cancer patients receiving (neo-)adjuvant chemotherapy with 5-fluorouracil, epirubicin and cyclophosphamide (FEC). Fluorouracil 183-197 ATP binding cassette subfamily C member 1 Homo sapiens 76-80 23314856-2 2013 AIM: To investigate whether nuclear factor erythroid 2-related factor 2 (Nrf2) was associated with drug resistance in 5-FU resistant Bel-7402 (Bel-7402/5-FU) cells, and if sorafenib, an oral multikinase inhibitor targeting the tumor and vasculature, could reverse drug resistance in Bel-7402/5-FU cells at the noncytotoxic dosage. Fluorouracil 118-122 NFE2 like bZIP transcription factor 2 Homo sapiens 28-71 23719766-1 2013 S-1 (Teysuno( )) is an oral anticancer agent comprising the 5-fluorouracil (5-FU) prodrug tegafur and targeted modulators, gimeracil and oteracil. Fluorouracil 60-74 proteasome 26S subunit, non-ATPase 1 Homo sapiens 0-3 23719766-1 2013 S-1 (Teysuno( )) is an oral anticancer agent comprising the 5-fluorouracil (5-FU) prodrug tegafur and targeted modulators, gimeracil and oteracil. Fluorouracil 76-80 proteasome 26S subunit, non-ATPase 1 Homo sapiens 0-3 23314856-2 2013 AIM: To investigate whether nuclear factor erythroid 2-related factor 2 (Nrf2) was associated with drug resistance in 5-FU resistant Bel-7402 (Bel-7402/5-FU) cells, and if sorafenib, an oral multikinase inhibitor targeting the tumor and vasculature, could reverse drug resistance in Bel-7402/5-FU cells at the noncytotoxic dosage. Fluorouracil 118-122 NFE2 like bZIP transcription factor 2 Homo sapiens 73-77 23314856-5 2013 However, Nrf2 expression levels were increased by 5-FU treatment in Bel-7402/5-FU cells higher than that in Bel-7402 cells, which is to highlight the Nrf2 contribution to the enhanced resistance of Bel-7402/5-FU cells to 5-FU. Fluorouracil 50-54 NFE2 like bZIP transcription factor 2 Homo sapiens 9-13 23314856-5 2013 However, Nrf2 expression levels were increased by 5-FU treatment in Bel-7402/5-FU cells higher than that in Bel-7402 cells, which is to highlight the Nrf2 contribution to the enhanced resistance of Bel-7402/5-FU cells to 5-FU. Fluorouracil 50-54 NFE2 like bZIP transcription factor 2 Homo sapiens 150-154 23314856-5 2013 However, Nrf2 expression levels were increased by 5-FU treatment in Bel-7402/5-FU cells higher than that in Bel-7402 cells, which is to highlight the Nrf2 contribution to the enhanced resistance of Bel-7402/5-FU cells to 5-FU. Fluorouracil 77-81 NFE2 like bZIP transcription factor 2 Homo sapiens 9-13 23314856-5 2013 However, Nrf2 expression levels were increased by 5-FU treatment in Bel-7402/5-FU cells higher than that in Bel-7402 cells, which is to highlight the Nrf2 contribution to the enhanced resistance of Bel-7402/5-FU cells to 5-FU. Fluorouracil 77-81 NFE2 like bZIP transcription factor 2 Homo sapiens 150-154 23314856-5 2013 However, Nrf2 expression levels were increased by 5-FU treatment in Bel-7402/5-FU cells higher than that in Bel-7402 cells, which is to highlight the Nrf2 contribution to the enhanced resistance of Bel-7402/5-FU cells to 5-FU. Fluorouracil 77-81 NFE2 like bZIP transcription factor 2 Homo sapiens 9-13 23314856-5 2013 However, Nrf2 expression levels were increased by 5-FU treatment in Bel-7402/5-FU cells higher than that in Bel-7402 cells, which is to highlight the Nrf2 contribution to the enhanced resistance of Bel-7402/5-FU cells to 5-FU. Fluorouracil 77-81 NFE2 like bZIP transcription factor 2 Homo sapiens 150-154 23314856-5 2013 However, Nrf2 expression levels were increased by 5-FU treatment in Bel-7402/5-FU cells higher than that in Bel-7402 cells, which is to highlight the Nrf2 contribution to the enhanced resistance of Bel-7402/5-FU cells to 5-FU. Fluorouracil 77-81 NFE2 like bZIP transcription factor 2 Homo sapiens 9-13 23314856-5 2013 However, Nrf2 expression levels were increased by 5-FU treatment in Bel-7402/5-FU cells higher than that in Bel-7402 cells, which is to highlight the Nrf2 contribution to the enhanced resistance of Bel-7402/5-FU cells to 5-FU. Fluorouracil 77-81 NFE2 like bZIP transcription factor 2 Homo sapiens 150-154 23314856-6 2013 Moreover, intracellular Nrf2 protein level was significantly down-regulated by Nrf2-shRNA in Bel-7402/5-FU cells, resulting in partial reversal of 5-FU resistance. Fluorouracil 102-106 NFE2 like bZIP transcription factor 2 Homo sapiens 24-28 23314856-6 2013 Moreover, intracellular Nrf2 protein level was significantly down-regulated by Nrf2-shRNA in Bel-7402/5-FU cells, resulting in partial reversal of 5-FU resistance. Fluorouracil 102-106 NFE2 like bZIP transcription factor 2 Homo sapiens 79-83 23314856-6 2013 Moreover, intracellular Nrf2 protein level was significantly down-regulated by Nrf2-shRNA in Bel-7402/5-FU cells, resulting in partial reversal of 5-FU resistance. Fluorouracil 147-151 NFE2 like bZIP transcription factor 2 Homo sapiens 24-28 23314856-6 2013 Moreover, intracellular Nrf2 protein level was significantly down-regulated by Nrf2-shRNA in Bel-7402/5-FU cells, resulting in partial reversal of 5-FU resistance. Fluorouracil 147-151 NFE2 like bZIP transcription factor 2 Homo sapiens 79-83 23314856-7 2013 Sorafenib down-regulated the increased expression of Nrf2 induced by 5-FU treatment and partly reversed 5-FU resistance in Bel-7402/5-FU cells. Fluorouracil 69-73 NFE2 like bZIP transcription factor 2 Homo sapiens 53-57 23314856-8 2013 CONCLUSIONS: These results suggested that more sensitive cell defense mediated by Nrf2 was associated with drug resistance of Bel-7402/5-FU cells. Fluorouracil 135-139 NFE2 like bZIP transcription factor 2 Homo sapiens 82-86 23314856-9 2013 Sorafenib reversed drug resistance, and its reversal mechanism might be due to the suppression of Nrf2 expression induced by 5-FU, indicating the feasibility of using Nrf2 inhibitors to increase efficacy of chemotherapeutic drugs in HCC patients. Fluorouracil 125-129 NFE2 like bZIP transcription factor 2 Homo sapiens 98-102 23314856-9 2013 Sorafenib reversed drug resistance, and its reversal mechanism might be due to the suppression of Nrf2 expression induced by 5-FU, indicating the feasibility of using Nrf2 inhibitors to increase efficacy of chemotherapeutic drugs in HCC patients. Fluorouracil 125-129 NFE2 like bZIP transcription factor 2 Homo sapiens 167-171 23403306-2 2013 In this study, we introduced the human parental neural stem cells, HB1.F3, with the human interferon beta (IFN-beta) gene which is a typical cytokine gene that has an antitumor effect and the cytosine deaminase (CD) gene from Escherichia coli (E. coli) that could convert the non-toxic prodrug, 5-fluorocytosine (5-FC), to a toxic metabolite, 5-fluorouracil (5-FU). Fluorouracil 343-357 histocompatibility minor HB-1 Homo sapiens 67-70 23403306-2 2013 In this study, we introduced the human parental neural stem cells, HB1.F3, with the human interferon beta (IFN-beta) gene which is a typical cytokine gene that has an antitumor effect and the cytosine deaminase (CD) gene from Escherichia coli (E. coli) that could convert the non-toxic prodrug, 5-fluorocytosine (5-FC), to a toxic metabolite, 5-fluorouracil (5-FU). Fluorouracil 359-363 histocompatibility minor HB-1 Homo sapiens 67-70 23403306-6 2013 In particular, HB1.F3.CD.IFN-beta cells showed the synergistic cytotoxic activity of 5-FU and IFN-beta. Fluorouracil 85-89 histocompatibility minor HB-1 Homo sapiens 15-18 23562851-0 2013 Silencing the EZH2 gene by RNA interference reverses the drug resistance of human hepatic multidrug-resistant cancer cells to 5-Fu. Fluorouracil 126-130 enhancer of zeste 2 polycomb repressive complex 2 subunit Homo sapiens 14-18 23359275-0 2013 Fluorouracil selectively enriches stem-like cells in the lung adenocarcinoma cell line SPC. Fluorouracil 0-12 proline rich protein gene cluster Homo sapiens 87-90 23359275-3 2013 This study sought to enrich cancer stem cells and explore cancer stem-like cell clones using 5-fluorouracil (5-FU) in the lung adenocarcinoma cell line, SPC. Fluorouracil 109-113 proline rich protein gene cluster Homo sapiens 153-156 23562851-5 2013 After EZH2-depleted Bel/Fu cells were treated with 5-Fu, the cell proliferation was inhibited, the cell cycle arrested at G1, which may be associated with the alteration of G1/S checkpoint regulators, meanwhile the apoptotic rate of the cells increased. Fluorouracil 51-55 enhancer of zeste 2 polycomb repressive complex 2 subunit Homo sapiens 6-10 23658244-3 2013 We used a cytosine deaminase (CD)-expressing clonal human NSC line, HB1.F3.CD, to home to gliomas in mice and locally convert the prodrug 5-fluorocytosine to the active chemotherapeutic 5-fluorouracil. Fluorouracil 186-200 histocompatibility minor HB-1 Homo sapiens 68-71 23348694-5 2013 This compound was found to exert anti-cancer effects stronger than those of 5-fluorouracil (5-FU) on gastric cancer cells, especially cell lines that overexpressed c-Met. Fluorouracil 92-96 MET proto-oncogene, receptor tyrosine kinase Homo sapiens 164-169 23454010-5 2013 The blockade of A(2A)-AR with ZM 241385 (0.1 muM) significantly increased the cytotoxicity of 5-FU (1 muM) in HCT 116 cells but not in HT-29 cells. Fluorouracil 94-98 latexin Homo sapiens 45-48 23454010-5 2013 The blockade of A(2A)-AR with ZM 241385 (0.1 muM) significantly increased the cytotoxicity of 5-FU (1 muM) in HCT 116 cells but not in HT-29 cells. Fluorouracil 94-98 latexin Homo sapiens 102-105 23454010-6 2013 The suppression of A(3)-AR with MRS 1523 (1 muM) increased the sensitivity of HT-29 cells to 5-FU while response of HCT 116 cells to 5-FU decreased. Fluorouracil 93-97 adenosine A3 receptor Homo sapiens 19-26 23645743-8 2013 RESULTS: We demonstrated a significant reduction of VEGF and PDGFRbeta expression after incubation with docetaxel by ELISA and of PDGF by immunohistochemistry, irrespective of the HPV status, whereas the application of 5-FU had a significantly weaker impact on the expression of angiogenic peptides. Fluorouracil 219-223 vascular endothelial growth factor A Homo sapiens 52-56 23454010-6 2013 The suppression of A(3)-AR with MRS 1523 (1 muM) increased the sensitivity of HT-29 cells to 5-FU while response of HCT 116 cells to 5-FU decreased. Fluorouracil 93-97 latexin Homo sapiens 44-47 23454010-6 2013 The suppression of A(3)-AR with MRS 1523 (1 muM) increased the sensitivity of HT-29 cells to 5-FU while response of HCT 116 cells to 5-FU decreased. Fluorouracil 133-137 adenosine A3 receptor Homo sapiens 19-26 23645743-0 2013 Chemotherapeutic alteration of VEGF, PDGF and PDGFRalpha/beta expression under 5-FU vs. docetaxel in HPV-transformed squamous cell carcinoma compared to HPV-negative HNSCC in vitro. Fluorouracil 79-83 vascular endothelial growth factor A Homo sapiens 31-35 23645743-0 2013 Chemotherapeutic alteration of VEGF, PDGF and PDGFRalpha/beta expression under 5-FU vs. docetaxel in HPV-transformed squamous cell carcinoma compared to HPV-negative HNSCC in vitro. Fluorouracil 79-83 platelet derived growth factor receptor beta Homo sapiens 46-61 23558238-6 2013 and most interestingly, all the compounds revealed preferred cytotoxicities on the HT-1080 cell line and displayed much stronger inhibitory activities (IC50<29.94 muM) compared with positive control 5-fluorouracil (IC50=35.62 muM), particularly, compounds 9-11, 13, 16 and 19 exhibited the strongest cytotoxicity activities against the HT-1080 cell line (IC50<0.1 muM). Fluorouracil 202-216 latexin Homo sapiens 166-169 23661467-6 2013 The participation of Htz1p in 5-FU toxicity was also evaluated in single- and double-mutants of CR and HAT; the most significant effect was on cell cycle distribution. Fluorouracil 30-34 histone H2AZ Saccharomyces cerevisiae S288C 21-26 23055106-5 2013 CaSR null cells were highly resistant to fluorouracil and expressed abundant amount of thymidylate synthase and survivin. Fluorouracil 41-53 calcium sensing receptor Homo sapiens 0-4 22963136-6 2013 Most of the p53 negative cases with Maspin nuclear predominance, which seems to respond to 5-Fluorouracil, were microsatellite instability (MSI) cases. Fluorouracil 91-105 tumor protein p53 Homo sapiens 12-15 22963136-10 2013 CONCLUSIONS: Maspin nuclear expression, associated with p53 ones, might be used either to select the high-risk microsatellite stable (MSS) colorectal carcinomas diagnosed in Stage II or those MSI cases which can respond to 5-Fluorouracil. Fluorouracil 223-237 tumor protein p53 Homo sapiens 56-59 23525256-0 2013 microRNA expression profiling in multidrug resistance of the 5-Fu-induced SGC-7901 human gastric cancer cell line. Fluorouracil 61-65 sarcoglycan beta Homo sapiens 74-77 23761814-1 2013 S-1 has been developed as a new oral anticancer drug based on the biological modulation of 5-fluorouracil. Fluorouracil 91-105 proteasome 26S subunit, non-ATPase 1 Homo sapiens 0-3 23423487-0 2013 Effect of TP53 codon 72 and MDM2 SNP309 polymorphisms on survival of gastric cancer among patients who receiving 5-fluorouracil-based postoperative adjuvant chemotherapy. Fluorouracil 113-127 tumor protein p53 Homo sapiens 10-14 23637542-5 2013 Effects on interferon-gamma production in fluorouracil/doxorubicin-treated mice were tested with enzyme-linked immunosorbent assay. Fluorouracil 42-54 interferon gamma Mus musculus 11-27 23637542-8 2013 Interferon-gamma levels, reduced following fluorouracil treatment, were corrected in treated animals. Fluorouracil 43-55 interferon gamma Mus musculus 0-16 23423487-8 2013 CONCLUSIONS: Our findings showed that TP53 codon 72 polymorphism was associated with survival of gastric cancer patients treated with 5-Fu-based postoperative chemotherapy. Fluorouracil 134-138 tumor protein p53 Homo sapiens 38-42 23423487-5 2013 However, the TP53 codon 72 polymorphism had a prominent correlation with clinical outcome of patients receiving 5-fluorouracil (5-Fu)-based postoperative chemotherapy [Arg/Arg + Arg/Pro vs. Pro/Pro, adjusted hazard ratio (HR) = 1.63, 95 % confidence interval (CI) = 1.08-2.44]. Fluorouracil 112-126 tumor protein p53 Homo sapiens 13-17 23423487-5 2013 However, the TP53 codon 72 polymorphism had a prominent correlation with clinical outcome of patients receiving 5-fluorouracil (5-Fu)-based postoperative chemotherapy [Arg/Arg + Arg/Pro vs. Pro/Pro, adjusted hazard ratio (HR) = 1.63, 95 % confidence interval (CI) = 1.08-2.44]. Fluorouracil 128-132 tumor protein p53 Homo sapiens 13-17 24250621-9 2013 5-FU also induced HMGB1 secretion, Cas3 and PARP activity and these effects were stronger in cells expressing WT TLR4 than the other cells. Fluorouracil 0-4 poly(ADP-ribose) polymerase 1 Homo sapiens 44-48 23373735-0 2013 Regulation of carboxylesterase-2 expression by p53 family proteins and enhanced anti-cancer activities among 5-fluorouracil, irinotecan and doxazolidine prodrug. Fluorouracil 109-123 carboxylesterase 2 Homo sapiens 14-32 23373735-4 2013 5-FU, on the other hand, reportedly induces CES2 in colorectal tumour lines. Fluorouracil 0-4 carboxylesterase 2 Homo sapiens 44-48 23328075-3 2013 The aim of this study was to examine any modulations in the DDC mRNA levels in gastric cancer cells after their treatment with the chemotherapeutic agents 5-fluorouracil, leucovorin, irinotecan, etoposide, cisplatin, and taxol. Fluorouracil 155-169 dopa decarboxylase Homo sapiens 60-63 22841540-1 2013 Colorectal carcinomas (CRCs) with P53 mutations have been shown to be resistant to chemotherapy with 5-fluorouracil (5-FU), the most widely used chemotherapeutic drug for CRC treatment. Fluorouracil 101-115 tumor protein p53 Homo sapiens 34-37 22841540-1 2013 Colorectal carcinomas (CRCs) with P53 mutations have been shown to be resistant to chemotherapy with 5-fluorouracil (5-FU), the most widely used chemotherapeutic drug for CRC treatment. Fluorouracil 117-121 tumor protein p53 Homo sapiens 34-37 23519428-9 2013 HBV replication or 5-fluorouracil-induced cell death was suppressed by treatment of IFN-lambda or IL-22 in an IL-10RB K47E-independent manner. Fluorouracil 19-33 interleukin 10 receptor subunit beta Homo sapiens 110-117 23072534-10 2013 The up-regulation of TNF-alpha, IL-1beta and IL-6 following 5-FU treatment was also attenuated by ramosetron. Fluorouracil 60-64 tumor necrosis factor Mus musculus 21-30 23072534-10 2013 The up-regulation of TNF-alpha, IL-1beta and IL-6 following 5-FU treatment was also attenuated by ramosetron. Fluorouracil 60-64 interleukin 1 beta Mus musculus 32-40 22052826-4 2013 Cetuximab, a monoclonal antibody against epidermal growth factor receptor (EGFR), significantly improved median survival in combination with platinum/5-FU compared with chemotherapy alone, establishing it as a new standard for patients with recurrent or metastatic disease. Fluorouracil 150-154 epidermal growth factor receptor Homo sapiens 75-79 23426065-6 2013 A drug resistance assay revealed that SP cells have a high survival rate when exposed to the chemotherapy drug 5-fluorouracil; the results of western blot analysis suggest that this stems from the abundant expression of the chemoresistance-associated proteins ABCG2 and Bcl-2. Fluorouracil 111-125 ATP binding cassette subfamily G member 2 (Junior blood group) Homo sapiens 260-265 22791308-12 2013 Mice receiving FYG alone or FYG plus 5-FU had higher serum levels of TNF-a (P <0.01) compared with the vehicle. Fluorouracil 37-41 tumor necrosis factor Mus musculus 69-74 22983756-10 2013 Interestingly, treatment with either sorafenib or 5-FU resulted in a significant decrease of VEGFR1 and PDGFRbeta expression intensity. Fluorouracil 50-54 fms related receptor tyrosine kinase 1 Homo sapiens 93-99 22983756-10 2013 Interestingly, treatment with either sorafenib or 5-FU resulted in a significant decrease of VEGFR1 and PDGFRbeta expression intensity. Fluorouracil 50-54 platelet derived growth factor receptor beta Homo sapiens 104-113 23428176-8 2013 RESULTS: The CCK results showed that the half inhibition dose (ID50) of the HLECs in 5-Fu-CSNP group and in 5-Fu solution group was 0.2 mug/mL and 1 mug/mL, respectively. Fluorouracil 108-112 cholecystokinin Homo sapiens 13-16 23291714-4 2013 Moreover, siRNA targeting EZH2 sensitized Bel/FU cells to 5-fluorouracil treatment. Fluorouracil 70-84 enhancer of zeste 2 polycomb repressive complex 2 subunit Homo sapiens 38-42 23426065-6 2013 A drug resistance assay revealed that SP cells have a high survival rate when exposed to the chemotherapy drug 5-fluorouracil; the results of western blot analysis suggest that this stems from the abundant expression of the chemoresistance-associated proteins ABCG2 and Bcl-2. Fluorouracil 111-125 BCL2 apoptosis regulator Homo sapiens 270-275 23374220-1 2013 BACKGROUND: The aim of this study is to evaluate the associations between vascular endothelial growth factor (VEGF) Single-nucleotide polymorphisms (SNPs) and clinical outcome in advanced gastric cancer patients treated with oxaliplatin, 5-fluorouracil, and leucovorin (FOLFOX). Fluorouracil 238-252 vascular endothelial growth factor A Homo sapiens 74-108 23429289-6 2013 Consequently, when we generated MSCs that secreted TRAIL-R2-specific variants of soluble TRAIL (sTRAIL), we found that such engineered MSCs, labeled MSC.sTRAIL(DR5), had enhanced antitumor activity in combination with 5-FU when compared with MSC.sTRAIL. Fluorouracil 218-222 TNF superfamily member 10 Homo sapiens 51-56 23322208-8 2013 The gene induction of REG Ialpha conferred resistance to cell death induced by 5-FU or CDDP in GC cells. Fluorouracil 79-83 regenerating family member 1 alpha Homo sapiens 22-25 23253900-5 2013 UNG and SMUG1 are the two human UDGs most likely to combat the genomic incorporation of uracil and 5-FU during replication. Fluorouracil 99-103 uracil DNA glycosylase Homo sapiens 0-3 23253900-7 2013 Loss of UNG did not alter cellular sensitivity to 5-FU in two human cell lines, despite its predominant biochemical activity for uracil and 5-FU in DNA. Fluorouracil 140-144 uracil DNA glycosylase Homo sapiens 8-11 23253900-10 2013 We observed that 5-FU treatment induced an enhanced S-phase arrest and CHK1 activation plus an increase in the formation of strand breaks and alkali-labile sites in all sublines. Fluorouracil 17-21 checkpoint kinase 1 Homo sapiens 71-75 23446022-9 2013 RESULTS: The presence of the V600E mutation in the BRAF gene was a poor prognostic factor for disease free and overall survival (DFS; hazard ratio [HR], 2.57; 95% CI: 1.03 -6.37; p = 0.04 and OS; HR, 3.68; 95% CI: 1.43-9.47; p < 0.01 respectively), independently of 5-FU treatment. Fluorouracil 269-273 B-Raf proto-oncogene, serine/threonine kinase Homo sapiens 51-55 23322208-5 2013 The effects of REG Ialpha gene induction on resistance to 5-FU or CDDP treatment were examined by cell survival assay and flow cytometry. Fluorouracil 58-62 regenerating family member 1 alpha Homo sapiens 15-18 23393346-0 2013 COX-2 overexpression Induced by gene transfer reduces sensitivity of TE13 esophageal carcinoma cells to 5-fluorouracil and cisplatin. Fluorouracil 104-118 prostaglandin-endoperoxide synthase 2 Homo sapiens 0-5 23393346-5 2013 Chemosensitivity testing revealed that sensitivity of COX-2 transfectants to 5-fluorouracil and cisplatin was significantly lower than in control vector-only transfectants, and that sensitivity of COX-2 transfectants was restored by the transfection of COX-2-specific siRNA. Fluorouracil 77-91 prostaglandin-endoperoxide synthase 2 Homo sapiens 54-59 23393346-5 2013 Chemosensitivity testing revealed that sensitivity of COX-2 transfectants to 5-fluorouracil and cisplatin was significantly lower than in control vector-only transfectants, and that sensitivity of COX-2 transfectants was restored by the transfection of COX-2-specific siRNA. Fluorouracil 77-91 prostaglandin-endoperoxide synthase 2 Homo sapiens 197-202 23393346-5 2013 Chemosensitivity testing revealed that sensitivity of COX-2 transfectants to 5-fluorouracil and cisplatin was significantly lower than in control vector-only transfectants, and that sensitivity of COX-2 transfectants was restored by the transfection of COX-2-specific siRNA. Fluorouracil 77-91 prostaglandin-endoperoxide synthase 2 Homo sapiens 197-202 23374220-1 2013 BACKGROUND: The aim of this study is to evaluate the associations between vascular endothelial growth factor (VEGF) Single-nucleotide polymorphisms (SNPs) and clinical outcome in advanced gastric cancer patients treated with oxaliplatin, 5-fluorouracil, and leucovorin (FOLFOX). Fluorouracil 238-252 vascular endothelial growth factor A Homo sapiens 110-114 23108452-7 2013 In the 5-FU-treated group, the expressions of two proteins were not affected by any of the doses at day 10 and 22, whereas the GATA-4 expression was decreased (P < 0.05) by more than 400 nM of 5-FU at days 28 and 40. Fluorouracil 7-11 GATA binding protein 4 Mus musculus 127-133 23096219-0 2013 Effect of topical chamomile on immunohistochemical levels of IL-1beta and TNF-alpha in 5-fluorouracil-induced oral mucositis in hamsters. Fluorouracil 87-101 tumor necrosis factor Homo sapiens 74-83 23096219-1 2013 PURPOSE: The aim of the present study was to evaluate the effect of topical chamomile and corticosteroid treatment on the profile of tissue cytokines (IL-1beta and TNF-alpha) in 5-fluorouracil-induced oral mucositis in hamsters. Fluorouracil 178-192 interleukin 1 beta Homo sapiens 151-159 23108452-7 2013 In the 5-FU-treated group, the expressions of two proteins were not affected by any of the doses at day 10 and 22, whereas the GATA-4 expression was decreased (P < 0.05) by more than 400 nM of 5-FU at days 28 and 40. Fluorouracil 196-200 GATA binding protein 4 Mus musculus 127-133 23096219-1 2013 PURPOSE: The aim of the present study was to evaluate the effect of topical chamomile and corticosteroid treatment on the profile of tissue cytokines (IL-1beta and TNF-alpha) in 5-fluorouracil-induced oral mucositis in hamsters. Fluorouracil 178-192 tumor necrosis factor Homo sapiens 164-173 23103836-6 2013 The silencing of MGAT5 in MHCC97-H cells inhibited invasion and increased sensitivity to 5-fluorouracil in vitro. Fluorouracil 89-103 alpha-1,6-mannosylglycoprotein 6-beta-N-acetylglucosaminyltransferase Homo sapiens 17-22 23348635-6 2013 Nonetheless, cells exposed to 5-FU, CPT-11, TNF-alpha or HSV-1 activate NF-kappaB. Fluorouracil 30-34 nuclear factor kappa B subunit 1 Homo sapiens 72-81 23420099-9 2013 In conclusion, mRNA levels of SLC22A2, SLC23A2, ABCB1, ABCC2, Rad51, MSH2 and DPYD were confirmed to be strongly correlated with IC50 values for 5-FU, and mRNA levels of ABCC2, MSH2 and DPYD were confirmed to be strongly correlated with IC(50) values for CDDP. Fluorouracil 145-149 ATP binding cassette subfamily B member 1 Homo sapiens 48-53 22820863-10 2013 In a mouse model, we also found that the combination of 5-fluorouracil and doxorubicin with AdBB-IL24 completely inhibited the growth of colon cancer cells. Fluorouracil 56-70 interleukin 24 Mus musculus 97-101 22820863-0 2013 Conditionally replicative adenovirus-based mda-7/IL-24 expression enhances sensitivity of colon cancer cells to 5-fluorouracil and doxorubicin. Fluorouracil 112-126 interleukin 24 Mus musculus 43-48 22820863-0 2013 Conditionally replicative adenovirus-based mda-7/IL-24 expression enhances sensitivity of colon cancer cells to 5-fluorouracil and doxorubicin. Fluorouracil 112-126 interleukin 24 Mus musculus 49-54 22820863-8 2013 Consistently, 5-fluorouracil and doxorubicin induced more apoptosis in AdBB-IL24-infected colon cancer cells compared with that in the Ad-IL24-infected cells. Fluorouracil 14-28 interleukin 24 Mus musculus 76-80 22820863-9 2013 A cell viability assay showed that AdBB-IL24 could enhance the growth-inhibitory effect of 5-fluorouracil and doxorubicin on colon cancer cells more effectively than Ad-IL24 in vitro. Fluorouracil 91-105 interleukin 24 Mus musculus 40-44 23076534-6 2013 Periostin-overexpressing cells treated with cisplatin or 5-FU showed significantly (p < 0.05) decreased expression of Bax and p53 proteins and increased expression of Bcl-2 protein, when compared to drug-treated mock counterparts. Fluorouracil 57-61 BCL2 associated X, apoptosis regulator Homo sapiens 121-124 23076534-6 2013 Periostin-overexpressing cells treated with cisplatin or 5-FU showed significantly (p < 0.05) decreased expression of Bax and p53 proteins and increased expression of Bcl-2 protein, when compared to drug-treated mock counterparts. Fluorouracil 57-61 tumor protein p53 Homo sapiens 129-132 23076534-6 2013 Periostin-overexpressing cells treated with cisplatin or 5-FU showed significantly (p < 0.05) decreased expression of Bax and p53 proteins and increased expression of Bcl-2 protein, when compared to drug-treated mock counterparts. Fluorouracil 57-61 BCL2 apoptosis regulator Homo sapiens 170-175 23076534-10 2013 Taken together, our data indicate that periostin confers protection against cisplatin or 5-FU-induced apoptosis in SGC-7901 cells, likely through modulating the Akt/p53 pathway, and thus represents a potential therapeutic target in gastric cancer. Fluorouracil 89-93 sarcoglycan beta Homo sapiens 115-118 23076534-10 2013 Taken together, our data indicate that periostin confers protection against cisplatin or 5-FU-induced apoptosis in SGC-7901 cells, likely through modulating the Akt/p53 pathway, and thus represents a potential therapeutic target in gastric cancer. Fluorouracil 89-93 AKT serine/threonine kinase 1 Homo sapiens 161-164 23076534-10 2013 Taken together, our data indicate that periostin confers protection against cisplatin or 5-FU-induced apoptosis in SGC-7901 cells, likely through modulating the Akt/p53 pathway, and thus represents a potential therapeutic target in gastric cancer. Fluorouracil 89-93 tumor protein p53 Homo sapiens 165-168 23089579-0 2013 Nanogels fabricated by lysozyme and sodium carboxymethyl cellulose for 5-fluorouracil controlled release. Fluorouracil 71-85 lysozyme Homo sapiens 23-31 23232555-2 2013 Various antimetabolites such as 5-fluorouracil often increase ENT1 activity and [(18)F]FLT uptake (flare) in spite of cell death. Fluorouracil 32-46 fms related receptor tyrosine kinase 1 Homo sapiens 87-90 23229803-7 2013 The antitumor activity of capecitabine and 5"-DFUR correlated significantly with the mRNA levels of TP and with the TP/DPD ratio, whereas the activity of 5-FU correlated significantly with OPRT, TMPK, UMPK and CD. Fluorouracil 178-182 deoxythymidylate kinase Homo sapiens 219-223 23267153-0 2013 CEA fluctuation during a single fluorouracil-based chemotherapy cycle for metastatic colorectal cancer. Fluorouracil 32-44 CEA cell adhesion molecule 3 Homo sapiens 0-3 23347845-8 2013 Cyclooxygenase-2 (COX-2) were decreased after treatment with celecoxib only or combined with 5-FU. Fluorouracil 93-97 prostaglandin-endoperoxide synthase 2 Homo sapiens 0-16 23347845-8 2013 Cyclooxygenase-2 (COX-2) were decreased after treatment with celecoxib only or combined with 5-FU. Fluorouracil 93-97 prostaglandin-endoperoxide synthase 2 Homo sapiens 18-23 23347845-10 2013 CONCLUSIONS: Celecoxib combined with 5-FU could inhibit the growth of tumors in vivo by inducing apoptosis and activation of the cytochrome C dependency apoptosis signal pathway. Fluorouracil 37-41 cytochrome c, somatic Homo sapiens 129-141 23125179-3 2013 This study investigated the effect of TFPI-2 in 5-fluorouracil (5-FU)-resistant human hepatocellular cancer BEL-7402/5-FU cells in vitro. Fluorouracil 48-62 tissue factor pathway inhibitor 2 Homo sapiens 38-44 23125179-3 2013 This study investigated the effect of TFPI-2 in 5-fluorouracil (5-FU)-resistant human hepatocellular cancer BEL-7402/5-FU cells in vitro. Fluorouracil 64-68 tissue factor pathway inhibitor 2 Homo sapiens 38-44 23125179-5 2013 We found that TFPI-2 improved the RI of 5-FU and inhibited P-gp function. Fluorouracil 40-44 tissue factor pathway inhibitor 2 Homo sapiens 14-20 23085145-9 2013 Plasma MCP-1 was increased following 5-FU treatment on both days 5 (p=0.10) and 14 (p<0.05). Fluorouracil 37-41 mast cell protease 1 Mus musculus 7-12 24175806-13 2013 Taken together, Nrf2 is a potential prognostic marker and predictive for 5-FU resistance in GC. Fluorouracil 73-77 NFE2 like bZIP transcription factor 2 Homo sapiens 16-20 24324958-0 2013 The synergistic effects of low dose fluorouracil and TRAIL on TRAIL-resistant human gastric adenocarcinoma AGS cells. Fluorouracil 36-48 TNF superfamily member 10 Homo sapiens 62-67 24324958-3 2013 In this study, we had investigated the synergistic effects of low dose fluorouracil (5-Fu) and TRAIL on TRAIL-resistant human gastric adenocarcinoma AGS cells and explored the potential mechanisms. Fluorouracil 71-83 TNF superfamily member 10 Homo sapiens 104-109 24324958-3 2013 In this study, we had investigated the synergistic effects of low dose fluorouracil (5-Fu) and TRAIL on TRAIL-resistant human gastric adenocarcinoma AGS cells and explored the potential mechanisms. Fluorouracil 85-89 TNF superfamily member 10 Homo sapiens 104-109 24324958-6 2013 Our results showed that there were significant synergistic effects of low dose 5-Fu and TRAIL on TRAIL-resistant AGS cells, and this effect was supposed to be mediated by decreasing DcR2 expression and increasing DR5 expression. Fluorouracil 79-83 TNF superfamily member 10 Homo sapiens 97-102 24175806-10 2013 The gene silencing of Nrf2 reduced resistance to cell death induced by 5-FU in GC cell lines. Fluorouracil 71-75 NFE2 like bZIP transcription factor 2 Homo sapiens 22-26 24175806-12 2013 Furthermore, Nrf2 confers resistance to chemotherapeutic drug 5-FU in GC cells. Fluorouracil 62-66 NFE2 like bZIP transcription factor 2 Homo sapiens 13-17 23359317-6 2013 More importantly, mice lacking p15Ink4b have lower numbers of primitive red cell progenitors and a severely impaired response to 5-fluorouracil- and phenylhydrazine-induced hematopoietic stress. Fluorouracil 129-143 cyclin dependent kinase inhibitor 2B Mus musculus 31-39 23202296-3 2013 Here we show that two clinically used chemotherapeutic agents, gemcitabine (Gem) and 5-fluorouracil (5FU), activate the NOD-like receptor family, pyrin domain containing-3 protein (Nlrp3)-dependent caspase-1 activation complex (termed the inflammasome) in myeloid-derived suppressor cells (MDSCs), leading to production of interleukin-1beta (IL-1beta), which curtails anticancer immunity. Fluorouracil 85-99 interleukin 1 beta Mus musculus 323-340 23107827-9 2013 5-FU-induced epithelial damage increased the MPO activity (neutrophil number) and the level of pro-inflammatory cytokines (IL-4, TNF-alpha, IL-1beta and CXCL-8) in the duodenum. Fluorouracil 0-4 tumor necrosis factor Mus musculus 129-138 23107827-9 2013 5-FU-induced epithelial damage increased the MPO activity (neutrophil number) and the level of pro-inflammatory cytokines (IL-4, TNF-alpha, IL-1beta and CXCL-8) in the duodenum. Fluorouracil 0-4 interleukin 1 beta Mus musculus 140-148 22895366-0 2013 Topical 5-fluorouracil elicits regressions of BRAF inhibitor-induced cutaneous squamous cell carcinoma. Fluorouracil 8-22 B-Raf proto-oncogene, serine/threonine kinase Homo sapiens 46-50 23202296-3 2013 Here we show that two clinically used chemotherapeutic agents, gemcitabine (Gem) and 5-fluorouracil (5FU), activate the NOD-like receptor family, pyrin domain containing-3 protein (Nlrp3)-dependent caspase-1 activation complex (termed the inflammasome) in myeloid-derived suppressor cells (MDSCs), leading to production of interleukin-1beta (IL-1beta), which curtails anticancer immunity. Fluorouracil 85-99 interleukin 1 beta Mus musculus 342-350 23202296-3 2013 Here we show that two clinically used chemotherapeutic agents, gemcitabine (Gem) and 5-fluorouracil (5FU), activate the NOD-like receptor family, pyrin domain containing-3 protein (Nlrp3)-dependent caspase-1 activation complex (termed the inflammasome) in myeloid-derived suppressor cells (MDSCs), leading to production of interleukin-1beta (IL-1beta), which curtails anticancer immunity. Fluorouracil 101-104 interleukin 1 beta Mus musculus 323-340 23202296-3 2013 Here we show that two clinically used chemotherapeutic agents, gemcitabine (Gem) and 5-fluorouracil (5FU), activate the NOD-like receptor family, pyrin domain containing-3 protein (Nlrp3)-dependent caspase-1 activation complex (termed the inflammasome) in myeloid-derived suppressor cells (MDSCs), leading to production of interleukin-1beta (IL-1beta), which curtails anticancer immunity. Fluorouracil 101-104 interleukin 1 beta Mus musculus 342-350 23441616-0 2013 Nobiletin induces apoptosis and potentiates the effects of the anticancer drug 5-fluorouracil in p53-mutated SNU-16 human gastric cancer cells. Fluorouracil 79-93 tumor protein p53 Homo sapiens 97-100 23255931-0 2013 RhoGDI2 confers resistance to 5-fluorouracil in human gastric cancer cells. Fluorouracil 30-44 Rho GDP dissociation inhibitor beta Homo sapiens 0-7 23255931-3 2013 The expression of RhoGDI2 in seven gastric cancer cell lines was positively correlated with resistance to 5-FU. Fluorouracil 106-110 Rho GDP dissociation inhibitor beta Homo sapiens 18-25 23255931-4 2013 Lower 5-FU sensitivity of isolated tumor cells from patients with gastric cancer was also associated with higher RhoGDI2 expression. Fluorouracil 6-10 Rho GDP dissociation inhibitor beta Homo sapiens 113-120 23255931-5 2013 Ectopic expression of RhoGDI2 in gastric cancer cells increased the resistance to 5-FU and reverted low dose 5-FU-induced G2/M phase arrest without affecting the population of sub-G1 cells. Fluorouracil 82-86 Rho GDP dissociation inhibitor beta Homo sapiens 22-29 23255931-5 2013 Ectopic expression of RhoGDI2 in gastric cancer cells increased the resistance to 5-FU and reverted low dose 5-FU-induced G2/M phase arrest without affecting the population of sub-G1 cells. Fluorouracil 109-113 Rho GDP dissociation inhibitor beta Homo sapiens 22-29 23255931-6 2013 Overall, these findings suggest that RhoGDI2 is associated with 5-FU resistance and is a potential therapeutic target for enhancing chemotherapy efficacy in gastric cancer. Fluorouracil 64-68 Rho GDP dissociation inhibitor beta Homo sapiens 37-44 24154628-3 2013 Here we show that the BER AP endonucleases APN-1 and EXO-3 function in the same pathway as MMR, to elicit DNA-directed toxicity in response to 5-fluorouracil, a mainstay of systemic adjuvant treatment of solid cancers. Fluorouracil 143-157 Apurinic-apyrimidinic endonuclease Caenorhabditis elegans 43-48 24154628-3 2013 Here we show that the BER AP endonucleases APN-1 and EXO-3 function in the same pathway as MMR, to elicit DNA-directed toxicity in response to 5-fluorouracil, a mainstay of systemic adjuvant treatment of solid cancers. Fluorouracil 143-157 DNA-(apurinic or apyrimidinic site) endonuclease Caenorhabditis elegans 53-58 23441616-5 2013 The expression of p53 protein increased after treatment with 5-FU, but not nobiletin, whereas the expression of p21 (WAF1/CIP1) protein increased after treatment with nobiletin, but not 5-FU. Fluorouracil 61-65 tumor protein p53 Homo sapiens 18-21 23441616-7 2013 The results of this study suggest the potential application of nobiletin to the enhancement of 5-FU efficiency in p53 mutant tumors. Fluorouracil 95-99 tumor protein p53 Homo sapiens 114-117 23451189-9 2013 Curcumin potentiated 5-FU-induced expression or cleavage of pro-apoptotic proteins (caspase-8, -9, -3, PARP and Bax), and down-regulated anti-apoptotic (Bcl-xL) and proliferative (cyclin D1) proteins. Fluorouracil 21-25 poly(ADP-ribose) polymerase 1 Homo sapiens 103-107 23451189-9 2013 Curcumin potentiated 5-FU-induced expression or cleavage of pro-apoptotic proteins (caspase-8, -9, -3, PARP and Bax), and down-regulated anti-apoptotic (Bcl-xL) and proliferative (cyclin D1) proteins. Fluorouracil 21-25 BCL2 associated X, apoptosis regulator Homo sapiens 112-115 23451189-9 2013 Curcumin potentiated 5-FU-induced expression or cleavage of pro-apoptotic proteins (caspase-8, -9, -3, PARP and Bax), and down-regulated anti-apoptotic (Bcl-xL) and proliferative (cyclin D1) proteins. Fluorouracil 21-25 BCL2 like 1 Homo sapiens 153-159 23451189-10 2013 Although 5-FU activated NF-kappaB/PI-3K/Src pathway in CRC cells, this was down-regulated by curcumin treatment through inhibition of IkappaBalpha kinase activation and IkappaBalpha phosphorylation. Fluorouracil 9-13 nuclear factor kappa B subunit 1 Homo sapiens 24-33 23451189-10 2013 Although 5-FU activated NF-kappaB/PI-3K/Src pathway in CRC cells, this was down-regulated by curcumin treatment through inhibition of IkappaBalpha kinase activation and IkappaBalpha phosphorylation. Fluorouracil 9-13 SRC proto-oncogene, non-receptor tyrosine kinase Homo sapiens 40-43 23409141-0 2013 Notch1 is a 5-fluorouracil resistant and poor survival marker in human esophagus squamous cell carcinomas. Fluorouracil 12-26 notch receptor 1 Homo sapiens 0-6 23409141-7 2013 Additional studies demonstrated that the KYSE70 cell line was more 5-FU resistant than the KYSE450 cell line and such 5-FU resistance is correlated to Notch1 expression verified by Notch1 knockdown experiments. Fluorouracil 118-122 notch receptor 1 Homo sapiens 151-157 23409141-7 2013 Additional studies demonstrated that the KYSE70 cell line was more 5-FU resistant than the KYSE450 cell line and such 5-FU resistance is correlated to Notch1 expression verified by Notch1 knockdown experiments. Fluorouracil 118-122 notch receptor 1 Homo sapiens 181-187 23235459-6 2012 The induction of PRAP1 expression by p53 may promote resistance of cancer cells to chemotherapeutic drugs such as 5-fluorouracil (5-FU), as knockdown of PRAP1 increases apoptosis in cancer cells after 5-FU treatment. Fluorouracil 114-128 proline rich acidic protein 1 Homo sapiens 17-22 23457527-10 2013 In conclusion, we identified three genes that chemosensitize the effects of 5-FU and IFN-alpha/5-FU on HCC cells and demonstrated that PRKAG2 mRNA can serve as a prognostic marker for IFN-alpha/5-FU therapy. Fluorouracil 76-80 interferon alpha 1 Homo sapiens 184-195 23241148-11 2012 In line with, l-CaD positive human colon cancer cell lines were more resistant to 5-fluorouracil (5-FU) and radiation treatment compared to l-CaD negative cell lines. Fluorouracil 82-96 caldesmon 1 Homo sapiens 14-19 23241148-11 2012 In line with, l-CaD positive human colon cancer cell lines were more resistant to 5-fluorouracil (5-FU) and radiation treatment compared to l-CaD negative cell lines. Fluorouracil 98-102 caldesmon 1 Homo sapiens 14-19 23382968-3 2013 In the present study, the expressions of mRNAs that encode inflammatory cytokines, TNF-alpha, IL-1beta, IL-6, Il-17A and IL-22, were significantly increased throughout the entire colon of mice that exhibited diarrhea following 5-FU administration. Fluorouracil 227-231 tumor necrosis factor Mus musculus 83-92 23382968-3 2013 In the present study, the expressions of mRNAs that encode inflammatory cytokines, TNF-alpha, IL-1beta, IL-6, Il-17A and IL-22, were significantly increased throughout the entire colon of mice that exhibited diarrhea following 5-FU administration. Fluorouracil 227-231 interleukin 6 Mus musculus 104-108 23349734-11 2013 The cleaved caspase-3 expression was significantly decreased (2.09 and 2.47 folds respectively for 5-Fluorouracil and Camptothecin) in H460 spheroid cultures compared to 2D culture system. Fluorouracil 99-113 caspase 3 Homo sapiens 12-21 23355249-0 2013 [Effect of 5-fluorouracil on the expression of ATP-binding cassette superfamily G member 2 in human colon cancer cell SW480]. Fluorouracil 11-25 ATP binding cassette subfamily G member 2 (Junior blood group) Homo sapiens 47-90 23355249-1 2013 OBJECTIVE: To investigate the effect of 5-fluorouracil (5-FU) on the expression of ATP-binding cassette superfamily G member 2 (ABCG2) in human colon cancer cell SW480. Fluorouracil 40-54 ATP binding cassette subfamily G member 2 (Junior blood group) Homo sapiens 83-126 23355249-1 2013 OBJECTIVE: To investigate the effect of 5-fluorouracil (5-FU) on the expression of ATP-binding cassette superfamily G member 2 (ABCG2) in human colon cancer cell SW480. Fluorouracil 40-54 ATP binding cassette subfamily G member 2 (Junior blood group) Homo sapiens 128-133 23355249-1 2013 OBJECTIVE: To investigate the effect of 5-fluorouracil (5-FU) on the expression of ATP-binding cassette superfamily G member 2 (ABCG2) in human colon cancer cell SW480. Fluorouracil 56-60 ATP binding cassette subfamily G member 2 (Junior blood group) Homo sapiens 83-126 23355249-1 2013 OBJECTIVE: To investigate the effect of 5-fluorouracil (5-FU) on the expression of ATP-binding cassette superfamily G member 2 (ABCG2) in human colon cancer cell SW480. Fluorouracil 56-60 ATP binding cassette subfamily G member 2 (Junior blood group) Homo sapiens 128-133 23355249-7 2013 Immediately after treatment with 5-FU for 48 hours, the positive expression rate of ABCG2 (group B) was (3.43+-1.18)% (P<0.05). Fluorouracil 33-37 ATP binding cassette subfamily G member 2 (Junior blood group) Homo sapiens 84-89 23355249-8 2013 In the second passage of cells after treatment with 5-FU for 48 hours, the positive expression rate of ABCG2 (group C) was (12.91+-3.42)% (P<0.05). Fluorouracil 52-56 ATP binding cassette subfamily G member 2 (Junior blood group) Homo sapiens 103-108 23355249-10 2013 CONCLUSION: Expression of ABCG2 in SW480 cells can be affected by various concentrations of 5-FU. Fluorouracil 92-96 ATP binding cassette subfamily G member 2 (Junior blood group) Homo sapiens 26-31 23235459-6 2012 The induction of PRAP1 expression by p53 may promote resistance of cancer cells to chemotherapeutic drugs such as 5-fluorouracil (5-FU), as knockdown of PRAP1 increases apoptosis in cancer cells after 5-FU treatment. Fluorouracil 114-128 tumor protein p53 Homo sapiens 37-40 23235459-6 2012 The induction of PRAP1 expression by p53 may promote resistance of cancer cells to chemotherapeutic drugs such as 5-fluorouracil (5-FU), as knockdown of PRAP1 increases apoptosis in cancer cells after 5-FU treatment. Fluorouracil 130-134 proline rich acidic protein 1 Homo sapiens 17-22 23235459-6 2012 The induction of PRAP1 expression by p53 may promote resistance of cancer cells to chemotherapeutic drugs such as 5-fluorouracil (5-FU), as knockdown of PRAP1 increases apoptosis in cancer cells after 5-FU treatment. Fluorouracil 130-134 tumor protein p53 Homo sapiens 37-40 23235459-6 2012 The induction of PRAP1 expression by p53 may promote resistance of cancer cells to chemotherapeutic drugs such as 5-fluorouracil (5-FU), as knockdown of PRAP1 increases apoptosis in cancer cells after 5-FU treatment. Fluorouracil 130-134 proline rich acidic protein 1 Homo sapiens 153-158 23235459-6 2012 The induction of PRAP1 expression by p53 may promote resistance of cancer cells to chemotherapeutic drugs such as 5-fluorouracil (5-FU), as knockdown of PRAP1 increases apoptosis in cancer cells after 5-FU treatment. Fluorouracil 201-205 proline rich acidic protein 1 Homo sapiens 17-22 23235459-6 2012 The induction of PRAP1 expression by p53 may promote resistance of cancer cells to chemotherapeutic drugs such as 5-fluorouracil (5-FU), as knockdown of PRAP1 increases apoptosis in cancer cells after 5-FU treatment. Fluorouracil 201-205 tumor protein p53 Homo sapiens 37-40 23235459-6 2012 The induction of PRAP1 expression by p53 may promote resistance of cancer cells to chemotherapeutic drugs such as 5-fluorouracil (5-FU), as knockdown of PRAP1 increases apoptosis in cancer cells after 5-FU treatment. Fluorouracil 201-205 proline rich acidic protein 1 Homo sapiens 153-158 22790872-3 2012 Our analysis of genome-wide chromatin occupancy by p53 using chromatin immunoprecipitation (ChIP)-seq revealed "p53 default program", that is, the pattern of major p53-bound sites that is similar upon p53 activation by nutlin3a, reactivation of p53 and induction of tumor cell apoptosis (RITA) or 5-fluorouracil in breast cancer cells, despite different biological outcomes. Fluorouracil 297-311 tumor protein p53 Homo sapiens 51-54 22286760-3 2012 The MTA1 promoter contains two putative p53 response elements (p53REs), which were repressed by the p53-inducing drug 5-fluorouracil (5-FU). Fluorouracil 118-132 tumor protein p53 Homo sapiens 40-43 22286760-3 2012 The MTA1 promoter contains two putative p53 response elements (p53REs), which were repressed by the p53-inducing drug 5-fluorouracil (5-FU). Fluorouracil 118-132 tumor protein p53 Homo sapiens 63-66 22286760-3 2012 The MTA1 promoter contains two putative p53 response elements (p53REs), which were repressed by the p53-inducing drug 5-fluorouracil (5-FU). Fluorouracil 134-138 tumor protein p53 Homo sapiens 40-43 22286760-3 2012 The MTA1 promoter contains two putative p53 response elements (p53REs), which were repressed by the p53-inducing drug 5-fluorouracil (5-FU). Fluorouracil 134-138 tumor protein p53 Homo sapiens 63-66 22286760-4 2012 Notably, 5-FU treatment decreased MTA1 expression only in p53 wild-type cells. Fluorouracil 9-13 tumor protein p53 Homo sapiens 58-61 22286760-5 2012 p53 and histone deacetylases 1/2 were recruited, and acetylation of H3K9 was decreased on the promoter region including the p53REs after 5-FU treatment. Fluorouracil 137-141 tumor protein p53 Homo sapiens 0-3 22286760-5 2012 p53 and histone deacetylases 1/2 were recruited, and acetylation of H3K9 was decreased on the promoter region including the p53REs after 5-FU treatment. Fluorouracil 137-141 histone deacetylase 1 Homo sapiens 8-32 22286760-5 2012 p53 and histone deacetylases 1/2 were recruited, and acetylation of H3K9 was decreased on the promoter region including the p53REs after 5-FU treatment. Fluorouracil 137-141 tumor protein p53 Homo sapiens 124-127 22790872-3 2012 Our analysis of genome-wide chromatin occupancy by p53 using chromatin immunoprecipitation (ChIP)-seq revealed "p53 default program", that is, the pattern of major p53-bound sites that is similar upon p53 activation by nutlin3a, reactivation of p53 and induction of tumor cell apoptosis (RITA) or 5-fluorouracil in breast cancer cells, despite different biological outcomes. Fluorouracil 297-311 tumor protein p53 Homo sapiens 112-115 22790872-3 2012 Our analysis of genome-wide chromatin occupancy by p53 using chromatin immunoprecipitation (ChIP)-seq revealed "p53 default program", that is, the pattern of major p53-bound sites that is similar upon p53 activation by nutlin3a, reactivation of p53 and induction of tumor cell apoptosis (RITA) or 5-fluorouracil in breast cancer cells, despite different biological outcomes. Fluorouracil 297-311 tumor protein p53 Homo sapiens 112-115 22790872-3 2012 Our analysis of genome-wide chromatin occupancy by p53 using chromatin immunoprecipitation (ChIP)-seq revealed "p53 default program", that is, the pattern of major p53-bound sites that is similar upon p53 activation by nutlin3a, reactivation of p53 and induction of tumor cell apoptosis (RITA) or 5-fluorouracil in breast cancer cells, despite different biological outcomes. Fluorouracil 297-311 tumor protein p53 Homo sapiens 112-115 22790872-3 2012 Our analysis of genome-wide chromatin occupancy by p53 using chromatin immunoprecipitation (ChIP)-seq revealed "p53 default program", that is, the pattern of major p53-bound sites that is similar upon p53 activation by nutlin3a, reactivation of p53 and induction of tumor cell apoptosis (RITA) or 5-fluorouracil in breast cancer cells, despite different biological outcomes. Fluorouracil 297-311 tumor protein p53 Homo sapiens 112-115 22252310-5 2012 The EGFR-targeted monoclonal antibody cetuximab is approved for the treatment of locally advanced SCCHN in combination with radiotherapy, for first-line treatment of recurrent or metastatic SCCHN in combination with platinum-based chemotherapy and 5-fluorouracil, and for recurrent or metastatic SCCHN following progression with platinum-based chemotherapy. Fluorouracil 248-262 epidermal growth factor receptor Homo sapiens 4-8 22960985-1 2012 PURPOSE: We investigated the efficacy and toxicity of a novel oral 5-fluorouracil (5-FU) formulation (S-1), administered according to a tailored dose regimen. Fluorouracil 67-81 proteasome 26S subunit, non-ATPase 1 Homo sapiens 102-105 22960985-1 2012 PURPOSE: We investigated the efficacy and toxicity of a novel oral 5-fluorouracil (5-FU) formulation (S-1), administered according to a tailored dose regimen. Fluorouracil 83-87 proteasome 26S subunit, non-ATPase 1 Homo sapiens 102-105 22516806-11 2012 In vitro experiments showed that DLD-1 cells stably transfected with TFF3 were significantly less sensitive to 5-fluorouracil and showed upregulation of genes involved in the transcriptional machinery and in resistance to apoptosis. Fluorouracil 111-125 trefoil factor 3 Homo sapiens 69-73 23108049-6 2012 5"-FU treatment dephosphorylated ERK in a DUSP6-dependent manner, resulting in destabilization of Bcl-2 and stabilization of Bad. Fluorouracil 0-5 mitogen-activated protein kinase 1 Homo sapiens 33-36 23169477-8 2012 After being combined with 5-Fu, the suppressing effect of Ad/Bcl-XL shRNA was enhanced further. Fluorouracil 26-30 BCL2 like 1 Homo sapiens 61-67 23169477-9 2012 In addition, the data also showed that Ad/Bcl-XL shRNA combined with 5-Fu could significantly increase the apoptotic ratio in the rectal cancer xenograft. Fluorouracil 69-73 BCL2 like 1 Homo sapiens 42-48 23169477-10 2012 CONCLUSIONS: These data indicate that Ad/Bcl-XL shRNA with or without 5-Fu has effective anti-tumor effects on the patient tumor-derived rectal cancer xenografts, suggesting that it could be a potential strategy for rectal cancer therapy. Fluorouracil 70-74 BCL2 like 1 Homo sapiens 41-47 22544540-5 2012 Epidemiological studies have also associated elevated tumor tissue TIMP-1 levels with a poor response to cyclophosphamide/methotrexate/5-fluorouracil and anthracycline-based chemotherapy. Fluorouracil 135-149 TIMP metallopeptidase inhibitor 1 Homo sapiens 67-73 23108049-6 2012 5"-FU treatment dephosphorylated ERK in a DUSP6-dependent manner, resulting in destabilization of Bcl-2 and stabilization of Bad. Fluorouracil 0-5 BCL2 apoptosis regulator Homo sapiens 98-103 23152059-8 2012 miR-204 targeted Bcl-2 messenger RNA and increased responsiveness of GC cells to 5-fluorouracil and oxaliplatin treatment. Fluorouracil 81-95 BCL2 apoptosis regulator Homo sapiens 17-22 23152059-9 2012 Ectopic expression of Bcl-2 protein counteracted miR-204 pro-apoptotic activity in response to 5-fluorouracil. Fluorouracil 95-109 BCL2 apoptosis regulator Homo sapiens 22-27 22767582-0 2012 VEGF remains an interesting target in advanced pancreas cancer (APCA): results of a multi-institutional phase II study of bevacizumab, gemcitabine, and infusional 5-fluorouracil in patients with APCA. Fluorouracil 163-177 vascular endothelial growth factor A Homo sapiens 0-4 23085230-6 2012 Here, we adopted a prodrug system that uses 5-fluorocytosine (5-FC) and human EGF (hEGF) fused with yeast cytosine deaminase (Fcy) to target EGFR-overexpressing cancer cells and to convert 5-FC to a significantly more toxic chemotherapeutic, 5-fluorouracil (5-FU). Fluorouracil 242-256 epidermal growth factor receptor Homo sapiens 141-145 23085230-6 2012 Here, we adopted a prodrug system that uses 5-fluorocytosine (5-FC) and human EGF (hEGF) fused with yeast cytosine deaminase (Fcy) to target EGFR-overexpressing cancer cells and to convert 5-FC to a significantly more toxic chemotherapeutic, 5-fluorouracil (5-FU). Fluorouracil 258-262 epidermal growth factor receptor Homo sapiens 141-145 22172707-5 2012 Following treatment with 5-FU, JAK1 and STAT5 immunoreactivities were decreased in MCF-7 cells in comparison with both gemcitabine-treated and non-treated groups. Fluorouracil 25-29 Janus kinase 1 Homo sapiens 31-35 22424872-2 2012 We conducted a multicenter feasibility study using S-1, an oral derivative of 5-fluorouracil, as postoperative adjuvant chemotherapy in patients with curatively resected pathologically stage IB-IIIA non-small-cell lung cancer. Fluorouracil 78-92 proteasome 26S subunit, non-ATPase 1 Homo sapiens 51-54 22292507-0 2012 Immunohistochemical study of nuclear factor-kappaB expression in esophageal squamous cell carcinoma: prognostic significance and sensitivity to treatment with 5-FU. Fluorouracil 159-163 nuclear factor kappa B subunit 1 Homo sapiens 29-50 22292507-8 2012 The sensitivity of esophageal squamous cell carcinoma cell lines to 5-fluorouracil (5-FU) was analyzed by their NF-kappaB expression, and the effect of 5-FU was evaluated on the proliferation and activity of two cell lines of cultured ESCCs expressing NF-kappaB. Fluorouracil 84-88 nuclear factor kappa B subunit 1 Homo sapiens 112-121 22292507-9 2012 ESCCs with activated NF-kappaB had poor sensitivity to 5-FU. Fluorouracil 55-59 nuclear factor kappa B subunit 1 Homo sapiens 21-30 23033004-1 2012 BACKGROUND: Combination of S-1, an oral fluorouracil derivative, plus docetaxel against non-small cell lung cancer (NSCLC) showed promising efficacy but clinically problematic emesis. Fluorouracil 40-52 proteasome 26S subunit, non-ATPase 1 Homo sapiens 27-30 22534547-2 2012 METHODOLOGY: Twenty-two meta-static gastric cancer patients with HER2 over-expression (3+ by immunohistochemistry or HER2 amplification by fluorescence in situ hybridization) previously treated with 5-fluorouracil-based chemotherapy were eligible. Fluorouracil 199-213 erb-b2 receptor tyrosine kinase 2 Homo sapiens 65-69 23291139-12 2012 CONCLUSIONS: Oral administration of S-1 is an alternative option of venous infusional fluorouracil. Fluorouracil 86-98 proteasome 26S subunit, non-ATPase 1 Homo sapiens 36-39 23170132-1 2012 This study aimed to investigate the impact of the combined use of the nuclear factor-kappaB (NF-kappaB) inhibitors pyrrolidine dithiocarbamate (PDTC), bortezomib or SN50, and the chemotherapy agents arsenic acid (As(2)O(3)), fluorouracil (5FU), oxaliplatin or paclitaxel on the growth and apoptosis of HT-29 cells. Fluorouracil 225-237 nuclear factor kappa B subunit 1 Homo sapiens 70-91 22983008-9 2012 In addition, CREBZF expression confers sensitivity to 5-fluorouracil, a p53-activating chemotherapeutic drug. Fluorouracil 54-68 CREB/ATF bZIP transcription factor Homo sapiens 13-19 22983008-9 2012 In addition, CREBZF expression confers sensitivity to 5-fluorouracil, a p53-activating chemotherapeutic drug. Fluorouracil 54-68 tumor protein p53 Homo sapiens 72-75 22899557-9 2012 The drug sensitivity of 5-FU or DOX, the apoptotic rate, and the intracellular accumulation of Rhodamine-123 and DOX were increased, while the mRNA and protein expression levels of MDR1, LRP, and MRP1 were reduced. Fluorouracil 24-28 ATP binding cassette subfamily B member 1 Homo sapiens 181-185 22955854-7 2012 Pre-miR144 treatment and the resultant repression of ZFX in GC cell lines moderately upregulated their susceptibility to 5-fluorouracil chemotherapy. Fluorouracil 121-135 microRNA 144 Homo sapiens 4-10 23170132-1 2012 This study aimed to investigate the impact of the combined use of the nuclear factor-kappaB (NF-kappaB) inhibitors pyrrolidine dithiocarbamate (PDTC), bortezomib or SN50, and the chemotherapy agents arsenic acid (As(2)O(3)), fluorouracil (5FU), oxaliplatin or paclitaxel on the growth and apoptosis of HT-29 cells. Fluorouracil 239-242 nuclear factor kappa B subunit 1 Homo sapiens 70-91 22895565-6 2012 In addition, knockdown of MMS22L expression also enhanced the apoptosis of cancer cells that were exposed to DNA-damaging agents including 5-FU and CDDP. Fluorouracil 139-143 MMS22 like, DNA repair protein Homo sapiens 26-32 22825128-5 2012 The expression of apoptosis related proteins was also affected in cells treated with the combination of OA and 5-FU, including activation of caspases-3 and the expression of Bcl-2/Bax, survivin and NF-kappaB. Fluorouracil 123-127 BCL2 apoptosis regulator Homo sapiens 198-203 22825128-5 2012 The expression of apoptosis related proteins was also affected in cells treated with the combination of OA and 5-FU, including activation of caspases-3 and the expression of Bcl-2/Bax, survivin and NF-kappaB. Fluorouracil 123-127 BCL2 associated X, apoptosis regulator Homo sapiens 204-207 22825128-5 2012 The expression of apoptosis related proteins was also affected in cells treated with the combination of OA and 5-FU, including activation of caspases-3 and the expression of Bcl-2/Bax, survivin and NF-kappaB. Fluorouracil 123-127 nuclear factor kappa B subunit 1 Homo sapiens 222-231 22192364-3 2012 Anti-EGFR agents can be added to first-line FOLFIRI (5-fluorouracil, leucovorin [folinic acid], irinotecan) or FOLFOX (5-fluorouracil, leucovorin [folinic acid], oxaliplatin) in patients whose tumors express wild-type KRAS. Fluorouracil 53-67 epidermal growth factor receptor Homo sapiens 5-9 22817133-2 2012 ETIOLOGY: 5-Fluorouracil"s mechanism of action revolves around the metabolism of 5-FU into fluorouridine triphosphate which then interferes with RNA synthesis and function as well as the inhibition of thymidylate synthase which ultimately impairs DNA stability. Fluorouracil 10-24 thymidylate synthetase Canis lupus familiaris 201-221 22817133-2 2012 ETIOLOGY: 5-Fluorouracil"s mechanism of action revolves around the metabolism of 5-FU into fluorouridine triphosphate which then interferes with RNA synthesis and function as well as the inhibition of thymidylate synthase which ultimately impairs DNA stability. Fluorouracil 81-85 thymidylate synthetase Canis lupus familiaris 201-221 23020798-9 2012 CONCLUSION: Polymorphisms of ERCC1, GSTs, TS and MTHFR were closely associated with clinical outcomes of GC patients treated with platinum/5-Fu-based chemotherapy. Fluorouracil 139-143 hematopoietic prostaglandin D synthase Homo sapiens 36-40 22192364-3 2012 Anti-EGFR agents can be added to first-line FOLFIRI (5-fluorouracil, leucovorin [folinic acid], irinotecan) or FOLFOX (5-fluorouracil, leucovorin [folinic acid], oxaliplatin) in patients whose tumors express wild-type KRAS. Fluorouracil 119-133 epidermal growth factor receptor Homo sapiens 5-9 22864933-6 2012 This SNP is located upstream of the 5 methyltetrahydrofolate-homocysteine methyltransferase reductase (MTRR) gene, and it is known that the enzyme for MTRR is involved in the methionine-folate biosynthesis and metabolism pathway, which is the primary target of 5-FU-related compounds, although the authors were unable to identify a direct relation between rs4702484 and MTRR expression in a tested subset of cells. Fluorouracil 261-265 5-methyltetrahydrofolate-homocysteine methyltransferase reductase Homo sapiens 36-101 22684338-0 2012 Prospective impact of 5-FU in the induction of endoplasmic reticulum stress, modulation of GRP78 expression and autophagy in Sk-Hep1 cells. Fluorouracil 22-26 heat shock protein family A (Hsp70) member 5 Homo sapiens 103-108 22684338-5 2012 We found that 5-FU profoundly induces ER stress in Sk-Hep1 cells and upregulates p53 and activates CHOP/GADD153 and caspase-12. Fluorouracil 14-18 tumor protein p53 Homo sapiens 93-96 22684338-5 2012 We found that 5-FU profoundly induces ER stress in Sk-Hep1 cells and upregulates p53 and activates CHOP/GADD153 and caspase-12. Fluorouracil 14-18 DNA damage inducible transcript 3 Homo sapiens 111-115 22684338-5 2012 We found that 5-FU profoundly induces ER stress in Sk-Hep1 cells and upregulates p53 and activates CHOP/GADD153 and caspase-12. Fluorouracil 14-18 DNA damage inducible transcript 3 Homo sapiens 116-123 22684338-9 2012 Our study demonstrates that 5-FU-induced ER stress suppresses autophagy and also downregulates GRP78 expression. Fluorouracil 28-32 heat shock protein family A (Hsp70) member 5 Homo sapiens 107-112 22684338-12 2012 Taken together, these results indicate that 5-FU-induced ER stress activates the mitochondrial apoptotic cell death pathway by downregulating GRP78 and protective autophagy proteins in Sk-Hep1 cells, raising the possibility of using 5-FU as a therapeutic agent to target human HCC. Fluorouracil 44-48 heat shock protein family A (Hsp70) member 5 Homo sapiens 154-159 23181119-0 2012 siRNA targeting decoy receptor 3 enhances the sensitivity of gastric carcinoma cells to 5-fluorouracil. Fluorouracil 88-102 TNF receptor superfamily member 6b Homo sapiens 16-32 23181119-1 2012 In order to investigate the effects of RNA interference of decoy receptor 3 (DcR3) on the sensitivity of gastric cancer cells to 5-fluorouracil (5-FU) and the relevant mechanisms, siRNA against DcR3 was transfected into the gastric cancer cell line AGS. Fluorouracil 129-143 TNF receptor superfamily member 6b Homo sapiens 59-75 23181119-1 2012 In order to investigate the effects of RNA interference of decoy receptor 3 (DcR3) on the sensitivity of gastric cancer cells to 5-fluorouracil (5-FU) and the relevant mechanisms, siRNA against DcR3 was transfected into the gastric cancer cell line AGS. Fluorouracil 129-143 TNF receptor superfamily member 6b Homo sapiens 77-81 23181119-1 2012 In order to investigate the effects of RNA interference of decoy receptor 3 (DcR3) on the sensitivity of gastric cancer cells to 5-fluorouracil (5-FU) and the relevant mechanisms, siRNA against DcR3 was transfected into the gastric cancer cell line AGS. Fluorouracil 145-149 TNF receptor superfamily member 6b Homo sapiens 59-75 23181119-1 2012 In order to investigate the effects of RNA interference of decoy receptor 3 (DcR3) on the sensitivity of gastric cancer cells to 5-fluorouracil (5-FU) and the relevant mechanisms, siRNA against DcR3 was transfected into the gastric cancer cell line AGS. Fluorouracil 145-149 TNF receptor superfamily member 6b Homo sapiens 77-81 23181119-11 2012 Downregulation of DcR3 enhances the sensitivity of gastric cancer cells to 5-FU and increased the expression of Fas, FasL and caspase-3/8. Fluorouracil 75-79 TNF receptor superfamily member 6b Homo sapiens 18-22 22864933-6 2012 This SNP is located upstream of the 5 methyltetrahydrofolate-homocysteine methyltransferase reductase (MTRR) gene, and it is known that the enzyme for MTRR is involved in the methionine-folate biosynthesis and metabolism pathway, which is the primary target of 5-FU-related compounds, although the authors were unable to identify a direct relation between rs4702484 and MTRR expression in a tested subset of cells. Fluorouracil 261-265 5-methyltetrahydrofolate-homocysteine methyltransferase reductase Homo sapiens 103-107 22864933-6 2012 This SNP is located upstream of the 5 methyltetrahydrofolate-homocysteine methyltransferase reductase (MTRR) gene, and it is known that the enzyme for MTRR is involved in the methionine-folate biosynthesis and metabolism pathway, which is the primary target of 5-FU-related compounds, although the authors were unable to identify a direct relation between rs4702484 and MTRR expression in a tested subset of cells. Fluorouracil 261-265 5-methyltetrahydrofolate-homocysteine methyltransferase reductase Homo sapiens 151-155 22864933-6 2012 This SNP is located upstream of the 5 methyltetrahydrofolate-homocysteine methyltransferase reductase (MTRR) gene, and it is known that the enzyme for MTRR is involved in the methionine-folate biosynthesis and metabolism pathway, which is the primary target of 5-FU-related compounds, although the authors were unable to identify a direct relation between rs4702484 and MTRR expression in a tested subset of cells. Fluorouracil 261-265 5-methyltetrahydrofolate-homocysteine methyltransferase reductase Homo sapiens 151-155 22614071-0 2012 Inhibition of the mTOR/S6K signal is necessary to enhance fluorouracil-induced apoptosis in gastric cancer cells with HER2 amplification. Fluorouracil 58-70 mechanistic target of rapamycin kinase Homo sapiens 18-22 22809558-4 2012 Particularly, compound 37 had four-fold improvement compared to Fluorouracil in inhibiting A549 and HepG2 cell proliferation with IC(50) values of 6.76 and 9.44 muM, respectively. Fluorouracil 64-76 latexin Homo sapiens 161-164 22908043-5 2012 Diploids lacking Blm10 also were sensitized to doxorubicin, hydroxyurea, 5-fluorouracil, rapamycin, hydrogen peroxide, methyl methanesulfonate, and calcofluor. Fluorouracil 73-87 Blm10p Saccharomyces cerevisiae S288C 17-22 22607196-0 2012 Oroxylin A improves the sensitivity of HT-29 human colon cancer cells to 5-FU through modulation of the COX-2 signaling pathway. Fluorouracil 73-77 mitochondrially encoded cytochrome c oxidase II Homo sapiens 104-109 22607196-4 2012 A correlation between COX-2 inhibition by oroxylin A and a synergistic effect of 5-FU on the growth of HT-29 cells was observed, and a COX-2 pathway for this effect was recognized; oroxylin A evidently elevated the level of reactive oxygen species in HT-29 cells, which subsequently inhibited COX-2 expression and enhanced the susceptibility of HT-29 cells to 5-FU. Fluorouracil 81-85 mitochondrially encoded cytochrome c oxidase II Homo sapiens 22-27 22607196-4 2012 A correlation between COX-2 inhibition by oroxylin A and a synergistic effect of 5-FU on the growth of HT-29 cells was observed, and a COX-2 pathway for this effect was recognized; oroxylin A evidently elevated the level of reactive oxygen species in HT-29 cells, which subsequently inhibited COX-2 expression and enhanced the susceptibility of HT-29 cells to 5-FU. Fluorouracil 360-364 mitochondrially encoded cytochrome c oxidase II Homo sapiens 22-27 22607196-4 2012 A correlation between COX-2 inhibition by oroxylin A and a synergistic effect of 5-FU on the growth of HT-29 cells was observed, and a COX-2 pathway for this effect was recognized; oroxylin A evidently elevated the level of reactive oxygen species in HT-29 cells, which subsequently inhibited COX-2 expression and enhanced the susceptibility of HT-29 cells to 5-FU. Fluorouracil 360-364 mitochondrially encoded cytochrome c oxidase II Homo sapiens 135-140 22607196-4 2012 A correlation between COX-2 inhibition by oroxylin A and a synergistic effect of 5-FU on the growth of HT-29 cells was observed, and a COX-2 pathway for this effect was recognized; oroxylin A evidently elevated the level of reactive oxygen species in HT-29 cells, which subsequently inhibited COX-2 expression and enhanced the susceptibility of HT-29 cells to 5-FU. Fluorouracil 360-364 mitochondrially encoded cytochrome c oxidase II Homo sapiens 135-140 22607196-6 2012 The synergistic effect of 5-FU induced by oroxylin A was also found in the suppression of Bcl-2 and in the activation of P53, Bax, PARP, and procaspase-3 proteins in HT-29 cells. Fluorouracil 26-30 BCL2 apoptosis regulator Homo sapiens 90-95 22607196-6 2012 The synergistic effect of 5-FU induced by oroxylin A was also found in the suppression of Bcl-2 and in the activation of P53, Bax, PARP, and procaspase-3 proteins in HT-29 cells. Fluorouracil 26-30 tumor protein p53 Homo sapiens 121-124 22607196-6 2012 The synergistic effect of 5-FU induced by oroxylin A was also found in the suppression of Bcl-2 and in the activation of P53, Bax, PARP, and procaspase-3 proteins in HT-29 cells. Fluorouracil 26-30 BCL2 associated X, apoptosis regulator Homo sapiens 126-129 22607196-6 2012 The synergistic effect of 5-FU induced by oroxylin A was also found in the suppression of Bcl-2 and in the activation of P53, Bax, PARP, and procaspase-3 proteins in HT-29 cells. Fluorouracil 26-30 caspase 3 Homo sapiens 141-153 22614071-0 2012 Inhibition of the mTOR/S6K signal is necessary to enhance fluorouracil-induced apoptosis in gastric cancer cells with HER2 amplification. Fluorouracil 58-70 erb-b2 receptor tyrosine kinase 2 Homo sapiens 130-134 22614071-4 2012 Fluorouracil-induced apoptosis was evaluated using western blot for poly (ADP-ribose) polymerase (PARP). Fluorouracil 0-12 poly(ADP-ribose) polymerase 1 Homo sapiens 68-96 22614071-4 2012 Fluorouracil-induced apoptosis was evaluated using western blot for poly (ADP-ribose) polymerase (PARP). Fluorouracil 0-12 poly(ADP-ribose) polymerase 1 Homo sapiens 98-102 22614071-6 2012 While the mTOR inhibitor everolimus enhanced fluorouracil-induced apoptosis in both HER2-amplified cell lines, this was not the case in the gastric cancer cell lines without HER2 amplification. Fluorouracil 45-57 mechanistic target of rapamycin kinase Homo sapiens 10-14 22614071-6 2012 While the mTOR inhibitor everolimus enhanced fluorouracil-induced apoptosis in both HER2-amplified cell lines, this was not the case in the gastric cancer cell lines without HER2 amplification. Fluorouracil 45-57 erb-b2 receptor tyrosine kinase 2 Homo sapiens 84-88 22614071-8 2012 In summary, inhibition of the mTOR/S6K signal may be a key molecular event in enhancing fluorouracil-induced apoptosis specifically in gastric cancer cells with HER2 amplification. Fluorouracil 88-100 mechanistic target of rapamycin kinase Homo sapiens 30-34 22614071-8 2012 In summary, inhibition of the mTOR/S6K signal may be a key molecular event in enhancing fluorouracil-induced apoptosis specifically in gastric cancer cells with HER2 amplification. Fluorouracil 88-100 erb-b2 receptor tyrosine kinase 2 Homo sapiens 161-165 22313545-0 2012 Opsin3 sensitizes hepatocellular carcinoma cells to 5-fluorouracil treatment by regulating the apoptotic pathway. Fluorouracil 52-66 opsin 3 Homo sapiens 0-6 22445862-0 2012 Docetaxel and 5-fluorouracil induce human p53 tumor suppressor gene transcription via a short sequence at core promoter element. Fluorouracil 14-28 tumor protein p53 Homo sapiens 42-45 22445862-9 2012 The same mutations also inhibited 5-fluorouracil (5-FU)-inducible p53 expression. Fluorouracil 34-48 tumor protein p53 Homo sapiens 66-69 22445862-9 2012 The same mutations also inhibited 5-fluorouracil (5-FU)-inducible p53 expression. Fluorouracil 50-54 tumor protein p53 Homo sapiens 66-69 22524518-0 2012 Apolipoprotein E COG 133 mimetic peptide improves 5-fluorouracil-induced intestinal mucositis. Fluorouracil 50-64 apolipoprotein E Rattus norvegicus 0-16 22524518-2 2012 In this study we addressed the role of the novel apolipoprotein E (ApoE) COG 133 mimetic peptide in 5-fluorouracil (5-FU)-challenged Swiss mice and IEC-6 cell monolayers. Fluorouracil 100-114 apolipoprotein E Mus musculus 49-65 22524518-2 2012 In this study we addressed the role of the novel apolipoprotein E (ApoE) COG 133 mimetic peptide in 5-fluorouracil (5-FU)-challenged Swiss mice and IEC-6 cell monolayers. Fluorouracil 100-114 apolipoprotein E Mus musculus 67-71 22524518-2 2012 In this study we addressed the role of the novel apolipoprotein E (ApoE) COG 133 mimetic peptide in 5-fluorouracil (5-FU)-challenged Swiss mice and IEC-6 cell monolayers. Fluorouracil 116-120 apolipoprotein E Mus musculus 49-65 22524518-2 2012 In this study we addressed the role of the novel apolipoprotein E (ApoE) COG 133 mimetic peptide in 5-fluorouracil (5-FU)-challenged Swiss mice and IEC-6 cell monolayers. Fluorouracil 116-120 apolipoprotein E Mus musculus 67-71 22524518-14 2012 RESULTS: Villus blunting and heavy inflammatory infiltrates were seen in the 5-FU-challenged group, findings that were partially ameliorated by the ApoE peptide. Fluorouracil 77-81 apolipoprotein E Rattus norvegicus 148-152 22524518-17 2012 CONCLUSION: Altogether, these findings suggest that the novel ApoE COG 133 mimetic peptide can reduce 5-FU-induced intestinal changes and potentially benefit mucositis. Fluorouracil 102-106 apolipoprotein E Rattus norvegicus 62-66 22313545-3 2012 The expression of opsin3 (OPN3), also called encephalopsin or panopsin, is lower in 5-fluorouracil (5-FU)-resistant Bel7402(5-FU) cells compared to 5-FU-sensitive Bel7402 cells. Fluorouracil 84-98 opsin 3 Homo sapiens 18-24 22313545-3 2012 The expression of opsin3 (OPN3), also called encephalopsin or panopsin, is lower in 5-fluorouracil (5-FU)-resistant Bel7402(5-FU) cells compared to 5-FU-sensitive Bel7402 cells. Fluorouracil 84-98 opsin 3 Homo sapiens 26-30 22313545-3 2012 The expression of opsin3 (OPN3), also called encephalopsin or panopsin, is lower in 5-fluorouracil (5-FU)-resistant Bel7402(5-FU) cells compared to 5-FU-sensitive Bel7402 cells. Fluorouracil 84-98 opsin 3 Homo sapiens 45-58 22313545-3 2012 The expression of opsin3 (OPN3), also called encephalopsin or panopsin, is lower in 5-fluorouracil (5-FU)-resistant Bel7402(5-FU) cells compared to 5-FU-sensitive Bel7402 cells. Fluorouracil 100-104 opsin 3 Homo sapiens 18-24 22313545-3 2012 The expression of opsin3 (OPN3), also called encephalopsin or panopsin, is lower in 5-fluorouracil (5-FU)-resistant Bel7402(5-FU) cells compared to 5-FU-sensitive Bel7402 cells. Fluorouracil 100-104 opsin 3 Homo sapiens 26-30 22313545-3 2012 The expression of opsin3 (OPN3), also called encephalopsin or panopsin, is lower in 5-fluorouracil (5-FU)-resistant Bel7402(5-FU) cells compared to 5-FU-sensitive Bel7402 cells. Fluorouracil 100-104 opsin 3 Homo sapiens 45-58 22313545-3 2012 The expression of opsin3 (OPN3), also called encephalopsin or panopsin, is lower in 5-fluorouracil (5-FU)-resistant Bel7402(5-FU) cells compared to 5-FU-sensitive Bel7402 cells. Fluorouracil 124-128 opsin 3 Homo sapiens 18-24 22313545-3 2012 The expression of opsin3 (OPN3), also called encephalopsin or panopsin, is lower in 5-fluorouracil (5-FU)-resistant Bel7402(5-FU) cells compared to 5-FU-sensitive Bel7402 cells. Fluorouracil 124-128 opsin 3 Homo sapiens 26-30 22313545-3 2012 The expression of opsin3 (OPN3), also called encephalopsin or panopsin, is lower in 5-fluorouracil (5-FU)-resistant Bel7402(5-FU) cells compared to 5-FU-sensitive Bel7402 cells. Fluorouracil 124-128 opsin 3 Homo sapiens 45-58 22313545-3 2012 The expression of opsin3 (OPN3), also called encephalopsin or panopsin, is lower in 5-fluorouracil (5-FU)-resistant Bel7402(5-FU) cells compared to 5-FU-sensitive Bel7402 cells. Fluorouracil 124-128 opsin 3 Homo sapiens 18-24 22313545-3 2012 The expression of opsin3 (OPN3), also called encephalopsin or panopsin, is lower in 5-fluorouracil (5-FU)-resistant Bel7402(5-FU) cells compared to 5-FU-sensitive Bel7402 cells. Fluorouracil 124-128 opsin 3 Homo sapiens 26-30 22313545-3 2012 The expression of opsin3 (OPN3), also called encephalopsin or panopsin, is lower in 5-fluorouracil (5-FU)-resistant Bel7402(5-FU) cells compared to 5-FU-sensitive Bel7402 cells. Fluorouracil 124-128 opsin 3 Homo sapiens 45-58 22313545-5 2012 Bel7402(5-FU)-OPN3 cells were more sensitive to 5-FU treatment than controls, while OPN3 knockdown resulted in a significant increase in 5-FU resistance. Fluorouracil 8-12 opsin 3 Homo sapiens 14-18 22313545-5 2012 Bel7402(5-FU)-OPN3 cells were more sensitive to 5-FU treatment than controls, while OPN3 knockdown resulted in a significant increase in 5-FU resistance. Fluorouracil 48-52 opsin 3 Homo sapiens 14-18 22313545-5 2012 Bel7402(5-FU)-OPN3 cells were more sensitive to 5-FU treatment than controls, while OPN3 knockdown resulted in a significant increase in 5-FU resistance. Fluorouracil 48-52 opsin 3 Homo sapiens 14-18 22648862-7 2012 Mice from the 5FU (5-Fluorouracil) group presented weight loss, ulcerations and inflammatory infiltration of neutrophils and eosinophils, increased expression of IL6 and TNF-alpha and increased intestinal permeability. Fluorouracil 20-34 interleukin 6 Mus musculus 163-166 22729158-8 2012 STUDY 2: Rats were treated with GLP-2 or control vehicle 2 days before a single injection of 5-FU or saline. Fluorouracil 93-97 mast cell protease 10 Rattus norvegicus 32-37 22773580-9 2012 None of the compounds induced internucleosomal DNA fragmentation and only 5-FU induced slight activation of caspase-3 in an oral squamous cell carcinoma cell line (HSC-2). Fluorouracil 74-78 caspase 3 Homo sapiens 108-117 22552543-0 2012 Impaired death-associated protein kinase-mediated survival signals in 5-fluorouracil-resistant human endometrial adenocarcinoma cells. Fluorouracil 82-96 death associated protein kinase 1 Homo sapiens 9-40 22552543-1 2012 A recent study showed that both 5-fluorouracil (5FU)-stimulated apoptosis and Fas-mediated apoptosis in human endometrial adenocarcinoma cells are enhanced by targeted knockdown of endogenous death-associated protein kinase (DAPK) with DAPK small-interfering RNAs. Fluorouracil 32-46 death associated protein kinase 1 Homo sapiens 216-247 22552543-1 2012 A recent study showed that both 5-fluorouracil (5FU)-stimulated apoptosis and Fas-mediated apoptosis in human endometrial adenocarcinoma cells are enhanced by targeted knockdown of endogenous death-associated protein kinase (DAPK) with DAPK small-interfering RNAs. Fluorouracil 32-46 death associated protein kinase 1 Homo sapiens 249-253 22552543-1 2012 A recent study showed that both 5-fluorouracil (5FU)-stimulated apoptosis and Fas-mediated apoptosis in human endometrial adenocarcinoma cells are enhanced by targeted knockdown of endogenous death-associated protein kinase (DAPK) with DAPK small-interfering RNAs. Fluorouracil 32-46 death associated protein kinase 1 Homo sapiens 272-276 22552543-1 2012 A recent study showed that both 5-fluorouracil (5FU)-stimulated apoptosis and Fas-mediated apoptosis in human endometrial adenocarcinoma cells are enhanced by targeted knockdown of endogenous death-associated protein kinase (DAPK) with DAPK small-interfering RNAs. Fluorouracil 48-51 death associated protein kinase 1 Homo sapiens 216-247 22552543-1 2012 A recent study showed that both 5-fluorouracil (5FU)-stimulated apoptosis and Fas-mediated apoptosis in human endometrial adenocarcinoma cells are enhanced by targeted knockdown of endogenous death-associated protein kinase (DAPK) with DAPK small-interfering RNAs. Fluorouracil 48-51 death associated protein kinase 1 Homo sapiens 249-253 22552543-1 2012 A recent study showed that both 5-fluorouracil (5FU)-stimulated apoptosis and Fas-mediated apoptosis in human endometrial adenocarcinoma cells are enhanced by targeted knockdown of endogenous death-associated protein kinase (DAPK) with DAPK small-interfering RNAs. Fluorouracil 48-51 death associated protein kinase 1 Homo sapiens 272-276 22716215-11 2012 The combination of 5-FU and chloroquine induced G1 arrest, up-regulation of p27 and p53, and down-regulation of CDK2 and cyclin D1. Fluorouracil 19-23 tumor protein p53 Homo sapiens 84-87 22649198-7 2012 Immunohistochemical analyses showed that most ESAM(hi) HSC were located near vascular endothelium in the BM after 5-fluorouracil treatment. Fluorouracil 114-128 endothelial cell-specific adhesion molecule Mus musculus 46-50 22648862-7 2012 Mice from the 5FU (5-Fluorouracil) group presented weight loss, ulcerations and inflammatory infiltration of neutrophils and eosinophils, increased expression of IL6 and TNF-alpha and increased intestinal permeability. Fluorouracil 20-34 tumor necrosis factor Mus musculus 171-180 22623418-7 2012 For example, the detoxification enzyme NQO1 was increased with treatment in both cell lines, while disparate members of the peroxiredoxin family, PRDX2 or PRDX5 and PRDX6, were elevated with 5-FU exposure in either SW480 or SW620, respectively. Fluorouracil 191-195 NAD(P)H quinone dehydrogenase 1 Homo sapiens 39-43 22673314-3 2012 METHODS: Apoptosis was induced by 5-fluorouracil (5-FU) in pcDNA3.0/PEG10 transiently transfected HEK293T cells and PEG10-suppressed Raji cells. Fluorouracil 34-48 paternally expressed 10 Homo sapiens 68-73 22673314-3 2012 METHODS: Apoptosis was induced by 5-fluorouracil (5-FU) in pcDNA3.0/PEG10 transiently transfected HEK293T cells and PEG10-suppressed Raji cells. Fluorouracil 50-54 paternally expressed 10 Homo sapiens 68-73 22673314-9 2012 RESULTS: HEK293T cells that overexpressed PEG10 exhibited greater viability 48 h following treatment with 5-FU, relative to control cells. Fluorouracil 106-110 paternally expressed 10 Homo sapiens 42-47 22905486-0 2012 cRGD conjugated mPEG-PLGA-PLL nanoparticles for SGC-7901 gastric cancer cells-targeted Delivery of fluorouracil. Fluorouracil 99-111 sarcoglycan beta Homo sapiens 48-51 24750599-5 2012 Meanwhile a synergistic effect was observed in boosting various immunity functions when the tumor bearing mice receiving BRP plus 5-FU administration, such as stimulating lymphocytes proliferation, increasing NK cell cytotoxicity, enhancing serum interleukin-2 (IL-2) and interferon-gamma (TNF-gamma) secretion, as well as augmenting CD4+ and CD8+ spleen T lymphocytes subsets. Fluorouracil 130-134 interferon gamma Mus musculus 272-288 22623418-7 2012 For example, the detoxification enzyme NQO1 was increased with treatment in both cell lines, while disparate members of the peroxiredoxin family, PRDX2 or PRDX5 and PRDX6, were elevated with 5-FU exposure in either SW480 or SW620, respectively. Fluorouracil 191-195 peroxiredoxin 2 Homo sapiens 124-137 22623418-7 2012 For example, the detoxification enzyme NQO1 was increased with treatment in both cell lines, while disparate members of the peroxiredoxin family, PRDX2 or PRDX5 and PRDX6, were elevated with 5-FU exposure in either SW480 or SW620, respectively. Fluorouracil 191-195 peroxiredoxin 2 Homo sapiens 146-151 22623418-8 2012 Cell adhesion-associated proteins CTNNB1 and RhoA showed decreased expression with 5-FU treatment in both cell lines. Fluorouracil 83-87 ras homolog family member A Homo sapiens 45-49 22654430-9 2012 Semi-quantitative RT-PCR indicated that 5-FU at the concentration of 5 mumol/L in combination with HHC at the concentration of 25 mumol/L significantly down-regulates COX-2 mRNA expression when compared with values in cells treated with 5-FU or HHC alone (HHC + 5-FU: 31.93% +- 5.69%, 5-FU: 100.66% +- 4.52% vs HHC: 61.01% +- 0.35%, P < 0.05). Fluorouracil 40-44 mitochondrially encoded cytochrome c oxidase II Homo sapiens 167-172 22322462-0 2012 MicroRNA-21-mediated regulation of Sprouty2 protein expression enhances the cytotoxic effect of 5-fluorouracil and metformin in colon cancer cells. Fluorouracil 96-110 sprouty RTK signaling antagonist 2 Homo sapiens 35-43 22441128-4 2012 In the present study, the early therapeutic response of rAd/p53, combined with 5-fluorouracil (5-FU) or with iodized oil, was observed in a human colon cancer model. Fluorouracil 79-93 tumor protein p53 Homo sapiens 60-63 22441128-8 2012 p53 expression reached its peak at 120 h in the rAd/p53 group, at 72 h in the rAd/p53+5-FU group, and at 48 h in the rAd/p53+iodized oil group. Fluorouracil 86-90 tumor protein p53 Homo sapiens 0-3 22441128-10 2012 The KI of the rAd/p53+5-FU group increased significantly at 24 h. 5-FU and iodized oil increase the anticancer effect of rAd/p53, and 5-FU combined with rAd/p53 has a synergistic anticancer effect. Fluorouracil 22-26 tumor protein p53 Homo sapiens 125-128 22441128-10 2012 The KI of the rAd/p53+5-FU group increased significantly at 24 h. 5-FU and iodized oil increase the anticancer effect of rAd/p53, and 5-FU combined with rAd/p53 has a synergistic anticancer effect. Fluorouracil 22-26 tumor protein p53 Homo sapiens 125-128 22441128-10 2012 The KI of the rAd/p53+5-FU group increased significantly at 24 h. 5-FU and iodized oil increase the anticancer effect of rAd/p53, and 5-FU combined with rAd/p53 has a synergistic anticancer effect. Fluorouracil 66-70 tumor protein p53 Homo sapiens 18-21 22441128-10 2012 The KI of the rAd/p53+5-FU group increased significantly at 24 h. 5-FU and iodized oil increase the anticancer effect of rAd/p53, and 5-FU combined with rAd/p53 has a synergistic anticancer effect. Fluorouracil 66-70 tumor protein p53 Homo sapiens 125-128 22441128-10 2012 The KI of the rAd/p53+5-FU group increased significantly at 24 h. 5-FU and iodized oil increase the anticancer effect of rAd/p53, and 5-FU combined with rAd/p53 has a synergistic anticancer effect. Fluorouracil 66-70 tumor protein p53 Homo sapiens 125-128 22441128-10 2012 The KI of the rAd/p53+5-FU group increased significantly at 24 h. 5-FU and iodized oil increase the anticancer effect of rAd/p53, and 5-FU combined with rAd/p53 has a synergistic anticancer effect. Fluorouracil 66-70 tumor protein p53 Homo sapiens 18-21 22441128-10 2012 The KI of the rAd/p53+5-FU group increased significantly at 24 h. 5-FU and iodized oil increase the anticancer effect of rAd/p53, and 5-FU combined with rAd/p53 has a synergistic anticancer effect. Fluorouracil 66-70 tumor protein p53 Homo sapiens 125-128 22441128-10 2012 The KI of the rAd/p53+5-FU group increased significantly at 24 h. 5-FU and iodized oil increase the anticancer effect of rAd/p53, and 5-FU combined with rAd/p53 has a synergistic anticancer effect. Fluorouracil 66-70 tumor protein p53 Homo sapiens 125-128 22403796-7 2012 Furthermore, the 5-FU-mediated upregulation of TNF-alpha, IL-1beta, and NOX1 and the production of reactive oxygen species were significantly attenuated in Nox1KO mice compared with that in WT mice. Fluorouracil 17-21 tumor necrosis factor Mus musculus 47-56 22403796-7 2012 Furthermore, the 5-FU-mediated upregulation of TNF-alpha, IL-1beta, and NOX1 and the production of reactive oxygen species were significantly attenuated in Nox1KO mice compared with that in WT mice. Fluorouracil 17-21 interleukin 1 beta Mus musculus 58-66 21822560-8 2012 CONCLUSION: Neoadjuvant chemotherapy utilizing 5-fluorouracil and cisplatin in esophageal squamous cell carcinoma is useful to induce CD4 and CD8 T lymphocytes in the tumor microenvironment and to maintain HLA class I expression levels in combination with its direct cytotoxic effects. Fluorouracil 47-61 CD4 molecule Homo sapiens 134-137 22322462-3 2012 Expression of Spry2 inhibited the growth of a colon cancer cell line, HCT116, and induced sensitization to fluorouracil (5-FU) and metformin. Fluorouracil 119-131 sprouty RTK signaling antagonist 2 Homo sapiens 14-19 22322462-3 2012 Expression of Spry2 inhibited the growth of a colon cancer cell line, HCT116, and induced sensitization to fluorouracil (5-FU) and metformin. Fluorouracil 145-149 sprouty RTK signaling antagonist 2 Homo sapiens 14-19 22222640-1 2012 Trastuzumab in combination with capecitabine or 5-fluorouracil and cisplatin is approved by the European Medicines Agency for the treatment of patients with human epidermal growth factor receptor 2 (HER2)-positive (immunohistochemistry 3+ or immunohistochemistry 2+/fluorescence in situ hybridization-positive or immunohistochemistry 2+/silver in situ hybridization-positive) metastatic adenocarcinoma of the stomach or gastro-esophageal junction. Fluorouracil 48-62 erb-b2 receptor tyrosine kinase 2 Homo sapiens 163-197 22221825-12 2012 Furthermore, the combination of EGCG and 5-FU abrogated the COX-2 overexpression and PGE(2) secretion induced by 5-FU. Fluorouracil 41-45 prostaglandin-endoperoxide synthase 2 Homo sapiens 60-65 22221825-12 2012 Furthermore, the combination of EGCG and 5-FU abrogated the COX-2 overexpression and PGE(2) secretion induced by 5-FU. Fluorouracil 114-118 prostaglandin-endoperoxide synthase 2 Homo sapiens 60-65 22366766-0 2012 EBP50 gene transfection promotes 5-fluorouracil-induced apoptosis in gastric cancer cells through Bax- and Bcl-2-triggered mitochondrial pathways. Fluorouracil 33-47 BCL2 associated X, apoptosis regulator Homo sapiens 110-113 22366766-0 2012 EBP50 gene transfection promotes 5-fluorouracil-induced apoptosis in gastric cancer cells through Bax- and Bcl-2-triggered mitochondrial pathways. Fluorouracil 33-47 BCL2 apoptosis regulator Homo sapiens 119-124 22353201-9 2012 CONCLUSIONS: A "5-day on/2-day off" low-dose (40 mg twice daily) regimen of S-1 is feasible for the treatment of NSCLC, with acceptable plasma 5-FU concentrations and minimal adverse effects. Fluorouracil 143-147 proteasome 26S subunit, non-ATPase 1 Homo sapiens 76-79 22293713-9 2012 The potentiation effect of combined treatment was associated with downregulation of EGFR and HER2 signaling pathways because data from western blot analysis showed that lapatinib in combination with 5-Fu markedly reduced the phosphorylation of EGFR and HER2, and inhibited the activation of downstream signaling molecules, such as AKT and ERK. Fluorouracil 223-227 epidermal growth factor receptor Homo sapiens 96-100 22293713-9 2012 The potentiation effect of combined treatment was associated with downregulation of EGFR and HER2 signaling pathways because data from western blot analysis showed that lapatinib in combination with 5-Fu markedly reduced the phosphorylation of EGFR and HER2, and inhibited the activation of downstream signaling molecules, such as AKT and ERK. Fluorouracil 223-227 erb-b2 receptor tyrosine kinase 2 Homo sapiens 105-109 22293713-9 2012 The potentiation effect of combined treatment was associated with downregulation of EGFR and HER2 signaling pathways because data from western blot analysis showed that lapatinib in combination with 5-Fu markedly reduced the phosphorylation of EGFR and HER2, and inhibited the activation of downstream signaling molecules, such as AKT and ERK. Fluorouracil 223-227 epidermal growth factor receptor Homo sapiens 280-284 22293713-9 2012 The potentiation effect of combined treatment was associated with downregulation of EGFR and HER2 signaling pathways because data from western blot analysis showed that lapatinib in combination with 5-Fu markedly reduced the phosphorylation of EGFR and HER2, and inhibited the activation of downstream signaling molecules, such as AKT and ERK. Fluorouracil 223-227 erb-b2 receptor tyrosine kinase 2 Homo sapiens 289-293 22293713-9 2012 The potentiation effect of combined treatment was associated with downregulation of EGFR and HER2 signaling pathways because data from western blot analysis showed that lapatinib in combination with 5-Fu markedly reduced the phosphorylation of EGFR and HER2, and inhibited the activation of downstream signaling molecules, such as AKT and ERK. Fluorouracil 223-227 AKT serine/threonine kinase 1 Homo sapiens 379-382 22293713-11 2012 These results indicate that the combination of the lapatinib and 5-Fu is a promising treatment option for esophageal carcinoma with HER2 amplification. Fluorouracil 77-81 erb-b2 receptor tyrosine kinase 2 Homo sapiens 156-160 22322240-1 2012 S-1 is an oral antitumor agent that contains tegafur, which is converted to fluorouracil (5-FU) in the human body. Fluorouracil 88-100 proteasome 26S subunit, non-ATPase 1 Homo sapiens 0-3 22322240-1 2012 S-1 is an oral antitumor agent that contains tegafur, which is converted to fluorouracil (5-FU) in the human body. Fluorouracil 102-106 proteasome 26S subunit, non-ATPase 1 Homo sapiens 0-3 22322320-0 2012 Prognostic significance of p16 in locoregionally advanced head and neck cancer treated with concurrent 5-fluorouracil, hydroxyurea, cetuximab and intensity-modulated radiation therapy. Fluorouracil 115-129 cyclin dependent kinase inhibitor 2A Homo sapiens 27-30 22322320-11 2012 Concurrent 5-FU, HU, cetuximab and SIB-IMRT is a highly active regimen, particularly in patients with p16-positive disease. Fluorouracil 11-15 cyclin dependent kinase inhibitor 2A Homo sapiens 102-105 21947696-0 2012 Prognosis of esophageal squamous cell carcinoma in patients positive for human epidermal growth factor receptor family can be improved by initial chemotherapy with docetaxel, fluorouracil, and cisplatin. Fluorouracil 175-187 epidermal growth factor receptor Homo sapiens 79-111 21706156-0 2012 MDM2 SNP309 and TP53 R72P associated with severe and febrile neutropenia in breast cancer patients treated with 5-FU/epirubicin/cyclophosphamide. Fluorouracil 112-116 tumor protein p53 Homo sapiens 16-20 21706156-1 2012 The aim of this study was to investigate the association of two genetic polymorphisms, MDM2 SNP309 and TP53 R72P, with incidence of neutropenia in breast cancer patients treated with 5-FU/epirubicin/cyclophosphamide (FEC). Fluorouracil 183-187 tumor protein p53 Homo sapiens 103-107 22227409-9 2012 Moreover, Gli3 siRNA sensitized colon cancer cells to treatment with anti-cancer agents (5-FU and bevacizumab). Fluorouracil 89-93 GLI family zinc finger 3 Homo sapiens 10-14 22139134-9 2012 The combination of 5FU and cetuximab synergistically inhibited cell proliferation and exhibited an enhanced proapoptotic effect in GC cells with EGFR overexpression. Fluorouracil 19-22 epidermal growth factor receptor Homo sapiens 145-149 22308296-3 2012 Deletion of Cited2 using Mx1-Cre resulted in increased hematopoietic stem cell (HSC) apoptosis, loss of quiescence, and increased cycling, leading to a severely impaired reconstitution capacity as assessed by 5-fluorouracil treatment and long-term transplantation. Fluorouracil 209-223 Cbp/p300-interacting transactivator, with Glu/Asp-rich carboxy-terminal domain, 2 Mus musculus 12-18 22265575-3 2012 After 54 passages, treatments with 5-FU and gemcitabine reduced virus infectivity, p24 and RT activity. Fluorouracil 35-39 transmembrane p24 trafficking protein 2 Homo sapiens 83-86 23422737-10 2012 HM781-36B combined with 5-fluorouracil, cisplatin, paclitaxel, or gemcitabine showed a synergistic inhibitory effect on the HER2-amplified and on some of the HER2-nonamplified breast cancer cells. Fluorouracil 24-38 erb-b2 receptor tyrosine kinase 2 Homo sapiens 124-128 23422737-10 2012 HM781-36B combined with 5-fluorouracil, cisplatin, paclitaxel, or gemcitabine showed a synergistic inhibitory effect on the HER2-amplified and on some of the HER2-nonamplified breast cancer cells. Fluorouracil 24-38 erb-b2 receptor tyrosine kinase 2 Homo sapiens 158-162 22188649-0 2012 ATR-Chk1 signaling pathway and homologous recombinational repair protect cells from 5-fluorouracil cytotoxicity. Fluorouracil 84-98 opsin, green sensitive (rhodopsin-like) Gallus gallus 4-8 22188649-6 2012 Inhibition of Chk1 kinase by UCN-01 increased 5-FU-induced gammaH2AX and enhanced 5-FU cytotoxicity not only in wild-type cells but also in Rad54- or BRCA2-deficient cells, suggesting that HRR and Chk1 kinase have non-overlapping roles in 5-FU tolerance. Fluorouracil 46-50 opsin, green sensitive (rhodopsin-like) Gallus gallus 14-18 22188649-6 2012 Inhibition of Chk1 kinase by UCN-01 increased 5-FU-induced gammaH2AX and enhanced 5-FU cytotoxicity not only in wild-type cells but also in Rad54- or BRCA2-deficient cells, suggesting that HRR and Chk1 kinase have non-overlapping roles in 5-FU tolerance. Fluorouracil 46-50 opsin, green sensitive (rhodopsin-like) Gallus gallus 197-201 22189143-8 2012 Finally, Gal-3-targeted conjugates significantly improved the anti-tumor activity of 5-Fu in nude mice bearing PC-3 tumor xenografts. Fluorouracil 85-89 lectin, galactose binding, soluble 3 Mus musculus 9-14 22188649-6 2012 Inhibition of Chk1 kinase by UCN-01 increased 5-FU-induced gammaH2AX and enhanced 5-FU cytotoxicity not only in wild-type cells but also in Rad54- or BRCA2-deficient cells, suggesting that HRR and Chk1 kinase have non-overlapping roles in 5-FU tolerance. Fluorouracil 82-86 opsin, green sensitive (rhodopsin-like) Gallus gallus 14-18 22244588-0 2012 Synthesis and biological evaluation of conjugates of deoxypodophyllotoxin and 5-FU as inducer of caspase-3 and -7. Fluorouracil 78-82 caspase 3 Homo sapiens 97-113 22188649-6 2012 Inhibition of Chk1 kinase by UCN-01 increased 5-FU-induced gammaH2AX and enhanced 5-FU cytotoxicity not only in wild-type cells but also in Rad54- or BRCA2-deficient cells, suggesting that HRR and Chk1 kinase have non-overlapping roles in 5-FU tolerance. Fluorouracil 82-86 opsin, green sensitive (rhodopsin-like) Gallus gallus 14-18 22188649-7 2012 5-FU-induced Chk1 phosphorylation was significantly impaired in Rad9- or Rad17-deficient cells, and severe gammaH2AX nuclear foci and DSBs were formed, which was followed by apoptosis. Fluorouracil 0-4 opsin, green sensitive (rhodopsin-like) Gallus gallus 13-17 22188649-8 2012 Finally, inhibition of Chk1 kinase by UCN-01 increased 5-FU-induced gammaH2AX nuclear foci and enhanced 5-FU cytotoxicity in Rad9- or Rad17-deficient cells. Fluorouracil 55-59 opsin, green sensitive (rhodopsin-like) Gallus gallus 23-27 22188649-8 2012 Finally, inhibition of Chk1 kinase by UCN-01 increased 5-FU-induced gammaH2AX nuclear foci and enhanced 5-FU cytotoxicity in Rad9- or Rad17-deficient cells. Fluorouracil 104-108 opsin, green sensitive (rhodopsin-like) Gallus gallus 23-27 22188649-9 2012 These results suggest that Rad9- and Rad17-independent activation of the ATR-Chk1 signaling pathway also significantly contributes to 5-FU tolerance. Fluorouracil 134-138 opsin, green sensitive (rhodopsin-like) Gallus gallus 77-81 22235991-4 2012 Furthermore, the alternate-day S-1 administration can reduce the GI toxicities and myelotoxicities of 5-FU without reducing its anticancer efficacy, enabling patients to continue the oral administration for 6 - 12 months. Fluorouracil 102-106 proteasome 26S subunit, non-ATPase 1 Homo sapiens 31-34 22235991-5 2012 EXPERT OPINION: Replacement of regimens with infusional 5-FU and other fluoropyrimidines by the alternate-day S-1 administration may be recommended because the latter procedure is efficient for patients while sustaining the enhanced anticancer efficacy of 5-FU and without reducing its dose intensity. Fluorouracil 256-260 proteasome 26S subunit, non-ATPase 1 Homo sapiens 110-113 22291191-5 2012 Administration of these 5-FU-resistant CD11b(-)CD45(-) MSCs 6 d after myelin oligodendrocyte glycoprotein (MOG) immunization completely remitted MOG-induced experimental autoimmune encephalomyelitis after initial development of mild disease. Fluorouracil 24-28 integrin alpha M Mus musculus 39-44 22969929-0 2012 Tanshinone IIA potentiates the efficacy of 5-FU in Colo205 colon cancer cells in vivo through downregulation of P-gp and LC3-II. Fluorouracil 43-47 ATP binding cassette subfamily B member 1 Homo sapiens 112-116 22969929-8 2012 Our results showed that the Colo205 xenograft model co-treated with Tan-IIA plus 5-FU caused a reduction in the xenograft tumor volumes and decreased P-glycoprotein (P-gp) and microtubule-associated protein light chain 3 (LC3)-II expression compared to 5-FU alone. Fluorouracil 81-85 ATP binding cassette subfamily B member 1 Homo sapiens 150-164 22969929-8 2012 Our results showed that the Colo205 xenograft model co-treated with Tan-IIA plus 5-FU caused a reduction in the xenograft tumor volumes and decreased P-glycoprotein (P-gp) and microtubule-associated protein light chain 3 (LC3)-II expression compared to 5-FU alone. Fluorouracil 81-85 ATP binding cassette subfamily B member 1 Homo sapiens 166-170 22291191-11 2012 Together, our findings suggested that immunosuppression by 5-FU-MSC is mediated by a combination of elevated IL-1ra, IL-10, and PGE(2), anti-inflammatory Th2 cytokines, and decreased IL-17. Fluorouracil 59-63 interleukin 10 Mus musculus 117-122 22265744-6 2012 Furthermore, CDy::UPRT-MSCs were significantly more sensitive to 5-fluorouracil (5FU), cisplatin, cyclophosphamide and cytosine arabinoside as determined by increased Caspase 3/7 activation and/or decreased relative proliferation. Fluorouracil 65-79 chromodomain Y-linked 1B Homo sapiens 13-16 21841826-5 2012 Activation of p38MAPK by 5-FU was dependent on canonical MAP2K, MAPK kinase (MKK)-3 and MKK6. Fluorouracil 25-29 mitogen-activated protein kinase kinase 6 Homo sapiens 88-92 22226896-1 2012 The binding of anticancer drugs (i) Uracil (U), (ii) 5-Fluorouracil (5FU) and (iii) 5-Chlorouracil (5ClU), to bovine serum albumin (BSA) at two levels of temperature was studied by the fluorescence of quenching method. Fluorouracil 53-67 albumin Homo sapiens 117-130 22265744-6 2012 Furthermore, CDy::UPRT-MSCs were significantly more sensitive to 5-fluorouracil (5FU), cisplatin, cyclophosphamide and cytosine arabinoside as determined by increased Caspase 3/7 activation and/or decreased relative proliferation. Fluorouracil 65-79 caspase 3 Homo sapiens 167-176 22265744-6 2012 Furthermore, CDy::UPRT-MSCs were significantly more sensitive to 5-fluorouracil (5FU), cisplatin, cyclophosphamide and cytosine arabinoside as determined by increased Caspase 3/7 activation and/or decreased relative proliferation. Fluorouracil 81-84 chromodomain Y-linked 1B Homo sapiens 13-16 22265744-6 2012 Furthermore, CDy::UPRT-MSCs were significantly more sensitive to 5-fluorouracil (5FU), cisplatin, cyclophosphamide and cytosine arabinoside as determined by increased Caspase 3/7 activation and/or decreased relative proliferation. Fluorouracil 81-84 caspase 3 Homo sapiens 167-176 22265744-7 2012 CDy::UPRT-MSCs in direct cocultures with breast cancer cells MDA-MB-231 increased tumor cell killing induced by low concentrations of 5FU. Fluorouracil 134-137 chromodomain Y-linked 1B Homo sapiens 0-3 22309939-15 2012 Finally, whereas paclitaxel, doxorubicin, and 5-fluorouracil enriched the CD44high/CD24-/low population compared with control in SUM149, subsequent treatment with BI 2536 killed the emergent population, suggesting that it could potentially be used to prevent relapse. Fluorouracil 46-60 CD24 molecule Homo sapiens 83-87 22205702-8 2012 Knockdown of STAT3 dramatically enhanced chemosensitivity of CRC cells to fluorouracil. Fluorouracil 74-86 signal transducer and activator of transcription 3 Homo sapiens 13-18 22416214-5 2012 We found that the fraction of ABCG2-positive(+) cells was significantly increased by treatment with both 5-FU and MTX in NSCLC cells, and the elevation of abcg2, il-6r and cd133 expressions in response to these drugs was also confirmed using RT-PCR. Fluorouracil 105-109 ATP binding cassette subfamily G member 2 (Junior blood group) Homo sapiens 30-35 22154421-0 2012 Interaction of 5-Fluorouracil and its derivatives with bovine serum albumin. Fluorouracil 15-29 albumin Homo sapiens 62-75 22416214-6 2012 Also, the number of IL-6R(+) cells was increased by MTX in the 3 cell lines mentioned and increased by 5-FU in the H460 cell line. Fluorouracil 103-107 interleukin 6 receptor Homo sapiens 20-25 22192357-0 2012 14-3-3sigma regulation by p53 mediates a chemotherapy response to 5-fluorouracil in MCF-7 breast cancer cells via Akt inactivation. Fluorouracil 66-80 tumor protein p53 Homo sapiens 26-29 22192357-0 2012 14-3-3sigma regulation by p53 mediates a chemotherapy response to 5-fluorouracil in MCF-7 breast cancer cells via Akt inactivation. Fluorouracil 66-80 AKT serine/threonine kinase 1 Homo sapiens 114-117 22192357-5 2012 Meanwhile, initial treatments with high concentrations of 5-Fu clearly induced 14-3-3sigma and p53 expression in a time-dependent manner. Fluorouracil 58-62 tumor protein p53 Homo sapiens 95-98 22166209-0 2012 Chemoresistance to 5-fluorouracil induces epithelial-mesenchymal transition via up-regulation of Snail in MCF7 human breast cancer cells. Fluorouracil 19-33 snail family transcriptional repressor 1 Homo sapiens 97-102 21351099-1 2012 S-1 is a recently developed dihydropyrimidine dehydrogenase inhibitor fluoropyrimidine and has demonstrated high maximum plasma 5-Fluorouracil (5-FU) levels with mild toxicity, and an oral formulation has resulted in an improvement in patient quality of life. Fluorouracil 128-142 proteasome 26S subunit, non-ATPase 1 Homo sapiens 0-3 21351099-1 2012 S-1 is a recently developed dihydropyrimidine dehydrogenase inhibitor fluoropyrimidine and has demonstrated high maximum plasma 5-Fluorouracil (5-FU) levels with mild toxicity, and an oral formulation has resulted in an improvement in patient quality of life. Fluorouracil 144-148 proteasome 26S subunit, non-ATPase 1 Homo sapiens 0-3 22186294-4 2012 5-FU was used to investigate whether knockdown NF-kappaB p65 can potentiate 5-FU"s antitumor effect. Fluorouracil 0-4 nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105 Mus musculus 47-56 22186294-4 2012 5-FU was used to investigate whether knockdown NF-kappaB p65 can potentiate 5-FU"s antitumor effect. Fluorouracil 76-80 nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105 Mus musculus 47-56 22206670-5 2012 Moreover, we found that TQ enhanced the 5-FU-induced killing of gastric cancer cells by mediating the downregulation of the anti-apoptotic protein bcl-2, the upregulation of the pro-apoptotic protein bax, and the activation of both caspase-3 and caspase-9. Fluorouracil 40-44 BCL2 apoptosis regulator Homo sapiens 147-152 22166209-7 2012 We also showed that inhibition of Snail increased the sensitivity of 5-FU-resistant cells to 5-FU. Fluorouracil 69-73 snail family transcriptional repressor 1 Homo sapiens 34-39 22206670-5 2012 Moreover, we found that TQ enhanced the 5-FU-induced killing of gastric cancer cells by mediating the downregulation of the anti-apoptotic protein bcl-2, the upregulation of the pro-apoptotic protein bax, and the activation of both caspase-3 and caspase-9. Fluorouracil 40-44 BCL2 associated X, apoptosis regulator Homo sapiens 200-203 22206670-5 2012 Moreover, we found that TQ enhanced the 5-FU-induced killing of gastric cancer cells by mediating the downregulation of the anti-apoptotic protein bcl-2, the upregulation of the pro-apoptotic protein bax, and the activation of both caspase-3 and caspase-9. Fluorouracil 40-44 caspase 3 Homo sapiens 232-241 22186294-7 2012 Overall, our work indicates that downregulation of p65 can increase tumor apoptosis and potentiates the effects of 5-FU by suppressing NF-kappaB signaling pathway. Fluorouracil 115-119 nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105 Mus musculus 135-144 22166209-7 2012 We also showed that inhibition of Snail increased the sensitivity of 5-FU-resistant cells to 5-FU. Fluorouracil 93-97 snail family transcriptional repressor 1 Homo sapiens 34-39 22206670-7 2012 These data suggest that the TQ/5-FU combined treatment induces apoptosis by enhancing the activation of both caspase-3 and caspase-9 in gastric cancer cells. Fluorouracil 31-35 caspase 3 Homo sapiens 109-118 22166209-9 2012 We believed that down-regulation of Snail could be a potential novel therapeutic approach to overcoming chemoresistance and preventing metastasis during 5-FU chemotherapy. Fluorouracil 153-157 snail family transcriptional repressor 1 Homo sapiens 36-41 22206670-8 2012 These results, which provide molecular evidence both in vitro and in vivo, support our conclusion that thymoquinone can activate caspase-3 and caspase-9 and thus result in the chemosensitisation of gastric cancer cells to 5-FU-induced cell death. Fluorouracil 222-226 caspase 3 Homo sapiens 129-138 21713761-9 2012 In addition, FBI-1 could inhibit cell death induced by 5-fluorouracil or doxorubicin through suppressing the activation of p53. Fluorouracil 55-69 tumor protein p53 Homo sapiens 123-126 22213289-6 2012 In p53-null cells, the combination of low dose 5-FU with up to 6 muM quercetin promoted clonogenic survival. Fluorouracil 47-51 tumor protein p53 Homo sapiens 3-6 22213289-6 2012 In p53-null cells, the combination of low dose 5-FU with up to 6 muM quercetin promoted clonogenic survival. Fluorouracil 47-51 latexin Homo sapiens 65-68 22525470-9 2012 The differential responses to 5-FU between these cell lines appeared to be due to the difference in the TP53 gene status, thus providing a molecular basis for the bioassays using these cell lines in the toxicology field. Fluorouracil 30-34 tumor protein p53 Homo sapiens 104-108 22525470-10 2012 Our results indicate that the clinical efficacy of 5-FU chemotherapy may depend on the TP53 genotype. Fluorouracil 51-55 tumor protein p53 Homo sapiens 87-91 23167424-13 2012 P-glycoprotein (P-gp) might play a limited role in the MDR of BEL-7402/5-FU. Fluorouracil 71-75 ATP binding cassette subfamily B member 1 Homo sapiens 0-14 23167424-13 2012 P-glycoprotein (P-gp) might play a limited role in the MDR of BEL-7402/5-FU. Fluorouracil 71-75 ATP binding cassette subfamily B member 1 Homo sapiens 16-20 22336586-0 2012 Pharmacologic synergy between dual phosphoinositide-3-kinase and mammalian target of rapamycin inhibition and 5-fluorouracil in PIK3CA mutant gastric cancer cells. Fluorouracil 110-124 phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha Homo sapiens 128-134 22336586-2 2012 Here, we tested the hypothesis that the dual PI3K/mTOR inhibitor, PI103, could synergize with the chemotherapeutic agent, 5-fluorouracil (5-FU) by inhibiting E2F1, thymidylate synthase (TS) and enhancing DNA damage. Fluorouracil 138-142 mechanistic target of rapamycin kinase Homo sapiens 50-54 22336586-10 2012 Inhibition of PI3K and mTOR alone enhanced 5-FU cytotoxicity in only 2/3 cell lines that displayed synergy each. Fluorouracil 43-47 mechanistic target of rapamycin kinase Homo sapiens 23-27 23295255-4 2012 The aim of this study was to evaluate the prognostic significance of serum VEGF and IGF-1 levels in advanced gastric cancer patients who were treated with oxaliplatin/5-fluorouracil (FOLFOX). Fluorouracil 167-181 vascular endothelial growth factor A Homo sapiens 75-79 22336586-14 2012 PI3K/mTOR inhibitors can enhance 5-FU cytotoxicity in vitro and in vivo, especially in PIK3CA mutant tumor cells. Fluorouracil 33-37 mechanistic target of rapamycin kinase Homo sapiens 5-9 22336586-14 2012 PI3K/mTOR inhibitors can enhance 5-FU cytotoxicity in vitro and in vivo, especially in PIK3CA mutant tumor cells. Fluorouracil 33-37 phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha Homo sapiens 87-93 22336586-15 2012 Dual, rather than single, PI3K/mTOR inhibitors may combine better with 5-FU due to cellular heterogeneity in sensitivity to PI3K and mTOR inhibition. Fluorouracil 71-75 mechanistic target of rapamycin kinase Homo sapiens 133-137 22632387-2 2012 In this study, the effect of locally applied 5-FU on cell death was evaluated both in a SCC4/HEK001 model and in a newly proposed 3D outgrowth model of oral squamous cell carcinoma (OSCC). Fluorouracil 45-49 MAU2 sister chromatid cohesion factor Homo sapiens 88-92 23481572-8 2012 While 5-florouracil did not inhibit the VEGF secretion of HT-29 cell line, irinotecan, oxaliplatin, docetaxel and paclitaxel significantly decreased the levels of secreted VEGF. Fluorouracil 6-19 vascular endothelial growth factor A Homo sapiens 172-176 23549021-2 2012 In this study, PR81-conjugated bovine serum albumin (BSA) nanoparticles loaded with anticancer drug 5-fluorouracil (5-FU) were developed. Fluorouracil 100-114 albumin Homo sapiens 38-51 23155356-0 2012 VEGF -634C/G genotype is predictive of long-term survival after treatment with a definitive 5-fluorouracil/cisplatin-based chemoradiotherapy in Japanese patients with esophageal squamous cell carcinoma. Fluorouracil 92-106 vascular endothelial growth factor A Homo sapiens 0-4 23155356-12 2012 CONCLUSIONS: VEGF -634C/G is possibly predictive of long-term survival after treatment with a definitive 5-FU/CDDP-based CRT. Fluorouracil 105-109 vascular endothelial growth factor A Homo sapiens 13-17 23549021-2 2012 In this study, PR81-conjugated bovine serum albumin (BSA) nanoparticles loaded with anticancer drug 5-fluorouracil (5-FU) were developed. Fluorouracil 116-120 albumin Homo sapiens 38-51 22531515-0 2012 Overexpression of interferon regulatory factor 1 enhances chemosensitivity to 5-fluorouracil in gastric cancer cells. Fluorouracil 78-92 interferon regulatory factor 1 Homo sapiens 18-48 22531515-6 2012 Compared with control cells, the growth inhibition rate of cells with IRF-1 overexpression was significantly increased when treated with 5-FU (P<0.01). Fluorouracil 137-141 interferon regulatory factor 1 Homo sapiens 70-75 22531515-9 2012 CONCLUSIONS: Overexpression of IRF-1 enhanced the chemosensitivity of gastric cancer cells to 5-FU through induction of apoptosis. Fluorouracil 94-98 interferon regulatory factor 1 Homo sapiens 31-36 22027693-0 2012 A systems biology approach identifies SART1 as a novel determinant of both 5-fluorouracil and SN38 drug resistance in colorectal cancer. Fluorouracil 75-89 spliceosome associated factor 1, recruiter of U4/U6.U5 tri-snRNP Homo sapiens 38-43 22002472-5 2012 Treatment with Tan-IIA 30 mg/-kg or with 30 mg/-kg of 5-FU resulted in a reduction in tumor size and weight compared with the control group. Fluorouracil 54-58 ATPase, class II, type 9A Mus musculus 19-22 22002472-6 2012 The protein expression of Bax and caspase-3 in the J5 xenograft tumors treated with Tan-IIA 30 mg/-kg or with 30 mg/kg of 5-FU was upregulated, whereas that of CD31 was downregulated compared with the control group. Fluorouracil 122-126 BCL2 associated X, apoptosis regulator Homo sapiens 26-29 22002472-6 2012 The protein expression of Bax and caspase-3 in the J5 xenograft tumors treated with Tan-IIA 30 mg/-kg or with 30 mg/kg of 5-FU was upregulated, whereas that of CD31 was downregulated compared with the control group. Fluorouracil 122-126 caspase 3 Homo sapiens 34-43 22027693-6 2012 Silencing SART1 sensitized all 5 cell lines to 5-FU treatment and 4/5 cell lines to SN38 treatment. Fluorouracil 47-51 spliceosome associated factor 1, recruiter of U4/U6.U5 tri-snRNP Homo sapiens 10-15 21910008-9 2011 Treating cells with PP2 and 5-FU resulted in reduced interaction of Par-4 with Akt1 and with the scaffolding protein 14-3-3sigma, and mobilization of Par-4 to the nucleus. Fluorouracil 28-32 AKT serine/threonine kinase 1 Homo sapiens 79-83 22740861-1 2012 Irinotecan hydrochloride (CPT-11) is reported to be involved in the downregulation of thymidylate synthase (TS), a target molecule of 5-fluorouracil (5-FU) and oral fluoropyrimidine S-1. Fluorouracil 134-148 proteasome 26S subunit, non-ATPase 1 Homo sapiens 182-185 23238479-2 2012 The beta-ureidopropionase (BUP1) enzyme catalyzes the final step in the 5-FU catabolic pathway; however, alterations in the UPB1 gene coding for the BUP1 enzyme have not yet been analyzed in fluoropyrimidine (FP)-treated patients suffering from 5-FU-related toxicity. Fluorouracil 72-76 beta-ureidopropionase 1 Homo sapiens 4-25 23238479-2 2012 The beta-ureidopropionase (BUP1) enzyme catalyzes the final step in the 5-FU catabolic pathway; however, alterations in the UPB1 gene coding for the BUP1 enzyme have not yet been analyzed in fluoropyrimidine (FP)-treated patients suffering from 5-FU-related toxicity. Fluorouracil 72-76 beta-ureidopropionase 1 Homo sapiens 27-31 23238479-2 2012 The beta-ureidopropionase (BUP1) enzyme catalyzes the final step in the 5-FU catabolic pathway; however, alterations in the UPB1 gene coding for the BUP1 enzyme have not yet been analyzed in fluoropyrimidine (FP)-treated patients suffering from 5-FU-related toxicity. Fluorouracil 72-76 beta-ureidopropionase 1 Homo sapiens 124-128 23238479-2 2012 The beta-ureidopropionase (BUP1) enzyme catalyzes the final step in the 5-FU catabolic pathway; however, alterations in the UPB1 gene coding for the BUP1 enzyme have not yet been analyzed in fluoropyrimidine (FP)-treated patients suffering from 5-FU-related toxicity. Fluorouracil 72-76 beta-ureidopropionase 1 Homo sapiens 149-153 23238479-2 2012 The beta-ureidopropionase (BUP1) enzyme catalyzes the final step in the 5-FU catabolic pathway; however, alterations in the UPB1 gene coding for the BUP1 enzyme have not yet been analyzed in fluoropyrimidine (FP)-treated patients suffering from 5-FU-related toxicity. Fluorouracil 245-249 beta-ureidopropionase 1 Homo sapiens 4-25 23238479-2 2012 The beta-ureidopropionase (BUP1) enzyme catalyzes the final step in the 5-FU catabolic pathway; however, alterations in the UPB1 gene coding for the BUP1 enzyme have not yet been analyzed in fluoropyrimidine (FP)-treated patients suffering from 5-FU-related toxicity. Fluorouracil 245-249 beta-ureidopropionase 1 Homo sapiens 27-31 23238479-2 2012 The beta-ureidopropionase (BUP1) enzyme catalyzes the final step in the 5-FU catabolic pathway; however, alterations in the UPB1 gene coding for the BUP1 enzyme have not yet been analyzed in fluoropyrimidine (FP)-treated patients suffering from 5-FU-related toxicity. Fluorouracil 245-249 beta-ureidopropionase 1 Homo sapiens 124-128 23238479-2 2012 The beta-ureidopropionase (BUP1) enzyme catalyzes the final step in the 5-FU catabolic pathway; however, alterations in the UPB1 gene coding for the BUP1 enzyme have not yet been analyzed in fluoropyrimidine (FP)-treated patients suffering from 5-FU-related toxicity. Fluorouracil 245-249 beta-ureidopropionase 1 Homo sapiens 149-153 23238479-6 2012 An analysis of UPB1 variants on 5-FU-related toxicity in the population of all analyzed patients revealed an association between the c.-80C>G (rs2070474) variant and gastrointestinal toxicity. Fluorouracil 32-36 beta-ureidopropionase 1 Homo sapiens 15-19 23238479-8 2012 CONCLUSION: Our results suggest that UPB1 variants may contribute to the development of 5-FU-related toxicity in some FP-treated patients; however, the role of UPB1 alterations is probably less significant than that of DPYD alterations. Fluorouracil 88-92 beta-ureidopropionase 1 Homo sapiens 37-41 22927913-10 2012 Viability of both XB130-silenced SGC7901 cells and wild-type cells was suppressed by 5-fluorouracil (5-FU), cisplatin, and irinotecan in a dose-dependent way, but cisplatin and irinotecan were more sensitive against sXB130-silenced GC cells and 5-FU showed higher sensitivity to wild-type cells. Fluorouracil 85-99 actin filament associated protein 1 like 2 Homo sapiens 18-23 22927913-10 2012 Viability of both XB130-silenced SGC7901 cells and wild-type cells was suppressed by 5-fluorouracil (5-FU), cisplatin, and irinotecan in a dose-dependent way, but cisplatin and irinotecan were more sensitive against sXB130-silenced GC cells and 5-FU showed higher sensitivity to wild-type cells. Fluorouracil 101-105 actin filament associated protein 1 like 2 Homo sapiens 18-23 22927913-10 2012 Viability of both XB130-silenced SGC7901 cells and wild-type cells was suppressed by 5-fluorouracil (5-FU), cisplatin, and irinotecan in a dose-dependent way, but cisplatin and irinotecan were more sensitive against sXB130-silenced GC cells and 5-FU showed higher sensitivity to wild-type cells. Fluorouracil 245-249 actin filament associated protein 1 like 2 Homo sapiens 18-23 22927913-11 2012 When treated by 5-FU, patients with high expression of XB130 tumors had a higher survival rate than those with low expression tumors. Fluorouracil 16-20 actin filament associated protein 1 like 2 Homo sapiens 55-60 22905237-6 2012 Baseline expression of these proteins using gastric cancer cell lines demonstrated the reciprocal patterns between NF-kappaB and JNK, while 5-FU exposure of these cell lines only induced NF-kappaB, suggesting that NF-kappaB plays a dominant role in the response to 5-FU. Fluorouracil 140-144 nuclear factor kappa B subunit 1 Homo sapiens 187-196 22905237-6 2012 Baseline expression of these proteins using gastric cancer cell lines demonstrated the reciprocal patterns between NF-kappaB and JNK, while 5-FU exposure of these cell lines only induced NF-kappaB, suggesting that NF-kappaB plays a dominant role in the response to 5-FU. Fluorouracil 140-144 nuclear factor kappa B subunit 1 Homo sapiens 187-196 21947305-0 2012 miRNA-195 sensitizes human hepatocellular carcinoma cells to 5-FU by targeting BCL-w. Fluorouracil 61-65 microRNA 195 Homo sapiens 0-9 22590561-4 2012 RESULTS: Administration of 5-FU but not pemetrexed potentiated CXCL8 secretion and increased CXCR1 and CXCR2 gene expression in metastatic PC3 cells. Fluorouracil 27-31 C-X-C motif chemokine ligand 8 Homo sapiens 63-68 22590561-5 2012 Consistent with this, the inhibition of CXCL8 signaling using a CXCR2 antagonist, AZ10397767, increased the cytotoxicity of 5-FU by 4-fold (P<0.001), and increased 5-FU-induced apoptosis in PC3 cells (P<0.01). Fluorouracil 124-128 C-X-C motif chemokine ligand 8 Homo sapiens 40-45 22590561-5 2012 Consistent with this, the inhibition of CXCL8 signaling using a CXCR2 antagonist, AZ10397767, increased the cytotoxicity of 5-FU by 4-fold (P<0.001), and increased 5-FU-induced apoptosis in PC3 cells (P<0.01). Fluorouracil 167-171 C-X-C motif chemokine ligand 8 Homo sapiens 40-45 22590561-8 2012 Moreover, siRNA-mediated knockdown of the CXCL8-target gene Bcl-2 increased the sensitivity of PC3 cells to 5-FU. Fluorouracil 108-112 C-X-C motif chemokine ligand 8 Homo sapiens 42-47 22590561-8 2012 Moreover, siRNA-mediated knockdown of the CXCL8-target gene Bcl-2 increased the sensitivity of PC3 cells to 5-FU. Fluorouracil 108-112 BCL2 apoptosis regulator Homo sapiens 60-65 22412841-0 2012 5-Fluorouracil induced intestinal mucositis via nuclear factor-kappaB activation by transcriptomic analysis and in vivo bioluminescence imaging. Fluorouracil 0-14 nuclear factor kappa B subunit 1 Homo sapiens 48-69 22412841-6 2012 Our data showed that 5-FU induced inflammation in the small intestine, characterized by the increased intestinal wall thickness and crypt length, the decreased villus height, and the increased myeloperoxidase activity in tissues and proinflammatory cytokine production in sera. Fluorouracil 21-25 myeloperoxidase Homo sapiens 193-208 22412841-7 2012 Network analysis of 5-FU-affected genes by transcriptomic tool showed that the expression of genes was regulated by nuclear factor-kappaB (NF-kappaB), and NF-kappaB was the central molecule in the 5-FU-regulated biological network. Fluorouracil 20-24 nuclear factor kappa B subunit 1 Homo sapiens 116-137 22412841-7 2012 Network analysis of 5-FU-affected genes by transcriptomic tool showed that the expression of genes was regulated by nuclear factor-kappaB (NF-kappaB), and NF-kappaB was the central molecule in the 5-FU-regulated biological network. Fluorouracil 20-24 nuclear factor kappa B subunit 1 Homo sapiens 139-148 22412841-7 2012 Network analysis of 5-FU-affected genes by transcriptomic tool showed that the expression of genes was regulated by nuclear factor-kappaB (NF-kappaB), and NF-kappaB was the central molecule in the 5-FU-regulated biological network. Fluorouracil 20-24 nuclear factor kappa B subunit 1 Homo sapiens 155-164 22412841-7 2012 Network analysis of 5-FU-affected genes by transcriptomic tool showed that the expression of genes was regulated by nuclear factor-kappaB (NF-kappaB), and NF-kappaB was the central molecule in the 5-FU-regulated biological network. Fluorouracil 197-201 nuclear factor kappa B subunit 1 Homo sapiens 116-137 22412841-7 2012 Network analysis of 5-FU-affected genes by transcriptomic tool showed that the expression of genes was regulated by nuclear factor-kappaB (NF-kappaB), and NF-kappaB was the central molecule in the 5-FU-regulated biological network. Fluorouracil 197-201 nuclear factor kappa B subunit 1 Homo sapiens 139-148 22412841-7 2012 Network analysis of 5-FU-affected genes by transcriptomic tool showed that the expression of genes was regulated by nuclear factor-kappaB (NF-kappaB), and NF-kappaB was the central molecule in the 5-FU-regulated biological network. Fluorouracil 197-201 nuclear factor kappa B subunit 1 Homo sapiens 155-164 22412841-8 2012 NF-kappaB activity was activated by 5-FU in the intestine, which was judged by in vivo bioluminescence imaging and immunohistochemical staining. Fluorouracil 36-40 nuclear factor kappa B subunit 1 Homo sapiens 0-9 22412841-9 2012 However, 5-aminosalicylic acid (5-ASA) inhibited 5-FU-induced NF-kappaB activation and proinflammatory cytokine production. Fluorouracil 49-53 nuclear factor kappa B subunit 1 Homo sapiens 62-71 22412841-11 2012 In conclusion, our findings suggested that NF-kappaB was the critical molecule associated with the pathogenesis of 5-FU-induced mucositis, and inhibition of NF-kappaB activity ameliorated the mucosal damage caused by 5-FU. Fluorouracil 115-119 nuclear factor kappa B subunit 1 Homo sapiens 43-52 22412841-11 2012 In conclusion, our findings suggested that NF-kappaB was the critical molecule associated with the pathogenesis of 5-FU-induced mucositis, and inhibition of NF-kappaB activity ameliorated the mucosal damage caused by 5-FU. Fluorouracil 217-221 nuclear factor kappa B subunit 1 Homo sapiens 157-166 21910008-13 2011 The activation of the pro-apoptotic protein Par-4 as reported in this study is a novel mechanism by which apoptosis occurs with a Src kinase inhibitor and 5-FU. Fluorouracil 155-159 SRC proto-oncogene, non-receptor tyrosine kinase Homo sapiens 130-133 21479885-0 2011 Quercetin enhances 5-fluorouracil-induced apoptosis in MSI colorectal cancer cells through p53 modulation. Fluorouracil 19-33 tumor protein p53 Homo sapiens 91-94 21479885-6 2011 RESULTS: CO115 p53-wt cells are more sensitive to 5-FU than the p53-mutated HCT15. Fluorouracil 50-54 tumor protein p53 Homo sapiens 15-18 20734163-11 2011 In the hepatocellular carcinoma cell line, Hep G2, insulin rather than glucose was more important for promoting cell proliferation and enhancing the drug resistance of cisplatin or fluorouracil. Fluorouracil 181-193 insulin Homo sapiens 51-58 21903448-3 2011 We demonstrated that down-regulation of MRP1 in MC3/5FU, a drug-resistant MEC cell line, by RNA interference increased the drug sensitivity of the cells to 5-fluorouracil, doxorubicin, pharmorubicin, bleomycin-A5, cis-platinum and taxol. Fluorouracil 156-170 ATP binding cassette subfamily C member 1 Homo sapiens 40-44 21374737-1 2011 We have previously reported that activation of the G protein coupled calcium-sensing receptor (CaSR) by extracellular Ca(2+) down-modulates the expression of thymidylate synthase (TS) and survivin and promotes sensitivity to fluorouracil in human colon carcinoma cells. Fluorouracil 225-237 calcium sensing receptor Homo sapiens 95-99 21374737-6 2011 siRNAs targeting TS or survivin or both could mimic the effect of CaSR activation in promoting sensitivity to 5-FU. Fluorouracil 110-114 calcium sensing receptor Homo sapiens 66-70 21801281-0 2011 Combination treatment with fulvestrant and various cytotoxic agents (doxorubicin, paclitaxel, docetaxel, vinorelbine, and 5-fluorouracil) has a synergistic effect in estrogen receptor-positive breast cancer. Fluorouracil 122-136 estrogen receptor 1 Homo sapiens 166-183 22384554-11 2011 RESULTS: Compared with the model control group, the tumor volume was markedly reduced in the small, medium, large dose RKY groups, and the medium dose RKY +5-FU group, the expressions of VEGF-C and VEGFR-3 were significantly down-regulated and LMVD were obviously lowered, showing statistical difference (P < 0.05, P < 0.01). Fluorouracil 156-160 vascular endothelial growth factor C Mus musculus 187-193 22312705-0 2011 MiR-122 increases sensitivity of drug-resistant BEL-7402/5-FU cells to 5-fluorouracil via down-regulation of bcl-2 family proteins. Fluorouracil 71-85 BCL2 apoptosis regulator Homo sapiens 109-114 22312705-7 2011 Accordingly, P53 protein expression showed a significant up-regulation; MTT results showed that after incubation with 5-FU, miR-122 transfectants had higher cell inhibitory rates than negative miRNA or untreated cells; flow cytometry results demonstrated that apoptosis rate increased in miR-122 transfected cells, compared with negative miRNA or untreated cells. Fluorouracil 118-122 tumor protein p53 Homo sapiens 13-16 22312705-9 2011 MiR-122 can specifically down-regulate the expression of Bcl-2 and Bcl-XL, and increase P53 activity in BEL-7402/5-FU cells, which increased cells spontaneous apoptosis and sensitize cells to 5-FU. Fluorouracil 113-117 tumor protein p53 Homo sapiens 88-91 21718388-9 2011 Notably, 5-fluorouracil-based chemotherapy conferred significant survival benefit to patients with tumors negative for Nr-CAM overexpression but not to those with Nr-CAM overexpressed tumors. Fluorouracil 9-23 neuronal cell adhesion molecule Homo sapiens 119-125 21878904-2 2011 However, 5-FU resistance, mainly caused by the overexpression of antiapoptotic proteins such as Bcl-2, often leads ultimately to treatment failure. Fluorouracil 9-13 BCL2 apoptosis regulator Homo sapiens 96-101 21878904-3 2011 We here investigated the effect of Bcl-2 gene silencing, using small interfering RNA (siRNA) (siBcl-2), on the efficacy of 5-FU in CRC. Fluorouracil 123-127 BCL2 apoptosis regulator Homo sapiens 35-40 21878904-4 2011 Transfection of siBcl-2 by a Lipofectamine2000/siRNA lipoplex effectively downregulated Bcl-2 expression in the DLD-1 cell line (a CRC), resulting in significant cell growth inhibition in vitro upon treatment with 5-FU. Fluorouracil 214-218 BCL2 apoptosis regulator Homo sapiens 18-23 21718388-11 2011 Nr-CAM overexpression is an independent marker of poor prognosis among advanced CRC patients, and is a possible predictive marker for non-beneficence to 5-fluorouracil- based chemotherapy. Fluorouracil 153-167 neuronal cell adhesion molecule Homo sapiens 0-6 21807902-8 2011 Interestingly, treatment of cells with the ribosomal stress-inducing agent actinomycin D or 5-fluorouracil significantly decreased the c-myc mRNA levels in an L11- and Ago2-dependent manner. Fluorouracil 92-106 argonaute RISC catalytic component 2 Homo sapiens 168-172 21745813-0 2011 UNG-initiated base excision repair is the major repair route for 5-fluorouracil in DNA, but 5-fluorouracil cytotoxicity depends mainly on RNA incorporation. Fluorouracil 65-79 uracil DNA glycosylase Homo sapiens 0-3 21745813-0 2011 UNG-initiated base excision repair is the major repair route for 5-fluorouracil in DNA, but 5-fluorouracil cytotoxicity depends mainly on RNA incorporation. Fluorouracil 92-106 uracil DNA glycosylase Homo sapiens 0-3 21342712-1 2011 OBJECTIVE: The aim of this study was to evaluate the efficacy and toxicity of a novel oral 5-fluorouracil formulation (S-1) as second-line therapy after platinum agent chemotherapy for advanced non-small cell lung cancer (NSCLC). Fluorouracil 91-105 proteasome 26S subunit, non-ATPase 1 Homo sapiens 119-122 21710497-5 2011 Ad-FZ33 expressing uracil phosphoribosyl transferase (UPRT), an enzyme which greatly enhances the toxicity of 5-fluorouracil (FU), combined with antibodies against EpCAM or EGFR, remarkably enhanced the sensitivity of biliary cancer cells to 5-FU. Fluorouracil 242-246 epithelial cell adhesion molecule Homo sapiens 164-169 22006582-7 2011 Furthermore, Matrigel assays indicated that low concentrations of propranolol (10 - 50 muM) potentiated the anti-angiogenic effects of 5-FU and paclitaxel. Fluorouracil 135-139 latexin Homo sapiens 87-90 21572321-0 2011 Predictive values of 5-fluorouracil pathway genes for S-1 treatment in patients with advanced gastric cancer. Fluorouracil 21-35 proteasome 26S subunit, non-ATPase 1 Homo sapiens 54-57 21572321-2 2011 We investigated the mRNA expression of 5-fluorouracil (5-FU) pathway genes in prechemotherapeutic tumor samples of primary gastric cancer to try to predict the treatment outcome of S-1 monotherapy. Fluorouracil 39-53 proteasome 26S subunit, non-ATPase 1 Homo sapiens 181-184 21572321-2 2011 We investigated the mRNA expression of 5-fluorouracil (5-FU) pathway genes in prechemotherapeutic tumor samples of primary gastric cancer to try to predict the treatment outcome of S-1 monotherapy. Fluorouracil 55-59 proteasome 26S subunit, non-ATPase 1 Homo sapiens 181-184 21153821-9 2011 RESULTS: 5-FU treatment decreased the duodenal villus height/crypt depth ratio, increased MPO activity, and increased the concentration of TNF-alpha, IL-1beta and KC in comparison with saline-treated animals. Fluorouracil 9-13 tumor necrosis factor Mus musculus 139-148 21153821-9 2011 RESULTS: 5-FU treatment decreased the duodenal villus height/crypt depth ratio, increased MPO activity, and increased the concentration of TNF-alpha, IL-1beta and KC in comparison with saline-treated animals. Fluorouracil 9-13 interleukin 1 beta Mus musculus 150-158 21868535-6 2011 RESULTS: Selective COX-2 inhibitor, etodolac, sensitized UM-SCC-23F/R cells to 5-FU. Fluorouracil 79-83 prostaglandin-endoperoxide synthase 2 Homo sapiens 19-24 21710497-5 2011 Ad-FZ33 expressing uracil phosphoribosyl transferase (UPRT), an enzyme which greatly enhances the toxicity of 5-fluorouracil (FU), combined with antibodies against EpCAM or EGFR, remarkably enhanced the sensitivity of biliary cancer cells to 5-FU. Fluorouracil 242-246 epidermal growth factor receptor Homo sapiens 173-177 21931533-3 2011 Cd81(-/-) HSCs showed a marked engraftment defect when transplanted into secondary recipient mice and a significantly delayed return to quiescence when stimulated to proliferate with 5-fluorouracil (5FU). Fluorouracil 183-197 CD81 antigen Mus musculus 0-4 21674128-0 2011 DNA damage signaling in response to 5-fluorouracil in three colorectal cancer cell lines with different mismatch repair and TP53 status. Fluorouracil 36-50 tumor protein p53 Homo sapiens 124-128 21674128-3 2011 The pattern of DNA damage checkpoint activation in bolus 5-FU-treated HT29 (TP53-deficient/MMR-proficient) cultures suggested SSB formation (CHEK1 activation) followed by DSB formation (CHEK2 activation and increased phospho-H2AX levels), but no cell death suggested that DNA repair capacity was not overwhelmed. Fluorouracil 57-61 tumor protein p53 Homo sapiens 76-80 21674128-3 2011 The pattern of DNA damage checkpoint activation in bolus 5-FU-treated HT29 (TP53-deficient/MMR-proficient) cultures suggested SSB formation (CHEK1 activation) followed by DSB formation (CHEK2 activation and increased phospho-H2AX levels), but no cell death suggested that DNA repair capacity was not overwhelmed. Fluorouracil 57-61 checkpoint kinase 1 Homo sapiens 141-146 21674128-4 2011 High-dose 5-FU treatment led to activation of ATM/CHEK2/TP53 (not CHEK1) in TP53-proficient and TP53-depleted HCT116 (later CHEK2 activation relative to TP53-proficient) cultures; HCT15 cultures had ATM activation only. Fluorouracil 10-14 tumor protein p53 Homo sapiens 56-60 21674128-4 2011 High-dose 5-FU treatment led to activation of ATM/CHEK2/TP53 (not CHEK1) in TP53-proficient and TP53-depleted HCT116 (later CHEK2 activation relative to TP53-proficient) cultures; HCT15 cultures had ATM activation only. Fluorouracil 10-14 tumor protein p53 Homo sapiens 76-80 21674128-4 2011 High-dose 5-FU treatment led to activation of ATM/CHEK2/TP53 (not CHEK1) in TP53-proficient and TP53-depleted HCT116 (later CHEK2 activation relative to TP53-proficient) cultures; HCT15 cultures had ATM activation only. Fluorouracil 10-14 tumor protein p53 Homo sapiens 76-80 21674128-4 2011 High-dose 5-FU treatment led to activation of ATM/CHEK2/TP53 (not CHEK1) in TP53-proficient and TP53-depleted HCT116 (later CHEK2 activation relative to TP53-proficient) cultures; HCT15 cultures had ATM activation only. Fluorouracil 10-14 tumor protein p53 Homo sapiens 76-80 21674128-6 2011 TP53-depleted HCT116 cultures also had DSBs after high-dose 5-FU treatment but experienced a (transient) G1/S cell cycle arrest that protected them from apoptosis. Fluorouracil 60-64 tumor protein p53 Homo sapiens 0-4 21674128-8 2011 Overall, activation of ATM, CHEK1 and/or CHEK2 and phospho-H2AX levels reflected the nature of 5-FU-induced DNA damage and indi-cated when DNA damage was significant (5-FU-dose-dependent). Fluorouracil 95-99 checkpoint kinase 1 Homo sapiens 28-33 21674128-9 2011 DNA repair and cell cycle responses to 5-FU-induced DNA damage were distinctly affected by MMR and TP53 (role in BER/NER) functionalities, but MMR deficiency especially seemed to confer less overall sensitivity to 5-FU. Fluorouracil 39-43 tumor protein p53 Homo sapiens 99-103 21617867-6 2011 ESCCs with activated NF-kappaB had poor sensitivity to 5-FU. Fluorouracil 55-59 nuclear factor kappa B subunit 1 Homo sapiens 21-30 21617867-8 2011 Transcriptional activity of NF-kappaB was significantly suppressed in cells treated with 5-FU and NF-kappaB siRNA compared to cells treated with 5-FU alone. Fluorouracil 89-93 nuclear factor kappa B subunit 1 Homo sapiens 28-37 21617867-8 2011 Transcriptional activity of NF-kappaB was significantly suppressed in cells treated with 5-FU and NF-kappaB siRNA compared to cells treated with 5-FU alone. Fluorouracil 145-149 nuclear factor kappa B subunit 1 Homo sapiens 28-37 21617867-8 2011 Transcriptional activity of NF-kappaB was significantly suppressed in cells treated with 5-FU and NF-kappaB siRNA compared to cells treated with 5-FU alone. Fluorouracil 145-149 nuclear factor kappa B subunit 1 Homo sapiens 98-107 21931533-3 2011 Cd81(-/-) HSCs showed a marked engraftment defect when transplanted into secondary recipient mice and a significantly delayed return to quiescence when stimulated to proliferate with 5-fluorouracil (5FU). Fluorouracil 199-202 CD81 antigen Mus musculus 0-4 21712253-6 2011 Furthermore, we found that HER2 overexpression led to an increased resistance of MCF7 cells to multiple antitumor drugs such as paclitaxel (Taxol), cisplatin (DDP), etoposide (VP-16), adriamycin (ADM), mitoxantrone (MX), and 5-fluorouracil (5-FU). Fluorouracil 225-239 erb-b2 receptor tyrosine kinase 2 Homo sapiens 27-31 21514041-0 2011 Gene expression signature of TP53 but not its mutation status predicts response to sequential paclitaxel and 5-FU/epirubicin/cyclophosphamide in human breast cancer. Fluorouracil 109-113 tumor protein p53 Homo sapiens 29-33 21945777-1 2011 OBJECTIVE: To investigate the effects of lentivirus-mediated RNA interference (RNAi) targeting a proliferation-inducing ligand (APRIL) on the chemosensitivity to 5-FU of colorectal cancer cell line LoVo. Fluorouracil 162-166 TNF superfamily member 13 Homo sapiens 95-126 21945777-1 2011 OBJECTIVE: To investigate the effects of lentivirus-mediated RNA interference (RNAi) targeting a proliferation-inducing ligand (APRIL) on the chemosensitivity to 5-FU of colorectal cancer cell line LoVo. Fluorouracil 162-166 TNF superfamily member 13 Homo sapiens 128-133 21945777-11 2011 CONCLUSION: Lentivirus-mediated RNAi targeting APRIL can effectively suppress the expression of APRIL in LoVo cells and enhance the chemosensitivity of the cells to 5-FU. Fluorouracil 165-169 TNF superfamily member 13 Homo sapiens 47-52 21969819-6 2011 Short hairpin RNA-mediated down-regulation of NRF2 in ESC cells that harbor only mutated Nrf2 allele revealed that themutant NRF2 conferred increased cell proliferation, attachment-independent survival, and resistance to 5-fluorouracil and gamma-irradiation. Fluorouracil 221-235 NFE2 like bZIP transcription factor 2 Homo sapiens 89-93 21969819-6 2011 Short hairpin RNA-mediated down-regulation of NRF2 in ESC cells that harbor only mutated Nrf2 allele revealed that themutant NRF2 conferred increased cell proliferation, attachment-independent survival, and resistance to 5-fluorouracil and gamma-irradiation. Fluorouracil 221-235 NFE2 like bZIP transcription factor 2 Homo sapiens 125-129 21712253-6 2011 Furthermore, we found that HER2 overexpression led to an increased resistance of MCF7 cells to multiple antitumor drugs such as paclitaxel (Taxol), cisplatin (DDP), etoposide (VP-16), adriamycin (ADM), mitoxantrone (MX), and 5-fluorouracil (5-FU). Fluorouracil 241-245 erb-b2 receptor tyrosine kinase 2 Homo sapiens 27-31 21690569-0 2011 Enhancement of 5-fluorouracil-induced in vitro and in vivo radiosensitization with MEK inhibition. Fluorouracil 15-29 mitogen-activated protein kinase kinase 7 Homo sapiens 83-86 21555362-0 2011 VEGF gene polymorphisms may be associated with an increased risk of fluorouracil-induced diarrhea. Fluorouracil 68-80 vascular endothelial growth factor A Homo sapiens 0-4 21079960-2 2011 S-1 has been developed as a novel oral antineoplastic agent based on the modulation of 5-fluorouracil (5-FU) bioactivity. Fluorouracil 87-101 proteasome 26S subunit, non-ATPase 1 Homo sapiens 0-3 21079960-2 2011 S-1 has been developed as a novel oral antineoplastic agent based on the modulation of 5-fluorouracil (5-FU) bioactivity. Fluorouracil 103-107 proteasome 26S subunit, non-ATPase 1 Homo sapiens 0-3 21673602-1 2011 INTRODUCTION: S-1 is a rationally designed oral agent that combines the 5-fluorouracil prodrug tegafur with gimeracil and oteracil, which inhibit 5-fluorouracil degradation by dihydropyrimidine dehydronase and phosphorylation within the gastrointestinal tract, respectively, to increase antineoplastic activity while reducing gastrointestinal toxicity. Fluorouracil 72-86 proteasome 26S subunit, non-ATPase 1 Homo sapiens 14-17 22066110-0 2011 Up-regulation of cyclooxygenase-2-derived prostaglandin E(2) in colon cancer cells resistant to 5-fluorouracil. Fluorouracil 96-110 prostaglandin-endoperoxide synthase 2 Homo sapiens 17-33 22066110-3 2011 However, little is known about the role of COX-2 in acquired resistance to 5-FU in colon cancer. Fluorouracil 75-79 mitochondrially encoded cytochrome c oxidase II Homo sapiens 43-48 22066110-4 2011 METHODS: Hence we investigated whether COX-2 contribute to acquired resistance to 5-FU in colon cancer cells, using cytotoxicity assay for cell survival, reverse transcription-polymerase chain reaction (RT-PCR) for vascular endothelial growth factor (VEGF), quantitative RT-PCR for COX-1 and COX-2, and enzyme-linked immunosorbent assay for PGE(2). Fluorouracil 82-86 mitochondrially encoded cytochrome c oxidase II Homo sapiens 39-44 22066110-5 2011 RESULTS: The 5-FU resistant colon cancer cells, SNU-C5/5FUR, showed increased expression of COX-2, prostaglandin E(2) (PGE(2)), and VEGF, compared to its parental cell (SNU-C5). Fluorouracil 13-17 mitochondrially encoded cytochrome c oxidase II Homo sapiens 92-97 22066110-5 2011 RESULTS: The 5-FU resistant colon cancer cells, SNU-C5/5FUR, showed increased expression of COX-2, prostaglandin E(2) (PGE(2)), and VEGF, compared to its parental cell (SNU-C5). Fluorouracil 13-17 vascular endothelial growth factor A Homo sapiens 132-136 22066110-7 2011 CONCLUSION: These results demonstrate that COX-2 derived PGE(2) is up-regulated and COX-2 inhibitor may have an anti-angiogenic effect in the colon cancer cells resistant to 5-FU. Fluorouracil 174-178 mitochondrially encoded cytochrome c oxidase II Homo sapiens 43-48 22066110-7 2011 CONCLUSION: These results demonstrate that COX-2 derived PGE(2) is up-regulated and COX-2 inhibitor may have an anti-angiogenic effect in the colon cancer cells resistant to 5-FU. Fluorouracil 174-178 mitochondrially encoded cytochrome c oxidase II Homo sapiens 84-89 21828290-3 2011 T-DNA insertions in UKL1 and UKL2 reduced transcript expression and increased plant tolerance to toxic analogs 5-fluorouridine and 5-fluorouracil. Fluorouracil 131-145 uridine kinase/uracil phosphoribosyltransferase 1 Arabidopsis thaliana 20-24 21673602-1 2011 INTRODUCTION: S-1 is a rationally designed oral agent that combines the 5-fluorouracil prodrug tegafur with gimeracil and oteracil, which inhibit 5-fluorouracil degradation by dihydropyrimidine dehydronase and phosphorylation within the gastrointestinal tract, respectively, to increase antineoplastic activity while reducing gastrointestinal toxicity. Fluorouracil 146-160 proteasome 26S subunit, non-ATPase 1 Homo sapiens 14-17 20844880-6 2011 The expression of IL-1beta induced by 5-FU in local intestinal tissue was examined by RT-PCR and immunohistochemistry. Fluorouracil 38-42 interleukin 1 beta Mus musculus 18-26 21709442-4 2011 DR5, Fas, Bax, Bad, Puma and Bnip3L were induced by 5-FU and adriamycin (ADR) in HCT116 cells in a p53-dependent manner. Fluorouracil 52-56 tumor protein p53 Homo sapiens 99-102 21613406-2 2011 These agents cause imbalances in deoxynucleotide triphosphate levels and the accumulation of uracil and 5-FU in the genome, events that activate the ATR- and ATM-dependent checkpoint signaling pathways and the base excision repair (BER) pathway. Fluorouracil 104-108 ATR serine/threonine kinase Homo sapiens 149-152 21613406-6 2011 Consistent with a role for the BER pathway, the poly(ADP-ribose) polymerase (PARP) inhibitors ABT-888 (veliparib) and AZD2281 (olaparib) markedly synergized with FdUrd but not with 5-FU in ovarian cancer cell lines. Fluorouracil 181-185 poly(ADP-ribose) polymerase 1 Homo sapiens 48-75 21613406-6 2011 Consistent with a role for the BER pathway, the poly(ADP-ribose) polymerase (PARP) inhibitors ABT-888 (veliparib) and AZD2281 (olaparib) markedly synergized with FdUrd but not with 5-FU in ovarian cancer cell lines. Fluorouracil 181-185 poly(ADP-ribose) polymerase 1 Homo sapiens 77-81 21613406-8 2011 These findings underscore differences in the cytotoxic mechanisms of 5-FU and FdUrd and suggest that combining FdUrd and PARP inhibitors may be an innovative therapeutic strategy for ovarian tumors. Fluorouracil 69-73 poly(ADP-ribose) polymerase 1 Homo sapiens 121-125 20844880-12 2011 RESULTS: The variation of IL-1beta expression induced by 5-FU was in accordance with the changes in intestinal apoptosis. Fluorouracil 57-61 interleukin 1 beta Mus musculus 26-34 20844880-18 2011 CONCLUSIONS: Our studies elucidate that IL-1beta is quite possibly involved in and mediated the course of intestinal apoptosis after 5-FU chemotherapy. Fluorouracil 133-137 interleukin 1 beta Mus musculus 40-48 21568934-4 2011 The elimination of MDSC by 5-FU increased IFNgamma secretion by tumor specific CD8(+) T cells infiltrating the tumor and promoted T-cell dependent antitumor responses in vivo, suggesting that some anticancer therapies can reverse tumor-mediated immunosuppression. Fluorouracil 27-31 interferon gamma Homo sapiens 42-50 21424124-11 2011 Western blotting data revealed that SB203580 sensitises cancer cells to 5-FU due to an increase in Bax expression. Fluorouracil 72-76 BCL2 associated X, apoptosis regulator Homo sapiens 99-102 21375586-9 2011 Caspase-3 activation was significantly lower in the co-treated group than in the group treated with 5-FU alone. Fluorouracil 100-104 caspase 3 Homo sapiens 0-9 21375586-10 2011 In addition, ghrelin reversed the 5-FU-induced Bcl-2/Bax protein ratio. Fluorouracil 34-38 BCL2 apoptosis regulator Homo sapiens 47-52 21375586-10 2011 In addition, ghrelin reversed the 5-FU-induced Bcl-2/Bax protein ratio. Fluorouracil 34-38 BCL2 associated X, apoptosis regulator Homo sapiens 53-56 21375586-11 2011 CONCLUSION: Ghrelin inhibits 5-FU-induced apoptosis in colon cancer cells through the regulation of the Bcl-2/Bax protein ratio. Fluorouracil 29-33 BCL2 apoptosis regulator Homo sapiens 104-109 21375586-11 2011 CONCLUSION: Ghrelin inhibits 5-FU-induced apoptosis in colon cancer cells through the regulation of the Bcl-2/Bax protein ratio. Fluorouracil 29-33 BCL2 associated X, apoptosis regulator Homo sapiens 110-113 20714726-1 2011 PURPOSE: To evaluate the efficacy, safety and pharmacokinetic profiles of S-1, which composed of tegafur (FT, a prodrug of 5-FU), 5-chloro-2,4-dihydroxypyridine and potassium oxonate (Oxo), in Taiwanese advanced gastric cancer (AGC) patients. Fluorouracil 123-127 proteasome 26S subunit, non-ATPase 1 Homo sapiens 74-77 21561866-5 2011 Knockdown of S27a significantly attenuates the p53 activation in cells in response to treatment with ribosomal stress-inducing agent actinomycin D or 5-fluorouracil. Fluorouracil 150-164 tumor protein p53 Homo sapiens 47-50 21444628-8 2011 Combined treatment with 5-FU could decrease cisplatin-induced ERK1/2 activation and the induction of TS and TP, which subsequently resulted in synergistic cytotoxic effects. Fluorouracil 24-28 mitogen-activated protein kinase 3 Homo sapiens 62-68 21444628-9 2011 Enforced expression of constitutive active MKK1/2 vectors rescued the protein levels of phospho-ERK1/2, TS, and TP, and the cell viability that were decreased by cisplatin and 5-FU combination. Fluorouracil 176-180 mitogen-activated protein kinase 3 Homo sapiens 96-102 21737644-8 2011 On 5-FU treatment, phosphorylation of Akt and Erk1/2 was suppressed in CT26/NK4 less than in mock-transfected cells. Fluorouracil 3-7 thymoma viral proto-oncogene 1 Mus musculus 38-41 21513489-6 2011 The insulin-induced resistance to cycloheximide and 5-fluorouracil can be used in drug screening to overcome the inefficacy of chemotherapy in obesity-associated colon cancer. Fluorouracil 52-66 insulin Homo sapiens 4-11 21651859-9 2011 CONCLUSION: The siRNA expression vector can active inhibit expression of STAT3 gene in SMMC7721 cells, enhance its sensitivity to chemotherapeutics 5-Fu, to provide experiment based on for the biological therapy of tumor. Fluorouracil 148-152 signal transducer and activator of transcription 3 Homo sapiens 73-78 21455575-4 2011 Furthermore, 5-FU inhibited the phosphorylation of Akt and p70 S6K, while the knockdown of IGFBP3 reduced the levels of poly (ADP-ribose) polymerase cleaved by 5-FU in PC3 cells. Fluorouracil 13-17 AKT serine/threonine kinase 1 Homo sapiens 51-54 21455575-5 2011 Therefore, the up-regulation of IGFBP3 by 5-FU not only inhibits cell growth by reducing the IGF1 signal but also induces apoptosis in PC3 cells. Fluorouracil 42-46 insulin like growth factor 1 Homo sapiens 93-97 21317879-9 2011 Disruption of CASR expression in CASR-unmethylated HCT-8 cells blocked the enhancing effect of Ca2+ on the cytotoxic response to 5-fluorouracil. Fluorouracil 129-143 calcium sensing receptor Homo sapiens 33-37 21317879-9 2011 Disruption of CASR expression in CASR-unmethylated HCT-8 cells blocked the enhancing effect of Ca2+ on the cytotoxic response to 5-fluorouracil. Fluorouracil 129-143 calcium sensing receptor Homo sapiens 14-18 21619678-0 2011 A predicted protein, KIAA0247, is a cell cycle modulator in colorectal cancer cells under 5-FU treatment. Fluorouracil 90-94 sushi domain containing 6 Homo sapiens 21-29 21619678-10 2011 Immunofluorescent staining revealed that the cytoplasm of CRC cells evenly expresses KIAA0247 without 5-FU treatment, and KIAA0247 accumulates in the nucleus after 40 muM 5-FU treatment. Fluorouracil 171-175 sushi domain containing 6 Homo sapiens 122-130 21619678-11 2011 In HCT116 p53(-/-) cells, which lack p53 cell cycle control, the proportion of cells in the G2/M phase was larger (13%) in KIAA0247-silent cells than in the respective shLuc control (10%) and KIAA0247-overexpressing cells (7%) after the addition of low dose (40 muM) 5-FU. Fluorouracil 267-271 sushi domain containing 6 Homo sapiens 123-131 21354366-5 2011 Furthermore, the IC(50) of DOX and epirubicin (EPI) in HepG2 cells, both of which are known to be exported by MDR1, were higher in spheroid compared with monolayer cells, while IC(50) of 5-fluorouracil (5-FU), which is not exported by MDR1 protein, was almost the same in both types of culture. Fluorouracil 203-207 ATP binding cassette subfamily B member 1 Homo sapiens 110-114 21566434-6 2011 Here, we investigated whether blood DAO activity can be a biomarker for the gastrointestinal (GI) mucosal disorder caused by 5-FU anti-cancer drugs, both in rats and humans. Fluorouracil 125-129 D-amino-acid oxidase Rattus norvegicus 36-39 21566434-7 2011 From results of the rat study, the degree of jejunal mucosal disorder caused by the 5-FU anti-cancer drug was well correlated with a decrease in blood DAO activity. Fluorouracil 84-88 D-amino-acid oxidase Rattus norvegicus 151-154 21354366-5 2011 Furthermore, the IC(50) of DOX and epirubicin (EPI) in HepG2 cells, both of which are known to be exported by MDR1, were higher in spheroid compared with monolayer cells, while IC(50) of 5-fluorouracil (5-FU), which is not exported by MDR1 protein, was almost the same in both types of culture. Fluorouracil 187-201 ATP binding cassette subfamily B member 1 Homo sapiens 110-114 24367220-0 2011 Type 1 interferon receptor in peripheral blood mononuclear cells may predict response to intra-arterial 5-fluorouracil + interferon therapy for advanced hepatocellular carcinoma. Fluorouracil 104-118 interferon alpha 1 Homo sapiens 7-17 21522149-0 2011 Co-overexpression of Bag-1 and heat shock protein 70 in human epidermal squamous cell carcinoma: Bag-1-mediated resistance to 5-fluorouracil-induced apoptosis. Fluorouracil 126-140 BAG cochaperone 1 Homo sapiens 21-26 21522149-0 2011 Co-overexpression of Bag-1 and heat shock protein 70 in human epidermal squamous cell carcinoma: Bag-1-mediated resistance to 5-fluorouracil-induced apoptosis. Fluorouracil 126-140 BAG cochaperone 1 Homo sapiens 97-102 21522149-6 2011 Bag-1 knockdown resulted in markedly reduced SCC-13 cell yield, increased spontaneous apoptosis and enhanced sensitivity to 5-FU-induced apoptosis. Fluorouracil 124-128 BAG cochaperone 1 Homo sapiens 0-5 24367220-1 2011 BACKGROUND: Type 1 interferon alpha receptor 2 (IFNAR2) in the liver has been reported to be a predictive factor for the response to intra-arterial 5-fluorouracil (5-FU) + systemic interferon (IFN)-alpha combination therapy in patients with advanced hepatocellular carcinoma. Fluorouracil 148-162 interferon alpha 1 Homo sapiens 19-29 21522149-7 2011 Apoptosis induced by 5-FU in the Bag-1-knockdown cells was significantly greater than the additive apoptotic effect of 5-FU or Bag-1 knockdown alone. Fluorouracil 21-25 BAG cochaperone 1 Homo sapiens 33-38 21522149-7 2011 Apoptosis induced by 5-FU in the Bag-1-knockdown cells was significantly greater than the additive apoptotic effect of 5-FU or Bag-1 knockdown alone. Fluorouracil 119-123 BAG cochaperone 1 Homo sapiens 33-38 24367220-1 2011 BACKGROUND: Type 1 interferon alpha receptor 2 (IFNAR2) in the liver has been reported to be a predictive factor for the response to intra-arterial 5-fluorouracil (5-FU) + systemic interferon (IFN)-alpha combination therapy in patients with advanced hepatocellular carcinoma. Fluorouracil 148-162 interferon alpha 1 Homo sapiens 181-203 24367220-1 2011 BACKGROUND: Type 1 interferon alpha receptor 2 (IFNAR2) in the liver has been reported to be a predictive factor for the response to intra-arterial 5-fluorouracil (5-FU) + systemic interferon (IFN)-alpha combination therapy in patients with advanced hepatocellular carcinoma. Fluorouracil 164-168 interferon alpha 1 Homo sapiens 19-29 24367220-2 2011 We tested whether IFNAR2 expression in peripheral blood mononuclear cells could predict the response to 5-FU + IFN. Fluorouracil 104-108 interferon alpha 1 Homo sapiens 18-21 24367220-10 2011 CONCLUSION: IFNAR2 expression in peripheral blood mononuclear cells may predict the response to 5-FU + IFN therapy in patients with advanced hepatocellular carcinoma, although these data are preliminary. Fluorouracil 96-100 interferon alpha 1 Homo sapiens 12-15 21037557-8 2011 However, such sensitization was not achieved in vivo as treatment of mixed HT29/TRAIL-MSC xenografts with 5-FU rather resulted in enhanced growth. Fluorouracil 106-110 TNF superfamily member 10 Homo sapiens 80-85 21544729-7 2011 Immunofluorescence assay and Western blot showed that 5-FU induced the expression of EBV-lytic genes including BZLF1, BRLF1, BMRF1 and BHRF1. Fluorouracil 54-58 apoptosis regulator BHRF1 Human gammaherpesvirus 4 135-140 21289297-0 2011 The incorporation of 5-fluorouracil into RNA affects the ribonucleolytic activity of the exosome subunit Rrp6. Fluorouracil 21-35 exosome component 10 Homo sapiens 105-109 21161336-3 2011 The current study examines whether difluorinated-curcumin (CDF), a novel analog of the dietary ingredient of curcumin, in combination with 5-fluorouracil and oxaliplatin (5-FU + Ox), the mainstay of colon cancer chemotherapeutic, would be effective in eliminating colon CSCs. Fluorouracil 139-153 interleukin 6 Homo sapiens 59-62 20863677-9 2011 Since the antiproliferative action of micromolar bisabololoxide A on cancerous cells was expected to be beneficial to cancer treatment, the modification of antiproliferative action of 5-fluorouracil (3-30 muM) by bisabololoxide A was studied. Fluorouracil 184-198 latexin Homo sapiens 205-208 21057529-4 2011 Loss of VEGF also increased the in vitro sensitivity of cells to the cytotoxic effects of the chemotherapeutic drug 5-fluorouracil, as shown by increased apoptosis (P<0.05). Fluorouracil 116-130 vascular endothelial growth factor A Homo sapiens 8-12 21243325-8 2011 This suggested that OH-flutamide enhanced the growth-inhibitory activity of 5-FU in CDX25R cells by reducing TS expression through the AR pathway. Fluorouracil 76-80 androgen receptor Homo sapiens 135-137 21480341-9 2011 5-FU inhibited CD90+ proliferating CSCs, some of which produce CD13+ semiquiescent CSCs, while CD13 inhibition suppressed the self-renewing and tumor-initiating ability of dormant CSCs. Fluorouracil 0-4 thymus cell antigen 1, theta Mus musculus 15-19 21369800-9 2011 Expression of p21(WAF1) in colorectal tumor cells identifies a subgroup of Astler-Coller stage B2 patients who could benefit significantly from 5FU-based chemotherapy and may improve the selection of patients for adjuvant chemotherapy. Fluorouracil 144-147 cyclin dependent kinase inhibitor 1A Homo sapiens 14-17 21369800-9 2011 Expression of p21(WAF1) in colorectal tumor cells identifies a subgroup of Astler-Coller stage B2 patients who could benefit significantly from 5FU-based chemotherapy and may improve the selection of patients for adjuvant chemotherapy. Fluorouracil 144-147 cyclin dependent kinase inhibitor 1A Homo sapiens 18-22 21205083-1 2011 We previously reported that mitochondrial transcription factor A (mtTFA) preferentially recognizes cisplatin-damaged DNA via physical interaction with p53 and is upregulated by treatment with cisplatin and fluorouracil (5-FU). Fluorouracil 206-218 transcription factor A, mitochondrial Homo sapiens 28-64 21205083-1 2011 We previously reported that mitochondrial transcription factor A (mtTFA) preferentially recognizes cisplatin-damaged DNA via physical interaction with p53 and is upregulated by treatment with cisplatin and fluorouracil (5-FU). Fluorouracil 206-218 transcription factor A, mitochondrial Homo sapiens 66-71 21205083-1 2011 We previously reported that mitochondrial transcription factor A (mtTFA) preferentially recognizes cisplatin-damaged DNA via physical interaction with p53 and is upregulated by treatment with cisplatin and fluorouracil (5-FU). Fluorouracil 206-218 tumor protein p53 Homo sapiens 151-154 21205083-1 2011 We previously reported that mitochondrial transcription factor A (mtTFA) preferentially recognizes cisplatin-damaged DNA via physical interaction with p53 and is upregulated by treatment with cisplatin and fluorouracil (5-FU). Fluorouracil 220-224 transcription factor A, mitochondrial Homo sapiens 28-64 21205083-1 2011 We previously reported that mitochondrial transcription factor A (mtTFA) preferentially recognizes cisplatin-damaged DNA via physical interaction with p53 and is upregulated by treatment with cisplatin and fluorouracil (5-FU). Fluorouracil 220-224 transcription factor A, mitochondrial Homo sapiens 66-71 21205083-2 2011 The aim of the present study was to evaluate whether expression of mtTFA predicts the clinical outcome in patients with metastatic colorectal cancer treated with modified 5-fluorouracil, leucovorin and oxaliplatin 6 (mFOLFOX6). Fluorouracil 171-185 transcription factor A, mitochondrial Homo sapiens 67-72 21449674-4 2011 RESULTS: Of the 24 genes analyzed, 13 produced significant changes on the phenotype of sensitivity to 5-FU (DHFR, DPYS, DTYMK, DUT, FPGS, GGH, NME1, NT5C, RRM1, TYMS, UCK2, UNG and UMPS). Fluorouracil 102-106 dihydropyrimidinase Homo sapiens 114-118 21449674-4 2011 RESULTS: Of the 24 genes analyzed, 13 produced significant changes on the phenotype of sensitivity to 5-FU (DHFR, DPYS, DTYMK, DUT, FPGS, GGH, NME1, NT5C, RRM1, TYMS, UCK2, UNG and UMPS). Fluorouracil 102-106 deoxythymidylate kinase Homo sapiens 120-125 21449674-4 2011 RESULTS: Of the 24 genes analyzed, 13 produced significant changes on the phenotype of sensitivity to 5-FU (DHFR, DPYS, DTYMK, DUT, FPGS, GGH, NME1, NT5C, RRM1, TYMS, UCK2, UNG and UMPS). Fluorouracil 102-106 uridine-cytidine kinase 2 Homo sapiens 167-171 21449674-4 2011 RESULTS: Of the 24 genes analyzed, 13 produced significant changes on the phenotype of sensitivity to 5-FU (DHFR, DPYS, DTYMK, DUT, FPGS, GGH, NME1, NT5C, RRM1, TYMS, UCK2, UNG and UMPS). Fluorouracil 102-106 uracil DNA glycosylase Homo sapiens 173-176 20811948-2 2011 We previously reported the efficacy of interferon-alpha and 5-fluorouracil combination (IFN/5-FU) therapy for these patients and the potential mechanism via the regulation of vascular endothelial growth factor (VEGF). Fluorouracil 60-74 vascular endothelial growth factor A Homo sapiens 175-209 21487460-0 2011 Transient effectiveness of an oral 5-Fluorouracil derivative, s-1, for epirubicin, cyclophosphamide and Paclitaxel refractory skin metastases from possible occult breast cancer in a male. Fluorouracil 35-49 proteasome 26S subunit, non-ATPase 1 Homo sapiens 62-65 21222484-2 2011 In budding yeast, 5-FU promotes a large increase in the dUMP/dTMP ratio leading to massive polymerase-catalyzed incorporation of uracil (U) into genomic DNA, and to a lesser extent 5-FU, which are both excised by yeast uracil DNA glycosylase (UNG), leading to DNA fragmentation and cell death. Fluorouracil 18-22 uracil DNA glycosylase Gallus gallus 243-246 21442486-13 2011 CONCLUSIONS: Depletion of PI3K P85alpha can significantly induce SW480 cell cycle arrest and sensitize SW480 cells to 5-FU induced apoptosis. Fluorouracil 118-122 phosphoinositide-3-kinase regulatory subunit 1 Homo sapiens 31-39 21326246-11 2011 Biotransformation of S-1 (AUC(0-24 h) of 5-fluorouracil/AUC(0-24 h) of tegafur) was 1.85-fold higher for the *1/*1 group than for the other groups (90% confidence interval 1.37-2.49). Fluorouracil 41-55 proteasome 26S subunit, non-ATPase 1 Homo sapiens 21-24 21222484-8 2011 In vitro kinetic analyses of the purified human enzymes show that hUNG2 is the most powerful catalyst for excision of 5-FU and U regardless of whether it is found in base pairs with A or G or present in single-stranded DNA. Fluorouracil 118-122 uracil DNA glycosylase Homo sapiens 66-71 21222484-9 2011 Fully consistent with the in vitro activity assays, nuclear extracts isolated from human and chicken cell cultures show that hUNG2 is the overwhelming activity for removal of both U and 5-FU, despite its bystander status with respect to drug toxicity in these cell lines. Fluorouracil 186-190 uracil DNA glycosylase Homo sapiens 125-130 20811948-2 2011 We previously reported the efficacy of interferon-alpha and 5-fluorouracil combination (IFN/5-FU) therapy for these patients and the potential mechanism via the regulation of vascular endothelial growth factor (VEGF). Fluorouracil 60-74 vascular endothelial growth factor A Homo sapiens 211-215 20811948-6 2011 PTK/ZK enhanced the IFN/5-FU induced apoptosis, based on increased proteins levels of Bax and reduced Bcl-xL and Bcl-2. Fluorouracil 24-28 BCL2 associated X, apoptosis regulator Homo sapiens 86-89 21378348-12 2011 CONCLUSION: Despite the differences in the FT dose administered, exposure to 5-FU was significantly greater following S-1 administration compared to FT administration. Fluorouracil 77-81 proteasome 26S subunit, non-ATPase 1 Homo sapiens 118-121 21378348-0 2011 A phase I study evaluating the effect of CDHP as a component of S-1 on the pharmacokinetics of 5-fluorouracil. Fluorouracil 95-109 proteasome 26S subunit, non-ATPase 1 Homo sapiens 64-67 21082354-0 2011 Insulin-like growth factor 1 mediates 5-fluorouracil chemoresistance in esophageal carcinoma cells through increasing survivin stability. Fluorouracil 38-52 insulin like growth factor 1 Homo sapiens 0-28 21378348-1 2011 UNLABELLED: The purpose of this study was to investigate the effect of gimeracil (CDHP), a reversible dihydropyrimidine dehydrogenase (DPD) inhibitor, on the pharmacokinetics of 5-fluorouracil (5-FU) and other related metabolites by comparing the pharmacokinetic (PK) profile of S-1 (tegafur [FT] + CDHP + oteracil potassium [Oxo]) to that of FT alone. Fluorouracil 178-192 proteasome 26S subunit, non-ATPase 1 Homo sapiens 279-282 21378348-8 2011 Following S-1 administration, 5-FU exposure was significantly greater (approximately 3-fold) compared to FT alone (p <= 0.0007 for AUC0-inf, AUC0-last, and C(max) of 5-FU) despite the 16-fold higher dose of FT administered alone compared to S-1, while plasma concentrations of FT and FBAL were significantly lower with S-1 (p < 0.0001 for all comparisons). Fluorouracil 30-34 proteasome 26S subunit, non-ATPase 1 Homo sapiens 10-13 21378348-8 2011 Following S-1 administration, 5-FU exposure was significantly greater (approximately 3-fold) compared to FT alone (p <= 0.0007 for AUC0-inf, AUC0-last, and C(max) of 5-FU) despite the 16-fold higher dose of FT administered alone compared to S-1, while plasma concentrations of FT and FBAL were significantly lower with S-1 (p < 0.0001 for all comparisons). Fluorouracil 30-34 proteasome 26S subunit, non-ATPase 1 Homo sapiens 244-247 21378348-8 2011 Following S-1 administration, 5-FU exposure was significantly greater (approximately 3-fold) compared to FT alone (p <= 0.0007 for AUC0-inf, AUC0-last, and C(max) of 5-FU) despite the 16-fold higher dose of FT administered alone compared to S-1, while plasma concentrations of FT and FBAL were significantly lower with S-1 (p < 0.0001 for all comparisons). Fluorouracil 30-34 proteasome 26S subunit, non-ATPase 1 Homo sapiens 244-247 21378348-8 2011 Following S-1 administration, 5-FU exposure was significantly greater (approximately 3-fold) compared to FT alone (p <= 0.0007 for AUC0-inf, AUC0-last, and C(max) of 5-FU) despite the 16-fold higher dose of FT administered alone compared to S-1, while plasma concentrations of FT and FBAL were significantly lower with S-1 (p < 0.0001 for all comparisons). Fluorouracil 169-173 proteasome 26S subunit, non-ATPase 1 Homo sapiens 10-13 21809488-1 2011 Bevacizumab, a recombinant humanized monoclonal antibody against vascular endothelial growth factor (VEGF), was the first angiogenesis inhibitor approved for the first-line treatment of metastatic colorectal cancer in combination with intravenous fluorouracil-based chemotherapy. Fluorouracil 247-259 vascular endothelial growth factor A Homo sapiens 101-105 21143703-1 2011 S-1 is an oral fluoropyrimidine anti-neoplastic agent that is converted by CYP2A6 to 5-fluorouracil (5FU). Fluorouracil 85-99 proteasome 26S subunit, non-ATPase 1 Homo sapiens 0-3 21143703-1 2011 S-1 is an oral fluoropyrimidine anti-neoplastic agent that is converted by CYP2A6 to 5-fluorouracil (5FU). Fluorouracil 101-104 proteasome 26S subunit, non-ATPase 1 Homo sapiens 0-3 20876774-8 2011 Similarly, primary cultured pancreatic cancer cells are primed for TRAIL-induced apoptosis by pre-exposure to 5-FU or cisplatin. Fluorouracil 110-114 TNF superfamily member 10 Homo sapiens 67-72 20876774-9 2011 Mechanistic studies revealed that 5-FU-mediated suppression of c-FLIP results in increased TRAIL-induced recruitment and activation of caspase-8 at the death-inducing signalling complex (DISC), leading to caspase-3 activation and caspase-dependent cell death. Fluorouracil 34-38 CASP8 and FADD like apoptosis regulator Homo sapiens 63-69 20876774-9 2011 Mechanistic studies revealed that 5-FU-mediated suppression of c-FLIP results in increased TRAIL-induced recruitment and activation of caspase-8 at the death-inducing signalling complex (DISC), leading to caspase-3 activation and caspase-dependent cell death. Fluorouracil 34-38 TNF superfamily member 10 Homo sapiens 91-96 20876774-9 2011 Mechanistic studies revealed that 5-FU-mediated suppression of c-FLIP results in increased TRAIL-induced recruitment and activation of caspase-8 at the death-inducing signalling complex (DISC), leading to caspase-3 activation and caspase-dependent cell death. Fluorouracil 34-38 caspase 3 Homo sapiens 205-214 20876774-10 2011 Overexpression of c-FLIP(L) rescues cells from 5-FU- or cisplatin-mediated sensitisation for TRAIL-induced apoptosis, indicating that c-FLIP suppression is a key event in this chemotherapy-mediated sensitisation to TRAIL. Fluorouracil 47-51 CASP8 and FADD like apoptosis regulator Homo sapiens 18-24 20876774-10 2011 Overexpression of c-FLIP(L) rescues cells from 5-FU- or cisplatin-mediated sensitisation for TRAIL-induced apoptosis, indicating that c-FLIP suppression is a key event in this chemotherapy-mediated sensitisation to TRAIL. Fluorouracil 47-51 TNF superfamily member 10 Homo sapiens 93-98 20876774-10 2011 Overexpression of c-FLIP(L) rescues cells from 5-FU- or cisplatin-mediated sensitisation for TRAIL-induced apoptosis, indicating that c-FLIP suppression is a key event in this chemotherapy-mediated sensitisation to TRAIL. Fluorouracil 47-51 TNF superfamily member 10 Homo sapiens 215-220 21188390-0 2011 Predictive value of VEGF gene polymorphisms for metastatic colorectal cancer patients receiving first-line treatment including fluorouracil, irinotecan, and bevacizumab. Fluorouracil 127-139 vascular endothelial growth factor A Homo sapiens 20-24 20425122-2 2011 In the present study, we have investigated the effects of 5-FU treatment on apoptosis induction in wild-type and mutant p53 urinary bladder cancer cells. Fluorouracil 58-62 tumor protein p53 Homo sapiens 120-123 20425122-4 2011 RESULTS: In the urothelial bladder cancer cell lines RT4 and T24, 5-FU-induced TS inhibition proved to be associated with cell type-dependent (a) sensitivity to the drug, (b) Caspase-mediated apoptosis, (c) p53 stabilization and activation, as well as Rb phosphorylation and E2F1 expression and (d) transcriptional regulation of p53 target genes and their cognate proteins, while an E2F-dependent transcriptional network did not seem to be critically engaged in such type of responses. Fluorouracil 66-70 tumor protein p53 Homo sapiens 207-210 20425122-4 2011 RESULTS: In the urothelial bladder cancer cell lines RT4 and T24, 5-FU-induced TS inhibition proved to be associated with cell type-dependent (a) sensitivity to the drug, (b) Caspase-mediated apoptosis, (c) p53 stabilization and activation, as well as Rb phosphorylation and E2F1 expression and (d) transcriptional regulation of p53 target genes and their cognate proteins, while an E2F-dependent transcriptional network did not seem to be critically engaged in such type of responses. Fluorouracil 66-70 tumor protein p53 Homo sapiens 329-332 20425122-5 2011 CONCLUSIONS: We have shown that in the wild-type p53 context of RT4 cells, 5-FU-triggered apoptosis was prominently efficient and mainly regulated by p53-dependent mechanisms, whereas the mutant p53 environment of T24 cells was able to provide notable levels of resistance to apoptosis, basically ascribed to E2F-independent, and still unidentified, pathways. Fluorouracil 75-79 tumor protein p53 Homo sapiens 49-52 20425122-5 2011 CONCLUSIONS: We have shown that in the wild-type p53 context of RT4 cells, 5-FU-triggered apoptosis was prominently efficient and mainly regulated by p53-dependent mechanisms, whereas the mutant p53 environment of T24 cells was able to provide notable levels of resistance to apoptosis, basically ascribed to E2F-independent, and still unidentified, pathways. Fluorouracil 75-79 tumor protein p53 Homo sapiens 150-153 20425122-5 2011 CONCLUSIONS: We have shown that in the wild-type p53 context of RT4 cells, 5-FU-triggered apoptosis was prominently efficient and mainly regulated by p53-dependent mechanisms, whereas the mutant p53 environment of T24 cells was able to provide notable levels of resistance to apoptosis, basically ascribed to E2F-independent, and still unidentified, pathways. Fluorouracil 75-79 tumor protein p53 Homo sapiens 150-153 21332314-5 2011 We examined the ABCB1 gene polymorphism C3435T to predict response and prognosis to neoadjuvant radiochemotherapy (cisplatin, 5-fluorouracil and 36 Gy) in locally advanced esophageal cancer patients. Fluorouracil 126-140 ATP binding cassette subfamily B member 1 Homo sapiens 16-21 21067862-2 2011 Exposure to 5-FU at 30 muM activated phosphoinositide 3-kinase (PI3K)/Akt signaling markedly from 12h up to 48 h in the 5-FU-resistant cells compared with that in the parental cells and resulted in an overt difference in growth at those times. Fluorouracil 12-16 AKT serine/threonine kinase 1 Homo sapiens 70-73 21067862-2 2011 Exposure to 5-FU at 30 muM activated phosphoinositide 3-kinase (PI3K)/Akt signaling markedly from 12h up to 48 h in the 5-FU-resistant cells compared with that in the parental cells and resulted in an overt difference in growth at those times. Fluorouracil 120-124 AKT serine/threonine kinase 1 Homo sapiens 70-73 21067862-5 2011 The ectopic expression of miR-34a in the 5-FU-resistant cells inhibited growth, as in the parental cells, and attenuated the resistance to 5-FU through the down-regulation of Sirt1 and E2F3. Fluorouracil 41-45 E2F transcription factor 3 Homo sapiens 185-189 21067862-7 2011 These findings suggest that miR-34a targeting the Sirt1 and E2F3 genes could negatively regulate, at least in part, the resistance to 5-FU in human colorectal cancer DLD-1 cells. Fluorouracil 134-138 E2F transcription factor 3 Homo sapiens 60-64 21273614-2 2011 S-1, a newly developed oral fluorouracil antitumor drug, has been reported to be effective in the treatment of gastrointestinal tumors and non-small cell lung cancer. Fluorouracil 28-40 proteasome 26S subunit, non-ATPase 1 Homo sapiens 0-3 20722640-6 2011 The 5-FU-mediated decrease in the myeloid colony formation was intensified in Nrf2(-/-) mice, in which antioxidant proteins were down-regulated. Fluorouracil 4-8 nuclear factor, erythroid derived 2, like 2 Mus musculus 78-82 20722640-9 2011 Therefore, Nrf2-dependent genes as well as glutathione levels in bone marrow could be therapeutic targets for decreasing such side-effects in 5-FU-based chemotherapy. Fluorouracil 142-146 nuclear factor, erythroid derived 2, like 2 Mus musculus 11-15 20798686-6 2011 Furthermore, all patients who received cyclophosphamide (CP), epirubicin plus taxotere/CP, epirubicin plus 5-fluorouracil chemotherapy showed miR-448 suppression, an increased SATB1, Twist1 expression and acquisition of mesenchymal phenotypes. Fluorouracil 107-121 microRNA 448 Homo sapiens 142-149 20798686-6 2011 Furthermore, all patients who received cyclophosphamide (CP), epirubicin plus taxotere/CP, epirubicin plus 5-fluorouracil chemotherapy showed miR-448 suppression, an increased SATB1, Twist1 expression and acquisition of mesenchymal phenotypes. Fluorouracil 107-121 twist family bHLH transcription factor 1 Homo sapiens 183-189 20503071-0 2011 Bax predicts outcome in gastric cancer patients treated with 5-fluorouracil, leucovorin, and oxaliplatin palliative chemotherapy. Fluorouracil 61-75 BCL2 associated X, apoptosis regulator Homo sapiens 0-3 21196321-9 2011 Separate treatments and drug combinations significantly decreased DNA binding activity of NF-kappaB which led to the potentiation of cell death induced by the colon cancer drugs oxaliplatin and 5-FU. Fluorouracil 194-198 nuclear factor kappa B subunit 1 Homo sapiens 90-99 20951698-11 2011 Administration of BMP4 to immunocompromised mice with tumors that arose from CRC-SCs increased the antitumor effects of 5-fluorouracil and oxaliplatin. Fluorouracil 120-134 bone morphogenetic protein 4 Mus musculus 18-22 21403907-9 2011 Moreover, compared with 5-FU alone, the apoptosis of CRC cells treated with DCA and 5-FU was enhanced and demonstrated with the changes of Bcl-2, Bax, and caspase-3 proteins. Fluorouracil 84-88 BCL2 apoptosis regulator Homo sapiens 139-144 21403907-9 2011 Moreover, compared with 5-FU alone, the apoptosis of CRC cells treated with DCA and 5-FU was enhanced and demonstrated with the changes of Bcl-2, Bax, and caspase-3 proteins. Fluorouracil 84-88 BCL2 associated X, apoptosis regulator Homo sapiens 146-149 21403907-9 2011 Moreover, compared with 5-FU alone, the apoptosis of CRC cells treated with DCA and 5-FU was enhanced and demonstrated with the changes of Bcl-2, Bax, and caspase-3 proteins. Fluorouracil 84-88 caspase 3 Homo sapiens 155-164 20451285-1 2011 S-1, an oral 5-fluorouracil derivative, is effective against advanced non-small cell lung cancer (NSCLC) with mild toxicity and synergistic effects with radiation in preclinical trials. Fluorouracil 13-27 proteasome 26S subunit, non-ATPase 1 Homo sapiens 0-3 21461573-0 2011 Chan-Yu-Bao-Yuan-Tang and 5-fluorouracil synergistically induce apoptosis by means of the caspase-3 signaling pathway in lung and cervical cancer cells. Fluorouracil 26-40 caspase 3 Homo sapiens 90-99 21461573-7 2011 CYBYT and 5-Fu, alone or in combination, up-regulated cleaved caspase-3 expression in a time-dependent manner, with CYBYT being more effective than 5-Fu. Fluorouracil 10-14 caspase 3 Homo sapiens 62-71 21963999-1 2011 The product Teysuno (S-1) contains tegafur, a prodrug of 5-fluorouracil (5-FU), and two modulators of 5-FU metabolism, gimeracil and oteracil. Fluorouracil 58-72 proteasome 26S subunit, non-ATPase 1 Homo sapiens 22-25 21963999-1 2011 The product Teysuno (S-1) contains tegafur, a prodrug of 5-fluorouracil (5-FU), and two modulators of 5-FU metabolism, gimeracil and oteracil. Fluorouracil 74-78 proteasome 26S subunit, non-ATPase 1 Homo sapiens 22-25 21963999-1 2011 The product Teysuno (S-1) contains tegafur, a prodrug of 5-fluorouracil (5-FU), and two modulators of 5-FU metabolism, gimeracil and oteracil. Fluorouracil 103-107 proteasome 26S subunit, non-ATPase 1 Homo sapiens 22-25 21968463-1 2011 BACKGROUND: S-1 is a novel oral agent combining the 5-fluorouracil (FU) prodrug tegafur with gimeracil and oteracil, which inhibit 5-FU degradation by dihydropyrimidine dehydrogenase and phosphorylation within the gastrointestinal tract, respectively. Fluorouracil 52-66 proteasome 26S subunit, non-ATPase 1 Homo sapiens 12-15 21968463-1 2011 BACKGROUND: S-1 is a novel oral agent combining the 5-fluorouracil (FU) prodrug tegafur with gimeracil and oteracil, which inhibit 5-FU degradation by dihydropyrimidine dehydrogenase and phosphorylation within the gastrointestinal tract, respectively. Fluorouracil 131-135 proteasome 26S subunit, non-ATPase 1 Homo sapiens 12-15 21985855-0 2011 Successful treatment of a patient with HER2-positive metastatic gastric cancer with third-line combination therapy with irinotecan, 5-fluorouracil, leucovorin and trastuzumab (FOLFIRI-T). Fluorouracil 132-146 erb-b2 receptor tyrosine kinase 2 Homo sapiens 39-43 21109480-8 2011 In combination therapy, p53RA small molecules enhanced the anti-tumor activity of cisplatin, 5-fluorouracil, paclitaxel, and erlotinib against HNSCC cells. Fluorouracil 93-107 tumor protein p53 Homo sapiens 24-27 21849809-9 2011 Knockdown of CDON in DU145 cells induced 5-fluorouracil-induced apoptosis and inhibited invasion ability. Fluorouracil 41-55 cell adhesion associated, oncogene regulated Homo sapiens 13-17 22216150-0 2011 Induction of Bcl-2 expression by hepatitis B virus pre-S2 mutant large surface protein resistance to 5-fluorouracil treatment in Huh-7 cells. Fluorouracil 101-115 BCL2 apoptosis regulator Homo sapiens 13-18 22216150-8 2011 Induction of Bcl-2 expression by HBV pre-S2Delta protein resulted in resistance to 5-fluorouracil treatment in colony formation, caspase-3 assay, and cell apoptosis, and can enhance cell death by co-incubation with Bcl-2 inhibitor. Fluorouracil 83-97 BCL2 apoptosis regulator Homo sapiens 13-18 22216150-8 2011 Induction of Bcl-2 expression by HBV pre-S2Delta protein resulted in resistance to 5-fluorouracil treatment in colony formation, caspase-3 assay, and cell apoptosis, and can enhance cell death by co-incubation with Bcl-2 inhibitor. Fluorouracil 83-97 caspase 3 Homo sapiens 129-138 22216150-8 2011 Induction of Bcl-2 expression by HBV pre-S2Delta protein resulted in resistance to 5-fluorouracil treatment in colony formation, caspase-3 assay, and cell apoptosis, and can enhance cell death by co-incubation with Bcl-2 inhibitor. Fluorouracil 83-97 BCL2 apoptosis regulator Homo sapiens 215-220 22216150-10 2011 CONCLUSION/SIGNIFICANCE: Our result demonstrates that HBV pre-S2Delta increased Bcl-2 expression which plays an important role in resistance to 5-fluorouracil-caused cell death. Fluorouracil 144-158 BCL2 apoptosis regulator Homo sapiens 80-85 22194930-4 2011 These studies demonstrate that both FdUrd and 5-FU activate the ATR and ATM checkpoint signaling pathways, indicating that they cause genotoxic damage. Fluorouracil 46-50 ATR serine/threonine kinase Homo sapiens 64-67 21887339-0 2011 The chemotherapeutic drug 5-fluorouracil promotes PKR-mediated apoptosis in a p53-independent manner in colon and breast cancer cells. Fluorouracil 26-40 tumor protein p53 Homo sapiens 78-81 21887339-5 2011 PKR protein was activated by 5-FU treatment in a p53-independent manner, inducing phosphorylation of the protein synthesis translation initiation factor eIF-2alpha and cell death by apoptosis. Fluorouracil 29-33 tumor protein p53 Homo sapiens 49-52 21629657-9 2011 Gene expression of the autophagy-related LC3 gene as well as of Bad, Mdr-1, Atg12 and the vATPase was analysed after treatment of cells with 5-fluorouracil and omeprazole and confirmed the above mentioned results. Fluorouracil 141-155 ATP binding cassette subfamily B member 1 Homo sapiens 69-74 21629657-9 2011 Gene expression of the autophagy-related LC3 gene as well as of Bad, Mdr-1, Atg12 and the vATPase was analysed after treatment of cells with 5-fluorouracil and omeprazole and confirmed the above mentioned results. Fluorouracil 141-155 autophagy related 12 Homo sapiens 76-81 21629658-0 2011 Calbindin 2 (CALB2) regulates 5-fluorouracil sensitivity in colorectal cancer by modulating the intrinsic apoptotic pathway. Fluorouracil 30-44 calbindin 2 Homo sapiens 0-11 21629658-0 2011 Calbindin 2 (CALB2) regulates 5-fluorouracil sensitivity in colorectal cancer by modulating the intrinsic apoptotic pathway. Fluorouracil 30-44 calbindin 2 Homo sapiens 13-18 21629658-1 2011 The role of the calcium binding protein, Calbindin 2 (CALB2), in regulating the response of colorectal cancer (CRC) cells to 5-Fluorouracil (5-FU) was investigated. Fluorouracil 125-139 calbindin 2 Homo sapiens 41-52 21629658-1 2011 The role of the calcium binding protein, Calbindin 2 (CALB2), in regulating the response of colorectal cancer (CRC) cells to 5-Fluorouracil (5-FU) was investigated. Fluorouracil 125-139 calbindin 2 Homo sapiens 54-59 21629658-1 2011 The role of the calcium binding protein, Calbindin 2 (CALB2), in regulating the response of colorectal cancer (CRC) cells to 5-Fluorouracil (5-FU) was investigated. Fluorouracil 141-145 calbindin 2 Homo sapiens 41-52 21629658-1 2011 The role of the calcium binding protein, Calbindin 2 (CALB2), in regulating the response of colorectal cancer (CRC) cells to 5-Fluorouracil (5-FU) was investigated. Fluorouracil 141-145 calbindin 2 Homo sapiens 54-59 21629658-2 2011 Real-time RT-PCR and Western blot analysis revealed that CALB2 mRNA and protein expression were down-regulated in p53 wild-type and p53 null isogenic HCT116 CRC cell lines following 48 h and 72 h 5-FU treatment. Fluorouracil 196-200 calbindin 2 Homo sapiens 57-62 21629658-2 2011 Real-time RT-PCR and Western blot analysis revealed that CALB2 mRNA and protein expression were down-regulated in p53 wild-type and p53 null isogenic HCT116 CRC cell lines following 48 h and 72 h 5-FU treatment. Fluorouracil 196-200 tumor protein p53 Homo sapiens 114-117 21629658-3 2011 Moreover, 5-FU-induced apoptosis was significantly reduced in HCT116 and LS174T CRC cell lines in which CALB2 expression had been silenced. Fluorouracil 10-14 calbindin 2 Homo sapiens 104-109 21629658-4 2011 Further investigation revealed that CALB2 translocated to the mitochondria following 5-FU treatment and that 5-FU-induced loss of mitochondrial membrane potential (Deltapsi(m)) was abrogated in CALB2-silenced cells. Fluorouracil 85-89 calbindin 2 Homo sapiens 36-41 21629658-4 2011 Further investigation revealed that CALB2 translocated to the mitochondria following 5-FU treatment and that 5-FU-induced loss of mitochondrial membrane potential (Deltapsi(m)) was abrogated in CALB2-silenced cells. Fluorouracil 85-89 calbindin 2 Homo sapiens 194-199 21629658-4 2011 Further investigation revealed that CALB2 translocated to the mitochondria following 5-FU treatment and that 5-FU-induced loss of mitochondrial membrane potential (Deltapsi(m)) was abrogated in CALB2-silenced cells. Fluorouracil 109-113 calbindin 2 Homo sapiens 36-41 21629658-4 2011 Further investigation revealed that CALB2 translocated to the mitochondria following 5-FU treatment and that 5-FU-induced loss of mitochondrial membrane potential (Deltapsi(m)) was abrogated in CALB2-silenced cells. Fluorouracil 109-113 calbindin 2 Homo sapiens 194-199 21629658-5 2011 Furthermore, CALB2 silencing decreased 5-FU-induced cytochrome c and smac release from the mitochondria and also decreased 5-FU-induced activation of caspases 9 and 3/7. Fluorouracil 39-43 calbindin 2 Homo sapiens 13-18 21629658-5 2011 Furthermore, CALB2 silencing decreased 5-FU-induced cytochrome c and smac release from the mitochondria and also decreased 5-FU-induced activation of caspases 9 and 3/7. Fluorouracil 39-43 cytochrome c, somatic Homo sapiens 52-64 21629658-5 2011 Furthermore, CALB2 silencing decreased 5-FU-induced cytochrome c and smac release from the mitochondria and also decreased 5-FU-induced activation of caspases 9 and 3/7. Fluorouracil 123-127 calbindin 2 Homo sapiens 13-18 21629658-6 2011 Of note, co-silencing of XIAP overcame 5-FU resistance in CALB2-silenced cells. Fluorouracil 39-43 calbindin 2 Homo sapiens 58-63 21629658-7 2011 Collectively, these results suggest that following 5-FU treatment in CRC cell lines, CALB2 is involved in apoptosis induction through the intrinsic mitochondrial pathway. Fluorouracil 51-55 calbindin 2 Homo sapiens 85-90 21629658-8 2011 This indicates that CALB2 may be an important mediator of 5-FU-induced cell death. Fluorouracil 58-62 calbindin 2 Homo sapiens 20-25 21629658-9 2011 Moreover, down-regulation of CALB2 in response to 5-FU may represent an intrinsic mechanism of resistance to this anti-cancer drug. Fluorouracil 50-54 calbindin 2 Homo sapiens 29-34 21080742-4 2010 In patients with HER2-positive metastatic gastric cancer (n = 584), median overall survival (primary endpoint) was significantly longer for recipients of intravenous trastuzumab plus chemotherapy (comprising cisplatin and either fluorouracil or capecitabine) than in those receiving chemotherapy alone in the ToGA trial. Fluorouracil 229-241 erb-b2 receptor tyrosine kinase 2 Homo sapiens 17-21 20585871-4 2010 METHODS: HDAC1/2 expression was analyzed immunohistochemically in 127 pretherapeutic biopsy samples of neoadjuvant (platinum/5-fluorouracil) chemotherapy-treated GC patients and correlated with response and overall survival (OS). Fluorouracil 125-139 histone deacetylase 1 Homo sapiens 9-14 20633010-6 2010 5-FU induced p53 and p21 accumulation together with a decrease in cyclin B1 and Bcl-2 levels in treated keloid fibroblasts. Fluorouracil 0-4 tumor protein p53 Homo sapiens 13-16 20633010-6 2010 5-FU induced p53 and p21 accumulation together with a decrease in cyclin B1 and Bcl-2 levels in treated keloid fibroblasts. Fluorouracil 0-4 BCL2 apoptosis regulator Homo sapiens 80-85 21160270-0 2010 [A case of HER2 overexpressing advanced breast cancer with CTF therapy [cyclophosphamide, pirarubicin (THPADM), fluorouracil] showed long-term effectiveness after paclitaxel shock]. Fluorouracil 112-124 erb-b2 receptor tyrosine kinase 2 Homo sapiens 11-15 21160270-0 2010 [A case of HER2 overexpressing advanced breast cancer with CTF therapy [cyclophosphamide, pirarubicin (THPADM), fluorouracil] showed long-term effectiveness after paclitaxel shock]. Fluorouracil 112-124 nuclear factor I C Homo sapiens 59-62 22811811-10 2010 CONCLUSION: These findings are the first to demonstrate that high Bax expression is a good prognosticator for patients who underwent surgery alone, and that patient with low Bax/Bcl-2 expression ratio benefit from 5-FU-based adjuvant therapies. Fluorouracil 214-218 BCL2 associated X, apoptosis regulator Homo sapiens 66-69 22811811-10 2010 CONCLUSION: These findings are the first to demonstrate that high Bax expression is a good prognosticator for patients who underwent surgery alone, and that patient with low Bax/Bcl-2 expression ratio benefit from 5-FU-based adjuvant therapies. Fluorouracil 214-218 BCL2 associated X, apoptosis regulator Homo sapiens 174-177 22811811-10 2010 CONCLUSION: These findings are the first to demonstrate that high Bax expression is a good prognosticator for patients who underwent surgery alone, and that patient with low Bax/Bcl-2 expression ratio benefit from 5-FU-based adjuvant therapies. Fluorouracil 214-218 BCL2 apoptosis regulator Homo sapiens 178-183 21139340-10 2010 5-fluorouracil treatment decreased not only the number of field potential detecting electrodes and beating area, but also cTnT expression, and the area of these parameters was also nearly identical. Fluorouracil 0-14 troponin T2, cardiac Mus musculus 122-126 21163769-7 2010 The main purpose of our experiments was to investigate the effect of COX inhibitors on the efficacy of 5-FU on high and low COX-2 expressing HCA-7 and HT-29 human colon adenocarcinoma cell lines, respectively, and also on xenografts derived from HT-29 cells. Fluorouracil 103-107 prostaglandin-endoperoxide synthase 2 Homo sapiens 124-129 21163769-10 2010 Our data indicated that the elevated COX-2 expression of HCA-7, the collagen-induced HT-29-C cells and of the HT-29 xenograft were associated with reduced 5-FU sensitivity. Fluorouracil 155-159 prostaglandin-endoperoxide synthase 2 Homo sapiens 37-42 21163769-11 2010 Based on the fact that at the same time DPD activity was also increased it might be conceivable that a possible explanation for the decrease of 5-FU sensitivity is the co-existence of high COX-2 and DPD activity. Fluorouracil 144-148 prostaglandin-endoperoxide synthase 2 Homo sapiens 189-194 21163769-12 2010 Indomethacin or NS-398 enhanced in a simultaneous and significant manner the sensitivity and cytotoxic effect of 5-FU on high COX-2 expressing cells and xenografts through the modulation of DPD - decrease of its mRNA expression and/or enzyme activity. Fluorouracil 113-117 prostaglandin-endoperoxide synthase 2 Homo sapiens 126-131 21163769-13 2010 Based on our results it could be presumable that 5-FU efficacy is limited by the COX-2 associated high DPD expression and activity in patients with colorectal cancer as well, therefore further clinical studies are warranted to decide if NSAIDs in the therapeutic protocol might improve the antitumor potency of 5-FU. Fluorouracil 49-53 prostaglandin-endoperoxide synthase 2 Homo sapiens 81-86 21163769-13 2010 Based on our results it could be presumable that 5-FU efficacy is limited by the COX-2 associated high DPD expression and activity in patients with colorectal cancer as well, therefore further clinical studies are warranted to decide if NSAIDs in the therapeutic protocol might improve the antitumor potency of 5-FU. Fluorouracil 311-315 prostaglandin-endoperoxide synthase 2 Homo sapiens 81-86 21142915-1 2010 AIM: To find out whether SNPs in the transporter gene ATP-binding casette B1 (ABCB1) were related to adverse effects in colorectal cancer patients treated with 5-fluorouracil (5-FU) or capecitabine. Fluorouracil 160-174 ATP binding cassette subfamily B member 1 Homo sapiens 54-76 21142915-1 2010 AIM: To find out whether SNPs in the transporter gene ATP-binding casette B1 (ABCB1) were related to adverse effects in colorectal cancer patients treated with 5-fluorouracil (5-FU) or capecitabine. Fluorouracil 160-174 ATP binding cassette subfamily B member 1 Homo sapiens 78-83 21142915-1 2010 AIM: To find out whether SNPs in the transporter gene ATP-binding casette B1 (ABCB1) were related to adverse effects in colorectal cancer patients treated with 5-fluorouracil (5-FU) or capecitabine. Fluorouracil 176-180 ATP binding cassette subfamily B member 1 Homo sapiens 54-76 21142915-1 2010 AIM: To find out whether SNPs in the transporter gene ATP-binding casette B1 (ABCB1) were related to adverse effects in colorectal cancer patients treated with 5-fluorouracil (5-FU) or capecitabine. Fluorouracil 176-180 ATP binding cassette subfamily B member 1 Homo sapiens 78-83 20723540-0 2010 Induction of thymidine kinase 1 after 5-fluorouracil as a mechanism for 3"-deoxy-3"-[18F]fluorothymidine flare. Fluorouracil 38-52 thymidine kinase 1 Homo sapiens 13-31 20723540-3 2010 We investigated the induction of thymidine kinase 1 (TK1) after 5-fluorouracil (5-FU) treatment as one of mechanisms for [(18)F]FLT flare. Fluorouracil 64-78 thymidine kinase 1 Homo sapiens 33-51 20723540-3 2010 We investigated the induction of thymidine kinase 1 (TK1) after 5-fluorouracil (5-FU) treatment as one of mechanisms for [(18)F]FLT flare. Fluorouracil 64-78 thymidine kinase 1 Homo sapiens 53-56 20723540-3 2010 We investigated the induction of thymidine kinase 1 (TK1) after 5-fluorouracil (5-FU) treatment as one of mechanisms for [(18)F]FLT flare. Fluorouracil 80-84 thymidine kinase 1 Homo sapiens 33-51 20723540-3 2010 We investigated the induction of thymidine kinase 1 (TK1) after 5-fluorouracil (5-FU) treatment as one of mechanisms for [(18)F]FLT flare. Fluorouracil 80-84 thymidine kinase 1 Homo sapiens 53-56 20723540-5 2010 The increase of [(18)F]FLT uptake 24h after 5-FU exposure accompanied TK1 induction in most cell lines. Fluorouracil 44-48 thymidine kinase 1 Homo sapiens 70-73 20723540-7 2010 Cycloheximide treatment and knockdown of TK1 completely inhibited 5-FU-induced [(18)F]FLT flare. Fluorouracil 66-70 thymidine kinase 1 Homo sapiens 41-44 20723540-8 2010 On the other hand, HCT8 cells showed a biphasic [(18)F]FLT flare with lacked TK1 induction in response to the dosage of 5-FU. Fluorouracil 120-124 thymidine kinase 1 Homo sapiens 77-80 20723540-11 2010 Conclusively, 5-FU induced TK1 and TK1-mediated high [(18)F]FLT flare in most of cell lines. Fluorouracil 14-18 thymidine kinase 1 Homo sapiens 27-30 20723540-11 2010 Conclusively, 5-FU induced TK1 and TK1-mediated high [(18)F]FLT flare in most of cell lines. Fluorouracil 14-18 thymidine kinase 1 Homo sapiens 35-38 20978511-1 2010 BACKGROUND: We reported recently the clinical efficiency of interferon (IFN)-alpha/5-fluorouracil (5-FU) combination therapy in advanced hepatocellular carcinoma (HCC). Fluorouracil 99-103 interferon alpha 1 Homo sapiens 60-82 20876284-4 2010 Although, DNA-damaging agents such as 5-fluorouracil (5-FU), etoposide and adriamycin have been successfully employed due to their ability to trigger cFLIP(L) and cFLIP(s) down-regulation the molecular mechanisms underneath their action have been only partially elucidated. Fluorouracil 38-52 CASP8 and FADD like apoptosis regulator Homo sapiens 150-155 20876284-4 2010 Although, DNA-damaging agents such as 5-fluorouracil (5-FU), etoposide and adriamycin have been successfully employed due to their ability to trigger cFLIP(L) and cFLIP(s) down-regulation the molecular mechanisms underneath their action have been only partially elucidated. Fluorouracil 38-52 CASP8 and FADD like apoptosis regulator Homo sapiens 163-168 20876284-4 2010 Although, DNA-damaging agents such as 5-fluorouracil (5-FU), etoposide and adriamycin have been successfully employed due to their ability to trigger cFLIP(L) and cFLIP(s) down-regulation the molecular mechanisms underneath their action have been only partially elucidated. Fluorouracil 54-58 CASP8 and FADD like apoptosis regulator Homo sapiens 150-155 20876284-4 2010 Although, DNA-damaging agents such as 5-fluorouracil (5-FU), etoposide and adriamycin have been successfully employed due to their ability to trigger cFLIP(L) and cFLIP(s) down-regulation the molecular mechanisms underneath their action have been only partially elucidated. Fluorouracil 54-58 CASP8 and FADD like apoptosis regulator Homo sapiens 163-168 20876284-6 2010 Here, we provide genetic evidence that ATM kinase activity is required to trigger 5-FU- and neocarzinostatin-dependent cFLIP(L) and cFLIP(S) down-regulation, which in turn sensitize hepatocellular carcinoma (HCC) cell lines to TRAIL. Fluorouracil 82-86 CASP8 and FADD like apoptosis regulator Homo sapiens 119-124 20876284-6 2010 Here, we provide genetic evidence that ATM kinase activity is required to trigger 5-FU- and neocarzinostatin-dependent cFLIP(L) and cFLIP(S) down-regulation, which in turn sensitize hepatocellular carcinoma (HCC) cell lines to TRAIL. Fluorouracil 82-86 CASP8 and FADD like apoptosis regulator Homo sapiens 132-140 20876284-6 2010 Here, we provide genetic evidence that ATM kinase activity is required to trigger 5-FU- and neocarzinostatin-dependent cFLIP(L) and cFLIP(S) down-regulation, which in turn sensitize hepatocellular carcinoma (HCC) cell lines to TRAIL. Fluorouracil 82-86 TNF superfamily member 10 Homo sapiens 227-232 21224577-0 2010 [A case of liver metastasis of pancreatic cancer that was resistant to S-1 and gemcitabine successfully treated by 5-FU and cisplatin hepatic arterial infusion]. Fluorouracil 115-119 proteasome 26S subunit, non-ATPase 1 Homo sapiens 71-74 21224577-1 2010 We report a case of postoperative liver metastasis of pancreatic cancer that was resistant to S-1 and gemcitabine (GEM) successfully treated by hepatic arterial infusion of 5-fluorouracil (5-FU) and cisplatin (CDDP). Fluorouracil 173-187 proteasome 26S subunit, non-ATPase 1 Homo sapiens 94-97 20878137-4 2010 DAPK siRNA transfections strongly enhanced 5-fluorouracil (5FU)-sensitivity, but not etoposide-sensitivity, of HHUA cells compared with control siRNA-transfected cells. Fluorouracil 43-57 death associated protein kinase 1 Homo sapiens 0-4 20878137-4 2010 DAPK siRNA transfections strongly enhanced 5-fluorouracil (5FU)-sensitivity, but not etoposide-sensitivity, of HHUA cells compared with control siRNA-transfected cells. Fluorouracil 59-62 death associated protein kinase 1 Homo sapiens 0-4 20878137-6 2010 Moreover, 5FU-combined chemotherapy with DAPK siRNA transfection may show stronger anticancer effects on patients with endometrial adenocarcinoma than does chemotherapy alone. Fluorouracil 10-13 death associated protein kinase 1 Homo sapiens 41-45 20943624-8 2010 After decades without real progress, a recent European randomized trial showed that adding cetuximab, the first clinically available EGFR-directed monoclonal antibody, to a standard chemotherapy regimen (platinum/5-fluorouracil) leads to an important survival benefit and this, with support of an additional smaller study in the US, has changed practice. Fluorouracil 213-227 epidermal growth factor receptor Homo sapiens 133-137 21036698-2 2010 Previous studies with 5-FU suggest that proapoptotic protein BAX and tumor suppressor protein TP53 are central factors in this process. Fluorouracil 22-26 BCL2 associated X, apoptosis regulator Homo sapiens 61-64 21036698-2 2010 Previous studies with 5-FU suggest that proapoptotic protein BAX and tumor suppressor protein TP53 are central factors in this process. Fluorouracil 22-26 tumor protein p53 Homo sapiens 94-98 21036698-7 2010 Furthermore, we observed 5-FU induced PARP cleavage and notably, reduced expression of antiapoptotic MCL-1L associated with the appearance of proapoptotic MCL-1S. Fluorouracil 25-29 poly(ADP-ribose) polymerase 1 Homo sapiens 38-42 21036698-8 2010 Our results demonstrate the activation of alternative death pathways following treatment with 5-FU, despite mutations in the TP53 and BAX genes. Fluorouracil 94-98 tumor protein p53 Homo sapiens 125-129 21036698-8 2010 Our results demonstrate the activation of alternative death pathways following treatment with 5-FU, despite mutations in the TP53 and BAX genes. Fluorouracil 94-98 BCL2 associated X, apoptosis regulator Homo sapiens 134-137 20638924-4 2010 CONCLUSION: We introduced new data related to the contribution of p53 codon 72 to toxicity due to 5-fluorouracil and cyclophosphamide-based neoadjuvant chemotherapy in patients with breast cancer. Fluorouracil 98-112 tumor protein p53 Homo sapiens 66-69 20920994-0 2010 Routine dihydropyrimidine dehydrogenase testing for anticipating 5-fluorouracil-related severe toxicities: hype or hope? Fluorouracil 65-79 FIC domain protein adenylyltransferase Homo sapiens 107-111 20811704-9 2010 The activity of Akt3/PKBgamma was inhibited with 5-FU alone and trastuzumab, indicating that trastuzumab may inhibit colon cancer growth through ErbB2-Akt3/PKBgamma signaling. Fluorouracil 49-53 erb-b2 receptor tyrosine kinase 2 Homo sapiens 145-150 21180996-1 2010 OBJECTIVE: To evaluate the immunohistochemical expression of cox-2 before primary chemotherapy with 5-fluorouracil, epirubicin and cyclophosphamide (FEC) and its association with initial tumor size, lymph node status, hormone receptors, expression of HER2 and the clinical and pathological response in patients with breast cancer. Fluorouracil 100-114 mitochondrially encoded cytochrome c oxidase II Homo sapiens 61-66 21410040-0 2010 Involvement of RhoGDI2 in the resistance of colon cancer cells to 5-fluorouracil. Fluorouracil 66-80 Rho GDP dissociation inhibitor beta Homo sapiens 15-22 21410040-6 2010 The cytotoxicity of 5-FU was measured in LoVo/5-FU after knockdown of RhoGDI2 (one of the identified protien). Fluorouracil 20-24 Rho GDP dissociation inhibitor beta Homo sapiens 70-77 21410040-9 2010 Furthermore, knockdown of RhoGDI2 expression by transfection with the RhoGDI2-specific siRNA significantly reduced the resistance to 5-FU in LoVo/5-FU (p < 0.05). Fluorouracil 133-137 Rho GDP dissociation inhibitor beta Homo sapiens 26-33 21410040-9 2010 Furthermore, knockdown of RhoGDI2 expression by transfection with the RhoGDI2-specific siRNA significantly reduced the resistance to 5-FU in LoVo/5-FU (p < 0.05). Fluorouracil 133-137 Rho GDP dissociation inhibitor beta Homo sapiens 70-77 21410040-9 2010 Furthermore, knockdown of RhoGDI2 expression by transfection with the RhoGDI2-specific siRNA significantly reduced the resistance to 5-FU in LoVo/5-FU (p < 0.05). Fluorouracil 146-150 Rho GDP dissociation inhibitor beta Homo sapiens 26-33 21410040-9 2010 Furthermore, knockdown of RhoGDI2 expression by transfection with the RhoGDI2-specific siRNA significantly reduced the resistance to 5-FU in LoVo/5-FU (p < 0.05). Fluorouracil 146-150 Rho GDP dissociation inhibitor beta Homo sapiens 70-77 20020496-0 2010 HIF-1alpha is an unfavorable determinant of relapse in gastric cancer patients who underwent curative surgery followed by adjuvant 5-FU chemotherapy. Fluorouracil 131-135 hypoxia inducible factor 1 subunit alpha Homo sapiens 0-10 20020496-10 2010 In conclusion, the current study confirmed, for the first time that HIF-1alpha expression is an independent risk factor for relapse in high-risk gastric cancer patients who underwent curative surgery followed by adjuvant 5-FU chemotherapy. Fluorouracil 221-225 hypoxia inducible factor 1 subunit alpha Homo sapiens 68-78 20697159-9 2010 5-FU inhibited CD90+ proliferating CSCs, some of which produce CD13+ semiquiescent CSCs, while CD13 inhibition suppressed the self-renewing and tumor-initiating ability of dormant CSCs. Fluorouracil 0-4 thymus cell antigen 1, theta Mus musculus 15-19 20816370-0 2010 S-1 for advanced colorectal cancer: do we need another oral fluorouracil prodrug? Fluorouracil 60-72 proteasome 26S subunit, non-ATPase 1 Homo sapiens 0-3 20570612-0 2010 Wogonin potentiates the antitumor effects of low dose 5-fluorouracil against gastric cancer through induction of apoptosis by down-regulation of NF-kappaB and regulation of its metabolism. Fluorouracil 54-68 nuclear factor kappa B subunit 1 Homo sapiens 145-154 20704765-5 2010 When 5-FU and LY were treated in single and sequential combinations, the expression of p-AKT, p-NFkB, p-p53 and bcl-2 was observed on different concentrations by Western blot analysis. Fluorouracil 5-9 AKT serine/threonine kinase 1 Homo sapiens 89-92 20704765-5 2010 When 5-FU and LY were treated in single and sequential combinations, the expression of p-AKT, p-NFkB, p-p53 and bcl-2 was observed on different concentrations by Western blot analysis. Fluorouracil 5-9 tumor protein p53 Homo sapiens 104-107 20704765-5 2010 When 5-FU and LY were treated in single and sequential combinations, the expression of p-AKT, p-NFkB, p-p53 and bcl-2 was observed on different concentrations by Western blot analysis. Fluorouracil 5-9 BCL2 apoptosis regulator Homo sapiens 112-117 20704765-9 2010 The expression of p-AKT and p-NF kappaB was upregulated by 5-FU alone but sequential treatment of 5-FU and LY decreased the expression of both p-AKT and p-NF kappaB. Fluorouracil 59-63 AKT serine/threonine kinase 1 Homo sapiens 20-23 20704765-9 2010 The expression of p-AKT and p-NF kappaB was upregulated by 5-FU alone but sequential treatment of 5-FU and LY decreased the expression of both p-AKT and p-NF kappaB. Fluorouracil 98-102 AKT serine/threonine kinase 1 Homo sapiens 20-23 20704765-9 2010 The expression of p-AKT and p-NF kappaB was upregulated by 5-FU alone but sequential treatment of 5-FU and LY decreased the expression of both p-AKT and p-NF kappaB. Fluorouracil 98-102 AKT serine/threonine kinase 1 Homo sapiens 145-148 20704765-11 2010 When 5-FU was added to the cells transfected with LMP2A siRNA, its anti-proliferative effect increased and the expression of p-AKT decreased. Fluorouracil 5-9 AKT serine/threonine kinase 1 Homo sapiens 127-130 20704765-12 2010 In sequential combination of 5-FU and LY, the expression of p-p53 was increased and bcl-2 expression was diminished compared to 5-FU alone. Fluorouracil 29-33 tumor protein p53 Homo sapiens 62-65 20704765-12 2010 In sequential combination of 5-FU and LY, the expression of p-p53 was increased and bcl-2 expression was diminished compared to 5-FU alone. Fluorouracil 29-33 BCL2 apoptosis regulator Homo sapiens 84-89 20704765-13 2010 CONCLUSION: These data suggest that sequential combination of 5-FU and LY induce synergistic cytotoxicity and overcome intrinsic and acquired resistance of 5-FU via downregulation of activated p-AKT and mitochondria-dependent apoptosis in EBV gastric cancer cell line, SNU-719. Fluorouracil 62-66 AKT serine/threonine kinase 1 Homo sapiens 195-198 21082354-1 2011 Insulin-like growth factor 1 (IGF-1) inhibits 5-fluorouracil (5-Fu)-induced apoptosis in esophageal carcinoma cells; however, the mechanisms for IGF-1-induced 5-Fu chemoresistance remain unknown. Fluorouracil 46-60 insulin like growth factor 1 Homo sapiens 0-28 21082354-1 2011 Insulin-like growth factor 1 (IGF-1) inhibits 5-fluorouracil (5-Fu)-induced apoptosis in esophageal carcinoma cells; however, the mechanisms for IGF-1-induced 5-Fu chemoresistance remain unknown. Fluorouracil 46-60 insulin like growth factor 1 Homo sapiens 30-35 21082354-1 2011 Insulin-like growth factor 1 (IGF-1) inhibits 5-fluorouracil (5-Fu)-induced apoptosis in esophageal carcinoma cells; however, the mechanisms for IGF-1-induced 5-Fu chemoresistance remain unknown. Fluorouracil 46-60 insulin like growth factor 1 Homo sapiens 145-150 21082354-1 2011 Insulin-like growth factor 1 (IGF-1) inhibits 5-fluorouracil (5-Fu)-induced apoptosis in esophageal carcinoma cells; however, the mechanisms for IGF-1-induced 5-Fu chemoresistance remain unknown. Fluorouracil 62-66 insulin like growth factor 1 Homo sapiens 0-28 21082354-1 2011 Insulin-like growth factor 1 (IGF-1) inhibits 5-fluorouracil (5-Fu)-induced apoptosis in esophageal carcinoma cells; however, the mechanisms for IGF-1-induced 5-Fu chemoresistance remain unknown. Fluorouracil 62-66 insulin like growth factor 1 Homo sapiens 30-35 21082354-1 2011 Insulin-like growth factor 1 (IGF-1) inhibits 5-fluorouracil (5-Fu)-induced apoptosis in esophageal carcinoma cells; however, the mechanisms for IGF-1-induced 5-Fu chemoresistance remain unknown. Fluorouracil 62-66 insulin like growth factor 1 Homo sapiens 145-150 21082354-1 2011 Insulin-like growth factor 1 (IGF-1) inhibits 5-fluorouracil (5-Fu)-induced apoptosis in esophageal carcinoma cells; however, the mechanisms for IGF-1-induced 5-Fu chemoresistance remain unknown. Fluorouracil 159-163 insulin like growth factor 1 Homo sapiens 0-28 21082354-1 2011 Insulin-like growth factor 1 (IGF-1) inhibits 5-fluorouracil (5-Fu)-induced apoptosis in esophageal carcinoma cells; however, the mechanisms for IGF-1-induced 5-Fu chemoresistance remain unknown. Fluorouracil 159-163 insulin like growth factor 1 Homo sapiens 30-35 21082354-1 2011 Insulin-like growth factor 1 (IGF-1) inhibits 5-fluorouracil (5-Fu)-induced apoptosis in esophageal carcinoma cells; however, the mechanisms for IGF-1-induced 5-Fu chemoresistance remain unknown. Fluorouracil 159-163 insulin like growth factor 1 Homo sapiens 145-150 21082354-3 2011 We then examine whether IGF-1-induced 5-Fu chemoresistance is mediated through up-regulation of survivin. Fluorouracil 38-42 insulin like growth factor 1 Homo sapiens 24-29 21082354-4 2011 Ectopic expression of survivin inhibits 5-Fu-induced apoptosis; furthermore, the abolition of survivin expression sensitizes cells to 5-Fu treatment and prevents the anti-apoptotic function of IGF-1 in esophageal carcinoma cell lines. Fluorouracil 40-44 insulin like growth factor 1 Homo sapiens 193-198 21082354-5 2011 We also found that ectopic expression of survivin or treatment with IGF-1 inhibits the release of Smac/DIABLO and caspases activation after 5-Fu treatment. Fluorouracil 140-144 insulin like growth factor 1 Homo sapiens 68-73 21082354-6 2011 Our results strongly suggest that IGF-1 inhibits 5-Fu induced apoptosis through increasing survivin levels, which prevents Smac/DIABLO release and blocks the activation of caspases. Fluorouracil 49-53 insulin like growth factor 1 Homo sapiens 34-39 20463005-9 2010 Furthermore, the amount of 5-FU and GBL/GHB formed in the hepatic S9 was markedly decreased in the presence of a CYP2A6 inhibitor, suggesting that GBL/GHB may be mainly generated through the CYP2A6-mediated formation of SA. Fluorouracil 27-31 MTOR associated protein, LST8 homolog Homo sapiens 147-154 20714440-3 2010 In this study, CD34(+)CD38(-)stem-like cell subsets in human KG-1a leukemic cell line were enriched by cytotoxic agent 5-fluorouracil (5-FU). Fluorouracil 119-133 CD34 molecule Homo sapiens 15-19 20714440-3 2010 In this study, CD34(+)CD38(-)stem-like cell subsets in human KG-1a leukemic cell line were enriched by cytotoxic agent 5-fluorouracil (5-FU). Fluorouracil 135-139 CD34 molecule Homo sapiens 15-19 20714440-4 2010 After 4 days incubation of KG-1a cell line with 5-FU (50 microg/ml), the CD34(+)CD38(-) subpopulation of cell lines was enriched more than 10 times. Fluorouracil 48-52 CD34 molecule Homo sapiens 73-77 20716879-7 2010 Interestingly, a pathway analysis revealed that expressions of p53-related genes were up-regulated in the 5-FU-sensitive groups. Fluorouracil 106-110 tumor protein p53 Homo sapiens 63-66 19960436-5 2010 PRL-3 small interfering RNA robustly repressed cell proliferation, anchorage-independent colony formation and invasion and augmented 5-FU-induced apoptosis in all the tested ESCC cell lines with PRL-3 overexpression, irrespective of its gene amplification status. Fluorouracil 133-137 protein tyrosine phosphatase 4A3 Homo sapiens 0-5 20684155-3 2010 The authors report six cases of early stage CTCL responded to topical 5-FU. Fluorouracil 70-74 TSPY like 2 Homo sapiens 44-48 20684155-4 2010 All of these patients (four females and two males) with early stage CTCL (1A = 4; 18 = 1; 2B = 1) had good response to topical 5-FU following three to 18 months" treatment. Fluorouracil 127-131 TSPY like 2 Homo sapiens 68-72 20684155-7 2010 The overall efficacy, relatively modest price and low incidence of side effects indicate that topical 5-FU has a place for treatment of early stage CTCL. Fluorouracil 102-106 TSPY like 2 Homo sapiens 148-152 20346742-1 2010 We document an EGFR mutation in a patient with papillary renal cell cancer with a history of multiple therapies, including interferon-alpha, interleukin-2, 5-fluorouracil, and interferon-alpha together with 13-cis-retinoic acid, to which floxuridine was later added, and thalidomide maintenance therapy for six years. Fluorouracil 156-170 epidermal growth factor receptor Homo sapiens 15-19 20647341-0 2010 miR-192/miR-215 influence 5-fluorouracil resistance through cell cycle-mediated mechanisms complementary to its post-transcriptional thymidilate synthase regulation. Fluorouracil 26-40 microRNA 192 Homo sapiens 0-7 20630104-12 2010 The potentiation of the inhibitory effect of 5-FU by CQ was dependent on the increase of p21Cip1 and p27Kip1 and the decrease of CDK2. Fluorouracil 45-49 cyclin dependent kinase inhibitor 1A Homo sapiens 89-96 20682991-0 2010 Combination therapy of 5-fluorouracil with rapamycin for hormone receptor-negative human breast cancer. Fluorouracil 23-37 nuclear receptor subfamily 4 group A member 1 Homo sapiens 57-73 20682991-8 2010 CONCLUSION: 5-FU is more effective in combination with the TS-reducing action of Rap, even for highly HER2-expressing breast cancer cells. Fluorouracil 12-16 erb-b2 receptor tyrosine kinase 2 Homo sapiens 102-106 19830428-0 2010 Enhanced 5-fluorouracil cytotoxicity in high cyclooxygenase-2 expressing colorectal cancer cells and xenografts induced by non-steroidal anti-inflammatory drugs via downregulation of dihydropyrimidine dehydrogenase. Fluorouracil 9-23 prostaglandin-endoperoxide synthase 2 Homo sapiens 45-61 19921195-1 2010 PURPOSE: S-1 is an oral anticancer drug containing tegafur (FT), a pro-drug of fluorouracil, combined with two modulators, 5-chloro-2,4-dihydroxypyridine and potassium oxonate (Oxo), at a molar ratio of 1:0.4:1. Fluorouracil 79-91 proteasome 26S subunit, non-ATPase 1 Homo sapiens 9-12 20367642-6 2010 We found that the DNA-damaging reagent 5-fluorouracil (5-FU) increased TLR3 mRNA expression and potentiated poly I:C-induced apoptosis in HCT116 p53(+/+) cells but had only minimal effect in p53(-/-) cells, indicating a p53-dependent pathway. Fluorouracil 39-53 tumor protein p53 Homo sapiens 145-148 20367642-6 2010 We found that the DNA-damaging reagent 5-fluorouracil (5-FU) increased TLR3 mRNA expression and potentiated poly I:C-induced apoptosis in HCT116 p53(+/+) cells but had only minimal effect in p53(-/-) cells, indicating a p53-dependent pathway. Fluorouracil 39-53 tumor protein p53 Homo sapiens 191-194 20367642-6 2010 We found that the DNA-damaging reagent 5-fluorouracil (5-FU) increased TLR3 mRNA expression and potentiated poly I:C-induced apoptosis in HCT116 p53(+/+) cells but had only minimal effect in p53(-/-) cells, indicating a p53-dependent pathway. Fluorouracil 39-53 tumor protein p53 Homo sapiens 191-194 20367642-6 2010 We found that the DNA-damaging reagent 5-fluorouracil (5-FU) increased TLR3 mRNA expression and potentiated poly I:C-induced apoptosis in HCT116 p53(+/+) cells but had only minimal effect in p53(-/-) cells, indicating a p53-dependent pathway. Fluorouracil 55-59 tumor protein p53 Homo sapiens 145-148 20367642-6 2010 We found that the DNA-damaging reagent 5-fluorouracil (5-FU) increased TLR3 mRNA expression and potentiated poly I:C-induced apoptosis in HCT116 p53(+/+) cells but had only minimal effect in p53(-/-) cells, indicating a p53-dependent pathway. Fluorouracil 55-59 tumor protein p53 Homo sapiens 191-194 20367642-6 2010 We found that the DNA-damaging reagent 5-fluorouracil (5-FU) increased TLR3 mRNA expression and potentiated poly I:C-induced apoptosis in HCT116 p53(+/+) cells but had only minimal effect in p53(-/-) cells, indicating a p53-dependent pathway. Fluorouracil 55-59 tumor protein p53 Homo sapiens 191-194 20367642-8 2010 Furthermore, the combination of poly I:C, 5-FU and IFN-alpha induced the highest apoptosis in HCT116 p53(+/+) and p53(-/-) cells. Fluorouracil 42-46 tumor protein p53 Homo sapiens 101-104 20367642-8 2010 Furthermore, the combination of poly I:C, 5-FU and IFN-alpha induced the highest apoptosis in HCT116 p53(+/+) and p53(-/-) cells. Fluorouracil 42-46 tumor protein p53 Homo sapiens 114-117 19830428-1 2010 PURPOSE: To prove that 5-FU cytotoxicity could be increased by combination with low-dose non-steroidal anti-inflammatory drugs (NSAIDs) (indomethacin or NS-398) in high cyclooxygenase-2- (COX-2) expressing cells and xenografts through the modulation of dihydropyrimidine dehydrogenase (DPD) mRNA expression and/or enzyme activity. Fluorouracil 23-27 prostaglandin-endoperoxide synthase 2 Homo sapiens 169-185 20514446-6 2010 5-FU (400 microM) induced apoptosis in MCF-7 cell monolayer as determined by HO/PI staining, PARP cleavage, p53 induction, Bax induction, and Bcl-2 down-regulation. Fluorouracil 0-4 tumor protein p53 Homo sapiens 108-111 20570921-7 2010 RESULTS: Chemotherapy (5-fluorouracil) treatment resulted in acute increases in transforming growth factor-alpha, amphiregulin, and heregulin ligand shedding in vitro and in vivo that correlated with significantly increased ADAM-17 activity. Fluorouracil 23-37 tumor necrosis factor Homo sapiens 80-112 19904749-0 2010 The effect of focal adhesion kinase gene silencing on 5-fluorouracil chemosensitivity involves an Akt/NF-kappaB signaling pathway in colorectal carcinomas. Fluorouracil 54-68 AKT serine/threonine kinase 1 Homo sapiens 98-101 19904749-0 2010 The effect of focal adhesion kinase gene silencing on 5-fluorouracil chemosensitivity involves an Akt/NF-kappaB signaling pathway in colorectal carcinomas. Fluorouracil 54-68 nuclear factor kappa B subunit 1 Homo sapiens 102-111 20514446-6 2010 5-FU (400 microM) induced apoptosis in MCF-7 cell monolayer as determined by HO/PI staining, PARP cleavage, p53 induction, Bax induction, and Bcl-2 down-regulation. Fluorouracil 0-4 BCL2 associated X, apoptosis regulator Homo sapiens 123-126 20514446-6 2010 5-FU (400 microM) induced apoptosis in MCF-7 cell monolayer as determined by HO/PI staining, PARP cleavage, p53 induction, Bax induction, and Bcl-2 down-regulation. Fluorouracil 0-4 BCL2 apoptosis regulator Homo sapiens 142-147 20514446-10 2010 Furthermore, most of p53 induced by 5-FU was aggregated in MTS with necrotic core. Fluorouracil 36-40 tumor protein p53 Homo sapiens 21-24 20206682-4 2010 Interestingly, 5-FU represses levels of mRNA encoding LIN-29, a transcription factor that affects vulva development and egg laying system. Fluorouracil 15-19 Zinc finger transcription factor lin-29 Caenorhabditis elegans 54-60 20616597-4 2010 Recently, the combination therapy of subcutaneous interferon (IFN)-alpha and intraarterial 5-fluorouracil (5-FU) showed an outstanding response rate for intractable HCC (with portal vein thrombosis). Fluorouracil 107-111 interferon alpha 1 Homo sapiens 50-72 20484035-7 2010 Noticeably, combination of OSM treatment with the chemotherapeutic agent 5-fluorouracil (5-FU), which eradicates EpCAM-negative non-CSCs, dramatically increased the number of apoptotic cells in vitro and suppressed tumor growth in vivo compared with either saline control, OSM, or 5-FU treatment alone. Fluorouracil 73-87 epithelial cell adhesion molecule Homo sapiens 113-118 20484035-7 2010 Noticeably, combination of OSM treatment with the chemotherapeutic agent 5-fluorouracil (5-FU), which eradicates EpCAM-negative non-CSCs, dramatically increased the number of apoptotic cells in vitro and suppressed tumor growth in vivo compared with either saline control, OSM, or 5-FU treatment alone. Fluorouracil 89-93 epithelial cell adhesion molecule Homo sapiens 113-118 20368736-0 2010 BNIP3 is essential for mediating 6-thioguanine- and 5-fluorouracil-induced autophagy following DNA mismatch repair processing. Fluorouracil 52-66 BCL2 interacting protein 3 Homo sapiens 0-5 20368736-4 2010 We found that BNIP3 protein levels are upregulated in a MLH1 (MMR(+))-dependent manner following 6-TG and 5-FU treatment. Fluorouracil 106-110 BCL2 interacting protein 3 Homo sapiens 14-19 20368736-6 2010 We also found that p53 knockdown or inhibition of mTOR activity by rapamycin cotreatment impairs 6-TG- and 5-FU-induced upregulation of BNIP3 protein levels and autophagy. Fluorouracil 107-111 tumor protein p53 Homo sapiens 19-22 19856312-2 2010 In this study, to elucidate whether the rapamycin, the inhibitor of the mTOR (mammalian target of rapamaycin), can enhance the potentiation of TXT and 5-fluorouracil (5-Fu) in gastric carcinoma cells. Fluorouracil 151-165 mechanistic target of rapamycin kinase Homo sapiens 72-76 20368736-6 2010 We also found that p53 knockdown or inhibition of mTOR activity by rapamycin cotreatment impairs 6-TG- and 5-FU-induced upregulation of BNIP3 protein levels and autophagy. Fluorouracil 107-111 mechanistic target of rapamycin kinase Homo sapiens 50-54 20368736-6 2010 We also found that p53 knockdown or inhibition of mTOR activity by rapamycin cotreatment impairs 6-TG- and 5-FU-induced upregulation of BNIP3 protein levels and autophagy. Fluorouracil 107-111 BCL2 interacting protein 3 Homo sapiens 136-141 20368736-8 2010 These findings suggest that BNIP3 mediates 6-TG- and 5-FU-induced autophagy in a p53- and mTOR-dependent manner. Fluorouracil 53-57 BCL2 interacting protein 3 Homo sapiens 28-33 20368736-8 2010 These findings suggest that BNIP3 mediates 6-TG- and 5-FU-induced autophagy in a p53- and mTOR-dependent manner. Fluorouracil 53-57 tumor protein p53 Homo sapiens 81-84 20368736-8 2010 These findings suggest that BNIP3 mediates 6-TG- and 5-FU-induced autophagy in a p53- and mTOR-dependent manner. Fluorouracil 53-57 mechanistic target of rapamycin kinase Homo sapiens 90-94 20399639-6 2010 These drugs were able to up-regulate EGFR expression on the surface of all the colon cancer cell lines with a maximal effect observed few hours after the exposure to GILF regimen (Gem, Iri, Levofolinic acid and 5-FU). Fluorouracil 211-215 epidermal growth factor receptor Homo sapiens 37-41 19856312-2 2010 In this study, to elucidate whether the rapamycin, the inhibitor of the mTOR (mammalian target of rapamaycin), can enhance the potentiation of TXT and 5-fluorouracil (5-Fu) in gastric carcinoma cells. Fluorouracil 151-165 mechanistic target of rapamycin kinase Homo sapiens 78-108 19856312-2 2010 In this study, to elucidate whether the rapamycin, the inhibitor of the mTOR (mammalian target of rapamaycin), can enhance the potentiation of TXT and 5-fluorouracil (5-Fu) in gastric carcinoma cells. Fluorouracil 167-171 mechanistic target of rapamycin kinase Homo sapiens 72-76 19856312-2 2010 In this study, to elucidate whether the rapamycin, the inhibitor of the mTOR (mammalian target of rapamaycin), can enhance the potentiation of TXT and 5-fluorouracil (5-Fu) in gastric carcinoma cells. Fluorouracil 167-171 mechanistic target of rapamycin kinase Homo sapiens 78-108 19856312-8 2010 These results strongly indicate that the mTOR inhibitor can enhance the potentiation of TXT and 5-Fu or S-1 and can serve as a new therapeutic tool for advanced and recurrent gastric cancer patients. Fluorouracil 96-100 mechanistic target of rapamycin kinase Homo sapiens 41-45 19903580-5 2010 PG490 and 5-FU treatment induced activated caspase 3 and Bax expression and inhibited Bcl-2 expression. Fluorouracil 10-14 caspase 3 Homo sapiens 43-52 20463601-0 2010 Combined treatment with dendritic cells and 5-fluorouracil elicits augmented NK cell-mediated antitumor activity through the tumor necrosis factor-alpha pathway. Fluorouracil 44-58 tumor necrosis factor Mus musculus 125-152 20463601-7 2010 MC38 cells pretreated with 5-FU exhibited enhanced expression of procaspase 8 and efficiently underwent apoptosis by TNF-alpha with activation of caspase 8. Fluorouracil 27-31 tumor necrosis factor Mus musculus 117-126 20463601-9 2010 These results indicate that combined therapy with a DC vaccine and 5-FU is a promising strategy for cancer treatment mediated by the tumoricidal activity of NK cells through the TNF-alpha pathway. Fluorouracil 67-71 tumor necrosis factor Mus musculus 178-187 19415535-3 2010 In this study, we aimed to evaluate the influence of 5-FU administration on the diameter of the brachial artery and the levels of angiotensin II. Fluorouracil 53-57 angiotensinogen Homo sapiens 130-144 19903580-5 2010 PG490 and 5-FU treatment induced activated caspase 3 and Bax expression and inhibited Bcl-2 expression. Fluorouracil 10-14 BCL2 associated X, apoptosis regulator Homo sapiens 57-60 19903580-5 2010 PG490 and 5-FU treatment induced activated caspase 3 and Bax expression and inhibited Bcl-2 expression. Fluorouracil 10-14 BCL2 apoptosis regulator Homo sapiens 86-91 20372793-0 2010 The role of thymidine phosphorylase in the induction of early growth response protein-1 and thrombospondin-1 by 5-fluorouracil in human cancer carcinoma cells. Fluorouracil 112-126 thrombospondin 1 Homo sapiens 92-108 20407444-6 2010 The correlation between immunohistochemically determined IGFBP7 expression and the response to IFN-alpha/5-fluorouracil (5-FU) therapy was investigated in surgically resected HCC specimens. Fluorouracil 105-119 insulin like growth factor binding protein 7 Homo sapiens 57-63 20407444-6 2010 The correlation between immunohistochemically determined IGFBP7 expression and the response to IFN-alpha/5-fluorouracil (5-FU) therapy was investigated in surgically resected HCC specimens. Fluorouracil 121-125 insulin like growth factor binding protein 7 Homo sapiens 57-63 20407444-9 2010 In resected specimens, IGFBP7 expression significantly correlated with the response to IFN-alpha/5-FU therapy. Fluorouracil 97-101 insulin like growth factor binding protein 7 Homo sapiens 23-29 20407444-9 2010 In resected specimens, IGFBP7 expression significantly correlated with the response to IFN-alpha/5-FU therapy. Fluorouracil 97-101 interferon alpha 1 Homo sapiens 87-90 20372793-5 2010 TPI, a newly synthesized inhibitor for TP (Ki=2.36 x 10(-9) M), decreased the sensitivity to 5-FU of the TP expressing cells but not of the parental cells. Fluorouracil 93-97 triosephosphate isomerase 1 Homo sapiens 0-3 20372793-8 2010 5-FU increased the expression of early growth response protein-1 (Egr-1) and an angiogenesis inhibitor, thrombospondin-1 (TSP-1), in KB/TP cells but only slightly in KB/CV cells, if any. Fluorouracil 0-4 thrombospondin 1 Homo sapiens 104-120 20372793-8 2010 5-FU increased the expression of early growth response protein-1 (Egr-1) and an angiogenesis inhibitor, thrombospondin-1 (TSP-1), in KB/TP cells but only slightly in KB/CV cells, if any. Fluorouracil 0-4 thrombospondin 1 Homo sapiens 122-127 20107315-5 2010 MK-1775 enhanced the cytotoxic effects of 5-FU in p53-deficient human colon cancer cells. Fluorouracil 42-46 tumor protein p53 Homo sapiens 50-53 20501401-0 2010 [PI3K p85alpha gene silencing by RNA interference promotes 5-fluorouracil-induced apoptosis of colorectal cancer LoVo cells]. Fluorouracil 59-73 phosphoinositide-3-kinase regulatory subunit 1 Homo sapiens 6-14 20501401-1 2010 OBJECTIVE: To explore the effect of PI3K p85alpha gene silencing on the 5-fluorouracil (5-FU)-induced apoptosis of colorectal cancer cells. Fluorouracil 72-86 phosphoinositide-3-kinase regulatory subunit 1 Homo sapiens 41-49 20501401-1 2010 OBJECTIVE: To explore the effect of PI3K p85alpha gene silencing on the 5-fluorouracil (5-FU)-induced apoptosis of colorectal cancer cells. Fluorouracil 88-92 phosphoinositide-3-kinase regulatory subunit 1 Homo sapiens 41-49 20501401-5 2010 RESULTS: Compared with the untransfected LoVo cells, PI3K p85alpha/RNAi-LoVo showed obviously decreased IC(50) of 5-FU (P=0.000). Fluorouracil 114-118 phosphoinositide-3-kinase regulatory subunit 1 Homo sapiens 58-66 20501401-6 2010 The mitochondrial membrane potential of PI3K p85alpha/RNAi-LoVo cells was significantly lower than that of LoVo cells, suggesting that silencing PI3K p85alpha expression increased the sensitivity of LoVo cells to 5-FU. Fluorouracil 213-217 phosphoinositide-3-kinase regulatory subunit 1 Homo sapiens 45-53 20501401-6 2010 The mitochondrial membrane potential of PI3K p85alpha/RNAi-LoVo cells was significantly lower than that of LoVo cells, suggesting that silencing PI3K p85alpha expression increased the sensitivity of LoVo cells to 5-FU. Fluorouracil 213-217 phosphoinositide-3-kinase regulatory subunit 1 Homo sapiens 150-158 20501401-7 2010 The expression of apoptotic protein Bcl-6 and Bim were significantly higher in PI3K p85alpha/RNAi-LoVo cells treated with 5-FU than LoVo cells (P=0.000). Fluorouracil 122-126 phosphoinositide-3-kinase regulatory subunit 1 Homo sapiens 84-92 20568543-7 2010 As for metastasis, as well as MMP-9 and VEGF expression OD values, significant difference was observed between the 5-FU group (Group B) and the control group (Group A) with p<0.05, but not between the HBO2 group (Group C) and the control group (Group A). Fluorouracil 115-119 vascular endothelial growth factor A Homo sapiens 40-44 20433755-0 2010 Prostate apoptosis response protein 4 sensitizes human colon cancer cells to chemotherapeutic 5-FU through mediation of an NF kappaB and microRNA network. Fluorouracil 94-98 nuclear factor kappa B subunit 1 Homo sapiens 123-132 20422012-4 2010 Surprisingly, unlike the case for other p53 target promoters, p53-mediated transactivation of FLT1-T constructs or expression of the endogenous FLT1 gene, as well as binding of p53 and ER at the promoter constructs, was inducible by doxorubicin but not by 5-fluorouracil. Fluorouracil 256-270 tumor protein p53 Homo sapiens 62-65 20422012-4 2010 Surprisingly, unlike the case for other p53 target promoters, p53-mediated transactivation of FLT1-T constructs or expression of the endogenous FLT1 gene, as well as binding of p53 and ER at the promoter constructs, was inducible by doxorubicin but not by 5-fluorouracil. Fluorouracil 256-270 fms related receptor tyrosine kinase 1 Homo sapiens 94-98 20422012-4 2010 Surprisingly, unlike the case for other p53 target promoters, p53-mediated transactivation of FLT1-T constructs or expression of the endogenous FLT1 gene, as well as binding of p53 and ER at the promoter constructs, was inducible by doxorubicin but not by 5-fluorouracil. Fluorouracil 256-270 tumor protein p53 Homo sapiens 62-65 20422012-4 2010 Surprisingly, unlike the case for other p53 target promoters, p53-mediated transactivation of FLT1-T constructs or expression of the endogenous FLT1 gene, as well as binding of p53 and ER at the promoter constructs, was inducible by doxorubicin but not by 5-fluorouracil. Fluorouracil 256-270 estrogen receptor 1 Homo sapiens 185-187 20354524-7 2010 RESULTS: Oncogenic KRAS sensitised colorectal tumour cells to oxaliplatin and 5-FU in a p53-dependent manner and promoted p53 phosphorylation at Ser37 and Ser392, without affecting p53 stabilisation, p21 induction, or cell-cycle arrest. Fluorouracil 78-82 tumor protein p53 Homo sapiens 88-91 20354524-11 2010 CONCLUSION: Oncogenic KRAS determines the cellular response to p53 activation by oxaliplatin or 5-FU, by facilitating apoptosis induction through Noxa. Fluorouracil 96-100 tumor protein p53 Homo sapiens 63-66 20354524-11 2010 CONCLUSION: Oncogenic KRAS determines the cellular response to p53 activation by oxaliplatin or 5-FU, by facilitating apoptosis induction through Noxa. Fluorouracil 96-100 phorbol-12-myristate-13-acetate-induced protein 1 Homo sapiens 146-150 20180626-13 2010 DISCUSSION: Potential reasons for the disappointing results of EGFR inhibition with fluoropyrimidine-based preoperative chemoradiation include a less critical role of repopulation in rectal adenocarcinoma using a non-curative radiation dose; or antagonistic effects on 5FU-based chemoradiation and oxaliplatin, if some cells arrest in G1 or G2-M and fail to pass through S phase. Fluorouracil 269-272 epidermal growth factor receptor Homo sapiens 63-67 20106511-0 2010 Docetaxel, carboplatin and 5-fluorouracil (TCF) chemotherapy in patients with unresectable metastatic carcinoma of cervix. Fluorouracil 27-41 hepatocyte nuclear factor 4 alpha Homo sapiens 43-46 19782464-2 2010 The NFkappaB activity can be induced by dFdC and 5-FU exposure. Fluorouracil 49-53 nuclear factor kappa B subunit 1 Homo sapiens 4-12 20106511-1 2010 OBJECTIVES: This retrospective study evaluates the efficacy and safety of chemotherapy with docetaxel, carboplatin and 5-FU (TCF) in patients with metastatic cervical carcinoma. Fluorouracil 119-123 hepatocyte nuclear factor 4 alpha Homo sapiens 125-128 20106511-10 2010 CONCLUSIONS: The combination of docetaxel, carboplatin and 5-fluorouracil (TCF) appears to have activity in metastatic cervical carcinoma with acceptable toxicity profile. Fluorouracil 59-73 hepatocyte nuclear factor 4 alpha Homo sapiens 75-78 19810096-0 2010 Combination of p53 codon 72 polymorphism and inactive p53 mutation predicts chemosensitivity to 5-fluorouracil in colorectal cancer. Fluorouracil 96-110 tumor protein p53 Homo sapiens 15-18 19810096-0 2010 Combination of p53 codon 72 polymorphism and inactive p53 mutation predicts chemosensitivity to 5-fluorouracil in colorectal cancer. Fluorouracil 96-110 tumor protein p53 Homo sapiens 54-57 19810096-2 2010 We investigated whether p53 polymorphism and mutation were associated with in vitro sensitivity to 5-fluorouracil (5-FU) in patients with colorectal cancer. Fluorouracil 99-113 tumor protein p53 Homo sapiens 24-27 19810096-2 2010 We investigated whether p53 polymorphism and mutation were associated with in vitro sensitivity to 5-fluorouracil (5-FU) in patients with colorectal cancer. Fluorouracil 115-119 tumor protein p53 Homo sapiens 24-27 19810096-4 2010 5-FU sensitivity of tumor cells without inactive p53 mutation in the arginine/arginine (Arg/Arg) variant was significantly higher than that of tumor cells with or without inactive p53 mutation in other variants (p = 0.022), whereas the 5-FU sensitivity of tumor cells with inactive p53 mutation in the Arg/Arg variant was significantly lower than that of tumor cells with or without inactive p53 mutation in other variants (p = 0.002). Fluorouracil 0-4 tumor protein p53 Homo sapiens 49-52 19810096-5 2010 In the Arg/Arg variant, apoptotic cells induced by 5-FU treatment in patients without inactive p53 mutation were more markedly increased than those in patients with inactive p53 mutation (p = 0.037). Fluorouracil 51-55 tumor protein p53 Homo sapiens 95-98 19810096-5 2010 In the Arg/Arg variant, apoptotic cells induced by 5-FU treatment in patients without inactive p53 mutation were more markedly increased than those in patients with inactive p53 mutation (p = 0.037). Fluorouracil 51-55 tumor protein p53 Homo sapiens 174-177 19810096-6 2010 Bax and Bcl-2 protein expressions in tumor tissue treated with 5-FU were associated with both 5-FU sensitivity and the apoptotic cell count. Fluorouracil 63-67 BCL2 associated X, apoptosis regulator Homo sapiens 0-3 19810096-6 2010 Bax and Bcl-2 protein expressions in tumor tissue treated with 5-FU were associated with both 5-FU sensitivity and the apoptotic cell count. Fluorouracil 63-67 BCL2 apoptosis regulator Homo sapiens 8-13 19810096-6 2010 Bax and Bcl-2 protein expressions in tumor tissue treated with 5-FU were associated with both 5-FU sensitivity and the apoptotic cell count. Fluorouracil 94-98 BCL2 associated X, apoptosis regulator Homo sapiens 0-3 19810096-6 2010 Bax and Bcl-2 protein expressions in tumor tissue treated with 5-FU were associated with both 5-FU sensitivity and the apoptotic cell count. Fluorouracil 94-98 BCL2 apoptosis regulator Homo sapiens 8-13 19810096-8 2010 The combination of the p53 codon 72 polymorphism and p53 mutation status is a potential predictive marker of sensitivity to 5-FU in CRC. Fluorouracil 124-128 tumor protein p53 Homo sapiens 23-26 19810096-8 2010 The combination of the p53 codon 72 polymorphism and p53 mutation status is a potential predictive marker of sensitivity to 5-FU in CRC. Fluorouracil 124-128 tumor protein p53 Homo sapiens 53-56 20414030-13 2010 Differences in the 5-fluorouracil concentration of UFT and that of S-1 may explain the effectiveness of S-1 for recurrence of gastric cancer after adjuvant chemotherapy with UFT. Fluorouracil 19-33 proteasome 26S subunit, non-ATPase 1 Homo sapiens 104-107 20339982-2 2010 Recently developed agents such as irinotecan, taxanes (docetaxel), and new oral fluorouracil (S-1) have yielded more promising results, with a response rate of over 50% and a median survival time of over 10 months in combination studies. Fluorouracil 80-92 proteasome 26S subunit, non-ATPase 1 Homo sapiens 94-97 20012971-2 2010 In the present study, expression of members of the transforming growth factor-beta1 (TGF-beta1) signaling pathway was investigated in pretherapeutic biopsies from 97 ESCCs (cT3, cN0/+, cM0) in patients who underwent neoadjuvant chemoradiotherapy (45 Gy plus cisplatin and 5-fluorouracil) and subsequent esophagectomy in the setting of a single-center prospective treatment trial. Fluorouracil 272-286 transforming growth factor beta 1 Homo sapiens 51-83 20012971-2 2010 In the present study, expression of members of the transforming growth factor-beta1 (TGF-beta1) signaling pathway was investigated in pretherapeutic biopsies from 97 ESCCs (cT3, cN0/+, cM0) in patients who underwent neoadjuvant chemoradiotherapy (45 Gy plus cisplatin and 5-fluorouracil) and subsequent esophagectomy in the setting of a single-center prospective treatment trial. Fluorouracil 272-286 transforming growth factor beta 1 Homo sapiens 85-94 20360934-9 2010 In addition, curcumin, a well-known inhibitor of NF-kappaB activity, was shown to increase apoptosis and enhance both 5-FU- and CDDP-mediated chemosensitivity, suggesting that it may have potential application in the therapy of patients with EAC. Fluorouracil 118-122 nuclear factor kappa B subunit 1 Homo sapiens 49-58 20238327-19 2010 Two and three-drug regimens including 5-FU, cisplatin, with or without an anthracycline, as well as irinotecan or docetaxel-containing regimens are reasonable treatment options for HER-2 negative patients. Fluorouracil 38-42 erb-b2 receptor tyrosine kinase 2 Homo sapiens 181-186 20037758-9 2010 RESULTS: Area under the concentration-time curve (AUC)of 5-FU was 2647.2 ng h/mL after administration of S-1 of 23.5 mg/m(2) (40 mg/body). Fluorouracil 57-61 proteasome 26S subunit, non-ATPase 1 Homo sapiens 105-108 20181235-1 2010 BACKGROUND: The combination of gemcitabine (GEM) and S-1, an oral 5-fluorouracil (5-FU) derivative, has been shown to be a promising regimen for patients with unresectable pancreatic cancer. Fluorouracil 66-80 proteasome 26S subunit, non-ATPase 1 Homo sapiens 53-56 20450582-0 2010 [Insulin induces anticancer cytotoxicity of 5-Fu to two human colon cancer cell lines]. Fluorouracil 44-48 insulin Homo sapiens 1-8 20450582-1 2010 OBJECTIVE: To explore the possibility of use of insulin as a potentiator of 5-Fu to human colon cancer cell lines HCT-8 and HT-29 and study its mechanism. Fluorouracil 76-80 insulin Homo sapiens 48-55 20450582-4 2010 RESULTS: Insulin showed an enhancing effect on the chemotherapeutic response of 5-Fu when insulin was applied at a dose of exceeding 0.8 mU/ml 0 approximately 8 h before 5-Fu. Fluorouracil 80-84 insulin Homo sapiens 9-16 20450582-4 2010 RESULTS: Insulin showed an enhancing effect on the chemotherapeutic response of 5-Fu when insulin was applied at a dose of exceeding 0.8 mU/ml 0 approximately 8 h before 5-Fu. Fluorouracil 80-84 insulin Homo sapiens 90-97 20450582-4 2010 RESULTS: Insulin showed an enhancing effect on the chemotherapeutic response of 5-Fu when insulin was applied at a dose of exceeding 0.8 mU/ml 0 approximately 8 h before 5-Fu. Fluorouracil 170-174 insulin Homo sapiens 9-16 20450582-4 2010 RESULTS: Insulin showed an enhancing effect on the chemotherapeutic response of 5-Fu when insulin was applied at a dose of exceeding 0.8 mU/ml 0 approximately 8 h before 5-Fu. Fluorouracil 170-174 insulin Homo sapiens 90-97 20450582-9 2010 CONCLUSION: Insulin can enhance the anticancer toxicity of 5-Fu to human colon cancer cell lines HCT-8 and HT-29 cells. Fluorouracil 59-63 insulin Homo sapiens 12-19 20450582-10 2010 Insulin increases the percentage of S phase cells, which may be one of the main mechanisms of insulin-induced enhancement of anticancer response of cancer cells to 5-Fu chemotherapy. Fluorouracil 164-168 insulin Homo sapiens 0-7 20450582-10 2010 Insulin increases the percentage of S phase cells, which may be one of the main mechanisms of insulin-induced enhancement of anticancer response of cancer cells to 5-Fu chemotherapy. Fluorouracil 164-168 insulin Homo sapiens 94-101 20042597-8 2010 It was also suggested by studies of the inhibitory effect on rSNBT1-mediated uracil transport that several nucleobase analogs such as 5-fluorouracil are recognized by rSNBT1, but cytosine and nucleosides are not or only poorly recognized. Fluorouracil 134-148 similar to Solute carrier family 23, member 2 (Sodium-dependent vitamin C transporter 2) Rattus norvegicus 61-67 20042597-8 2010 It was also suggested by studies of the inhibitory effect on rSNBT1-mediated uracil transport that several nucleobase analogs such as 5-fluorouracil are recognized by rSNBT1, but cytosine and nucleosides are not or only poorly recognized. Fluorouracil 134-148 similar to Solute carrier family 23, member 2 (Sodium-dependent vitamin C transporter 2) Rattus norvegicus 167-173 20181235-1 2010 BACKGROUND: The combination of gemcitabine (GEM) and S-1, an oral 5-fluorouracil (5-FU) derivative, has been shown to be a promising regimen for patients with unresectable pancreatic cancer. Fluorouracil 82-86 proteasome 26S subunit, non-ATPase 1 Homo sapiens 53-56 19941080-3 2010 METHODS: Genomic mutation and protein expression of p53 were investigated retrospectively by polymerase chain reaction (PCR) single-strand conformation polymorphism (SSCP) and immunohistochemistry (IHC) using biopsy specimens from 77 ESCC patients before chemotherapy with 5-fluorouracil, adriamycin, and cisplatin. Fluorouracil 273-287 tumor protein p53 Homo sapiens 52-55 20048189-0 2010 TP53 mutations and pathologic complete response to neoadjuvant cisplatin and fluorouracil chemotherapy in resected oral cavity squamous cell carcinoma. Fluorouracil 77-89 tumor protein p53 Homo sapiens 0-4 19585117-10 2010 Western blotting assay revealed oroxylin A enhanced 5-FU-induced apoptosis in HepG2 cells by elevating the expressions of apoptotic-inducing proteins P53 and cleaved PARP and decreasing the expression of apoptotic-inhibitory proteins COX-2, Bcl-2, and pro-caspase3. Fluorouracil 52-56 tumor protein p53 Homo sapiens 150-153 19585117-10 2010 Western blotting assay revealed oroxylin A enhanced 5-FU-induced apoptosis in HepG2 cells by elevating the expressions of apoptotic-inducing proteins P53 and cleaved PARP and decreasing the expression of apoptotic-inhibitory proteins COX-2, Bcl-2, and pro-caspase3. Fluorouracil 52-56 mitochondrially encoded cytochrome c oxidase II Homo sapiens 234-239 19585117-10 2010 Western blotting assay revealed oroxylin A enhanced 5-FU-induced apoptosis in HepG2 cells by elevating the expressions of apoptotic-inducing proteins P53 and cleaved PARP and decreasing the expression of apoptotic-inhibitory proteins COX-2, Bcl-2, and pro-caspase3. Fluorouracil 52-56 BCL2 apoptosis regulator Homo sapiens 241-246 19585117-10 2010 Western blotting assay revealed oroxylin A enhanced 5-FU-induced apoptosis in HepG2 cells by elevating the expressions of apoptotic-inducing proteins P53 and cleaved PARP and decreasing the expression of apoptotic-inhibitory proteins COX-2, Bcl-2, and pro-caspase3. Fluorouracil 52-56 caspase 3 Homo sapiens 252-264 19621386-0 2010 Vitamin D mediates its action in human colon carcinoma cells in a calcium-sensing receptor-dependent manner: downregulates malignant cell behavior and the expression of thymidylate synthase and survivin and promotes cellular sensitivity to 5-FU. Fluorouracil 240-244 calcium sensing receptor Homo sapiens 66-90 19621386-9 2010 We now demonstrate, for the first time, that VD suppressed the expression of TS and survivin, TS and survivin gene transcriptional activities and promoted a cytotoxic response to 5-FU in a CaSR-dependent manner. Fluorouracil 179-183 calcium sensing receptor Homo sapiens 189-193 19621386-10 2010 Ectopic expression of wild-type CaSR in colon carcinoma cells also inhibited the expression of TS and survivin and enhanced cellular sensitivity to 5-FU. Fluorouracil 148-152 calcium sensing receptor Homo sapiens 32-36 19074180-11 2010 Conversely, Il6 null mice exhibited impaired recovery following massive enterectomy and increased apoptosis after 5-fluorouracil chemotherapy relative to wild-type controls. Fluorouracil 114-128 interleukin 6 Mus musculus 12-15 19712668-9 2010 Interestingly, deficiencies in HR (rad52) and PPR (rad6, rad18) were associated with increased sensitivity to 5-FU, but not to FdUMP. Fluorouracil 110-114 E3 ubiquitin-protein ligase RAD18 Saccharomyces cerevisiae S288C 57-62 20522971-4 2010 Here, we examined the effects of dCyd on the cytotoxicity of 5FU on mouse myeloma SP2/0-Ag14 (SP2/0) cells lacking hypoxanthine-guanine-phosphoribosyl transferase (HGPRT) and RH4 hybridomas with HGPRT under asynchronized conditions. Fluorouracil 61-64 Sp2 transcription factor Mus musculus 82-87 20522971-4 2010 Here, we examined the effects of dCyd on the cytotoxicity of 5FU on mouse myeloma SP2/0-Ag14 (SP2/0) cells lacking hypoxanthine-guanine-phosphoribosyl transferase (HGPRT) and RH4 hybridomas with HGPRT under asynchronized conditions. Fluorouracil 61-64 Sp2 transcription factor Mus musculus 94-99 20437857-2 2010 In metastatic gastric cancer, chemotherapy with docetaxel, cisplatin and 5-fluorouracil (TCF) q3w is very active, and, even though there is no international consensus on the subject, it is the regimen of choice of many European centers as first-line chemotherapy in this subset of patients. Fluorouracil 73-87 hepatocyte nuclear factor 4 alpha Homo sapiens 89-92 20058135-1 2010 UFT and S-1 are oral 5-fluorouracil (5-FU) derivative drugs containing an inhibitor of dihydropyrimidine dehydrogenase (DPD); they are defined as DPD-inhibitory fluoropyrimidine (DIF). Fluorouracil 21-35 proteasome 26S subunit, non-ATPase 1 Homo sapiens 8-11 20058135-1 2010 UFT and S-1 are oral 5-fluorouracil (5-FU) derivative drugs containing an inhibitor of dihydropyrimidine dehydrogenase (DPD); they are defined as DPD-inhibitory fluoropyrimidine (DIF). Fluorouracil 37-41 proteasome 26S subunit, non-ATPase 1 Homo sapiens 8-11 19629643-6 2010 In contrast, Apak was not phosphorylated at Ser68 after 5-fluorouracil or alpha-lipoic acid treatment and persistently inhibited p53 activity. Fluorouracil 56-70 zinc finger protein 420 Homo sapiens 13-17 21372603-2 2010 The current retrospective study was conducted to find whether S-1, an orally administered 5-FU agent, can produce a therapeutic result in patients with recurrent metastatic breast cancer while maintaining their QOL. Fluorouracil 90-94 proteasome 26S subunit, non-ATPase 1 Homo sapiens 62-65 20437857-3 2010 Based on these studies, we tested for the first time the feasibility and activity of an intensified dose-dense TCF regimen (q2w) modifying the 5-fluorouracil infusion with 1-folinic acid/5-fluorouracil according to the "De Gramont regimen". Fluorouracil 143-157 hepatocyte nuclear factor 4 alpha Homo sapiens 111-114 20437857-3 2010 Based on these studies, we tested for the first time the feasibility and activity of an intensified dose-dense TCF regimen (q2w) modifying the 5-fluorouracil infusion with 1-folinic acid/5-fluorouracil according to the "De Gramont regimen". Fluorouracil 187-201 hepatocyte nuclear factor 4 alpha Homo sapiens 111-114 20057904-1 2009 PURPOSE: S-1 is an oral antineoplastic agent that contains a prodrug of 5-fluorouracil and has adverse effects on skin, alimentary tract mucosa, and the ocular surface. Fluorouracil 72-86 proteasome 26S subunit, non-ATPase 1 Homo sapiens 9-12 19861116-7 2009 Chemoresistance to 5-fluorouracil (IC50) was higher in SNAI1-6SA and SNAI1-8SA transfectants compared with SNAI1-WT and NC. Fluorouracil 19-33 snail family transcriptional repressor 1 Homo sapiens 55-60 19861116-7 2009 Chemoresistance to 5-fluorouracil (IC50) was higher in SNAI1-6SA and SNAI1-8SA transfectants compared with SNAI1-WT and NC. Fluorouracil 19-33 snail family transcriptional repressor 1 Homo sapiens 69-74 19861116-7 2009 Chemoresistance to 5-fluorouracil (IC50) was higher in SNAI1-6SA and SNAI1-8SA transfectants compared with SNAI1-WT and NC. Fluorouracil 19-33 snail family transcriptional repressor 1 Homo sapiens 69-74 19920821-1 2009 BACKGROUND: Both irinotecan (CPT-11) and S-1 are active against colorectal cancer; however, as S-1 is a prodrug of 5-fluorouracil (5-FU), 5-FU and its metabolites might inhibit the antitumour effect of CPT-11. Fluorouracil 115-129 proteasome 26S subunit, non-ATPase 1 Homo sapiens 41-44 20014456-8 2009 Apoptosis resistance towards TRAIL could be considerably reduced by adding the chemotherapeutic drugs 5-fluorouracil and doxorubicin as well as the kinase inhibitors LY294002 [inhibition of phosphoinositol-3-kinase (PI3K)], AG1478 (epidermal growth factor receptor kinase), PD98059 (MEK1), rapamycin (mammalian target of rapamycin) and the multi-kinase inhibitor Sorafenib. Fluorouracil 102-116 TNF superfamily member 10 Homo sapiens 29-34 20014456-8 2009 Apoptosis resistance towards TRAIL could be considerably reduced by adding the chemotherapeutic drugs 5-fluorouracil and doxorubicin as well as the kinase inhibitors LY294002 [inhibition of phosphoinositol-3-kinase (PI3K)], AG1478 (epidermal growth factor receptor kinase), PD98059 (MEK1), rapamycin (mammalian target of rapamycin) and the multi-kinase inhibitor Sorafenib. Fluorouracil 102-116 mechanistic target of rapamycin kinase Homo sapiens 301-330 19920821-1 2009 BACKGROUND: Both irinotecan (CPT-11) and S-1 are active against colorectal cancer; however, as S-1 is a prodrug of 5-fluorouracil (5-FU), 5-FU and its metabolites might inhibit the antitumour effect of CPT-11. Fluorouracil 115-129 proteasome 26S subunit, non-ATPase 1 Homo sapiens 95-98 19920821-1 2009 BACKGROUND: Both irinotecan (CPT-11) and S-1 are active against colorectal cancer; however, as S-1 is a prodrug of 5-fluorouracil (5-FU), 5-FU and its metabolites might inhibit the antitumour effect of CPT-11. Fluorouracil 131-135 proteasome 26S subunit, non-ATPase 1 Homo sapiens 41-44 19920821-1 2009 BACKGROUND: Both irinotecan (CPT-11) and S-1 are active against colorectal cancer; however, as S-1 is a prodrug of 5-fluorouracil (5-FU), 5-FU and its metabolites might inhibit the antitumour effect of CPT-11. Fluorouracil 131-135 proteasome 26S subunit, non-ATPase 1 Homo sapiens 95-98 19920821-1 2009 BACKGROUND: Both irinotecan (CPT-11) and S-1 are active against colorectal cancer; however, as S-1 is a prodrug of 5-fluorouracil (5-FU), 5-FU and its metabolites might inhibit the antitumour effect of CPT-11. Fluorouracil 138-142 proteasome 26S subunit, non-ATPase 1 Homo sapiens 41-44 19920821-1 2009 BACKGROUND: Both irinotecan (CPT-11) and S-1 are active against colorectal cancer; however, as S-1 is a prodrug of 5-fluorouracil (5-FU), 5-FU and its metabolites might inhibit the antitumour effect of CPT-11. Fluorouracil 138-142 proteasome 26S subunit, non-ATPase 1 Homo sapiens 95-98 19837844-5 2009 In wild-type D. vulgaris, growth was shown to be inhibited by the toxic pyrimidine analog 5-fluorouracil (5-FU), whereas a mutant bearing a deletion of the upp gene was resistant to 5-FU. Fluorouracil 106-110 upp Desulfovibrio vulgaris str. Hildenborough 156-159 19954513-0 2009 Identification of colorectal cancer patients with tumors carrying the TP53 mutation on the codon 72 proline allele that benefited most from 5-fluorouracil (5-FU) based postoperative chemotherapy. Fluorouracil 140-154 tumor protein p53 Homo sapiens 70-74 19954513-0 2009 Identification of colorectal cancer patients with tumors carrying the TP53 mutation on the codon 72 proline allele that benefited most from 5-fluorouracil (5-FU) based postoperative chemotherapy. Fluorouracil 156-160 tumor protein p53 Homo sapiens 70-74 19837844-5 2009 In wild-type D. vulgaris, growth was shown to be inhibited by the toxic pyrimidine analog 5-fluorouracil (5-FU), whereas a mutant bearing a deletion of the upp gene was resistant to 5-FU. Fluorouracil 182-186 upp Desulfovibrio vulgaris str. Hildenborough 156-159 19764996-6 2009 mTOR inhibitors with 5FU showed a synergistic antiproliferative effect in scirrhous gastric cancer, whereas the other signal inhibitors showed no synergistic effect with any anticancer drugs. Fluorouracil 21-24 mechanistic target of rapamycin kinase Homo sapiens 0-4 19954513-2 2009 Previous in vitro and clinical investigations reported that CRC patients with wild-type p53 gene (TP53)-tumors benefit from 5-fluorouracil (5-FU) based chemotherapy, while those with mutated TP53-tumors do not. Fluorouracil 124-138 tumor protein p53 Homo sapiens 88-91 19954513-2 2009 Previous in vitro and clinical investigations reported that CRC patients with wild-type p53 gene (TP53)-tumors benefit from 5-fluorouracil (5-FU) based chemotherapy, while those with mutated TP53-tumors do not. Fluorouracil 124-138 tumor protein p53 Homo sapiens 98-102 19954513-2 2009 Previous in vitro and clinical investigations reported that CRC patients with wild-type p53 gene (TP53)-tumors benefit from 5-fluorouracil (5-FU) based chemotherapy, while those with mutated TP53-tumors do not. Fluorouracil 140-144 tumor protein p53 Homo sapiens 88-91 19954513-2 2009 Previous in vitro and clinical investigations reported that CRC patients with wild-type p53 gene (TP53)-tumors benefit from 5-fluorouracil (5-FU) based chemotherapy, while those with mutated TP53-tumors do not. Fluorouracil 140-144 tumor protein p53 Homo sapiens 98-102 19954513-10 2009 We raised a possibility that Dukes" stage C colorectal cancer patients with tumors carrying TP53 mutation, especially the P72 allele, benefited from 5-FU based postoperative chemotherapy. Fluorouracil 149-153 tumor protein p53 Homo sapiens 92-96 19954513-10 2009 We raised a possibility that Dukes" stage C colorectal cancer patients with tumors carrying TP53 mutation, especially the P72 allele, benefited from 5-FU based postoperative chemotherapy. Fluorouracil 149-153 DEAD-box helicase 17 Homo sapiens 122-125 19764996-12 2009 Therefore, mTOR inhibitor is a promising therapeutic agent in combination with 5FU in scirrhous gastric cancer. Fluorouracil 79-82 mechanistic target of rapamycin kinase Homo sapiens 11-15 19666095-3 2009 For example, P-CS/GA (0.1 wt.%) gels have swelling ratios of 13.2+/-1.0, which are maintained for approximately 18 h in water at 37 degrees C. In vitro releases of 5-FU from P-CS/GA (0.1 wt.%) gels had significantly lower initial burst release (P<0.01) and lasted much longer than those from gels without a CS network. Fluorouracil 164-168 PCS Homo sapiens 13-20 19666095-3 2009 For example, P-CS/GA (0.1 wt.%) gels have swelling ratios of 13.2+/-1.0, which are maintained for approximately 18 h in water at 37 degrees C. In vitro releases of 5-FU from P-CS/GA (0.1 wt.%) gels had significantly lower initial burst release (P<0.01) and lasted much longer than those from gels without a CS network. Fluorouracil 164-168 PCS Homo sapiens 174-181 19952114-0 2009 COMP-Ang1 potentiates the antitumor activity of 5-fluorouracil by improving tissue perfusion in murine Lewis lung carcinoma. Fluorouracil 48-62 angiopoietin 1 Mus musculus 5-9 19952114-4 2009 The combination of COMP-Ang1 with the cytotoxic drug 5-fluorouracil potentiated the effect of 5-fluorouracil on tumor growth without increasing animal toxicity. Fluorouracil 94-108 angiopoietin 1 Mus musculus 24-28 19885597-5 2009 In the present study, treatment of colorectal cancer cells with PI3K p85alpha-specific siRNA inhibited cell proliferation, induced G1 phase cell cycle arrest and sensitized colorectal cancer cells to 5-FU-induced apoptosis. Fluorouracil 200-204 phosphoinositide-3-kinase regulatory subunit 1 Homo sapiens 69-77 19885610-8 2009 Moreover, compared with 5-fluorouracil alone, 5-fluorouracil in combination with apigenin at concentrations >10 microM exerted a pro-apoptotic effect via the inhibition of Akt expression. Fluorouracil 46-60 AKT serine/threonine kinase 1 Homo sapiens 175-178 19885610-2 2009 The MDA-MB-453 cells, which have been shown to overexpress ErbB2, were resistant to 5-fluorouracil; 5-fluorouracil exhibited a small dose-dependent anti-proliferative effect, with an IC50 of 90 microM. Fluorouracil 100-114 erb-b2 receptor tyrosine kinase 2 Homo sapiens 59-64 19885610-9 2009 Taken together, our results suggest that 5-fluorouracil acts synergistically with apigenin inhibiting cell growth and inducing apoptosis via the down-regulation of ErbB2 expression and Akt signaling. Fluorouracil 41-55 erb-b2 receptor tyrosine kinase 2 Homo sapiens 164-169 19885610-9 2009 Taken together, our results suggest that 5-fluorouracil acts synergistically with apigenin inhibiting cell growth and inducing apoptosis via the down-regulation of ErbB2 expression and Akt signaling. Fluorouracil 41-55 AKT serine/threonine kinase 1 Homo sapiens 185-188 19885610-7 2009 The level of ErbB2 was unchanged by 5-fluorouracil alone but was drastically reduced in cells treated with 5-fluorouracil plus apigenin. Fluorouracil 36-50 erb-b2 receptor tyrosine kinase 2 Homo sapiens 13-18 19885610-7 2009 The level of ErbB2 was unchanged by 5-fluorouracil alone but was drastically reduced in cells treated with 5-fluorouracil plus apigenin. Fluorouracil 107-121 erb-b2 receptor tyrosine kinase 2 Homo sapiens 13-18 19461675-4 2009 RAd-hCD40L is also found to be superior to recombinant CD40L in inducing carcinoma cell death and in amplifying the cytotoxic effects of the chemotherapeutic agents 5-fluorouracil, cis-platin and mitomycin C. Fluorouracil 165-179 CD40 ligand Homo sapiens 4-10 19461675-4 2009 RAd-hCD40L is also found to be superior to recombinant CD40L in inducing carcinoma cell death and in amplifying the cytotoxic effects of the chemotherapeutic agents 5-fluorouracil, cis-platin and mitomycin C. Fluorouracil 165-179 CD40 ligand Homo sapiens 5-10 19793002-6 2009 The downregulation of cIAP2 efficiently enhances apoptosis through the activation of caspase 3/7 and 5-fluorouracil (5-FU) sensitivity in colorectal cancer cells exposed to 5-FU. Fluorouracil 173-177 caspase 3 Homo sapiens 85-94 19901540-0 2009 Inhibition of Hsp27 and Hsp40 potentiates 5-fluorouracil and carboplatin mediated cell killing in hepatoma cells. Fluorouracil 42-56 DnaJ heat shock protein family (Hsp40) member B1 pseudogene 1 Homo sapiens 24-29 19901540-4 2009 We for the first time report that 5-fluorouracil (5-FU) and carboplatin specifically induce expression of Hsp40 in addition to Hsp27 in Hep3B and HepG2 cells. Fluorouracil 34-48 DnaJ heat shock protein family (Hsp40) member B1 pseudogene 1 Homo sapiens 106-111 19901540-4 2009 We for the first time report that 5-fluorouracil (5-FU) and carboplatin specifically induce expression of Hsp40 in addition to Hsp27 in Hep3B and HepG2 cells. Fluorouracil 50-54 DnaJ heat shock protein family (Hsp40) member B1 pseudogene 1 Homo sapiens 106-111 19901540-11 2009 Collectively, our novel findings on compelling action of 5-FU or carboplatin following knockdown of Hsp40 and that of Hsp27 highlights their strategic implications towards an effective therapy against HCC. Fluorouracil 57-61 DnaJ heat shock protein family (Hsp40) member B1 pseudogene 1 Homo sapiens 100-105 19923910-0 2009 The combination of 5-fluorouracil plus p53 pathway restoration is associated with depletion of p53-deficient or mutant p53-expressing putative colon cancer stem cells. Fluorouracil 19-33 tumor protein p53 Homo sapiens 95-98 19923910-0 2009 The combination of 5-fluorouracil plus p53 pathway restoration is associated with depletion of p53-deficient or mutant p53-expressing putative colon cancer stem cells. Fluorouracil 19-33 tumor protein p53 Homo sapiens 95-98 19843160-7 2009 In addition, extracellular-regulated protein kinase 5, nuclear factor-kappaB and Bcl-2 protein expression was down-regulated by miR-143, and further reduced by exposure to 5-fluorouracil. Fluorouracil 172-186 BCL2 apoptosis regulator Homo sapiens 81-86 19210287-3 2009 By using gene-deficient mice, we found that plasmin and its activators tPA and uPA play a role in the haematopoietic recovery upon delivery of the cytotoxic agent 5-fluoro-uracil (5-FU). Fluorouracil 163-178 promotion susceptibility QTL 1 Mus musculus 71-74 19731257-3 2009 The dependence of p53-mediated chemosensitivity on pRb status was first investigated in a prospective study on the prognostic relevance of p53 in breast cancer patients treated with adjuvant chemotherapy (5-fluorouracil, methotrexate and cyclophosphamide). Fluorouracil 205-219 tumor protein p53 Homo sapiens 18-21 19731257-6 2009 We then studied the role of pRb status in the p53-mediated response to 5-fluorouracil and methotrexate or doxorubicin treatment in three human cancer cell lines. Fluorouracil 71-85 tumor protein p53 Homo sapiens 46-49 19210287-3 2009 By using gene-deficient mice, we found that plasmin and its activators tPA and uPA play a role in the haematopoietic recovery upon delivery of the cytotoxic agent 5-fluoro-uracil (5-FU). Fluorouracil 180-184 promotion susceptibility QTL 1 Mus musculus 71-74 19821965-1 2009 BACKGROUND: The combination therapy of interferon (IFN)-alpha and 5-fluorouracil (5-FU) improved the prognosis of the patients with hepatocellular carcinoma (HCC). Fluorouracil 82-86 interferon alpha 1 Homo sapiens 39-61 19821965-5 2009 RESULTS: IFN-alpha and 5-FU alone had anti-proliferative properties on HUVEC and their combination significantly inhibited the growth (compared with control, 5-FU or IFN alone). Fluorouracil 158-162 interferon alpha 1 Homo sapiens 9-18 19846930-4 2009 5-FU substantially reduced TS activity by 50% in IL-2-activated PBMCs. Fluorouracil 0-4 interleukin 2 Homo sapiens 49-53 19846930-0 2009 Effects of 5-FU on DNA synthesis and cytotoxicity of human lymphocytes induced by IL-2, TGF-beta3 and PGE2. Fluorouracil 11-15 interleukin 2 Homo sapiens 82-86 19846930-5 2009 5-FU combined with TGF-beta3 and PGE(2) did not alter their inhibitory effects on IL-2-activated natural killer cell cytotoxicity, but substantially affected increased DNA synthesis of cells cultured in IL-2 and co-cultured with 10 ng/ml TGF-beta3 and 10 microM PGE(2). Fluorouracil 0-4 interleukin 2 Homo sapiens 203-207 19846930-2 2009 MATERIALS AND METHODS: We explored 2.5 microM 5-FU-induced DNA synthesis by testing 5-FU activity in hypoxanthine-aminopterin-thymidine (HAT)-containing medium, and its effect on thymidylate synthase (TS) activity and CD25 expression in interleukin (IL)-2-activated human peripheral blood mononuclear cells (PBMCs) and the combined effects with prostaglandin E(2) (PGE(2)) and transforming growth factor (TGF)-beta3. Fluorouracil 46-50 interleukin 2 Homo sapiens 237-255 19846930-6 2009 CONCLUSION: Low 5-FU concentrations increase DNA synthesis in lymphocytes and exert a co-stimulatory activity on TGF-beta3 and PGE(2) modulation of IL-2-activated lymphocytes. Fluorouracil 16-20 interleukin 2 Homo sapiens 148-152 19846936-7 2009 During the first 48 h of incubation, VEGF and EGF induced a near 30% reduction in 5-FU antitumour activity, while exposure to HGF abrogated the drug-induced growth inhibition. Fluorouracil 82-86 vascular endothelial growth factor A Homo sapiens 37-41 19565301-0 2009 Effective treatment of advanced colorectal cancer by rapamycin and 5-FU/oxaliplatin monitored by TIMP-1. Fluorouracil 67-71 tissue inhibitor of metalloproteinase 1 Mus musculus 97-103 19846936-9 2009 Moreover, the addition of either of the GSH modulators to 5-FU produced an increase of nearly 40% in the 5-FU activity in the case of HGF or VEGF, and a 25% increase in the case of EGF. Fluorouracil 58-62 vascular endothelial growth factor A Homo sapiens 141-145 19846936-9 2009 Moreover, the addition of either of the GSH modulators to 5-FU produced an increase of nearly 40% in the 5-FU activity in the case of HGF or VEGF, and a 25% increase in the case of EGF. Fluorouracil 105-109 vascular endothelial growth factor A Homo sapiens 141-145 19838025-2 2009 SUBJECTS AND METHODS: The efficacy of treatment with S-1 (initial dosage: 80 mg/m(2)) was studied in 19 patients with advanced recurrent colon cancer in whom PD was observed after pretreatment with 5-FU-based combination chemotherapy had been performed during the period from December 2003 to April 2006. Fluorouracil 198-202 proteasome 26S subunit, non-ATPase 1 Homo sapiens 53-56 19856075-1 2009 S-1 is an oral 5-fluorouracil (5-FU) anticancer agent and has shown promising effects in the treatment of a wide range of carcinomas, including head and neck cancer. Fluorouracil 15-29 proteasome 26S subunit, non-ATPase 1 Homo sapiens 0-3 19856075-1 2009 S-1 is an oral 5-fluorouracil (5-FU) anticancer agent and has shown promising effects in the treatment of a wide range of carcinomas, including head and neck cancer. Fluorouracil 31-35 proteasome 26S subunit, non-ATPase 1 Homo sapiens 0-3 19724845-0 2009 Hypoxia-inducible factor-1alpha expression predicts the response to 5-fluorouracil-based adjuvant chemotherapy in advanced gastric cancer. Fluorouracil 68-82 hypoxia inducible factor 1 subunit alpha Homo sapiens 0-31 19605487-5 2009 Both HCV core protein and a chemotherapeutic agent for HCC, 5-flouorouracil (5-FU), are known to modulate p53. Fluorouracil 77-81 tumor protein p53 Homo sapiens 106-109 19605487-6 2009 We examined here whether an association between core and HAX-1 has any functional relevance to p53 modulation in 5-FU-treated cells. Fluorouracil 113-117 tumor protein p53 Homo sapiens 95-98 19605487-9 2009 Further, 5-FU-mediated p53 expression was reduced with concurrent HAX-1 suppression in core- or polyprotein-expressing cells compared to control HepG2 cells, and caspase-2 and -7 activities were diminished. Fluorouracil 9-13 tumor protein p53 Homo sapiens 23-26 19605487-11 2009 These observations underscore an association between HCV core and HAX-1, which promotes 5-FU mediated p53-dependent caspase-7 activation and hepatocyte growth inhibition. Fluorouracil 88-92 tumor protein p53 Homo sapiens 102-105 19724845-10 2009 These results indicated that the diffuse expression of HIF-1alpha in gastric tumors might lead to drug resistance against adjuvant chemotherapy using 5-FU. Fluorouracil 150-154 hypoxia inducible factor 1 subunit alpha Homo sapiens 55-65 19724845-11 2009 In conclusion, the assessment of the HIF-1alpha expression in the resected tissues might predict the drug response to adjuvant 5-FU chemotherapy in advanced gastric cancer patients. Fluorouracil 127-131 hypoxia inducible factor 1 subunit alpha Homo sapiens 37-47 19724848-1 2009 S-1, an oral fluorouracil antitumor drug, is composed of three agents: tegafur (FT), 5-chloro-2,4-dihydroxypyridine (CDHP), and potassium oxonate (Oxo). Fluorouracil 13-25 eukaryotic translation elongation factor 1 alpha 2 Mus musculus 0-3 19724848-10 2009 Western blot analysis revealed that treatment with 5-FU and CDHP suppressed expression of integrins alphav, alpha3, alpha6, beta1, beta3, beta4, beta5, and beta6. Fluorouracil 51-55 cholinergic receptor, nicotinic, alpha polypeptide 3 Mus musculus 108-136 19724848-10 2009 Western blot analysis revealed that treatment with 5-FU and CDHP suppressed expression of integrins alphav, alpha3, alpha6, beta1, beta3, beta4, beta5, and beta6. Fluorouracil 51-55 integrin beta 5 Mus musculus 145-161 19362768-7 2009 With the changes in caspase-6 and cell cycle, ZBP-89 greatly enhanced the killing effectiveness of 5-fluorouracil or staurosporine in HCC cells. Fluorouracil 99-113 zinc finger protein 148 Homo sapiens 46-52 19765320-15 2009 Supernatants from HFCL/EF cell cultures treated with 5-FU increased CD34+ cell growth significantly. Fluorouracil 53-57 CD34 molecule Homo sapiens 68-72 19638344-11 2009 BCRP down-regulation could partially reverse 5-fluorouracil but not cisplatin resistance induced by GAS1 suppression, suggesting 5-fluorouracil but not cisplatin was a BCRP substrate. Fluorouracil 45-59 ATP binding cassette subfamily G member 2 (Junior blood group) Homo sapiens 0-4 19638344-11 2009 BCRP down-regulation could partially reverse 5-fluorouracil but not cisplatin resistance induced by GAS1 suppression, suggesting 5-fluorouracil but not cisplatin was a BCRP substrate. Fluorouracil 129-143 ATP binding cassette subfamily G member 2 (Junior blood group) Homo sapiens 0-4 19638344-11 2009 BCRP down-regulation could partially reverse 5-fluorouracil but not cisplatin resistance induced by GAS1 suppression, suggesting 5-fluorouracil but not cisplatin was a BCRP substrate. Fluorouracil 129-143 ATP binding cassette subfamily G member 2 (Junior blood group) Homo sapiens 168-172 19684609-0 2009 Rosiglitazone sensitizes hepatocellular carcinoma cell lines to 5-fluorouracil antitumor activity through activation of the PPARgamma signaling pathway. Fluorouracil 64-78 peroxisome proliferator activated receptor gamma Homo sapiens 124-133 19561488-0 2009 Involvement of N-acetyltransferase human in the cytotoxic activity of 5-fluorouracil. Fluorouracil 70-84 N-alpha-acetyltransferase 15, NatA auxiliary subunit Homo sapiens 15-40 19561488-2 2009 In this study, the involvement of NATH in the cytotoxic action of 5-fluorouracil (5-FU) in human squamous cell carcinoma HEp-2 cells was examined. Fluorouracil 66-80 N-alpha-acetyltransferase 15, NatA auxiliary subunit Homo sapiens 34-38 19561488-2 2009 In this study, the involvement of NATH in the cytotoxic action of 5-fluorouracil (5-FU) in human squamous cell carcinoma HEp-2 cells was examined. Fluorouracil 82-86 N-alpha-acetyltransferase 15, NatA auxiliary subunit Homo sapiens 34-38 19561488-3 2009 We found that 5-FU decreased NATH expression in a dose-dependent and time-dependent manner. Fluorouracil 14-18 N-alpha-acetyltransferase 15, NatA auxiliary subunit Homo sapiens 29-33 19561488-9 2009 The results of this study suggest that NATH plays an important role in the cytotoxic activity of 5-FU. Fluorouracil 97-101 N-alpha-acetyltransferase 15, NatA auxiliary subunit Homo sapiens 39-43 19684609-8 2009 RESULTS: Rosiglitazone facilitates the anti-tumor effect of 5-FU in HCC cell lines, which is mediated by the PPARgamma signaling pathway. Fluorouracil 60-64 peroxisome proliferator activated receptor gamma Homo sapiens 109-118 19684609-11 2009 Moreover, down-regulation of COX-2 is implicated in the synergistic effect of 5-FU. Fluorouracil 78-82 mitochondrially encoded cytochrome c oxidase II Homo sapiens 29-34 19684609-12 2009 CONCLUSION: Rosiglitazone sensitizes hepatocellular carcinoma cell lines to 5-FU antitumor activity through the activation of PPARgamma. Fluorouracil 76-80 peroxisome proliferator activated receptor gamma Homo sapiens 126-135 19500106-6 2009 However, silencing of FAK combined with 5-FU treatment significantly decreased the 50% inhibitory concentration (IC(50)) of 5-FU and markedly increased the population of apoptosis cells, which was associated with the reduction of the levels of Akt and nuclear factor-kappa B (NF-kappaB). Fluorouracil 40-44 thymoma viral proto-oncogene 1 Mus musculus 244-247 19500106-6 2009 However, silencing of FAK combined with 5-FU treatment significantly decreased the 50% inhibitory concentration (IC(50)) of 5-FU and markedly increased the population of apoptosis cells, which was associated with the reduction of the levels of Akt and nuclear factor-kappa B (NF-kappaB). Fluorouracil 40-44 nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105 Mus musculus 252-274 19500106-6 2009 However, silencing of FAK combined with 5-FU treatment significantly decreased the 50% inhibitory concentration (IC(50)) of 5-FU and markedly increased the population of apoptosis cells, which was associated with the reduction of the levels of Akt and nuclear factor-kappa B (NF-kappaB). Fluorouracil 40-44 nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105 Mus musculus 276-285 19500106-8 2009 These results indicate that while not affecting cellular proliferation in the absence of 5-FU, RNA interference targeting FAK potentiated 5-FU-induced cytotoxicity in vitro and in vivo, and partially reversed multicellular resistance, which may contribute to its chemosensitizing effect through efficiently suppressing Akt/NF-kappaB activity. Fluorouracil 138-142 thymoma viral proto-oncogene 1 Mus musculus 319-322 19500106-8 2009 These results indicate that while not affecting cellular proliferation in the absence of 5-FU, RNA interference targeting FAK potentiated 5-FU-induced cytotoxicity in vitro and in vivo, and partially reversed multicellular resistance, which may contribute to its chemosensitizing effect through efficiently suppressing Akt/NF-kappaB activity. Fluorouracil 138-142 nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105 Mus musculus 323-332 19531543-7 2009 Cases with AR expression showed higher cell death rates than those without in 5-FU and MTX (P = 0.012 and 0.014, respectively). Fluorouracil 78-82 androgen receptor Homo sapiens 11-13 19723887-6 2009 Exposure of ESCC cells to two NF-kappaB inhibitors, Bay11-7082 and sulfasalazine, not only reduced cancer cell proliferation, but also induced apoptosis and enhanced sensitivity to chemotherapeutic drugs, 5-fluorouracil, and cisplatin. Fluorouracil 205-219 nuclear factor kappa B subunit 1 Homo sapiens 30-39 19723892-2 2009 A clear p53-dependent expression pattern of PDF was shown in a panel of colorectal cancer cell lines following acute exposure to oxaliplatin, 5-fluorouracil, and SN38. Fluorouracil 142-156 tumor protein p53 Homo sapiens 8-11 19048402-0 2009 Enhancement of 5-fluorouracil efficacy on high COX-2 expressing HCA-7 cells by low dose indomethacin and NS-398 but not on low COX-2 expressing HT-29 cells. Fluorouracil 15-29 prostaglandin-endoperoxide synthase 2 Homo sapiens 47-52 19570909-7 2009 Moreover, disruption of ATR and Chk1 in MMR-deficient cells enhanced the sensitivity to treatment with the commonly used colorectal chemotherapeutic compound, 5-fluorouracil. Fluorouracil 159-173 ATR serine/threonine kinase Homo sapiens 24-27 19570909-7 2009 Moreover, disruption of ATR and Chk1 in MMR-deficient cells enhanced the sensitivity to treatment with the commonly used colorectal chemotherapeutic compound, 5-fluorouracil. Fluorouracil 159-173 checkpoint kinase 1 Homo sapiens 32-36 19048402-1 2009 The antiproliferative effect of 5-fluorouracil (5-FU) in the presence of low dose non-steroidal anti-inflammatory drugs (NSAIDs) on high cyclooxygenase-2 (COX-2)-expressing HCA-7 and low COX-2-expressing HT-29 colon carcinoma cell lines was investigated. Fluorouracil 32-46 prostaglandin-endoperoxide synthase 2 Homo sapiens 137-153 19048402-1 2009 The antiproliferative effect of 5-fluorouracil (5-FU) in the presence of low dose non-steroidal anti-inflammatory drugs (NSAIDs) on high cyclooxygenase-2 (COX-2)-expressing HCA-7 and low COX-2-expressing HT-29 colon carcinoma cell lines was investigated. Fluorouracil 32-46 prostaglandin-endoperoxide synthase 2 Homo sapiens 155-160 19048402-1 2009 The antiproliferative effect of 5-fluorouracil (5-FU) in the presence of low dose non-steroidal anti-inflammatory drugs (NSAIDs) on high cyclooxygenase-2 (COX-2)-expressing HCA-7 and low COX-2-expressing HT-29 colon carcinoma cell lines was investigated. Fluorouracil 48-52 prostaglandin-endoperoxide synthase 2 Homo sapiens 137-153 19048402-1 2009 The antiproliferative effect of 5-fluorouracil (5-FU) in the presence of low dose non-steroidal anti-inflammatory drugs (NSAIDs) on high cyclooxygenase-2 (COX-2)-expressing HCA-7 and low COX-2-expressing HT-29 colon carcinoma cell lines was investigated. Fluorouracil 48-52 prostaglandin-endoperoxide synthase 2 Homo sapiens 155-160 19048402-11 2009 The presented data suggested that the enhancement of 5-FU cytotoxicity by indomethacin or NS-398 applied in low dose is related to the potency of NSAIDs to modulate the cell-cycle distribution and the apoptosis; however, it seems that this effect might be dependent on cell phenotype, namely on the COX-2 expression. Fluorouracil 53-57 prostaglandin-endoperoxide synthase 2 Homo sapiens 299-304 19714313-0 2009 Enhanced cytotoxicity of 5-FU by bFGF through up-regulation of uridine phosphorylase 1. Fluorouracil 25-29 fibroblast growth factor 2 Homo sapiens 33-37 19622726-2 2009 AEG-1 is known to augment invasion, metastasis, and angiogenesis, and we now demonstrate that AEG-1 directly contributes to another important hallmark of aggressive cancers, that is, resistance to chemotherapeutic drugs, such as 5-fluorouracil (5-FU). Fluorouracil 229-243 metadherin Homo sapiens 94-99 19542220-6 2009 The kinase activity of Mirk was increased by the chemotherapeutic drug 5-fluorouracil (5-FU). Fluorouracil 71-85 dual specificity tyrosine phosphorylation regulated kinase 1B Homo sapiens 23-27 19542220-6 2009 The kinase activity of Mirk was increased by the chemotherapeutic drug 5-fluorouracil (5-FU). Fluorouracil 87-91 dual specificity tyrosine phosphorylation regulated kinase 1B Homo sapiens 23-27 19542220-7 2009 Treatment of p53 mutant colon cancer cells with 5-FU led to an elongated G1 in a Mirk-dependent manner, as G1 was shortened by ectopic overexpression of cyclin D1 mutated at the Mirk phosphorylation site (T288A), but not by wild-type cyclin D1. Fluorouracil 48-52 tumor protein p53 Homo sapiens 13-16 19542220-7 2009 Treatment of p53 mutant colon cancer cells with 5-FU led to an elongated G1 in a Mirk-dependent manner, as G1 was shortened by ectopic overexpression of cyclin D1 mutated at the Mirk phosphorylation site (T288A), but not by wild-type cyclin D1. Fluorouracil 48-52 dual specificity tyrosine phosphorylation regulated kinase 1B Homo sapiens 81-85 19542220-7 2009 Treatment of p53 mutant colon cancer cells with 5-FU led to an elongated G1 in a Mirk-dependent manner, as G1 was shortened by ectopic overexpression of cyclin D1 mutated at the Mirk phosphorylation site (T288A), but not by wild-type cyclin D1. Fluorouracil 48-52 dual specificity tyrosine phosphorylation regulated kinase 1B Homo sapiens 178-182 19622726-2 2009 AEG-1 is known to augment invasion, metastasis, and angiogenesis, and we now demonstrate that AEG-1 directly contributes to another important hallmark of aggressive cancers, that is, resistance to chemotherapeutic drugs, such as 5-fluorouracil (5-FU). Fluorouracil 245-249 metadherin Homo sapiens 94-99 19622726-5 2009 siRNA-mediated inhibition of AEG-1, LSF, or DPYD significantly increased the sensitivity of HCC cells to 5-FU in vitro and a lentivirus delivering AEG-1 siRNA in combination with 5-FU markedly inhibited growth of HCC cells xenotransplanted in athymic nude mice when compared to either agent alone. Fluorouracil 105-109 transcription factor CP2 Mus musculus 36-39 19622726-7 2009 Inhibition of AEG-1 might be exploited as a therapeutic strategy along with 5-FU-based combinatorial chemotherapy for HCC, a highly fatal cancer with currently very limited therapeutic options. Fluorouracil 76-80 metadherin Homo sapiens 14-19 19493271-10 2009 Dkk-3 overexpression in endothelial cells resulted in significantly enhanced growth inhibition after 5-fluorouracil or gemcitabine treatment compared to control endothelial cells and cancer cell lines. Fluorouracil 101-115 dickkopf WNT signaling pathway inhibitor 3 Homo sapiens 0-5 20641233-17 2004 The CDy part of the recombinant fusion protein deaminates 5-fluorocytosine (5-FC), the prodrug, to produce cytotoxic 5-fluorouracil after the A33scFv part binds to the A33 antigen on the cell surface. Fluorouracil 117-131 chromodomain Y-linked 1B Homo sapiens 4-7 19661313-1 2009 BACKGROUND: We have reported that resveratrol (RSV) and 5-fluorouracil (5-FU) evoked apoptosis through caspase-6 activation in wild-type (p53+/+) and knockout (p53(-/-)) HCT116 human colon cancer cells. Fluorouracil 56-70 tumor protein p53 Homo sapiens 138-141 19661313-1 2009 BACKGROUND: We have reported that resveratrol (RSV) and 5-fluorouracil (5-FU) evoked apoptosis through caspase-6 activation in wild-type (p53+/+) and knockout (p53(-/-)) HCT116 human colon cancer cells. Fluorouracil 56-70 tumor protein p53 Homo sapiens 160-163 19661313-1 2009 BACKGROUND: We have reported that resveratrol (RSV) and 5-fluorouracil (5-FU) evoked apoptosis through caspase-6 activation in wild-type (p53+/+) and knockout (p53(-/-)) HCT116 human colon cancer cells. Fluorouracil 72-76 tumor protein p53 Homo sapiens 138-141 19661313-1 2009 BACKGROUND: We have reported that resveratrol (RSV) and 5-fluorouracil (5-FU) evoked apoptosis through caspase-6 activation in wild-type (p53+/+) and knockout (p53(-/-)) HCT116 human colon cancer cells. Fluorouracil 72-76 tumor protein p53 Homo sapiens 160-163 19661313-4 2009 RESULTS: SC (100 microM) sensitized RSV- (200 microM) and 5-FU (500 microM)-evoked apoptosis in p53+/+ but not p53(-/-) cells. Fluorouracil 58-62 tumor protein p53 Homo sapiens 96-99 19574900-1 2009 PURPOSE: To evaluate matrix metalloproteinases (MMP)-2, MMP-9, and tissue inhibitor of metalloproteinase (TIMP)-1 expression in a case of conjunctival intraepithelial squamous cell carcinoma (SCC) treated with topical 5-fluorouracil (5-FU) chemotherapy. Fluorouracil 218-232 TIMP metallopeptidase inhibitor 1 Homo sapiens 67-113 19661313-7 2009 CONCLUSION: SC is a novel sensitizing agent for both RSV- and 5-FU-evoked apoptosis, through the enhancement of caspase-6 activation in a p53-dependent manner. Fluorouracil 62-66 tumor protein p53 Homo sapiens 138-141 19661321-3 2009 It was demonstrated that elevated dihydropyrimidine dehydrogenase (DPD) and COX-2 activities influence the response to 5-fluorouracil (5-FU). Fluorouracil 119-133 prostaglandin-endoperoxide synthase 2 Homo sapiens 76-81 19661321-3 2009 It was demonstrated that elevated dihydropyrimidine dehydrogenase (DPD) and COX-2 activities influence the response to 5-fluorouracil (5-FU). Fluorouracil 135-139 prostaglandin-endoperoxide synthase 2 Homo sapiens 76-81 19661321-4 2009 We previously showed that NSAIDs increased 5-FU sensitivity only in high COX-2-expressing cancer cells. Fluorouracil 43-47 prostaglandin-endoperoxide synthase 2 Homo sapiens 73-78 19661321-8 2009 CONCLUSION: NSAIDs could be promising modulators of fluorouracil-based chemotherapy, especially in high COX-2-expressing tumours. Fluorouracil 52-64 prostaglandin-endoperoxide synthase 2 Homo sapiens 104-109 19574900-7 2009 Clinical resolution of the neoplasm obtained using topical 5-FU was accompanied by a reduction in the expression of MMP-2, MMP-9, and TIMP-1 in tears and dysplastic conjunctival epithelium. Fluorouracil 59-63 TIMP metallopeptidase inhibitor 1 Homo sapiens 134-140 19415305-1 2009 PURPOSE: The aim of this study was to determine the significance of three most common single-nucleotide polymorphisms (SNPs) of ABCB1 gene in the development of colorectal cancer and to estimate the influence of these SNPs to surviving patients" treatment combination adjuvant therapy 5-fluorouracil/leucovorin. Fluorouracil 285-299 ATP binding cassette subfamily B member 1 Homo sapiens 128-133 19524433-0 2009 Involvement of Nrf2 activation in resistance to 5-fluorouracil in human colon cancer HT-29 cells. Fluorouracil 48-62 NFE2 like bZIP transcription factor 2 Homo sapiens 15-19 19524433-7 2009 Translocation of Nrf2 into the nucleus after 5-FU exposure was demonstrated by immunocytochemistry and western blotting. Fluorouracil 45-49 NFE2 like bZIP transcription factor 2 Homo sapiens 17-21 19524433-9 2009 Moreover, transfection of HT-29 cells with siRNA directed against Nrf2 inhibited induction of Nrf2 target genes and increased 5-FU cytotoxicity. Fluorouracil 126-130 NFE2 like bZIP transcription factor 2 Homo sapiens 66-70 19524433-10 2009 In conclusion, we demonstrate for the first time that 5-FU activates the Nrf2/ARE pathway which in turn induces cytoprotective genes and modulates chemosensitivity of HT-29 colon cancer cells. Fluorouracil 54-58 NFE2 like bZIP transcription factor 2 Homo sapiens 73-77 19524433-11 2009 Therefore, we postulate that Nrf2 might represent a potential therapeutic target in 5-FU treatment of colon cancer. Fluorouracil 84-88 NFE2 like bZIP transcription factor 2 Homo sapiens 29-33 19698236-5 2009 It is concluded that cis-elements including T-Ag, PU.1, c-Ets, XPF-1, P2 alphaA, IL6-6RE and RAR may inhibit lrp16 expression and hormone or its inhibitor such as corticosteroid, tamoxifen, forskolin, phenylephrine, inflammatory factors such as IL6, IFNgamma and TNFalpha, and chemotherapeutics 5-fluorouracil may participate in the regulation of lrp16 gene expression in negative manner. Fluorouracil 295-309 interleukin 6 Homo sapiens 81-84 19470942-1 2009 PURPOSE We have demonstrated that patients with HER2-amplified tumors derive more benefit from higher doses of doxorubicin-containing chemotherapy (cyclophosphamide, doxorubicin, and fluorouracil [CAF]). Fluorouracil 183-195 erb-b2 receptor tyrosine kinase 2 Homo sapiens 48-52 19698236-5 2009 It is concluded that cis-elements including T-Ag, PU.1, c-Ets, XPF-1, P2 alphaA, IL6-6RE and RAR may inhibit lrp16 expression and hormone or its inhibitor such as corticosteroid, tamoxifen, forskolin, phenylephrine, inflammatory factors such as IL6, IFNgamma and TNFalpha, and chemotherapeutics 5-fluorouracil may participate in the regulation of lrp16 gene expression in negative manner. Fluorouracil 295-309 interleukin 6 Homo sapiens 245-248 19698236-5 2009 It is concluded that cis-elements including T-Ag, PU.1, c-Ets, XPF-1, P2 alphaA, IL6-6RE and RAR may inhibit lrp16 expression and hormone or its inhibitor such as corticosteroid, tamoxifen, forskolin, phenylephrine, inflammatory factors such as IL6, IFNgamma and TNFalpha, and chemotherapeutics 5-fluorouracil may participate in the regulation of lrp16 gene expression in negative manner. Fluorouracil 295-309 interferon gamma Homo sapiens 250-258 19698236-5 2009 It is concluded that cis-elements including T-Ag, PU.1, c-Ets, XPF-1, P2 alphaA, IL6-6RE and RAR may inhibit lrp16 expression and hormone or its inhibitor such as corticosteroid, tamoxifen, forskolin, phenylephrine, inflammatory factors such as IL6, IFNgamma and TNFalpha, and chemotherapeutics 5-fluorouracil may participate in the regulation of lrp16 gene expression in negative manner. Fluorouracil 295-309 tumor necrosis factor Homo sapiens 263-271 19584296-6 2009 Independent validation experiment using five new pancreatic cancer cell lines confirmed that an inverse correlation between E-cadherin and Zeb-1 correlated closely with resistance to gemcitabine, 5-FU, and cisplatin. Fluorouracil 196-200 cadherin 1 Homo sapiens 124-134 19371262-0 2009 Protective effects of amifostine and cyclooxygenase-1 inhibitor against normal human epidermal keratinocyte toxicity induced by methotrexate and 5-fluorouracil. Fluorouracil 145-159 prostaglandin-endoperoxide synthase 1 Homo sapiens 37-53 19371262-12 2009 However, the cell injury induced by 5-fluorouracil was markedly recovered by a selective cyclooxygenase-1 inhibitor compared to amifostine. Fluorouracil 36-50 prostaglandin-endoperoxide synthase 1 Homo sapiens 89-105 19371262-13 2009 It was suggested that amifostine and cyclooxygenase-1 inhibitor could be useful protective agents against methotrexate and 5-fluorouracil chemotherapeutic toxicity. Fluorouracil 123-137 prostaglandin-endoperoxide synthase 1 Homo sapiens 37-53 19364972-12 2009 CONCLUSION High GGI is associated with increased sensitivity to neoadjuvant paclitaxel plus fluorouracil, adriamycin, and cyclophosphamide chemotherapy in both ER-negative and ER-positive patients, but it remains a predictor of worse survival in ER-positive patients. Fluorouracil 92-104 estrogen receptor 1 Homo sapiens 160-162 19056143-1 2009 A combination of S-1, a newly developed oral 5-fluorouracil derivative, and cisplatin is reported to show anti-tumour activity against advanced non-small cell lung cancer (NSCLC). Fluorouracil 45-59 proteasome 26S subunit, non-ATPase 1 Homo sapiens 17-20 19364972-12 2009 CONCLUSION High GGI is associated with increased sensitivity to neoadjuvant paclitaxel plus fluorouracil, adriamycin, and cyclophosphamide chemotherapy in both ER-negative and ER-positive patients, but it remains a predictor of worse survival in ER-positive patients. Fluorouracil 92-104 estrogen receptor 1 Homo sapiens 176-178 19364972-12 2009 CONCLUSION High GGI is associated with increased sensitivity to neoadjuvant paclitaxel plus fluorouracil, adriamycin, and cyclophosphamide chemotherapy in both ER-negative and ER-positive patients, but it remains a predictor of worse survival in ER-positive patients. Fluorouracil 92-104 estrogen receptor 1 Homo sapiens 176-178 21475874-0 2009 AKT plays a pivotal role in the acquisition of resistance to 5-fluorouracil in human squamous carcinoma cells. Fluorouracil 61-75 AKT serine/threonine kinase 1 Homo sapiens 0-3 21475874-7 2009 5-FU induced the activation of the ERK and Akt kinases in UM-SCC-23 human squamous carcinoma cells, indicating that this anticancer drug activates survival signaling pathways as well as apoptotic signals. Fluorouracil 0-4 mitogen-activated protein kinase 1 Homo sapiens 35-38 21475874-7 2009 5-FU induced the activation of the ERK and Akt kinases in UM-SCC-23 human squamous carcinoma cells, indicating that this anticancer drug activates survival signaling pathways as well as apoptotic signals. Fluorouracil 0-4 AKT serine/threonine kinase 1 Homo sapiens 43-46 21475874-8 2009 In 5-FU-resistant UM-SCC-23 cells established by our group, ERK and Akt signals were constitutively activated. Fluorouracil 3-7 mitogen-activated protein kinase 1 Homo sapiens 60-63 21475874-8 2009 In 5-FU-resistant UM-SCC-23 cells established by our group, ERK and Akt signals were constitutively activated. Fluorouracil 3-7 AKT serine/threonine kinase 1 Homo sapiens 68-71 21475874-13 2009 These results indicate that the Akt survival signal plays an important role in the resistance of squamous carcinoma cells to 5-FU treatment, and suggest that the modification of Akt activity might provide a new strategy for human 5-FU-resistant squamous carcinoma therapy. Fluorouracil 125-129 AKT serine/threonine kinase 1 Homo sapiens 32-35 21475874-13 2009 These results indicate that the Akt survival signal plays an important role in the resistance of squamous carcinoma cells to 5-FU treatment, and suggest that the modification of Akt activity might provide a new strategy for human 5-FU-resistant squamous carcinoma therapy. Fluorouracil 125-129 AKT serine/threonine kinase 1 Homo sapiens 178-181 21475874-13 2009 These results indicate that the Akt survival signal plays an important role in the resistance of squamous carcinoma cells to 5-FU treatment, and suggest that the modification of Akt activity might provide a new strategy for human 5-FU-resistant squamous carcinoma therapy. Fluorouracil 230-234 AKT serine/threonine kinase 1 Homo sapiens 32-35 21475874-13 2009 These results indicate that the Akt survival signal plays an important role in the resistance of squamous carcinoma cells to 5-FU treatment, and suggest that the modification of Akt activity might provide a new strategy for human 5-FU-resistant squamous carcinoma therapy. Fluorouracil 230-234 AKT serine/threonine kinase 1 Homo sapiens 178-181 19217205-6 2009 Furthermore, 5-FU has significantly lower inhibition effect on Huh7-EGFRvIII cells then on both Huh-7 and Huh7-EGFR cells in vitro and in vivo. Fluorouracil 13-17 epidermal growth factor receptor Homo sapiens 68-72 19052713-0 2009 5-FU pretreatment potentiates cisplatin-induced apoptosis through up-regulation of thrombospondin-1 in head and neck squamous cell carcinomas. Fluorouracil 0-4 thrombospondin 1 Homo sapiens 83-99 19401692-1 2009 Type I IFN receptor type 2 (IFNAR2) expression correlates significantly with clinical response to interferon (IFN)-alpha/5-fluorouracil (5-FU) combination therapy for hepatocellular carcinoma (HCC). Fluorouracil 137-141 interferon alpha 1 Homo sapiens 98-120 19401692-10 2009 The results indicate that activation of Wnt/beta-catenin signalling pathway induces chemoresistance to IFN-alpha/5-FU therapy and suggest that Ep-CAM is a potentially useful marker for resistance to such therapy, especially in IFNAR2-positive cases. Fluorouracil 113-117 epithelial cell adhesion molecule Homo sapiens 143-149 19302291-6 2009 The down-regulation of cIAP2 efficiently enhanced 5-FU sensitivity, the activation of caspase 3/7 and apoptosis under exposure to 5-FU. Fluorouracil 130-134 caspase 3 Homo sapiens 86-95 19270508-0 2009 Modulation of thymidilate synthase and p53 expression by HDAC inhibitor vorinostat resulted in synergistic antitumor effect in combination with 5FU or raltitrexed. Fluorouracil 144-147 tumor protein p53 Homo sapiens 39-42 19366444-1 2009 BACKGROUND: This study was designed to investigate the efficacy and safety of the epidermal growth factor receptor (EGFR) inhibitor cetuximab combined with irinotecan, folinic acid (FA) and two different doses of infusional 5-fluorouracil (5-FU) in the first-line treatment of EGFR-detectable metastatic colorectal cancer. Fluorouracil 224-238 epidermal growth factor receptor Homo sapiens 116-120 19420978-4 2009 The German Rectal Cancer study CAO/ARO/AIO-94 showed a full remission rate of 8% after a 5-fluorouracil (5-FU)based chemotherapy added to a conventional fractional radiation therapy (50.4 Gy). Fluorouracil 89-103 cytochrome P450 family 19 subfamily A member 1 Homo sapiens 35-38 19420978-4 2009 The German Rectal Cancer study CAO/ARO/AIO-94 showed a full remission rate of 8% after a 5-fluorouracil (5-FU)based chemotherapy added to a conventional fractional radiation therapy (50.4 Gy). Fluorouracil 105-109 cytochrome P450 family 19 subfamily A member 1 Homo sapiens 35-38 19402749-0 2009 Base excision by thymine DNA glycosylase mediates DNA-directed cytotoxicity of 5-fluorouracil. Fluorouracil 79-93 thymine DNA glycosylase Homo sapiens 17-40 19402749-3 2009 In this study, we investigated a possible role of thymine DNA glycosylase (TDG), one of four mammalian uracil DNA glycosylases (UDGs), in the cellular response to 5-FU. Fluorouracil 163-167 thymine DNA glycosylase Homo sapiens 50-73 19402749-3 2009 In this study, we investigated a possible role of thymine DNA glycosylase (TDG), one of four mammalian uracil DNA glycosylases (UDGs), in the cellular response to 5-FU. Fluorouracil 163-167 thymine DNA glycosylase Homo sapiens 75-78 19402749-5 2009 We show that excision of DNA-incorporated 5-FU by TDG generates persistent DNA strand breaks, delays S-phase progression, and activates DNA damage signaling, and that the repair of 5-FU-induced DNA strand breaks is more efficient in the absence of TDG. Fluorouracil 42-46 thymine DNA glycosylase Homo sapiens 50-53 19402749-6 2009 Hence, excision of 5-FU by TDG, but not by other UDGs (UNG2 and SMUG1), prevents efficient downstream processing of the repair intermediate, thereby mediating DNA-directed cytotoxicity. Fluorouracil 19-23 thymine DNA glycosylase Homo sapiens 27-30 19402749-7 2009 The status of TDG expression in a cancer is therefore likely to determine its response to 5-FU-based chemotherapy. Fluorouracil 90-94 thymine DNA glycosylase Homo sapiens 14-17 19097688-0 2009 Andrographolide enhances 5-fluorouracil-induced apoptosis via caspase-8-dependent mitochondrial pathway involving p53 participation in hepatocellular carcinoma (SMMC-7721) cells. Fluorouracil 25-39 tumor protein p53 Homo sapiens 114-117 19097688-8 2009 Surprisingly, the addition of ANDRO to 5-FU induces synergistic apoptosis, which could be corroborated to the increased caspase-8, p53 activity and the significant changes of Bax conformation in these cells, resulting in increased losses of mitochondrial membrane potential, increased release of cytochrome c, and activation of caspase-9 and caspase-3. Fluorouracil 39-43 tumor protein p53 Homo sapiens 131-134 19097688-8 2009 Surprisingly, the addition of ANDRO to 5-FU induces synergistic apoptosis, which could be corroborated to the increased caspase-8, p53 activity and the significant changes of Bax conformation in these cells, resulting in increased losses of mitochondrial membrane potential, increased release of cytochrome c, and activation of caspase-9 and caspase-3. Fluorouracil 39-43 BCL2 associated X, apoptosis regulator Homo sapiens 175-178 19097688-8 2009 Surprisingly, the addition of ANDRO to 5-FU induces synergistic apoptosis, which could be corroborated to the increased caspase-8, p53 activity and the significant changes of Bax conformation in these cells, resulting in increased losses of mitochondrial membrane potential, increased release of cytochrome c, and activation of caspase-9 and caspase-3. Fluorouracil 39-43 cytochrome c, somatic Homo sapiens 296-308 19097688-8 2009 Surprisingly, the addition of ANDRO to 5-FU induces synergistic apoptosis, which could be corroborated to the increased caspase-8, p53 activity and the significant changes of Bax conformation in these cells, resulting in increased losses of mitochondrial membrane potential, increased release of cytochrome c, and activation of caspase-9 and caspase-3. Fluorouracil 39-43 caspase 3 Homo sapiens 342-351 19380024-5 2009 The function of P-glycoprotein, the protein product of the ABCB1 gene, was assessed by rhodamine 123 (Rh123)-retention assay, and chemosensitivity was determined by evaluating the cytotoxicity of 5-fluorouracil (5-FU) on the tumor cells. Fluorouracil 212-216 ATP binding cassette subfamily B member 1 Homo sapiens 16-30 19366444-1 2009 BACKGROUND: This study was designed to investigate the efficacy and safety of the epidermal growth factor receptor (EGFR) inhibitor cetuximab combined with irinotecan, folinic acid (FA) and two different doses of infusional 5-fluorouracil (5-FU) in the first-line treatment of EGFR-detectable metastatic colorectal cancer. Fluorouracil 240-244 epidermal growth factor receptor Homo sapiens 82-114 19366444-1 2009 BACKGROUND: This study was designed to investigate the efficacy and safety of the epidermal growth factor receptor (EGFR) inhibitor cetuximab combined with irinotecan, folinic acid (FA) and two different doses of infusional 5-fluorouracil (5-FU) in the first-line treatment of EGFR-detectable metastatic colorectal cancer. Fluorouracil 240-244 epidermal growth factor receptor Homo sapiens 116-120 19150257-9 2009 Furthermore, silencing of p53 with siRNA and inactivation of p53 with a dominant negative mutant rescued the hypersensitive response to kinases inhibitors, 5-fluorouracil and adriamycin in HCT116p21(-/-) cells. Fluorouracil 156-170 tumor protein p53 Homo sapiens 26-29 19381049-4 2009 In patients whose urinary uracil values exceeded the standard, 5-FU tended to be accumulated when S-1, a DIF product, was administered and side effects, such as anorexia, vomiting and diarrhea occurred immediately after the start of S-1 administration. Fluorouracil 63-67 tumor necrosis factor Homo sapiens 105-108 25949315-0 2009 Severe adverse effects of 5-fluorouracil in S-1 were lessened by haemodialysis due to elimination of the drug. Fluorouracil 26-40 proteasome 26S subunit, non-ATPase 1 Homo sapiens 44-47 25949315-2 2009 The plasma concentration of 5-fluorouracil (5-FU) is increased in patients with renal dysfunction because gimeracil in S-1 inhibits the degradation of 5-FU and about 50% of gimeracil is excreted in the urine. Fluorouracil 28-42 proteasome 26S subunit, non-ATPase 1 Homo sapiens 119-122 25949315-2 2009 The plasma concentration of 5-fluorouracil (5-FU) is increased in patients with renal dysfunction because gimeracil in S-1 inhibits the degradation of 5-FU and about 50% of gimeracil is excreted in the urine. Fluorouracil 44-48 proteasome 26S subunit, non-ATPase 1 Homo sapiens 119-122 25949315-2 2009 The plasma concentration of 5-fluorouracil (5-FU) is increased in patients with renal dysfunction because gimeracil in S-1 inhibits the degradation of 5-FU and about 50% of gimeracil is excreted in the urine. Fluorouracil 151-155 proteasome 26S subunit, non-ATPase 1 Homo sapiens 119-122 25949315-3 2009 We describe a 35-year-old man with acute kidney injury while taking S-1 and cisplatin for advanced gastric cancer and who presented severe adverse effects of 5-FU. Fluorouracil 158-162 proteasome 26S subunit, non-ATPase 1 Homo sapiens 68-71 19259093-0 2009 Biomarker analysis in stage III-IV (M0) gastric cancer patients who received curative surgery followed by adjuvant 5-fluorouracil and cisplatin chemotherapy: epidermal growth factor receptor (EGFR) associated with favourable survival. Fluorouracil 115-129 epidermal growth factor receptor Homo sapiens 192-196 19095777-0 2009 Epidermal growth factor receptor gene copy number, K-ras mutation and pathological response to preoperative cetuximab, 5-FU and radiation therapy in locally advanced rectal cancer. Fluorouracil 119-123 epidermal growth factor receptor Homo sapiens 0-32 19095777-10 2009 CONCLUSIONS: In pts with LARC, EGFR GCN is predictive of high TRG to cetuximab plus 5-FU radiotherapy. Fluorouracil 84-88 epidermal growth factor receptor Homo sapiens 31-35 19150257-9 2009 Furthermore, silencing of p53 with siRNA and inactivation of p53 with a dominant negative mutant rescued the hypersensitive response to kinases inhibitors, 5-fluorouracil and adriamycin in HCT116p21(-/-) cells. Fluorouracil 156-170 tumor protein p53 Homo sapiens 61-64 18618519-0 2009 Calcium and calcium sensing receptor modulates the expression of thymidylate synthase, NAD(P)H:quinone oxidoreductase 1 and survivin in human colon carcinoma cells: promotion of cytotoxic response to mitomycin C and fluorouracil. Fluorouracil 216-228 calcium sensing receptor Homo sapiens 12-36 19171477-0 2009 Effect of HIF-1 modulation on the response of two- and three-dimensional cultures of human colon cancer cells to 5-fluorouracil. Fluorouracil 113-127 hypoxia inducible factor 1 subunit alpha Homo sapiens 10-15 19171477-3 2009 In the present study we investigate the effects of HIF-1 modulation on the response of the human colon adenocarcinoma cell line HCT116 to 5-fluorouracil (5FU). Fluorouracil 138-152 hypoxia inducible factor 1 subunit alpha Homo sapiens 51-56 19243284-1 2009 S-1 is an oral fluoropyrimidine that is designed to improve the antitumor activity of 5-fluorouracil (5-FU) concomitantly with an intent to reduce its toxicity. Fluorouracil 86-100 proteasome 26S subunit, non-ATPase 1 Homo sapiens 0-3 19243284-1 2009 S-1 is an oral fluoropyrimidine that is designed to improve the antitumor activity of 5-fluorouracil (5-FU) concomitantly with an intent to reduce its toxicity. Fluorouracil 102-106 proteasome 26S subunit, non-ATPase 1 Homo sapiens 0-3 19243284-2 2009 S-1 consists of tegafur, a prodrug of 5-FU combined with two 5-FU biochemical modulators:5-chloro-2,4-dihydroxypyridine (gimeracil or CDHP), a competitive inhibitor of dihydropyrimidine dehydrogenase and oteracil potassium which inhibits phosphorylation of 5-FU in the gastrointestinal tract decreasing serious gastrointestinal toxicities,including nausea, vomiting, stomatitis and diarrhea. Fluorouracil 38-42 proteasome 26S subunit, non-ATPase 1 Homo sapiens 0-3 19243284-2 2009 S-1 consists of tegafur, a prodrug of 5-FU combined with two 5-FU biochemical modulators:5-chloro-2,4-dihydroxypyridine (gimeracil or CDHP), a competitive inhibitor of dihydropyrimidine dehydrogenase and oteracil potassium which inhibits phosphorylation of 5-FU in the gastrointestinal tract decreasing serious gastrointestinal toxicities,including nausea, vomiting, stomatitis and diarrhea. Fluorouracil 61-65 proteasome 26S subunit, non-ATPase 1 Homo sapiens 0-3 19243284-2 2009 S-1 consists of tegafur, a prodrug of 5-FU combined with two 5-FU biochemical modulators:5-chloro-2,4-dihydroxypyridine (gimeracil or CDHP), a competitive inhibitor of dihydropyrimidine dehydrogenase and oteracil potassium which inhibits phosphorylation of 5-FU in the gastrointestinal tract decreasing serious gastrointestinal toxicities,including nausea, vomiting, stomatitis and diarrhea. Fluorouracil 61-65 proteasome 26S subunit, non-ATPase 1 Homo sapiens 0-3 19295262-2 2009 S-1, developed by the scientific theory of both potentiating antitumor activity of 5-fluorouracil(5-FU)and reducing gastrointestinal toxicity induced by 5-FU, is an active agent for squamous cell carcinoma of the head and neck(HNSCC). Fluorouracil 83-97 proteasome 26S subunit, non-ATPase 1 Homo sapiens 0-3 19295262-2 2009 S-1, developed by the scientific theory of both potentiating antitumor activity of 5-fluorouracil(5-FU)and reducing gastrointestinal toxicity induced by 5-FU, is an active agent for squamous cell carcinoma of the head and neck(HNSCC). Fluorouracil 98-102 proteasome 26S subunit, non-ATPase 1 Homo sapiens 0-3 19295262-2 2009 S-1, developed by the scientific theory of both potentiating antitumor activity of 5-fluorouracil(5-FU)and reducing gastrointestinal toxicity induced by 5-FU, is an active agent for squamous cell carcinoma of the head and neck(HNSCC). Fluorouracil 153-157 proteasome 26S subunit, non-ATPase 1 Homo sapiens 0-3 18618519-2 2009 Here we show that activation of CaSR by extracellular Ca(2+) (or CaSR agonists) enhanced the sensitivity of human colon carcinoma cells to mitomycin C (MMC) and fluorouracil (5-FU). Fluorouracil 161-173 calcium sensing receptor Homo sapiens 32-36 18618519-2 2009 Here we show that activation of CaSR by extracellular Ca(2+) (or CaSR agonists) enhanced the sensitivity of human colon carcinoma cells to mitomycin C (MMC) and fluorouracil (5-FU). Fluorouracil 161-173 calcium sensing receptor Homo sapiens 65-69 18618519-2 2009 Here we show that activation of CaSR by extracellular Ca(2+) (or CaSR agonists) enhanced the sensitivity of human colon carcinoma cells to mitomycin C (MMC) and fluorouracil (5-FU). Fluorouracil 175-179 calcium sensing receptor Homo sapiens 32-36 18618519-2 2009 Here we show that activation of CaSR by extracellular Ca(2+) (or CaSR agonists) enhanced the sensitivity of human colon carcinoma cells to mitomycin C (MMC) and fluorouracil (5-FU). Fluorouracil 175-179 calcium sensing receptor Homo sapiens 65-69 18618519-6 2009 It is concluded that activation of CaSR can enhance colon cancer cell sensitivity to MMC and 5-FU and can modulate the expression of molecules involved in the cellular responses to these cytotoxic drugs. Fluorouracil 93-97 calcium sensing receptor Homo sapiens 35-39 18844240-5 2009 The ACC-M and ACC-2 cells exhibited relative resistant to 5-Fu. Fluorouracil 58-62 BCL2 related protein A1 Homo sapiens 14-19 19091861-5 2009 Thymidine phosphorylase, a cellular enzyme markedly induced by ORFK13/vFLIP, can metabolize the prodrug 5-fluoro-5-deoxyuridine (5-dFUrd) to 5-fluouridine (5-FU), a potent thymidine synthase inhibitor, which blocks DNA and RNA synthesis. Fluorouracil 156-160 K13 Human gammaherpesvirus 8 70-75 19212626-9 2009 DDP and 5-FU increased the growth-inhibiting ability of rh-TRAIL to SGC7901 cells. Fluorouracil 8-12 TNF superfamily member 10 Homo sapiens 59-64 19052037-5 2009 S-1 is an oral anticancer agent containing two biochemical modulators for 5-FU and tegafur (FT), a metabolically activated prodrug of 5-FU. Fluorouracil 74-78 proteasome 26S subunit, non-ATPase 1 Homo sapiens 0-3 19155291-1 2009 The major determinants of 5-flurouracil (5-FU) response would seem, based on accumulated literature, to be thymidylate synthase (TYMS, TS) expression levels, TS gene modifications, and TP53 status. Fluorouracil 41-45 tumor protein p53 Homo sapiens 185-189 19155291-2 2009 We tested 5-FU sensitivity in yeast and human cancer cell models in which TS or TP53 alleles and expression were varied. Fluorouracil 10-14 tumor protein p53 Homo sapiens 80-84 18984863-5 2009 Whereas young PSF1(+/-) mutant mice develop normally, are fertile, and have no obvious differences in hematopoiesis in the steady state compared with wild-type mice, intravenous injection of 5-fluorouracil (5-FU) is lethal in PSF1(+/-) mice, resulting from a delay in induction of HSC proliferation during ablated BM reconstitution. Fluorouracil 191-205 GINS complex subunit 1 (Psf1 homolog) Mus musculus 226-230 20691103-12 2010 Respectively, the rate of inhibition of EADM,5- Fu, NVB and DDP were significantly higher in the BCL-2 negative cancer cells than in the BCL-2 positive cancer cells. Fluorouracil 45-50 BCL2 apoptosis regulator Homo sapiens 97-102 19342998-11 2009 Twenty-five-day subcutaneous administration of a three-peptide cocktail (3 mg/kg) in combination with 5-fluorouracil in Rag-2 mice with established CCRF-CEM leukemia significantly reduces splenomegaly and bone marrow cancer cell burden. Fluorouracil 102-116 recombination activating gene 2 Mus musculus 120-125 19118048-5 2009 Combining rNAPc2 with the cytotoxic agent 5-fluorouracil or bevacizumab (humanized anti-vascular endothelial growth factor monoclonal antibody) resulted in additive growth inhibition and simultaneous reduction of microvessel density in HCT116 human colorectal tumor xenografts in nude mice. Fluorouracil 42-56 vascular endothelial growth factor A Homo sapiens 88-122 19013060-1 2009 The chitosan-coated magnetic nanoparticles (CS MNPs) were prepared as carriers of 5-Fluorouracil (CS-5-Fu MNPs) through a reverse microemulsion method. Fluorouracil 82-96 chorionic somatomammotropin hormone like 1 Homo sapiens 98-102 19390930-2 2009 A pilot study of S-1 (TS-1; Taiho Pharmaceutical, Tokyo, Japan), an oral 5-fluorouracil derivative, for neoadjuvant chemotherapy unexpectedly showed good response and a promising effect on survival. Fluorouracil 73-87 proteasome 26S subunit, non-ATPase 1 Homo sapiens 17-20 19052037-5 2009 S-1 is an oral anticancer agent containing two biochemical modulators for 5-FU and tegafur (FT), a metabolically activated prodrug of 5-FU. Fluorouracil 134-138 proteasome 26S subunit, non-ATPase 1 Homo sapiens 0-3 19052037-11 2009 Furthermore, "alternate-day S-1 regimen" may improve the dosing schedule for 5-FU by utilizing its strongly time-dependent mode of action; the former is characterized by the low incidences of myelotoxicity and non-hematologic toxicities (e.g. < or =Grade 1 anorexia, fatigue, stomatitis, nausea, vomiting and taste alteration). Fluorouracil 77-81 proteasome 26S subunit, non-ATPase 1 Homo sapiens 28-31 19077464-5 2009 We studied ATP-binding cassette (ABC) transporter expression in human pancreatic carcinoma cell lines as compared to primary pancreatic duct cells, and analyzed the MRP expression profile in 5-fluorouracil-resistant cells. Fluorouracil 191-205 ATP binding cassette subfamily C member 1 Homo sapiens 165-168 18626508-3 2009 Taking advantage of this prostate cancer-specific property of PSMA(E/P), we successfully introduced bacterial UPRT into LNCaP cells where the tumoricidal effect of 5-fluorouracil (5-FU) was significantly increased when compared with the cells without the exogenous UPRT. Fluorouracil 164-178 folate hydrolase 1 Homo sapiens 62-66 18626508-3 2009 Taking advantage of this prostate cancer-specific property of PSMA(E/P), we successfully introduced bacterial UPRT into LNCaP cells where the tumoricidal effect of 5-fluorouracil (5-FU) was significantly increased when compared with the cells without the exogenous UPRT. Fluorouracil 180-184 folate hydrolase 1 Homo sapiens 62-66 18626508-4 2009 We conclude that the efficacy of 5-FU-based chemotherapy in prostate cancers can be significantly improved by targeted expression of the suicide gene UPRT under the control of PSMA(E/P). Fluorouracil 33-37 folate hydrolase 1 Homo sapiens 176-180 18854306-7 2008 During 5-fluorouracil-induced anemia, both reticulocyte and red cell formation in DYRK3-/- mice were elevated. Fluorouracil 7-21 dual-specificity tyrosine-(Y)-phosphorylation regulated kinase 3 Mus musculus 82-87 19440006-3 2009 The aim of this study was to investigate the modulations in the BAX, BCL2 and BCL2L12 mRNA levels in gastric cancer cells, after their treatment with the anticancer drugs 5-fluorouracil and irinotecan as well as the antioxidant substance leucovorin. Fluorouracil 171-185 BCL2 associated X, apoptosis regulator Homo sapiens 64-67 19521145-6 2009 In combination therapy experiments, antibodies to PrP enhanced the effect of irinotecan, 5-FU, cisplatin and doxorubicin to varying degrees. Fluorouracil 89-93 prion protein Homo sapiens 50-53 18794807-0 2008 Inhibition of Src tyrosine kinase reverts chemoresistance toward 5-fluorouracil in human pancreatic carcinoma cells: an involvement of epidermal growth factor receptor signaling. Fluorouracil 65-79 SRC proto-oncogene, non-receptor tyrosine kinase Homo sapiens 14-17 19074875-8 2008 Antagonizing endogenous miR-192 attenuated 5-fluorouracil-induced accumulation of p21. Fluorouracil 43-57 microRNA 192 Homo sapiens 24-31 19074875-8 2008 Antagonizing endogenous miR-192 attenuated 5-fluorouracil-induced accumulation of p21. Fluorouracil 43-57 cyclin dependent kinase inhibitor 1A Homo sapiens 82-85 18794807-3 2008 We tested the hypothesis that Src tyrosine kinase inhibition could augment the chemosensitivity of 5-fluorouracil (5-FU)-resistant human pancreatic cancer cells to 5-FU. Fluorouracil 99-113 SRC proto-oncogene, non-receptor tyrosine kinase Homo sapiens 30-33 18794807-3 2008 We tested the hypothesis that Src tyrosine kinase inhibition could augment the chemosensitivity of 5-fluorouracil (5-FU)-resistant human pancreatic cancer cells to 5-FU. Fluorouracil 115-119 SRC proto-oncogene, non-receptor tyrosine kinase Homo sapiens 30-33 18794807-3 2008 We tested the hypothesis that Src tyrosine kinase inhibition could augment the chemosensitivity of 5-fluorouracil (5-FU)-resistant human pancreatic cancer cells to 5-FU. Fluorouracil 164-168 SRC proto-oncogene, non-receptor tyrosine kinase Homo sapiens 30-33 18794807-5 2008 Furthermore, when small-interfering RNA approach to silence Src gene expression was applied, the degree of 5-FU-induced apoptosis was increased in all cell lines independently of the chemoresistance status. Fluorouracil 107-111 SRC proto-oncogene, non-receptor tyrosine kinase Homo sapiens 60-63 18794807-7 2008 Furthermore, the combination of 5-FU+PP2 decreased the 5-FU-induced activation of epidermal growth factor receptor (EGFR)-AKT pathway. Fluorouracil 32-36 epidermal growth factor receptor Homo sapiens 82-114 18794807-7 2008 Furthermore, the combination of 5-FU+PP2 decreased the 5-FU-induced activation of epidermal growth factor receptor (EGFR)-AKT pathway. Fluorouracil 32-36 epidermal growth factor receptor Homo sapiens 116-120 18794807-7 2008 Furthermore, the combination of 5-FU+PP2 decreased the 5-FU-induced activation of epidermal growth factor receptor (EGFR)-AKT pathway. Fluorouracil 55-59 epidermal growth factor receptor Homo sapiens 82-114 18794807-7 2008 Furthermore, the combination of 5-FU+PP2 decreased the 5-FU-induced activation of epidermal growth factor receptor (EGFR)-AKT pathway. Fluorouracil 55-59 epidermal growth factor receptor Homo sapiens 116-120 18794807-9 2008 Taken together, 5-FU chemoresistance can be reversed through indirect TS regulation by inhibiting Src tyrosine kinase. Fluorouracil 16-20 SRC proto-oncogene, non-receptor tyrosine kinase Homo sapiens 98-101 18794807-10 2008 A potential mechanism of action of Src kinase inhibitors on 5-FU chemosensitivity might be linked to the inhibition of 5-FU-induced EGFR-AKT activation. Fluorouracil 60-64 SRC proto-oncogene, non-receptor tyrosine kinase Homo sapiens 35-38 18794807-10 2008 A potential mechanism of action of Src kinase inhibitors on 5-FU chemosensitivity might be linked to the inhibition of 5-FU-induced EGFR-AKT activation. Fluorouracil 60-64 epidermal growth factor receptor Homo sapiens 132-136 18794807-10 2008 A potential mechanism of action of Src kinase inhibitors on 5-FU chemosensitivity might be linked to the inhibition of 5-FU-induced EGFR-AKT activation. Fluorouracil 119-123 SRC proto-oncogene, non-receptor tyrosine kinase Homo sapiens 35-38 18794807-10 2008 A potential mechanism of action of Src kinase inhibitors on 5-FU chemosensitivity might be linked to the inhibition of 5-FU-induced EGFR-AKT activation. Fluorouracil 119-123 epidermal growth factor receptor Homo sapiens 132-136 19020740-1 2008 To elucidate the mechanism of resistance to 5-fluorouracil (5-FU) in human gastric cancer cells, we established a cell line MKN45/F2R, which acquired 5-FU resistance as a result of continuous exposure to increasing dosages of 5-FU over a year. Fluorouracil 44-58 coagulation factor II thrombin receptor Homo sapiens 130-133 18996727-1 2008 BACKGROUND: Recent studies give rise to the hypothesis, that adjuvant chemoradioimmunotherapy with 5-fluorouracil (5-FU), cisplatin and interferon-alpha (IFN-alpha) might be a possible new treatment of pancreatic cancer in resected patients. Fluorouracil 99-113 interferon alpha 1 Homo sapiens 154-163 19020740-1 2008 To elucidate the mechanism of resistance to 5-fluorouracil (5-FU) in human gastric cancer cells, we established a cell line MKN45/F2R, which acquired 5-FU resistance as a result of continuous exposure to increasing dosages of 5-FU over a year. Fluorouracil 150-154 coagulation factor II thrombin receptor Homo sapiens 130-133 19020740-1 2008 To elucidate the mechanism of resistance to 5-fluorouracil (5-FU) in human gastric cancer cells, we established a cell line MKN45/F2R, which acquired 5-FU resistance as a result of continuous exposure to increasing dosages of 5-FU over a year. Fluorouracil 150-154 coagulation factor II thrombin receptor Homo sapiens 130-133 19000447-12 2008 The inhibition rates of 5-fluorouracil (5-FU), VCR, epirubicin (EADM) and OXA on cancer cells were lower in the group with strong expression of bcl-2 than in that with weak expression of bcl-2 (P<0.05). Fluorouracil 24-38 BCL2 apoptosis regulator Homo sapiens 144-149 19000447-12 2008 The inhibition rates of 5-fluorouracil (5-FU), VCR, epirubicin (EADM) and OXA on cancer cells were lower in the group with strong expression of bcl-2 than in that with weak expression of bcl-2 (P<0.05). Fluorouracil 40-44 BCL2 apoptosis regulator Homo sapiens 144-149 18814928-5 2008 Bevacizumab is a recombinant humanized monoclonal antibody directed against VEGF which is used for the treatment of metastatic colorectal cancer in combination with 5-fluorouracil-based regimens. Fluorouracil 165-179 vascular endothelial growth factor A Homo sapiens 76-80 19189638-6 2008 Conversely, RKO cells expressing wildtype p53, proteolytically activated caspase-8, -9, -7 and -3 and unmethylated caspase-8 were more responsive to 5-FU and selenous acid-induced apoptosis. Fluorouracil 149-153 tumor protein p53 Homo sapiens 42-45 18941179-4 2008 Tgfb2(+/-) mice have a smaller and more slowly cycling HSPC compartment, which has a decreased serial repopulation capacity, and are less susceptible to the lethal effect of high doses of 5-fluorouracil. Fluorouracil 188-202 transforming growth factor, beta 2 Mus musculus 0-5 18779317-5 2008 Activation of p53 by 5-fluorouracil increased the TLR3 mRNA in epithelial cell lines with wild-type p53 but not in cell lines harboring mutant p53. Fluorouracil 21-35 tumor protein p53 Homo sapiens 14-17 18779317-5 2008 Activation of p53 by 5-fluorouracil increased the TLR3 mRNA in epithelial cell lines with wild-type p53 but not in cell lines harboring mutant p53. Fluorouracil 21-35 tumor protein p53 Homo sapiens 100-103 18779317-5 2008 Activation of p53 by 5-fluorouracil increased the TLR3 mRNA in epithelial cell lines with wild-type p53 but not in cell lines harboring mutant p53. Fluorouracil 21-35 tumor protein p53 Homo sapiens 100-103 18583030-0 2008 Down regulation of c-Myc and induction of an angiogenesis inhibitor, thrombospondin-1, by 5-FU in human colon cancer KM12C cells. Fluorouracil 90-94 thrombospondin 1 Homo sapiens 69-85 21479491-4 2008 Two representative chemotherapeutic agents for pancreatic cancer, 5-fluorouracil and gemcitabine, promoted cell death in a p53-dependent manner; however, 1% hypoxia caused chemoresistance to these drugs. Fluorouracil 66-80 tumor protein p53 Homo sapiens 123-126 18949393-6 2008 Bcl-2/MMR expression was significantly (p=0.030 for whole series; p=0.018 for the 5-FU-treated cases) related to the response to treatment; tumours with low levels of both Bcl-2 and MMR responded better (n=18/31, 58%) than those with high Bcl-2 and MMR (n=3/16, 18%). Fluorouracil 82-86 BCL2 apoptosis regulator Homo sapiens 0-5 18612238-4 2008 Overexpression of the worm DPD and TS homologs (DPYD-1 and Y110A7A.4, respectively) suppressed germ cell death following 5-FU exposure. Fluorouracil 121-125 Dihydropyrimidine dehydrogenase [NADP(+)] Caenorhabditis elegans 48-54 18612238-5 2008 In addition, DPYD-1 depletion by RNAi resulted in 5-FU sensitivity, while treatment with Y110A7A.4 RNAi and 5-FU resulted in similar patterns of embryonic death. Fluorouracil 50-54 Dihydropyrimidine dehydrogenase [NADP(+)] Caenorhabditis elegans 13-19 18583030-2 2008 We have previously demonstrated that Egr-1 induced by 5-FU enhanced TSP-1 expression in human colon cancer KM12C cells. Fluorouracil 54-58 thrombospondin 1 Homo sapiens 68-73 18583030-5 2008 Since 5-FU induced the expression of TSP-1, we examined the effect of c-Myc on the TSP-1 promoter. Fluorouracil 6-10 thrombospondin 1 Homo sapiens 37-42 18583030-8 2008 These findings suggest that 5-FU decreased the expression of c-Myc and consequently miR-17-92 cluster and increased the expression of TSP-1 mRNA. Fluorouracil 28-32 thrombospondin 1 Homo sapiens 134-139 18834353-8 2008 When cells were treated with 20 microM 5-fluorouracil and 200 microg/ml Bupleuri Radix simultaneously, Bax protein increased in HepG2 cells at 24 hr; however, p21 and p53 proteins were up-regulated in normal human lymphocytes. Fluorouracil 39-53 BCL2 associated X, apoptosis regulator Homo sapiens 103-106 18834353-8 2008 When cells were treated with 20 microM 5-fluorouracil and 200 microg/ml Bupleuri Radix simultaneously, Bax protein increased in HepG2 cells at 24 hr; however, p21 and p53 proteins were up-regulated in normal human lymphocytes. Fluorouracil 39-53 tumor protein p53 Homo sapiens 167-170 18755584-4 2008 We analysed TRAIL-R 1, -2, -3 and -4 expression by immuno-histochemistry in CRC, using tissue micro arrays, and found that concomitant low/medium TRAIL-R1 and high TRAIL-R3 expression in primary CRC is significantly associated with a poor response to 5-FU-based first-line chemotherapy and with shorter progression-free survival. Fluorouracil 251-255 TNF receptor superfamily member 10c Homo sapiens 164-172 18246360-0 2008 Topical application of 5-fluorouracil on attic cholesteatoma results in downregulation of keratinocyte growth factor and reduction of proliferative activity. Fluorouracil 23-37 fibroblast growth factor 7 Homo sapiens 90-116 18246360-4 2008 5-FU significantly reduced the expression of KGF, did not change KGFR expression, and significantly reduced the Ki-67 labeling index, relative to the control group. Fluorouracil 0-4 fibroblast growth factor 7 Homo sapiens 45-48 18246360-5 2008 The effect of 5-FU on cholesteatoma seems to be mediated, at least in part, through downregulation of KGF in stromal cells and reduction of the proliferative activity of epithelial cells. Fluorouracil 14-18 fibroblast growth factor 7 Homo sapiens 102-105 18755584-6 2008 Thus, the combination of TRAIL-R1 and TRAIL-R3 expression might represent a predictive and prognostic factor of the response to 5-FU-based first-line chemotherapy in patients with metastatic CRC. Fluorouracil 128-132 TNF receptor superfamily member 10c Homo sapiens 38-46 18357466-0 2008 Prognostic role of p53 codon 72 polymorphism in gastric cancer patients treated with fluorouracil-based adjuvant chemotherapy. Fluorouracil 85-97 tumor protein p53 Homo sapiens 19-22 18931578-2 2008 He was treated with concomitant chemoradiotherapy (CRT)with low-dose FP(5-FU, CDDP)and 60 Gy of irradiation. Fluorouracil 72-76 calcitonin receptor Homo sapiens 51-54 18692501-5 2008 Functional analysis of cancer-related mutant Keap1 in Nrf2 repression and the association between Nrf2 activation and resistance to 5-fluorouracil (5-FU) were investigated. Fluorouracil 148-152 NFE2 like bZIP transcription factor 2 Homo sapiens 98-102 18692501-8 2008 Down-regulation of Nrf2 activity by either Keap1 complementation or Nrf2 short interference RNA increased sensitivity to 5-FU in Keap1-altered BTC cells. Fluorouracil 121-125 NFE2 like bZIP transcription factor 2 Homo sapiens 19-23 18692501-8 2008 Down-regulation of Nrf2 activity by either Keap1 complementation or Nrf2 short interference RNA increased sensitivity to 5-FU in Keap1-altered BTC cells. Fluorouracil 121-125 NFE2 like bZIP transcription factor 2 Homo sapiens 68-72 18692501-8 2008 Down-regulation of Nrf2 activity by either Keap1 complementation or Nrf2 short interference RNA increased sensitivity to 5-FU in Keap1-altered BTC cells. Fluorouracil 121-125 kelch like ECH associated protein 1 Homo sapiens 129-134 18692501-10 2008 Aberrant Nrf2 activation provoked by Keap1 alteration is one of the molecular mechanisms for chemotherapeutic resistance in GBC and will be a novel therapeutic target as an enhancer of sensitivity to 5-FU-based regimens. Fluorouracil 200-204 NFE2 like bZIP transcription factor 2 Homo sapiens 9-13 18692501-10 2008 Aberrant Nrf2 activation provoked by Keap1 alteration is one of the molecular mechanisms for chemotherapeutic resistance in GBC and will be a novel therapeutic target as an enhancer of sensitivity to 5-FU-based regimens. Fluorouracil 200-204 kelch like ECH associated protein 1 Homo sapiens 37-42 18357466-2 2008 Our aim was to investigate the association of p53 Arg72Pro polymorphism with the clinical outcome of gastric cancer patients treated with 5-FU-based adjuvant chemotherapy. Fluorouracil 138-142 tumor protein p53 Homo sapiens 46-49 18357466-3 2008 METHODS: The p53 codon 72 genotype was determined in blood samples from 110 Chinese patients with gastric cancer treated with 5-fluorouracil (5-FU)-based adjuvant chemotherapy, using polymerase chain reaction-ligation detection reaction (PCR-LDR) method. Fluorouracil 126-140 tumor protein p53 Homo sapiens 13-16 18357466-3 2008 METHODS: The p53 codon 72 genotype was determined in blood samples from 110 Chinese patients with gastric cancer treated with 5-fluorouracil (5-FU)-based adjuvant chemotherapy, using polymerase chain reaction-ligation detection reaction (PCR-LDR) method. Fluorouracil 142-146 tumor protein p53 Homo sapiens 13-16 18357466-6 2008 CONCLUSION: These results suggested that p53 codon 72 polymorphism appears to be an independent prognostic factor in gastric cancer patients treated with 5-FU-based adjuvant chemotherapy. Fluorouracil 154-158 tumor protein p53 Homo sapiens 41-44 18813834-6 2008 LC-antisense molecules to EIF3EIP and AFP were simultaneously treated with 5-FU to Huh-7 cells. Fluorouracil 75-79 alpha fetoprotein Homo sapiens 38-41 18757417-9 2008 Blockade of the p38 MAPK pathway by SB203580 remarkably inhibited the phosphorylation of HSP27 induced by 5-FU and decreased the induction of Egr-1 and TSP-1 by 5-FU in KM12C cells. Fluorouracil 161-165 thrombospondin 1 Homo sapiens 152-157 18776995-5 2008 The expression and subcellular location of PTC1 protein in Hep3B cells treated by 5-FU were also investigated by Western blot analysis and immunofluorescent microscopy. Fluorouracil 82-86 patched 1 Homo sapiens 43-47 18776995-8 2008 Furthermore, 5-FU treatment affects the subcellular localization of PTC1 protein, a key member in SHh signaling pathway. Fluorouracil 13-17 patched 1 Homo sapiens 68-72 18757417-0 2008 Molecular basis for the induction of an angiogenesis inhibitor, thrombospondin-1, by 5-fluorouracil. Fluorouracil 85-99 thrombospondin 1 Homo sapiens 64-80 18757417-2 2008 5-FU dose-dependently increased the expression levels of intrinsic antiangiogenic factor thrombospondin-1 (TSP-1) in human colon carcinoma KM12C cells and human breast cancer MCF7 cells. Fluorouracil 0-4 thrombospondin 1 Homo sapiens 89-105 18757417-2 2008 5-FU dose-dependently increased the expression levels of intrinsic antiangiogenic factor thrombospondin-1 (TSP-1) in human colon carcinoma KM12C cells and human breast cancer MCF7 cells. Fluorouracil 0-4 thrombospondin 1 Homo sapiens 107-112 18546291-2 2008 The role of nonhomologous end joining (NHEJ) genes (Ku70, Ku80 and DNA-PKcs) in double-strand break (DSB) repair, genomic instability and apoptosis suggest a possible impact on tumor response to radiotherapy, 5-fluorouracil or cisplatin, as these agents are direct or indirect inductors of DSBs. Fluorouracil 209-223 protein kinase, DNA-activated, catalytic subunit Homo sapiens 67-75 18757417-3 2008 We investigated the molecular basis for the induction of TSP-1 by 5-FU in KM12C cells. Fluorouracil 66-70 thrombospondin 1 Homo sapiens 57-62 18757417-4 2008 Promoter assays showed that the region with the Egr-1 binding site is critical for the induction of TSP-1 promoter activity by 5-FU. Fluorouracil 127-131 thrombospondin 1 Homo sapiens 100-105 18757417-5 2008 The binding of Egr-1 to the TSP-1 promoter was increased in KM12C cells treated with 5-FU. Fluorouracil 85-89 thrombospondin 1 Homo sapiens 28-33 18757417-8 2008 Furthermore, 5-FU induced the phosphorylation of p38 mitogen-activated protein kinase (MAPK) and heat shock protein 27 (HSP27). Fluorouracil 13-17 mitogen-activated protein kinase 14 Homo sapiens 49-85 18930000-2 2008 The commonly used anti-tumor drug, 5-fluorouracil (5-FU), blocks the cell cycle by inhibiting thymidylate synthase, and is also known to induce TXNIP gene expression. Fluorouracil 35-49 thioredoxin interacting protein Homo sapiens 144-149 18930000-2 2008 The commonly used anti-tumor drug, 5-fluorouracil (5-FU), blocks the cell cycle by inhibiting thymidylate synthase, and is also known to induce TXNIP gene expression. Fluorouracil 51-55 thioredoxin interacting protein Homo sapiens 144-149 18930000-6 2008 5-FU suppressed the expression of p27(kip1), p53, and cyclin E, whereas d-allose induced p53 and reduced cyclins D, A, and E. The expression of p27(kip1) remained unchanged by d-allose at transcriptional level, but increased at the protein level suggesting an increase in protein stability by TXNIP. Fluorouracil 0-4 tumor protein p53 Homo sapiens 45-48 18930000-7 2008 d-Allose and to a lesser extent 5-FU induced TXNIP expression significantly (808.4+/-122.9% and 186.8+/-32.9%, respectively) and the combination of both further enhanced TXNIP expression. Fluorouracil 32-36 thioredoxin interacting protein Homo sapiens 45-50 18930000-7 2008 d-Allose and to a lesser extent 5-FU induced TXNIP expression significantly (808.4+/-122.9% and 186.8+/-32.9%, respectively) and the combination of both further enhanced TXNIP expression. Fluorouracil 32-36 thioredoxin interacting protein Homo sapiens 170-175 18698031-5 2008 RESULTS: Transient Chk1 down-regulation sensitized HCT-116 cells, p53-/- more than the p53 wild-type counterpart, to DNA-damaging agents 5-fluorouracil (5-FU), doxorubicin, and etoposide treatments, with no modification of Taxol and PS341 cytotoxic activities. Fluorouracil 137-151 checkpoint kinase 1 Homo sapiens 19-23 18758304-1 2008 INTRODUCTION: The aim of this study was to determine and evaluate the recommended dose of docetaxel in combination with a novel oral 5-fluorouracil analogue S-1 and evaluate the efficacy and safety in patients with previously treated non-small cell lung cancer. Fluorouracil 133-147 proteasome 26S subunit, non-ATPase 1 Homo sapiens 157-160 18420342-7 2008 These results suggest that 5-FU-based drugs inhibit tumor progression through different modes of action, including cytotoxic activity derived from 5-FU and the inhibition of angiogenesis through the induction of TSP-1. Fluorouracil 27-31 thrombospondin 1 Homo sapiens 212-217 18698031-5 2008 RESULTS: Transient Chk1 down-regulation sensitized HCT-116 cells, p53-/- more than the p53 wild-type counterpart, to DNA-damaging agents 5-fluorouracil (5-FU), doxorubicin, and etoposide treatments, with no modification of Taxol and PS341 cytotoxic activities. Fluorouracil 153-157 checkpoint kinase 1 Homo sapiens 19-23 18665170-7 2008 Compared with untreated cells, 5-FU and doxorubicin increased TK-1 levels by >300. Fluorouracil 31-35 thymidine kinase 1 Homo sapiens 62-64 18497562-7 2008 Moreover, G(1)-arrest of the p53+/+ cells was elicited by lower doses of RSV and 5-FU in combination, but not with either agent alone. Fluorouracil 81-85 tumor protein p53 Homo sapiens 29-32 18837291-5 2008 RESULTS: MTT assay showed that the expression of BCRP increased with the increasing resistance of 5-fluorouracil (5-Fu) (P<0.05, n=3) in the cell model, while HPLC assay indicated that the intracellular retention dose of 5-Fu was significantly correlated with the expression of BCRP (r=-0.897, P<0.05, n=3). Fluorouracil 98-112 ATP binding cassette subfamily G member 2 (Junior blood group) Homo sapiens 49-53 18837291-5 2008 RESULTS: MTT assay showed that the expression of BCRP increased with the increasing resistance of 5-fluorouracil (5-Fu) (P<0.05, n=3) in the cell model, while HPLC assay indicated that the intracellular retention dose of 5-Fu was significantly correlated with the expression of BCRP (r=-0.897, P<0.05, n=3). Fluorouracil 114-118 ATP binding cassette subfamily G member 2 (Junior blood group) Homo sapiens 49-53 18837291-5 2008 RESULTS: MTT assay showed that the expression of BCRP increased with the increasing resistance of 5-fluorouracil (5-Fu) (P<0.05, n=3) in the cell model, while HPLC assay indicated that the intracellular retention dose of 5-Fu was significantly correlated with the expression of BCRP (r=-0.897, P<0.05, n=3). Fluorouracil 224-228 ATP binding cassette subfamily G member 2 (Junior blood group) Homo sapiens 49-53 18837291-8 2008 As shown by MTT assay subsequently, the resistance index (RI) of 47 BCRP-positive breast cancer tissue specimens to 5-Fu was 7-12 times as high as that of adjacent normal tissue samples. Fluorouracil 116-120 ATP binding cassette subfamily G member 2 (Junior blood group) Homo sapiens 68-72 18837291-9 2008 BCRP expression was related to 5-Fu resistance (R2=0.8124, P<0.01). Fluorouracil 31-35 ATP binding cassette subfamily G member 2 (Junior blood group) Homo sapiens 0-4 18837291-10 2008 CONCLUSION: Resistance to 5-Fu can be mediated by BCRP. Fluorouracil 26-30 ATP binding cassette subfamily G member 2 (Junior blood group) Homo sapiens 50-54 18497562-9 2008 At lower doses (25 or 50 microM), it interacted with 5-FU in antagonistic (mean CI > 1.1) and additive manners (0.9 < mean CI < 1.1) in p53+/+ and p53-/- cells respectively. Fluorouracil 53-57 tumor protein p53 Homo sapiens 145-148 18690847-3 2008 The aim of the study was to investigate the induction by celecoxib of some multidrug resistance proteins, MRP1, MRP2, MRP4 and MRP5, involved in the transport of irinotecan and 5-FU. Fluorouracil 177-181 ATP binding cassette subfamily C member 1 Homo sapiens 106-110 18497562-9 2008 At lower doses (25 or 50 microM), it interacted with 5-FU in antagonistic (mean CI > 1.1) and additive manners (0.9 < mean CI < 1.1) in p53+/+ and p53-/- cells respectively. Fluorouracil 53-57 tumor protein p53 Homo sapiens 156-159 18497562-13 2008 Conversely, it inhibits 5-FU-triggered apoptosis at lower concentrations in p53+/+ cells. Fluorouracil 24-28 tumor protein p53 Homo sapiens 76-79 18704308-8 2008 It is concluded that the targeted magnetic nanoparticles containing 5-Fu can improve the chemotherapeutic effect of 5-Fu by decreasing bcl-2 expression, increasing bax expression and inducing apoptosis of the liver cancer cells. Fluorouracil 68-72 BCL2 apoptosis regulator Homo sapiens 135-140 18498133-10 2008 A SNP in codon 72 of TP53 was revealed to be a key regulator of 5-FU metabolizing genes such as DHFR and MTHFR, constituting 50% of all significant associations observed after FUMI therapy. Fluorouracil 64-68 tumor protein p53 Homo sapiens 21-25 18704308-8 2008 It is concluded that the targeted magnetic nanoparticles containing 5-Fu can improve the chemotherapeutic effect of 5-Fu by decreasing bcl-2 expression, increasing bax expression and inducing apoptosis of the liver cancer cells. Fluorouracil 68-72 BCL2 associated X, apoptosis regulator Homo sapiens 164-167 18704308-8 2008 It is concluded that the targeted magnetic nanoparticles containing 5-Fu can improve the chemotherapeutic effect of 5-Fu by decreasing bcl-2 expression, increasing bax expression and inducing apoptosis of the liver cancer cells. Fluorouracil 116-120 BCL2 apoptosis regulator Homo sapiens 135-140 18704308-8 2008 It is concluded that the targeted magnetic nanoparticles containing 5-Fu can improve the chemotherapeutic effect of 5-Fu by decreasing bcl-2 expression, increasing bax expression and inducing apoptosis of the liver cancer cells. Fluorouracil 116-120 BCL2 associated X, apoptosis regulator Homo sapiens 164-167 18687176-13 2008 The level of IL-6 in 5-FU group was lower than that in severe sepsis group, but with no difference compared with that of control group. Fluorouracil 21-25 interleukin 6 Rattus norvegicus 13-17 18632807-0 2008 Colorectal tumor cells treated with 5-FU, oxaliplatin, irinotecan, and cetuximab exhibit changes in 18F-FDG incorporation corresponding to hexokinase activity and glucose transport. Fluorouracil 36-40 hexokinase 1 Homo sapiens 139-149 18641541-1 2008 This study was conducted to evaluate the association between systemic exposure to 5-fluorouracil (5-FU) and genetic polymorphisms of vascular endothelial growth factor (VEGF) with clinical outcomes to a 5-FU/cisplatin-based chemoradiotherapy in Japanese patients with esophageal squamous cell carcinoma (ESCC). Fluorouracil 203-207 vascular endothelial growth factor A Homo sapiens 133-167 18641541-1 2008 This study was conducted to evaluate the association between systemic exposure to 5-fluorouracil (5-FU) and genetic polymorphisms of vascular endothelial growth factor (VEGF) with clinical outcomes to a 5-FU/cisplatin-based chemoradiotherapy in Japanese patients with esophageal squamous cell carcinoma (ESCC). Fluorouracil 203-207 vascular endothelial growth factor A Homo sapiens 169-173 18641541-7 2008 In conclusion, VEGF G-1154A was a predictor of severe acute toxicities during 5-FU/cisplatin-based chemoradiotherapy in Japanese ESCC patients, whereas the AUC480h value of 5-FU was predictive of the clinical response. Fluorouracil 78-82 vascular endothelial growth factor A Homo sapiens 15-19 18687176-15 2008 CONCLUSION: 5-FU may lower simultaneously the level of proinflammatory IL-6 and anti-inflammatory IL-10, alleviate lung edema and inflammation. Fluorouracil 12-16 interleukin 6 Rattus norvegicus 71-75 19035187-0 2008 [Study on the relationship between breast cancer resistance protein expression and 5-fluorouracil resistance]. Fluorouracil 83-97 ATP binding cassette subfamily G member 2 (Junior blood group) Homo sapiens 35-67 18325917-2 2008 We analysed the efficacy of a preoperative combination between 5-fluorouracil, anthracyclines and cyclophosphamide according to both p53 status and molecular classification. Fluorouracil 63-77 tumor protein p53 Homo sapiens 133-136 18535404-7 2008 In most instances, peaks in serum levels occurred following initial histological changes, Although following MTX administration, serum IL-1beta peaked before histological changes and following 5-FU administration, serum NFkappaB, TNF, IL-1beta and IL-6 all peaked before histological evidence of tissue damage. Fluorouracil 193-197 interleukin 1 beta Homo sapiens 135-143 19343150-8 2008 In a randomized trial comparing 5-FU vs. irinotecan plus cisplatin vs. S-1, conducted by the Japan Clinical Oncology Group, S-1 was associated with a favorable safety profile, response rate, and time-to-treatment failure with longer survival compared with 5-FU. Fluorouracil 32-36 proteasome 26S subunit, non-ATPase 1 Homo sapiens 124-127 19343150-8 2008 In a randomized trial comparing 5-FU vs. irinotecan plus cisplatin vs. S-1, conducted by the Japan Clinical Oncology Group, S-1 was associated with a favorable safety profile, response rate, and time-to-treatment failure with longer survival compared with 5-FU. Fluorouracil 256-260 proteasome 26S subunit, non-ATPase 1 Homo sapiens 124-127 18609706-11 2008 Furthermore, cells with reduced Bcl-x(L) or Mcl-1 expression was more sensitive towards oxaliplatin- and irinotecan-induced apoptosis, and in the case of Bcl-x(L) also towards 5-FU-induced apoptosis. Fluorouracil 176-180 BCL2 like 1 Homo sapiens 32-40 18609706-11 2008 Furthermore, cells with reduced Bcl-x(L) or Mcl-1 expression was more sensitive towards oxaliplatin- and irinotecan-induced apoptosis, and in the case of Bcl-x(L) also towards 5-FU-induced apoptosis. Fluorouracil 176-180 BCL2 like 1 Homo sapiens 154-162 18575591-4 2008 It has been also hypothesized that its specific ligand, KGF, might contribute to the development of resistance to 5-fluorouracil (5-FU) in epithelial cancers and tamoxifen in estrogen-positive breast cancers. Fluorouracil 114-128 fibroblast growth factor 7 Homo sapiens 56-59 18575591-4 2008 It has been also hypothesized that its specific ligand, KGF, might contribute to the development of resistance to 5-fluorouracil (5-FU) in epithelial cancers and tamoxifen in estrogen-positive breast cancers. Fluorouracil 130-134 fibroblast growth factor 7 Homo sapiens 56-59 18575591-9 2008 The capacity of 5-FU to induce cell death is abrogated by co-treatment with KGF, whereas in KGFR silenced cells 5-FU efficiently induces cell death even combined to KGF, as determined by evaluating cell viability. Fluorouracil 16-20 fibroblast growth factor 7 Homo sapiens 76-79 18575591-9 2008 The capacity of 5-FU to induce cell death is abrogated by co-treatment with KGF, whereas in KGFR silenced cells 5-FU efficiently induces cell death even combined to KGF, as determined by evaluating cell viability. Fluorouracil 112-116 fibroblast growth factor 7 Homo sapiens 92-95 19035187-7 2008 RESULTS: MT assay showed that increasing resistance of 5-fluorouracil (5-Fu) climbed with the increases of the BCRP expressions by 10.58 times (P < 0.05, n = 3) in cell model. Fluorouracil 55-69 ATP binding cassette subfamily G member 2 (Junior blood group) Homo sapiens 111-115 19035187-7 2008 RESULTS: MT assay showed that increasing resistance of 5-fluorouracil (5-Fu) climbed with the increases of the BCRP expressions by 10.58 times (P < 0.05, n = 3) in cell model. Fluorouracil 71-75 ATP binding cassette subfamily G member 2 (Junior blood group) Homo sapiens 111-115 19035187-8 2008 HPLC assay also proved that a significant negative correlation between the intracellular retention dose of 5-Fu with different expression of BCRP (r = -0.897, P < 0.05, n = 3). Fluorouracil 107-111 ATP binding cassette subfamily G member 2 (Junior blood group) Homo sapiens 141-145 19035187-10 2008 Subsequently, the resistance index (RI) for 47 BCRP-positive clinical breast cancer tissues to 5-Fu was shown from 7 to 12 times compared with normal cancer-side tissues through MT assay. Fluorouracil 95-99 ATP binding cassette subfamily G member 2 (Junior blood group) Homo sapiens 47-51 19035187-11 2008 The statistical correlation between BCRP expression and 5-Fu resistance was observed in clinical breast cancer tissue specimens (R2 = 0.8124, P < 0.01). Fluorouracil 56-60 ATP binding cassette subfamily G member 2 (Junior blood group) Homo sapiens 36-40 19035187-12 2008 CONCLUSION: This study results showed that there is a significant relationship between BCRP expression and 5-Fu resistance. Fluorouracil 107-111 ATP binding cassette subfamily G member 2 (Junior blood group) Homo sapiens 87-91 18497986-8 2008 This study shows the feasibility of constructing fusion proteins in a prokaryotic cell based system consisting of a human scFv antibody and yCD to convert the antifungal agent 5-FC to 5-FU, one of the widely used anticancer agent. Fluorouracil 184-188 immunglobulin heavy chain variable region Homo sapiens 122-126 18497992-1 2008 To understand one of the mechanisms of resistance to chemoradiation in colon cancer cells, we investigated whether 5-fluorouracil (5-FU) mediated the expression of epidermal growth factor receptor (EGFR) and modified repair of radiation-induced DNA damage, especially in a p53 independent pathway. Fluorouracil 115-129 epidermal growth factor receptor Homo sapiens 164-196 18497992-1 2008 To understand one of the mechanisms of resistance to chemoradiation in colon cancer cells, we investigated whether 5-fluorouracil (5-FU) mediated the expression of epidermal growth factor receptor (EGFR) and modified repair of radiation-induced DNA damage, especially in a p53 independent pathway. Fluorouracil 115-129 epidermal growth factor receptor Homo sapiens 198-202 18497992-1 2008 To understand one of the mechanisms of resistance to chemoradiation in colon cancer cells, we investigated whether 5-fluorouracil (5-FU) mediated the expression of epidermal growth factor receptor (EGFR) and modified repair of radiation-induced DNA damage, especially in a p53 independent pathway. Fluorouracil 131-135 epidermal growth factor receptor Homo sapiens 164-196 18497992-1 2008 To understand one of the mechanisms of resistance to chemoradiation in colon cancer cells, we investigated whether 5-fluorouracil (5-FU) mediated the expression of epidermal growth factor receptor (EGFR) and modified repair of radiation-induced DNA damage, especially in a p53 independent pathway. Fluorouracil 131-135 epidermal growth factor receptor Homo sapiens 198-202 18497992-1 2008 To understand one of the mechanisms of resistance to chemoradiation in colon cancer cells, we investigated whether 5-fluorouracil (5-FU) mediated the expression of epidermal growth factor receptor (EGFR) and modified repair of radiation-induced DNA damage, especially in a p53 independent pathway. Fluorouracil 131-135 tumor protein p53 Homo sapiens 273-276 18497992-6 2008 5-FU-induced activation of EGFR followed by radiation in SW480 cells resulted in up-regulation of ERCC1. Fluorouracil 0-4 epidermal growth factor receptor Homo sapiens 27-31 18497992-7 2008 In contrast, 5-FU-induced degradation of EGFR followed by radiation in the other radiosensitive cell lines resulted in down-regulation of ERCC1. Fluorouracil 13-17 epidermal growth factor receptor Homo sapiens 41-45 18497992-8 2008 This suggested a complementary interaction between EGFR and ERCC1, and that 5-FU-induced EGFR activation conferred protection against radiation, through activation of DNA repair. Fluorouracil 76-80 epidermal growth factor receptor Homo sapiens 89-93 18497992-9 2008 Interaction of EGFR and ERCC1 might correlate with radiation-induced DNA damage when p53 mutant colon cancer cell lines are exposed to 5-FU followed by radiation. Fluorouracil 135-139 epidermal growth factor receptor Homo sapiens 15-19 18497992-9 2008 Interaction of EGFR and ERCC1 might correlate with radiation-induced DNA damage when p53 mutant colon cancer cell lines are exposed to 5-FU followed by radiation. Fluorouracil 135-139 tumor protein p53 Homo sapiens 85-88 18566238-4 2008 Our data indicate that methylnaltrexone (MNTX), a peripheral antagonist of the mu-opioid receptor, exerts a synergistic effect with 5-FU and bevacizumab on inhibition of vascular endothelial growth factor (VEGF)-induced human pulmonary microvascular endothelial cell (EC) proliferation and migration, two key components in cancer-associated angiogenesis. Fluorouracil 132-136 vascular endothelial growth factor A Homo sapiens 170-204 18606591-5 2008 CDDP and 5-FU induced apoptosis mediated by the intrinsic pathway in colon cancer cells, as demonstrated by morphological analyses, mitochondrial cytochrome c release and cleavage of caspase 3. Fluorouracil 9-13 cytochrome c, somatic Homo sapiens 146-158 18606591-5 2008 CDDP and 5-FU induced apoptosis mediated by the intrinsic pathway in colon cancer cells, as demonstrated by morphological analyses, mitochondrial cytochrome c release and cleavage of caspase 3. Fluorouracil 9-13 caspase 3 Homo sapiens 183-192 18567802-0 2008 The RNA exosome component hRrp6 is a target for 5-fluorouracil in human cells. Fluorouracil 48-62 exosome component 10 Homo sapiens 26-31 18566238-4 2008 Our data indicate that methylnaltrexone (MNTX), a peripheral antagonist of the mu-opioid receptor, exerts a synergistic effect with 5-FU and bevacizumab on inhibition of vascular endothelial growth factor (VEGF)-induced human pulmonary microvascular endothelial cell (EC) proliferation and migration, two key components in cancer-associated angiogenesis. Fluorouracil 132-136 vascular endothelial growth factor A Homo sapiens 206-210 18567802-4 2008 HeLa cells depleted of the inessential exosome component hRrp6, also called PM/Scl100, are significantly growth impaired relative to control cells after 5-FU administration. Fluorouracil 153-157 exosome component 10 Homo sapiens 57-62 18567802-4 2008 HeLa cells depleted of the inessential exosome component hRrp6, also called PM/Scl100, are significantly growth impaired relative to control cells after 5-FU administration. Fluorouracil 153-157 exosome component 10 Homo sapiens 76-85 18567802-5 2008 The selective stabilization of bona fide hRrp6 RNA substrates on 5-FU treatment suggests that this exosome component is specifically targeted. Fluorouracil 65-69 exosome component 10 Homo sapiens 41-46 18567802-6 2008 Consistently, levels of hRrp6 substrates are increased in two 5-FU-sensitive cell lines. Fluorouracil 62-66 exosome component 10 Homo sapiens 24-29 18600534-0 2008 Functional inactivity and mutations of p53 differentially affect sensitivity to 5-fluorouracil and antifolate inhibitors of thymidylate synthase (TS) by altering TS levels in colorectal cancer cells. Fluorouracil 80-94 tumor protein p53 Homo sapiens 39-42 18071320-2 2008 Using cervical carcinoma cells (HeLa), the present study investigates the involvement of COX-2 in apoptosis elicited by the chemotherapeutics paclitaxel, cisplatin and 5-fluorouracil. Fluorouracil 168-182 prostaglandin-endoperoxide synthase 2 Homo sapiens 89-94 21136888-1 2008 The monoclonal antibody cetuximab directed against the epidermal growth factor receptor (EGFR) is an attractive agent for targeted therapy in advanced colorectal cancer (CRC), especially when combined with 5-fluorouracil (5-FU)-based chemotherapy. Fluorouracil 222-226 epidermal growth factor receptor Homo sapiens 55-87 21136888-1 2008 The monoclonal antibody cetuximab directed against the epidermal growth factor receptor (EGFR) is an attractive agent for targeted therapy in advanced colorectal cancer (CRC), especially when combined with 5-fluorouracil (5-FU)-based chemotherapy. Fluorouracil 222-226 epidermal growth factor receptor Homo sapiens 89-93 21136888-7 2008 Combined treatment with cetuximab and 5-FU revealed a synergistic anti-tumor response that is closely correlated with functional activity of EGFR/mitogen-activated protein kinase (MAPK) pathway. Fluorouracil 38-42 epidermal growth factor receptor Homo sapiens 141-145 21136888-9 2008 We demonstrated that only EGFR expression with high functional activity of EGFR/MAPK pathway is important for the synergistic effects between cetuximab and 5-FU in the investigated cell lines. Fluorouracil 156-160 epidermal growth factor receptor Homo sapiens 26-30 21136888-9 2008 We demonstrated that only EGFR expression with high functional activity of EGFR/MAPK pathway is important for the synergistic effects between cetuximab and 5-FU in the investigated cell lines. Fluorouracil 156-160 epidermal growth factor receptor Homo sapiens 75-79 18494554-4 2008 METHODS AND FINDINGS: Knockdown of VEGF with vegf-targeting small-interfering (si) RNAs increased susceptibility of human colon cancer cell line (HCT116) to apoptosis caused with 5-fluorouracil, etoposide, or doxorubicin. Fluorouracil 179-193 vascular endothelial growth factor A Homo sapiens 35-39 18494554-4 2008 METHODS AND FINDINGS: Knockdown of VEGF with vegf-targeting small-interfering (si) RNAs increased susceptibility of human colon cancer cell line (HCT116) to apoptosis caused with 5-fluorouracil, etoposide, or doxorubicin. Fluorouracil 179-193 vascular endothelial growth factor A Homo sapiens 45-49 18577244-0 2008 Combined effects of 5-fluorouracil, folinic acid and oxaliplatin on the expression of carcinoembryonic antigen in human colon cancer cells: pharmacological basis to develop an active antitumor immunochemotherapy. Fluorouracil 20-34 CEA cell adhesion molecule 3 Homo sapiens 86-110 18390970-0 2008 Influence of activation state of ErbB-2 (HER-2) on response to adjuvant cyclophosphamide, doxorubicin, and fluorouracil for stage II, node-positive breast cancer: study 8541 from the Cancer and Leukemia Group B. Fluorouracil 107-119 erb-b2 receptor tyrosine kinase 2 Homo sapiens 33-39 18390970-0 2008 Influence of activation state of ErbB-2 (HER-2) on response to adjuvant cyclophosphamide, doxorubicin, and fluorouracil for stage II, node-positive breast cancer: study 8541 from the Cancer and Leukemia Group B. Fluorouracil 107-119 erb-b2 receptor tyrosine kinase 2 Homo sapiens 41-46 18390970-2 2008 Results from a previous study from the Cancer and Leukemia Group B (CALGB 8541) demonstrated an interaction between ErbB-2 and increasing dose of adjuvant cyclophosphamide, doxorubicin, and fluorouracil (CAF) chemotherapy. Fluorouracil 190-202 erb-b2 receptor tyrosine kinase 2 Homo sapiens 116-122 18575323-1 2008 OBJECTIVE: To study the bystander effect of Uracil Phosphoribosyltransferase (UPRT )/5-fluorouracil (5-FU) suicide gene system, which is regulated by PSMA enhancer/promoter, on prostate cancer cell. Fluorouracil 85-99 folate hydrolase 1 Homo sapiens 150-154 18473752-1 2008 Capecitabine is a drug that requires the consecutive action of three enzymes: carboxylesterase 2 (CES 2), cytidine deaminase (CDD), and thymidine phosphorylase (TP) for transformation into 5-fluorouracil (5FU). Fluorouracil 189-203 carboxylesterase 2 Homo sapiens 78-96 18473752-1 2008 Capecitabine is a drug that requires the consecutive action of three enzymes: carboxylesterase 2 (CES 2), cytidine deaminase (CDD), and thymidine phosphorylase (TP) for transformation into 5-fluorouracil (5FU). Fluorouracil 189-203 carboxylesterase 2 Homo sapiens 98-103 18473752-1 2008 Capecitabine is a drug that requires the consecutive action of three enzymes: carboxylesterase 2 (CES 2), cytidine deaminase (CDD), and thymidine phosphorylase (TP) for transformation into 5-fluorouracil (5FU). Fluorouracil 205-208 carboxylesterase 2 Homo sapiens 78-96 21479426-0 2008 A Phase II study of 5-fluorouracil and cisplatin systemic chemotherapy for inoperable hepatocellular carcinoma with alpha fetoprotein as a predictive and prognostic marker. Fluorouracil 20-34 alpha fetoprotein Homo sapiens 116-133 18575323-1 2008 OBJECTIVE: To study the bystander effect of Uracil Phosphoribosyltransferase (UPRT )/5-fluorouracil (5-FU) suicide gene system, which is regulated by PSMA enhancer/promoter, on prostate cancer cell. Fluorouracil 101-105 folate hydrolase 1 Homo sapiens 150-154 20731894-16 2008 The IC50 of pEGFP-p53(RS)-801D cell line to 5-Fluorouracil(5FU) is 2.08+/-0.18 mug/mL, which is obviously lower than that of 801D(4.90+/-1.12 mug/mL,P <0.05) and pEGFP-801D(3.41+/-0.86 mug/mL,P <0.05). Fluorouracil 59-62 tumor protein p53 Homo sapiens 18-21 18478476-7 2008 Positive expression rate of Bcl-2 was 80% and the positive cells showed resistance to 5-FU, ADM and MMC. Fluorouracil 86-90 BCL2 apoptosis regulator Homo sapiens 28-33 20731894-16 2008 The IC50 of pEGFP-p53(RS)-801D cell line to 5-Fluorouracil(5FU) is 2.08+/-0.18 mug/mL, which is obviously lower than that of 801D(4.90+/-1.12 mug/mL,P <0.05) and pEGFP-801D(3.41+/-0.86 mug/mL,P <0.05). Fluorouracil 44-58 tumor protein p53 Homo sapiens 18-21 18329632-6 2008 Treatment of cultured NIH3T3 cells with 5-FU for 48 h resulted in a significant reduction of mRNA levels of Period1 (Per1) and Period2 (Per2) without affecting cell viability; however, treatment with the same amount of uracil, a structural analog of 5-FU, had little effect on the expression of clock genes. Fluorouracil 40-44 period circadian clock 2 Mus musculus 127-134 17982488-6 2008 5-Fluorouracil treatment of colon carcinoma HCT116 cells expressing WT p53 results in a reduction of the cyclin B2 protein level suggesting that DNA damage may indeed cause repression of these genes. Fluorouracil 0-14 tumor protein p53 Homo sapiens 71-74 18329632-7 2008 Consistent with its inhibitory actions, continuous administration of 5-FU (2 mg/kg/h) to mice attenuated the oscillation in the expressions of Per1 and Per2 in the liver and suprachiasmatic nuclei, the center of the mammalian circadian clock. Fluorouracil 69-73 period circadian clock 2 Mus musculus 152-156 18329632-6 2008 Treatment of cultured NIH3T3 cells with 5-FU for 48 h resulted in a significant reduction of mRNA levels of Period1 (Per1) and Period2 (Per2) without affecting cell viability; however, treatment with the same amount of uracil, a structural analog of 5-FU, had little effect on the expression of clock genes. Fluorouracil 40-44 period circadian clock 2 Mus musculus 136-140 18191509-4 2008 5-FU-loaded bola-niosomes were tested on SKMEL-28 (human melanoma) and HaCaT (non-melanoma skin cancer with a specific mutations in the p53 tumor suppressor gene) to assess the cytotoxic activity with respect to the free drug. Fluorouracil 0-4 tumor protein p53 Homo sapiens 136-139 18423122-2 2008 This research was to detect the expression of APRIL in colorectal carcinoma tissues, and to compare the effects of 5-fluorouracil (5-FU) and cisplatin (DDP) on the expression of APRIL in colorectal carcinoma SW480 cells. Fluorouracil 115-129 TNF superfamily member 13 Homo sapiens 178-183 18423122-2 2008 This research was to detect the expression of APRIL in colorectal carcinoma tissues, and to compare the effects of 5-fluorouracil (5-FU) and cisplatin (DDP) on the expression of APRIL in colorectal carcinoma SW480 cells. Fluorouracil 131-135 TNF superfamily member 13 Homo sapiens 178-183 18423122-4 2008 SW480 cells were treated with 5-FU and DDP at various concentrations for 24 h, 48 h and 72 h. The changes of APRIL mRNA level were analyzed by FQ-RT-PCR. Fluorouracil 30-34 TNF superfamily member 13 Homo sapiens 109-114 18423122-7 2008 When treated with different concentrations of 5-FU, the mRNA level of APRIL in SW480 cells raised gradually and reached the highest levels at 72 h after treatment (0.85+/-0.10, 0.81+/-0.09, 0.83+/-0.11, and 0.90+/-0.12 at the concentrations of 25, 50, 100 and 200 microg/mL, respectively), which were significantly higher than those in blank control group (P<0.001). Fluorouracil 46-50 TNF superfamily member 13 Homo sapiens 70-75 18212800-1 2008 S-1 is an oral fluorouracil anticancer drug that contains the 5-FU prodrug tegafur. Fluorouracil 15-27 proteasome 26S subunit, non-ATPase 1 Homo sapiens 0-3 18377724-6 2008 CAS overexpression enhanced p53 accumulation induced by doxorubicin, 5-fluorouracil, cisplatin, tamoxifen, and etoposide. Fluorouracil 69-83 tumor protein p53 Homo sapiens 28-31 18312275-3 2008 RNAi knockdown of DHODH expression in bloodstream form T. brucei did not inhibit growth in normal medium, but profoundly retarded growth in pyrimidine-depleted media or in the presence of the known pyrimidine uptake antagonist 5-fluorouracil (5-FU). Fluorouracil 227-241 dihydroorotate dehydrogenase (quinone) Homo sapiens 18-23 18312275-3 2008 RNAi knockdown of DHODH expression in bloodstream form T. brucei did not inhibit growth in normal medium, but profoundly retarded growth in pyrimidine-depleted media or in the presence of the known pyrimidine uptake antagonist 5-fluorouracil (5-FU). Fluorouracil 243-247 dihydroorotate dehydrogenase (quinone) Homo sapiens 18-23 18191533-5 2008 In vitro toxicity assays where mitomycin C, 5-fluorouracil and vincristine were preincubated with microsomes expressing recombinant P450R showed that this effect was not a result of direct metabolism by P450R. Fluorouracil 44-58 cytochrome p450 oxidoreductase Homo sapiens 132-137 18191533-7 2008 P450R overexpression appears therefore to be detrimental to MDA 231 cells, depleting NADPH and increasing ROS levels; the increased oxidative stress observed in MDA R4 cells might explain the enhanced sensitivity to 5-fluorouracil. Fluorouracil 216-230 cytochrome p450 oxidoreductase Homo sapiens 0-5 18344684-0 2008 A new trick for an old drug: mTOR inhibitor rapamycin augments the effect of fluorouracil on hepatocellular carcinoma by inducing cell senescence. Fluorouracil 77-89 mechanistic target of rapamycin kinase Homo sapiens 29-33 18075305-7 2008 Further study showed rapamycin plus 5-Fu-induced senescence-like growth arrest was accompanied by down-regulation of AP-1 and NF kappa B transcription activity. Fluorouracil 36-40 nuclear factor kappa B subunit 1 Homo sapiens 126-136 18075305-8 2008 These results suggest that inhibitors of mTOR may have anticancer potential when used together with some other chemotherapeutic agents, and that down-regulation of AP-1 and NF kappa B transcription activity might take part in a senescence-like growth arrest program induced by rapamycin plus 5-Fu. Fluorouracil 292-296 mechanistic target of rapamycin kinase Homo sapiens 41-45 18075305-8 2008 These results suggest that inhibitors of mTOR may have anticancer potential when used together with some other chemotherapeutic agents, and that down-regulation of AP-1 and NF kappa B transcription activity might take part in a senescence-like growth arrest program induced by rapamycin plus 5-Fu. Fluorouracil 292-296 nuclear factor kappa B subunit 1 Homo sapiens 173-183 18501075-1 2008 Bevacizumab is the fi rst vascular endothelial growth factor-targeted agent shown to increase survival in patients receiving first- and second-line intravenous 5-FU-based chemotherapy for the treatment of metastatic colorectal cancer. Fluorouracil 160-164 vascular endothelial growth factor A Homo sapiens 26-60 18310281-9 2008 Our findings support the notion that expression of ABCC11 in ER-alpha-positive breast cancers may contribute to decreased sensitivity to chemotherapy combinations that include 5-FU. Fluorouracil 176-180 estrogen receptor 1 Homo sapiens 61-69 18319335-8 2008 Linkage of a repression domain to the selected ATF resulted in enhanced sensitivity to multiple drugs, particularly vincristine, cisplatinum, and 5-fluorouracil. Fluorouracil 146-160 glial cell derived neurotrophic factor Homo sapiens 47-50 18205257-18 2008 By using SP immunohistochemical method the expression of Phospho-Stat3 (Tyr705) and Bcl-2 in WCA group and 5-FU group was significantly decreased compared with the control group respectively. Fluorouracil 107-111 signal transducer and activator of transcription 3 Homo sapiens 65-70 18082672-0 2008 The immunocytokine scFv23/TNF targeting HER-2/neu induces synergistic cytotoxic effects with 5-fluorouracil in TNF-resistant pancreatic cancer cell lines. Fluorouracil 93-107 tumor necrosis factor Homo sapiens 26-29 18082672-0 2008 The immunocytokine scFv23/TNF targeting HER-2/neu induces synergistic cytotoxic effects with 5-fluorouracil in TNF-resistant pancreatic cancer cell lines. Fluorouracil 93-107 erb-b2 receptor tyrosine kinase 2 Homo sapiens 40-49 18082672-0 2008 The immunocytokine scFv23/TNF targeting HER-2/neu induces synergistic cytotoxic effects with 5-fluorouracil in TNF-resistant pancreatic cancer cell lines. Fluorouracil 93-107 tumor necrosis factor Homo sapiens 111-114 18082672-6 2008 Combination studies demonstrated a synergistic cytotoxic effect of scFv23/TNF with 5-fluorouracil (5-FU) in TNF-resistant pancreatic cancer cell lines. Fluorouracil 83-97 tumor necrosis factor Homo sapiens 108-111 18082672-6 2008 Combination studies demonstrated a synergistic cytotoxic effect of scFv23/TNF with 5-fluorouracil (5-FU) in TNF-resistant pancreatic cancer cell lines. Fluorouracil 99-103 tumor necrosis factor Homo sapiens 108-111 18082672-7 2008 Mechanistic studies demonstrated that the 5-FU plus scFv23/TNF combination specifically resulted in a down-regulation of HER-2/neu, p-Akt and Bcl-2 and up-regulation of TNF-R1. Fluorouracil 42-46 tumor necrosis factor Homo sapiens 59-62 18082672-7 2008 Mechanistic studies demonstrated that the 5-FU plus scFv23/TNF combination specifically resulted in a down-regulation of HER-2/neu, p-Akt and Bcl-2 and up-regulation of TNF-R1. Fluorouracil 42-46 erb-b2 receptor tyrosine kinase 2 Homo sapiens 121-130 18082672-7 2008 Mechanistic studies demonstrated that the 5-FU plus scFv23/TNF combination specifically resulted in a down-regulation of HER-2/neu, p-Akt and Bcl-2 and up-regulation of TNF-R1. Fluorouracil 42-46 BCL2 apoptosis regulator Homo sapiens 142-147 18082672-8 2008 In addition, the combination 5-FU plus scFv23/TNF induced apoptosis and this synergistic effect was dependent on activation of caspase-8 and caspase-3. Fluorouracil 29-33 tumor necrosis factor Homo sapiens 46-49 18082672-8 2008 In addition, the combination 5-FU plus scFv23/TNF induced apoptosis and this synergistic effect was dependent on activation of caspase-8 and caspase-3. Fluorouracil 29-33 caspase 3 Homo sapiens 141-150 18082672-9 2008 Delivery of the cytokine TNF to HER-2/neu expressing pancreatic tumor cells, which are inherently resistant to TNF using scFv23/TNF may be an effective therapy for pancreatic cancer especially when utilized in combination with 5-FU. Fluorouracil 227-231 tumor necrosis factor Homo sapiens 25-28 18082672-9 2008 Delivery of the cytokine TNF to HER-2/neu expressing pancreatic tumor cells, which are inherently resistant to TNF using scFv23/TNF may be an effective therapy for pancreatic cancer especially when utilized in combination with 5-FU. Fluorouracil 227-231 erb-b2 receptor tyrosine kinase 2 Homo sapiens 32-37 17704804-6 2008 Moreover, tumor necrosis factor alpha (TNFalpha)- or 5-FU-induced apoptosis that is greatly enhanced by G17 treatment in Colo320wt cells was prevented if IEX-1 expression was repressed. Fluorouracil 53-57 immediate early response 3 Homo sapiens 154-159 17704804-8 2008 Conversely, IEX-1 overexpression in Colo320mut cells caused an increase of basal and TNFalpha- or 5-FU-induced apoptosis, an effect not further triggered by G17 treatment. Fluorouracil 98-102 immediate early response 3 Homo sapiens 12-17 18047833-4 2008 Although LRCs expressed very low level of a well-known HSC marker, c-kit in normal circumstances, myeloablation by 5-FU treatment caused LRCs to abundantly express c-kit and proliferate actively. Fluorouracil 115-119 KIT proto-oncogene, receptor tyrosine kinase Homo sapiens 164-169 17637740-2 2008 We found that the cytotoxic drugs methotrexate (MTX) and 5-fluorouracil (5-FU) were both able to sensitize resistant tumor cells for induction of apoptosis by p53-mediated upregulation of caspase-8. Fluorouracil 57-71 tumor protein p53 Homo sapiens 159-162 17637740-2 2008 We found that the cytotoxic drugs methotrexate (MTX) and 5-fluorouracil (5-FU) were both able to sensitize resistant tumor cells for induction of apoptosis by p53-mediated upregulation of caspase-8. Fluorouracil 73-77 tumor protein p53 Homo sapiens 159-162 17918158-0 2008 Curcumin enhances the effects of 5-fluorouracil and oxaliplatin in mediating growth inhibition of colon cancer cells by modulating EGFR and IGF-1R. Fluorouracil 33-47 epidermal growth factor receptor Homo sapiens 131-135 18850275-3 2008 Herein, phase separation method was used to prepare 5-fluorouracil-loaded bovine serum albumin (BSA) nanoparticles. Fluorouracil 52-66 albumin Homo sapiens 81-94 18383902-1 2008 S-1 is a novel oral anticancer drug, composed of tegafur (FT), gimestat (CDHP) and otastat potassium (Oxo), based on the biochemical modulation of 5-fluorouracil (5-FU). Fluorouracil 147-161 proteasome 26S subunit, non-ATPase 1 Homo sapiens 0-3 17851877-0 2008 Effect of interferon and 5-fluorouracil on serum VEGF levels in neuroendocrine tumours. Fluorouracil 25-39 vascular endothelial growth factor A Homo sapiens 49-53 18383843-0 2008 Pretreatment with S-1, an oral derivative of 5-fluorouracil, enhances gemcitabine effects in pancreatic cancer xenografts. Fluorouracil 45-59 proteasome 26S subunit, non-ATPase 1 Homo sapiens 18-21 18383902-1 2008 S-1 is a novel oral anticancer drug, composed of tegafur (FT), gimestat (CDHP) and otastat potassium (Oxo), based on the biochemical modulation of 5-fluorouracil (5-FU). Fluorouracil 163-167 proteasome 26S subunit, non-ATPase 1 Homo sapiens 0-3 17885815-6 2008 Methotrexate (MTX), 5-florouracil (5-Fu), and cisplatin (CDDP) are commonly used for breast carcinoma treatment in clinics; however, patients with HER2/neu overexpression exhibit resistance to these anticancer drugs. Fluorouracil 20-33 erb-b2 receptor tyrosine kinase 2 Homo sapiens 147-155 17885815-6 2008 Methotrexate (MTX), 5-florouracil (5-Fu), and cisplatin (CDDP) are commonly used for breast carcinoma treatment in clinics; however, patients with HER2/neu overexpression exhibit resistance to these anticancer drugs. Fluorouracil 35-39 erb-b2 receptor tyrosine kinase 2 Homo sapiens 147-155 18172823-0 2008 Transferrin-conjugated liposomal system for improved delivery of 5-fluorouracil to brain. Fluorouracil 65-79 transferrin Homo sapiens 0-11 17786445-7 2008 Patients who received regimens containing oxaliplatin and infusional 5-fluorouracil (5-FU) demonstrated mTTP up to 7 months and a mOS of 16 months. Fluorouracil 69-83 Moloney sarcoma oncogene Mus musculus 130-133 17786445-7 2008 Patients who received regimens containing oxaliplatin and infusional 5-fluorouracil (5-FU) demonstrated mTTP up to 7 months and a mOS of 16 months. Fluorouracil 85-89 Moloney sarcoma oncogene Mus musculus 130-133 17698398-8 2008 Furthermore, upon exposure to 5-Fluorouracil and UV irradiation, Cyr61 was rapidly induced in both p53(+/+) HepG2 and p53(-/-) Hep3B cells. Fluorouracil 30-44 tumor protein p53 Homo sapiens 99-102 17698398-8 2008 Furthermore, upon exposure to 5-Fluorouracil and UV irradiation, Cyr61 was rapidly induced in both p53(+/+) HepG2 and p53(-/-) Hep3B cells. Fluorouracil 30-44 tumor protein p53 Homo sapiens 118-121 17805550-2 2008 This study evaluates the putative clinical usefulness of measuring caspase-3 activity as a prognostic factor in colonic cancer patients receiving 5-fluoracil adjuvant chemotherapy. Fluorouracil 146-157 caspase 3 Homo sapiens 67-76 17805550-11 2008 CONCLUSION: Low caspase-3 activity in the normal mucosa and tumour are independent prognostic factors of tumour recurrence in patients receiving adjuvant 5-fluoracil-based treatment in colon cancer, correlating with poor disease-free survival and higher recurrence rate. Fluorouracil 154-165 caspase 3 Homo sapiens 16-25 18172823-1 2008 The objective of this study is to achieve the enhanced delivery of 5-fluorouracil to brain through transferrin-coupled liposomes. Fluorouracil 67-81 transferrin Homo sapiens 99-110 18172823-9 2008 An average of 10-fold increase in the brain uptake of the drug was observed after the liposomal delivery of 5-fluorouracil, while the transferrin-coupled liposomes caused a 17-fold increase in the brain uptake of 5-fluorouracil. Fluorouracil 213-227 transferrin Homo sapiens 134-145 18172823-10 2008 Therefore, it can be concluded that transferrin-coupled liposomes enhance the brain uptake of the drug, like 5-fluorouracil. Fluorouracil 109-123 transferrin Homo sapiens 36-47 18389626-4 2008 The down-regulation of CIAPIN1 significantly enhanced the sensitivity of SGC7901/VCR cells to vincristine (VCR), adriamycin (ADR) and etoposide (VP-16), but not to 5-fluorouracil (5-FU) and cisplatin (CDDP). Fluorouracil 180-184 cytokine induced apoptosis inhibitor 1 Homo sapiens 23-30 17951356-7 2008 We have demonstrated for the first time that Hmgb1 is an essential activator of cellular response to genotoxic stress caused by chemotherapeutic agents (thiopurines, cytarabine, and 5-fluorouracil), which acts at early steps of antimetabolite-induced stress by stimulating phosphorylation of two DNA damage markers, p53 and H2AX. Fluorouracil 182-196 H2A.X variant histone Mus musculus 324-328 18216719-2 2008 There remains, however, a subset of patients presenting with 5-FU-associated toxicity despite normal DPD activity, suggesting possible deficiencies in enzymes downstream of DPD: dihydropyrimidinase (DHP), encoded by the DPYS gene, and/or beta-ureidopropionase (BUP-1), encoded by the UPB1 gene. Fluorouracil 61-65 dihydropyrimidinase Homo sapiens 199-202 18216719-2 2008 There remains, however, a subset of patients presenting with 5-FU-associated toxicity despite normal DPD activity, suggesting possible deficiencies in enzymes downstream of DPD: dihydropyrimidinase (DHP), encoded by the DPYS gene, and/or beta-ureidopropionase (BUP-1), encoded by the UPB1 gene. Fluorouracil 61-65 dihydropyrimidinase Homo sapiens 220-224 20020938-4 2008 Our studies showed that CAS over-expression increased p53 accumulation and apoptosis induced by 5-fluorouracil, doxorubicin, cisplatin, and tamoxifen in HT-29 cancer cells. Fluorouracil 96-110 tumor protein p53 Homo sapiens 54-57 18544999-8 2008 Ectopic overexpression of XAF1 induced apoptosis in MS1 and also sensitized cells to 5-fluorouracil-induced apoptosis. Fluorouracil 85-99 XIAP associated factor 1 Mus musculus 26-30 17971768-2 2007 Here, we examined the role p53 plays in the antitumour effect of combination treatment with pegylated interferon (PEG-IFN)-alpha and 5-fluorouracil (5-FU), which has been shown to effectively treat advanced hepatocellular carcinoma (HCC). Fluorouracil 133-147 tumor protein p53 Homo sapiens 27-30 17971768-2 2007 Here, we examined the role p53 plays in the antitumour effect of combination treatment with pegylated interferon (PEG-IFN)-alpha and 5-fluorouracil (5-FU), which has been shown to effectively treat advanced hepatocellular carcinoma (HCC). Fluorouracil 149-153 tumor protein p53 Homo sapiens 27-30 17971768-7 2007 The antitumour effects of combination treatment is due in part to the elevation by PEG-IFN of p53 protein and mRNA expression and in part to the DNA damage that is generated by 5-FU, which induces p53 serine46 phosphorylation, which in turn upregulates p53AIP1 expression. Fluorouracil 177-181 tumor protein p53 Homo sapiens 197-200 17982676-0 2007 Apoptosis, cell cycle progression and gene expression in TP53-depleted HCT116 colon cancer cells in response to short-term 5-fluorouracil treatment. Fluorouracil 123-137 tumor protein p53 Homo sapiens 57-61 17941012-1 2007 BACKGROUND: The authors reported previously the beneficial effects of interferon (IFN)-alpha/5-fluorouracil (5-FU) combination therapy for patients with advanced hepatocellular carcinoma (HCC) who have tumor thrombi in the major portal branches. Fluorouracil 109-113 interferon alpha 1 Homo sapiens 70-92 17982676-7 2007 Alterations in gene expression in 5-FU-treated TP53-depleted HCT116 cultures confirmed previously-reported TP53 target genes and suggested potentially novel TP53 target genes (e.g. APOBEC3C, BIRC3, JMJD2B, LAMP3, MYO1E, PRRG1, SULF2, TACSTD2, TncRNA, ZFYVE20) that may play a role in mediating the 5-FU-induced DNA damage response in TP53-proficient cells. Fluorouracil 34-38 tumor protein p53 Homo sapiens 47-51 17982676-1 2007 Loss of TP53 function may contribute to 5-fluorouracil (5-FU) resistance in colorectal cancer since TP53-deficient cells may be unable to undergo apoptosis in response to 5-FU-induced DNA damage. Fluorouracil 40-54 tumor protein p53 Homo sapiens 8-12 17982676-7 2007 Alterations in gene expression in 5-FU-treated TP53-depleted HCT116 cultures confirmed previously-reported TP53 target genes and suggested potentially novel TP53 target genes (e.g. APOBEC3C, BIRC3, JMJD2B, LAMP3, MYO1E, PRRG1, SULF2, TACSTD2, TncRNA, ZFYVE20) that may play a role in mediating the 5-FU-induced DNA damage response in TP53-proficient cells. Fluorouracil 34-38 tumor protein p53 Homo sapiens 107-111 17982676-1 2007 Loss of TP53 function may contribute to 5-fluorouracil (5-FU) resistance in colorectal cancer since TP53-deficient cells may be unable to undergo apoptosis in response to 5-FU-induced DNA damage. Fluorouracil 56-60 tumor protein p53 Homo sapiens 8-12 17982676-7 2007 Alterations in gene expression in 5-FU-treated TP53-depleted HCT116 cultures confirmed previously-reported TP53 target genes and suggested potentially novel TP53 target genes (e.g. APOBEC3C, BIRC3, JMJD2B, LAMP3, MYO1E, PRRG1, SULF2, TACSTD2, TncRNA, ZFYVE20) that may play a role in mediating the 5-FU-induced DNA damage response in TP53-proficient cells. Fluorouracil 34-38 tumor protein p53 Homo sapiens 107-111 17982676-7 2007 Alterations in gene expression in 5-FU-treated TP53-depleted HCT116 cultures confirmed previously-reported TP53 target genes and suggested potentially novel TP53 target genes (e.g. APOBEC3C, BIRC3, JMJD2B, LAMP3, MYO1E, PRRG1, SULF2, TACSTD2, TncRNA, ZFYVE20) that may play a role in mediating the 5-FU-induced DNA damage response in TP53-proficient cells. Fluorouracil 34-38 lysine demethylase 4B Homo sapiens 198-204 17982676-1 2007 Loss of TP53 function may contribute to 5-fluorouracil (5-FU) resistance in colorectal cancer since TP53-deficient cells may be unable to undergo apoptosis in response to 5-FU-induced DNA damage. Fluorouracil 56-60 tumor protein p53 Homo sapiens 100-104 17982676-7 2007 Alterations in gene expression in 5-FU-treated TP53-depleted HCT116 cultures confirmed previously-reported TP53 target genes and suggested potentially novel TP53 target genes (e.g. APOBEC3C, BIRC3, JMJD2B, LAMP3, MYO1E, PRRG1, SULF2, TACSTD2, TncRNA, ZFYVE20) that may play a role in mediating the 5-FU-induced DNA damage response in TP53-proficient cells. Fluorouracil 34-38 tumor associated calcium signal transducer 2 Homo sapiens 234-241 17982676-1 2007 Loss of TP53 function may contribute to 5-fluorouracil (5-FU) resistance in colorectal cancer since TP53-deficient cells may be unable to undergo apoptosis in response to 5-FU-induced DNA damage. Fluorouracil 171-175 tumor protein p53 Homo sapiens 8-12 17982676-7 2007 Alterations in gene expression in 5-FU-treated TP53-depleted HCT116 cultures confirmed previously-reported TP53 target genes and suggested potentially novel TP53 target genes (e.g. APOBEC3C, BIRC3, JMJD2B, LAMP3, MYO1E, PRRG1, SULF2, TACSTD2, TncRNA, ZFYVE20) that may play a role in mediating the 5-FU-induced DNA damage response in TP53-proficient cells. Fluorouracil 34-38 tumor protein p53 Homo sapiens 107-111 17982676-7 2007 Alterations in gene expression in 5-FU-treated TP53-depleted HCT116 cultures confirmed previously-reported TP53 target genes and suggested potentially novel TP53 target genes (e.g. APOBEC3C, BIRC3, JMJD2B, LAMP3, MYO1E, PRRG1, SULF2, TACSTD2, TncRNA, ZFYVE20) that may play a role in mediating the 5-FU-induced DNA damage response in TP53-proficient cells. Fluorouracil 298-302 tumor protein p53 Homo sapiens 47-51 17982676-2 2007 5-FU treatment of TP53-deficient cells would provide useful information on the apoptotic response to drug-induced DNA damage in the absence of TP53 and its transcriptional targets. Fluorouracil 0-4 tumor protein p53 Homo sapiens 18-22 17982676-8 2007 Abrogation of TP53 function in 5-FU-treated HCT116 cultures results in reduced apoptosis, TP53- and CDKN1A-independent G1/S phase arrests that may be protective against apoptosis, smaller intra-S phase arrests, and transcript level decreases of both reported TP53 target genes as well as potentially novel TP53 target genes. Fluorouracil 31-35 tumor protein p53 Homo sapiens 14-18 17982676-6 2007 Compared to 5-FU-treated TP53-proficient HCT116 cultures, 5-FU-treated TP53-depleted HCT116 cultures showed lack of CDKN1A induction, decreased apoptotic levels, decreased FAS and TNFRSF10B transcript levels and cleaved PARP protein levels, G1/S transition arrests, decreased CCND1 protein levels, and smaller intra-S phase arrests. Fluorouracil 12-16 tumor protein p53 Homo sapiens 25-29 17982676-8 2007 Abrogation of TP53 function in 5-FU-treated HCT116 cultures results in reduced apoptosis, TP53- and CDKN1A-independent G1/S phase arrests that may be protective against apoptosis, smaller intra-S phase arrests, and transcript level decreases of both reported TP53 target genes as well as potentially novel TP53 target genes. Fluorouracil 31-35 tumor protein p53 Homo sapiens 90-94 17982676-8 2007 Abrogation of TP53 function in 5-FU-treated HCT116 cultures results in reduced apoptosis, TP53- and CDKN1A-independent G1/S phase arrests that may be protective against apoptosis, smaller intra-S phase arrests, and transcript level decreases of both reported TP53 target genes as well as potentially novel TP53 target genes. Fluorouracil 31-35 cyclin dependent kinase inhibitor 1A Homo sapiens 100-106 17982676-6 2007 Compared to 5-FU-treated TP53-proficient HCT116 cultures, 5-FU-treated TP53-depleted HCT116 cultures showed lack of CDKN1A induction, decreased apoptotic levels, decreased FAS and TNFRSF10B transcript levels and cleaved PARP protein levels, G1/S transition arrests, decreased CCND1 protein levels, and smaller intra-S phase arrests. Fluorouracil 58-62 tumor protein p53 Homo sapiens 71-75 17982676-8 2007 Abrogation of TP53 function in 5-FU-treated HCT116 cultures results in reduced apoptosis, TP53- and CDKN1A-independent G1/S phase arrests that may be protective against apoptosis, smaller intra-S phase arrests, and transcript level decreases of both reported TP53 target genes as well as potentially novel TP53 target genes. Fluorouracil 31-35 tumor protein p53 Homo sapiens 90-94 17982676-8 2007 Abrogation of TP53 function in 5-FU-treated HCT116 cultures results in reduced apoptosis, TP53- and CDKN1A-independent G1/S phase arrests that may be protective against apoptosis, smaller intra-S phase arrests, and transcript level decreases of both reported TP53 target genes as well as potentially novel TP53 target genes. Fluorouracil 31-35 tumor protein p53 Homo sapiens 90-94 17982676-6 2007 Compared to 5-FU-treated TP53-proficient HCT116 cultures, 5-FU-treated TP53-depleted HCT116 cultures showed lack of CDKN1A induction, decreased apoptotic levels, decreased FAS and TNFRSF10B transcript levels and cleaved PARP protein levels, G1/S transition arrests, decreased CCND1 protein levels, and smaller intra-S phase arrests. Fluorouracil 58-62 cyclin dependent kinase inhibitor 1A Homo sapiens 116-122 17996122-0 2007 Coupled down-regulation of mTOR and telomerase activity during fluorouracil-induced apoptosis of hepatocarcinoma cells. Fluorouracil 63-75 mechanistic target of rapamycin kinase Homo sapiens 27-31 17996122-4 2007 METHODS: This study investigated changes in mTOR pathway and telomerase activity in hepatocarcinoma cell line SMMC-7721 treated with chemotherapeutic agent 5-fluorouracil (5-Fu). Fluorouracil 156-170 mechanistic target of rapamycin kinase Homo sapiens 44-48 17996122-4 2007 METHODS: This study investigated changes in mTOR pathway and telomerase activity in hepatocarcinoma cell line SMMC-7721 treated with chemotherapeutic agent 5-fluorouracil (5-Fu). Fluorouracil 172-176 mechanistic target of rapamycin kinase Homo sapiens 44-48 17996122-7 2007 RESULTS: Treating SMMC-7721 cells with 5-Fu leads to apoptosis of the cells, and reduction in telomerase activity, as well as a dramatic reduction in the activated form of p70 S6 kinase, a mTOR substrate. Fluorouracil 39-43 mechanistic target of rapamycin kinase Homo sapiens 189-193 17996122-11 2007 CONCLUSION: These results suggest that chemotherapeutic agent 5-Fu may down-regulate telomerase activity at both transcriptional level and PI3K/Akt/mTOR pathway-dependent post-transcriptional level to facilitate hepatocellular carcinoma cell apoptosis. Fluorouracil 62-66 AKT serine/threonine kinase 1 Homo sapiens 144-147 17996122-11 2007 CONCLUSION: These results suggest that chemotherapeutic agent 5-Fu may down-regulate telomerase activity at both transcriptional level and PI3K/Akt/mTOR pathway-dependent post-transcriptional level to facilitate hepatocellular carcinoma cell apoptosis. Fluorouracil 62-66 mechanistic target of rapamycin kinase Homo sapiens 148-152 18225584-0 2007 In vitro modulation of interleukin-2-mediated human peripheral mononuclear cell proliferation and antitumor cytotoxicity by 5-fluorouracil. Fluorouracil 124-138 interleukin 2 Homo sapiens 23-36 18225584-3 2007 RESULTS: Activation of PBMCs with IL-2, PHA and PWM in the presence of 250 and 2500 microM of 5-FU caused a marked decrease in both the induction of activated natural killer (ANK) cell cytotoxic activity and DNA synthesis, while 2.5 microM increased DNA synthesis by 195%, 58% and 222% for IL-2, PHA and PWM, respectively, more than cells cultured without the drug. Fluorouracil 94-98 interleukin 2 Homo sapiens 34-38 18225534-4 2007 The aim of this investigation was to evaluate the 5-fluorouracil (5-FU) and methotrexate (MTX) combination to determine the most effective regimen considering the mechanism of action in treating ER-negative human breast cancer cells and at the same time mitigating methotrexate cytotoxicity in human bone marrow cells. Fluorouracil 66-70 estrogen receptor 1 Homo sapiens 195-197 18225584-3 2007 RESULTS: Activation of PBMCs with IL-2, PHA and PWM in the presence of 250 and 2500 microM of 5-FU caused a marked decrease in both the induction of activated natural killer (ANK) cell cytotoxic activity and DNA synthesis, while 2.5 microM increased DNA synthesis by 195%, 58% and 222% for IL-2, PHA and PWM, respectively, more than cells cultured without the drug. Fluorouracil 94-98 interleukin 2 Homo sapiens 290-294 17511782-4 2007 Using these methods, we show that EGFR kinase inhibitors sensitize colorectal SW-480 tumor cells for 5-fluorouracil-induced apoptosis, indicating that EGFR-mediated survival signaling contributes to apoptosis resistance via its intrinsic kinase activity. Fluorouracil 101-115 epidermal growth factor receptor Homo sapiens 34-38 17511782-4 2007 Using these methods, we show that EGFR kinase inhibitors sensitize colorectal SW-480 tumor cells for 5-fluorouracil-induced apoptosis, indicating that EGFR-mediated survival signaling contributes to apoptosis resistance via its intrinsic kinase activity. Fluorouracil 101-115 epidermal growth factor receptor Homo sapiens 151-155 17970874-6 2007 The regulation detection of S100A6 with flurouracil and doxorubicin at the mRNA and protein level was performed in the SGC7901 cell line. Fluorouracil 40-51 S100 calcium binding protein A6 Homo sapiens 28-34 18008030-0 2007 Aberrant methylation of p16 predicts candidates for 5-fluorouracil-based adjuvant therapy in gastric cancer patients. Fluorouracil 52-66 cyclin dependent kinase inhibitor 2A Homo sapiens 24-27 18008030-7 2007 A multivariate analysis identified p16INK4a methylation to be an independent factor predicting a longer recurrence-free period under 5-FU-based adjuvant chemotherapy. Fluorouracil 133-137 cyclin dependent kinase inhibitor 2A Homo sapiens 35-43 18008030-8 2007 CONCLUSIONS: The present study demonstrated for the first time that gastric cancer patients with p16INK4a methylation specifically benefit from 5-FU-based adjuvant chemotherapy. Fluorouracil 144-148 cyclin dependent kinase inhibitor 2A Homo sapiens 97-105 17942911-9 2007 Knockdown of GRP78 also sensitizes glioma cells to 5-fluorouracil and CPT-11. Fluorouracil 51-65 heat shock protein family A (Hsp70) member 5 Homo sapiens 13-18 18075467-2 2007 There, however, remain a number of patients presenting with 5-fluorouracil-associated toxicity despite normal DPD enzyme activity, suggesting possible deficiencies in dihydropyrimidinase (DHP), encoded by the DPYS gene, and/or beta-ureidopropionase (BUP-1), encoded by the UPB1 gene. Fluorouracil 60-74 dihydropyrimidinase Homo sapiens 188-191 17909293-1 2007 Beta-alanine synthase catalyzes the last step in the reductive degradation pathway for uracil and thymine, which represents the main clearance route for the widely used anticancer drug 5-fluorouracil. Fluorouracil 185-199 pyd3 Drosophila melanogaster 0-21 17499351-3 2007 Unlike the tumour suppressor gene encoding p53 that is notoriously prone to inactivating mutations but whose function is essential for induction of apoptosis by DNA-targeting agents (such as doxorubicin or 5-fluorouracil), mitochondria present targets that are not so compromised by genetic mutation and whose targeting overcomes problems with mutations of upstream targets such as p53. Fluorouracil 206-220 tumor protein p53 Homo sapiens 43-46 17690883-5 2007 RESULTS: At day 4 from the initial preoperative administration of S-1, the AUC of 5-FU was 1,055 +/- 304 ng h/ml. Fluorouracil 82-86 proteasome 26S subunit, non-ATPase 1 Homo sapiens 66-69 17275163-0 2007 Synergy of interferon-alpha and 5-fluorouracil in human renal cell carcinoma requires p53 activity. Fluorouracil 32-46 tumor protein p53 Homo sapiens 86-89 17275163-5 2007 RESULTS: We demonstrated synergy of IFN-alpha and 5-FU in five RCC cell lines with wild-type p53. Fluorouracil 50-54 tumor protein p53 Homo sapiens 93-96 17275163-7 2007 IFN-alpha enhanced the apoptosis of RCC cells induced by 5-FU, whereas 5-FU did not increase the antiproliferative effect of IFN-alpha. Fluorouracil 57-61 interferon alpha 1 Homo sapiens 0-9 17275163-8 2007 However, the synergistic inhibition by IFN-alpha and 5-FU was abolished when the cell lines were transfected with p53 dominant-negative vector. Fluorouracil 53-57 tumor protein p53 Homo sapiens 114-117 17275163-9 2007 CONCLUSIONS: The synergy of IFN-alpha and 5-FU requires p53 activity, suggesting that p53 status may serve as a predictive factor for response to the combination therapy. Fluorouracil 42-46 tumor protein p53 Homo sapiens 56-59 17275163-9 2007 CONCLUSIONS: The synergy of IFN-alpha and 5-FU requires p53 activity, suggesting that p53 status may serve as a predictive factor for response to the combination therapy. Fluorouracil 42-46 tumor protein p53 Homo sapiens 86-89 17275163-10 2007 Because metastatic RCC frequently has p53 mutations, therapy restoring p53 may markedly improve the response rate of immunochemical therapy combining IFN-alpha and 5-FU. Fluorouracil 164-168 tumor protein p53 Homo sapiens 38-41 17275163-10 2007 Because metastatic RCC frequently has p53 mutations, therapy restoring p53 may markedly improve the response rate of immunochemical therapy combining IFN-alpha and 5-FU. Fluorouracil 164-168 tumor protein p53 Homo sapiens 71-74 17786339-0 2007 Combination therapy of interferon-alpha and 5-fluorouracil inhibits tumor angiogenesis in human hepatocellular carcinoma cells by regulating vascular endothelial growth factor and angiopoietins. Fluorouracil 44-58 vascular endothelial growth factor A Homo sapiens 141-175 17687334-0 2007 In vitro evaluation of cancer-specific NF-kappaB-CEA enhancer-promoter system for 5-fluorouracil prodrug gene therapy in colon cancer cell lines. Fluorouracil 82-96 nuclear factor kappa B subunit 1 Homo sapiens 39-48 17687334-0 2007 In vitro evaluation of cancer-specific NF-kappaB-CEA enhancer-promoter system for 5-fluorouracil prodrug gene therapy in colon cancer cell lines. Fluorouracil 82-96 CEA cell adhesion molecule 3 Homo sapiens 49-52 17881904-5 2007 SP-cells from multiple tumorigenic human cell lines, which are most often resistant to chemotherapeutic agents such as etoposide, cisplatin and 5-FU, are more sensitive to TRAIL than non-SP cells. Fluorouracil 144-148 TNF superfamily member 10 Homo sapiens 172-177 17470401-3 2007 Up-regulation of DARPP-32 could significantly enhance the sensitivity of SGC7901/VCR cells towards vincristine, adriamycin, 5-fluorouracil and cisplatin, and could decrease the capacity of cells to efflux adriamycin. Fluorouracil 124-138 protein phosphatase 1 regulatory inhibitor subunit 1B Homo sapiens 17-25 17761979-5 2007 The antiproliferative effect of fluorouracil (FU) on adenocarcinoma cell lines with EGFR wild-type or mutant type status was examined by measuring the inhibitory concentrations at 50% (IC(50)s). Fluorouracil 32-44 epidermal growth factor receptor Homo sapiens 84-88 17923759-5 2007 Cell cytotoxicity, the change of telomerase activity, and hTERT mRNA and hTR expression by 5-FU and cisplatin exposure were assessed by MTT assay, TRAP assay, and real-time RT-PCR, respectively. Fluorouracil 91-95 telomerase RNA component Homo sapiens 73-76 17495129-6 2007 The effect of megakaryocyte damage and release of PF4 on 5-fluorouracil-induced marrow failure was then examined. Fluorouracil 57-71 platelet factor 4 Mus musculus 50-53 17851795-0 2007 [Study of the anti-tumor effect of anti-vascular endothelial growth factor McAb 5-fluorouracil loaded polylactic acid nanoparticles]. Fluorouracil 80-94 vascular endothelial growth factor A Homo sapiens 40-74 17851795-1 2007 OBJECTIVE: To explore the anti-tumor efficacy of anti- vascular endothelial growth factor (VEGF) McAb 5-fluorouracil (5-FU) loaded polylactic acid (PLA) nanoparticles (NPS) in human gastric carcinoma xenografts of nude mice. Fluorouracil 102-116 vascular endothelial growth factor A Homo sapiens 55-89 17851795-1 2007 OBJECTIVE: To explore the anti-tumor efficacy of anti- vascular endothelial growth factor (VEGF) McAb 5-fluorouracil (5-FU) loaded polylactic acid (PLA) nanoparticles (NPS) in human gastric carcinoma xenografts of nude mice. Fluorouracil 102-116 vascular endothelial growth factor A Homo sapiens 91-95 17851795-1 2007 OBJECTIVE: To explore the anti-tumor efficacy of anti- vascular endothelial growth factor (VEGF) McAb 5-fluorouracil (5-FU) loaded polylactic acid (PLA) nanoparticles (NPS) in human gastric carcinoma xenografts of nude mice. Fluorouracil 118-122 vascular endothelial growth factor A Homo sapiens 55-89 17851795-1 2007 OBJECTIVE: To explore the anti-tumor efficacy of anti- vascular endothelial growth factor (VEGF) McAb 5-fluorouracil (5-FU) loaded polylactic acid (PLA) nanoparticles (NPS) in human gastric carcinoma xenografts of nude mice. Fluorouracil 118-122 vascular endothelial growth factor A Homo sapiens 91-95 17851795-6 2007 Compared with control group and anti-VEGF McAb 5-FU loaded nanosphere group, the 5-FU group decreased by 34.43% and 37.38% respectively in WBC count (P< 0.05), and increased by 93.17% and 66.56% respectively in alanine transferase. Fluorouracil 47-51 vascular endothelial growth factor A Homo sapiens 37-41 17851795-6 2007 Compared with control group and anti-VEGF McAb 5-FU loaded nanosphere group, the 5-FU group decreased by 34.43% and 37.38% respectively in WBC count (P< 0.05), and increased by 93.17% and 66.56% respectively in alanine transferase. Fluorouracil 81-85 vascular endothelial growth factor A Homo sapiens 37-41 17851795-7 2007 There were significant differences between experimental groups and control group in apoptosis index, especially between anti-VEGF McAb 5-FU loaded nanosphere group and control group (P< 0.05). Fluorouracil 135-139 vascular endothelial growth factor A Homo sapiens 125-129 17851795-9 2007 CONCLUSION: Anti-VEGF McAb 5-FU loaded nanosphere can increase the tumor inhibitory rate of 5-FU, induce apoptosis by inhibiting tumor angiogenesis with less side effect, and then enhance therapeutic effect, which indicate its potential as a novel, safe nano-tumor-targeting drug. Fluorouracil 27-31 vascular endothelial growth factor A Homo sapiens 17-21 17851795-9 2007 CONCLUSION: Anti-VEGF McAb 5-FU loaded nanosphere can increase the tumor inhibitory rate of 5-FU, induce apoptosis by inhibiting tumor angiogenesis with less side effect, and then enhance therapeutic effect, which indicate its potential as a novel, safe nano-tumor-targeting drug. Fluorouracil 92-96 vascular endothelial growth factor A Homo sapiens 17-21 17450522-0 2007 Synergistic antitumor effects of celecoxib with 5-fluorouracil depend on IFN-gamma. Fluorouracil 48-62 interferon gamma Mus musculus 73-82 17450522-8 2007 5FU/celecoxib also enhanced IFN-gamma levels in tumor tissue, which could be involved in the potent antitumor effects of 5FU/celecoxib. Fluorouracil 0-3 interferon gamma Mus musculus 28-37 17450522-8 2007 5FU/celecoxib also enhanced IFN-gamma levels in tumor tissue, which could be involved in the potent antitumor effects of 5FU/celecoxib. Fluorouracil 121-124 interferon gamma Mus musculus 28-37 17450522-9 2007 This hypothesis was proven, because in IFN-gamma knockout (IFN-gamma(-/-)) mice, the inhibitory effects of 5FU/celecoxib on angiogenesis and tumor growth were significantly impaired compared with that in wild type mice. Fluorouracil 107-110 interferon gamma Mus musculus 39-48 17450522-9 2007 This hypothesis was proven, because in IFN-gamma knockout (IFN-gamma(-/-)) mice, the inhibitory effects of 5FU/celecoxib on angiogenesis and tumor growth were significantly impaired compared with that in wild type mice. Fluorouracil 107-110 interferon gamma Mus musculus 59-68 17699714-7 2007 Bevacizumab/5-FU-induced growth suppression was associated with reduction in microvessel density, inhibition of cell proliferation; up-regulation of phosphatase and tensin homologue, p21(Cip1/Waf1), p16(INK4a), and p27(Kip1); hypophosphorylation of retinoblastoma protein; and inhibition of Akt/mammalian target of rapamycin pathway. Fluorouracil 12-16 cyclin dependent kinase inhibitor 1A Homo sapiens 183-186 17988526-10 2007 IC(50) of 5-FU was (5.8 +/- 2.0) micromol/L and (6.3 +/- 1.4) micromol/L in with IFN-alpha (10 000 U/ml) and control group, respectively. Fluorouracil 10-14 interferon alpha 1 Homo sapiens 81-90 17697537-12 2007 The proportions of immune T cells were lower in 5-FU-pretreated PBMCs than in control PBMCs (0.7% vs. 2.1% for CD4+IFN-gamma+ T cells, 2.2% vs. 3.9% for CD8+IFN-gamma+ T cells, 0.7% vs. 2.5% for CD4+IL-2+ T cells, 0.2% vs. 0.4% for CD8+IL-2+ T cells). Fluorouracil 48-52 CD4 molecule Homo sapiens 111-124 17699714-7 2007 Bevacizumab/5-FU-induced growth suppression was associated with reduction in microvessel density, inhibition of cell proliferation; up-regulation of phosphatase and tensin homologue, p21(Cip1/Waf1), p16(INK4a), and p27(Kip1); hypophosphorylation of retinoblastoma protein; and inhibition of Akt/mammalian target of rapamycin pathway. Fluorouracil 12-16 cyclin dependent kinase inhibitor 1A Homo sapiens 187-191 17699714-7 2007 Bevacizumab/5-FU-induced growth suppression was associated with reduction in microvessel density, inhibition of cell proliferation; up-regulation of phosphatase and tensin homologue, p21(Cip1/Waf1), p16(INK4a), and p27(Kip1); hypophosphorylation of retinoblastoma protein; and inhibition of Akt/mammalian target of rapamycin pathway. Fluorouracil 12-16 cyclin dependent kinase inhibitor 1A Homo sapiens 192-196 17699714-7 2007 Bevacizumab/5-FU-induced growth suppression was associated with reduction in microvessel density, inhibition of cell proliferation; up-regulation of phosphatase and tensin homologue, p21(Cip1/Waf1), p16(INK4a), and p27(Kip1); hypophosphorylation of retinoblastoma protein; and inhibition of Akt/mammalian target of rapamycin pathway. Fluorouracil 12-16 cyclin dependent kinase inhibitor 2A Homo sapiens 199-202 17699714-7 2007 Bevacizumab/5-FU-induced growth suppression was associated with reduction in microvessel density, inhibition of cell proliferation; up-regulation of phosphatase and tensin homologue, p21(Cip1/Waf1), p16(INK4a), and p27(Kip1); hypophosphorylation of retinoblastoma protein; and inhibition of Akt/mammalian target of rapamycin pathway. Fluorouracil 12-16 cyclin dependent kinase inhibitor 2A Homo sapiens 203-208 17699714-7 2007 Bevacizumab/5-FU-induced growth suppression was associated with reduction in microvessel density, inhibition of cell proliferation; up-regulation of phosphatase and tensin homologue, p21(Cip1/Waf1), p16(INK4a), and p27(Kip1); hypophosphorylation of retinoblastoma protein; and inhibition of Akt/mammalian target of rapamycin pathway. Fluorouracil 12-16 AKT serine/threonine kinase 1 Homo sapiens 291-294 17699714-7 2007 Bevacizumab/5-FU-induced growth suppression was associated with reduction in microvessel density, inhibition of cell proliferation; up-regulation of phosphatase and tensin homologue, p21(Cip1/Waf1), p16(INK4a), and p27(Kip1); hypophosphorylation of retinoblastoma protein; and inhibition of Akt/mammalian target of rapamycin pathway. Fluorouracil 12-16 mechanistic target of rapamycin kinase Homo sapiens 295-324 17699726-0 2007 Alteration of dihydropyrimidine dehydrogenase expression by IFN-alpha affects the antiproliferative effects of 5-fluorouracil in human hepatocellular carcinoma cells. Fluorouracil 111-125 interferon alpha 1 Homo sapiens 60-69 17583745-11 2007 Chemosensitivity of Panc-1 cells to 5-fluorouracil or gemcitabine after Snail transfection was assayed by MTT cell proliferation assay. Fluorouracil 36-50 snail family transcriptional repressor 1 Homo sapiens 72-77 17583745-12 2007 Overexpression of Snail enhanced the chemoresistance to 5-fluorouracil of gemcitabine at different dosages. Fluorouracil 56-70 snail family transcriptional repressor 1 Homo sapiens 18-23 17699726-9 2007 The antiproliferative effect of 5-FU could thus be modulated by IFN-alpha, possibly through DPD expression, in HCC cells. Fluorouracil 32-36 interferon alpha 1 Homo sapiens 64-73 17715009-0 2007 [Biodistribution of (99m)Tc-labeled anti-VEGF mAb 5-FU loaded polylactic acid nanoparticles in human gastric carcinoma xenografts]. Fluorouracil 50-54 vascular endothelial growth factor A Homo sapiens 41-45 17715009-1 2007 OBJECTIVE: To prepare (99m)Tc-labeled Anti-VEGF mAb 5-FU loaded polylactic acid nanoparticles ((99m)Tc-Ab-5-FU-NPs) and investigate its biodistribution in human gastric carcinoma xenografts. Fluorouracil 52-56 vascular endothelial growth factor A Homo sapiens 43-47 17680227-12 2007 With respect to the current literature and the clinical findings it is discussed that both increased leukocyte/endothelial cell adhesion and altered release of reactive oxygen species or inducible nitric oxide synthase (iNOS) may play a role in 5-FU-induced colitis. Fluorouracil 245-249 nitric oxide synthase 2 Homo sapiens 187-218 17680227-12 2007 With respect to the current literature and the clinical findings it is discussed that both increased leukocyte/endothelial cell adhesion and altered release of reactive oxygen species or inducible nitric oxide synthase (iNOS) may play a role in 5-FU-induced colitis. Fluorouracil 245-249 nitric oxide synthase 2 Homo sapiens 220-224 17553452-8 2007 The results showed that 10 mM fluorouracil (5-FU) and gentamicin are inhibitors to UDG. Fluorouracil 30-42 uracil DNA glycosylase Homo sapiens 83-86 17537404-4 2007 However, tumor cells that adapt to oxidative stress by increasing manganese superoxide dismutase (MnSOD), Prx I, and Bcl-2 showed drug resistance to 5-FU. Fluorouracil 149-153 BCL2 apoptosis regulator Homo sapiens 117-122 17553452-8 2007 The results showed that 10 mM fluorouracil (5-FU) and gentamicin are inhibitors to UDG. Fluorouracil 44-48 uracil DNA glycosylase Homo sapiens 83-86 17634542-10 2007 CONCLUSIONS: Low expression of Bax was significantly associated with the poor survival of patients with locally advanced esophageal cancer treated with chemoradiotherapy using 5-fluorouracil and cisplatin. Fluorouracil 176-190 BCL2 associated X, apoptosis regulator Homo sapiens 31-34 17634538-0 2007 TIMP-1 is significantly associated with objective response and survival in metastatic colorectal cancer patients receiving combination of irinotecan, 5-fluorouracil, and folinic acid. Fluorouracil 150-164 TIMP metallopeptidase inhibitor 1 Homo sapiens 0-6 17634554-0 2007 Regulation of p53 expression in response to 5-fluorouracil in human cancer RKO cells. Fluorouracil 44-58 tumor protein p53 Homo sapiens 14-17 17634554-10 2007 Levels of both the acetylated and phosphorylated forms of p53 were markedly increased upon doxorubicin exposure when compared with treatment with 5-FU, resulting in a significantly prolonged half-life of p53 (120 versus 20 min). Fluorouracil 146-150 tumor protein p53 Homo sapiens 204-207 17634554-1 2007 PURPOSE: The purpose of the study is to investigate the regulation of p53 expression in response to 5-fluorouracil (5-FU) in human colon cancer cells. Fluorouracil 100-114 tumor protein p53 Homo sapiens 70-73 17634554-1 2007 PURPOSE: The purpose of the study is to investigate the regulation of p53 expression in response to 5-fluorouracil (5-FU) in human colon cancer cells. Fluorouracil 116-120 tumor protein p53 Homo sapiens 70-73 17634554-13 2007 Studies are under way to define the specific mechanism(s) that control 5-FU-mediated translational regulation of p53. Fluorouracil 71-75 tumor protein p53 Homo sapiens 113-116 17634554-3 2007 The levels of p53 expression and p53 protein stability in response to 5-FU and doxorubicin were investigated. Fluorouracil 70-74 tumor protein p53 Homo sapiens 14-17 17634554-4 2007 In addition, the acetylation and phosphorylation status of p53 after 5-FU and doxorubicin treatment was analyzed by Western immunoblot analysis. Fluorouracil 69-73 tumor protein p53 Homo sapiens 59-62 17634554-5 2007 RESULTS: Treatment of human colon cancer RKO cells with 10 micromol/L 5-FU resulted in significantly increased levels of p53 protein with maximal induction observed at 24 h. The level of acetylated p53 after 5-FU exposure remained unchanged, whereas the phosphorylated form of p53 was expressed only after 24 h drug treatment. Fluorouracil 70-74 tumor protein p53 Homo sapiens 121-124 17634554-5 2007 RESULTS: Treatment of human colon cancer RKO cells with 10 micromol/L 5-FU resulted in significantly increased levels of p53 protein with maximal induction observed at 24 h. The level of acetylated p53 after 5-FU exposure remained unchanged, whereas the phosphorylated form of p53 was expressed only after 24 h drug treatment. Fluorouracil 70-74 tumor protein p53 Homo sapiens 198-201 17634554-5 2007 RESULTS: Treatment of human colon cancer RKO cells with 10 micromol/L 5-FU resulted in significantly increased levels of p53 protein with maximal induction observed at 24 h. The level of acetylated p53 after 5-FU exposure remained unchanged, whereas the phosphorylated form of p53 was expressed only after 24 h drug treatment. Fluorouracil 70-74 tumor protein p53 Homo sapiens 198-201 17634554-5 2007 RESULTS: Treatment of human colon cancer RKO cells with 10 micromol/L 5-FU resulted in significantly increased levels of p53 protein with maximal induction observed at 24 h. The level of acetylated p53 after 5-FU exposure remained unchanged, whereas the phosphorylated form of p53 was expressed only after 24 h drug treatment. Fluorouracil 208-212 tumor protein p53 Homo sapiens 198-201 17634554-5 2007 RESULTS: Treatment of human colon cancer RKO cells with 10 micromol/L 5-FU resulted in significantly increased levels of p53 protein with maximal induction observed at 24 h. The level of acetylated p53 after 5-FU exposure remained unchanged, whereas the phosphorylated form of p53 was expressed only after 24 h drug treatment. Fluorouracil 208-212 tumor protein p53 Homo sapiens 198-201 17634554-7 2007 No differences were observed in the half-life of p53 protein in control and 5-FU-treated cells, suggesting that the increase in p53 was the direct result of newly synthesized protein. Fluorouracil 76-80 tumor protein p53 Homo sapiens 128-131 17124594-8 2007 5-fluorouracil combined with PXD101 also increased DNA fragmentation and PARP cleavage in HCT116 cells. Fluorouracil 0-14 poly(ADP-ribose) polymerase 1 Homo sapiens 73-77 17399942-8 2007 Treatment with 5-FU also down-regulated Bcl-xL in HepG2 cells. Fluorouracil 15-19 BCL2 like 1 Homo sapiens 40-46 17399942-13 2007 Using an antibody that recognizes unprocessed caspase-3, we observed that the enzyme was assumingly activated in HepG2 cells treated with 5FU and paclitaxel, but only weakly after treatment with cisplatin. Fluorouracil 138-141 caspase 3 Homo sapiens 46-55 17673469-1 2007 BACKGROUND: We have reported that vascular endothelial growth factor (VEGF) expression in gastric cancers might be a selective marker between 5-fluorouracil (5-FU) and a combination of 5-FU plus cisplatin (CDDP). Fluorouracil 142-156 vascular endothelial growth factor A Homo sapiens 34-68 17673469-1 2007 BACKGROUND: We have reported that vascular endothelial growth factor (VEGF) expression in gastric cancers might be a selective marker between 5-fluorouracil (5-FU) and a combination of 5-FU plus cisplatin (CDDP). Fluorouracil 142-156 vascular endothelial growth factor A Homo sapiens 70-74 17673469-1 2007 BACKGROUND: We have reported that vascular endothelial growth factor (VEGF) expression in gastric cancers might be a selective marker between 5-fluorouracil (5-FU) and a combination of 5-FU plus cisplatin (CDDP). Fluorouracil 158-162 vascular endothelial growth factor A Homo sapiens 34-68 17673469-1 2007 BACKGROUND: We have reported that vascular endothelial growth factor (VEGF) expression in gastric cancers might be a selective marker between 5-fluorouracil (5-FU) and a combination of 5-FU plus cisplatin (CDDP). Fluorouracil 158-162 vascular endothelial growth factor A Homo sapiens 70-74 17673469-1 2007 BACKGROUND: We have reported that vascular endothelial growth factor (VEGF) expression in gastric cancers might be a selective marker between 5-fluorouracil (5-FU) and a combination of 5-FU plus cisplatin (CDDP). Fluorouracil 185-189 vascular endothelial growth factor A Homo sapiens 34-68 17673469-1 2007 BACKGROUND: We have reported that vascular endothelial growth factor (VEGF) expression in gastric cancers might be a selective marker between 5-fluorouracil (5-FU) and a combination of 5-FU plus cisplatin (CDDP). Fluorouracil 185-189 vascular endothelial growth factor A Homo sapiens 70-74 17589894-0 2007 Effect of targeted magnetic nanoparticles containing 5-FU on expression of bcl-2, bax and caspase 3 in nude mice with transplanted human liver cancer. Fluorouracil 53-57 B cell leukemia/lymphoma 2 Mus musculus 75-80 17589894-9 2007 CONCLUSION: The targeted magnetic nanoparticles containing 5-FU can improve the chemotherapeutic effect of 5-FU against hepatocellular carcinoma by decreasing the expression of bcl-2 gene, and increasing the expression of bax and caspase 3 genes. Fluorouracil 59-63 B cell leukemia/lymphoma 2 Mus musculus 177-182 17589894-9 2007 CONCLUSION: The targeted magnetic nanoparticles containing 5-FU can improve the chemotherapeutic effect of 5-FU against hepatocellular carcinoma by decreasing the expression of bcl-2 gene, and increasing the expression of bax and caspase 3 genes. Fluorouracil 107-111 B cell leukemia/lymphoma 2 Mus musculus 177-182 17725105-0 2007 Schedule-dependent cytotoxicity of 5-fluorouracil and irinotecan in p53 mutant human colon cancer. Fluorouracil 35-49 tumor protein p53 Homo sapiens 68-71 17725105-2 2007 We evaluated cytotoxic effects of a sequentially administered a combination of 5-FU with CPT-11 in human p53 mutant colon cancer. Fluorouracil 79-83 tumor protein p53 Homo sapiens 105-108 17531112-9 2007 Silencing of endogenous PLC-gamma 1 resulted in efficient inhibition of the adhesion and migration of LoVo cells in vitro and a great increase of 5-fluorouracil induced apoptosis (30%-40%) of LoVo cells. Fluorouracil 146-160 phospholipase C gamma 1 Homo sapiens 24-35 17671767-1 2007 We report two cases of hepatocellular carcinoma (HCC) with portal vein tumor thrombus (PVTT) and lymph node (LN) metastases successfully treated by hepatic arterial infusion of 5-fluorouracil (5-FU) combined with systemic injection of interferon (IFN)-alpha following hepatic resection for the liver tumor. Fluorouracil 177-191 interferon alpha 1 Homo sapiens 235-257 17426704-11 2007 BAX protein expression may be of central significance for clinical outcome to 5-FU-based adjuvant chemotherapy in stage III colon cancer, and bivariate analysis of p53/BAX possibly may provide further prognostic evidence. Fluorouracil 78-82 BCL2 associated X, apoptosis regulator Homo sapiens 0-3 17439729-0 2007 Pretreatment with insulin enhances anticancer functions of 5-fluorouracil in human esophageal and colonic cancer cells. Fluorouracil 59-73 insulin Homo sapiens 18-25 17439729-1 2007 AIM: To investigate the effects of insulin on enhancing 5-fluorouracil (5-FU) anticancer functions and its mechanisms in the human esophageal cancer cell line (Eca 109) and human colonic cancer cell line (Ls-174-t). Fluorouracil 56-70 insulin Homo sapiens 35-42 17439729-1 2007 AIM: To investigate the effects of insulin on enhancing 5-fluorouracil (5-FU) anticancer functions and its mechanisms in the human esophageal cancer cell line (Eca 109) and human colonic cancer cell line (Ls-174-t). Fluorouracil 72-76 insulin Homo sapiens 35-42 17439729-6 2007 Moreover, the changes of 5-FU uptake after insulin pretreatment were detected by HPLC assay and Western blot analysis. Fluorouracil 25-29 insulin Homo sapiens 43-50 17439729-7 2007 RESULTS: We found that insulin enhanced the inhibitory effect of 5- FU on cell proliferation when Eca 109 cells and Ls-174-t cells were pretreated with insulin for the appropriate time. Fluorouracil 65-70 insulin Homo sapiens 23-30 19147571-3 2009 We then report that chemotherapy induces Notch-1, as oxaliplatin, 5-fluorouracil (5-FU), or SN-38 (the active metabolite of irinotecan) induced Notch-1 intracellular domain (NICD) protein and activated Hes-1. Fluorouracil 66-80 notch receptor 1 Homo sapiens 41-48 19147571-3 2009 We then report that chemotherapy induces Notch-1, as oxaliplatin, 5-fluorouracil (5-FU), or SN-38 (the active metabolite of irinotecan) induced Notch-1 intracellular domain (NICD) protein and activated Hes-1. Fluorouracil 66-80 notch receptor 1 Homo sapiens 144-151 19147571-3 2009 We then report that chemotherapy induces Notch-1, as oxaliplatin, 5-fluorouracil (5-FU), or SN-38 (the active metabolite of irinotecan) induced Notch-1 intracellular domain (NICD) protein and activated Hes-1. Fluorouracil 82-86 notch receptor 1 Homo sapiens 41-48 17439729-7 2007 RESULTS: We found that insulin enhanced the inhibitory effect of 5- FU on cell proliferation when Eca 109 cells and Ls-174-t cells were pretreated with insulin for the appropriate time. Fluorouracil 65-70 insulin Homo sapiens 152-159 17439729-8 2007 Insulin increased the cell number of the S phase and the uptake of 5-FU. Fluorouracil 67-71 insulin Homo sapiens 0-7 17439729-9 2007 Insulin/5-FU treatment enhanced apoptosis of tumor cells and upregulated the expression of cleaved caspase-3 compared with 5-FU treatment. Fluorouracil 8-12 caspase 3 Homo sapiens 99-108 17439729-9 2007 Insulin/5-FU treatment enhanced apoptosis of tumor cells and upregulated the expression of cleaved caspase-3 compared with 5-FU treatment. Fluorouracil 123-127 insulin Homo sapiens 0-7 19147571-3 2009 We then report that chemotherapy induces Notch-1, as oxaliplatin, 5-fluorouracil (5-FU), or SN-38 (the active metabolite of irinotecan) induced Notch-1 intracellular domain (NICD) protein and activated Hes-1. Fluorouracil 82-86 notch receptor 1 Homo sapiens 144-151 17439729-10 2007 Moreover, insulin/5-FU treatment induced the changes of free TS and the TS ternary complex level compared with 5-FU treatment in Eca 109 and Ls-174-t cells. Fluorouracil 111-115 insulin Homo sapiens 10-17 19147571-6 2009 Blocking the activation of Notch signaling with GSI34 sensitized cells to chemotherapy and was synergistic with oxaliplatin, 5-FU, and SN-38. Fluorouracil 125-129 notch receptor 1 Homo sapiens 27-32 17439729-11 2007 CONCLUSION: These data suggest that insulin enhances anticancer functions of 5- FU when it is treated before 5-FU for the appropriate time in human esophageal and colonic cancer cell lines. Fluorouracil 77-82 insulin Homo sapiens 36-43 17439729-11 2007 CONCLUSION: These data suggest that insulin enhances anticancer functions of 5- FU when it is treated before 5-FU for the appropriate time in human esophageal and colonic cancer cell lines. Fluorouracil 109-113 insulin Homo sapiens 36-43 17119966-10 2007 NF-kappaB transfected MCF-7 and p53 knockout HCT116 cells were resistant to 5-FU (4.4- and 2.4-fold, respectively) but not to TDX. Fluorouracil 76-80 nuclear factor kappa B subunit 1 Homo sapiens 0-9 17119966-10 2007 NF-kappaB transfected MCF-7 and p53 knockout HCT116 cells were resistant to 5-FU (4.4- and 2.4-fold, respectively) but not to TDX. Fluorouracil 76-80 tumor protein p53 Homo sapiens 32-35 17119966-13 2007 Loss of p53 function and NF-kappaB over-expression may be involved in TS-independent 5-FU chemoresistance in some cancer cell lines. Fluorouracil 85-89 tumor protein p53 Homo sapiens 8-11 17119966-13 2007 Loss of p53 function and NF-kappaB over-expression may be involved in TS-independent 5-FU chemoresistance in some cancer cell lines. Fluorouracil 85-89 nuclear factor kappa B subunit 1 Homo sapiens 25-34 17186550-2 2007 However, it is not fully understood to what extent NFkappaB contributes to induction of the metastasis-associated matrix metalloprotease-9 (MMP-9) gene and sensitivity to the commonly used chemotherapeutic 5-fluorouracil (5-Fu) in CRC. Fluorouracil 206-220 nuclear factor kappa B subunit 1 Homo sapiens 51-59 17439414-10 2007 The MTT results demonstrated that Bcl-2 and Bcl-xl transfected cells exhibited increased sensitivity to 5-FU or HCPT. Fluorouracil 104-108 BCL2 apoptosis regulator Homo sapiens 34-39 17439414-10 2007 The MTT results demonstrated that Bcl-2 and Bcl-xl transfected cells exhibited increased sensitivity to 5-FU or HCPT. Fluorouracil 104-108 BCL2 like 1 Homo sapiens 44-50 17186550-2 2007 However, it is not fully understood to what extent NFkappaB contributes to induction of the metastasis-associated matrix metalloprotease-9 (MMP-9) gene and sensitivity to the commonly used chemotherapeutic 5-fluorouracil (5-Fu) in CRC. Fluorouracil 222-226 nuclear factor kappa B subunit 1 Homo sapiens 51-59 17186550-3 2007 Using the RKO human CRC cell line and two NFkappaB signaling deficient RKO mutants, we investigated NFkappaB"s role in the induction of MMP-9 and 5-Fu sensitivity in RKO CRC cells. Fluorouracil 146-150 nuclear factor kappa B subunit 1 Homo sapiens 100-108 17186550-7 2007 5-Fu only activated NFkappaB in the parental RKO cells through induction of IkappaB-kinase (IKK) activity and increased sensitivity to 5-Fu is observed in both NFkappaB mutant lines. Fluorouracil 0-4 nuclear factor kappa B subunit 1 Homo sapiens 20-28 17186550-7 2007 5-Fu only activated NFkappaB in the parental RKO cells through induction of IkappaB-kinase (IKK) activity and increased sensitivity to 5-Fu is observed in both NFkappaB mutant lines. Fluorouracil 135-139 nuclear factor kappa B subunit 1 Homo sapiens 160-168 17186550-8 2007 Our results suggest that TNFalpha-dependent induction of MMP-9 gene expression is tightly regulated by oscillatory/cumulative activation of NFkappaB and that 5-Fu stimulates NFkappaB and RKO CRC cell survival through induction of IKK activity. Fluorouracil 158-162 nuclear factor kappa B subunit 1 Homo sapiens 174-182 17351391-12 2007 Multidrug resistance protein 1 expression correlates positively with the GI50 values of several drugs, e.g. vinblastine and etoposide, and negatively with the GI50 values of 5-fluorouracil. Fluorouracil 174-188 ATP binding cassette subfamily B member 1 Homo sapiens 0-30 17290426-8 2007 We modulated checkpoint-related gene expression in testis using the anti-metabolite, 5-fluorouracil, resulting in increased apoptosis and upregulation of Chk1 (P<0.0001) and Cdc2 (P<0.02) mRNA. Fluorouracil 85-99 checkpoint kinase 1 Homo sapiens 154-158 16924496-0 2007 A phase I study of paclitaxel, cisplatin, and fluorouracil (TCF) for advanced gastric cancer. Fluorouracil 46-58 hepatocyte nuclear factor 4 alpha Homo sapiens 60-63 16924496-1 2007 PURPOSE: A phase I study of TCF therapy, which consists of paclitaxel (TXL: Taxol) + cisplatin (CDDP) + 5-fluorouracil (5-FU), in advanced gastric cancer patients was performed to determine the recommended dose (RD) for a phase II study by checking the dose-limiting toxicity (DLT) and maximum-tolerated dose (MTD) of 5-FU above the fixed dose of TXL and CDDP. Fluorouracil 104-118 hepatocyte nuclear factor 4 alpha Homo sapiens 28-31 16924496-1 2007 PURPOSE: A phase I study of TCF therapy, which consists of paclitaxel (TXL: Taxol) + cisplatin (CDDP) + 5-fluorouracil (5-FU), in advanced gastric cancer patients was performed to determine the recommended dose (RD) for a phase II study by checking the dose-limiting toxicity (DLT) and maximum-tolerated dose (MTD) of 5-FU above the fixed dose of TXL and CDDP. Fluorouracil 120-124 hepatocyte nuclear factor 4 alpha Homo sapiens 28-31 16924496-1 2007 PURPOSE: A phase I study of TCF therapy, which consists of paclitaxel (TXL: Taxol) + cisplatin (CDDP) + 5-fluorouracil (5-FU), in advanced gastric cancer patients was performed to determine the recommended dose (RD) for a phase II study by checking the dose-limiting toxicity (DLT) and maximum-tolerated dose (MTD) of 5-FU above the fixed dose of TXL and CDDP. Fluorouracil 318-322 hepatocyte nuclear factor 4 alpha Homo sapiens 28-31 16924496-11 2007 CONCLUSIONS: Although the MTD level was not determined, based on the observed efficacy and the results of other clinical trials, the recommended doses of TXL, CDDP, and 5-FU for the TCF regimen were set as 80, 25, and 600 mg/m(2), respectively, and a phase II study to investigate the clinical effectiveness and safety of this regimen has now begun. Fluorouracil 169-173 hepatocyte nuclear factor 4 alpha Homo sapiens 182-185 17522103-1 2007 BACKGROUND: Our previous phase II study of 5-fluorouracil (5-FU) and cisplatin (FP) for treatment of advanced gastric cancer showed that strong immunoreactivity for vascular endothelial growth factor (VEGF) is associated with chemoresponse. Fluorouracil 43-57 vascular endothelial growth factor A Homo sapiens 165-199 17522103-1 2007 BACKGROUND: Our previous phase II study of 5-fluorouracil (5-FU) and cisplatin (FP) for treatment of advanced gastric cancer showed that strong immunoreactivity for vascular endothelial growth factor (VEGF) is associated with chemoresponse. Fluorouracil 43-57 vascular endothelial growth factor A Homo sapiens 201-205 17522103-1 2007 BACKGROUND: Our previous phase II study of 5-fluorouracil (5-FU) and cisplatin (FP) for treatment of advanced gastric cancer showed that strong immunoreactivity for vascular endothelial growth factor (VEGF) is associated with chemoresponse. Fluorouracil 59-63 vascular endothelial growth factor A Homo sapiens 165-199 17063488-3 2007 We report that Carb or 5-FU upregulate Gadd45alpha and p53 in both these cells. Fluorouracil 23-27 tumor protein p53 Homo sapiens 55-58 17522103-1 2007 BACKGROUND: Our previous phase II study of 5-fluorouracil (5-FU) and cisplatin (FP) for treatment of advanced gastric cancer showed that strong immunoreactivity for vascular endothelial growth factor (VEGF) is associated with chemoresponse. Fluorouracil 59-63 vascular endothelial growth factor A Homo sapiens 201-205 17242401-0 2007 5-fluorouracil activation of p53 involves an MDM2-ribosomal protein interaction. Fluorouracil 0-14 tumor protein p53 Homo sapiens 29-32 17242401-2 2007 The anti-tumor activity of 5-FU has been attributed in part to its ability to induce p53-dependent cell growth arrest and apoptosis. Fluorouracil 27-31 tumor protein p53 Homo sapiens 85-88 17242401-3 2007 However, the molecular mechanisms underlying p53 activation by 5-FU remain largely obscure. Fluorouracil 63-67 tumor protein p53 Homo sapiens 45-48 17242401-4 2007 Here we report that 5-FU treatment leads to p53 stabilization and activation by blocking MDM2 feedback inhibition through ribosomal proteins. Fluorouracil 20-24 tumor protein p53 Homo sapiens 44-47 17242401-5 2007 5-FU treatment increased the fraction of ribosome-free L5, L11, and L23 ribosomal proteins and their interaction with MDM2, leading to p53 activation and G1/S arrest. Fluorouracil 0-4 tumor protein p53 Homo sapiens 135-138 17242401-6 2007 Conversely, individual knockdown of these ribosomal proteins by small interfering RNA prevented the 5-FU-induced p53 activation and reversed the 5-FU-induced G1/S arrest. Fluorouracil 100-104 tumor protein p53 Homo sapiens 113-116 17242401-7 2007 These results demonstrate that 5-FU treatment triggers a ribosomal stress response so that ribosomal proteins L5, L11, and L23 are released from ribosome to activate p53 by ablating the MDM2-p53 feedback circuit. Fluorouracil 31-35 tumor protein p53 Homo sapiens 166-169 17242401-7 2007 These results demonstrate that 5-FU treatment triggers a ribosomal stress response so that ribosomal proteins L5, L11, and L23 are released from ribosome to activate p53 by ablating the MDM2-p53 feedback circuit. Fluorouracil 31-35 tumor protein p53 Homo sapiens 191-194 17363540-3 2007 In this study, we examined the use of 5-fluorouracil (5-FU) for sensitizing D54 tumors to tumor necrosis factor alpha-related apoptosis-inducing ligand (TRAIL) therapy by monitoring apoptotic activity in vivo using bioluminescence imaging. Fluorouracil 38-52 TNF superfamily member 10 Homo sapiens 90-151 17363540-3 2007 In this study, we examined the use of 5-fluorouracil (5-FU) for sensitizing D54 tumors to tumor necrosis factor alpha-related apoptosis-inducing ligand (TRAIL) therapy by monitoring apoptotic activity in vivo using bioluminescence imaging. Fluorouracil 38-52 TNF superfamily member 10 Homo sapiens 153-158 17363540-3 2007 In this study, we examined the use of 5-fluorouracil (5-FU) for sensitizing D54 tumors to tumor necrosis factor alpha-related apoptosis-inducing ligand (TRAIL) therapy by monitoring apoptotic activity in vivo using bioluminescence imaging. Fluorouracil 54-58 TNF superfamily member 10 Homo sapiens 90-151 17363540-3 2007 In this study, we examined the use of 5-fluorouracil (5-FU) for sensitizing D54 tumors to tumor necrosis factor alpha-related apoptosis-inducing ligand (TRAIL) therapy by monitoring apoptotic activity in vivo using bioluminescence imaging. Fluorouracil 54-58 TNF superfamily member 10 Homo sapiens 153-158 17363540-11 2007 Moreover, this technique sheds light on the synergy of 5-FU and TRAIL as evidenced by differences in the temporal activation of caspase-3 resulting from the different therapeutic regimens. Fluorouracil 55-59 caspase 3 Homo sapiens 128-137 17339891-4 2007 Lovo 175X2 cells (transfected with mt p53) were more resistant to 5-fluorouracil (5-FU; 2-fold), nolatrexed (3-fold), raltitrexed (3-fold) and pemetrexed (10-fold) in comparison with the wt p53 parental cells Lovo 92. Fluorouracil 66-80 tumor protein p53 Homo sapiens 38-41 17461445-0 2007 Rosiglitazone enhances fluorouracil-induced apoptosis of HT-29 cells by activating peroxisome proliferator-activated receptor gamma. Fluorouracil 23-35 peroxisome proliferator activated receptor gamma Homo sapiens 83-131 17461445-11 2007 CONCLUSION: Rosiglitazone enhances fluorouracil-induced apoptosis of HT-29 cells by activating PPARgamma. Fluorouracil 35-47 peroxisome proliferator activated receptor gamma Homo sapiens 95-104 17303011-8 2007 After the treatment with MK-AS or with 5-Fu, the plasma AFP concentration decreased in a dose-dependent manner. Fluorouracil 39-43 alpha fetoprotein Homo sapiens 56-59 17339891-4 2007 Lovo 175X2 cells (transfected with mt p53) were more resistant to 5-fluorouracil (5-FU; 2-fold), nolatrexed (3-fold), raltitrexed (3-fold) and pemetrexed (10-fold) in comparison with the wt p53 parental cells Lovo 92. Fluorouracil 82-86 tumor protein p53 Homo sapiens 38-41 17237997-7 2007 %CD90 was significantly lower in 5-FU-treated controls compared with that in saline-treated controls on day 10. Fluorouracil 33-37 Thy-1 cell surface antigen Rattus norvegicus 1-5 16900372-3 2007 METHODS: Estrogen receptor (ER)-alpha-positive or -negative breast cancer cells were treated with 4-hydroxy TAM (4OHT), 5-fluorouracil (FU) and/or doxorubicin (Dox). Fluorouracil 120-134 estrogen receptor 1 Homo sapiens 9-26 16900372-3 2007 METHODS: Estrogen receptor (ER)-alpha-positive or -negative breast cancer cells were treated with 4-hydroxy TAM (4OHT), 5-fluorouracil (FU) and/or doxorubicin (Dox). Fluorouracil 120-134 estrogen receptor 1 Homo sapiens 28-30 16900372-5 2007 RESULTS: Concurrent treatment of 4OHT with 5-FU but not with Dox additively inhibited the growth of ER-alpha-positive cells. Fluorouracil 43-47 estrogen receptor 1 Homo sapiens 100-108 17169374-0 2007 Combining siRNAs at two different sites in the EGFR to suppress its expression, induce apoptosis, and enhance 5-fluorouracil sensitivity of colon cancer cells. Fluorouracil 110-124 epidermal growth factor receptor Homo sapiens 47-51 17169374-11 2007 CONCLUSIONS: Both pU6-EGFR-shRNA-1 and pU6-EGFR-shRNA-2 are capable of suppressing EGFR expression of the LoVo cell and can promote apoptosis and increase the cell toxicity of 5-FU. Fluorouracil 176-180 epidermal growth factor receptor Homo sapiens 22-26 17169374-11 2007 CONCLUSIONS: Both pU6-EGFR-shRNA-1 and pU6-EGFR-shRNA-2 are capable of suppressing EGFR expression of the LoVo cell and can promote apoptosis and increase the cell toxicity of 5-FU. Fluorouracil 176-180 epidermal growth factor receptor Homo sapiens 43-47 17169374-11 2007 CONCLUSIONS: Both pU6-EGFR-shRNA-1 and pU6-EGFR-shRNA-2 are capable of suppressing EGFR expression of the LoVo cell and can promote apoptosis and increase the cell toxicity of 5-FU. Fluorouracil 176-180 epidermal growth factor receptor Homo sapiens 43-47 16724238-0 2007 5-Fluorouracil prevents lipopolysaccharide-induced nitric oxide production in RAW 264.7 macrophage cells by inhibiting Akt-dependent nuclear factor-kappaB activation. Fluorouracil 0-14 thymoma viral proto-oncogene 1 Mus musculus 119-122 16724238-4 2007 5-FU inhibited the activation of nuclear factor (NF)-kappaB and the subsequent nuclear translocation. Fluorouracil 0-4 nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105 Mus musculus 33-59 16724238-5 2007 Furthermore, 5-FU inhibited the phosphorylation of Akt, an upstream molecule of NF-kappaB signaling. Fluorouracil 13-17 thymoma viral proto-oncogene 1 Mus musculus 51-54 16724238-7 2007 Therefore, 5-FU was suggested to inhibit the LPS-induced NO production in activated macrophages through preventing Akt-dependent NF-kappaB activation. Fluorouracil 11-15 thymoma viral proto-oncogene 1 Mus musculus 115-118 17327702-7 2007 Furthermore, MDMX overexpression promotes resistance to the chemotherapeutic agent 5-FU, which at low concentrations activates p53 by inhibiting RNA metabolism. Fluorouracil 83-87 tumor protein p53 Homo sapiens 127-130 17203218-4 2007 The S-1 component (5-FU plus CDHP) significantly suppressed the growth and migration of OSCC cells and BAEC, which inhibited tubule formation in HUVECs in vitro. Fluorouracil 19-23 proteasome 26S subunit, non-ATPase 1 Homo sapiens 4-7 17045692-7 2007 Caspase-3 activation was exclusively increased by IFNalpha/5-FU combination treatment, which was compatible with enhancement of the synergistic apoptotic effect, and other caspases and apoptotic factors (FLIP, BCL-xl, and Bax) were also regulated by IFNalpha/5-FU. Fluorouracil 59-63 caspase 3 Homo sapiens 0-9 17200359-1 2007 PURPOSE: Findings from our previously published phase III randomized trial showed a high pathologic complete remission (CR) rate in patients with human epidermal growth factor receptor 2-positive breast cancer after the concurrent administration of trastuzumab and paclitaxel, followed by concurrent trastuzumab and 5-fluorouracil, epirubicin, and cyclophosphamide (FEC) preoperative chemotherapy. Fluorouracil 316-330 erb-b2 receptor tyrosine kinase 2 Homo sapiens 152-186 17922560-8 2007 RESULTS: The AUC(24)values of fluorouracil (p < 0.0001), uracil (p < 0.0001) and tegafur (p = 0.058) were greater with the bid schedule than the tid schedule. Fluorouracil 30-42 BH3 interacting domain death agonist Homo sapiens 129-132 17922560-9 2007 The bid : tid AUC(24) ratio (90% CI) was 1.8 (1.55, 2.10) with fluorouracil, 2.0 (1.59, 2.57) with uracil and 1.2 (1.02, 1.36) with tegafur, indicating that the bid and tid schedules were not bioequivalent. Fluorouracil 63-75 BH3 interacting domain death agonist Homo sapiens 4-7 17922560-12 2007 CONCLUSION: A 2-fold increase in the fluorouracil and uracil AUC values was observed with UFT administered bid compared with tid, without a significant impact on tolerability, suggesting that the more convenient bid schedule may improve the UFT therapeutic index. Fluorouracil 37-49 BH3 interacting domain death agonist Homo sapiens 107-110 17922560-12 2007 CONCLUSION: A 2-fold increase in the fluorouracil and uracil AUC values was observed with UFT administered bid compared with tid, without a significant impact on tolerability, suggesting that the more convenient bid schedule may improve the UFT therapeutic index. Fluorouracil 37-49 BH3 interacting domain death agonist Homo sapiens 212-215 17066447-4 2007 In this study, we investigated the influence of HIF-1alpha expression on the susceptibility of oral squamous cell carcinoma (OSCC) cells to chemotherapeutic drugs (cis-diamminedichloroplatinum and 5-fluorouracil) and gamma-rays. Fluorouracil 197-211 hypoxia inducible factor 1 subunit alpha Homo sapiens 48-58 17056233-0 2007 Inhibition of Fas expression by RNAi modulates 5-fluorouracil-induced apoptosis in HCT116 cells expressing wild-type p53. Fluorouracil 47-61 tumor protein p53 Homo sapiens 117-120 17056233-2 2007 In addition, the clinical value of p53 as a predictive marker for 5-FU-based chemotherapy remains a matter of debate. Fluorouracil 66-70 tumor protein p53 Homo sapiens 35-38 17056233-9 2007 Nuclear fragmentation and caspase-3, -8 and -9 activities were also markedly increased in HCT116 cells after 5-FU (p<0.001). Fluorouracil 109-113 caspase 3 Homo sapiens 26-46 17056233-12 2007 Finally, western blot analysis of mitochondrial extracts from HCT116 cells exposed to 5-FU showed a 6-fold increase in Bax, together with a 3-fold decrease in cytochrome c (p<0.001). Fluorouracil 86-90 BCL2 associated X, apoptosis regulator Homo sapiens 119-122 17056233-12 2007 Finally, western blot analysis of mitochondrial extracts from HCT116 cells exposed to 5-FU showed a 6-fold increase in Bax, together with a 3-fold decrease in cytochrome c (p<0.001). Fluorouracil 86-90 cytochrome c, somatic Homo sapiens 159-171 17056233-13 2007 In conclusion, 5-FU exerts its cytotoxic effects, in part, through a p53/Fas-dependent apoptotic pathway that involves Bax translocation and mitochondrial permeabilization. Fluorouracil 15-19 tumor protein p53 Homo sapiens 69-72 17056233-13 2007 In conclusion, 5-FU exerts its cytotoxic effects, in part, through a p53/Fas-dependent apoptotic pathway that involves Bax translocation and mitochondrial permeabilization. Fluorouracil 15-19 BCL2 associated X, apoptosis regulator Homo sapiens 119-122 17045692-7 2007 Caspase-3 activation was exclusively increased by IFNalpha/5-FU combination treatment, which was compatible with enhancement of the synergistic apoptotic effect, and other caspases and apoptotic factors (FLIP, BCL-xl, and Bax) were also regulated by IFNalpha/5-FU. Fluorouracil 59-63 interferon alpha 1 Homo sapiens 50-58 17045692-7 2007 Caspase-3 activation was exclusively increased by IFNalpha/5-FU combination treatment, which was compatible with enhancement of the synergistic apoptotic effect, and other caspases and apoptotic factors (FLIP, BCL-xl, and Bax) were also regulated by IFNalpha/5-FU. Fluorouracil 59-63 BCL2 like 1 Homo sapiens 210-216 17045692-7 2007 Caspase-3 activation was exclusively increased by IFNalpha/5-FU combination treatment, which was compatible with enhancement of the synergistic apoptotic effect, and other caspases and apoptotic factors (FLIP, BCL-xl, and Bax) were also regulated by IFNalpha/5-FU. Fluorouracil 59-63 BCL2 associated X, apoptosis regulator Homo sapiens 222-225 17045692-7 2007 Caspase-3 activation was exclusively increased by IFNalpha/5-FU combination treatment, which was compatible with enhancement of the synergistic apoptotic effect, and other caspases and apoptotic factors (FLIP, BCL-xl, and Bax) were also regulated by IFNalpha/5-FU. Fluorouracil 59-63 interferon alpha 1 Homo sapiens 250-258 17045692-7 2007 Caspase-3 activation was exclusively increased by IFNalpha/5-FU combination treatment, which was compatible with enhancement of the synergistic apoptotic effect, and other caspases and apoptotic factors (FLIP, BCL-xl, and Bax) were also regulated by IFNalpha/5-FU. Fluorouracil 259-263 caspase 3 Homo sapiens 0-9 17045692-7 2007 Caspase-3 activation was exclusively increased by IFNalpha/5-FU combination treatment, which was compatible with enhancement of the synergistic apoptotic effect, and other caspases and apoptotic factors (FLIP, BCL-xl, and Bax) were also regulated by IFNalpha/5-FU. Fluorouracil 259-263 interferon alpha 1 Homo sapiens 50-58 17045692-9 2007 The largest interaction was observed when both PBMC and HCC cells were pretreated with the combination of IFNalpha/5-FU. Fluorouracil 115-119 interferon alpha 1 Homo sapiens 106-114 17045692-11 2007 CONCLUSIONS: Our results indicated that IFNalpha/5-FU combination treatment enhances the induction of apoptosis and the cytotoxic effect of PBMCs via the Fas/FasL pathway. Fluorouracil 49-53 interferon alpha 1 Homo sapiens 40-48 17045692-12 2007 The Fas/FasL pathway seems, at least in part, to contribute to the anti-tumor effects of IFNalpha/5-FU against HCCs. Fluorouracil 98-102 interferon alpha 1 Homo sapiens 89-97 18337622-4 2007 RESULTS: Statistically significant associations were found between 5-fluorouracil (5-FU) sensitivity in HDRA and HER-2 mRNA expression level (p = 0.0030). Fluorouracil 67-81 erb-b2 receptor tyrosine kinase 2 Homo sapiens 113-118 17237273-7 2007 Western blot analyses showed that SSAT protein expression was dramatically enhanced when DENSpm was combined with oxaliplatin or 5-FU in HCT116 p53(+/+) cells. Fluorouracil 129-133 tumor protein p53 Homo sapiens 144-147 18337622-4 2007 RESULTS: Statistically significant associations were found between 5-fluorouracil (5-FU) sensitivity in HDRA and HER-2 mRNA expression level (p = 0.0030). Fluorouracil 83-87 erb-b2 receptor tyrosine kinase 2 Homo sapiens 113-118 17088986-1 2006 Combination therapy with interferon (IFN)-alpha and 5-fluorouracil (5-FU) has been reported to show an improved therapeutic efficacy in patients with advanced hepatocellular carcinoma (HCC) but the mechanism behind this has not been completely elucidated. Fluorouracil 68-72 interferon alpha 1 Homo sapiens 25-47 17114213-5 2006 RESULTS: When analyzed as a continuous log-transformed variable, increasing TIMP-1 levels were significantly associated with lack of response to cyclophosphamide/methotrexate/5-fluorouracil and anthracycline-based chemotherapy (P = 0.01; odds ratio, 2.0; 95% confidence interval, 1.1-3.3). Fluorouracil 175-189 TIMP metallopeptidase inhibitor 1 Homo sapiens 76-82 17114213-8 2006 By using TIMP-1, we identified a group of patients with metastatic breast cancer, which hardly respond to the most frequently used chemotherapy regimes (i.e., cyclophosphamide/methotrexate/5-fluorouracil and anthracyclines). Fluorouracil 189-203 TIMP metallopeptidase inhibitor 1 Homo sapiens 9-15 16528528-1 2006 PURPOSE: Ferredoxin reductase (FDXR) is a putative contributor to p53-mediated apoptosis from 5-fluorouracil (5-FU) through the generation of oxidative stress in the mitochondria. Fluorouracil 94-108 tumor protein p53 Homo sapiens 66-69 16528528-1 2006 PURPOSE: Ferredoxin reductase (FDXR) is a putative contributor to p53-mediated apoptosis from 5-fluorouracil (5-FU) through the generation of oxidative stress in the mitochondria. Fluorouracil 110-114 tumor protein p53 Homo sapiens 66-69 16528528-10 2006 FDXR gene expression, which is regulated at least in part by p53, is associated with both response and survival when metastatic colorectal cancer is treated with 5-FU plus LV. Fluorouracil 162-166 tumor protein p53 Homo sapiens 61-64 16528528-11 2006 In addition, analysis of p53 mutation combined with FDXR gene expression might be useful in estimating the outcome in 5-FU-treated patients. Fluorouracil 118-122 tumor protein p53 Homo sapiens 25-28 17088986-5 2006 IFN-alpha modulated the protein expression levels of six enzymes regulating sensitivity to 5-FU, but none of them were down- or up-regulated in the same way in all members of the S- or A-group. Fluorouracil 91-95 interferon alpha 1 Homo sapiens 0-9 17287894-5 2006 Reverse transcription-polymerase chain reaction analysis revealed that exposure to 5-FU downregulated both MDR1 and bcl-2 mRNA and simultaneously upregulated CE2 mRNA expression, suggesting enhancement of subsequent CPT-11 cytotoxicity. Fluorouracil 83-87 ATP binding cassette subfamily B member 1 Homo sapiens 107-111 17287894-5 2006 Reverse transcription-polymerase chain reaction analysis revealed that exposure to 5-FU downregulated both MDR1 and bcl-2 mRNA and simultaneously upregulated CE2 mRNA expression, suggesting enhancement of subsequent CPT-11 cytotoxicity. Fluorouracil 83-87 BCL2 apoptosis regulator Homo sapiens 116-121 17287894-5 2006 Reverse transcription-polymerase chain reaction analysis revealed that exposure to 5-FU downregulated both MDR1 and bcl-2 mRNA and simultaneously upregulated CE2 mRNA expression, suggesting enhancement of subsequent CPT-11 cytotoxicity. Fluorouracil 83-87 carboxylesterase 2 Homo sapiens 158-161 17054996-5 2006 Inhibition of the ERK pathway by PD98059 sensitized cells to 5-fluorouracil (5-FU), whereas cells became more resistant to Adriamycin (ADM; Meiji Seika, Tokyo, Japan) and gemcitabine (GEM). Fluorouracil 61-75 mitogen-activated protein kinase 1 Homo sapiens 18-21 17054996-5 2006 Inhibition of the ERK pathway by PD98059 sensitized cells to 5-fluorouracil (5-FU), whereas cells became more resistant to Adriamycin (ADM; Meiji Seika, Tokyo, Japan) and gemcitabine (GEM). Fluorouracil 77-81 mitogen-activated protein kinase 1 Homo sapiens 18-21 17088986-6 2006 In conclusion, the 5-FU-induced modulation of IFN receptor expression could play a pivotal role in the therapeutic efficacy of IFN-alpha combined with 5-FU. Fluorouracil 19-23 interferon alpha 1 Homo sapiens 127-136 17213586-2 2006 METHODS: MDR1j targeted small interfering RNA duplexes were introduced into multidrug-resistant hepatocellular carcinoma cell line Bel7402/5-Fu. Fluorouracil 139-143 ATP binding cassette subfamily B member 1 Homo sapiens 9-13 16963839-3 2006 We examined whether p53 activated by the DNA-damaging drug 5-fluorouracil (5-FU) also induces CES-2 expression. Fluorouracil 59-73 tumor protein p53 Homo sapiens 20-23 16963839-3 2006 We examined whether p53 activated by the DNA-damaging drug 5-fluorouracil (5-FU) also induces CES-2 expression. Fluorouracil 59-73 carboxylesterase 2 Homo sapiens 94-99 16963839-3 2006 We examined whether p53 activated by the DNA-damaging drug 5-fluorouracil (5-FU) also induces CES-2 expression. Fluorouracil 75-79 tumor protein p53 Homo sapiens 20-23 16963839-3 2006 We examined whether p53 activated by the DNA-damaging drug 5-fluorouracil (5-FU) also induces CES-2 expression. Fluorouracil 75-79 carboxylesterase 2 Homo sapiens 94-99 16963839-4 2006 Our experiments showed that 5-FU induced CES-2 expression in two colon carcinoma cell lines that express wild-type p53 (HCT116 p53(+/+) and RKO) but not in five lines that are p53-null (HCT116 p53(-/- )) or express mutated p53 (HT29, KM12C, KM12SM, and KM12L4A). Fluorouracil 28-32 carboxylesterase 2 Homo sapiens 41-46 16963839-4 2006 Our experiments showed that 5-FU induced CES-2 expression in two colon carcinoma cell lines that express wild-type p53 (HCT116 p53(+/+) and RKO) but not in five lines that are p53-null (HCT116 p53(-/- )) or express mutated p53 (HT29, KM12C, KM12SM, and KM12L4A). Fluorouracil 28-32 tumor protein p53 Homo sapiens 115-118 16963839-4 2006 Our experiments showed that 5-FU induced CES-2 expression in two colon carcinoma cell lines that express wild-type p53 (HCT116 p53(+/+) and RKO) but not in five lines that are p53-null (HCT116 p53(-/- )) or express mutated p53 (HT29, KM12C, KM12SM, and KM12L4A). Fluorouracil 28-32 tumor protein p53 Homo sapiens 127-130 16963839-4 2006 Our experiments showed that 5-FU induced CES-2 expression in two colon carcinoma cell lines that express wild-type p53 (HCT116 p53(+/+) and RKO) but not in five lines that are p53-null (HCT116 p53(-/- )) or express mutated p53 (HT29, KM12C, KM12SM, and KM12L4A). Fluorouracil 28-32 tumor protein p53 Homo sapiens 127-130 16963839-4 2006 Our experiments showed that 5-FU induced CES-2 expression in two colon carcinoma cell lines that express wild-type p53 (HCT116 p53(+/+) and RKO) but not in five lines that are p53-null (HCT116 p53(-/- )) or express mutated p53 (HT29, KM12C, KM12SM, and KM12L4A). Fluorouracil 28-32 tumor protein p53 Homo sapiens 127-130 17207318-0 2006 5-fluorouracil mediates apoptosis and G1/S arrest in laryngeal squamous cell carcinoma via a p53-independent pathway. Fluorouracil 0-14 tumor protein p53 Homo sapiens 93-96 17207318-2 2006 5-FU can induce cell cycle arrest or apoptosis in various cancers via either a p53-dependent or a p53-independent pathway; however, its pathway of action in laryngeal carcinoma is unknown. Fluorouracil 0-4 tumor protein p53 Homo sapiens 79-82 17207318-2 2006 5-FU can induce cell cycle arrest or apoptosis in various cancers via either a p53-dependent or a p53-independent pathway; however, its pathway of action in laryngeal carcinoma is unknown. Fluorouracil 0-4 tumor protein p53 Homo sapiens 98-101 17207318-3 2006 In this study, we aim to investigate the role that p53 plays in the cytotoxic effect of 5-FU on laryngeal squamous carcinoma cells. Fluorouracil 88-92 tumor protein p53 Homo sapiens 51-54 17207318-8 2006 RESULTS: 5-FU induces apoptosis in both UMSCC12 and UMSCC11A cells in a dose- and time-dependent manner, suggesting that the pathway was p53-independent. Fluorouracil 9-13 tumor protein p53 Homo sapiens 137-140 16963839-4 2006 Our experiments showed that 5-FU induced CES-2 expression in two colon carcinoma cell lines that express wild-type p53 (HCT116 p53(+/+) and RKO) but not in five lines that are p53-null (HCT116 p53(-/- )) or express mutated p53 (HT29, KM12C, KM12SM, and KM12L4A). Fluorouracil 28-32 tumor protein p53 Homo sapiens 127-130 16963839-6 2006 A reporter gene assay showed that the luciferase construct with the p53-binding element responded to 5-FU treatment, whereas the reporter construct without the binding element did not. Fluorouracil 101-105 tumor protein p53 Homo sapiens 68-71 16963839-7 2006 Chromatin immunoprecipitation assay confirmed that p53 bound the CES-2 fragment containing the p53-binding element after 5-FU treatment, whereas p21 binding to p53 was present with or without chemotherapy. Fluorouracil 121-125 tumor protein p53 Homo sapiens 51-54 16963839-7 2006 Chromatin immunoprecipitation assay confirmed that p53 bound the CES-2 fragment containing the p53-binding element after 5-FU treatment, whereas p21 binding to p53 was present with or without chemotherapy. Fluorouracil 121-125 carboxylesterase 2 Homo sapiens 65-70 16963839-7 2006 Chromatin immunoprecipitation assay confirmed that p53 bound the CES-2 fragment containing the p53-binding element after 5-FU treatment, whereas p21 binding to p53 was present with or without chemotherapy. Fluorouracil 121-125 tumor protein p53 Homo sapiens 95-98 17207318-9 2006 5-FU induced the accumulation of retinoblastoma protein and a cyclin dependent kinase inhibitor, p21WAF1/CIP1, in both UMSCC12 and UMSCC11A cells. Fluorouracil 0-4 cyclin dependent kinase inhibitor 1A Homo sapiens 97-109 17207318-12 2006 In order to gain an insight into the role p53 plays in response to 5-FU treatment in laryngeal carcinoma, we further transfected either a wildtype p53 plasmid or an empty pcDNA3.1 vector into UMSCC12 cells. Fluorouracil 67-71 tumor protein p53 Homo sapiens 42-45 16963839-7 2006 Chromatin immunoprecipitation assay confirmed that p53 bound the CES-2 fragment containing the p53-binding element after 5-FU treatment, whereas p21 binding to p53 was present with or without chemotherapy. Fluorouracil 121-125 tumor protein p53 Homo sapiens 95-98 17207318-13 2006 We found that 5-FU increased pRb and p21WAF1/CIP1 expression in both p53-transfected and vector-transfected cells without the significant accumulation of p53. Fluorouracil 14-18 cyclin dependent kinase inhibitor 1A Homo sapiens 45-49 17099286-9 2006 These results propose that IFN-alpha subtypes induce cells to undergo apoptosis through p53 activation directly and indirectly, in collaboration with 5-FU, further suggesting the presence of distinct signal pathways for IFN-alpha-induced apoptosis. Fluorouracil 150-154 interferon alpha 1 Homo sapiens 27-36 17207318-13 2006 We found that 5-FU increased pRb and p21WAF1/CIP1 expression in both p53-transfected and vector-transfected cells without the significant accumulation of p53. Fluorouracil 14-18 tumor protein p53 Homo sapiens 69-72 17207318-14 2006 DISCUSSION: Our results suggest that 5-FU mediates apoptosis and G1/S cell cycle phase arrest in laryngeal carcinoma via a p53-independent but p21WAF1/CIP1-dependent or p21WAF1/CIP1-Rb-dependent pathway. Fluorouracil 37-41 tumor protein p53 Homo sapiens 123-126 17207318-14 2006 DISCUSSION: Our results suggest that 5-FU mediates apoptosis and G1/S cell cycle phase arrest in laryngeal carcinoma via a p53-independent but p21WAF1/CIP1-dependent or p21WAF1/CIP1-Rb-dependent pathway. Fluorouracil 37-41 cyclin dependent kinase inhibitor 1A Homo sapiens 151-155 17207318-14 2006 DISCUSSION: Our results suggest that 5-FU mediates apoptosis and G1/S cell cycle phase arrest in laryngeal carcinoma via a p53-independent but p21WAF1/CIP1-dependent or p21WAF1/CIP1-Rb-dependent pathway. Fluorouracil 37-41 cyclin dependent kinase inhibitor 1A Homo sapiens 177-181 17016659-3 2006 In this study, we investigated the molecular mechanisms of apoptosis induction in hepatoma cell lines with IFNalpha and 5-FU combination therapy from the view point of 5-FU"s additive effect on interferon-related signaling pathways. Fluorouracil 120-124 interferon alpha 1 Homo sapiens 194-204 17016659-3 2006 In this study, we investigated the molecular mechanisms of apoptosis induction in hepatoma cell lines with IFNalpha and 5-FU combination therapy from the view point of 5-FU"s additive effect on interferon-related signaling pathways. Fluorouracil 168-172 interferon alpha 1 Homo sapiens 194-204 17016659-6 2006 The JAK/STAT pathway transcriptional factor ISRE was activated more synergistically when 5-FU was added to IFNalpha treatments. Fluorouracil 89-93 interferon alpha 1 Homo sapiens 107-115 17016659-7 2006 Caspase-3, -9, and especially caspase-8 activity was higher with IFN alpha plus 5-FU than IFN or 5-FU alone. Fluorouracil 80-84 caspase 3 Homo sapiens 0-13 17016659-8 2006 Inhibition of caspase-8, -9, c-Jun N-terminal kinase (JNK), phosphatidylinositide 3-kinase (PI3K), and p38 mitogen-activated protein kinase (p38 MAPK) revealed that caspase-8 inhibition was the most effective at decreasing the apoptotic effects of IFN and/or 5-FU. Fluorouracil 259-263 mitogen-activated protein kinase 14 Homo sapiens 141-149 17016659-9 2006 In JAK1 and ISGF3gamma-silenced Hep3B cells, the apoptosis induction and caspase-8 activation levels by IFN, even in combination with 5-FU, were abrogated. Fluorouracil 134-138 Janus kinase 1 Homo sapiens 3-7 17016659-9 2006 In JAK1 and ISGF3gamma-silenced Hep3B cells, the apoptosis induction and caspase-8 activation levels by IFN, even in combination with 5-FU, were abrogated. Fluorouracil 134-138 interferon regulatory factor 9 Homo sapiens 12-22 17033717-0 2006 Bcl-XL small interfering RNA enhances sensitivity of Hepg2 hepatocellular carcinoma cells to 5-fluorouracil and hydroxycamptothecin. Fluorouracil 93-107 BCL2 like 1 Homo sapiens 0-6 17033717-8 2006 Flow cytometry (FCM) results demonstrated that the sub-G1 population increased in the Bcl-XL siRNA group, compared with the negative siRNA group and untreated control group, after the addition of 5-FU (1300 mg/L) and HCPT (0.72 mg/L). Fluorouracil 196-200 BCL2 like 1 Homo sapiens 86-92 17033717-9 2006 siRNA targeting Bcl-XL gene can specifically down-regulate Bcl-XL expression in Hepg2 cells, and can increase spontaneous cell apoptosis and sensitize cells to 5-FU or HCPT. Fluorouracil 160-164 BCL2 like 1 Homo sapiens 16-22 17099286-9 2006 These results propose that IFN-alpha subtypes induce cells to undergo apoptosis through p53 activation directly and indirectly, in collaboration with 5-FU, further suggesting the presence of distinct signal pathways for IFN-alpha-induced apoptosis. Fluorouracil 150-154 interferon alpha 1 Homo sapiens 220-229 16557594-0 2006 Transcriptional profiling of MCF7 breast cancer cells in response to 5-Fluorouracil: relationship with cell cycle changes and apoptosis, and identification of novel targets of p53. Fluorouracil 69-83 tumor protein p53 Homo sapiens 176-179 16984384-0 2006 Small interfering RNA targeting epidermal growth factor receptor enhances chemosensitivity to cisplatin, 5-fluorouracil and docetaxel in head and neck squamous cell carcinoma. Fluorouracil 105-119 epidermal growth factor receptor Homo sapiens 32-64 16984384-7 2006 Treatment with EGFR siRNA in combination with cisplatin, 5-FU and docetaxel enhanced chemosensitivity with a significant increase in apoptosis. Fluorouracil 57-61 epidermal growth factor receptor Homo sapiens 15-19 16984384-9 2006 These cumulative results suggest that EGFR siRNA combined with cisplatin, 5-FU and docetaxel may be a feasible strategy to enhance the effects of chemotherapy in patients with HNSCC. Fluorouracil 74-78 epidermal growth factor receptor Homo sapiens 38-42 17023760-3 2006 Systemic administration of 5FU and CDDP caused her CEA level to decrease gradually and abdominal computed tomography revealed considerable reduction of the metastatic tumors and ascites. Fluorouracil 27-30 CEA cell adhesion molecule 3 Homo sapiens 51-54 16984202-7 2006 We find that hTDG removes 5-fluorouracil 78-fold faster than uracil, and 5-chlorouracil, 572-fold faster than thymine, differences that can be attributed predominantly to leaving-group ability. Fluorouracil 26-40 thymine DNA glycosylase Homo sapiens 13-17 16652156-11 2006 As suppression of caspase-2 expression in 5-FU-treated cells also affects the level of the p53 protein, possibilities of a reciprocal interaction between these proteins are discussed. Fluorouracil 42-46 tumor protein p53 Homo sapiens 91-94 16931914-4 2006 In this study we have uncovered a novel positive feedback that involves the transcriptional activation of the anti-apoptotic molecule deltaNp63 by the anti-apoptotic molecules deltaNp73 and mutant p53, and that is put into motion upon treatment with a subset of DNA damaging agents such as Doxorubicin and 5-FU. Fluorouracil 306-310 tumor protein p53 Homo sapiens 197-200 16929163-5 2006 Moreover, while telomerase activity was reduced equally by both drugs, 5-FU but not GEM effectively downregulated NFkappaB binding activity. Fluorouracil 71-75 nuclear factor kappa B subunit 1 Homo sapiens 114-122 17003427-4 2006 The contribution of AQP3-facilitated cell migration to corneal re-epithelialization was assessed using an organ culture model, in which initial resurfacing results from epithelial cell migration, as shown by BrdU analysis and 5-fluorouracil insensitivity, and by scratch wound assay using primary cultures of corneal epithelial cells from wild-type versus AQP3-null mice. Fluorouracil 226-240 aquaporin 3 Mus musculus 20-24 16951200-7 2006 Evidence presented here indicates that both the nuclear and the mitochondrial isoforms of UDG are modulated by FdUrd (and 5-FU) treatment in certain cell lines but not in others. Fluorouracil 122-126 uracil DNA glycosylase Homo sapiens 90-93 16557594-6 2006 High dose 5-FU also induced a higher regulation of the mitochondrial death genes APAF1, BAK1 and BCL2, and induction of genes of the ID family. Fluorouracil 10-14 apoptotic peptidase activating factor 1 Homo sapiens 81-86 16557594-6 2006 High dose 5-FU also induced a higher regulation of the mitochondrial death genes APAF1, BAK1 and BCL2, and induction of genes of the ID family. Fluorouracil 10-14 BCL2 apoptosis regulator Homo sapiens 97-101 16619043-0 2006 Chk1-dependent slowing of S-phase progression protects DT40 B-lymphoma cells against killing by the nucleoside analogue 5-fluorouracil. Fluorouracil 120-134 opsin, green sensitive (rhodopsin-like) Gallus gallus 0-4 16924531-5 2006 RESULTS: Patients in the CRT group were given cisplatin and 5-FU (143 and 6,000 mg on average, respectively) plus an average of 35 Gy of radiation. Fluorouracil 60-64 calcitonin receptor Homo sapiens 25-28 16865244-0 2006 S-1, an oral fluoropyrimidine, enhances radiation response of DLD-1/FU human colon cancer xenografts resistant to 5-FU. Fluorouracil 114-118 proteasome 26S subunit, non-ATPase 1 Homo sapiens 0-3 16865244-10 2006 Combined S-1 plus radiation treatment resulted in a synergistic effect in the therapy of 5-FU resistant human colon carcinoma xenografts (EF = 2.06). Fluorouracil 89-93 proteasome 26S subunit, non-ATPase 1 Homo sapiens 9-12 16619043-3 2006 We show that 5FU activates Chk1 in wild-type DT40 cells and that 5FU-treated cells accumulate in the S phase of the cell cycle due to slowing of the overall rate of DNA replication. Fluorouracil 13-16 opsin, green sensitive (rhodopsin-like) Gallus gallus 27-31 16619043-6 2006 Taken together, these results demonstrate that a Chk1-dependent replication checkpoint which slows S phase progression can protect tumour cells against the cytotoxic effects of 5FU. Fluorouracil 177-180 opsin, green sensitive (rhodopsin-like) Gallus gallus 49-53 16928813-7 2006 Our result showed that only the down-regulation of Chk1, but not of Chk2 or MK2, abrogated camptothecin- or 5-fluorouracil-induced S-phase arrest or doxorubicin-induced G(2)-phase arrest. Fluorouracil 108-122 checkpoint kinase 1 Homo sapiens 51-55 16820916-9 2006 After administration of S-1 to gastric cancer patients with peritoneal dissemination, 5-FU and CDHP in the serum linearly pass through the peritoneum and enter the ascites. Fluorouracil 86-90 proteasome 26S subunit, non-ATPase 1 Homo sapiens 24-27 16953072-0 2006 A case of early relapsed multiple lung metastases after esophagectomy successfully treated with S-1/cisplatin therapy after docetaxel/5-fluorouracil/cisplatin therapy. Fluorouracil 134-148 proteasome 26S subunit, non-ATPase 1 Homo sapiens 96-99 16584912-0 2006 Relationship between p53 status and 5-fluorouracil sensitivity in 3 cell lines. Fluorouracil 36-50 tumor protein p53 Homo sapiens 21-24 16881736-7 2006 In vitro, PF4 also promoted survival and proliferation of 5-fluorouracil-resistant hematopoietic stem/progenitor cells after irradiation. Fluorouracil 58-72 platelet factor 4 Mus musculus 10-13 16897968-5 2006 In combination with other anticancer drugs such as CPT-11 and taxanes, S-1 exercised synergistic antitumor efficacy not only on 5-FU-sensitive tumors with low expression levels of thymidylate synthase (TS) but also on 5-FU-resistant tumors with originally higher and/or elevated levels of TS expression. Fluorouracil 128-132 proteasome 26S subunit, non-ATPase 1 Homo sapiens 71-74 16838650-4 2006 Concerning the mechanism of FAIT, we reported the synergistic effects of IFNalpha and 5-FU, in terms of the influence to cell cycle progression leading into the S phase via p27Kip1, an apoptosis-inducing effect through a reduction of Bcl-xl, and an immuno-modulatory effect via the TRAIL/TRAIL-receptor pathway. Fluorouracil 86-90 BCL2 like 1 Homo sapiens 234-240 16838650-4 2006 Concerning the mechanism of FAIT, we reported the synergistic effects of IFNalpha and 5-FU, in terms of the influence to cell cycle progression leading into the S phase via p27Kip1, an apoptosis-inducing effect through a reduction of Bcl-xl, and an immuno-modulatory effect via the TRAIL/TRAIL-receptor pathway. Fluorouracil 86-90 TNF superfamily member 10 Homo sapiens 282-287 16838650-4 2006 Concerning the mechanism of FAIT, we reported the synergistic effects of IFNalpha and 5-FU, in terms of the influence to cell cycle progression leading into the S phase via p27Kip1, an apoptosis-inducing effect through a reduction of Bcl-xl, and an immuno-modulatory effect via the TRAIL/TRAIL-receptor pathway. Fluorouracil 86-90 TNF superfamily member 10 Homo sapiens 288-293 16721360-2 2006 The present study evaluated the relationship between C-reactive protein concentrations and survival in a cohort of patients receiving adjuvant 5-fluorouracil (5-FU) chemotherapy following potentially curative resection for colorectal cancer. Fluorouracil 143-157 C-reactive protein Homo sapiens 53-71 16721360-2 2006 The present study evaluated the relationship between C-reactive protein concentrations and survival in a cohort of patients receiving adjuvant 5-fluorouracil (5-FU) chemotherapy following potentially curative resection for colorectal cancer. Fluorouracil 159-163 C-reactive protein Homo sapiens 53-71 16639731-1 2006 BACKGROUND: The authors previously reported results from a randomized trial of standard-dose chemotherapy with combined 5-fluorouracil (1000 mg/m2 per cycle), doxorubicin (50 mg/m2 per cycle), and cyclophosphamide (500 mg/m2 per cycle) (FAC) versus FAC followed by high-dose chemotherapy (HDCT) and autologous stem cell support (ASCS) for patients with high-risk primary breast carcinoma. Fluorouracil 120-134 FA complementation group C Homo sapiens 237-240 16639731-1 2006 BACKGROUND: The authors previously reported results from a randomized trial of standard-dose chemotherapy with combined 5-fluorouracil (1000 mg/m2 per cycle), doxorubicin (50 mg/m2 per cycle), and cyclophosphamide (500 mg/m2 per cycle) (FAC) versus FAC followed by high-dose chemotherapy (HDCT) and autologous stem cell support (ASCS) for patients with high-risk primary breast carcinoma. Fluorouracil 120-134 FA complementation group C Homo sapiens 249-252 16897970-6 2006 The area under the curve (AUC0-10h) of 5-FU on day 5 was 728 +/- 113 ng x hr/ml for PVI of 5-FU and 1,364 +/- 374 ng x hr/ml for S-1. Fluorouracil 39-43 proteasome 26S subunit, non-ATPase 1 Homo sapiens 129-132 16897968-1 2006 TS-1 (S-1), developed by the scientific theory of both potentiating antitumor activity of 5-fluorouracil (5-FU) and reducing gastrointestinal toxicity induced by 5-FU, is a new oral formulation consisting of 1 M tegafur, 0.4 M gimeracil and 1 M oteracil potassium. Fluorouracil 90-104 proteasome 26S subunit, non-ATPase 1 Homo sapiens 1-4 16897968-1 2006 TS-1 (S-1), developed by the scientific theory of both potentiating antitumor activity of 5-fluorouracil (5-FU) and reducing gastrointestinal toxicity induced by 5-FU, is a new oral formulation consisting of 1 M tegafur, 0.4 M gimeracil and 1 M oteracil potassium. Fluorouracil 106-110 proteasome 26S subunit, non-ATPase 1 Homo sapiens 1-4 16897968-1 2006 TS-1 (S-1), developed by the scientific theory of both potentiating antitumor activity of 5-fluorouracil (5-FU) and reducing gastrointestinal toxicity induced by 5-FU, is a new oral formulation consisting of 1 M tegafur, 0.4 M gimeracil and 1 M oteracil potassium. Fluorouracil 162-166 proteasome 26S subunit, non-ATPase 1 Homo sapiens 1-4 16897968-5 2006 In combination with other anticancer drugs such as CPT-11 and taxanes, S-1 exercised synergistic antitumor efficacy not only on 5-FU-sensitive tumors with low expression levels of thymidylate synthase (TS) but also on 5-FU-resistant tumors with originally higher and/or elevated levels of TS expression. Fluorouracil 218-222 proteasome 26S subunit, non-ATPase 1 Homo sapiens 71-74 16897970-0 2006 [Plasma concentrations of 5-fluorouracil and F-beta-alanine following oral administration of S-1, a dihydropyrimidine dehydrogenase inhibitory fluoropyrimidine, as compared with protracted venous infusion of 5-fluorouracil]. Fluorouracil 26-40 proteasome 26S subunit, non-ATPase 1 Homo sapiens 93-96 16407826-0 2006 Overexpression of hRFI inhibits 5-fluorouracil-induced apoptosis in colorectal cancer cells via activation of NF-kappaB and upregulation of BCL-2 and BCL-XL. Fluorouracil 32-46 ring finger protein 34 Homo sapiens 18-22 16898000-0 2006 [Phase II study of S-1, a novel oral fluorouracil, in advanced non-small-cell lung cancer]. Fluorouracil 37-49 proteasome 26S subunit, non-ATPase 1 Homo sapiens 19-22 16898001-1 2006 S-1 is a newly developed oral anti-tumor agent, which contains 5-chloro-2, 4-dihydroxypyridine and potassium oxonate to strengthen biological activities of 5-fluorouracil. Fluorouracil 156-170 proteasome 26S subunit, non-ATPase 1 Homo sapiens 0-3 16898006-5 2006 Under these circumstances, we conducted a phase I /II trial of gemcitabine with S-1, an oral fluorouracil derivative, to determine the maximum tolerated dose and to evaluate the activity and toxicity of such a combination in patients with APC. Fluorouracil 93-105 proteasome 26S subunit, non-ATPase 1 Homo sapiens 80-83 16898008-3 2006 Even though there has been no effective chemotherapy against hepatocellular carcinoma with distant metastases, we performed S-1 and interferon-alpha combination chemotherapy for the cases where good results were exhibited from interferon-alpha combined with arterial 5-FU infusion. Fluorouracil 267-271 proteasome 26S subunit, non-ATPase 1 Homo sapiens 124-127 16818496-6 2006 Indeed, the inactivation of p53 may explain the relative resistance to 5-fluorouracil, whereas Bcl-2 overexpression is associated with reduced sensitivity to gemcitabine. Fluorouracil 71-85 tumor protein p53 Homo sapiens 28-31 16794239-3 2006 DESIGN: This review summarizes current clinical data for EGFR-TKIs as monotherapy or in combination with 5-fluorouracil/leucovorin, irinotecan, or oxaliplatin, focusing on the rapidly developing area of colorectal, gastroesophageal, and pancreatic cancers. Fluorouracil 105-119 epidermal growth factor receptor Homo sapiens 57-61 16836928-0 2006 [Double sites short hairpin RNAs targeting epidermal growth factor receptor to promote colon cancer cells apoptosis and enhance 5-fluorouracil chemotherapy effect]. Fluorouracil 128-142 epidermal growth factor receptor Homo sapiens 43-75 16836928-8 2006 CONCLUSIONS: Both pU6-EGFR-shRNA-1 and pU6-EGFR-shRNA-2 were capable of suppressing EGFR expression of LoVo cells, and therefore promoting apoptosis and increasing the cell toxicity of 5-FU. Fluorouracil 185-189 epidermal growth factor receptor Homo sapiens 22-26 16836928-8 2006 CONCLUSIONS: Both pU6-EGFR-shRNA-1 and pU6-EGFR-shRNA-2 were capable of suppressing EGFR expression of LoVo cells, and therefore promoting apoptosis and increasing the cell toxicity of 5-FU. Fluorouracil 185-189 epidermal growth factor receptor Homo sapiens 43-47 16836928-8 2006 CONCLUSIONS: Both pU6-EGFR-shRNA-1 and pU6-EGFR-shRNA-2 were capable of suppressing EGFR expression of LoVo cells, and therefore promoting apoptosis and increasing the cell toxicity of 5-FU. Fluorouracil 185-189 epidermal growth factor receptor Homo sapiens 43-47 16836929-9 2006 CONCLUSIONS: Combined MDR1 antisense RNA with oxaliplatin and 5-FU has a synergistic effect of killing drug-resistant cancer cells and may be a promising method for treating drug-resistant rectal carcinoma. Fluorouracil 62-66 ATP binding cassette subfamily B member 1 Homo sapiens 22-26 16897978-11 2006 The mechanisms underlying these synergistic effects of S-1 and docetaxel were examined by expression and activity analyses of 5-FU metabolic enzymes. Fluorouracil 126-130 proteasome 26S subunit, non-ATPase 1 Homo sapiens 55-58 16897985-10 2006 In addition, considerable ethnic differences in the tolerated doses of S-1 have been considered related to varying efficiency rates of conversion of tegafur to 5-fluorouracil by the CYP450 enzyme system. Fluorouracil 160-174 proteasome 26S subunit, non-ATPase 1 Homo sapiens 71-74 16897986-3 2006 S-1 is an oral 5-FU anti-tumor drug that combines three pharmacological agents: tegafur, 5-chloro-2,4-dihydroxypyridine, which inhibits dihydropyrimidine dehydrogenase activity, and potassium oxonate, which reduces gastrointestinal toxicity. Fluorouracil 15-19 proteasome 26S subunit, non-ATPase 1 Homo sapiens 0-3 16897987-10 2006 It will be essential to prove that the combination of S-1 plus CPT-11 can replace the combination of infusional 5-FU and LV plus CPT-11 without negatively affecting efficacy and toxicity. Fluorouracil 112-116 proteasome 26S subunit, non-ATPase 1 Homo sapiens 54-57 16897989-2 2006 S-1 was a newly developed 5-FU derivative and was orally administered. Fluorouracil 26-30 proteasome 26S subunit, non-ATPase 1 Homo sapiens 0-3 16793607-6 2006 Treatment with diclofenac or 5-Fu resulted in elevated COX-2 mRNA expression both in HepG2 and Hep3B cells. Fluorouracil 29-33 prostaglandin-endoperoxide synthase 2 Homo sapiens 55-60 16643889-0 2006 Effects of adenosine A(3) receptor agonist on bone marrow granulocytic system in 5-fluorouracil-treated mice. Fluorouracil 81-95 adenosine A3 receptor Mus musculus 11-34 16407826-0 2006 Overexpression of hRFI inhibits 5-fluorouracil-induced apoptosis in colorectal cancer cells via activation of NF-kappaB and upregulation of BCL-2 and BCL-XL. Fluorouracil 32-46 BCL2 apoptosis regulator Homo sapiens 140-145 16407826-0 2006 Overexpression of hRFI inhibits 5-fluorouracil-induced apoptosis in colorectal cancer cells via activation of NF-kappaB and upregulation of BCL-2 and BCL-XL. Fluorouracil 32-46 BCL2 like 1 Homo sapiens 150-156 16407826-4 2006 In order to investigate the molecular function of hRFI in the regulation of 5-FU-induced apoptosis in colorectal cancer cells, HCT116 cells were stably transfected with hRFI or LacZ as a control. Fluorouracil 76-80 ring finger protein 34 Homo sapiens 50-54 16407826-5 2006 hRFI overexpression resulted in cellular resistance to 5-FU through an inhibition of the mitochondrial apoptotic pathway and specific upregulation of Bcl-2 and Bcl-XL. Fluorouracil 55-59 ring finger protein 34 Homo sapiens 0-4 16407826-8 2006 Overexpression of hRFI in SW480 and COLO320 colorectal cancer cells similarly resulted in resistance to 5-FU with the activation of NF-kappaB and upregulation of Bcl-2 and Bcl-XL. Fluorouracil 104-108 ring finger protein 34 Homo sapiens 18-22 15996812-2 2006 The present work reports the involvement of Bcl-2 in response to the exposure of HEp-2 and KB cells to Carb or 5-FU. Fluorouracil 111-115 BCL2 apoptosis regulator Homo sapiens 44-49 16709241-5 2006 RESULTS: 5-FU treatment for 24 hours resulted in S phase arrests, p53 accumulation, up-regulation of p53-target genes on DNA damage response (ATF3, GADD34, GADD45A, PCNA), cell cycle-regulatory (CDKN1A), and apoptosis-regulatory pathways (FAS), and apoptosis induction in the parental and resistant cell lines. Fluorouracil 9-13 tumor protein p53 Homo sapiens 66-69 16709241-5 2006 RESULTS: 5-FU treatment for 24 hours resulted in S phase arrests, p53 accumulation, up-regulation of p53-target genes on DNA damage response (ATF3, GADD34, GADD45A, PCNA), cell cycle-regulatory (CDKN1A), and apoptosis-regulatory pathways (FAS), and apoptosis induction in the parental and resistant cell lines. Fluorouracil 9-13 tumor protein p53 Homo sapiens 101-104 16709241-5 2006 RESULTS: 5-FU treatment for 24 hours resulted in S phase arrests, p53 accumulation, up-regulation of p53-target genes on DNA damage response (ATF3, GADD34, GADD45A, PCNA), cell cycle-regulatory (CDKN1A), and apoptosis-regulatory pathways (FAS), and apoptosis induction in the parental and resistant cell lines. Fluorouracil 9-13 protein phosphatase 1 regulatory subunit 15A Homo sapiens 148-154 16709241-5 2006 RESULTS: 5-FU treatment for 24 hours resulted in S phase arrests, p53 accumulation, up-regulation of p53-target genes on DNA damage response (ATF3, GADD34, GADD45A, PCNA), cell cycle-regulatory (CDKN1A), and apoptosis-regulatory pathways (FAS), and apoptosis induction in the parental and resistant cell lines. Fluorouracil 9-13 cyclin dependent kinase inhibitor 1A Homo sapiens 195-201 16709241-8 2006 The strongly 5-FU-resistant ContinD cell line had the smallest S phase arrests, the lowest CDKN1A levels, and the lowest levels of 5-FU-induced apoptosis throughout the treatment and recovery periods, and the fastest recovery of exponential growth (10 days) compared to the other two cell lines. Fluorouracil 13-17 cyclin dependent kinase inhibitor 1A Homo sapiens 91-97 16709241-11 2006 Differential expression in response to 5-FU treatment was demonstrated for genes involved in regulation of nucleotide binding/metabolism (ATAD2, GNL2, GNL3, MATR3), amino acid metabolism (AHCY, GSS, IVD, OAT), cytoskeleton organization (KRT7, KRT8, KRT19, MAST1), transport (MTCH1, NCBP1, SNAPAP, VPS52), and oxygen metabolism (COX5A, COX7C). Fluorouracil 39-43 ATPase family AAA domain containing 2 Homo sapiens 138-143 16709241-11 2006 Differential expression in response to 5-FU treatment was demonstrated for genes involved in regulation of nucleotide binding/metabolism (ATAD2, GNL2, GNL3, MATR3), amino acid metabolism (AHCY, GSS, IVD, OAT), cytoskeleton organization (KRT7, KRT8, KRT19, MAST1), transport (MTCH1, NCBP1, SNAPAP, VPS52), and oxygen metabolism (COX5A, COX7C). Fluorouracil 39-43 keratin 7 Homo sapiens 237-241 16709241-11 2006 Differential expression in response to 5-FU treatment was demonstrated for genes involved in regulation of nucleotide binding/metabolism (ATAD2, GNL2, GNL3, MATR3), amino acid metabolism (AHCY, GSS, IVD, OAT), cytoskeleton organization (KRT7, KRT8, KRT19, MAST1), transport (MTCH1, NCBP1, SNAPAP, VPS52), and oxygen metabolism (COX5A, COX7C). Fluorouracil 39-43 mitochondrial carrier 1 Homo sapiens 275-280 16709241-11 2006 Differential expression in response to 5-FU treatment was demonstrated for genes involved in regulation of nucleotide binding/metabolism (ATAD2, GNL2, GNL3, MATR3), amino acid metabolism (AHCY, GSS, IVD, OAT), cytoskeleton organization (KRT7, KRT8, KRT19, MAST1), transport (MTCH1, NCBP1, SNAPAP, VPS52), and oxygen metabolism (COX5A, COX7C). Fluorouracil 39-43 nuclear cap binding protein subunit 1 Homo sapiens 282-287 16364925-4 2006 Interestingly, while the susceptibilities of Tbeta4 overexpressers to 5-FU and irinotecan remained unchanged, they were more resistant to doxorubicin and etoposide which triggered apoptosis via a mitochondrial pathway. Fluorouracil 70-74 thymosin beta 4 X-linked Homo sapiens 45-51 16680372-11 2006 RNA interference targeting at p65 increased the sensitivity of the ESCC cell lines to 5-fluorouracil, suggesting that NF-kappaB might be a good target for cancer treatment. Fluorouracil 86-100 nuclear factor kappa B subunit 1 Homo sapiens 118-127 16631755-1 2006 Doxorubicin, cis-diamminedichloroplatinum (II) and 5-fluorouracil used in chemotherapy induce apoptosis in Hep3B cells in the absence of p53, p73, and functional Fas. Fluorouracil 51-65 tumor protein p53 Homo sapiens 137-140 16686938-2 2006 Here, we address the individual role of p53 and its transcriptional targets, p21CIP/WAF-1 and Bax, on apoptosis induced by individual components of multimodal anticancer therapy, i.e. 5-fluorouracil (5-FU), ionising gamma-radiation (IR) and heat shock/hyperthermia. Fluorouracil 184-198 tumor protein p53 Homo sapiens 40-43 16686938-2 2006 Here, we address the individual role of p53 and its transcriptional targets, p21CIP/WAF-1 and Bax, on apoptosis induced by individual components of multimodal anticancer therapy, i.e. 5-fluorouracil (5-FU), ionising gamma-radiation (IR) and heat shock/hyperthermia. Fluorouracil 200-204 tumor protein p53 Homo sapiens 40-43 16686938-10 2006 In contrast, loss of p21CIP/WAF-1 or, to a lesser extent, p53 sensitized predominantly for 5-FU and IR. Fluorouracil 91-95 cyclin dependent kinase inhibitor 1A Homo sapiens 28-33 16686938-10 2006 In contrast, loss of p21CIP/WAF-1 or, to a lesser extent, p53 sensitized predominantly for 5-FU and IR. Fluorouracil 91-95 tumor protein p53 Homo sapiens 58-61 16596200-0 2006 hRFI overexpressed in HCT116 cells modulates Bcl-2 family proteins when treated with 5-fluorouracil. Fluorouracil 85-99 ring finger protein 34 Homo sapiens 0-4 16596200-0 2006 hRFI overexpressed in HCT116 cells modulates Bcl-2 family proteins when treated with 5-fluorouracil. Fluorouracil 85-99 BCL2 apoptosis regulator Homo sapiens 45-50 16596200-1 2006 Exogenous overexpression of hRFI, originally isolated in our laboratory, inhibits not only death receptor-mediated apoptosis but also the mitochondrial apoptosis induced by several chemotherapeutic agents including 5-fluorouracil (5-FU). Fluorouracil 215-229 ring finger protein 34 Homo sapiens 28-32 16596200-1 2006 Exogenous overexpression of hRFI, originally isolated in our laboratory, inhibits not only death receptor-mediated apoptosis but also the mitochondrial apoptosis induced by several chemotherapeutic agents including 5-fluorouracil (5-FU). Fluorouracil 231-235 ring finger protein 34 Homo sapiens 28-32 16596200-5 2006 As a result, we identified four genes (Bcl-2, Bcl-XL, cIAP2, and CFLAR) whose expression was four or more times higher in HCT116/ hRFI cells than in HCT116/LacZ cells, and found that Bcl-2 and the ratio of Bcl-2/Bax or Bcl-2/Bak were upregulated when HCT116/hRFI cells were treated with 5-FU. Fluorouracil 287-291 BCL2 apoptosis regulator Homo sapiens 39-44 16596200-5 2006 As a result, we identified four genes (Bcl-2, Bcl-XL, cIAP2, and CFLAR) whose expression was four or more times higher in HCT116/ hRFI cells than in HCT116/LacZ cells, and found that Bcl-2 and the ratio of Bcl-2/Bax or Bcl-2/Bak were upregulated when HCT116/hRFI cells were treated with 5-FU. Fluorouracil 287-291 BCL2 like 1 Homo sapiens 46-52 16596200-5 2006 As a result, we identified four genes (Bcl-2, Bcl-XL, cIAP2, and CFLAR) whose expression was four or more times higher in HCT116/ hRFI cells than in HCT116/LacZ cells, and found that Bcl-2 and the ratio of Bcl-2/Bax or Bcl-2/Bak were upregulated when HCT116/hRFI cells were treated with 5-FU. Fluorouracil 287-291 CASP8 and FADD like apoptosis regulator Homo sapiens 65-70 16596200-5 2006 As a result, we identified four genes (Bcl-2, Bcl-XL, cIAP2, and CFLAR) whose expression was four or more times higher in HCT116/ hRFI cells than in HCT116/LacZ cells, and found that Bcl-2 and the ratio of Bcl-2/Bax or Bcl-2/Bak were upregulated when HCT116/hRFI cells were treated with 5-FU. Fluorouracil 287-291 ring finger protein 34 Homo sapiens 130-134 16596200-6 2006 Furthermore, we also validated the up-regulation of Bcl-2 and Bcl-XL in HCT116/hRFI cells treated with 5-FU by Western blot analysis. Fluorouracil 103-107 BCL2 apoptosis regulator Homo sapiens 52-57 16596200-6 2006 Furthermore, we also validated the up-regulation of Bcl-2 and Bcl-XL in HCT116/hRFI cells treated with 5-FU by Western blot analysis. Fluorouracil 103-107 BCL2 like 1 Homo sapiens 62-68 16596200-6 2006 Furthermore, we also validated the up-regulation of Bcl-2 and Bcl-XL in HCT116/hRFI cells treated with 5-FU by Western blot analysis. Fluorouracil 103-107 ring finger protein 34 Homo sapiens 79-83 16596200-7 2006 Such evidence suggests that the modulation of Bcl-2 family proteins seen in 5-FU treatment plays an important role in the anti-apoptotic function of HCT116/hRFI cells. Fluorouracil 76-80 BCL2 apoptosis regulator Homo sapiens 46-51 16596200-7 2006 Such evidence suggests that the modulation of Bcl-2 family proteins seen in 5-FU treatment plays an important role in the anti-apoptotic function of HCT116/hRFI cells. Fluorouracil 76-80 ring finger protein 34 Homo sapiens 156-160 16809149-1 2006 UNLABELLED: Thymidylate synthase (TS), dihydropyrimidine dehydrogenase (DPD), and vascular endothelial growth factor (VEGF) are associated with the effect of 5-fluorouracil (5-FU) based adjuvant chemotherapy. Fluorouracil 158-172 vascular endothelial growth factor A Homo sapiens 82-116 16677934-8 2006 Furthermore, we show that treatment with 5-FU and ultrasound increased the levels of the Bax and p27kip1 proteins, but the addition of Optison appears to suppress apoptotic protein expression. Fluorouracil 41-45 BCL2 associated X, apoptosis regulator Homo sapiens 89-92 16609087-13 2006 CONCLUSION: Among patients with node-positive tumors, ER-negative breast cancer, biweekly doxorubicin/cyclophosphamide plus paclitaxel lowers the rate of recurrence and death by more than 50% in comparison with low-dose cyclophosphamide, doxorubicin, and fluorouracil as used in the first study. Fluorouracil 255-267 estrogen receptor 1 Homo sapiens 54-56 16809149-1 2006 UNLABELLED: Thymidylate synthase (TS), dihydropyrimidine dehydrogenase (DPD), and vascular endothelial growth factor (VEGF) are associated with the effect of 5-fluorouracil (5-FU) based adjuvant chemotherapy. Fluorouracil 174-178 vascular endothelial growth factor A Homo sapiens 82-116 16809149-1 2006 UNLABELLED: Thymidylate synthase (TS), dihydropyrimidine dehydrogenase (DPD), and vascular endothelial growth factor (VEGF) are associated with the effect of 5-fluorouracil (5-FU) based adjuvant chemotherapy. Fluorouracil 158-172 vascular endothelial growth factor A Homo sapiens 118-122 16809149-1 2006 UNLABELLED: Thymidylate synthase (TS), dihydropyrimidine dehydrogenase (DPD), and vascular endothelial growth factor (VEGF) are associated with the effect of 5-fluorouracil (5-FU) based adjuvant chemotherapy. Fluorouracil 174-178 vascular endothelial growth factor A Homo sapiens 118-122 16303861-0 2006 Cetuximab and irinotecan/5-fluorouracil/folinic acid is a safe combination for the first-line treatment of patients with epidermal growth factor receptor expressing metastatic colorectal carcinoma. Fluorouracil 25-39 epidermal growth factor receptor Homo sapiens 121-153 16563096-3 2006 For example: 5-fluorouracil-derived agents would be used for tumors with a low expression of thymidylate synthase; gefitinib and erlotinib for tumors with epidermal growth factor receptor (EGFR) mutations or increased EGFR gene copy numbers; cisplatin and carboplatin for tumors with a low expression of excision repair cross complementing-1; and gemcitabine for tumors with a low expression of ribonucleotide reductase. Fluorouracil 13-27 epidermal growth factor receptor Homo sapiens 189-193 16563096-3 2006 For example: 5-fluorouracil-derived agents would be used for tumors with a low expression of thymidylate synthase; gefitinib and erlotinib for tumors with epidermal growth factor receptor (EGFR) mutations or increased EGFR gene copy numbers; cisplatin and carboplatin for tumors with a low expression of excision repair cross complementing-1; and gemcitabine for tumors with a low expression of ribonucleotide reductase. Fluorouracil 13-27 epidermal growth factor receptor Homo sapiens 218-222 16500647-5 2006 The CB1 antagonist N-(piperidin-1-1yl)-5-(4-iodophenyl)-1-(2,4-dichlorophenyl)-4-methyl-1H-pyrazole-3-carboxamide (AM251) was the most active compound with an IC50 of 8.6 +/- 1.3 microM after 72 h. AM251 induces apoptosis, causes transcriptional changes of genes in janus kinase/signal transducers and activators of transcription signaling network and synergistically interacts with the pyrimidine analogue, 5-fluorouracil. Fluorouracil 408-422 cannabinoid receptor 1 Homo sapiens 4-7 16490547-11 2006 The addition of IFNs significantly enhanced the cytotoxic effects of 5-FU and gemcitabine in those cell lines that expressed the corresponding IFN-alpha, -beta, or -gamma receptors. Fluorouracil 69-73 interferon alpha 1 Homo sapiens 143-152 16549996-0 2006 Effect of gastrectomy on the pharmacokinetics of 5-fluorouracil and gimeracil after oral administration of S-1. Fluorouracil 49-63 proteasome 26S subunit, non-ATPase 1 Homo sapiens 107-110 16549996-7 2006 Thus, the results of the present study showed that around post-operative hospital day 14, when total oral feeding had become possible after surgery for gastric cancer, the AUC0-8 h values of 5-FU and CDHP after S-1 administration were almost the same as before surgery and that gastrectomy had hardly any effect on the pharmacokinetics of S-1. Fluorouracil 191-195 proteasome 26S subunit, non-ATPase 1 Homo sapiens 211-214 16373718-2 2005 We assessed the roles of p53, TRAIL receptors, and cellular Fas-associated death domain-like interleukin-1beta-converting enzyme inhibitory protein (c-FLIP) in regulating the cytotoxic effects of recombinant TRAIL (rTRAIL) alone and in combination with chemotherapy [5-fluorouracil (5-FU), oxaliplatin, and irinotecan] in a panel of colon cancer cell lines. Fluorouracil 267-281 CASP8 and FADD like apoptosis regulator Homo sapiens 149-155 16511603-3 2006 In mice expressing a phosphotyrosine-null (PY-null) Epo receptor allele (EpoR-HM), severe and persistent anemia was induced by hemolysis or 5-fluorouracil. Fluorouracil 140-154 erythropoietin Homo sapiens 52-55 16412276-0 2006 Inhibition of Bcl-2 expression by a novel tumor-specific RNA interference system increases chemosensitivity to 5-fluorouracil in Hela cells. Fluorouracil 111-125 BCL2 apoptosis regulator Homo sapiens 14-19 16412276-12 2006 Inhibition of Bcl-2 did not affect cell proliferation, but increased the chemosensitivity of HeLa cells to 5-fluorouracil. Fluorouracil 107-121 BCL2 apoptosis regulator Homo sapiens 14-19 16412276-14 2006 Suppression of Bcl-2 by using this system sensitized HeLa cells to 5-fluorouracil. Fluorouracil 67-81 BCL2 apoptosis regulator Homo sapiens 15-20 16075279-9 2006 Western blotting showed that PXL exposure followed by 5-FU up-regulated Chk1 and Wee1 protein expressions until PXL removal and 5-FU exposure, when these expressions gradually decreased to their basal levels. Fluorouracil 54-58 checkpoint kinase 1 Homo sapiens 72-76 16538045-4 2006 On the other hand, 5-FU 20 mg/kg also caused a significant decline in the amount of produced TNF-alpha but it showed no apparent effects on the number of leukocytes and the body weight. Fluorouracil 19-23 tumor necrosis factor Mus musculus 93-102 16538045-5 2006 These results indicate that LPS-induced TNF-alpha production is a more sensitive measure than leukocyte count used conventionally to detect the immunotoxicity of two anticancer drugs, CDDP and 5-FU, and suggest that it might be a more practical index for hazard identification in clinical treatment with anticancer drugs. Fluorouracil 193-197 toll-like receptor 4 Mus musculus 28-31 16538045-5 2006 These results indicate that LPS-induced TNF-alpha production is a more sensitive measure than leukocyte count used conventionally to detect the immunotoxicity of two anticancer drugs, CDDP and 5-FU, and suggest that it might be a more practical index for hazard identification in clinical treatment with anticancer drugs. Fluorouracil 193-197 tumor necrosis factor Mus musculus 40-49 16434701-6 2006 Reporter gene assays confirmed the expected responsiveness of the respective promoter regions to the p53 inducer 5-fluorouracil and 1alpha,25(OH)2D3. Fluorouracil 113-127 tumor protein p53 Homo sapiens 101-104 16755122-13 2006 S-1 is a combined formulation containing 5-chloro-2, 4-dihydroxypyrimidine (CDHP; gimestat), which inhibits an enzyme that metabolites 5-FU, dihydropyrimidine dehydrogenase (DPD). Fluorouracil 135-139 proteasome 26S subunit, non-ATPase 1 Homo sapiens 0-3 16755122-14 2006 Therefore, high 5-FU concentrations are maintained with S-1, and S-1 may be effective in the patients who do not respond to other fluoropyrimidine agents. Fluorouracil 16-20 proteasome 26S subunit, non-ATPase 1 Homo sapiens 56-59 16755122-16 2006 Since S-1 contains potassium oxonate (OXO; otastat), gastrointestinal toxicities, the main adverse events of 5-FU agents, could be reduced. Fluorouracil 109-113 proteasome 26S subunit, non-ATPase 1 Homo sapiens 6-9 17318948-6 2006 FAC (5 fluorouracil/doxorubicin/cyclophosphamide/methotrexate/5 fluorouracil), higher doses of epirubicin in FE(100)C are twice as high compared with FAC. Fluorouracil 5-19 FA complementation group C Homo sapiens 0-3 17318948-6 2006 FAC (5 fluorouracil/doxorubicin/cyclophosphamide/methotrexate/5 fluorouracil), higher doses of epirubicin in FE(100)C are twice as high compared with FAC. Fluorouracil 7-19 FA complementation group C Homo sapiens 0-3 16706824-5 2006 RESULTS: In vitro growth of HAK-1B cells was suppressed dose-dependently to 5-FU, but the addition of IFN-alpha did not induce additional or synergic effects. Fluorouracil 76-80 alpha kinase 2 Homo sapiens 28-31 16706824-6 2006 In vivo growth in terms of tumor diameter and weight was suppressed at most in the IFN-alpha + 5-FU (combination) group, that is, the tumor volume became 29.3% and the tumor weight became 54.7% of the control. Fluorouracil 95-99 interferon alpha 1 Homo sapiens 83-92 16518803-14 2006 Also, GSH, GSH-Px, and SOD enzyme activities were significantly increased in the cyclophosphamide and 5-fluorouracil groups, compared to the other two antineoplastic agent groups (P < 0.01). Fluorouracil 102-116 glutathione peroxidase 1 Rattus norvegicus 11-17 16470928-5 2006 SGC-7901 cells with mutant p53 showed higher chemotherapeutic sensitivity to 5-Fu than that with mp53+sv40Tag and control (P<0.05), but no difference between those with mp53+sv40Tag and control (P>0.05). Fluorouracil 77-81 tumor protein p53 Homo sapiens 27-30 16332177-0 2005 Enhanced sensitivity of human hepatoma cells to 5-fluorouracil by small interfering RNA targeting Bcl-2. Fluorouracil 48-62 BCL2 apoptosis regulator Homo sapiens 98-103 16332177-1 2005 This study was designed to reveal whether the apoptosis induced in human hepatocellular carcinoma (HCC) cell lines by 5-fluorouracil (5-FU) could be enhanced by transfecting Bcl-2 small interfering RNA (siRNA). Fluorouracil 118-132 BCL2 apoptosis regulator Homo sapiens 174-179 16332177-1 2005 This study was designed to reveal whether the apoptosis induced in human hepatocellular carcinoma (HCC) cell lines by 5-fluorouracil (5-FU) could be enhanced by transfecting Bcl-2 small interfering RNA (siRNA). Fluorouracil 134-138 BCL2 apoptosis regulator Homo sapiens 174-179 16332177-2 2005 Bcl-2 siRNA and control siRNA were transfected into cells following treatment with or without 5-FU. Fluorouracil 94-98 BCL2 apoptosis regulator Homo sapiens 0-5 16332177-5 2005 Incubation of all cell lines with Bcl-2 siRNA reduced cell viability 96 h after 5-FU treatment compared with all other controls: Huh-7 (P < 0.01), Huh-7 with hepatitis C replicon (P < 0.01), HepG2 (P < 0.01), HLE (P < 0.05). Fluorouracil 80-84 BCL2 apoptosis regulator Homo sapiens 34-39 16332177-7 2005 The Bcl-2 siRNA prior to 5-FU treatment group showed the strongest effect of inducing apoptosis. Fluorouracil 25-29 BCL2 apoptosis regulator Homo sapiens 4-9 16471319-4 2005 Apoptosis of HepG2 cells exposed to hypoxia or transfected by plasmid pcDNA3/HIF-1alpha was detected by Flow Cytometry after administration of chemotherapeutic drug (5-Fu). Fluorouracil 166-170 hypoxia inducible factor 1 subunit alpha Homo sapiens 77-87 16471319-9 2005 Apoptosis index of HIF-1alpha transfected cells was obviously less than that of control cells when they were simultaneously exposed to 5-Fu for 24hrs. Fluorouracil 135-139 hypoxia inducible factor 1 subunit alpha Homo sapiens 19-29 16406507-0 2006 Phase I study of the thrombospondin-1-mimetic angiogenesis inhibitor ABT-510 with 5-fluorouracil and leucovorin: a safe combination. Fluorouracil 82-96 thrombospondin 1 Homo sapiens 21-37 16875599-0 2006 [Bcl-XL antisense oligodeoxynucleotide sensitizes human esophageal cancer cell line to 5-fluorouracil]. Fluorouracil 87-101 BCL2 like 1 Homo sapiens 1-7 16875599-3 2006 RESULTS: In the group of ASODN combined with 5-Fu, the proliferation inhibitory rate of esophageal cancer cells was 71.58%, the expression inhibitory rate of Bcl-XL mRNA was 81.25%, the expression of Bcl-XL protein was decreased significantly. Fluorouracil 45-49 BCL2 like 1 Homo sapiens 200-206 16875599-7 2006 Bcl-XL ASODN can significantly increase the sensitivity of esophageal cancer cells to 5-Fu through suppressing the expression of Bcl-XL. Fluorouracil 86-90 BCL2 like 1 Homo sapiens 0-6 16875599-7 2006 Bcl-XL ASODN can significantly increase the sensitivity of esophageal cancer cells to 5-Fu through suppressing the expression of Bcl-XL. Fluorouracil 86-90 BCL2 like 1 Homo sapiens 129-135 16391804-8 2006 Microarray analysis revealed that expressions of some apoptosis related genes such as Bcl-2 changed, and were correlated with sequence-dependent cytotoxicity of the 5-FU --> CPT-11 sequence. Fluorouracil 165-169 BCL2 apoptosis regulator Homo sapiens 86-91 16603448-0 2006 Bcl-2 siRNA induced apoptosis and increased sensitivity to 5-fluorouracil and HCPT in HepG2 cells. Fluorouracil 59-73 BCL2 apoptosis regulator Homo sapiens 0-5 16603448-7 2006 Accordingly, Bax protein expression had no change and caspase-3 protein expression showed significantly be up regulated; (2) MTT results showed that Bcl-2 siRNA transfectants had higher cell inhibitory rates after treated with 5-FU or HCPT; (3) flow cytometry results demonstrated that sub G1 population increased in Bcl-2 siRNA transfected cells compared with negative siRNA or untreated cells. Fluorouracil 227-231 BCL2 apoptosis regulator Homo sapiens 149-154 16603448-8 2006 After addition 5-FU (1300 mg/l) and HCPT (0.72 mg/l), Bcl-2 siRNA cells showed higher sub G1 population than negative siRNA or untreated cells. Fluorouracil 15-19 BCL2 apoptosis regulator Homo sapiens 54-59 16603448-9 2006 siRNA targeting Bcl-2 gene can specifically down-regulate Bcl-2 expression, increased Bax/Bcl-2 ratio expression and caspase-3 activity in HepG2 cells, which lead to increase cells spontaneous apoptosis and sensitize cells to 5-FU or HCPT. Fluorouracil 226-230 BCL2 apoptosis regulator Homo sapiens 16-21 17219956-9 2006 After HIF-1alpha being transfected into A549, the activity of MDR-1 was increased and the effect of 5-Fu was weakened. Fluorouracil 100-104 hypoxia inducible factor 1 subunit alpha Homo sapiens 6-16 17219956-10 2006 In conclusion, HIF-1alpha can promote chemoresistance by increasing the activation of MDRI and suppressing apoptosis during lung cancer cells A549 induced with 5-Fu. Fluorouracil 160-164 hypoxia inducible factor 1 subunit alpha Homo sapiens 15-25 16253763-6 2005 In conclusion, PEPT1 expressed in MKN45 cells are resistant against the cellular injury induced by 5-fluorouracil and cisplatin. Fluorouracil 99-113 solute carrier family 15 member 1 Homo sapiens 15-20 16047145-10 2005 There was a significant reduction of 5-FU Cmax in plasma the second day of treatment if vasopressin was used (3.4+/-2.5 and 6.1+/-5.4 mumol/l, respectively, p<0.05). Fluorouracil 37-41 arginine vasopressin Homo sapiens 88-99 16369751-12 2005 S-1 may be administered safely to patients with 5-FU-induced cardiotoxicity. Fluorouracil 48-52 proteasome 26S subunit, non-ATPase 1 Homo sapiens 0-3 16373718-7 2005 In addition, treatment of a 5-FU-resistant cell line with 5-FU down-regulated c-FLIP expression and sensitized the chemotherapy-resistant cell line to rTRAIL. Fluorouracil 28-32 CASP8 and FADD like apoptosis regulator Homo sapiens 78-84 16373718-7 2005 In addition, treatment of a 5-FU-resistant cell line with 5-FU down-regulated c-FLIP expression and sensitized the chemotherapy-resistant cell line to rTRAIL. Fluorouracil 58-62 CASP8 and FADD like apoptosis regulator Homo sapiens 78-84 16373718-2 2005 We assessed the roles of p53, TRAIL receptors, and cellular Fas-associated death domain-like interleukin-1beta-converting enzyme inhibitory protein (c-FLIP) in regulating the cytotoxic effects of recombinant TRAIL (rTRAIL) alone and in combination with chemotherapy [5-fluorouracil (5-FU), oxaliplatin, and irinotecan] in a panel of colon cancer cell lines. Fluorouracil 283-287 CASP8 and FADD like apoptosis regulator Homo sapiens 149-155 15900596-8 2005 When the chemotherapeutic sensibilities of these patients were studied in an MTT assay, it was found that the activated AKT was associated with increased resistance to multiple chemotherapeutic agents (5-fluorouracil, adriamycin, mitomycin C and cis-platinum). Fluorouracil 202-216 AKT serine/threonine kinase 1 Homo sapiens 120-123 16243820-4 2005 RNA expression levels of 5-FU metabolism-associated genes thymidylate synthase, thymidine phosphorylase, dihydropyrimidine dehydrogenase, methylenetetrahydrofolate reductase, MAP7, and ELF3, of platinum- and taxane-related genes caldesmon, ERCC1, ERCC4, HER-2/neu, and GADD45, and of multidrug resistance gene MRP1 were determined using real-time reverse transcriptase-PCR. Fluorouracil 25-29 caldesmon 1 Homo sapiens 229-238 16224030-0 2005 5-Fluorouracil infusion reduces gut-associated lymphoid tissue cell number and mucosal immunoglobulin A levels. Fluorouracil 0-14 CD79A antigen (immunoglobulin-associated alpha) Mus musculus 87-103 16224030-8 2005 Intestinal and respiratory tract IgA levels were lower in the 5-FU than in the control group. Fluorouracil 62-66 CD79A antigen (immunoglobulin-associated alpha) Mus musculus 33-36 16224030-9 2005 CONCLUSIONS: A small dose of 5-FU reduces GALT cell number and mucosal IgA levels, regardless of food intake. Fluorouracil 29-33 CD79A antigen (immunoglobulin-associated alpha) Mus musculus 71-74 16277025-0 2005 Enhancement of the efficacy of chemotherapy with oxaliplatin plus 5-fluorouracil by pretreatment with IL-2 subcutaneous immunotherapy in metastatic colorectal cancer patients with lymphocytopenia prior to therapy. Fluorouracil 66-80 interleukin 2 Homo sapiens 102-106 16213483-11 2005 In vitro rosiglitazone enhanced the survival of both murine progenitor and human mobilized blood stem cells in the presence of 5-fluorouracil, the effect of which was neutralized by a peroxisome-proliferator-activated receptor-gamma antagonist. Fluorouracil 127-141 peroxisome proliferator activated receptor gamma Homo sapiens 184-232 16243822-9 2005 In contrast to oxaliplatin, 5-FU treatment increased EGFR phosphorylation in all cell lines and this correlated with synergistic decreases in cell viability when 5-FU was combined with gefitinib. Fluorouracil 28-32 epidermal growth factor receptor Homo sapiens 53-57 16243822-9 2005 In contrast to oxaliplatin, 5-FU treatment increased EGFR phosphorylation in all cell lines and this correlated with synergistic decreases in cell viability when 5-FU was combined with gefitinib. Fluorouracil 162-166 epidermal growth factor receptor Homo sapiens 53-57 16243820-4 2005 RNA expression levels of 5-FU metabolism-associated genes thymidylate synthase, thymidine phosphorylase, dihydropyrimidine dehydrogenase, methylenetetrahydrofolate reductase, MAP7, and ELF3, of platinum- and taxane-related genes caldesmon, ERCC1, ERCC4, HER-2/neu, and GADD45, and of multidrug resistance gene MRP1 were determined using real-time reverse transcriptase-PCR. Fluorouracil 25-29 erb-b2 receptor tyrosine kinase 2 Homo sapiens 254-263 16204068-2 2005 We found that 5-fluorouracil (5-FU) and oxaliplatin only sensitized p53 wild-type (WT) colorectal cancer cell lines to Fas-mediated apoptosis. Fluorouracil 14-28 tumor protein p53 Homo sapiens 68-71 16204068-2 2005 We found that 5-fluorouracil (5-FU) and oxaliplatin only sensitized p53 wild-type (WT) colorectal cancer cell lines to Fas-mediated apoptosis. Fluorouracil 30-34 tumor protein p53 Homo sapiens 68-71 16315867-6 2005 Radiation and 5-FU induce Th1-dominant state by inhibiting the OK-432-induced production of IL-10 and TGF-beta mediated by regulation of SOCS-1 and SOCS-3 expression, and are suggested to increase anti-cancer immunity. Fluorouracil 14-18 transforming growth factor beta 1 Homo sapiens 102-110 16315942-1 2005 PURPOSE: We report two patients with refractory recurrent breast cancer (HER2/neu: +) postoperatively, who had failed response to the available conventional chemotherapy of CAF (cyclophosphamide, adriamycin, 5-fluorouracil) and docetaxel, etc. Fluorouracil 208-222 erb-b2 receptor tyrosine kinase 2 Homo sapiens 73-77 16315867-0 2005 [Radiation, 5-FU and OK-432: inhibitory effect of IL-10 and TGF-beta]. Fluorouracil 12-16 transforming growth factor beta 1 Homo sapiens 60-68 16315867-3 2005 When the PBMCs were stimulated by 5-FU (5 microg/ml) or X-ray (2 Gy) simultaneously with OK-432, production of IL-10 and TGF-beta was significantly inhibited, while no significant change in Th1 cytokine production was observed. Fluorouracil 34-38 transforming growth factor beta 1 Homo sapiens 121-129 16101138-5 2005 Among them, three IFN-related genes, an IFN receptor gene (IFNAR2) and two IFN-stimulated genes (ISG15K, ISG-54K), that were up-regulated following addition of 5-FU, were investigated. Fluorouracil 160-164 interferon alpha 1 Homo sapiens 18-21 16145059-0 2005 Just when you thought the fluorouracil debate was over: S-1 and gastric cancer. Fluorouracil 26-38 proteasome 26S subunit, non-ATPase 1 Homo sapiens 56-59 16149157-1 2005 We report a case of hepatocellular carcinoma (HCC) treated successfully by transarterial chemoembolization (TACE) followed by combination therapy of 5-fluorouracil (5-FU) and pegylated interferon-alpha (PEG-IFN-alpha). Fluorouracil 149-163 interferon alpha 1 Homo sapiens 207-216 16149157-1 2005 We report a case of hepatocellular carcinoma (HCC) treated successfully by transarterial chemoembolization (TACE) followed by combination therapy of 5-fluorouracil (5-FU) and pegylated interferon-alpha (PEG-IFN-alpha). Fluorouracil 165-169 interferon alpha 1 Homo sapiens 207-216 16149157-6 2005 Although it has been reported that the combined use of conventional IFN-alpha and 5-FU showed striking effects on HCC in some cases, this case may suggest the more promising effect of PEG-IFN-alpha with a long-lasting effect, in the combined use with 5-FU for the treatment of massive advanced HCC. Fluorouracil 251-255 interferon alpha 1 Homo sapiens 68-77 16149157-6 2005 Although it has been reported that the combined use of conventional IFN-alpha and 5-FU showed striking effects on HCC in some cases, this case may suggest the more promising effect of PEG-IFN-alpha with a long-lasting effect, in the combined use with 5-FU for the treatment of massive advanced HCC. Fluorouracil 251-255 interferon alpha 1 Homo sapiens 188-197 16101138-5 2005 Among them, three IFN-related genes, an IFN receptor gene (IFNAR2) and two IFN-stimulated genes (ISG15K, ISG-54K), that were up-regulated following addition of 5-FU, were investigated. Fluorouracil 160-164 interferon alpha 1 Homo sapiens 40-43 16101138-8 2005 The growth of esophageal SCC cells with 5-FU was suppressed synergistically or semi-additively by IFN-alpha and -beta, but not by IFN-gamma. Fluorouracil 40-44 interferon alpha 1 Homo sapiens 98-117 16101138-9 2005 These findings indicated that 5-FU stimulated IFN pathways in esophageal SCC cells following up-regulation of the IFN type I receptor. Fluorouracil 30-34 interferon alpha 1 Homo sapiens 46-49 16101138-9 2005 These findings indicated that 5-FU stimulated IFN pathways in esophageal SCC cells following up-regulation of the IFN type I receptor. Fluorouracil 30-34 interferon alpha 1 Homo sapiens 114-117 16323444-7 2005 Treatment of esophageal cancer cells with 5-Fu and cisplatin induced NF-kappaB and AP-1 activation. Fluorouracil 42-46 JunB proto-oncogene, AP-1 transcription factor subunit Homo sapiens 83-87 16323444-9 2005 Vitamin C also inhibited 5-Fu- and cisplatin-induced AP-1 activation. Fluorouracil 25-29 JunB proto-oncogene, AP-1 transcription factor subunit Homo sapiens 53-57 16323444-10 2005 Our data demonstrate that vitamin C enhances the antitumor activity of 5-Fu and cisplatin, in part by inhibiting translocation of NF-kappaB and AP-1, and sensitizes cancer cells to drug-induced cell death. Fluorouracil 71-75 JunB proto-oncogene, AP-1 transcription factor subunit Homo sapiens 144-148 16202244-3 2005 Here we showed that etoposide can induce the similar degree of cell death in p53-deficient HCT 116 cells, whereas 5"-FU-mediated cell death is strongly dependent on the existence of functional p53 in HCT 116 cells. Fluorouracil 114-119 tumor protein p53 Homo sapiens 193-196 16101138-5 2005 Among them, three IFN-related genes, an IFN receptor gene (IFNAR2) and two IFN-stimulated genes (ISG15K, ISG-54K), that were up-regulated following addition of 5-FU, were investigated. Fluorouracil 160-164 interferon alpha 1 Homo sapiens 40-43 16184937-0 2005 [A case of colon cancer with liver and lung metastases-efficacy of CPT-11/5-FU/l-LV (IFL) as part of ambulatory treatment]. Fluorouracil 74-78 interferon alpha 1 Homo sapiens 85-88 16101140-2 2005 PATIENTS AND METHODS: The impact of gemcitabine, irinotecan and oxaliplatin + 5-FU upon the serum markers vascular endothelial growth factor (VEGF) (pro-angiogenic) and IFN-gamma-inducible protein (IP)-10 (anti-angiogenic) was evaluated by ELISA in locally advanced and/or metastatic cancer versus clinical efficacy and survival. Fluorouracil 78-82 vascular endothelial growth factor A Homo sapiens 106-140 16101140-2 2005 PATIENTS AND METHODS: The impact of gemcitabine, irinotecan and oxaliplatin + 5-FU upon the serum markers vascular endothelial growth factor (VEGF) (pro-angiogenic) and IFN-gamma-inducible protein (IP)-10 (anti-angiogenic) was evaluated by ELISA in locally advanced and/or metastatic cancer versus clinical efficacy and survival. Fluorouracil 78-82 vascular endothelial growth factor A Homo sapiens 142-146 16184937-2 2005 Hepatic intraarterial injection therapy with 5-FU/CDDP was not only ineffective against a liver metastasis but a lung metastasis was also found, and therefore systemic chemotherapy with CPT-11/5-FU/l-LV (IFL) was administered. Fluorouracil 45-49 interferon alpha 1 Homo sapiens 204-207 15975592-10 2005 The plasma endotoxin, tumor necrosis factor-alpha and interleukin-6 levels in the 5-FU and GM-CSF groups were significantly increased at day 7 compared with the control groups (P < 0.01), but these levels were significantly lower in the GM-CSF group compared to the 5-FU group (P < 0.01). Fluorouracil 82-86 tumor necrosis factor Rattus norvegicus 11-49 16037944-7 2005 In contrast to the previously reported mechanism of sensitization by 5-fluorouracil (5-FU), cellular FLICE-inhibitory protein (cFLIP)(L) and cFLIP(S) were markedly upregulated in the TRAIL death inducing signaling complex (DISC) by proteasome inhibitor pretreatment. Fluorouracil 69-83 TNF superfamily member 10 Homo sapiens 183-188 16270526-2 2005 In this study, we sought to determine the potential effect of hRFI expression on the sensitivity to 5-fluorouracil (5-FU) and/or other fluoropyrimidines. Fluorouracil 100-114 ring finger protein 34 Homo sapiens 62-66 16270526-2 2005 In this study, we sought to determine the potential effect of hRFI expression on the sensitivity to 5-fluorouracil (5-FU) and/or other fluoropyrimidines. Fluorouracil 116-120 ring finger protein 34 Homo sapiens 62-66 16270526-3 2005 For the whole lysates of 8 colon cancer cell lines, we performed Western blotting with anti-hRFI antibody and analyzed the correlations between the expression level of hRFI and the cell lines" sensitivity to 5-FU induced apoptosis. Fluorouracil 208-212 ring finger protein 34 Homo sapiens 168-172 16270526-5 2005 Both in colon cancer cell lines and in xenografts, the expression level of hRFI was correlated with resistance to 5-FU and its derivatives. Fluorouracil 114-118 ring finger protein 34 Homo sapiens 75-79 16270526-6 2005 This evidence suggests that hRFI may be a marker predicting the response to fluorouracil derived chemotherapeutic agents and that the reduction of the expression level of hRFI might improve the outcome of chemotherapy. Fluorouracil 76-88 ring finger protein 34 Homo sapiens 28-32 16118771-1 2005 BACKGROUND: Bevacizumab (Avastin; rhuMab VEGF), a humanized monoclonal antibody against vascular endothelial growth factor (VEGF), significantly prolongs survival when added to intravenous 5-fluorouracil-based chemotherapy in first-line metastatic colorectal cancer (CRC) treatment. Fluorouracil 189-203 vascular endothelial growth factor A Homo sapiens 41-45 16118771-1 2005 BACKGROUND: Bevacizumab (Avastin; rhuMab VEGF), a humanized monoclonal antibody against vascular endothelial growth factor (VEGF), significantly prolongs survival when added to intravenous 5-fluorouracil-based chemotherapy in first-line metastatic colorectal cancer (CRC) treatment. Fluorouracil 189-203 vascular endothelial growth factor A Homo sapiens 88-122 15975592-10 2005 The plasma endotoxin, tumor necrosis factor-alpha and interleukin-6 levels in the 5-FU and GM-CSF groups were significantly increased at day 7 compared with the control groups (P < 0.01), but these levels were significantly lower in the GM-CSF group compared to the 5-FU group (P < 0.01). Fluorouracil 82-86 interleukin 6 Rattus norvegicus 54-67 16118771-1 2005 BACKGROUND: Bevacizumab (Avastin; rhuMab VEGF), a humanized monoclonal antibody against vascular endothelial growth factor (VEGF), significantly prolongs survival when added to intravenous 5-fluorouracil-based chemotherapy in first-line metastatic colorectal cancer (CRC) treatment. Fluorouracil 189-203 vascular endothelial growth factor A Homo sapiens 124-128 15975592-10 2005 The plasma endotoxin, tumor necrosis factor-alpha and interleukin-6 levels in the 5-FU and GM-CSF groups were significantly increased at day 7 compared with the control groups (P < 0.01), but these levels were significantly lower in the GM-CSF group compared to the 5-FU group (P < 0.01). Fluorouracil 269-273 tumor necrosis factor Rattus norvegicus 11-49 19956517-0 2005 Thymidylate synthase, thymidine phosphorylase, VEGF and p53 protein expression in primary colorectal cancer for predicting response to 5-fluorouracil-based chemotherapy. Fluorouracil 135-149 tumor protein p53 Homo sapiens 56-59 16077963-0 2005 The evaluation of gastric cancer sensitivity to 5-FU/CDDP in terms of induction of apoptosis: time- and p53 expression-dependency of anti-cancer drugs. Fluorouracil 48-52 tumor protein p53 Homo sapiens 104-107 15856005-2 2005 Here, we demonstrate that FGF-2 is also a potent stimulator of breast cancer cell survival, as it counteracts the apoptotic activity of the C2 ceramide analogue and various chemotherapeutic agents (5-fluorouracil, camptothecin, etoposide) in MCF-7, T47-D and BT-20 cells. Fluorouracil 198-212 fibroblast growth factor 2 Homo sapiens 26-31 19956517-3 2005 The expression levels of thymidylate synthase (TS), thymidine phosphorylase (TP) and p53 have been known to be associated with the clinical response to 5-FU-based therapy as well as the prognosis, and that of vascular endothelial growth factor (VEGF) is associated with poor survival. Fluorouracil 152-156 tumor protein p53 Homo sapiens 85-88 19956517-3 2005 The expression levels of thymidylate synthase (TS), thymidine phosphorylase (TP) and p53 have been known to be associated with the clinical response to 5-FU-based therapy as well as the prognosis, and that of vascular endothelial growth factor (VEGF) is associated with poor survival. Fluorouracil 152-156 vascular endothelial growth factor A Homo sapiens 209-243 19956517-3 2005 The expression levels of thymidylate synthase (TS), thymidine phosphorylase (TP) and p53 have been known to be associated with the clinical response to 5-FU-based therapy as well as the prognosis, and that of vascular endothelial growth factor (VEGF) is associated with poor survival. Fluorouracil 152-156 vascular endothelial growth factor A Homo sapiens 245-249 19956523-5 2005 RESULTS: RhoA significantly enhanced the resistance to lovastatin, 5-FU, taxol and vincristine, but did not affect the sensitivity to cisplatin or etoposide in SNU638. Fluorouracil 67-71 ras homolog family member A Homo sapiens 9-13 16137437-0 2005 HER2 overexpression as a predictive marker in a randomized trial comparing adjuvant cyclophosphamide/methotrexate/5-fluorouracil with epirubicin in patients with stage I/II breast cancer: long-term results. Fluorouracil 114-128 erb-b2 receptor tyrosine kinase 2 Homo sapiens 0-4 16026610-6 2005 RESULTS: In 8/16 paired esophageal biopsies, there was an increase in the expression of multi-drug resistance gene 1 (MDR1) following epirubicin + cisplatin + 5-fluorouracil (ECF) chemotherapy and this was accompanied by increased expression of the MDR-1 encoded protein, P-gp. Fluorouracil 159-173 ATP binding cassette subfamily B member 1 Homo sapiens 88-116 16041207-3 2005 The aim of this study was to investigate the efficacy of modulating 5-FU+ LEV by either FA or IFN-alpha in the adjuvant treatment of high-risk colon cancer. Fluorouracil 68-72 interferon alpha 1 Homo sapiens 94-103 15967383-0 2005 Combined effects of protein kinase inhibitors and 5-fluorouracil on CEA expression in human colon cancer cells. Fluorouracil 50-64 CEA cell adhesion molecule 3 Homo sapiens 68-71 15967383-1 2005 Previous studies showed that 5-fluorouracil (5-FU) and Staurosporine (ST), a protein kinase inhibitor (PKI), were able to increase the expression of carcinoembryonic antigen (CEA) in human colon cancer cells. Fluorouracil 29-43 CEA cell adhesion molecule 3 Homo sapiens 149-173 15967383-1 2005 Previous studies showed that 5-fluorouracil (5-FU) and Staurosporine (ST), a protein kinase inhibitor (PKI), were able to increase the expression of carcinoembryonic antigen (CEA) in human colon cancer cells. Fluorouracil 29-43 CEA cell adhesion molecule 3 Homo sapiens 175-178 15967383-1 2005 Previous studies showed that 5-fluorouracil (5-FU) and Staurosporine (ST), a protein kinase inhibitor (PKI), were able to increase the expression of carcinoembryonic antigen (CEA) in human colon cancer cells. Fluorouracil 45-49 CEA cell adhesion molecule 3 Homo sapiens 149-173 15967383-1 2005 Previous studies showed that 5-fluorouracil (5-FU) and Staurosporine (ST), a protein kinase inhibitor (PKI), were able to increase the expression of carcinoembryonic antigen (CEA) in human colon cancer cells. Fluorouracil 45-49 CEA cell adhesion molecule 3 Homo sapiens 175-178 15967383-6 2005 Flow cytometric analysis showed that treatment of cells with 5-FU + ST resulted in a synergistic increase of CEA expression, being higher than that obtainable with both agents alone. Fluorouracil 61-65 CEA cell adhesion molecule 3 Homo sapiens 109-112 16026610-6 2005 RESULTS: In 8/16 paired esophageal biopsies, there was an increase in the expression of multi-drug resistance gene 1 (MDR1) following epirubicin + cisplatin + 5-fluorouracil (ECF) chemotherapy and this was accompanied by increased expression of the MDR-1 encoded protein, P-gp. Fluorouracil 159-173 ATP binding cassette subfamily B member 1 Homo sapiens 118-122 16026610-6 2005 RESULTS: In 8/16 paired esophageal biopsies, there was an increase in the expression of multi-drug resistance gene 1 (MDR1) following epirubicin + cisplatin + 5-fluorouracil (ECF) chemotherapy and this was accompanied by increased expression of the MDR-1 encoded protein, P-gp. Fluorouracil 159-173 ATP binding cassette subfamily B member 1 Homo sapiens 249-254 15942645-6 2005 Overexpression of p21cip1/waf1 caused an appreciable growth inhibition in monolayer and soft agar cultures and it significantly reduced sodium butyrate- but not 5-fluorouracil-induced apoptosis. Fluorouracil 161-175 cyclin dependent kinase inhibitor 1A Homo sapiens 18-25 15817675-6 2005 However, after 5-fluorouracil (5-FU) treatment, there was a rapid increase in plasma vascular endothelial growth factor A (VEGF-A) levels and expansion of Tie2-positive neovessels. Fluorouracil 15-29 TEK receptor tyrosine kinase Mus musculus 155-159 15817675-6 2005 However, after 5-fluorouracil (5-FU) treatment, there was a rapid increase in plasma vascular endothelial growth factor A (VEGF-A) levels and expansion of Tie2-positive neovessels. Fluorouracil 31-35 TEK receptor tyrosine kinase Mus musculus 155-159 16080558-4 2005 RESULTS: The response rate was significantly higher in patients with DPD-positive tumors than in those with DPD-negative tumors in the S-1 group (45.5%, 10.0%: p < 0.05), as compared to the 5-FU group (0%, 5.6%: p = 0.398). Fluorouracil 193-197 proteasome 26S subunit, non-ATPase 1 Homo sapiens 135-138 15896711-0 2005 Combination of 5-fluorouracil and genistein induces apoptosis synergistically in chemo-resistant cancer cells through the modulation of AMPK and COX-2 signaling pathways. Fluorouracil 15-29 prostaglandin-endoperoxide synthase 2 Homo sapiens 145-150 15896711-5 2005 The present study focused on the correlation of AMPK and COX-2 in combined cytotoxicity of 5-FU and genistein, since AMPK is known as a primary cellular homeostasis regulator and a possible target molecule of cancer treatment, and COX-2 as cell proliferation and anti-apoptotic molecule. Fluorouracil 91-95 prostaglandin-endoperoxide synthase 2 Homo sapiens 57-62 15896711-5 2005 The present study focused on the correlation of AMPK and COX-2 in combined cytotoxicity of 5-FU and genistein, since AMPK is known as a primary cellular homeostasis regulator and a possible target molecule of cancer treatment, and COX-2 as cell proliferation and anti-apoptotic molecule. Fluorouracil 91-95 prostaglandin-endoperoxide synthase 2 Homo sapiens 231-236 15896711-6 2005 Our results demonstrated that the combination of 5-FU and genistein abolished the up-regulated state of COX-2 and prostaglandin secretion caused by 5-FU treatment in HT-29 colon cancer cells. Fluorouracil 49-53 prostaglandin-endoperoxide synthase 2 Homo sapiens 104-109 15896711-6 2005 Our results demonstrated that the combination of 5-FU and genistein abolished the up-regulated state of COX-2 and prostaglandin secretion caused by 5-FU treatment in HT-29 colon cancer cells. Fluorouracil 148-152 prostaglandin-endoperoxide synthase 2 Homo sapiens 104-109 16531325-8 2005 Cx43 expression in Cx43-/- BM was markedly reduced (> 90%) as analyzed on day +14 post-5-FU treatment. Fluorouracil 90-94 gap junction protein, alpha 1 Mus musculus 0-4 16531325-8 2005 Cx43 expression in Cx43-/- BM was markedly reduced (> 90%) as analyzed on day +14 post-5-FU treatment. Fluorouracil 90-94 gap junction protein, alpha 1 Mus musculus 19-23 16008516-8 2005 Our data further show that 5-FU upregulates serum levels of IL-6, known to contribute to weight loss, in tumor-free mice, and that this increase in IL-6 is significantly less in mice that received Bing De Ling in addition to 5-FU. Fluorouracil 27-31 interleukin 6 Mus musculus 60-64 15942645-6 2005 Overexpression of p21cip1/waf1 caused an appreciable growth inhibition in monolayer and soft agar cultures and it significantly reduced sodium butyrate- but not 5-fluorouracil-induced apoptosis. Fluorouracil 161-175 cyclin dependent kinase inhibitor 1A Homo sapiens 26-30 15944764-1 2005 The purposes of this study were to evaluate the antitumor activity of S-1 (1 M tegafur, 0.4 M 5-chloro-2,4-dihydroxypyridine and 1 M potassium oxonate) on human lung tumor xenografts, as compared with other fluoro-pyrimidines, and to investigate the relationships between fluoropyrimidine antitumor activities and four distinct enzymatic activities involved in the phosphorylation and degradation pathways of 5-fluorouracil (5-FU) metabolism. Fluorouracil 409-423 proteasome 26S subunit, non-ATPase 1 Homo sapiens 70-73 15944764-1 2005 The purposes of this study were to evaluate the antitumor activity of S-1 (1 M tegafur, 0.4 M 5-chloro-2,4-dihydroxypyridine and 1 M potassium oxonate) on human lung tumor xenografts, as compared with other fluoro-pyrimidines, and to investigate the relationships between fluoropyrimidine antitumor activities and four distinct enzymatic activities involved in the phosphorylation and degradation pathways of 5-fluorouracil (5-FU) metabolism. Fluorouracil 425-429 proteasome 26S subunit, non-ATPase 1 Homo sapiens 70-73 15930305-1 2005 FdUMP[10], a 10mer of 5-fluoro-2"-deoxyuridine 5"-monophosphate (FdUMP), the thymidylate synthase inhibitory metabolite of 5-fluorouracil (FU), is most closely correlated with the DNA topoisomerase I (Top1) inhibitor camptothecin in the National Cancer Institute COMPARE analysis, but not with FU. Fluorouracil 123-137 topoisomerase (DNA) I Mus musculus 180-199 15856026-12 2005 Downregulation of BNIP3 resulted in increased resistance to 5-fluoro-uracil and gemcitabine. Fluorouracil 60-75 BCL2 interacting protein 3 Homo sapiens 18-23 15856030-6 2005 Using isogenic colon cancer cell lines that differ only by the presence of the mutant Ras allele, HCT116 and Hke-3 cells, we demonstrated that signaling by oncogenic Ras promotes both accumulation of p53 and its phosphorylation on serine15 in response to 5-FU, a situation that favors apoptosis over growth arrest. Fluorouracil 255-259 tumor protein p53 Homo sapiens 200-203 15846114-0 2005 Rapid up-regulation of cyclooxygenase-2 by 5-fluorouracil in human solid tumors. Fluorouracil 43-57 prostaglandin-endoperoxide synthase 2 Homo sapiens 23-39 15846114-3 2005 COX-2 expression was measured by quantitative RT-PCR in biopsies from a series of 14 esophageal carcinomas, six of which had paired samples taken before and after chemotherapy, and in tumor-derived cells exposed to 5-FU in vitro from a series of 44 tumors, including breast, ovarian, esophageal and colonic carcinomas. Fluorouracil 215-219 mitochondrially encoded cytochrome c oxidase II Homo sapiens 0-5 15846114-4 2005 COX-2 expression was increased by exposure to 5-FU or 5-FU combination chemotherapy in all the tumor types studied, whether measured in biopsies taken before and after 5-FU-based chemotherapy (4-fold increase, p<0.015) or in primary cells exposed to drugs in vitro (24-fold increase, p<0.001). Fluorouracil 46-50 mitochondrially encoded cytochrome c oxidase II Homo sapiens 0-5 15846114-4 2005 COX-2 expression was increased by exposure to 5-FU or 5-FU combination chemotherapy in all the tumor types studied, whether measured in biopsies taken before and after 5-FU-based chemotherapy (4-fold increase, p<0.015) or in primary cells exposed to drugs in vitro (24-fold increase, p<0.001). Fluorouracil 54-58 mitochondrially encoded cytochrome c oxidase II Homo sapiens 0-5 15846114-4 2005 COX-2 expression was increased by exposure to 5-FU or 5-FU combination chemotherapy in all the tumor types studied, whether measured in biopsies taken before and after 5-FU-based chemotherapy (4-fold increase, p<0.015) or in primary cells exposed to drugs in vitro (24-fold increase, p<0.001). Fluorouracil 54-58 mitochondrially encoded cytochrome c oxidase II Homo sapiens 0-5 15916744-10 2005 After the treatment with Cantide alone or combined with 5-fluorouracil, plasma AFP concentration decreased in a dose-dependent manner. Fluorouracil 56-70 alpha fetoprotein Homo sapiens 79-82 15986848-7 2005 Cells treated with ASA, both alone and in combination with 5-FU, demonstrated apoptotic activity with the up-regulation of Bax protein, which is consistent with 5-FU anticancer treatment. Fluorouracil 59-63 BCL2 associated X, apoptosis regulator Homo sapiens 123-126 15886465-5 2005 The expression of p53 protein was increased after treatment with cisplatin and 5-FU, but not radiation. Fluorouracil 79-83 tumor protein p53 Homo sapiens 18-21 15914960-1 2005 BACKGROUND: Myelosuppressives such as cyclophosphamide (Cy) and 5-fluorouracil (5FU), which can increase circulating CD34+ cells, may have a beneficial effect in the post-infarct heart. Fluorouracil 64-78 hematopoietic progenitor cell antigen CD34 Oryctolagus cuniculus 117-121 15914960-1 2005 BACKGROUND: Myelosuppressives such as cyclophosphamide (Cy) and 5-fluorouracil (5FU), which can increase circulating CD34+ cells, may have a beneficial effect in the post-infarct heart. Fluorouracil 80-83 hematopoietic progenitor cell antigen CD34 Oryctolagus cuniculus 117-121 15849826-1 2005 AIM: To study the anti-hepatocarcinoma effects of 5-fluorouracil (5-Fu) encapsulated by galactosylceramide liposomes (5-Fu-GCL) in vivo and in vitro. Fluorouracil 50-64 germ cell-less, spermatogenesis associated 1 Mus musculus 123-126 15849826-1 2005 AIM: To study the anti-hepatocarcinoma effects of 5-fluorouracil (5-Fu) encapsulated by galactosylceramide liposomes (5-Fu-GCL) in vivo and in vitro. Fluorouracil 66-70 germ cell-less, spermatogenesis associated 1 Mus musculus 123-126 15849826-1 2005 AIM: To study the anti-hepatocarcinoma effects of 5-fluorouracil (5-Fu) encapsulated by galactosylceramide liposomes (5-Fu-GCL) in vivo and in vitro. Fluorouracil 118-122 germ cell-less, spermatogenesis associated 1 Mus musculus 123-126 15849826-2 2005 METHODS: Tumor-bearing animal model and HepA cell line were respectively adopted to evaluate the anti-tumor effects of 5-Fu-GCL in vivo and in vitro. Fluorouracil 119-123 germ cell-less, spermatogenesis associated 1 Mus musculus 124-127 15849826-3 2005 Tumor cell growth inhibition effects of 5-Fu-GCL in vitro were assessed by cell viability assay and MTT assay. Fluorouracil 40-44 germ cell-less, spermatogenesis associated 1 Mus musculus 45-48 15849826-5 2005 High performance liquid chromatography was used to detect the concentration-time course of 5-Fu-GCL in intracellular fluid in vitro and the distribution of 5-Fu-GCL in liver tumor tissues in vivo. Fluorouracil 91-95 germ cell-less, spermatogenesis associated 1 Mus musculus 96-99 15849826-5 2005 High performance liquid chromatography was used to detect the concentration-time course of 5-Fu-GCL in intracellular fluid in vitro and the distribution of 5-Fu-GCL in liver tumor tissues in vivo. Fluorouracil 156-160 germ cell-less, spermatogenesis associated 1 Mus musculus 161-164 15849826-7 2005 RESULTS: In vitro experiment, 5-Fu-GCL (6.25-100 micromol/L) and free 5-Fu significantly inhibited HepA cell growth. Fluorouracil 30-34 germ cell-less, spermatogenesis associated 1 Mus musculus 35-38 15849826-8 2005 Furthermore, IC50 of 5-Fu-GCL (34.5 micromol/L) was lower than that of free 5-Fu (51.2 micromol/L). Fluorouracil 21-25 germ cell-less, spermatogenesis associated 1 Mus musculus 26-29 15849826-9 2005 In vivo experiment, 5-Fu-GCL (20, 40, 80 mg/kg) significantly suppressed the tumor growth in HepA bearing mice model. Fluorouracil 20-24 germ cell-less, spermatogenesis associated 1 Mus musculus 25-28 15849826-10 2005 Compared with free 5-Fu, the area under curve of 5-Fu-GCL in intracellular fluid increased 2.6 times. Fluorouracil 19-23 germ cell-less, spermatogenesis associated 1 Mus musculus 54-57 15849826-10 2005 Compared with free 5-Fu, the area under curve of 5-Fu-GCL in intracellular fluid increased 2.6 times. Fluorouracil 49-53 germ cell-less, spermatogenesis associated 1 Mus musculus 54-57 15849826-11 2005 Similarly, the distribution of 5-Fu-GCL in liver tumor tissues was significantly higher than that of free 5-Fu. Fluorouracil 31-35 germ cell-less, spermatogenesis associated 1 Mus musculus 36-39 15849826-12 2005 After being treated with 5-Fu-GCL, the apoptotic rate and the proportion of HepA cells in the S phase increased, while the proportion in the G0/G1 and G2/M phases decreased. Fluorouracil 25-29 germ cell-less, spermatogenesis associated 1 Mus musculus 30-33 15849826-13 2005 CONCLUSION: 5-Fu-GCL appears to have anti-hepato-carcinoma effects and its drug action is better than free 5-Fu. Fluorouracil 12-16 germ cell-less, spermatogenesis associated 1 Mus musculus 17-20 15867225-2 2005 Recently, we reported that mGluR4 mediates 5-fluorouracil resistance in a human colon cancer cell line. Fluorouracil 43-57 glutamate receptor, ionotropic, AMPA4 (alpha 4) Mus musculus 27-33 15870870-0 2005 Apoptosis induced by 5-fluorouracil, cisplatin and paclitaxel are associated with p53 gene status in gastric cancer cell lines. Fluorouracil 21-35 tumor protein p53 Homo sapiens 82-85 15687373-2 2005 A three-step in vivo-targeted activation process requiring carboxylesterases, cytidine deaminase, and thymidine phosphorylase converts capecitabine to 5-fluorouracil. Fluorouracil 151-165 carboxylesterase 2 Homo sapiens 59-76 15750632-0 2005 YB-1 facilitates basal and 5-fluorouracil-inducible expression of the human major vault protein (MVP) gene. Fluorouracil 27-41 Y-box binding protein 1 Homo sapiens 0-4 15750632-4 2005 Treatment with 5-FU amplified the binding activity and interaction of the transcription factor Y-box binding protein-1 (YB-1) with the Y-box of the human MVP gene promoter in a time-dependent manner. Fluorouracil 15-19 Y-box binding protein 1 Homo sapiens 95-118 15750632-4 2005 Treatment with 5-FU amplified the binding activity and interaction of the transcription factor Y-box binding protein-1 (YB-1) with the Y-box of the human MVP gene promoter in a time-dependent manner. Fluorouracil 15-19 Y-box binding protein 1 Homo sapiens 120-124 15750632-6 2005 Interestingly, stably YB-1 overexpressing cell clones showed enhanced binding of YB-1 to the Y-box motif, associated with enhanced basal as well as 5-FU-inducible MVP promoter-driven reporter expressions. Fluorouracil 148-152 Y-box binding protein 1 Homo sapiens 22-26 15750632-9 2005 In summary, our data demonstrate a direct involvement of YB-1 in controlling basal and 5-FU-induced MVP promoter activity. Fluorouracil 87-91 Y-box binding protein 1 Homo sapiens 57-61 15902120-7 2005 Constitutive AKT levels are the lowest in cell lines that are the most resistant to CDDP, 5-FU, and radiation. Fluorouracil 90-94 AKT serine/threonine kinase 1 Homo sapiens 13-16 15786421-13 2005 CONCLUSIONS: STI571 was an effective chemosensitizer of antitumor drugs, such as 5-FU and paclitaxel for gastric carcinoma, targeting the PDGF/PDGFR-signaling pathway of tumor cells and stromal cells in disease progression and angiogenesis. Fluorouracil 81-85 platelet derived growth factor receptor beta Homo sapiens 143-148 15886465-6 2005 The expression of p21(WAF1/CIP1) protein was increased only after treatment with 5-FU, not cisplatin or radiation. Fluorouracil 81-85 cyclin dependent kinase inhibitor 1A Homo sapiens 18-21 15886465-6 2005 The expression of p21(WAF1/CIP1) protein was increased only after treatment with 5-FU, not cisplatin or radiation. Fluorouracil 81-85 cyclin dependent kinase inhibitor 1A Homo sapiens 22-31 15886465-10 2005 Cisplatin induced p53-dependent apoptosis and p21(WAF1/CIP1)-independent S-phase cell cycle arrest and 5-FU induced p53 and p21(WAF1/CIP1)-dependent G1-phase cell cycle arrest, not apoptosis. Fluorouracil 103-107 tumor protein p53 Homo sapiens 116-119 15886465-10 2005 Cisplatin induced p53-dependent apoptosis and p21(WAF1/CIP1)-independent S-phase cell cycle arrest and 5-FU induced p53 and p21(WAF1/CIP1)-dependent G1-phase cell cycle arrest, not apoptosis. Fluorouracil 103-107 cyclin dependent kinase inhibitor 1A Homo sapiens 124-127 15886465-10 2005 Cisplatin induced p53-dependent apoptosis and p21(WAF1/CIP1)-independent S-phase cell cycle arrest and 5-FU induced p53 and p21(WAF1/CIP1)-dependent G1-phase cell cycle arrest, not apoptosis. Fluorouracil 103-107 cyclin dependent kinase inhibitor 1A Homo sapiens 128-137 15886465-11 2005 Cisplatin and 5-FU induced p53-dependent pathways, but radiation p53-independent pathway. Fluorouracil 14-18 tumor protein p53 Homo sapiens 27-30 15886465-11 2005 Cisplatin and 5-FU induced p53-dependent pathways, but radiation p53-independent pathway. Fluorouracil 14-18 tumor protein p53 Homo sapiens 65-68 15774934-13 2005 p53 as an antiproliferative drug has the potential to replace mitomycin C and 5-fluorouracil in glaucoma surgery. Fluorouracil 78-92 tumor protein p53 Homo sapiens 0-3 15850837-4 2005 METHODS: TbetaRI null and control bone marrow chimeras were subjected to repeated treatments with the cell cycle-specific cytotoxic drug 5-fluorouracil (5-FU) and surviving HSCs were assayed by competitive transplantation experiments. Fluorouracil 137-151 transforming growth factor, beta receptor I Mus musculus 9-16 16051536-0 2005 Transferrin coupled liposomes as drug delivery carriers for brain targeting of 5-florouracil. Fluorouracil 79-92 transferrin Homo sapiens 0-11 16051536-3 2005 In the present work, a transferrin-coupled liposomal system for brain delivery of 5-florouracil has been investigated.5-florouracil and (99m)Tc-DTPA bearing non-coupled liposomes were prepared by cast film method, which were coupled with the transferrin by incubating these liposomes with transferrin in the presence of the 1-ethyl-3-(3-dimethylaminopropyl) carbodiimide hydrochloride in saline phosphate buffer (pH 7.4). Fluorouracil 82-95 transferrin Homo sapiens 23-34 16051536-3 2005 In the present work, a transferrin-coupled liposomal system for brain delivery of 5-florouracil has been investigated.5-florouracil and (99m)Tc-DTPA bearing non-coupled liposomes were prepared by cast film method, which were coupled with the transferrin by incubating these liposomes with transferrin in the presence of the 1-ethyl-3-(3-dimethylaminopropyl) carbodiimide hydrochloride in saline phosphate buffer (pH 7.4). Fluorouracil 118-131 transferrin Homo sapiens 23-34 15937643-7 2005 In addition, IFN-evoked TP enzyme activity enhanced the cytotoxicity of 5-fluorouracil (5-FU). Fluorouracil 72-86 interferon alpha 1 Homo sapiens 13-16 15937643-7 2005 In addition, IFN-evoked TP enzyme activity enhanced the cytotoxicity of 5-fluorouracil (5-FU). Fluorouracil 88-92 interferon alpha 1 Homo sapiens 13-16 15703814-10 2005 Interestingly, we found that patients who were on a chemotherapy regime which contained an anthracycline (a Pgp substrate) and subsequently developed recurrence, had a higher YB-1 score compared to patients on the Cyclophosphamide/Methotrexate/5-Fluorouracil regime (P=0.024). Fluorouracil 244-258 ATP binding cassette subfamily B member 1 Homo sapiens 108-111 15703814-10 2005 Interestingly, we found that patients who were on a chemotherapy regime which contained an anthracycline (a Pgp substrate) and subsequently developed recurrence, had a higher YB-1 score compared to patients on the Cyclophosphamide/Methotrexate/5-Fluorouracil regime (P=0.024). Fluorouracil 244-258 Y-box binding protein 1 Homo sapiens 175-179 15767554-5 2005 Even so, knockdown of Bcl-XL protein expression by Bcl-XL-specific small interfering RNA could inhibit proliferation more effectively in 5-FU-resistant cells than in 5-FU-sensitive cells, and the combination of Bcl-XL-specific small interfering RNA and 5-FU had additive effect on the inhibition of 5-FU-resistant cells. Fluorouracil 137-141 BCL2 like 1 Homo sapiens 22-28 15625077-8 2005 Thus, in HepG2 cells pravastatin and simvastatin pretreatment attenuated the p53 response to DNA damage induced by 5-fluorouracil and benzo(a)pyrene. Fluorouracil 115-129 tumor protein p53 Homo sapiens 77-80 15767554-0 2005 Bcl-XL small interfering RNA suppresses the proliferation of 5-fluorouracil-resistant human colon cancer cells. Fluorouracil 61-75 BCL2 like 1 Homo sapiens 0-6 15767554-5 2005 Even so, knockdown of Bcl-XL protein expression by Bcl-XL-specific small interfering RNA could inhibit proliferation more effectively in 5-FU-resistant cells than in 5-FU-sensitive cells, and the combination of Bcl-XL-specific small interfering RNA and 5-FU had additive effect on the inhibition of 5-FU-resistant cells. Fluorouracil 137-141 BCL2 like 1 Homo sapiens 51-57 15767554-3 2005 Western blot analysis revealed that these resistant cells overexpressed the proteins Bcl-XL, Bcl-Xs, and Bik, and further data showed that the cells were resistant to 5-FU-induced DNA damage and cell cycle disorder. Fluorouracil 167-171 BCL2 like 1 Homo sapiens 85-91 15767554-5 2005 Even so, knockdown of Bcl-XL protein expression by Bcl-XL-specific small interfering RNA could inhibit proliferation more effectively in 5-FU-resistant cells than in 5-FU-sensitive cells, and the combination of Bcl-XL-specific small interfering RNA and 5-FU had additive effect on the inhibition of 5-FU-resistant cells. Fluorouracil 137-141 BCL2 like 1 Homo sapiens 51-57 15767554-3 2005 Western blot analysis revealed that these resistant cells overexpressed the proteins Bcl-XL, Bcl-Xs, and Bik, and further data showed that the cells were resistant to 5-FU-induced DNA damage and cell cycle disorder. Fluorouracil 167-171 BCL2 interacting killer Homo sapiens 105-108 15767554-5 2005 Even so, knockdown of Bcl-XL protein expression by Bcl-XL-specific small interfering RNA could inhibit proliferation more effectively in 5-FU-resistant cells than in 5-FU-sensitive cells, and the combination of Bcl-XL-specific small interfering RNA and 5-FU had additive effect on the inhibition of 5-FU-resistant cells. Fluorouracil 166-170 BCL2 like 1 Homo sapiens 22-28 15767554-5 2005 Even so, knockdown of Bcl-XL protein expression by Bcl-XL-specific small interfering RNA could inhibit proliferation more effectively in 5-FU-resistant cells than in 5-FU-sensitive cells, and the combination of Bcl-XL-specific small interfering RNA and 5-FU had additive effect on the inhibition of 5-FU-resistant cells. Fluorouracil 166-170 BCL2 like 1 Homo sapiens 51-57 15767554-5 2005 Even so, knockdown of Bcl-XL protein expression by Bcl-XL-specific small interfering RNA could inhibit proliferation more effectively in 5-FU-resistant cells than in 5-FU-sensitive cells, and the combination of Bcl-XL-specific small interfering RNA and 5-FU had additive effect on the inhibition of 5-FU-resistant cells. Fluorouracil 166-170 BCL2 like 1 Homo sapiens 51-57 15767554-5 2005 Even so, knockdown of Bcl-XL protein expression by Bcl-XL-specific small interfering RNA could inhibit proliferation more effectively in 5-FU-resistant cells than in 5-FU-sensitive cells, and the combination of Bcl-XL-specific small interfering RNA and 5-FU had additive effect on the inhibition of 5-FU-resistant cells. Fluorouracil 166-170 BCL2 like 1 Homo sapiens 22-28 15767554-5 2005 Even so, knockdown of Bcl-XL protein expression by Bcl-XL-specific small interfering RNA could inhibit proliferation more effectively in 5-FU-resistant cells than in 5-FU-sensitive cells, and the combination of Bcl-XL-specific small interfering RNA and 5-FU had additive effect on the inhibition of 5-FU-resistant cells. Fluorouracil 166-170 BCL2 like 1 Homo sapiens 51-57 15767554-5 2005 Even so, knockdown of Bcl-XL protein expression by Bcl-XL-specific small interfering RNA could inhibit proliferation more effectively in 5-FU-resistant cells than in 5-FU-sensitive cells, and the combination of Bcl-XL-specific small interfering RNA and 5-FU had additive effect on the inhibition of 5-FU-resistant cells. Fluorouracil 166-170 BCL2 like 1 Homo sapiens 51-57 15767554-5 2005 Even so, knockdown of Bcl-XL protein expression by Bcl-XL-specific small interfering RNA could inhibit proliferation more effectively in 5-FU-resistant cells than in 5-FU-sensitive cells, and the combination of Bcl-XL-specific small interfering RNA and 5-FU had additive effect on the inhibition of 5-FU-resistant cells. Fluorouracil 166-170 BCL2 like 1 Homo sapiens 22-28 15767554-5 2005 Even so, knockdown of Bcl-XL protein expression by Bcl-XL-specific small interfering RNA could inhibit proliferation more effectively in 5-FU-resistant cells than in 5-FU-sensitive cells, and the combination of Bcl-XL-specific small interfering RNA and 5-FU had additive effect on the inhibition of 5-FU-resistant cells. Fluorouracil 166-170 BCL2 like 1 Homo sapiens 51-57 15767554-5 2005 Even so, knockdown of Bcl-XL protein expression by Bcl-XL-specific small interfering RNA could inhibit proliferation more effectively in 5-FU-resistant cells than in 5-FU-sensitive cells, and the combination of Bcl-XL-specific small interfering RNA and 5-FU had additive effect on the inhibition of 5-FU-resistant cells. Fluorouracil 166-170 BCL2 like 1 Homo sapiens 51-57 15754409-11 2005 The production of IL-12 and IFN-gamma was suppressed moderately in 5-FU-treated mice (IL-12: 166.67+/-53.22 pg/mL; 53.33+/-16.98 pg/mL) compared to control mice (P>0.05), whereas the combination of CpG ODN and 5-FU significantly increased the serum levels of IL-12 and IFN-gamma compared to 5-FU alone (P<0.05). Fluorouracil 67-71 interferon gamma Mus musculus 28-37 15688169-9 2005 MCC1 is sensitive to 5-fluorouracil, representing the first assessment of drug sensitivity for MCC. Fluorouracil 21-35 MCC regulator of WNT signaling pathway Homo sapiens 0-4 15754409-11 2005 The production of IL-12 and IFN-gamma was suppressed moderately in 5-FU-treated mice (IL-12: 166.67+/-53.22 pg/mL; 53.33+/-16.98 pg/mL) compared to control mice (P>0.05), whereas the combination of CpG ODN and 5-FU significantly increased the serum levels of IL-12 and IFN-gamma compared to 5-FU alone (P<0.05). Fluorouracil 67-71 interferon gamma Mus musculus 272-281 15754409-11 2005 The production of IL-12 and IFN-gamma was suppressed moderately in 5-FU-treated mice (IL-12: 166.67+/-53.22 pg/mL; 53.33+/-16.98 pg/mL) compared to control mice (P>0.05), whereas the combination of CpG ODN and 5-FU significantly increased the serum levels of IL-12 and IFN-gamma compared to 5-FU alone (P<0.05). Fluorouracil 213-217 interferon gamma Mus musculus 28-37 15754409-11 2005 The production of IL-12 and IFN-gamma was suppressed moderately in 5-FU-treated mice (IL-12: 166.67+/-53.22 pg/mL; 53.33+/-16.98 pg/mL) compared to control mice (P>0.05), whereas the combination of CpG ODN and 5-FU significantly increased the serum levels of IL-12 and IFN-gamma compared to 5-FU alone (P<0.05). Fluorouracil 213-217 interferon gamma Mus musculus 28-37 15670580-0 2005 Modulation of 5-fluorouracil cytotoxicity through thymidylate synthase and NF-kappaB down-regulation and its application on the radiolabelled iododeoxyuridine therapy on human hepatoma cell. Fluorouracil 14-28 nuclear factor kappa B subunit 1 Homo sapiens 75-84 15608686-5 2005 Similarly, constitutive hTERT expression inhibited wild-type p53-dependent apoptosis in response to mitomycin C or 5-fluorouracil in HCT116 colon carcinoma cells carrying endogenous p53. Fluorouracil 115-129 tumor protein p53 Homo sapiens 61-64 15608676-5 2005 Here we demonstrate that 5-FU activates Chk1 and induces an early S-phase arrest. Fluorouracil 25-29 checkpoint kinase 1 Homo sapiens 40-44 15608676-6 2005 Chk1 downregulation abrogates this arrest and dramatically sensitizes tumor cells to the cytotoxic effects of 5-FU. Fluorouracil 110-114 checkpoint kinase 1 Homo sapiens 0-4 15608676-7 2005 5-FU confers S-phase arrest through Chk1-mediated Cdc25A proteolysis leading to inhibition of Cdk2. Fluorouracil 0-4 checkpoint kinase 1 Homo sapiens 36-40 15608676-9 2005 As a result, downregulation of Chk1 potentiates 5-FU efficacy through induction of premature chromosomal condensation followed by apoptosis. Fluorouracil 48-52 checkpoint kinase 1 Homo sapiens 31-35 15608676-14 2005 Additionally, we show that Chk1 deficiency potentiates 5-FU efficacy through the preferential induction of the caspase-8 pathway and subsequent caspase-3 activation. Fluorouracil 55-59 checkpoint kinase 1 Homo sapiens 27-31 15608676-14 2005 Additionally, we show that Chk1 deficiency potentiates 5-FU efficacy through the preferential induction of the caspase-8 pathway and subsequent caspase-3 activation. Fluorouracil 55-59 caspase 3 Homo sapiens 144-153 15682485-1 2005 AIM: To investigate the difference in activation of STAT3 signaling between two human stomach adenocarcinoma cell lines: 5-fluorouracil resistant cell line and its parental cell line, and to evaluate its relationship with the expression of vascular endothelial growth factor (VEGF). Fluorouracil 121-135 signal transducer and activator of transcription 3 Homo sapiens 52-57 15682485-2 2005 METHODS: Western blot and electrophoretic mobility shift assay (EMSA) were used to detect the expression of phospho-STAT3 protein and constitutive activation of STAT3 in two human stomach adenocarcinoma cell lines, 5-fluorouracil resistant cell line SGC7901/R and its parental cell line SGC7901, respectively. Fluorouracil 215-229 signal transducer and activator of transcription 3 Homo sapiens 116-121 15748688-4 2005 We genetically fused P67 to the carboxyl terminus of the yeast enzyme FCU1, a derivative of cytosine deaminase that can convert the non-toxic prodrug 5-fluorocytosine to the cytotoxic agent 5-fluorouracil. Fluorouracil 190-204 CD33 molecule Homo sapiens 21-24 15546879-3 2005 We therefore examined whether combinations of 5-FU with drugs that specifically target polyamine metabolism, i.e. N1,N11-diethylnorspermine (DENSPM) or alpha-difluoromethylornithine (DFMO), have synergistic effects in killing HCT116 colon carcinoma cells with wild-type or absent p53. Fluorouracil 46-50 tumor protein p53 Homo sapiens 280-283 15546879-4 2005 Our results showed that simultaneous 5-FU and DENSPM, a spermine analogue, synergistically increased transcript levels of the polyamine catabolism enzyme spermidine/spermine N1-acetyltransferase, depleted spermine and spermidine, increased acetylated spermidine, and produced synergistic tumor cell apoptosis in both p53 wild-type and p53-null variants. Fluorouracil 37-41 tumor protein p53 Homo sapiens 317-320 15546879-4 2005 Our results showed that simultaneous 5-FU and DENSPM, a spermine analogue, synergistically increased transcript levels of the polyamine catabolism enzyme spermidine/spermine N1-acetyltransferase, depleted spermine and spermidine, increased acetylated spermidine, and produced synergistic tumor cell apoptosis in both p53 wild-type and p53-null variants. Fluorouracil 37-41 tumor protein p53 Homo sapiens 335-338 15546879-6 2005 Some pre-treatment and post-treatment regimens of DENSPM and DFMO were antagonistic to 5-FU depending on cellular p53 status. Fluorouracil 87-91 tumor protein p53 Homo sapiens 114-117 15546879-7 2005 Protein and transcriptome expression analysis showed that combined 5-FU and DENSPM treatment activated caspase 9, but not caspase 3, and significantly suppressed NADH dehydrogenases and cytochrome c oxidases, consistent with the observed increase in hydrogen peroxide, loss of mitochondrial membrane potential, and release of cytochrome c. Fluorouracil 67-71 caspase 3 Homo sapiens 122-131 15546879-7 2005 Protein and transcriptome expression analysis showed that combined 5-FU and DENSPM treatment activated caspase 9, but not caspase 3, and significantly suppressed NADH dehydrogenases and cytochrome c oxidases, consistent with the observed increase in hydrogen peroxide, loss of mitochondrial membrane potential, and release of cytochrome c. Fluorouracil 67-71 cytochrome c, somatic Homo sapiens 186-198 15546879-7 2005 Protein and transcriptome expression analysis showed that combined 5-FU and DENSPM treatment activated caspase 9, but not caspase 3, and significantly suppressed NADH dehydrogenases and cytochrome c oxidases, consistent with the observed increase in hydrogen peroxide, loss of mitochondrial membrane potential, and release of cytochrome c. Fluorouracil 67-71 cytochrome c, somatic Homo sapiens 326-338 15691646-1 2005 We measured the expression of the p53 nuclear protein and epidermal growth factor receptor (EGFR) in 46 biopsy samples from patients with advanced head and neck cancer treated with induction combination chemotherapy of 5-fluorouracil, cisplatin, and paclitaxel. Fluorouracil 219-233 tumor protein p53 Homo sapiens 34-37 15663907-1 2005 AIM: To study the pharmacokinetics and tissue distribution of 5-fluorouracil encapsulated by galactosylceramide liposomes (5-Fu-GCL) in mice. Fluorouracil 62-76 germ cell-less, spermatogenesis associated 1 Mus musculus 128-131 15663907-2 2005 METHODS: The concentration of 5-fluorouracil (5-Fu) in serum was detected by high performance liquid chromatography after 5-Fu-GCL (80, 40, 20 mg/kg) and free 5-Fu (40 mg/kg) were injected intravenously into mice. Fluorouracil 30-44 germ cell-less, spermatogenesis associated 1 Mus musculus 127-130 15663907-2 2005 METHODS: The concentration of 5-fluorouracil (5-Fu) in serum was detected by high performance liquid chromatography after 5-Fu-GCL (80, 40, 20 mg/kg) and free 5-Fu (40 mg/kg) were injected intravenously into mice. Fluorouracil 46-50 germ cell-less, spermatogenesis associated 1 Mus musculus 127-130 15663907-3 2005 The tissue distribution of 5-Fu-GCL (40 mg/kg) and free 5-Fu (40 mg/kg) was investigated, and concentration-time profile of the two preparations in the liver were studied. Fluorouracil 27-31 germ cell-less, spermatogenesis associated 1 Mus musculus 32-35 15663907-5 2005 RESULTS: Serum concentration-time curves of 5-Fu-GCL and free 5-Fu conformed to one compartment model of first order absorption. Fluorouracil 44-48 germ cell-less, spermatogenesis associated 1 Mus musculus 49-52 15663907-8 2005 The tissue distribution of 5-Fu-GCL in the liver and immune organs was significantly increased, while in heart and kidney it was remarkably decreased. Fluorouracil 27-31 germ cell-less, spermatogenesis associated 1 Mus musculus 32-35 15663907-9 2005 The AUC of 5-Fu-GCL in the liver was 3 times higher than that of free 5-Fu. Fluorouracil 11-15 germ cell-less, spermatogenesis associated 1 Mus musculus 16-19 15684607-7 2005 However, the chemotherapeutic agent 5-FU, by inducing Caspase-1 and Caspase-3 activation, induced secretion of proteolytically processed mature and degraded IL-18 species, respectively, in Capan-2 cells. Fluorouracil 36-40 caspase 1 Homo sapiens 54-63 15684607-7 2005 However, the chemotherapeutic agent 5-FU, by inducing Caspase-1 and Caspase-3 activation, induced secretion of proteolytically processed mature and degraded IL-18 species, respectively, in Capan-2 cells. Fluorouracil 36-40 caspase 3 Homo sapiens 68-77 15684607-8 2005 Conditioned medium from 5-FU-treated but not control Capan-2 cells induced IFN-gamma production by activated T cells in an IL-18-dependent manner. Fluorouracil 24-28 interferon gamma Homo sapiens 75-84 15641988-4 2005 METHODS: In three oral SCC cell lines, Bax expression before and after treatment with chemotherapeutic agents [docetaxel (TXT), cisplatin and 5-fluorouracil] was examined by reverse transcriptase-polymerase chain reaction and immunoblotting. Fluorouracil 142-156 BCL2 associated X, apoptosis regulator Homo sapiens 39-42 15709199-11 2005 Furthermore, IFN-alpha/type 2 IFN receptor long form-transfected HuH7 cells treated with combination therapy showed strong DNA fragmentation compared with nontransfected or transfected with IFN-alpha- and 5-FU-treated HuH7. Fluorouracil 205-209 interferon alpha 1 Homo sapiens 13-22 15709199-11 2005 Furthermore, IFN-alpha/type 2 IFN receptor long form-transfected HuH7 cells treated with combination therapy showed strong DNA fragmentation compared with nontransfected or transfected with IFN-alpha- and 5-FU-treated HuH7. Fluorouracil 205-209 interferon alpha 1 Homo sapiens 13-16 15709199-12 2005 CONCLUSIONS: Our results showed that combination of IFN-alpha plus 5-FU strongly induced cell growth inhibition of human hepatocellular carcinoma cells and indicated that one of the direct mechanisms of combination therapy may in part be attributable to alterations in induction of apoptosis through IFN-alpha/betaR. Fluorouracil 67-71 interferon alpha 1 Homo sapiens 300-315 15698412-2 2005 The aim of this study was to investigate whether interferon (IFN)-alpha influences expression of 5-FU catabolic or target-related enzymes in human hepatoma cells. Fluorouracil 97-101 interferon alpha 1 Homo sapiens 49-71 15709211-14 2005 There it was reported that the combination of 5-fluorouracil, leucovorin, and irinotecan (Camptosar; Pfizer Pharmaceuticals; New York, NY) with anti-vascular endothelial growth factor antibody (bevacizumab-Avastin; Genentech, Inc.; South San Francisco, CA) was superior to the chemotherapy regimen alone when used to treat patients with metastatic colorectal cancer. Fluorouracil 46-60 vascular endothelial growth factor A Homo sapiens 149-183 15643515-3 2005 Specifically, both RhoA and caRhoA induce statistically significant resistance to statin, etoposide, 5-FU and taxol while increasing sensitivity to vincristine (all p<0.001). Fluorouracil 101-105 ras homolog family member A Homo sapiens 19-23 15365767-3 2005 In the work reported here we investigated the ability of docosahexaenoic acid (DHA) to potentiate the antineoplastic activity of 5-fluorouracil (5-FU) in p53-wildtype (LS-174 and Colo 320) and p53-mutant (HT-29 and Colo 205) human colon cancer cells. Fluorouracil 129-143 tumor protein p53 Homo sapiens 154-157 16168113-9 2005 The sequence Dox-->Pacl-->48-h washout-->5-FU produced a synergistic and highly schedule-dependent interaction (combination index < 1), resulting in an induction of apoptosis in both experimental models regardless of hormonal, p53, bcl-2 or bax status. Fluorouracil 50-54 tumor protein p53 Homo sapiens 239-242 16168113-9 2005 The sequence Dox-->Pacl-->48-h washout-->5-FU produced a synergistic and highly schedule-dependent interaction (combination index < 1), resulting in an induction of apoptosis in both experimental models regardless of hormonal, p53, bcl-2 or bax status. Fluorouracil 50-54 BCL2 apoptosis regulator Homo sapiens 244-249 16168113-9 2005 The sequence Dox-->Pacl-->48-h washout-->5-FU produced a synergistic and highly schedule-dependent interaction (combination index < 1), resulting in an induction of apoptosis in both experimental models regardless of hormonal, p53, bcl-2 or bax status. Fluorouracil 50-54 BCL2 associated X, apoptosis regulator Homo sapiens 253-256 15365767-9 2005 DHA markedly increased the inhibitory effect of 5-FU on the expression of the antiapoptotic proteins BCL-2 and BCL-XL, and induced overexpression of c-MYC which has recently been shown to drive apoptosis and, when overexpressed, to sensitize cancer cells to the action of proapoptotic agents, including 5-FU. Fluorouracil 48-52 BCL2 apoptosis regulator Homo sapiens 101-106 15365767-9 2005 DHA markedly increased the inhibitory effect of 5-FU on the expression of the antiapoptotic proteins BCL-2 and BCL-XL, and induced overexpression of c-MYC which has recently been shown to drive apoptosis and, when overexpressed, to sensitize cancer cells to the action of proapoptotic agents, including 5-FU. Fluorouracil 48-52 BCL2 like 1 Homo sapiens 111-117 15365767-3 2005 In the work reported here we investigated the ability of docosahexaenoic acid (DHA) to potentiate the antineoplastic activity of 5-fluorouracil (5-FU) in p53-wildtype (LS-174 and Colo 320) and p53-mutant (HT-29 and Colo 205) human colon cancer cells. Fluorouracil 145-149 tumor protein p53 Homo sapiens 154-157 15611226-7 2005 Moreover, we demonstrate that chemotherapeutic agents that suppress protein synthesis and reverse the CD40-mediated dissociation of the translational repressor eukaryotic initiation factor 4E-binding protein from the initiation factor eukaryotic initiation factor 4E, such as 5-fluorouracil, etoposide, and quercetin, dramatically increase the susceptibility of cervical carcinoma cells to CD40L-induced apoptosis. Fluorouracil 276-290 CD40 ligand Homo sapiens 390-395 15796184-6 2005 In the Paca-2 cell, an equivalent cytotoxic activity to 5-FU (10 microg/ml) was observed at about 40 microg/ml of apoE 133-162 peptide, but no synergistic effect of apoE 133-162 (40 microg/ml ) with 5-FU (10 microg/ml), nor inhibitory effect by heparin(100 microg/ml), was observed. Fluorouracil 56-60 apolipoprotein E Homo sapiens 114-118 15675582-0 2005 [Phase I study of the combination of nedaplatin (NED), adriamycin (ADM), and 5-fluorouracil (5-FU) (NAF) for treatment of unresectable advanced esophageal cancer]. Fluorouracil 77-91 C-X-C motif chemokine ligand 8 Homo sapiens 100-103 15675582-0 2005 [Phase I study of the combination of nedaplatin (NED), adriamycin (ADM), and 5-fluorouracil (5-FU) (NAF) for treatment of unresectable advanced esophageal cancer]. Fluorouracil 93-97 C-X-C motif chemokine ligand 8 Homo sapiens 100-103 15489892-2 2004 The time course of p53 activation by mithramycin A was similar to the known chemotherapeutic compound 5-fluorouracil (5-FU). Fluorouracil 118-122 tumor protein p53 Homo sapiens 19-22 16491956-8 2005 In these cells, both caspase-3 and -9 were involved in the activation of apoptosis after CPT-11/5-FU treatment. Fluorouracil 96-100 caspase 3 Homo sapiens 21-37 15611505-0 2004 Prediction of TP53 status for primary cisplatin, fluorouracil, and leucovorin chemotherapy in ethmoid sinus intestinal-type adenocarcinoma. Fluorouracil 49-61 tumor protein p53 Homo sapiens 14-18 15720820-0 2005 CF101, an agonist to the A3 adenosine receptor, enhances the chemotherapeutic effect of 5-fluorouracil in a colon carcinoma murine model. Fluorouracil 88-102 adenosine A3 receptor Mus musculus 25-46 15720820-6 2005 Downregulation of PKB/Akt, NF-kappaB, and cyclin D1, and upregulation of caspase-3 protein expression level were observed in cells and tumor lesions on treatment with a combination of CF101 and 5-FU. Fluorouracil 194-198 thymoma viral proto-oncogene 1 Mus musculus 18-21 15720820-6 2005 Downregulation of PKB/Akt, NF-kappaB, and cyclin D1, and upregulation of caspase-3 protein expression level were observed in cells and tumor lesions on treatment with a combination of CF101 and 5-FU. Fluorouracil 194-198 nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105 Mus musculus 27-36 15489892-3 2004 Both 5-FU and mithramycin A induced site-specific phosphorylation of p53 at serine 15. Fluorouracil 5-9 tumor protein p53 Homo sapiens 69-72 15489892-4 2004 However, in contrast to 5-FU, mithramycin A failed to activate p53 target genes including the cell cycle inhibitor p21Cip1 gene as well as the proapoptotic genes PUMA (p53-upregulated mediator of apotosis) and BAK (bcl2-homologous antagonist/killer) and blocked the induction of the above genes by 5-FU. Fluorouracil 298-302 tumor protein p53 Homo sapiens 168-171 15489892-6 2004 Using chromatin immunoprecipitation assays and a novel protein-protein interaction assay based on biotinylation in vivo, we established that 5-FU enhanced the formation of p53-Sp1 complexes in solution and the subsequent recruitment of both factors to the p21Cip1 promoter. Fluorouracil 141-145 tumor protein p53 Homo sapiens 172-175 15489892-6 2004 Using chromatin immunoprecipitation assays and a novel protein-protein interaction assay based on biotinylation in vivo, we established that 5-FU enhanced the formation of p53-Sp1 complexes in solution and the subsequent recruitment of both factors to the p21Cip1 promoter. Fluorouracil 141-145 cyclin dependent kinase inhibitor 1A Homo sapiens 256-263 15585071-5 2004 Similarly, in the multicenter prospective Chemo N0 trial, administration of cyclophosphamide/methotrexate/5-fluorouracil-based chemotherapy led to a substantial reduction in risk of disease recurrence in patients with high uPA/PAI-1. Fluorouracil 106-120 plasminogen activator, urokinase Homo sapiens 223-226 15585621-0 2004 Partial contribution of tumor necrosis factor-related apoptosis-inducing ligand (TRAIL)/TRAIL receptor pathway to antitumor effects of interferon-alpha/5-fluorouracil against Hepatocellular Carcinoma. Fluorouracil 152-166 TNF superfamily member 10 Homo sapiens 24-79 15585621-1 2004 PURPOSE: Our purpose was to explore the contribution of tumor necrosis factor-related apoptosis-inducing ligand (TRAIL)/TRAIL receptor pathway to antitumor effects of IFNalpha and 5-fluorouracil (5-FU) combination therapy for hepatocellular carcinoma (HCC). Fluorouracil 196-200 TNF superfamily member 10 Homo sapiens 120-125 15585621-0 2004 Partial contribution of tumor necrosis factor-related apoptosis-inducing ligand (TRAIL)/TRAIL receptor pathway to antitumor effects of interferon-alpha/5-fluorouracil against Hepatocellular Carcinoma. Fluorouracil 152-166 TNF superfamily member 10 Homo sapiens 81-86 15585621-3 2004 The effects of 5-FU, IFNalpha, or both on the expression of TRAIL receptors (R1, R2, R3, and R4) on HCC cells or TRAIL in peripheral blood mononuclear cells (PBMC) were examined by flow cytometry. Fluorouracil 15-19 TNF superfamily member 10 Homo sapiens 60-65 15585621-0 2004 Partial contribution of tumor necrosis factor-related apoptosis-inducing ligand (TRAIL)/TRAIL receptor pathway to antitumor effects of interferon-alpha/5-fluorouracil against Hepatocellular Carcinoma. Fluorouracil 152-166 TNF superfamily member 10 Homo sapiens 88-93 15585621-7 2004 5-FU had synergistic effect on TRAIL in HLF and additive effect in four other HCC cell lines. Fluorouracil 0-4 TNF superfamily member 10 Homo sapiens 31-36 15585621-1 2004 PURPOSE: Our purpose was to explore the contribution of tumor necrosis factor-related apoptosis-inducing ligand (TRAIL)/TRAIL receptor pathway to antitumor effects of IFNalpha and 5-fluorouracil (5-FU) combination therapy for hepatocellular carcinoma (HCC). Fluorouracil 180-194 TNF superfamily member 10 Homo sapiens 56-111 15585621-9 2004 Treatment of effector cells by IFNalpha and target HCC cells by 5-FU enhanced the cytotoxicity of CD14(+) monocytes and CD56(+) NK cells against HCC cells via a TRAIL-mediated pathway. Fluorouracil 64-68 interferon alpha 1 Homo sapiens 31-39 15585621-1 2004 PURPOSE: Our purpose was to explore the contribution of tumor necrosis factor-related apoptosis-inducing ligand (TRAIL)/TRAIL receptor pathway to antitumor effects of IFNalpha and 5-fluorouracil (5-FU) combination therapy for hepatocellular carcinoma (HCC). Fluorouracil 180-194 TNF superfamily member 10 Homo sapiens 113-118 15585621-9 2004 Treatment of effector cells by IFNalpha and target HCC cells by 5-FU enhanced the cytotoxicity of CD14(+) monocytes and CD56(+) NK cells against HCC cells via a TRAIL-mediated pathway. Fluorouracil 64-68 TNF superfamily member 10 Homo sapiens 161-166 15585621-1 2004 PURPOSE: Our purpose was to explore the contribution of tumor necrosis factor-related apoptosis-inducing ligand (TRAIL)/TRAIL receptor pathway to antitumor effects of IFNalpha and 5-fluorouracil (5-FU) combination therapy for hepatocellular carcinoma (HCC). Fluorouracil 180-194 TNF superfamily member 10 Homo sapiens 120-125 15585621-10 2004 TRAIL mRNA overexpression was noted in PBMC of HCC patients who clinically responded to IFNalpha/5-FU combination therapy, and TRAIL(+) mononuclear cells were found in cancer tissue of a responder. Fluorouracil 97-101 TNF superfamily member 10 Homo sapiens 0-5 15585621-11 2004 CONCLUSION: Our results suggest that modulation of TRAIL/TRAIL receptor-mediated cytotoxic pathway might partially contribute to the anti-HCC effect of IFNalpha and 5-FU combination therapy. Fluorouracil 165-169 TNF superfamily member 10 Homo sapiens 51-56 15585621-1 2004 PURPOSE: Our purpose was to explore the contribution of tumor necrosis factor-related apoptosis-inducing ligand (TRAIL)/TRAIL receptor pathway to antitumor effects of IFNalpha and 5-fluorouracil (5-FU) combination therapy for hepatocellular carcinoma (HCC). Fluorouracil 196-200 TNF superfamily member 10 Homo sapiens 56-111 15585621-11 2004 CONCLUSION: Our results suggest that modulation of TRAIL/TRAIL receptor-mediated cytotoxic pathway might partially contribute to the anti-HCC effect of IFNalpha and 5-FU combination therapy. Fluorouracil 165-169 TNF superfamily member 10 Homo sapiens 57-62 15585621-1 2004 PURPOSE: Our purpose was to explore the contribution of tumor necrosis factor-related apoptosis-inducing ligand (TRAIL)/TRAIL receptor pathway to antitumor effects of IFNalpha and 5-fluorouracil (5-FU) combination therapy for hepatocellular carcinoma (HCC). Fluorouracil 196-200 TNF superfamily member 10 Homo sapiens 113-118 15730734-0 2004 [The impact of decreased Stat3 activation on 5-fluorouracil resistance of human gastric cancer cell line]. Fluorouracil 45-59 signal transducer and activator of transcription 3 Homo sapiens 25-30 15588950-6 2004 RESULTS: We confirmed that the number of Sca-1+lin- cells and the LTRA of marrow from paired dose 5-FU-treated animals were diminished. Fluorouracil 98-102 ataxin 1 Homo sapiens 41-46 15364927-9 2004 As p53 is required for 5-fluorouracil-induced cell death, our data show that Daxx can suppress cell death induced by p53 overexpression and p53-dependent stress response. Fluorouracil 23-37 tumor protein p53 Homo sapiens 3-6 15364927-9 2004 As p53 is required for 5-fluorouracil-induced cell death, our data show that Daxx can suppress cell death induced by p53 overexpression and p53-dependent stress response. Fluorouracil 23-37 tumor protein p53 Homo sapiens 117-120 15364927-9 2004 As p53 is required for 5-fluorouracil-induced cell death, our data show that Daxx can suppress cell death induced by p53 overexpression and p53-dependent stress response. Fluorouracil 23-37 tumor protein p53 Homo sapiens 117-120 15640503-0 2004 Prognostic implications of the expression of erbB2, topoisomerase II alpha and thymidylate synthase in metastatic gastric cancer after fluorouracil-based therapy. Fluorouracil 135-147 erb-b2 receptor tyrosine kinase 2 Homo sapiens 45-50 15640503-7 2004 CONCLUSION: High dose fluorouracil/leucovorin-based chemotherapy may have the potential to reverse the adverse effects resulting from erbB2 gene amplification in gastric cancer. Fluorouracil 22-34 erb-b2 receptor tyrosine kinase 2 Homo sapiens 134-139 15730734-1 2004 OBJECTIVE: To investigate the relationship between different activation of Stat3 signaling and the drug resistance mechanisms in two human gastric cancer cell lines, 5-fluorouracil (5-FU) resistant cell line and its parental cell line. Fluorouracil 166-180 signal transducer and activator of transcription 3 Homo sapiens 75-80 15730734-1 2004 OBJECTIVE: To investigate the relationship between different activation of Stat3 signaling and the drug resistance mechanisms in two human gastric cancer cell lines, 5-fluorouracil (5-FU) resistant cell line and its parental cell line. Fluorouracil 182-186 signal transducer and activator of transcription 3 Homo sapiens 75-80 15730734-8 2004 CONCLUSIONS: The decreased Stat3 activation in 5-FU resistant human gastric cancer cell line SGC7901/R is related to the drug resistance mechanisms and may be correlated with the lower VEGF expression. Fluorouracil 47-51 signal transducer and activator of transcription 3 Homo sapiens 27-32 15730734-8 2004 CONCLUSIONS: The decreased Stat3 activation in 5-FU resistant human gastric cancer cell line SGC7901/R is related to the drug resistance mechanisms and may be correlated with the lower VEGF expression. Fluorouracil 47-51 vascular endothelial growth factor A Homo sapiens 185-189 15516750-3 2004 Composite polymeric prodrugs were synthesized by the mechanochemical solid-state polymerization of a vinyl monomer of 5-fluorouracil (I) in the presence of Mgst or HCO. Fluorouracil 118-132 microsomal glutathione S-transferase 1 Homo sapiens 156-160 15548681-7 2004 The 5-FU-resistant cell lines also showed high NFkappaB DNA-binding activity. Fluorouracil 4-8 nuclear factor kappa B subunit 1 Homo sapiens 47-55 15548681-8 2004 Cotransfection of NFkappaB p50 and p65 cDNA induced 5-FU resistance in MCF-7 cells. Fluorouracil 52-56 nuclear factor kappa B subunit 1 Homo sapiens 18-26 15548681-8 2004 Cotransfection of NFkappaB p50 and p65 cDNA induced 5-FU resistance in MCF-7 cells. Fluorouracil 52-56 nuclear factor kappa B subunit 1 Homo sapiens 27-30 15585135-7 2004 Our experiments showed that 5-FU engaged the mitochondrial apoptotic pathway involving cytosolic cytochrome c release and subsequent activation of caspase-9 and caspase-3 as well as the membrane death receptor (DR)-mediated apoptotic pathway involving activation of caspase-8 with an Apo-1/CD95 (Fas)-dependent fashion. Fluorouracil 28-32 cytochrome c, somatic Homo sapiens 97-109 15585135-8 2004 In addition, we could observe reduction of HPV-18 E6/E7 gene expression and activation of p53, pRb, and p21waf1 proteins by 5-FU treatment in HeLa cervical carcinoma cells. Fluorouracil 124-128 tumor protein p53 Homo sapiens 90-93 15585135-7 2004 Our experiments showed that 5-FU engaged the mitochondrial apoptotic pathway involving cytosolic cytochrome c release and subsequent activation of caspase-9 and caspase-3 as well as the membrane death receptor (DR)-mediated apoptotic pathway involving activation of caspase-8 with an Apo-1/CD95 (Fas)-dependent fashion. Fluorouracil 28-32 caspase 3 Homo sapiens 161-170 15492816-7 2004 Of the eight cells tested, five showed increased susceptibility to 5-FU plus IFN-alpha compared with 5-FU treatment alone. Fluorouracil 101-105 interferon alpha 1 Homo sapiens 77-86 15492816-9 2004 The relevance networks revealed that sensitivity to 5-FU plus IFN-alpha involved the expression of 27 independent genes, which included 10 genes that are commonly associated with sensitivity to 5-FU alone. Fluorouracil 194-198 interferon alpha 1 Homo sapiens 62-71 15467752-0 2004 Multidomain Bcl-2 homolog Bax but not Bak mediates synergistic induction of apoptosis by TRAIL and 5-FU through the mitochondrial apoptosis pathway. Fluorouracil 99-103 BCL2 apoptosis regulator Homo sapiens 12-17 15509204-5 2004 RESULTS: Triple combination therapy (5-FU, IFN alpha/beta and IFN gamma) showed a synergistic antitumor effect on RENCA tumors, because triple combination therapy suppressed growth significantly compared to combination therapy (IFN alpha/beta and IFN gamma, P = 0.0258) and 5-FU (P < 0.0001). Fluorouracil 37-41 interferon gamma Mus musculus 238-256 15509204-5 2004 RESULTS: Triple combination therapy (5-FU, IFN alpha/beta and IFN gamma) showed a synergistic antitumor effect on RENCA tumors, because triple combination therapy suppressed growth significantly compared to combination therapy (IFN alpha/beta and IFN gamma, P = 0.0258) and 5-FU (P < 0.0001). Fluorouracil 274-278 interferon gamma Mus musculus 53-71 15467752-4 2004 In contrast, TRAIL sensitized for 5-FU-induced apoptosis and vice versa upon reconstitution of Bax expression. Fluorouracil 34-38 TNF superfamily member 10 Homo sapiens 13-18 15507659-4 2004 Treatment with tumor necrosis factor alpha did not induce apoptosis of EBNA2- or EBNA2DeltaCR4-expressing cells, but EBNA2DeltaCR4 cells were susceptible to etoposide and 5-fluorouracil, Nur77-mediated inducers of apoptosis. Fluorouracil 171-185 tumor necrosis factor Homo sapiens 15-42 15467752-0 2004 Multidomain Bcl-2 homolog Bax but not Bak mediates synergistic induction of apoptosis by TRAIL and 5-FU through the mitochondrial apoptosis pathway. Fluorouracil 99-103 BCL2 associated X, apoptosis regulator Homo sapiens 26-29 15467752-5 2004 Isobolographic analyses of ED50 doses for 5-FU at increasing TRAIL concentrations showed a clear synergism of TRAIL and 5-FU in Bax-expressing cells. Fluorouracil 42-46 TNF superfamily member 10 Homo sapiens 61-66 15467752-5 2004 Isobolographic analyses of ED50 doses for 5-FU at increasing TRAIL concentrations showed a clear synergism of TRAIL and 5-FU in Bax-expressing cells. Fluorouracil 42-46 TNF superfamily member 10 Homo sapiens 110-115 15467752-2 2004 Here, we show that the synergism of TRAIL and 5-fluorouracil (5-FU) and cross-sensitization between TRAIL and 5-FU for induction of apoptosis, entirely depend on Bax proficiency in human DU145 and HCT116 carcinoma cells. Fluorouracil 46-60 BCL2 associated X, apoptosis regulator Homo sapiens 162-165 15467752-5 2004 Isobolographic analyses of ED50 doses for 5-FU at increasing TRAIL concentrations showed a clear synergism of TRAIL and 5-FU in Bax-expressing cells. Fluorouracil 42-46 BCL2 associated X, apoptosis regulator Homo sapiens 128-131 15467752-5 2004 Isobolographic analyses of ED50 doses for 5-FU at increasing TRAIL concentrations showed a clear synergism of TRAIL and 5-FU in Bax-expressing cells. Fluorouracil 120-124 TNF superfamily member 10 Homo sapiens 61-66 15467752-5 2004 Isobolographic analyses of ED50 doses for 5-FU at increasing TRAIL concentrations showed a clear synergism of TRAIL and 5-FU in Bax-expressing cells. Fluorouracil 120-124 BCL2 associated X, apoptosis regulator Homo sapiens 128-131 15467752-2 2004 Here, we show that the synergism of TRAIL and 5-fluorouracil (5-FU) and cross-sensitization between TRAIL and 5-FU for induction of apoptosis, entirely depend on Bax proficiency in human DU145 and HCT116 carcinoma cells. Fluorouracil 62-66 TNF superfamily member 10 Homo sapiens 36-41 15467752-10 2004 Moreover, we show by the use of EGFP-tagged Bax and Bak that TRAIL and 5-FU synergistically trigger oligomerization and clustering of Bax but not Bak. Fluorouracil 71-75 BCL2 associated X, apoptosis regulator Homo sapiens 44-47 15467752-2 2004 Here, we show that the synergism of TRAIL and 5-fluorouracil (5-FU) and cross-sensitization between TRAIL and 5-FU for induction of apoptosis, entirely depend on Bax proficiency in human DU145 and HCT116 carcinoma cells. Fluorouracil 62-66 BCL2 associated X, apoptosis regulator Homo sapiens 162-165 15467752-10 2004 Moreover, we show by the use of EGFP-tagged Bax and Bak that TRAIL and 5-FU synergistically trigger oligomerization and clustering of Bax but not Bak. Fluorouracil 71-75 BCL2 associated X, apoptosis regulator Homo sapiens 134-137 15467752-2 2004 Here, we show that the synergism of TRAIL and 5-fluorouracil (5-FU) and cross-sensitization between TRAIL and 5-FU for induction of apoptosis, entirely depend on Bax proficiency in human DU145 and HCT116 carcinoma cells. Fluorouracil 110-114 BCL2 associated X, apoptosis regulator Homo sapiens 162-165 15467752-3 2004 DU145 prostate carcinoma cells that have lost Bax protein expression due to mutation fail to release cytochrome c and to activate caspase-3 and -9 when exposed to TRAIL and 5-FU. Fluorouracil 173-177 BCL2 associated X, apoptosis regulator Homo sapiens 46-49 15448013-8 2004 Both RhoA-specific siRNA and dominant-negative RhoA expressions could significantly inhibit the proliferation and tumorigenicity of AGS cells and enhance chemosensitivity of the cancer cells to Adriamycin and 5-fluorouracil. Fluorouracil 209-223 ras homolog family member A Homo sapiens 5-9 15475457-15 2004 CONCLUSIONS: These results for FAU incorporation into DNA in vitro and in vivo further support clinical evaluation of FAU as a therapeutic agent in tumors with high concentrations of thymidylate synthase that are less likely to respond to 5-fluorouracil treatment. Fluorouracil 239-253 Finkel-Biskis-Reilly murine sarcoma virus (FBR-MuSV) ubiquitously expressed (fox derived) Mus musculus 31-34 15475457-15 2004 CONCLUSIONS: These results for FAU incorporation into DNA in vitro and in vivo further support clinical evaluation of FAU as a therapeutic agent in tumors with high concentrations of thymidylate synthase that are less likely to respond to 5-fluorouracil treatment. Fluorouracil 239-253 Finkel-Biskis-Reilly murine sarcoma virus (FBR-MuSV) ubiquitously expressed (fox derived) Mus musculus 118-121 15591457-1 2004 BACKGROUND: Our previous analyses on the expression of thymidylate synthase (TS) and p16(INK4a) in colorectal cancer patients administered 5-fluorouracil (5-FU) pre-operatively demonstrated that a high level of TS expression was a predictor of 5-FU resistance, and that the combination of a low level of TS expression and induction of p16(INK4a) after chemotherapy implicated chemosensitivity. Fluorouracil 139-153 cyclin dependent kinase inhibitor 2A Homo sapiens 85-88 15591457-1 2004 BACKGROUND: Our previous analyses on the expression of thymidylate synthase (TS) and p16(INK4a) in colorectal cancer patients administered 5-fluorouracil (5-FU) pre-operatively demonstrated that a high level of TS expression was a predictor of 5-FU resistance, and that the combination of a low level of TS expression and induction of p16(INK4a) after chemotherapy implicated chemosensitivity. Fluorouracil 139-153 cyclin dependent kinase inhibitor 2A Homo sapiens 89-94 15591457-1 2004 BACKGROUND: Our previous analyses on the expression of thymidylate synthase (TS) and p16(INK4a) in colorectal cancer patients administered 5-fluorouracil (5-FU) pre-operatively demonstrated that a high level of TS expression was a predictor of 5-FU resistance, and that the combination of a low level of TS expression and induction of p16(INK4a) after chemotherapy implicated chemosensitivity. Fluorouracil 139-153 cyclin dependent kinase inhibitor 2A Homo sapiens 335-338 15591457-1 2004 BACKGROUND: Our previous analyses on the expression of thymidylate synthase (TS) and p16(INK4a) in colorectal cancer patients administered 5-fluorouracil (5-FU) pre-operatively demonstrated that a high level of TS expression was a predictor of 5-FU resistance, and that the combination of a low level of TS expression and induction of p16(INK4a) after chemotherapy implicated chemosensitivity. Fluorouracil 139-153 cyclin dependent kinase inhibitor 2A Homo sapiens 339-344 15591457-1 2004 BACKGROUND: Our previous analyses on the expression of thymidylate synthase (TS) and p16(INK4a) in colorectal cancer patients administered 5-fluorouracil (5-FU) pre-operatively demonstrated that a high level of TS expression was a predictor of 5-FU resistance, and that the combination of a low level of TS expression and induction of p16(INK4a) after chemotherapy implicated chemosensitivity. Fluorouracil 155-159 cyclin dependent kinase inhibitor 2A Homo sapiens 85-88 15591457-1 2004 BACKGROUND: Our previous analyses on the expression of thymidylate synthase (TS) and p16(INK4a) in colorectal cancer patients administered 5-fluorouracil (5-FU) pre-operatively demonstrated that a high level of TS expression was a predictor of 5-FU resistance, and that the combination of a low level of TS expression and induction of p16(INK4a) after chemotherapy implicated chemosensitivity. Fluorouracil 155-159 cyclin dependent kinase inhibitor 2A Homo sapiens 89-94 15591457-1 2004 BACKGROUND: Our previous analyses on the expression of thymidylate synthase (TS) and p16(INK4a) in colorectal cancer patients administered 5-fluorouracil (5-FU) pre-operatively demonstrated that a high level of TS expression was a predictor of 5-FU resistance, and that the combination of a low level of TS expression and induction of p16(INK4a) after chemotherapy implicated chemosensitivity. Fluorouracil 155-159 cyclin dependent kinase inhibitor 2A Homo sapiens 335-338 15591457-1 2004 BACKGROUND: Our previous analyses on the expression of thymidylate synthase (TS) and p16(INK4a) in colorectal cancer patients administered 5-fluorouracil (5-FU) pre-operatively demonstrated that a high level of TS expression was a predictor of 5-FU resistance, and that the combination of a low level of TS expression and induction of p16(INK4a) after chemotherapy implicated chemosensitivity. Fluorouracil 155-159 cyclin dependent kinase inhibitor 2A Homo sapiens 339-344 15591457-1 2004 BACKGROUND: Our previous analyses on the expression of thymidylate synthase (TS) and p16(INK4a) in colorectal cancer patients administered 5-fluorouracil (5-FU) pre-operatively demonstrated that a high level of TS expression was a predictor of 5-FU resistance, and that the combination of a low level of TS expression and induction of p16(INK4a) after chemotherapy implicated chemosensitivity. Fluorouracil 244-248 cyclin dependent kinase inhibitor 2A Homo sapiens 85-88 15591457-1 2004 BACKGROUND: Our previous analyses on the expression of thymidylate synthase (TS) and p16(INK4a) in colorectal cancer patients administered 5-fluorouracil (5-FU) pre-operatively demonstrated that a high level of TS expression was a predictor of 5-FU resistance, and that the combination of a low level of TS expression and induction of p16(INK4a) after chemotherapy implicated chemosensitivity. Fluorouracil 244-248 cyclin dependent kinase inhibitor 2A Homo sapiens 89-94 15591457-2 2004 The present study aimed to assess the relationship between the biological behavior of advanced colorectal cancer treated post-operatively by 5-FU-based chemotherapy and the expression of TS and p16(INK4a) in primary tumors. Fluorouracil 141-145 cyclin dependent kinase inhibitor 2A Homo sapiens 194-197 15591457-2 2004 The present study aimed to assess the relationship between the biological behavior of advanced colorectal cancer treated post-operatively by 5-FU-based chemotherapy and the expression of TS and p16(INK4a) in primary tumors. Fluorouracil 141-145 cyclin dependent kinase inhibitor 2A Homo sapiens 198-203 15470036-5 2004 Our results show that methotrexate and 5-fluorouracil prevent the acquisition of effector functions, such as IFN-gamma, granzyme B expression, and cytotoxic function following antigenic stimulation of naive cells. Fluorouracil 39-53 interferon gamma Mus musculus 109-118 15448013-8 2004 Both RhoA-specific siRNA and dominant-negative RhoA expressions could significantly inhibit the proliferation and tumorigenicity of AGS cells and enhance chemosensitivity of the cancer cells to Adriamycin and 5-fluorouracil. Fluorouracil 209-223 ras homolog family member A Homo sapiens 47-51 15138707-13 2004 Intraperitoneal 5-FU abrogated the reduction in peritoneal blood flow with intravenous vasopressin the first day after treatment. Fluorouracil 16-20 arginine vasopressin Rattus norvegicus 87-98 15367711-2 2004 We report here that Ad.Egr-TNF.11D is activated by the clinically important anticancer agents cisplatin, cyclophosphamide, doxorubicin, 5-fluorouracil, gemcitabine, and paclitaxel. Fluorouracil 136-150 tumor necrosis factor Homo sapiens 27-30 15138707-0 2004 Effect of carcinomatosis and intraperitoneal 5-fluorouracil on peritoneal blood flow modulated by vasopressin in the rat as measured with the 133Xe-clearance technique. Fluorouracil 45-59 arginine vasopressin Rattus norvegicus 98-109 15138707-5 2004 The aim of the present study was to explore whether intraperitoneal 5-FU or peritoneal carcinomatosis affects the peritoneal blood flow and its reactivity to intravenous vasopressin, as measured indirectly with the 133Xe-clearance technique. Fluorouracil 68-72 arginine vasopressin Rattus norvegicus 170-181 15342418-1 2004 We have demonstrated previously that interferon (IFN)-gamma sensitizes human colon carcinoma cell lines to the cytotoxic effects of 5-fluorouracil combined with leucovorin and to the thymidylate synthase inhibitor, ZD9331, dependent on thymineless stress-induced DNA damage, independent of p53. Fluorouracil 132-146 interferon gamma Homo sapiens 37-59 15342418-1 2004 We have demonstrated previously that interferon (IFN)-gamma sensitizes human colon carcinoma cell lines to the cytotoxic effects of 5-fluorouracil combined with leucovorin and to the thymidylate synthase inhibitor, ZD9331, dependent on thymineless stress-induced DNA damage, independent of p53. Fluorouracil 132-146 tumor protein p53 Homo sapiens 290-293 15289866-9 2004 Overexpression of Bid or tBid sensitized HCC cells to 5-FU and doxorubicin (Dox) treatments. Fluorouracil 54-58 BH3 interacting domain death agonist Homo sapiens 18-21 15342418-7 2004 P21Cip1, cdk1, cdk2, and cyclin E mRNA expression increased coincident with S-phase accumulation in HT29 cells treated with ZD9331 or 5fluorouracil/leucovorin, as demonstrated by cDNA microarray analyses. Fluorouracil 134-147 cyclin dependent kinase inhibitor 1A Homo sapiens 0-7 15247902-5 2004 Here, we document that human HCT116 colorectal carcinoma cells treated with adriamycin or 5-fluorouracil (5FU) can accumulate total p53 to equally high levels, and mitochondrial p53 to proportionate levels, although only 5FU treatment provoked p53-dependent apoptosis. Fluorouracil 90-104 tumor protein p53 Homo sapiens 132-135 15247902-5 2004 Here, we document that human HCT116 colorectal carcinoma cells treated with adriamycin or 5-fluorouracil (5FU) can accumulate total p53 to equally high levels, and mitochondrial p53 to proportionate levels, although only 5FU treatment provoked p53-dependent apoptosis. Fluorouracil 90-104 tumor protein p53 Homo sapiens 178-181 15247902-5 2004 Here, we document that human HCT116 colorectal carcinoma cells treated with adriamycin or 5-fluorouracil (5FU) can accumulate total p53 to equally high levels, and mitochondrial p53 to proportionate levels, although only 5FU treatment provoked p53-dependent apoptosis. Fluorouracil 90-104 tumor protein p53 Homo sapiens 178-181 15247902-5 2004 Here, we document that human HCT116 colorectal carcinoma cells treated with adriamycin or 5-fluorouracil (5FU) can accumulate total p53 to equally high levels, and mitochondrial p53 to proportionate levels, although only 5FU treatment provoked p53-dependent apoptosis. Fluorouracil 106-109 tumor protein p53 Homo sapiens 132-135 15247902-5 2004 Here, we document that human HCT116 colorectal carcinoma cells treated with adriamycin or 5-fluorouracil (5FU) can accumulate total p53 to equally high levels, and mitochondrial p53 to proportionate levels, although only 5FU treatment provoked p53-dependent apoptosis. Fluorouracil 106-109 tumor protein p53 Homo sapiens 178-181 15247902-5 2004 Here, we document that human HCT116 colorectal carcinoma cells treated with adriamycin or 5-fluorouracil (5FU) can accumulate total p53 to equally high levels, and mitochondrial p53 to proportionate levels, although only 5FU treatment provoked p53-dependent apoptosis. Fluorouracil 106-109 tumor protein p53 Homo sapiens 178-181 15301717-0 2004 [Enhancement effect of interferon gamma on the sensitivity of RT4 bladder cancer cells to 5"-deoxy-5-fluorouridine,and 5-fluorouracil through up-regulation of PD-ECGF/TP]. Fluorouracil 119-133 interferon gamma Homo sapiens 23-39 15265716-7 2004 5-Fluorouracil (5-FU) causes pro-apoptotic Bax levels to increase 2-fold during the drug exposure. Fluorouracil 0-14 BCL2 associated X, apoptosis regulator Homo sapiens 43-46 15265716-7 2004 5-Fluorouracil (5-FU) causes pro-apoptotic Bax levels to increase 2-fold during the drug exposure. Fluorouracil 16-20 BCL2 associated X, apoptosis regulator Homo sapiens 43-46 15265716-8 2004 The increase in Bax was also apparent following the combination of 5-FU/freezing, while Bcl-2 levels were maintained at or below control levels. Fluorouracil 67-71 BCL2 associated X, apoptosis regulator Homo sapiens 16-19 15254702-6 2004 In this study, we examined induced apoptosis in colon cancer cell lines and the status of p53 expression in response to treatment of HCT116, COLO320, SW480 and DLD1 with 5-FU alone, CDDP alone and FP treatment under flow cytometric analysis. Fluorouracil 170-174 tumor protein p53 Homo sapiens 90-93 15313921-8 2004 PKCalpha-AS and PKCbeta1-AS cells were more responsive to mitomycin C- or 5-fluorouracil-induced apoptosis. Fluorouracil 74-88 protein kinase C, alpha Mus musculus 0-8 15282376-6 2004 Finally, 5-fluorouracil and docetaxel were shown to cause apoptotic cell death involving caspase-3 cleavage in Centre d"Etude du Polymorphisme Humain lymphoblastoid cells. Fluorouracil 9-23 caspase 3 Homo sapiens 89-98 15297391-1 2004 PURPOSE: The oral fluoropyrimidine S-1, which consists of a mixture of a 5-fluorouracil (5-FU) prodrug (tegafur), a dihydropyrimidine dehydrogenase inhibitor [5-chloro-2,4-dihydroxypyrimidine (CDHP)], and an inhibitor of orotate phosphoribosyltransferase [potassium oxonate (oxonic acid)], was developed to increase the feasibility and therapeutic index of 5-FU administered orally. Fluorouracil 89-93 proteasome 26S subunit, non-ATPase 1 Homo sapiens 35-38 15297391-1 2004 PURPOSE: The oral fluoropyrimidine S-1, which consists of a mixture of a 5-fluorouracil (5-FU) prodrug (tegafur), a dihydropyrimidine dehydrogenase inhibitor [5-chloro-2,4-dihydroxypyrimidine (CDHP)], and an inhibitor of orotate phosphoribosyltransferase [potassium oxonate (oxonic acid)], was developed to increase the feasibility and therapeutic index of 5-FU administered orally. Fluorouracil 357-361 proteasome 26S subunit, non-ATPase 1 Homo sapiens 35-38 15275881-2 2004 Inhibition of NF-kappaB by adenoviral delivery of an IkappaBalpha superrepressor (Ad.IkappaBalpha-SR) should potentiate 5-fluorouracil (5-FU) and irinotecan chemotherapy in gastric cancer cells. Fluorouracil 120-134 nuclear factor kappa B subunit 1 Homo sapiens 14-23 15275881-2 2004 Inhibition of NF-kappaB by adenoviral delivery of an IkappaBalpha superrepressor (Ad.IkappaBalpha-SR) should potentiate 5-fluorouracil (5-FU) and irinotecan chemotherapy in gastric cancer cells. Fluorouracil 120-134 NFKB inhibitor alpha Homo sapiens 53-65 15275881-2 2004 Inhibition of NF-kappaB by adenoviral delivery of an IkappaBalpha superrepressor (Ad.IkappaBalpha-SR) should potentiate 5-fluorouracil (5-FU) and irinotecan chemotherapy in gastric cancer cells. Fluorouracil 120-134 NFKB inhibitor alpha Homo sapiens 85-97 15275881-2 2004 Inhibition of NF-kappaB by adenoviral delivery of an IkappaBalpha superrepressor (Ad.IkappaBalpha-SR) should potentiate 5-fluorouracil (5-FU) and irinotecan chemotherapy in gastric cancer cells. Fluorouracil 136-140 nuclear factor kappa B subunit 1 Homo sapiens 14-23 15275881-2 2004 Inhibition of NF-kappaB by adenoviral delivery of an IkappaBalpha superrepressor (Ad.IkappaBalpha-SR) should potentiate 5-fluorouracil (5-FU) and irinotecan chemotherapy in gastric cancer cells. Fluorouracil 136-140 NFKB inhibitor alpha Homo sapiens 53-65 15275881-2 2004 Inhibition of NF-kappaB by adenoviral delivery of an IkappaBalpha superrepressor (Ad.IkappaBalpha-SR) should potentiate 5-fluorouracil (5-FU) and irinotecan chemotherapy in gastric cancer cells. Fluorouracil 136-140 NFKB inhibitor alpha Homo sapiens 85-97 15275881-8 2004 RESULTS: 5-FU and SN-38 significantly induced NF-kappaB activation as measured by luciferase reporter assay (p < 0.001). Fluorouracil 9-13 nuclear factor kappa B subunit 1 Homo sapiens 46-55 15275881-10 2004 In AGS cells, pretreatment with Ad.IkappaBalpha-SR followed by 5-FU (0.005 mmol/L) or SN-38 (10 ng/mL) led to increased growth inhibition of 13% and 59%, respectively (p < 0.001). Fluorouracil 63-67 NFKB inhibitor alpha Homo sapiens 35-47 15234211-0 2004 Inhibition of NF-kappa B augments sensitivity to 5-fluorouracil/folinic acid in colon cancer. Fluorouracil 49-63 nuclear factor kappa B subunit 1 Homo sapiens 14-24 15234211-9 2004 RESULTS: Treatment with 5-FU (0.001-10 mm), not only inhibited growth and induced apoptosis but significantly activated NF-kappaB in SW48 cells. Fluorouracil 24-28 nuclear factor kappa B subunit 1 Homo sapiens 120-129 15234211-11 2004 Likewise, folinic acid alone did not activate NF-kappaB or induce apoptosis but enhanced 5-FU-mediated NF-kappaB activation and cell apoptosis. Fluorouracil 89-93 nuclear factor kappa B subunit 1 Homo sapiens 103-112 15234211-13 2004 CONCLUSIONS: Treatment with 5-FU activates NF-kappaB. Fluorouracil 28-32 nuclear factor kappa B subunit 1 Homo sapiens 43-52 15234211-14 2004 Folinic acid enhances 5-FU-mediated activation of NF-kappaB. Fluorouracil 22-26 nuclear factor kappa B subunit 1 Homo sapiens 50-59 15234211-15 2004 Inhibition of NF-kappaB enhances the cytotoxic effect of 5-FU with or without Folinic acid in colon cancer cells. Fluorouracil 57-61 nuclear factor kappa B subunit 1 Homo sapiens 14-23 15301717-1 2004 BACKGROUND & OBJECTIVE: Platelet-derived endothelial cell growth factor/thymidine phosphorylase (PD-ECGF/TP) is an essential enzyme in converting 5"-deoxy-5-fluorouridine (5"-DFUR), and 5-fluorouracil (5-FU) to their active metabolites in vivo, and can be up-regulated by some cytokines such as interleukin-1, and interferon gamma (INFgamma). Fluorouracil 190-204 interferon gamma Homo sapiens 318-334 15301717-1 2004 BACKGROUND & OBJECTIVE: Platelet-derived endothelial cell growth factor/thymidine phosphorylase (PD-ECGF/TP) is an essential enzyme in converting 5"-deoxy-5-fluorouridine (5"-DFUR), and 5-fluorouracil (5-FU) to their active metabolites in vivo, and can be up-regulated by some cytokines such as interleukin-1, and interferon gamma (INFgamma). Fluorouracil 206-210 interferon gamma Homo sapiens 318-334 15172127-0 2004 p53 is an independent pre-treatment markers for long-term survival in stage II and III colorectal cancers: an analysis of interaction between genetic markers and fluorouracil-based adjuvant therapy. Fluorouracil 162-174 tumor protein p53 Homo sapiens 0-3 15260847-4 2004 We immunohistochemically evaluated the relationship between the expression of TS, p16(INK4a), CDK4 and cyclin D1 and the effect of 5-FU-based chemotherapy in colorectal cancers. Fluorouracil 131-135 cyclin dependent kinase inhibitor 2A Homo sapiens 82-85 15260847-4 2004 We immunohistochemically evaluated the relationship between the expression of TS, p16(INK4a), CDK4 and cyclin D1 and the effect of 5-FU-based chemotherapy in colorectal cancers. Fluorouracil 131-135 cyclin dependent kinase inhibitor 2A Homo sapiens 86-91 15260847-12 2004 In conclusion, the combination of low expression of TS and induction of p16(INK4a) after chemotherapy can be important indicators of the sensitivity to 5-FU-based chemotherapy in colorectal cancers. Fluorouracil 152-156 cyclin dependent kinase inhibitor 2A Homo sapiens 72-75 15260847-12 2004 In conclusion, the combination of low expression of TS and induction of p16(INK4a) after chemotherapy can be important indicators of the sensitivity to 5-FU-based chemotherapy in colorectal cancers. Fluorouracil 152-156 cyclin dependent kinase inhibitor 2A Homo sapiens 76-81 15217955-6 2004 RESULTS: 5-FU-resistant human colon cancer cells were found to overexpress metabotropic glutamate receptor 4 (mGluR4). Fluorouracil 9-13 glutamate receptor, ionotropic, AMPA4 (alpha 4) Mus musculus 110-116 15105837-5 2004 Pretreatment with chemotherapeutic drugs, for example, 5-fluorouracil (5-FU), rendered the TRAIL-resistant HCC cell lines sensitive to TRAIL-induced apoptosis. Fluorouracil 55-69 TNF superfamily member 10 Homo sapiens 91-96 15105837-5 2004 Pretreatment with chemotherapeutic drugs, for example, 5-fluorouracil (5-FU), rendered the TRAIL-resistant HCC cell lines sensitive to TRAIL-induced apoptosis. Fluorouracil 55-69 TNF superfamily member 10 Homo sapiens 135-140 15105837-5 2004 Pretreatment with chemotherapeutic drugs, for example, 5-fluorouracil (5-FU), rendered the TRAIL-resistant HCC cell lines sensitive to TRAIL-induced apoptosis. Fluorouracil 71-75 TNF superfamily member 10 Homo sapiens 91-96 15105837-5 2004 Pretreatment with chemotherapeutic drugs, for example, 5-fluorouracil (5-FU), rendered the TRAIL-resistant HCC cell lines sensitive to TRAIL-induced apoptosis. Fluorouracil 71-75 TNF superfamily member 10 Homo sapiens 135-140 15105837-8 2004 5-FU pretreatment downregulated cellular FLICE-inhibitory protein (cFLIP) and specific cFLIP downregulation by small interfering RNA was sufficient to sensitise TRAIL-resistant HCC cell lines for TRAIL-induced apoptosis. Fluorouracil 0-4 CASP8 and FADD like apoptosis regulator Homo sapiens 67-72 15105837-8 2004 5-FU pretreatment downregulated cellular FLICE-inhibitory protein (cFLIP) and specific cFLIP downregulation by small interfering RNA was sufficient to sensitise TRAIL-resistant HCC cell lines for TRAIL-induced apoptosis. Fluorouracil 0-4 CASP8 and FADD like apoptosis regulator Homo sapiens 87-92 15105837-8 2004 5-FU pretreatment downregulated cellular FLICE-inhibitory protein (cFLIP) and specific cFLIP downregulation by small interfering RNA was sufficient to sensitise TRAIL-resistant HCC cell lines for TRAIL-induced apoptosis. Fluorouracil 0-4 TNF superfamily member 10 Homo sapiens 161-166 15105837-8 2004 5-FU pretreatment downregulated cellular FLICE-inhibitory protein (cFLIP) and specific cFLIP downregulation by small interfering RNA was sufficient to sensitise TRAIL-resistant HCC cell lines for TRAIL-induced apoptosis. Fluorouracil 0-4 TNF superfamily member 10 Homo sapiens 196-201 15105837-9 2004 Thus, a potential mechanism for TRAIL sensitisation by 5-FU is the increased effectiveness of caspase-8 recruitment to and activation at the DISC facilitated by the downregulation of cFLIP and the consequent shift in the ratio of caspase-8 to cFLIP at the DISC. Fluorouracil 55-59 TNF superfamily member 10 Homo sapiens 32-37 15105837-9 2004 Thus, a potential mechanism for TRAIL sensitisation by 5-FU is the increased effectiveness of caspase-8 recruitment to and activation at the DISC facilitated by the downregulation of cFLIP and the consequent shift in the ratio of caspase-8 to cFLIP at the DISC. Fluorouracil 55-59 CASP8 and FADD like apoptosis regulator Homo sapiens 183-188 15105837-9 2004 Thus, a potential mechanism for TRAIL sensitisation by 5-FU is the increased effectiveness of caspase-8 recruitment to and activation at the DISC facilitated by the downregulation of cFLIP and the consequent shift in the ratio of caspase-8 to cFLIP at the DISC. Fluorouracil 55-59 CASP8 and FADD like apoptosis regulator Homo sapiens 243-248 15330158-5 2004 MATERIALS AND METHODS: The effect of chemotherapeutic agents (Cisplatin, Carboplatin and 5-FU) on the production of VEGF was investigated on established human HNSCC cell lines at both mRNA and protein levels. Fluorouracil 89-93 vascular endothelial growth factor A Homo sapiens 116-120 15280064-3 2004 The aim of this study was to estimate quantitatively the apparent permeability-surface area product (K(PS)) in tumors to a macromolecular contrast medium (MMCM), to follow changes in K(PS) induced by antibodies to vascular endothelial growth factor (anti-VEGF), and to correlate the findings with tumor accumulation of cisplatin, a highly protein-bound cytotoxin, and 5-fluorouracil (5-FU), a small unbound cytotoxin. Fluorouracil 368-382 vascular endothelial growth factor A Homo sapiens 214-248 15280064-3 2004 The aim of this study was to estimate quantitatively the apparent permeability-surface area product (K(PS)) in tumors to a macromolecular contrast medium (MMCM), to follow changes in K(PS) induced by antibodies to vascular endothelial growth factor (anti-VEGF), and to correlate the findings with tumor accumulation of cisplatin, a highly protein-bound cytotoxin, and 5-fluorouracil (5-FU), a small unbound cytotoxin. Fluorouracil 384-388 vascular endothelial growth factor A Homo sapiens 214-248 15222051-1 2004 AIM: To observe the reversal effects of wide-type p53 gene on multi-drug resistance to 5-FU (LOVO/5-FU). Fluorouracil 87-91 tumor protein p53 Homo sapiens 50-53 15222051-1 2004 AIM: To observe the reversal effects of wide-type p53 gene on multi-drug resistance to 5-FU (LOVO/5-FU). Fluorouracil 98-102 tumor protein p53 Homo sapiens 50-53 15222051-2 2004 METHODS: After treatment with Ad-p53, LOVO/5-FU sensitivity to 5-Fu was investigated using tetrazolium dye assay. Fluorouracil 63-67 tumor protein p53 Homo sapiens 33-36 15217955-7 2004 Other experiments showed cellular resistance to 5-FU (i.e., cell survival) was altered by the mGluR4 agonist l-2-amino-4-phosphonobutyric acid (L-AP 4), and by the mGluR4 antagonist (S)-amino-2-methyl-4-phosphonobutanoic acid (MAP 4), in that L-AP 4 increased 5-FU resistance in SNU-769A cells, whereas MAP 4 ablated 5-FU resistance in 5-FU-resistant cells. Fluorouracil 48-52 glutamate receptor, ionotropic, AMPA4 (alpha 4) Mus musculus 94-100 15217955-7 2004 Other experiments showed cellular resistance to 5-FU (i.e., cell survival) was altered by the mGluR4 agonist l-2-amino-4-phosphonobutyric acid (L-AP 4), and by the mGluR4 antagonist (S)-amino-2-methyl-4-phosphonobutanoic acid (MAP 4), in that L-AP 4 increased 5-FU resistance in SNU-769A cells, whereas MAP 4 ablated 5-FU resistance in 5-FU-resistant cells. Fluorouracil 48-52 growth differentiation factor 5 Homo sapiens 144-150 15217955-7 2004 Other experiments showed cellular resistance to 5-FU (i.e., cell survival) was altered by the mGluR4 agonist l-2-amino-4-phosphonobutyric acid (L-AP 4), and by the mGluR4 antagonist (S)-amino-2-methyl-4-phosphonobutanoic acid (MAP 4), in that L-AP 4 increased 5-FU resistance in SNU-769A cells, whereas MAP 4 ablated 5-FU resistance in 5-FU-resistant cells. Fluorouracil 48-52 glutamate receptor, ionotropic, AMPA4 (alpha 4) Mus musculus 164-170 15217955-7 2004 Other experiments showed cellular resistance to 5-FU (i.e., cell survival) was altered by the mGluR4 agonist l-2-amino-4-phosphonobutyric acid (L-AP 4), and by the mGluR4 antagonist (S)-amino-2-methyl-4-phosphonobutanoic acid (MAP 4), in that L-AP 4 increased 5-FU resistance in SNU-769A cells, whereas MAP 4 ablated 5-FU resistance in 5-FU-resistant cells. Fluorouracil 48-52 growth differentiation factor 5 Homo sapiens 243-249 15217955-7 2004 Other experiments showed cellular resistance to 5-FU (i.e., cell survival) was altered by the mGluR4 agonist l-2-amino-4-phosphonobutyric acid (L-AP 4), and by the mGluR4 antagonist (S)-amino-2-methyl-4-phosphonobutanoic acid (MAP 4), in that L-AP 4 increased 5-FU resistance in SNU-769A cells, whereas MAP 4 ablated 5-FU resistance in 5-FU-resistant cells. Fluorouracil 260-264 glutamate receptor, ionotropic, AMPA4 (alpha 4) Mus musculus 164-170 15217955-7 2004 Other experiments showed cellular resistance to 5-FU (i.e., cell survival) was altered by the mGluR4 agonist l-2-amino-4-phosphonobutyric acid (L-AP 4), and by the mGluR4 antagonist (S)-amino-2-methyl-4-phosphonobutanoic acid (MAP 4), in that L-AP 4 increased 5-FU resistance in SNU-769A cells, whereas MAP 4 ablated 5-FU resistance in 5-FU-resistant cells. Fluorouracil 260-264 glutamate receptor, ionotropic, AMPA4 (alpha 4) Mus musculus 164-170 15217955-7 2004 Other experiments showed cellular resistance to 5-FU (i.e., cell survival) was altered by the mGluR4 agonist l-2-amino-4-phosphonobutyric acid (L-AP 4), and by the mGluR4 antagonist (S)-amino-2-methyl-4-phosphonobutanoic acid (MAP 4), in that L-AP 4 increased 5-FU resistance in SNU-769A cells, whereas MAP 4 ablated 5-FU resistance in 5-FU-resistant cells. Fluorouracil 260-264 glutamate receptor, ionotropic, AMPA4 (alpha 4) Mus musculus 164-170 15217955-9 2004 Interestingly, 5-FU down-regulated mGluR4 expression, and MAP 4 suppressed proliferation in both cell lines. Fluorouracil 15-19 glutamate receptor, ionotropic, AMPA4 (alpha 4) Mus musculus 35-41 15217955-11 2004 Overexpression of mGluR4 may tentatively be responsible for 5-FU resistance and, although activation by agonist promotes cell survival in the presence of 5-FU, decreased mGluR4 expression or inactivation by antagonist contributes to cell death. Fluorouracil 60-64 glutamate receptor, ionotropic, AMPA4 (alpha 4) Mus musculus 18-24 15217955-11 2004 Overexpression of mGluR4 may tentatively be responsible for 5-FU resistance and, although activation by agonist promotes cell survival in the presence of 5-FU, decreased mGluR4 expression or inactivation by antagonist contributes to cell death. Fluorouracil 154-158 glutamate receptor, ionotropic, AMPA4 (alpha 4) Mus musculus 18-24 15161699-3 2004 We investigated p21 and p21B for mutations and epigenetic silencing in locally advanced breast cancers treated with doxorubicin or 5-fluorouracil/mitomycin and correlated our findings with treatment response and TP53 status. Fluorouracil 131-145 cyclin dependent kinase inhibitor 1A Homo sapiens 16-19 15136595-1 2004 PURPOSE: The goal of this study was to examine the feasibility of developing a multigene predictor of pathologic complete response (pCR) to sequential weekly paclitaxel and fluorouracil + doxorubicin + cyclophosphamide (T/FAC) neoadjuvant chemotherapy regimen for breast cancer. Fluorouracil 173-185 FA complementation group C Homo sapiens 222-225 15177426-1 2004 This study was designed to observe whether the rates of apoptosis induced in the breast cancer cell line MCF-7 by 5-fluorouracil (5-FU) could be enhanced by transfecting bcl-2 antisense oligonucleotide (ASODN). Fluorouracil 114-128 BCL2 apoptosis regulator Homo sapiens 170-175 15177426-1 2004 This study was designed to observe whether the rates of apoptosis induced in the breast cancer cell line MCF-7 by 5-fluorouracil (5-FU) could be enhanced by transfecting bcl-2 antisense oligonucleotide (ASODN). Fluorouracil 130-134 BCL2 apoptosis regulator Homo sapiens 170-175 15177426-5 2004 Moreover, incubation of MCF-7 with bcl-2 ASODN prior to 5-FU treatment caused remarkable loss of viable cells compared with all other control ODNs (P < 0.01). Fluorouracil 56-60 BCL2 apoptosis regulator Homo sapiens 35-40 15161716-8 2004 Inactivation of p53 in MCF-7 and HCT116 cell lines blocked 5-FU- and antifolate-mediated up-regulation of Fas. Fluorouracil 59-63 tumor protein p53 Homo sapiens 16-19 15161716-10 2004 Lack of Fas up-regulation in the p53-null and -mutant lines abolished the synergistic interaction between 5-FU and CH-11. Fluorouracil 106-110 tumor protein p53 Homo sapiens 33-36 15150801-1 2004 The mechanism of cooperative binding of both cytarabine and fluorouracil, used in combination therapy, to the transporting protein [bovine serum albumin (BSA)] has been investigated. Fluorouracil 60-72 albumin Homo sapiens 139-152 15150801-7 2004 The competition of these two drugs and the removal of 5-fluorouracil by cytarabine from the common binding site in serum albumin tertiary structure are observed. Fluorouracil 54-68 albumin Homo sapiens 115-128 15016801-2 2004 To this end, we assessed the transcriptional response of HCT116 colorectal cancer cells during apoptosis induced by the anticancer drug 5-fluorouracil as the function of p53 status, and we identified 230 potential targets that are regulated by p53. Fluorouracil 136-150 tumor protein p53 Homo sapiens 170-173 15016801-2 2004 To this end, we assessed the transcriptional response of HCT116 colorectal cancer cells during apoptosis induced by the anticancer drug 5-fluorouracil as the function of p53 status, and we identified 230 potential targets that are regulated by p53. Fluorouracil 136-150 tumor protein p53 Homo sapiens 244-247 15016801-4 2004 Strikingly, we found that p53 regulates gene expression primarily through transcriptional repression (n = 189) rather than activation (n = 41), and selective blockade of p53-dependent gene repression resulted in the reduction in 5-fluorouracil-induced apoptosis. Fluorouracil 229-243 tumor protein p53 Homo sapiens 26-29 15016801-4 2004 Strikingly, we found that p53 regulates gene expression primarily through transcriptional repression (n = 189) rather than activation (n = 41), and selective blockade of p53-dependent gene repression resulted in the reduction in 5-fluorouracil-induced apoptosis. Fluorouracil 229-243 tumor protein p53 Homo sapiens 170-173 15082204-1 2004 OBJECTIVE: To analyse the long-term efficacy of combined interferon-alpha (IFN-alpha) and interleukin-2 (IL-2) subcutaneously, with 5-fluorouracil (5-FU) intravenously in a general multicentre setting, as treatment for metastatic renal cell carcinoma (RCC). Fluorouracil 132-146 interferon alpha 1 Homo sapiens 75-84 15124184-5 2004 In the present experiments, we examined the expression of caspase-3, p53 and Bid in the three cell lines induced by 5-FU and/or anti-CD8 antibody. Fluorouracil 116-120 caspase 3 Homo sapiens 58-67 15124184-6 2004 We found high expression of p53 during activation-induced cell death of TJK cells mediated by anti-CD8 antibody and apoptosis of TJK and T3JK induced by 5-FU, implicating p53 involvement in apoptosis of leukemia cells induced by anti-CD8 antibody and 5-FU. Fluorouracil 153-157 tumor protein p53 Homo sapiens 171-174 15124184-6 2004 We found high expression of p53 during activation-induced cell death of TJK cells mediated by anti-CD8 antibody and apoptosis of TJK and T3JK induced by 5-FU, implicating p53 involvement in apoptosis of leukemia cells induced by anti-CD8 antibody and 5-FU. Fluorouracil 251-255 tumor protein p53 Homo sapiens 28-31 15124184-6 2004 We found high expression of p53 during activation-induced cell death of TJK cells mediated by anti-CD8 antibody and apoptosis of TJK and T3JK induced by 5-FU, implicating p53 involvement in apoptosis of leukemia cells induced by anti-CD8 antibody and 5-FU. Fluorouracil 251-255 tumor protein p53 Homo sapiens 171-174 15124184-7 2004 We also detected the active form of caspase-3 and Bid in apoptotic leukemia cells after treatment with 5-FU and/or anti-CD8 antibody, indicating that the drug and antibody induced cell death through caspase-3 and the signal pathway may involve the Bcl-2 protein family. Fluorouracil 103-107 caspase 3 Homo sapiens 36-45 15124184-7 2004 We also detected the active form of caspase-3 and Bid in apoptotic leukemia cells after treatment with 5-FU and/or anti-CD8 antibody, indicating that the drug and antibody induced cell death through caspase-3 and the signal pathway may involve the Bcl-2 protein family. Fluorouracil 103-107 BH3 interacting domain death agonist Homo sapiens 50-53 15124184-7 2004 We also detected the active form of caspase-3 and Bid in apoptotic leukemia cells after treatment with 5-FU and/or anti-CD8 antibody, indicating that the drug and antibody induced cell death through caspase-3 and the signal pathway may involve the Bcl-2 protein family. Fluorouracil 103-107 caspase 3 Homo sapiens 199-208 15124184-7 2004 We also detected the active form of caspase-3 and Bid in apoptotic leukemia cells after treatment with 5-FU and/or anti-CD8 antibody, indicating that the drug and antibody induced cell death through caspase-3 and the signal pathway may involve the Bcl-2 protein family. Fluorouracil 103-107 BCL2 apoptosis regulator Homo sapiens 248-253 15124184-8 2004 Our results showed that combined treatment with 5-FU and anti-CD8 antibody could enhance the rate of apoptosis induced by 5-FU or anti-CD8 antibody through increased expression of p53 and by promoting activation of caspase-3 and Bid. Fluorouracil 48-52 tumor protein p53 Homo sapiens 180-183 15124184-8 2004 Our results showed that combined treatment with 5-FU and anti-CD8 antibody could enhance the rate of apoptosis induced by 5-FU or anti-CD8 antibody through increased expression of p53 and by promoting activation of caspase-3 and Bid. Fluorouracil 48-52 caspase 3 Homo sapiens 215-224 15124184-8 2004 Our results showed that combined treatment with 5-FU and anti-CD8 antibody could enhance the rate of apoptosis induced by 5-FU or anti-CD8 antibody through increased expression of p53 and by promoting activation of caspase-3 and Bid. Fluorouracil 48-52 BH3 interacting domain death agonist Homo sapiens 229-232 15124184-8 2004 Our results showed that combined treatment with 5-FU and anti-CD8 antibody could enhance the rate of apoptosis induced by 5-FU or anti-CD8 antibody through increased expression of p53 and by promoting activation of caspase-3 and Bid. Fluorouracil 122-126 tumor protein p53 Homo sapiens 180-183 15124184-8 2004 Our results showed that combined treatment with 5-FU and anti-CD8 antibody could enhance the rate of apoptosis induced by 5-FU or anti-CD8 antibody through increased expression of p53 and by promoting activation of caspase-3 and Bid. Fluorouracil 122-126 caspase 3 Homo sapiens 215-224 15124184-8 2004 Our results showed that combined treatment with 5-FU and anti-CD8 antibody could enhance the rate of apoptosis induced by 5-FU or anti-CD8 antibody through increased expression of p53 and by promoting activation of caspase-3 and Bid. Fluorouracil 122-126 BH3 interacting domain death agonist Homo sapiens 229-232 15067352-9 2004 5-FU metabolism-associated genes (e.g., TYMS, DTYMK, UP) and DNA repair genes (e.g., FEN1, FANCG, RAD23B) were also up-regulated in one or both resistant derivatives, suggesting that the resistant derivatives might be able to overcome both 5-FU inhibition of thymidylate synthase and the DNA damage caused by 5-FU, respectively. Fluorouracil 0-4 deoxythymidylate kinase Homo sapiens 46-51 15200906-21 2004 40.2 micro mol/L and 29.5 micro mol/L of 5-Fu were detected in the medium containing 400 micro mol/L of 5"-DFUR treated with THP-1 and U937 cells, respectively. Fluorouracil 41-45 GLI family zinc finger 2 Homo sapiens 125-130 15082204-1 2004 OBJECTIVE: To analyse the long-term efficacy of combined interferon-alpha (IFN-alpha) and interleukin-2 (IL-2) subcutaneously, with 5-fluorouracil (5-FU) intravenously in a general multicentre setting, as treatment for metastatic renal cell carcinoma (RCC). Fluorouracil 132-146 interleukin 2 Homo sapiens 90-103 15082204-1 2004 OBJECTIVE: To analyse the long-term efficacy of combined interferon-alpha (IFN-alpha) and interleukin-2 (IL-2) subcutaneously, with 5-fluorouracil (5-FU) intravenously in a general multicentre setting, as treatment for metastatic renal cell carcinoma (RCC). Fluorouracil 132-146 interleukin 2 Homo sapiens 105-109 15082204-13 2004 CONCLUSION: IL-2 and IFN-alpha with 5-FU based immunotherapy achieve durable survival rates at 3 years in a minority of patients. Fluorouracil 36-40 interferon alpha 1 Homo sapiens 21-30 15206578-3 2004 After repeated administration of 5-FU at 50 mg/kg/day for 1-5 days, a time-dependent decrease in cells expressing CD45Low, CD71 and CD90 was observed, whereas a decrease in the CD45High expressing cells was not observed. Fluorouracil 33-37 Thy-1 cell surface antigen Rattus norvegicus 132-136 15133762-0 2004 5-Fluorouracil or gemcitabine combined with adenoviral-mediated reintroduction of p16INK4A greatly enhanced cytotoxicity in Panc-1 pancreatic adenocarcinoma cells. Fluorouracil 0-14 cyclin dependent kinase inhibitor 2A Homo sapiens 82-90 15133762-12 2004 Incubation of Suit-2 cells with 5-FU followed by Ad-mediated overexpression of p16(INK4A) also resulted in a significant reduction in cell viability. Fluorouracil 32-36 cyclin dependent kinase inhibitor 2A Homo sapiens 83-88 15206578-4 2004 Furthermore, the decrease was dose-dependent in CD45Low, CD71 and CD90 expressing cells after administration of 5-FU between 2 and 50 mg/kg/day for 4 days. Fluorouracil 112-116 Thy-1 cell surface antigen Rattus norvegicus 66-70 15206578-5 2004 After 4-day repeated dose of 5-FU at 50 mg/kg/day followed by a recovery period, the change in number of CD45Low, CD45R, CD71 and CD90 cells to the bottom and in recovery showed different kinetics. Fluorouracil 29-33 Thy-1 cell surface antigen Rattus norvegicus 130-134 15120327-5 2004 Whereas treatment with the combination of TRAIL and 5-FU or mitomycin led to enhanced activation of caspase-3, the combination of TRAIL and calpain inhibitor I resulted in enhanced activation of both caspase-8 and caspase-3. Fluorouracil 52-56 caspase 3 Homo sapiens 100-109 15120327-3 2004 Here we demonstrate that several chemotherapeutic agents, including 5-fluorouracil (5-FU) and mitomycin, and calpain inhibitor I, an NFkappaB inhibitor, can overcome acquired resistance to TRAIL in DLD1 colon cancer cells. Fluorouracil 68-82 TNF superfamily member 10 Homo sapiens 189-194 15120327-3 2004 Here we demonstrate that several chemotherapeutic agents, including 5-fluorouracil (5-FU) and mitomycin, and calpain inhibitor I, an NFkappaB inhibitor, can overcome acquired resistance to TRAIL in DLD1 colon cancer cells. Fluorouracil 84-88 TNF superfamily member 10 Homo sapiens 189-194 15231865-13 2004 Pharmacokinetic studies after administration of S-1 revealed high and prolonged plasma 5-FU levels. Fluorouracil 87-91 proteasome 26S subunit, non-ATPase 1 Homo sapiens 48-51 15279063-3 2004 Patients underwent low-dose CDDP+5-FU monitoring continual CEA level. Fluorouracil 33-37 CEA cell adhesion molecule 3 Homo sapiens 59-62 14998932-5 2004 In this study we report that three different mutations of murine Hip1 lead to hematopoietic abnormalities reflected by diminished early progenitor frequencies and resistance to 5-FU-induced bone marrow toxicity. Fluorouracil 177-181 huntingtin interacting protein 1 Mus musculus 65-69 14998548-4 2004 Actually, it has been shown that the expression of CEA can be up-regulated by pharmacological agents including, antineoplastic drugs (i.e. 5-fluorouracil), cytokines (i.e. interferons or interleukin-6), differentiating agents (i.e. sodium butyrate) and protein kinase inhibitors (i.e. staurosporine). Fluorouracil 139-153 CEA cell adhesion molecule 3 Homo sapiens 51-54 15087041-6 2004 METHOD: Serum analysis of p53 antibodies was performed by enzyme-linked immunosorbent assay (ELISA) in 38 patients with esophageal cancer preoperatively, then surgically resected specimens were analyzed for their chemosensitivity to cisdichlorodiammineplatinum (DDP),5-fluorouracil (5-FU), and Adriamycin (ADM) by in vitro drug response assay MTT colorimetry. Fluorouracil 267-281 tumor protein p53 Homo sapiens 26-29 15102660-10 2004 A multivariate analysis, including tumor stage, gender, TP53 mutations, and MMP3 polymorphism, showed that the 6A/6A genotype was an independent factor of response to 5-fluorouracil-cisplatin chemotherapy in head and neck cancer patients with an odds ratio of 6.7 as compared with the 5A/5A genotype. Fluorouracil 167-181 tumor protein p53 Homo sapiens 56-60 15102660-10 2004 A multivariate analysis, including tumor stage, gender, TP53 mutations, and MMP3 polymorphism, showed that the 6A/6A genotype was an independent factor of response to 5-fluorouracil-cisplatin chemotherapy in head and neck cancer patients with an odds ratio of 6.7 as compared with the 5A/5A genotype. Fluorouracil 167-181 matrix metallopeptidase 3 Homo sapiens 76-80 15087041-6 2004 METHOD: Serum analysis of p53 antibodies was performed by enzyme-linked immunosorbent assay (ELISA) in 38 patients with esophageal cancer preoperatively, then surgically resected specimens were analyzed for their chemosensitivity to cisdichlorodiammineplatinum (DDP),5-fluorouracil (5-FU), and Adriamycin (ADM) by in vitro drug response assay MTT colorimetry. Fluorouracil 283-287 tumor protein p53 Homo sapiens 26-29 15087041-12 2004 The chemosensitivity to DDP, 5-FU, and ADM (11.1%,16.1%,and 16.1%, respectively) of the patients with positive serum p53-Ab was significantly lower than that of the patients with negative p53-Ab (60%, 45%, and 35%; P< 0.01,P< 0.05, and P< 0.05, respectively). Fluorouracil 29-33 tumor protein p53 Homo sapiens 117-120 14726695-6 2004 It was found that overexpression of ZNRD1 could sensitize SGC7901 cells to P-glycoprotein (P-gp)-related anticancer drugs (vincristine, adriamycin, etoposide) but not to P-gp-nonrelated drugs (5-fluorouracil and cisplatin), which was accompanied with significantly decreased adriamycin accumulation and retention and increased adriamycin releasing in SGC7901 cells. Fluorouracil 193-207 ATP binding cassette subfamily B member 1 Homo sapiens 91-95 15144595-0 2004 [Effects of selective cyclooxygenase-2 inhibitor NS-398 on 5-fluorouracil chemotherapy and progression of colon cells: an experimental study]. Fluorouracil 59-73 prostaglandin-endoperoxide synthase 2 Homo sapiens 22-38 15144595-1 2004 OBJECTIVE: To investigate the effects of selective cyclooxygenase-2 (COX-2) inhibitor NS-398 on 5-fluorouracil (5-Fu) chemotherapy and on the progression of colon cells. Fluorouracil 96-110 prostaglandin-endoperoxide synthase 2 Homo sapiens 51-67 15144595-1 2004 OBJECTIVE: To investigate the effects of selective cyclooxygenase-2 (COX-2) inhibitor NS-398 on 5-fluorouracil (5-Fu) chemotherapy and on the progression of colon cells. Fluorouracil 96-110 prostaglandin-endoperoxide synthase 2 Homo sapiens 69-74 15144595-1 2004 OBJECTIVE: To investigate the effects of selective cyclooxygenase-2 (COX-2) inhibitor NS-398 on 5-fluorouracil (5-Fu) chemotherapy and on the progression of colon cells. Fluorouracil 112-116 prostaglandin-endoperoxide synthase 2 Homo sapiens 51-67 15144595-1 2004 OBJECTIVE: To investigate the effects of selective cyclooxygenase-2 (COX-2) inhibitor NS-398 on 5-fluorouracil (5-Fu) chemotherapy and on the progression of colon cells. Fluorouracil 112-116 prostaglandin-endoperoxide synthase 2 Homo sapiens 69-74 15144568-5 2004 By transmission electron microscopy (TEM) assay, most tumor cells treated with ONYX015 or with ZD55-hTRAIL singly or in combination with 5-FU were lysed due to viral propagation. Fluorouracil 137-141 TNF superfamily member 10 Homo sapiens 100-106 15010816-0 2004 Expression of p53 protein as a predictor of the response to 5-fluorouracil and cisplatin chemotherapy in human gastrointestinal cancer cell lines evaluated with apoptosis by use of thin layer collagen gel. Fluorouracil 60-74 tumor protein p53 Homo sapiens 14-17 15041737-9 2004 Using semiquantitative reverse transcription-PCR, we have demonstrated down-regulation of thymidine phosphorylase mRNA in both p53(+/+) and p53(-/-) 5-FU-resistant cells, suggesting that decreased production of 5-FU active metabolites may be an important resistance mechanism in these lines. Fluorouracil 149-153 tumor protein p53 Homo sapiens 140-143 15041737-9 2004 Using semiquantitative reverse transcription-PCR, we have demonstrated down-regulation of thymidine phosphorylase mRNA in both p53(+/+) and p53(-/-) 5-FU-resistant cells, suggesting that decreased production of 5-FU active metabolites may be an important resistance mechanism in these lines. Fluorouracil 211-215 tumor protein p53 Homo sapiens 127-130 15041737-8 2004 These data suggest that p53 may be an important determinant of sensitivity to 5-FU and oxaliplatin but not CPT-11. Fluorouracil 78-82 tumor protein p53 Homo sapiens 24-27 15014363-0 2004 Sequence-dependent effect of a cyclooxygenase-2 inhibitor on topoisomerase I inhibitor and 5-fluorouracil-induced cytotoxicity of colon cancer cells. Fluorouracil 91-105 prostaglandin-endoperoxide synthase 2 Homo sapiens 31-47 15041737-0 2004 Characterization of p53 wild-type and null isogenic colorectal cancer cell lines resistant to 5-fluorouracil, oxaliplatin, and irinotecan. Fluorouracil 94-108 tumor protein p53 Homo sapiens 20-23 15041737-5 2004 In addition, we found that resistance to 5-FU and oxaliplatin was higher in parental p53(-/-) cells compared with parental p53(+/+) cells, with an approximately 5-fold increase in IC(50 (72 h)) for each drug. Fluorouracil 41-45 tumor protein p53 Homo sapiens 85-88 15041737-5 2004 In addition, we found that resistance to 5-FU and oxaliplatin was higher in parental p53(-/-) cells compared with parental p53(+/+) cells, with an approximately 5-fold increase in IC(50 (72 h)) for each drug. Fluorouracil 41-45 tumor protein p53 Homo sapiens 123-126 15041737-7 2004 Furthermore, apoptosis after treatment with 5-FU and oxaliplatin, but not CPT-11, was significantly reduced in parental p53(-/-) cells compared with parental p53(+/+) cells. Fluorouracil 44-48 tumor protein p53 Homo sapiens 120-123 15041737-7 2004 Furthermore, apoptosis after treatment with 5-FU and oxaliplatin, but not CPT-11, was significantly reduced in parental p53(-/-) cells compared with parental p53(+/+) cells. Fluorouracil 44-48 tumor protein p53 Homo sapiens 158-161 15152939-6 2004 Inactivation of wild-type p53 abrogated the 5-FU-mediated induction of SSAT and annexin II. Fluorouracil 44-48 tumor protein p53 Homo sapiens 26-29 14648016-1 2004 PURPOSE: The study objectives were to define subcutaneous (s.c.) interferon gamma (IFN-gamma) disposition in patients with gastrointestinal malignancies receiving 5-fluorouracil (5-FU) and leucovorin (LV) and to examine the relationship between IFN-gamma exposures and Fas upregulation in vivo and in vitro. Fluorouracil 163-177 interferon gamma Homo sapiens 65-92 14648016-1 2004 PURPOSE: The study objectives were to define subcutaneous (s.c.) interferon gamma (IFN-gamma) disposition in patients with gastrointestinal malignancies receiving 5-fluorouracil (5-FU) and leucovorin (LV) and to examine the relationship between IFN-gamma exposures and Fas upregulation in vivo and in vitro. Fluorouracil 163-177 interferon gamma Homo sapiens 83-92 14648016-2 2004 METHODS: Patients received IFN-gamma (10, 25, 50, 75, and 100 microg/m(2)) with LV and 5-FU, and serial samples were collected after the first dose. Fluorouracil 87-91 interferon gamma Homo sapiens 27-36 14648016-1 2004 PURPOSE: The study objectives were to define subcutaneous (s.c.) interferon gamma (IFN-gamma) disposition in patients with gastrointestinal malignancies receiving 5-fluorouracil (5-FU) and leucovorin (LV) and to examine the relationship between IFN-gamma exposures and Fas upregulation in vivo and in vitro. Fluorouracil 179-183 interferon gamma Homo sapiens 65-92 14648016-9 2004 In vitro studies in HT29 cells demonstrated that clinically relevant IFN-gamma concentrations (1 to 10 U/ml for 6.5 h) with 5-FU/LV upregulated Fas expression 3.5-fold, similar to that in PBMC in vivo. Fluorouracil 124-128 interferon gamma Homo sapiens 69-78 14648016-1 2004 PURPOSE: The study objectives were to define subcutaneous (s.c.) interferon gamma (IFN-gamma) disposition in patients with gastrointestinal malignancies receiving 5-fluorouracil (5-FU) and leucovorin (LV) and to examine the relationship between IFN-gamma exposures and Fas upregulation in vivo and in vitro. Fluorouracil 179-183 interferon gamma Homo sapiens 83-92 14712497-0 2004 Enhanced radiosensitization and chemosensitization in NF-kappaB-suppressed human oral cancer cells via the inhibition of gamma-irradiation- and 5-FU-induced production of IL-6 and IL-8. Fluorouracil 144-148 interleukin 6 Homo sapiens 171-175 15014017-0 2004 Combination phase I trial of a novel oral fluorouracil derivative S-1 with low-dose cisplatin for unresectable and recurrent gastric cancer (JFMC27-9902). Fluorouracil 42-54 proteasome 26S subunit, non-ATPase 1 Homo sapiens 66-69 15014017-1 2004 PURPOSE: The Japanese Foundation for Multidisciplinary Treatment of Cancer conducted a Phase I study of a novel oral fluorouracil derivative, S-1, combined with a low dose of cisplatin in unresectable and recurrent gastric cancer. Fluorouracil 117-129 proteasome 26S subunit, non-ATPase 1 Homo sapiens 142-145 14712497-0 2004 Enhanced radiosensitization and chemosensitization in NF-kappaB-suppressed human oral cancer cells via the inhibition of gamma-irradiation- and 5-FU-induced production of IL-6 and IL-8. Fluorouracil 144-148 C-X-C motif chemokine ligand 8 Homo sapiens 180-184 14712497-7 2004 ELISA analysis indicated that although a remarkable increase in production of IL-6 and IL-8 was observed in B88 and B88neo after in vitro exposure to IR or treatment with 5-FU, radiotherapy and chemotherapy-induced production of these cytokines was significantly suppressed in B88mI cell clones. Fluorouracil 171-175 interleukin 6 Homo sapiens 78-82 14712497-7 2004 ELISA analysis indicated that although a remarkable increase in production of IL-6 and IL-8 was observed in B88 and B88neo after in vitro exposure to IR or treatment with 5-FU, radiotherapy and chemotherapy-induced production of these cytokines was significantly suppressed in B88mI cell clones. Fluorouracil 171-175 C-X-C motif chemokine ligand 8 Homo sapiens 87-91 15076784-10 2004 CONCLUSION: Exercise training enhances endothelium-dependent vasorelaxation after 5-FU-induced vasoconstriction, and this may be due, at least in part, to an increase in aortic eNOS protein content and activity. Fluorouracil 82-86 nitric oxide synthase 3 Homo sapiens 177-181 14985455-4 2004 In so doing, we found that disruption of E-cadherin-mediated adhesion sensitizes multicellular spheroids of HT29 in vitro to treatment with 5-fluorouracil, paclitaxel, vinblastine, and etoposide but not cisplatin. Fluorouracil 140-154 cadherin 1 Homo sapiens 41-51 14665630-4 2004 Compared with cells expressing exogenous wild type p53, the apoptotic response to 5-fluorouracil (5FU) was >50% reduced in cells expressing S15A or S20A mutant p53, and even more reduced by combined mutation of serines 6, 9, 15, 20, 33, and 37 (N6A). Fluorouracil 82-96 tumor protein p53 Homo sapiens 51-54 14665630-4 2004 Compared with cells expressing exogenous wild type p53, the apoptotic response to 5-fluorouracil (5FU) was >50% reduced in cells expressing S15A or S20A mutant p53, and even more reduced by combined mutation of serines 6, 9, 15, 20, 33, and 37 (N6A). Fluorouracil 82-96 tumor protein p53 Homo sapiens 163-166 14665630-4 2004 Compared with cells expressing exogenous wild type p53, the apoptotic response to 5-fluorouracil (5FU) was >50% reduced in cells expressing S15A or S20A mutant p53, and even more reduced by combined mutation of serines 6, 9, 15, 20, 33, and 37 (N6A). Fluorouracil 98-101 tumor protein p53 Homo sapiens 51-54 14665630-4 2004 Compared with cells expressing exogenous wild type p53, the apoptotic response to 5-fluorouracil (5FU) was >50% reduced in cells expressing S15A or S20A mutant p53, and even more reduced by combined mutation of serines 6, 9, 15, 20, 33, and 37 (N6A). Fluorouracil 98-101 tumor protein p53 Homo sapiens 163-166 14719102-0 2004 Cyclin A correlates with the sensitivity of human cancer cells to cytotoxic effects of 5-FU. Fluorouracil 87-91 cyclin A2 Homo sapiens 0-8 14719102-1 2004 We investigated the role of cyclin A in the cytotoxic effect of 5-fluorouracil (5-FU) on cancer cell lines. Fluorouracil 64-78 cyclin A2 Homo sapiens 28-36 14719102-1 2004 We investigated the role of cyclin A in the cytotoxic effect of 5-fluorouracil (5-FU) on cancer cell lines. Fluorouracil 80-84 cyclin A2 Homo sapiens 28-36 14719102-7 2004 5-FU increased cyclin A mRNA level in NUGC3 cells but not NUGC3/5FU/L cells. Fluorouracil 0-4 cyclin A2 Homo sapiens 15-23 14719102-8 2004 In the presence of 100 micro M 5-FU, cyclin A protein level increased 2.6-fold in NUGC3 and 1.47-fold in NUGC3/5FU/L. Fluorouracil 31-35 cyclin A2 Homo sapiens 37-45 14719102-9 2004 5-FU dose-dependently increased the percentage of cyclin A-positive NUGC3 cells, but not NUGC3/5FU/L cells. Fluorouracil 0-4 cyclin A2 Homo sapiens 50-58 14719102-10 2004 The percentage of cyclin A-positive cells in other 5-FU sensitive esophageal, colon and gastric cancer cell lines (T.Tn, LOVO, DLD-1, MKN-7), increased in the presence of 1 and 10 micro M 5-FU, while cyclin A-positive cells in 5-FU resitant hepatocellular and colon carcinoma cell lines (HCC50 and C-1), did not increase with the same treatment. Fluorouracil 51-55 cyclin A2 Homo sapiens 18-26 14719102-10 2004 The percentage of cyclin A-positive cells in other 5-FU sensitive esophageal, colon and gastric cancer cell lines (T.Tn, LOVO, DLD-1, MKN-7), increased in the presence of 1 and 10 micro M 5-FU, while cyclin A-positive cells in 5-FU resitant hepatocellular and colon carcinoma cell lines (HCC50 and C-1), did not increase with the same treatment. Fluorouracil 188-192 cyclin A2 Homo sapiens 18-26 14719102-10 2004 The percentage of cyclin A-positive cells in other 5-FU sensitive esophageal, colon and gastric cancer cell lines (T.Tn, LOVO, DLD-1, MKN-7), increased in the presence of 1 and 10 micro M 5-FU, while cyclin A-positive cells in 5-FU resitant hepatocellular and colon carcinoma cell lines (HCC50 and C-1), did not increase with the same treatment. Fluorouracil 188-192 cyclin A2 Homo sapiens 18-26 14719102-11 2004 Our results indicate that the cytotoxic effects of 5-FU in human cancer cell lines correlate with cyclin A and it may be used as a predictive factor for chemotherapy response. Fluorouracil 51-55 cyclin A2 Homo sapiens 98-106 15075664-7 2004 This review will focus on the oral fluoropyrimidine S-1, which consists of the 5-FU prodrug tegafur (ftorafur, FT) and two enzyme inhibitors, i.e. CDHP (5-chloro-2,4-dihydroxypyridine) and OXO (potassium oxonate), in a molar ratio of 1(FT):0.4 (CDHP):1(OXO). Fluorouracil 79-83 proteasome 26S subunit, non-ATPase 1 Homo sapiens 52-55 15520875-10 2004 In addition to the increase of apoptosis rate, the expression of p53 protein, caused by 5-FU was further potentiated by UdR. Fluorouracil 88-92 tumor protein p53 Homo sapiens 65-68 14704126-1 2004 AIM: To study the effect of wild type (wt) p53 gene transfection on drug resistant human hepatocellular carcinoma (HCC) cells induced by 5-Fluorouracil (5-FU). Fluorouracil 137-151 tumor protein p53 Homo sapiens 43-46 14704126-1 2004 AIM: To study the effect of wild type (wt) p53 gene transfection on drug resistant human hepatocellular carcinoma (HCC) cells induced by 5-Fluorouracil (5-FU). Fluorouracil 153-157 tumor protein p53 Homo sapiens 43-46 14704126-10 2004 CONCLUSION: These results indicated that the wt p53 gene transfection not only induced suppression of cell growth, but also increased the sensitivity of Bel7402/5-FU cells to 5-FU, vincristine, and doxorubicin. Fluorouracil 161-165 tumor protein p53 Homo sapiens 48-51 12827409-8 2004 CONCLUSION: Considering also our own findings, this review presents the latest developments in the scientific discussion of the tumor suppressor/oncogenes p53, k-ras, and DCC, biochemical determinants of the 5-fluorouracil metabolism, and defects of the DNA repair system. Fluorouracil 208-222 tumor protein p53 Homo sapiens 155-158 15520875-7 2004 One hundred muM concentration of EUdR resulted in a 40% decrease of the IC50 value of 5-FU. Fluorouracil 86-90 latexin Homo sapiens 12-15 14704126-10 2004 CONCLUSION: These results indicated that the wt p53 gene transfection not only induced suppression of cell growth, but also increased the sensitivity of Bel7402/5-FU cells to 5-FU, vincristine, and doxorubicin. Fluorouracil 175-179 tumor protein p53 Homo sapiens 48-51 15224197-1 2004 BACKGROUND: We conducted a feasibility study using S-1, a novel oral derivative of 5-fluorouracil, as postoperative adjuvant chemotherapy for curatively resected gastric cancer patients. Fluorouracil 83-97 proteasome 26S subunit, non-ATPase 1 Homo sapiens 51-54 15520875-11 2004 CONCLUSION: This study demonstrated a potential novel approach to increase the efficacy of 5-FU by EUdR, which incorporated two complementary molecular actions, the selective modulation of TS inhibition and potentiation of the p53 protein expression, consequently leading to an increase in the apoptotic rate. Fluorouracil 91-95 tumor protein p53 Homo sapiens 227-230 15138368-0 2004 Effect of wild-type and mutant E-cadherin on cell proliferation and responsiveness to the chemotherapeutic agents cisplatin, etoposide, and 5-fluorouracil. Fluorouracil 140-154 cadherin 1 Homo sapiens 31-41 15331922-0 2004 Safety and efficacy of S-1, a novel oral fluorouracil antitumor drug, for a chronic renal failure patient maintained on hemodialysis. Fluorouracil 41-53 proteasome 26S subunit, non-ATPase 1 Homo sapiens 23-26 15138368-2 2004 The aim of the present study was to investigate the impact of wild-type (wt) E-cadherin and tumor-derived mutant E-cadherin variants on the proliferation rate of MDA-MB-435S mammary carcinoma cells and the sensitivity of the cells to the chemotherapeutic drugs cisplatin, etoposide and 5-fluorouracil (5-FU) and whether p53 is involved in the chemotherapeutic response. Fluorouracil 286-300 cadherin 1 Homo sapiens 113-123 15331922-1 2004 OBJECTIVE: S-1 is a novel oral fluorouracil antitumor drug that combines three pharmacological agents: tegafur (FT), a prodrug of 5-fluorouracil (5-FU); 5-chloro-2,4-dihydroxypyridine (CDHP), an inhibitor of dihydropyrimidine dehydrogenase, and potassium oxonate (Oxo), a reducer of gastrointestinal toxicity. Fluorouracil 31-43 proteasome 26S subunit, non-ATPase 1 Homo sapiens 11-14 15138368-2 2004 The aim of the present study was to investigate the impact of wild-type (wt) E-cadherin and tumor-derived mutant E-cadherin variants on the proliferation rate of MDA-MB-435S mammary carcinoma cells and the sensitivity of the cells to the chemotherapeutic drugs cisplatin, etoposide and 5-fluorouracil (5-FU) and whether p53 is involved in the chemotherapeutic response. Fluorouracil 302-306 cadherin 1 Homo sapiens 113-123 15331922-1 2004 OBJECTIVE: S-1 is a novel oral fluorouracil antitumor drug that combines three pharmacological agents: tegafur (FT), a prodrug of 5-fluorouracil (5-FU); 5-chloro-2,4-dihydroxypyridine (CDHP), an inhibitor of dihydropyrimidine dehydrogenase, and potassium oxonate (Oxo), a reducer of gastrointestinal toxicity. Fluorouracil 130-144 proteasome 26S subunit, non-ATPase 1 Homo sapiens 11-14 15331922-1 2004 OBJECTIVE: S-1 is a novel oral fluorouracil antitumor drug that combines three pharmacological agents: tegafur (FT), a prodrug of 5-fluorouracil (5-FU); 5-chloro-2,4-dihydroxypyridine (CDHP), an inhibitor of dihydropyrimidine dehydrogenase, and potassium oxonate (Oxo), a reducer of gastrointestinal toxicity. Fluorouracil 146-150 proteasome 26S subunit, non-ATPase 1 Homo sapiens 11-14 15138368-10 2004 In contrast, chemosensitivity of parental, wt or mutant E-cadherin-expressing MDA-MB-435S cells measured after etoposide or 5-FU exposure was found to be similar in all tested cell lines. Fluorouracil 124-128 cadherin 1 Homo sapiens 56-66 14676797-1 2003 The association of interleukin-2 (IL-2), interferon alpha-2a (IFNalpha), 5-fluorouracil (5-FU) has been reported to induce response in metastatic renal cell carcinoma (MRCC). Fluorouracil 73-87 interleukin 2 Homo sapiens 19-32 14662417-5 2004 p21 expression was augmented by 5-FU without any notable changes in p53 expression. Fluorouracil 32-36 cyclin dependent kinase inhibitor 1A Homo sapiens 0-3 15031593-10 2004 The VEGF antibody bevacizumab prolongs survival when given in combination with 5-FU/FA and irinotecan. Fluorouracil 79-83 vascular endothelial growth factor A Homo sapiens 4-8 14695155-2 2003 Importantly, the cytotoxic effects of thymidine deprivation induced by 5-fluorouracil (FUra) combined with leucovorin (LV) was enhanced by IFN-gamma, and the synergism was shown to be dependent on Fas, FUra-induced DNA damage, and independent of p53. Fluorouracil 71-85 interferon gamma Homo sapiens 139-148 14676797-1 2003 The association of interleukin-2 (IL-2), interferon alpha-2a (IFNalpha), 5-fluorouracil (5-FU) has been reported to induce response in metastatic renal cell carcinoma (MRCC). Fluorouracil 89-93 interleukin 2 Homo sapiens 19-32 14695155-2 2003 Importantly, the cytotoxic effects of thymidine deprivation induced by 5-fluorouracil (FUra) combined with leucovorin (LV) was enhanced by IFN-gamma, and the synergism was shown to be dependent on Fas, FUra-induced DNA damage, and independent of p53. Fluorouracil 71-85 tumor protein p53 Homo sapiens 246-249 14695155-2 2003 Importantly, the cytotoxic effects of thymidine deprivation induced by 5-fluorouracil (FUra) combined with leucovorin (LV) was enhanced by IFN-gamma, and the synergism was shown to be dependent on Fas, FUra-induced DNA damage, and independent of p53. Fluorouracil 87-91 interferon gamma Homo sapiens 139-148 26680985-2 2003 We undertook this study to determine whether the introduction of the wild type p53 gene into GBCE (human gallbladder cancer cell line with a heterozygous p53 mutation) by an adenoviral vector could increase the sensitivity of the cell to 5-FU, a commonly used drug in the treatment of gallbladder cancer. Fluorouracil 238-242 tumor protein p53 Homo sapiens 79-82 14695155-2 2003 Importantly, the cytotoxic effects of thymidine deprivation induced by 5-fluorouracil (FUra) combined with leucovorin (LV) was enhanced by IFN-gamma, and the synergism was shown to be dependent on Fas, FUra-induced DNA damage, and independent of p53. Fluorouracil 87-91 tumor protein p53 Homo sapiens 246-249 14695155-2 2003 Importantly, the cytotoxic effects of thymidine deprivation induced by 5-fluorouracil (FUra) combined with leucovorin (LV) was enhanced by IFN-gamma, and the synergism was shown to be dependent on Fas, FUra-induced DNA damage, and independent of p53. Fluorouracil 202-206 interferon gamma Homo sapiens 139-148 26680985-9 2003 Tumor colony formation was more inhibited with p53 gene transfection than with mock transfection in the presence of 5-FU. Fluorouracil 116-120 tumor protein p53 Homo sapiens 47-50 14751837-6 2003 The antisense oligonucleotides also potentiated the effects of p53 activation and p21 induction by chemotherapeutic agents 10-hydroxycamptothecin, adriamycin, 5-fluorouracil, and paclitaxel. Fluorouracil 159-173 tumor protein p53 Homo sapiens 63-66 14671431-5 2003 However, cisplatin, 5-FU and cyclophosphamide are not P-gp substrates, yet cisplatin, 5-FU and possibly cyclophosphamide are purported substrates for multidrug resistance proteins (MRPs) 1 and 2 (known to cause chemotherapy resistance). Fluorouracil 86-90 ATP binding cassette subfamily B member 1 Homo sapiens 150-194 14654539-0 2003 TP53 gene mutations predict the response to neoadjuvant treatment with 5-fluorouracil and mitomycin in locally advanced breast cancer. Fluorouracil 71-85 tumor protein p53 Homo sapiens 0-4 14599546-3 2003 5-FU increased interleukin-8 production and induced morphological signs of irritation. Fluorouracil 0-4 C-X-C motif chemokine ligand 8 Homo sapiens 15-28 14564514-6 2003 However, expression of CEA mRNA was only induced upon exposure to 5-FU, in contrast to obscure induction following CDDP and SN-38 treatment. Fluorouracil 66-70 carcinoembryonic antigen gene family Mus musculus 23-26 14564514-7 2003 Combined treatment with 5-FU and CDDP gave additional effect on CEA expression in COLO201 cells. Fluorouracil 24-28 CEA cell adhesion molecule 3 Homo sapiens 64-67 14703431-1 2003 OBJECTIVE: To investigate the relationship between apoptosis induced by CD3epsilon and 5-fluorouracil (5-FU), and study the P53 expression in the apoptosis process provide a novel insight and useful information of the apoptosis signaling pathway induced by CD3epsilon and/or 5-FU, and an important implication for the treatment of T-lymphocyte leukemia. Fluorouracil 275-279 tumor protein p53 Homo sapiens 124-127 14703431-5 2003 RESULTS: CD3epsilon or 5-FU induced apoptosis of TJK with increase of P53 expression. Fluorouracil 23-27 tumor protein p53 Homo sapiens 70-73 14703431-6 2003 Co-treatment with CD3epsilon specific antibody and 5-FU elevated the apoptotic rates and P53 expression in TJK cells remarkably. Fluorouracil 51-55 tumor protein p53 Homo sapiens 89-92 14703431-7 2003 The cells transfected with wild-type p53 exhibited more sensitivity to 5-FU than that transfected with mutant p53. Fluorouracil 71-75 tumor protein p53 Homo sapiens 37-40 14703431-8 2003 CONCLUSION: Co-treatment of CD3epsilon and 5-FU increases the apoptosis and p53 expression, suggesting that there is a synergetic role of CD3epsilon and 5-FU on T lymphocytes. Fluorouracil 43-47 tumor protein p53 Homo sapiens 76-79 14703431-8 2003 CONCLUSION: Co-treatment of CD3epsilon and 5-FU increases the apoptosis and p53 expression, suggesting that there is a synergetic role of CD3epsilon and 5-FU on T lymphocytes. Fluorouracil 153-157 tumor protein p53 Homo sapiens 76-79 14654539-6 2003 CONCLUSION: This study revealed a significant association between lack of response to 5-fluorouracil and mitomycin and mutations affecting the L2/L3 domains of the p53 protein. Fluorouracil 86-100 tumor protein p53 Homo sapiens 164-167 14561585-9 2003 Finally, pharmacological studies have shown that the expression of Pept-1 can be upregulated by agents such as 5 fluorouracil and downregulated by agents such as cyclosporine. Fluorouracil 113-125 solute carrier family 15 member 1 Homo sapiens 67-73 12973835-0 2003 ErbB2 overexpression in human breast carcinoma is correlated with p21Cip1 up-regulation and tyrosine-15 hyperphosphorylation of p34Cdc2: poor responsiveness to chemotherapy with cyclophoshamide methotrexate, and 5-fluorouracil is associated with Erb2 overexpression and with p21Cip1 overexpression. Fluorouracil 212-226 erb-b2 receptor tyrosine kinase 2 Homo sapiens 0-5 14597879-6 2003 In contrast, only DC that had been taken up 5-FU- or LAK-treated tumors up-modulated IL-12 and presented tumor-associated antigens with increased efficiency, as shown by class I MHC-restricted interferon-gamma release and cytotoxic responses by autologous lymphocytes. Fluorouracil 44-48 interferon gamma Homo sapiens 193-209 14559799-1 2003 Ferredoxin reductase (FDXR) is a putative contributor to TP53-mediated apoptosis from 5-fluorouracil chemotherapy through the generation of oxidative stress. Fluorouracil 86-100 tumor protein p53 Homo sapiens 57-61 14555537-7 2003 Between courses of treatment with either 5-FU or MTX, repopulation of ER+ cells was specifically inhibited by the SERMs, whereas repopulation of ER- MDA-231 was not affected. Fluorouracil 41-45 estrogen receptor 1 Homo sapiens 70-72 14555537-7 2003 Between courses of treatment with either 5-FU or MTX, repopulation of ER+ cells was specifically inhibited by the SERMs, whereas repopulation of ER- MDA-231 was not affected. Fluorouracil 41-45 estrogen receptor 1 Homo sapiens 115-117 14619538-5 2003 These results indicate that the type of p53 expression might play an important role in the determination of response to low-dose CDDP + 5-FU therapy in colon cancer patients. Fluorouracil 136-140 tumor protein p53 Homo sapiens 40-43 14724945-2 2003 MTT assay was used to determine IC50 of K562/ADR cells to adriamycin (ADR), cisplatin (DDP), 5-fluorouracil (5-FU) and vincristin (VCR). Fluorouracil 93-107 aldo-keto reductase family 1 member B Homo sapiens 45-48 14724945-2 2003 MTT assay was used to determine IC50 of K562/ADR cells to adriamycin (ADR), cisplatin (DDP), 5-fluorouracil (5-FU) and vincristin (VCR). Fluorouracil 109-113 aldo-keto reductase family 1 member B Homo sapiens 40-48 14724945-2 2003 MTT assay was used to determine IC50 of K562/ADR cells to adriamycin (ADR), cisplatin (DDP), 5-fluorouracil (5-FU) and vincristin (VCR). Fluorouracil 109-113 aldo-keto reductase family 1 member B Homo sapiens 45-48 14724945-7 2003 The IC50 of K562/ADR cells to ADR, DDP, 5-FU, VDR were much higher than those of K562. Fluorouracil 40-44 aldo-keto reductase family 1 member B Homo sapiens 12-20 14724945-7 2003 The IC50 of K562/ADR cells to ADR, DDP, 5-FU, VDR were much higher than those of K562. Fluorouracil 40-44 aldo-keto reductase family 1 member B Homo sapiens 17-20 14581279-0 2003 Phase I clinical study of infusional 5-fluorouracil with oxaliplatin and gemcitabine (FOG regimen) in patients with solid tumors. Fluorouracil 37-51 zinc finger protein, FOG family member 1 Homo sapiens 86-89 14562041-4 2003 Mice deficient for MBD4 showed significantly reduced apoptotic responses 6 h following treatment with a range of cytotoxic agents including gamma-irradiation, cisplatin, temozolomide and 5-fluorouracil (5-FU). Fluorouracil 187-201 methyl-CpG binding domain protein 4 Mus musculus 19-23 14562041-4 2003 Mice deficient for MBD4 showed significantly reduced apoptotic responses 6 h following treatment with a range of cytotoxic agents including gamma-irradiation, cisplatin, temozolomide and 5-fluorouracil (5-FU). Fluorouracil 203-207 methyl-CpG binding domain protein 4 Mus musculus 19-23 14562041-5 2003 This leads to increased clonogenic survival in vivo in Mbd4(-/-) mice following exposure to either 5-FU or cisplatin. Fluorouracil 99-103 methyl-CpG binding domain protein 4 Mus musculus 55-59 14562041-6 2003 We next analysed the apoptotic response to 5-FU and temozolomide in doubly mutant Mbd4(-/-), Mlh1(-/-) mice but observed no additive decrease. Fluorouracil 43-47 methyl-CpG binding domain protein 4 Mus musculus 82-86 14555507-1 2003 Dihydropyrimidinase (DHP) is the second enzyme in the catabolism of 5-fluorouracil (5FU), and it has been suggested that patients with a deficiency of this enzyme are at risk from developing severe 5FU-associated toxicity. Fluorouracil 68-82 dihydropyrimidinase Homo sapiens 0-19 14555507-1 2003 Dihydropyrimidinase (DHP) is the second enzyme in the catabolism of 5-fluorouracil (5FU), and it has been suggested that patients with a deficiency of this enzyme are at risk from developing severe 5FU-associated toxicity. Fluorouracil 68-82 dihydropyrimidinase Homo sapiens 21-24 14555507-1 2003 Dihydropyrimidinase (DHP) is the second enzyme in the catabolism of 5-fluorouracil (5FU), and it has been suggested that patients with a deficiency of this enzyme are at risk from developing severe 5FU-associated toxicity. Fluorouracil 84-87 dihydropyrimidinase Homo sapiens 0-19 14555507-1 2003 Dihydropyrimidinase (DHP) is the second enzyme in the catabolism of 5-fluorouracil (5FU), and it has been suggested that patients with a deficiency of this enzyme are at risk from developing severe 5FU-associated toxicity. Fluorouracil 84-87 dihydropyrimidinase Homo sapiens 21-24 14555507-1 2003 Dihydropyrimidinase (DHP) is the second enzyme in the catabolism of 5-fluorouracil (5FU), and it has been suggested that patients with a deficiency of this enzyme are at risk from developing severe 5FU-associated toxicity. Fluorouracil 198-201 dihydropyrimidinase Homo sapiens 0-19 14555507-1 2003 Dihydropyrimidinase (DHP) is the second enzyme in the catabolism of 5-fluorouracil (5FU), and it has been suggested that patients with a deficiency of this enzyme are at risk from developing severe 5FU-associated toxicity. Fluorouracil 198-201 dihydropyrimidinase Homo sapiens 21-24 14502645-2 2003 Accordingly, HDAC inhibitors such as trichostatin A (TSA) have potential utility in pancreatic cancer, as most of these tumors possess mutations in p53, which in fact is the main cause of chemoresistance to 5-fluorouracil. Fluorouracil 207-221 tumor protein p53 Homo sapiens 148-151 14724945-2 2003 MTT assay was used to determine IC50 of K562/ADR cells to adriamycin (ADR), cisplatin (DDP), 5-fluorouracil (5-FU) and vincristin (VCR). Fluorouracil 93-107 aldo-keto reductase family 1 member B Homo sapiens 40-48 14680567-7 2003 Chemotherapeutic agents, mitomycin (M), 5-FU and actinomycin D (AcD) dramatically augmented TRAIL induced cytotoxic function. Fluorouracil 40-44 TNF superfamily member 10 Homo sapiens 92-97 12941601-0 2003 Inhibition of inducible NF-kappaB activity reduces chemoresistance to 5-fluorouracil in human stomach cancer cell line. Fluorouracil 70-84 nuclear factor kappa B subunit 1 Homo sapiens 24-33 12941601-2 2003 5-FU induces apoptosis of several cancer cell lines, while some chemotherapeutic agents are known to activate the transcriptional factor NF-kappaB, which strongly suppresses apoptosis in vitro. Fluorouracil 0-4 nuclear factor kappa B subunit 1 Homo sapiens 137-146 12941601-3 2003 In the present study, we investigated the relationship between activation of NF-kappaB and chemoresistance to 5-FU in human stomach cancer cell lines, NUGC3 (5-FU sensitive) and NUGC3/5FU/L (5-FU resistant). Fluorouracil 110-114 nuclear factor kappa B subunit 1 Homo sapiens 77-86 12941601-3 2003 In the present study, we investigated the relationship between activation of NF-kappaB and chemoresistance to 5-FU in human stomach cancer cell lines, NUGC3 (5-FU sensitive) and NUGC3/5FU/L (5-FU resistant). Fluorouracil 158-162 nuclear factor kappa B subunit 1 Homo sapiens 77-86 12941601-3 2003 In the present study, we investigated the relationship between activation of NF-kappaB and chemoresistance to 5-FU in human stomach cancer cell lines, NUGC3 (5-FU sensitive) and NUGC3/5FU/L (5-FU resistant). Fluorouracil 158-162 nuclear factor kappa B subunit 1 Homo sapiens 77-86 12941601-4 2003 Treatment with 5-FU for 9-12 h caused activation of inducible NF-kappaB in NUGC3/5FU/L cells but not in NUGC3 cells. Fluorouracil 15-19 nuclear factor kappa B subunit 1 Homo sapiens 62-71 12941601-5 2003 5-FU also resulted in an increase in the number of TUNEL-positive cells and enhanced caspase-3 activity 3- to 5-fold in NUGC3 cells but not NUGC3/5FU/L cells. Fluorouracil 0-4 caspase 3 Homo sapiens 85-94 12941601-6 2003 Moreover we also demonstrated that the inhibition of inducible NF-kappaB activation by using a NF-kappaB decoy could induce apoptosis and reduce chemoresistance against 5-FU. Fluorouracil 169-173 nuclear factor kappa B subunit 1 Homo sapiens 63-72 12941601-6 2003 Moreover we also demonstrated that the inhibition of inducible NF-kappaB activation by using a NF-kappaB decoy could induce apoptosis and reduce chemoresistance against 5-FU. Fluorouracil 169-173 nuclear factor kappa B subunit 1 Homo sapiens 95-104 12941601-7 2003 Our results suggest that 5-FU chemoresistance can be overcome by inhibition of inducible NF-kappaB activation, and that the use of the NF-kappaB decoy combined with 5-FU treatment is a new molecular and gene therapeutic strategy aimed at treatment of human stomach cancers resistant to 5-FU. Fluorouracil 25-29 nuclear factor kappa B subunit 1 Homo sapiens 89-98 12942110-7 2003 The area under the curve (AUC(0-10 h)) of 5-FU on day 5 was 728+/-113 ng h ml(-1) for PVI of 5-FU and 1364+/-374 ng h ml(-1) for S-1. Fluorouracil 42-46 proteasome 26S subunit, non-ATPase 1 Homo sapiens 129-132 12920208-0 2003 5-fluorouracil blocks transforming growth factor-beta-induced alpha 2 type I collagen gene (COL1A2) expression in human fibroblasts via c-Jun NH2-terminal kinase/activator protein-1 activation. Fluorouracil 0-14 collagen type I alpha 2 chain Homo sapiens 92-98 12920208-3 2003 Using various molecular approaches to study the mechanisms underlying 5-FU effects, we have demonstrated that 5-FU antagonizes TGF-beta-driven COL1A2 transcription and associated type I collagen production by dermal fibroblasts. Fluorouracil 70-74 collagen type I alpha 2 chain Homo sapiens 143-149 12920208-3 2003 Using various molecular approaches to study the mechanisms underlying 5-FU effects, we have demonstrated that 5-FU antagonizes TGF-beta-driven COL1A2 transcription and associated type I collagen production by dermal fibroblasts. Fluorouracil 110-114 collagen type I alpha 2 chain Homo sapiens 143-149 12920208-6 2003 Overexpression of an antisense c-jun expression vector, or that of a dominant-negative form of MKK4 that interferes with c-Jun N-terminal kinase (JNK) activation, blocks the inhibitory activity of 5-FU on TGF-beta-induced COL1A2 transcription. Fluorouracil 197-201 mitogen-activated protein kinase kinase 4 Homo sapiens 95-99 12920208-6 2003 Overexpression of an antisense c-jun expression vector, or that of a dominant-negative form of MKK4 that interferes with c-Jun N-terminal kinase (JNK) activation, blocks the inhibitory activity of 5-FU on TGF-beta-induced COL1A2 transcription. Fluorouracil 197-201 mitogen-activated protein kinase 8 Homo sapiens 121-144 12920208-6 2003 Overexpression of an antisense c-jun expression vector, or that of a dominant-negative form of MKK4 that interferes with c-Jun N-terminal kinase (JNK) activation, blocks the inhibitory activity of 5-FU on TGF-beta-induced COL1A2 transcription. Fluorouracil 197-201 mitogen-activated protein kinase 8 Homo sapiens 146-149 12920208-6 2003 Overexpression of an antisense c-jun expression vector, or that of a dominant-negative form of MKK4 that interferes with c-Jun N-terminal kinase (JNK) activation, blocks the inhibitory activity of 5-FU on TGF-beta-induced COL1A2 transcription. Fluorouracil 197-201 collagen type I alpha 2 chain Homo sapiens 222-228 12920208-8 2003 Together, these results identify 5-FU as a potent inhibitor of TGF-beta/SMAD signaling, capable of blocking TGF-beta-induced, SMAD-driven up-regulation of COL1A2 gene expression in a JNK-dependent manner. Fluorouracil 33-37 collagen type I alpha 2 chain Homo sapiens 155-161 12920208-8 2003 Together, these results identify 5-FU as a potent inhibitor of TGF-beta/SMAD signaling, capable of blocking TGF-beta-induced, SMAD-driven up-regulation of COL1A2 gene expression in a JNK-dependent manner. Fluorouracil 33-37 mitogen-activated protein kinase 8 Homo sapiens 183-186 12845662-9 2003 These results suggest that CDDP and 5-FU may enhance the susceptibility to Fas-mediated apoptosis through down-regulation of c-FLIP. Fluorouracil 36-40 CASP8 and FADD like apoptosis regulator Homo sapiens 125-131 12967482-1 2003 We previously demonstrated that epidermal growth factor (EGF) induces a decrease in dihydropyrimidine dehydrogenase (DPD), which is the first and rate-limiting enzyme in the catabolism of 5-fluorouracil (5-FU), in EGF receptor (EGFR)-positive human SKG-IIIb uterine cervical carcinoma cells, and thereby increased the sensitivity of the cells to 5-FU. Fluorouracil 188-202 epidermal growth factor receptor Homo sapiens 214-226 12967482-1 2003 We previously demonstrated that epidermal growth factor (EGF) induces a decrease in dihydropyrimidine dehydrogenase (DPD), which is the first and rate-limiting enzyme in the catabolism of 5-fluorouracil (5-FU), in EGF receptor (EGFR)-positive human SKG-IIIb uterine cervical carcinoma cells, and thereby increased the sensitivity of the cells to 5-FU. Fluorouracil 188-202 epidermal growth factor receptor Homo sapiens 228-232 12967482-1 2003 We previously demonstrated that epidermal growth factor (EGF) induces a decrease in dihydropyrimidine dehydrogenase (DPD), which is the first and rate-limiting enzyme in the catabolism of 5-fluorouracil (5-FU), in EGF receptor (EGFR)-positive human SKG-IIIb uterine cervical carcinoma cells, and thereby increased the sensitivity of the cells to 5-FU. Fluorouracil 204-208 epidermal growth factor receptor Homo sapiens 214-226 12967482-1 2003 We previously demonstrated that epidermal growth factor (EGF) induces a decrease in dihydropyrimidine dehydrogenase (DPD), which is the first and rate-limiting enzyme in the catabolism of 5-fluorouracil (5-FU), in EGF receptor (EGFR)-positive human SKG-IIIb uterine cervical carcinoma cells, and thereby increased the sensitivity of the cells to 5-FU. Fluorouracil 204-208 epidermal growth factor receptor Homo sapiens 228-232 12967482-1 2003 We previously demonstrated that epidermal growth factor (EGF) induces a decrease in dihydropyrimidine dehydrogenase (DPD), which is the first and rate-limiting enzyme in the catabolism of 5-fluorouracil (5-FU), in EGF receptor (EGFR)-positive human SKG-IIIb uterine cervical carcinoma cells, and thereby increased the sensitivity of the cells to 5-FU. Fluorouracil 346-350 epidermal growth factor receptor Homo sapiens 214-226 12967482-1 2003 We previously demonstrated that epidermal growth factor (EGF) induces a decrease in dihydropyrimidine dehydrogenase (DPD), which is the first and rate-limiting enzyme in the catabolism of 5-fluorouracil (5-FU), in EGF receptor (EGFR)-positive human SKG-IIIb uterine cervical carcinoma cells, and thereby increased the sensitivity of the cells to 5-FU. Fluorouracil 346-350 epidermal growth factor receptor Homo sapiens 228-232 12904931-0 2003 Inhibitory effect of 5-fluorouracil on human cytochrome P(450) isoforms in human liver microsomes. Fluorouracil 21-35 cytochrome P450 family 4 subfamily F member 3 Homo sapiens 45-62 12904931-2 2003 However, little is known regarding the inhibitory potential of 5-FU on the metabolism of co-administered drugs by cytochrome P(450) (CYP). Fluorouracil 63-67 cytochrome P450 family 4 subfamily F member 3 Homo sapiens 114-131 12904931-2 2003 However, little is known regarding the inhibitory potential of 5-FU on the metabolism of co-administered drugs by cytochrome P(450) (CYP). Fluorouracil 63-67 cytochrome P450 family 4 subfamily F member 3 Homo sapiens 133-136 12904931-3 2003 The aim of the present study was to elucidate the inhibitory effect of 5-FU on CYP isoforms using human liver microsomes. Fluorouracil 71-75 cytochrome P450 family 4 subfamily F member 3 Homo sapiens 79-82 12904931-4 2003 METHODS: The inhibitory effect of 5-FU on CYP1A2, CYP2C9, CYP2C19, CYP2C8, CYP2E1, CYP2D6, and CYP3A4 activities was examined with specific probe drugs in human liver microsomes. Fluorouracil 34-38 cytochrome P450 family 2 subfamily E member 1 Homo sapiens 75-81 12904931-4 2003 METHODS: The inhibitory effect of 5-FU on CYP1A2, CYP2C9, CYP2C19, CYP2C8, CYP2E1, CYP2D6, and CYP3A4 activities was examined with specific probe drugs in human liver microsomes. Fluorouracil 34-38 cytochrome P450 family 2 subfamily D member 6 Homo sapiens 83-89 12904931-4 2003 METHODS: The inhibitory effect of 5-FU on CYP1A2, CYP2C9, CYP2C19, CYP2C8, CYP2E1, CYP2D6, and CYP3A4 activities was examined with specific probe drugs in human liver microsomes. Fluorouracil 34-38 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 95-101 14680567-9 2003 CONCLUSIONS: The combination of human TRAIL and chemotherapeutic agents, such as mitomycin, 5-FU and actinomycin D, seemed to exert a synergistic effect compared with either agent alone, and it might have therapeutic potential in the treatment of human HCC. Fluorouracil 92-96 TNF superfamily member 10 Homo sapiens 38-43 12763215-2 2003 S-1 is a new oral fluorinated pyrimidine derivate, in which the oral 5-fluorouracil (5-FU) prodrug, tegafur, was combined with two 5-FU-modulating substances, 5-chloro-2,4-dihydroxypyridine (gimeracil), and potassium oxonate (oteracil), at a molar ratio of 1:0.4:1. Fluorouracil 69-83 proteasome 26S subunit, non-ATPase 1 Homo sapiens 0-3 12915131-2 2003 Further studies revealed that the cells susceptible to 5-FU treatment died of apoptosis, which was demonstrated by caspase-3 activation, loss of mitochondria membrane potential (MMP), and DNA fragmentation. Fluorouracil 55-59 caspase 3 Homo sapiens 115-124 12915131-5 2003 These results indicate that Ras, Bcl-2, as well as Raf-1 and PI3K pathways play pivotal roles in 5-FU-induced apoptosis under Ha-ras-overexpressed condition. Fluorouracil 97-101 BCL2 apoptosis regulator Homo sapiens 33-38 12915131-8 2003 Through understanding the mechanism of 5-FU induced apoptosis in tumor cells, a new direction toward the treatment of Ha-ras oncogene-related cancers with 5-FU at more optimal dosages is possible and combinational therapy with other drugs that suppress PI3K and Bcl-2 activities can also be considered. Fluorouracil 39-43 BCL2 apoptosis regulator Homo sapiens 262-267 12888834-3 2003 We have previously demonstrated a synergistic interaction between ZD1839 and cisplatin/5-fluorouracil (5FU) in CAL33, a human head and neck cancer cell line that markedly expresses EGFR. Fluorouracil 87-101 epidermal growth factor receptor Homo sapiens 181-185 12888834-3 2003 We have previously demonstrated a synergistic interaction between ZD1839 and cisplatin/5-fluorouracil (5FU) in CAL33, a human head and neck cancer cell line that markedly expresses EGFR. Fluorouracil 103-106 epidermal growth factor receptor Homo sapiens 181-185 12935400-0 2003 p14ARF upregulation of p53 and enhanced effects of 5-fluorouracil in pancreatic cancer. Fluorouracil 51-65 cyclin dependent kinase inhibitor 2A Homo sapiens 0-6 12935400-6 2003 PC-3/p14ARF cells that underwent 5-Fu treatment had significantly greater G(2)/M phase accumulation, from 11.48% to 53.47%. Fluorouracil 33-37 cyclin dependent kinase inhibitor 2A Homo sapiens 5-11 12935400-8 2003 The MTT assay showed p14ARF-expressing cells were significantly more sensitive to 5-Fu (0.01 - 10 mg/L) than those devoid of p14ARF expression (P < 0.01). Fluorouracil 82-86 cyclin dependent kinase inhibitor 2A Homo sapiens 21-27 12865931-9 2003 Exposure of the cell lines to 5-FU, cisplatin and interferon-gamma left TRAIL-receptor membrane expression and TRAIL sensitivity unaffected. Fluorouracil 30-34 TNF superfamily member 10 Homo sapiens 72-77 12865931-9 2003 Exposure of the cell lines to 5-FU, cisplatin and interferon-gamma left TRAIL-receptor membrane expression and TRAIL sensitivity unaffected. Fluorouracil 30-34 TNF superfamily member 10 Homo sapiens 111-116 12807744-6 2003 Furthermore, caffeine also inhibited the accumulation of p53 by a variety of stress-inducing agents in vivo, such as 5-fluorouracil, doxorubicin, mitomycin C, camptothecin and roscovitine. Fluorouracil 117-131 tumor protein p53 Homo sapiens 57-60 12792779-1 2003 5-Fluorouracil (5FU) exposure can lead to both G1/S arrest and apoptosis induction which are dependent of P53 induction. Fluorouracil 0-14 tumor protein p53 Homo sapiens 106-109 12792779-1 2003 5-Fluorouracil (5FU) exposure can lead to both G1/S arrest and apoptosis induction which are dependent of P53 induction. Fluorouracil 16-19 tumor protein p53 Homo sapiens 106-109 12907638-7 2003 The 5-FU-induced activation of MAT-8, thymosin-beta-10, and chaperonin-10 was abrogated by inactivation of p53 in MCF-7 cells, whereas induction of SSAT and annexin II was significantly reduced in the absence of p53. Fluorouracil 4-8 FXYD domain containing ion transport regulator 3 Homo sapiens 31-36 12907638-7 2003 The 5-FU-induced activation of MAT-8, thymosin-beta-10, and chaperonin-10 was abrogated by inactivation of p53 in MCF-7 cells, whereas induction of SSAT and annexin II was significantly reduced in the absence of p53. Fluorouracil 4-8 tumor protein p53 Homo sapiens 107-110 12907638-7 2003 The 5-FU-induced activation of MAT-8, thymosin-beta-10, and chaperonin-10 was abrogated by inactivation of p53 in MCF-7 cells, whereas induction of SSAT and annexin II was significantly reduced in the absence of p53. Fluorouracil 4-8 tumor protein p53 Homo sapiens 212-215 12907638-8 2003 Moreover, each of these genes contained more than one potential p53-binding site, suggesting that p53 may play an important regulatory role in 5-FU-induced expression of these genes. Fluorouracil 143-147 tumor protein p53 Homo sapiens 64-67 12907638-8 2003 Moreover, each of these genes contained more than one potential p53-binding site, suggesting that p53 may play an important regulatory role in 5-FU-induced expression of these genes. Fluorouracil 143-147 tumor protein p53 Homo sapiens 98-101 14650374-1 2003 OBJECTIVE: S-1 is an oral anticancer agent combining tegafur (FT), a prodrug of 5-fluorouracil (5-FU), with potassium oxonate (oteracil) and gimeracil (CDHP) respectively to mitigate gastrointestinal toxicity and increase the half-life of 5-FU. Fluorouracil 80-94 proteasome 26S subunit, non-ATPase 1 Homo sapiens 11-14 14650374-1 2003 OBJECTIVE: S-1 is an oral anticancer agent combining tegafur (FT), a prodrug of 5-fluorouracil (5-FU), with potassium oxonate (oteracil) and gimeracil (CDHP) respectively to mitigate gastrointestinal toxicity and increase the half-life of 5-FU. Fluorouracil 96-100 proteasome 26S subunit, non-ATPase 1 Homo sapiens 11-14 14650374-1 2003 OBJECTIVE: S-1 is an oral anticancer agent combining tegafur (FT), a prodrug of 5-fluorouracil (5-FU), with potassium oxonate (oteracil) and gimeracil (CDHP) respectively to mitigate gastrointestinal toxicity and increase the half-life of 5-FU. Fluorouracil 239-243 proteasome 26S subunit, non-ATPase 1 Homo sapiens 11-14 12838322-4 2003 Although inhibition of MEK/MAPK or PI-3K/Akt can each enhance the cytotoxicity of paclitaxel, doxorubicin, or 5-fluorouracil, inhibition of the PI-3K/Akt pathway seems to have a greater effect than inhibition of the MEK/MAPK pathway in reversing Ras-mediated drug resistance. Fluorouracil 110-124 mitogen-activated protein kinase kinase 7 Homo sapiens 23-26 12838322-4 2003 Although inhibition of MEK/MAPK or PI-3K/Akt can each enhance the cytotoxicity of paclitaxel, doxorubicin, or 5-fluorouracil, inhibition of the PI-3K/Akt pathway seems to have a greater effect than inhibition of the MEK/MAPK pathway in reversing Ras-mediated drug resistance. Fluorouracil 110-124 AKT serine/threonine kinase 1 Homo sapiens 41-44 12739060-11 2003 In conclusion, oral S-1 administration resulted in prolonged exposure to micromolar 5-FU concentrations due to DPD inhibition, and the decrease in uracil levels after 6 h followed the pattern of CDHP and indicates reversible DPD inhibition. Fluorouracil 84-88 proteasome 26S subunit, non-ATPase 1 Homo sapiens 20-23 12842708-11 2003 bcl-2 overexpression also prevents the dramatic changes in HSC following 5-FU treatment (downregulation of c-kit, upregulation of Lin, less efficient long-term reconstitution). Fluorouracil 73-77 B cell leukemia/lymphoma 2 Mus musculus 0-5 12763215-2 2003 S-1 is a new oral fluorinated pyrimidine derivate, in which the oral 5-fluorouracil (5-FU) prodrug, tegafur, was combined with two 5-FU-modulating substances, 5-chloro-2,4-dihydroxypyridine (gimeracil), and potassium oxonate (oteracil), at a molar ratio of 1:0.4:1. Fluorouracil 85-89 proteasome 26S subunit, non-ATPase 1 Homo sapiens 0-3 12829029-9 2003 Moderate reductions in L-selectin and CD11a expression were observed on stem cells of 5-FU-treated mice. Fluorouracil 86-90 selectin, lymphocyte Mus musculus 23-33 12763215-2 2003 S-1 is a new oral fluorinated pyrimidine derivate, in which the oral 5-fluorouracil (5-FU) prodrug, tegafur, was combined with two 5-FU-modulating substances, 5-chloro-2,4-dihydroxypyridine (gimeracil), and potassium oxonate (oteracil), at a molar ratio of 1:0.4:1. Fluorouracil 131-135 proteasome 26S subunit, non-ATPase 1 Homo sapiens 0-3 12684687-4 2003 We report that Brca1-deficiency in p53-null cells was associated with increased sensitivity to the topoisomerase I poisons camptothecin and topotecan, the topoisomerase II poisons doxorubicin, mitoxantrone and etoposide, and to the platinum compounds carboplatin and oxaliplatin, but not to the antimetabolites 5-fluorouracil and gemcitabine and the taxanes docetaxel and paclitaxel. Fluorouracil 311-325 tumor protein p53 Homo sapiens 35-38 12776195-6 2003 In contrast to hypoxia, 5-flourouracil (5-FU)-induced p53-dependent cell death correlated with enhanced Ser(392) phosphorylation of p53 and elevated p21(WAF1) protein levels. Fluorouracil 40-44 tumor protein p53 Homo sapiens 54-57 12776195-6 2003 In contrast to hypoxia, 5-flourouracil (5-FU)-induced p53-dependent cell death correlated with enhanced Ser(392) phosphorylation of p53 and elevated p21(WAF1) protein levels. Fluorouracil 40-44 tumor protein p53 Homo sapiens 132-135 12776195-6 2003 In contrast to hypoxia, 5-flourouracil (5-FU)-induced p53-dependent cell death correlated with enhanced Ser(392) phosphorylation of p53 and elevated p21(WAF1) protein levels. Fluorouracil 40-44 cyclin dependent kinase inhibitor 1A Homo sapiens 149-152 12776195-6 2003 In contrast to hypoxia, 5-flourouracil (5-FU)-induced p53-dependent cell death correlated with enhanced Ser(392) phosphorylation of p53 and elevated p21(WAF1) protein levels. Fluorouracil 40-44 cyclin dependent kinase inhibitor 1A Homo sapiens 153-157 12776195-7 2003 Hypoxia inhibited 5-FU-induced p53-dependent cell death and attenuated p53 phosphorylation at the ATM and CK2/FACT phosphorylation sites. Fluorouracil 18-22 tumor protein p53 Homo sapiens 31-34 12761490-4 2003 Transfection of HER2 in MCF7 breast cancer cells that express HER3 caused a phosphoinoside-3 kinase (PI-3K)-dependent activation of Akt, and was associated with an increased resistance of the cells to multiple chemotherapeutic agents (paclitaxel, doxorubicin, 5-fluorouracil, etoposide, and camptothecin). Fluorouracil 260-274 erb-b2 receptor tyrosine kinase 2 Homo sapiens 16-20 12761490-4 2003 Transfection of HER2 in MCF7 breast cancer cells that express HER3 caused a phosphoinoside-3 kinase (PI-3K)-dependent activation of Akt, and was associated with an increased resistance of the cells to multiple chemotherapeutic agents (paclitaxel, doxorubicin, 5-fluorouracil, etoposide, and camptothecin). Fluorouracil 260-274 AKT serine/threonine kinase 1 Homo sapiens 132-135 12773255-0 2003 [Role of caspase-8 and caspase-3 in hepatoma cells apoptosis induced by 5-fluorouracil]. Fluorouracil 72-86 caspase 3 Homo sapiens 23-32 12655514-8 2003 However, in the lymph node negative population, the benefit of one course of perioperative chemotherapy with cyclophosphamide, methotrexate, and 5-fluorouracil was confined exclusively to patients with tumors that showed reduced p27 immunoreactivity (P = 0.03; test for interaction). Fluorouracil 145-159 zinc ribbon domain containing 2 Homo sapiens 229-232 12584740-0 2003 Treatment of colon and breast carcinoma cells with 5-fluorouracil enhances expression of carcinoembryonic antigen and susceptibility to HLA-A(*)02.01 restricted, CEA-peptide-specific cytotoxic T cells in vitro. Fluorouracil 51-65 major histocompatibility complex, class I, A Homo sapiens 136-141 12584740-0 2003 Treatment of colon and breast carcinoma cells with 5-fluorouracil enhances expression of carcinoembryonic antigen and susceptibility to HLA-A(*)02.01 restricted, CEA-peptide-specific cytotoxic T cells in vitro. Fluorouracil 51-65 CEA cell adhesion molecule 3 Homo sapiens 162-165 12584740-3 2003 Previous studies have shown that 5-fluorouracil (5-FU) can upregulate the expression of membrane-associated carcino-embryonic antigen (CEA), and MHC molecules in colon and breast carcinoma cell lines. Fluorouracil 33-47 CEA cell adhesion molecule 3 Homo sapiens 135-138 12584740-3 2003 Previous studies have shown that 5-fluorouracil (5-FU) can upregulate the expression of membrane-associated carcino-embryonic antigen (CEA), and MHC molecules in colon and breast carcinoma cell lines. Fluorouracil 49-53 CEA cell adhesion molecule 3 Homo sapiens 135-138 12584740-6 2003 The treatment of target cells with 5-FU, enhanced their CEA expression and susceptibility to CTL-mediated lysis. Fluorouracil 35-39 CEA cell adhesion molecule 3 Homo sapiens 56-59 12584740-7 2003 Cold competition assays confirmed these results, thus supporting the hypothesis that immune target cell lysis and 5-FU mediated enhancement were dependent on CEA peptide presentation by cancer cells. Fluorouracil 114-118 CEA cell adhesion molecule 3 Homo sapiens 158-161 12584740-9 2003 These results provide a rationale for investigating a possible new role of 5-FU as an immuno targeting amplifier agent in breast and colorectal cancer patients immunized with CEA-directed cancer vaccines. Fluorouracil 75-79 CEA cell adhesion molecule 3 Homo sapiens 175-178 12584750-0 2003 Disulfiram-mediated inhibition of NF-kappaB activity enhances cytotoxicity of 5-fluorouracil in human colorectal cancer cell lines. Fluorouracil 78-92 nuclear factor kappa B subunit 1 Homo sapiens 34-43 12584750-5 2003 We demonstrated that nuclear NF-kappaB activity in CRC cell lines, DLD-1 and RKO(WT), was significantly induced by 5-FU in a concentration- and time-dependent manner. Fluorouracil 115-119 nuclear factor kappa B subunit 1 Homo sapiens 29-38 12584750-6 2003 5-FU induced IkappaBalpha degradation and promoted both NF-kappaB nuclear translocation and its DNA binding activity. Fluorouracil 0-4 NFKB inhibitor alpha Homo sapiens 13-25 12584750-6 2003 5-FU induced IkappaBalpha degradation and promoted both NF-kappaB nuclear translocation and its DNA binding activity. Fluorouracil 0-4 nuclear factor kappa B subunit 1 Homo sapiens 56-65 12584750-8 2003 Disulfiram (DS), a clinically used anti-alcoholism drug, strongly inhibited constitutive and 5-FU-induced NF-kappaB activity in a dose-dependent manner. Fluorouracil 93-97 nuclear factor kappa B subunit 1 Homo sapiens 106-115 12692863-9 2003 A potentiating effect of adenoviral treatment was also seen when 5-FU treatment was substituted by the overexpression of cyclin-dependent kinase inhibitors, p21(WAF1/CIP1) and p27(KIP1), suggesting that the cytostatic effect of 5-FU augmented apoptosis induced by caspase-8 gene transduction by inhibiting the dilution of gene products associated with cell division. Fluorouracil 228-232 cyclin dependent kinase inhibitor 1A Homo sapiens 161-165 12697866-1 2003 PURPOSE: To evaluate the safety of recombinant human keratinocyte growth factor (KGF) when administered with fluorouracil (FU) in patients with metastatic colorectal cancer. Fluorouracil 109-121 fibroblast growth factor 7 Homo sapiens 53-79 12697866-1 2003 PURPOSE: To evaluate the safety of recombinant human keratinocyte growth factor (KGF) when administered with fluorouracil (FU) in patients with metastatic colorectal cancer. Fluorouracil 109-121 fibroblast growth factor 7 Homo sapiens 81-84 12655533-0 2003 Correlation between HER-2 expression and response to neoadjuvant chemotherapy with 5-fluorouracil, doxorubicin, and cyclophosphamide in patients with breast carcinoma. Fluorouracil 83-97 erb-b2 receptor tyrosine kinase 2 Homo sapiens 20-25 12655533-1 2003 BACKGROUND: The objective of this study was to determine whether HER-2 overexpression is associated with improved response to neoadjuvant chemotherapy with 5-fluorouracil, doxorubicin, cyclophosphamide (FAC) in patients with breast carcinoma. Fluorouracil 156-170 erb-b2 receptor tyrosine kinase 2 Homo sapiens 65-70 12592379-7 2003 Transient exposure of wild-type RKO(WT) and H630(WT) cells to 5-FU induced NF-kappa B DNA-binding activity but had no effect on NF-kappa B protein expression in these cells. Fluorouracil 62-66 nuclear factor kappa B subunit 1 Homo sapiens 75-85 12934351-1 2003 OBJECTIVES: To study the change of caspase-3 activity on the neoadjuvant chemotherapy-induced apoptosis by hydroxycamptothecin (HCPT) with 5-fluorouracil (5-Fu)/leucovorin (CF) in large-intestinal carcinoma, and to explore its mechanism. Fluorouracil 139-153 caspase 3 Homo sapiens 35-44 12934351-1 2003 OBJECTIVES: To study the change of caspase-3 activity on the neoadjuvant chemotherapy-induced apoptosis by hydroxycamptothecin (HCPT) with 5-fluorouracil (5-Fu)/leucovorin (CF) in large-intestinal carcinoma, and to explore its mechanism. Fluorouracil 155-159 caspase 3 Homo sapiens 35-44 12619112-4 2003 Several in vitro, animal and clinical studies have shown that normal p53 is required for the response of colorectal cancers to 5-fluorouracil-based chemotherapy. Fluorouracil 127-141 tumor protein p53 Homo sapiens 69-72 12812659-11 2003 GLC cell cycle assay showed that the S phase block induced by etopside, cisplatin and 5-FU and the G(2)/M block induced by 5-FU were enhanced by insulin with the increased block rates of 80% and 90% respectively. Fluorouracil 86-90 insulin Homo sapiens 145-152 12518324-7 2003 The antisense oligonucleotide also potentiated the effects of p53 activation and p21 induction by chemotherapeutic agents 10-hydroxycamptothecin, adriamycin, 5-fluorouracil, and paclitaxel. Fluorouracil 158-172 tumor protein p53 Homo sapiens 62-65 12812659-11 2003 GLC cell cycle assay showed that the S phase block induced by etopside, cisplatin and 5-FU and the G(2)/M block induced by 5-FU were enhanced by insulin with the increased block rates of 80% and 90% respectively. Fluorouracil 123-127 insulin Homo sapiens 145-152 12576456-8 2003 However, in the subgroup of patients treated with anthracycline-based chemotherapy (5-fluorouracil, Adriamycin/epirubicin, and cyclophosphamide), a correlation between response and the expression of BCRP and MRP1 (only PFS) was found, whereas such an association was not present in the cyclophosphamide, methotrexate, and 5-fluorouracil-treated group of patients. Fluorouracil 84-98 ATP binding cassette subfamily C member 1 Homo sapiens 208-212 12775014-7 2003 RESULTS: Maintenance of high 5-FU concentrations in the intraperitoneal tumors was confirmed in the S-1 group, and survival time was prolonged without any decrease in oral food intake or body weight. Fluorouracil 29-33 eukaryotic translation elongation factor 1 alpha 2 Mus musculus 100-103 12810457-8 2003 The addition of 5-FU, by this schedule, to TC (TCF) does not increase hematological toxicity, and does not compromise the tolerability of TC. Fluorouracil 16-20 hepatocyte nuclear factor 4 alpha Homo sapiens 47-50 12775012-2 2003 S-1 is a novel oral dihydropyrimidine dehydrogenase (DPD) inhibitory fluoropyrimidine (DIF) based on a biochemical modulation of 5-fluorouracil (5-FU); S-1 contains tegafur (FF) and two types of enzyme inhibitor, 5-chloro-2,4-dihydroxypyridine (CDHP) and potassium oxonate (Oxo) in a molar ratio of 1:0.4:1. Fluorouracil 129-143 proteasome 26S subunit, non-ATPase 1 Homo sapiens 0-3 12775012-2 2003 S-1 is a novel oral dihydropyrimidine dehydrogenase (DPD) inhibitory fluoropyrimidine (DIF) based on a biochemical modulation of 5-fluorouracil (5-FU); S-1 contains tegafur (FF) and two types of enzyme inhibitor, 5-chloro-2,4-dihydroxypyridine (CDHP) and potassium oxonate (Oxo) in a molar ratio of 1:0.4:1. Fluorouracil 129-143 tumor necrosis factor Homo sapiens 87-90 12775012-2 2003 S-1 is a novel oral dihydropyrimidine dehydrogenase (DPD) inhibitory fluoropyrimidine (DIF) based on a biochemical modulation of 5-fluorouracil (5-FU); S-1 contains tegafur (FF) and two types of enzyme inhibitor, 5-chloro-2,4-dihydroxypyridine (CDHP) and potassium oxonate (Oxo) in a molar ratio of 1:0.4:1. Fluorouracil 145-149 proteasome 26S subunit, non-ATPase 1 Homo sapiens 0-3 12775012-2 2003 S-1 is a novel oral dihydropyrimidine dehydrogenase (DPD) inhibitory fluoropyrimidine (DIF) based on a biochemical modulation of 5-fluorouracil (5-FU); S-1 contains tegafur (FF) and two types of enzyme inhibitor, 5-chloro-2,4-dihydroxypyridine (CDHP) and potassium oxonate (Oxo) in a molar ratio of 1:0.4:1. Fluorouracil 145-149 tumor necrosis factor Homo sapiens 87-90 12775012-3 2003 In pharmacokinetic studies, S-1 showed high 5-FU concentration in blood for long periods of time. Fluorouracil 44-48 proteasome 26S subunit, non-ATPase 1 Homo sapiens 28-31 12469202-0 2003 Bcl-2 in cancer and normal tissue cells as a prediction marker of response to 5-fluorouracil. Fluorouracil 78-92 BCL2 apoptosis regulator Homo sapiens 0-5 12469202-1 2003 Bcl-2 in cancer cells was shown to be a potent indicator of 5-FU efficacy, but the protein in normal tissue cells appeared not to be a marker of 5-FU toxicity probably due to the functional alteration of Bcl-2 associated with cell senescence. Fluorouracil 60-64 BCL2 apoptosis regulator Homo sapiens 0-5 12566916-0 2003 Prevention of peritoneal metastasis of human gastric cancer cells in nude mice by S-1, a novel oral derivative of 5-Fluorouracil. Fluorouracil 114-128 eukaryotic translation elongation factor 1 alpha 2 Mus musculus 82-85 14520533-1 2003 S-1 has been developed as a new oral anticancer drug, based on the biological modulation of 5-fluorouracil. Fluorouracil 92-106 proteasome 26S subunit, non-ATPase 1 Homo sapiens 0-3 15015643-7 2003 Compared with normal group, 5-Fu and antisense survivin group, the cells growth inhibition, apoptosis index, and caspase-3 activity were increased in antisense survivin transfected + 5-Fu group. Fluorouracil 183-187 caspase 3 Homo sapiens 113-122 12459384-2 2002 METHODS AND MATERIALS: 5-FU was incorporated into a polyanhydride-based polymer, bis(p-carboxyphenoxy)propane sebacic acid (CPP:SA) and implanted in RIF-1 mouse fibrosarcoma growing s.c. Fluorouracil 23-27 replication timing regulatory factor 1 Mus musculus 149-154 12743424-2 2003 This report addressed the time-dependent dynamic alterations in the expression of three tumor-associated antigens: carcinoembryonic antigen (CEA), colon-specific antigen (CSAp) and mucin-1 (MUC-1) following chemotherapy with 5-fluorouracil (5-FU) or radioimmunotherapy (RAIT; (131)I-labeled anti-CEA IgG) in human colonic tumor xenografts. Fluorouracil 225-239 CEA cell adhesion molecule 3 Homo sapiens 115-139 12520739-10 2002 Expression of VEGF in tumors was clearly inhibited by TNP-470 in combination with 5-FU or 5-FU alone compared to the control. Fluorouracil 82-86 vascular endothelial growth factor A Homo sapiens 14-18 12520739-10 2002 Expression of VEGF in tumors was clearly inhibited by TNP-470 in combination with 5-FU or 5-FU alone compared to the control. Fluorouracil 90-94 vascular endothelial growth factor A Homo sapiens 14-18 12743424-3 2003 Immunoassay results show that CEA and MUC-1 expression all increase rapidly after either 5-FU or RAIT. Fluorouracil 89-93 CEA cell adhesion molecule 3 Homo sapiens 30-33 12506484-0 2002 [A case of recurrent breast cancer with carcinomatous pleurisy successfully treated with combined chemoendocrine-therapy of CTF (CPA, THP and 5-FU) and anastrozole following instillation therapy 12 years after radical mastectomy]. Fluorouracil 142-146 nuclear factor I C Homo sapiens 124-127 12397465-6 2002 Strikingly, FLT uptake per 10(5) viable cells was increased seven- to tenfold 24 h after treatment with 5-FU or MTX irrespective of dose. Fluorouracil 104-108 fms related receptor tyrosine kinase 1 Homo sapiens 12-15 12442003-15 2002 Treating HT1197 cells with 5-FU enhanced expression of the pro-apoptotic molecule Bax, while JTE-522 treatment reduced expression of the anti-apoptotic molecule Bcl-XL, resulting in a significantly higher ratio of Bax-to-Bcl-XL. Fluorouracil 27-31 BCL2 associated X, apoptosis regulator Homo sapiens 82-85 12442003-16 2002 CONCLUSIONS: This study shows that combination treatment of bladder cancer cells with the selective COX-2 inhibitor JTE-522 and 5-FU results in synergistic cytotoxicity and apoptosis due to the enhanced Bax-to-Bcl-XL expression ratio. Fluorouracil 128-132 prostaglandin-endoperoxide synthase 2 Homo sapiens 100-105 12442003-16 2002 CONCLUSIONS: This study shows that combination treatment of bladder cancer cells with the selective COX-2 inhibitor JTE-522 and 5-FU results in synergistic cytotoxicity and apoptosis due to the enhanced Bax-to-Bcl-XL expression ratio. Fluorouracil 128-132 BCL2 associated X, apoptosis regulator Homo sapiens 203-206 12442003-16 2002 CONCLUSIONS: This study shows that combination treatment of bladder cancer cells with the selective COX-2 inhibitor JTE-522 and 5-FU results in synergistic cytotoxicity and apoptosis due to the enhanced Bax-to-Bcl-XL expression ratio. Fluorouracil 128-132 BCL2 like 1 Homo sapiens 210-216 12397645-0 2002 DCR3 locus is a predictive marker for 5-fluorouracil-based adjuvant chemotherapy in colorectal cancer. Fluorouracil 38-52 TNF receptor superfamily member 6b Homo sapiens 0-4 12530065-0 2002 Reduced expression of p53 and p21WAF1/CIP1 sensitizes human breast cancer cells to paclitaxel and its combination with 5-fluorouracil. Fluorouracil 119-133 tumor protein p53 Homo sapiens 22-25 12530065-0 2002 Reduced expression of p53 and p21WAF1/CIP1 sensitizes human breast cancer cells to paclitaxel and its combination with 5-fluorouracil. Fluorouracil 119-133 cyclin dependent kinase inhibitor 1A Homo sapiens 30-42 12530065-3 2002 Biochemical examination also revealed that 5-FU inhibited expression of p21WAF1/CIP1 that may contribute to paclitaxel cytotoxicity. Fluorouracil 43-47 cyclin dependent kinase inhibitor 1A Homo sapiens 80-84 12530065-7 2002 The reduced protein levels of p53 and p21WAF1/CIP1 were also found to abrogate the inhibitory effects of 5-FU on paclitaxel-induced mitotic arrest and apoptosis. Fluorouracil 105-109 tumor protein p53 Homo sapiens 30-33 12530065-7 2002 The reduced protein levels of p53 and p21WAF1/CIP1 were also found to abrogate the inhibitory effects of 5-FU on paclitaxel-induced mitotic arrest and apoptosis. Fluorouracil 105-109 cyclin dependent kinase inhibitor 1A Homo sapiens 46-50 12530065-8 2002 CONCLUSION: These findings suggest that the status of p53 and p21WAF1/CIP1 might play an important role in tumor cell susceptibility to paclitaxel and its combination with other drugs such as 5-FU. Fluorouracil 192-196 tumor protein p53 Homo sapiens 54-57 12530065-8 2002 CONCLUSION: These findings suggest that the status of p53 and p21WAF1/CIP1 might play an important role in tumor cell susceptibility to paclitaxel and its combination with other drugs such as 5-FU. Fluorouracil 192-196 cyclin dependent kinase inhibitor 1A Homo sapiens 70-74 12484016-1 2002 We administered interleukin (IL)-2 with mitomycin C (MMC) and 5-fluorouracil (5-FU) by hepatic arterial infusion for the treatment of liver recurrence from colorectal cancer. Fluorouracil 78-82 interleukin 2 Homo sapiens 16-34 12484016-7 2002 We herein report 3 patients treated with hepatic arterial infusion of IL-2 with MMC and 5-FU for liver recurrence from colorectal cancer. Fluorouracil 88-92 interleukin 2 Homo sapiens 70-74 12530074-4 2002 RESULTS: p53 wild-type fibroblasts, in contrast to p53-deficient cells, survive much higher doses of 5-fluorouracil when incubated at 28 degrees C than at 37 degrees C. Among tumor cells, the loss of the p53 function coincides with the inability to arrest cell cycle progression at low temperature and with increased sensitivity to prolonged hypothermia as a single modality. Fluorouracil 101-115 tumor protein p53 Homo sapiens 9-12 12414664-7 2002 NSAIDs and 5-FU induced the mitochondrial release of cytochrome c as well as caspase-3 and -9 activation, and to a much lesser extent, caspase-8. Fluorouracil 11-15 cytochrome c, somatic Homo sapiens 53-65 12414664-7 2002 NSAIDs and 5-FU induced the mitochondrial release of cytochrome c as well as caspase-3 and -9 activation, and to a much lesser extent, caspase-8. Fluorouracil 11-15 caspase 3 Homo sapiens 77-93 12414664-11 2002 In conclusion, forced COX-2 expression significantly attenuates apoptosis induction by NSAIDs and 5-FU through predominant inhibition of the cytochrome c-dependent apoptotic pathway. Fluorouracil 98-102 prostaglandin-endoperoxide synthase 2 Homo sapiens 22-27 12414664-11 2002 In conclusion, forced COX-2 expression significantly attenuates apoptosis induction by NSAIDs and 5-FU through predominant inhibition of the cytochrome c-dependent apoptotic pathway. Fluorouracil 98-102 cytochrome c, somatic Homo sapiens 141-153 12397465-13 2002 The antimetabolites 5-FU and MTX massively increase FLT accumulation per cell independent of dose, i.e. cytotoxicity. Fluorouracil 20-24 fms related receptor tyrosine kinase 1 Homo sapiens 52-55 12432233-10 2002 Finally, we found that IGF-I prevented the apoptosis of CE81T/VGH cells induced by chemotherapeutic drugs, such as cisplatin, 5-fluorouracil and camptothecin. Fluorouracil 126-140 insulin like growth factor 1 Homo sapiens 23-28 12677090-11 2002 Ad-E2F-1 treatment alone results in 3.4-fold increase of cyclin A kinase activity compared to Ad-LacZ control (p < 0.05); when combined with chemotherapeutic agents, cyclin A kinase activity was inhibited significantly by VIN, actinomycin D, and etoposide (p < 0.005), but not with CPT, CIS, and 5-FU (p > 0.1) compared to Ad-E2F-1 treatment alone. Fluorouracil 302-306 cyclin A2 Homo sapiens 57-65 12487851-1 2002 OBJECTIVE: To study target killing of 5-FU drug-fast cancer cells with thymidylate synthase (TS) and p16 gene promoters inducting TK gene expression. Fluorouracil 38-42 cyclin dependent kinase inhibitor 2A Homo sapiens 101-104 12677090-11 2002 Ad-E2F-1 treatment alone results in 3.4-fold increase of cyclin A kinase activity compared to Ad-LacZ control (p < 0.05); when combined with chemotherapeutic agents, cyclin A kinase activity was inhibited significantly by VIN, actinomycin D, and etoposide (p < 0.005), but not with CPT, CIS, and 5-FU (p > 0.1) compared to Ad-E2F-1 treatment alone. Fluorouracil 302-306 cyclin A2 Homo sapiens 169-177 12677090-12 2002 Combination of Ad-LacZ/5-FU and Ad-LacZ/actinomycin D significantly inhibited cyclin A kinase activity compared to Ad-LacZ treatment alone (p < 0.005). Fluorouracil 23-27 cyclin A2 Homo sapiens 78-86 12402433-5 2002 The treatment resulted in a fall in serum PIVKA-II (protein induced by vitamin K antagonism) levels from 337 mAU/ml to 65 mAU/ml and disappearance of tumor stain in enhanced CT. 5-FU is usually administered by arterial infusion in a combination therapy of IFN-alpha and 5-FU. Fluorouracil 178-182 interferon alpha 1 Homo sapiens 256-265 12384541-5 2002 Combining TRAIL with either 5-fluorouracil (5-FU) or CPT-11 (irinotecan hydrochloride) produced a greatly enhanced antitumor effect over that of either agent alone, with 50% of the animals achieving complete tumor regression with a combination of TRAIL and CPT-11. Fluorouracil 28-42 TNF superfamily member 10 Homo sapiens 247-252 12384541-5 2002 Combining TRAIL with either 5-fluorouracil (5-FU) or CPT-11 (irinotecan hydrochloride) produced a greatly enhanced antitumor effect over that of either agent alone, with 50% of the animals achieving complete tumor regression with a combination of TRAIL and CPT-11. Fluorouracil 44-48 TNF superfamily member 10 Homo sapiens 10-15 12402433-6 2002 However, 5-FU infusion may be possible intravenously in the combination therapy of IFN-alpha and 5-FU for the treatment of advanced HCC. Fluorouracil 9-13 interferon alpha 1 Homo sapiens 83-92 12529971-0 2002 IFN gamma-induced up-regulation of PD-ECGF/TP enhances the cytotoxicity of 5-fluorouracil and 5"-deoxy-5-fluorouridine in bladder cancer cells. Fluorouracil 75-89 interferon gamma Homo sapiens 0-9 12209689-7 2002 CONCLUSIONS: The current data suggest that combined outpatient sc IFN-alpha and sc IL-2, according to the Atzpodien regimen, achieves long-term survival benefits in a subset of patients with metastatic renal cell carcinoma, both with and without 13-cis-retinoic acid and/or 5-fluorouracil. Fluorouracil 274-288 interferon alpha 1 Homo sapiens 66-75 12209689-7 2002 CONCLUSIONS: The current data suggest that combined outpatient sc IFN-alpha and sc IL-2, according to the Atzpodien regimen, achieves long-term survival benefits in a subset of patients with metastatic renal cell carcinoma, both with and without 13-cis-retinoic acid and/or 5-fluorouracil. Fluorouracil 274-288 interleukin 2 Homo sapiens 83-87 12168112-1 2002 We investigated supra-additive cytotoxic effects of 5-fluorouracil (5FU) on gastric and colon cancer cells with tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) in vitro. Fluorouracil 52-66 TNF superfamily member 10 Homo sapiens 112-167 12168112-1 2002 We investigated supra-additive cytotoxic effects of 5-fluorouracil (5FU) on gastric and colon cancer cells with tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) in vitro. Fluorouracil 52-66 TNF superfamily member 10 Homo sapiens 169-174 12168112-1 2002 We investigated supra-additive cytotoxic effects of 5-fluorouracil (5FU) on gastric and colon cancer cells with tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) in vitro. Fluorouracil 68-71 TNF superfamily member 10 Homo sapiens 112-167 12168112-2 2002 p53 wild- and mutant-type gastric and colon cancer cell lines were treated by 5FU alone, TRAIL alone, and a combination of 5FU and TRAIL, and cell viability after each treatment was determined by MTT assay. Fluorouracil 78-81 tumor protein p53 Homo sapiens 0-3 12168112-2 2002 p53 wild- and mutant-type gastric and colon cancer cell lines were treated by 5FU alone, TRAIL alone, and a combination of 5FU and TRAIL, and cell viability after each treatment was determined by MTT assay. Fluorouracil 123-126 tumor protein p53 Homo sapiens 0-3 12168112-4 2002 The cell growth inhibitory effects of the combined treatment were supra-additive and more significant in proportion to the increasing concentrations of TRAIL as compared with 5FU alone both in p53 wild- and mutant-type cells. Fluorouracil 175-178 TNF superfamily member 10 Homo sapiens 152-157 12168112-6 2002 This is the first demonstration of the supra-additive antitumor activity of 5FU with TRAIL on gastric cancer cells, giving evidence that TRAIL can reduce the requirement for 5FU that ultimately results in minimizing risks for systemic side effects while increasing the antitumor activity of 5FU, suggesting the clinical applicability of this combination for gastric and colon cancers. Fluorouracil 76-79 TNF superfamily member 10 Homo sapiens 137-142 12115540-2 2002 We found that there was a slight tendency (not statistically significant) for the p53 inactivated cells to be less sensitive to 5-FU after 6 days continuous treatment. Fluorouracil 128-132 tumor protein p53 Homo sapiens 82-85 12420861-5 2002 Using this approach, we demonstrated an ST-mediated increase in CEA transcript in blood specimens collected from a patient with metastatic colon cancer before receiving treatment with 5-fluorouracil/leucovorin. Fluorouracil 184-198 CEA cell adhesion molecule 3 Homo sapiens 64-67 12171874-0 2002 Modulation of the Fas signaling pathway by IFN-gamma in therapy of colon cancer: phase I trial and correlative studies of IFN-gamma, 5-fluorouracil, and leucovorin. Fluorouracil 133-147 interferon gamma Homo sapiens 43-52 12171874-1 2002 Potentiation of 5-fluorouracil/leucovorin (FUra/LV) cytotoxicity by IFN-gamma in colon carcinoma cells is dependent on FUra-induced DNA damage, the Fas death receptor, and independent of p53 and RNA-mediated FUra toxicity, which occurs in normal gastrointestinal tissues. Fluorouracil 16-30 interferon gamma Homo sapiens 68-77 12171874-1 2002 Potentiation of 5-fluorouracil/leucovorin (FUra/LV) cytotoxicity by IFN-gamma in colon carcinoma cells is dependent on FUra-induced DNA damage, the Fas death receptor, and independent of p53 and RNA-mediated FUra toxicity, which occurs in normal gastrointestinal tissues. Fluorouracil 16-30 tumor protein p53 Homo sapiens 187-190 12115540-3 2002 Simultaneous administration of RPR-115135 and 5-FU, at subtoxic concentrations, resulted in a synergistic enhancement of 5-FU cytotoxicity in the p53 wildtype cells (HCT-116, RKO, DLD-1, Colo-320, LoVo). Fluorouracil 46-50 tumor protein p53 Homo sapiens 146-149 12115540-3 2002 Simultaneous administration of RPR-115135 and 5-FU, at subtoxic concentrations, resulted in a synergistic enhancement of 5-FU cytotoxicity in the p53 wildtype cells (HCT-116, RKO, DLD-1, Colo-320, LoVo). Fluorouracil 121-125 tumor protein p53 Homo sapiens 146-149 12115540-9 2002 Although RPR-115135 can potentiate the effect of 5-FU in cells in which p53 function is disrupted, these data suggest strongly that RPR-115135 significantly enhances the efficacy of 5-FU only when p53 is functioning. Fluorouracil 49-53 tumor protein p53 Homo sapiens 72-75 12115540-9 2002 Although RPR-115135 can potentiate the effect of 5-FU in cells in which p53 function is disrupted, these data suggest strongly that RPR-115135 significantly enhances the efficacy of 5-FU only when p53 is functioning. Fluorouracil 182-186 tumor protein p53 Homo sapiens 197-200 12084458-9 2002 The enzyme uridine-cytidine monophosphate kinase (UMPK) is an essential and rate-limiting enzyme in 5-FU activation while dihydropyrimidine dehydrogenase (DPD) is a catabolic enzyme that inactivates 5-FU. Fluorouracil 100-104 uridine-cytidine kinase 2 Homo sapiens 50-54 12084458-7 2002 Studies thus far involving colorectal tumors obtained from patients have focused predominantly on the predictive value of levels of TS expression and p53 mutations in determining response to 5-FU. Fluorouracil 191-195 tumor protein p53 Homo sapiens 150-153 12174943-5 2002 On the other hand, the inhibitory effect on tumor growth in rats administered with both TNF-SAM2 and 5-FU (10 mg/kg) was 65%, which was equal to, or less than, that in rats administered with only TNF-SAM2 or 5-FU. Fluorouracil 101-105 tumor necrosis factor Rattus norvegicus 196-199 12084458-9 2002 The enzyme uridine-cytidine monophosphate kinase (UMPK) is an essential and rate-limiting enzyme in 5-FU activation while dihydropyrimidine dehydrogenase (DPD) is a catabolic enzyme that inactivates 5-FU. Fluorouracil 100-104 uridine-cytidine kinase 2 Homo sapiens 11-48 12096336-0 2002 Novel gain of function activity of p53 mutants: activation of the dUTPase gene expression leading to resistance to 5-fluorouracil. Fluorouracil 115-129 tumor protein p53 Homo sapiens 35-38 12096336-6 2002 Using tetracycline-regulated retroviral vectors for conditional expression of p53 mutants, we found that transcription of the dUTPase gene is increased within 24 h after tetracycline withdrawal, and the cells acquire higher resistance to 5-FU. Fluorouracil 238-242 tumor protein p53 Homo sapiens 78-81 12084458-9 2002 The enzyme uridine-cytidine monophosphate kinase (UMPK) is an essential and rate-limiting enzyme in 5-FU activation while dihydropyrimidine dehydrogenase (DPD) is a catabolic enzyme that inactivates 5-FU. Fluorouracil 199-203 uridine-cytidine kinase 2 Homo sapiens 11-48 12084458-9 2002 The enzyme uridine-cytidine monophosphate kinase (UMPK) is an essential and rate-limiting enzyme in 5-FU activation while dihydropyrimidine dehydrogenase (DPD) is a catabolic enzyme that inactivates 5-FU. Fluorouracil 199-203 uridine-cytidine kinase 2 Homo sapiens 50-54 12084458-10 2002 Alterations in UMPK and DPD may therefore explain failure of 5-FU response in the absence of alterations in TS or p53. Fluorouracil 61-65 uridine-cytidine kinase 2 Homo sapiens 15-19 12174943-5 2002 On the other hand, the inhibitory effect on tumor growth in rats administered with both TNF-SAM2 and 5-FU (10 mg/kg) was 65%, which was equal to, or less than, that in rats administered with only TNF-SAM2 or 5-FU. Fluorouracil 208-212 tumor necrosis factor Rattus norvegicus 88-91 12174947-3 2002 After administration of chemotherapy consisting of 5-fluorouracil (4000 mg) and epirubicin (280 mg), the pulmonary metastases disappeared and this was associated with a decrease of serum CEA levels and tumor size. Fluorouracil 51-65 CEA cell adhesion molecule 3 Homo sapiens 187-190 12182321-0 2002 Radiation could induce p53-independent and cell cycle--unrelated apoptosis in 5-fluorouracil radiosensitized head and neck carcinoma cells. Fluorouracil 78-92 tumor protein p53 Homo sapiens 23-26 12150722-3 2002 We observed the expression of inducible nitric oxide synthase (iNOS) and apoptosis of cells induced by 5-FU with L-Arg added to the medium. Fluorouracil 103-107 nitric oxide synthase 2 Homo sapiens 30-61 12111108-0 2002 Pharmacokinetic study of S-1, a novel oral fluorouracil antitumor agent in animal model and in patients with impaired renal function. Fluorouracil 43-55 proteasome 26S subunit, non-ATPase 1 Homo sapiens 25-28 12111108-1 2002 PURPOSE: S-1 is a novel oral fluorouracil antitumor drug that combines tegafur (FT), 5-chloro-2,4-dihydroxypyridine (CDHP), which inhibits dihydropyrimidine dehydrogenase (DPD), and potassium oxonate (Oxo). Fluorouracil 29-41 proteasome 26S subunit, non-ATPase 1 Homo sapiens 9-12 12085207-0 2002 Expression of multidrug resistance-associated protein1,P-glycoprotein, and thymidylate synthase in gastric cancer patients treated with 5-fluorouracil and doxorubicin-based adjuvant chemotherapy after curative resection. Fluorouracil 136-150 ATP binding cassette subfamily C member 1 Homo sapiens 14-54 12085207-0 2002 Expression of multidrug resistance-associated protein1,P-glycoprotein, and thymidylate synthase in gastric cancer patients treated with 5-fluorouracil and doxorubicin-based adjuvant chemotherapy after curative resection. Fluorouracil 136-150 ATP binding cassette subfamily B member 1 Homo sapiens 55-69 12173327-10 2002 CONCLUSIONS: The addition of gemcitabine and 5-FU to subcutaneous IL2 and IFNA results in a similar response rate to what was observed in previous studies of IL2-based therapy. Fluorouracil 45-49 interleukin 2 Homo sapiens 66-69 12173327-0 2002 A phase II trial of intravenous gemcitabine and 5-fluorouracil with subcutaneous interleukin-2 and interferon-alpha in patients with metastatic renal cell carcinoma. Fluorouracil 48-62 interleukin 2 Homo sapiens 81-94 12173327-10 2002 CONCLUSIONS: The addition of gemcitabine and 5-FU to subcutaneous IL2 and IFNA results in a similar response rate to what was observed in previous studies of IL2-based therapy. Fluorouracil 45-49 interleukin 2 Homo sapiens 158-161 26680854-12 2002 Furthermore, 5-FU increased the enzymatic activity of caspase-3 protease with PARP digestion in HepG2 cells. Fluorouracil 13-17 caspase 3 Homo sapiens 54-63 11920608-0 2002 Resistance of colon cancer cells to long-term 5-fluorouracil exposure is correlated to the relative level of Bcl-2 and Bcl-X(L) in addition to Bax and p53 status. Fluorouracil 46-60 BCL2 apoptosis regulator Homo sapiens 109-114 11920608-0 2002 Resistance of colon cancer cells to long-term 5-fluorouracil exposure is correlated to the relative level of Bcl-2 and Bcl-X(L) in addition to Bax and p53 status. Fluorouracil 46-60 BCL2 like 1 Homo sapiens 119-127 11920608-0 2002 Resistance of colon cancer cells to long-term 5-fluorouracil exposure is correlated to the relative level of Bcl-2 and Bcl-X(L) in addition to Bax and p53 status. Fluorouracil 46-60 BCL2 associated X, apoptosis regulator Homo sapiens 143-146 11920608-0 2002 Resistance of colon cancer cells to long-term 5-fluorouracil exposure is correlated to the relative level of Bcl-2 and Bcl-X(L) in addition to Bax and p53 status. Fluorouracil 46-60 tumor protein p53 Homo sapiens 151-154 11920608-5 2002 In p53(+/+) cell lines but not in p53(-/0) cell lines, a low level of the pro-apoptotic Bax protein was correlated with a greater resistance of cells to 5-FU. Fluorouracil 153-157 tumor protein p53 Homo sapiens 3-6 11920608-5 2002 In p53(+/+) cell lines but not in p53(-/0) cell lines, a low level of the pro-apoptotic Bax protein was correlated with a greater resistance of cells to 5-FU. Fluorouracil 153-157 BCL2 associated X, apoptosis regulator Homo sapiens 88-91 11920608-6 2002 In addition, we found that high levels of anti-apoptotic Bcl-2 and Bcl-x(L) proteins combined with a low level of Bax were correlated to high 5-FU resistance of wild-type p53 cell lines. Fluorouracil 142-146 BCL2 apoptosis regulator Homo sapiens 57-62 11920608-6 2002 In addition, we found that high levels of anti-apoptotic Bcl-2 and Bcl-x(L) proteins combined with a low level of Bax were correlated to high 5-FU resistance of wild-type p53 cell lines. Fluorouracil 142-146 BCL2 like 1 Homo sapiens 67-75 11920608-6 2002 In addition, we found that high levels of anti-apoptotic Bcl-2 and Bcl-x(L) proteins combined with a low level of Bax were correlated to high 5-FU resistance of wild-type p53 cell lines. Fluorouracil 142-146 BCL2 associated X, apoptosis regulator Homo sapiens 114-117 11920608-6 2002 In addition, we found that high levels of anti-apoptotic Bcl-2 and Bcl-x(L) proteins combined with a low level of Bax were correlated to high 5-FU resistance of wild-type p53 cell lines. Fluorouracil 142-146 tumor protein p53 Homo sapiens 171-174 11920608-8 2002 In conclusion, the relative levels of Bcl-2, Bcl-x(L) and Bax may altogether contribute to determine the resistance of a majority of colon tumor cells to long-term 5-FU treatment, whatever their p53 status. Fluorouracil 164-168 BCL2 apoptosis regulator Homo sapiens 38-43 11920608-8 2002 In conclusion, the relative levels of Bcl-2, Bcl-x(L) and Bax may altogether contribute to determine the resistance of a majority of colon tumor cells to long-term 5-FU treatment, whatever their p53 status. Fluorouracil 164-168 BCL2 like 1 Homo sapiens 45-53 11920608-8 2002 In conclusion, the relative levels of Bcl-2, Bcl-x(L) and Bax may altogether contribute to determine the resistance of a majority of colon tumor cells to long-term 5-FU treatment, whatever their p53 status. Fluorouracil 164-168 BCL2 associated X, apoptosis regulator Homo sapiens 58-61 11980662-0 2002 The role of thymidylate synthase induction in modulating p53-regulated gene expression in response to 5-fluorouracil and antifolates. Fluorouracil 102-116 tumor protein p53 Homo sapiens 57-60 11980662-6 2002 Inactivation of p53 significantly increased resistance to 5-FU and the antifolates with IC-50(72 h) doses for 5-FU and TDX of >100 and >10 microM, respectively, in the M7TS90-E6 cell line. Fluorouracil 58-62 tumor protein p53 Homo sapiens 16-19 11980662-6 2002 Inactivation of p53 significantly increased resistance to 5-FU and the antifolates with IC-50(72 h) doses for 5-FU and TDX of >100 and >10 microM, respectively, in the M7TS90-E6 cell line. Fluorouracil 110-114 tumor protein p53 Homo sapiens 16-19 11980662-7 2002 Furthermore, p53 inactivation completely abrogated the cell cycle arrest and apoptosis induced by 5-FU. Fluorouracil 98-102 tumor protein p53 Homo sapiens 13-16 11927016-0 2002 The roles of JNK1 and Stat3 in the response of head and neck cancer cell lines to combined treatment with all-trans-retinoic acid and 5-fluorouracil. Fluorouracil 134-148 mitogen-activated protein kinase 8 Homo sapiens 13-17 12014658-2 2002 This study was undertaken to evaluate the impact of wild-type or mutant p53 status on the synergistic effects of 5-Fluorouracil (5-FU) and radiation (XRT) in pancreatic tumors. Fluorouracil 113-127 tumor protein p53 Homo sapiens 72-75 12014658-10 2002 Clonogenic assays showed enhanced radiosensitizing effect when 5-Fluorouracil was added to cell lines lacking functional p53. Fluorouracil 63-77 tumor protein p53 Homo sapiens 121-124 11836567-15 2002 Although the receptor signaling pathway in apoptosis was not observed by 5-FU, Bax-induced cytochrome c and caspase 3 was also observed in a receptor-independent pathway by 5-FU and CDDP. Fluorouracil 73-77 BCL2 associated X, apoptosis regulator Homo sapiens 79-82 11836567-15 2002 Although the receptor signaling pathway in apoptosis was not observed by 5-FU, Bax-induced cytochrome c and caspase 3 was also observed in a receptor-independent pathway by 5-FU and CDDP. Fluorouracil 173-177 BCL2 associated X, apoptosis regulator Homo sapiens 79-82 11836567-15 2002 Although the receptor signaling pathway in apoptosis was not observed by 5-FU, Bax-induced cytochrome c and caspase 3 was also observed in a receptor-independent pathway by 5-FU and CDDP. Fluorouracil 173-177 cytochrome c, somatic Homo sapiens 91-103 11836567-15 2002 Although the receptor signaling pathway in apoptosis was not observed by 5-FU, Bax-induced cytochrome c and caspase 3 was also observed in a receptor-independent pathway by 5-FU and CDDP. Fluorouracil 173-177 caspase 3 Homo sapiens 108-117 11912124-1 2002 The cornerstone of the systemic treatment of advanced colorectal cancer is 5-fluorouracil.However, 5-fluorouracil-induced apoptosis is dependent on p53, a tumor suppressor gene that is lost or inactivated in at least 85% of human colorectal cancers. Fluorouracil 99-113 tumor protein p53 Homo sapiens 148-151 11872346-3 2002 The purpose of this study was to assess whether c-erbB-2 expression is associated with clinical sensitivity to docetaxel (T) or sequential methotrexate and 5-fluorouracil (MF). Fluorouracil 156-170 erb-b2 receptor tyrosine kinase 2 Homo sapiens 48-56 11927016-7 2002 Both ATRA and 5-FU activated c-Jun N-terminal kinase (JNK) 1 and the combination of both agents resulted in additive or synergistic activation of JNK1, and also enhanced the induction of apoptosis. Fluorouracil 14-18 mitogen-activated protein kinase 8 Homo sapiens 29-60 11927016-7 2002 Both ATRA and 5-FU activated c-Jun N-terminal kinase (JNK) 1 and the combination of both agents resulted in additive or synergistic activation of JNK1, and also enhanced the induction of apoptosis. Fluorouracil 14-18 mitogen-activated protein kinase 8 Homo sapiens 146-150 11927016-8 2002 The YCU-H891 cells, in which the epidermal growth factor receptor (EGFR)-signal transducer and activator of transcription 3 (Stat3) pathway is constitutively activated, were more resistant to treatments with ATRA, 5-FU and the combination of both agents than YCU-N861 cells. Fluorouracil 214-218 epidermal growth factor receptor Homo sapiens 33-65 11927016-8 2002 The YCU-H891 cells, in which the epidermal growth factor receptor (EGFR)-signal transducer and activator of transcription 3 (Stat3) pathway is constitutively activated, were more resistant to treatments with ATRA, 5-FU and the combination of both agents than YCU-N861 cells. Fluorouracil 214-218 epidermal growth factor receptor Homo sapiens 67-71 11927016-8 2002 The YCU-H891 cells, in which the epidermal growth factor receptor (EGFR)-signal transducer and activator of transcription 3 (Stat3) pathway is constitutively activated, were more resistant to treatments with ATRA, 5-FU and the combination of both agents than YCU-N861 cells. Fluorouracil 214-218 signal transducer and activator of transcription 3 Homo sapiens 125-130 11927016-9 2002 A dominant negative Stat3 construct strongly enhanced the cellular sensitivity of this cell line to 5-FU but not to ATRA. Fluorouracil 100-104 signal transducer and activator of transcription 3 Homo sapiens 20-25 11927016-0 2002 The roles of JNK1 and Stat3 in the response of head and neck cancer cell lines to combined treatment with all-trans-retinoic acid and 5-fluorouracil. Fluorouracil 134-148 signal transducer and activator of transcription 3 Homo sapiens 22-27 11854447-4 2002 In cross-resistance studies, we observed resistance of yeast sky1 Delta cells (i.e., cells from which the SKY1 gene had been disrupted) to cisplatin, carboplatin (but not oxaliplatin), doxorubicin and daunorubicin, and hypersensitivity to cadmium chloride and 5-fluorouracil. Fluorouracil 260-274 serine/threonine protein kinase SKY1 Saccharomyces cerevisiae S288C 61-65 11854447-4 2002 In cross-resistance studies, we observed resistance of yeast sky1 Delta cells (i.e., cells from which the SKY1 gene had been disrupted) to cisplatin, carboplatin (but not oxaliplatin), doxorubicin and daunorubicin, and hypersensitivity to cadmium chloride and 5-fluorouracil. Fluorouracil 260-274 serine/threonine protein kinase SKY1 Saccharomyces cerevisiae S288C 106-110 11990524-6 2002 There were significant increases in tumour vascularity, vessel length density and blood flow with both interstitial and systemic bFGF infusions, and a significant increase in tumour fluorouracil uptake after systemic bFGF infusion of liver tumours. Fluorouracil 182-194 fibroblast growth factor 2 Homo sapiens 217-221 11802206-0 2002 P53 overexpression predicts poor chemosensitivity to high-dose 5-fluorouracil plus leucovorin chemotherapy for stage IV colorectal cancers after palliative bowel resection. Fluorouracil 63-77 tumor protein p53 Homo sapiens 0-3 11791172-6 2002 Our results with 5-FU thus show that genetically separable functions of p53 are involved in its ability to respond to DNA-damaging agents to induce apoptosis. Fluorouracil 17-21 tumor protein p53 Homo sapiens 72-75 11990524-8 2002 bFGF infusion increased tumour fluorouracil uptake. Fluorouracil 31-43 fibroblast growth factor 2 Homo sapiens 0-4 11748447-4 2002 Introduction of HER-2 oncoprotein in vitro induces resistance to several anticancer drugs, including taxanes, cisplatin (CDDP) and 5-fluorouracil (5-FU) in breast cancer cells. Fluorouracil 131-145 erb-b2 receptor tyrosine kinase 2 Homo sapiens 16-21 11750847-0 2002 Potentiation of the sensitivity of renal cell carcinoma cells to TRAIL-mediated apoptosis by subtoxic concentrations of 5-fluorouracil. Fluorouracil 120-134 TNF superfamily member 10 Homo sapiens 65-70 11750847-5 2002 Since several cytotoxic anticancer drugs including 5-fluorouracil (5-FU) also mediate apoptosis, we reasoned that combined treatment of cancer cells with TRAIL and drugs might result in synergy and overcome the resistance of the cancer cell. Fluorouracil 51-65 TNF superfamily member 10 Homo sapiens 154-159 11750847-5 2002 Since several cytotoxic anticancer drugs including 5-fluorouracil (5-FU) also mediate apoptosis, we reasoned that combined treatment of cancer cells with TRAIL and drugs might result in synergy and overcome the resistance of the cancer cell. Fluorouracil 67-71 TNF superfamily member 10 Homo sapiens 154-159 11750847-14 2002 Treatment of Caki-1 cells with 5-FU enhanced the expression of p53 and bax, but had no effect on the expression of bcl-2. Fluorouracil 31-35 tumor protein p53 Homo sapiens 63-66 11750847-14 2002 Treatment of Caki-1 cells with 5-FU enhanced the expression of p53 and bax, but had no effect on the expression of bcl-2. Fluorouracil 31-35 BCL2 associated X, apoptosis regulator Homo sapiens 71-74 11750847-15 2002 Incubation of Caki-1 cells with TRAIL enhanced the intracellular accumulation of 5-FU and 5-fluoro-2"-deoxyuridine 5"-monophosphate (FdUMP). Fluorouracil 81-85 TNF superfamily member 10 Homo sapiens 32-37 11750847-20 2002 These findings support the potential application in vivo of a combination of TRAIL and 5-FU in the treatment of TRAIL/5-FU-resistant RCC. Fluorouracil 87-91 TNF superfamily member 10 Homo sapiens 112-117 11750847-20 2002 These findings support the potential application in vivo of a combination of TRAIL and 5-FU in the treatment of TRAIL/5-FU-resistant RCC. Fluorouracil 118-122 TNF superfamily member 10 Homo sapiens 77-82 12065876-2 2002 METHODS: The expression of p53 and mdm2 was analyzed by an immunohistochemical assay in 80 formalin-fixed paraffin embedded primary tumour samples and related to the clinical response to 5-fluorouracil therapy and to the prognosis of the patients. Fluorouracil 187-201 tumor protein p53 Homo sapiens 27-30 11918083-8 2002 Collagen 1, fibronectin and fibroblast-derived ECM rendered LiM6 cells, but not LS174T, more sensitive to the harmful effect of 5-FU. Fluorouracil 128-132 fibronectin 1 Homo sapiens 12-23 12378342-8 2002 After incubation with MGr1 antibody, SGC7901/VCR cells showed significantly decreased IC(50) values for adriamycin (from 0.887 +/- 0.081 mg/l to 0.607 +/- 0.084 mg/l; P, 0.05), vincristine (from 0.707 +/- 0.055 mg/l to 0.557 +/- 0.042 mg/l; P, 0.05), and 5-fluorouracil (from 4.367 +/- 0.407 mg/l to 2.630 +/- 0.644 mg/l; P, 0.05), as well as slightly increased IC(50) values for mitomycin (from 0.183 +/- 0.045 mg/l to 0.198 +/- 0.048 mg/l; P. 0.05). Fluorouracil 255-269 MGR1 Homo sapiens 22-26 11752120-3 2002 We found that, relative to control transfectants, there was a slight tendency for the p53 inactivated cells to be less sensitive to 5-FU after 6 days of continuous treatment. Fluorouracil 132-136 tumor protein p53 Homo sapiens 86-89 11748447-4 2002 Introduction of HER-2 oncoprotein in vitro induces resistance to several anticancer drugs, including taxanes, cisplatin (CDDP) and 5-fluorouracil (5-FU) in breast cancer cells. Fluorouracil 147-151 erb-b2 receptor tyrosine kinase 2 Homo sapiens 16-21 11748447-7 2002 In contrast, a correlation between the response to a cyclophosphamide + methotrexate + 5-FU regimen and overexpression of HER-2 is not certain. Fluorouracil 87-91 erb-b2 receptor tyrosine kinase 2 Homo sapiens 122-127 11748459-0 2002 Up-regulation of vitamin D3 up-regulated protein 1 gene in response to 5-fluorouracil in colon carcinoma SW620. Fluorouracil 71-85 thioredoxin interacting protein Homo sapiens 17-50 12138244-3 2002 METHODS: The cytotoxic effects of 5-FU and gemcitabine in AsPC-1, Capan-1, Mia-PaCa-2 and T3M4 pancreatic cancer cell lines were assessed by growth assays, and mRNA expression levels of pro-apoptotic and anti-apoptotic genes of the Bcl-2 family were analyzed by RNAse protection assays. Fluorouracil 34-38 BCL2 apoptosis regulator Homo sapiens 232-237 12138244-7 2002 RNase protection assay showed a negative correlation between bcl-x(L) and mcl-1 mRNA expression levels and the sensitivity to 5-FU and gemcitabine after 5-FU and gemcitabine treatment. Fluorouracil 126-130 BCL2 like 1 Homo sapiens 61-69 11748459-3 2002 The microarray showed that the most strongly up-regulated gene by 5-FU was vitamin D3 up-regulated protein 1 (VDUP1), an interesting stress response gene, which was originally reported as a vitamin D3 inducible gene in HL-60. Fluorouracil 66-70 thioredoxin interacting protein Homo sapiens 75-108 11724902-1 2001 Aquaporin-9 (AQP9) is a water channel membrane protein also permeable to small solutes such as urea, glycerol, and 5-fluorouracil, a chemotherapeutic agent. Fluorouracil 115-129 aquaporin 9 Rattus norvegicus 0-11 11748459-3 2002 The microarray showed that the most strongly up-regulated gene by 5-FU was vitamin D3 up-regulated protein 1 (VDUP1), an interesting stress response gene, which was originally reported as a vitamin D3 inducible gene in HL-60. Fluorouracil 66-70 thioredoxin interacting protein Homo sapiens 110-115 11748459-4 2002 TaqMan RT-PCR assay confirmed that VDUP1 gene expression was significantly increased after 24 h of 5-FU treatment compared with untreated control (p<0.01). Fluorouracil 99-103 thioredoxin interacting protein Homo sapiens 35-40 11748459-7 2002 Therefore, VDUP1 not only may be induced by stress response as a result of 5-FU cytotoxicity, but may also play a key role in 5-FU cytotoxicity in colon cancers. Fluorouracil 75-79 thioredoxin interacting protein Homo sapiens 11-16 11748459-7 2002 Therefore, VDUP1 not only may be induced by stress response as a result of 5-FU cytotoxicity, but may also play a key role in 5-FU cytotoxicity in colon cancers. Fluorouracil 126-130 thioredoxin interacting protein Homo sapiens 11-16 11781659-8 2001 Infection of human CD34+-enriched cells with this construct and incubation with 5-FU (10(-6) M) for 14 days also resulted in an increased number of 5-FU-resistant colonies. Fluorouracil 80-84 CD34 molecule Homo sapiens 19-23 11781659-8 2001 Infection of human CD34+-enriched cells with this construct and incubation with 5-FU (10(-6) M) for 14 days also resulted in an increased number of 5-FU-resistant colonies. Fluorouracil 148-152 CD34 molecule Homo sapiens 19-23 12138244-7 2002 RNase protection assay showed a negative correlation between bcl-x(L) and mcl-1 mRNA expression levels and the sensitivity to 5-FU and gemcitabine after 5-FU and gemcitabine treatment. Fluorouracil 153-157 BCL2 like 1 Homo sapiens 61-69 12138244-8 2002 The bax/bcl-2 ratio maintained relatively stable following 5-FU/gemcitabine treatment and reflected the chemotherapeutic sensitivity of these cell lines. Fluorouracil 59-63 BCL2 associated X, apoptosis regulator Homo sapiens 4-7 12138244-8 2002 The bax/bcl-2 ratio maintained relatively stable following 5-FU/gemcitabine treatment and reflected the chemotherapeutic sensitivity of these cell lines. Fluorouracil 59-63 BCL2 apoptosis regulator Homo sapiens 8-13 12138244-10 2002 The bax/bcl-2 ratio is predictive of chemotherapy sensitivity, whereas bcl-x(L) and mcl-1 mRNA levels following repeated exposure to 5-FU or gemcitabine are associated with resistance to these drugs. Fluorouracil 133-137 BCL2 like 1 Homo sapiens 71-79 12185293-0 2002 Clinical studies of three oral prodrugs of 5-fluorouracil (capecitabine, UFT, S-1): a review. Fluorouracil 43-57 proteasome 26S subunit, non-ATPase 1 Homo sapiens 78-81 11791389-0 2001 [A case of AFP producing early gastric cancer successfully treated with small dose CDDP and 5-FU (PF) therapy]. Fluorouracil 92-96 alpha fetoprotein Homo sapiens 11-14 11791389-1 2001 A case of AFP producing early gastric cancer successfully treated with a small dose of CDDP and 5-FU therapy administered intermittedly is reported with a review of the literature. Fluorouracil 96-100 alpha fetoprotein Homo sapiens 10-13 11724902-1 2001 Aquaporin-9 (AQP9) is a water channel membrane protein also permeable to small solutes such as urea, glycerol, and 5-fluorouracil, a chemotherapeutic agent. Fluorouracil 115-129 aquaporin 9 Rattus norvegicus 13-17 11592762-0 2001 Phase II study of S-1, a novel oral fluorouracil, in advanced non-small-cell lung cancer. Fluorouracil 36-48 proteasome 26S subunit, non-ATPase 1 Homo sapiens 18-21 11791891-0 2001 In vitro and in vivo inhibition of myeloperoxidase with 5-fluorouracil. Fluorouracil 56-70 myeloperoxidase Homo sapiens 35-50 11791891-3 2001 The aim of the present study was to investigate whether 5-fluorouracil (5-FU), a chemotherapeutic agent, has a direct inhibitory effect on MPO and to evaluate some properties of this inhibition. Fluorouracil 56-70 myeloperoxidase Homo sapiens 139-142 11791891-3 2001 The aim of the present study was to investigate whether 5-fluorouracil (5-FU), a chemotherapeutic agent, has a direct inhibitory effect on MPO and to evaluate some properties of this inhibition. Fluorouracil 72-76 myeloperoxidase Homo sapiens 139-142 11791891-7 2001 RESULTS: 5-FU inhibited tissue-associated MPO activity in a dose-dependent but not time-dependent manner with an IC50 value of 0.6 mg/ml. Fluorouracil 9-13 myeloperoxidase Homo sapiens 42-45 11791891-8 2001 5-FU also inhibited MPO activity in isolated human leukocytes in a dose-dependent manner, and the IC50 value was 0.75 mg/ml. Fluorouracil 0-4 myeloperoxidase Homo sapiens 20-23 11791891-10 2001 Leukocyte MPO activities of patients receiving 5-FU therapy were compared before treatment and after the first, second, and third administration cycles. Fluorouracil 47-51 myeloperoxidase Homo sapiens 10-13 11791891-11 2001 5-FU treatment resulted in a significant decrease in leukocyte MPO activity, and repeated 5-FU treatment caused additional decrease. Fluorouracil 0-4 myeloperoxidase Homo sapiens 63-66 11791891-12 2001 CONCLUSION: Our data showed that 5-FU directly inhibited the MPO activity of human leukocytes in vitro and in vivo. Fluorouracil 33-37 myeloperoxidase Homo sapiens 61-64 11745442-2 2001 We examined the effect of transfection of Mn-SOD antisense on apoptosis by 5-FU, PLM, CDDP and gamma-rays using nu/nu mice. Fluorouracil 75-79 superoxide dismutase 2, mitochondrial Mus musculus 42-48 11689601-0 2001 Complete response achieved following administration of S-1 in a patient with adrenal gland metastasis of 5-FU-resistant gastric cancer: a case report. Fluorouracil 105-109 proteasome 26S subunit, non-ATPase 1 Homo sapiens 55-58 11590433-0 2001 Ferredoxin reductase affects p53-dependent, 5-fluorouracil-induced apoptosis in colorectal cancer cells. Fluorouracil 44-58 tumor protein p53 Homo sapiens 29-32 11590433-1 2001 Loss of p53 gene function, which occurs in most colon cancer cells, has been shown to abolish the apoptotic response to 5-fluorouracil (5-FU). Fluorouracil 120-134 tumor protein p53 Homo sapiens 8-11 11590433-1 2001 Loss of p53 gene function, which occurs in most colon cancer cells, has been shown to abolish the apoptotic response to 5-fluorouracil (5-FU). Fluorouracil 136-140 tumor protein p53 Homo sapiens 8-11 11590433-2 2001 To identify genes downstream of p53 that might mediate these effects, we assessed global patterns of gene expression following 5-FU treatment of isogenic cells differing only in their p53 status. Fluorouracil 127-131 tumor protein p53 Homo sapiens 32-35 11590433-3 2001 The gene encoding mitochondrial ferredoxin reductase (protein, FR; gene, FDXR) was one of the few genes significantly induced by p53 after 5-FU treatment. Fluorouracil 139-143 tumor protein p53 Homo sapiens 129-132 11759828-2 2001 It was the purpose of this in vitro study to define the association between HER-2/neu overexpression and the sensitivity to the chemotherapeutic drug combinations of cyclophosphamide, methotrexate and 5-fluorouracil (CMF) and 5-fluorouracil, epirubicin and cyclophosphamide (FEC) of breast cancer cells derived from 140 chemotherapy-naive patients at the time of primary surgery. Fluorouracil 201-215 erb-b2 receptor tyrosine kinase 2 Homo sapiens 82-85 11759828-2 2001 It was the purpose of this in vitro study to define the association between HER-2/neu overexpression and the sensitivity to the chemotherapeutic drug combinations of cyclophosphamide, methotrexate and 5-fluorouracil (CMF) and 5-fluorouracil, epirubicin and cyclophosphamide (FEC) of breast cancer cells derived from 140 chemotherapy-naive patients at the time of primary surgery. Fluorouracil 226-240 erb-b2 receptor tyrosine kinase 2 Homo sapiens 82-85 11554164-4 2001 Positivity for p53 was associated with shorter survival in 5-fluorouracil-treated and untreated patients. Fluorouracil 59-73 tumor protein p53 Homo sapiens 15-18 11689601-9 2001 There has been no previous report of S-1 showing remarkable effectiveness in a patient with 5-FU-resistant gastric cancer metastasizing to the adrenal gland. Fluorouracil 92-96 proteasome 26S subunit, non-ATPase 1 Homo sapiens 37-40 11689601-10 2001 We consider that the efficacy of S-1 for treatment of 5-FU-resistant gastric cancer should be verified. Fluorouracil 54-58 proteasome 26S subunit, non-ATPase 1 Homo sapiens 33-36 11445854-9 2001 In conclusion, our observations suggested that p53 mutation may be associated with apoptotic induction by 5-FU; however, p53 status may not strongly affect TS induction by 5-FU. Fluorouracil 106-110 tumor protein p53 Homo sapiens 47-50 11489535-3 2001 IL-6 protects PC12 cells from the death induced by serum deprivation or anticancer agents, such as cisplatin, paclitaxel and 5-fluorouracil. Fluorouracil 125-139 interleukin 6 Rattus norvegicus 0-4 11603002-4 2001 However, IFN-gamma attenuated the anti-tumor effect of 5-FU at the concentrations of 0.1-10 IU/ml. Fluorouracil 55-59 interferon gamma Homo sapiens 9-18 11603002-6 2001 As low as 0.1 IU/ml of IFN-gamma attenuated the anti-tumor effect of 5-FU in another experimental system where HCT-15 cells were exposed to 0.1 IU/ml of IFN-gamma before and during the treatment with 5-FU. Fluorouracil 69-73 interferon gamma Homo sapiens 23-32 11603002-6 2001 As low as 0.1 IU/ml of IFN-gamma attenuated the anti-tumor effect of 5-FU in another experimental system where HCT-15 cells were exposed to 0.1 IU/ml of IFN-gamma before and during the treatment with 5-FU. Fluorouracil 69-73 interferon gamma Homo sapiens 153-162 11603002-6 2001 As low as 0.1 IU/ml of IFN-gamma attenuated the anti-tumor effect of 5-FU in another experimental system where HCT-15 cells were exposed to 0.1 IU/ml of IFN-gamma before and during the treatment with 5-FU. Fluorouracil 200-204 interferon gamma Homo sapiens 23-32 11899785-0 2001 Meta-analysis of adjuvant cyclophosphamide/methotrexate/5-fluorouracil chemotherapy in postmenopausal women with estrogen receptor-positive, node-positive breast cancer. Fluorouracil 56-70 estrogen receptor 1 Homo sapiens 113-130 11448920-9 2001 However, CEA significantly protected HT29 cells from undergoing apoptosis under various conditions, including confluent growth, UV light, IFN-gamma treatment, and treatment with 5-fluorouracil. Fluorouracil 178-192 CEA cell adhesion molecule 3 Homo sapiens 9-12 11408917-0 2001 Activation of caspase-3 in renal cell carcinoma cells by anthracyclines or 5-fluorouracil. Fluorouracil 75-89 caspase 3 Homo sapiens 14-23 11408917-5 2001 Treatment of ACHN cells with CDDP, VLB, IFN-alpha, or IFN-gamma did not activate caspase-3, but its activity was increased 7.2-fold (p = 0.0001) with ADR and 2.8-fold (p = 0.0385) with 5-FU in comparison with control. Fluorouracil 185-189 interferon gamma Homo sapiens 54-63 11408917-8 2001 Of the six freshly derived RCC cells treated with 5-FU, caspase-3 activity was increased 3.1-fold (p = 0.0051) and 2.4-fold (p = 0.0346) in two of them, respectively. Fluorouracil 50-54 caspase 3 Homo sapiens 56-65 11408917-11 2001 Furthermore, both active caspase-3 and apoptosis triggered by either ADR or 5-FU were inhibited significantly by the general caspase inhibitor Z-VAD-FMK, or a specific caspase-3 inhibitor DMQD-CHO. Fluorouracil 76-80 caspase 3 Homo sapiens 25-34 11408917-11 2001 Furthermore, both active caspase-3 and apoptosis triggered by either ADR or 5-FU were inhibited significantly by the general caspase inhibitor Z-VAD-FMK, or a specific caspase-3 inhibitor DMQD-CHO. Fluorouracil 76-80 caspase 3 Homo sapiens 168-177 11899785-1 2001 Conflicting results have been published regarding the efficacy of adjuvant cyclophosphamide/methotrexate/5-fluorouracil (CMF)-type chemotherapy in postmenopausal, estrogen receptor (ER)-positive women. Fluorouracil 105-119 estrogen receptor 1 Homo sapiens 163-180 11899785-1 2001 Conflicting results have been published regarding the efficacy of adjuvant cyclophosphamide/methotrexate/5-fluorouracil (CMF)-type chemotherapy in postmenopausal, estrogen receptor (ER)-positive women. Fluorouracil 105-119 estrogen receptor 1 Homo sapiens 182-184 11484952-6 2001 RESULTS: Expression of both p53 and Rb correlated with survival benefit after 5-FU treatment. Fluorouracil 78-82 tumor protein p53 Homo sapiens 28-31 11406570-0 2001 c-myc/p53 interaction determines sensitivity of human colon carcinoma cells to 5-fluorouracil in vitro and in vivo. Fluorouracil 79-93 tumor protein p53 Homo sapiens 6-9 11410796-2 2001 MKN-1 gastric cancer cells were treated with the IC50 of 5-FU in the presence of interferon-gamma (IFN-gamma). Fluorouracil 57-61 interferon gamma Homo sapiens 81-97 11410796-2 2001 MKN-1 gastric cancer cells were treated with the IC50 of 5-FU in the presence of interferon-gamma (IFN-gamma). Fluorouracil 57-61 interferon gamma Homo sapiens 99-108 11410796-5 2001 After 5-FU treatment in the presence of IFN-gamma, NO and TNF-alpha were produced and anti-tumor activity was enhanced. Fluorouracil 6-10 interferon gamma Homo sapiens 40-49 11410796-5 2001 After 5-FU treatment in the presence of IFN-gamma, NO and TNF-alpha were produced and anti-tumor activity was enhanced. Fluorouracil 6-10 tumor necrosis factor Homo sapiens 58-67 11406570-6 2001 Finally, the in vitro data predicted that only patients with both amplified c-myc and wild-type p53 in their primary tumors would be responsive to 5FU-based therapy, which was borne out by analysis of tumors from 135 patients entered into a Phase III clinical trial of 5FU-based adjuvant therapy. Fluorouracil 147-150 tumor protein p53 Homo sapiens 96-99 11267993-4 2001 MED1 acts as a mismatch-specific DNA N-glycosylase active on thymine, uracil, 5-fluorouracil and, weakly, 3,N(4)-ethenocytosine paired with guanine. Fluorouracil 78-92 methyl-CpG binding domain 4, DNA glycosylase Homo sapiens 15-50 11353746-4 2001 The contributions of CYP1A, CYP2C, and CYP3A enzymes to 5-FU formation in male rat liver microsomes were supported by immunoinhibition studies. Fluorouracil 56-60 cytochrome P450, family 3, subfamily a, polypeptide 62 Rattus norvegicus 39-44 11353746-7 2001 These results suggest that CYP1A and CYP3A enzymes, autoinduced by tegafur, have important roles in 5-FU formation from tegafur in rat liver microsomes. Fluorouracil 100-104 cytochrome P450, family 3, subfamily a, polypeptide 62 Rattus norvegicus 37-42 11497250-0 2001 Possible regulation of 5-fluorouracil-induced neuro- and oral toxicities by two biochemical modulators consisting of S-1, a new oral formulation of 5-fluorouracil. Fluorouracil 23-37 proteasome 26S subunit, non-ATPase 1 Homo sapiens 117-120 11497250-0 2001 Possible regulation of 5-fluorouracil-induced neuro- and oral toxicities by two biochemical modulators consisting of S-1, a new oral formulation of 5-fluorouracil. Fluorouracil 148-162 proteasome 26S subunit, non-ATPase 1 Homo sapiens 117-120 11497250-1 2001 S-1 is a new oral formulation of 5-fluorouracil (5-FU) containing 1 M tegafur and 0.4 M 5-chloro-2,4-dihydroxypyridine (CDHP) and 1 M potassium oxonate (Oxo). Fluorouracil 33-47 proteasome 26S subunit, non-ATPase 1 Homo sapiens 0-3 11497250-1 2001 S-1 is a new oral formulation of 5-fluorouracil (5-FU) containing 1 M tegafur and 0.4 M 5-chloro-2,4-dihydroxypyridine (CDHP) and 1 M potassium oxonate (Oxo). Fluorouracil 49-53 proteasome 26S subunit, non-ATPase 1 Homo sapiens 0-3 11497250-6 2001 Another advantage of the use of S-1 was protection through Oxo against the development of 5-FU-induced mucositis, which occurs frequently in cancer patients. Fluorouracil 90-94 proteasome 26S subunit, non-ATPase 1 Homo sapiens 32-35 11497250-8 2001 One of the possible mechanisms of the decreased incidence of mucositis associated with oral S-1 administration is the decreased formation of 5-fluoronucleotides from 5-FU in the mucosal tissues of the oral cavity. Fluorouracil 166-170 proteasome 26S subunit, non-ATPase 1 Homo sapiens 92-95 11350904-12 2001 CONCLUSIONS: Our findings suggest that p53 alteration and MSI could be clinically useful molecular predictive markers for the identification of CRC patients who might benefit from 5-fluorouracil-based chemotherapy. Fluorouracil 180-194 tumor protein p53 Homo sapiens 39-42 11311495-4 2001 5-fluorouracil (5FU) treatment resulted in a substantial increase in the p53-positive signet-ring cell population (from 17% to 45%) and in an increased Mdm2 immunoreactivity. Fluorouracil 0-14 tumor protein p53 Homo sapiens 73-76 11311495-4 2001 5-fluorouracil (5FU) treatment resulted in a substantial increase in the p53-positive signet-ring cell population (from 17% to 45%) and in an increased Mdm2 immunoreactivity. Fluorouracil 16-19 tumor protein p53 Homo sapiens 73-76 11286477-1 2001 Dexrazoxane combined with doxorubicin (+ 5-fluorouracil + cyclophosphamide - the FAC regime) leads to a significant decrease in doxorubicin cardiotoxicity and a significant increase in median survival time for patients with advanced breast cancer responsive to FAC. Fluorouracil 41-55 FA complementation group C Homo sapiens 81-84 11295077-0 2001 Effect of a combined administration of 5-fluorouracil and medroxyprogesterone acetate on pyrimidine nucleoside phosphorylases and thymidylate synthetase in 7,12-dimethylbenz. Fluorouracil 39-53 thymidylate synthetase Rattus norvegicus 130-152 11309634-8 2001 CONCLUSIONS: Retention of 18q alleles in microsatellite-stable cancers and mutation of the gene for the type II receptor for TGF-beta1 in cancers with high levels of microsatellite instability point to a favorable outcome after adjuvant chemotherapy with fluorouracil-based regimens for stage III colon cancer. Fluorouracil 255-267 transforming growth factor beta 1 Homo sapiens 125-134 11419451-14 2001 IFN-alpha modulation of 5-FU (plus LEV) adds to the toxicity with no therapeutic benefit. Fluorouracil 24-28 interferon alpha 1 Homo sapiens 0-9 11286477-1 2001 Dexrazoxane combined with doxorubicin (+ 5-fluorouracil + cyclophosphamide - the FAC regime) leads to a significant decrease in doxorubicin cardiotoxicity and a significant increase in median survival time for patients with advanced breast cancer responsive to FAC. Fluorouracil 41-55 FA complementation group C Homo sapiens 261-264 11264006-0 2001 5-Fluorouracil suppression of NF-KappaB is mediated by the inhibition of IKappab kinase activity in human salivary gland cancer cells. Fluorouracil 0-14 nuclear factor kappa B subunit 1 Homo sapiens 30-39 11309351-8 2001 Cell lines with faster doubling times and wild-type p53 were significantly more sensitive to 5-FU and FDURD: CONCLUSIONS: The lack of correlation may in part be attributable to the influence of downstream factors such as p53, the observation that the more sensitive cell lines with faster doubling times also had higher TS levels, and the standard procedure of the screen that uses a relatively short (48-h) drug exposure. Fluorouracil 93-97 tumor protein p53 Homo sapiens 52-55 11329775-5 2001 The importance of DIF in 5-FU-based therapy is reviewed herein. Fluorouracil 25-29 tumor necrosis factor Homo sapiens 18-21 11706756-2 2001 The aim of this study was to determine the predictive value of p53 mutation or the expression of GML, a target of p53, for sensitivity to 5-FU and MMC. Fluorouracil 138-142 tumor protein p53 Homo sapiens 63-66 11706756-2 2001 The aim of this study was to determine the predictive value of p53 mutation or the expression of GML, a target of p53, for sensitivity to 5-FU and MMC. Fluorouracil 138-142 tumor protein p53 Homo sapiens 114-117 11264006-1 2001 We have recently shown that 5-Fluorouracil (5-FU) suppresses the transcription factor NF-kappaB in human salivary gland cancer cells (cl-1) by mediating upregulation of IkappaB-alpha expression. Fluorouracil 28-42 nuclear factor kappa B subunit 1 Homo sapiens 86-95 11264006-1 2001 We have recently shown that 5-Fluorouracil (5-FU) suppresses the transcription factor NF-kappaB in human salivary gland cancer cells (cl-1) by mediating upregulation of IkappaB-alpha expression. Fluorouracil 28-42 NFKB inhibitor alpha Homo sapiens 169-182 11264006-1 2001 We have recently shown that 5-Fluorouracil (5-FU) suppresses the transcription factor NF-kappaB in human salivary gland cancer cells (cl-1) by mediating upregulation of IkappaB-alpha expression. Fluorouracil 44-48 nuclear factor kappa B subunit 1 Homo sapiens 86-95 11264006-1 2001 We have recently shown that 5-Fluorouracil (5-FU) suppresses the transcription factor NF-kappaB in human salivary gland cancer cells (cl-1) by mediating upregulation of IkappaB-alpha expression. Fluorouracil 44-48 NFKB inhibitor alpha Homo sapiens 169-182 11264006-5 2001 Thus, we investigated the molecular mechanisms involved in the suppression of NF-kappaB by 5-FU. Fluorouracil 91-95 nuclear factor kappa B subunit 1 Homo sapiens 78-87 11264006-8 2001 The expression of Fas-associated death domain-like interleukin 1-converting enzyme-inhibitory protein (FLIP), which acts as an inhibitor of an initiator caspase (caspase-8), was down-regulated by 5-FU treatment in cl-1 cells. Fluorouracil 196-200 CASP8 and FADD like apoptosis regulator Homo sapiens 18-101 11264006-10 2001 Thus, these results suggest that 5-FU induction of apoptosis in cl-1 cells may be mediated by suppression of NF-kappaB via inhibition of IKK activity. Fluorouracil 33-37 nuclear factor kappa B subunit 1 Homo sapiens 109-118 11745907-12 2001 The active cytotoxic moiety, 5-FU, exhibited formation rate limited kinetics from R-FT because the T-HALF of 5-FU (3.4 h) was similar to that of R-FT (2.4 h). Fluorouracil 29-33 methyl-CpG binding domain protein 1 Homo sapiens 82-86 11745907-12 2001 The active cytotoxic moiety, 5-FU, exhibited formation rate limited kinetics from R-FT because the T-HALF of 5-FU (3.4 h) was similar to that of R-FT (2.4 h). Fluorouracil 29-33 methyl-CpG binding domain protein 1 Homo sapiens 145-149 11745907-12 2001 The active cytotoxic moiety, 5-FU, exhibited formation rate limited kinetics from R-FT because the T-HALF of 5-FU (3.4 h) was similar to that of R-FT (2.4 h). Fluorouracil 109-113 methyl-CpG binding domain protein 1 Homo sapiens 82-86 11300328-0 2001 CEA and CA 19-9 measurement as a monitoring parameter in metastatic colorectal cancer (CRC) under palliative first-line chemotherapy with weekly 24-hour infusion of high-dose 5-fluorouracil (5-FU) and folinic acid (FA). Fluorouracil 175-189 CEA cell adhesion molecule 3 Homo sapiens 0-15 11289281-4 2001 METHODS: Mutation screening of the hot spots of the K-ras gene and of the evolutionarily conserved regions of the TP53 gene was performed by denaturing gradient gel electrophoresis technique in formalin-fixed paraffin-embedded specimens of 55 consecutive patients with Dukes C colon cancer treated with adjuvant 5-fluorouracil-based chemotherapy. Fluorouracil 312-326 tumor protein p53 Homo sapiens 114-118 11370832-5 2001 Furthermore, examination of U937 cell apoptotic trend in parallel with PAP activity measurements and isoforms detection by immunoblotting, revealed both partial enzyme inactivation and dephosphorylation, in particular after the combined drug action of 5-FU and IFN on U937 cells. Fluorouracil 252-256 interferon alpha 1 Homo sapiens 261-264 11179210-0 2001 Crystal structure of dihydropyrimidine dehydrogenase, a major determinant of the pharmacokinetics of the anti-cancer drug 5-fluorouracil. Fluorouracil 122-136 dihydropyrimidine dehydrogenase Sus scrofa 21-52 11300328-0 2001 CEA and CA 19-9 measurement as a monitoring parameter in metastatic colorectal cancer (CRC) under palliative first-line chemotherapy with weekly 24-hour infusion of high-dose 5-fluorouracil (5-FU) and folinic acid (FA). Fluorouracil 191-195 CEA cell adhesion molecule 3 Homo sapiens 0-15 11172605-8 2001 The antitumor effect of 5-FU and CDDP was significantly enhanced in the combination with intra-tumoral administration of bax gene as compared to that of CDDP and 5-FU alone (p<0.05, Student"s t-test). Fluorouracil 24-28 BCL2 associated X, apoptosis regulator Homo sapiens 121-124 11172605-8 2001 The antitumor effect of 5-FU and CDDP was significantly enhanced in the combination with intra-tumoral administration of bax gene as compared to that of CDDP and 5-FU alone (p<0.05, Student"s t-test). Fluorouracil 162-166 BCL2 associated X, apoptosis regulator Homo sapiens 121-124 11172899-8 2001 The SRB assay revealed a 8-fold increased IC(50) for cisplatin and a 2.5-fold increase for 5-FU in DU 145 MN1 as compared to DU 145 cells. Fluorouracil 91-95 MN1 proto-oncogene, transcriptional regulator Homo sapiens 106-109 11167147-0 2001 Effect of a mutant form of IkappaB-alpha on 5-fluorouracil-induced apoptosis in transformed human salivary gland cells. Fluorouracil 44-58 NFKB inhibitor alpha Homo sapiens 27-40 11167147-4 2001 Thus, we investigated whether NF-kappaB suppression in transformed human salivary gland (NS-SV-AC) cells leads to a marked reduction in cell growth in response to 5-FU treatment. Fluorouracil 163-167 nuclear factor kappa B subunit 1 Homo sapiens 30-39 11212269-4 2001 We report here that a human degradation-resistant GLP-2 analogue, h[Gly2]-GLP-2 significantly improves survival, reduces bacteremia, attenuates epithelial injury, and inhibits crypt apoptosis in the murine gastrointestinal tract after administration of topoisomerase I inhibitor irinotecan hydrochloride or the antimetabolite 5-fluorouracil. Fluorouracil 326-340 glucagon Homo sapiens 50-55 11212269-4 2001 We report here that a human degradation-resistant GLP-2 analogue, h[Gly2]-GLP-2 significantly improves survival, reduces bacteremia, attenuates epithelial injury, and inhibits crypt apoptosis in the murine gastrointestinal tract after administration of topoisomerase I inhibitor irinotecan hydrochloride or the antimetabolite 5-fluorouracil. Fluorouracil 326-340 glucagon Homo sapiens 74-79 11208823-0 2001 Response to cyclophosphamide, methotrexate, and fluorouracil in lymph node-positive breast cancer according to HER2 overexpression and other tumor biologic variables. Fluorouracil 48-60 erb-b2 receptor tyrosine kinase 2 Homo sapiens 111-115 11299739-6 2001 We therefore concluded that immunohistochemical studies for p53 and p21 were useful for predicting the chemosensitivities of colon and gastric cancer to MMC and 5-FU. Fluorouracil 161-165 tumor protein p53 Homo sapiens 60-63 11208823-3 2001 However, the significance of HER2 overexpression in responsiveness to cyclophosphamide, methotrexate, and fluorouracil (CMF) has remained unclear. Fluorouracil 106-118 erb-b2 receptor tyrosine kinase 2 Homo sapiens 29-33 11911014-0 2001 gamma-Hydroxybutyric acid and 5-fluorouracil, metabolites of UFT, inhibit the angiogenesis induced by vascular endothelial growth factor. Fluorouracil 30-44 vascular endothelial growth factor A Homo sapiens 102-136 11911014-8 2001 On the other hand, 5-FU inhibited DNA synthesis and migration of HUVECs stimulated by both VEGF and FGF-2, and tube formation driven by VEGF, suggesting that 5-FU is cytotoxic to endothelial cells. Fluorouracil 19-23 vascular endothelial growth factor A Homo sapiens 91-95 11911014-8 2001 On the other hand, 5-FU inhibited DNA synthesis and migration of HUVECs stimulated by both VEGF and FGF-2, and tube formation driven by VEGF, suggesting that 5-FU is cytotoxic to endothelial cells. Fluorouracil 19-23 fibroblast growth factor 2 Homo sapiens 100-105 11911014-8 2001 On the other hand, 5-FU inhibited DNA synthesis and migration of HUVECs stimulated by both VEGF and FGF-2, and tube formation driven by VEGF, suggesting that 5-FU is cytotoxic to endothelial cells. Fluorouracil 158-162 vascular endothelial growth factor A Homo sapiens 91-95 11911014-8 2001 On the other hand, 5-FU inhibited DNA synthesis and migration of HUVECs stimulated by both VEGF and FGF-2, and tube formation driven by VEGF, suggesting that 5-FU is cytotoxic to endothelial cells. Fluorouracil 158-162 fibroblast growth factor 2 Homo sapiens 100-105 11911014-8 2001 On the other hand, 5-FU inhibited DNA synthesis and migration of HUVECs stimulated by both VEGF and FGF-2, and tube formation driven by VEGF, suggesting that 5-FU is cytotoxic to endothelial cells. Fluorouracil 158-162 vascular endothelial growth factor A Homo sapiens 136-140 11911014-10 2001 The VEGF-mediated angiogenesis was significantly inhibited by UFT, 5-FU, and especially by GHB. Fluorouracil 67-71 vascular endothelial growth factor A Homo sapiens 4-8 11167991-7 2001 In additional experiments with chemotherapeutic drugs commonly used for the treatment of colorectal cancer, we found that 5-fluorouracil, mitomycin-C and oxaliplatin up-regulated EpCAM and LewisY antigen expression. Fluorouracil 122-136 epithelial cell adhesion molecule Homo sapiens 179-184 11196169-3 2001 We have shown previously that 5-fluorouracil (5-FU) induces apoptosis in vitro via the activation of the CD95/CD95L system. Fluorouracil 46-50 Fas (TNF receptor superfamily member 6) Mus musculus 105-109 11196169-13 2001 Thus, a significant portion of apoptosis of thymocytes in vivo on treatment with 5-FU is mediated via the CD95/CD95L pathway. Fluorouracil 81-85 Fas (TNF receptor superfamily member 6) Mus musculus 106-110 11196169-0 2001 The chemotherapeutic drug 5-fluorouracil induces apoptosis in mouse thymocytes in vivo via activation of the CD95(APO-1/Fas) system. Fluorouracil 26-40 Fas (TNF receptor superfamily member 6) Mus musculus 109-113 11196169-0 2001 The chemotherapeutic drug 5-fluorouracil induces apoptosis in mouse thymocytes in vivo via activation of the CD95(APO-1/Fas) system. Fluorouracil 26-40 Fas (TNF receptor superfamily member 6) Mus musculus 114-119 11196169-3 2001 We have shown previously that 5-fluorouracil (5-FU) induces apoptosis in vitro via the activation of the CD95/CD95L system. Fluorouracil 30-44 Fas (TNF receptor superfamily member 6) Mus musculus 105-109 11167991-9 2001 The highest expression for EpCAM on HT29 cells was achieved by the combination of IFN-alpha, 5-fluorouracil and MoAb 17-1A. Fluorouracil 93-107 epithelial cell adhesion molecule Homo sapiens 27-32 11474243-1 2001 TS-1(S-1) has been developed as a new oral anticancer drug based on the biological modulation of 5-fluorouracil. Fluorouracil 97-111 proteasome 26S subunit, non-ATPase 1 Homo sapiens 1-4 11773294-3 2001 Findings from NSABP B-13 demonstrated, through 14 years of follow-up, improvements in disease-free survival (DFS) and overall survival from methotrexate and fluorouracil (MF), regardless of age, in women with estrogen receptor (ER)-negative tumors. Fluorouracil 157-169 estrogen receptor 1 Homo sapiens 209-226 11095583-3 2000 In fourteen cDNA-expressed human P450 enzymes having measurable activities, CYP1A2, CYP2A6, CYP2E1, and CYP3A5 were highly active in catalyzing 5-FU formation at a tegafur concentration of 100 microM. Fluorouracil 144-148 cytochrome P450 family 2 subfamily E member 1 Homo sapiens 92-98 11589301-8 2001 The C18 and C29 cell lines were in general resistant to the other agents tested (methotrexate, 5-fluorouracil, nolatrexed) when compared with the C85 and C86 cell lines. Fluorouracil 95-109 Bardet-Biedl syndrome 9 Homo sapiens 4-7 11134542-10 2001 On the other hand, 5-FU produced dose-dependent inhibition of thymidylate synthetase in the whole embryo, and recovery from enzyme inhibition was also related to the administered dose. Fluorouracil 19-23 thymidylate synthetase Rattus norvegicus 62-84 11121461-2 2000 This has led some clinicians to propose that HER2 should be used as a predictive marker in choosing between anthracycline-based regimens and combination chemotherapy with cyclophosphamide, methotrexate, and 5-fluorouracil (CMF). Fluorouracil 207-221 erb-b2 receptor tyrosine kinase 2 Homo sapiens 45-49 11694791-5 2001 It has not yet been demonstrated conclusively that HER2 positivity increases resistance to adjuvant cyclophosphamide, methotrexate, 5-FU (CMF), but there are indications that HER2-positive patients benefit more from adequately dosed anthracyclines than from CMF. Fluorouracil 132-136 erb-b2 receptor tyrosine kinase 2 Homo sapiens 51-55 11495153-11 2001 The presence of serum p53-Abs was associated with decreased in vitro chemosensitivity to CDDP and 5-FU. Fluorouracil 98-102 tumor protein p53 Homo sapiens 22-25 11095583-3 2000 In fourteen cDNA-expressed human P450 enzymes having measurable activities, CYP1A2, CYP2A6, CYP2E1, and CYP3A5 were highly active in catalyzing 5-FU formation at a tegafur concentration of 100 microM. Fluorouracil 144-148 cytochrome P450 family 3 subfamily A member 5 Homo sapiens 104-110 11056019-3 2000 Indeed, MED1 acts as a mismatch-specific DNA N-glycosylase active on thymine, uracil, and 5-fluorouracil paired with guanine. Fluorouracil 90-104 methyl-CpG binding domain 4, DNA glycosylase Homo sapiens 23-58 11277324-1 2000 Treatment with 5-fluorouracil (5-FU) or recombinant interferon-gamma (IFN), alone or in combination, was found to increase carcinoembryonic antigen (CEA) expression in several carcinoma cell lines. Fluorouracil 15-29 CEA cell adhesion molecule 3 Homo sapiens 123-147 11099325-5 2000 RESULTS: Dose-limiting toxicity (diarrhea, neutropenia, and fatigue) was seen with 5-FU 15 mg/m(2) PO bid on day 2 given weekly for either 6 of 8 weeks or 3 of 4 weeks, whereas five of seven patients tolerated 5-FU 10 mg/m(2) PO bid given weekly for 3 of 4 weeks. Fluorouracil 83-87 BH3 interacting domain death agonist Homo sapiens 229-232 11099325-9 2000 CONCLUSION: The recommended oral dosage of 5-FU (10 mg/m(2) PO bid) given with eniluracil and leucovorin is approximately 115-fold lower than the reference dosage for 24-hour infusional 5-FU. Fluorouracil 43-47 BH3 interacting domain death agonist Homo sapiens 63-66 11277324-1 2000 Treatment with 5-fluorouracil (5-FU) or recombinant interferon-gamma (IFN), alone or in combination, was found to increase carcinoembryonic antigen (CEA) expression in several carcinoma cell lines. Fluorouracil 15-29 CEA cell adhesion molecule 3 Homo sapiens 149-152 11277324-1 2000 Treatment with 5-fluorouracil (5-FU) or recombinant interferon-gamma (IFN), alone or in combination, was found to increase carcinoembryonic antigen (CEA) expression in several carcinoma cell lines. Fluorouracil 31-35 CEA cell adhesion molecule 3 Homo sapiens 123-147 11277324-1 2000 Treatment with 5-fluorouracil (5-FU) or recombinant interferon-gamma (IFN), alone or in combination, was found to increase carcinoembryonic antigen (CEA) expression in several carcinoma cell lines. Fluorouracil 31-35 CEA cell adhesion molecule 3 Homo sapiens 149-152 11277324-3 2000 The results showed that exposure of cancer cells to 5-FU or to IFN resulted in increased CEA levels in terms of percentage of CEA-positive cells and mean fluorescence values, as indicated by FACS analysis. Fluorouracil 52-56 CEA cell adhesion molecule 3 Homo sapiens 89-92 11277324-3 2000 The results showed that exposure of cancer cells to 5-FU or to IFN resulted in increased CEA levels in terms of percentage of CEA-positive cells and mean fluorescence values, as indicated by FACS analysis. Fluorouracil 52-56 CEA cell adhesion molecule 3 Homo sapiens 126-129 11236028-3 2000 Chemotherapy trials have supported an interaction between HER-2 overexpression and chemotherapy sensitivity (cyclophosphamide/methotrexate/5-fluorouracil resistance and doxorubicin sensitivity) which is compelling. Fluorouracil 139-153 erb-b2 receptor tyrosine kinase 2 Homo sapiens 58-63 11123425-5 2000 Apoptosis induced by a chemotherapeutic agent, 5-fluorouracil, mitomycin C, paclitaxel, doxorubicin, or cisplatin, was enhanced by Bax overexpression. Fluorouracil 47-61 BCL2 associated X, apoptosis regulator Homo sapiens 131-134 11044365-0 2000 Bcl-2/Bax protein ratio predicts 5-fluorouracil sensitivity independently of p53 status. Fluorouracil 33-47 BCL2 apoptosis regulator Homo sapiens 0-5 11071927-4 2000 We show that upon treatment of HepG2 cells with 5-fluorouracil or methotrexate, p53 levels increase while concentrations of cyclin B2 mRNA, measured by RT-PCR with the LightCycler system, are reduced. Fluorouracil 48-62 tumor protein p53 Homo sapiens 80-83 11044365-9 2000 Moreover, after 5-FU exposure, Bax and Bcl-2 proteins regulation was under p53 protein control and a statistically significant relationship (r = 0.880, P = 0.0097) was observed between Bcl-2/Bax ratio and 5-FU sensitivity. Fluorouracil 16-20 BCL2 associated X, apoptosis regulator Homo sapiens 31-34 11044365-0 2000 Bcl-2/Bax protein ratio predicts 5-fluorouracil sensitivity independently of p53 status. Fluorouracil 33-47 BCL2 associated X, apoptosis regulator Homo sapiens 6-9 11044365-9 2000 Moreover, after 5-FU exposure, Bax and Bcl-2 proteins regulation was under p53 protein control and a statistically significant relationship (r = 0.880, P = 0.0097) was observed between Bcl-2/Bax ratio and 5-FU sensitivity. Fluorouracil 16-20 BCL2 apoptosis regulator Homo sapiens 39-44 11044365-9 2000 Moreover, after 5-FU exposure, Bax and Bcl-2 proteins regulation was under p53 protein control and a statistically significant relationship (r = 0.880, P = 0.0097) was observed between Bcl-2/Bax ratio and 5-FU sensitivity. Fluorouracil 16-20 tumor protein p53 Homo sapiens 75-78 11044365-2 2000 Nevertheless cell cycle arrest and apoptosis induction can be observed in p53-defective cells after exposure to DNA-damaging agents such as 5-fluorouracil (5-FU) suggesting the importance of alternative pathways via p53-independent mechanisms. Fluorouracil 140-154 tumor protein p53 Homo sapiens 74-77 11044365-9 2000 Moreover, after 5-FU exposure, Bax and Bcl-2 proteins regulation was under p53 protein control and a statistically significant relationship (r = 0.880, P = 0.0097) was observed between Bcl-2/Bax ratio and 5-FU sensitivity. Fluorouracil 16-20 BCL2 apoptosis regulator Homo sapiens 185-190 11044365-2 2000 Nevertheless cell cycle arrest and apoptosis induction can be observed in p53-defective cells after exposure to DNA-damaging agents such as 5-fluorouracil (5-FU) suggesting the importance of alternative pathways via p53-independent mechanisms. Fluorouracil 140-154 tumor protein p53 Homo sapiens 216-219 11044365-9 2000 Moreover, after 5-FU exposure, Bax and Bcl-2 proteins regulation was under p53 protein control and a statistically significant relationship (r = 0.880, P = 0.0097) was observed between Bcl-2/Bax ratio and 5-FU sensitivity. Fluorouracil 16-20 BCL2 associated X, apoptosis regulator Homo sapiens 191-194 11044365-9 2000 Moreover, after 5-FU exposure, Bax and Bcl-2 proteins regulation was under p53 protein control and a statistically significant relationship (r = 0.880, P = 0.0097) was observed between Bcl-2/Bax ratio and 5-FU sensitivity. Fluorouracil 205-209 BCL2 associated X, apoptosis regulator Homo sapiens 31-34 11044365-2 2000 Nevertheless cell cycle arrest and apoptosis induction can be observed in p53-defective cells after exposure to DNA-damaging agents such as 5-fluorouracil (5-FU) suggesting the importance of alternative pathways via p53-independent mechanisms. Fluorouracil 156-160 tumor protein p53 Homo sapiens 74-77 11044365-9 2000 Moreover, after 5-FU exposure, Bax and Bcl-2 proteins regulation was under p53 protein control and a statistically significant relationship (r = 0.880, P = 0.0097) was observed between Bcl-2/Bax ratio and 5-FU sensitivity. Fluorouracil 205-209 BCL2 apoptosis regulator Homo sapiens 39-44 11044365-9 2000 Moreover, after 5-FU exposure, Bax and Bcl-2 proteins regulation was under p53 protein control and a statistically significant relationship (r = 0.880, P = 0.0097) was observed between Bcl-2/Bax ratio and 5-FU sensitivity. Fluorouracil 205-209 BCL2 apoptosis regulator Homo sapiens 185-190 11044365-2 2000 Nevertheless cell cycle arrest and apoptosis induction can be observed in p53-defective cells after exposure to DNA-damaging agents such as 5-fluorouracil (5-FU) suggesting the importance of alternative pathways via p53-independent mechanisms. Fluorouracil 156-160 tumor protein p53 Homo sapiens 216-219 11044365-9 2000 Moreover, after 5-FU exposure, Bax and Bcl-2 proteins regulation was under p53 protein control and a statistically significant relationship (r = 0.880, P = 0.0097) was observed between Bcl-2/Bax ratio and 5-FU sensitivity. Fluorouracil 205-209 BCL2 associated X, apoptosis regulator Homo sapiens 191-194 11044365-5 2000 5-FU induced a rise in p53 mRNA expression in mt p53 cell lines and in human papilloma virus positive wt p53 cell line, whereas significant decrease in p53 mRNA expression was found in wt p53 cell line. Fluorouracil 0-4 tumor protein p53 Homo sapiens 23-26 11044365-10 2000 In conclusion, whatever p53 status, Bcl-2 or Bax induction and Bcl-2/Bax protein ratio were correlated to 5-FU sensitivity. Fluorouracil 106-110 BCL2 apoptosis regulator Homo sapiens 36-41 11044365-10 2000 In conclusion, whatever p53 status, Bcl-2 or Bax induction and Bcl-2/Bax protein ratio were correlated to 5-FU sensitivity. Fluorouracil 106-110 BCL2 associated X, apoptosis regulator Homo sapiens 45-48 11044365-10 2000 In conclusion, whatever p53 status, Bcl-2 or Bax induction and Bcl-2/Bax protein ratio were correlated to 5-FU sensitivity. Fluorouracil 106-110 BCL2 apoptosis regulator Homo sapiens 63-68 11044365-10 2000 In conclusion, whatever p53 status, Bcl-2 or Bax induction and Bcl-2/Bax protein ratio were correlated to 5-FU sensitivity. Fluorouracil 106-110 BCL2 associated X, apoptosis regulator Homo sapiens 69-72 11044365-5 2000 5-FU induced a rise in p53 mRNA expression in mt p53 cell lines and in human papilloma virus positive wt p53 cell line, whereas significant decrease in p53 mRNA expression was found in wt p53 cell line. Fluorouracil 0-4 tumor protein p53 Homo sapiens 49-52 11044365-5 2000 5-FU induced a rise in p53 mRNA expression in mt p53 cell lines and in human papilloma virus positive wt p53 cell line, whereas significant decrease in p53 mRNA expression was found in wt p53 cell line. Fluorouracil 0-4 tumor protein p53 Homo sapiens 49-52 11044365-5 2000 5-FU induced a rise in p53 mRNA expression in mt p53 cell lines and in human papilloma virus positive wt p53 cell line, whereas significant decrease in p53 mRNA expression was found in wt p53 cell line. Fluorouracil 0-4 tumor protein p53 Homo sapiens 49-52 11044365-5 2000 5-FU induced a rise in p53 mRNA expression in mt p53 cell lines and in human papilloma virus positive wt p53 cell line, whereas significant decrease in p53 mRNA expression was found in wt p53 cell line. Fluorouracil 0-4 tumor protein p53 Homo sapiens 49-52 11044365-7 2000 In relation with p53 functionality, but independently of p53 mutational status, after exposure to 5-FU equitoxic concentration, all cell lines were able to arrest in G1. Fluorouracil 98-102 tumor protein p53 Homo sapiens 17-20 11106261-2 2000 It is bioactivated to 5-FU via 5"-hydroxylation mediated by cytochrome P-450 (CYP). Fluorouracil 22-26 cytochrome P450 family 4 subfamily F member 3 Homo sapiens 60-76 11106261-2 2000 It is bioactivated to 5-FU via 5"-hydroxylation mediated by cytochrome P-450 (CYP). Fluorouracil 22-26 cytochrome P450 family 4 subfamily F member 3 Homo sapiens 78-81 11106264-1 2000 We examined the patterns of induction of apoptosis, Fas expression, and the influence of the status of the p53 tumor suppressor gene, in response to treatment of human colon carcinoma cell lines to 5-fluorouracil (FUra) combined with leucovorin (LV) under conditions of both DNA-directed (HT29, VRC5/c1, and RKO) and RNA-directed (HCT8 and HCT116) cytotoxicity. Fluorouracil 198-212 tumor protein p53 Homo sapiens 107-110 11106264-1 2000 We examined the patterns of induction of apoptosis, Fas expression, and the influence of the status of the p53 tumor suppressor gene, in response to treatment of human colon carcinoma cell lines to 5-fluorouracil (FUra) combined with leucovorin (LV) under conditions of both DNA-directed (HT29, VRC5/c1, and RKO) and RNA-directed (HCT8 and HCT116) cytotoxicity. Fluorouracil 214-218 tumor protein p53 Homo sapiens 107-110 11095436-7 2000 Furthermore, wt-p53 expression renders two out of four carcinoma cell lines (FRO and NPA) more sensitive to doxorubicin and one (FRO) to 5-fluorouracil, independent of treatment schedule. Fluorouracil 137-151 tumor protein p53 Homo sapiens 16-19 10930409-3 2000 We show that MED1 functions as a mismatch-specific DNA N-glycosylase active on thymine, uracil, and 5-fluorouracil when these bases are opposite to guanine. Fluorouracil 100-114 methyl-CpG binding domain 4, DNA glycosylase Homo sapiens 33-68 10974399-1 2000 1 M Tegafur (FT)-0.4 M 5-chloro-2,4-dihydroxypridine (CHDP)-1 M potassium oxonate (Oxo) (S-1), was developed as a new oral antineoplastic agent based on biochemical modulation of fluorouracil (5-FU) by CHDP and Oxo. Fluorouracil 179-191 eukaryotic translation elongation factor 1 alpha 2 Mus musculus 89-92 10974399-1 2000 1 M Tegafur (FT)-0.4 M 5-chloro-2,4-dihydroxypridine (CHDP)-1 M potassium oxonate (Oxo) (S-1), was developed as a new oral antineoplastic agent based on biochemical modulation of fluorouracil (5-FU) by CHDP and Oxo. Fluorouracil 193-197 eukaryotic translation elongation factor 1 alpha 2 Mus musculus 89-92 11038295-6 2000 The IC(50) for 5-FU was reassessed in the presence of IGF-I. Fluorouracil 15-19 insulin like growth factor 1 Homo sapiens 54-59 11038295-8 2000 RESULTS: The addition of 100 ng/ml IGF-I 1 h prior to 5-FU or radiation significantly blunted the expected cytotoxicity, resulting in a 10-fold increase in the IC(50) (from 0.5 to 5 microg/ml). Fluorouracil 54-58 insulin like growth factor 1 Homo sapiens 35-40 11038295-11 2000 CONCLUSIONS: IGF-I-R activation blocks the expected cytotoxic effects of 5-FU and external beam radiation. Fluorouracil 73-77 insulin like growth factor 1 Homo sapiens 13-18 10974399-3 2000 Mice treatment with S-1 showed a significant higher concentration of 5-FU in the tumor and the serum than UFT treated mice. Fluorouracil 69-73 eukaryotic translation elongation factor 1 alpha 2 Mus musculus 20-23 11098498-8 2000 In vitro analysis revealed that 5-FU and gamma-hydroxybutyric acid regulated VEGF-dependent responses of human umbilical vein endothelial cells. Fluorouracil 32-36 vascular endothelial growth factor A Homo sapiens 77-81 11086424-6 2000 The total dose of 5-FU was 30.0 +/- 7.6 g in the normal CEA level group and 19.1 +/- 6.9 g in the high CEA level group. Fluorouracil 18-22 CEA cell adhesion molecule 3 Homo sapiens 56-59 11000583-7 2000 These findings suggest that multiple factors, including p53 and DNA mismatch repair, participate in diverse cell growth modulations in cells treated with 5-FU. Fluorouracil 154-158 tumor protein p53 Homo sapiens 56-59 11098498-9 2000 Dorsal air sac assay revealed that UFT, 5-FU, and gamma-hydroxybutyric acid strongly inhibited the angiogenesis induced by recombinant human VEGF. Fluorouracil 40-44 vascular endothelial growth factor A Homo sapiens 141-145 10993958-6 2000 Radiation sensitivity was unaffected by combined treatments, except for Taxol, irradiation, and 5-FU sequence in the HCT116 p53-/- and 40-16 cell lines, where radiation sensitivity determined by clonogenic survival curve slopes was doubled or quadrupled, respectively. Fluorouracil 96-100 tumor protein p53 Homo sapiens 124-127 11027414-5 2000 We describe here our analysis of the PSMA enhancer for the most active region(s) and present a way of using the enhancer in combination with the E. coli cytosine deaminase gene for suicide-driven gene therapy that converts the nontoxic prodrug 5-fluorocytosine (5-FC) into the cytotoxic drug 5-fluorouracil (5-FU) in prostate cancer cells. Fluorouracil 292-306 folate hydrolase 1 Homo sapiens 37-41 11027414-5 2000 We describe here our analysis of the PSMA enhancer for the most active region(s) and present a way of using the enhancer in combination with the E. coli cytosine deaminase gene for suicide-driven gene therapy that converts the nontoxic prodrug 5-fluorocytosine (5-FC) into the cytotoxic drug 5-fluorouracil (5-FU) in prostate cancer cells. Fluorouracil 308-312 folate hydrolase 1 Homo sapiens 37-41 11819671-6 2000 MTT assay showed increased sensitization of fas-SGC7901/VCR to DDP, MMC and 5-FU, but same sensitization to VCR according to pBK-SGC7901/VCR. Fluorouracil 76-80 sarcoglycan beta Homo sapiens 48-51 11131650-0 2000 Effect of 5-fluorouracil on carcinoembryonic antigen expression and shedding at clonal level in colon cancer cells. Fluorouracil 10-24 CEA cell adhesion molecule 3 Homo sapiens 28-52 11131650-2 2000 In preclinical models CEA has been found to be up-regulated after exposure of cancer cells to 5-fluorouracil (5-FU). Fluorouracil 94-108 CEA cell adhesion molecule 3 Homo sapiens 22-25 11131650-2 2000 In preclinical models CEA has been found to be up-regulated after exposure of cancer cells to 5-fluorouracil (5-FU). Fluorouracil 110-114 CEA cell adhesion molecule 3 Homo sapiens 22-25 11131650-3 2000 In the present study, the clonal distribution of CEA and its regulation by 5-FU at clonal level was investigated using human HT-29 colon cancer cells. Fluorouracil 75-79 CEA cell adhesion molecule 3 Homo sapiens 49-52 11131650-6 2000 In all cases 5-FU was able to increase the percentage of CEA-positive cells, the amount of antigen, either in the membrane or cytosolic fractions, and the corresponding transcript. Fluorouracil 13-17 CEA cell adhesion molecule 3 Homo sapiens 57-60 10965024-0 2000 Bcl-X(L) antisense sensitizes human colon cancer cell line to 5-fluorouracil. Fluorouracil 62-76 BCL2 like 1 Homo sapiens 0-8 10930966-8 2000 RESULTS: An increase in Epo levels occurred following every course of 5-FU or platinum based chemotherapy in patients with steady concentrations of creatinine and decreased levels of haemoglobin (Hb). Fluorouracil 70-74 erythropoietin Homo sapiens 24-27 11038045-1 2000 BACKGROUND: We assessed the hypothesis that a compromised p53 function could account for the non response of colon cancer patients with low thymidylate synthase (TS) expression receiving a bolus 5-fluorouracil (5-FU) leucovorin (LV) combination. Fluorouracil 195-209 tumor protein p53 Homo sapiens 58-61 11038045-1 2000 BACKGROUND: We assessed the hypothesis that a compromised p53 function could account for the non response of colon cancer patients with low thymidylate synthase (TS) expression receiving a bolus 5-fluorouracil (5-FU) leucovorin (LV) combination. Fluorouracil 211-215 tumor protein p53 Homo sapiens 58-61 10965024-2 2000 Our previous study suggested that high expression of endogenous Bcl-X(L), might be associated with resistance to 5-FU in colorectal cancer. Fluorouracil 113-117 BCL2 like 1 Homo sapiens 64-72 10965024-3 2000 The aim of this study is to analyze the role of Bcl-X(L) in 5-FU resistance and to explore a new therapeutic strategy using Bcl-X(L) antisense. Fluorouracil 60-64 BCL2 like 1 Homo sapiens 48-53 10965024-3 2000 The aim of this study is to analyze the role of Bcl-X(L) in 5-FU resistance and to explore a new therapeutic strategy using Bcl-X(L) antisense. Fluorouracil 60-64 BCL2 like 1 Homo sapiens 48-56 10965024-5 2000 Second, when Colo320 cells, with undetectable endogenous Bcl-XL expression, were transfected with Bcl-XL gene, they acquired high resistance to 5-FU. Fluorouracil 144-148 BCL2 like 1 Homo sapiens 98-104 10965024-8 2000 5-FU treatment induced a level of apoptosis 10-fold higher in DLD1 cells than in untreated control cells, while the same dose of 5-FU induced a 55-fold higher level of apoptosis in DLD1 cells treated with Bcl-XL antisense oligodeoxynucleotides (P = 0.0003). Fluorouracil 0-4 BCL2 like 1 Homo sapiens 205-211 10965024-8 2000 5-FU treatment induced a level of apoptosis 10-fold higher in DLD1 cells than in untreated control cells, while the same dose of 5-FU induced a 55-fold higher level of apoptosis in DLD1 cells treated with Bcl-XL antisense oligodeoxynucleotides (P = 0.0003). Fluorouracil 129-133 BCL2 like 1 Homo sapiens 205-211 10965024-10 2000 These results suggest that Bcl-X(L) is an important factor for 5-FU resistance and the suppression of Bcl-X(L) expression by the specific antisense ODNs can increase the sensitivity of colon cancer cells to 5-FU. Fluorouracil 63-67 BCL2 like 1 Homo sapiens 27-35 10965024-10 2000 These results suggest that Bcl-X(L) is an important factor for 5-FU resistance and the suppression of Bcl-X(L) expression by the specific antisense ODNs can increase the sensitivity of colon cancer cells to 5-FU. Fluorouracil 207-211 BCL2 like 1 Homo sapiens 27-35 10965024-10 2000 These results suggest that Bcl-X(L) is an important factor for 5-FU resistance and the suppression of Bcl-X(L) expression by the specific antisense ODNs can increase the sensitivity of colon cancer cells to 5-FU. Fluorouracil 207-211 BCL2 like 1 Homo sapiens 102-110 10894878-3 2000 5-FU pharmacokinetics were investigated after a single initial dose of S-1 during the first 24 hours and weekly thereafter. Fluorouracil 0-4 proteasome 26S subunit, non-ATPase 1 Homo sapiens 71-74 10891390-0 2000 5-Fluorouracil induces apoptosis through the suppression of NF-kappaB activity in human salivary gland cancer cells. Fluorouracil 0-14 nuclear factor kappa B subunit 1 Homo sapiens 60-69 10891390-2 2000 Thus, we examined whether 5-FU could induce apoptosis through the suppression of NF-kappaB activity. Fluorouracil 26-30 nuclear factor kappa B subunit 1 Homo sapiens 81-90 10891390-3 2000 We found that upon treatment of a human salivary gland cancer cell line (cl-1) with 5-FU, the NF-kappaB activity was suppressed in a time-dependent manner. Fluorouracil 84-88 nuclear factor kappa B subunit 1 Homo sapiens 94-103 10891390-5 2000 In addition, the expression of TRAF-2 and cIAP-1, which are transcriptionally regulated by NF-kappaB and function as anti-apoptotic molecules through the interruption of caspase pathway, was also inhibited by 5-FU. Fluorouracil 209-213 nuclear factor kappa B subunit 1 Homo sapiens 91-100 10891390-6 2000 Finally, the activity of caspase-8 and caspase-3 showed a significant increase in response to 5-FU. Fluorouracil 94-98 caspase 3 Homo sapiens 39-48 10891390-8 2000 Thus, our results suggest that one of the molecular mechanisms involved in 5-FU-induced apoptosis in cl-1 cells may be due to the suppression of NF-kappaB activity, resulting in the activation of the pro-apoptotic pathway. Fluorouracil 75-79 nuclear factor kappa B subunit 1 Homo sapiens 145-154 10914738-3 2000 However, the underlying mechanism by which IFN-alpha modulates the effects of 5-FU is unknown. Fluorouracil 78-82 interferon alpha 1 Homo sapiens 43-52 10914738-5 2000 IFN-alpha significantly enhanced the growth inhibitory effect of 5-FU in PLC/PRF/5 cells but not in HuH7 cells, and the isobolographic analysis indicated that this effect was synergistic. Fluorouracil 65-69 interferon alpha 1 Homo sapiens 0-9 10853031-1 2000 We have previously reported that HT29 human colon cancer cells selected by adaptation to 5-fluorouracil (5FU) (HT29-5FU cells) express increased levels of a major intestinal mucin MUC2 mRNA compared with parental HT29 cells. Fluorouracil 89-103 mucin 2, oligomeric mucus/gel-forming Homo sapiens 180-184 10853031-1 2000 We have previously reported that HT29 human colon cancer cells selected by adaptation to 5-fluorouracil (5FU) (HT29-5FU cells) express increased levels of a major intestinal mucin MUC2 mRNA compared with parental HT29 cells. Fluorouracil 105-108 mucin 2, oligomeric mucus/gel-forming Homo sapiens 180-184 10901361-2 2000 This study set out to evaluate, in patients with metastatic colorectal carcinoma, the efficacy and toxicity of S-1, which contains tegafur, 5-chloro-2,4-dihydroxypyridine (CDHP) and potassium oxonate, based on a biochemical modulation of 5-fluorouracil (5-FU) targeted at inhibition of dihydropyrimidine dehydrogenase (DPD). Fluorouracil 238-252 proteasome 26S subunit, non-ATPase 1 Homo sapiens 111-114 10901361-2 2000 This study set out to evaluate, in patients with metastatic colorectal carcinoma, the efficacy and toxicity of S-1, which contains tegafur, 5-chloro-2,4-dihydroxypyridine (CDHP) and potassium oxonate, based on a biochemical modulation of 5-fluorouracil (5-FU) targeted at inhibition of dihydropyrimidine dehydrogenase (DPD). Fluorouracil 254-258 proteasome 26S subunit, non-ATPase 1 Homo sapiens 111-114 10901374-11 2000 5-FU/folinic acid alone did not induce TP activity but a single dose of IFNalpha led to upregulation of TP within 2 h of administration with a further increase by 24 h (signed rank test, P = 0.006). Fluorouracil 0-4 interferon alpha 1 Homo sapiens 72-80 10901374-14 2000 A single dose of IFNalpha as low as 3 MIU m(-2) can cause sustained elevation of PBL TP activity in vivo indicating that biochemical markers are important pharmacodynamic endpoints for developing optimal schedules of IFNalpha for biomodulation of 5-FU. Fluorouracil 247-251 interferon alpha 1 Homo sapiens 17-25 10894878-9 2000 Plasma pharmacokinetics of 5-FU were linear; at the highest S-1 dose level, 5-FU plasma peak concentrations reached 1 to 2 micromol/L, and the half-life of 5-FU was 3 to 4 hours. Fluorouracil 27-31 proteasome 26S subunit, non-ATPase 1 Homo sapiens 60-63 10894878-9 2000 Plasma pharmacokinetics of 5-FU were linear; at the highest S-1 dose level, 5-FU plasma peak concentrations reached 1 to 2 micromol/L, and the half-life of 5-FU was 3 to 4 hours. Fluorouracil 76-80 proteasome 26S subunit, non-ATPase 1 Homo sapiens 60-63 10894878-9 2000 Plasma pharmacokinetics of 5-FU were linear; at the highest S-1 dose level, 5-FU plasma peak concentrations reached 1 to 2 micromol/L, and the half-life of 5-FU was 3 to 4 hours. Fluorouracil 76-80 proteasome 26S subunit, non-ATPase 1 Homo sapiens 60-63 10866311-0 2000 Regrowth of 5-fluorouracil-treated human colon cancer cells is prevented by the combination of interferon gamma, indomethacin, and phenylbutyrate. Fluorouracil 12-26 interferon gamma Homo sapiens 95-111 10866311-10 2000 The finding that the readily reversible growth inhibition and decrease in clonogenicity of FUra-treated HCC are prolonged by subsequent treatment with the three cytostatic agents in all HCCs may be of clinical importance because FUra continues to be the most widely used cytotoxic agent in the treatment of colon carcinoma. Fluorouracil 91-95 holocytochrome c synthase Homo sapiens 186-190 10897215-7 2000 Furthermore, significant statistical differences in chemosensitivity to 5-FU and CDDP were revealed depending on the presence of serum p53 antibodies. Fluorouracil 72-76 tumor protein p53 Homo sapiens 135-138 10854555-0 2000 Immunohistochemical expression of vascular endothelial growth factor can predict response to 5-fluorouracil and cisplatin in patients with gastric adenocarcinoma. Fluorouracil 93-107 vascular endothelial growth factor A Homo sapiens 34-68 10914823-3 2000 METHODS: Six nonoperated esophageal cancer patients were treated by daily concurrent CRT, which consisted of continuous 5-fluorouracil administration with leucovorin, combined with a low dose of daily cisplatin administration before each fraction of radiation. Fluorouracil 120-134 calcitonin receptor Homo sapiens 85-88 10785598-0 2000 Molecular downstream events and induction of thymidylate synthase in mutant and wild-type p53 colon cancer cell lines after treatment with 5-fluorouracil and the thymidylate synthase inhibitor raltitrexed. Fluorouracil 139-153 tumor protein p53 Homo sapiens 90-93 10785598-4 2000 Exposure to 5-FU (50 and 100 microM) and ZD1694 (50 and 100 nM) for 24 and 48 h induced p53 and p21 expression in wt p53 cells, but not in mt p53 cells. Fluorouracil 12-16 tumor protein p53 Homo sapiens 88-91 10785598-4 2000 Exposure to 5-FU (50 and 100 microM) and ZD1694 (50 and 100 nM) for 24 and 48 h induced p53 and p21 expression in wt p53 cells, but not in mt p53 cells. Fluorouracil 12-16 tumor protein p53 Homo sapiens 117-120 10785598-4 2000 Exposure to 5-FU (50 and 100 microM) and ZD1694 (50 and 100 nM) for 24 and 48 h induced p53 and p21 expression in wt p53 cells, but not in mt p53 cells. Fluorouracil 12-16 tumor protein p53 Homo sapiens 117-120 10786672-0 2000 Metabolites of 2"-fluoro-2"-deoxy-D-glucose detected by 19F magnetic resonance spectroscopy in vivo predict response of murine RIF-1 tumors to 5-fluorouracil. Fluorouracil 143-157 replication timing regulatory factor 1 Mus musculus 127-132 10832444-4 2000 Combined chemotherapy consisting of cisplatin and 5-FU was given, and was so effective that the patient recovered well and both serum AFP level and the size of the swollen liver decreased markedly. Fluorouracil 50-54 alpha fetoprotein Homo sapiens 134-137 10765119-0 2000 Phase II study of S-1, a novel oral derivative of 5-fluorouracil, in advanced gastric cancer. Fluorouracil 50-64 proteasome 26S subunit, non-ATPase 1 Homo sapiens 18-21 10847455-8 2000 TS inhibition by either 5-FU or antifolates can also result in a depression of TS protein mediated inhibition of TS mRNA translation leading to induction of more TS protein synthesis, and p53 protein may further deregulate this process. Fluorouracil 24-28 tumor protein p53 Homo sapiens 188-191 10762745-1 2000 The aim of this study was to evaluate the efficacy and toxicity of ifosfamide, 5-fluorouracil (5-FU) and leucovorin (IFL) as a second-line chemotherapy regimen in patients with recurrent undifferentiated nasopharyngeal carcinoma (NPC) previously treated with platinum/5-FU. Fluorouracil 268-272 interferon alpha 1 Homo sapiens 117-120 10883892-4 2000 The therapeutic agents interferon (IFN), 5-fluorouracil (5-FU) and tamoxifen (Tam) with different mechanisms of action mediate both partial dephosphorylation and inactivation of PAP, detected by immunoblotting analysis and PAP enzyme assay, respectively. Fluorouracil 57-61 interferon alpha 1 Homo sapiens 23-33 10790998-1 2000 S-1 is a novel oral anticancer drug, composed of tegafur (FT), gimestat (CDHP) and otastat potassium (Oxo) in a molar ratio of 1:0.4:1, based on the biochemical modulation of 5-fluorouracil (5-FU). Fluorouracil 175-189 eukaryotic translation elongation factor 1 alpha 2 Mus musculus 0-3 10790998-1 2000 S-1 is a novel oral anticancer drug, composed of tegafur (FT), gimestat (CDHP) and otastat potassium (Oxo) in a molar ratio of 1:0.4:1, based on the biochemical modulation of 5-fluorouracil (5-FU). Fluorouracil 191-195 eukaryotic translation elongation factor 1 alpha 2 Mus musculus 0-3 10733124-0 2000 Selective augmentations of intratumoral 5-fluorouracil concentration by local immunotherapy with OK-432 and fibrinogen. Fluorouracil 40-54 fibrinogen beta chain Homo sapiens 108-118 12849612-12 2000 It is also possible that HER2-overexpressing patients may respond better to dose-intense anthracycline therapy and worse to cyclophosphamide/methotrexate/5-fluorouracil than non-overexpressing patients. Fluorouracil 154-168 erb-b2 receptor tyrosine kinase 2 Homo sapiens 25-29 10733124-12 2000 CONCLUSION: In patients with colorectal cancer, selective high 5-fluorouracil concentration in the cancer tissue could be achieved by a combination of 5"-deoxy-5-fluorouridine and local immunotherapy with a mixture of OK-432 and fibrinogen. Fluorouracil 63-77 fibrinogen beta chain Homo sapiens 218-239 10757421-0 2000 Effects of pegylated recombinant human megakaryocyte growth and development factor on 5-fluorouracil-induced thrombocytopenia in balloon-injured rats. Fluorouracil 86-100 thrombopoietin Homo sapiens 39-82 12579728-7 2000 The inhibition rate of IFN-gamma in two experiments was smaller than MMC and 5-Fu (P < 0.05). Fluorouracil 77-81 interferon gamma Homo sapiens 23-32 10791219-0 2000 Interleukin-2 as a modulator of 5-fluorouracil in hepatic arterial immunochemotherapy for liver metastases. Fluorouracil 32-46 interleukin 2 Homo sapiens 0-13 10791219-2 2000 In order to clarify the mechanisms that underlie the apparent benefit of combination treatment, the role of IL-2 as a modulator of 5-fluorouracil metabolism was investigated. Fluorouracil 131-145 interleukin 2 Homo sapiens 108-112 10791219-6 2000 Although the addition of IL-2 reduced 5-fluorouracil levels in both tumor and normal liver tissues by the activation of dihydropyrimidine dehydrogenase, the ratio of tumor/normal liver 5-fluorouracil levels was unchanged. Fluorouracil 38-52 interleukin 2 Homo sapiens 25-29 10791219-8 2000 CONCLUSIONS: IL-2 increases 5-fluorouracil cytotoxicity through the inhibition of thymidylate synthase/thymidine kinase activities in the hepatic arterial infusion. Fluorouracil 28-42 interleukin 2 Homo sapiens 13-17 10757421-1 2000 We examined whether pegylated recombinant human megakaryocyte growth and development factor (PEG-rHuMGDF) affected 5-fluorouracil-induced thrombocytopenia without inducing more severe intimal thickening after injury to rat carotid arteries. Fluorouracil 115-129 thrombopoietin Homo sapiens 48-91 10623878-6 2000 HER2 overexpression is associated with breast cancer patient responsiveness to doxorubicin, to cyclophosphamide, methotrexate, and fluorouracil (CMF), and to paclitaxel, whereas tamoxifen was found to be ineffective and even detrimental in patients with HER2-positive tumors. Fluorouracil 131-143 erb-b2 receptor tyrosine kinase 2 Homo sapiens 0-4 10770640-11 2000 These findings suggest that CPT-11 and 5-FU may thus be useful as possible anticancer agents for use in a combination therapy regimen using wt p53 gene transfer. Fluorouracil 39-43 tumor protein p53 Homo sapiens 143-146 10682666-1 2000 The purpose of this work was to analyse the ability of p53 and thymidilate synthase (TS) primary tumour expression to retrospectively predict clinical response to chemotherapy and long-term prognosis in patients with advanced colorectal cancers homogeneously treated by methotrexate (MTX)-modulated-5-fluorouracil (5-FU-FA). Fluorouracil 299-313 tumor protein p53 Homo sapiens 55-58 11129987-3 2000 When the MTX and 5-FU concentrations are 10 microM, antiproliferative effects of MTX 2 hr before 5-FU (MTX/5-FU) and 5-FU 2 h before MTX (5-FU/MTX) are 25.17+/-1.23% and 25.60+/-1.28% of the control rate, respectively. Fluorouracil 17-21 metaxin 2 Homo sapiens 81-86 10771466-0 2000 Influence of adjuvant chemotherapy with cyclophosphamide, methotrexate and 5-fluorouracil on plasma insulin-like growth factor-I and chosen hormones in breast cancer pre-menopausal patients. Fluorouracil 75-89 insulin like growth factor 1 Homo sapiens 100-128 10585597-0 2000 Role for alpha1,2-fucosyltransferase and histo-blood group antigen H type 2 in resistance of rat colon carcinoma cells to 5-fluorouracil. Fluorouracil 122-136 fucosyltransferase 2 Homo sapiens 9-36 10623435-5 2000 Moreover, we have previously demonstrated that 5-fluorouracile (5-FU) resistant HSC require a combination of interleukin 12 (IL-12), IL-6 and SCF for the production of morphologically recognizable clonogenic elements at day 14 in semisolid medium. Fluorouracil 64-68 interleukin 6 Homo sapiens 133-137 10912578-0 2000 Reduction of 5-fluorouracil (5-FU) gastrointestinal (GI) toxicity resulting from the protection of thymidylate synthase (TS) in GI tissue by repeated simultaneous administration of potassium oxonate (Oxo) in rats. Fluorouracil 13-27 thymidylate synthetase Rattus norvegicus 99-119 10912578-0 2000 Reduction of 5-fluorouracil (5-FU) gastrointestinal (GI) toxicity resulting from the protection of thymidylate synthase (TS) in GI tissue by repeated simultaneous administration of potassium oxonate (Oxo) in rats. Fluorouracil 29-33 thymidylate synthetase Rattus norvegicus 99-119 10912578-1 2000 PURPOSE: An important cytotoxic effect of 5-fluorouracil (5-FU) is the inactivation of thymidylate synthase (TS) (EC 2.1.1.45) activity by the formation of a ternary complex consisting of covalently bound 5-fluorodeoxyuridine 5"-monophosphate (FdUMP), TS and 5,10-methylenetetrahydrofolate (CH2FH4). Fluorouracil 42-56 thymidylate synthetase Rattus norvegicus 87-107 10912578-1 2000 PURPOSE: An important cytotoxic effect of 5-fluorouracil (5-FU) is the inactivation of thymidylate synthase (TS) (EC 2.1.1.45) activity by the formation of a ternary complex consisting of covalently bound 5-fluorodeoxyuridine 5"-monophosphate (FdUMP), TS and 5,10-methylenetetrahydrofolate (CH2FH4). Fluorouracil 58-62 thymidylate synthetase Rattus norvegicus 87-107 10585597-6 2000 The increase was also observed after in vitro short-term exposure to 5-FU, as well as on a cell-resistant variant selected by continuous exposure to the drug, and was accompanied by an increase in alpha1,2-fucosyltransferase activity, the key enzyme involved in synthesis of H antigens. Fluorouracil 69-73 fucosyltransferase 2 Homo sapiens 197-224 10585597-7 2000 Transfection of cells devoid of this enzymatic activity by an alpha1, 2-fucosyltransferase cDNA allowed expression of H type 2 antigen and increased resistance to 5-FU. Fluorouracil 163-167 fucosyltransferase 2 Homo sapiens 62-90 10585597-9 2000 These results demonstrate that, in this experimental model, alpha1,2-fucosyltransferase and H type 2 antigen are involved in cellular resistance to 5-FU. Fluorouracil 148-152 fucosyltransferase 2 Homo sapiens 60-87 11417748-7 2000 Western blotting showed that p53 induction was not detectable in mutant (mt) p53 WiDr and increased much earlier in wild-type (wt) Lovo cells after 5-FU and MTA (24 h) than after AG337 exposure (72 h). Fluorouracil 148-152 tumor protein p53 Homo sapiens 29-32 10637237-1 2000 PURPOSE: To study whether two modulators, high-dose methotrexate (MTX) and interferon alfa-2a (IFNalpha-2a) will alter the intratumoral pharmacokinetics of fluorouracil (5-FU). Fluorouracil 156-168 interferon alpha 1 Homo sapiens 95-103 10637237-5 2000 Four of the five patients exhibited increases in the t(1/2) of 5-FU after intravenous (IV) administration of MTX or IFNalpha-2a. Fluorouracil 63-67 interferon alpha 1 Homo sapiens 116-124 10637237-7 2000 In the three patients with colorectal cancer who received IV IFNalpha-2a followed by IV 5-FU, the two patients with partial responses had increases in the t(1/2) of 5-FU of 41% and 30.2%, whereas the nonresponder had a nonsignificant increase (5.6%) in the t(1/2) of 5-FU. Fluorouracil 165-169 interferon alpha 1 Homo sapiens 61-69 10637237-7 2000 In the three patients with colorectal cancer who received IV IFNalpha-2a followed by IV 5-FU, the two patients with partial responses had increases in the t(1/2) of 5-FU of 41% and 30.2%, whereas the nonresponder had a nonsignificant increase (5.6%) in the t(1/2) of 5-FU. Fluorouracil 165-169 interferon alpha 1 Homo sapiens 61-69 10637237-9 2000 The findings also indicate that IFNalpha-2a and high-dose MTX can increase the intratumoral 5-FU in some patients. Fluorouracil 92-96 interferon alpha 1 Homo sapiens 32-40 10637254-1 2000 PURPOSE: To determine whether p53 gene status predicts tumor responses to platinum- and fluorouracil-based induction chemotherapy in locoregionally advanced squamous cell carcinomas of the head and neck. Fluorouracil 88-100 tumor protein p53 Homo sapiens 30-33 10983383-3 2000 The aim of the presented work is to asses the plasma GH levels in 24 pre-menopausal women after mastectomy for breast cancer on adjuvant chemotherapy with cyclophosphamide, methotrexate, 5-fluorouracil (CMF). Fluorouracil 187-201 growth hormone 1 Homo sapiens 53-55 11007917-1 2000 CD34(+) cells and megakaryocyte progenitors were lower in marrow from patients after hematological recovery from the first cycle of 5-fluorouracil, leucovorin, adriamycin, cyclophosphamide (FLAC) chemotherapy plus PIXY321 (GM-CSF/interleukin 3; IL-3 hybrid) than in FLAC + GM-CSF or pre-FLAC marrows. Fluorouracil 132-146 CD34 molecule Homo sapiens 0-4 10602483-4 1999 The colonic epithelia of 5FU treated bcl-2-null mice showed elevated levels of apoptosis at 4.5 h: from 48 apoptotic events in wild-type mice to 273 in the nulls, scoring 200 half crypts. Fluorouracil 25-28 B cell leukemia/lymphoma 2 Mus musculus 37-42 10487550-1 1999 PURPOSE: To assess the prognostic significance of p53 protein expression in patients with primary epidermoid carcinoma of the anal canal managed by radiation therapy (XRT), 5-fluorouracil (5-FU), and mitomycin C (MMC). Fluorouracil 173-187 tumor protein p53 Homo sapiens 50-53 10606259-7 1999 Randomized trials of 5-FU double-modulated by both IFN-alpha and LV showed no response or survival advantage compared with 5-FU/LV, and greater toxicity. Fluorouracil 21-25 interferon alpha 1 Homo sapiens 51-60 11829914-8 1999 5-FU plus sandostatin would be helpful in the biotherapy of breast cancer patients with positive ER and PR. Fluorouracil 0-4 estrogen receptor 1 Homo sapiens 97-99 10650785-4 1999 Here we report the first P-gp+ MDR MM with brain metastasis in the literature, demonstrating a remarkable response to IL-2, interferon-alpha (IFN), 5-fluorouracil (5FU) regimen. Fluorouracil 148-162 ATP binding cassette subfamily B member 1 Homo sapiens 25-29 10650785-4 1999 Here we report the first P-gp+ MDR MM with brain metastasis in the literature, demonstrating a remarkable response to IL-2, interferon-alpha (IFN), 5-fluorouracil (5FU) regimen. Fluorouracil 164-167 ATP binding cassette subfamily B member 1 Homo sapiens 25-29 10499633-8 1999 In addition, biochemical examination revealed that 5-FU and HU blocked the antimitotic agent-induced increase of p21WAF1/CIP1 protein levels, as well as prevented the hyperphosphorylation of the bcl-2 and c-raf-1 proteins. Fluorouracil 51-55 cyclin dependent kinase inhibitor 1A Homo sapiens 121-125 10499633-8 1999 In addition, biochemical examination revealed that 5-FU and HU blocked the antimitotic agent-induced increase of p21WAF1/CIP1 protein levels, as well as prevented the hyperphosphorylation of the bcl-2 and c-raf-1 proteins. Fluorouracil 51-55 BCL2 apoptosis regulator Homo sapiens 195-200 10568827-0 1999 Apoptosis of colorectal adenocarcinoma induced by 5-FU and/or IFN-gamma through caspase 3 and caspase 8. Fluorouracil 50-54 caspase 3 Homo sapiens 80-89 10568827-1 1999 The cytotoxic effect of 5-FU has been shown by the induction of apoptosis in cancer cells, and reported to be enhanced by IFN-gamma. Fluorouracil 24-28 interferon gamma Homo sapiens 122-131 10568827-3 1999 The activities of caspase 3 and caspase 8 increased when apoptosis was induced by 5-FU and/or IFN-gamma. Fluorouracil 82-86 caspase 3 Homo sapiens 18-27 10568827-6 1999 Thus, caspase 3 and caspase 8 play crucial roles in apoptosis induced by 5-FU and/or IFN-gamma, regardless of the Fas-Fas ligand system. Fluorouracil 73-77 caspase 3 Homo sapiens 6-15 10565860-8 1999 These cells also exhibited a drug resistance profile commensurate with the previously described MRP1 overexpressing phenotype, with resistance to Vinca alkaloids, epipodophyllotoxins, and anthracyclines; additional cross-resistance to paclitaxel (Taxol), mitoxantrone, and 5-fluorouracil was observed. Fluorouracil 273-287 ATP binding cassette subfamily C member 1 Homo sapiens 96-100 10697613-6 1999 CONCLUSION: The present results suggest that TP is important for remodeling the existing vasculature early in tumor development and intraductal extension, expressions of TP and Bcl-2 are tightly linked and TP status can not generally predict chemotherapeutic sensitivity for 5-FU as a single molecular marker. Fluorouracil 275-279 BCL2 apoptosis regulator Homo sapiens 177-182 11829914-6 1999 When samples were divided into 2 groups according to the sensitivity of ER and PR, the apoptotic rate of 5-FU plus sandostatin was (32.2 +/- 7.9)%, in positive ER and PR group, but (20.5 +/- 5.5)% in negative ER and PR group (P < 0.05). Fluorouracil 105-109 estrogen receptor 1 Homo sapiens 72-74 11829914-6 1999 When samples were divided into 2 groups according to the sensitivity of ER and PR, the apoptotic rate of 5-FU plus sandostatin was (32.2 +/- 7.9)%, in positive ER and PR group, but (20.5 +/- 5.5)% in negative ER and PR group (P < 0.05). Fluorouracil 105-109 estrogen receptor 1 Homo sapiens 160-162 11829914-6 1999 When samples were divided into 2 groups according to the sensitivity of ER and PR, the apoptotic rate of 5-FU plus sandostatin was (32.2 +/- 7.9)%, in positive ER and PR group, but (20.5 +/- 5.5)% in negative ER and PR group (P < 0.05). Fluorouracil 105-109 estrogen receptor 1 Homo sapiens 160-162 11829914-7 1999 CONCLUSIONS: 5-FU plus sandostatin is more sensitive in the positive ER and PR group than in the negative ER and PR group. Fluorouracil 13-17 estrogen receptor 1 Homo sapiens 69-71 11829914-7 1999 CONCLUSIONS: 5-FU plus sandostatin is more sensitive in the positive ER and PR group than in the negative ER and PR group. Fluorouracil 13-17 estrogen receptor 1 Homo sapiens 106-108 10545788-0 1999 An early phase II study of oral S-1, a newly developed 5-fluorouracil derivative for advanced and recurrent gastrointestinal cancers. Fluorouracil 55-69 proteasome 26S subunit, non-ATPase 1 Homo sapiens 32-35 10487550-1 1999 PURPOSE: To assess the prognostic significance of p53 protein expression in patients with primary epidermoid carcinoma of the anal canal managed by radiation therapy (XRT), 5-fluorouracil (5-FU), and mitomycin C (MMC). Fluorouracil 189-193 tumor protein p53 Homo sapiens 50-53 10487550-20 1999 For patients managed with combined XRT, 5-FU, and MMC, percent p53 protein expression is of prognostic value for DFS independent of other clinical factors such as T category, gender, and histology. Fluorouracil 40-44 tumor protein p53 Homo sapiens 63-66 10440197-6 1999 5-FU was administered at 750 mg/m2 on days 1, 8, 15, 22, and 29 after the administration of IFN and cisplatin. Fluorouracil 0-4 interferon alpha 1 Homo sapiens 92-95 10473078-0 1999 Pharmacokinetic study of S-1, a novel oral fluorouracil antitumor drug. Fluorouracil 43-55 proteasome 26S subunit, non-ATPase 1 Homo sapiens 25-28 10424768-6 1999 FUra exposure resulted in transient induction of p53 and p21, which returned to basal levels 24 hr after drug removal. Fluorouracil 0-4 tumor protein p53 Homo sapiens 49-52 10850313-6 1999 It is even more noteworthy that combined treatment with MSC and one of the following antineoplastic agents (5-FU and DTIC)--both in wide use in every day clinical practice--exhibited a significantly enhanced antimetastatic effect in appropriate metastasis models (established from C38 mouse colon carcinoma and B16 mouse melanoma respectively) as compared to the effect elicited by any component of these therapeutic compositions (MSC + 5-FU and MSC + DTIC) administered alone. Fluorouracil 108-112 musculin Mus musculus 56-59 10850313-6 1999 It is even more noteworthy that combined treatment with MSC and one of the following antineoplastic agents (5-FU and DTIC)--both in wide use in every day clinical practice--exhibited a significantly enhanced antimetastatic effect in appropriate metastasis models (established from C38 mouse colon carcinoma and B16 mouse melanoma respectively) as compared to the effect elicited by any component of these therapeutic compositions (MSC + 5-FU and MSC + DTIC) administered alone. Fluorouracil 108-112 musculin Mus musculus 431-434 10850313-6 1999 It is even more noteworthy that combined treatment with MSC and one of the following antineoplastic agents (5-FU and DTIC)--both in wide use in every day clinical practice--exhibited a significantly enhanced antimetastatic effect in appropriate metastasis models (established from C38 mouse colon carcinoma and B16 mouse melanoma respectively) as compared to the effect elicited by any component of these therapeutic compositions (MSC + 5-FU and MSC + DTIC) administered alone. Fluorouracil 108-112 musculin Mus musculus 431-434 10850313-6 1999 It is even more noteworthy that combined treatment with MSC and one of the following antineoplastic agents (5-FU and DTIC)--both in wide use in every day clinical practice--exhibited a significantly enhanced antimetastatic effect in appropriate metastasis models (established from C38 mouse colon carcinoma and B16 mouse melanoma respectively) as compared to the effect elicited by any component of these therapeutic compositions (MSC + 5-FU and MSC + DTIC) administered alone. Fluorouracil 437-441 musculin Mus musculus 56-59 11601286-7 1999 The combined treatment with AFP antisense oligomers and 5-FU showed significantly enhanced hepatoma cell growth inhibition than either AFP antisense or 5-FU treated cells alone (P < 0.05). Fluorouracil 152-156 alpha fetoprotein Homo sapiens 28-31 11601286-7 1999 The combined treatment with AFP antisense oligomers and 5-FU showed significantly enhanced hepatoma cell growth inhibition than either AFP antisense or 5-FU treated cells alone (P < 0.05). Fluorouracil 56-60 alpha fetoprotein Homo sapiens 135-138 10473078-1 1999 S-1 is a novel oral fluorouracil antitumor drug that combines three pharmacological agents: tegafur (FT), which is a prodrug of 5-fluorouracil (5-FU); 5-chloro-2,4-dihydroxypyridine (CDHP), which inhibits dihydropyrimidine dehydrogenase (DPD) activity; and potassium oxonate (Oxo), which reduces gastrointestinal toxicity. Fluorouracil 144-148 proteasome 26S subunit, non-ATPase 1 Homo sapiens 0-3 10473078-13 1999 infusion of 5-FU, we concluded that S-1 may improve patients" quality of life. Fluorouracil 12-16 proteasome 26S subunit, non-ATPase 1 Homo sapiens 36-39 10473078-1 1999 S-1 is a novel oral fluorouracil antitumor drug that combines three pharmacological agents: tegafur (FT), which is a prodrug of 5-fluorouracil (5-FU); 5-chloro-2,4-dihydroxypyridine (CDHP), which inhibits dihydropyrimidine dehydrogenase (DPD) activity; and potassium oxonate (Oxo), which reduces gastrointestinal toxicity. Fluorouracil 20-32 proteasome 26S subunit, non-ATPase 1 Homo sapiens 0-3 10473078-1 1999 S-1 is a novel oral fluorouracil antitumor drug that combines three pharmacological agents: tegafur (FT), which is a prodrug of 5-fluorouracil (5-FU); 5-chloro-2,4-dihydroxypyridine (CDHP), which inhibits dihydropyrimidine dehydrogenase (DPD) activity; and potassium oxonate (Oxo), which reduces gastrointestinal toxicity. Fluorouracil 128-142 proteasome 26S subunit, non-ATPase 1 Homo sapiens 0-3 11091713-9 1999 CONCLUSION: A false-positive increase in CEA, NCC-ST-439 or BCA225 might be caused by treatment with oral 5-FU or its derivatives. Fluorouracil 106-110 CEA cell adhesion molecule 3 Homo sapiens 41-44 10430607-4 1999 In contrast, p53 disruption rendered cells strikingly resistant to the effects of the antimetabolite 5-fluorouracil (5-FU), the mainstay of adjuvant therapy for colorectal cancer. Fluorouracil 101-115 tumor protein p53 Homo sapiens 13-16 10430607-4 1999 In contrast, p53 disruption rendered cells strikingly resistant to the effects of the antimetabolite 5-fluorouracil (5-FU), the mainstay of adjuvant therapy for colorectal cancer. Fluorouracil 117-121 tumor protein p53 Homo sapiens 13-16 10430607-5 1999 The effects on 5-FU sensitivity were observed both in vitro and in vivo, were independent of p21, and appeared to be the result of perturbations in RNA, rather than DNA, metabolism. Fluorouracil 15-19 cyclin dependent kinase inhibitor 1A Homo sapiens 93-96 10357907-12 1999 CONCLUSIONS: Wound healing following a colonic anastomosis is associated with local increases in TGF-beta1 expression, which in turn is diminished by the administration of 5-FU. Fluorouracil 172-176 transforming growth factor, beta 1 Rattus norvegicus 97-106 10573108-9 1999 MCF-7 cells overexpressing FGF-2 had a greater rate of programmed cell death at baseline and in response to etoposide and 5-fluorouracil in a TUNEL assay by immunofluorescent microphotography and by flow cytometric quantitation. Fluorouracil 122-136 fibroblast growth factor 2 Homo sapiens 27-32 10561274-4 1999 The genetic prodrug activation therapy is specifically targeted to erbB-2-overexpressing breast cancer cells by use of a therapeutic cassette that contains the Escherichia coli cytosine deaminase gene driven by the tumor-specific erbB-2 promoter, thus allowing activation of fluorocytosine to the active cytotoxic fluorouracil only within tumor cells that express the oncogene. Fluorouracil 314-326 erb-b2 receptor tyrosine kinase 2 Homo sapiens 67-73 10561274-4 1999 The genetic prodrug activation therapy is specifically targeted to erbB-2-overexpressing breast cancer cells by use of a therapeutic cassette that contains the Escherichia coli cytosine deaminase gene driven by the tumor-specific erbB-2 promoter, thus allowing activation of fluorocytosine to the active cytotoxic fluorouracil only within tumor cells that express the oncogene. Fluorouracil 314-326 erb-b2 receptor tyrosine kinase 2 Homo sapiens 230-236 10470656-10 1999 The BCL-2/BAX mRNA ratio was decreased in response to 5-FU in IMR90. Fluorouracil 54-58 BCL2 apoptosis regulator Homo sapiens 4-9 10470656-10 1999 The BCL-2/BAX mRNA ratio was decreased in response to 5-FU in IMR90. Fluorouracil 54-58 BCL2 associated X, apoptosis regulator Homo sapiens 10-13 10362102-10 1999 These findings indicate that treatment with CDDP and 5-FU induces ICAM-1 expression by a NF-kappaB independent regulatory mechanism involving PTK. Fluorouracil 53-57 nuclear factor kappa B subunit 1 Homo sapiens 89-98 10339671-6 1999 Moreover, IFN-alpha-transduced cells acquired less resistance to 5-FU induced apoptosis. Fluorouracil 65-69 interferon alpha 1 Homo sapiens 10-19 10362102-0 1999 Synergistic induction of ICAM-1 expression by cisplatin and 5-fluorouracil in a cancer cell line via a NF-kappaB independent pathway. Fluorouracil 60-74 nuclear factor kappa B subunit 1 Homo sapiens 103-112 10334547-1 1999 PURPOSE: To evaluate the effect of N-phosphonacetyl-L-aspartate (PALA), folinic acid (FA), and interferon alfa (IFN-alpha) biomodulation on plasma fluorouracil (5FU) pharmacokinetics and tumor and liver radioactivity uptake and retention after [18F]-fluorouracil (5-[18F]-FU) administration. Fluorouracil 147-159 interferon alpha 1 Homo sapiens 112-121 10403552-5 1999 TGF-beta1 secretion was not changed in KATOIII cells by tamoxifen plus 5-FU treatment but was down-regulated in MKN28 cells. Fluorouracil 71-75 transforming growth factor beta 1 Homo sapiens 0-9 10429661-2 1999 5-FU inhibited cell growth dose-dependently and this growth inhibition was accompanied with cell cycle accumulation in early S phase and increased expression of cyclin A. Fluorouracil 0-4 cyclin A2 Homo sapiens 161-169 10429661-3 1999 When cells were released from short-term treatment (3 or 24 h) with 5-FU, the cell cycle started to progress again and cyclin A protein levels decreased. Fluorouracil 68-72 cyclin A2 Homo sapiens 119-127 10429661-4 1999 Cyclin A-associated kinase activity assay showed that cyclin A-cyclin-dependent kinase (Cdk) 2 kinase activity was altered by 5-FU treatment concomitantly with the changes in cell cycle state seen in flow cytometric analysis. Fluorouracil 126-130 cyclin A2 Homo sapiens 0-8 10429661-4 1999 Cyclin A-associated kinase activity assay showed that cyclin A-cyclin-dependent kinase (Cdk) 2 kinase activity was altered by 5-FU treatment concomitantly with the changes in cell cycle state seen in flow cytometric analysis. Fluorouracil 126-130 cyclin A2 Homo sapiens 54-62 10429661-5 1999 Furthermore, the elevation of cyclin A protein level by 5-FU treatment was observed in three other human cancer cell lines, DLD-1, H226Br and T.Tn. Fluorouracil 56-60 cyclin A2 Homo sapiens 30-38 10429661-6 1999 These results suggest that cyclin A protein levels in cancer cells are increased by 5-FU, and the cyclin A function and degradation mechanism remain normal. Fluorouracil 84-88 cyclin A2 Homo sapiens 27-35 10389868-7 1999 Furthermore, significant statistical differences in chemosensitivity to 5-fluorouracil and CDDP were revealed depending on the presence of serum p53 antibodies. Fluorouracil 72-86 tumor protein p53 Homo sapiens 145-148 10430334-0 1999 A case of colon cancer recurrence with P-glycoprotein treated by methotrexate, fluorouracil, and leucovorin. Fluorouracil 79-91 ATP binding cassette subfamily B member 1 Homo sapiens 39-53 10189126-10 1999 Among those patients whose tumors overexpressed p53, there was a trend toward improved outcome in the arm that received 5-FU and mitomycin-C compared with the arm that received 5-FU only. Fluorouracil 120-124 tumor protein p53 Homo sapiens 48-51 10233360-2 1999 In vitro proliferation of 5-FU-resistant CD34+ (G0) peripheral blood stem cells (PBSC) in response to sequential cytokine stimulation was examined in the presence and absence of 100 ng/ml IL-12. Fluorouracil 26-30 CD34 molecule Homo sapiens 41-45 10363584-1 1999 S-1 [1 M tegafur (FT)-0.4 M 5-chloro-2,4-dihydroxypyridine (CDHP)-1 M potassium oxonate (Oxo)], was developed as a new oral antineoplastic agent based on biochemical modulation of fluorouracil (5-FU) by CDHP and Oxo. Fluorouracil 180-192 proteasome 26S subunit, non-ATPase 1 Homo sapiens 0-3 10363584-1 1999 S-1 [1 M tegafur (FT)-0.4 M 5-chloro-2,4-dihydroxypyridine (CDHP)-1 M potassium oxonate (Oxo)], was developed as a new oral antineoplastic agent based on biochemical modulation of fluorouracil (5-FU) by CDHP and Oxo. Fluorouracil 194-198 proteasome 26S subunit, non-ATPase 1 Homo sapiens 0-3 10363584-7 1999 Analysis of AUC (area under the curve) revealed that S-1 yielded higher 5-FU levels in both tumor tissue (1.6 times) and plasma (2.5 times) than UFT. Fluorouracil 72-76 proteasome 26S subunit, non-ATPase 1 Homo sapiens 53-56 10206306-0 1999 A multifactorial approach including tumoural epidermal growth factor receptor, p53, thymidylate synthase and dihydropyrimidine dehydrogenase to predict treatment outcome in head and neck cancer patients receiving 5-fluorouracil. Fluorouracil 213-227 epidermal growth factor receptor Homo sapiens 45-77 11593534-8 1999 5-Fu could also inhibit the expression of MRP, but had no effect on the expression of GST pi. Fluorouracil 0-4 ATP binding cassette subfamily C member 1 Homo sapiens 42-45 11593534-10 1999 CONCLUSION: Scheduled administration of 5-Fu can reverse CDDP resistance completely through reduction of GSH and inhibition of MRP expression. Fluorouracil 40-44 ATP binding cassette subfamily C member 1 Homo sapiens 127-130 10327070-5 1999 One drug, 5-fluorouracil, was found to be antagonistic with rhuMAb HER2 in vitro (CI=2.87, P=0.0001). Fluorouracil 10-24 erb-b2 receptor tyrosine kinase 2 Homo sapiens 67-71 10189126-10 1999 Among those patients whose tumors overexpressed p53, there was a trend toward improved outcome in the arm that received 5-FU and mitomycin-C compared with the arm that received 5-FU only. Fluorouracil 177-181 tumor protein p53 Homo sapiens 48-51 10448286-2 1999 Improved therapeutic efficacy has been reported using biochemical modulation of 5-FU by leucovorin (LV) or interferon alpha (IFN), the combination of 5-FU/LV frequently considered as standard therapy in metastatic colorectal cancer. Fluorouracil 80-84 interferon alpha 1 Homo sapiens 125-128 10368642-3 1999 The combinations of 5-FU 2 h prior to MTX or MTX 2 h prior to 5-FU followed by a 48 h incubation, respectively, gave growth rates of 20.96 +/- 2.44% and 19.86 +/- 2.56% of the control rate for MCF-7 cells. Fluorouracil 62-66 metaxin 2 Homo sapiens 45-50 10368642-4 1999 In bone marrow cells, the combinations of 5-FU 2 h prior to MTX or MTX 2 h prior to 5-FU followed by a 48 h incubation, respectively, gave growth rates of 79.66 +/- 7.41% (protection) and 31.39 +/- 1.77% of the control rate. Fluorouracil 84-88 metaxin 2 Homo sapiens 67-72 10048975-3 1999 Compared with parental or mock-transfected HAG-1 cells, v-src-transfected HAG/src3-1 cells showed a 3.5-fold resistance to cis-diamminedichloroplatinum (II) (CDDP) but not to doxorubicin, etoposide or 5-fluorouracil. Fluorouracil 201-215 SRC proto-oncogene, non-receptor tyrosine kinase Homo sapiens 58-61 10037174-14 1999 Studies on TS inhibition indicated that, although both S-1 and FUra caused a 4- to 6-fold induction of total TS protein, single oral administration of S-1 was superior to 24-h infusion of FUra in suppressing free TS. Fluorouracil 63-67 thymidylate synthetase Rattus norvegicus 109-111 10225695-3 1999 METHODS: Based on recent advances in knowledge on the radiosensitizing and biochemical modulation effects of chemotherapeutic agents, we have recently developed concurrent CRT which consisted of continuous 5-fluorouracil (5FU) administration (600 mg/m2/day, days 1-5) combined with a low dose of daily cisplatin administration (10 mg/m2/day, days 1-5, and 5 or 10 mg/m2/day, days 8-12 and 15-19) before each fraction of radiation (2 Gy each). Fluorouracil 206-220 calcitonin receptor Homo sapiens 172-175 10225695-3 1999 METHODS: Based on recent advances in knowledge on the radiosensitizing and biochemical modulation effects of chemotherapeutic agents, we have recently developed concurrent CRT which consisted of continuous 5-fluorouracil (5FU) administration (600 mg/m2/day, days 1-5) combined with a low dose of daily cisplatin administration (10 mg/m2/day, days 1-5, and 5 or 10 mg/m2/day, days 8-12 and 15-19) before each fraction of radiation (2 Gy each). Fluorouracil 222-225 calcitonin receptor Homo sapiens 172-175 9973225-9 1999 Incubation of cell lines with doxorubicin or 5-fluorouracil significantly augmented TRAIL-induced apoptosis in most breast cell lines. Fluorouracil 45-59 TNF superfamily member 10 Homo sapiens 84-89 9973225-12 1999 Augmentation of TRAIL-induced apoptosis by doxorubicin or 5-fluorouracil was mediated through caspase activation. Fluorouracil 58-72 TNF superfamily member 10 Homo sapiens 16-21 10037174-14 1999 Studies on TS inhibition indicated that, although both S-1 and FUra caused a 4- to 6-fold induction of total TS protein, single oral administration of S-1 was superior to 24-h infusion of FUra in suppressing free TS. Fluorouracil 63-67 thymidylate synthetase Rattus norvegicus 109-111 10037193-11 1999 Like HT29 cells, this cytotoxicity was potentiated by IFN-gamma in GC3/c1 and VRC5/c1 but not in Caco2, which fails to express Fas, nor in HCT8 and HCT116, in which no dThd-dependent FUra-induced cytotoxicity was demonstrated. Fluorouracil 183-187 interferon gamma Homo sapiens 54-63 10037174-15 1999 The data are consistent with the observation that the therapeutic efficacy of S-1 (100% cure) over FUra is associated with high and sustained levels of drug-induced apoptosis, greater suppression of mitosis, and inhibition of free TS in tumor tissues. Fluorouracil 99-103 thymidylate synthetase Rattus norvegicus 231-233 10070877-7 1999 The induction of MDR1 mRNA expression by IDA, MX2 and 5-FU was analysed by Northern blotting and semiquantitatively assessed by scanning Northern blots on a phosphorimager. Fluorouracil 54-58 ATP binding cassette subfamily B member 1 Homo sapiens 17-21 10070877-10 1999 Both IDA and MX2 induced MDR1 expression within 4 h. 5-FU up-regulated MDR1 expression only when drug exposure was prolonged to 24 h. Based on MRK 16 binding, flow cytometric analysis of P-glycoprotein (Pgp) expression paralleled the increase in MDR1 mRNA levels. Fluorouracil 53-57 ATP binding cassette subfamily B member 1 Homo sapiens 71-75 10070877-10 1999 Both IDA and MX2 induced MDR1 expression within 4 h. 5-FU up-regulated MDR1 expression only when drug exposure was prolonged to 24 h. Based on MRK 16 binding, flow cytometric analysis of P-glycoprotein (Pgp) expression paralleled the increase in MDR1 mRNA levels. Fluorouracil 53-57 ATP binding cassette subfamily B member 1 Homo sapiens 187-201 10070877-10 1999 Both IDA and MX2 induced MDR1 expression within 4 h. 5-FU up-regulated MDR1 expression only when drug exposure was prolonged to 24 h. Based on MRK 16 binding, flow cytometric analysis of P-glycoprotein (Pgp) expression paralleled the increase in MDR1 mRNA levels. Fluorouracil 53-57 ATP binding cassette subfamily B member 1 Homo sapiens 203-206 10070877-10 1999 Both IDA and MX2 induced MDR1 expression within 4 h. 5-FU up-regulated MDR1 expression only when drug exposure was prolonged to 24 h. Based on MRK 16 binding, flow cytometric analysis of P-glycoprotein (Pgp) expression paralleled the increase in MDR1 mRNA levels. Fluorouracil 53-57 ATP binding cassette subfamily B member 1 Homo sapiens 71-75 10070877-12 1999 The induction of MDR1 expression by 5-FU was transient, associated with a rapid decrease in the increased Pgp levels which returned to baseline 72 h after the removal of 5-FU. Fluorouracil 36-40 ATP binding cassette subfamily B member 1 Homo sapiens 17-21 10070877-12 1999 The induction of MDR1 expression by 5-FU was transient, associated with a rapid decrease in the increased Pgp levels which returned to baseline 72 h after the removal of 5-FU. Fluorouracil 36-40 ATP binding cassette subfamily B member 1 Homo sapiens 106-109 10070877-12 1999 The induction of MDR1 expression by 5-FU was transient, associated with a rapid decrease in the increased Pgp levels which returned to baseline 72 h after the removal of 5-FU. Fluorouracil 170-174 ATP binding cassette subfamily B member 1 Homo sapiens 17-21 10048591-5 1999 The SICs detected in our culture system were present only in Mac-1(-)CD45(-) cells, and the M-CSF treatment of 5-FU-pretreated mice actually increased the number of Mac-1(-)CD45(-) SICs. Fluorouracil 111-115 integrin alpha M Mus musculus 165-170 10048591-6 1999 The Mac-1(-)CD45(-) SICs collected from mice that were pretreated with 5-FU and then treated with M-CSF formed stromal colonies under in vitro culture conditions that did not contain M-CSF but did contain a high concentration of fetal calf serum. Fluorouracil 71-75 integrin alpha M Mus musculus 4-9 11819386-0 1999 Expression of IL 1betaconverting enzyme in 5-FU induced apoptosis in esophageal carcinoma cells. Fluorouracil 43-47 interleukin 1 beta Homo sapiens 14-18 11819386-2 1999 Expression of ICE in the tumor cells exposed to 5-FU was examined by the immunocytochemical method.RESULTS:The cells treated with 5-FU displayed disappearance of nucleoli, chromatin gathering under nuclear envelope, karyorrhexis, budding and the formation of apoptotic bodies.The expression of ICE was negative in control cells, and 5-FU could induce the ICE expression in Eca-109 cells undergoing apoptosis. Fluorouracil 48-52 caspase 1 Homo sapiens 14-17 11819386-2 1999 Expression of ICE in the tumor cells exposed to 5-FU was examined by the immunocytochemical method.RESULTS:The cells treated with 5-FU displayed disappearance of nucleoli, chromatin gathering under nuclear envelope, karyorrhexis, budding and the formation of apoptotic bodies.The expression of ICE was negative in control cells, and 5-FU could induce the ICE expression in Eca-109 cells undergoing apoptosis. Fluorouracil 130-134 caspase 1 Homo sapiens 14-17 11819386-2 1999 Expression of ICE in the tumor cells exposed to 5-FU was examined by the immunocytochemical method.RESULTS:The cells treated with 5-FU displayed disappearance of nucleoli, chromatin gathering under nuclear envelope, karyorrhexis, budding and the formation of apoptotic bodies.The expression of ICE was negative in control cells, and 5-FU could induce the ICE expression in Eca-109 cells undergoing apoptosis. Fluorouracil 130-134 caspase 1 Homo sapiens 294-297 11819386-2 1999 Expression of ICE in the tumor cells exposed to 5-FU was examined by the immunocytochemical method.RESULTS:The cells treated with 5-FU displayed disappearance of nucleoli, chromatin gathering under nuclear envelope, karyorrhexis, budding and the formation of apoptotic bodies.The expression of ICE was negative in control cells, and 5-FU could induce the ICE expression in Eca-109 cells undergoing apoptosis. Fluorouracil 130-134 caspase 1 Homo sapiens 294-297 11819386-2 1999 Expression of ICE in the tumor cells exposed to 5-FU was examined by the immunocytochemical method.RESULTS:The cells treated with 5-FU displayed disappearance of nucleoli, chromatin gathering under nuclear envelope, karyorrhexis, budding and the formation of apoptotic bodies.The expression of ICE was negative in control cells, and 5-FU could induce the ICE expression in Eca-109 cells undergoing apoptosis. Fluorouracil 130-134 caspase 1 Homo sapiens 14-17 11819386-2 1999 Expression of ICE in the tumor cells exposed to 5-FU was examined by the immunocytochemical method.RESULTS:The cells treated with 5-FU displayed disappearance of nucleoli, chromatin gathering under nuclear envelope, karyorrhexis, budding and the formation of apoptotic bodies.The expression of ICE was negative in control cells, and 5-FU could induce the ICE expression in Eca-109 cells undergoing apoptosis. Fluorouracil 130-134 caspase 1 Homo sapiens 294-297 11819386-2 1999 Expression of ICE in the tumor cells exposed to 5-FU was examined by the immunocytochemical method.RESULTS:The cells treated with 5-FU displayed disappearance of nucleoli, chromatin gathering under nuclear envelope, karyorrhexis, budding and the formation of apoptotic bodies.The expression of ICE was negative in control cells, and 5-FU could induce the ICE expression in Eca-109 cells undergoing apoptosis. Fluorouracil 130-134 caspase 1 Homo sapiens 294-297 11819386-3 1999 The number and the staining intensity of positive cells increased with the extension of action time.CONCLUSION: 5-FU may induce apoptosis in human esophageal carcinoma Eca-109 cells; ICE gene may be involved in the regulation of 5-FU induced apoptosis; and ICE protein may mediate apoptosis induced by 5-FU. Fluorouracil 112-116 caspase 1 Homo sapiens 183-186 11819386-3 1999 The number and the staining intensity of positive cells increased with the extension of action time.CONCLUSION: 5-FU may induce apoptosis in human esophageal carcinoma Eca-109 cells; ICE gene may be involved in the regulation of 5-FU induced apoptosis; and ICE protein may mediate apoptosis induced by 5-FU. Fluorouracil 112-116 caspase 1 Homo sapiens 257-260 11819386-3 1999 The number and the staining intensity of positive cells increased with the extension of action time.CONCLUSION: 5-FU may induce apoptosis in human esophageal carcinoma Eca-109 cells; ICE gene may be involved in the regulation of 5-FU induced apoptosis; and ICE protein may mediate apoptosis induced by 5-FU. Fluorouracil 229-233 caspase 1 Homo sapiens 183-186 11819386-3 1999 The number and the staining intensity of positive cells increased with the extension of action time.CONCLUSION: 5-FU may induce apoptosis in human esophageal carcinoma Eca-109 cells; ICE gene may be involved in the regulation of 5-FU induced apoptosis; and ICE protein may mediate apoptosis induced by 5-FU. Fluorouracil 229-233 caspase 1 Homo sapiens 183-186 10023694-2 1999 Although biochemical modulation of 5-fluorouracil (5-FU) by leucovorin (LV) and interferon-alpha (IFN-alpha) has improved the outcomes of patients with metastatic colorectal carcinoma compared with 5-FU alone, this approach has not been extensively evaluated in the treatment of advanced gastric carcinoma. Fluorouracil 35-49 interferon alpha 1 Homo sapiens 98-107 10023694-2 1999 Although biochemical modulation of 5-fluorouracil (5-FU) by leucovorin (LV) and interferon-alpha (IFN-alpha) has improved the outcomes of patients with metastatic colorectal carcinoma compared with 5-FU alone, this approach has not been extensively evaluated in the treatment of advanced gastric carcinoma. Fluorouracil 51-55 interferon alpha 1 Homo sapiens 98-107 10023697-11 1999 The ratio of SPF (after 5-FU/before 5-FU) was higher in the 5-day group (2.35+/-0.78) than in the 3-day (1.71+/-0.48), 7-day (1.68+/-0.55), or 10-day (1.20+/-0.20) groups (P < 0.05). Fluorouracil 24-28 SEC14 like lipid binding 2 Homo sapiens 13-16 10023697-11 1999 The ratio of SPF (after 5-FU/before 5-FU) was higher in the 5-day group (2.35+/-0.78) than in the 3-day (1.71+/-0.48), 7-day (1.68+/-0.55), or 10-day (1.20+/-0.20) groups (P < 0.05). Fluorouracil 36-40 SEC14 like lipid binding 2 Homo sapiens 13-16 10226560-1 1999 Combined treatment of interleukin-2 (IL-2), 5-fluorouracil (5-FU) and mitomycin C (MMC) is reported to be effective against hepatic metastasis of colon carcinoma. Fluorouracil 60-64 interleukin 2 Homo sapiens 22-35 10412941-4 1999 RESULTS: IFN-alpha enhanced the sensitivity of three of five RCC cell lines to 5-FU in a dose- and schedule-dependent manner. Fluorouracil 79-83 interferon alpha 1 Homo sapiens 9-18 10412941-5 1999 When IFN-alpha was given prior to 5-FU, sensitivity to 5-FU was significantly higher than when IFN-alpha was given simultaneously (P < 0.05). Fluorouracil 55-59 interferon alpha 1 Homo sapiens 5-14 10412941-7 1999 The relative IFN-alpha-induced increase in sensitivity to 5-FU correlated with the relative IFN-alpha-induced increase in TP expression (P < 0.05). Fluorouracil 58-62 interferon alpha 1 Homo sapiens 13-22 10412941-7 1999 The relative IFN-alpha-induced increase in sensitivity to 5-FU correlated with the relative IFN-alpha-induced increase in TP expression (P < 0.05). Fluorouracil 58-62 interferon alpha 1 Homo sapiens 92-101 10412941-8 1999 In addition, two of three RCC cell lines with more than a twofold increase in sensitivity to 5-FU induced by IFN-alpha showed a higher TP expression without IFN-alpha stimulation. Fluorouracil 93-97 interferon alpha 1 Homo sapiens 109-118 10412941-9 1999 CONCLUSIONS: These results suggest that IFN-alpha upregulates TP expression and modulates 5-FU anabolism thus enhancing 5-FU cytotoxicity in a dose- and schedule-dependent manner in some RCC cells. Fluorouracil 90-94 interferon alpha 1 Homo sapiens 40-49 10412941-9 1999 CONCLUSIONS: These results suggest that IFN-alpha upregulates TP expression and modulates 5-FU anabolism thus enhancing 5-FU cytotoxicity in a dose- and schedule-dependent manner in some RCC cells. Fluorouracil 120-124 interferon alpha 1 Homo sapiens 40-49 10412949-9 1999 RESULTS: p53 Ad combined with cisplatin, doxorubicin, 5-fluorouracil, methotrexate, or etoposide inhibited cell proliferation more effectively than chemotherapy alone in SCC-9 head and neck, SCC-15 head and neck, SCC-25 head and neck, SK-OV-3 ovarian, DU-145 prostate, MDA-MB-468 breast, and MDA-MB-231 breast tumor cells. Fluorouracil 54-68 tumor protein p53 Homo sapiens 9-12 10449942-4 1999 Thus, intravenous 5-FU was found to be an effective therapeutic modality for the Witten and Zak type of KA. Fluorouracil 18-22 mitogen-activated protein kinase kinase kinase 20 Homo sapiens 92-95 9923446-2 1999 Thy-1.2lo Sca-1+ H-2Khi stem cells enriched from the bone marrow of 5-fluorouracil-treated (Ly5-2) mice were infected with the bcl-2 retrovirus and injected into (Ly5-1) irradiated recipients. Fluorouracil 68-82 thymus cell antigen 1, theta Mus musculus 0-7 10363568-2 1999 The aim of this work was to investigate the role of p53 in the apoptosis of colorectal cancer cells in vitro, induced by 5-fluorouracil (5-FU) and hydroxy-camptothecin (HCPT). Fluorouracil 121-135 tumor protein p53 Homo sapiens 52-55 10363568-2 1999 The aim of this work was to investigate the role of p53 in the apoptosis of colorectal cancer cells in vitro, induced by 5-fluorouracil (5-FU) and hydroxy-camptothecin (HCPT). Fluorouracil 137-141 tumor protein p53 Homo sapiens 52-55 10489165-3 1999 A253/Bax cells exhibited a significant increase in in vitro sensitivity to various anticancer drugs, including tomudex (9.5-fold), SN-38 (13.8-fold), doxorubicin (7.9-fold), taxol (3.1-fold), 5-FU (2.7-fold), and 5-FU/LV (4.5-fold). Fluorouracil 192-196 BCL2 associated X, apoptosis regulator Homo sapiens 5-8 10489165-3 1999 A253/Bax cells exhibited a significant increase in in vitro sensitivity to various anticancer drugs, including tomudex (9.5-fold), SN-38 (13.8-fold), doxorubicin (7.9-fold), taxol (3.1-fold), 5-FU (2.7-fold), and 5-FU/LV (4.5-fold). Fluorouracil 213-217 BCL2 associated X, apoptosis regulator Homo sapiens 5-8 11498842-5 1999 CONCLUSION: PF4 or AcSDKP accelerate the recovery in vivo of HPP-CFC, CFU-GM and BFU-E after 5-FU treatment but their effect may be different on megakaryocytic progenitors. Fluorouracil 93-97 platelet factor 4 Mus musculus 12-15 9839521-2 1998 Preclinical and clinical phase I/II data suggested that interferon alfa-2a (IFN) enhanced the efficacy of 5-FU therapy. Fluorouracil 106-110 interferon alpha 1 Homo sapiens 76-79 9856651-1 1998 The objective of this phase I-II study was to determine the efficacy and toxicity of combination chemotherapy with 5-fluorouracil, leucovorin, doxorubicin, methotrexate, and oral etoposide (FLAME) in patients with measurable unresectable or metastatic gastric cancer. Fluorouracil 115-129 CASP8 and FADD like apoptosis regulator Homo sapiens 190-195 9875677-3 1998 The cultivation of human peripheral blood mononuclear cells (PBMC) in the presence of cisplatin (0-1.0 microg/ml) or 5-FU (0-5.0 microg/ml) resulted in the significant augmentation of natural killer (NK) and lymphokine-activated killer (LAK) cell activities as well as generation of interferon (IFN) gamma, tumor necrosis factor (TNF) alpha, beta interleukin(IL)-1beta, IL-6 and IL-12 in vitro. Fluorouracil 117-121 interferon gamma Homo sapiens 283-305 9875677-3 1998 The cultivation of human peripheral blood mononuclear cells (PBMC) in the presence of cisplatin (0-1.0 microg/ml) or 5-FU (0-5.0 microg/ml) resulted in the significant augmentation of natural killer (NK) and lymphokine-activated killer (LAK) cell activities as well as generation of interferon (IFN) gamma, tumor necrosis factor (TNF) alpha, beta interleukin(IL)-1beta, IL-6 and IL-12 in vitro. Fluorouracil 117-121 tumor necrosis factor Homo sapiens 307-340 9875677-3 1998 The cultivation of human peripheral blood mononuclear cells (PBMC) in the presence of cisplatin (0-1.0 microg/ml) or 5-FU (0-5.0 microg/ml) resulted in the significant augmentation of natural killer (NK) and lymphokine-activated killer (LAK) cell activities as well as generation of interferon (IFN) gamma, tumor necrosis factor (TNF) alpha, beta interleukin(IL)-1beta, IL-6 and IL-12 in vitro. Fluorouracil 117-121 interleukin 6 Homo sapiens 370-374 9824638-3 1998 Treatment of KTFU-4 cells with 5-FU resulted in increased amounts of activated phosphorylated ERK1/2 and p38 MAP kinases, but not in the parent KT cells. Fluorouracil 31-35 mitogen-activated protein kinase 3 Homo sapiens 94-100 9824638-3 1998 Treatment of KTFU-4 cells with 5-FU resulted in increased amounts of activated phosphorylated ERK1/2 and p38 MAP kinases, but not in the parent KT cells. Fluorouracil 31-35 mitogen-activated protein kinase 1 Homo sapiens 105-108 9829841-6 1998 Preliminary in vitro studies indicated that IL-2 or IFN antagonized the severe inhibition of NKA induced by hydroxy-peroxy-cyclophosphamide (in vitro active derivative of cyclophosphamide), alone or associated with methotrexate + 5-fluorouracil. Fluorouracil 230-244 interleukin 2 Homo sapiens 44-55 10037193-7 1999 The objective of this study was to elucidate whether a Fas-dependent component exists in 5-fluorouracil (FUra)/leucovorin (LV)-induced cytotoxicity of colon carcinoma cells, and whether this may be potentiated by IFN-gamma-induced elevation in Fas expression, using the HT29 cell line as a model. Fluorouracil 89-103 interferon gamma Homo sapiens 213-222 10037193-12 1999 Data suggest that a Fas-dependent component, potentiated by IFN-gamma, exists in FUra/LV-induced cytotoxicity but requires FUra/LV-induced DNA damage for IFN-gamma-induced potentiation to occur. Fluorouracil 81-85 interferon gamma Homo sapiens 60-69 10037193-12 1999 Data suggest that a Fas-dependent component, potentiated by IFN-gamma, exists in FUra/LV-induced cytotoxicity but requires FUra/LV-induced DNA damage for IFN-gamma-induced potentiation to occur. Fluorouracil 81-86 interferon gamma Homo sapiens 60-69 9796980-0 1998 Effect of the combined treatment with 5-fluorouracil, gamma-interferon or folinic acid on carcinoembryonic antigen expression in colon cancer cells. Fluorouracil 38-52 CEA cell adhesion molecule 3 Homo sapiens 90-114 9930367-0 1998 p53- and p21-independent apoptosis of squamous cell carcinoma cells induced by 5-fluorouracil and radiation. Fluorouracil 79-93 tumor protein p53 Homo sapiens 0-3 9930367-12 1998 These findings indicate that 5-FU and gamma-rays induce apoptosis of squamous cell carcinoma cells in p53- and p21-independent manners, in the S and G2/M phases, respectively. Fluorouracil 29-33 tumor protein p53 Homo sapiens 102-105 9792140-0 1998 5-Fluorouracil induces apoptosis in human colon cancer cell lines with modulation of Bcl-2 family proteins. Fluorouracil 0-14 BCL2 apoptosis regulator Homo sapiens 85-90 9792140-3 1998 We sought to determine the roles played by the p53 and Bcl-2 family of proteins in 5-fluorouracil (5-FU)-induced apoptosis of human colon cancer cell lines. Fluorouracil 83-97 tumor protein p53 Homo sapiens 47-50 9792140-3 1998 We sought to determine the roles played by the p53 and Bcl-2 family of proteins in 5-fluorouracil (5-FU)-induced apoptosis of human colon cancer cell lines. Fluorouracil 83-97 BCL2 apoptosis regulator Homo sapiens 55-60 9792140-3 1998 We sought to determine the roles played by the p53 and Bcl-2 family of proteins in 5-fluorouracil (5-FU)-induced apoptosis of human colon cancer cell lines. Fluorouracil 99-103 tumor protein p53 Homo sapiens 47-50 9792140-3 1998 We sought to determine the roles played by the p53 and Bcl-2 family of proteins in 5-fluorouracil (5-FU)-induced apoptosis of human colon cancer cell lines. Fluorouracil 99-103 BCL2 apoptosis regulator Homo sapiens 55-60 9792140-6 1998 Using five human colon cancer cell lines, we found that equitoxic (IC50) doses of 5-FU induced apoptosis in both wild-type p53 and mutant p53 cells. Fluorouracil 82-86 tumor protein p53 Homo sapiens 123-126 9792140-6 1998 Using five human colon cancer cell lines, we found that equitoxic (IC50) doses of 5-FU induced apoptosis in both wild-type p53 and mutant p53 cells. Fluorouracil 82-86 tumor protein p53 Homo sapiens 138-141 9792140-11 1998 In cells containing wild-type p53 (e.g. LoVo), 5-FU-induced apoptosis was accompanied by increased expression of Bax and Bak without consistent modulation of other bcl-2 family proteins. Fluorouracil 47-51 tumor protein p53 Homo sapiens 30-33 9792140-11 1998 In cells containing wild-type p53 (e.g. LoVo), 5-FU-induced apoptosis was accompanied by increased expression of Bax and Bak without consistent modulation of other bcl-2 family proteins. Fluorouracil 47-51 BCL2 associated X, apoptosis regulator Homo sapiens 113-116 9792140-11 1998 In cells containing wild-type p53 (e.g. LoVo), 5-FU-induced apoptosis was accompanied by increased expression of Bax and Bak without consistent modulation of other bcl-2 family proteins. Fluorouracil 47-51 BCL2 apoptosis regulator Homo sapiens 164-169 9792140-14 1998 In conclusion, these results suggest that some members of the Bcl-2 family of proteins, in human colon cancer cell lines, are modulated by 5-FU and that the ratio of Bcl-X(L) to Bax may be related to chemosensitivity to 5-FU. Fluorouracil 139-143 BCL2 apoptosis regulator Homo sapiens 62-67 9792140-14 1998 In conclusion, these results suggest that some members of the Bcl-2 family of proteins, in human colon cancer cell lines, are modulated by 5-FU and that the ratio of Bcl-X(L) to Bax may be related to chemosensitivity to 5-FU. Fluorouracil 220-224 BCL2 apoptosis regulator Homo sapiens 62-67 9792140-14 1998 In conclusion, these results suggest that some members of the Bcl-2 family of proteins, in human colon cancer cell lines, are modulated by 5-FU and that the ratio of Bcl-X(L) to Bax may be related to chemosensitivity to 5-FU. Fluorouracil 220-224 BCL2 like 1 Homo sapiens 166-174 9796980-1 1998 5-Fluorouracil (5-FU) and human recombinant gamma-interferon (gamma-IFN) were found to increase the expression of carcinoembryonic antigen (CEA) in human cancer cells in vitro. Fluorouracil 0-14 CEA cell adhesion molecule 3 Homo sapiens 114-138 9796980-1 1998 5-Fluorouracil (5-FU) and human recombinant gamma-interferon (gamma-IFN) were found to increase the expression of carcinoembryonic antigen (CEA) in human cancer cells in vitro. Fluorouracil 0-14 CEA cell adhesion molecule 3 Homo sapiens 140-143 9796980-1 1998 5-Fluorouracil (5-FU) and human recombinant gamma-interferon (gamma-IFN) were found to increase the expression of carcinoembryonic antigen (CEA) in human cancer cells in vitro. Fluorouracil 16-20 CEA cell adhesion molecule 3 Homo sapiens 114-138 9796980-1 1998 5-Fluorouracil (5-FU) and human recombinant gamma-interferon (gamma-IFN) were found to increase the expression of carcinoembryonic antigen (CEA) in human cancer cells in vitro. Fluorouracil 16-20 CEA cell adhesion molecule 3 Homo sapiens 140-143 9796980-3 1998 Treatment of two human colon cancer cell lines (HT-29 and WiDr) with 5-FU + gamma-IFN resulted in an increase of CEA expression higher than that obtainable with both agents alone, although no synergistic effects were obtained. Fluorouracil 69-73 CEA cell adhesion molecule 3 Homo sapiens 113-116 9796980-9 1998 In vivo studies showed, for the first time, that 5-FU, alone or combined with gamma-IFN, increases the amount of CEA protein over controls, either in cancer cells or in peripheral blood of nude mice bearing HT-29 cells. Fluorouracil 49-53 carcinoembryonic antigen gene family Mus musculus 113-116 9735397-0 1998 Preclinical antitumor efficacy of S-1: a new oral formulation of 5-fluorouracil on human tumor xenografts. Fluorouracil 65-79 proteasome 26S subunit, non-ATPase 1 Homo sapiens 34-37 9840729-2 1998 S-1 is an oral combined form of 1 M tegafur [a prodrug of 5-fluorouracil (5-FU)], 0.4 M 5-chloro-2,4-dihydroxypyridine (a reversible inhibitor of dihydropyrimidine dehydrogenase) and 1 M potassium oxonate (an inhibitor of orotate phosphoribosyltransferase). Fluorouracil 58-72 proteasome 26S subunit, non-ATPase 1 Homo sapiens 0-3 9840729-2 1998 S-1 is an oral combined form of 1 M tegafur [a prodrug of 5-fluorouracil (5-FU)], 0.4 M 5-chloro-2,4-dihydroxypyridine (a reversible inhibitor of dihydropyrimidine dehydrogenase) and 1 M potassium oxonate (an inhibitor of orotate phosphoribosyltransferase). Fluorouracil 74-78 proteasome 26S subunit, non-ATPase 1 Homo sapiens 0-3 9893658-1 1998 S-1 is a novel oral anticancer drug, composed of tegafur (FT), gimestat (CDHP) and otastat potassium (Oxo) in a molar ratio of 1:0.4:1, based on the biochemical modulation of 5-fluorouracil (5-FU). Fluorouracil 175-189 proteasome 26S subunit, non-ATPase 1 Homo sapiens 0-3 9893658-1 1998 S-1 is a novel oral anticancer drug, composed of tegafur (FT), gimestat (CDHP) and otastat potassium (Oxo) in a molar ratio of 1:0.4:1, based on the biochemical modulation of 5-fluorouracil (5-FU). Fluorouracil 191-195 proteasome 26S subunit, non-ATPase 1 Homo sapiens 0-3 9893658-4 1998 S-1 improves the tumour-selective toxicity of 5-FU by the actions of two modulators, CDHP and Oxo. Fluorouracil 46-50 proteasome 26S subunit, non-ATPase 1 Homo sapiens 0-3 9735397-6 1998 The reason of the discrepancy in the efficacy of S-1 between rats and mice was found to be that the 5-FU levels in the blood and tumor tissue of rats after oral administration of S-1 persisted much longer than in mice, and this prolonged maintenance of plasma 5-FU levels was significantly related to the potent antitumor activity of S-1. Fluorouracil 100-104 proteasome 26S subunit, non-ATPase 1 Homo sapiens 49-52 9735397-6 1998 The reason of the discrepancy in the efficacy of S-1 between rats and mice was found to be that the 5-FU levels in the blood and tumor tissue of rats after oral administration of S-1 persisted much longer than in mice, and this prolonged maintenance of plasma 5-FU levels was significantly related to the potent antitumor activity of S-1. Fluorouracil 100-104 proteasome 26S subunit, non-ATPase 1 Homo sapiens 179-182 9735397-6 1998 The reason of the discrepancy in the efficacy of S-1 between rats and mice was found to be that the 5-FU levels in the blood and tumor tissue of rats after oral administration of S-1 persisted much longer than in mice, and this prolonged maintenance of plasma 5-FU levels was significantly related to the potent antitumor activity of S-1. Fluorouracil 100-104 eukaryotic translation elongation factor 1 alpha 2 Mus musculus 179-182 9735397-6 1998 The reason of the discrepancy in the efficacy of S-1 between rats and mice was found to be that the 5-FU levels in the blood and tumor tissue of rats after oral administration of S-1 persisted much longer than in mice, and this prolonged maintenance of plasma 5-FU levels was significantly related to the potent antitumor activity of S-1. Fluorouracil 260-264 proteasome 26S subunit, non-ATPase 1 Homo sapiens 49-52 9735397-6 1998 The reason of the discrepancy in the efficacy of S-1 between rats and mice was found to be that the 5-FU levels in the blood and tumor tissue of rats after oral administration of S-1 persisted much longer than in mice, and this prolonged maintenance of plasma 5-FU levels was significantly related to the potent antitumor activity of S-1. Fluorouracil 260-264 proteasome 26S subunit, non-ATPase 1 Homo sapiens 179-182 9735397-6 1998 The reason of the discrepancy in the efficacy of S-1 between rats and mice was found to be that the 5-FU levels in the blood and tumor tissue of rats after oral administration of S-1 persisted much longer than in mice, and this prolonged maintenance of plasma 5-FU levels was significantly related to the potent antitumor activity of S-1. Fluorouracil 260-264 eukaryotic translation elongation factor 1 alpha 2 Mus musculus 179-182 9726437-20 1998 IFN-alpha2b preceding 5-FU has shown an interesting profile of activity in a patient population with clearly unfavorable characteristics. Fluorouracil 22-26 interferon alpha 1 Homo sapiens 0-9 9788412-0 1998 Role of a DT-diaphorase mutation in the response of anal canal carcinoma to radiation, 5-fluorouracil, and mitomycin C. Fluorouracil 87-101 NAD(P)H quinone dehydrogenase 1 Homo sapiens 10-23 9788412-1 1998 PURPOSE: To determine, retrospectively, the status of the bp 609 mutation in the DT-diaphorase gene in anal canal carcinoma patients who have undergone radical radiotherapy with concurrent 5-fluorouracil (5-FU) and mitomycin C (MMC), to determine the relationship of the mutant form of the gene to treatment outcomes. Fluorouracil 189-203 NAD(P)H quinone dehydrogenase 1 Homo sapiens 81-94 9788412-1 1998 PURPOSE: To determine, retrospectively, the status of the bp 609 mutation in the DT-diaphorase gene in anal canal carcinoma patients who have undergone radical radiotherapy with concurrent 5-fluorouracil (5-FU) and mitomycin C (MMC), to determine the relationship of the mutant form of the gene to treatment outcomes. Fluorouracil 205-209 NAD(P)H quinone dehydrogenase 1 Homo sapiens 81-94 9826123-0 1998 Effects of fibroblast-mediated interleukin 3 and interleukin 6 gene therapy on hematopoiesis in mice treated with 5-fluorouracil. Fluorouracil 114-128 interleukin 6 Mus musculus 49-62 9826123-7 1998 In hematopoiesis-depressed mice induced by preinjection with 5-fluorouracil at the dose of 150 mg/kg before cell implantation, the platelets, neutrophils, and white blood cells showed accelerated recovery, and the numbers of CFU-GM and CFU-MK formed by bone marrow cells were also markedly higher after the combined implantation of NIH3T3-IL-3 and NIH3T3-IL-6 cells than in control groups. Fluorouracil 61-75 interleukin 3 Mus musculus 339-343 9826123-7 1998 In hematopoiesis-depressed mice induced by preinjection with 5-fluorouracil at the dose of 150 mg/kg before cell implantation, the platelets, neutrophils, and white blood cells showed accelerated recovery, and the numbers of CFU-GM and CFU-MK formed by bone marrow cells were also markedly higher after the combined implantation of NIH3T3-IL-3 and NIH3T3-IL-6 cells than in control groups. Fluorouracil 61-75 interleukin 6 Homo sapiens 355-359 11819336-1 1998 AIM:To compare the expression level of Fas gene and Bcl-2 gene in gastric cancer cells SGC7901 and gastric cancer MDR (multidrug resistant) cells SGC7901/VCR,to transduce Fas cDNA and Bcl-2 antisense nucleic acid into SGC7901/VCR cells respectively, and to observe the expression of two genes in transfectants and non-transfectants as well as their drug sensitivity.METHODS:Eukaryotic expression vector pBK-Fas cDNA and pDOR-anti Bcl-2 were constructed and transfected into SGC7901/VCR cells by lipofectamine,respectively.Northern blot and Western blot were used to detect the expression of mRNA and protein in SGC7901/VCR and SGC7901 cells and transfectants, and drug sensitivity of transfectants for VCR, CDDP and 5-FU was analyzed with MTT assay.RESULTS:After gene transfection, 80 for Fas and 120 for antisense Bcl-2 drug-resistant clones were selected from 2 X10(5) cells, transfection rate being 0.04% and 0.06%. Fluorouracil 716-720 BCL2 apoptosis regulator Homo sapiens 52-57 9751613-2 1998 We have demonstrated the feasibility of noninvasive magnetic resonance spectroscopy and spectroscopic imaging (chemical shift imaging) to detect activation of the prodrug 5-fluorocytosine (5-FCyt) to the cytotoxic species 5-fluorouracil (5-FU) by monoclonal antibody-cytosine deaminase (CD) conjugates. Fluorouracil 222-236 PKHD1 ciliary IPT domain containing fibrocystin/polyductin Homo sapiens 191-195 9751613-2 1998 We have demonstrated the feasibility of noninvasive magnetic resonance spectroscopy and spectroscopic imaging (chemical shift imaging) to detect activation of the prodrug 5-fluorocytosine (5-FCyt) to the cytotoxic species 5-fluorouracil (5-FU) by monoclonal antibody-cytosine deaminase (CD) conjugates. Fluorouracil 238-242 PKHD1 ciliary IPT domain containing fibrocystin/polyductin Homo sapiens 191-195 9751613-4 1998 After pretreatment of H2981 tumor-bearing mice with L6-CD, in vivo metabolism of 5-FCyt to 5-FU within the tumors was detected by 19F magnetic resonance spectroscopy; the chemical shift separation between 5-FCyt and 5-FU resonances was approximately 1.2 ppm. Fluorouracil 216-220 PKHD1 ciliary IPT domain containing fibrocystin/polyductin Homo sapiens 83-87 9751613-5 1998 5-FU levels were 50-100% of 5-FCyt levels in tumors 10-60 min after 5-FCyt administration. Fluorouracil 0-4 PKHD1 ciliary IPT domain containing fibrocystin/polyductin Homo sapiens 30-34 9751613-5 1998 5-FU levels were 50-100% of 5-FCyt levels in tumors 10-60 min after 5-FCyt administration. Fluorouracil 0-4 PKHD1 ciliary IPT domain containing fibrocystin/polyductin Homo sapiens 70-74 9679577-3 1998 To achieve high activity and low toxicity, S-1 was designed, in which tegafur, prodrug of 5-FU, was combined with two classes of modulators. Fluorouracil 90-94 proteasome 26S subunit, non-ATPase 1 Homo sapiens 43-46 9662268-0 1998 IL-12 indirectly enhances proliferation of 5-FU-treated human hematopoietic peripheral blood CD34+ cells. Fluorouracil 43-47 CD34 molecule Homo sapiens 93-97 9662268-6 1998 We evaluated 5-FU-treated human CD34+ PBSC proliferation in cultures with Epo, G-CSF, and IL-3, in the presence or absence of IL-12. Fluorouracil 13-17 CD34 molecule Homo sapiens 32-36 9662268-6 1998 We evaluated 5-FU-treated human CD34+ PBSC proliferation in cultures with Epo, G-CSF, and IL-3, in the presence or absence of IL-12. Fluorouracil 13-17 erythropoietin Homo sapiens 74-77 9733602-0 1998 Vasopressin selectively increases 5-fluorouracil uptake by colorectal liver metastases following hepatic artery bolus infusion. Fluorouracil 34-48 arginine vasopressin Rattus norvegicus 0-11 9662268-7 1998 No cytokine combination enhanced colony formation from 5-FU-treated CD34+ cells. Fluorouracil 55-59 CD34 molecule Homo sapiens 68-72 9662268-8 1998 However, in cultures of 5-FU-treated human CD34+ cells, the most efficient combination was IL-3 + Epo + G-CSF + Accessory cells (CD34-). Fluorouracil 24-28 CD34 molecule Homo sapiens 43-47 9662268-8 1998 However, in cultures of 5-FU-treated human CD34+ cells, the most efficient combination was IL-3 + Epo + G-CSF + Accessory cells (CD34-). Fluorouracil 24-28 erythropoietin Homo sapiens 98-101 9662268-10 1998 To investigate whether immature CD34+ cells were responsible for FL or SCF, 5-FU-treated human CD34+ cells were cultured with or without IL-12. Fluorouracil 76-80 CD34 molecule Homo sapiens 95-99 9667258-2 1998 METHODS: We determined plasma levels of c-erbB-2 in 79 stages II and III breast cancer patients who received cyclophosphamide, methotrexate, and flourouracil (CMF)/cyclophosphamide, methotrexate, fluorouracil, vincristine, and prednisone (CMFVP) chemotherapy. Fluorouracil 196-208 erb-b2 receptor tyrosine kinase 2 Homo sapiens 40-48 9733602-3 1998 The aim of this study was to determine whether vasopressin could selectively increase tumor uptake of 5-FU. Fluorouracil 102-106 arginine vasopressin Rattus norvegicus 47-58 9733602-15 1998 CONCLUSIONS: The results of this study show that vasopressin selectively enhances the uptake of 5-FU by colorectal liver metastases in a rat model of hepatic artery infusion. Fluorouracil 96-100 arginine vasopressin Rattus norvegicus 49-60 9607583-9 1998 In this study, we also present data linking specific p53 point mutations to TS expression levels and resistance to 5-FU. Fluorouracil 115-119 tumor protein p53 Homo sapiens 53-56 9612600-10 1998 CONCLUSION: Patients with unresectable alpha-fetoprotein-positive hepatocellular carcinoma experienced improved survival and decreased toxicity when managed with post-induction cycles of intra-arterial cisplatin as compared with intravenous doxorubicin and 5-FU. Fluorouracil 257-261 alpha fetoprotein Homo sapiens 39-56 9610658-7 1998 CONCLUSIONS: Immunohistochemically detected p53 protein status in NSCLC patients may be a promising indicator in determining in vitro chemosensitivity to some anticancer drugs, especially 5-Fu and ADM. Fluorouracil 188-192 tumor protein p53 Homo sapiens 44-47 9617733-8 1998 Plasma concentrations of 5-FU and 1-LV in this study overwhelmed the concentrations that enhancement of thymidylate synthetase (TS) inhibition due to 5-FU was observed by addition of 1-LV in vitro. Fluorouracil 25-29 thymidylate synthetase Rattus norvegicus 104-126 9617733-8 1998 Plasma concentrations of 5-FU and 1-LV in this study overwhelmed the concentrations that enhancement of thymidylate synthetase (TS) inhibition due to 5-FU was observed by addition of 1-LV in vitro. Fluorouracil 150-154 thymidylate synthetase Rattus norvegicus 104-126 9515799-12 1998 In stage III, adjuvant therapy with 5FU plus levamisole improved 7-year survival in patients with wild-type Ki-ras (76 versus 44%; HR, 0.4; 95% CI, 0.2-0.8) and in those without p53 overexpression (64 versus 26%; HR, 0.3; 95% CI, 0.1-0.7). Fluorouracil 36-39 tumor protein p53 Homo sapiens 178-181 9607502-7 1998 With three courses of cisplatin, vincristine, and 5-fluorouracil after the hepatectomy, the serum alpha-fetoprotein level returned to normal, and the patient has remained well 4 months postoperation. Fluorouracil 50-64 alpha fetoprotein Homo sapiens 98-115 9531612-2 1998 We examined the role of the p53 tumor suppressor gene in hematopoietic recovery in vivo after treatment with the cytotoxic drug 5-fluorouracil (5-FU). Fluorouracil 128-142 tumor protein p53 Homo sapiens 28-31 9531612-2 1998 We examined the role of the p53 tumor suppressor gene in hematopoietic recovery in vivo after treatment with the cytotoxic drug 5-fluorouracil (5-FU). Fluorouracil 144-148 tumor protein p53 Homo sapiens 28-31 9531612-4 1998 Analysis of the repopulation ability and clonogenic activity of hematopoietic stem cells (HSCs) and their lineage-committed descendants showed a greater number of HSCs responsible for reconstitution of lethally irradiated recipients in p53-/- bone marrow cells (BMCs) recovering after 5-FU treatment than in the corresponding p53+/+ BMCs. Fluorouracil 285-289 tumor protein p53 Homo sapiens 236-239 9531612-7 1998 The pool of HSCs from 5-FU-treated p53-/- BMCs was exhausted more slowly than that from the p53+/+ population as shown in vivo using pre-spleen colony-forming unit (CFU-S) assay and in vitro using long-term culture-initiating cells (LTC-ICs) and methylcellulose replating assays. Fluorouracil 22-26 tumor protein p53 Homo sapiens 35-38 9531612-9 1998 Despite all these changes and the dramatic difference in sensitivity of p53-/- and p53+/+ BMCs to 5-FU-induced apoptosis, lineage commitment and differentiation of hematopoietic progenitors appeared to be independent of p53 status. Fluorouracil 98-102 tumor protein p53 Homo sapiens 72-75 9531612-9 1998 Despite all these changes and the dramatic difference in sensitivity of p53-/- and p53+/+ BMCs to 5-FU-induced apoptosis, lineage commitment and differentiation of hematopoietic progenitors appeared to be independent of p53 status. Fluorouracil 98-102 tumor protein p53 Homo sapiens 83-86 9531612-9 1998 Despite all these changes and the dramatic difference in sensitivity of p53-/- and p53+/+ BMCs to 5-FU-induced apoptosis, lineage commitment and differentiation of hematopoietic progenitors appeared to be independent of p53 status. Fluorouracil 98-102 tumor protein p53 Homo sapiens 83-86 9568724-4 1998 To observe the protective effects of NIH3T3-IL-6 cells on hematopoietic depression in chemotherapy-treated mice, the mice were preinjected with 5-FU at a dosage of 150 mg/kg before implantation of NIH3T3-IL-6 cells. Fluorouracil 144-148 interleukin 6 Mus musculus 44-48 9508190-12 1998 CONCLUSION: Modulation of CDDP and 5-FU with IFNalpha as used in this study does not improve the RR or the median survival in patients with RMHNC. Fluorouracil 35-39 interferon alpha 1 Homo sapiens 45-53 9492838-3 1998 After the operation, 5-FU alone and low doses of CDDP and 5-FU were administered, but the level of serum CEA elevated and CT scanning showed multiple liver metastases. Fluorouracil 58-62 CEA cell adhesion molecule 3 Homo sapiens 105-108 9472799-2 1998 Analysis of cultures established with BM cells collected 2 and 4 days after 5-FU treatment (2d and 4d 5-FU BM, respectively) and stimulated with IL-3 + IL-6 and IL-3 + SCF resulted in the generation of samples highly enriched for colony-forming units granulocyte/macrophage (CFU-GMs). Fluorouracil 102-106 interleukin 3 Mus musculus 145-149 9463483-8 1998 FUra-mediated thymidylate synthase inhibition was accompanied by a 124-fold increase in total deoxyuridylate immunoreactivity and a 31-fold increase in dUTP pools, but the addition of IFN-alpha + gamma attenuated the accumulation. Fluorouracil 0-4 interferon alpha 1 Homo sapiens 184-193 9501824-9 1998 Although the myeloperoxidase and hydroxyproline content were significantly lower after 5-FU therapy (P < 0.01, compared with others), the clinical outcome was similar. Fluorouracil 87-91 myeloperoxidase Homo sapiens 13-28 9589033-3 1998 Modulation of 5-FU by methotrexate (MTX), trimetrexate (TMTX), interferon-alpha (IFN-alpha), leucovorin (LV), or N-(phosphonacetyl)-L-asparte acid (PALA) has produced higher response rates than those observed with 5-FU alone. Fluorouracil 14-18 interferon alpha 1 Homo sapiens 81-90 9463483-0 1998 Modulation of fluorouracil cytotoxicity by interferon-alpha and -gamma. Fluorouracil 14-26 interferon gamma Homo sapiens 43-70 9463483-4 1998 When cells were exposed to IFN-alpha + gamma and FUra, free FdUMP levels became detectable, whereas [3H]FUra-RNA incorporation decreased. Fluorouracil 104-108 interferon alpha 1 Homo sapiens 27-36 9457070-9 1998 Basic FGF promoted apoptosis and increased the rate of drug-induced cell death with both etoposide and 5-fluorouracil. Fluorouracil 103-117 fibroblast growth factor 2 Homo sapiens 6-9 9589033-6 1998 IFN-alpha has shown therapeutic efficiency when combined with 5-FU alone or with 5-FU and leucovorin, but latest studies with these combinations have shown increased toxicity. Fluorouracil 81-85 interferon alpha 1 Homo sapiens 0-9 9619746-2 1998 Interferon-alpha (IFNalpha) is a cytokine that is able to influence the pharmacodynamics of 5-fluorouracil (5FU) through a number of mechanisms. Fluorouracil 92-106 interferon alpha 1 Homo sapiens 18-26 9516963-6 1998 Data demonstrated p53-dependent sensitization (> or = 4-fold) to bleomycin, actinomycin D, and 5-fluorouracil and considerably less p53-dependence (< or = 2-fold) for doxorubicin, topotecan, etoposide, and cisplatin in Cl.#27 compared to an equivalent clone containing the pGRE5-EBV vector alone (VC#3). Fluorouracil 98-112 tumor protein p53 Homo sapiens 18-21 9619746-2 1998 Interferon-alpha (IFNalpha) is a cytokine that is able to influence the pharmacodynamics of 5-fluorouracil (5FU) through a number of mechanisms. Fluorouracil 108-111 interferon alpha 1 Homo sapiens 18-26 9392545-0 1997 Original p53 status predicts for pathological response in locally advanced breast cancer patients treated preoperatively with continuous infusion 5-fluorouracil and radiation therapy. Fluorouracil 146-160 tumor protein p53 Homo sapiens 9-12 10388104-11 1998 Gene modulation by IFN-&agr; or IFN-&bgr; of thymidine phosphorylase, an enzyme important in DNA synthesis, has been suggested to be the basis for enhancing 5-fluorouracil (5-FU) effectiveness in preclinical models and may augment effectiveness in adenocarcinomas. Fluorouracil 165-179 interferon alpha 1 Homo sapiens 19-22 10388104-11 1998 Gene modulation by IFN-&agr; or IFN-&bgr; of thymidine phosphorylase, an enzyme important in DNA synthesis, has been suggested to be the basis for enhancing 5-fluorouracil (5-FU) effectiveness in preclinical models and may augment effectiveness in adenocarcinomas. Fluorouracil 165-179 interferon alpha 1 Homo sapiens 36-39 10388104-11 1998 Gene modulation by IFN-&agr; or IFN-&bgr; of thymidine phosphorylase, an enzyme important in DNA synthesis, has been suggested to be the basis for enhancing 5-fluorouracil (5-FU) effectiveness in preclinical models and may augment effectiveness in adenocarcinomas. Fluorouracil 181-185 interferon alpha 1 Homo sapiens 19-22 10388104-11 1998 Gene modulation by IFN-&agr; or IFN-&bgr; of thymidine phosphorylase, an enzyme important in DNA synthesis, has been suggested to be the basis for enhancing 5-fluorouracil (5-FU) effectiveness in preclinical models and may augment effectiveness in adenocarcinomas. Fluorouracil 181-185 interferon alpha 1 Homo sapiens 36-39 9399677-7 1997 Resistance to 5-FU was accompanied by a 2-fold increase in thymidylate synthase activity and a substantially higher incorporation of thymidine in the presence of 5-FU, compared with parental PROb cells. Fluorouracil 14-18 thymidylate synthetase Rattus norvegicus 59-79 9479870-0 1997 A 13-24 C-terminal peptide related to PF4 accelerates hematopoietic recovery of progenitor cells in vivo in mice treated with 5-fluorouracil. Fluorouracil 126-140 platelet factor 4 Mus musculus 38-41 9687887-3 1998 We found high plasma levels of ET-1, a potent natural vasoconstrictor, in two patients who experienced two of the commonest clinical manifestations of 5-FU-induced cardiac toxicity--i.e., angina pectoris and chronic heart failure. Fluorouracil 151-155 endothelin 1 Homo sapiens 31-35 9687887-5 1998 Finally, another important question still remains unresolved: is the release of ET-1 from normal coronary endothelial cells the prime cause or simply the consequence of 5-FU-related cardiotoxicity? Fluorouracil 169-173 endothelin 1 Homo sapiens 80-84 9479870-2 1997 In addition, PF4 accelerated the recovery of the marrow precursor cells in 5-fluorouracil (5-FU) treated mice. Fluorouracil 75-89 platelet factor 4 Mus musculus 13-16 9479870-2 1997 In addition, PF4 accelerated the recovery of the marrow precursor cells in 5-fluorouracil (5-FU) treated mice. Fluorouracil 91-95 platelet factor 4 Mus musculus 13-16 9479870-5 1997 These data indicate that the C13-24DE peptide related to PF4 accelerated the in vivo recovery of stem cells, progenitors (CFU-GM, CFU-MK) and single MK after 5-FU treatment and may have a hemoprotective effect against chemotherapeutic agents. Fluorouracil 158-162 platelet factor 4 Mus musculus 57-60 9815814-1 1997 We have used pulsed-field gel electrophoresis to examine 5-fluorouracil (5FU)-induced DNA double-strand breaks (DSBs), both with and without modulation by IFN-alpha2a (IFNalpha), in HT29 human colon adenocarcinoma cells. Fluorouracil 57-71 interferon alpha 1 Homo sapiens 168-176 9331263-6 1997 Exposure to 5FU or MMC resulted in an initial significant increase (P < 0.05) in the production of TGFbeta and bFGF, with levels then decreasing toward those of controls. Fluorouracil 12-15 transforming growth factor beta 1 Homo sapiens 102-109 9331263-6 1997 Exposure to 5FU or MMC resulted in an initial significant increase (P < 0.05) in the production of TGFbeta and bFGF, with levels then decreasing toward those of controls. Fluorouracil 12-15 fibroblast growth factor 2 Homo sapiens 114-118 9242554-4 1997 In addition, Bcl-XL provided significantly greater cell viability than Bcl-2 against methotrexate, fluorouracil, and hydroxyurea, three S-phase specific agents. Fluorouracil 99-111 B cell leukemia/lymphoma 2 Mus musculus 71-76 9279352-8 1997 5-FU, CDDP and Leucovorin were administered, but the CEA level became more and more elevated. Fluorouracil 0-4 CEA cell adhesion molecule 3 Homo sapiens 53-56 9388485-5 1997 These results suggest that 5-FU has the capacity to induce apoptosis in COLO 201, resulting from the up-regulation of Bax; the apoptosis-inducing signal of 5-FU seems to be different from that of IFN-gamma. Fluorouracil 27-31 interferon gamma Homo sapiens 196-205 9570369-4 1997 In wt-p53 transfected cells, the expression of MDRI gene was significantly increased, accumulation of adriamycin (ADM) was decreased, and the sensitivity to vincristine (VCR), ADM and 5-fluorouracil (5-FU) was increased compared with the parent KBv200 cells. Fluorouracil 184-198 tumor protein p53 Homo sapiens 6-9 9570369-4 1997 In wt-p53 transfected cells, the expression of MDRI gene was significantly increased, accumulation of adriamycin (ADM) was decreased, and the sensitivity to vincristine (VCR), ADM and 5-fluorouracil (5-FU) was increased compared with the parent KBv200 cells. Fluorouracil 200-204 tumor protein p53 Homo sapiens 6-9 9362454-5 1997 Bak wt or Bak deltaBH3 were also able to abrogate the protective effect of Bcl-2 in cells expressing Bcl-2 and Bak wt or Bak deltaBH3 when challenged by etoposide or fluorouracil. Fluorouracil 166-178 B cell leukemia/lymphoma 2 Mus musculus 75-80 9266952-0 1997 Ex vivo cytokine expansion of peripheral blood 5-fluorouracil-treated CD34-positive chronic myeloid leukaemia cells increases the selection of Ph-negative cells. Fluorouracil 47-61 CD34 molecule Homo sapiens 70-74 9266952-4 1997 CD34-positive (progenitor) cells from the peripheral blood (PB) of CML patients were pretreated with 5-fluorouracil (5FU) (5 microg/ml) to suppress Ph-positive cells and then grown in suspension culture for 7 d with a combination of cytokines. Fluorouracil 117-120 CD34 molecule Homo sapiens 0-4 9299183-4 1997 In the colon, the "toxicology" of 5 fluorouracil (5FU) is entirely dependent on p53, since p53 knockouts lose the pathology of 5FU damage. Fluorouracil 36-48 tumor protein p53 Homo sapiens 80-83 9299183-4 1997 In the colon, the "toxicology" of 5 fluorouracil (5FU) is entirely dependent on p53, since p53 knockouts lose the pathology of 5FU damage. Fluorouracil 36-48 tumor protein p53 Homo sapiens 91-94 9379509-5 1997 These results suggest that 5-fluorouracil alone can induce apoptosis in RPMI 4788 tumor cells and that this effect can be enhanced by combination with natural human tumor necrosis factor-alpha and natural human interferon-alpha. Fluorouracil 27-41 tumor necrosis factor Homo sapiens 165-192 9219846-1 1997 In tissue culture conditions, exogeneous active transforming growth factor-beta1 (TGF-beta1) enhances the lethal effect of DNA-damaging agents (UV-C, gamma rays, cisplatin, methotrexate and 5-fluorouracil) toward human A549 cells and mink Mv1Lu cells, as detected by the loss of their capacity to give rise to colonies; both these cell lines harbor a wild-type p53, as determined by immunoprecipitation. Fluorouracil 190-204 transforming growth factor beta 1 Homo sapiens 48-80 11596302-1 1997 Recent studies indicate that wild-type p53 can trigger cell apoptosis induced by many chemotherapeutic agents which induce DNA damage or cause disruptions of DNA metabolism, such as ADM, 5-FU, VP-16 and radiation. Fluorouracil 187-191 tumor protein p53 Homo sapiens 39-42 9219846-1 1997 In tissue culture conditions, exogeneous active transforming growth factor-beta1 (TGF-beta1) enhances the lethal effect of DNA-damaging agents (UV-C, gamma rays, cisplatin, methotrexate and 5-fluorouracil) toward human A549 cells and mink Mv1Lu cells, as detected by the loss of their capacity to give rise to colonies; both these cell lines harbor a wild-type p53, as determined by immunoprecipitation. Fluorouracil 190-204 transforming growth factor beta 1 Homo sapiens 82-91 9205078-2 1997 IGF-1 increased cell survival of HBL100 cells treated with 5-fluorouracil (antimetabolite), methotrexate (antimetabolite), tamoxifen (antiestrogen/antiproliferative), or camptothecin (topoisomerase 1 inhibitor) and after serum withdrawal. Fluorouracil 59-73 insulin like growth factor 1 Homo sapiens 0-5 9137428-3 1997 The administration of 5-Fu and CNG suppressed the production of IL-1 alpha and PGE2, and induced the production of IL-4 and IL-10 earlier than 5-Fu alone did. Fluorouracil 22-26 interleukin 10 Mus musculus 124-129 9815792-1 1997 The combination of IFN-alpha-2a (IFN-alpha) and IFN-gamma-1b (IFN-gamma) has been found to produce more than additive cytotoxicity with fluorouracil (5-FU) in HT 29 colon cancer cells due to enhanced DNA-directed effects. Fluorouracil 136-148 interferon alpha 1 Homo sapiens 19-28 9815792-1 1997 The combination of IFN-alpha-2a (IFN-alpha) and IFN-gamma-1b (IFN-gamma) has been found to produce more than additive cytotoxicity with fluorouracil (5-FU) in HT 29 colon cancer cells due to enhanced DNA-directed effects. Fluorouracil 136-148 interferon alpha 1 Homo sapiens 33-42 9815792-1 1997 The combination of IFN-alpha-2a (IFN-alpha) and IFN-gamma-1b (IFN-gamma) has been found to produce more than additive cytotoxicity with fluorouracil (5-FU) in HT 29 colon cancer cells due to enhanced DNA-directed effects. Fluorouracil 136-148 interferon gamma Homo sapiens 48-57 9815792-1 1997 The combination of IFN-alpha-2a (IFN-alpha) and IFN-gamma-1b (IFN-gamma) has been found to produce more than additive cytotoxicity with fluorouracil (5-FU) in HT 29 colon cancer cells due to enhanced DNA-directed effects. Fluorouracil 136-148 interferon gamma Homo sapiens 62-71 9815792-1 1997 The combination of IFN-alpha-2a (IFN-alpha) and IFN-gamma-1b (IFN-gamma) has been found to produce more than additive cytotoxicity with fluorouracil (5-FU) in HT 29 colon cancer cells due to enhanced DNA-directed effects. Fluorouracil 150-154 interferon alpha 1 Homo sapiens 19-28 9815792-1 1997 The combination of IFN-alpha-2a (IFN-alpha) and IFN-gamma-1b (IFN-gamma) has been found to produce more than additive cytotoxicity with fluorouracil (5-FU) in HT 29 colon cancer cells due to enhanced DNA-directed effects. Fluorouracil 150-154 interferon alpha 1 Homo sapiens 33-42 9815792-1 1997 The combination of IFN-alpha-2a (IFN-alpha) and IFN-gamma-1b (IFN-gamma) has been found to produce more than additive cytotoxicity with fluorouracil (5-FU) in HT 29 colon cancer cells due to enhanced DNA-directed effects. Fluorouracil 150-154 interferon gamma Homo sapiens 48-57 9815792-1 1997 The combination of IFN-alpha-2a (IFN-alpha) and IFN-gamma-1b (IFN-gamma) has been found to produce more than additive cytotoxicity with fluorouracil (5-FU) in HT 29 colon cancer cells due to enhanced DNA-directed effects. Fluorouracil 150-154 interferon gamma Homo sapiens 62-71 9815792-9 1997 5-FU clearance was higher in 14 cycles with IFN-gamma compared to the patient"s prior cycle with the same doses of 5-FU/LV/IFN-alpha: 798 +/- 309 versus 601 +/- 250 ml/min/m2 (mean +/- SD; P = 0.04). Fluorouracil 0-4 interferon gamma Homo sapiens 44-53 9815792-9 1997 5-FU clearance was higher in 14 cycles with IFN-gamma compared to the patient"s prior cycle with the same doses of 5-FU/LV/IFN-alpha: 798 +/- 309 versus 601 +/- 250 ml/min/m2 (mean +/- SD; P = 0.04). Fluorouracil 0-4 interferon alpha 1 Homo sapiens 123-132 9815792-15 1997 Compared to our previous experience with 5-FU/LV/IFN-alpha, IFN-gamma and IFN-alpha appeared to have opposite effects on 5-FU clearance. Fluorouracil 121-125 interferon gamma Homo sapiens 60-69 9815792-15 1997 Compared to our previous experience with 5-FU/LV/IFN-alpha, IFN-gamma and IFN-alpha appeared to have opposite effects on 5-FU clearance. Fluorouracil 121-125 interferon alpha 1 Homo sapiens 74-83 9192825-11 1997 Treatment of cells with 5-FU increased p53 protein levels, whereas sulindac metabolites did not induce expression. Fluorouracil 24-28 tumor protein p53 Homo sapiens 39-42 9238541-2 1997 In this report, we show that 5-Fluorouracil increases the Interleukin-1 expression upto 2.66 folds without significantly affecting the levels of surface expression of p55 IL-2 receptor on human Peripheral blood mononuclear cells, CD4 and CD8 T cells. Fluorouracil 29-43 CD4 molecule Homo sapiens 230-233 9238541-4 1997 In earlier studies we have shown that 5-fluorouracil increases the IL-2 expression both at mRNA and protein levels. Fluorouracil 38-52 interleukin 2 Homo sapiens 67-71 9238541-5 1997 Taken together, 5-fluorouracil differentially affects the expression of Interleukin-1, Interferon-gamma and Interleukin-2 receptor. Fluorouracil 16-30 interferon gamma Homo sapiens 87-103 9552441-2 1997 Two different molecular weight polymers of L-PLA [L-PLA1 (152,500 Da) and L-PLA2 (52,000 Da)] were used to prepare 5-FU-loaded microspheres. Fluorouracil 115-119 phospholipase A2 group IB Homo sapiens 76-80 9057636-0 1997 Transgenic mice overexpressing human c-mpl ligand exhibit chronic thrombocytosis and display enhanced recovery from 5-fluorouracil or antiplatelet serum treatment. Fluorouracil 116-130 thrombopoietin Homo sapiens 37-49 9248088-4 1997 More recently, the prognostic role of biological parameters such as p53 gene or enzymes implicated in 5-fluorouracil metabolisms has been identified. Fluorouracil 102-116 tumor protein p53 Homo sapiens 68-71 9209521-6 1997 There was an inverse relationship between bcl-2 oncoprotein expression and apoptosis in 5-FU-treated patients, but no significant correlation between histological effect and apoptosis. Fluorouracil 88-92 BCL2 apoptosis regulator Homo sapiens 42-47 9209521-8 1997 CONCLUSIONS: Apoptosis may be induced by 5-FU administered preoperatively and bcl-2 oncogene expression may suppress 5-FU-induced apoptosis. Fluorouracil 117-121 BCL2 apoptosis regulator Homo sapiens 78-83 9092685-3 1997 The finding that endogenous IL-6 levels in serum increased after 5-fluorouracil (5-FU) treatment suggests that IL-6 may play some role in the recovery of hematopoietic systems. Fluorouracil 65-79 interleukin 6 Homo sapiens 28-32 9092685-3 1997 The finding that endogenous IL-6 levels in serum increased after 5-fluorouracil (5-FU) treatment suggests that IL-6 may play some role in the recovery of hematopoietic systems. Fluorouracil 65-79 interleukin 6 Homo sapiens 111-115 9092685-3 1997 The finding that endogenous IL-6 levels in serum increased after 5-fluorouracil (5-FU) treatment suggests that IL-6 may play some role in the recovery of hematopoietic systems. Fluorouracil 81-85 interleukin 6 Homo sapiens 28-32 9092685-3 1997 The finding that endogenous IL-6 levels in serum increased after 5-fluorouracil (5-FU) treatment suggests that IL-6 may play some role in the recovery of hematopoietic systems. Fluorouracil 81-85 interleukin 6 Homo sapiens 111-115 9140762-1 1997 A high-performance liquid chromatography (HPLC) and gas chromatography-negative ion chemical ionization mass spectrometry (GC-NICI-MS) method was developed for the analysis of the combined antitumor drug S-1 (tegafur, 5-chloro-2,4-dihydroxypyridine and potassium oxonate) and active metabolite 5-fluorouracil in human plasma and urine. Fluorouracil 294-308 proteasome 26S subunit, non-ATPase 1 Homo sapiens 204-207 9070485-2 1997 UNLABELLED: BACKGROUND; The rationale for the modulation of 5-fluorouracil (5-FU) with interferon-alpha (IFN) is inhibition of 5-FU catabolism and 5-FU resistance. Fluorouracil 60-74 interferon alpha 1 Homo sapiens 87-109 9070485-2 1997 UNLABELLED: BACKGROUND; The rationale for the modulation of 5-fluorouracil (5-FU) with interferon-alpha (IFN) is inhibition of 5-FU catabolism and 5-FU resistance. Fluorouracil 76-80 interferon alpha 1 Homo sapiens 87-109 9070485-2 1997 UNLABELLED: BACKGROUND; The rationale for the modulation of 5-fluorouracil (5-FU) with interferon-alpha (IFN) is inhibition of 5-FU catabolism and 5-FU resistance. Fluorouracil 127-131 interferon alpha 1 Homo sapiens 87-109 9070485-2 1997 UNLABELLED: BACKGROUND; The rationale for the modulation of 5-fluorouracil (5-FU) with interferon-alpha (IFN) is inhibition of 5-FU catabolism and 5-FU resistance. Fluorouracil 127-131 interferon alpha 1 Homo sapiens 87-109 9070485-3 1997 Clinical trials have shown debatable results when IFN is given in high doses with 5-FU used as a bolus alone or in combination with leucovorin (LV). Fluorouracil 82-86 interferon alpha 1 Homo sapiens 50-53 9070485-11 1997 However, as in other schedules of LV and 5-FU, IFN induces high grade toxicity. Fluorouracil 41-45 interferon alpha 1 Homo sapiens 47-50 9155534-1 1997 The antiproliferative effect of 5-fluorouracil (5-FU) in colon cancer can be enhanced by interferons (IFN-alpha and IFN-gamma). Fluorouracil 32-46 interferon alpha 1 Homo sapiens 102-111 9155534-1 1997 The antiproliferative effect of 5-fluorouracil (5-FU) in colon cancer can be enhanced by interferons (IFN-alpha and IFN-gamma). Fluorouracil 32-46 interferon gamma Homo sapiens 116-125 9155534-1 1997 The antiproliferative effect of 5-fluorouracil (5-FU) in colon cancer can be enhanced by interferons (IFN-alpha and IFN-gamma). Fluorouracil 48-52 interferon alpha 1 Homo sapiens 102-111 9155534-1 1997 The antiproliferative effect of 5-fluorouracil (5-FU) in colon cancer can be enhanced by interferons (IFN-alpha and IFN-gamma). Fluorouracil 48-52 interferon gamma Homo sapiens 116-125 9155534-3 1997 IFN-alpha may elevate the levels of the active 5-FU metabolite 5-fluoro-2"-deoxyuridine-5"-monophosphate (FdUMP) in the cell, possibly leading to increased inhibition of the target enzyme thymidylate synthase (TS), which might enhance DNA damage. Fluorouracil 47-51 interferon alpha 1 Homo sapiens 0-9 9155534-4 1997 It has been shown that IFN-gamma can prevent 5-FU induced overexpression of TS. Fluorouracil 45-49 interferon gamma Homo sapiens 23-32 9155534-6 1997 A 1.5-fold increase in 5-FU sensitivity was observed in C26-10 and C26-10/F (by murine IFN-alpha, beta); in SW948, WiDr and WiDr/F (by human IFN-gamma) and in SW948 and WiDr/ F (by human IFN-alpha). Fluorouracil 23-27 interferon gamma Homo sapiens 141-150 9155534-6 1997 A 1.5-fold increase in 5-FU sensitivity was observed in C26-10 and C26-10/F (by murine IFN-alpha, beta); in SW948, WiDr and WiDr/F (by human IFN-gamma) and in SW948 and WiDr/ F (by human IFN-alpha). Fluorouracil 23-27 interferon alpha 1 Homo sapiens 187-196 9155534-11 1997 Human IFN-alpha alone caused minimal DNA damage (95% dss DNA), but increased 5-FU-induced effects to 35-50% dss DNA. Fluorouracil 77-81 interferon alpha 1 Homo sapiens 6-15 9155534-14 1997 It is concluded that one of the mechanisms involved in modulation of 5-FU activity is the effect of IFN-alpha on 5-FU-mediated DNA damage, but for IFN-gamma no mechanism of action was found. Fluorouracil 69-73 interferon alpha 1 Homo sapiens 100-109 9155534-14 1997 It is concluded that one of the mechanisms involved in modulation of 5-FU activity is the effect of IFN-alpha on 5-FU-mediated DNA damage, but for IFN-gamma no mechanism of action was found. Fluorouracil 113-117 interferon alpha 1 Homo sapiens 100-109 9137428-8 1997 These results indicate that CNG modulates inflammatory responses induced by 5-Fu through production of anti-inflammatory cytokines such as IL-4 and IL-10. Fluorouracil 76-80 interleukin 10 Mus musculus 148-153 9020295-1 1997 Previous laboratory and clinical studies support the ability of interferon (IFN) to enhance the antitumor properties of chemotherapy agents, including cisplatin and 5-fluorouracil (5-FU). Fluorouracil 165-179 interferon alpha 1 Homo sapiens 64-74 9032231-8 1997 However, Bcl-2 also prevented apoptosis of these cells upon exposure to 5-fluorouracil and doxorubicin, which were also cytotoxic for control cells. Fluorouracil 72-86 B cell leukemia/lymphoma 2 Mus musculus 9-14 9110342-2 1997 HER2 overexpression has been linked to sensitivity and/or resistance to hormone therapy and chemotherapeutic regimens, including CMF (cyclophosphamide, methotrexate, and fluoruracil) and anthracyclines. Fluorouracil 170-181 erb-b2 receptor tyrosine kinase 2 Homo sapiens 0-4 9020295-1 1997 Previous laboratory and clinical studies support the ability of interferon (IFN) to enhance the antitumor properties of chemotherapy agents, including cisplatin and 5-fluorouracil (5-FU). Fluorouracil 165-179 interferon alpha 1 Homo sapiens 76-79 9020295-1 1997 Previous laboratory and clinical studies support the ability of interferon (IFN) to enhance the antitumor properties of chemotherapy agents, including cisplatin and 5-fluorouracil (5-FU). Fluorouracil 181-185 interferon alpha 1 Homo sapiens 64-74 9020295-1 1997 Previous laboratory and clinical studies support the ability of interferon (IFN) to enhance the antitumor properties of chemotherapy agents, including cisplatin and 5-fluorouracil (5-FU). Fluorouracil 181-185 interferon alpha 1 Homo sapiens 76-79 9020491-7 1997 In the group of patients receiving 5-fluorouracil-based chemotherapy bcl-2 expression did not influence response to chemotherapy; nor did it effect failure-free or overall survival. Fluorouracil 35-49 BCL2 apoptosis regulator Homo sapiens 69-74 14646558-0 1997 5-Fluorouracil (5-FU) induced apoptosis in gastric cancer cell lines: role of the p53 gene. Fluorouracil 0-14 tumor protein p53 Homo sapiens 82-85 14646558-0 1997 5-Fluorouracil (5-FU) induced apoptosis in gastric cancer cell lines: role of the p53 gene. Fluorouracil 16-20 tumor protein p53 Homo sapiens 82-85 14646558-1 1997 We examined chemosensitivity to 5-fluorouracil (5-FU) in four human gastric cancer cell lines, by analyzing the expression of p53 and its related genes. Fluorouracil 32-46 tumor protein p53 Homo sapiens 126-129 14646558-1 1997 We examined chemosensitivity to 5-fluorouracil (5-FU) in four human gastric cancer cell lines, by analyzing the expression of p53 and its related genes. Fluorouracil 48-52 tumor protein p53 Homo sapiens 126-129 14646558-4 1997 On the other hand, 50 microM 5-FU had little effect on the induction of apoptosis in MKN-74 cells, the value being approximately 2% after 72 h. Induction of P53 expression was noted 3 h after initiating the treatment, followed by the induction of P21/Waf1 after 6 h in both MKN-74 and MKN-45 cells. Fluorouracil 29-33 tumor protein p53 Homo sapiens 157-160 14646558-7 1997 The Bax/Bcl-2 expression ratio was gradually elevated for up to 72 h in MKN-74 and MKN-45 cells treated with 1mM 5-FU; in contrast, it was unchanged in MKN-28 and KATO-III cells, and MKN-74 treated with 50 microM 5-FU. Fluorouracil 113-117 BCL2 associated X, apoptosis regulator Homo sapiens 4-7 14646558-7 1997 The Bax/Bcl-2 expression ratio was gradually elevated for up to 72 h in MKN-74 and MKN-45 cells treated with 1mM 5-FU; in contrast, it was unchanged in MKN-28 and KATO-III cells, and MKN-74 treated with 50 microM 5-FU. Fluorouracil 113-117 BCL2 apoptosis regulator Homo sapiens 8-13 14646558-7 1997 The Bax/Bcl-2 expression ratio was gradually elevated for up to 72 h in MKN-74 and MKN-45 cells treated with 1mM 5-FU; in contrast, it was unchanged in MKN-28 and KATO-III cells, and MKN-74 treated with 50 microM 5-FU. Fluorouracil 213-217 BCL2 associated X, apoptosis regulator Homo sapiens 4-7 14646558-7 1997 The Bax/Bcl-2 expression ratio was gradually elevated for up to 72 h in MKN-74 and MKN-45 cells treated with 1mM 5-FU; in contrast, it was unchanged in MKN-28 and KATO-III cells, and MKN-74 treated with 50 microM 5-FU. Fluorouracil 213-217 BCL2 apoptosis regulator Homo sapiens 8-13 14646558-8 1997 These results might indicate that (1) 1mM 5-FU induces apoptosis in cultured gastric cancer cells carrying the wild-type p53 gene, but not those carrying the mutated type or a gene deletion, and (2) the elevated Bax/Bcl-2 expression ratio plays a more crucial role than the higher expression of P21/Waf1 in the induction of p53- gene dependent apoptosis. Fluorouracil 42-46 tumor protein p53 Homo sapiens 121-124 14646558-8 1997 These results might indicate that (1) 1mM 5-FU induces apoptosis in cultured gastric cancer cells carrying the wild-type p53 gene, but not those carrying the mutated type or a gene deletion, and (2) the elevated Bax/Bcl-2 expression ratio plays a more crucial role than the higher expression of P21/Waf1 in the induction of p53- gene dependent apoptosis. Fluorouracil 42-46 BCL2 associated X, apoptosis regulator Homo sapiens 212-215 14646558-8 1997 These results might indicate that (1) 1mM 5-FU induces apoptosis in cultured gastric cancer cells carrying the wild-type p53 gene, but not those carrying the mutated type or a gene deletion, and (2) the elevated Bax/Bcl-2 expression ratio plays a more crucial role than the higher expression of P21/Waf1 in the induction of p53- gene dependent apoptosis. Fluorouracil 42-46 BCL2 apoptosis regulator Homo sapiens 216-221 14646558-8 1997 These results might indicate that (1) 1mM 5-FU induces apoptosis in cultured gastric cancer cells carrying the wild-type p53 gene, but not those carrying the mutated type or a gene deletion, and (2) the elevated Bax/Bcl-2 expression ratio plays a more crucial role than the higher expression of P21/Waf1 in the induction of p53- gene dependent apoptosis. Fluorouracil 42-46 cyclin dependent kinase inhibitor 1A Homo sapiens 295-298 14646558-8 1997 These results might indicate that (1) 1mM 5-FU induces apoptosis in cultured gastric cancer cells carrying the wild-type p53 gene, but not those carrying the mutated type or a gene deletion, and (2) the elevated Bax/Bcl-2 expression ratio plays a more crucial role than the higher expression of P21/Waf1 in the induction of p53- gene dependent apoptosis. Fluorouracil 42-46 cyclin dependent kinase inhibitor 1A Homo sapiens 299-303 14646558-8 1997 These results might indicate that (1) 1mM 5-FU induces apoptosis in cultured gastric cancer cells carrying the wild-type p53 gene, but not those carrying the mutated type or a gene deletion, and (2) the elevated Bax/Bcl-2 expression ratio plays a more crucial role than the higher expression of P21/Waf1 in the induction of p53- gene dependent apoptosis. Fluorouracil 42-46 tumor protein p53 Homo sapiens 324-327 9020491-3 1997 We analysed bcl-2 expression in 231 colorectal tumours from patients that were treated by surgery alone or with 5-fluorouracil-based chemotherapy. Fluorouracil 112-126 BCL2 apoptosis regulator Homo sapiens 12-17 9020952-3 1997 After arterial infusion chemotherapy consisting of CDDP, epirubicin and 5-FU, the tumor size and serum level of CEA were significantly decreased. Fluorouracil 72-76 CEA cell adhesion molecule 3 Homo sapiens 112-115 9116319-2 1997 The de novo p-gp expression rate was 26% and increased up to 58% (p = 0.03) with the FAC (5-fluorouracil, adriamycin, cyclophosphamide) regimen. Fluorouracil 90-104 ATP binding cassette subfamily B member 1 Homo sapiens 12-16 9547673-9 1997 In contrast with [14C]Adriamycin and [3H] vincristine uptake, [3H] 5-fluorouracil uptake by the cells was unaffected by TPA and reduced by the PKC-inhibitory peptides. Fluorouracil 67-81 protein kinase C alpha Homo sapiens 143-146 8996200-2 1997 We studied the effects of TPA on interleukin-3 (IL-3)-dependent colony formation of mouse bone marrow cells from mice injected with 5-fluorouracil 2 days before examination in order to clarify the significance of PKC in the proliferation of primitive hematopoietic progenitors. Fluorouracil 132-146 interleukin 3 Mus musculus 33-46 8996200-2 1997 We studied the effects of TPA on interleukin-3 (IL-3)-dependent colony formation of mouse bone marrow cells from mice injected with 5-fluorouracil 2 days before examination in order to clarify the significance of PKC in the proliferation of primitive hematopoietic progenitors. Fluorouracil 132-146 interleukin 3 Mus musculus 48-52 8996200-6 1997 Because TPA enhanced IL-3-dependent colony formation derived from lineage-negative marrow cells obtained from mice that received 5-FU 2 days before, it is possible that it might act directly on primitive progenitors. Fluorouracil 129-133 interleukin 3 Mus musculus 21-25 9268987-0 1997 Inhibition by 5-fluorouracil of ERCC1 and gamma-glutamylcysteine synthetase messenger RNA expression in a cisplatin-resistant HST-1 human squamous carcinoma cell line. Fluorouracil 14-28 fibroblast growth factor 4 Homo sapiens 126-131 9253112-4 1997 A strong correlation between the number of CFU-Mk and HPP-CFC formation from 5-fluorouracil bone marrow cells was observed when these cells were stimulated with EPO in the presence of SCF and IL-3. Fluorouracil 77-91 interleukin 3 Mus musculus 192-196 9031469-6 1997 MPEG-IL-6 significantly stimulated platelet recovery in mice treated with 5-fluorouracil, whereas the administration of native IL-6 had a negligible effect. Fluorouracil 74-88 interleukin 6 Mus musculus 5-9 8980242-4 1996 The probability of clinical response to biochemically modulated 5-FU was independent of p53 and PCNA expression. Fluorouracil 64-68 tumor protein p53 Homo sapiens 88-91 8931668-2 1996 Evidence suggests that interferon-alpha (IFN-alpha) augments the antineoplastic activity of 5-fluorouracil (5-FU) in human adenocarcinoma cell lines in vitro and may enhance the efficacy of 5-FU in patients with advanced colorectal carcinoma. Fluorouracil 92-106 interferon alpha 1 Homo sapiens 41-50 8931668-2 1996 Evidence suggests that interferon-alpha (IFN-alpha) augments the antineoplastic activity of 5-fluorouracil (5-FU) in human adenocarcinoma cell lines in vitro and may enhance the efficacy of 5-FU in patients with advanced colorectal carcinoma. Fluorouracil 108-112 interferon alpha 1 Homo sapiens 41-50 8931668-2 1996 Evidence suggests that interferon-alpha (IFN-alpha) augments the antineoplastic activity of 5-fluorouracil (5-FU) in human adenocarcinoma cell lines in vitro and may enhance the efficacy of 5-FU in patients with advanced colorectal carcinoma. Fluorouracil 190-194 interferon alpha 1 Homo sapiens 41-50 21541641-4 1996 Increased p53 protein levels have previously been shown to correlate with disease progression in a series of colorectal carcinoma patients treated with 5-FU/folinic acid biomodulated chemotherapy. Fluorouracil 152-156 tumor protein p53 Homo sapiens 10-13 8968385-1 1996 Previous studies showed that 5-fluorouracil (5-FU) is capable of enhancing the membrane reactivity of the human colon carcinoma cell line HT-29 with a monoclonal antibody (COL-1) directed against carcinoembryonic antigen (CEA). Fluorouracil 29-43 CEA cell adhesion molecule 3 Homo sapiens 196-220 8968385-1 1996 Previous studies showed that 5-fluorouracil (5-FU) is capable of enhancing the membrane reactivity of the human colon carcinoma cell line HT-29 with a monoclonal antibody (COL-1) directed against carcinoembryonic antigen (CEA). Fluorouracil 29-43 CEA cell adhesion molecule 3 Homo sapiens 222-225 8968385-1 1996 Previous studies showed that 5-fluorouracil (5-FU) is capable of enhancing the membrane reactivity of the human colon carcinoma cell line HT-29 with a monoclonal antibody (COL-1) directed against carcinoembryonic antigen (CEA). Fluorouracil 45-49 CEA cell adhesion molecule 3 Homo sapiens 196-220 8968385-1 1996 Previous studies showed that 5-fluorouracil (5-FU) is capable of enhancing the membrane reactivity of the human colon carcinoma cell line HT-29 with a monoclonal antibody (COL-1) directed against carcinoembryonic antigen (CEA). Fluorouracil 45-49 CEA cell adhesion molecule 3 Homo sapiens 222-225 8968385-2 1996 In the present study, we show that short-term exposure (i.e., 1 hr) of cancer cells to 5-FU mediates a marked increase of CEA expression, that is concentration-dependent and lasts up to day 5 after treatment. Fluorouracil 87-91 CEA cell adhesion molecule 3 Homo sapiens 122-125 8968385-4 1996 This is supported by the finding that the increase of the CEA expression detected by cytofluorimetric analysis is observed not only in the parental HT-29 line, but also in its C22.20 subclone, endowed with a low basal level of CEA and with chemosensitivity to 5-FU lower than that of the parental cell line. Fluorouracil 260-264 CEA cell adhesion molecule 3 Homo sapiens 58-61 8968385-6 1996 Northern blot analysis of total RNA extracted from 5-FU-treated HT-29 or C22.20 cells shows an increase in the steady-state levels of CEA and CEA-related transcripts (e.g., biliary glycoprotein). Fluorouracil 51-55 carcinoembryonic antigen gene family Mus musculus 134-137 8968385-6 1996 Northern blot analysis of total RNA extracted from 5-FU-treated HT-29 or C22.20 cells shows an increase in the steady-state levels of CEA and CEA-related transcripts (e.g., biliary glycoprotein). Fluorouracil 51-55 CEA cell adhesion molecule 3 Homo sapiens 142-145 8968385-7 1996 Moreover 5-FU-mediated augmentation of the CEA transcript appears to be attributable mainly to enhanced transcription rather than to increased mRNA stability. Fluorouracil 9-13 CEA cell adhesion molecule 3 Homo sapiens 43-46 8968385-8 1996 It is concluded that induction of enhanced CEA protein expression in cancer cells treated with 5-FU could be of clinical interest for the development of immunochemotherapeutic protocols based on CEA protein as the target molecule. Fluorouracil 95-99 CEA cell adhesion molecule 3 Homo sapiens 43-46 8968385-8 1996 It is concluded that induction of enhanced CEA protein expression in cancer cells treated with 5-FU could be of clinical interest for the development of immunochemotherapeutic protocols based on CEA protein as the target molecule. Fluorouracil 95-99 CEA cell adhesion molecule 3 Homo sapiens 195-198 9021668-1 1996 S-1 is a new antineoplastic agent of a fluorinated pyrimidine derivative containing tegafur (FT), 5-chloro-2,4-dihydroxypyridine (CDHP) and potassium oxonate (Oxo) in a molar ratio of 1:0.4:1 with the aim of prolonging the effective plasma concentration of 5-fluorouracil (5-FU) and reducing its dose-limiting gastrointestinal toxicity. Fluorouracil 257-271 proteasome 26S subunit, non-ATPase 1 Homo sapiens 0-3 9021668-1 1996 S-1 is a new antineoplastic agent of a fluorinated pyrimidine derivative containing tegafur (FT), 5-chloro-2,4-dihydroxypyridine (CDHP) and potassium oxonate (Oxo) in a molar ratio of 1:0.4:1 with the aim of prolonging the effective plasma concentration of 5-fluorouracil (5-FU) and reducing its dose-limiting gastrointestinal toxicity. Fluorouracil 273-277 proteasome 26S subunit, non-ATPase 1 Homo sapiens 0-3 9816112-6 1996 However, we find that the induction of wild-type p53 powerfully potentiates the cytotoxicity of both irradiation and 5-fluorouracil, two agents that are used clinically in the treatment of colorectal cancer. Fluorouracil 117-131 tumor protein p53 Homo sapiens 49-52 21541578-1 1996 We investigated whether carcinoembryonic antigen (CEA) could be used to predict the response and survival of patients treated with 5-FU. Fluorouracil 131-135 CEA cell adhesion molecule 3 Homo sapiens 24-48 21541578-1 1996 We investigated whether carcinoembryonic antigen (CEA) could be used to predict the response and survival of patients treated with 5-FU. Fluorouracil 131-135 CEA cell adhesion molecule 3 Homo sapiens 50-53 8874326-7 1996 CONCLUSION: The combination IFN/5-FU produced a response rate, response duration, and survival duration similar to that of 5-FU alone. Fluorouracil 123-127 interferon alpha 1 Homo sapiens 28-31 8795571-1 1996 We assessed the cytotoxic interaction between paclitaxel and 5-fluorouracil administered at various schedules against four human carcinoma cell lines, A549, MCF7, PA1 and WiDr. Fluorouracil 61-75 PAXIP1 associated glutamate rich protein 1 Homo sapiens 163-166 8795571-9 1996 Sequential exposure to 5-fluorouracil followed by paclitaxel showed subadditive effects in A549, MCF7 and PA1 cells. Fluorouracil 23-37 PAXIP1 associated glutamate rich protein 1 Homo sapiens 106-109 8795571-12 1996 Interestingly, the continuous (5-day) exposure to paclitaxel and 5-fluorouracil had additive effects in A549, PA1 and WiDr cells, indicating that the prolonged simultaneous administration of these agents may circumvent the antagonistic interaction produced by short-term simultaneous administration. Fluorouracil 65-79 PAXIP1 associated glutamate rich protein 1 Homo sapiens 110-113 8887054-1 1996 We have demonstrated previously that interferon-gamma (IFN-gamma) accelerates platelet recovery in mice with 5-FU induced-marrow aplasia in vivo. Fluorouracil 109-113 interferon gamma Mus musculus 37-53 8887054-1 1996 We have demonstrated previously that interferon-gamma (IFN-gamma) accelerates platelet recovery in mice with 5-FU induced-marrow aplasia in vivo. Fluorouracil 109-113 interferon gamma Mus musculus 55-64 8759880-5 1996 TPO in combination with the ligand for c-kit (SF) or interleukin-3 (IL-3) supported colony formation by marrow cells of 5-fluorouracil (5-FU)-treated mice whereas TPO alone yielded no colony. Fluorouracil 120-134 interleukin 3 Mus musculus 53-66 8759880-5 1996 TPO in combination with the ligand for c-kit (SF) or interleukin-3 (IL-3) supported colony formation by marrow cells of 5-fluorouracil (5-FU)-treated mice whereas TPO alone yielded no colony. Fluorouracil 120-134 interleukin 3 Mus musculus 68-72 8759880-5 1996 TPO in combination with the ligand for c-kit (SF) or interleukin-3 (IL-3) supported colony formation by marrow cells of 5-fluorouracil (5-FU)-treated mice whereas TPO alone yielded no colony. Fluorouracil 136-140 interleukin 3 Mus musculus 68-72 8911121-0 1996 Effect of regional angiotensin II infusion on the relationship between tumour blood flow and fluorouracil uptake in a liver metastasis animal model. Fluorouracil 93-105 angiotensinogen Homo sapiens 19-33 8911121-6 1996 There was a poor correlation (r = 0.51, P = 0.13) between tumour:liver blood flow and 5-FU uptake ratios with angiotensin II infusion. Fluorouracil 86-90 angiotensinogen Homo sapiens 110-124 8712699-1 1996 This study was performed to investigate the direct effects of recombinant human tumor necrosis factor (rH-TNF) and recombinant human interleukin-2 (rH-IL-2), either alone or in combination, on the cytotoxicity of 5-FU measured by MTT assay against human gastric adenocarcinoma cell lines (MKN-28 and MKN-45), and also to determine the optimal schedule for their combination. Fluorouracil 213-217 interleukin 2 Homo sapiens 133-146 9414406-3 1996 Therefore, in this study we determined the effect of downregulating PKC alpha expression by transfecting human colon carcinoma cells with an antisense PKC alpha expression vector and then determined the sensitivity of these cells to the anticancer drugs mitomycin C (MMC), 5-fluorouracil (5-FU) and vincristine (Vin). Fluorouracil 273-287 protein kinase C alpha Homo sapiens 68-77 9414406-3 1996 Therefore, in this study we determined the effect of downregulating PKC alpha expression by transfecting human colon carcinoma cells with an antisense PKC alpha expression vector and then determined the sensitivity of these cells to the anticancer drugs mitomycin C (MMC), 5-fluorouracil (5-FU) and vincristine (Vin). Fluorouracil 289-293 protein kinase C alpha Homo sapiens 68-77 9414406-4 1996 Transiently transfecting the human colon carcinoma cell lines Moser, SW480 and HT29 with antisense PKC alpha expression vector (but not antisense PKC beta expression vector) consistently increased the sensitivity of these cells to MMC, 5-FU and VIN by several-fold. Fluorouracil 236-240 protein kinase C alpha Homo sapiens 99-108 8807498-0 1996 IFN-gamma in combination with IL-3 accelerates platelet recovery in mice with 5-fluorouracil-induced marrow aplasia. Fluorouracil 78-92 interleukin 3 Mus musculus 30-34 8689103-1 1996 OBJECTIVE: To confirm the activity and evaluate the toxicity of the combination of subcutaneous interferon-alpha (IFN-alpha) and interleukin-2 (IL-2) with intravenous 5-fluorouracil (5-FU) in patients with advanced and recurrent renal carcinoma and of performance status 0-2. Fluorouracil 167-181 interleukin 2 Homo sapiens 129-142 8689103-1 1996 OBJECTIVE: To confirm the activity and evaluate the toxicity of the combination of subcutaneous interferon-alpha (IFN-alpha) and interleukin-2 (IL-2) with intravenous 5-fluorouracil (5-FU) in patients with advanced and recurrent renal carcinoma and of performance status 0-2. Fluorouracil 167-181 interleukin 2 Homo sapiens 144-148 8697140-8 1996 Furthermore, the data presented are consistent with the hypothesis that IL-1 + M-CSF initially acts on a multilineage, 5-FU-resistant target cell and that IL-6 (and possibly IL-3 and GM-CSF) serves as a secondary cytokine further to enhance platelet production during rebound thrombopoiesis in the 5-FU-treated mouse. Fluorouracil 298-302 interleukin 6 Mus musculus 155-159 8758793-9 1996 Transfection with pDOR-erbB-neo rendered the cells significantly, more sensitive to chemotherapeutic drugs (5-fluorouracil, cisplatinum) than the parental cells. Fluorouracil 108-122 epidermal growth factor receptor Homo sapiens 23-27 8723027-0 1996 Modulation of the expression on constitutive rat hepatic cytochrome P450 isozymes by 5-fluorouracil. Fluorouracil 85-99 cytochrome P450, family 2, subfamily g, polypeptide 1 Rattus norvegicus 57-72 8723027-1 1996 The objective of this study was to determine the effects of 5-fluorouracil (5FU) on the expression of individual cytochrome P450 (CYP) isozymes in rat liver at the catalytic activity and apoprotein levels. Fluorouracil 60-74 cytochrome P450, family 2, subfamily g, polypeptide 1 Rattus norvegicus 113-128 8723027-1 1996 The objective of this study was to determine the effects of 5-fluorouracil (5FU) on the expression of individual cytochrome P450 (CYP) isozymes in rat liver at the catalytic activity and apoprotein levels. Fluorouracil 60-74 cytochrome P450, family 2, subfamily g, polypeptide 1 Rattus norvegicus 130-133 8723027-1 1996 The objective of this study was to determine the effects of 5-fluorouracil (5FU) on the expression of individual cytochrome P450 (CYP) isozymes in rat liver at the catalytic activity and apoprotein levels. Fluorouracil 76-79 cytochrome P450, family 2, subfamily g, polypeptide 1 Rattus norvegicus 113-128 8723027-1 1996 The objective of this study was to determine the effects of 5-fluorouracil (5FU) on the expression of individual cytochrome P450 (CYP) isozymes in rat liver at the catalytic activity and apoprotein levels. Fluorouracil 76-79 cytochrome P450, family 2, subfamily g, polypeptide 1 Rattus norvegicus 130-133 8723027-8 1996 Two days following 5FU exposure, CYP3A immunoreactive protein was increased compared with vehicle control; however, 7 days after treatment, both CYP3A immunoreactivity and catalytic activity (progesterone 6 beta-hydroxylase) were suppressed by 5FU. Fluorouracil 19-22 cytochrome P450, family 3, subfamily a, polypeptide 62 Rattus norvegicus 33-38 8554139-7 1996 The EGF receptor expression was reduced by 30% in cells treated with PYY/5-FU/leucovorin and by 45% in cells treated with BIM/5-FU/leucovorin as compared with control cells without treatment. Fluorouracil 73-77 peptide YY Homo sapiens 69-72 8823494-1 1996 Interferon (IFN) augments the anabolism of 5-fluorouracil (5FU) to its active metabolite, fluorodeoxyuridylate (FdUMP), which inhibits thymidylate synthase (TS). Fluorouracil 59-62 interferon alpha 1 Homo sapiens 0-10 8823494-1 1996 Interferon (IFN) augments the anabolism of 5-fluorouracil (5FU) to its active metabolite, fluorodeoxyuridylate (FdUMP), which inhibits thymidylate synthase (TS). Fluorouracil 59-62 interferon alpha 1 Homo sapiens 12-15 8823494-5 1996 The addition of IFN to 5FU resulted in greater depletion of dTTP levels over treatment with 5FU alone by up to fourfold, and markedly augmented the dATP/dTTP ratio. Fluorouracil 23-26 interferon alpha 1 Homo sapiens 16-19 8824349-1 1996 The ribonucleotide reductase inhibitor, hydroxyurea (HU), augments the cytotoxic effects of 5-fluorouracil (5FU) in vitro; both drugs are synergistic with interferon-alpha (IFN) in vitro. Fluorouracil 92-106 interferon alpha 1 Homo sapiens 173-176 8824349-1 1996 The ribonucleotide reductase inhibitor, hydroxyurea (HU), augments the cytotoxic effects of 5-fluorouracil (5FU) in vitro; both drugs are synergistic with interferon-alpha (IFN) in vitro. Fluorouracil 108-111 interferon alpha 1 Homo sapiens 173-176 8542939-0 1995 5-Fluorouracil-resistant CD34+ cell population from peripheral blood of CML patients contains BCR-ABL-negative progenitor cells. Fluorouracil 0-14 CD34 molecule Homo sapiens 25-29 8542939-3 1995 The CD34+ cells isolated from the PB of 12 CML patients in the chronic phase were treated with low doses (5 or 10 micrograms/mL) of 5-fluorouracil (5-FU). Fluorouracil 132-146 CD34 molecule Homo sapiens 4-8 8731973-6 1995 Moreover, incubation of CD34+ cells with PF 4 in liquid culture caused an increase in the number of both stem cell factor (SCF)-binding cells and CD34 antigen-bearing cells, and exhibited greater capacity to form MK colonies than control after the treatment of 5-FU. Fluorouracil 261-265 CD34 molecule Homo sapiens 24-28 8731973-7 1995 In vivo in mice, twice injections of PF 4 at 40 micrograms/kg with an interval of 6 h followed by one injection of 5-FU at 150 mg/kg resulted in a significant increase in the number of colony-forming cells with high proliferative potential (HPP-CFC) and colony-forming unit-megakaryocyte (CFU-MK) in bone marrow. Fluorouracil 115-119 platelet factor 4 Mus musculus 37-41 7563172-0 1995 Accumulation of p53 protein as a possible predictor of response to adjuvant combination chemotherapy with cyclophosphamide, methotrexate, fluorouracil, and prednisone for breast cancer. Fluorouracil 138-150 tumor protein p53 Homo sapiens 16-19 7634247-5 1995 IFN-alpha-induced protection of ACHN from lysis by IFN-alpha-activated NK cells weakened in the presence of 5FU at 0.2 microgram/ml. Fluorouracil 108-111 interferon alpha 1 Homo sapiens 0-9 7634247-5 1995 IFN-alpha-induced protection of ACHN from lysis by IFN-alpha-activated NK cells weakened in the presence of 5FU at 0.2 microgram/ml. Fluorouracil 108-111 interferon alpha 1 Homo sapiens 51-60 7795216-2 1995 Cells expressing Sca-1 but no lineage-specific or major histocompatibility complex (MHC) class II antigens (Lin-MHC II-Sca-1+) were enriched from 5-fluorouracil-pretreated bone marrow by Ficoll density-gradient and immunomagnetic sorting. Fluorouracil 146-160 histocompatibility-2, MHC Mus musculus 112-118 7611752-1 1995 The biomodulation (BM) of 5-fluorouracil (5-FU) by interferon (IFN) is reviewed both preclinically and clinically, stressing clinical relevance. Fluorouracil 26-40 interferon alpha 1 Homo sapiens 63-66 7611752-1 1995 The biomodulation (BM) of 5-fluorouracil (5-FU) by interferon (IFN) is reviewed both preclinically and clinically, stressing clinical relevance. Fluorouracil 42-46 interferon alpha 1 Homo sapiens 63-66 7611752-4 1995 However, extensive preclinical investigations have been performed very recently showing that IFN can enhance cytotoxic effects of 5-FU through various mechanisms, not only by increased anabolism of 5-FU to 5-fluoro 2"-deoxyuridine monophosphate (FdUMP) or 5-fluorouridine (FUR), inhibition of thymidine kinase activity, possible alternation of pharmacokinetics of 5-FU, but also by biological response modification. Fluorouracil 130-134 interferon alpha 1 Homo sapiens 93-96 7611752-4 1995 However, extensive preclinical investigations have been performed very recently showing that IFN can enhance cytotoxic effects of 5-FU through various mechanisms, not only by increased anabolism of 5-FU to 5-fluoro 2"-deoxyuridine monophosphate (FdUMP) or 5-fluorouridine (FUR), inhibition of thymidine kinase activity, possible alternation of pharmacokinetics of 5-FU, but also by biological response modification. Fluorouracil 198-202 interferon alpha 1 Homo sapiens 93-96 7611752-4 1995 However, extensive preclinical investigations have been performed very recently showing that IFN can enhance cytotoxic effects of 5-FU through various mechanisms, not only by increased anabolism of 5-FU to 5-fluoro 2"-deoxyuridine monophosphate (FdUMP) or 5-fluorouridine (FUR), inhibition of thymidine kinase activity, possible alternation of pharmacokinetics of 5-FU, but also by biological response modification. Fluorouracil 198-202 interferon alpha 1 Homo sapiens 93-96 7611752-9 1995 The role of biomodulating chemotherapy of 5-FU by IFN or IFN and LV must also be investigated in the field of head and neck cancers, esophageal cancer, biliary tract cancer, all of which are relatively sensitive to the effector of 5-FU. Fluorouracil 42-46 interferon alpha 1 Homo sapiens 50-53 7794002-5 1995 With re-elevated serum CEA level, subsequent intrahepatic arterial infusion of CDDP and 5-FU the nodule size reduced with normalization of the serum CEA level. Fluorouracil 88-92 CEA cell adhesion molecule 3 Homo sapiens 23-26 7759157-1 1995 5"-deoxy-5-fluorouridine (5"-FUdR) is a cytostatic that is biotransformed to 5-fluorouracil (5-FUra) by pyrimidine nucleoside phosphorylase (PyNPase), the expression of which is up-regulated by tumor necrosis factor alpha (TNF alpha), interleukin-1 alpha (IL-1 alpha) and interferon gamma (IFN gamma). Fluorouracil 77-91 tumor necrosis factor Mus musculus 194-221 7759157-1 1995 5"-deoxy-5-fluorouridine (5"-FUdR) is a cytostatic that is biotransformed to 5-fluorouracil (5-FUra) by pyrimidine nucleoside phosphorylase (PyNPase), the expression of which is up-regulated by tumor necrosis factor alpha (TNF alpha), interleukin-1 alpha (IL-1 alpha) and interferon gamma (IFN gamma). Fluorouracil 77-91 tumor necrosis factor Mus musculus 223-232 7759157-1 1995 5"-deoxy-5-fluorouridine (5"-FUdR) is a cytostatic that is biotransformed to 5-fluorouracil (5-FUra) by pyrimidine nucleoside phosphorylase (PyNPase), the expression of which is up-regulated by tumor necrosis factor alpha (TNF alpha), interleukin-1 alpha (IL-1 alpha) and interferon gamma (IFN gamma). Fluorouracil 77-91 interferon gamma Mus musculus 272-299 7759157-1 1995 5"-deoxy-5-fluorouridine (5"-FUdR) is a cytostatic that is biotransformed to 5-fluorouracil (5-FUra) by pyrimidine nucleoside phosphorylase (PyNPase), the expression of which is up-regulated by tumor necrosis factor alpha (TNF alpha), interleukin-1 alpha (IL-1 alpha) and interferon gamma (IFN gamma). Fluorouracil 93-99 tumor necrosis factor Mus musculus 194-221 7759157-1 1995 5"-deoxy-5-fluorouridine (5"-FUdR) is a cytostatic that is biotransformed to 5-fluorouracil (5-FUra) by pyrimidine nucleoside phosphorylase (PyNPase), the expression of which is up-regulated by tumor necrosis factor alpha (TNF alpha), interleukin-1 alpha (IL-1 alpha) and interferon gamma (IFN gamma). Fluorouracil 93-99 tumor necrosis factor Mus musculus 223-232 7759157-1 1995 5"-deoxy-5-fluorouridine (5"-FUdR) is a cytostatic that is biotransformed to 5-fluorouracil (5-FUra) by pyrimidine nucleoside phosphorylase (PyNPase), the expression of which is up-regulated by tumor necrosis factor alpha (TNF alpha), interleukin-1 alpha (IL-1 alpha) and interferon gamma (IFN gamma). Fluorouracil 93-99 interferon gamma Mus musculus 272-299 7669711-3 1995 Interferon-alpha (IFN) either alone or in combination with FA has also improved treatment results by modulating 5-FU activity. Fluorouracil 112-116 interferon alpha 1 Homo sapiens 18-21 8542509-1 1995 A case of primarily inoperable hepatoid adenocarcinoma of the stomach is reported, which, after chemotherapy with farmorubicin, 5-fluorouracil and leucovorin, showed an impressive regression resulting in an improvement of the overall condition of the patient and a decrease of the serum AFP level from initially 79.120 ng/ml to 3.728 ng/ml. Fluorouracil 128-142 alpha fetoprotein Homo sapiens 287-290 21556603-4 1995 Using a 4-channel microcalorimeter, it could be shown, that the combination of 5-FU with IFN-alpha-2a or IFN-alpha-2a plus IL-2 led to a significant reduction in thermal cell activity, compared with the addition of 5-FU on its own. Fluorouracil 215-219 interferon alpha 1 Homo sapiens 105-114 21556603-4 1995 Using a 4-channel microcalorimeter, it could be shown, that the combination of 5-FU with IFN-alpha-2a or IFN-alpha-2a plus IL-2 led to a significant reduction in thermal cell activity, compared with the addition of 5-FU on its own. Fluorouracil 215-219 interleukin 2 Homo sapiens 123-127 7850703-13 1995 CONCLUSIONS: The high response rate of this 5-FU/LV/IFN regimen holds true in a larger group of patients. Fluorouracil 44-48 interferon alpha 1 Homo sapiens 52-55 8542247-5 1995 Combination of 5-FU and IFN resulted in a significant increase of the AUC of 5-FU (80%) and the fictive initial concentration (C0, 65%) obviously caused by a reduction of 5-FU clearance by 50%. Fluorouracil 77-81 interferon alpha 1 Homo sapiens 24-27 8542247-5 1995 Combination of 5-FU and IFN resulted in a significant increase of the AUC of 5-FU (80%) and the fictive initial concentration (C0, 65%) obviously caused by a reduction of 5-FU clearance by 50%. Fluorouracil 77-81 interferon alpha 1 Homo sapiens 24-27 7532407-5 1995 The NF-kappa B binding activity was found to be enhanced in ACH2 cells exposed to 5-FU (but not in those exposed to 5-AZC) as assessed by the mobility shift assay using an oligonucleotide containing two NF-kappa B binding sites. Fluorouracil 82-86 nuclear factor kappa B subunit 1 Homo sapiens 4-14 7532407-5 1995 The NF-kappa B binding activity was found to be enhanced in ACH2 cells exposed to 5-FU (but not in those exposed to 5-AZC) as assessed by the mobility shift assay using an oligonucleotide containing two NF-kappa B binding sites. Fluorouracil 82-86 nuclear factor kappa B subunit 1 Homo sapiens 203-213 7720172-4 1995 A 5-FU/epi injectable gel was designed, providing drug release in vitro of 50% by approximately 4 h and of 80% by 24 h. The retention of 5-FU in RIF-1 mouse tumors was determined after intratumoral administration of 5-FU/epi gel or various combinations of the formulation components. Fluorouracil 137-141 replication timing regulatory factor 1 Mus musculus 145-150 7640050-0 1995 The effect of different routes of administration of 5-fluorouracil on thymidylate synthase inhibition in the rat. Fluorouracil 52-66 thymidylate synthetase Rattus norvegicus 70-90 7640050-5 1995 A pronounced inhibition of TS was observed 3 h after 5FU administration by all routes, but was followed by a recovery of TS activity within 24 and 48 h. Effects of 5FU on normal tissues were diverse. Fluorouracil 53-56 thymidylate synthetase Rattus norvegicus 27-29 7654318-3 1994 Using the phosphatase inhibitor okadaic acid (OA) or chemotherapeutic agents such as Taxol and 5"-fluorouracil, we found that bcl-2 can be phosphorylated. Fluorouracil 95-110 BCL2 apoptosis regulator Homo sapiens 126-131 7654318-8 1994 Treatment with the phosphatase inhibitor or with chemotherapeutic agents (Taxol, 5"-fluorouracil) led to severe apoptosis of these cells, along with hyperphosphorylation of bcl-2. Fluorouracil 81-96 BCL2 apoptosis regulator Homo sapiens 173-178 7847809-3 1994 The results show that: (a) IFN-alpha inhibited MNC and HT-29 cells by 13.4% and 32.9%, respectively; (b) 5-FU inhibited MNC and HT-29 cells by 54.7% and 87.0%, respectively; (c) IFN-alpha + 5-FU resulted in a stronger inhibition of HT-29 cells (i.e., 96.1%). Fluorouracil 105-109 interferon alpha 1 Homo sapiens 178-187 7847809-3 1994 The results show that: (a) IFN-alpha inhibited MNC and HT-29 cells by 13.4% and 32.9%, respectively; (b) 5-FU inhibited MNC and HT-29 cells by 54.7% and 87.0%, respectively; (c) IFN-alpha + 5-FU resulted in a stronger inhibition of HT-29 cells (i.e., 96.1%). Fluorouracil 190-194 interferon alpha 1 Homo sapiens 27-36 7847809-6 1994 Moreover, treatment with IFN-alpha, 5-FU or IFN-alpha + 5-FU resulted in a marked increase in the number of HT-29 cells positive for the CEA surface antigen. Fluorouracil 56-60 interferon alpha 1 Homo sapiens 25-34 7847809-6 1994 Moreover, treatment with IFN-alpha, 5-FU or IFN-alpha + 5-FU resulted in a marked increase in the number of HT-29 cells positive for the CEA surface antigen. Fluorouracil 56-60 interferon alpha 1 Homo sapiens 44-53 8077282-8 1994 When BM cells from mice given 5-fluorouracil were cocultured with FHC-4D2 cells under the limiting dilution condition, interleukin-3 (IL-3)-responsive CFU-GM were induced from immature hematopoietic progenitor cells that were otherwise unresponsive to IL-3. Fluorouracil 30-44 interleukin 3 Mus musculus 119-132 8077282-8 1994 When BM cells from mice given 5-fluorouracil were cocultured with FHC-4D2 cells under the limiting dilution condition, interleukin-3 (IL-3)-responsive CFU-GM were induced from immature hematopoietic progenitor cells that were otherwise unresponsive to IL-3. Fluorouracil 30-44 interleukin 3 Mus musculus 134-138 8077282-8 1994 When BM cells from mice given 5-fluorouracil were cocultured with FHC-4D2 cells under the limiting dilution condition, interleukin-3 (IL-3)-responsive CFU-GM were induced from immature hematopoietic progenitor cells that were otherwise unresponsive to IL-3. Fluorouracil 30-44 interleukin 3 Mus musculus 252-256 8064224-2 1994 Initial studies showed that whereas administration of TGF-beta 1 or TGF-beta 2 did not prevent death in normal mice treated with high doses of 5-fluorouracil (5-FU), those mice that received TGF-beta 2 did exhibit the beginning of a hematologic recovery by day 11 after administration of 5-FU, and were preferentially rescued by a suboptimal number of transplanted bone marrow cells. Fluorouracil 288-292 transforming growth factor, beta 2 Mus musculus 191-201 8064224-3 1994 Subsequently, it was found that the administration of TGF-beta 2 protected recovering progenitor cells from high concentrations of 5-FU in vitro. Fluorouracil 131-135 transforming growth factor, beta 2 Mus musculus 54-64 7812360-2 1994 Combining IFN-alpha with either IL-2 or 5-fluorouracil (5-FU) enhanced IFN-alpha activity. Fluorouracil 56-60 interferon alpha 1 Homo sapiens 71-80 8026229-1 1994 PURPOSE: To determine whether interferon: alpha 2b can improve results of 5-fluorouracil adjuvant treatment of Dukes C colorectal cancer patients, we compared the outcome of patients receiving a fluorouracil-interferon combination to that of historic controls treated with fluorouracil alone. Fluorouracil 74-88 interferon alpha 1 Homo sapiens 30-40 8026229-1 1994 PURPOSE: To determine whether interferon: alpha 2b can improve results of 5-fluorouracil adjuvant treatment of Dukes C colorectal cancer patients, we compared the outcome of patients receiving a fluorouracil-interferon combination to that of historic controls treated with fluorouracil alone. Fluorouracil 76-88 interferon alpha 1 Homo sapiens 30-40 8026229-2 1994 METHODS: Fifty-seven Dukes C colorectal cancer patients were given 5-fluorouracil-interferon-alpha 2b adjuvant treatment from October 1986 to September 1990. Fluorouracil 67-81 interferon alpha 1 Homo sapiens 82-92 7524887-6 1994 However, as well as showing inhibitory effects, IFN-gamma increased the number of pure and mixed megakaryocyte colonies formed by post-5-fluorouracil treated bone marrow cells and, moreover, the addition of IFN-gamma to culture containing stem cell factor resulted in a synergistic effect on the development of both primitive hematopoietic progenitors and mature populations. Fluorouracil 135-149 interferon gamma Homo sapiens 48-57 8192103-6 1994 In conclusion, our study demonstrates that IFN-alpha 2B at doses higher than 6 x 10(6) IU intramuscularly three times per week in the combination with 5-fluorouracil and folinic acid we used is too toxic for the majority of patients; this combination has moderate activity in metastatic colorectal cancer, although similar response rates have been reported, with less toxicity, with 5-fluorouracil plus folinic acid without IFN-alpha. Fluorouracil 151-165 interferon alpha 1 Homo sapiens 43-52 8192103-6 1994 In conclusion, our study demonstrates that IFN-alpha 2B at doses higher than 6 x 10(6) IU intramuscularly three times per week in the combination with 5-fluorouracil and folinic acid we used is too toxic for the majority of patients; this combination has moderate activity in metastatic colorectal cancer, although similar response rates have been reported, with less toxicity, with 5-fluorouracil plus folinic acid without IFN-alpha. Fluorouracil 383-397 interferon alpha 1 Homo sapiens 43-52 7908410-9 1994 CONCLUSIONS: There is a significant dose-response effect of adjuvant chemotherapy with cyclophosphamide, doxorubicin, and fluorouracil in patients with overexpression of c-erbB-2 but not in patients with no c-erbB-2 expression or minimal c-erbB-2 expression. Fluorouracil 122-134 erb-b2 receptor tyrosine kinase 2 Homo sapiens 170-178 7908410-9 1994 CONCLUSIONS: There is a significant dose-response effect of adjuvant chemotherapy with cyclophosphamide, doxorubicin, and fluorouracil in patients with overexpression of c-erbB-2 but not in patients with no c-erbB-2 expression or minimal c-erbB-2 expression. Fluorouracil 122-134 erb-b2 receptor tyrosine kinase 2 Homo sapiens 207-215 7908410-9 1994 CONCLUSIONS: There is a significant dose-response effect of adjuvant chemotherapy with cyclophosphamide, doxorubicin, and fluorouracil in patients with overexpression of c-erbB-2 but not in patients with no c-erbB-2 expression or minimal c-erbB-2 expression. Fluorouracil 122-134 erb-b2 receptor tyrosine kinase 2 Homo sapiens 207-215 8074466-1 1994 The modulating effect of recombinant human interferon alpha (IFN-alpha) on the antitumor efficacy of 5-fluorouracil (5-FU) against human carcinoma cell lines was investigated in vitro and in vivo. Fluorouracil 101-115 interferon alpha 1 Homo sapiens 43-70 8074466-1 1994 The modulating effect of recombinant human interferon alpha (IFN-alpha) on the antitumor efficacy of 5-fluorouracil (5-FU) against human carcinoma cell lines was investigated in vitro and in vivo. Fluorouracil 117-121 interferon alpha 1 Homo sapiens 43-70 7584078-7 1994 We have constructed a chimeric minigene consisting of the proximal ERBB2 promoter linked to the gene encoding cytosine deaminase, an enzyme that can deaminate the prodrug 5-fluorocytosine (5-FC) to form cytotoxic 5-fluorouracil (5-FU). Fluorouracil 213-227 erb-b2 receptor tyrosine kinase 2 Homo sapiens 67-72 7584078-7 1994 We have constructed a chimeric minigene consisting of the proximal ERBB2 promoter linked to the gene encoding cytosine deaminase, an enzyme that can deaminate the prodrug 5-fluorocytosine (5-FC) to form cytotoxic 5-fluorouracil (5-FU). Fluorouracil 229-233 erb-b2 receptor tyrosine kinase 2 Homo sapiens 67-72 8184423-5 1994 5-FU inhibits thymidylate synthetase (TS), resulting in inhibited growth of rapidly proliferating tissues. Fluorouracil 0-4 thymidylate synthetase Rattus norvegicus 14-36 8137250-1 1994 alpha-Interferon (IFN alpha) potentiates the cytotoxicity of 5-fluorouracil (FUra) in vitro, and the combination has clinical efficacy in advanced colorectal cancer. Fluorouracil 61-75 interferon alpha 1 Homo sapiens 0-27 8137250-1 1994 alpha-Interferon (IFN alpha) potentiates the cytotoxicity of 5-fluorouracil (FUra) in vitro, and the combination has clinical efficacy in advanced colorectal cancer. Fluorouracil 77-81 interferon alpha 1 Homo sapiens 0-27 8137250-10 1994 IFN alpha potentiated the cytotoxicity of FUra by 1.8-fold, and the combination of IFN alpha and PO-dUrd produced a 25-fold increase in the cytotoxicity of FUra. Fluorouracil 42-46 interferon alpha 1 Homo sapiens 0-9 8137250-10 1994 IFN alpha potentiated the cytotoxicity of FUra by 1.8-fold, and the combination of IFN alpha and PO-dUrd produced a 25-fold increase in the cytotoxicity of FUra. Fluorouracil 156-160 interferon alpha 1 Homo sapiens 83-92 8137250-12 1994 There was a significant correlation between the ability of a nucleoside and/or IFN alpha combination to increase thymine incorporation and to reduce the 50% inhibitory concentration for FUra. Fluorouracil 186-190 interferon alpha 1 Homo sapiens 79-88 8137250-13 1994 IFN alpha and PO-dUrd also potentiated the inhibition by FUra of thymidylate synthase activity. Fluorouracil 57-61 interferon alpha 1 Homo sapiens 0-9 8137250-14 1994 These findings suggest that the use of a deoxyribonucleoside to provide the rate limiting cosubstrate would complement the stimulation of TP by IFN alpha, and together they should further enhance the antitumor activity of FUra. Fluorouracil 222-226 interferon alpha 1 Homo sapiens 144-153 7516637-8 1994 The results appear to indicate that IFN-alpha modulation of a DDP, 5-FU combination induces an acceptable degree of toxicity. Fluorouracil 67-71 interferon alpha 1 Homo sapiens 36-45 8181904-9 1994 Therefore, the effects of the antitumor polysaccharide SPR-901 used in combination with 5-FU were augmented as compared with single drug use. Fluorouracil 88-92 sepiapterin reductase Mus musculus 55-58 8032955-0 1994 Alpha interferon, leucovorin, and 5-fluorouracil (ALF) in advanced cancer: results of a dose-finding study and evidence of activity in non-small cell lung cancer. Fluorouracil 34-48 general transcription factor IIA subunit 1 like Homo sapiens 50-53 7691392-0 1993 Low serum alpha-fetoprotein level in patients with hepatocellular carcinoma as a predictor of response to 5-FU and interferon-alpha-2b. Fluorouracil 106-110 alpha fetoprotein Homo sapiens 10-27 7691392-15 1993 5-FU and SC rIFN-alpha-2b was well tolerated and induced durable partial response in 31% (5 of 16) of patients with HCC who had low levels of serum AFP and in those with 50% or less of liver replacement. Fluorouracil 0-4 alpha fetoprotein Homo sapiens 148-151 8292812-1 1993 Increased activity against colorectal cancer by 5-fluorouracil (5-Fu) modulation with leucovorin (LV) and/or interferon (IFN) has been reported. Fluorouracil 48-62 interferon alpha 1 Homo sapiens 109-125 8292812-1 1993 Increased activity against colorectal cancer by 5-fluorouracil (5-Fu) modulation with leucovorin (LV) and/or interferon (IFN) has been reported. Fluorouracil 64-68 interferon alpha 1 Homo sapiens 109-125 8379671-0 1993 [Etoposide, doxorubicin, cisplatin and 5-FU (EAP-F) therapy of advanced gastric cancer--its antitumor effect and evaluation of quality of life]. Fluorouracil 39-43 pleckstrin homology and FYVE domain containing 2 Homo sapiens 45-50 8336197-12 1993 Our findings suggest that under certain conditions, mechanisms other than altered 5-FU pharmacokinetics may be responsible for the ability of IFN-alpha to enhance the toxic effects of 5-FU. Fluorouracil 184-188 interferon alpha 1 Homo sapiens 142-151 8100781-3 1993 H-7, a protein kinase C inhibitor, at more than 40 microM inhibited activation of the MDR1 promoter that was induced by ethylmethane sulfonate, 5-fluorouracil or UV irradiation. Fluorouracil 144-158 ATP binding cassette subfamily B member 1 Homo sapiens 86-90 7686504-1 1993 The monoclonal rat anti-c-kit antibody (ACK2), which abrogates colony growth supported by stem cell factor (SCF), significantly inhibited the interleukin-6 (IL-6)-dependent growth of hematopoietic progenitors derived from spleen cells of normal and 5-fluorouracil (5-FU)-treated mice and from bone marrow cells of normal mice in serum-containing culture. Fluorouracil 249-263 interleukin 6 Mus musculus 142-155 7686504-1 1993 The monoclonal rat anti-c-kit antibody (ACK2), which abrogates colony growth supported by stem cell factor (SCF), significantly inhibited the interleukin-6 (IL-6)-dependent growth of hematopoietic progenitors derived from spleen cells of normal and 5-fluorouracil (5-FU)-treated mice and from bone marrow cells of normal mice in serum-containing culture. Fluorouracil 249-263 interleukin 6 Mus musculus 157-161 7686504-1 1993 The monoclonal rat anti-c-kit antibody (ACK2), which abrogates colony growth supported by stem cell factor (SCF), significantly inhibited the interleukin-6 (IL-6)-dependent growth of hematopoietic progenitors derived from spleen cells of normal and 5-fluorouracil (5-FU)-treated mice and from bone marrow cells of normal mice in serum-containing culture. Fluorouracil 265-269 interleukin 6 Mus musculus 142-155 7686504-1 1993 The monoclonal rat anti-c-kit antibody (ACK2), which abrogates colony growth supported by stem cell factor (SCF), significantly inhibited the interleukin-6 (IL-6)-dependent growth of hematopoietic progenitors derived from spleen cells of normal and 5-fluorouracil (5-FU)-treated mice and from bone marrow cells of normal mice in serum-containing culture. Fluorouracil 265-269 interleukin 6 Mus musculus 157-161 8501906-9 1993 FAC regimen (5-fluorouracil, Adriamycin, and cyclophosphamide) was given to 6 patients (40%). Fluorouracil 13-27 FA complementation group C Homo sapiens 0-3 8173197-2 1993 In a first step, the 5-FU pharmacokinetic and pharmacodynamic analysis of 25 cycles for 14 patients revealed that both the time-concentration product (ASC) for the entire cycle and the half-cycle were predictive of cycle toxicity and a dose adjustment diagram was established. Fluorouracil 21-25 PYD and CARD domain containing Homo sapiens 151-154 8443377-4 1993 In addition, formation of multilineage colonies from J11d.2+ in both 5-FU-treated and normal mice was augmented by interleukin 6. Fluorouracil 69-73 interleukin 6 Mus musculus 115-128 8427959-5 1993 Similarly, in vitro treatment with IL-1 of bone marrow cells isolated from 5-fluorouracil-treated mice results in elevated levels of MnSOD RNA. Fluorouracil 75-89 superoxide dismutase 2, mitochondrial Mus musculus 133-138 8435370-1 1993 BACKGROUND: On the basis of data suggesting the possibility of maximizing the efficacy of 5-FU by LV and IFN, a pilot clinical trial was initiated in advanced pancreatic cancer. Fluorouracil 90-94 interferon alpha 1 Homo sapiens 105-108 8500219-2 1993 The reduced folate 5,10-methylenetetrahydrofolate (CH2FH4) and its precursor tetrahydrofolate (FH4) are essential cofactors for the formation of a tight ternary complex of thymidylate synthase (TS) and 5-fluoro-2"-deoxyuridine-5"-monophosphate (FdUMP) derived from FUra. Fluorouracil 265-269 thymidylate synthetase Rattus norvegicus 172-192 8418225-1 1993 PURPOSE: Diarrhea is a prominent feature of fluorouracil (5FU) gastrointestinal toxicity, especially when 5FU is combined with leucovorin (LV) or interferon (IFN). Fluorouracil 44-56 interferon alpha 1 Homo sapiens 146-162 8418225-1 1993 PURPOSE: Diarrhea is a prominent feature of fluorouracil (5FU) gastrointestinal toxicity, especially when 5FU is combined with leucovorin (LV) or interferon (IFN). Fluorouracil 58-61 interferon alpha 1 Homo sapiens 146-162 1333262-5 1992 Preliminary 1H studies of the RIF-1 tumor indicate that: (i) there are no significant changes in metabolite levels relative to tumor water during 4 days of untreated tumor growth; (ii) tumor response to chemotherapy with 5-fluorouracil results in a decrease in intensity of all metabolite 1H resonances relative to tumor water, with total choline decreasing the most and lactate the least; and (iii) acute tumor blood flow reduction induced by administration of hydralazine results in doubling of the lactate intensity relative to water. Fluorouracil 221-235 replication timing regulatory factor 1 Mus musculus 30-35 9268987-1 1997 Pretreatment of 5-fluorouracil (5-FU), but not posttreatment, has been shown to augment the cytotoxicity of cisplatin (CDDP) or even circumvent CDDP resistance by inhibiting repair of platinum-DNA interstrand crosslinks as well as by reducing the cellular glutathione (GSH) contents in CDDP-resistant HST-1/CP0.2 human squamous carcinoma cells. Fluorouracil 16-30 fibroblast growth factor 4 Homo sapiens 301-306 9268987-1 1997 Pretreatment of 5-fluorouracil (5-FU), but not posttreatment, has been shown to augment the cytotoxicity of cisplatin (CDDP) or even circumvent CDDP resistance by inhibiting repair of platinum-DNA interstrand crosslinks as well as by reducing the cellular glutathione (GSH) contents in CDDP-resistant HST-1/CP0.2 human squamous carcinoma cells. Fluorouracil 32-36 fibroblast growth factor 4 Homo sapiens 301-306 9268987-9 1997 Although not convinced, our data suggest that 5-FU, when incorporated into RNA, may inhibit both GSH synthesis and repair of platinum-DNA adducts by downregulating the ERCC1 and gamma-GCS genes, thereby enhancing antitumor activity of CDDP and reversing resistance to CDDP in HST-1/CP0.2 cells. Fluorouracil 46-50 fibroblast growth factor 4 Homo sapiens 276-281 9042268-4 1996 In contrast, DNA synthesis blockers such as fluorouracil can induce apoptosis through p53-dependent mechanisms. Fluorouracil 44-56 tumor protein p53 Homo sapiens 86-89 9021669-15 1996 This finding might reflect the fact that S-1 induced continuous high levels of 5-FU in the blood. Fluorouracil 79-83 eukaryotic translation elongation factor 1 alpha 2 Mus musculus 41-44 9017443-3 1996 Data from 53 patients with high risk primary breast cancer who had undergone adjuvant or neoadjuvant 5FU-containing chemotherapy (FAC or FAC plus G-CSF) for 3 to 12 months were reviewed. Fluorouracil 101-104 FA complementation group C Homo sapiens 130-133 21541578-5 1996 Patients with CEA values reduced by greater than or equal to 30% at 2 months after the start of 5-FU infusion had a significantly longer survival period than patients with a decrease of <30%. Fluorouracil 96-100 CEA cell adhesion molecule 3 Homo sapiens 14-17 8790139-7 1996 These data indicate that PF4 or AcSDKP accelerate the recovery in vivo of HPP-CFC, CFU-GM and BFU-E after 5-FU treatment but their effect may be different on megakaryocytic progenitors and suggests that both molecules may have a haemoprotective effect against chemotherapeutic agents. Fluorouracil 106-110 platelet factor 4 Mus musculus 25-28 8826868-1 1996 With the association of 5-fluorouracil (5-FU) and alpha-interferon (IFN), objective responses as high as 26 63% have been reported in untreated patients with advanced colorectal cancer. Fluorouracil 24-38 interferon alpha 1 Homo sapiens 50-72 8826868-17 1996 At least at this dosage and schedule, the association of 5-FU and IFN is no better than 5-FU alone and is of no clinical interest. Fluorouracil 57-61 interferon alpha 1 Homo sapiens 66-69 8879370-13 1996 CONCLUSION: 5-FU plus IFN is more effective than 5-FU alone in terms of response rate, event free survival but not of overall survival. Fluorouracil 49-53 interferon alpha 1 Homo sapiens 22-25 8751810-0 1996 [A case of AFP (alpha-fetoprotein) producing gastric cancer successfully treated with FEP (5-FU, Epirubicin, cisplatin) therapy by continuous venous daily infusion of 5-FU and low-dose CDDP]. Fluorouracil 91-95 alpha fetoprotein Homo sapiens 11-14 8751810-0 1996 [A case of AFP (alpha-fetoprotein) producing gastric cancer successfully treated with FEP (5-FU, Epirubicin, cisplatin) therapy by continuous venous daily infusion of 5-FU and low-dose CDDP]. Fluorouracil 91-95 alpha fetoprotein Homo sapiens 16-33 8751810-0 1996 [A case of AFP (alpha-fetoprotein) producing gastric cancer successfully treated with FEP (5-FU, Epirubicin, cisplatin) therapy by continuous venous daily infusion of 5-FU and low-dose CDDP]. Fluorouracil 167-171 alpha fetoprotein Homo sapiens 11-14 8751810-0 1996 [A case of AFP (alpha-fetoprotein) producing gastric cancer successfully treated with FEP (5-FU, Epirubicin, cisplatin) therapy by continuous venous daily infusion of 5-FU and low-dose CDDP]. Fluorouracil 167-171 alpha fetoprotein Homo sapiens 16-33 8751810-1 1996 We reported our experience with a case of AFP producing gastric cancer with liver metastasis successfully treated with FEP therapy by continuous daily venous infusion of 5-FU and low-dose CDDP. Fluorouracil 170-174 alpha fetoprotein Homo sapiens 42-45 8764108-0 1996 Alternate splicing of the rTS gene product and its overexpression in a 5-fluorouracil-resistant cell line. Fluorouracil 71-85 RT1 class Ib, locus EC2 Rattus norvegicus 26-29 8764108-6 1996 rTSbeta is overexpressed 40-70-fold in a 5-fluorouracil-resistant H630 subline compared with 7-8-fold for TS and rTSalpha. Fluorouracil 41-55 RT1 class Ib, locus EC2 Rattus norvegicus 1-3 8862717-10 1996 Our results show that doses of IFN of 18 MU/m2 given by a 24 h infusion can be administered safely to an established and active schedule of weekly 24 h infusion of 5-FU and LV. Fluorouracil 164-168 interferon alpha 1 Homo sapiens 31-34 8646722-1 1996 BACKGROUND: Recombinant interferon-alpha (IFN) augments the cytotoxicity of both 5-fluorouracil (5-FU) and cisplatin in vitro. Fluorouracil 81-95 interferon alpha 1 Homo sapiens 42-45 8646722-1 1996 BACKGROUND: Recombinant interferon-alpha (IFN) augments the cytotoxicity of both 5-fluorouracil (5-FU) and cisplatin in vitro. Fluorouracil 97-101 interferon alpha 1 Homo sapiens 42-45 8683228-0 1996 Sequential methotrexate and fluorouracil for the treatment of node-negative breast cancer patients with estrogen receptor-negative tumors: eight-year results from National Surgical Adjuvant Breast and Bowel Project (NSABP) B-13 and first report of findings from NSABP B-19 comparing methotrexate and fluorouracil with conventional cyclophosphamide, methotrexate, and fluorouracil. Fluorouracil 28-40 estrogen receptor 1 Homo sapiens 104-121 9229325-1 1996 To improve the therapeutic ratio of palliative chemotherapy in patients with metastatic colorectal and gastric cancer 5-fluorouracil (5-FU) was administered as weekly high-dose 24-hour continuous infusion in combination with leucovorin (LV) and interferon-alpha-2b (IFN) as biomodulating agents: Chemotherapy consisted of a weekly schedule of 500 mg/m2 leucovorin as a 2-hour infusion, followed by a 24-hour continuous infusion of 2500 mg/m2 5-FU. Fluorouracil 134-138 interferon alpha 1 Homo sapiens 266-269 8673929-4 1996 In vitro investigations have shown intact p53 to play a critical role executing cell death in response to treatment with cytotoxic drugs like 5-fluorouracil, etoposide and doxorubicin. Fluorouracil 142-156 tumor protein p53 Homo sapiens 42-45 8758262-1 1996 The aspartate transcarbamoylase inhibitor, N-(phosphonacetyl)-L-aspartate (PALA), synergistically enhanced the cytotoxicity of a combination of 5-fluorouracil (5-FU) and interferon-alpha (IFN) against human colon cancer cell lines in vitro. Fluorouracil 144-158 interferon alpha 1 Homo sapiens 170-192 8807498-0 1996 IFN-gamma in combination with IL-3 accelerates platelet recovery in mice with 5-fluorouracil-induced marrow aplasia. Fluorouracil 78-92 interferon gamma Mus musculus 0-9 8639415-6 1996 In addition, PF4-preincubated CD34+ cells exhibited a higher potential in MK colony formation in the presence of 5-fluorouracil (5FU). Fluorouracil 113-127 CD34 molecule Homo sapiens 30-34 8639415-6 1996 In addition, PF4-preincubated CD34+ cells exhibited a higher potential in MK colony formation in the presence of 5-fluorouracil (5FU). Fluorouracil 129-132 CD34 molecule Homo sapiens 30-34 8616835-7 1996 Treatment of DLD-1 cells with concentrations of 5-FUra that are not growth inhibitory or cytotoxic strongly inhibited their ability to express nitric oxide synthase and produce nitric oxide in response to IFN-gamma. Fluorouracil 48-54 interferon gamma Homo sapiens 205-214 8608838-0 1996 p53 protein overexpression and response to biomodulated 5-fluorouracil chemotherapy in patients with advanced colorectal cancer. Fluorouracil 56-70 tumor protein p53 Homo sapiens 0-3 8613443-10 1996 Dose survival studies with use of a tetrazolium colorimetric assay showed that the MOS/ADR1 cells were cross-resistant to vincristine, vinblastine, etoposide, bleomycin, mitomycin C, and actinomycin D but not to dacarbazine, cisplatin, carboplatin, cytosine arabinoside, carmustine, cyclophosphamide, ifosfamide, methotrexate, and 5-fluorouracil. Fluorouracil 331-345 Moloney sarcoma oncogene Mus musculus 83-86 8620460-3 1996 To obtain a maximal inhibition of cell metabolism without causing cell toxicity, we were able to decrease the dose of 5-FU by simultaneously adding IFN-alpha. Fluorouracil 118-122 interferon alpha 1 Homo sapiens 148-157 8621231-0 1996 Schedule-dependent reversion of acquired cisplatin resistance by 5-fluorouracil in a newly established cisplatin-resistant HST-1 human squamous carcinoma cell line. Fluorouracil 65-79 fibroblast growth factor 4 Homo sapiens 123-128 8621231-5 1996 Pretreatment of HST-1/CP0.2 cells with 5-FU, with drug-free intervals of 24 to 48 hr before exposure to CDDP, completely reversed CDDP resistance, or even increased the sensitivity to a level greater than that of parental cells, whereas the opposite sequence had no effect on resistance. Fluorouracil 39-43 fibroblast growth factor 4 Homo sapiens 16-21 9816174-8 1996 Drug concentrations in peritoneal fluid, plasma, and thoracic duct lymph were monitored over the ensuing 6 h. The pharmacokinetics of 5-fluorouracil were not altered by vasopressin; however, vasopressin increased the peritoneal fluid:plasma AUC ratio for CBDCA from 30.6 +/- 5.6 to 70. Fluorouracil 134-148 vasopressin Sus scrofa 191-202 8529283-4 1996 5-FU/LV was administered 2-3 days before TNF and CP, followed 1 h later by HTX. Fluorouracil 0-4 tumor necrosis factor Homo sapiens 41-44 8823488-0 1996 Erythropoietin and granulocyte-macrophage colony-stimulating factor allow acceleration and dose escalation of cyclophosphamide/epidoxorubicin/5-fluorouracil chemotherapy: a dose-finding study in patients with advanced breast cancer. Fluorouracil 142-156 erythropoietin Homo sapiens 0-14 8823488-11 1996 Increasing the doses of Ctx and Epidx while maintaining a fixed dose of 5-Fu with the support of both EPO and GM-CSF allows safe acceleration and dose escalation of CEF chemotherapy. Fluorouracil 72-76 erythropoietin Homo sapiens 102-105 8823494-0 1996 Effect of interferon on 5-fluorouracil-induced perturbations in pools of deoxynucleotide triphosphates and DNA strand breaks. Fluorouracil 24-38 interferon alpha 1 Homo sapiens 10-20 8823494-1 1996 Interferon (IFN) augments the anabolism of 5-fluorouracil (5FU) to its active metabolite, fluorodeoxyuridylate (FdUMP), which inhibits thymidylate synthase (TS). Fluorouracil 43-57 interferon alpha 1 Homo sapiens 0-10 8823494-1 1996 Interferon (IFN) augments the anabolism of 5-fluorouracil (5FU) to its active metabolite, fluorodeoxyuridylate (FdUMP), which inhibits thymidylate synthase (TS). Fluorouracil 43-57 interferon alpha 1 Homo sapiens 12-15 8747891-2 1996 Inositol 1,4,5-trisphosphate and diacyl glycerol levels in formyl-methionyl-leucyl-phenylalanine (FMLP)-stimulated PMN were decreased by cis-diammine-dichloroplatinum (CDDP), 5-fluorouracil (5-FU), 137Cs, and peplomycin (PLM, a bleomycin analog) in this order. Fluorouracil 175-189 formyl peptide receptor 1 Homo sapiens 98-102 8747891-2 1996 Inositol 1,4,5-trisphosphate and diacyl glycerol levels in formyl-methionyl-leucyl-phenylalanine (FMLP)-stimulated PMN were decreased by cis-diammine-dichloroplatinum (CDDP), 5-fluorouracil (5-FU), 137Cs, and peplomycin (PLM, a bleomycin analog) in this order. Fluorouracil 191-195 formyl peptide receptor 1 Homo sapiens 98-102 8747891-8 1996 In conclusion, these results indicate that long term treatment of PMN with 5-FU and CDDP inhibit respiratory burst, suppressing intracellular calcium mobilization, PKC translocation and tyrosine kinase activation, in adverse, short term treatment with PLM enhances PKC translocation and tyrosine kinase activation, but inhibits myeloperoxidase (MPO) activity, and radiation causes weak inhibition of signal transduction for respiratory burst. Fluorouracil 75-79 myeloperoxidase Homo sapiens 328-343 8747891-8 1996 In conclusion, these results indicate that long term treatment of PMN with 5-FU and CDDP inhibit respiratory burst, suppressing intracellular calcium mobilization, PKC translocation and tyrosine kinase activation, in adverse, short term treatment with PLM enhances PKC translocation and tyrosine kinase activation, but inhibits myeloperoxidase (MPO) activity, and radiation causes weak inhibition of signal transduction for respiratory burst. Fluorouracil 75-79 myeloperoxidase Homo sapiens 345-348 8542939-8 1995 5-FU pretreatment of CML CD34+ cells markedly reduced their clonogenic potential and growth factor-mediated cell proliferation but favored higher frequency of BCR-ABL-free colonies. Fluorouracil 0-4 CD34 molecule Homo sapiens 25-29 8542939-9 1995 In conclusion, these data show that 5-FU-resistant CD34+ cells from the PB of CML patients contain normal progenitor cells, which can be selected and expanded in short-term cytokine-mediated cultures. Fluorouracil 36-40 CD34 molecule Homo sapiens 51-55 8717183-4 1995 Moreover, incubation of CD34+ cells with PF4 in liquid culture caused an increase in the number of both stem cell factor (SCF)-binding cells and CD34 antigen-bearing cells, and exhibited greater capacity to form MK colonies than control after the treatment of 5-FU. Fluorouracil 260-264 CD34 molecule Homo sapiens 24-28 7574817-5 1995 Treatment with 5-FU (iv; once a week) and epirubicin (20 mg/body once every 2 weeks iv) resulted in disappearance of the pulmonary metastases and a marked decrease in the AFP level. Fluorouracil 15-19 alpha fetoprotein Homo sapiens 171-174 7666089-1 1995 PURPOSE: The aim of this study was to investigate the effects of adding interferon alfa-2b (IFN) to protracted venous infusion fluorouracil (PVI 5-FU) from the start of treatment in patients with advanced colorectal cancer. Fluorouracil 127-139 interferon alpha 1 Homo sapiens 92-95 8680797-1 1995 Interferon-alpha (IFN-alpha) exhibits synergistic antitumor activity when combined with tumor necrosis factor-alpha (TNF-alpha) in vitro and in vivo and increases the cytotoxicity of 5-fluorouracil (5-FU) in vitro. Fluorouracil 199-203 tumor necrosis factor Mus musculus 117-126 8680797-2 1995 Using a colon cancer cell line transplanted into nude mice, we examined the effects of pretreatment for 3 days with IFN-alpha (10(6) IU) and/or TNF-alpha (2.9 x 10(3) JRU) on 5-FU metabolism. Fluorouracil 175-179 tumor necrosis factor Mus musculus 144-153 7482555-12 1995 These results further suggest that TS inhibition, resultant deficits in DNA synthesis and cell cycle perturbations represent a critical mechanistic pathway in the developmental toxicity of 5-FU. Fluorouracil 189-193 thymidylate synthetase Rattus norvegicus 35-37 7627962-3 1995 Since TP catalyzes the first step in the direct conversion of FUra to deoxyribonucleotides, its induction by IFN is a potential biochemical mechanism for the modulation of the antitumor activity of FUra. Fluorouracil 198-202 interferon alpha 1 Homo sapiens 109-112 7642571-1 1995 Interferon-alpha (IFN alpha) potentiates the antitumor activity of 5-fluorouracil (FUra) in colon cancer in vitro, in vivo, and clinically. Fluorouracil 67-81 interferon alpha 1 Homo sapiens 18-27 7642571-1 1995 Interferon-alpha (IFN alpha) potentiates the antitumor activity of 5-fluorouracil (FUra) in colon cancer in vitro, in vivo, and clinically. Fluorouracil 83-87 interferon alpha 1 Homo sapiens 18-27 7642571-2 1995 A likely mechanism for this action is the induction by IFN alpha of thymidine phosphorylase (TP), the first enzyme in one pathway for the metabolic activation of FUra to fluorodeoxyribonucleotides. Fluorouracil 162-166 interferon alpha 1 Homo sapiens 55-64 7642571-9 1995 These studies provide direct evidence for the role of TP in mediating the sensitivity of colon carcinoma cells to FUra, and further support the importance of the induction of TP in the biomodulating action of IFN alpha on FUra chemosensitivity. Fluorouracil 114-118 interferon alpha 1 Homo sapiens 209-218 7642571-9 1995 These studies provide direct evidence for the role of TP in mediating the sensitivity of colon carcinoma cells to FUra, and further support the importance of the induction of TP in the biomodulating action of IFN alpha on FUra chemosensitivity. Fluorouracil 222-226 interferon alpha 1 Homo sapiens 209-218 8573632-0 1995 The binding of 5-fluorouracil to native and modified human serum albumin: UV, CD, and 1H and 19F NMR investigation. Fluorouracil 15-29 albumin Homo sapiens 59-72 7623839-2 1995 We show that exposure of cells to various genotoxic agents, including anticancer drugs such as mitomycin and 5-fluorouracil, results in an increase in p53 mRNA levels and in p53 promoter activation, indicating that the p53 genotoxic stress response is partly regulated at the transcriptional level. Fluorouracil 109-123 tumor protein p53 Homo sapiens 151-154 7623839-2 1995 We show that exposure of cells to various genotoxic agents, including anticancer drugs such as mitomycin and 5-fluorouracil, results in an increase in p53 mRNA levels and in p53 promoter activation, indicating that the p53 genotoxic stress response is partly regulated at the transcriptional level. Fluorouracil 109-123 tumor protein p53 Homo sapiens 174-177 7623839-2 1995 We show that exposure of cells to various genotoxic agents, including anticancer drugs such as mitomycin and 5-fluorouracil, results in an increase in p53 mRNA levels and in p53 promoter activation, indicating that the p53 genotoxic stress response is partly regulated at the transcriptional level. Fluorouracil 109-123 tumor protein p53 Homo sapiens 174-177 7577043-3 1995 These preclinical studies stimulated clinical evaluation of IFN-alpha in combination with 5-fluorouracil (5-FU) with and without leucovorin (LV), and the initial clinical results appeared promising. Fluorouracil 106-110 interferon alpha 1 Homo sapiens 60-69 7577043-4 1995 We summarise preclinical research concerning the interaction of 5-FU and IFN-alpha. Fluorouracil 64-68 interferon alpha 1 Homo sapiens 73-82 7646900-2 1995 Experimental findings suggesting that interferon-alpha (IFN-alpha) enhances 5-FU cytotoxicity have stimulated an increasing number of clinical trials to evaluate the therapeutic potential of this combination. Fluorouracil 76-80 interferon alpha 1 Homo sapiens 56-65 7715908-5 1995 On the basis, we have performed a clinical trial to evaluate the impact of low-dose IL-2 plus melatonin on the survival time in metastatic colon cancer, which progressed in response to 5-FU plus folates. Fluorouracil 185-189 interleukin 2 Homo sapiens 84-88 7715908-11 1995 This study suggests that low-dose subcutaneous IL-2 plus melatonin may be effective as a second-line therapy to induce tumor regression and to prolong percent survival at 1 year in metastatic colorectal cancer patients progressing under 5-FU and folates. Fluorouracil 237-241 interleukin 2 Homo sapiens 47-51 7534710-2 1995 We found a significant increase in the proportion of CD34+ cells in the PBSC fraction resistant to 25 micrograms/mL 5-FU after 7-day incubation with IL-1 plus IL-3 plus SCF as compared with the untreated fraction (p = 0.011). Fluorouracil 116-120 CD34 molecule Homo sapiens 53-57 7896881-8 1995 ErbB-2-transformed MCF10-A cells responded to mitomycin, cisplatin, and 5-Fl-uracil, suggesting that signaling from activated ErbB-2 enhances the cells ability to respond to DNA damage. Fluorouracil 72-83 erb-b2 receptor tyrosine kinase 2 Homo sapiens 0-6 7896881-8 1995 ErbB-2-transformed MCF10-A cells responded to mitomycin, cisplatin, and 5-Fl-uracil, suggesting that signaling from activated ErbB-2 enhances the cells ability to respond to DNA damage. Fluorouracil 72-83 erb-b2 receptor tyrosine kinase 2 Homo sapiens 126-132 9815973-11 1995 In the cyclophosphamide-methotrexate-fluorouracil-treated group, bcl-2 absence was significant for poor overall survival (P = 0.02) as well as a number of nodes above 3 (P = 0.04) and a tumor size above 2 cm (P = 0.05). Fluorouracil 37-49 BCL2 apoptosis regulator Homo sapiens 65-70 7865240-5 1995 The study showed a decrease in blood and plasma viscosity during treatment with 5-FU, probably caused by a decrease of plasma fibrinogen. Fluorouracil 80-84 fibrinogen beta chain Homo sapiens 126-136 7720172-2 1995 In vitro chemosensitivity studies with 5-FU in RIF-1 fibrosarcoma cells showed less than 1 log of cell kill at 1 mM after 2 h of exposure. Fluorouracil 39-43 replication timing regulatory factor 1 Mus musculus 47-52 7720172-4 1995 A 5-FU/epi injectable gel was designed, providing drug release in vitro of 50% by approximately 4 h and of 80% by 24 h. The retention of 5-FU in RIF-1 mouse tumors was determined after intratumoral administration of 5-FU/epi gel or various combinations of the formulation components. Fluorouracil 137-141 replication timing regulatory factor 1 Mus musculus 145-150 7882458-1 1995 To determine the maximum tolerated dose (MTD) of escalating doses of interferon-alpha-2b (IFN, Intron A) with 5-fluorouracil (5-FU) and cisplatin (DDP) in patients with advanced cancer, 15 patients were accrued between May 1990 and July 1991. Fluorouracil 110-124 interferon alpha 1 Homo sapiens 90-93 7882458-3 1995 IFN was given s.c. on days 1-5 and then three times weekly with DDP (75 mg/m2, day 1) and 5-FU [750 mg/m2, days 1-5, continuous infusion (CI) on a 28-day cycle. Fluorouracil 90-94 interferon alpha 1 Homo sapiens 0-3 7882458-10 1995 The combination of IFN is possible with 5-FU and DDP. Fluorouracil 40-44 interferon alpha 1 Homo sapiens 19-22 7597304-6 1995 A major mechanism involved in the synergistic interaction of interferon (IFN) and 5-fluorouracil (5-FU) seems to be the increase of active 5-FU metabolites by IFN. Fluorouracil 82-96 interferon alpha 1 Homo sapiens 159-162 7597304-6 1995 A major mechanism involved in the synergistic interaction of interferon (IFN) and 5-fluorouracil (5-FU) seems to be the increase of active 5-FU metabolites by IFN. Fluorouracil 98-102 interferon alpha 1 Homo sapiens 61-71 7597304-6 1995 A major mechanism involved in the synergistic interaction of interferon (IFN) and 5-fluorouracil (5-FU) seems to be the increase of active 5-FU metabolites by IFN. Fluorouracil 98-102 interferon alpha 1 Homo sapiens 159-162 7597304-6 1995 A major mechanism involved in the synergistic interaction of interferon (IFN) and 5-fluorouracil (5-FU) seems to be the increase of active 5-FU metabolites by IFN. Fluorouracil 139-143 interferon alpha 1 Homo sapiens 61-71 7597304-6 1995 A major mechanism involved in the synergistic interaction of interferon (IFN) and 5-fluorouracil (5-FU) seems to be the increase of active 5-FU metabolites by IFN. Fluorouracil 139-143 interferon alpha 1 Homo sapiens 73-76 7597304-6 1995 A major mechanism involved in the synergistic interaction of interferon (IFN) and 5-fluorouracil (5-FU) seems to be the increase of active 5-FU metabolites by IFN. Fluorouracil 139-143 interferon alpha 1 Homo sapiens 159-162 7597304-7 1995 Moreover, IFN can reverse resistance against 5-FU by inhibiting the overexpression of thymidylate synthase. Fluorouracil 45-49 interferon alpha 1 Homo sapiens 10-13 7957712-0 1994 Serum erythropoietin increase in patients receiving adjuvant therapy with 5-fluorouracil and leucovorin. Fluorouracil 74-88 erythropoietin Homo sapiens 6-20 7947102-1 1994 Interferon alpha (IFN-alpha) enhances the activity of 5-fluorouracil (5-FU) in the treatment of advanced colorectal cancer although the mechanism is not understood. Fluorouracil 54-68 interferon alpha 1 Homo sapiens 0-27 7947102-1 1994 Interferon alpha (IFN-alpha) enhances the activity of 5-fluorouracil (5-FU) in the treatment of advanced colorectal cancer although the mechanism is not understood. Fluorouracil 70-74 interferon alpha 1 Homo sapiens 0-27 7947102-3 1994 This study has demonstrated an enhancement of the cellular immune response in patients given 5-FU/IFN-alpha with augmentation of natural killer (NK) cell function and abrogation of 5-FU-induced suppression of lymphokine-activated killer (LAK) cell activity. Fluorouracil 93-97 interferon alpha 1 Homo sapiens 98-107 7947102-3 1994 This study has demonstrated an enhancement of the cellular immune response in patients given 5-FU/IFN-alpha with augmentation of natural killer (NK) cell function and abrogation of 5-FU-induced suppression of lymphokine-activated killer (LAK) cell activity. Fluorouracil 181-185 interferon alpha 1 Homo sapiens 98-107 7930877-8 1994 Furthermore, when administered to 5-fluorouracil-treated mice, 5 micrograms/day of Peg-IL-6 diminished the platelet nadir and increased platelet counts on individual days during the recovery phase. Fluorouracil 34-48 interleukin 6 Homo sapiens 87-91 7923102-6 1994 IFN-alpha increased the anti-neoplastic activity of cisplatin and 5-FU against T2/CUHK cells, but the effect was less evident in PWH-S1 cells. Fluorouracil 66-70 interferon alpha 1 Homo sapiens 0-9 8085851-0 1994 [Innate resistance to thymidylate synthase inhibition after 5-fluorouracil treatment--a rationale of combined use of cisplatin and its optimal administration dose]. Fluorouracil 60-74 thymidylate synthetase Rattus norvegicus 22-42 8085853-4 1994 Inhibition of thymidylate synthase activity in tumor tissue after dosing of AO-90 (nitrogen 0.68g/kg on the 1st day and 1.36 g/kg for the remaining 6 days) by TPN along with daily intraperitoneal dosing of 5-FU (10 mg/kg) was also evaluated with the inoculation of 10(6) tumor cells. Fluorouracil 206-210 thymidylate synthetase Rattus norvegicus 14-34 7812360-2 1994 Combining IFN-alpha with either IL-2 or 5-fluorouracil (5-FU) enhanced IFN-alpha activity. Fluorouracil 40-54 interferon alpha 1 Homo sapiens 71-80 7522897-5 1994 We demonstrated a significantly greater increase in the percentage of CD34+ cells in the 5-FU-resistant PBSC fraction as compared to 5-FU-resistant BM cells (p = 0.012). Fluorouracil 89-93 CD34 molecule Homo sapiens 70-74 8169845-3 1994 In this report we describe for the first time a mechanism by which 5-FlUra as the free base specifically binds in vivo to the UDG in noncycling human cells, thereby inhibiting its activity. Fluorouracil 67-74 uracil DNA glycosylase Homo sapiens 126-129 8169845-4 1994 By using 5-FlUra concentrations which did not elicit demonstrable cell toxicity, a dose-dependent decrease in UDG activity was detected which approached 30% of that observed in control cells. Fluorouracil 9-16 uracil DNA glycosylase Homo sapiens 110-113 8169845-7 1994 Kinetic analysis using nonlinear regression analysis demonstrated a competitive mode of inhibition and indicated a tight binding of 5-FlUra to UDG in vivo, although the 5-FlUra-UDG complex was easily dissociated in vitro. Fluorouracil 132-139 uracil DNA glycosylase Homo sapiens 143-146 8169845-7 1994 Kinetic analysis using nonlinear regression analysis demonstrated a competitive mode of inhibition and indicated a tight binding of 5-FlUra to UDG in vivo, although the 5-FlUra-UDG complex was easily dissociated in vitro. Fluorouracil 132-139 uracil DNA glycosylase Homo sapiens 177-180 8186172-1 1994 BACKGROUND: Due to the possibility of a synergistic effect between Interferon (IFN-alpha) and 5-fluorouracil (5-FU), a phase II trial was conducted in metastatic renal cell carcinoma (MRCC) combining recombinant IFN-alpha, 5-FU and prednisone. Fluorouracil 94-108 interferon alpha 1 Homo sapiens 212-221 8186172-1 1994 BACKGROUND: Due to the possibility of a synergistic effect between Interferon (IFN-alpha) and 5-fluorouracil (5-FU), a phase II trial was conducted in metastatic renal cell carcinoma (MRCC) combining recombinant IFN-alpha, 5-FU and prednisone. Fluorouracil 110-114 interferon alpha 1 Homo sapiens 212-221 8186172-1 1994 BACKGROUND: Due to the possibility of a synergistic effect between Interferon (IFN-alpha) and 5-fluorouracil (5-FU), a phase II trial was conducted in metastatic renal cell carcinoma (MRCC) combining recombinant IFN-alpha, 5-FU and prednisone. Fluorouracil 223-227 interferon alpha 1 Homo sapiens 79-88 21607382-3 1994 However, significant enhancement in NKCMC and ADCC was observed when PBMC from patients were cultured in RPMI-1640 containing 200 IU/ml of Interleukin-2 (IL-2) for 4 days in 5% CO2 atmosphere at 37 degrees C. Augmentation of NKCMC and ADCC was also detected when a follow-up study of the patients was conducted after one month following initial trial of chemotherapy with 5-fluorouracil (5-Fu). Fluorouracil 372-386 interleukin 2 Homo sapiens 139-152 21607382-3 1994 However, significant enhancement in NKCMC and ADCC was observed when PBMC from patients were cultured in RPMI-1640 containing 200 IU/ml of Interleukin-2 (IL-2) for 4 days in 5% CO2 atmosphere at 37 degrees C. Augmentation of NKCMC and ADCC was also detected when a follow-up study of the patients was conducted after one month following initial trial of chemotherapy with 5-fluorouracil (5-Fu). Fluorouracil 372-386 interleukin 2 Homo sapiens 154-158 21607382-3 1994 However, significant enhancement in NKCMC and ADCC was observed when PBMC from patients were cultured in RPMI-1640 containing 200 IU/ml of Interleukin-2 (IL-2) for 4 days in 5% CO2 atmosphere at 37 degrees C. Augmentation of NKCMC and ADCC was also detected when a follow-up study of the patients was conducted after one month following initial trial of chemotherapy with 5-fluorouracil (5-Fu). Fluorouracil 388-392 interleukin 2 Homo sapiens 139-152 21607382-3 1994 However, significant enhancement in NKCMC and ADCC was observed when PBMC from patients were cultured in RPMI-1640 containing 200 IU/ml of Interleukin-2 (IL-2) for 4 days in 5% CO2 atmosphere at 37 degrees C. Augmentation of NKCMC and ADCC was also detected when a follow-up study of the patients was conducted after one month following initial trial of chemotherapy with 5-fluorouracil (5-Fu). Fluorouracil 388-392 interleukin 2 Homo sapiens 154-158 21607382-4 1994 Patients, who had undergone clinical trial with 5-Fu were better responders of IL-2 activation as reflected on NK cell and ADCC potential of these patients. Fluorouracil 48-52 interleukin 2 Homo sapiens 79-83 8181904-6 1994 LAK activity of spleen cells from mice treated with both SPR-901 and 5-FU was higher than that from the untreated control group and either the SPR-901 or 5-FU treated group. Fluorouracil 69-73 sepiapterin reductase Mus musculus 143-146 8181904-6 1994 LAK activity of spleen cells from mice treated with both SPR-901 and 5-FU was higher than that from the untreated control group and either the SPR-901 or 5-FU treated group. Fluorouracil 154-158 sepiapterin reductase Mus musculus 57-60 8181904-8 1994 Furthermore, spleen cells from both the SPR-901- and 5-FU-treated groups exhibited higher growth responses to IL-2 than that from the untreated control group and either of the SPR-901- or 5-FU-treated groups. Fluorouracil 53-57 sepiapterin reductase Mus musculus 176-179 7896537-2 1994 Among 8 compounds tested at nontoxic concentrations, flupentixol, a piperazine-substituted thioxanthene, was the most potent in enhancing the cytotoxicity of anticancer drugs commonly associated with the multidrug resistant (MDR) phenotype, such as Adriamycin, actinomycin D, vinblastine, and vincristine, but not 5-fluorouracil, a drug usually unaffected by MDR. Fluorouracil 314-328 ATP-binding cassette, sub-family B (MDR/TAP), member 1B Mus musculus 225-228 7787251-1 1994 Recombinant human interleukin-1 alpha (rIL-1 alpha), at concentrations that were not growth-inhibitory when given alone (100-10,000 U/ml), enhanced the growth inhibition resulting from a 72-h fluorouracil (FUra) exposure in HCT116 colon cancer cells. Fluorouracil 192-204 interleukin 1 alpha Rattus norvegicus 39-50 7787251-1 1994 Recombinant human interleukin-1 alpha (rIL-1 alpha), at concentrations that were not growth-inhibitory when given alone (100-10,000 U/ml), enhanced the growth inhibition resulting from a 72-h fluorouracil (FUra) exposure in HCT116 colon cancer cells. Fluorouracil 206-210 interleukin 1 alpha Rattus norvegicus 39-50 7787251-2 1994 Median-effect analysis of clonogenic assays indicated that rIL-1 alpha, given 24 h prior to and following a 24-h exposure to FUra, increased lethality in a more than additive fashion. Fluorouracil 125-129 interleukin 1 alpha Rattus norvegicus 59-70 7787251-4 1994 During continuous exposure to rIL-1 alpha, transient stimulation of RNA and DNA synthesis was observed at 72 h, with a return to normal by 96 h. A 24-h exposure to 10 microM FUra altered the elution profile of newly synthesized DNA as monitored by pH step alkaline elution. Fluorouracil 174-178 interleukin 1 alpha Rattus norvegicus 30-41 7787251-8 1994 FUra prevented the stimulatory effect of rIL-1 alpha on RNA synthesis, and net RNA synthesis was significantly inhibited (by 64-79% after 72 and 96 h) with the combination compared to rIL-1 alpha alone. Fluorouracil 0-4 interleukin 1 alpha Rattus norvegicus 41-52 8054813-9 1994 These data indicate that EGF may be a potent agent as a biological response modifier for 5-FU against the tumors which express the EGF/EGFR autocrine mechanism, and that the TSG6 cell line is useful in furthering our understanding of the interaction between anticancer drugs and EGF. Fluorouracil 89-93 epidermal growth factor receptor Homo sapiens 135-139 7904537-4 1993 Presence of 5FU at 2 micrograms/ml but not at 0.2 microgram/ml in media blocked LAK activity induction by IL-2. Fluorouracil 12-15 interleukin 2 Homo sapiens 106-110 8221681-1 1993 Interferon (IFN) has been shown to enhance the cytotoxic effects of 5-fluorouracil (5FUra) in colorectal cancer, and clinical trials with this combination resulted in higher response rate with respect to 5FUra alone. Fluorouracil 68-82 interferon alpha 1 Homo sapiens 0-16 8221681-1 1993 Interferon (IFN) has been shown to enhance the cytotoxic effects of 5-fluorouracil (5FUra) in colorectal cancer, and clinical trials with this combination resulted in higher response rate with respect to 5FUra alone. Fluorouracil 84-89 interferon alpha 1 Homo sapiens 0-16 8221681-1 1993 Interferon (IFN) has been shown to enhance the cytotoxic effects of 5-fluorouracil (5FUra) in colorectal cancer, and clinical trials with this combination resulted in higher response rate with respect to 5FUra alone. Fluorouracil 204-209 interferon alpha 1 Homo sapiens 0-16 8246910-1 1993 Recombinant interferon-alpha (IFN) enhances the cytotoxic effects of the fluorinated pyrimidine, 5-fluorouracil (5FU), against two human colon cancer cell lines. Fluorouracil 97-111 interferon alpha 1 Homo sapiens 12-34 8246910-1 1993 Recombinant interferon-alpha (IFN) enhances the cytotoxic effects of the fluorinated pyrimidine, 5-fluorouracil (5FU), against two human colon cancer cell lines. Fluorouracil 113-116 interferon alpha 1 Homo sapiens 12-34 8239524-4 1993 These results suggest that the changes observed in vivo of 5-FU toxicity induced by IFN-alpha should be attributed to indirect effects of the latter. Fluorouracil 59-63 interferon alpha 1 Homo sapiens 84-93 8339255-1 1993 alpha-Interferon (IFN-alpha) enhances the activity of 5-fluorouracil in patients with advanced colorectal carcinoma. Fluorouracil 54-68 interferon alpha 1 Homo sapiens 18-27 8336197-1 1993 PURPOSE: To determine the maximum-tolerable dose (MTD) of fluorouracil (5-FU) administered as a low-dose, prolonged continuous intravenous infusion (PCI) plus interferon-alfa (IFN-alpha) that would permit treatment for at least 28 consecutive days, and to determine the effect of IFN-alpha on 5-FU pharmacokinetics. Fluorouracil 58-70 interferon alpha 1 Homo sapiens 280-289 8336197-11 1993 CONCLUSION: IFN-alpha substantially enhanced the gastrointestinal toxicity of low-dose PCI 5-FU without affecting 5-FU pharmacokinetics, contrary to previous reports using alternative 5-FU schedules in which IFN-alpha-related enhancement of 5-FU toxicity was attributable to reduced 5-FU clearance. Fluorouracil 91-95 interferon alpha 1 Homo sapiens 12-21 8221817-8 1993 Electron microscopic analysis of the resected liver of a patient receiving the IL-2-mitomycin-C/5-fluorouracil (IL-2.MF) infusion showed a pronounced accumulation of lymphocytes, penetrating from the space of Disse, around the cancer cells. Fluorouracil 96-110 interleukin 2 Homo sapiens 79-83 8221817-8 1993 Electron microscopic analysis of the resected liver of a patient receiving the IL-2-mitomycin-C/5-fluorouracil (IL-2.MF) infusion showed a pronounced accumulation of lymphocytes, penetrating from the space of Disse, around the cancer cells. Fluorouracil 96-110 interleukin 2 Homo sapiens 112-116 8316218-0 1993 Mechanisms of excision of 5-fluorouracil by uracil DNA glycosylase in normal human cells. Fluorouracil 26-40 uracil DNA glycosylase Homo sapiens 44-66 8316218-1 1993 Recent evidence indicates that 5-fluorouracil (5-FlUra) is incorporated into DNA and is removed by the DNA repair enzyme uracil DNA glycosylase. Fluorouracil 31-45 uracil DNA glycosylase Homo sapiens 121-143 8316218-1 1993 Recent evidence indicates that 5-fluorouracil (5-FlUra) is incorporated into DNA and is removed by the DNA repair enzyme uracil DNA glycosylase. Fluorouracil 47-54 uracil DNA glycosylase Homo sapiens 121-143 8485705-2 1993 Activation of p53-DNA binding was seen for treatment with radiation, hydrogen peroxide, actinomycin D, Adriamycin, etoposide, camptothecin, 5-fluorouracil, mitomycin C, and cisplatin. Fluorouracil 140-154 tumor protein p53 Homo sapiens 14-17 8479746-3 1993 To examine the BCR/ABL-sensitive target cells present in the marrow of mice treated with 5-fluorouracil, we used a single-step in vitro assay. Fluorouracil 89-103 BCR activator of RhoGEF and GTPase Mus musculus 15-18 8470917-4 1993 The effectiveness of this MTX/3-dose 5-FU regimen was compared retrospectively with that of the standard sequential regimen consisting of the IV administration of MTX 100 mg/m2 followed by a single IV dose of 5-FU 800 mg/m2 one hr. Fluorouracil 37-41 metaxin 3 Homo sapiens 26-31 8470917-9 1993 There were no significant difference in the patient characteristics between the two groups, and the toxic effects were much lower in the MTX/3-dose 5-FU than in the MTX/1-dose 5-FU regimen. Fluorouracil 148-152 metaxin 3 Homo sapiens 137-142 8470917-10 1993 It is therefore, concluded that the MTX/3-dose 5-FU regimen is superior to the standard MTX/1-dose 5-FU regimen. Fluorouracil 47-51 metaxin 3 Homo sapiens 36-41 8474431-4 1993 A 24-hr exposure to 1 microM 5-FU resulted in a 4.5-fold increase in the level of TS protein, whereas in 5-FU/IFN-gamma-treated cells TS protein was increased by only 1.8-fold, compared with control cells. Fluorouracil 29-33 interferon gamma Homo sapiens 110-119 8474431-7 1993 Pulse-labeling studies with [35S]methionine demonstrated a 3.5-fold increase in net synthesis of TS in cells treated with 1 microM 5-FU, whereas the level of newly synthesized TS increased only 1.5-fold in cells treated with 5-FU/IFN-gamma, compared with control cells. Fluorouracil 131-135 interferon gamma Homo sapiens 230-239 8474431-9 1993 These findings demonstrate that the increase in TS protein after 5-FU exposure and the subsequent inhibitory effect of IFN-gamma on TS protein expression are both regulated at the post-transcriptional level. Fluorouracil 65-69 interferon gamma Homo sapiens 119-128 8486533-7 1993 Consequently, the anabolism of 5"-dFUrd to fluoronucleotides and the incorporation of 5-FUra into RNA in colon 26 cells were increased by TNF alpha treatment. Fluorouracil 86-92 tumor necrosis factor Mus musculus 138-147 8426214-2 1993 PATIENTS AND METHODS: Escalating doses of IFN (0.5 to 4.0 x 10(6) U/m2/d x 6) were added to cisplatin 100 mg/m2, continuous infusion 5-FU 800 or 640 mg/m2/d x 5, and leucovorin 100 mg orally every 4 hours. Fluorouracil 133-137 interferon alpha 1 Homo sapiens 42-45 8426214-6 1993 After decreasing the 5-FU dose to 640 mg/m2/d, the maximally tolerated dose (MTD) of IFN was 2.0 x 10(6) U/m2/d. Fluorouracil 21-25 interferon alpha 1 Homo sapiens 85-88 8426214-12 1993 CONCLUSION: The recommended doses for PFL-IFN are 640 mg/m2/d for 5-FU and 2.0 x 10(6) U/m2/d for IFN. Fluorouracil 66-70 interferon alpha 1 Homo sapiens 42-45 8339382-1 1993 The present study shows that various cytokines such as tumor necrosis factor (TNF alpha), interleukin-1 alpha (IL-1 alpha), and interferon-gamma (IFN gamma) make tumor cells much more susceptible to the cytostatic 5"-deoxy-5-fluorouridine (5"-dFUrd) than to 5-fluorouracil (5-FUra) and other cytostatics. Fluorouracil 258-272 interferon gamma Homo sapiens 128-144 8339382-1 1993 The present study shows that various cytokines such as tumor necrosis factor (TNF alpha), interleukin-1 alpha (IL-1 alpha), and interferon-gamma (IFN gamma) make tumor cells much more susceptible to the cytostatic 5"-deoxy-5-fluorouridine (5"-dFUrd) than to 5-fluorouracil (5-FUra) and other cytostatics. Fluorouracil 258-272 interferon gamma Homo sapiens 146-155 8339382-1 1993 The present study shows that various cytokines such as tumor necrosis factor (TNF alpha), interleukin-1 alpha (IL-1 alpha), and interferon-gamma (IFN gamma) make tumor cells much more susceptible to the cytostatic 5"-deoxy-5-fluorouridine (5"-dFUrd) than to 5-fluorouracil (5-FUra) and other cytostatics. Fluorouracil 274-280 interferon gamma Homo sapiens 128-144 8339382-1 1993 The present study shows that various cytokines such as tumor necrosis factor (TNF alpha), interleukin-1 alpha (IL-1 alpha), and interferon-gamma (IFN gamma) make tumor cells much more susceptible to the cytostatic 5"-deoxy-5-fluorouridine (5"-dFUrd) than to 5-fluorouracil (5-FUra) and other cytostatics. Fluorouracil 274-280 interferon gamma Homo sapiens 146-155 8509231-2 1993 Five clinical trials in humans with advanced colorectal carcinoma have demonstrated responses ranging from 26 to 63% in patients treated with 5-fluorouracil (5-FU) plus interferon-alpha (IFN-alpha), suggesting improved response with the combination as compared with 5-FU alone. Fluorouracil 266-270 interferon alpha 1 Homo sapiens 187-196 8509231-3 1993 In addition, responses have been observed in patients with adenocarcinomas of the lung, pancreas, breast, and kidney, squamous cell carcinoma of the oesophagus, and urothelial carcinoma treated with 5-FU/IFN-alpha. Fluorouracil 199-203 interferon alpha 1 Homo sapiens 204-213 7688612-2 1993 Recombinant IL-1 beta restored bone marrow cell proliferation reduced after 5-fluorouracil treatment and significantly increased the survival rates of lethally irradiated mice. Fluorouracil 76-90 interleukin 1 beta Mus musculus 12-21 1423296-0 1992 Inhibition by 5-fluorouracil of cis-diamminedichloroplatinum(II)-induced DNA interstrand cross-link removal in a HST-1 human squamous carcinoma cell line. Fluorouracil 14-28 fibroblast growth factor 4 Homo sapiens 113-118 1423296-1 1992 To elucidate the mechanism of the synergistic cytotoxicity of 5-fluorouracil (5-FU) and cis-diamminedichloroplatinum(II) (CDDP), we studied the interaction of these agents using a human squamous carcinoma cell line (HST-1). Fluorouracil 78-82 fibroblast growth factor 4 Homo sapiens 216-221 1447313-3 1992 However, the number of IL-3-dependent GM colonies formed by the bone marrow cells of 5-fluorouracil (5-FU)-treated mice was not influenced by the addition of IFN-gamma. Fluorouracil 85-99 interleukin 3 Mus musculus 23-27 1447313-3 1992 However, the number of IL-3-dependent GM colonies formed by the bone marrow cells of 5-fluorouracil (5-FU)-treated mice was not influenced by the addition of IFN-gamma. Fluorouracil 101-105 interleukin 3 Mus musculus 23-27 1382702-4 1992 The stimulatory effect of SCF was approximately three to four times as high as that of IL-6 on the primitive progenitors capable of megakaryocytic-lineage expression derived from 5-FU-treated mice. Fluorouracil 179-183 interleukin 6 Mus musculus 87-91 1525760-1 1992 BACKGROUND: Preclinical and clinical data suggest that both leucovorin (LV) and interferon (IFN) can augment the cytotoxic effects of 5-fluorouracil (5-FU). Fluorouracil 134-148 interferon alpha 1 Homo sapiens 60-96 1525760-1 1992 BACKGROUND: Preclinical and clinical data suggest that both leucovorin (LV) and interferon (IFN) can augment the cytotoxic effects of 5-fluorouracil (5-FU). Fluorouracil 150-154 interferon alpha 1 Homo sapiens 60-96 1351538-12 1992 CONCLUSION: We conclude that tumors with overexpression of the c-erbB-2 oncogene are less responsive to cyclophosphamide, methotrexate, and fluorouracil (CMF)-containing adjuvant therapy regimens than those with a normal amount of gene product. Fluorouracil 140-152 erb-b2 receptor tyrosine kinase 2 Homo sapiens 63-71 1619944-0 1992 Schedule dependent inhibition of thymidylate synthase and tumor growth by 5-fluorouracil in Yoshida sarcoma bearing rats. Fluorouracil 74-88 thymidylate synthetase Rattus norvegicus 33-53 1517151-10 1992 On the other hand, the antitumor effect of PSK was enhanced by previous intravenous administration of an anti-metabolite, 5-fluorouracil. Fluorouracil 122-136 TAO kinase 2 Mus musculus 43-46 1498068-1 1992 Because of the different sites and mechanisms of biochemical interaction among 5-fluorouracil (5-FU), leucovorin (LV) and interferon (IFN), we hypothesized that the concomitant use of IFN could increase the activity of the 5-FU/LV combination in colorectal cancer patients. Fluorouracil 223-227 interferon alpha 1 Homo sapiens 102-138 1498068-1 1992 Because of the different sites and mechanisms of biochemical interaction among 5-fluorouracil (5-FU), leucovorin (LV) and interferon (IFN), we hypothesized that the concomitant use of IFN could increase the activity of the 5-FU/LV combination in colorectal cancer patients. Fluorouracil 223-227 interferon alpha 1 Homo sapiens 134-137 1587307-2 1992 Murine bone marrow (BM) harvested 24 h after 5-fluorouracil (5-FU) administration (d1 5-FU BM) was stimulated with IL-1 and IL-3 to expand its progenitor pool during 7 days of suspension culture (delta-culture), and this in vitro expanded BM was compared to fresh d1 5-FU BM in its ability to reconstitute lethally irradiated or high-dose 5-FU-treated hosts. Fluorouracil 61-65 interleukin 3 Mus musculus 124-128 1587307-2 1992 Murine bone marrow (BM) harvested 24 h after 5-fluorouracil (5-FU) administration (d1 5-FU BM) was stimulated with IL-1 and IL-3 to expand its progenitor pool during 7 days of suspension culture (delta-culture), and this in vitro expanded BM was compared to fresh d1 5-FU BM in its ability to reconstitute lethally irradiated or high-dose 5-FU-treated hosts. Fluorouracil 86-90 interleukin 3 Mus musculus 124-128 1587307-2 1992 Murine bone marrow (BM) harvested 24 h after 5-fluorouracil (5-FU) administration (d1 5-FU BM) was stimulated with IL-1 and IL-3 to expand its progenitor pool during 7 days of suspension culture (delta-culture), and this in vitro expanded BM was compared to fresh d1 5-FU BM in its ability to reconstitute lethally irradiated or high-dose 5-FU-treated hosts. Fluorouracil 86-90 interleukin 3 Mus musculus 124-128 1587307-2 1992 Murine bone marrow (BM) harvested 24 h after 5-fluorouracil (5-FU) administration (d1 5-FU BM) was stimulated with IL-1 and IL-3 to expand its progenitor pool during 7 days of suspension culture (delta-culture), and this in vitro expanded BM was compared to fresh d1 5-FU BM in its ability to reconstitute lethally irradiated or high-dose 5-FU-treated hosts. Fluorouracil 86-90 interleukin 3 Mus musculus 124-128 1568463-0 1992 Effects of interleukin 3 and interleukin 6 on platelet recovery in mice treated with 5-fluorouracil. Fluorouracil 85-99 interleukin 6 Mus musculus 29-42 1568463-7 1992 The combination of IL-3 and IL-6, initiated immediately or 2 days following 5-FU, diminished the platelet nadir and increased platelet counts on individual days during the recovery phase, thus apparently decreasing the time required for recovery to a normal platelet level. Fluorouracil 76-80 interleukin 3 Mus musculus 19-23 1568463-7 1992 The combination of IL-3 and IL-6, initiated immediately or 2 days following 5-FU, diminished the platelet nadir and increased platelet counts on individual days during the recovery phase, thus apparently decreasing the time required for recovery to a normal platelet level. Fluorouracil 76-80 interleukin 6 Mus musculus 28-32 1568463-11 1992 We propose that IL-3 and IL-6 can act synergistically to enhance platelet recovery following 5-FU-mediated thrombocytopenia, but their modification of the response to 5-FU is modest. Fluorouracil 93-97 interleukin 3 Mus musculus 16-20 1568463-11 1992 We propose that IL-3 and IL-6 can act synergistically to enhance platelet recovery following 5-FU-mediated thrombocytopenia, but their modification of the response to 5-FU is modest. Fluorouracil 93-97 interleukin 6 Mus musculus 25-29 1553576-2 1992 In a phase I trial, we recently showed that interferon alpha-2b (IFN), folinic acid and 5-FU can be safely administered with a 4-hour infusion of 5-FU. Fluorouracil 146-150 interferon alpha 1 Homo sapiens 65-68 1553576-14 1992 From these data we conclude that modulation of 5-FU with both folinic acid and IFN induces an overall response rate of 31% in disseminated colorectal cancer. Fluorouracil 47-51 interferon alpha 1 Homo sapiens 79-82 1557647-1 1992 Preclinical data suggest that both folinic acid and interferon may enhance the efficacy of 5-fluorouracil (5-FU) in colorectal carcinoma. Fluorouracil 91-105 interferon alpha 1 Homo sapiens 52-62 1557647-1 1992 Preclinical data suggest that both folinic acid and interferon may enhance the efficacy of 5-fluorouracil (5-FU) in colorectal carcinoma. Fluorouracil 107-111 interferon alpha 1 Homo sapiens 52-62 1557648-2 1992 Therefore a pilot study was initiated to evaluate the effects of the combination 5-FU/FA/interferon alfa (IFN-alpha) in colorectal adenocarcinomas refractory to first-line therapy with 5-FU/FA. Fluorouracil 185-189 interferon alpha 1 Homo sapiens 86-115 1557648-6 1992 Looking at the sensitivity of lung metastases (three of three), the regressions can be explained through the additive effect of IFN-alpha to 5-FU/FA. Fluorouracil 141-145 interferon alpha 1 Homo sapiens 128-137 1557649-1 1992 Several reports on fluorouracil (5-FU) and alfa interferon (IFN-alpha) combination therapy in patients with advanced colorectal cancer have been published. Fluorouracil 19-31 interferon alpha 1 Homo sapiens 60-69 1557650-13 1992 Our preliminary data suggest that biochemical modulation of 5-FU with FA and IFN-alpha (reduced dosage) is effective in pancreatic cancer with moderate toxicity, warranting further study. Fluorouracil 60-64 interferon alpha 1 Homo sapiens 77-86 1557651-2 1992 The biochemical modulation of 5-FU by various drugs has brought about the two combinations of 5-FU/folinic acid (FA) and 5-FU/alpha-interferon (IFN), which have shown clinical activity in phase II and III trials, especially in colorectal cancer. Fluorouracil 30-34 interferon alpha 1 Homo sapiens 121-148 1557651-4 1992 In esophageal cancer, two phase II studies with 5-FU/IFN reported seven (27%) objective remissions in 26 patients, indicating superiority of 5-FU/IFN over 5-FU monotherapy. Fluorouracil 48-52 interferon alpha 1 Homo sapiens 146-149 1557651-4 1992 In esophageal cancer, two phase II studies with 5-FU/IFN reported seven (27%) objective remissions in 26 patients, indicating superiority of 5-FU/IFN over 5-FU monotherapy. Fluorouracil 141-145 interferon alpha 1 Homo sapiens 53-56 1557651-4 1992 In esophageal cancer, two phase II studies with 5-FU/IFN reported seven (27%) objective remissions in 26 patients, indicating superiority of 5-FU/IFN over 5-FU monotherapy. Fluorouracil 141-145 interferon alpha 1 Homo sapiens 53-56 1557651-7 1992 However, in gastric cancer, 5-FU/FA and 5-FU/IFN seem to induce higher complete and overall remission rates in advanced gastric cancer compared with 5-FU alone. Fluorouracil 40-44 interferon alpha 1 Homo sapiens 45-48 1557651-7 1992 However, in gastric cancer, 5-FU/FA and 5-FU/IFN seem to induce higher complete and overall remission rates in advanced gastric cancer compared with 5-FU alone. Fluorouracil 40-44 interferon alpha 1 Homo sapiens 45-48 1557656-7 1992 Interferon gamma interacts with 5-FU in H630 colon cancer cells at the level of thymidylate synthase and enhances cytotoxicity of 5-FU by eliminating the 5-FU-induced acute overexpression of the target enzyme. Fluorouracil 32-36 interferon gamma Homo sapiens 0-16 1557656-7 1992 Interferon gamma interacts with 5-FU in H630 colon cancer cells at the level of thymidylate synthase and enhances cytotoxicity of 5-FU by eliminating the 5-FU-induced acute overexpression of the target enzyme. Fluorouracil 130-134 interferon gamma Homo sapiens 0-16 1557656-7 1992 Interferon gamma interacts with 5-FU in H630 colon cancer cells at the level of thymidylate synthase and enhances cytotoxicity of 5-FU by eliminating the 5-FU-induced acute overexpression of the target enzyme. Fluorouracil 130-134 interferon gamma Homo sapiens 0-16 1372764-1 1992 Interferon (IFN) is capable of modulating the cytotoxic effects and clinical activity of the fluorinated pyrimidine, 5-fluorouracil (5-FU). Fluorouracil 117-131 interferon alpha 1 Homo sapiens 0-10 1372764-1 1992 Interferon (IFN) is capable of modulating the cytotoxic effects and clinical activity of the fluorinated pyrimidine, 5-fluorouracil (5-FU). Fluorouracil 117-131 interferon alpha 1 Homo sapiens 12-15 1372764-1 1992 Interferon (IFN) is capable of modulating the cytotoxic effects and clinical activity of the fluorinated pyrimidine, 5-fluorouracil (5-FU). Fluorouracil 133-137 interferon alpha 1 Homo sapiens 0-10 1372764-1 1992 Interferon (IFN) is capable of modulating the cytotoxic effects and clinical activity of the fluorinated pyrimidine, 5-fluorouracil (5-FU). Fluorouracil 133-137 interferon alpha 1 Homo sapiens 12-15 1372764-3 1992 Pharmacokinetic studies have also demonstrated that IFN can increase serum levels of 5-FU. Fluorouracil 85-89 interferon alpha 1 Homo sapiens 52-55 1536940-6 1992 Further studies showed that the administration of IL-7 to mice that had been rendered leukopenic by the injection of cyclophosphamide (Cy) or 5-fluorouracil (5FU) exhibited a more rapid recovery and/or overshoot in their peripheral blood lymphocytes when compared with mice treated with Cy or 5FU alone. Fluorouracil 142-156 interleukin 7 Mus musculus 50-54 1536940-6 1992 Further studies showed that the administration of IL-7 to mice that had been rendered leukopenic by the injection of cyclophosphamide (Cy) or 5-fluorouracil (5FU) exhibited a more rapid recovery and/or overshoot in their peripheral blood lymphocytes when compared with mice treated with Cy or 5FU alone. Fluorouracil 158-161 interleukin 7 Mus musculus 50-54 1536940-6 1992 Further studies showed that the administration of IL-7 to mice that had been rendered leukopenic by the injection of cyclophosphamide (Cy) or 5-fluorouracil (5FU) exhibited a more rapid recovery and/or overshoot in their peripheral blood lymphocytes when compared with mice treated with Cy or 5FU alone. Fluorouracil 293-296 interleukin 7 Mus musculus 50-54 1523983-5 1992 5-FU, CPM and ADM enhanced the antitumor effect when combined with TNF, but CDDP did not. Fluorouracil 0-4 tumor necrosis factor Mus musculus 67-70 1564955-2 1992 Multilineage colony formation from mice that had been treated with 150 mg/kg 5-fluorouracil was assayed in cultures containing interleukin-3, interleukin-6, and erythropoietin. Fluorouracil 77-91 interleukin 3 Mus musculus 127-140 1564955-2 1992 Multilineage colony formation from mice that had been treated with 150 mg/kg 5-fluorouracil was assayed in cultures containing interleukin-3, interleukin-6, and erythropoietin. Fluorouracil 77-91 interleukin 6 Mus musculus 142-155 1540167-1 1992 Interferon-alpha (IFN alpha) increases the cytotoxicity of 5-fluorouracil (FUra) in vitro, and the combination has clinical efficacy against advanced colorectal cancer. Fluorouracil 59-73 interferon alpha 1 Homo sapiens 18-27 1540167-1 1992 Interferon-alpha (IFN alpha) increases the cytotoxicity of 5-fluorouracil (FUra) in vitro, and the combination has clinical efficacy against advanced colorectal cancer. Fluorouracil 75-79 interferon alpha 1 Homo sapiens 18-27 1540167-2 1992 IFN alpha treatment of HT-29 colon carcinoma cells induced a greater than two-fold increase in the intracellular levels of the active metabolite of FUra, FdUMP. Fluorouracil 148-152 interferon alpha 1 Homo sapiens 0-9 1540167-3 1992 Using cell extracts from HT-29 cells and FUra as substrate, IFN alpha produced a 1.9- and 8.7-fold increase, respectively, in the activities of uridine phosphorylase and pyrimidine nucleoside phosphorylase (PyNP). Fluorouracil 41-45 interferon alpha 1 Homo sapiens 60-69 1540167-4 1992 Furthermore, the effect was selective for the conversion of FUra to FdUMP, as IFN alpha did not increase the cellular levels of FUTP, nor did it change the extent of incorporation of FUra into RNA (or DNA). Fluorouracil 60-64 interferon alpha 1 Homo sapiens 78-87 1540167-5 1992 IFN alpha also had no effect on thymidine kinase activity, the second step in the activation of FUra. Fluorouracil 96-100 interferon alpha 1 Homo sapiens 0-9 1540167-6 1992 Hence the effect of IFN alpha on PyNP activity is likely a critical biochemical event that modulates the cytotoxicity of FUra. Fluorouracil 121-125 interferon alpha 1 Homo sapiens 20-29 1537072-0 1992 In vivo comparative therapeutic study of optimal administration of 5-fluorouracil and cisplatin using a newly established HST-1 human squamous-carcinoma cell line. Fluorouracil 67-81 fibroblast growth factor 4 Homo sapiens 122-127 1537082-6 1992 Although alpha IFN may enhance the toxicity of 5FU, the toxicity of this regimen remained manageable. Fluorouracil 47-50 interferon alpha 1 Homo sapiens 15-18 1370257-4 1992 However, pretreatment of target cells with 5-FU increased their susceptibility to NK activity and abolished the protective effect induced by IFN against NK-CMC. Fluorouracil 43-47 interferon alpha 1 Homo sapiens 141-144 1374741-6 1992 The serum level of IL-6 in 5-FU-treated mice was increased by SPR-901. Fluorouracil 27-31 interleukin 6 Mus musculus 19-23 1406088-6 1992 TdR-pretreated mice had higher 5FU anabolite (fluoronucleotide + fluoronucleoside) levels in their RIF-1 tumors than nonpretreated mice that received the same 5FU doses (56 +/- 15 SEM vs. 0 arbitrary units at the 5FU dose of 65 mg/kg, and 88 +/- 21 vs. 10 +/- 3 arbitrary units at 130 mg/kg 5FU; P less than .0001). Fluorouracil 31-34 replication timing regulatory factor 1 Mus musculus 99-104 1406460-6 1992 Oral administration of the skim-milk fraction to mice significantly reduced the susceptibility to the lethal toxicity of 5-fluorouracil (5 FU). Fluorouracil 121-135 Weaning weight-maternal milk Bos taurus 32-36 1421872-3 1992 Although IFN, given as 600,000 units/mouse daily sc x 14, and 5-FU, given as 60 mg/kg q4d x 3 ip, showed additive antitumor activity against Co-4, the thymidylate synthetase (TS) inhibition rate was unchanged in the tumors treated with the IFN/5-FU combination in comparison with those treated with 5-FU alone. Fluorouracil 62-66 interferon alpha 1 Homo sapiens 240-243 1421872-3 1992 Although IFN, given as 600,000 units/mouse daily sc x 14, and 5-FU, given as 60 mg/kg q4d x 3 ip, showed additive antitumor activity against Co-4, the thymidylate synthetase (TS) inhibition rate was unchanged in the tumors treated with the IFN/5-FU combination in comparison with those treated with 5-FU alone. Fluorouracil 244-248 interferon alpha 1 Homo sapiens 9-12 1421872-3 1992 Although IFN, given as 600,000 units/mouse daily sc x 14, and 5-FU, given as 60 mg/kg q4d x 3 ip, showed additive antitumor activity against Co-4, the thymidylate synthetase (TS) inhibition rate was unchanged in the tumors treated with the IFN/5-FU combination in comparison with those treated with 5-FU alone. Fluorouracil 244-248 interferon alpha 1 Homo sapiens 9-12 1940339-10 1991 This inhibition of the recovery of the bone marrow from 5FU treatment induced by rTGF-beta 1 was a delayed transient response because by day 16 the progenitor cell numbers and bone marrow cellularity were identical to the 5FU-treated marrow controls. Fluorouracil 56-59 transforming growth factor, beta 1 Rattus norvegicus 81-92 1940339-10 1991 This inhibition of the recovery of the bone marrow from 5FU treatment induced by rTGF-beta 1 was a delayed transient response because by day 16 the progenitor cell numbers and bone marrow cellularity were identical to the 5FU-treated marrow controls. Fluorouracil 222-225 transforming growth factor, beta 1 Rattus norvegicus 81-92 1798394-0 1991 Tumor bioenergetics and blood flow in RIF-1 murine tumors treated with 5-fluorouracil. Fluorouracil 71-85 replication timing regulatory factor 1 Mus musculus 38-43 1931710-5 1991 Due to multiplicity of mechanisms of action postulated for IFN alpha, the role of IFN alpha in the modulation of the cytotoxicity and therapeutic efficacy of FUra alone and in combination with CF has been evaluated in patients with advanced colorectal cancer and also in a variety of human cell lines in culture, including human colorectal cell lines, HCT-8, human bladder cell line RT-4 and leukaemia CEM cells. Fluorouracil 158-162 interferon alpha 1 Homo sapiens 82-91 1931710-6 1991 The results obtained in patients demonstrated that indeed the antitumour activity of FUra can be improved by the addition of IFN alpha with a response range from 26% to 76%. Fluorouracil 85-89 interferon alpha 1 Homo sapiens 125-134 1719644-13 1991 5-Fluorouracil also reverses the induction of human leukocyte antigens by IFN. Fluorouracil 0-14 interferon alpha 1 Homo sapiens 74-77 1719644-14 1991 Studies in the resistance model suggest that high doses of 5-FU by infusion for several days might be the optimal method for modulation of IFN-induced effects. Fluorouracil 59-63 interferon alpha 1 Homo sapiens 139-142 1781811-2 1991 IFN causes a highly significant change of the pharmacokinetic parameters of 5FU (p less than 0.001) compared to 5FU administration without IFN. Fluorouracil 76-79 interferon alpha 1 Homo sapiens 0-3 2060021-7 1991 The injection of 5-FU also decreased the cell numbers of whole spleen cells, B cells, and non-T non-B cells (Ig- and Thy-1- cells). Fluorouracil 17-21 thymus cell antigen 1, theta Mus musculus 117-122 1626952-6 1992 Furthermore, side effects of IFN/5-FU combination and dual modulation of 5-FU with IFN and LV were referred. Fluorouracil 73-77 interferon alpha 1 Homo sapiens 83-86 1355336-0 1992 Overexpression of erbB-2 protein in gastric adenocarcinoma--a potential role in therapeutic response to adjuvant 5-FU-doxorubicin regimen. Fluorouracil 113-117 erb-b2 receptor tyrosine kinase 2 Homo sapiens 18-24 1355336-4 1992 However, erbB-2 overexpression was an indicator for poor disease free survival (p = 0.0474), local relapse free survival (p = 0.0293), and overall survival (p = 0.0310) of the patients treated with surgery only (N = 51), while it did not show any effect on outcome of patients treated with 5-FU plus Doxorubicin (FA) as adjuvant chemotherapy (N = 58). Fluorouracil 290-294 erb-b2 receptor tyrosine kinase 2 Homo sapiens 9-15 1830034-4 1991 When 50 U/ml IFN-gamma were combined with 5-FU or FUdR, the antiproliferative effects were synergistic in those cell lines with sensitivity to IFN-gamma as a single agent, but not in the IFN-gamma-insensitive cell lines. Fluorouracil 42-46 interferon gamma Homo sapiens 143-152 1830034-4 1991 When 50 U/ml IFN-gamma were combined with 5-FU or FUdR, the antiproliferative effects were synergistic in those cell lines with sensitivity to IFN-gamma as a single agent, but not in the IFN-gamma-insensitive cell lines. Fluorouracil 42-46 interferon gamma Homo sapiens 143-152 1908937-0 1991 Multinuclear MR investigation of the metabolic response of the murine RIF-1 tumor to 5-fluorouracil chemotherapy. Fluorouracil 85-99 replication timing regulatory factor 1 Mus musculus 70-75 2043679-1 1991 The injection of 5-fluorouracil to partial hepatectomized rat prevented the rise of activities of thymidylate synthase and thymidine kinase as well as DNA synthesis in 24-h regenerating liver in a dose-dependent manner. Fluorouracil 17-31 thymidylate synthetase Rattus norvegicus 98-118 2043679-3 1991 The immunoblotting assay showed the existence of fluorodeoxyuridine monophosphate bound thymidylate synthase in 5-fluorouracil injected rat liver. Fluorouracil 112-126 thymidylate synthetase Rattus norvegicus 88-108 2043679-4 1991 These results indicate that the reduction of DNA synthesis in regenerating liver by 5-fluorouracil result from the inhibitions of the rise of activities of both thymidylate synthase and thymidine kinase, while the mechanisms in their inhibitions may be different. Fluorouracil 84-98 thymidylate synthetase Rattus norvegicus 161-181 1886590-5 1991 5-FU with AT-II (n = 5), Group C; i.a. Fluorouracil 0-4 angiotensinogen Homo sapiens 10-15 1886590-9 1991 5-FU with AT-II (n = 5). Fluorouracil 0-4 angiotensinogen Homo sapiens 10-15 1908937-1 1991 The metabolic response of the RIF-1 tumor to 5-fluorouracil (a single dose of 260 mg 5FU/kg, ip) was monitored in 10 mice using 19F and 31P MR spectroscopy. Fluorouracil 45-59 replication timing regulatory factor 1 Mus musculus 30-35 2285584-2 1990 The therapeutic regimen consisted of: (a) estrogenic suppression by aminoglutethimide 1 g/day + hydrocortisone 40 mg/day; surgical castration in premenopausal patients only; (b) FAC (5FU 500 mg/m2; ADM 50 mg/m2; CPA 500 mg/m2) for 3 weeks; (c) following randomization, exactly 24 h prior to chemotherapy, patients had to take 1 tablet of either placebo (PL) or 50 microgram ethinylestradiol (EE2). Fluorouracil 183-186 FA complementation group C Homo sapiens 178-181 1997177-1 1991 The metabolism of 5-fluorouracil (5FU) in tumors and livers of RIF-1 tumor-bearing C3H mice given i.p. Fluorouracil 18-32 replication timing regulatory factor 1 Mus musculus 63-68 1997177-1 1991 The metabolism of 5-fluorouracil (5FU) in tumors and livers of RIF-1 tumor-bearing C3H mice given i.p. Fluorouracil 34-37 replication timing regulatory factor 1 Mus musculus 63-68 1825140-3 1991 When tested with marrow cells harvested 2 days after injection of 5-fluorouracil at 150 mg/kg, IL-11 enhanced interleukin 3-dependent colony formation, whereas IL-11 alone supported only scant colony formation. Fluorouracil 66-80 interleukin 3 Mus musculus 110-123 1703493-9 1991 When sorted WGA+Lin- spleen cells of the 5-FU-treated mice were cultured in vitro in the presence of recombinant interleukin 3 (IL-3), interleukin 6 (IL-6), and granulocyte colony-stimulating factor (G-CSF), colony formation was observed only in wells with IL-3, whereas unfractionated spleen cells formed colonies in the presence of IL-3, IL-6, or G-CSF. Fluorouracil 41-45 interleukin 3 Mus musculus 113-132 1703493-9 1991 When sorted WGA+Lin- spleen cells of the 5-FU-treated mice were cultured in vitro in the presence of recombinant interleukin 3 (IL-3), interleukin 6 (IL-6), and granulocyte colony-stimulating factor (G-CSF), colony formation was observed only in wells with IL-3, whereas unfractionated spleen cells formed colonies in the presence of IL-3, IL-6, or G-CSF. Fluorouracil 41-45 interleukin 6 Mus musculus 135-148 1703493-9 1991 When sorted WGA+Lin- spleen cells of the 5-FU-treated mice were cultured in vitro in the presence of recombinant interleukin 3 (IL-3), interleukin 6 (IL-6), and granulocyte colony-stimulating factor (G-CSF), colony formation was observed only in wells with IL-3, whereas unfractionated spleen cells formed colonies in the presence of IL-3, IL-6, or G-CSF. Fluorouracil 41-45 interleukin 6 Mus musculus 150-154 1703493-9 1991 When sorted WGA+Lin- spleen cells of the 5-FU-treated mice were cultured in vitro in the presence of recombinant interleukin 3 (IL-3), interleukin 6 (IL-6), and granulocyte colony-stimulating factor (G-CSF), colony formation was observed only in wells with IL-3, whereas unfractionated spleen cells formed colonies in the presence of IL-3, IL-6, or G-CSF. Fluorouracil 41-45 interleukin 3 Mus musculus 128-132 1703493-9 1991 When sorted WGA+Lin- spleen cells of the 5-FU-treated mice were cultured in vitro in the presence of recombinant interleukin 3 (IL-3), interleukin 6 (IL-6), and granulocyte colony-stimulating factor (G-CSF), colony formation was observed only in wells with IL-3, whereas unfractionated spleen cells formed colonies in the presence of IL-3, IL-6, or G-CSF. Fluorouracil 41-45 interleukin 3 Mus musculus 257-261 1703493-9 1991 When sorted WGA+Lin- spleen cells of the 5-FU-treated mice were cultured in vitro in the presence of recombinant interleukin 3 (IL-3), interleukin 6 (IL-6), and granulocyte colony-stimulating factor (G-CSF), colony formation was observed only in wells with IL-3, whereas unfractionated spleen cells formed colonies in the presence of IL-3, IL-6, or G-CSF. Fluorouracil 41-45 interleukin 6 Mus musculus 340-344 2249187-2 1990 Preclinical data showed that the cytotoxic effects of 5-fluorouracil (5-FU) are augmented by interferon (IFN). Fluorouracil 54-68 interferon alpha 1 Homo sapiens 93-109 2249187-2 1990 Preclinical data showed that the cytotoxic effects of 5-fluorouracil (5-FU) are augmented by interferon (IFN). Fluorouracil 70-74 interferon alpha 1 Homo sapiens 93-109 2249187-3 1990 In a small study, 13 of 17 patients with advanced colorectal cancer responded to a regimen of 5-FU with IFN. Fluorouracil 94-98 interferon alpha 1 Homo sapiens 104-107 2131049-3 1990 This system was used to study ways in which to improve the efficacy of 5-FU, which was used in combination with alpha-2a interferon. Fluorouracil 71-75 adrenergic receptor, alpha 2a Mus musculus 112-120 2206997-3 1990 In 5-FU-induced anaemia, marked serum erythropoietin (Epo) elevation was observed in inverse correlation to blood Hb concentration and Hb concentration rapidly recovered to normal levels. Fluorouracil 3-7 erythropoietin Homo sapiens 38-52 1697499-2 1990 To determine whether interferon (IFN) is capable of augmenting the cytotoxic and cytokinetic effects of FUra, combinations of FUra and IFN alpha, -beta, and -gamma were tested against 2 human colon cancer cell lines in vitro. Fluorouracil 104-108 interferon alpha 1 Homo sapiens 21-31 1697499-3 1990 In a clonogenic assay, IFN alpha and -beta, at concentrations that produced less than 1 log cell kill, significantly increased the cytotoxic effects of FUra in both cell lines. Fluorouracil 152-156 interferon alpha 1 Homo sapiens 23-42 1697499-4 1990 IFN gamma also enhanced the cytotoxic effects of FUra, but unlike IFN alpha and -beta, only at the highest concentrations tested. Fluorouracil 49-53 interferon gamma Homo sapiens 0-9 1697499-10 1990 These results indicate that IFN is capable of increasing the cytotoxic actions of FUra and that this is separable from any cytokinetic effects produced by the interferons. Fluorouracil 82-86 interferon alpha 1 Homo sapiens 28-31 2402230-7 1990 Cesium sulfate gradient centrifugation was used to more accurately separate and analyze for DNA-incorporated 5-FU metabolites and confirmed that the absolute level of 5-FU in the DNA of the PEO4 cells was markedly decreased (6.5-fold) compared with that of the sensitive PEO1 cell line. Fluorouracil 167-171 twinkle mtDNA helicase Homo sapiens 271-275 2402230-8 1990 Moreover, time course studies demonstrated that the accumulated 5-FU in the DNA of the PEO4 cells was more rapidly removed compared with that in the PEO1 cells. Fluorouracil 64-68 twinkle mtDNA helicase Homo sapiens 149-153 2257211-1 1990 The effects of treatment with 5-FU/folinic acid on interleukin-2 related lymphocyte responses was investigated in 21 patients with advanced colorectal cancer. Fluorouracil 30-34 interleukin 2 Homo sapiens 51-64 1697502-4 1990 Simultaneous treatment of H630 with subinhibitory concentrations of IFN-gamma and 5-FU produced a significant enhancement of the 5-FU-associated growth inhibition. Fluorouracil 129-133 interferon gamma Homo sapiens 68-77 1697502-7 1990 A 24-h exposure to 1 microM 5-FU in the H630 line resulted in a 3.1-fold increase in the total amount of TS, while in the 5-FU/IFN-gamma-treated cells TS remained unchanged from non-drug-treated control levels. Fluorouracil 28-32 interferon gamma Homo sapiens 127-136 1697502-7 1990 A 24-h exposure to 1 microM 5-FU in the H630 line resulted in a 3.1-fold increase in the total amount of TS, while in the 5-FU/IFN-gamma-treated cells TS remained unchanged from non-drug-treated control levels. Fluorouracil 122-126 interferon gamma Homo sapiens 127-136 1697502-8 1990 Moreover, we found that free thymidylate synthase in the 5-FU/IFN-gamma-treated cells was significantly decreased, as compared to the cells treated with 5-FU alone. Fluorouracil 57-61 interferon gamma Homo sapiens 62-71 1697502-8 1990 Moreover, we found that free thymidylate synthase in the 5-FU/IFN-gamma-treated cells was significantly decreased, as compared to the cells treated with 5-FU alone. Fluorouracil 153-157 interferon gamma Homo sapiens 62-71 1697502-12 1990 These studies contribute to a growing understanding of the complex interaction between 5-FU and IFN-gamma. Fluorouracil 87-91 interferon gamma Homo sapiens 96-105 2206997-3 1990 In 5-FU-induced anaemia, marked serum erythropoietin (Epo) elevation was observed in inverse correlation to blood Hb concentration and Hb concentration rapidly recovered to normal levels. Fluorouracil 3-7 erythropoietin Homo sapiens 54-57 2114374-9 1990 The addition of TNF/IFN-gamma to clinically achievable concentrations of 5-FU in both schedules resulted in additive cytotoxicity. Fluorouracil 73-77 interferon gamma Homo sapiens 16-29 2114374-10 1990 For example, the addition of 10 ng/ml of both TNF and IFN-gamma to 96 hr of 0.1 microgram/ml 5-FU resulted in 10%, 5%, and 20% of control growth for the HCT 116 cell line, SKCO1 cell line, and VACO 9P cell line, respectively. Fluorouracil 93-97 tumor necrosis factor Homo sapiens 46-49 2114374-10 1990 For example, the addition of 10 ng/ml of both TNF and IFN-gamma to 96 hr of 0.1 microgram/ml 5-FU resulted in 10%, 5%, and 20% of control growth for the HCT 116 cell line, SKCO1 cell line, and VACO 9P cell line, respectively. Fluorouracil 93-97 interferon gamma Homo sapiens 54-63 2114374-11 1990 The addition of 10 ng/ml of both TNF and IFN-gamma to 1 hr of 50 micrograms/ml of 5-FU inhibited all cell growth in all 3 cell lines. Fluorouracil 82-86 tumor necrosis factor Homo sapiens 33-36 2114374-11 1990 The addition of 10 ng/ml of both TNF and IFN-gamma to 1 hr of 50 micrograms/ml of 5-FU inhibited all cell growth in all 3 cell lines. Fluorouracil 82-86 interferon gamma Homo sapiens 41-50 2138912-5 1990 Conversely, 5-FU given on days 5-8 after implantation augmented the antitumor effects of rTNF-alpha. Fluorouracil 12-16 tumor necrosis factor Rattus norvegicus 89-99 2111746-3 1990 Recurrent widespread metastatic lesions have been treated over a 10-year period by repeated cycles of the nitrosourea CCNU and 5-fluorouracil with evidence of tumour regression and reduction of circulating growth hormone (GH) and urinary 5HIAA excretion. Fluorouracil 127-141 growth hormone 1 Homo sapiens 206-220 2111746-3 1990 Recurrent widespread metastatic lesions have been treated over a 10-year period by repeated cycles of the nitrosourea CCNU and 5-fluorouracil with evidence of tumour regression and reduction of circulating growth hormone (GH) and urinary 5HIAA excretion. Fluorouracil 127-141 growth hormone 1 Homo sapiens 222-224 2350576-3 1990 The megakaryocytic progenitors that survive exposure to 5-fluorouracil (5-FU) exhibited a more significant response to IL-6 and IL-3. Fluorouracil 56-70 interleukin 6 Mus musculus 119-123 2350576-3 1990 The megakaryocytic progenitors that survive exposure to 5-fluorouracil (5-FU) exhibited a more significant response to IL-6 and IL-3. Fluorouracil 56-70 interleukin 3 Mus musculus 128-132 2350576-3 1990 The megakaryocytic progenitors that survive exposure to 5-fluorouracil (5-FU) exhibited a more significant response to IL-6 and IL-3. Fluorouracil 72-76 interleukin 6 Mus musculus 119-123 2350576-3 1990 The megakaryocytic progenitors that survive exposure to 5-fluorouracil (5-FU) exhibited a more significant response to IL-6 and IL-3. Fluorouracil 72-76 interleukin 3 Mus musculus 128-132 2350576-7 1990 The combination of granulocyte colony-stimulating factor or granulocyte-macrophage colony stimulating factor with IL-3 resulted in an increase in the granulocyte-macrophage colony growth of bone marrow cells of 5-FU-treated mice or normal mice, respectively, but had little effect on the enhancement of pure and mixed megakaryocyte colony growth. Fluorouracil 211-215 interleukin 3 Mus musculus 114-118 2334892-0 1990 Interleukin 6 perfusion stimulates reconstitution of the immune and hematopoietic systems after 5-fluorouracil treatment. Fluorouracil 96-110 interleukin 6 Mus musculus 0-13 2334892-3 1990 IL-6 perfusion significantly augmented anti-sheep RBC antibody responses depressed by 5-FU (150 mg/kg) treatment. Fluorouracil 86-90 interleukin 6 Mus musculus 0-4 2334892-4 1990 IL-6 also was shown to stimulate hematological recovery in mice treated with 5-FU. Fluorouracil 77-81 interleukin 6 Mus musculus 0-4 2334892-7 1990 Furthermore, it was found that the endogenous IL-6 level in serum increased after 5-FU treatment, which suggests that IL-6 may play some role in the recovery of the immune and hematopoietic systems. Fluorouracil 82-86 interleukin 6 Mus musculus 46-50 2334892-7 1990 Furthermore, it was found that the endogenous IL-6 level in serum increased after 5-FU treatment, which suggests that IL-6 may play some role in the recovery of the immune and hematopoietic systems. Fluorouracil 82-86 interleukin 6 Mus musculus 118-122 2106500-1 1990 In Bloom"s syndrome (BS) the regulation of uracil-DNA glycosylase, an enzyme involved in the repair of DNA containing 5-FU, is altered. Fluorouracil 118-122 uracil DNA glycosylase Homo sapiens 43-65 2105896-6 1990 Inhibition of RNA or protein synthesis by actinomycin D or cycloheximide did not prevent the antiproliferative action of IFN gamma nor the induction of monocytic differentiation, yet these two compounds blocked the priming effect of IFN gamma on the potentiation of 5-FU action. Fluorouracil 266-270 interferon gamma Homo sapiens 233-242 2138912-7 1990 The results show that the timing of 5-FU treatment is important when attempting to enhance the antitumor effects of rTNF-alpha, and suggest that these effects are directly associated with newly formed fine capillaries in the tumor. Fluorouracil 36-40 tumor necrosis factor Rattus norvegicus 116-126 33822896-8 2021 Moreover, andrographis significantly downregulated 5FU-induced DKK1 overexpression, accompanied with enhanced anti-tumor effects by abrogating downstream Akt-phosphorylation. Fluorouracil 51-54 AKT serine/threonine kinase 1 Homo sapiens 154-157 2300389-1 1990 We tried to study the protection of allopurinol (HPP) from the toxicity of 5-fluorouracil (5-FU). Fluorouracil 75-89 familial progressive hyperpigmentation 1 Homo sapiens 49-52 2300389-1 1990 We tried to study the protection of allopurinol (HPP) from the toxicity of 5-fluorouracil (5-FU). Fluorouracil 91-95 familial progressive hyperpigmentation 1 Homo sapiens 49-52 2300389-8 1990 We conclude that HPP can diminish the side effects, especially myelosuppression, allowing an increase in the maximum tolerated dose of 5-FU; even if combined with other cytostatic drugs. Fluorouracil 135-139 familial progressive hyperpigmentation 1 Homo sapiens 17-20 33794252-11 2021 The propolis combined with 5FU reduced the expression of Cox-2, iNOS, and beta-catenin proteins. Fluorouracil 27-30 nitric oxide synthase 2, inducible Mus musculus 64-68 33814416-9 2021 Following 5-FU treatment, Tie2-Cre; Etv2 CKO mice revealed a significant reduction in capillary density, anagen induction, and hair restoration when compared with controls. Fluorouracil 10-14 TEK receptor tyrosine kinase Mus musculus 26-30 33798968-4 2021 We showed that Pos3Aa-mediated delivery of tumor suppressor p53 protein, a promising therapeutic candidate found to be inactivated in nearly half of human cancers, resulted in the restoration of p53 function in p53-deficient cancer cells, and thereby sensitized them to 5-fluorouracil chemotherapy as demonstrated in in vitro and in vivo models. Fluorouracil 270-284 tumor protein p53 Homo sapiens 60-63 33798968-4 2021 We showed that Pos3Aa-mediated delivery of tumor suppressor p53 protein, a promising therapeutic candidate found to be inactivated in nearly half of human cancers, resulted in the restoration of p53 function in p53-deficient cancer cells, and thereby sensitized them to 5-fluorouracil chemotherapy as demonstrated in in vitro and in vivo models. Fluorouracil 270-284 tumor protein p53 Homo sapiens 195-198 33798968-4 2021 We showed that Pos3Aa-mediated delivery of tumor suppressor p53 protein, a promising therapeutic candidate found to be inactivated in nearly half of human cancers, resulted in the restoration of p53 function in p53-deficient cancer cells, and thereby sensitized them to 5-fluorouracil chemotherapy as demonstrated in in vitro and in vivo models. Fluorouracil 270-284 tumor protein p53 Homo sapiens 195-198 33808326-7 2021 Substitution of either of these two residues to alanine or inhibition of ATR/ATM kinase activity abolished nuclear localization of SRPK1 and conferred tolerance to 5-FU treatment. Fluorouracil 164-168 ATR serine/threonine kinase Homo sapiens 73-76 33816278-0 2021 CMPK1 Regulated by miR-130b Attenuates Response to 5-FU Treatment in Gastric Cancer. Fluorouracil 51-55 microRNA 130b Homo sapiens 19-27 33764853-4 2021 To understand pre-binding factors contributing to the temporal gene regulation by p53, we performed time-course RNA sequencing experiments in human colon cancer cell line HCT116 treated with fluorouracil to identify early and late genes. Fluorouracil 191-203 tumor protein p53 Homo sapiens 82-85 33816278-5 2021 Further analysis demonstrated that miR-130b as a key epigenetic regulator of CMPK1, and miR-130b-mediated attenuation of CMPK1 resulted in resistance of gastric cancer cells to DNA damage and cell death after treatment with 5-FU. Fluorouracil 224-228 microRNA 130b Homo sapiens 35-43 33816278-5 2021 Further analysis demonstrated that miR-130b as a key epigenetic regulator of CMPK1, and miR-130b-mediated attenuation of CMPK1 resulted in resistance of gastric cancer cells to DNA damage and cell death after treatment with 5-FU. Fluorouracil 224-228 microRNA 130b Homo sapiens 88-96 33816278-7 2021 Thus, this newly identified miR-130b-CMPK1 axis suggests a potentially new chemotherapeutic strategy for improved response to 5-FU therapy. Fluorouracil 126-130 microRNA 130b Homo sapiens 28-36 33793771-0 2021 miR-424-5p reduces 5-fluorouracil resistance possibly by inhibiting Src/focal adhesion kinase signalling-mediated epithelial-mesenchymal transition in colon cancer cells. Fluorouracil 19-33 microRNA 424 Homo sapiens 0-7 33793771-9 2021 Furthermore, the miR-424-5p mimic downregulated vimentin and upregulated E-cadherin in 5-fluorouracil-resistant HT-29 cells, whereas the miR-424-5p inhibitor exhibited opposite effects. Fluorouracil 87-101 cadherin 1 Homo sapiens 73-83 33793771-0 2021 miR-424-5p reduces 5-fluorouracil resistance possibly by inhibiting Src/focal adhesion kinase signalling-mediated epithelial-mesenchymal transition in colon cancer cells. Fluorouracil 19-33 SRC proto-oncogene, non-receptor tyrosine kinase Homo sapiens 68-71 33793771-10 2021 The miR-424-5p inhibitor significantly inhibited 5-fluorouracil-induced HT-29 cell apoptosis and Src and focal adhesion kinase phosphorylation, whereas the miR-424-5p mimic showed opposite effects. Fluorouracil 49-63 microRNA 424 Homo sapiens 4-11 33793771-7 2021 KEY FINDINGS: miR-424-5p was downregulated in 5-fluorouracil-resistant HT-29 cells. Fluorouracil 46-60 microRNA 424 Homo sapiens 14-21 33793771-10 2021 The miR-424-5p inhibitor significantly inhibited 5-fluorouracil-induced HT-29 cell apoptosis and Src and focal adhesion kinase phosphorylation, whereas the miR-424-5p mimic showed opposite effects. Fluorouracil 49-63 SRC proto-oncogene, non-receptor tyrosine kinase Homo sapiens 97-100 33793771-12 2021 CONCLUSIONS: miR-424-5p suppressed epithelial-mesenchymal transition by inhibiting the Src/focal adhesion kinase signalling pathway to reduce 5-fluorouracil resistance in colon cancer cells. Fluorouracil 142-156 microRNA 424 Homo sapiens 13-20 33793771-8 2021 A miR-424-5p mimic enhanced the sensitivity of the resistant cells to 5-fluorouracil, whereas a miR-424-5p inhibitor promoted 5-fluorouracil resistance in HT-29 cells. Fluorouracil 70-84 microRNA 424 Homo sapiens 2-9 33793771-12 2021 CONCLUSIONS: miR-424-5p suppressed epithelial-mesenchymal transition by inhibiting the Src/focal adhesion kinase signalling pathway to reduce 5-fluorouracil resistance in colon cancer cells. Fluorouracil 142-156 SRC proto-oncogene, non-receptor tyrosine kinase Homo sapiens 87-90 33793771-9 2021 Furthermore, the miR-424-5p mimic downregulated vimentin and upregulated E-cadherin in 5-fluorouracil-resistant HT-29 cells, whereas the miR-424-5p inhibitor exhibited opposite effects. Fluorouracil 87-101 microRNA 424 Homo sapiens 17-24 33030957-8 2021 Knockout of PD-L1 was shown to attenuate the induction of DNA double-strand breaks (pH2AX) and caspase-3 cleavage by 5-fluorouracil (5-FU) and paclitaxel compared to parental CRC cells. Fluorouracil 117-131 caspase 3 Homo sapiens 95-104 33030957-8 2021 Knockout of PD-L1 was shown to attenuate the induction of DNA double-strand breaks (pH2AX) and caspase-3 cleavage by 5-fluorouracil (5-FU) and paclitaxel compared to parental CRC cells. Fluorouracil 133-137 caspase 3 Homo sapiens 95-104 26640560-0 2015 Hedyotis diffusa Willd overcomes 5-fluorouracil resistance in human colorectal cancer HCT-8/5-FU cells by downregulating the expression of P-glycoprotein and ATP-binding casette subfamily G member 2. Fluorouracil 33-47 ATP binding cassette subfamily B member 1 Homo sapiens 139-153 33790159-6 2021 She was treated with weekly infusion of methotrexate 100 mg/m2 plus 5-fluorouracil 600 mg/m2 for 4 courses; and she completely recovered from DIC. Fluorouracil 68-82 solute carrier family 25 member 10 Homo sapiens 142-145 33033330-8 2020 This study demonstrated that the VLNP can be used to deliver chemically modified 5-FU derivatives to cancer cells overexpressing EGFR, expanding the applications of the VLNP in targeted delivery of chemotherapeutic agents to cancer cells overexpressing this transmembrane receptor. Fluorouracil 81-85 epidermal growth factor receptor Homo sapiens 129-133 33816780-0 2021 The lncRNA DLGAP1-AS1/miR-149-5p/TGFB2 axis contributes to colorectal cancer progression and 5-FU resistance by regulating smad2 pathway. Fluorouracil 93-97 arylsulfatase B Mus musculus 18-21 33816780-0 2021 The lncRNA DLGAP1-AS1/miR-149-5p/TGFB2 axis contributes to colorectal cancer progression and 5-FU resistance by regulating smad2 pathway. Fluorouracil 93-97 transforming growth factor, beta 2 Mus musculus 33-38 33816780-0 2021 The lncRNA DLGAP1-AS1/miR-149-5p/TGFB2 axis contributes to colorectal cancer progression and 5-FU resistance by regulating smad2 pathway. Fluorouracil 93-97 SMAD family member 2 Mus musculus 123-128 33816780-3 2021 This work aims to analyze the functions and molecular basis of DLGAP1-AS1 in CRC progression and 5-fluorouracil resistance. Fluorouracil 97-111 arylsulfatase B Mus musculus 70-73 33816780-10 2021 These new findings indicate that DLGAP1-AS1 knockdown inhibited the progression of CRC and enhanced the 5-FU sensitivity of CRC cells through miR-149-5p/TGFB2 regulatory axis, suggesting that DLGAP1-AS1 may be a promising therapeutic target for CRC. Fluorouracil 104-108 arylsulfatase B Mus musculus 40-43 33816780-10 2021 These new findings indicate that DLGAP1-AS1 knockdown inhibited the progression of CRC and enhanced the 5-FU sensitivity of CRC cells through miR-149-5p/TGFB2 regulatory axis, suggesting that DLGAP1-AS1 may be a promising therapeutic target for CRC. Fluorouracil 104-108 transforming growth factor, beta 2 Mus musculus 153-158 33816780-10 2021 These new findings indicate that DLGAP1-AS1 knockdown inhibited the progression of CRC and enhanced the 5-FU sensitivity of CRC cells through miR-149-5p/TGFB2 regulatory axis, suggesting that DLGAP1-AS1 may be a promising therapeutic target for CRC. Fluorouracil 104-108 arylsulfatase B Mus musculus 199-202 26386386-3 2015 Overexpression of a multidrug resistance (MDR) transporter ABCG2 in vitro has been shown to cause resistance to 5-fluorouracil (5-FU) and irinotecan, components of the most commonly adopted regimens for treating CRC. Fluorouracil 112-126 ATP binding cassette subfamily G member 2 (Junior blood group) Homo sapiens 59-64 26386386-3 2015 Overexpression of a multidrug resistance (MDR) transporter ABCG2 in vitro has been shown to cause resistance to 5-fluorouracil (5-FU) and irinotecan, components of the most commonly adopted regimens for treating CRC. Fluorouracil 128-132 ATP binding cassette subfamily G member 2 (Junior blood group) Homo sapiens 59-64 26386386-8 2015 On the contrary, the tumors from patients not responding to 5-FU-based chemotherapy have higher ABCG2 level than the adjacent normal tissues. Fluorouracil 60-64 ATP binding cassette subfamily G member 2 (Junior blood group) Homo sapiens 96-101 22233820-2 2011 5-FU blocks thymidylate synthase (TS) which cross-links p53 mRNA, inhibiting its synthesis. Fluorouracil 0-4 tumor protein p53 Homo sapiens 56-59 25175038-9 2014 In addition, we found that IGF-1R was associated with the response to standard chemotherapy drugs 5-FU and cisplatin in an ESCC cell line. Fluorouracil 98-102 insulin-like growth factor I receptor Mus musculus 27-33 22233820-4 2011 Enough p53 mutations can confer resistance to chemotherapy using anthracyclines and 5-FU, while are associated with improved responses to TXT. Fluorouracil 84-88 tumor protein p53 Homo sapiens 7-10 34883427-2 2022 Manuka honey, alone and more in combination with 5-Fu, reduced the weight, the diameter and mass density of the spheroids and induced apoptosis through the downregulation of many apoptosis inhibitors, including IAPs (Livin, Survivin, XIAP), IGFs (IGF-I, IGF-II and IGF-IR) and HSPs (HSP-27, HSP-60 and HSP-70). Fluorouracil 49-53 insulin like growth factor 1 Homo sapiens 247-252 34658120-12 2022 Rescue experiments demonstrated that restoration of miR-338-3p in HAGLR-overexpressing HGC27 5-Fu R cells successfully overrode the HAGLR-promoted 5-Fu resistance through targeting LDHA. Fluorouracil 93-97 lactate dehydrogenase A Homo sapiens 181-185 34633539-9 2022 Groups with EP and treated with 5-FU or CIS showed high immunolabelling pattern of RANKL, TNF-alpha, and IL-1beta, moderate of BAX, and low of HIF-1alpha. Fluorouracil 32-36 tumor necrosis factor Rattus norvegicus 90-99 34633539-9 2022 Groups with EP and treated with 5-FU or CIS showed high immunolabelling pattern of RANKL, TNF-alpha, and IL-1beta, moderate of BAX, and low of HIF-1alpha. Fluorouracil 32-36 interleukin 1 alpha Rattus norvegicus 105-113 34196940-2 2022 The present study demonstrated that estrogen-related receptor alpha (ERRalpha) was upregulated in cisplatin- and fluorouracil-resistant NPC cells. Fluorouracil 113-125 estrogen related receptor alpha Homo sapiens 36-67 34196940-2 2022 The present study demonstrated that estrogen-related receptor alpha (ERRalpha) was upregulated in cisplatin- and fluorouracil-resistant NPC cells. Fluorouracil 113-125 estrogen related receptor alpha Homo sapiens 69-77 34658120-12 2022 Rescue experiments demonstrated that restoration of miR-338-3p in HAGLR-overexpressing HGC27 5-Fu R cells successfully overrode the HAGLR-promoted 5-Fu resistance through targeting LDHA. Fluorouracil 147-151 lactate dehydrogenase A Homo sapiens 181-185 34363017-6 2022 In addition, CD63-deficient HSCs exhibit impaired quiescence and long-term repopulating capacity, accompanied by increased sensitivity to irradiation and 5-fluorouracil treatment. Fluorouracil 154-168 CD63 antigen Mus musculus 13-17 34800596-7 2022 Our data revealed that 5-FU could induce cardiotoxicity which was detected as significant increases of troponin I, lactate dehydrogenase (LDH), creatine kinase- MB (CK-MB), endothelin receptors, malondialdehyde (MDA), toll like receptor4 (TLR4), myeloid differentiation primary response 88 (MyD88), nuclear factor kappa B (NFkappaB), and caspase 3 levels. Fluorouracil 23-27 toll-like receptor 4 Rattus norvegicus 218-237 34800596-7 2022 Our data revealed that 5-FU could induce cardiotoxicity which was detected as significant increases of troponin I, lactate dehydrogenase (LDH), creatine kinase- MB (CK-MB), endothelin receptors, malondialdehyde (MDA), toll like receptor4 (TLR4), myeloid differentiation primary response 88 (MyD88), nuclear factor kappa B (NFkappaB), and caspase 3 levels. Fluorouracil 23-27 toll-like receptor 4 Rattus norvegicus 239-243 34370147-0 2022 Synergistic effects of Rapamycin and Fluorouracil to treat a gastric tumor in a PTEN conditional deletion mouse model. Fluorouracil 37-49 phosphatase and tensin homolog Mus musculus 80-84 34370147-3 2022 The purpose of the study was to investigate the combined treatment of gastric tumorigenesis using Rapamycin and Fluorouracil (5-Fu) through interfering with the Akt/mTOR pathway in a mouse model with PTEN conditional deletion. Fluorouracil 112-124 thymoma viral proto-oncogene 1 Mus musculus 161-164 34370147-3 2022 The purpose of the study was to investigate the combined treatment of gastric tumorigenesis using Rapamycin and Fluorouracil (5-Fu) through interfering with the Akt/mTOR pathway in a mouse model with PTEN conditional deletion. Fluorouracil 112-124 phosphatase and tensin homolog Mus musculus 200-204 34370147-3 2022 The purpose of the study was to investigate the combined treatment of gastric tumorigenesis using Rapamycin and Fluorouracil (5-Fu) through interfering with the Akt/mTOR pathway in a mouse model with PTEN conditional deletion. Fluorouracil 126-130 thymoma viral proto-oncogene 1 Mus musculus 161-164 34370147-3 2022 The purpose of the study was to investigate the combined treatment of gastric tumorigenesis using Rapamycin and Fluorouracil (5-Fu) through interfering with the Akt/mTOR pathway in a mouse model with PTEN conditional deletion. Fluorouracil 126-130 phosphatase and tensin homolog Mus musculus 200-204 34821902-6 2021 Moreover, GA could up-regulate the expression of neuronal survival and growth-related proteins, such as BDNF, p-ERK, p-CREB, p-Akt, p-GSK3beta, Nrf2, p-mTOR, and p-S6, in the hippocampi of 5-FU-treated mice. Fluorouracil 189-193 mitogen-activated protein kinase 1 Mus musculus 112-115 34738322-3 2022 However, the ability of 5-FU to induce TNT formation in cancer cells and potentially enhance survival has not been explored. Fluorouracil 24-28 chromosome 16 open reading frame 82 Homo sapiens 39-42 34738322-4 2022 In this study, we examined whether 5-FU can induce TNT formation in MCF-7 breast cancer cells. Fluorouracil 35-39 chromosome 16 open reading frame 82 Homo sapiens 51-54 34738322-5 2022 Cytotoxic doses of 5-FU (150 - 350 muM) were observed to significantly induce TNT formation beginning at 24 hours after exposure. Fluorouracil 19-23 chromosome 16 open reading frame 82 Homo sapiens 78-81 34738322-8 2022 5-FU-induced TNT formation was inhibited by over 80% following treatment with the F-actin-depolymerizing agent, cytochalasin B (cytoB). Fluorouracil 0-4 chromosome 16 open reading frame 82 Homo sapiens 13-16 34738322-9 2022 The inhibition of TNTs by cytoB corresponded with increased 5-FU-induced cytotoxicity by 30-62% starting at 48 hours, suggesting TNT formation aides in MCF-7 cell survival against 5-FU. Fluorouracil 60-64 chromosome 16 open reading frame 82 Homo sapiens 129-132 34738322-9 2022 The inhibition of TNTs by cytoB corresponded with increased 5-FU-induced cytotoxicity by 30-62% starting at 48 hours, suggesting TNT formation aides in MCF-7 cell survival against 5-FU. Fluorouracil 180-184 chromosome 16 open reading frame 82 Homo sapiens 129-132 34954811-8 2022 For most skin reactions, severe ones were more common in patients treated with 5-fluorouracil 5% cream BID than in those treated with 5-fluorouracil 4% cream OD (P < 0.05). Fluorouracil 79-93 BH3 interacting domain death agonist Homo sapiens 103-106 34970530-8 2021 Mechanistically, 2b induced apoptosis-dependent anticancer effect (43%) higher than that of 5-fluorouracil (34.95%) in three studied cancer cell lines, activated p53 (47%), downregulated the Bcl2 gene (1.25-fold), and upregulated p21 (2-fold) in the treated cancer cells. Fluorouracil 92-106 tumor protein p53 Homo sapiens 162-165 34970530-8 2021 Mechanistically, 2b induced apoptosis-dependent anticancer effect (43%) higher than that of 5-fluorouracil (34.95%) in three studied cancer cell lines, activated p53 (47%), downregulated the Bcl2 gene (1.25-fold), and upregulated p21 (2-fold) in the treated cancer cells. Fluorouracil 92-106 BCL2 apoptosis regulator Homo sapiens 191-195 34312098-2 2022 The aim of this study is to compare the efficacy and late-onset cardiac toxicity of neoadjuvant chemotherapy regimens, trastuzumab plus paclitaxel followed by 5-fluorouracil, epirubicin, and cyclophosphamide (PH-FECH) versus trastuzumab plus docetaxel and carboplatin (TCH), for human epidermal growth factor receptor 2-positive (HER2+) breast cancer (BC). Fluorouracil 159-173 erb-b2 receptor tyrosine kinase 2 Homo sapiens 285-319 34312098-2 2022 The aim of this study is to compare the efficacy and late-onset cardiac toxicity of neoadjuvant chemotherapy regimens, trastuzumab plus paclitaxel followed by 5-fluorouracil, epirubicin, and cyclophosphamide (PH-FECH) versus trastuzumab plus docetaxel and carboplatin (TCH), for human epidermal growth factor receptor 2-positive (HER2+) breast cancer (BC). Fluorouracil 159-173 erb-b2 receptor tyrosine kinase 2 Homo sapiens 330-334 34665902-10 2022 The immunoblotting analysis also showed that thymol significantly inhibited the 5-FU-induced expression of nuclear factor-kappaB, tumor necrosis factor-alpha, and transforming growth factor beta-1 (TGF-beta1), in addition to the suppression of p38 and phosphorylated c-Jun N-terminal kinases (p-JNK) mitogen-activated protein kinase proteins" expressions. Fluorouracil 80-84 tumor necrosis factor Rattus norvegicus 130-157 34665902-10 2022 The immunoblotting analysis also showed that thymol significantly inhibited the 5-FU-induced expression of nuclear factor-kappaB, tumor necrosis factor-alpha, and transforming growth factor beta-1 (TGF-beta1), in addition to the suppression of p38 and phosphorylated c-Jun N-terminal kinases (p-JNK) mitogen-activated protein kinase proteins" expressions. Fluorouracil 80-84 transforming growth factor, beta 1 Rattus norvegicus 163-196 34665902-10 2022 The immunoblotting analysis also showed that thymol significantly inhibited the 5-FU-induced expression of nuclear factor-kappaB, tumor necrosis factor-alpha, and transforming growth factor beta-1 (TGF-beta1), in addition to the suppression of p38 and phosphorylated c-Jun N-terminal kinases (p-JNK) mitogen-activated protein kinase proteins" expressions. Fluorouracil 80-84 transforming growth factor, beta 1 Rattus norvegicus 198-207 34951582-7 2022 EGFR and KRAS gene expression analysis under the influence of PFNPs, FGNPs, PFGNPs, and 5-FU was studied and observed maximum potency for PFNPs. Fluorouracil 88-92 epidermal growth factor receptor Homo sapiens 0-4 34916479-0 2021 Galangin Enhances Anticancer Efficacy of 5-Fluorouracil in Esophageal Cancer Cells and Xenografts Through NLR Family Pyrin Domain Containing 3 (NLRP3) Downregulation. Fluorouracil 41-55 NLR family pyrin domain containing 3 Homo sapiens 106-142 34916479-8 2021 NLRP3 was identified as being significantly activated by 5-FU, but galangin treatment reversed the effect and inhibited NLRP3 expression, which was accompanied by downregulated interleukin-1b levels. Fluorouracil 57-61 NLR family pyrin domain containing 3 Homo sapiens 0-5 34916479-8 2021 NLRP3 was identified as being significantly activated by 5-FU, but galangin treatment reversed the effect and inhibited NLRP3 expression, which was accompanied by downregulated interleukin-1b levels. Fluorouracil 57-61 NLR family pyrin domain containing 3 Homo sapiens 120-125 34916479-8 2021 NLRP3 was identified as being significantly activated by 5-FU, but galangin treatment reversed the effect and inhibited NLRP3 expression, which was accompanied by downregulated interleukin-1b levels. Fluorouracil 57-61 interleukin 1 beta Homo sapiens 177-191 34821902-6 2021 Moreover, GA could up-regulate the expression of neuronal survival and growth-related proteins, such as BDNF, p-ERK, p-CREB, p-Akt, p-GSK3beta, Nrf2, p-mTOR, and p-S6, in the hippocampi of 5-FU-treated mice. Fluorouracil 189-193 cAMP responsive element binding protein 1 Mus musculus 119-123 34821902-6 2021 Moreover, GA could up-regulate the expression of neuronal survival and growth-related proteins, such as BDNF, p-ERK, p-CREB, p-Akt, p-GSK3beta, Nrf2, p-mTOR, and p-S6, in the hippocampi of 5-FU-treated mice. Fluorouracil 189-193 thymoma viral proto-oncogene 1 Mus musculus 127-130 34821902-6 2021 Moreover, GA could up-regulate the expression of neuronal survival and growth-related proteins, such as BDNF, p-ERK, p-CREB, p-Akt, p-GSK3beta, Nrf2, p-mTOR, and p-S6, in the hippocampi of 5-FU-treated mice. Fluorouracil 189-193 nuclear factor, erythroid derived 2, like 2 Mus musculus 144-148 34710829-0 2021 Affibody-conjugated 5-fluorouracil prodrug system preferentially targets and inhibits HER2-expressing cancer cells. Fluorouracil 20-34 erb-b2 receptor tyrosine kinase 2 Homo sapiens 86-90 34034636-0 2021 Insulin reverses choriocarcinoma 5- fluorouracil resistance. Fluorouracil 33-48 insulin Homo sapiens 0-7 34890366-0 2021 Anemoside B4 sensitizes human colorectal cancer to fluorouracil-based chemotherapy through src-mediated cell apoptosis. Fluorouracil 51-63 SRC proto-oncogene, non-receptor tyrosine kinase Homo sapiens 91-94 34607103-11 2021 Moreover, the CS2 group could also respond to 5-fluorouracil, cisplatin, and paclitaxel. Fluorouracil 46-60 chorionic somatomammotropin hormone 2 Homo sapiens 14-17 34338150-8 2021 Further, associated in vitro experiments confirmed that CEMIP downregulation suppressed the proliferation and migration of GC cells and impaired the chemoresistance of GC cells to 5-fluorouracil.Our study effectively identified and validated prognostic biomarkers for GC, laying a new foundation for the therapeutic target, occurrence, and development of gastric cancer. Fluorouracil 180-194 cell migration inducing hyaluronidase 1 Homo sapiens 56-61 34546854-0 2021 Exosomal-mediated transfer of APCDD1L-AS1 induces 5-fluorouracil resistance in oral squamous cell carcinoma via miR-1224-5p/nuclear receptor binding SET domain protein 2 (NSD2) axis. Fluorouracil 50-64 nuclear receptor binding SET domain protein 2 Homo sapiens 171-175 34546854-8 2021 Herein, high APCDD1L-AS1 expression was shown in OSCC tissues and cells resistant to 5-FU and related to the worse prognosis of OSCC patients. Fluorouracil 85-89 APCDD1L divergent transcript Homo sapiens 13-24 34546854-10 2021 Besides, extracellular APCDD1L-AS1 could be transferred to sensitive cells via exosome incorporation, thereby transmitting 5-FU resistance in OSCC cells. Fluorouracil 123-127 APCDD1L divergent transcript Homo sapiens 23-34 34546854-11 2021 Besides, miR-1224-5p was a molecular target of APCDD1L-AS1 and directly targeted NSD2 in 5-FU-resistant cells. Fluorouracil 89-93 APCDD1L divergent transcript Homo sapiens 47-58 34546854-11 2021 Besides, miR-1224-5p was a molecular target of APCDD1L-AS1 and directly targeted NSD2 in 5-FU-resistant cells. Fluorouracil 89-93 nuclear receptor binding SET domain protein 2 Homo sapiens 81-85 34546854-13 2021 Moreover, NSD2 upregulation neutralized the influence of blocking APCDD1L-AS1 in HSC-3/5-FU and HN-4/5-FU cells on 5-FU resistance. Fluorouracil 101-105 nuclear receptor binding SET domain protein 2 Homo sapiens 10-14 34546854-13 2021 Moreover, NSD2 upregulation neutralized the influence of blocking APCDD1L-AS1 in HSC-3/5-FU and HN-4/5-FU cells on 5-FU resistance. Fluorouracil 115-119 nuclear receptor binding SET domain protein 2 Homo sapiens 10-14 34546854-13 2021 Moreover, NSD2 upregulation neutralized the influence of blocking APCDD1L-AS1 in HSC-3/5-FU and HN-4/5-FU cells on 5-FU resistance. Fluorouracil 115-119 APCDD1L divergent transcript Homo sapiens 66-77 34546854-14 2021 To sum up, our study demonstrated that exosomal APCDD1L-AS1 conferred resistance to 5-FU in HSC-3/5-FU and HN-4/5-FU cells via the miR-1224-5p/NSD2 axis, thus providing a novel target for OSCC chemoresistance. Fluorouracil 84-88 APCDD1L divergent transcript Homo sapiens 48-59 34546854-14 2021 To sum up, our study demonstrated that exosomal APCDD1L-AS1 conferred resistance to 5-FU in HSC-3/5-FU and HN-4/5-FU cells via the miR-1224-5p/NSD2 axis, thus providing a novel target for OSCC chemoresistance. Fluorouracil 98-102 APCDD1L divergent transcript Homo sapiens 48-59 34546854-14 2021 To sum up, our study demonstrated that exosomal APCDD1L-AS1 conferred resistance to 5-FU in HSC-3/5-FU and HN-4/5-FU cells via the miR-1224-5p/NSD2 axis, thus providing a novel target for OSCC chemoresistance. Fluorouracil 112-116 APCDD1L divergent transcript Homo sapiens 48-59 34034636-5 2021 Our purpose was to explore insulin effect on 5-fluorouracil (5-FU) resistance in CC and elucidate its potential mechanism in vitro and in vivo. Fluorouracil 45-59 insulin Homo sapiens 27-34 34034636-5 2021 Our purpose was to explore insulin effect on 5-fluorouracil (5-FU) resistance in CC and elucidate its potential mechanism in vitro and in vivo. Fluorouracil 61-65 insulin Homo sapiens 27-34 34034636-6 2021 CKK-8, colony formation, Transwell, and flow cytometry were used to detect the effect of insulin on 5-FU resistance in CC cells JEG-3 and JARS. Fluorouracil 100-104 insulin Homo sapiens 89-96 34034636-7 2021 Xenograft mice were used to evaluate the effect of insulin on 5-FU resistance. Fluorouracil 62-66 insulin Homo sapiens 51-58 34034636-8 2021 Results showed that insulin combined with 5-FU suppressed cell viability by 30% in JEG-3 and 43% in JAR compared with 5-FU alone in 72 h. What"s more, insulin combined with 5-FU promoted cell apoptosis, inhibited cell proliferation, migration, and phosphorylation of survivin at residue threonine 34 (Thr34) and drug resistance-related proteins, P-GP and MRP1 levels (p < 0.05). Fluorouracil 42-46 insulin Homo sapiens 151-158 34034636-8 2021 Results showed that insulin combined with 5-FU suppressed cell viability by 30% in JEG-3 and 43% in JAR compared with 5-FU alone in 72 h. What"s more, insulin combined with 5-FU promoted cell apoptosis, inhibited cell proliferation, migration, and phosphorylation of survivin at residue threonine 34 (Thr34) and drug resistance-related proteins, P-GP and MRP1 levels (p < 0.05). Fluorouracil 42-46 ATP binding cassette subfamily C member 1 Homo sapiens 355-359 34034636-8 2021 Results showed that insulin combined with 5-FU suppressed cell viability by 30% in JEG-3 and 43% in JAR compared with 5-FU alone in 72 h. What"s more, insulin combined with 5-FU promoted cell apoptosis, inhibited cell proliferation, migration, and phosphorylation of survivin at residue threonine 34 (Thr34) and drug resistance-related proteins, P-GP and MRP1 levels (p < 0.05). Fluorouracil 118-122 insulin Homo sapiens 20-27 34034636-8 2021 Results showed that insulin combined with 5-FU suppressed cell viability by 30% in JEG-3 and 43% in JAR compared with 5-FU alone in 72 h. What"s more, insulin combined with 5-FU promoted cell apoptosis, inhibited cell proliferation, migration, and phosphorylation of survivin at residue threonine 34 (Thr34) and drug resistance-related proteins, P-GP and MRP1 levels (p < 0.05). Fluorouracil 118-122 insulin Homo sapiens 151-158 34034636-8 2021 Results showed that insulin combined with 5-FU suppressed cell viability by 30% in JEG-3 and 43% in JAR compared with 5-FU alone in 72 h. What"s more, insulin combined with 5-FU promoted cell apoptosis, inhibited cell proliferation, migration, and phosphorylation of survivin at residue threonine 34 (Thr34) and drug resistance-related proteins, P-GP and MRP1 levels (p < 0.05). Fluorouracil 118-122 ATP binding cassette subfamily C member 1 Homo sapiens 355-359 34794098-7 2021 The most balanced potent and safe derivatives; 5i and 5q were more active than 5-fluorouracil, exhibited low mumrange MDM2 binding (KD=1.32and 1.72 mum, respectively), induced apoptosis-dependent anticancer activities up to 50%, activated p53 by 47-63%, downregulated the BCL2 gene to 59.8%, and reduced its protein level (13.75%) in the treated cancer cells. Fluorouracil 79-93 tumor protein p53 Homo sapiens 239-242 34034636-8 2021 Results showed that insulin combined with 5-FU suppressed cell viability by 30% in JEG-3 and 43% in JAR compared with 5-FU alone in 72 h. What"s more, insulin combined with 5-FU promoted cell apoptosis, inhibited cell proliferation, migration, and phosphorylation of survivin at residue threonine 34 (Thr34) and drug resistance-related proteins, P-GP and MRP1 levels (p < 0.05). Fluorouracil 173-177 insulin Homo sapiens 20-27 34034636-8 2021 Results showed that insulin combined with 5-FU suppressed cell viability by 30% in JEG-3 and 43% in JAR compared with 5-FU alone in 72 h. What"s more, insulin combined with 5-FU promoted cell apoptosis, inhibited cell proliferation, migration, and phosphorylation of survivin at residue threonine 34 (Thr34) and drug resistance-related proteins, P-GP and MRP1 levels (p < 0.05). Fluorouracil 173-177 ATP binding cassette subfamily C member 1 Homo sapiens 355-359 34794098-7 2021 The most balanced potent and safe derivatives; 5i and 5q were more active than 5-fluorouracil, exhibited low mumrange MDM2 binding (KD=1.32and 1.72 mum, respectively), induced apoptosis-dependent anticancer activities up to 50%, activated p53 by 47-63%, downregulated the BCL2 gene to 59.8%, and reduced its protein level (13.75%) in the treated cancer cells. Fluorouracil 79-93 BCL2 apoptosis regulator Homo sapiens 272-276 34034636-10 2021 In summary, the findings of this study show that insulin reversed chemoresistance of CC cells to 5-FU by inhibiting phosphorylation of survivin. Fluorouracil 97-101 insulin Homo sapiens 49-56 34530056-10 2021 In summary, we found that SPIB is a tumor suppressor in colorectal cancer cells and that SPIB sensitizes colorectal cancer cells to oxaliplatin and 5-FU, SPIB exerts its anti-colorectal cancer effect by activating the NFkB and JNK signaling pathways through MAP4K1. Fluorouracil 148-152 mitogen-activated protein kinase 8 Homo sapiens 227-230 34901834-9 2021 Factors other than DPYD polymorphisms (e.g., miR-27a, TYMS, ENOSF1, p53) also affect 5-FU toxicity. Fluorouracil 85-89 microRNA 27a Homo sapiens 45-52 34637097-6 2021 METHOD AND RESULTS: Different single and combined concentrations of 5-FU and Quer were applied to MCF 7 cells for 48 h. Cell viability, apoptosis, gene expression of Bax, Bcl2, and p53, caspase activity, and colony number were assessed using MTT assay, flow cytometry, quantitative real-time PCR, enzyme-linked immunosorbent (ELISA), and Colony formation assay, respectively. Fluorouracil 68-72 BCL2 associated X, apoptosis regulator Homo sapiens 166-169 34637097-6 2021 METHOD AND RESULTS: Different single and combined concentrations of 5-FU and Quer were applied to MCF 7 cells for 48 h. Cell viability, apoptosis, gene expression of Bax, Bcl2, and p53, caspase activity, and colony number were assessed using MTT assay, flow cytometry, quantitative real-time PCR, enzyme-linked immunosorbent (ELISA), and Colony formation assay, respectively. Fluorouracil 68-72 BCL2 apoptosis regulator Homo sapiens 171-175 34637097-7 2021 The combination of 5-FU and Quer compared to 5-FU alone improved apoptosis by increasing the gene expression of Bax and p53 and caspase-9 activity and decreasing the Bcl2 gene expression. Fluorouracil 19-23 BCL2 associated X, apoptosis regulator Homo sapiens 112-115 34637097-7 2021 The combination of 5-FU and Quer compared to 5-FU alone improved apoptosis by increasing the gene expression of Bax and p53 and caspase-9 activity and decreasing the Bcl2 gene expression. Fluorouracil 19-23 tumor protein p53 Homo sapiens 120-123 34637097-7 2021 The combination of 5-FU and Quer compared to 5-FU alone improved apoptosis by increasing the gene expression of Bax and p53 and caspase-9 activity and decreasing the Bcl2 gene expression. Fluorouracil 19-23 BCL2 apoptosis regulator Homo sapiens 166-170 34637097-7 2021 The combination of 5-FU and Quer compared to 5-FU alone improved apoptosis by increasing the gene expression of Bax and p53 and caspase-9 activity and decreasing the Bcl2 gene expression. Fluorouracil 45-49 BCL2 associated X, apoptosis regulator Homo sapiens 112-115 34637097-7 2021 The combination of 5-FU and Quer compared to 5-FU alone improved apoptosis by increasing the gene expression of Bax and p53 and caspase-9 activity and decreasing the Bcl2 gene expression. Fluorouracil 45-49 tumor protein p53 Homo sapiens 120-123 34637097-7 2021 The combination of 5-FU and Quer compared to 5-FU alone improved apoptosis by increasing the gene expression of Bax and p53 and caspase-9 activity and decreasing the Bcl2 gene expression. Fluorouracil 45-49 BCL2 apoptosis regulator Homo sapiens 166-170 34901834-9 2021 Factors other than DPYD polymorphisms (e.g., miR-27a, TYMS, ENOSF1, p53) also affect 5-FU toxicity. Fluorouracil 85-89 tumor protein p53 Homo sapiens 68-71 34843983-0 2022 Vesicular IFN-gamma as a cooperative attacker to enhance anti-cancer effect of 5-fluorouracil via thymidine phosphorylase upregulation and tumor microenvironment normalization. Fluorouracil 79-93 interferon gamma Homo sapiens 10-19 34843983-1 2022 On the basis of immuno-modulating effect and upregulating the activity of thymidine phosphorylase (TP), interferon-gamma (IFN-gamma) as a cooperative attacker was explored to enhance the anticancer activity of 5-FU. Fluorouracil 210-214 interferon gamma Homo sapiens 104-120 34843983-1 2022 On the basis of immuno-modulating effect and upregulating the activity of thymidine phosphorylase (TP), interferon-gamma (IFN-gamma) as a cooperative attacker was explored to enhance the anticancer activity of 5-FU. Fluorouracil 210-214 interferon gamma Homo sapiens 122-131 34843983-3 2022 The IFN-gamma-EDP vesicles allowed IFN-gamma to accumulate at the tumor site and be taken up by tumor cells, resulting in significantly upregulated expression level of TP, distinct inhibition of cell growth, more cellular apoptosis and more serious cell cycle arrest when administrated combined with 5-FU. Fluorouracil 300-304 interferon gamma Homo sapiens 4-13 34843983-3 2022 The IFN-gamma-EDP vesicles allowed IFN-gamma to accumulate at the tumor site and be taken up by tumor cells, resulting in significantly upregulated expression level of TP, distinct inhibition of cell growth, more cellular apoptosis and more serious cell cycle arrest when administrated combined with 5-FU. Fluorouracil 300-304 interferon gamma Homo sapiens 35-44 34843983-5 2022 As a consequence, the combination therapy of IFN-gamma-EDP with 5-FU achieved remarkably enhanced tumor inhibition rate of 56.9% against CT26 colorectal cancer. Fluorouracil 64-68 interferon gamma Homo sapiens 45-54 34785642-5 2021 We conducted in vitro experiments and found that in HCC cells, UBE2S overexpression increases the resistance to 5-FU and oxaliplatin, while UBE2S knockdown achieves an opposite effect. Fluorouracil 112-116 ubiquitin conjugating enzyme E2 S Homo sapiens 63-68 34866926-11 2021 Notably, overexpression of the LINC00909 increased the cell line resistance to the 5-FU and radiotherapy in vivo and in vitro. Fluorouracil 83-87 ZNF407 antisense RNA 1 Homo sapiens 31-40 34596215-0 2021 Syndecan-2, negatively regulated by miR-20b-5p, contributes to 5-fluorouracil resistance of colorectal cancer cells via the JNK/ERK signaling pathway. Fluorouracil 63-77 mitogen-activated protein kinase 8 Homo sapiens 124-127 34794379-16 2021 Mechanistically, TBHQ activated Nrf2 effectively and selective Nrf2 knockdown significantly reduced the anti-ferroptotic functions of TBHQ in 5-FU-treated HIECs. Fluorouracil 142-146 nuclear factor, erythroid derived 2, like 2 Mus musculus 32-36 34794379-16 2021 Mechanistically, TBHQ activated Nrf2 effectively and selective Nrf2 knockdown significantly reduced the anti-ferroptotic functions of TBHQ in 5-FU-treated HIECs. Fluorouracil 142-146 nuclear factor, erythroid derived 2, like 2 Mus musculus 63-67 34758839-0 2021 Lactate induces aberration in the miR-30a-DBF4 axis to promote the development of gastric cancer and weakens the sensitivity to 5-Fu. Fluorouracil 128-132 DBF4 zinc finger Homo sapiens 42-46 34758839-8 2021 Furthermore, functional experiments were applied to demonstrate that DBF4 promotes cell proliferation and migration in GC cell lines, moreover weakens the sensitivity of MGC803 and AGS cells to 5-Fu. Fluorouracil 194-198 DBF4 zinc finger Homo sapiens 69-73 34758839-10 2021 Furthermore, rescue experiments revealed that the miR-30a-DBF4 axis regulated the GC cell proliferation, migration and the sensitivity to 5-Fu. Fluorouracil 138-142 DBF4 zinc finger Homo sapiens 58-62 34758839-13 2021 Furthermore, our study identified the lactate-miR-30a-DBF4 axis as a crucial regulator of tumor progression and the tumor sensitivity to 5-Fu, which maybe serve useful for the development of novel therapeutic targets. Fluorouracil 137-141 DBF4 zinc finger Homo sapiens 54-58 34605863-7 2021 Moreover, exosome-incubated A549 cells were co-transfected with si-FOXD3-AS1 and pcDNA-ELAVL1, showing the same cell proliferation, invasion, and 5-FU resistance as those of A549 cells treated with lung cancer cell-derived exosomes alone. Fluorouracil 146-150 forkhead box D3 Homo sapiens 67-72 34596215-0 2021 Syndecan-2, negatively regulated by miR-20b-5p, contributes to 5-fluorouracil resistance of colorectal cancer cells via the JNK/ERK signaling pathway. Fluorouracil 63-77 mitogen-activated protein kinase 1 Homo sapiens 128-131 34596215-8 2021 We also confirmed that miR-20b-5p interacted with SDC2, which reversed the effect of SDC2 in SW480/5-FU cells via the c-Jun N-terminal kinase (JNK)/extracellular regulated protein kinases (ERK) signaling pathway. Fluorouracil 99-103 mitogen-activated protein kinase 8 Homo sapiens 118-141 34596215-8 2021 We also confirmed that miR-20b-5p interacted with SDC2, which reversed the effect of SDC2 in SW480/5-FU cells via the c-Jun N-terminal kinase (JNK)/extracellular regulated protein kinases (ERK) signaling pathway. Fluorouracil 99-103 mitogen-activated protein kinase 8 Homo sapiens 143-146 34596215-8 2021 We also confirmed that miR-20b-5p interacted with SDC2, which reversed the effect of SDC2 in SW480/5-FU cells via the c-Jun N-terminal kinase (JNK)/extracellular regulated protein kinases (ERK) signaling pathway. Fluorouracil 99-103 mitogen-activated protein kinase 1 Homo sapiens 189-192 34596215-9 2021 These findings showed that JNK/ERK signaling pathway is involved in miR-20b-5p/SDC2 axis-mediated 5-FU resistance in SW480/5-FU cells, indicating that the miR-20b-5p/SDC2 axis is a potential target for reversing 5-FU resistance in CRC. Fluorouracil 98-102 mitogen-activated protein kinase 8 Homo sapiens 27-30 34596215-9 2021 These findings showed that JNK/ERK signaling pathway is involved in miR-20b-5p/SDC2 axis-mediated 5-FU resistance in SW480/5-FU cells, indicating that the miR-20b-5p/SDC2 axis is a potential target for reversing 5-FU resistance in CRC. Fluorouracil 98-102 mitogen-activated protein kinase 1 Homo sapiens 31-34 34596215-9 2021 These findings showed that JNK/ERK signaling pathway is involved in miR-20b-5p/SDC2 axis-mediated 5-FU resistance in SW480/5-FU cells, indicating that the miR-20b-5p/SDC2 axis is a potential target for reversing 5-FU resistance in CRC. Fluorouracil 123-127 mitogen-activated protein kinase 8 Homo sapiens 27-30 34795760-0 2021 Nrf3 Promotes 5-FU Resistance in Colorectal Cancer Cells via the NF-kappaB/BCL-2 Signaling Pathway In Vitro and In Vivo. Fluorouracil 14-18 nuclear factor kappa B subunit 1 Homo sapiens 65-74 34596215-9 2021 These findings showed that JNK/ERK signaling pathway is involved in miR-20b-5p/SDC2 axis-mediated 5-FU resistance in SW480/5-FU cells, indicating that the miR-20b-5p/SDC2 axis is a potential target for reversing 5-FU resistance in CRC. Fluorouracil 123-127 mitogen-activated protein kinase 1 Homo sapiens 31-34 34795760-0 2021 Nrf3 Promotes 5-FU Resistance in Colorectal Cancer Cells via the NF-kappaB/BCL-2 Signaling Pathway In Vitro and In Vivo. Fluorouracil 14-18 BCL2 apoptosis regulator Homo sapiens 75-80 34596215-9 2021 These findings showed that JNK/ERK signaling pathway is involved in miR-20b-5p/SDC2 axis-mediated 5-FU resistance in SW480/5-FU cells, indicating that the miR-20b-5p/SDC2 axis is a potential target for reversing 5-FU resistance in CRC. Fluorouracil 212-216 mitogen-activated protein kinase 8 Homo sapiens 27-30 34795760-7 2021 Inhibition of NF-kappaB partly reversed the effects of Nrf3 overexpression, resulting in the resistance of colon cancer cells to 5-FU. Fluorouracil 129-133 nuclear factor kappa B subunit 1 Homo sapiens 14-23 34795760-8 2021 Overall, the study revealed that Nrf3 was connected to the sensitivity of colon cancer cells to 5-FU, and its possible mechanism was related to the NF-kappaB signaling pathway, which provided a new target for overcoming the resistance of colon cancer cells to 5-FU. Fluorouracil 96-100 nuclear factor kappa B subunit 1 Homo sapiens 148-157 34795760-8 2021 Overall, the study revealed that Nrf3 was connected to the sensitivity of colon cancer cells to 5-FU, and its possible mechanism was related to the NF-kappaB signaling pathway, which provided a new target for overcoming the resistance of colon cancer cells to 5-FU. Fluorouracil 260-264 nuclear factor kappa B subunit 1 Homo sapiens 148-157 34596215-9 2021 These findings showed that JNK/ERK signaling pathway is involved in miR-20b-5p/SDC2 axis-mediated 5-FU resistance in SW480/5-FU cells, indicating that the miR-20b-5p/SDC2 axis is a potential target for reversing 5-FU resistance in CRC. Fluorouracil 212-216 mitogen-activated protein kinase 1 Homo sapiens 31-34 34605863-0 2021 Exosomal lncRNA FOXD3-AS1 upregulates ELAVL1 expression and activates PI3K/Akt pathway to enhance lung cancer cell proliferation, invasion, and 5-fluorouracil resistance. Fluorouracil 144-158 forkhead box D3 Homo sapiens 16-21 34605863-1 2021 Long non-coding RNA (lncRNA) FOXD3-AS1 expression is upregulated in lung cancer; however, its effect and mechanism on 5-fluorouracil (5-FU) resistance remain unclear. Fluorouracil 118-132 forkhead box D3 Homo sapiens 29-34 34605863-1 2021 Long non-coding RNA (lncRNA) FOXD3-AS1 expression is upregulated in lung cancer; however, its effect and mechanism on 5-fluorouracil (5-FU) resistance remain unclear. Fluorouracil 134-138 forkhead box D3 Homo sapiens 29-34 34605863-2 2021 In this study, we determined the effects of FOXD3-AS1-enriched exosomes derived from lung cancer cells on the proliferation, invasion, and 5-FU resistance of lung cancer cells. Fluorouracil 139-143 forkhead box D3 Homo sapiens 44-49 34605226-7 2021 Moreover, NK-1R antagonists enhance the efficacy of chemotherapy by increasing the sensitivity and overcoming resistance to 5-fluorouracil in CRC cells through the induction of sustained ER stress and the consequent suppression of ERK-c-Myc signaling both in vitro and in vivo. Fluorouracil 124-138 mitogen-activated protein kinase 1 Homo sapiens 231-234 34747284-6 2021 5-FU injection caused marked elevation of MDA, NO, TNF-alpha, IL-1beta, IL-6, PAF, histamine, myeloperoxidase, caspase-3, and NF-kappaB expressions. Fluorouracil 0-4 tumor necrosis factor Rattus norvegicus 51-60 34747284-6 2021 5-FU injection caused marked elevation of MDA, NO, TNF-alpha, IL-1beta, IL-6, PAF, histamine, myeloperoxidase, caspase-3, and NF-kappaB expressions. Fluorouracil 0-4 interleukin 1 alpha Rattus norvegicus 62-70 34747284-6 2021 5-FU injection caused marked elevation of MDA, NO, TNF-alpha, IL-1beta, IL-6, PAF, histamine, myeloperoxidase, caspase-3, and NF-kappaB expressions. Fluorouracil 0-4 interleukin 6 Rattus norvegicus 72-76 34320879-10 2021 Drug response prediction suggested that patients with low CBS expression showed high drug sensitivity to 5-Fluorouracil. Fluorouracil 105-119 cystathionine beta-synthase Homo sapiens 58-61 34790580-0 2021 Restoring HOXD10 Exhibits Therapeutic Potential for Ameliorating Malignant Progression and 5-Fluorouracil Resistance in Colorectal Cancer. Fluorouracil 91-105 homeobox D10 Homo sapiens 10-16 34790580-10 2021 Restoration of the expression of HOXD10 in 5-fluorouracil (5-FU)-resistant cells significantly upregulates the expressions of miR-7 and IGFBP3 and enhances chemosensitivity to 5-FU. Fluorouracil 43-57 homeobox D10 Homo sapiens 33-39 34790580-10 2021 Restoration of the expression of HOXD10 in 5-fluorouracil (5-FU)-resistant cells significantly upregulates the expressions of miR-7 and IGFBP3 and enhances chemosensitivity to 5-FU. Fluorouracil 59-63 homeobox D10 Homo sapiens 33-39 34790580-10 2021 Restoration of the expression of HOXD10 in 5-fluorouracil (5-FU)-resistant cells significantly upregulates the expressions of miR-7 and IGFBP3 and enhances chemosensitivity to 5-FU. Fluorouracil 176-180 homeobox D10 Homo sapiens 33-39 34594423-0 2021 NDRG4 sensitizes CRC cells to 5-FU by upregulating DDIT3 expression. Fluorouracil 30-34 DNA damage inducible transcript 3 Homo sapiens 51-56 34857985-10 2021 Concerning inflammatory responses, resveratrol suppressed the 5-FU-induced expression of pro-inflammatory cytokines via NF-kappaB nuclear translocation. Fluorouracil 62-66 nuclear factor kappa B subunit 1 Homo sapiens 120-129 34588619-0 2021 Epigenetic induction of lipocalin 2 expression drives acquired resistance to 5-fluorouracil in colorectal cancer through integrin beta3/SRC pathway. Fluorouracil 77-91 integrin subunit beta 3 Homo sapiens 121-135 34588619-0 2021 Epigenetic induction of lipocalin 2 expression drives acquired resistance to 5-fluorouracil in colorectal cancer through integrin beta3/SRC pathway. Fluorouracil 77-91 SRC proto-oncogene, non-receptor tyrosine kinase Homo sapiens 136-139 34588619-5 2021 LCN2 attenuated the cytotoxicity of 5-FU by activating the SRC/AKT/ERK-mediated antiapoptotic program. Fluorouracil 36-40 SRC proto-oncogene, non-receptor tyrosine kinase Homo sapiens 59-62 34588619-5 2021 LCN2 attenuated the cytotoxicity of 5-FU by activating the SRC/AKT/ERK-mediated antiapoptotic program. Fluorouracil 36-40 AKT serine/threonine kinase 1 Homo sapiens 63-66 34588619-5 2021 LCN2 attenuated the cytotoxicity of 5-FU by activating the SRC/AKT/ERK-mediated antiapoptotic program. Fluorouracil 36-40 mitogen-activated protein kinase 1 Homo sapiens 67-70 34562873-10 2021 Therefore, apigenin may improve the therapeutic efficacy of 5-FU against CRC by suppressing TS, but apoptosis induction is mainly dependent on functional P53. Fluorouracil 60-64 tumor protein p53 Homo sapiens 154-157 34528330-3 2021 A significant positive correlation was observed between AEG-1, TS, ERCC1, EGFR, and VEGF gene expression levels in CRC cell lines, and low AEG-1 and TS expression were highly sensitive to 5-fluorouracil treatment. Fluorouracil 188-202 metadherin Homo sapiens 56-61 34528330-3 2021 A significant positive correlation was observed between AEG-1, TS, ERCC1, EGFR, and VEGF gene expression levels in CRC cell lines, and low AEG-1 and TS expression were highly sensitive to 5-fluorouracil treatment. Fluorouracil 188-202 metadherin Homo sapiens 139-144 34594423-3 2021 The results of the present study demonstrate that NDRG4 sensitized CRC cells to 5-FU by upregulating DNA damage inducible transcript 3 (DDIT3). Fluorouracil 80-84 DNA damage inducible transcript 3 Homo sapiens 101-134 34594423-3 2021 The results of the present study demonstrate that NDRG4 sensitized CRC cells to 5-FU by upregulating DNA damage inducible transcript 3 (DDIT3). Fluorouracil 80-84 DNA damage inducible transcript 3 Homo sapiens 136-141 34594423-6 2021 Mechanistic analyses revealed that NDRG4 upregulated DDIT3 expression, and that the proapoptotic effect of NDRG4 under 5-FU treatment conditions was dependent on DDIT3. Fluorouracil 119-123 DNA damage inducible transcript 3 Homo sapiens 162-167 34594423-7 2021 These findings support the biological value of the association between NDRG4, DDIT3 and 5-FU chemosensitivity in CRC, and may advance the clinical treatment of CRC in the future. Fluorouracil 88-92 DNA damage inducible transcript 3 Homo sapiens 78-83 34718327-8 2021 GPER was predominantly expressed in ileal crypts, and G-1 inhibited the DNA damage induced by 5-fluorouracil in vivo and vitro, as confirmed by the decrease in the number of gammaH2AX+ cells in the crypts and the comet assay results. Fluorouracil 94-108 H2A.X variant histone Mus musculus 174-183 34627212-9 2021 The activity of caspase 3 was increased by 5-FU but reduced by all concentrations of various extracts of BC. Fluorouracil 43-47 caspase 3 Homo sapiens 16-25 34827096-3 2021 This study was designed to evaluate the capacity of using first-line chemotherapies including cisplatin, 5-fluorouracil (5-FU) and vinorelbine to act as a chemo-sensitizer on CD133+ (prominin-1 positive) CSCs derived from NSCLC cell lines (A549, H460 and H2170) for the purpose of MSC-TRAIL-induced inhibition. Fluorouracil 105-119 TNF superfamily member 10 Homo sapiens 285-290 34827096-3 2021 This study was designed to evaluate the capacity of using first-line chemotherapies including cisplatin, 5-fluorouracil (5-FU) and vinorelbine to act as a chemo-sensitizer on CD133+ (prominin-1 positive) CSCs derived from NSCLC cell lines (A549, H460 and H2170) for the purpose of MSC-TRAIL-induced inhibition. Fluorouracil 121-125 TNF superfamily member 10 Homo sapiens 285-290 34827096-5 2021 Pre-treatment using either cisplatin or 5-FU, but not with vinorelbine, was able to increase the efficacy of MSC-TRAIL to kill the TRAIL-resistant A549-derived CSCs. Fluorouracil 40-44 TNF superfamily member 10 Homo sapiens 113-118 34827096-5 2021 Pre-treatment using either cisplatin or 5-FU, but not with vinorelbine, was able to increase the efficacy of MSC-TRAIL to kill the TRAIL-resistant A549-derived CSCs. Fluorouracil 40-44 TNF superfamily member 10 Homo sapiens 131-136 34827096-6 2021 The study also demonstrated that both 5-FU and vinorelbine were an effective chemo-sensitizer, used to increase the anti-tumor effect of MSC-TRAIL against H460- and H2170-derived CSCs. Fluorouracil 38-42 TNF superfamily member 10 Homo sapiens 141-146 34712612-0 2021 Adipocytic Glutamine Synthetase Upregulation via Altered Histone Methylation Promotes 5FU Chemoresistance in Peritoneal Carcinomatosis of Colorectal Cancer. Fluorouracil 86-89 glutamate-ammonia ligase Homo sapiens 11-31 34712612-3 2021 By performing metabolomics analysis, we identified glutamine (Gln), an important amino acid, inducing resistance to 5FU-triggered tumor suppression of CRC-PC through activating mTOR pathway. Fluorouracil 116-119 mechanistic target of rapamycin kinase Homo sapiens 177-181 34712612-4 2021 Noteworthily, genetic overexpression of glutamine synthetase (GS) in adipocytes increased chemoresistance to 5FU in vitro and in vivo while this effect was reversed by pharmacological blockage of GS. Fluorouracil 109-112 glutamate-ammonia ligase Homo sapiens 40-60 34712612-4 2021 Noteworthily, genetic overexpression of glutamine synthetase (GS) in adipocytes increased chemoresistance to 5FU in vitro and in vivo while this effect was reversed by pharmacological blockage of GS. Fluorouracil 109-112 glutamate-ammonia ligase Homo sapiens 62-64 34216375-6 2021 Next, hepatic arterial infusion chemotherapy using 5-fluorouracil and cisplatin decreased NSE and CYFRA levels and suppressed tumor growth. Fluorouracil 51-65 enolase 2 Homo sapiens 90-93 34685438-5 2021 It was shown that the level of sterol-regulatory element-binding protein-1 (SREBP-1), a critical transcription factor involved in lipid synthesis and metabolism, would be upregulated through Akt and p70S6K signaling pathways while CRC cells are cultured in ACM, which subsequently decreases the cell sensitivity to 5-FU cytotoxicity. Fluorouracil 315-319 AKT serine/threonine kinase 1 Homo sapiens 191-194 34638487-2 2021 The tumor suppressor microRNA (miR)-199b has been reported to play a key role determining 5-FU sensitivity of colorectal cancer cells through the regulation of several signaling pathways, and has emerged as a novel molecular target to overcome the 5-FU resistant phenotype. Fluorouracil 90-94 microRNA 199b Homo sapiens 21-40 34638487-2 2021 The tumor suppressor microRNA (miR)-199b has been reported to play a key role determining 5-FU sensitivity of colorectal cancer cells through the regulation of several signaling pathways, and has emerged as a novel molecular target to overcome the 5-FU resistant phenotype. Fluorouracil 248-252 microRNA 199b Homo sapiens 21-40 34261152-7 2021 We showed that WNT5A, MDR1, and DKK1 mRNA expression levels were down-regulated in the allicin- and allicin/5-FU-treated cells. Fluorouracil 108-112 Wnt family member 5A Homo sapiens 15-20 34261152-7 2021 We showed that WNT5A, MDR1, and DKK1 mRNA expression levels were down-regulated in the allicin- and allicin/5-FU-treated cells. Fluorouracil 108-112 ATP binding cassette subfamily B member 1 Homo sapiens 22-26 34261152-9 2021 CONCLUSION: Our findings indicate that the combination of allicin with 5-FU could reverse multidrug resistance in the GC cells by reducing the expression of WNT5A, DKK1, MDR1, P-gp, and CD44 levels. Fluorouracil 71-75 Wnt family member 5A Homo sapiens 157-162 34261152-8 2021 Indeed, the combination of allicin and 5-FU significantly decreased the expression of the P-gp and CD44 proteins (P<0.05). Fluorouracil 39-43 ATP binding cassette subfamily B member 1 Homo sapiens 90-94 34261152-9 2021 CONCLUSION: Our findings indicate that the combination of allicin with 5-FU could reverse multidrug resistance in the GC cells by reducing the expression of WNT5A, DKK1, MDR1, P-gp, and CD44 levels. Fluorouracil 71-75 ATP binding cassette subfamily B member 1 Homo sapiens 170-174 34265852-2 2021 Although inhibition of mTOR signaling promotes tumor cell death and several mTOR inhibitors have been used clinically, recent reports have shown that co-treatment with MHY1485, an mTOR activator, enhances the anti-cancer effects of anti-PD-1 antibody and 5-fluorouracil. Fluorouracil 255-269 mechanistic target of rapamycin kinase Homo sapiens 23-27 34261152-9 2021 CONCLUSION: Our findings indicate that the combination of allicin with 5-FU could reverse multidrug resistance in the GC cells by reducing the expression of WNT5A, DKK1, MDR1, P-gp, and CD44 levels. Fluorouracil 71-75 ATP binding cassette subfamily B member 1 Homo sapiens 176-180 34504596-0 2021 Decreased expression of miR-3135b reduces sensitivity to 5-fluorouracil in colorectal cancer by direct repression of PIM1. Fluorouracil 57-71 Pim-1 proto-oncogene, serine/threonine kinase Homo sapiens 117-121 34542064-0 2022 LncRNA HCG11 promotes 5-FU resistance of colon cancer cells through reprogramming glucose metabolism by targeting the miR-144-3p-PDK4 axis. Fluorouracil 22-26 HLA complex group 11 Homo sapiens 7-12 34542064-9 2022 Moreover, HCG11 was elevated in 5-FU resistant CRC tumors. Fluorouracil 32-36 HLA complex group 11 Homo sapiens 10-15 34542064-10 2022 Silencing HCG11 inhibited colon cancer cell proliferation, migration, invasion and glucose metabolism and sensitized CRC cells to 5-FU. Fluorouracil 130-134 HLA complex group 11 Homo sapiens 10-15 34542064-11 2022 In addition, we detected increased HCG11 expression level and glucose metabolism in the established 5-FU resistant CRC cell line (DLD-1 5-FU Res). Fluorouracil 100-104 HLA complex group 11 Homo sapiens 35-40 34542064-11 2022 In addition, we detected increased HCG11 expression level and glucose metabolism in the established 5-FU resistant CRC cell line (DLD-1 5-FU Res). Fluorouracil 136-140 HLA complex group 11 Homo sapiens 35-40 34542064-14 2022 Rescue studies validated that the miR-144-3p-inhibited glucose metabolism and 5-FU sensitization were through targeting PDK4. Fluorouracil 78-82 microRNA 144 Homo sapiens 34-41 34542064-14 2022 Rescue studies validated that the miR-144-3p-inhibited glucose metabolism and 5-FU sensitization were through targeting PDK4. Fluorouracil 78-82 pyruvate dehydrogenase kinase 4 Homo sapiens 120-124 34542064-15 2022 Finally, restoration of miR-144-3p in HCG11-overexpressing DLD-1 5-FU resistant cells successfully overcame the HCG11-faciliated 5-FU resistance via targeting PDK4. Fluorouracil 65-69 HLA complex group 11 Homo sapiens 38-43 34542064-15 2022 Finally, restoration of miR-144-3p in HCG11-overexpressing DLD-1 5-FU resistant cells successfully overcame the HCG11-faciliated 5-FU resistance via targeting PDK4. Fluorouracil 65-69 HLA complex group 11 Homo sapiens 112-117 34542064-15 2022 Finally, restoration of miR-144-3p in HCG11-overexpressing DLD-1 5-FU resistant cells successfully overcame the HCG11-faciliated 5-FU resistance via targeting PDK4. Fluorouracil 65-69 pyruvate dehydrogenase kinase 4 Homo sapiens 159-163 34542064-15 2022 Finally, restoration of miR-144-3p in HCG11-overexpressing DLD-1 5-FU resistant cells successfully overcame the HCG11-faciliated 5-FU resistance via targeting PDK4. Fluorouracil 129-133 HLA complex group 11 Homo sapiens 38-43 34542064-15 2022 Finally, restoration of miR-144-3p in HCG11-overexpressing DLD-1 5-FU resistant cells successfully overcame the HCG11-faciliated 5-FU resistance via targeting PDK4. Fluorouracil 129-133 HLA complex group 11 Homo sapiens 112-117 34542064-15 2022 Finally, restoration of miR-144-3p in HCG11-overexpressing DLD-1 5-FU resistant cells successfully overcame the HCG11-faciliated 5-FU resistance via targeting PDK4. Fluorouracil 129-133 pyruvate dehydrogenase kinase 4 Homo sapiens 159-163 34542064-16 2022 CONCLUSION: In summary, this study reveals critical roles and molecular mechanisms of the HCG11-mediated 5-FU resistance through modulating the miR-144-3p-PDK4-glucose metabolism pathway in CRC. Fluorouracil 105-109 HLA complex group 11 Homo sapiens 90-95 34542064-16 2022 CONCLUSION: In summary, this study reveals critical roles and molecular mechanisms of the HCG11-mediated 5-FU resistance through modulating the miR-144-3p-PDK4-glucose metabolism pathway in CRC. Fluorouracil 105-109 microRNA 144 Homo sapiens 144-151 34542064-16 2022 CONCLUSION: In summary, this study reveals critical roles and molecular mechanisms of the HCG11-mediated 5-FU resistance through modulating the miR-144-3p-PDK4-glucose metabolism pathway in CRC. Fluorouracil 105-109 pyruvate dehydrogenase kinase 4 Homo sapiens 155-159 34552824-6 2021 The high expression of APOBEC3B indicated inferior overall survival (OS, P < .001 and P = .003) and disease-free survival (DFS, P < .001 and P < .001), yet superior therapeutic responsiveness to fluorouracil-based adjuvant chemotherapy (ACT) in TNM stage II patients. Fluorouracil 195-207 apolipoprotein B mRNA editing enzyme catalytic subunit 3B Homo sapiens 23-31 34214754-8 2021 The cell cycle study found that, compared with the positive control 5-FU (48.05%), the compounds BP-2, BP-3 and BP-4 all increased the proportion of HeLa cells in the G1 phase, reaching 57.65%, 55.46% and 53.58%, respectively. Fluorouracil 68-72 BP2 Homo sapiens 97-101 34214754-8 2021 The cell cycle study found that, compared with the positive control 5-FU (48.05%), the compounds BP-2, BP-3 and BP-4 all increased the proportion of HeLa cells in the G1 phase, reaching 57.65%, 55.46% and 53.58%, respectively. Fluorouracil 68-72 BP3 Homo sapiens 103-107 34214754-8 2021 The cell cycle study found that, compared with the positive control 5-FU (48.05%), the compounds BP-2, BP-3 and BP-4 all increased the proportion of HeLa cells in the G1 phase, reaching 57.65%, 55.46% and 53.58%, respectively. Fluorouracil 68-72 BP4 Homo sapiens 112-116 34540836-7 2021 Dysfunction of MOF in hepatocellular carcinoma cells also results in chemoresistance to trichostatin A, sorafenib and 5-fluorouracil via HIF-1alpha. Fluorouracil 118-132 hypoxia inducible factor 1 subunit alpha Homo sapiens 137-147 34097885-0 2021 Tumor-specific delivery of 5FU-incorporated EGFR-targeted aptamers as an efficient treatment in pancreatic ductal adenocarcinoma models. Fluorouracil 27-30 epidermal growth factor receptor Homo sapiens 44-48 34097885-4 2021 METHODS: We designed, generated and characterized 5FU-incorporated SELEX-selected EGFR-targeted aptamers for tumor-specific delivery of 5FU to PDAC cells and tested their therapeutic efficacy in vitro and in vivo. Fluorouracil 50-53 epidermal growth factor receptor Homo sapiens 82-86 34097885-4 2021 METHODS: We designed, generated and characterized 5FU-incorporated SELEX-selected EGFR-targeted aptamers for tumor-specific delivery of 5FU to PDAC cells and tested their therapeutic efficacy in vitro and in vivo. Fluorouracil 136-139 epidermal growth factor receptor Homo sapiens 82-86 34097885-9 2021 Tumor growth was significantly attenuated during 5FU-EGFR-aptamer treatment in the course of follow-up. Fluorouracil 49-52 epidermal growth factor receptor Homo sapiens 53-57 34323266-0 2021 HDAC6 inhibitor WT161 performs antitumor effect on osteosarcoma and synergistically interacts with 5-FU. Fluorouracil 99-103 histone deacetylase 6 Homo sapiens 0-5 34502219-0 2021 S-Adenosylmethionine Increases the Sensitivity of Human Colorectal Cancer Cells to 5-Fluorouracil by Inhibiting P-Glycoprotein Expression and NF-kappaB Activation. Fluorouracil 83-97 nuclear factor kappa B subunit 1 Homo sapiens 142-151 34502219-6 2021 We demonstrate here that AdoMet was able to revert the 5-FU-induced upregulation of P-gp expression and to decrease levels of acetylated NF-kappaB, the activated form of NF-kappaB, the major antiapoptotic factor involved in P-gp-related chemoresistance. Fluorouracil 55-59 ATP binding cassette subfamily B member 1 Homo sapiens 84-88 34502219-6 2021 We demonstrate here that AdoMet was able to revert the 5-FU-induced upregulation of P-gp expression and to decrease levels of acetylated NF-kappaB, the activated form of NF-kappaB, the major antiapoptotic factor involved in P-gp-related chemoresistance. Fluorouracil 55-59 nuclear factor kappa B subunit 1 Homo sapiens 137-146 34502219-6 2021 We demonstrate here that AdoMet was able to revert the 5-FU-induced upregulation of P-gp expression and to decrease levels of acetylated NF-kappaB, the activated form of NF-kappaB, the major antiapoptotic factor involved in P-gp-related chemoresistance. Fluorouracil 55-59 nuclear factor kappa B subunit 1 Homo sapiens 170-179 34502219-6 2021 We demonstrate here that AdoMet was able to revert the 5-FU-induced upregulation of P-gp expression and to decrease levels of acetylated NF-kappaB, the activated form of NF-kappaB, the major antiapoptotic factor involved in P-gp-related chemoresistance. Fluorouracil 55-59 ATP binding cassette subfamily B member 1 Homo sapiens 224-228 34575034-0 2021 Dexamethasone Sensitizes Cancer Stem Cells to Gemcitabine and 5-Fluorouracil by Increasing Reactive Oxygen Species Production through NRF2 Reduction. Fluorouracil 62-76 NFE2 like bZIP transcription factor 2 Homo sapiens 134-138 34451244-6 2021 The distribution of 5-FU in micelles is related to the PEO and PPO segment length of Pluronic polymers and the environmental temperature. Fluorouracil 20-24 protoporphyrinogen oxidase Homo sapiens 63-66 34451244-7 2021 The drug release tests further confirm that if 5-FU medicines were loaded in the PPO segment inside the micelles, the purpose of the prolonged drug release carrier is achieved. Fluorouracil 47-51 protoporphyrinogen oxidase Homo sapiens 81-84 34379296-6 2022 Moreover, the effects of TMPRSS4 expression on cell migration and sensitivity to 5-FU were investigated. Fluorouracil 81-85 transmembrane serine protease 4 Homo sapiens 25-32 34379296-12 2022 TMPRSS4-silenced GC cells exhibited increased sensitivity to 5-FU when compared with the non-specific control siRNA-transfected cells. Fluorouracil 61-65 transmembrane serine protease 4 Homo sapiens 0-7 34422665-0 2021 ARTEMIN Promotes Oncogenicity and Resistance to 5-Fluorouracil in Colorectal Carcinoma by p44/42 MAPK Dependent Expression of CDH2. Fluorouracil 48-62 mitogen-activated protein kinase 3 Homo sapiens 90-101 34445183-0 2021 YY1 Silencing Induces 5-Fluorouracil-Resistance and BCL2L15 Downregulation in Colorectal Cancer Cells: Diagnostic and Prognostic Relevance. Fluorouracil 22-36 YY1 transcription factor Homo sapiens 0-3 34445183-6 2021 Silencing of YY1 increased the resistance to 5-Fluorouracil-induced cytotoxicity in two out of four CRC cells with different genotypes. Fluorouracil 45-59 YY1 transcription factor Homo sapiens 13-16 34170484-12 2021 After MTPN knockdown, the sensitivity of CCA cells to 5-FU and CDDP was increased. Fluorouracil 54-58 myotrophin Homo sapiens 6-10 34452150-3 2021 5-FU activity leads to caspase-1 activation, secretion and maturation of interleukins (IL)-1, IL-18 and reactive oxygen species (ROS) generation. Fluorouracil 0-4 caspase 1 Homo sapiens 23-32 34452150-5 2021 Exposure of tumor cells to P.CNF/5-FU resulted in a strong cytotoxic effect, an increased level of caspase-1 released in the culture media and ROS production-the latter directly proportional to the concentration of anti-tumor agent embedded in the scaffolds. Fluorouracil 33-37 caspase 1 Homo sapiens 99-108 34452150-6 2021 Simultaneously, 5-FU determined the increase of p53 and caspase-1 expressions, both at gene and protein levels. Fluorouracil 16-20 tumor protein p53 Homo sapiens 48-51 34452150-6 2021 Simultaneously, 5-FU determined the increase of p53 and caspase-1 expressions, both at gene and protein levels. Fluorouracil 16-20 caspase 1 Homo sapiens 56-65 34367280-11 2021 We also found that downregulation of ECT2 increased 5-FU sensitivity in GC cells by downregulating P-gp, MRP1, and Bcl-2. Fluorouracil 52-56 ATP binding cassette subfamily C member 1 Homo sapiens 105-109 34367280-11 2021 We also found that downregulation of ECT2 increased 5-FU sensitivity in GC cells by downregulating P-gp, MRP1, and Bcl-2. Fluorouracil 52-56 BCL2 apoptosis regulator Homo sapiens 115-120 34315857-3 2021 We observed that MCF7 and T47D BC-derived cells stably over-expressing ETV7 showed reduced sensitivity to the chemotherapeutic drug 5-fluorouracil and to radiotherapy, accompanied by an adaptive proliferative behavior observed in different culture conditions. Fluorouracil 132-146 ETS variant transcription factor 7 Homo sapiens 71-75 34360807-6 2021 In HCT116 cells, LMWF enhanced the suppressive effects of 5-FU on cell viability through the (1) induction of cell cycle arrest in the S phase and (2) late apoptosis mediated by the Jun-N-terminal kinase (JNK) signaling pathway. Fluorouracil 58-62 mitogen-activated protein kinase 8 Homo sapiens 182-203 34360807-6 2021 In HCT116 cells, LMWF enhanced the suppressive effects of 5-FU on cell viability through the (1) induction of cell cycle arrest in the S phase and (2) late apoptosis mediated by the Jun-N-terminal kinase (JNK) signaling pathway. Fluorouracil 58-62 mitogen-activated protein kinase 8 Homo sapiens 205-208 34360807-7 2021 In Caco-2 cells, LMWF enhanced the suppressive effects of 5-FU on cell viability through both the c-mesenchymal-epithelial transition (MET)/Kirsten rat sarcoma virus (KRAS)/extracellular signal-regulated kinase (ERK) and the c-MET/phosphatidyl-inositol 3-kinases (PI3K)/protein kinase B (AKT) signaling pathways. Fluorouracil 58-62 MET proto-oncogene, receptor tyrosine kinase Homo sapiens 225-230 34360807-7 2021 In Caco-2 cells, LMWF enhanced the suppressive effects of 5-FU on cell viability through both the c-mesenchymal-epithelial transition (MET)/Kirsten rat sarcoma virus (KRAS)/extracellular signal-regulated kinase (ERK) and the c-MET/phosphatidyl-inositol 3-kinases (PI3K)/protein kinase B (AKT) signaling pathways. Fluorouracil 58-62 AKT serine/threonine kinase 1 Homo sapiens 288-291 34309458-9 2022 The increase in p53, Bax, p38 MAPK, and PTEN gene expression levels compared to the control group was 1.71, 1.42, 3.26, and 3.29-fold with 5-FU + L treatment, respectively, while this increase was 8.43, 1.65, 3.55, and 3.54-fold with 5-FU + Q treatment, respectively. Fluorouracil 139-143 tumor protein p53 Homo sapiens 16-19 34309458-9 2022 The increase in p53, Bax, p38 MAPK, and PTEN gene expression levels compared to the control group was 1.71, 1.42, 3.26, and 3.29-fold with 5-FU + L treatment, respectively, while this increase was 8.43, 1.65, 3.55, and 3.54-fold with 5-FU + Q treatment, respectively. Fluorouracil 139-143 BCL2 associated X, apoptosis regulator Homo sapiens 21-24 34309458-9 2022 The increase in p53, Bax, p38 MAPK, and PTEN gene expression levels compared to the control group was 1.71, 1.42, 3.26, and 3.29-fold with 5-FU + L treatment, respectively, while this increase was 8.43, 1.65, 3.55, and 3.54-fold with 5-FU + Q treatment, respectively. Fluorouracil 234-238 tumor protein p53 Homo sapiens 16-19 34309458-9 2022 The increase in p53, Bax, p38 MAPK, and PTEN gene expression levels compared to the control group was 1.71, 1.42, 3.26, and 3.29-fold with 5-FU + L treatment, respectively, while this increase was 8.43, 1.65, 3.55, and 3.54-fold with 5-FU + Q treatment, respectively. Fluorouracil 234-238 BCL2 associated X, apoptosis regulator Homo sapiens 21-24 34309458-10 2022 In addition, when the anti-apoptotic Bcl-2, mTOR, and Akt gene expression levels were normalized as 1 in the control group, they were 0.28, 0.41, and 0.22 with 5-FU + L treatment, and 0.32, 0.46, and 0.39, respectively, with 5-FU + Q treatment. Fluorouracil 160-164 BCL2 apoptosis regulator Homo sapiens 37-42 34309458-10 2022 In addition, when the anti-apoptotic Bcl-2, mTOR, and Akt gene expression levels were normalized as 1 in the control group, they were 0.28, 0.41, and 0.22 with 5-FU + L treatment, and 0.32, 0.46, and 0.39, respectively, with 5-FU + Q treatment. Fluorouracil 160-164 mechanistic target of rapamycin kinase Homo sapiens 44-48 34309458-10 2022 In addition, when the anti-apoptotic Bcl-2, mTOR, and Akt gene expression levels were normalized as 1 in the control group, they were 0.28, 0.41, and 0.22 with 5-FU + L treatment, and 0.32, 0.46, and 0.39, respectively, with 5-FU + Q treatment. Fluorouracil 160-164 AKT serine/threonine kinase 1 Homo sapiens 54-57 34309458-10 2022 In addition, when the anti-apoptotic Bcl-2, mTOR, and Akt gene expression levels were normalized as 1 in the control group, they were 0.28, 0.41, and 0.22 with 5-FU + L treatment, and 0.32, 0.46, and 0.39, respectively, with 5-FU + Q treatment. Fluorouracil 225-229 BCL2 apoptosis regulator Homo sapiens 37-42 34309458-10 2022 In addition, when the anti-apoptotic Bcl-2, mTOR, and Akt gene expression levels were normalized as 1 in the control group, they were 0.28, 0.41, and 0.22 with 5-FU + L treatment, and 0.32, 0.46, and 0.39, respectively, with 5-FU + Q treatment. Fluorouracil 225-229 mechanistic target of rapamycin kinase Homo sapiens 44-48 34309458-10 2022 In addition, when the anti-apoptotic Bcl-2, mTOR, and Akt gene expression levels were normalized as 1 in the control group, they were 0.28, 0.41, and 0.22 with 5-FU + L treatment, and 0.32, 0.46, and 0.39, respectively, with 5-FU + Q treatment. Fluorouracil 225-229 AKT serine/threonine kinase 1 Homo sapiens 54-57 34589581-0 2021 Targeting EGFR sensitizes 5-Fu-resistant colon cancer cells through modification of the lncRNA-FGD5-AS1-miR-330-3p-Hexokinase 2 axis. Fluorouracil 26-30 epidermal growth factor receptor Homo sapiens 10-14 34589581-4 2021 Here we report that EGFR and lncRNA-FGD5-AS1 promoted 5-Fu resistance of CRC. Fluorouracil 54-58 epidermal growth factor receptor Homo sapiens 20-24 34589581-5 2021 By establishing the 5-Fu-resistant CRC cell line, we detected that EGFR, FGD5-AS1, and glucose metabolism were significantly elevated in 5-Fu-resistant CRC cells. Fluorouracil 20-24 epidermal growth factor receptor Homo sapiens 67-71 34589581-5 2021 By establishing the 5-Fu-resistant CRC cell line, we detected that EGFR, FGD5-AS1, and glucose metabolism were significantly elevated in 5-Fu-resistant CRC cells. Fluorouracil 137-141 epidermal growth factor receptor Homo sapiens 67-71 34589581-9 2021 Rescue experiments demonstrated that FGD5-AS1 promotes glycolysis through modulating the miR-330-3p-HK2 axis, leading to 5-Fu resistance of CRC cancer cells. Fluorouracil 121-125 FGD5 antisense RNA 1 Homo sapiens 37-45 34226586-9 2021 Upregulated IL-6 induced resistance to 5-FU with STAT3 and Akt activation in ECs in an autocrine manner. Fluorouracil 39-43 interleukin 6 Homo sapiens 12-16 34226586-9 2021 Upregulated IL-6 induced resistance to 5-FU with STAT3 and Akt activation in ECs in an autocrine manner. Fluorouracil 39-43 signal transducer and activator of transcription 3 Homo sapiens 49-54 34226586-9 2021 Upregulated IL-6 induced resistance to 5-FU with STAT3 and Akt activation in ECs in an autocrine manner. Fluorouracil 39-43 AKT serine/threonine kinase 1 Homo sapiens 59-62 34279763-3 2021 Here we examined the SIRT5 (Resveratrol and Suramin) and p53 (Nutlin3a) modulators alone or in combination with 5-FU on the proliferation of colon cancer cells and effect of 5-FU on the SIRT5 and FOXO3a protein expressions whether p53 dependent or independent manner. Fluorouracil 174-178 forkhead box O3 Homo sapiens 196-202 34279763-4 2021 METHODS AND RESULTS: According to our MTT assay results, Resveratrol (RSV), Nutlin3a and Suramin was found to be more effective in HCT-116 p53+/+ cells and these differences were evaluated together with the effect of 5-FU on the SIRT5, FOXO3a and Bim protein expressions in HCT-116 p53 +/+ and HCT-116 p53 -/- cells. Fluorouracil 217-221 forkhead box O3 Homo sapiens 236-242 34279763-6 2021 Our western blot experiment results showed that while Suramin decreased SIRT5 and RSV decreased FOXO3a protein expressions significantly in HCT-116 p53 -/- cells, 5-FU decreased significantly SIRT5 and FOXO3a protein expressions in a p53 independent manner. Fluorouracil 163-167 forkhead box O3 Homo sapiens 202-208 34279763-6 2021 Our western blot experiment results showed that while Suramin decreased SIRT5 and RSV decreased FOXO3a protein expressions significantly in HCT-116 p53 -/- cells, 5-FU decreased significantly SIRT5 and FOXO3a protein expressions in a p53 independent manner. Fluorouracil 163-167 tumor protein p53 Homo sapiens 234-237 34279763-7 2021 CONCLUSIONS: In this study, the effect of 5-FU on SIRT5 and FOXO 3a proteins was determined for the first time in HCT-116 p53 +/+ and HCT-116 p53 -/- cells. Fluorouracil 42-46 forkhead box O3 Homo sapiens 60-67 34157823-9 2021 Results: Administration of 5-FU at a dose of 20 mg/kg body weight resulted in a significant increase in the serum levels of hepatic biomarkers, including aspartate aminotransferase, alanine aminotransferase, alkaline phosphatase, direct bilirubin, and total bilirubin. Fluorouracil 27-31 glutamic-oxaloacetic transaminase 2 Rattus norvegicus 154-180 34306337-0 2021 Triamcinolone acetonide combined with 5-fluorouracil suppresses urethral scar fibroblasts autophagy and fibrosis by increasing miR-192-5p expression. Fluorouracil 38-52 microRNA 192 Homo sapiens 127-134 34306337-8 2021 MiR-192-5p level was downregulated in urethral stricture tissue and urethral tissue fibroblast, TA combined with 5-FU treatment rescue the expression of miR-192-5p. Fluorouracil 113-117 microRNA 192 Homo sapiens 153-160 34306337-10 2021 miR-192-5p mediated the improvement of urethral scar by triamcinolone acetonide combined with 5-FU by directly targeting ATG7, which is marker gene of autophagy. Fluorouracil 94-98 microRNA 192 Homo sapiens 0-7 34306337-11 2021 Our data demonstrated that TA combined with 5-FU suppresses urethral scar fibroblasts autophagy and fibrosis by increasing miR-192-5p expression, thus offering a new strategies and target for Urethral stricture. Fluorouracil 44-48 microRNA 192 Homo sapiens 123-130 34211552-6 2021 The results of CAT assay also showed a significant difference in nano-posttreatment (124.60 +- 10.85), posttreatment (135.4 +- 9.82), and nano-pretreatment groups (128.80 +- 7.20) compared to the 5-FU group (55.07 +- 8.91). Fluorouracil 196-200 catalase Mus musculus 15-18 34095137-0 2021 DCBLD2 Affects the Development of Colorectal Cancer via EMT and Angiogenesis and Modulates 5-FU Drug Resistance. Fluorouracil 91-95 discoidin, CUB and LCCL domain containing 2 Homo sapiens 0-6 34095137-6 2021 GDSC database was used to analyze the effect of DCBLD2 expression difference on 5-FU drug sensitivity on tumor cells. Fluorouracil 80-84 discoidin, CUB and LCCL domain containing 2 Homo sapiens 48-54 34095137-7 2021 CCK-8, clone formation, scratch, Transwell invasion and migration assays were used to assess DCBLD2 effects on the proliferation, metastasis, and 5-FU drug sensitivity on HCT116 and Caco-2 colorectal cancer cells. Fluorouracil 146-150 discoidin, CUB and LCCL domain containing 2 Homo sapiens 93-99 34095137-11 2021 GDSC database analysis showed that DCBLD2 overexpression caused tumor cell resistance to 5-FU. Fluorouracil 89-93 discoidin, CUB and LCCL domain containing 2 Homo sapiens 35-41 34095137-12 2021 The results of in vitro and in vivo experiments showed that the inhibition of DCBLD2 reduced the proliferation, migration and invasion of colorectal cancer cells, inhibited the angiogenesis of endothelial cells, and enhanced the drug sensitivity to 5-FU. Fluorouracil 249-253 discoidin, CUB and LCCL domain containing 2 Homo sapiens 78-84 34095137-16 2021 Conclusion: DCBLD2 may affect the development of colorectal cancer by regulating cell proliferation and motility, and modulate 5-FU resistance. Fluorouracil 127-131 discoidin, CUB and LCCL domain containing 2 Homo sapiens 12-18 34067869-8 2021 5FU reduced the expression of the key cytoskeletal proteins, desmin and dystrophin, which was not prevented by BGP-15. Fluorouracil 0-3 dystrophin, muscular dystrophy Mus musculus 72-82 34121975-9 2021 Treatment with Candesartan either alone, or in combination with 5-FU decreased tumor size in the mouse model, and also increased the level of oxidative markers MDA and reduced CAT, SOD, and thiols. Fluorouracil 64-68 catalase Mus musculus 176-179 34121975-9 2021 Treatment with Candesartan either alone, or in combination with 5-FU decreased tumor size in the mouse model, and also increased the level of oxidative markers MDA and reduced CAT, SOD, and thiols. Fluorouracil 64-68 superoxide dismutase 1 Homo sapiens 181-184 34602411-6 2021 In vitro, the protein and mRNA expressions of FAK, PI3K, AKT and mTOR in beta-carboline alkaloids groups were significantly lower than those in control and fluorouracil groups (P<0.05). Fluorouracil 156-168 mechanistic target of rapamycin kinase Homo sapiens 65-69 34602411-9 2021 FAK, PI3K, AKT and mTOR proteins in tumor tissues of beta-carboline alkaloids and fluorouracil groups were significantly lower than control group (P<0.05). Fluorouracil 82-94 AKT serine/threonine kinase 1 Homo sapiens 11-14 34602411-9 2021 FAK, PI3K, AKT and mTOR proteins in tumor tissues of beta-carboline alkaloids and fluorouracil groups were significantly lower than control group (P<0.05). Fluorouracil 82-94 mechanistic target of rapamycin kinase Homo sapiens 19-23 34981469-9 2021 The expression levels of all tested genes were altered in all treatment groups compared to the control, with that of WNT1, CTNNB1, TCF, MTOR, AKT1, BIRC5, and CCND1 showing the most robust changes in the combined curcumin/berberine/5-FU treatment. Fluorouracil 232-236 Wnt family member 1 Homo sapiens 117-121 34981469-9 2021 The expression levels of all tested genes were altered in all treatment groups compared to the control, with that of WNT1, CTNNB1, TCF, MTOR, AKT1, BIRC5, and CCND1 showing the most robust changes in the combined curcumin/berberine/5-FU treatment. Fluorouracil 232-236 hepatocyte nuclear factor 4 alpha Homo sapiens 131-134 34981469-9 2021 The expression levels of all tested genes were altered in all treatment groups compared to the control, with that of WNT1, CTNNB1, TCF, MTOR, AKT1, BIRC5, and CCND1 showing the most robust changes in the combined curcumin/berberine/5-FU treatment. Fluorouracil 232-236 mechanistic target of rapamycin kinase Homo sapiens 136-140 34981469-9 2021 The expression levels of all tested genes were altered in all treatment groups compared to the control, with that of WNT1, CTNNB1, TCF, MTOR, AKT1, BIRC5, and CCND1 showing the most robust changes in the combined curcumin/berberine/5-FU treatment. Fluorouracil 232-236 AKT serine/threonine kinase 1 Homo sapiens 142-146 34753130-11 2021 Enhancement of p38 MAPK activity by transfection with MKK6E (a constitutively active form of MKK6) vector increased the Rad52 protein level and cell survival by 5-FU. Fluorouracil 161-165 mitogen-activated protein kinase kinase 6 Homo sapiens 93-97 35320055-6 2022 This study discusses how the function of 5-fluorouracil in JAK/STAT, Wnt, Notch, NF-kappaB, and hedgehogs in some cancers. Fluorouracil 41-55 nuclear factor kappa B subunit 1 Homo sapiens 81-90 35609368-8 2022 In addition, C3G alone or combined with 5-FU affected the expression of the tumor microenvironment-related factors Ki67, CD45, PDL1, and CD73. Fluorouracil 40-44 CD274 antigen Mus musculus 127-131 35405270-4 2022 In addition, Met could inhibit 5-Fu-induced high expression of endoplasmic reticulum stress(ERS)-related proteins GRP78 and CHOP. Fluorouracil 31-35 heat shock protein 5 Mus musculus 114-119 35405270-8 2022 This study confirmed the protective effect of Met on 5-Fu-induced CIOM, which was achieved by inhibiting ERS and reducing the activity of NF-kappaB. Fluorouracil 53-57 nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105 Mus musculus 138-147 35490372-9 2022 Moreover, 5-FU and OxaPt treatments significantly modulate protein levels of core-autophagy proteins ATG7 and ATG12. Fluorouracil 10-14 autophagy related 12 Homo sapiens 110-115 35611809-7 2022 Ectopically expressed RASSF4 in LoVo cells inhibited cell growth, colony formation, cell cycle progression and increased the sensitivity to 5-FU treatment. Fluorouracil 140-144 Ras association domain family member 4 Homo sapiens 22-28 35611809-8 2022 Annexin V/PI apoptosis assay showed that RASSF4 overexpression increased 5-FU-induced apoptosis and downregulated the mitochondrial membrane potential. Fluorouracil 73-77 Ras association domain family member 4 Homo sapiens 41-47 35483272-4 2022 FNR associated genes (GPX4, SLC7A11, and FTH1) and STAT3 are upregulated in 5-FU resistant cells and xenografts. Fluorouracil 76-80 signal transducer and activator of transcription 3 Homo sapiens 51-56 35624466-16 2022 AP4-deficiency also sensitized CRC cells to 5-FU treatment, whereas ectopic AP4 conferred resistance to 5-FU in a miR-22-3p and MDC1-dependent manner. Fluorouracil 104-108 mediator of DNA damage checkpoint 1 Mus musculus 128-132 35624466-17 2022 CONCLUSIONS: In summary, AP4, miR-22-3p and MDC1 form a conserved and coherent, regulatory feed-forward loop to promote DNA repair, which suppresses DNA damage, senescence and CIN, and contributes to 5-FU resistance. Fluorouracil 200-204 mediator of DNA damage checkpoint 1 Mus musculus 44-48 35608750-0 2022 The epigenetic modifier HDAC2 and the checkpoint kinase ATM determine the responses of microsatellite instable colorectal cancer cells to 5-fluorouracil. Fluorouracil 138-152 histone deacetylase 2 Homo sapiens 24-29 35608750-8 2022 In contrast to this similarity, HDAC2-negative and HDAC2-positive RKO cells undergo differential cell cycle arrest and apoptosis induction in response to the frequently used chemotherapeutic 5-fluorouracil, which becomes incorporated into and damages RNA and DNA. Fluorouracil 191-205 histone deacetylase 2 Homo sapiens 32-37 35608750-8 2022 In contrast to this similarity, HDAC2-negative and HDAC2-positive RKO cells undergo differential cell cycle arrest and apoptosis induction in response to the frequently used chemotherapeutic 5-fluorouracil, which becomes incorporated into and damages RNA and DNA. Fluorouracil 191-205 histone deacetylase 2 Homo sapiens 51-56 35608750-9 2022 5-fluorouracil causes an enrichment of HDAC2-negative RKO cells in vitro and in a subset of primary colorectal tumors in mice. Fluorouracil 0-14 histone deacetylase 2 Homo sapiens 39-44 35608750-12 2022 These findings demonstrate that HDAC2 and ATM modulate the responses of colorectal cancer cells towards 5-FU. Fluorouracil 104-108 histone deacetylase 2 Homo sapiens 32-37 35634282-9 2022 The combination of 5-FU with ICB augmented an inflammatory tumor microenvironment with markedly increased CD8+ T cell activation and upregulation of IFNgamma, TNFalpha and IL-1beta signaling. Fluorouracil 19-23 interferon gamma Homo sapiens 149-157 35634282-9 2022 The combination of 5-FU with ICB augmented an inflammatory tumor microenvironment with markedly increased CD8+ T cell activation and upregulation of IFNgamma, TNFalpha and IL-1beta signaling. Fluorouracil 19-23 tumor necrosis factor Homo sapiens 159-167 35634282-10 2022 The effective anti-tumor immune response of 5-FU chemo-immunotherapy was dependent on CD8+ T cells but was unaffected when TNFalpha or IL-1beta cytokine signaling pathways were blocked. Fluorouracil 44-48 tumor necrosis factor Homo sapiens 123-131 35551770-0 2022 Influence of 6-shogaol potentiated on 5-fluorouracil treatment of liver cancer by promoting apoptosis and cell cycle arrest by regulating AKT/mTOR/MRP1 signalling. Fluorouracil 38-52 AKT serine/threonine kinase 1 Homo sapiens 138-141 35551770-0 2022 Influence of 6-shogaol potentiated on 5-fluorouracil treatment of liver cancer by promoting apoptosis and cell cycle arrest by regulating AKT/mTOR/MRP1 signalling. Fluorouracil 38-52 mechanistic target of rapamycin kinase Homo sapiens 142-146 35551770-8 2022 In cancer cells cotreated with 6-shogaol and 5-FU, AKT/mTOR pathway- and cell cycle-related protein expression levels were inhibited, and MRP1 expression was downregulated. Fluorouracil 45-49 AKT serine/threonine kinase 1 Homo sapiens 51-54 35551770-8 2022 In cancer cells cotreated with 6-shogaol and 5-FU, AKT/mTOR pathway- and cell cycle-related protein expression levels were inhibited, and MRP1 expression was downregulated. Fluorouracil 45-49 mechanistic target of rapamycin kinase Homo sapiens 55-59 35551770-8 2022 In cancer cells cotreated with 6-shogaol and 5-FU, AKT/mTOR pathway- and cell cycle-related protein expression levels were inhibited, and MRP1 expression was downregulated. Fluorouracil 45-49 ATP binding cassette subfamily B member 1 Homo sapiens 138-142 35551770-12 2022 In summary, our data demonstrated that 6-shogaol contributed to the curative outcome of 5-FU in liver cancer by inhibiting the AKT/mTOR/MRP1 signalling pathway. Fluorouracil 88-92 AKT serine/threonine kinase 1 Homo sapiens 127-130 35551770-12 2022 In summary, our data demonstrated that 6-shogaol contributed to the curative outcome of 5-FU in liver cancer by inhibiting the AKT/mTOR/MRP1 signalling pathway. Fluorouracil 88-92 mechanistic target of rapamycin kinase Homo sapiens 131-135 35551770-12 2022 In summary, our data demonstrated that 6-shogaol contributed to the curative outcome of 5-FU in liver cancer by inhibiting the AKT/mTOR/MRP1 signalling pathway. Fluorouracil 88-92 ATP binding cassette subfamily B member 1 Homo sapiens 136-140 35405096-9 2022 In addition, we showed that PP2A B56delta complexes directly dephosphorylated the multi-drug efflux pump MDR1, contributing to drug resistance against the chemotherapeutic 5-fluorouracil. Fluorouracil 172-186 malic enzyme complex, mitochondrial Mus musculus 105-109 35484214-5 2022 HIF-1alpha knockdown suppressed proliferation, migration/invasion and epithelial-mesenchymal transition (EMT) progression, induced G0/G1 cell cycle arrest, promoted apoptosis and inhibited 5-fluorouracil chemoresistance in vitro. Fluorouracil 189-203 hypoxia inducible factor 1 subunit alpha Homo sapiens 0-10 35484214-6 2022 In vivo assays showed that HIF-1alpha is essential in maintaining tumour growth, angiogenesis, and 5-fluorouracil chemoresistance. Fluorouracil 99-113 hypoxia inducible factor 1 subunit alpha Homo sapiens 27-37 35498037-14 2022 Finally, in human cardio myocytes, we observed 5-FU-induced upregulation of the inflammatory, senescence-associated cytokine IL6 and p16 genes, which expression was reduced by OMWW treatment. Fluorouracil 47-51 interleukin 6 Homo sapiens 125-128 35498037-14 2022 Finally, in human cardio myocytes, we observed 5-FU-induced upregulation of the inflammatory, senescence-associated cytokine IL6 and p16 genes, which expression was reduced by OMWW treatment. Fluorouracil 47-51 cyclin dependent kinase inhibitor 2A Homo sapiens 133-136 35411625-6 2022 5-FU resulted in significant cardiotoxicity, represented by an increase in the serum levels of cardiac enzymes and malondialdehyde, as well as cyclooxygenase-2 (COX-2) and tumor necrosis factor-alpha (TNF-alpha) expression, and histopathological degeneration. Fluorouracil 0-4 tumor necrosis factor Rattus norvegicus 172-199 35411625-6 2022 5-FU resulted in significant cardiotoxicity, represented by an increase in the serum levels of cardiac enzymes and malondialdehyde, as well as cyclooxygenase-2 (COX-2) and tumor necrosis factor-alpha (TNF-alpha) expression, and histopathological degeneration. Fluorouracil 0-4 tumor necrosis factor Rattus norvegicus 201-210 35462906-11 2022 Conclusion: Dormant CRC is associated with high glutamine metabolism and synergizes with CAFs in 5-FU resistance, and the key effectors are LMOD1, MAB21L2, and ASPN. Fluorouracil 97-101 asporin Homo sapiens 160-164 35379199-6 2022 Among nearly 350 KRAB-ZFPs, almost a quarter were downregulated after the induction of a 5-FU-resistance including a common one between the three CRC cell lines, ZNF649, whose role is still unknown. Fluorouracil 89-93 zinc finger protein 649 Homo sapiens 162-168 35416117-0 2022 Discoidin domain receptor 1a (DDR1a) confers 5-fluorouracil cytotoxicity in LoVo cell via PI3K/AKT/Bcl-2 pathway. Fluorouracil 45-59 AKT serine/threonine kinase 1 Homo sapiens 95-98 35416117-0 2022 Discoidin domain receptor 1a (DDR1a) confers 5-fluorouracil cytotoxicity in LoVo cell via PI3K/AKT/Bcl-2 pathway. Fluorouracil 45-59 BCL2 apoptosis regulator Homo sapiens 99-104 35416117-6 2022 When 5-FU (5 microM) was administered, the percentage of apoptotic cells, cytochrome C release and caspase-3 activity was found to be higher in the shDDR1a group than that in the control group. Fluorouracil 5-9 cytochrome c, somatic Homo sapiens 74-86 35416117-6 2022 When 5-FU (5 microM) was administered, the percentage of apoptotic cells, cytochrome C release and caspase-3 activity was found to be higher in the shDDR1a group than that in the control group. Fluorouracil 5-9 caspase 3 Homo sapiens 99-108 35191521-0 2022 ATR inhibitor AZD6738 increases the sensitivity of colorectal cancer cells to 5-fluorouracil by inhibiting repair of DNA damage. Fluorouracil 78-92 ATR serine/threonine kinase Homo sapiens 0-3 35191521-6 2022 In vitro, the AZD6738/5-FU combination increased the number of mitotic cells according to flow cytometry, decreased the checkpoint kinase 1 phosphorylation levels and increased cleaved caspase-3 and phosphorylated form of H2A.X variant histone levels according to western blotting, and decreased the proliferation rate of four colon cancer cell lines according to cell viability experiments. Fluorouracil 22-26 checkpoint kinase 1 Homo sapiens 120-139 35191521-6 2022 In vitro, the AZD6738/5-FU combination increased the number of mitotic cells according to flow cytometry, decreased the checkpoint kinase 1 phosphorylation levels and increased cleaved caspase-3 and phosphorylated form of H2A.X variant histone levels according to western blotting, and decreased the proliferation rate of four colon cancer cell lines according to cell viability experiments. Fluorouracil 22-26 caspase 3 Homo sapiens 185-194 35191521-8 2022 The present results suggested that AZD6738 enhanced the effect of 5-FU in p53-mutated colorectal cancer. Fluorouracil 66-70 tumor protein p53 Homo sapiens 74-77 35354250-5 2022 Mechanismly, PFKFB3 facilitated pro-apoptotic transcription factor FOXO3A and its downstream gene expressions, including p21, p27, FAS after 5FU treatment in vitro. Fluorouracil 141-144 forkhead box O3 Homo sapiens 67-73 35448163-7 2022 Furthermore, a few lncRNAs, such as AFAP1-AS1 and LINC01014, block the efficiency of chemotherapeutic drugs, including cisplatin, 5-fluorouracil, paclitaxel, and gefitinib, used for ESCC treatment. Fluorouracil 130-144 long intergenic non-protein coding RNA 1014 Homo sapiens 50-59 35408903-8 2022 In terms of mechanism, kaempferol promotes the expression of microRNA-326 (miR-326) in colon cancer cells, and miR-326 could inhibit the process of glycolysis by directly targeting pyruvate kinase M2 isoform (PKM2) 3"-UTR (untranslated region) to inhibit the expression of PKM2 or indirectly block the alternative splicing factors of PKM mRNA, and then reverse the resistance of colorectal cancer cells to 5-Fu. Fluorouracil 406-410 microRNA 326 Homo sapiens 61-73 35408903-8 2022 In terms of mechanism, kaempferol promotes the expression of microRNA-326 (miR-326) in colon cancer cells, and miR-326 could inhibit the process of glycolysis by directly targeting pyruvate kinase M2 isoform (PKM2) 3"-UTR (untranslated region) to inhibit the expression of PKM2 or indirectly block the alternative splicing factors of PKM mRNA, and then reverse the resistance of colorectal cancer cells to 5-Fu. Fluorouracil 406-410 microRNA 326 Homo sapiens 75-82 35408903-8 2022 In terms of mechanism, kaempferol promotes the expression of microRNA-326 (miR-326) in colon cancer cells, and miR-326 could inhibit the process of glycolysis by directly targeting pyruvate kinase M2 isoform (PKM2) 3"-UTR (untranslated region) to inhibit the expression of PKM2 or indirectly block the alternative splicing factors of PKM mRNA, and then reverse the resistance of colorectal cancer cells to 5-Fu. Fluorouracil 406-410 microRNA 326 Homo sapiens 111-118 35408903-9 2022 Taken together, our data suggest that kaempferol may play an important role in overcoming resistance to 5-Fu therapy by regulating the miR-326-hnRNPA1/A2/PTBP1-PKM2 axis. Fluorouracil 104-108 microRNA 326 Homo sapiens 135-142 35151644-3 2022 In vivo, 5-FU-induced oral mucositis model mice showed a higher level of glucose-regulated protein 78 kD (GRP78, a marker of ERS) than control mice. Fluorouracil 9-13 heat shock protein 5 Mus musculus 73-104 35151644-3 2022 In vivo, 5-FU-induced oral mucositis model mice showed a higher level of glucose-regulated protein 78 kD (GRP78, a marker of ERS) than control mice. Fluorouracil 9-13 heat shock protein 5 Mus musculus 106-111 35151644-5 2022 Moreover, inhibition of ERS significantly decreased the activation of nuclear factor kappa-B (NF-kappaB) in 5-FU-induced oral mucositis model mice following tissue damage reduction. Fluorouracil 108-112 nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105 Mus musculus 70-92 35151644-5 2022 Moreover, inhibition of ERS significantly decreased the activation of nuclear factor kappa-B (NF-kappaB) in 5-FU-induced oral mucositis model mice following tissue damage reduction. Fluorouracil 108-112 nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105 Mus musculus 94-103 35151644-6 2022 In the clinic, 5-FU could increase cell apoptosis and cause oral mucosa damage while increasing the expression of the ERS marker genes GRP78 and C/EBP-homologous protein (CHOP). Fluorouracil 15-19 heat shock protein 5 Mus musculus 135-140 35151644-7 2022 Our study found that 5-FU could induce severe ERS, upregulate the expression of GRP78 and CHOP, raise oxidative stress and increase the expression of inflammatory factors by activating the NF-kappaB pathway, thus causing cell apoptosis and finally leading to oral mucosal injury. Fluorouracil 21-25 heat shock protein 5 Mus musculus 80-85 35151644-7 2022 Our study found that 5-FU could induce severe ERS, upregulate the expression of GRP78 and CHOP, raise oxidative stress and increase the expression of inflammatory factors by activating the NF-kappaB pathway, thus causing cell apoptosis and finally leading to oral mucosal injury. Fluorouracil 21-25 nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105 Mus musculus 189-198 35326562-1 2022 The first-line therapy of patients with RAS wild-type (WT) non-resectable metastatic colorectal cancer (mCRC) is usually 5-fluorouracil-based chemotherapy with either bevacizumab or an anti-epidermal growth factor receptor (EGFR). Fluorouracil 121-135 epidermal growth factor receptor Homo sapiens 224-228 35170195-0 2022 Long noncoding RNA CCAT2 reduces chemosensitivity to 5-fluorouracil in breast cancer cells by activating the mTOR axis. Fluorouracil 53-67 mechanistic target of rapamycin kinase Homo sapiens 109-113 35112408-12 2022 The synergistic antitumor effect of Bio-A/ 5-FU combination can be, at least partly, attributed to Bio-A-mediated suppression of ER-alpha/Akt axis and the augmentation of 5-FU-mediated proapoptotic effects. Fluorouracil 43-47 estrogen receptor 1 Homo sapiens 129-137 35112408-12 2022 The synergistic antitumor effect of Bio-A/ 5-FU combination can be, at least partly, attributed to Bio-A-mediated suppression of ER-alpha/Akt axis and the augmentation of 5-FU-mediated proapoptotic effects. Fluorouracil 43-47 AKT serine/threonine kinase 1 Homo sapiens 138-141 35101590-17 2022 Both in vivo and in vitro experiments indicated that 5-FU increased the expression of ferroptosis, mainly by reducing the expression of glutathione peroxidase 4 (GPX4) and ferritin heavy chain 1 (FTH1), but enhancing the expression of transferrin receptor 1 (TfR1). Fluorouracil 53-57 ferritin heavy chain 1 Rattus norvegicus 172-194 35101590-17 2022 Both in vivo and in vitro experiments indicated that 5-FU increased the expression of ferroptosis, mainly by reducing the expression of glutathione peroxidase 4 (GPX4) and ferritin heavy chain 1 (FTH1), but enhancing the expression of transferrin receptor 1 (TfR1). Fluorouracil 53-57 ferritin heavy chain 1 Rattus norvegicus 196-200 35180871-0 2022 MeCP2 confers 5-fluorouracil resistance in gastric cancer via upregulating the NOX4/PKM2 pathway. Fluorouracil 14-28 methyl-CpG binding protein 2 Homo sapiens 0-5 35180871-3 2022 However, the function and molecular mechanisms of MeCP2 in GC 5-FU resistance remain unclear. Fluorouracil 62-66 methyl-CpG binding protein 2 Homo sapiens 50-55 35180871-4 2022 METHODS: We detected the expression of MeCP2 in 5-FU-resistant GC cells and examined cell behaviors when MeCP2 was silenced. Fluorouracil 48-52 methyl-CpG binding protein 2 Homo sapiens 39-44 35180871-6 2022 RESULTS: MeCP2 was up-regulated in 5-FU-resistant GC cells. Fluorouracil 35-39 methyl-CpG binding protein 2 Homo sapiens 9-14 35180871-7 2022 Knockdown of MeCP2 enhanced the sensitivity of the cells to 5-FU. Fluorouracil 60-64 methyl-CpG binding protein 2 Homo sapiens 13-18 35180871-9 2022 Silencing NOX4 rescued the inductive effect of MeCP2 overexpression on 5-FU sensitivity of GC cells and reduced the expression of NOX4 and PKM2 in MeCP2 overexpressed 5-FU-resistant GC cells. Fluorouracil 71-75 methyl-CpG binding protein 2 Homo sapiens 47-52 35180871-9 2022 Silencing NOX4 rescued the inductive effect of MeCP2 overexpression on 5-FU sensitivity of GC cells and reduced the expression of NOX4 and PKM2 in MeCP2 overexpressed 5-FU-resistant GC cells. Fluorouracil 167-171 methyl-CpG binding protein 2 Homo sapiens 47-52 35180871-9 2022 Silencing NOX4 rescued the inductive effect of MeCP2 overexpression on 5-FU sensitivity of GC cells and reduced the expression of NOX4 and PKM2 in MeCP2 overexpressed 5-FU-resistant GC cells. Fluorouracil 167-171 methyl-CpG binding protein 2 Homo sapiens 147-152 35180871-10 2022 In addition, our in vivo experiments demonstrated that MeCP2 knockdown enhanced 5-FU sensitivity in tumors. Fluorouracil 80-84 methyl-CpG binding protein 2 Homo sapiens 55-60 35180871-11 2022 CONCLUSION: MeCP2 confers 5-FU resistance in GC cells via upregulating the NOX4/PKM2 pathway, which may lead to a promising therapeutic strategy for GC. Fluorouracil 26-30 methyl-CpG binding protein 2 Homo sapiens 12-17 35110359-7 2022 RESULTS: High IL-1R1 expression predicted poor prognosis and inferior responsiveness to both 5-fluorouracil-based adjuvant chemotherapy (ACT) and immune checkpoint blockade (ICB). Fluorouracil 93-107 interleukin 1 receptor type 1 Homo sapiens 14-20 35039826-0 2022 Correction: Down-regulation of miR-543 expression increases the sensitivity of colorectal cancer cells to 5-Fluorouracil through the PTEN/PI3K/AKT pathway. Fluorouracil 106-120 AKT serine/threonine kinase 1 Homo sapiens 143-146 35207462-7 2022 Our findings demonstrate that down-regulation of C1GALT1 in CCA increases the expression of immature core 1 O-glycan, enhancing CCA progression, including growth and 5-fluorouracil resistance via the activation of the AKT/ERK signaling pathway. Fluorouracil 166-180 AKT serine/threonine kinase 1 Homo sapiens 218-221 35207462-7 2022 Our findings demonstrate that down-regulation of C1GALT1 in CCA increases the expression of immature core 1 O-glycan, enhancing CCA progression, including growth and 5-fluorouracil resistance via the activation of the AKT/ERK signaling pathway. Fluorouracil 166-180 mitogen-activated protein kinase 1 Homo sapiens 222-225 35083139-8 2021 Silence of CCDC144NL-AS1 and LINC01614 both significantly suppressed the cell proliferation and migration of gastric cancer cells, and also promoted the chemosensitivity of gastric cancer cells to 5-fluorouracil. Fluorouracil 197-211 CCDC144NL antisense RNA 1 Homo sapiens 11-24 34998404-0 2022 ROS/PI3K/Akt and Wnt/beta-catenin signalings activate HIF-1alpha-induced metabolic reprogramming to impart 5-fluorouracil resistance in colorectal cancer. Fluorouracil 107-121 AKT serine/threonine kinase 1 Homo sapiens 9-12 34998404-0 2022 ROS/PI3K/Akt and Wnt/beta-catenin signalings activate HIF-1alpha-induced metabolic reprogramming to impart 5-fluorouracil resistance in colorectal cancer. Fluorouracil 107-121 hypoxia inducible factor 1 subunit alpha Homo sapiens 54-64 34998404-7 2022 The influence of both HIF1A gene knockdown and pharmacological inhibition on 5-FU resistance in CRC was evaluated in cell models in vivo and in vitro. Fluorouracil 77-81 hypoxia inducible factor 1 subunit alpha Homo sapiens 22-27 34998404-10 2022 HIF-1alpha-induced glucose metabolic reprogramming imparted 5-FU resistance in CRC. Fluorouracil 60-64 hypoxia inducible factor 1 subunit alpha Homo sapiens 0-10 34998404-11 2022 HIF-1alpha showed enhanced expression in 5-FU-resistant CRC cell lines and clinical specimens, and increased HIF-1alpha levels were associated with failure of fluorouracil analog-based chemotherapy in CRC patients and poor survival. Fluorouracil 41-45 hypoxia inducible factor 1 subunit alpha Homo sapiens 0-10 34998404-11 2022 HIF-1alpha showed enhanced expression in 5-FU-resistant CRC cell lines and clinical specimens, and increased HIF-1alpha levels were associated with failure of fluorouracil analog-based chemotherapy in CRC patients and poor survival. Fluorouracil 159-171 hypoxia inducible factor 1 subunit alpha Homo sapiens 109-119 34998404-12 2022 Upregulation of HIF-1alpha in 5-FU-resistant CRC occurred through non-oxygen-dependent mechanisms of reactive oxygen species-mediated activation of PI3K/Akt signaling and aberrant activation of beta-catenin in the nucleus. Fluorouracil 30-34 hypoxia inducible factor 1 subunit alpha Homo sapiens 16-26 34998404-12 2022 Upregulation of HIF-1alpha in 5-FU-resistant CRC occurred through non-oxygen-dependent mechanisms of reactive oxygen species-mediated activation of PI3K/Akt signaling and aberrant activation of beta-catenin in the nucleus. Fluorouracil 30-34 AKT serine/threonine kinase 1 Homo sapiens 153-156 34998404-13 2022 Both HIF-1alpha gene knock-down and pharmacological inhibition restored the sensitivity of CRC to 5-FU. Fluorouracil 98-102 hypoxia inducible factor 1 subunit alpha Homo sapiens 5-15 34998404-14 2022 CONCLUSIONS: HIF-1alpha is a potential biomarker for 5-FU-resistant CRC, and targeting HIF-1a in combination with 5-FU may represent an effective therapeutic strategy in 5-FU-resistant CRC. Fluorouracil 53-57 hypoxia inducible factor 1 subunit alpha Homo sapiens 13-23 34998404-14 2022 CONCLUSIONS: HIF-1alpha is a potential biomarker for 5-FU-resistant CRC, and targeting HIF-1a in combination with 5-FU may represent an effective therapeutic strategy in 5-FU-resistant CRC. Fluorouracil 53-57 hypoxia inducible factor 1 subunit alpha Homo sapiens 87-93 35070952-0 2021 MicroRNA-155-5p Contributes to 5-Fluorouracil Resistance Through Down-Regulating TP53INP1 in Oral Squamous Cell Carcinoma. Fluorouracil 31-45 tumor protein p53 inducible nuclear protein 1 Homo sapiens 81-89 35070952-8 2021 The enhancement of cell viability (CCK-8 assay), migration (wound-healing and transwell assays) and invasion (transwell assay) by miR-155-5p after 5-FU treatment was reversed by TP53INP1 overexpression. Fluorouracil 147-151 tumor protein p53 inducible nuclear protein 1 Homo sapiens 178-186 35070952-10 2021 In conclusion, these results lead to the proposal that miR-155-5p enhances 5-FU resistance by decreasing TP53INP1 expression in OSCC. Fluorouracil 75-79 tumor protein p53 inducible nuclear protein 1 Homo sapiens 105-113 35154466-6 2022 Meanwhile, CP-25 and 5-Fu activated the intrinsic mitochondrial apoptosis pathway induced by P53, inhibited anti-apoptotic B-cell lymphoma (Bcl-2), induced the pro-apoptotic Bcl-2-associated X protein (Bax), Cytochrome-C and caspases. Fluorouracil 21-25 tumor protein p53 Homo sapiens 93-96 35154466-6 2022 Meanwhile, CP-25 and 5-Fu activated the intrinsic mitochondrial apoptosis pathway induced by P53, inhibited anti-apoptotic B-cell lymphoma (Bcl-2), induced the pro-apoptotic Bcl-2-associated X protein (Bax), Cytochrome-C and caspases. Fluorouracil 21-25 BCL2 apoptosis regulator Homo sapiens 140-145 35154466-6 2022 Meanwhile, CP-25 and 5-Fu activated the intrinsic mitochondrial apoptosis pathway induced by P53, inhibited anti-apoptotic B-cell lymphoma (Bcl-2), induced the pro-apoptotic Bcl-2-associated X protein (Bax), Cytochrome-C and caspases. Fluorouracil 21-25 BCL2 associated X, apoptosis regulator Homo sapiens 174-200 35154466-6 2022 Meanwhile, CP-25 and 5-Fu activated the intrinsic mitochondrial apoptosis pathway induced by P53, inhibited anti-apoptotic B-cell lymphoma (Bcl-2), induced the pro-apoptotic Bcl-2-associated X protein (Bax), Cytochrome-C and caspases. Fluorouracil 21-25 BCL2 associated X, apoptosis regulator Homo sapiens 202-205 34969360-11 2022 Intriguingly, HIF-1alpha overexpression reversed NORAD downregulation-mediated inhibition of VM formation and 5-FU resistance. Fluorouracil 110-114 hypoxia inducible factor 1 subunit alpha Homo sapiens 14-24 35103981-0 2022 5-fluorouracil suppresses stem cell-like properties by inhibiting p38 in pancreatic cancer cell line PANC-1. Fluorouracil 0-14 mitogen-activated protein kinase 14 Homo sapiens 66-69 35103981-4 2022 MATERIAL AND METHODS: PANC-1 human pancreatic cancer cells were treated with 5-fluorouracil (5-FU) at 0.5 IC50, IC50, and 2 IC50 for 24 h. PANC-1 cells were treated for 24 h with 5-FU at 0.5IC50, IC50, and 2IC50 with or without VX-702, p38 phosphorylation inhibitor. Fluorouracil 77-91 mitogen-activated protein kinase 14 Homo sapiens 236-239 35103981-4 2022 MATERIAL AND METHODS: PANC-1 human pancreatic cancer cells were treated with 5-fluorouracil (5-FU) at 0.5 IC50, IC50, and 2 IC50 for 24 h. PANC-1 cells were treated for 24 h with 5-FU at 0.5IC50, IC50, and 2IC50 with or without VX-702, p38 phosphorylation inhibitor. Fluorouracil 93-97 mitogen-activated protein kinase 14 Homo sapiens 236-239 35103981-12 2022 In addition, 5-FU inhibited the phosphorylation of p38 in PANC-1 cells. Fluorouracil 13-17 mitogen-activated protein kinase 14 Homo sapiens 51-54 35103981-13 2022 The phosphorylation of p38 was subsequently suppressed by VX-702, p38 mitogen-activated protein kinase inhibitor, which exhibited similar effects as those of 5-FU treatment. Fluorouracil 158-162 mitogen-activated protein kinase 14 Homo sapiens 23-26 35103981-17 2022 CONCLUSIONS: These findings indicate that the inhibition of p38 phosphorylation suppresses the stemness maintenance and 5-FU resistance of PANC-1 cells, providing a potential therapeutic target for the prevention and treatment of pancreatic cancer. Fluorouracil 120-124 mitogen-activated protein kinase 14 Homo sapiens 60-63 35145347-4 2022 Additionally, Diac, 5-FU and their combination suppressed colonic content/gene expression of IL-6, its downstream oncogene, Kirsten rat sarcoma viral oncogene homolog (K-Ras), and consequently Notch intracellular domain and nuclear factor-kappa B (NF-kappaB) p65. Fluorouracil 20-24 interleukin 6 Rattus norvegicus 93-97 35145347-10 2022 However, only 5-FU upregulated miR-200a, another K-Ras downstream factor. Fluorouracil 14-18 microRNA 200a Rattus norvegicus 31-39 34117917-5 2021 RESULTS: Our results demonstrated that co-administration of HPRP-A1 with iRGD increased the apoptosis, while these two peptides in combination with 5FU increased the intracellular level of p53 that upregulate the pro-apoptotic gene BAX and downregulate the anti-apoptotic gene BCL2. Fluorouracil 148-151 tumor protein p53 Homo sapiens 189-192 34117917-5 2021 RESULTS: Our results demonstrated that co-administration of HPRP-A1 with iRGD increased the apoptosis, while these two peptides in combination with 5FU increased the intracellular level of p53 that upregulate the pro-apoptotic gene BAX and downregulate the anti-apoptotic gene BCL2. Fluorouracil 148-151 BCL2 associated X, apoptosis regulator Homo sapiens 232-235 34117917-5 2021 RESULTS: Our results demonstrated that co-administration of HPRP-A1 with iRGD increased the apoptosis, while these two peptides in combination with 5FU increased the intracellular level of p53 that upregulate the pro-apoptotic gene BAX and downregulate the anti-apoptotic gene BCL2. Fluorouracil 148-151 BCL2 apoptosis regulator Homo sapiens 277-281 34683888-6 2021 The expression levels of E2F2 and Bcl-2 genes were found to be suppressed after treatment with both WO3-Cys and WO3-Trp NPs more than 5-FU-treated cells. Fluorouracil 134-138 BCL2 apoptosis regulator Homo sapiens 34-39 34391754-5 2021 In tumor tissues of groups that received 5-FU and andrographolide sulfonate, CD4+ and CD8+ T cell infiltration was increased, and the expression of IFN-gamma and Granzyme B detected by immunohistochemistry and qPCR was upregulated, reflecting improved antitumor immunity. Fluorouracil 41-45 interferon gamma Mus musculus 148-157 34535128-0 2021 LncRNA LBX2-AS1 promotes colorectal cancer progression and 5-fluorouracil resistance. Fluorouracil 59-73 ladybird homeobox 2 Homo sapiens 7-11 34535128-6 2021 In vitro and PDX models were used to determine if LBX2-AS1 promotes 5-fluorouracil resistance. Fluorouracil 68-82 ladybird homeobox 2 Homo sapiens 50-54 34535128-11 2021 Ex vivo analysis of patient-derived CRC xenografts showed that low LBX2-AS1 expression cases exhibited 5-FU responsiveness and clinical investigations confirmed that low LBX2-AS1 expression was associated with improved clinical benefits from 5-FU therapy. Fluorouracil 103-107 LBX2 antisense RNA 1 Homo sapiens 67-75 34535128-11 2021 Ex vivo analysis of patient-derived CRC xenografts showed that low LBX2-AS1 expression cases exhibited 5-FU responsiveness and clinical investigations confirmed that low LBX2-AS1 expression was associated with improved clinical benefits from 5-FU therapy. Fluorouracil 242-246 ladybird homeobox 2 Homo sapiens 170-174 34535128-12 2021 CONCLUSIONS: Together these results suggest that LBX2-AS1 may serve as a therapeutic target and predictor of 5-FU benefit in CRC patients. Fluorouracil 109-113 ladybird homeobox 2 Homo sapiens 49-53 34373709-0 2021 mRNA expression level of CDH2, LEP, POSTN, TIMP1 and VEGFC modulates 5-fluorouracil resistance in colon cancer cells. Fluorouracil 69-83 TIMP metallopeptidase inhibitor 1 Homo sapiens 43-48 34373709-0 2021 mRNA expression level of CDH2, LEP, POSTN, TIMP1 and VEGFC modulates 5-fluorouracil resistance in colon cancer cells. Fluorouracil 69-83 vascular endothelial growth factor C Homo sapiens 53-58 34373709-13 2021 Taken together, the results suggested that CDH2, LEP, POSTN, TIMP1 and VEGFC might play a role in chemotherapeutic resistance in colon cancer and represent potential targets for overcoming 5-FU resistance in colon cancer. Fluorouracil 189-193 vascular endothelial growth factor C Homo sapiens 71-76 34086111-8 2021 LINC00943 knockdown reduced GC cell proliferation, 5-FU resistance and in vivo explant growth. Fluorouracil 51-55 long intergenic non-protein coding RNA 943 Homo sapiens 0-9 34502219-0 2021 S-Adenosylmethionine Increases the Sensitivity of Human Colorectal Cancer Cells to 5-Fluorouracil by Inhibiting P-Glycoprotein Expression and NF-kappaB Activation. Fluorouracil 83-97 ATP binding cassette subfamily B member 1 Homo sapiens 112-126 34489705-14 2021 Compared with untreated group and 5-FU group, CHB-II-F also enhanced the expression of OX1R, GHSR, NPY, and AgRP protein and gene and decreased the expression of Ob-R, POMC, and CART protein and gene in hypothalamus of mice, and the gene expression was consistent with the protein expression. Fluorouracil 34-38 agouti related neuropeptide Mus musculus 108-112 34485154-0 2021 Angelica Polysaccharide Antagonizes 5-FU-Induced Oxidative Stress Injury to Reduce Apoptosis in the Liver Through Nrf2 Pathway. Fluorouracil 36-40 NFE2 like bZIP transcription factor 2 Homo sapiens 114-118 34485154-5 2021 Our results show that ASP inhibited 5-FU-induced the decrease in Bcl-2 protein and the increase in Bax protein. Fluorouracil 36-40 BCL2 apoptosis regulator Homo sapiens 65-70 34485154-5 2021 Our results show that ASP inhibited 5-FU-induced the decrease in Bcl-2 protein and the increase in Bax protein. Fluorouracil 36-40 BCL2 associated X, apoptosis regulator Homo sapiens 99-102 34485154-6 2021 ASP alleviated 5-FU-induced the increase in alanine aminotransferase (ALT), triglyceride (TG), and aspartate aminotransferase (AST) content; hepatic steatosis; and liver fibrosis. Fluorouracil 15-19 solute carrier family 17 member 5 Homo sapiens 99-125 34485154-6 2021 ASP alleviated 5-FU-induced the increase in alanine aminotransferase (ALT), triglyceride (TG), and aspartate aminotransferase (AST) content; hepatic steatosis; and liver fibrosis. Fluorouracil 15-19 solute carrier family 17 member 5 Homo sapiens 127-130 34485154-8 2021 5-FU promoted the expression of Keap1 and increased the binding to NF-E2-related factor 2 (Nrf2) to reduce the nuclear translocation of Nrf2, thereby weakening the transcriptional activity of Nrf2 to inhibit the expression of HO-1; reducing the activity of GSH, SOD, and CAT to increase ROS content; and aggravating DNA damage (indicated by the increase in 8-OHdG). Fluorouracil 0-4 kelch like ECH associated protein 1 Homo sapiens 32-37 34485154-8 2021 5-FU promoted the expression of Keap1 and increased the binding to NF-E2-related factor 2 (Nrf2) to reduce the nuclear translocation of Nrf2, thereby weakening the transcriptional activity of Nrf2 to inhibit the expression of HO-1; reducing the activity of GSH, SOD, and CAT to increase ROS content; and aggravating DNA damage (indicated by the increase in 8-OHdG). Fluorouracil 0-4 NFE2 like bZIP transcription factor 2 Homo sapiens 67-89 34485154-8 2021 5-FU promoted the expression of Keap1 and increased the binding to NF-E2-related factor 2 (Nrf2) to reduce the nuclear translocation of Nrf2, thereby weakening the transcriptional activity of Nrf2 to inhibit the expression of HO-1; reducing the activity of GSH, SOD, and CAT to increase ROS content; and aggravating DNA damage (indicated by the increase in 8-OHdG). Fluorouracil 0-4 NFE2 like bZIP transcription factor 2 Homo sapiens 91-95 34485154-8 2021 5-FU promoted the expression of Keap1 and increased the binding to NF-E2-related factor 2 (Nrf2) to reduce the nuclear translocation of Nrf2, thereby weakening the transcriptional activity of Nrf2 to inhibit the expression of HO-1; reducing the activity of GSH, SOD, and CAT to increase ROS content; and aggravating DNA damage (indicated by the increase in 8-OHdG). Fluorouracil 0-4 NFE2 like bZIP transcription factor 2 Homo sapiens 136-140 34485154-8 2021 5-FU promoted the expression of Keap1 and increased the binding to NF-E2-related factor 2 (Nrf2) to reduce the nuclear translocation of Nrf2, thereby weakening the transcriptional activity of Nrf2 to inhibit the expression of HO-1; reducing the activity of GSH, SOD, and CAT to increase ROS content; and aggravating DNA damage (indicated by the increase in 8-OHdG). Fluorouracil 0-4 NFE2 like bZIP transcription factor 2 Homo sapiens 192-196 34485154-8 2021 5-FU promoted the expression of Keap1 and increased the binding to NF-E2-related factor 2 (Nrf2) to reduce the nuclear translocation of Nrf2, thereby weakening the transcriptional activity of Nrf2 to inhibit the expression of HO-1; reducing the activity of GSH, SOD, and CAT to increase ROS content; and aggravating DNA damage (indicated by the increase in 8-OHdG). Fluorouracil 0-4 superoxide dismutase 1 Homo sapiens 262-265 34485154-8 2021 5-FU promoted the expression of Keap1 and increased the binding to NF-E2-related factor 2 (Nrf2) to reduce the nuclear translocation of Nrf2, thereby weakening the transcriptional activity of Nrf2 to inhibit the expression of HO-1; reducing the activity of GSH, SOD, and CAT to increase ROS content; and aggravating DNA damage (indicated by the increase in 8-OHdG). Fluorouracil 0-4 catalase Homo sapiens 271-274 34485154-10 2021 In conclusion, ASP attenuated the 5-FU-induced Nrf2 pathway barrier to reduce oxidative stress injury and thereby inhibit the disorder of lipid anabolism and apoptosis. Fluorouracil 34-38 NFE2 like bZIP transcription factor 2 Homo sapiens 47-51 34364387-11 2021 Targeting hexokinase and pyruvate dehydrogenase kinase enzymes may be an option to overcome 5-FU -mediated chemo-resistant in colorectal cancer. Fluorouracil 92-96 hexokinase 1 Homo sapiens 10-20 34151400-7 2021 Based on analysis of the differentially expressed genes, the most prominent molecular pathways affected by 5-FU included cell cycle, p53 signalling, mitochondrial ATP synthesis and apoptosis. Fluorouracil 107-111 tumor protein p53 Homo sapiens 133-136 34062410-10 2021 The influence of colossolactone-G alone or in combination with GCB or 5-FU on the apoptosis and autophagy were confirmed by qPCR analysis for the expression of several key apoptosis and autophagy genes such as, TRAIL, TP53INP1, BNIP3, hp62, ATG5, ATG7, Lamp2A and the golden standard for autophagy (LC3-II). Fluorouracil 70-74 TNF superfamily member 10 Homo sapiens 211-216 34062410-10 2021 The influence of colossolactone-G alone or in combination with GCB or 5-FU on the apoptosis and autophagy were confirmed by qPCR analysis for the expression of several key apoptosis and autophagy genes such as, TRAIL, TP53INP1, BNIP3, hp62, ATG5, ATG7, Lamp2A and the golden standard for autophagy (LC3-II). Fluorouracil 70-74 tumor protein p53 inducible nuclear protein 1 Homo sapiens 218-226 34062410-10 2021 The influence of colossolactone-G alone or in combination with GCB or 5-FU on the apoptosis and autophagy were confirmed by qPCR analysis for the expression of several key apoptosis and autophagy genes such as, TRAIL, TP53INP1, BNIP3, hp62, ATG5, ATG7, Lamp2A and the golden standard for autophagy (LC3-II). Fluorouracil 70-74 BCL2 interacting protein 3 Homo sapiens 228-233 34062410-10 2021 The influence of colossolactone-G alone or in combination with GCB or 5-FU on the apoptosis and autophagy were confirmed by qPCR analysis for the expression of several key apoptosis and autophagy genes such as, TRAIL, TP53INP1, BNIP3, hp62, ATG5, ATG7, Lamp2A and the golden standard for autophagy (LC3-II). Fluorouracil 70-74 autophagy related 5 Homo sapiens 241-245 34321321-7 2021 CD93 blockade in mice increased drug delivery, resulting in an improved antitumor response to gemcitabine or fluorouracil. Fluorouracil 109-121 CD93 antigen Mus musculus 0-4 34440086-7 2021 Our results reveal MEK signaling plays a pivotal role in loss-of-function, APC-mediated 5-FU resistance, and ROCK activation serves as a signature in APC-independent 5-FU resistance. Fluorouracil 88-92 mitogen-activated protein kinase kinase 7 Homo sapiens 19-22 34440086-7 2021 Our results reveal MEK signaling plays a pivotal role in loss-of-function, APC-mediated 5-FU resistance, and ROCK activation serves as a signature in APC-independent 5-FU resistance. Fluorouracil 166-170 mitogen-activated protein kinase kinase 7 Homo sapiens 19-22 34264023-5 2022 METHODS AND RESULTS: We immunolocalized Nrf2 signaling proteins in 69 patients with lymph node metastases, who received NACRT with 5-fluorouracil and cisplatin before esophagectomy. Fluorouracil 131-145 NFE2 like bZIP transcription factor 2 Homo sapiens 40-44 34589581-10 2021 Finally, in vitro and in vivo xenograft experiments consistently demonstrated that inhibition of EGFR by the specific inhibitor erlotinib effectively enhanced the anti-tumor toxicity of 5-Fu by targeting the EGFR-FGD5-AS1-miR-330-3p-HK2 pathway. Fluorouracil 186-190 epidermal growth factor receptor Homo sapiens 97-101 34589581-10 2021 Finally, in vitro and in vivo xenograft experiments consistently demonstrated that inhibition of EGFR by the specific inhibitor erlotinib effectively enhanced the anti-tumor toxicity of 5-Fu by targeting the EGFR-FGD5-AS1-miR-330-3p-HK2 pathway. Fluorouracil 186-190 epidermal growth factor receptor Homo sapiens 208-212 34589581-11 2021 In summary, this study demonstrates new mechanisms of the EGFR-modulated 5-Fu resistance through modulating the noncoding RNA network, contributing to development of new approaches against chemoresistant CRC. Fluorouracil 73-77 epidermal growth factor receptor Homo sapiens 58-62 34238199-8 2022 RESULTS: DTA3 and 5-FU synergized to induce apoptosis and repress proliferation of cervical cancer cells by downregulating the activation of PI3K/AKT and NF-kappaB signalling pathway. Fluorouracil 18-22 AKT serine/threonine kinase 1 Homo sapiens 146-149 34226296-0 2021 Age as a modifier of the effects of chemoradiotherapy with infusional 5-fluorouracil after D2 dissection in gastric cancer. Fluorouracil 70-84 renin binding protein Homo sapiens 0-3 34279763-0 2021 The role of SIRT5 and p53 proteins in the sensitivity of colon cancer cells to chemotherapeutic agent 5-Fluorouracil. Fluorouracil 102-116 tumor protein p53 Homo sapiens 22-25 34185243-0 2021 The IL-6/STAT Signaling Pathway and PPARalpha Are Involved in Mediating the Dose-Dependent Cardioprotective Effects of Fenofibrate in 5-Fluorouracil-Induced Cardiotoxicity. Fluorouracil 134-148 interleukin 6 Homo sapiens 4-8 34185243-7 2021 RESULTS: The current study showed that 5FU succeeded in inducing cardiotoxicity, manifested by significantly elevated levels of cardiac enzymes, tissue malondialdehyde (MDA), interleukin 6 (IL-6), signal transducer and activator of transcription 4 (STAT4), and caspase-3. Fluorouracil 39-42 interleukin 6 Homo sapiens 175-188 34185243-7 2021 RESULTS: The current study showed that 5FU succeeded in inducing cardiotoxicity, manifested by significantly elevated levels of cardiac enzymes, tissue malondialdehyde (MDA), interleukin 6 (IL-6), signal transducer and activator of transcription 4 (STAT4), and caspase-3. Fluorouracil 39-42 interleukin 6 Homo sapiens 190-194 34185243-7 2021 RESULTS: The current study showed that 5FU succeeded in inducing cardiotoxicity, manifested by significantly elevated levels of cardiac enzymes, tissue malondialdehyde (MDA), interleukin 6 (IL-6), signal transducer and activator of transcription 4 (STAT4), and caspase-3. Fluorouracil 39-42 caspase 3 Homo sapiens 261-270 34168410-10 2021 Moreover, NQO1 overexpression was correlated to a better response to 5-fluorouracil (5-FU)-based adjuvant chemotherapy. Fluorouracil 69-83 NAD(P)H quinone dehydrogenase 1 Homo sapiens 10-14 34168410-10 2021 Moreover, NQO1 overexpression was correlated to a better response to 5-fluorouracil (5-FU)-based adjuvant chemotherapy. Fluorouracil 85-89 NAD(P)H quinone dehydrogenase 1 Homo sapiens 10-14 34168410-11 2021 CONCLUSION: NQO1 overexpression is associated with a significantly poor prognosis and better response to 5-FU in patients with gastric cancer. Fluorouracil 105-109 NAD(P)H quinone dehydrogenase 1 Homo sapiens 12-16 34065602-0 2021 Targeting Lactate Dehydrogenase A with Catechin Resensitizes SNU620/5FU Gastric Cancer Cells to 5-Fluorouracil. Fluorouracil 96-110 lactate dehydrogenase A Homo sapiens 10-33 34065602-5 2021 SNU620/5FU, a gastric cancer cell harboring resistance to 5FU, showed much higher lactate production and expression of glycolysis-related enzymes, such as lactate dehydrogenase A (LDHA), than those of the parent SNU620 cells. Fluorouracil 7-10 lactate dehydrogenase A Homo sapiens 155-178 34065602-5 2021 SNU620/5FU, a gastric cancer cell harboring resistance to 5FU, showed much higher lactate production and expression of glycolysis-related enzymes, such as lactate dehydrogenase A (LDHA), than those of the parent SNU620 cells. Fluorouracil 7-10 lactate dehydrogenase A Homo sapiens 180-184 34065602-5 2021 SNU620/5FU, a gastric cancer cell harboring resistance to 5FU, showed much higher lactate production and expression of glycolysis-related enzymes, such as lactate dehydrogenase A (LDHA), than those of the parent SNU620 cells. Fluorouracil 58-61 lactate dehydrogenase A Homo sapiens 155-178 34065602-5 2021 SNU620/5FU, a gastric cancer cell harboring resistance to 5FU, showed much higher lactate production and expression of glycolysis-related enzymes, such as lactate dehydrogenase A (LDHA), than those of the parent SNU620 cells. Fluorouracil 58-61 lactate dehydrogenase A Homo sapiens 180-184 34065602-9 2021 Thus, based on these results, we suggest catechin as a candidate for the development of a novel adjuvant drug that reduces chemoresistance to 5FU by restricting LDHA. Fluorouracil 142-145 lactate dehydrogenase A Homo sapiens 161-165 34069731-5 2021 Exposure of HT-29 tumor cells and blood samples to 5-FU SF/PEG NPs augmented the tumor necrosis factor-alpha levels. Fluorouracil 51-55 tumor necrosis factor Homo sapiens 81-108 34268937-1 2021 PURPOSE: The purpose of this study was to investigate the effect of miR-183 on the sensitivity of laryngeal cancer cells to 5-fluorouracil (5-Fu) and its mechanism, so as to provide certain references for the clinical prevention of drug resistance in laryngeal cancer cells. Fluorouracil 124-138 microRNA 183 Homo sapiens 68-75 34268937-1 2021 PURPOSE: The purpose of this study was to investigate the effect of miR-183 on the sensitivity of laryngeal cancer cells to 5-fluorouracil (5-Fu) and its mechanism, so as to provide certain references for the clinical prevention of drug resistance in laryngeal cancer cells. Fluorouracil 140-144 microRNA 183 Homo sapiens 68-75 34268937-7 2021 RESULTS: MiR-183 declined remarkably in 5-Fu-RES group compared with that in Control group. Fluorouracil 40-44 microRNA 183 Homo sapiens 9-16 34268937-13 2021 CONCLUSIONS: The overexpression of miR-183 can inhibit the drug resistance of the human primary laryngeal cancer cells to 5-Fu, promote cancer cell apoptosis and inhibit their invasive and migratory abilities at the same time, whose mechanism may be associated with the targeted regulation of the TBX3/PTEN signaling pathway by miR-183. Fluorouracil 122-126 microRNA 183 Homo sapiens 35-42 34268937-13 2021 CONCLUSIONS: The overexpression of miR-183 can inhibit the drug resistance of the human primary laryngeal cancer cells to 5-Fu, promote cancer cell apoptosis and inhibit their invasive and migratory abilities at the same time, whose mechanism may be associated with the targeted regulation of the TBX3/PTEN signaling pathway by miR-183. Fluorouracil 122-126 microRNA 183 Homo sapiens 328-335 34380920-4 2021 5-FU exposure significantly reduced cytochrome P450 3A4 (CYP3A4) mRNA expression. Fluorouracil 0-4 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 36-55 34380920-4 2021 5-FU exposure significantly reduced cytochrome P450 3A4 (CYP3A4) mRNA expression. Fluorouracil 0-4 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 57-63 34380920-5 2021 Additionally, the mRNA expression of nuclear receptor subfamily 1 group I member 2 (also known as pregnane X receptor), a nuclear receptor transcription factor that promotes the expression of many CYP genes, was also decreased in HepaRG cells following 5-FU treatment. Fluorouracil 253-257 nuclear receptor subfamily 1 group I member 2 Homo sapiens 37-82 34380920-6 2021 The mRNA expressions of the CYP2B6 and ATP-binding cassette transporter genes were decreased after 5-FU treatment. Fluorouracil 99-103 ATP binding cassette subfamily A member 4 Homo sapiens 39-71 35506454-0 2022 Visfatin inhibits colon cancer cell apoptosis and decreases chemosensitivity to 5-FU by promoting the SDF-1/CXCR4/Akt axis. Fluorouracil 80-84 AKT serine/threonine kinase 1 Homo sapiens 114-117 35506454-7 2022 Rescue experiments and PI3K/Akt inhibitors were used to verify the role of the visfatin/SDF-1/Akt axis in the sensitivity of colon cancer cells to 5-FU. Fluorouracil 147-151 AKT serine/threonine kinase 1 Homo sapiens 94-97 35506454-11 2022 Furthermore, the Akt signalling pathway downstream of SDF-1/CXCR4 proved to be critical in the decreased sensitisation of colon cancer cells to 5-FU induced by visfatin. Fluorouracil 144-148 AKT serine/threonine kinase 1 Homo sapiens 17-20 35506454-12 2022 On the whole, the present study demonstrates that visatin can potentially decrease colon cancer cell apoptosis, promote proliferation and decrease colon cancer cell sensitivity to 5-FU via the visfatin/SDF-1/Akt axis. Fluorouracil 180-184 AKT serine/threonine kinase 1 Homo sapiens 208-211 35462225-0 2022 SPOCK1 silencing decreases 5-FU resistance through PRRX1 in colorectal cancer. Fluorouracil 27-31 paired related homeobox 1 Homo sapiens 51-56 35462225-7 2022 Mechanistically, SPOCK1 promoted 5-FU resistance by regulating PRRX1 expression and the downstream apoptosis signaling pathway. Fluorouracil 33-37 paired related homeobox 1 Homo sapiens 63-68 35606482-8 2022 5-FU resulted in significant cardiotoxicity represented by an increase in malondialdehyde (MDA) levels, cyclooxygenase-2 (COX-2) and tumor necrosis factor-alpha (TNF-alpha) expression, cardiac enzyme levels, and histopathological degenerations. Fluorouracil 0-4 tumor necrosis factor Rattus norvegicus 133-160 35606482-8 2022 5-FU resulted in significant cardiotoxicity represented by an increase in malondialdehyde (MDA) levels, cyclooxygenase-2 (COX-2) and tumor necrosis factor-alpha (TNF-alpha) expression, cardiac enzyme levels, and histopathological degenerations. Fluorouracil 0-4 tumor necrosis factor Rattus norvegicus 162-171 35606482-9 2022 5-FU treatment also decreased bodyweight, total anti-oxidant capacity (TAC), catalase (CAT) levels, blood cell counts, and hemoglobin (Hb) levels. Fluorouracil 0-4 catalase Rattus norvegicus 77-85 35606482-9 2022 5-FU treatment also decreased bodyweight, total anti-oxidant capacity (TAC), catalase (CAT) levels, blood cell counts, and hemoglobin (Hb) levels. Fluorouracil 0-4 catalase Rattus norvegicus 87-90 35596172-3 2022 This study aims to investigate the role of the hypoxia-induced miR-675-5p in 5-Fluorouracil (5-FU) resistance on colorectal cancer (CRC) cells. Fluorouracil 77-91 microRNA 675 Homo sapiens 63-70 35596172-3 2022 This study aims to investigate the role of the hypoxia-induced miR-675-5p in 5-Fluorouracil (5-FU) resistance on colorectal cancer (CRC) cells. Fluorouracil 93-97 microRNA 675 Homo sapiens 63-70 35596172-9 2022 RESULTS: Our data demonstrated that hypoxia-induced miR-675-5p counteracts the apoptotic signal induced by 5-FU, thus taking part in the drug resistance response. Fluorouracil 107-111 microRNA 675 Homo sapiens 52-59 35596172-10 2022 We showed that the apoptotic markers, cleaved PARP and cleaved caspase-3, increased combining miR-675-5p inhibition with 5-FU treatment. Fluorouracil 121-125 poly(ADP-ribose) polymerase 1 Homo sapiens 46-50 35596172-10 2022 We showed that the apoptotic markers, cleaved PARP and cleaved caspase-3, increased combining miR-675-5p inhibition with 5-FU treatment. Fluorouracil 121-125 caspase 3 Homo sapiens 63-72 35596172-10 2022 We showed that the apoptotic markers, cleaved PARP and cleaved caspase-3, increased combining miR-675-5p inhibition with 5-FU treatment. Fluorouracil 121-125 microRNA 675 Homo sapiens 94-101 35436101-1 2022 Thymine DNA glycosylase (TDG) is tasked with initiating DNA base excision repair by recognizing and removing T, U, the chemotherapeutic 5-fluorouracil (5-FU), and many other oxidized and halogenated pyrimidine bases. Fluorouracil 136-150 thymine DNA glycosylase Homo sapiens 0-23 35436101-1 2022 Thymine DNA glycosylase (TDG) is tasked with initiating DNA base excision repair by recognizing and removing T, U, the chemotherapeutic 5-fluorouracil (5-FU), and many other oxidized and halogenated pyrimidine bases. Fluorouracil 136-150 thymine DNA glycosylase Homo sapiens 25-28 35436101-1 2022 Thymine DNA glycosylase (TDG) is tasked with initiating DNA base excision repair by recognizing and removing T, U, the chemotherapeutic 5-fluorouracil (5-FU), and many other oxidized and halogenated pyrimidine bases. Fluorouracil 152-156 thymine DNA glycosylase Homo sapiens 0-23 35436101-1 2022 Thymine DNA glycosylase (TDG) is tasked with initiating DNA base excision repair by recognizing and removing T, U, the chemotherapeutic 5-fluorouracil (5-FU), and many other oxidized and halogenated pyrimidine bases. Fluorouracil 152-156 thymine DNA glycosylase Homo sapiens 25-28 35562738-8 2022 Interestingly, patient-derived scaffold cultures obtained from patients with disease recurrences showed a significantly less pronounced anti-proliferative effect of 5-fluorouracil and more pronounced increase of pluripotency, with MKI67 and POU5F1 being among the most significant genes linked to disease relapse in colorectal cancer. Fluorouracil 165-179 marker of proliferation Ki-67 Homo sapiens 231-236 35245520-0 2022 Enhanced in vitro tumoricidal effects of 5-Fluorouracil, thymoquinone, and active vitamin D3 triple therapy against colon cancer cells by attenuating the PI3K/AKT/mTOR pathway. Fluorouracil 41-55 AKT serine/threonine kinase 1 Homo sapiens 159-162 35245520-0 2022 Enhanced in vitro tumoricidal effects of 5-Fluorouracil, thymoquinone, and active vitamin D3 triple therapy against colon cancer cells by attenuating the PI3K/AKT/mTOR pathway. Fluorouracil 41-55 mechanistic target of rapamycin kinase Homo sapiens 163-167 35245520-3 2022 KEY FINDINGS: TQ monotherapy had greater anticancer effects to active VD3 or 5-FU, revealing higher expression of p21/p27/PTEN/BAX/Cyto-C/Casp-3 and increased levels of total glutathione, with inhibitions in CCND1/CCND3/BCL-2 and PI3K/AKT/mTOR molecules, alongside higher rates of apoptosis in HT29, SW480 and SW620 cells (P < 0.005 for all markers). Fluorouracil 77-81 dynactin subunit 6 Homo sapiens 118-121 35245520-3 2022 KEY FINDINGS: TQ monotherapy had greater anticancer effects to active VD3 or 5-FU, revealing higher expression of p21/p27/PTEN/BAX/Cyto-C/Casp-3 and increased levels of total glutathione, with inhibitions in CCND1/CCND3/BCL-2 and PI3K/AKT/mTOR molecules, alongside higher rates of apoptosis in HT29, SW480 and SW620 cells (P < 0.005 for all markers). Fluorouracil 77-81 BCL2 associated X, apoptosis regulator Homo sapiens 127-130 35245520-3 2022 KEY FINDINGS: TQ monotherapy had greater anticancer effects to active VD3 or 5-FU, revealing higher expression of p21/p27/PTEN/BAX/Cyto-C/Casp-3 and increased levels of total glutathione, with inhibitions in CCND1/CCND3/BCL-2 and PI3K/AKT/mTOR molecules, alongside higher rates of apoptosis in HT29, SW480 and SW620 cells (P < 0.005 for all markers). Fluorouracil 77-81 caspase 3 Homo sapiens 138-144 35525092-1 2022 We report on the fabrication of lysozyme microspheres (LyMs) incorporated with gold nanorods (NRs) as a distinctive approach for the encapsulation and release of an anticancer drug, 5-Fluorouracil (5-FU). Fluorouracil 182-196 lysozyme Homo sapiens 32-40 35525092-1 2022 We report on the fabrication of lysozyme microspheres (LyMs) incorporated with gold nanorods (NRs) as a distinctive approach for the encapsulation and release of an anticancer drug, 5-Fluorouracil (5-FU). Fluorouracil 198-202 lysozyme Homo sapiens 32-40 35582195-0 2022 miR-455-5p enhances 5-fluorouracil sensitivity in colorectal cancer cells by targeting PIK3R1 and DEPDC1. Fluorouracil 20-34 phosphoinositide-3-kinase regulatory subunit 1 Homo sapiens 87-93 35582195-0 2022 miR-455-5p enhances 5-fluorouracil sensitivity in colorectal cancer cells by targeting PIK3R1 and DEPDC1. Fluorouracil 20-34 DEP domain containing 1 Homo sapiens 98-104 35582195-3 2022 The expression of miR-455-5p, PIK3R1, and DEPDC1 was analyzed in HT-29 cells after treatment with different concentrations (0, 0.5, 2.5, and 12.5 muM) of 5-Fu. Fluorouracil 154-158 phosphoinositide-3-kinase regulatory subunit 1 Homo sapiens 30-36 35582195-3 2022 The expression of miR-455-5p, PIK3R1, and DEPDC1 was analyzed in HT-29 cells after treatment with different concentrations (0, 0.5, 2.5, and 12.5 muM) of 5-Fu. Fluorouracil 154-158 DEP domain containing 1 Homo sapiens 42-48 35582195-7 2022 We found that miR-455-5p decreased, while PIK3R1 and DEPDC1 increased after 5-Fu treatment. Fluorouracil 76-80 phosphoinositide-3-kinase regulatory subunit 1 Homo sapiens 42-48 35582195-7 2022 We found that miR-455-5p decreased, while PIK3R1 and DEPDC1 increased after 5-Fu treatment. Fluorouracil 76-80 DEP domain containing 1 Homo sapiens 53-59 35582195-9 2022 Overexpression of PIK3R1 and DEPDC1 could attenuate the effects of miR-455-5p mimic on the viability and apoptosis of 5-Fu-treated cells. Fluorouracil 118-122 phosphoinositide-3-kinase regulatory subunit 1 Homo sapiens 18-24 35582195-9 2022 Overexpression of PIK3R1 and DEPDC1 could attenuate the effects of miR-455-5p mimic on the viability and apoptosis of 5-Fu-treated cells. Fluorouracil 118-122 DEP domain containing 1 Homo sapiens 29-35 35582195-11 2022 In conclusion, miR-455-5p enhanced 5-Fu sensitivity by targeting PIK3R1 and DEPDC1 in CRC. Fluorouracil 35-39 phosphoinositide-3-kinase regulatory subunit 1 Homo sapiens 65-71 35582195-11 2022 In conclusion, miR-455-5p enhanced 5-Fu sensitivity by targeting PIK3R1 and DEPDC1 in CRC. Fluorouracil 35-39 DEP domain containing 1 Homo sapiens 76-82 35448938-6 2022 In our results, the three SCFAs could inhibit ROS expressions, NLRP3, Caspase-1, IL-1beta, IL-6, IL-18, Beclin-1 and LC3-II, when induced by 5-FU. Fluorouracil 141-145 NLR family pyrin domain containing 3 Homo sapiens 63-68 35448938-6 2022 In our results, the three SCFAs could inhibit ROS expressions, NLRP3, Caspase-1, IL-1beta, IL-6, IL-18, Beclin-1 and LC3-II, when induced by 5-FU. Fluorouracil 141-145 caspase 1 Homo sapiens 70-79 35448938-6 2022 In our results, the three SCFAs could inhibit ROS expressions, NLRP3, Caspase-1, IL-1beta, IL-6, IL-18, Beclin-1 and LC3-II, when induced by 5-FU. Fluorouracil 141-145 interleukin 6 Homo sapiens 91-95 35448938-7 2022 In a 5-FU-induced chemoentermuctis mouse model, Lactobacillus rhamnoides can increase the concentrations of three SCFAs in faeces and increase the concentrations of IL-1beta, IL-6 and IgA in serum, and decrease the expressions of NLRP3 and IL-17 in spleen cells. Fluorouracil 5-9 interleukin 6 Mus musculus 175-179 35410287-4 2022 RESULTS: By combining single-cell imaging and mathematical modeling of dose-dependent p53 dynamics induced by three chemotherapeutics of distinct mechanism-of-actions, including Etoposide, Nutlin-3a and 5-fluorouracil, and in five cancer cell types, we uncovered novel and highly variable p53 dynamic responses, in particular p53 transitional dynamics induced at intermediate drug concentrations, and identified the functional roles of distinct positive and negative feedback motifs of the p53 pathway in modulating the central p53-Mdm2 negative feedback to generate stimulus- and cell type-specific signaling responses. Fluorouracil 203-217 tumor protein p53 Homo sapiens 86-89 35394639-12 2022 In vitro and in vivo experiments showed that 5-FU and MR combined therapy further inhibited CD133+ cell activity and ATP binding cassette subfamily G member 2 (ABCG2) expression, and reduced tumor volume compared with drug administration alone. Fluorouracil 45-49 ATP binding cassette subfamily G member 2 (Junior blood group) Homo sapiens 117-158 35394639-12 2022 In vitro and in vivo experiments showed that 5-FU and MR combined therapy further inhibited CD133+ cell activity and ATP binding cassette subfamily G member 2 (ABCG2) expression, and reduced tumor volume compared with drug administration alone. Fluorouracil 45-49 ATP binding cassette subfamily G member 2 (Junior blood group) Homo sapiens 160-165 35157912-5 2022 Besides, Sch B could effectively inhibit the phosphorylation of STAT3 (signal transducer and activator of transcription 3), induce autophagy, and enhance the efficacy of chemotherapy drug 5-FU in vitro and in vivo. Fluorouracil 188-192 signal transducer and activator of transcription 3 Homo sapiens 64-69 35157912-5 2022 Besides, Sch B could effectively inhibit the phosphorylation of STAT3 (signal transducer and activator of transcription 3), induce autophagy, and enhance the efficacy of chemotherapy drug 5-FU in vitro and in vivo. Fluorouracil 188-192 signal transducer and activator of transcription 3 Homo sapiens 71-121 35253124-0 2022 Carvacrol Enhance Apoptotic Effect of 5-FU on MCF-7 Cell Line via inhibiting P-glycoprotein: An In-silco and In-vitro Study. Fluorouracil 38-42 ATP binding cassette subfamily B member 1 Homo sapiens 77-91 35235860-8 2022 RESULTS: Valsartan suppressed CRC cell-growth and synergistically enhanced the anti-tumor-activities of 5-FU by induction of apoptosis, BAX, BCL2, P53 and modulation of the cell cycle. Fluorouracil 104-108 B cell leukemia/lymphoma 2 Mus musculus 141-145 35326689-0 2022 In Vivo and In Vitro Enhanced Tumoricidal Effects of Metformin, Active Vitamin D3, and 5-Fluorouracil Triple Therapy against Colon Cancer by Modulating the PI3K/Akt/PTEN/mTOR Network. Fluorouracil 87-101 AKT serine/threonine kinase 1 Homo sapiens 161-164 35326689-0 2022 In Vivo and In Vitro Enhanced Tumoricidal Effects of Metformin, Active Vitamin D3, and 5-Fluorouracil Triple Therapy against Colon Cancer by Modulating the PI3K/Akt/PTEN/mTOR Network. Fluorouracil 87-101 mechanistic target of rapamycin kinase Homo sapiens 170-174 35326689-8 2022 All protocols decreased cell proliferation markers, inhibited PI3K/Akt/mTOR molecules, and increased proapoptotic molecules with an apoptosis index, and 5-FU/VD3/Met revealed the strongest effects. Fluorouracil 153-157 thymoma viral proto-oncogene 1 Mus musculus 67-70 35326689-11 2022 Moreover, 5-FU/VD3/Met revealed maximal inhibitions of cell cycle inducers (CCND1/CCND3), cell survival (BCL2), and the PI3K/Akt/mTOR molecules alongside the highest expression of cell cycle inhibitors (p21/p27), proapoptotic markers (BAX/cytochrome C/caspase-3), and PTEN in both cell lines. Fluorouracil 10-14 cyclin D3 Homo sapiens 82-87 35326689-11 2022 Moreover, 5-FU/VD3/Met revealed maximal inhibitions of cell cycle inducers (CCND1/CCND3), cell survival (BCL2), and the PI3K/Akt/mTOR molecules alongside the highest expression of cell cycle inhibitors (p21/p27), proapoptotic markers (BAX/cytochrome C/caspase-3), and PTEN in both cell lines. Fluorouracil 10-14 BCL2 apoptosis regulator Homo sapiens 105-109 35326689-11 2022 Moreover, 5-FU/VD3/Met revealed maximal inhibitions of cell cycle inducers (CCND1/CCND3), cell survival (BCL2), and the PI3K/Akt/mTOR molecules alongside the highest expression of cell cycle inhibitors (p21/p27), proapoptotic markers (BAX/cytochrome C/caspase-3), and PTEN in both cell lines. Fluorouracil 10-14 AKT serine/threonine kinase 1 Homo sapiens 125-128 35326689-11 2022 Moreover, 5-FU/VD3/Met revealed maximal inhibitions of cell cycle inducers (CCND1/CCND3), cell survival (BCL2), and the PI3K/Akt/mTOR molecules alongside the highest expression of cell cycle inhibitors (p21/p27), proapoptotic markers (BAX/cytochrome C/caspase-3), and PTEN in both cell lines. Fluorouracil 10-14 mechanistic target of rapamycin kinase Homo sapiens 129-133 35326689-11 2022 Moreover, 5-FU/VD3/Met revealed maximal inhibitions of cell cycle inducers (CCND1/CCND3), cell survival (BCL2), and the PI3K/Akt/mTOR molecules alongside the highest expression of cell cycle inhibitors (p21/p27), proapoptotic markers (BAX/cytochrome C/caspase-3), and PTEN in both cell lines. Fluorouracil 10-14 dynactin subunit 6 Homo sapiens 207-210 35326689-11 2022 Moreover, 5-FU/VD3/Met revealed maximal inhibitions of cell cycle inducers (CCND1/CCND3), cell survival (BCL2), and the PI3K/Akt/mTOR molecules alongside the highest expression of cell cycle inhibitors (p21/p27), proapoptotic markers (BAX/cytochrome C/caspase-3), and PTEN in both cell lines. Fluorouracil 10-14 BCL2 associated X, apoptosis regulator Homo sapiens 235-238 35326689-11 2022 Moreover, 5-FU/VD3/Met revealed maximal inhibitions of cell cycle inducers (CCND1/CCND3), cell survival (BCL2), and the PI3K/Akt/mTOR molecules alongside the highest expression of cell cycle inhibitors (p21/p27), proapoptotic markers (BAX/cytochrome C/caspase-3), and PTEN in both cell lines. Fluorouracil 10-14 cytochrome c, somatic Homo sapiens 239-251 35326689-11 2022 Moreover, 5-FU/VD3/Met revealed maximal inhibitions of cell cycle inducers (CCND1/CCND3), cell survival (BCL2), and the PI3K/Akt/mTOR molecules alongside the highest expression of cell cycle inhibitors (p21/p27), proapoptotic markers (BAX/cytochrome C/caspase-3), and PTEN in both cell lines. Fluorouracil 10-14 caspase 3 Homo sapiens 252-261 35326689-13 2022 However, the 5-FU/VD3/Met approach displayed the best in vivo and in vitro tumoricidal effects related to cell cycle arrest and apoptosis, justifiably by enhanced modulations of the PI3K/PTEN/Akt/mTOR pathway. Fluorouracil 13-17 AKT serine/threonine kinase 1 Homo sapiens 192-195 35326689-13 2022 However, the 5-FU/VD3/Met approach displayed the best in vivo and in vitro tumoricidal effects related to cell cycle arrest and apoptosis, justifiably by enhanced modulations of the PI3K/PTEN/Akt/mTOR pathway. Fluorouracil 13-17 mechanistic target of rapamycin kinase Homo sapiens 196-200 35399709-10 2022 These findings indicate that hinokitiol could enhance 5-Fluorouracil therapeutic effects in murine B16F10 and CT26 tumor cells via downregulation of the AKT/mTOR pathway. Fluorouracil 54-68 thymoma viral proto-oncogene 1 Mus musculus 153-156 35241559-2 2022 Our study investigated the association between epidermal growth factor receptor (EGFR) status in recurrent/metastatic SGC and the effectiveness of treatment with cisplatin/carboplatin and 5-fluorouracil plus cetuximab (EXTREME). Fluorouracil 188-202 epidermal growth factor receptor Homo sapiens 47-79 35241559-2 2022 Our study investigated the association between epidermal growth factor receptor (EGFR) status in recurrent/metastatic SGC and the effectiveness of treatment with cisplatin/carboplatin and 5-fluorouracil plus cetuximab (EXTREME). Fluorouracil 188-202 epidermal growth factor receptor Homo sapiens 81-85 35170195-4 2022 This study explored whether BC cell drug sensitivity to 5-Fu was related to lncRNA CCAT2-regulated mTOR pathway. Fluorouracil 56-60 mechanistic target of rapamycin kinase Homo sapiens 99-103 35170195-14 2022 p-mTOR/mTOR in 5-Fu-resistant BC cells with inhibited CCAT2 was decreased, while CCAT2 overexpression activated the mTOR pathway. Fluorouracil 15-19 mechanistic target of rapamycin kinase Homo sapiens 2-6 35170195-14 2022 p-mTOR/mTOR in 5-Fu-resistant BC cells with inhibited CCAT2 was decreased, while CCAT2 overexpression activated the mTOR pathway. Fluorouracil 15-19 mechanistic target of rapamycin kinase Homo sapiens 7-11 35170195-14 2022 p-mTOR/mTOR in 5-Fu-resistant BC cells with inhibited CCAT2 was decreased, while CCAT2 overexpression activated the mTOR pathway. Fluorouracil 15-19 mechanistic target of rapamycin kinase Homo sapiens 116-120 35170195-17 2022 CCAT2 may reduce BC cell chemosensitivity to 5-Fu by activating the mTOR pathway. Fluorouracil 45-49 mechanistic target of rapamycin kinase Homo sapiens 68-72 35252200-4 2022 Results: A total of 3,175 differentially expressed mRNAs (DEGs), lncRNAs (DELs), and miRNAs (DEMs) related to 5-FU resistance were identified, including significantly upregulated IL33, H19, and miR-17-5p; the downregulated AKR1B10, LINC01012, and miR-125b-5p; and chromatin modifiers such as INO80C, HDAC6, and KDM5A. Fluorouracil 110-114 INO80 complex subunit C Homo sapiens 292-298 35252200-4 2022 Results: A total of 3,175 differentially expressed mRNAs (DEGs), lncRNAs (DELs), and miRNAs (DEMs) related to 5-FU resistance were identified, including significantly upregulated IL33, H19, and miR-17-5p; the downregulated AKR1B10, LINC01012, and miR-125b-5p; and chromatin modifiers such as INO80C, HDAC6, and KDM5A. Fluorouracil 110-114 histone deacetylase 6 Homo sapiens 300-305 35151311-0 2022 UHMK1-dependent phosphorylation of Cajal body protein coilin alters 5-FU sensitivity in colon cancer cells. Fluorouracil 68-72 U2AF homology motif kinase 1 Homo sapiens 0-5 35126817-12 2022 5-Fluorouracil resulted in significant cardiotoxicity represented by an increase in cardiac enzymes, malondialdehyde levels, cyclooxygenase-2 and tumor necrosis factor-alpha expression, cardiac enzymes, and histopathological degenerations. Fluorouracil 0-14 tumor necrosis factor Rattus norvegicus 146-173 35096570-12 2021 HCT116 and SW480 cells stably overexpressing HIPK3 showed increased level of phosphorylated FADD, as well as retarded cell growth, migration, and increased sensitivity to 5-FU. Fluorouracil 171-175 homeodomain interacting protein kinase 3 Homo sapiens 45-50 35022331-0 2022 TIMP-2 regulates 5-Fu resistance via the ERK/MAPK signaling pathway in colorectal cancer. Fluorouracil 17-21 mitogen-activated protein kinase 1 Homo sapiens 41-44 35022331-7 2022 We established an autocrine mechanism through which elevated TIMP-2 protein levels sustained colorectal cancer cell resistance to 5-Fu by constitutively activating the ERK/MAPK signaling pathway. Fluorouracil 130-134 mitogen-activated protein kinase 1 Homo sapiens 168-171 35022331-8 2022 Inhibition of TIMP-2 using an anti-TIMP-2 antibody or ERK/MAPK inhibition by U0126 suppressed TIMP-2 mediated 5-Fu-resistance in CRC patients. Fluorouracil 110-114 mitogen-activated protein kinase 1 Homo sapiens 54-57 35022331-9 2022 In conclusion, a novel TIMP-2-ERK/MAPK mediated 5-Fu resistance mechanism is involved in colorectal cancer. Fluorouracil 48-52 mitogen-activated protein kinase 1 Homo sapiens 30-33 35022331-10 2022 Therefore, targeting TIMP-2 or ERK/MAPK may provide a new strategy to overcome 5-Fu resistance in colorectal cancer chemotherapy. Fluorouracil 79-83 mitogen-activated protein kinase 1 Homo sapiens 31-34 35096810-6 2021 Moreover, combination of HAUS6 knockdown and 5-FU treatment further enhanced the suppression of cell proliferation of CRC cells by increasing activation of the p53/p21 pathway. Fluorouracil 45-49 tumor protein p53 Homo sapiens 160-163 34998404-14 2022 CONCLUSIONS: HIF-1alpha is a potential biomarker for 5-FU-resistant CRC, and targeting HIF-1a in combination with 5-FU may represent an effective therapeutic strategy in 5-FU-resistant CRC. Fluorouracil 170-174 hypoxia inducible factor 1 subunit alpha Homo sapiens 87-93 35071232-0 2021 Deficient or R273H and R248W Mutations of p53 Promote Chemoresistance to 5-FU via TCF21/CD44 Axis-Mediated Enhanced Stemness in Colorectal Carcinoma. Fluorouracil 73-77 tumor protein p53 Homo sapiens 42-45 35071232-0 2021 Deficient or R273H and R248W Mutations of p53 Promote Chemoresistance to 5-FU via TCF21/CD44 Axis-Mediated Enhanced Stemness in Colorectal Carcinoma. Fluorouracil 73-77 transcription factor 21 Homo sapiens 82-87 35071232-14 2021 Xenografts also confirmed that HCT116 cells harboring deficient or mutant p53 promoted cancer growth and 5-FU tolerance. Fluorouracil 105-109 tumor protein p53 Homo sapiens 74-77 35071232-16 2021 Overexpression of TCF21 or knockdown of CD44 could rescue the sensitivity to 5-FU in deficient and mutant p53 HCT116 cell lines. Fluorouracil 77-81 transcription factor 21 Homo sapiens 18-23 35355718-0 2022 HIF1alpha/VEGF Feedback Loop Contributes to 5-Fluorouracil Resistance. Fluorouracil 44-58 hypoxia inducible factor 1 subunit alpha Homo sapiens 0-9 35355718-0 2022 HIF1alpha/VEGF Feedback Loop Contributes to 5-Fluorouracil Resistance. Fluorouracil 44-58 vascular endothelial growth factor A Homo sapiens 10-14 35355718-3 2022 In this study, hypoxia inducible factor 1alpha (HIF1alpha) was screened for high expression in 5-Fu resistant HCT115 cells, which displayed epithelial-mesenchymal transition (EMT) phenotype. Fluorouracil 95-99 hypoxia inducible factor 1 subunit alpha Homo sapiens 15-46 35355718-3 2022 In this study, hypoxia inducible factor 1alpha (HIF1alpha) was screened for high expression in 5-Fu resistant HCT115 cells, which displayed epithelial-mesenchymal transition (EMT) phenotype. Fluorouracil 95-99 hypoxia inducible factor 1 subunit alpha Homo sapiens 48-57 35355718-5 2022 Moreover, we unveiled that vascular endothelial growth factor (VEGF) was regulated by HIF1alpha and mediated HIF1alpha-maintained malignant phenotype of 5-Fu resistant cells. Fluorouracil 153-157 vascular endothelial growth factor A Homo sapiens 27-61 35355718-5 2022 Moreover, we unveiled that vascular endothelial growth factor (VEGF) was regulated by HIF1alpha and mediated HIF1alpha-maintained malignant phenotype of 5-Fu resistant cells. Fluorouracil 153-157 vascular endothelial growth factor A Homo sapiens 63-67 35355718-5 2022 Moreover, we unveiled that vascular endothelial growth factor (VEGF) was regulated by HIF1alpha and mediated HIF1alpha-maintained malignant phenotype of 5-Fu resistant cells. Fluorouracil 153-157 hypoxia inducible factor 1 subunit alpha Homo sapiens 109-118 35355718-9 2022 In conclusion, our findings proposed that HIF1alpha/VEGF feedback loop contributed to 5-Fu resistance, which might be potential therapeutic targets. Fluorouracil 86-90 hypoxia inducible factor 1 subunit alpha Homo sapiens 42-51 35355718-9 2022 In conclusion, our findings proposed that HIF1alpha/VEGF feedback loop contributed to 5-Fu resistance, which might be potential therapeutic targets. Fluorouracil 86-90 vascular endothelial growth factor A Homo sapiens 52-56 34265852-2 2021 Although inhibition of mTOR signaling promotes tumor cell death and several mTOR inhibitors have been used clinically, recent reports have shown that co-treatment with MHY1485, an mTOR activator, enhances the anti-cancer effects of anti-PD-1 antibody and 5-fluorouracil. Fluorouracil 255-269 mechanistic target of rapamycin kinase Homo sapiens 76-80 34265852-2 2021 Although inhibition of mTOR signaling promotes tumor cell death and several mTOR inhibitors have been used clinically, recent reports have shown that co-treatment with MHY1485, an mTOR activator, enhances the anti-cancer effects of anti-PD-1 antibody and 5-fluorouracil. Fluorouracil 255-269 mechanistic target of rapamycin kinase Homo sapiens 180-184 2510579-4 1989 When added in combination, IFN gamma potentiated synergistically the inhibitory action of 5-FU in both systems. Fluorouracil 90-94 interferon gamma Homo sapiens 27-36 2573433-3 1989 Bone marrow from mice treated with 5-fluorouracil was depleted of cells expressing Mac-1, CD4, and CD8 and incubated on lymphocyte-free monolayer cultures of adherent thymic stromal cells. Fluorouracil 35-49 integrin alpha M Mus musculus 83-88 2805072-8 1989 Importantly, IL 3 could induce the generation of NK activity from 5-FU-treated marrow cells in the presence of IL 2. Fluorouracil 66-70 interleukin 3 Mus musculus 13-17 2805072-9 1989 Kinetic studies indicated that NK activity was appreciably generated from 5-FU-treated marrow cells when preincubated with IL 3 at least for 12 hr and subsequently cultured with IL 2. Fluorouracil 74-78 interleukin 3 Mus musculus 123-127 2805072-10 1989 The cells bearing IL 2 receptors appeared in 5-FU-treated marrow cells, even though cultured only with IL 3, which implied that IL 3 could support the development of very primitive NK cells from IL 2-unresponsive to IL 2-responsive states. Fluorouracil 45-49 interleukin 3 Mus musculus 128-132 2669999-3 1989 When spleen cells from mice pretreated in vivo with 5-FU were cultured in the presence of methylcellulose medium containing recombinant interleukin-3 (rIL-3), small colonies consisting of blast cells with little sign of differentiation developed on day 7 of culture. Fluorouracil 52-56 interleukin 3 Mus musculus 136-149 2622477-0 1989 Effect of 5-fluorocytosine and 5-fluorouracil on human and rat hepatic cytochrome P 450. Fluorouracil 31-45 cytochrome P450, family 2, subfamily g, polypeptide 1 Rattus norvegicus 71-87 2622477-3 1989 The present in vitro study was, therefore, designed to assess the influence of 5-fluorocytosine and 5-fluorouracil on the hepatic cytochrome P 450 concentration in human and rat liver microsomes. Fluorouracil 100-114 cytochrome P450 family 4 subfamily F member 3 Homo sapiens 130-146 2811382-1 1989 To compare the activity of pyrimidine nucleoside phosphorylase (PNP), an enzyme involved in the metabolism of 5-fluorouracil (5-FU), we used uridine (Urd), deoxyuridine (dUrd), and thymidine (dThd) as substrates and human, rat, and mouse neoplastic and normal tissues. Fluorouracil 110-124 purine nucleoside phosphorylase Homo sapiens 27-62 2811382-1 1989 To compare the activity of pyrimidine nucleoside phosphorylase (PNP), an enzyme involved in the metabolism of 5-fluorouracil (5-FU), we used uridine (Urd), deoxyuridine (dUrd), and thymidine (dThd) as substrates and human, rat, and mouse neoplastic and normal tissues. Fluorouracil 110-124 purine nucleoside phosphorylase Homo sapiens 64-67 2811382-1 1989 To compare the activity of pyrimidine nucleoside phosphorylase (PNP), an enzyme involved in the metabolism of 5-fluorouracil (5-FU), we used uridine (Urd), deoxyuridine (dUrd), and thymidine (dThd) as substrates and human, rat, and mouse neoplastic and normal tissues. Fluorouracil 126-130 purine nucleoside phosphorylase Homo sapiens 27-62 2811382-1 1989 To compare the activity of pyrimidine nucleoside phosphorylase (PNP), an enzyme involved in the metabolism of 5-fluorouracil (5-FU), we used uridine (Urd), deoxyuridine (dUrd), and thymidine (dThd) as substrates and human, rat, and mouse neoplastic and normal tissues. Fluorouracil 126-130 purine nucleoside phosphorylase Homo sapiens 64-67 2811382-2 1989 As PNP activity was higher in the tumor tissues than in the normal ones in all species examined, the level of PNP activity is expected to be one critical factor linked to the effectiveness of 5-FU. Fluorouracil 192-196 purine nucleoside phosphorylase Homo sapiens 3-6 2811382-2 1989 As PNP activity was higher in the tumor tissues than in the normal ones in all species examined, the level of PNP activity is expected to be one critical factor linked to the effectiveness of 5-FU. Fluorouracil 192-196 purine nucleoside phosphorylase Homo sapiens 110-113 2476639-4 1989 Addition of IL-6 or granulocyte colony-stimulating factor (G-CSF), which act synergistically with IL-3 on dormant progenitors, partially neutralized the inhibition by TGF beta of colony formation from cells of 5-FU-treated mice. Fluorouracil 210-214 interleukin 6 Mus musculus 12-16 2506832-10 1989 Their pretreatment value of CEA was lower at 13.6 and 23.8 ng/ml, respectively, and these levels were decreased to 1.0 ng/ml with administration of 5-FU with ADM and 5-FU with MMC. Fluorouracil 148-152 CEA cell adhesion molecule 3 Homo sapiens 28-31 2506832-10 1989 Their pretreatment value of CEA was lower at 13.6 and 23.8 ng/ml, respectively, and these levels were decreased to 1.0 ng/ml with administration of 5-FU with ADM and 5-FU with MMC. Fluorouracil 166-170 CEA cell adhesion molecule 3 Homo sapiens 28-31 3264195-1 1988 Serial observations of blast cell colony development from spleen cells of mice treated with 5-fluorouracil (5-FU) four days earlier revealed that either form of human interleukin-1 (IL-1 alpha or IL-1 beta) hastens the emergence of interleukin-3 (IL-3)-dependent blast cell colonies. Fluorouracil 92-106 interleukin 1 beta Homo sapiens 196-205 2914273-9 1989 Differential sensitivities among the five cell lines to 5-fluorouracil, cisplatinum, and bleomycin appear to be mediated through other mechanism beside the mdr-1 gene. Fluorouracil 56-70 ATP binding cassette subfamily B member 1 Homo sapiens 156-161 3263278-4 1988 Recombinant IL-6 was able to support multilineage colony formation by spleen cells from 5-fluorouracil (5-FU)-treated mice. Fluorouracil 88-102 interleukin 6 Mus musculus 12-16 3263278-4 1988 Recombinant IL-6 was able to support multilineage colony formation by spleen cells from 5-fluorouracil (5-FU)-treated mice. Fluorouracil 104-108 interleukin 6 Mus musculus 12-16 2653457-1 1989 Post 5-fluorouracil-treated murine marrow cells were infected with a retroviral vector (MPZen) bearing a multi-potential colony stimulating factor (Multi-CSF) cDNA insert and then transplanted into lethally irradiated syngeneic recipients to study the effects of autocrine production of Multi-CSF in normal hematopoietic cells. Fluorouracil 5-19 interleukin 3 Mus musculus 105-146 2653457-1 1989 Post 5-fluorouracil-treated murine marrow cells were infected with a retroviral vector (MPZen) bearing a multi-potential colony stimulating factor (Multi-CSF) cDNA insert and then transplanted into lethally irradiated syngeneic recipients to study the effects of autocrine production of Multi-CSF in normal hematopoietic cells. Fluorouracil 5-19 interleukin 3 Mus musculus 148-157 2653457-1 1989 Post 5-fluorouracil-treated murine marrow cells were infected with a retroviral vector (MPZen) bearing a multi-potential colony stimulating factor (Multi-CSF) cDNA insert and then transplanted into lethally irradiated syngeneic recipients to study the effects of autocrine production of Multi-CSF in normal hematopoietic cells. Fluorouracil 5-19 interleukin 3 Mus musculus 287-296 2705401-5 1989 The fluorouracil, doxorubicin (Adriamycin), and cyclophosphamide (FAC) regimen was effective in improving disease and overall survival regardless of age of the patient, stage of disease, or extent of nodal involvement in comparison with the historical control patients treated with similar local therapy. Fluorouracil 4-16 FA complementation group C Homo sapiens 66-69 2492206-11 1989 Because the mouse r-IFN-gamma is devoid of direct antitumor effects (against human tumor cells) but is a potent macrophage activator, these results suggest that the antitumor effects were due to direct antitumor effects of FUra and to activation of host defense mechanisms by the r-IFN-gamma. Fluorouracil 223-227 interferon gamma Homo sapiens 20-29 3263940-5 1988 The biochemical properties of peak 1 were similar to those of murine IL-3 and stimulated multi-potential stem cell development in soft agar cultures of BM cells from rats treated with 5-fluorouracil (which enriches for haemopoietic stem cells). Fluorouracil 184-198 interleukin 3 Mus musculus 69-73 3337530-5 1988 UFT, 5-fluorouracil, mitomycin-C and adriamycin were administered to gastrointestinal cancer patients regularly, but our SRC-assay showed a high sensitivity rate for UFT and 5-fluorouracil but a low sensitivity rate for mitomycin-C and adriamycin. Fluorouracil 5-19 SRC proto-oncogene, non-receptor tyrosine kinase Homo sapiens 121-124 3201004-4 1988 After 150 mg/kg of 5-FU alone (i.e. the maximum tolerated dose, MTD), the stem cell survival rapidly decreased, reaching a minimum after 1-2 days. Fluorouracil 19-23 BCL2-related ovarian killer Mus musculus 64-67 3049908-4 1988 Addition of BSF-2 to the serum-free culture containing IL-3 resulted in a significant increase in the number of colonies formed from multipotential progenitors in spleen cells and bone marrow cells of 5-FU-treated mice, whereas no effects were seen on the number of single or oligolineage colonies formed by the spleen cells of normal mice. Fluorouracil 201-205 interleukin 3 Mus musculus 55-59 3255211-0 1988 Enhancement of 5-fluorouracil delivery to sarcoma 180 tissue under angiotensin II-induced hypertension chemotherapy. Fluorouracil 15-29 angiotensinogen Homo sapiens 67-81 3291772-11 1988 A synergistic increase in the cytotoxic effects of rH-TNF and anti-cancer drugs was demonstrated in vitro The cytotoxicity of rH-TNF against L-M cells in combination with MMC, ADM, Ara-C, ACD, DM, CDDP, VCR and 5-FU was 4 to 347 times as high as that of rH-TNF alone. Fluorouracil 211-215 tumor necrosis factor Homo sapiens 54-57 3291772-11 1988 A synergistic increase in the cytotoxic effects of rH-TNF and anti-cancer drugs was demonstrated in vitro The cytotoxicity of rH-TNF against L-M cells in combination with MMC, ADM, Ara-C, ACD, DM, CDDP, VCR and 5-FU was 4 to 347 times as high as that of rH-TNF alone. Fluorouracil 211-215 tumor necrosis factor Homo sapiens 129-132 3291772-11 1988 A synergistic increase in the cytotoxic effects of rH-TNF and anti-cancer drugs was demonstrated in vitro The cytotoxicity of rH-TNF against L-M cells in combination with MMC, ADM, Ara-C, ACD, DM, CDDP, VCR and 5-FU was 4 to 347 times as high as that of rH-TNF alone. Fluorouracil 211-215 tumor necrosis factor Homo sapiens 129-132 3265877-3 1988 Our serial observations (mapping studies) of the development of blast cell colonies from spleen cells harvested from mice 4 days after the injection of 150 mg/kg 5-fluorouracil revealed that the blast cell colonies appeared earlier in culture in the presence of Il-6 and Il-3 than with either factor alone. Fluorouracil 162-176 interleukin 6 Mus musculus 262-266 3265877-3 1988 Our serial observations (mapping studies) of the development of blast cell colonies from spleen cells harvested from mice 4 days after the injection of 150 mg/kg 5-fluorouracil revealed that the blast cell colonies appeared earlier in culture in the presence of Il-6 and Il-3 than with either factor alone. Fluorouracil 162-176 interleukin 3 Mus musculus 271-275 3281726-1 1988 Marrow cells from 5-fluorouracil (5-FU)-treated mice formed few or no mixed erythroid colonies when plated in semisolid medium with interleukin 3 (IL 3) and erythropoietin (Ep) alone. Fluorouracil 18-32 interleukin 3 Mus musculus 132-145 3281726-1 1988 Marrow cells from 5-fluorouracil (5-FU)-treated mice formed few or no mixed erythroid colonies when plated in semisolid medium with interleukin 3 (IL 3) and erythropoietin (Ep) alone. Fluorouracil 18-32 interleukin 3 Mus musculus 147-151 3281726-1 1988 Marrow cells from 5-fluorouracil (5-FU)-treated mice formed few or no mixed erythroid colonies when plated in semisolid medium with interleukin 3 (IL 3) and erythropoietin (Ep) alone. Fluorouracil 34-38 interleukin 3 Mus musculus 132-145 3281726-1 1988 Marrow cells from 5-fluorouracil (5-FU)-treated mice formed few or no mixed erythroid colonies when plated in semisolid medium with interleukin 3 (IL 3) and erythropoietin (Ep) alone. Fluorouracil 34-38 interleukin 3 Mus musculus 147-151 3416325-2 1988 In vitro immunochemistry studies showed that marked antitumor effects were obtained against cultured cancer cells when a widely used chemotherapeutic agent such as 5-FU was combined with nonsensitized spontaneously cytolytic MNC, preactivated in vitro with beta IFN. Fluorouracil 164-168 interferon alpha 1 Homo sapiens 262-265 3337530-5 1988 UFT, 5-fluorouracil, mitomycin-C and adriamycin were administered to gastrointestinal cancer patients regularly, but our SRC-assay showed a high sensitivity rate for UFT and 5-fluorouracil but a low sensitivity rate for mitomycin-C and adriamycin. Fluorouracil 174-188 SRC proto-oncogene, non-receptor tyrosine kinase Homo sapiens 121-124 3804036-1 1987 The adjuvant effect of calmodulin antagonists (W-5 and W-7) to 5-fluorouracil (5-FU) was studied by using two human cultured cell lines derived from ovarian adenocarcinoma. Fluorouracil 63-77 calmodulin 1 Homo sapiens 23-33 3257232-6 1988 Bone marrow from mice pre-treated with 5-fluorouracil is greatly depleted of progenitor cells directly responsive to IL-3 or IL-5. Fluorouracil 39-53 interleukin 3 Mus musculus 117-121 3257232-9 1988 Furthermore, pre-culture of 5-fluorouracil-treated marrow cells with a combination of IL-1 and IL-3 resulted in a more than 260-fold increase of CFU-eo over input numbers. Fluorouracil 28-42 interleukin 3 Mus musculus 95-99 3615855-2 1987 Responsiveness to chemotherapy, according to the MAF-schedule (Methotrexate, Adriamycin, 5-Fluorouracil) was reported to be successful in 50% of this cancer type. Fluorouracil 89-103 MAF bZIP transcription factor Homo sapiens 49-52 3804497-6 1987 The strongest anti-tumor effects in normal BALB/c mice were observed when TNF was combined with the following doses of chemotherapeutic agents: cyclophosphamide 100 mg/kg, adriamycin 5 mg/kg, 5-FU 30-100 mg/kg. Fluorouracil 192-196 tumor necrosis factor Mus musculus 74-77 3804497-10 1987 In this case TNF combinations with cyclophosphamide and 5-FU did not induce tumor regressions. Fluorouracil 56-60 tumor necrosis factor Mus musculus 13-16 3032726-6 1987 The rates of cytochrome P-450-dependent FUra formation in the microsomal fraction of liver tissue from two patients (1.1 and 1.3 nmol/mg microsomal protein/30 min) were dramatically reduced to less than half of those of two control subjects (2.4 and 2.7). Fluorouracil 40-44 cytochrome P450 family 4 subfamily F member 3 Homo sapiens 13-29 3660150-2 1987 The first combination, consisting of methotrexate, mitoxantrone (Novantrone) and 5-fluoro-uracil (MNF), gave a response rate of 17/48 (35%). Fluorouracil 81-96 forkhead box K1 Homo sapiens 98-101 3502358-2 1987 Results indicate that both IL-1 alpha and IL-1 beta (1-10 U/ml) are able to stimulate the generation of NK cells from 5-fluorouracil (5-FU) resistant BM progenitors. Fluorouracil 118-132 interleukin 1 beta Mus musculus 42-51 2448255-4 1987 Cytotoxic antitumor agents of 5-fluorouracil (5-FU), cyclophosphamide (CY) and bleomycin (BLM) suppressed TNF production in mice primed with CP and challenged with LPS. Fluorouracil 30-44 tumor necrosis factor Mus musculus 106-109 2448255-4 1987 Cytotoxic antitumor agents of 5-fluorouracil (5-FU), cyclophosphamide (CY) and bleomycin (BLM) suppressed TNF production in mice primed with CP and challenged with LPS. Fluorouracil 46-50 tumor necrosis factor Mus musculus 106-109 2448255-5 1987 TNF production suppressed by 5-FU, CY and BLM was partially restored by the combined treatment with OK-432 or PSK. Fluorouracil 29-33 tumor necrosis factor Mus musculus 0-3 3502358-2 1987 Results indicate that both IL-1 alpha and IL-1 beta (1-10 U/ml) are able to stimulate the generation of NK cells from 5-fluorouracil (5-FU) resistant BM progenitors. Fluorouracil 134-138 interleukin 1 beta Mus musculus 42-51 3455740-5 1986 The exposure of MIA PaCa-2 cells to 1.6 X 10(-5) M 5-fluorouracil (FUra) followed by 2 X 10(-8) M DHAD or 3 X 10(-7) M ADR had an additive (with DHAD) or synergistic (with ADR) effect when the two drugs were given simultaneously and a synergistic effect with either drug when they were given 2, 6, or 24 hours apart. Fluorouracil 51-65 MIA SH3 domain containing Homo sapiens 16-19 3547771-9 1986 In chemosensitivity test, all of PK cell lines were sensitive to aclacinomycin A (ACM), and PK-1 and PK-8 were sensitive to 5-Fluorouracil (5-Fu) at concentrations of 0.02 microgram/ml, ACM and 1 microgram/ml, 5-Fu, when the drugs were used for over 48 hr. Fluorouracil 124-138 pyruvate kinase L/R Homo sapiens 92-105 3547771-9 1986 In chemosensitivity test, all of PK cell lines were sensitive to aclacinomycin A (ACM), and PK-1 and PK-8 were sensitive to 5-Fluorouracil (5-Fu) at concentrations of 0.02 microgram/ml, ACM and 1 microgram/ml, 5-Fu, when the drugs were used for over 48 hr. Fluorouracil 140-144 pyruvate kinase L/R Homo sapiens 92-105 3547771-9 1986 In chemosensitivity test, all of PK cell lines were sensitive to aclacinomycin A (ACM), and PK-1 and PK-8 were sensitive to 5-Fluorouracil (5-Fu) at concentrations of 0.02 microgram/ml, ACM and 1 microgram/ml, 5-Fu, when the drugs were used for over 48 hr. Fluorouracil 210-214 pyruvate kinase L/R Homo sapiens 92-105 3081577-2 1986 When spleen cells of 5-fluorouracil (5-FU)-treated mice were cultured in the presence of interleukin 3 (IL-3), most colonies revealed IL-3 concentration-dependent colony formation except for mast cell colonies and blast cell colonies. Fluorouracil 21-35 interleukin 3 Mus musculus 89-108 3081577-2 1986 When spleen cells of 5-fluorouracil (5-FU)-treated mice were cultured in the presence of interleukin 3 (IL-3), most colonies revealed IL-3 concentration-dependent colony formation except for mast cell colonies and blast cell colonies. Fluorouracil 21-35 interleukin 3 Mus musculus 104-108 3081577-2 1986 When spleen cells of 5-fluorouracil (5-FU)-treated mice were cultured in the presence of interleukin 3 (IL-3), most colonies revealed IL-3 concentration-dependent colony formation except for mast cell colonies and blast cell colonies. Fluorouracil 37-41 interleukin 3 Mus musculus 89-108 3081577-2 1986 When spleen cells of 5-fluorouracil (5-FU)-treated mice were cultured in the presence of interleukin 3 (IL-3), most colonies revealed IL-3 concentration-dependent colony formation except for mast cell colonies and blast cell colonies. Fluorouracil 37-41 interleukin 3 Mus musculus 104-108 3081577-5 1986 This notion was supported by experiments in which IL-3 was added twice to cultures of spleen cells of 5-FU-treated mice. Fluorouracil 102-106 interleukin 3 Mus musculus 50-54 3082388-3 1986 CSF-1 supported more macrophage colonies from bone marrow cells of normal mice than IL 3, whereas in cultures of bone marrow cells of 5-fluorouracil-treated mice, IL 3 supported more macrophage colonies. Fluorouracil 134-148 interleukin 3 Mus musculus 163-167 3455740-5 1986 The exposure of MIA PaCa-2 cells to 1.6 X 10(-5) M 5-fluorouracil (FUra) followed by 2 X 10(-8) M DHAD or 3 X 10(-7) M ADR had an additive (with DHAD) or synergistic (with ADR) effect when the two drugs were given simultaneously and a synergistic effect with either drug when they were given 2, 6, or 24 hours apart. Fluorouracil 67-71 MIA SH3 domain containing Homo sapiens 16-19 3880810-2 1985 CBP (cyclophosphamide, bleomycin, and cisplatin) and AFP (doxorubicin, 5-fluorouracil, and cisplatin) had shown activity in generation II of this study (EST 2575). Fluorouracil 71-85 alpha fetoprotein Homo sapiens 53-56 3932469-11 1985 Finally, day 11 CFU-S persisting in the marrow of mice treated with 5-fluorouracil required IL-3 for proliferation in vitro. Fluorouracil 68-82 interleukin 3 Mus musculus 92-96 2994597-4 1985 Chemotherapy with streptozotocin and 5-fluorouracil was highly effective in ameliorating clinical symptoms, diminishing serum levels of gastrin and VIP, and greatly reducing the bulk of metastatic disease in this case. Fluorouracil 37-51 vasoactive intestinal peptide Homo sapiens 148-151 3934112-0 1985 [Experiences with polychemotherapy MAF (mitomycin C, adriablastine, 5-fluorouracil) in progressing metastasized prostate cancer]. Fluorouracil 68-82 MAF bZIP transcription factor Homo sapiens 35-38 2861227-1 1985 Expression of the Thy-1 alloantigen by hematopoietic stem and progenitor cells in post-5-fluorouracil (5-FU) murine bone marrow was investigated. Fluorouracil 87-101 thymus cell antigen 1, theta Mus musculus 18-23 2861227-1 1985 Expression of the Thy-1 alloantigen by hematopoietic stem and progenitor cells in post-5-fluorouracil (5-FU) murine bone marrow was investigated. Fluorouracil 103-107 thymus cell antigen 1, theta Mus musculus 18-23 2861227-6 1985 Ninety percent of all colony-forming cells surviving in vivo administration of 5-FU were Thy-1.2+. Fluorouracil 79-83 thymus cell antigen 1, theta Mus musculus 89-96 4004279-1 1985 5-FU and its analogs, Cyclophosphamide (CPA), Methotrexate (MTX), Adriamycin (ADM) and Vincristine (VCR) are among the many different anticancer agents that have proven effective by themselves against progressive recurrent carcinoma of the breast. Fluorouracil 0-4 carboxypeptidase A1 Homo sapiens 40-43 6436183-0 1984 Cytolytic activity of interferon-gamma and its synergism with 5-fluorouracil. Fluorouracil 62-76 interferon gamma Homo sapiens 22-38 6482418-9 1984 Of all agents or combinations of agents tested (L-PAM, 5-FU, MTX, adriamycin, vinblastine, cis-plat, FAC, CMF), only the response to 5-FU correlated significantly with ERA. Fluorouracil 133-137 FA complementation group C Homo sapiens 101-104 6436183-4 1984 A synergistic cytolysis on HT-29 cells of IFN-gamma and 5-fluorouracil (5-FU) was observed at 5-FU concentrations ranging from 64 to 640 micrograms/ml. Fluorouracil 72-76 interferon gamma Homo sapiens 42-51 6436183-4 1984 A synergistic cytolysis on HT-29 cells of IFN-gamma and 5-fluorouracil (5-FU) was observed at 5-FU concentrations ranging from 64 to 640 micrograms/ml. Fluorouracil 94-98 interferon gamma Homo sapiens 42-51 6436183-6 1984 The direct cytolytic activity and synergistic cytolysis with 5-FU of the IFN-gamma preparations used in the present study were abolished completely by treatment with a neutralizing monoclonal antibody specific for human IFN-gamma. Fluorouracil 61-65 interferon gamma Homo sapiens 73-82 6436183-6 1984 The direct cytolytic activity and synergistic cytolysis with 5-FU of the IFN-gamma preparations used in the present study were abolished completely by treatment with a neutralizing monoclonal antibody specific for human IFN-gamma. Fluorouracil 61-65 interferon gamma Homo sapiens 220-229 6409396-1 1983 There are two major R,S-1-(tetrahydro-2-furanyl)-5-fluorouracil (ftorafur) activation pathways to 5-fluorouracil, one that is mediated by microsomal cytochrome P-450 oxidation at C-5" of the tetrahydrofuran moiety and one that is mediated by soluble enzymes. Fluorouracil 49-63 cytochrome P450 family 4 subfamily F member 3 Homo sapiens 149-165 6438379-0 1984 Cytochrome P-450-dependent oxidative cleavage of 1-(tetrahydro-2-furanyl)-5-fluorouracil to 5-fluorouracil. Fluorouracil 74-88 cytochrome P450 family 4 subfamily F member 3 Homo sapiens 0-16 6438379-3 1984 Cytochrome P-450, NADPH-cytochrome P-450 reductase and NADPH were required for 5-FU production. Fluorouracil 79-83 cytochrome p450 oxidoreductase Homo sapiens 18-50 6861126-6 1983 The reduction of ER was reversible; regeneration of receptors to the control level occurred at either 4 hr (methotrexate and 5-fluorouracil) or 8 hr (vincristine) after removal of these drugs. Fluorouracil 125-139 estrogen receptor 1 Homo sapiens 17-19 6819375-5 1982 On the acute toxicity of tegafur or 5-FU, the lethality of the former was decreased and that of the latter was enhanced by the pretreatment with LPS 24 hr before. Fluorouracil 36-40 toll-like receptor 4 Mus musculus 145-148 6348483-5 1983 Moreover, the accumulation of RD mutants in the presence of berenil, 5-fluorouracil and basic fuchsin was higher in the mmc1 than in MMC1 strains. Fluorouracil 69-83 Mps2p Saccharomyces cerevisiae S288C 120-124 6348483-5 1983 Moreover, the accumulation of RD mutants in the presence of berenil, 5-fluorouracil and basic fuchsin was higher in the mmc1 than in MMC1 strains. Fluorouracil 69-83 Mps2p Saccharomyces cerevisiae S288C 133-137 6819375-6 1982 In LPS-treated mice, after the administration of tegafur, the level of tegafur in plasma was higher and the elevated level maintained longer than in untreated mice; and a small amount of 5-FU was released. Fluorouracil 187-191 toll-like receptor 4 Mus musculus 3-6 6819375-7 1982 A high level of 5-FU in plasma after the administration of 5-FU was also observed in LPS-treated mice. Fluorouracil 16-20 toll-like receptor 4 Mus musculus 85-88 6819375-7 1982 A high level of 5-FU in plasma after the administration of 5-FU was also observed in LPS-treated mice. Fluorouracil 59-63 toll-like receptor 4 Mus musculus 85-88 6819375-8 1982 In the liver and kidneys of LPS-treated mice, the level of 5-FU after the administration of tegafur or 5-FU was higher, and its conversion of 5-FU to fluorouridine (FUR) was lower than that of control mice. Fluorouracil 59-63 toll-like receptor 4 Mus musculus 28-31 6819375-8 1982 In the liver and kidneys of LPS-treated mice, the level of 5-FU after the administration of tegafur or 5-FU was higher, and its conversion of 5-FU to fluorouridine (FUR) was lower than that of control mice. Fluorouracil 103-107 toll-like receptor 4 Mus musculus 28-31 6819375-8 1982 In the liver and kidneys of LPS-treated mice, the level of 5-FU after the administration of tegafur or 5-FU was higher, and its conversion of 5-FU to fluorouridine (FUR) was lower than that of control mice. Fluorouracil 103-107 toll-like receptor 4 Mus musculus 28-31 6819375-10 1982 It can, therefore, be presumed that the antitumor activity of tegafur was affected with LPS as a result of inhibition of conversion from tegafur to 5-FU or from 5-FU to FUR mainly according to depression in the hepatic drug-metabolism. Fluorouracil 148-152 toll-like receptor 4 Mus musculus 88-91 6819375-10 1982 It can, therefore, be presumed that the antitumor activity of tegafur was affected with LPS as a result of inhibition of conversion from tegafur to 5-FU or from 5-FU to FUR mainly according to depression in the hepatic drug-metabolism. Fluorouracil 161-165 toll-like receptor 4 Mus musculus 88-91 6797104-1 1981 Phenobarbital stimulates the induction of liver microsomal drug-metabolizing enzyme, namely, cytochrome P-450, which enhances the rate of conversion of FT-207 to 5-FU, the active substance. Fluorouracil 162-166 cytochrome P450 family 4 subfamily F member 3 Homo sapiens 93-109 6820924-2 1982 The levels of 5-FU in the cancerous tissue of the stomach and the regional lymph nodes were higher in the cases who received 5-FU and ANG-II than in the cases received 5-FU alone. Fluorouracil 14-18 angiotensinogen Homo sapiens 134-140 6265056-9 1981 Chemotherapy, consisting of 5-FU given via intra-arterial hepatic infusion, was accompanied by significant transient clinical improvement which coincided with correction of thrombin clotting times and fibrin monomer aggregation. Fluorouracil 28-32 coagulation factor II, thrombin Homo sapiens 173-181 7397660-7 1980 The program that we have come to regard as our standard program in controlled clinical trials (CFP) employs cyclophosphamide, 5-fluorouracil, and prednisone. Fluorouracil 126-140 complement factor properdin Homo sapiens 95-98 510847-5 1979 Some regimens which did not include adriamycin, such as MFC (mitomycin-C, 5-fluorouracil, and cytosine arabinoside) had a good effect on the ER-positive cases, whereas the response to regimens including adriamycin was not influenced by the ER positiveness of the tumors. Fluorouracil 74-88 estrogen receptor 1 Homo sapiens 141-143 7003455-0 1980 Combination chemotherapy of advanced colorectal cancer with triazinate and ICRF-159 after failure of 5-Fluorouracil. Fluorouracil 101-115 regenerating family member 1 alpha Homo sapiens 75-79 11889-1 1976 Rats eating a diet containing casein hydrolysate (10% wt/wt)(diet 3) instead of whole casein (diet 1) exhibited increased tolerance to nine consecutive daily injections of 15 mg/kg of 5-fluorouracil (5-FU). Fluorouracil 184-198 MAM and LDL receptor class A domain containing 1 Rattus norvegicus 94-100 378934-1 1979 A leaky guaB mutant of Salmonella typhimurium LT-2 was obtained during a selection for mutants resistant to a combination of the two pyrimidine analogs, 5-fluorouracil and 5-fluorouridine. Fluorouracil 153-167 IMP dehydrogenase Salmonella enterica subsp. enterica serovar Typhimurium str. LT2 8-12 195585-4 1977 During the development of tumour-cell resistance to 5-fluorouracil or 5-fluorouridine in vivo there was an early differential increase in the activity of a low-affinity (high-Km) uridine kinase isoenzyme, as measured in cell extracts, and a 7-fold increase in the Km values for the uptake of both uridine and 5-fluorouridine into the intact resistant cells. Fluorouracil 52-66 uridine-cytidine kinase 2 Homo sapiens 179-193 132786-1 1976 In a prospective study eleven patients with metastasizing breast cancer were treated with 5-fluorouracil, adriamycin, and cyclophosphamide )FAC). Fluorouracil 90-104 FA complementation group C Homo sapiens 140-143 5775126-0 1969 Effect of erythropoietin on regeneration of hematopoietic stem cells after 5-fluorouracil administration. Fluorouracil 75-89 erythropoietin Homo sapiens 10-24 165496-3 1975 In 5-fluorouracil and 5-chlorouracil, however, the halogen is evidently abstracted by the Na to form NaF or NaC1 and the neutral uracil radical. Fluorouracil 3-17 C-X-C motif chemokine ligand 8 Homo sapiens 101-104 33906076-16 2021 CONCLUSION: TG potentiated 5-FU"s inhibitory activity to human colorectal cancer through arresting cell cycle progression and inducing p53-mediated apoptosis, which may present a novel strategy in CRC therapies and contribute to the optimizing clinical application of 5-FU. Fluorouracil 27-31 tumor protein p53 Homo sapiens 135-138 33901309-1 2021 Retraction: "Beta-elemene increases chemosensitivity to 5-fluorouracil through downregulating microRNA-191 expression in colorectal carcinoma cells", by Zongbing Guo, Zhenzhen Liu. Fluorouracil 56-70 microRNA 191 Homo sapiens 94-106 33727040-6 2021 Meanwhile, polarized M2 macrophages enhance 5-FU resistance in tumor cells by secreting CCL8 and activating phosphorylation of JAK1/STAT3 signaling pathway. Fluorouracil 44-48 Janus kinase 1 Homo sapiens 127-131 34042519-8 2021 Results: PD increased 5-FU-induced ICD in CRC cells, as demonstrated by the extracellular levels of adenosine triphosphate (ATP) and high-mobility group box 1 (HMGB1), and the surface levels of calreticulin (CRT). Fluorouracil 22-26 calreticulin Mus musculus 194-206 34042519-8 2021 Results: PD increased 5-FU-induced ICD in CRC cells, as demonstrated by the extracellular levels of adenosine triphosphate (ATP) and high-mobility group box 1 (HMGB1), and the surface levels of calreticulin (CRT). Fluorouracil 22-26 calreticulin Mus musculus 208-211 34042519-9 2021 Our mechanism study showed that PD promoted 5-FU-induced ICD by inactivating signal transducer and activator of transcription 3 (STAT3). Fluorouracil 44-48 signal transducer and activator of transcription 3 Mus musculus 77-127 34042519-9 2021 Our mechanism study showed that PD promoted 5-FU-induced ICD by inactivating signal transducer and activator of transcription 3 (STAT3). Fluorouracil 44-48 signal transducer and activator of transcription 3 Mus musculus 129-134 34042519-10 2021 Furthermore, the co-treatment of 5-FU and PD further promoted 5-FU-induced CRT expression and T cell infiltration in vivo. Fluorouracil 33-37 calreticulin Mus musculus 75-78 34042519-10 2021 Furthermore, the co-treatment of 5-FU and PD further promoted 5-FU-induced CRT expression and T cell infiltration in vivo. Fluorouracil 62-66 calreticulin Mus musculus 75-78 34042519-12 2021 Conclusion: This study indicated that PD enhances 5-FU-induced ICD and anti-tumor effect in CRC by inactivating STAT3. Fluorouracil 50-54 signal transducer and activator of transcription 3 Mus musculus 112-117 34003528-0 2021 Circular RNA PTGR1 regulates 5-FU resistance and development of hepatocellular carcinoma cells by modulating miR-129-5p/ABCC1 axis. Fluorouracil 29-33 prostaglandin reductase 1 Homo sapiens 13-18 33619534-5 2021 Twist1-deficient HSCs are more compromised in tolerance of irradiation and 5-fluorouracil-induced stresses, and exhibit typical phenotypes of senescence. Fluorouracil 75-89 twist family bHLH transcription factor 1 Homo sapiens 0-6 33727040-6 2021 Meanwhile, polarized M2 macrophages enhance 5-FU resistance in tumor cells by secreting CCL8 and activating phosphorylation of JAK1/STAT3 signaling pathway. Fluorouracil 44-48 signal transducer and activator of transcription 3 Homo sapiens 132-137 34003528-0 2021 Circular RNA PTGR1 regulates 5-FU resistance and development of hepatocellular carcinoma cells by modulating miR-129-5p/ABCC1 axis. Fluorouracil 29-33 ATP binding cassette subfamily C member 1 Homo sapiens 120-125 34003528-10 2021 Both circPTGR1 knockdown and miR-129-5p overexpression inhibited 5-FU resistance, migration, and invasion, and induced apoptosis of HCC cells. Fluorouracil 65-69 prostaglandin reductase 1 Homo sapiens 5-14 34026617-2 2021 In this review, we first summarize the molecular mechanisms of chemotherapy resistance that occur during the treatment with cisplatin, 5-fluorouracil, and docetaxel/paclitaxel, including DNA/RNA damage repair, drug efflux, apoptosis inhibition, and epidermal growth factor receptor/focal adhesion kinase/nuclear factor-kappaB activation. Fluorouracil 135-149 epidermal growth factor receptor Homo sapiens 249-281 34003528-14 2021 Our finding indicated that circPTGR1 modulated the 5-FU resistance, migration, invasion, and apoptosis of HCC cells via regulating miR-129-5p/ABCC1 axis, providing a theoretical basis for the treatment of HCC. Fluorouracil 51-55 prostaglandin reductase 1 Homo sapiens 27-36 34022544-9 2021 IL-8 and 5-FU increased MMP-2 and MMP-3 expression, while IL-6 and MTX augmented MMP-2 expression. Fluorouracil 9-13 matrix metallopeptidase 3 Homo sapiens 34-39 33662352-8 2021 Perifosine increases the efficacy of 5-FU and L-OHP by suppressing Akt activation. Fluorouracil 37-41 AKT serine/threonine kinase 1 Homo sapiens 67-70 33662352-9 2021 Thus, the use of an Akt inhibitor in combination with 5-FU and L-OHP may be beneficial in colon cancer with cells harboring the PIK3CA mutation. Fluorouracil 54-58 phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha Homo sapiens 128-134 33662352-0 2021 Perifosine enhances the potential antitumor effect of 5-fluorourasil and oxaliplatin in colon cancer cells harboring the PIK3CA mutation. Fluorouracil 54-68 phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha Homo sapiens 121-127 33931048-14 2021 Furthermore, the knockdown of S100A11 gene expression dramatically induces the cellular response of gastric cancer cells to the first-line chemotherapeutic drugs fluoropyrimidine 5-fluorouracil (5-FU) and cisplatin. Fluorouracil 179-193 S100 calcium binding protein A11 Homo sapiens 30-37 33662352-4 2021 The use of 5-FU or L-OHP alone or in combination induced significant death of Caco-2 cells (PIK3CA wild type), but only weakly decreased the viability of DLD-1 and SW948 cells harboring the PIK3CA mutation. Fluorouracil 11-15 phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha Homo sapiens 92-98 33662352-4 2021 The use of 5-FU or L-OHP alone or in combination induced significant death of Caco-2 cells (PIK3CA wild type), but only weakly decreased the viability of DLD-1 and SW948 cells harboring the PIK3CA mutation. Fluorouracil 11-15 phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha Homo sapiens 190-196 33662352-5 2021 The use of 5-FU and L-OHP, either alone or in combination, strongly suppressed Akt activation, Survivin, Bcl-2, and Bcl-xL expression, and enhanced Puma, phospho-p53, and p53 expression in Caco-2 cells than in DLD-1 cells. Fluorouracil 11-15 AKT serine/threonine kinase 1 Homo sapiens 79-82 33662352-5 2021 The use of 5-FU and L-OHP, either alone or in combination, strongly suppressed Akt activation, Survivin, Bcl-2, and Bcl-xL expression, and enhanced Puma, phospho-p53, and p53 expression in Caco-2 cells than in DLD-1 cells. Fluorouracil 11-15 BCL2 apoptosis regulator Homo sapiens 105-110 33662352-5 2021 The use of 5-FU and L-OHP, either alone or in combination, strongly suppressed Akt activation, Survivin, Bcl-2, and Bcl-xL expression, and enhanced Puma, phospho-p53, and p53 expression in Caco-2 cells than in DLD-1 cells. Fluorouracil 11-15 BCL2 like 1 Homo sapiens 116-122 33662352-5 2021 The use of 5-FU and L-OHP, either alone or in combination, strongly suppressed Akt activation, Survivin, Bcl-2, and Bcl-xL expression, and enhanced Puma, phospho-p53, and p53 expression in Caco-2 cells than in DLD-1 cells. Fluorouracil 11-15 tumor protein p53 Homo sapiens 162-165 33662352-5 2021 The use of 5-FU and L-OHP, either alone or in combination, strongly suppressed Akt activation, Survivin, Bcl-2, and Bcl-xL expression, and enhanced Puma, phospho-p53, and p53 expression in Caco-2 cells than in DLD-1 cells. Fluorouracil 11-15 tumor protein p53 Homo sapiens 171-174 33662352-6 2021 In addition, perifosine enhanced the cytotoxicity of the 5-FU and L-OHP combination, inhibited Akt activation and the expression of Survivin, Bcl-2, and Bcl-xL, and increased the expression of Puma, phospho-p53, and p53 in DLD-1 cells. Fluorouracil 57-61 AKT serine/threonine kinase 1 Homo sapiens 95-98 33662352-7 2021 These results indicate that PIK3CA mutation contributes to reduced sensitivity to 5-FU and L-OHP via Akt activation in colon cancer cells. Fluorouracil 82-86 phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha Homo sapiens 28-34 33662352-7 2021 These results indicate that PIK3CA mutation contributes to reduced sensitivity to 5-FU and L-OHP via Akt activation in colon cancer cells. Fluorouracil 82-86 AKT serine/threonine kinase 1 Homo sapiens 101-104 33951601-7 2021 The effect of 5-FU on PD-L1 expression was related to its genotoxic effect and was prevented by extracellular application of thymidine or using a chemical inhibitor of the DNA damage Response kinases ATM/ATR. Fluorouracil 14-18 ATR serine/threonine kinase Homo sapiens 204-207 33951601-10 2021 The induction of PD-L1 by 5-FU was partially prevented by Epidermal Growth Factor Receptor (EGFR) inhibition with cetuximab. Fluorouracil 26-30 epidermal growth factor receptor Homo sapiens 58-90 33951601-10 2021 The induction of PD-L1 by 5-FU was partially prevented by Epidermal Growth Factor Receptor (EGFR) inhibition with cetuximab. Fluorouracil 26-30 epidermal growth factor receptor Homo sapiens 92-96 33780262-7 2021 Eventually, xenograft transplantation was applied to confirm the effect of PITX2 knockdown on CRC chemoresistance to 5-FU. Fluorouracil 117-121 paired like homeodomain 2 Homo sapiens 75-80 33780262-8 2021 5-FU-resistant CRC cells were successfully established, in which CRC cell viability, proliferation, and cell cycle were all enhanced, while PITX2 knockout led to reversed results, indicating that resistance to 5-FU in CRC was restricted. Fluorouracil 0-4 paired like homeodomain 2 Homo sapiens 140-145 33780262-8 2021 5-FU-resistant CRC cells were successfully established, in which CRC cell viability, proliferation, and cell cycle were all enhanced, while PITX2 knockout led to reversed results, indicating that resistance to 5-FU in CRC was restricted. Fluorouracil 210-214 paired like homeodomain 2 Homo sapiens 140-145 33780262-11 2021 Additionally, xenograft transplantation further confirmed that PITX2 knockdown reduced the resistance of HCT116 cells to 5-FU. Fluorouracil 121-125 paired like homeodomain 2 Homo sapiens 63-68 33780262-12 2021 This study clarified that PITX2 enhanced resistance to 5-FU in CRC upregulating the Wnt/beta-catenin axis. Fluorouracil 55-59 paired like homeodomain 2 Homo sapiens 26-31 33938344-0 2021 LncRNA ENSG00000254615 Modulates Proliferation and 5-FU Resistance by Regulating p21 and Cyclin D1 in Colorectal Cancer. Fluorouracil 51-55 cyclin dependent kinase inhibitor 1A Homo sapiens 81-84 33938344-6 2021 Taken together, we proposed that ENSG00000254615 inhibits proliferation and attenuates 5-FU resistance of CRC by regulating p21 and Cyclin D1 expression. Fluorouracil 87-91 cyclin dependent kinase inhibitor 1A Homo sapiens 124-127 33931048-14 2021 Furthermore, the knockdown of S100A11 gene expression dramatically induces the cellular response of gastric cancer cells to the first-line chemotherapeutic drugs fluoropyrimidine 5-fluorouracil (5-FU) and cisplatin. Fluorouracil 195-199 S100 calcium binding protein A11 Homo sapiens 30-37 33995592-10 2021 Other oral fluoropyrimidines, such as FTD/TPI, are effective in patients with mCRC who are refractory, intolerant or ineligible for 5-FU. Fluorouracil 132-136 triosephosphate isomerase 1 Homo sapiens 42-45 33860796-0 2021 HDAC6 inhibitor WT161 performs antitumor effect on osteosarcoma and synergistically interacts with 5-FU. Fluorouracil 99-103 histone deacetylase 6 Homo sapiens 0-5 33927358-7 2021 We demonstrated that co-administration of GA ameliorated 5-FU-induced peripheral muscle fatigue-like behavior via improving muscle quality and mitochondria function, increasing glycogen content and ATP production, reducing lactic acid content and LDH activity, and inhibiting p-AMPK, IL-6 and TNF-alpha expression in skeletal muscle. Fluorouracil 57-61 interleukin 6 Mus musculus 284-288 33927358-7 2021 We demonstrated that co-administration of GA ameliorated 5-FU-induced peripheral muscle fatigue-like behavior via improving muscle quality and mitochondria function, increasing glycogen content and ATP production, reducing lactic acid content and LDH activity, and inhibiting p-AMPK, IL-6 and TNF-alpha expression in skeletal muscle. Fluorouracil 57-61 tumor necrosis factor Mus musculus 293-302 33927358-8 2021 Co-administration of GA also retarded the 5-FU-induced central fatigue-like behavior accompanied by down-regulating the expression of IL-6, iNOS and COX2 in the hippocampus through inhibiting TLR4/Myd88/NF-kappaB pathway. Fluorouracil 42-46 interleukin 6 Mus musculus 134-138 33927358-8 2021 Co-administration of GA also retarded the 5-FU-induced central fatigue-like behavior accompanied by down-regulating the expression of IL-6, iNOS and COX2 in the hippocampus through inhibiting TLR4/Myd88/NF-kappaB pathway. Fluorouracil 42-46 nitric oxide synthase 2, inducible Mus musculus 140-144 33927358-8 2021 Co-administration of GA also retarded the 5-FU-induced central fatigue-like behavior accompanied by down-regulating the expression of IL-6, iNOS and COX2 in the hippocampus through inhibiting TLR4/Myd88/NF-kappaB pathway. Fluorouracil 42-46 toll-like receptor 4 Mus musculus 192-196 33927358-8 2021 Co-administration of GA also retarded the 5-FU-induced central fatigue-like behavior accompanied by down-regulating the expression of IL-6, iNOS and COX2 in the hippocampus through inhibiting TLR4/Myd88/NF-kappaB pathway. Fluorouracil 42-46 nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105 Mus musculus 203-212 33948374-0 2021 Elevated LOXL2 expression by LINC01347/miR-328-5p axis contributes to 5-FU chemotherapy resistance of colorectal cancer. Fluorouracil 70-74 lysyl oxidase like 2 Homo sapiens 9-14 33925189-7 2021 In vitro genetic manipulation of IL-6 production by primary CAFs isolated from human CCA showed that IL-6 impairs the autophagy-associated apoptotic response to 5-FU in human CCA cells. Fluorouracil 161-165 interleukin 6 Homo sapiens 33-37 33925189-7 2021 In vitro genetic manipulation of IL-6 production by primary CAFs isolated from human CCA showed that IL-6 impairs the autophagy-associated apoptotic response to 5-FU in human CCA cells. Fluorouracil 161-165 interleukin 6 Homo sapiens 101-105 33886055-5 2021 Also, 5-FU-induced kidney damage, increased levels of malondialdehyde (MDA), decreased superoxide dismutase (SOD), catalase (CAT), glutathione reductase (GR) activity, and glutathione (GSH) level have been demonstrated. Fluorouracil 6-10 catalase Mus musculus 115-123 33886055-5 2021 Also, 5-FU-induced kidney damage, increased levels of malondialdehyde (MDA), decreased superoxide dismutase (SOD), catalase (CAT), glutathione reductase (GR) activity, and glutathione (GSH) level have been demonstrated. Fluorouracil 6-10 catalase Mus musculus 125-128 33923672-12 2021 The results showed that melatonin reduced the number of p21-positive cells in the SGZ of the dentate gyrus and increased Nrf2, DCX and BDNF protein expression in rats treated with 5-FU. Fluorouracil 180-184 NFE2 like bZIP transcription factor 2 Rattus norvegicus 121-125 33948374-0 2021 Elevated LOXL2 expression by LINC01347/miR-328-5p axis contributes to 5-FU chemotherapy resistance of colorectal cancer. Fluorouracil 70-74 microRNA 328 Homo sapiens 39-46 33948374-9 2021 LOXL2 knockdown impaired the LINC01347 overexpression induced 5-FU resistance in CRC cells. Fluorouracil 62-66 lysyl oxidase like 2 Homo sapiens 0-5 33948374-11 2021 Our study provided a molecular basis for the development of 5-FU based chemotherapy resistance in CRC by LINC01347/miR-328/LOXL2 axis. Fluorouracil 60-64 microRNA 328 Homo sapiens 115-122 33948374-11 2021 Our study provided a molecular basis for the development of 5-FU based chemotherapy resistance in CRC by LINC01347/miR-328/LOXL2 axis. Fluorouracil 60-64 lysyl oxidase like 2 Homo sapiens 123-128 33823840-11 2021 This observation supports that MUC2 is involved in resistance to fluorouracil-based adjuvant chemotherapy and might be a promising future predictive biomarker in stage II CRC patients. Fluorouracil 65-77 mucin 2, oligomeric mucus/gel-forming Homo sapiens 31-35 33471160-15 2021 A significantly higher gene expression for Bax and Bax/Bcl2 ratio was seen after 5-FU treatment. Fluorouracil 81-85 B cell leukemia/lymphoma 2 Mus musculus 55-59 33539818-3 2021 Our present study reveals that 5-FU and CDDP treatment increase the expression of histone deacetylase 1 (HDAC1) in LSCC cells. Fluorouracil 31-35 histone deacetylase 1 Homo sapiens 82-103 33539818-3 2021 Our present study reveals that 5-FU and CDDP treatment increase the expression of histone deacetylase 1 (HDAC1) in LSCC cells. Fluorouracil 31-35 histone deacetylase 1 Homo sapiens 105-110 33795638-7 2021 Significantly, UTD1 exhibited stronger effect on inducing apoptosis than paclitaxel and 5-FU, especially in HCT15 cells which is ABCB1 high-expression. Fluorouracil 88-92 ATP binding cassette subfamily B member 1 Homo sapiens 129-134 33970155-0 2021 Cashin and Graf: long-term intraperitoneal 5-fluorouracil is superior to adjuvant FOLFOX in a randomized trial. Fluorouracil 43-57 Rho GTPase activating protein 26 Homo sapiens 11-15 33472949-3 2021 Here we found that experimental YAP activation in 5FU-sensitive and 5FU-resistant HT29 CRC cells enhanced nuclear YAP localization and the transcript levels of the retinoic acid (RA) receptors RARalpha/gamma and RAR target genes CYP26A1, ALDH1A3 and LGR5 through RA Response Elements (RAREs). Fluorouracil 50-53 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 229-236 33472949-3 2021 Here we found that experimental YAP activation in 5FU-sensitive and 5FU-resistant HT29 CRC cells enhanced nuclear YAP localization and the transcript levels of the retinoic acid (RA) receptors RARalpha/gamma and RAR target genes CYP26A1, ALDH1A3 and LGR5 through RA Response Elements (RAREs). Fluorouracil 68-71 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 229-236 33593942-3 2021 The increased potency of CF10 relative to 5-FU correlated with enhanced TS inhibition and strong Top1 cleavage complex formation. Fluorouracil 42-46 DNA topoisomerase I Homo sapiens 97-101 33649858-0 2021 Melatonin sensitizes esophageal cancer cells to 5-fluorouracil via promotion of apoptosis by regulating EZH2 expression. Fluorouracil 48-62 enhancer of zeste 2 polycomb repressive complex 2 subunit Homo sapiens 104-108 33605536-5 2021 In endoscopic core ESCC biopsies taken from 61 patients who underwent neoadjuvant chemotherapy (5-fluorouracil and cisplatin), low MRE11A and high UBQLN4 protein levels were associated with reduced pathological response to neoadjuvant chemotherapy (p<0.001 and p<0.001, respectively). Fluorouracil 96-110 MRE11 homolog, double strand break repair nuclease Homo sapiens 131-137 33649858-8 2021 MLT and 5-FU combination inhibited cell proliferation and promoted apoptosis by regulating EZH2 expression. Fluorouracil 8-12 enhancer of zeste 2 polycomb repressive complex 2 subunit Homo sapiens 91-95 33649858-9 2021 In conclusion, MLT enhanced 5-FU-mediated inhibition of cell proliferation via promotion of apoptosis by regulating EZH2 expression in esophageal cancer. Fluorouracil 28-32 enhancer of zeste 2 polycomb repressive complex 2 subunit Homo sapiens 116-120 33538278-6 2021 Furthermore, delivery of 5-FU by using this nanoplatform can remarkably induce cytotoxicity, cell cycle arrest, and cell apoptosis for CRC cells with high EGFR expression. Fluorouracil 25-29 epidermal growth factor receptor Homo sapiens 155-159 33460610-5 2021 Furthermore, Nanog knockdown significantly increased CRC cell sensitivity to 5-FU drug via modulating Bax and Bcl-2 mRNA expression. Fluorouracil 77-81 BCL2 associated X, apoptosis regulator Homo sapiens 102-105 33720069-5 2021 In human epidermal growth factor receptor 2 (HER2)-positive oesophago-gastric adenocarcinoma, a phase II trial showed improved DFS when pertuzumab and trastuzumab were added to perioperative FLOT (5-fluorouracil/leucovorin, oxaliplatin, docetaxel). Fluorouracil 197-211 erb-b2 receptor tyrosine kinase 2 Homo sapiens 45-49 33460610-5 2021 Furthermore, Nanog knockdown significantly increased CRC cell sensitivity to 5-FU drug via modulating Bax and Bcl-2 mRNA expression. Fluorouracil 77-81 BCL2 apoptosis regulator Homo sapiens 110-115 32647340-8 2021 The activated ATF4 upregulated RNASET2-mediated uracil generation, which impaired exogenous 5-FU uptake to blunt 5-FU therapy. Fluorouracil 92-96 ribonuclease T2 Homo sapiens 31-38 33675849-1 2021 Human uracil DNA-glycosylase (UDG) is the prototypic and first identified DNA glycosylase with a vital role in removing deaminated cytosine and incorporated uracil and 5-fluorouracil (5-FU) from DNA. Fluorouracil 168-182 uracil DNA glycosylase Homo sapiens 6-28 33675849-1 2021 Human uracil DNA-glycosylase (UDG) is the prototypic and first identified DNA glycosylase with a vital role in removing deaminated cytosine and incorporated uracil and 5-fluorouracil (5-FU) from DNA. Fluorouracil 168-182 uracil DNA glycosylase Homo sapiens 30-33 33675849-1 2021 Human uracil DNA-glycosylase (UDG) is the prototypic and first identified DNA glycosylase with a vital role in removing deaminated cytosine and incorporated uracil and 5-fluorouracil (5-FU) from DNA. Fluorouracil 184-188 uracil DNA glycosylase Homo sapiens 6-28 33675849-1 2021 Human uracil DNA-glycosylase (UDG) is the prototypic and first identified DNA glycosylase with a vital role in removing deaminated cytosine and incorporated uracil and 5-fluorouracil (5-FU) from DNA. Fluorouracil 184-188 uracil DNA glycosylase Homo sapiens 30-33 33675849-2 2021 UDG depletion sensitizes cells to high APOBEC3B deaminase and to pemetrexed (PEM) and floxuridine (5-FdU), which are toxic to tumor cells through incorporation of uracil and 5-FU into DNA. Fluorouracil 174-178 uracil DNA glycosylase Homo sapiens 0-3 33674443-9 2021 We also demonstrated that 5-fluorouracil (5-FU)/cisplatin (CDDP) preferentially increased mRNA expression of IL-34 on human ESCC cell lines. Fluorouracil 26-40 interleukin 34 Homo sapiens 109-114 33674443-9 2021 We also demonstrated that 5-fluorouracil (5-FU)/cisplatin (CDDP) preferentially increased mRNA expression of IL-34 on human ESCC cell lines. Fluorouracil 42-46 interleukin 34 Homo sapiens 109-114 32647340-8 2021 The activated ATF4 upregulated RNASET2-mediated uracil generation, which impaired exogenous 5-FU uptake to blunt 5-FU therapy. Fluorouracil 113-117 ribonuclease T2 Homo sapiens 31-38 33838628-0 2021 Upregulation of NOX-2 and Nrf-2 Promotes 5-Fluorouracil Resistance of Human Colon Carcinoma (HCT-116) Cells. Fluorouracil 41-55 NFE2 like bZIP transcription factor 2 Homo sapiens 26-31 33361273-9 2021 CF10"s anti-tumor activity was associated with increased plasma levels of FP deoxynucleotide metabolites relative to 5-FU. Fluorouracil 117-121 coagulation factor X Mus musculus 0-4 33838628-12 2021 The treatment with HDC and ML-385 (specific inhibitor of Nrf-2) augmented the 5-FU-mediated apoptotic cell death of HCT-116/R cells, which suggests that NOX-2 and Nrf-2 are involved in the development of the chemoresistant phenotype of these cells. Fluorouracil 78-82 NFE2 like bZIP transcription factor 2 Homo sapiens 57-62 33838628-12 2021 The treatment with HDC and ML-385 (specific inhibitor of Nrf-2) augmented the 5-FU-mediated apoptotic cell death of HCT-116/R cells, which suggests that NOX-2 and Nrf-2 are involved in the development of the chemoresistant phenotype of these cells. Fluorouracil 78-82 NFE2 like bZIP transcription factor 2 Homo sapiens 163-168 33645623-16 2021 In summary, this study suggests a new molecular mechanism for the NEAT1-mediated 5-Fu resistance via the miR-34a/LDHA-glycolysis axis. Fluorouracil 81-85 lactate dehydrogenase A Homo sapiens 113-117 33392922-10 2021 Interestingly, the use of FO alongwith 5-FU also significantly declined the expression of drug transporters (ABCB1,ABCC5) and consequently resulted in an increased cellular uptake of 5-FU and its metabolite, 5-FdUMP at target site (colon). Fluorouracil 39-43 ATP-binding cassette, sub-family B (MDR/TAP), member 1B Mus musculus 109-114 33645623-0 2021 Inhibition of lncRNA-NEAT1 sensitizes 5-Fu resistant cervical cancer cells through de-repressing the microRNA-34a/LDHA axis. Fluorouracil 38-42 lactate dehydrogenase A Homo sapiens 114-118 33645623-15 2021 Finally, we demonstrated inhibition of NEAT1 significantly sensitized cervical cancer cells to 5-Fu through the miR-34a/LDHA pathway. Fluorouracil 95-99 lactate dehydrogenase A Homo sapiens 120-124 30990333-3 2021 The combination of PGG and 5-FU had synergistic effects on reversal the aggressive phenotypes of HepG2 cells, increasing the proportion of Bax/Bcl-2, promoting the activation of caspase-9 and caspase-3, and inducing apoptosis. Fluorouracil 27-31 BCL2 associated X, apoptosis regulator Homo sapiens 139-142 30990333-3 2021 The combination of PGG and 5-FU had synergistic effects on reversal the aggressive phenotypes of HepG2 cells, increasing the proportion of Bax/Bcl-2, promoting the activation of caspase-9 and caspase-3, and inducing apoptosis. Fluorouracil 27-31 BCL2 apoptosis regulator Homo sapiens 143-148 30990333-3 2021 The combination of PGG and 5-FU had synergistic effects on reversal the aggressive phenotypes of HepG2 cells, increasing the proportion of Bax/Bcl-2, promoting the activation of caspase-9 and caspase-3, and inducing apoptosis. Fluorouracil 27-31 caspase 3 Homo sapiens 192-201 30990333-5 2021 The combination significantly downregulated MDR1 and LRP1, suggesting the potential to reverse the resistance to 5-FU. Fluorouracil 113-117 ATP binding cassette subfamily B member 1 Homo sapiens 44-48 30990333-5 2021 The combination significantly downregulated MDR1 and LRP1, suggesting the potential to reverse the resistance to 5-FU. Fluorouracil 113-117 LDL receptor related protein 1 Homo sapiens 53-57 33452458-12 2021 GC cells treated with siNOTCH3, siPHLDB2, miR-491-5p, miR-875-5p, were more sensitive to Cisplatin and 5-FU. Fluorouracil 103-107 microRNA 875 Homo sapiens 54-61 33574948-7 2021 AKT1/CTNNB1 mutations were also associated with oxaliplatin, irinotecan, SN-38 and 5-fluorouracil resistance. Fluorouracil 83-97 AKT serine/threonine kinase 1 Homo sapiens 0-4 33613715-0 2021 p53 expression confers sensitivity to 5-fluorouracil via distinct chromatin accessibility dynamics in human colorectal cancer. Fluorouracil 38-52 tumor protein p53 Homo sapiens 0-3 33613715-7 2021 Notably, while treatment with 5-FU mediated global increases in chromatin accessibility, chromatin organization in several genomic regions differed depending on the expression status of p53. Fluorouracil 30-34 tumor protein p53 Homo sapiens 186-189 33613715-8 2021 Since the occupancy of p53 does not overlap with accessible chromatin regions, the 5-FU-mediated changes in chromatin accessibility were not regulated by direct binding of p53. Fluorouracil 83-87 tumor protein p53 Homo sapiens 23-26 33613715-9 2021 In the p53-expressing condition, the 5-FU-mediated accessible chromatin region was primarily associated with genes encoding cell death pathways. Fluorouracil 37-41 tumor protein p53 Homo sapiens 7-10 33613715-10 2021 Additionally, 5-FU was revealed to induce open chromatin conformation at regions containing binding motifs for AP-1 family transcription factors, which may drive expression of apoptosis pathway genes. Fluorouracil 14-18 JunB proto-oncogene, AP-1 transcription factor subunit Homo sapiens 111-115 33613715-11 2021 In conclusion, expression of p53 may confer 5-FU sensitivity by regulating chromatin accessibility of distinct genes associated with cell apoptosis in a transcription-independent manner. Fluorouracil 44-48 tumor protein p53 Homo sapiens 29-32 33613724-4 2021 In the present study, two CRC cell lines, including HT-29 and HCT-116 cells, were used to investigate the impact of miR-9-5p in overcoming 5-FU resistance. Fluorouracil 139-143 microRNA 95 Homo sapiens 116-124 33613724-5 2021 The results revealed that treatment with 5-FU decreased CRC cell viability and upregulated miR-9-5p expression in both CRC cells. Fluorouracil 41-45 microRNA 95 Homo sapiens 91-99 33613724-6 2021 Knockdown of miR-9-5p decreased HCT-116 cell sensitivity to 5-FU and inhibited apoptosis. Fluorouracil 60-64 microRNA 95 Homo sapiens 13-21 33613724-7 2021 By contrast, miR-9-5p overexpression enhanced the sensitivity of HT-29 cells to 5-FU and induced apoptosis. Fluorouracil 80-84 microRNA 95 Homo sapiens 13-21 33613724-10 2021 The present study indicated that miR-9-5p enhanced the sensitivity of CRC cells to 5-FU via downregulating HMGA2 expression. Fluorouracil 83-87 microRNA 95 Homo sapiens 33-41 33636347-3 2021 Here, we constructed an albumin-stabilized layered double hydroxide nanoparticle (BLDH) system to simultaneously load and deliver two widely used anti-tumor drugs, i.e. 5-fluorouracil (5FU) and albumin-bound PTX (Abraxane, ABX) for colorectal cancer treatment. Fluorouracil 169-183 albumin Homo sapiens 24-31 32959474-2 2021 In this study, we undertook ECG recording (Holter) and analyses of the biomarkers troponin and copeptin in patients receiving 5-FU to increase our understanding of the cardiotoxicity. Fluorouracil 126-130 arginine vasopressin Homo sapiens 95-103 32959474-7 2021 The ischemic burden per day (p = .001), the number of ST depression episodes per day (p = .003), and the total duration of ischemic episodes per day (p = .003) were higher during the first 5-FU infusion than before, as was plasma copeptin (p < .001), whereas plasma troponin I was similar (p = 1.). Fluorouracil 189-193 arginine vasopressin Homo sapiens 230-238 32959474-10 2021 According to biomarker analyses, 5-FU is associated with an increase in copeptin, but rarely with increases in cardiac troponin I. Fluorouracil 33-37 arginine vasopressin Homo sapiens 72-80 32959474-14 2021 Cardiac biomarker analyses suggested that 5-FU infusion results in endogenous stress (increased copeptin) but rarely induces myocyte injury (no change in troponin). Fluorouracil 42-46 arginine vasopressin Homo sapiens 96-104 33636347-3 2021 Here, we constructed an albumin-stabilized layered double hydroxide nanoparticle (BLDH) system to simultaneously load and deliver two widely used anti-tumor drugs, i.e. 5-fluorouracil (5FU) and albumin-bound PTX (Abraxane, ABX) for colorectal cancer treatment. Fluorouracil 185-188 albumin Homo sapiens 24-31 33599179-0 2021 JAK2/STAT3 inhibitor reduced 5-FU resistance and autophagy through ATF6-mediated ER stress. Fluorouracil 29-33 signal transducer and activator of transcription 3 Homo sapiens 5-10 33599179-3 2021 The mechanisms of action of JAK2/STAT3 pathway were investigated in AGS cells with drug resistance of 5-fluorouracil (5-FU) by corresponding inhibitors. Fluorouracil 102-116 signal transducer and activator of transcription 3 Homo sapiens 33-38 33599179-11 2021 These findings indicated that the involvement of JAK2/STAT3 pathway in regulating ER stress affected the 5-FU resistance of AGS cells and autophagy, which was mediated by ATF6. Fluorouracil 105-109 signal transducer and activator of transcription 3 Homo sapiens 54-59 33599179-12 2021 Targeting JAK2/STAT3 pathway could be a potential approach to decrease the 5-FU resistance of gastric cancer and enhance the sensitivity of gastric cancer to 5-FU. Fluorouracil 75-79 signal transducer and activator of transcription 3 Homo sapiens 15-20 33599179-12 2021 Targeting JAK2/STAT3 pathway could be a potential approach to decrease the 5-FU resistance of gastric cancer and enhance the sensitivity of gastric cancer to 5-FU. Fluorouracil 158-162 signal transducer and activator of transcription 3 Homo sapiens 15-20 33085122-9 2021 Moreover, 5-fluorouracil inhibited the proliferation, migration, and invasion of tumor cells, via the targeting of MARCH1 and the consequent downregulation of the PI3K/AKT pathway, impacting the progression of epithelial-mesenchymal transition. Fluorouracil 10-24 AKT serine/threonine kinase 1 Homo sapiens 168-171 33564015-0 2021 Retraction Note: JNK confers 5-fluorouracil resistance in p53-deficient and mutant p53-expressing colon cancer cells by inducing survival autophagy. Fluorouracil 29-43 mitogen-activated protein kinase 8 Homo sapiens 17-20 33564015-0 2021 Retraction Note: JNK confers 5-fluorouracil resistance in p53-deficient and mutant p53-expressing colon cancer cells by inducing survival autophagy. Fluorouracil 29-43 tumor protein p53 Homo sapiens 58-61 33564015-0 2021 Retraction Note: JNK confers 5-fluorouracil resistance in p53-deficient and mutant p53-expressing colon cancer cells by inducing survival autophagy. Fluorouracil 29-43 tumor protein p53 Homo sapiens 83-86 33567038-9 2021 Moreover, CDKN1A was upregulated, whereas CDK6 was downregulated in basal cell carcinoma treated with either 5-fluorouracil (p=0.0001 and p=0.01, respectively) or the combination of 5-fluorouracil and mitomycin C (p=0.007 and p=0.001, respectively). Fluorouracil 109-123 cyclin dependent kinase inhibitor 1A Homo sapiens 10-16 33567038-9 2021 Moreover, CDKN1A was upregulated, whereas CDK6 was downregulated in basal cell carcinoma treated with either 5-fluorouracil (p=0.0001 and p=0.01, respectively) or the combination of 5-fluorouracil and mitomycin C (p=0.007 and p=0.001, respectively). Fluorouracil 109-123 cyclin dependent kinase 6 Homo sapiens 42-46 33567038-9 2021 Moreover, CDKN1A was upregulated, whereas CDK6 was downregulated in basal cell carcinoma treated with either 5-fluorouracil (p=0.0001 and p=0.01, respectively) or the combination of 5-fluorouracil and mitomycin C (p=0.007 and p=0.001, respectively). Fluorouracil 182-196 cyclin dependent kinase 6 Homo sapiens 42-46 33373916-12 2021 In addition, MPH-966 prevented 5-FU-induced intestinal barrier dysfunction, as indicated by the modulated expression of the tight junction proteins zonula occludin-1 and occludin. Fluorouracil 31-35 occludin Mus musculus 155-163 33253919-2 2021 In some cases, however, some are stakeholders of the efficiency of the treatment and this combinatorial strategy is exploited by some drug associations, including levodopa (L-Dopa) and dopadecarboxylase inhibitors, beta-lactam antibiotics and clavulanic acid, 5-fluorouracil (5-FU) and folinic acid, and penicillin and probenecid. Fluorouracil 260-274 dopa decarboxylase Homo sapiens 185-202 33641785-0 2021 Jiedu Sangen decoction inhibits chemoresistance to 5-fluorouracil of colorectal cancer cells by suppressing glycolysis via PI3K/AKT/HIF-1alpha signaling pathway. Fluorouracil 51-65 AKT serine/threonine kinase 1 Homo sapiens 128-131 33641785-0 2021 Jiedu Sangen decoction inhibits chemoresistance to 5-fluorouracil of colorectal cancer cells by suppressing glycolysis via PI3K/AKT/HIF-1alpha signaling pathway. Fluorouracil 51-65 hypoxia inducible factor 1 subunit alpha Homo sapiens 132-142 33641785-9 2021 In HIF-1alpha silenced HCT-8/5-FU cells, synergistic group showed significantly reduced expression levels of PI3K, AKT, p-AKT. Fluorouracil 29-33 hypoxia inducible factor 1 subunit alpha Homo sapiens 3-13 33641785-9 2021 In HIF-1alpha silenced HCT-8/5-FU cells, synergistic group showed significantly reduced expression levels of PI3K, AKT, p-AKT. Fluorouracil 29-33 AKT serine/threonine kinase 1 Homo sapiens 115-118 33641785-9 2021 In HIF-1alpha silenced HCT-8/5-FU cells, synergistic group showed significantly reduced expression levels of PI3K, AKT, p-AKT. Fluorouracil 29-33 AKT serine/threonine kinase 1 Homo sapiens 122-125 33641785-12 2021 JSD may reverse 5-FU resistance by suppressing glycolysis via PI3K/AKT/HIF-1alpha signaling pathway, thereby inhibiting glycolysis and induce apoptosis to enhance anti-tumor activity. Fluorouracil 16-20 AKT serine/threonine kinase 1 Homo sapiens 67-70 33641785-12 2021 JSD may reverse 5-FU resistance by suppressing glycolysis via PI3K/AKT/HIF-1alpha signaling pathway, thereby inhibiting glycolysis and induce apoptosis to enhance anti-tumor activity. Fluorouracil 16-20 hypoxia inducible factor 1 subunit alpha Homo sapiens 71-81 33634982-8 2021 Synergistic inhibition of the LIF/JAK1/STAT3 and NF-kB signaling pathways by ATO and 5-FU/cisplatin is a potential molecular mechanism underlying the differentiation effect. Fluorouracil 85-89 Janus kinase 1 Homo sapiens 34-38 33634982-8 2021 Synergistic inhibition of the LIF/JAK1/STAT3 and NF-kB signaling pathways by ATO and 5-FU/cisplatin is a potential molecular mechanism underlying the differentiation effect. Fluorouracil 85-89 signal transducer and activator of transcription 3 Homo sapiens 39-44 33634982-9 2021 CONCLUSIONS: ATO induced the differentiation of HCC CSCs and potentiated the cytotoxic effects of 5-FU/cisplatin through synergistic inhibition of the LIF/JAK1/STAT3 and NF-kB signaling pathways. Fluorouracil 98-102 Janus kinase 1 Homo sapiens 155-159 33634982-9 2021 CONCLUSIONS: ATO induced the differentiation of HCC CSCs and potentiated the cytotoxic effects of 5-FU/cisplatin through synergistic inhibition of the LIF/JAK1/STAT3 and NF-kB signaling pathways. Fluorouracil 98-102 signal transducer and activator of transcription 3 Homo sapiens 160-165 33253919-2 2021 In some cases, however, some are stakeholders of the efficiency of the treatment and this combinatorial strategy is exploited by some drug associations, including levodopa (L-Dopa) and dopadecarboxylase inhibitors, beta-lactam antibiotics and clavulanic acid, 5-fluorouracil (5-FU) and folinic acid, and penicillin and probenecid. Fluorouracil 276-280 dopa decarboxylase Homo sapiens 185-202 33486902-12 2021 Signal transduction pathway analysis showed that after Bel-7402 cells acquired resistance to 5-Fu, CCND1, MCM2, and MCM3 gene expression was upregulated in the G1 to S cell cycle control signal transduction pathway, CDKN1C and CCNG2 gene expression was downregulated, and MCM2 and MCM3 gene expression was upregulated in the DNA replication signal transduction pathway. Fluorouracil 93-97 cyclin dependent kinase inhibitor 1C Homo sapiens 216-222 33129844-9 2021 The combination of 5-fluorouracil and oxaliplatin reduced MDSCs, increased numbers of intra-tumor CD8+ T cells, and increased the response of tumors to anti-PD1-however, this resulted in increased tumor expression of PDL1. Fluorouracil 19-33 programmed cell death 1 Mus musculus 157-160 33129844-9 2021 The combination of 5-fluorouracil and oxaliplatin reduced MDSCs, increased numbers of intra-tumor CD8+ T cells, and increased the response of tumors to anti-PD1-however, this resulted in increased tumor expression of PDL1. Fluorouracil 19-33 CD274 antigen Mus musculus 217-221 33129844-12 2021 CONCLUSIONS: In mouse models of gastric cancer, 5-fluorouracil and oxaliplatin reduce numbers of MDSCs to increase the effects of anti-PD1, which promotes tumor infiltration by CD8+ T cells. Fluorouracil 48-62 programmed cell death 1 Mus musculus 135-138 33416156-0 2021 Novel quinazolinone MJ-33 induces AKT/mTOR-mediated autophagy-associated apoptosis in 5FU-resistant colorectal cancer cells. Fluorouracil 86-89 AKT serine/threonine kinase 1 Homo sapiens 34-37 33321462-6 2021 The PFS benefit of 5-FU/LV added to panitumumab maintenance, reported in the study, was independent from ETS and DoR status (interaction tests NS for both PFS and OS). Fluorouracil 19-23 Moloney sarcoma oncogene Mus musculus 163-165 33645034-0 2021 [Curcumin mediates IL-6/STAT3 signaling pathway to repair intestinal mucosal injury induced by 5-FU chemotherapy for colon cancer]. Fluorouracil 95-99 interleukin 6 Rattus norvegicus 19-23 33323971-4 2021 Here, we investigate A3B expression upon treatment with chemotherapeutic drugs that activate p53, including 5-fluorouracil, etoposide and cisplatin. Fluorouracil 108-122 apolipoprotein B mRNA editing enzyme catalytic subunit 3B Homo sapiens 21-24 33645034-1 2021 This study aims to investigate the potential mechanism of curcumin in mediating interleukin-6(IL-6)/signal transducer and activator of transcription 3(STAT3) signaling pathway to repair intestinal mucosal injury induced by 5-fluorouracil(5-FU) chemotherapy for colon cancer. Fluorouracil 223-237 interleukin 6 Rattus norvegicus 80-93 33645034-1 2021 This study aims to investigate the potential mechanism of curcumin in mediating interleukin-6(IL-6)/signal transducer and activator of transcription 3(STAT3) signaling pathway to repair intestinal mucosal injury induced by 5-fluorouracil(5-FU) chemotherapy for colon cancer. Fluorouracil 223-237 interleukin 6 Rattus norvegicus 94-98 33645034-1 2021 This study aims to investigate the potential mechanism of curcumin in mediating interleukin-6(IL-6)/signal transducer and activator of transcription 3(STAT3) signaling pathway to repair intestinal mucosal injury induced by 5-fluorouracil(5-FU) chemotherapy for colon cancer. Fluorouracil 238-242 interleukin 6 Rattus norvegicus 80-93 33645034-1 2021 This study aims to investigate the potential mechanism of curcumin in mediating interleukin-6(IL-6)/signal transducer and activator of transcription 3(STAT3) signaling pathway to repair intestinal mucosal injury induced by 5-fluorouracil(5-FU) chemotherapy for colon cancer. Fluorouracil 238-242 interleukin 6 Rattus norvegicus 94-98 33500399-5 2021 Moreover, 4DPG boosts the tumor-suppressor protein, checkpoint kinase 2 (Chk2) via phosphorylation at Thr68 in a dose-dependent manner in 5-FU-R cells. Fluorouracil 138-142 trichoplein keratin filament binding Homo sapiens 26-50 33511942-0 2021 Current Perspectives on the Role of Nrf2 in 5-Fluorouracil Resistance in Colorectal Cancer. Fluorouracil 44-58 NFE2 like bZIP transcription factor 2 Homo sapiens 36-40 33511942-4 2021 Nuclear factor-erythroid 2-related factor 2 (Nrf2), a master regulator of cellular defense against oxidative and electrophilic stresses, is considered a major factor in 5-FU resistance. Fluorouracil 169-173 NFE2 like bZIP transcription factor 2 Homo sapiens 0-43 33511942-4 2021 Nuclear factor-erythroid 2-related factor 2 (Nrf2), a master regulator of cellular defense against oxidative and electrophilic stresses, is considered a major factor in 5-FU resistance. Fluorouracil 169-173 NFE2 like bZIP transcription factor 2 Homo sapiens 45-49 33511942-5 2021 OBJECTIVE: The current study was conducted to discuss the role and mechanisms of Nrf2 in 5-FU resistance and to search for medicines or compounds that can reverse Nrf2-mediated 5-FU resistance. Fluorouracil 89-93 NFE2 like bZIP transcription factor 2 Homo sapiens 81-85 33511942-5 2021 OBJECTIVE: The current study was conducted to discuss the role and mechanisms of Nrf2 in 5-FU resistance and to search for medicines or compounds that can reverse Nrf2-mediated 5-FU resistance. Fluorouracil 177-181 NFE2 like bZIP transcription factor 2 Homo sapiens 163-167 33511942-7 2021 RESULTS: Previous study suggested that overactivation of Nrf2 contributed to 5-FU resistance by regulating many cytoprotective genes. Fluorouracil 77-81 NFE2 like bZIP transcription factor 2 Homo sapiens 57-61 33511942-8 2021 Interestingly, several medicines and compounds can repress 5-FU resistance mediated of Nrf2. Fluorouracil 59-63 NFE2 like bZIP transcription factor 2 Homo sapiens 87-91 33511942-9 2021 CONCLUSION: This review describes the major 5-FU-resistance mechanisms of Nrf2 and summarized the medicines/compounds that can overcome them. Fluorouracil 44-48 NFE2 like bZIP transcription factor 2 Homo sapiens 74-78 33500399-7 2021 Furthermore, immunoprecipitation analysis unveiled that 4DPG prevents complex formation between Vimentin and p53 resulting in the rescue of p53 and its nuclear localization in aggressive 5-FU-R cells. Fluorouracil 187-191 tumor protein p53 Homo sapiens 109-112 33469286-12 2021 In addition, rapamycin liposomes and 5-FU can synergistically improve the efficacy of colorectal cancer via the Akt/mTOR and P53 pathways. Fluorouracil 37-41 thymoma viral proto-oncogene 1 Mus musculus 112-115 33564285-12 2021 Results demonstrated that miR-612 alongside 5-FU has an important role in the inhibition of migration and growth and also apoptosis induction in PANC-1 cells and could be considered as a supporting agent of chemotherapy and a novel therapeutic modality in pancreatic cancer treatment. Fluorouracil 44-48 microRNA 612 Homo sapiens 26-33 33402109-11 2021 Overexpression of miR-383 downregulated Bcl-2, resulting in reduced survival of Fluorouracil-treated GC cells. Fluorouracil 80-92 BCL2 apoptosis regulator Homo sapiens 40-45 33440689-0 2021 Chemosensitization of HT29 and HT29-5FU Cell Lines by a Combination of a Multi-Tyrosine Kinase Inhibitor and 5FU Downregulates ABCC1 and Inhibits PIK3CA in Light of Their Importance in Saudi Colorectal Cancer. Fluorouracil 36-39 ATP binding cassette subfamily C member 1 Homo sapiens 127-132 33440689-0 2021 Chemosensitization of HT29 and HT29-5FU Cell Lines by a Combination of a Multi-Tyrosine Kinase Inhibitor and 5FU Downregulates ABCC1 and Inhibits PIK3CA in Light of Their Importance in Saudi Colorectal Cancer. Fluorouracil 36-39 phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha Homo sapiens 146-152 33440689-0 2021 Chemosensitization of HT29 and HT29-5FU Cell Lines by a Combination of a Multi-Tyrosine Kinase Inhibitor and 5FU Downregulates ABCC1 and Inhibits PIK3CA in Light of Their Importance in Saudi Colorectal Cancer. Fluorouracil 109-112 ATP binding cassette subfamily C member 1 Homo sapiens 127-132 33440689-0 2021 Chemosensitization of HT29 and HT29-5FU Cell Lines by a Combination of a Multi-Tyrosine Kinase Inhibitor and 5FU Downregulates ABCC1 and Inhibits PIK3CA in Light of Their Importance in Saudi Colorectal Cancer. Fluorouracil 109-112 phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha Homo sapiens 146-152 33440689-10 2021 Additionally, HAA2020 with 5FU exerted significant inhibition of ABCC1 in the four CRC cells, and inhibition of PIK3CA/AKT/MAPK7/ERK in HT29 and HT29-5FU cells. Fluorouracil 27-30 ATP binding cassette subfamily C member 1 Homo sapiens 65-70 33440689-10 2021 Additionally, HAA2020 with 5FU exerted significant inhibition of ABCC1 in the four CRC cells, and inhibition of PIK3CA/AKT/MAPK7/ERK in HT29 and HT29-5FU cells. Fluorouracil 27-30 AKT serine/threonine kinase 1 Homo sapiens 119-122 33402109-13 2021 CONCLUSION: MiR-383 reduces survival of Fluorouracil-treated GC cells through downregulating of Bcl-2. Fluorouracil 40-52 BCL2 apoptosis regulator Homo sapiens 96-101 32838723-13 2021 Moreover, western blotting and molecular docking revealed that compounds 3 or 5 might promote 5-FU-induced apoptosis by regulating the expression of Caspase 9 and PARP. Fluorouracil 94-98 poly(ADP-ribose) polymerase 1 Homo sapiens 163-167 33569416-0 2021 Repressing PDCD4 activates JNK/ABCG2 pathway to induce chemoresistance to fluorouracil in colorectal cancer cells. Fluorouracil 74-86 mitogen-activated protein kinase 8 Homo sapiens 27-30 33569416-0 2021 Repressing PDCD4 activates JNK/ABCG2 pathway to induce chemoresistance to fluorouracil in colorectal cancer cells. Fluorouracil 74-86 ATP binding cassette subfamily G member 2 (Junior blood group) Homo sapiens 31-36 33569416-3 2021 Adenosine triphosphate (ATP)-binding cassette sub-family G member 2 (ABCG2) has been found highly expressed in CRC patients with poor responsiveness to folinic acid/5-FU/irinotecan. Fluorouracil 165-169 ATP binding cassette subfamily G member 2 (Junior blood group) Homo sapiens 0-67 33569416-3 2021 Adenosine triphosphate (ATP)-binding cassette sub-family G member 2 (ABCG2) has been found highly expressed in CRC patients with poor responsiveness to folinic acid/5-FU/irinotecan. Fluorouracil 165-169 ATP binding cassette subfamily G member 2 (Junior blood group) Homo sapiens 69-74 33569416-4 2021 However, the mechanisms of 5-FU resistance regulated by ABCG2 in CRC cells remain to be comprehensively understood. Fluorouracil 27-31 ATP binding cassette subfamily G member 2 (Junior blood group) Homo sapiens 56-61 33569416-8 2021 In order to investigate the efficacy of inhibiting the c-Jun NH2 terminal kinase (JNK) pathway to overcome 5-FU resistance, HCT116 and 5-FU-resistant HCT116 cells were inoculated into BALB/c-nu/nu mice to establish the cell-derived xenograft model. Fluorouracil 107-111 mitogen-activated protein kinase 8 Homo sapiens 82-85 33569416-10 2021 Overexpression of ABCG2 decreased sensitivity to 5-FU in HCT116 cells, but knockdown of ABCG2 decreased the survival rate in HCT116/FUR cells. Fluorouracil 49-53 ATP binding cassette subfamily G member 2 (Junior blood group) Homo sapiens 18-23 33569416-13 2021 Moreover, treatment with the JNK pathway inhibitor SP600125 downregulated ABCG2 expression and rescued sensitivity to 5-FU in HCT116/FUR cells. Fluorouracil 118-122 mitogen-activated protein kinase 8 Homo sapiens 29-32 33569416-16 2021 Conclusions: Our results demonstrated that 5-FU treatment upregulated miR-21, which directly repressed PDCD4, and subsequently activated the JNK pathway, leading to the upregulation of ABCG2 in CRC cells. Fluorouracil 43-47 mitogen-activated protein kinase 8 Homo sapiens 141-144 33569416-16 2021 Conclusions: Our results demonstrated that 5-FU treatment upregulated miR-21, which directly repressed PDCD4, and subsequently activated the JNK pathway, leading to the upregulation of ABCG2 in CRC cells. Fluorouracil 43-47 ATP binding cassette subfamily G member 2 (Junior blood group) Homo sapiens 185-190 33569416-17 2021 Inhibition of the JNK pathway overcame acquired 5-FU resistance both in vivo and in vitro. Fluorouracil 48-52 mitogen-activated protein kinase 8 Homo sapiens 18-21 33386794-9 2021 Nevertheless, miR-137 mimic attenuated the facilitating effect of pcDNA3.1-XIST on proliferation, migration, invasion, 5-FU/cisplatin-resistance and glycolysis of CRC cells (P< 0.05). Fluorouracil 119-123 microRNA 137 Homo sapiens 14-21 33240430-9 2021 5-FU induced apoptosis through p53-p21 activity, while chrysin arrested the cell cycle in the G2/M phase. Fluorouracil 0-4 tumor protein p53 Homo sapiens 31-34 31846964-0 2021 NOD-Like Receptor Family Pyrin Domain-Containing 3 Inflammasome Activation Exacerbates 5-Fluorouracil-Induced Small Intestinal Mucositis via Interleukin-1beta Activation. Fluorouracil 87-101 interleukin 1 beta Mus musculus 141-158 31846964-13 2021 CONCLUSIONS: NLRP3 inflammasome activation may exacerbate 5-FU-induced small intestinal mucositis via IL-1beta maturation. Fluorouracil 58-62 interleukin 1 beta Mus musculus 102-110 33240411-0 2021 Overexpression of microRNA-124-5p sensitizes non-small cell lung cancer cells to treatment with 5-fluorouracil via AEG-1 regulation. Fluorouracil 96-110 metadherin Homo sapiens 115-120 33240411-7 2021 Furthermore, AEG-1 was predicted as a target gene of miR-124-5p, and its expression was increased in A549/5-FU cells compared with A549 cells. Fluorouracil 106-110 metadherin Homo sapiens 13-18 33240411-8 2021 Additionally, the upregulation of miR-124-5p was associated with lower expression levels of AEG-1 in A549/5-FU cells, compared with parental A549 cells. Fluorouracil 106-110 metadherin Homo sapiens 92-97 33220257-7 2021 Finally, NMIIA protects CRC cells from 5-FU-induced apoptosis and proliferation inhibition through the AMPK/mTOR pathway. Fluorouracil 39-43 mechanistic target of rapamycin kinase Homo sapiens 108-112 33325631-0 2021 Overexpression of sortilin is associated with 5-FU resistance and poor prognosis in colorectal cancer. Fluorouracil 46-50 sortilin 1 Homo sapiens 18-26 33325631-4 2021 Sortilin, a vacuolar protein sorting 10 protein (Vps10p), implicated in protein trafficking, is over expressed in CRC cell lines cultured 72 hours in presence of 5-FU. Fluorouracil 162-166 sortilin 1 Homo sapiens 0-8 33240411-10 2021 Notably, the overexpression of AEG-1 reversed the ability of the miR-124-5p mimic to increase the sensitivity of A549/5-FU cells to 5-FU treatment. Fluorouracil 118-122 metadherin Homo sapiens 31-36 33408498-1 2020 Aim: The change in the levels of peripheral inflammatory markers together with EGFR in relation to 5- fluorouracil (5-FU) therapy was evaluated for their prognostic significance in colorectal cancer (CRC) patients. Fluorouracil 99-114 epidermal growth factor receptor Homo sapiens 79-83 33240411-10 2021 Notably, the overexpression of AEG-1 reversed the ability of the miR-124-5p mimic to increase the sensitivity of A549/5-FU cells to 5-FU treatment. Fluorouracil 132-136 metadherin Homo sapiens 31-36 33408498-6 2020 DFS and OS rates were reduced in patients with increased COX2, IL6, IL10, and TNFalpha expression with 5-FU therapy. Fluorouracil 103-107 tumor necrosis factor Homo sapiens 78-86 33408498-7 2020 Significant hazard of disease progression was associated with smoking (HR=1.27, P=0.004), 5-FU induction of COX2, and IL6 expression (HR=1.35, P=0.001 and HR=1.27, P=0.004, respectively). Fluorouracil 90-94 mitochondrially encoded cytochrome c oxidase II Homo sapiens 108-112 33730739-10 2021 RESULTS: TNFalpha affected viability of SCC-13 and HaCaT cells in combination with 5FU or TRAIL. Fluorouracil 83-86 tumor necrosis factor Homo sapiens 9-17 33730739-13 2021 In clear contrast, TNFalpha protected PNHK against TRAIL- and 5FU-induced apoptosis. Fluorouracil 62-65 tumor necrosis factor Homo sapiens 19-27 33091827-3 2021 Therefore, we identified the expression of eight genes closely associated with platinum and fluorouracil metabolism (RRM1, RRM2, RRM2B, POLH, DUT, TYMS, TYMP, MKI67) in the discovery cohort (N=291). Fluorouracil 92-104 marker of proliferation Ki-67 Homo sapiens 159-164 33414645-9 2020 Additionally, the increased ATG12 expression was more likely to get a satisfactory OS in patients who underwent surgery alone but was associated with poor OS for patients treated with 5-FU adjuvant. Fluorouracil 184-188 autophagy related 12 Homo sapiens 28-33 33408498-8 2020 Moreover, smoking, 5-FU induction of IL6, TNFalpha, and IL10 expression are found to be independent prognostic factors for OS (P=0.003, 0.003, 0.002, and 0.002, respectively). Fluorouracil 19-23 interleukin 6 Homo sapiens 37-40 33408498-1 2020 Aim: The change in the levels of peripheral inflammatory markers together with EGFR in relation to 5- fluorouracil (5-FU) therapy was evaluated for their prognostic significance in colorectal cancer (CRC) patients. Fluorouracil 116-120 epidermal growth factor receptor Homo sapiens 79-83 33408498-6 2020 DFS and OS rates were reduced in patients with increased COX2, IL6, IL10, and TNFalpha expression with 5-FU therapy. Fluorouracil 103-107 mitochondrially encoded cytochrome c oxidase II Homo sapiens 57-61 33408498-6 2020 DFS and OS rates were reduced in patients with increased COX2, IL6, IL10, and TNFalpha expression with 5-FU therapy. Fluorouracil 103-107 interleukin 6 Homo sapiens 63-66 33349222-11 2021 The optimized formulation (5-FU-PLGA-PEG-NP) was lyophilized using 4% trehalose (cryoprotectants) & conjugated with Anti-EGFR mAb on its surface to produce Anti-EGFR-5-FU-PLGA-PEG-NP; the final formulation, which increases target specificity and drug delivery system of nanoparticles. Fluorouracil 27-31 epidermal growth factor receptor Homo sapiens 121-125 33389946-0 2020 Combined Effects of Protocatechuic Acid and 5-Fluorouracil on p53 Gene Expression and Apoptosis in Gastric Adenocarcinoma Cells. Fluorouracil 44-58 tumor protein p53 Homo sapiens 62-65 33389946-4 2020 Moreover, the combined 5-FU/PCA exposure led to upregulation of p53 and downregulation of Bcl-2 protein when compared to the untreated control cells. Fluorouracil 23-27 tumor protein p53 Homo sapiens 64-67 33389946-4 2020 Moreover, the combined 5-FU/PCA exposure led to upregulation of p53 and downregulation of Bcl-2 protein when compared to the untreated control cells. Fluorouracil 23-27 BCL2 apoptosis regulator Homo sapiens 90-95 33389946-6 2020 The mechanisms by which the combined 5-FU/PCA exposure exerts its effects are associated with upregulation of p53 gene expression and downregulation of Bcl-2 level. Fluorouracil 37-41 tumor protein p53 Homo sapiens 110-113 33389946-6 2020 The mechanisms by which the combined 5-FU/PCA exposure exerts its effects are associated with upregulation of p53 gene expression and downregulation of Bcl-2 level. Fluorouracil 37-41 BCL2 apoptosis regulator Homo sapiens 152-157 33389946-7 2020 Therefore, the combination of 5-FU with PCA not only could be a promising approach to potentially reduce the dose requirements of 5-FU but also could promote apoptosis via p53 and Bcl-2 signaling pathways. Fluorouracil 30-34 tumor protein p53 Homo sapiens 172-175 33389946-7 2020 Therefore, the combination of 5-FU with PCA not only could be a promising approach to potentially reduce the dose requirements of 5-FU but also could promote apoptosis via p53 and Bcl-2 signaling pathways. Fluorouracil 30-34 BCL2 apoptosis regulator Homo sapiens 180-185 33564297-3 2020 Here, we report a case of AFP-producing lung HAC with brain metastasis with long-term disease control, treated with the 5-fluorouracil-derived regimen S-1. Fluorouracil 120-134 alpha fetoprotein Homo sapiens 26-29 33349222-15 2021 Therefore, Anti-EGFR-5-FU-PLGA-PEG-NP holds excellent potential for drug delivery to EGFR positive colorectal cancer cells. Fluorouracil 21-25 epidermal growth factor receptor Homo sapiens 16-20 32987067-3 2020 To meet this demand, 5-fluorouracil-chitosan-carbon quantum dot-aptamer (5-FU-CS-CQD-Apt) nanoparticle was successfully synthesized for specific targeted delivery of 5-FU anti-cancer drug used in breast cancer treatment and this was done by following facile water-in-oil (W/O) emulsification method. Fluorouracil 73-77 LYPLA2 pseudogene 1 Homo sapiens 85-88 32987067-3 2020 To meet this demand, 5-fluorouracil-chitosan-carbon quantum dot-aptamer (5-FU-CS-CQD-Apt) nanoparticle was successfully synthesized for specific targeted delivery of 5-FU anti-cancer drug used in breast cancer treatment and this was done by following facile water-in-oil (W/O) emulsification method. Fluorouracil 166-170 LYPLA2 pseudogene 1 Homo sapiens 85-88 33311453-0 2020 Inhibition of EZH2 enhances the therapeutic effect of 5-FU via PUMA upregulation in colorectal cancer. Fluorouracil 54-58 enhancer of zeste 2 polycomb repressive complex 2 subunit Homo sapiens 14-18 33335403-6 2020 The expression of some apoptotic and autophagy-related genes such as Bax, Bcl2, Beclin1 and ATG7 was significantly induced by carbon-ion beam irradiation alone and was further enhanced when the beam was combined with 5-FU. Fluorouracil 217-221 BCL2 associated X, apoptosis regulator Homo sapiens 69-72 33335403-6 2020 The expression of some apoptotic and autophagy-related genes such as Bax, Bcl2, Beclin1 and ATG7 was significantly induced by carbon-ion beam irradiation alone and was further enhanced when the beam was combined with 5-FU. Fluorouracil 217-221 BCL2 apoptosis regulator Homo sapiens 74-78 33364975-13 2020 Interestingly, 5FU reduced bone marrow CD45+ immune cells and CD45+CD11b+ monocytes. Fluorouracil 15-18 integrin alpha M Mus musculus 67-72 32727638-0 2020 Pyrotinib Sensitizes 5-Fluorouracil-resistant HER2+ Breast 4 Cancer Cells to 5-Fluorouracil. Fluorouracil 21-35 erb-b2 receptor tyrosine kinase 2 Homo sapiens 46-50 32727638-0 2020 Pyrotinib Sensitizes 5-Fluorouracil-resistant HER2+ Breast 4 Cancer Cells to 5-Fluorouracil. Fluorouracil 77-91 erb-b2 receptor tyrosine kinase 2 Homo sapiens 46-50 32790589-10 2020 CONCLUSION: In radically operated stage II to IV CRC patients who received adjuvant 5-FU-based chemotherapy, a postoperatively elevated CEA alone or in combination with CA19-9, YKL-40, CRP, or IL-6, or a normal CEA combined with an elevated YKL-40 or with an elevated CRP, may indicate patients at high risk of relapse. Fluorouracil 84-88 CEA cell adhesion molecule 3 Homo sapiens 136-139 33287255-1 2020 In this work, the nuclear magnetic resonance (NMR) and IR spectroscopic markers of the complexation between 5-fluorouracil (5-FU) and beta-cyclodextrin (beta-CD) in solid state and in aqueous solution are investigated. Fluorouracil 108-122 ACD shelterin complex subunit and telomerase recruitment factor Homo sapiens 153-160 33287255-1 2020 In this work, the nuclear magnetic resonance (NMR) and IR spectroscopic markers of the complexation between 5-fluorouracil (5-FU) and beta-cyclodextrin (beta-CD) in solid state and in aqueous solution are investigated. Fluorouracil 124-128 ACD shelterin complex subunit and telomerase recruitment factor Homo sapiens 153-160 33287255-2 2020 In the attenuated total reflectance(ATR) spectra of 5-FU/beta-CD products obtained by physical mixing, kneading and co-precipitation, we have identified the two most promising marker bands that could be used to detect complex formations: the C=O and C-F stretching bands of 5-FU that experience a blue shift by ca. Fluorouracil 52-56 ATR serine/threonine kinase Homo sapiens 36-39 33287255-2 2020 In the attenuated total reflectance(ATR) spectra of 5-FU/beta-CD products obtained by physical mixing, kneading and co-precipitation, we have identified the two most promising marker bands that could be used to detect complex formations: the C=O and C-F stretching bands of 5-FU that experience a blue shift by ca. Fluorouracil 274-278 ATR serine/threonine kinase Homo sapiens 36-39 33287255-2 2020 In the attenuated total reflectance(ATR) spectra of 5-FU/beta-CD products obtained by physical mixing, kneading and co-precipitation, we have identified the two most promising marker bands that could be used to detect complex formations: the C=O and C-F stretching bands of 5-FU that experience a blue shift by ca. Fluorouracil 274-278 ACD shelterin complex subunit and telomerase recruitment factor Homo sapiens 57-64 33287255-6 2020 The analysis has revealed that, at each moment, ~60% of 5-FU molecules form a complex with beta-CD and its lifetime is ca. Fluorouracil 56-60 ACD shelterin complex subunit and telomerase recruitment factor Homo sapiens 91-98 32866313-0 2020 Phase II study of de-intensified intensity-modulated radiotherapy and concurrent carboplatin/5-fluorouracil in lateralized p16-associated oropharyngeal carcinoma. Fluorouracil 93-107 cyclin dependent kinase inhibitor 2A Homo sapiens 123-126 32250192-10 2020 Targeting miR-195-5P reduced the sensitivity of MGC-803 cells to 5-FU, and miR-195-5P overexpression enhanced the sensitivity of MGC-803/5-FU cells to 5-FU. Fluorouracil 65-69 microRNA 195 Homo sapiens 10-17 32250192-10 2020 Targeting miR-195-5P reduced the sensitivity of MGC-803 cells to 5-FU, and miR-195-5P overexpression enhanced the sensitivity of MGC-803/5-FU cells to 5-FU. Fluorouracil 137-141 microRNA 195 Homo sapiens 75-82 33164645-0 2020 Matrine Inhibitory Effect on Self-renewal and Re-sensitization of 5-FU Resistant NSCLC Stem Cells were through Let-7b dependent Downregulation of CCND1. Fluorouracil 66-70 microRNA let7b Mus musculus 111-117 32377978-1 2020 5-fluorouracil (5-FU) and 5-FU derivatives, such as capecitabine, UFT, and S-1, are the mainstay of chemotherapy treatment for gastrointestinal cancers, and other solid tumors. Fluorouracil 0-14 proteasome 26S subunit, non-ATPase 1 Homo sapiens 75-78 32377978-1 2020 5-fluorouracil (5-FU) and 5-FU derivatives, such as capecitabine, UFT, and S-1, are the mainstay of chemotherapy treatment for gastrointestinal cancers, and other solid tumors. Fluorouracil 26-30 proteasome 26S subunit, non-ATPase 1 Homo sapiens 75-78 33257690-12 2020 Collectively, our study demonstrates that IAP inhibition is a promising modulator of response to oxaliplatin/5-FU in colorectal cancers of the CMS1 subtype, and may show promise as in the CMS2 subtype, suggesting that molecular subtyping may aid as a patient stratification tool for IAP antagonists in this disease. Fluorouracil 109-113 alkaline phosphatase, intestinal Homo sapiens 42-45 31897925-10 2020 Neoadjuvant chemotherapy with cisplatin, 5-fluorouracil and leucovorin may offer high response rates and long-term control in a subgroup of patients affected by intestinal-type adenocarcinoma, and in particular in those whose tumors harbor a functional p53 protein. Fluorouracil 41-55 tumor protein p53 Homo sapiens 253-256 33011221-0 2020 Diltiazem potentiates the cytotoxicity of gemcitabine and 5-fluorouracil in PANC-1 human pancreatic cancer cells through inhibition of P-glycoprotein. Fluorouracil 58-72 ATP binding cassette subfamily B member 1 Homo sapiens 135-149 33011221-2 2020 P-glycoprotein (P-gp) plays a pivotal role in PC response to gemcitabine and 5-fluorouracil (5-FU). Fluorouracil 77-91 ATP binding cassette subfamily B member 1 Homo sapiens 0-14 33011221-2 2020 P-glycoprotein (P-gp) plays a pivotal role in PC response to gemcitabine and 5-fluorouracil (5-FU). Fluorouracil 77-91 ATP binding cassette subfamily B member 1 Homo sapiens 16-20 33011221-2 2020 P-glycoprotein (P-gp) plays a pivotal role in PC response to gemcitabine and 5-fluorouracil (5-FU). Fluorouracil 93-97 ATP binding cassette subfamily B member 1 Homo sapiens 0-14 33011221-2 2020 P-glycoprotein (P-gp) plays a pivotal role in PC response to gemcitabine and 5-fluorouracil (5-FU). Fluorouracil 93-97 ATP binding cassette subfamily B member 1 Homo sapiens 16-20 33011221-4 2020 In the current study, we investigated the hypothesis that targeting of P-gp by diltiazem can enhance the cytotoxicity of gemcitabine and 5-FU against human pancreatic cancer cells. Fluorouracil 137-141 ATP binding cassette subfamily B member 1 Homo sapiens 71-75 32989391-10 2020 Furthermore, the knockdown of TC2N improved the sensitivity of AGS cells to cisplatin, paclitaxel and 5-fluorouracil, and downregulated the protein expression levels of P-gp. Fluorouracil 102-116 tandem C2 domains, nuclear Homo sapiens 30-34 33035787-5 2020 After stratifying by treatment, in the 5-Fluorouracil group, the DPYD rs17376848 AG genotype was associated with hematological toxicity (OR = 2.76; p = 0.003), ABCB1 rs1045642 T-allele with the need of treatment adjustment due to toxicity (OR = 3.06; p = 0.01), and rs1045642 CC genotype with gastrointestinal toxicity (OR = 5.80; p = 0.03). Fluorouracil 39-53 ATP binding cassette subfamily B member 1 Homo sapiens 160-165 33035787-8 2020 ABCB1 rs1045642 T-allele reduces the need for treatment modification with both 5FU and oxaliplatin. Fluorouracil 79-82 ATP binding cassette subfamily B member 1 Homo sapiens 0-5 33299895-0 2020 M2 Macrophages Mediate the Resistance of Gastric Adenocarcinoma Cells to 5-Fluorouracil through the Expression of Integrin beta3, Focal Adhesion Kinase, and Cofilin. Fluorouracil 73-87 integrin subunit beta 3 Homo sapiens 114-128 33299895-8 2020 These results reveal that integrin beta3, focal adhesion protein (FAK), and cofilin proteins are potential targets for the improvement of fluorouracil efficacy in gastric cancer treatment. Fluorouracil 138-150 integrin subunit beta 3 Homo sapiens 26-40 33312758-5 2020 We manifested that intratumoral CD103+CD4+ T cells in gastric cancer predicted poor overall survival and inferior responsiveness to fluorouracil-based ACT. Fluorouracil 132-144 CD4 molecule Homo sapiens 38-41 33312758-8 2020 Overall, this study revealed that intratumoral CD103+CD4+T cell infiltration defined immunoevasive contexture and predicted poor prognosis and inferior responsiveness to fluorouracil-based ACT. Fluorouracil 170-182 CD4 molecule Homo sapiens 53-56 32977944-7 2020 Generally speaking, our results indicated that miR-149 contributes to resistance of 5-FU in gastric cancer via targeting TREM2 and regulating beta-catenin pathway. Fluorouracil 84-88 triggering receptor expressed on myeloid cells 2 Homo sapiens 121-126 32961298-3 2020 In this study, we used a competitive transplantation mouse model to investigate how treatment with common preconditioning agents 5-fluorouracil (5-FU) or busulfan (BU) affects the prevalence of Dnmt3a -/- HSCs and progenitor cells in competition with WT cells. Fluorouracil 129-143 DNA methyltransferase 3A Mus musculus 194-200 32961298-3 2020 In this study, we used a competitive transplantation mouse model to investigate how treatment with common preconditioning agents 5-fluorouracil (5-FU) or busulfan (BU) affects the prevalence of Dnmt3a -/- HSCs and progenitor cells in competition with WT cells. Fluorouracil 145-149 DNA methyltransferase 3A Mus musculus 194-200 33256074-7 2020 Inhibition of TS alone or double inhibition of TS and TK1 using the siRNA technique increased susceptibility to 5-FU in IFIT2-knockdown cells. Fluorouracil 112-116 thymidine kinase 1 Homo sapiens 54-57 33205649-8 2020 Remarkably, the combination of CE and 5-FU treatment attenuated beta-catenin, MDR1, and ABCC1 expressions, while TFAP4 overexpression reversed their expressions by 2.68 +- 0.46-, 0.72 +- 0.44-, and 0.93 +- 0.21-fold, respectively. Fluorouracil 38-42 ATP binding cassette subfamily B member 1 Homo sapiens 78-82 33205649-8 2020 Remarkably, the combination of CE and 5-FU treatment attenuated beta-catenin, MDR1, and ABCC1 expressions, while TFAP4 overexpression reversed their expressions by 2.68 +- 0.46-, 0.72 +- 0.44-, and 0.93 +- 0.21-fold, respectively. Fluorouracil 38-42 ATP binding cassette subfamily C member 1 Homo sapiens 88-93 32561283-6 2020 Further mechanistic studies indicated that the 5-Fu + SATP group showed a decrease in hepatotoxicity caused by 5-Fu via a reduction in the levels of interleukin-1beta (IL-1beta), an increase in the expression of Bcl-2 and decreases in the expression of p-p38, p-JNK and Bax. Fluorouracil 47-51 interleukin 1 beta Mus musculus 149-166 32561283-6 2020 Further mechanistic studies indicated that the 5-Fu + SATP group showed a decrease in hepatotoxicity caused by 5-Fu via a reduction in the levels of interleukin-1beta (IL-1beta), an increase in the expression of Bcl-2 and decreases in the expression of p-p38, p-JNK and Bax. Fluorouracil 47-51 B cell leukemia/lymphoma 2 Mus musculus 212-217 32561283-6 2020 Further mechanistic studies indicated that the 5-Fu + SATP group showed a decrease in hepatotoxicity caused by 5-Fu via a reduction in the levels of interleukin-1beta (IL-1beta), an increase in the expression of Bcl-2 and decreases in the expression of p-p38, p-JNK and Bax. Fluorouracil 111-115 interleukin 1 beta Mus musculus 149-166 32977944-0 2020 miR-149 contributes to resistance of 5-FU in gastric cancer via targeting TREM2 and regulating beta-catenin pathway. Fluorouracil 37-41 triggering receptor expressed on myeloid cells 2 Homo sapiens 74-79 32977944-5 2020 Further experiments indicated that overexpression of miR-149 can alleviate 5-FU-induced apoptosis and proliferation inhibition by targeting TREM2. Fluorouracil 75-79 triggering receptor expressed on myeloid cells 2 Homo sapiens 140-145 32977944-6 2020 It was also confirmed that TREM2 regulated 5-FU resistance through beta-catenin pathway. Fluorouracil 43-47 triggering receptor expressed on myeloid cells 2 Homo sapiens 27-32 32907836-0 2020 5-Fluorouracil Enhances the Antitumor Activity of the Glutaminase Inhibitor CB-839 against PIK3CA-Mutant Colorectal Cancers. Fluorouracil 0-14 phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha Homo sapiens 91-97 32907836-4 2020 Moreover, the combination of CB-839 and 5-fluorouracil (5-FU) induces PIK3CA-mutant tumor regression in xenograft models. Fluorouracil 40-54 phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha Homo sapiens 70-76 32907836-4 2020 Moreover, the combination of CB-839 and 5-fluorouracil (5-FU) induces PIK3CA-mutant tumor regression in xenograft models. Fluorouracil 56-60 phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha Homo sapiens 70-76 33138139-7 2020 MSN-NH2 showed a relatively high loading capacity of 5-FU (12.6 +- 5.5) and DEX (44.72 +- 4.21) when using drug: MSN-NH2 ratios of 5:1 for both drugs. Fluorouracil 53-57 moesin Homo sapiens 0-3 32700606-4 2020 RESULTS: OMVs-MSN-5-FU with -18.22 +- 0.17mV zeta potential and 90.4 +- 9.1nm size were used for oral treatment of colon cancer. Fluorouracil 18-22 moesin Homo sapiens 14-17 32700606-8 2020 In vivo experiments results confirmed that OMVs-MSN-5-FU could be taken up by colon cancer cells. Fluorouracil 52-56 moesin Homo sapiens 48-51 32901850-5 2020 Specifically, the effects of exosomes derived from THP-1 cells and primary human macrophages (PHM) were assessed on the chemosensitivity of OSC-4 cells treated with 5-fluorouracil (5-FU) and cis-diamminedichloroplatinum (CDDP). Fluorouracil 165-179 GLI family zinc finger 2 Homo sapiens 51-56 32901850-6 2020 The THP-1- and PHM-derived exosomes promoted dose-dependent proliferation, decreased the proliferative inhibitory effects of 5-FU and CDDP and decreased apoptosis in OSC-4 cells through activation of the AKT/glycogen synthase kinase-3beta signaling pathway. Fluorouracil 125-129 GLI family zinc finger 2 Homo sapiens 4-9 33138139-7 2020 MSN-NH2 showed a relatively high loading capacity of 5-FU (12.6 +- 5.5) and DEX (44.72 +- 4.21) when using drug: MSN-NH2 ratios of 5:1 for both drugs. Fluorouracil 53-57 moesin Homo sapiens 113-116 33138139-9 2020 The skin permeability study revealed that enhancement ratio of 5-Fu and DEX using MSN-NH2 were 4.67 and 5.68, respectively, relative to their free drugs counterparts. Fluorouracil 63-67 moesin Homo sapiens 82-85 33138139-10 2020 In addition, the accumulation of drugs in skin layers where melanoma cells usually reside were enhanced approximately 10 times with 5-FU and 5 times with DEX when delivering drugs using MSN-NH2 compared to control. Fluorouracil 132-136 moesin Homo sapiens 186-189 33138139-12 2020 The combination of 5-FU MSN-NH2 and DEX MSN-NH2 showed significant increase in toxicity compared to their free dug counterparts and exhibited a synergetic effect as well as the ability to circumvent DEX induced 5-FU resistance in melanoma cells. Fluorouracil 19-23 moesin Homo sapiens 24-27 33138139-12 2020 The combination of 5-FU MSN-NH2 and DEX MSN-NH2 showed significant increase in toxicity compared to their free dug counterparts and exhibited a synergetic effect as well as the ability to circumvent DEX induced 5-FU resistance in melanoma cells. Fluorouracil 211-215 moesin Homo sapiens 24-27 33138139-12 2020 The combination of 5-FU MSN-NH2 and DEX MSN-NH2 showed significant increase in toxicity compared to their free dug counterparts and exhibited a synergetic effect as well as the ability to circumvent DEX induced 5-FU resistance in melanoma cells. Fluorouracil 211-215 moesin Homo sapiens 40-43 33117809-10 2020 Furthermore, STK35 overexpression could promote glycolysis, suppress apoptosis, upregulate p-AKT, and counteract the antitumor functions of 5-FU and neural precursor cell expressed developmentally downregulated gene 4-like (NEDD4L) in CRC cells. Fluorouracil 140-144 serine/threonine kinase 35 Homo sapiens 13-18 33087710-0 2020 5-FU promotes stemness of colorectal cancer via p53-mediated WNT/beta-catenin pathway activation. Fluorouracil 0-4 tumor protein p53 Homo sapiens 48-51 33087710-6 2020 These findings indicate p53 as a critical mediator of 5-FU-induced CSC activation via the WNT/beta-catenin signaling pathway and highlight the significance of combinatorial treatment of WNT inhibitor and 5-FU as a compelling therapeutic strategy to improve the poor outcomes of current 5-FU-based therapies for CRC patients. Fluorouracil 54-58 tumor protein p53 Homo sapiens 24-27 33087710-6 2020 These findings indicate p53 as a critical mediator of 5-FU-induced CSC activation via the WNT/beta-catenin signaling pathway and highlight the significance of combinatorial treatment of WNT inhibitor and 5-FU as a compelling therapeutic strategy to improve the poor outcomes of current 5-FU-based therapies for CRC patients. Fluorouracil 204-208 tumor protein p53 Homo sapiens 24-27 33087710-6 2020 These findings indicate p53 as a critical mediator of 5-FU-induced CSC activation via the WNT/beta-catenin signaling pathway and highlight the significance of combinatorial treatment of WNT inhibitor and 5-FU as a compelling therapeutic strategy to improve the poor outcomes of current 5-FU-based therapies for CRC patients. Fluorouracil 204-208 tumor protein p53 Homo sapiens 24-27 32483624-3 2020 Deletion of Yap1 and Taz induces a loss of HSC quiescence, symmetric self-renewal ability and renders HSC more vulnerable to serial myeloablative 5-fluorouracil treatment. Fluorouracil 146-160 tafazzin, phospholipid-lysophospholipid transacylase Homo sapiens 21-24 31983282-7 2020 Taken together, our data suggest that PRKDC-mediated phosphorylation of PRKAG1 primes AMPK complex to the lysosomal activation by STK11 in cancer cells thereby linking DNA damage response to autophagy and cellular metabolism.Abbreviations: AXIN1: axin 1; 3-MA: 3-methyladenine; 5-FU: 5-fluorouracil; AA mutant: double alanine mutant (S192A, T284A) of PRKAG1; ACACA: acetyl-CoA carboxylase alpha; AICAR: 5-Aminoimidazole-4-carboxamide ribonucleotide; AMPK: AMP-activated protein kinase; ATG: autophagy-related; ATM: ataxia telangiectasia mutated; ATR: ATM serine/threonine kinase; AV: autophagic vacuole; AVd: degradative autophagic vacuole; AVi: initial autophagic vacuole; BECN1: beclin 1; BSA: bovine serum albumin; CBS: cystathionine beta-synthase; CDK7: cyclin dependent kinase 7; CDKN1A: cyclin dependent kinase inhibitor 1A; EGFP: enhanced green fluorescent protein; GAPDH: glyceraldehyde-3-phosphate dehydrogenase; GST: glutathione S transferase; H2AX/H2AFX: H2A.X variant histone; HBSS: Hanks balanced salt solution; IP: immunopurification; IR: ionizing radiation; MAP1LC3/LC3: microtubule associated protein 1 light chain 3; MAP3K9: mitogen-activated protein kinase kinase kinase 9; mRFP: monomeric red fluorescent protein; mCh: mCherry; MCM7: minichromosome maintenance complex component 7; MTORC1: mechanistic target of rapamycin kinase complex 1; NHEJ: non-homologous end joining; NRBP2: nuclear receptor binding protein 2; NTC: non-targeting control; NUAK1: NUAK family kinase 1; PBS: phosphate-buffered saline; PIK3AP1: phosphoinositide-3-kinase adaptor protein 1; PIK3CA: phosphatidylinositol-4,5-biphosphate 3-kinase catalytic subunit alpha; PIKK: phosphatidylinositol 3-kinase-related kinase; PRKAA: protein kinase AMP-activated catalytic subunit alpha; PRKAB: protein kinase AMP-activated non-catalytic subunit beta; PRKAG: protein kinase AMP-activated non-catalytic subunit gamma; PRKDC: protein kinase, DNA-activated, catalytic subunit; RLuc: Renilla luciferase; RPS6KB1: ribosomal protein S6 kinase B1; SQSTM1: sequestosome 1; STK11/LKB1: serine/threonine kinase 11; TP53: tumor protein p53; TSKS: testis specific serine kinase substrate; ULK1: unc-51 like autophagy activating kinase 1; WIPI2: WD repeat domain, phosphoinositide interacting 2; WT: wild type. Fluorouracil 284-298 protein kinase, DNA-activated, catalytic subunit Homo sapiens 38-43 33082817-0 2020 Feng-Liao-Chang-Wei-Kang Combined with 5-Fluorouracil Synergistically Suppresses Colitis-Associated Colorectal Cancer via the IL-6/STAT3 Signalling Pathway. Fluorouracil 39-53 interleukin 6 Homo sapiens 126-130 33082817-0 2020 Feng-Liao-Chang-Wei-Kang Combined with 5-Fluorouracil Synergistically Suppresses Colitis-Associated Colorectal Cancer via the IL-6/STAT3 Signalling Pathway. Fluorouracil 39-53 signal transducer and activator of transcription 3 Homo sapiens 131-136 33082817-11 2020 Results: FLCWK enhanced the ability of 5-FU to promote apoptosis by inhibiting the proliferation of HCT116 cells and blocking the IL-6/STAT3 pathway. Fluorouracil 39-43 interleukin 6 Homo sapiens 130-134 33082817-11 2020 Results: FLCWK enhanced the ability of 5-FU to promote apoptosis by inhibiting the proliferation of HCT116 cells and blocking the IL-6/STAT3 pathway. Fluorouracil 39-43 signal transducer and activator of transcription 3 Homo sapiens 135-140 33082817-13 2020 In the CAC model, FLCWK synergized with 5-FU to inhibit the phosphorylation of STAT3, preventing IL-6/STAT3 signal transduction and thus further inducing apoptosis and inhibition of colon cancer cell proliferation. Fluorouracil 40-44 signal transducer and activator of transcription 3 Mus musculus 79-84 33082817-13 2020 In the CAC model, FLCWK synergized with 5-FU to inhibit the phosphorylation of STAT3, preventing IL-6/STAT3 signal transduction and thus further inducing apoptosis and inhibition of colon cancer cell proliferation. Fluorouracil 40-44 interleukin 6 Mus musculus 97-101 33082817-13 2020 In the CAC model, FLCWK synergized with 5-FU to inhibit the phosphorylation of STAT3, preventing IL-6/STAT3 signal transduction and thus further inducing apoptosis and inhibition of colon cancer cell proliferation. Fluorouracil 40-44 signal transducer and activator of transcription 3 Mus musculus 102-107 33082817-14 2020 Conclusion: FLCWK can inhibit the activation of STAT3 by reducing the production of IL-6, thereby increasing the occurrence of colitis-related colorectal cancer with 5-FU. Fluorouracil 166-170 signal transducer and activator of transcription 3 Mus musculus 48-53 31983282-7 2020 Taken together, our data suggest that PRKDC-mediated phosphorylation of PRKAG1 primes AMPK complex to the lysosomal activation by STK11 in cancer cells thereby linking DNA damage response to autophagy and cellular metabolism.Abbreviations: AXIN1: axin 1; 3-MA: 3-methyladenine; 5-FU: 5-fluorouracil; AA mutant: double alanine mutant (S192A, T284A) of PRKAG1; ACACA: acetyl-CoA carboxylase alpha; AICAR: 5-Aminoimidazole-4-carboxamide ribonucleotide; AMPK: AMP-activated protein kinase; ATG: autophagy-related; ATM: ataxia telangiectasia mutated; ATR: ATM serine/threonine kinase; AV: autophagic vacuole; AVd: degradative autophagic vacuole; AVi: initial autophagic vacuole; BECN1: beclin 1; BSA: bovine serum albumin; CBS: cystathionine beta-synthase; CDK7: cyclin dependent kinase 7; CDKN1A: cyclin dependent kinase inhibitor 1A; EGFP: enhanced green fluorescent protein; GAPDH: glyceraldehyde-3-phosphate dehydrogenase; GST: glutathione S transferase; H2AX/H2AFX: H2A.X variant histone; HBSS: Hanks balanced salt solution; IP: immunopurification; IR: ionizing radiation; MAP1LC3/LC3: microtubule associated protein 1 light chain 3; MAP3K9: mitogen-activated protein kinase kinase kinase 9; mRFP: monomeric red fluorescent protein; mCh: mCherry; MCM7: minichromosome maintenance complex component 7; MTORC1: mechanistic target of rapamycin kinase complex 1; NHEJ: non-homologous end joining; NRBP2: nuclear receptor binding protein 2; NTC: non-targeting control; NUAK1: NUAK family kinase 1; PBS: phosphate-buffered saline; PIK3AP1: phosphoinositide-3-kinase adaptor protein 1; PIK3CA: phosphatidylinositol-4,5-biphosphate 3-kinase catalytic subunit alpha; PIKK: phosphatidylinositol 3-kinase-related kinase; PRKAA: protein kinase AMP-activated catalytic subunit alpha; PRKAB: protein kinase AMP-activated non-catalytic subunit beta; PRKAG: protein kinase AMP-activated non-catalytic subunit gamma; PRKDC: protein kinase, DNA-activated, catalytic subunit; RLuc: Renilla luciferase; RPS6KB1: ribosomal protein S6 kinase B1; SQSTM1: sequestosome 1; STK11/LKB1: serine/threonine kinase 11; TP53: tumor protein p53; TSKS: testis specific serine kinase substrate; ULK1: unc-51 like autophagy activating kinase 1; WIPI2: WD repeat domain, phosphoinositide interacting 2; WT: wild type. Fluorouracil 278-282 protein kinase, DNA-activated, catalytic subunit Homo sapiens 38-43 32388677-3 2020 Here, we demonstrate that hypoxia-inducible factor 1alpha (HIF1alpha) in GC cells is activated upon 5-fluorouracil (5-FU) treatment and results in much more accumulation of M2-type TAMs which protect tumor cells from chemo-agents. Fluorouracil 100-114 hypoxia inducible factor 1 subunit alpha Homo sapiens 26-57 32505033-7 2020 In conclusion, we have identified LRP-1 as a signature protein of radio-resistant CRC and successfully developed LRP-1-targeting HSA-NP containing 5-FU that is a novel theranostic tool for both diagnostic imaging and neoadjuvant therapy of CRC patients. Fluorouracil 147-151 LDL receptor related protein 1 Homo sapiens 34-39 32505033-7 2020 In conclusion, we have identified LRP-1 as a signature protein of radio-resistant CRC and successfully developed LRP-1-targeting HSA-NP containing 5-FU that is a novel theranostic tool for both diagnostic imaging and neoadjuvant therapy of CRC patients. Fluorouracil 147-151 LDL receptor related protein 1 Homo sapiens 113-118 32388677-3 2020 Here, we demonstrate that hypoxia-inducible factor 1alpha (HIF1alpha) in GC cells is activated upon 5-fluorouracil (5-FU) treatment and results in much more accumulation of M2-type TAMs which protect tumor cells from chemo-agents. Fluorouracil 100-114 hypoxia inducible factor 1 subunit alpha Homo sapiens 59-68 32388677-3 2020 Here, we demonstrate that hypoxia-inducible factor 1alpha (HIF1alpha) in GC cells is activated upon 5-fluorouracil (5-FU) treatment and results in much more accumulation of M2-type TAMs which protect tumor cells from chemo-agents. Fluorouracil 116-120 hypoxia inducible factor 1 subunit alpha Homo sapiens 26-57 32388677-3 2020 Here, we demonstrate that hypoxia-inducible factor 1alpha (HIF1alpha) in GC cells is activated upon 5-fluorouracil (5-FU) treatment and results in much more accumulation of M2-type TAMs which protect tumor cells from chemo-agents. Fluorouracil 116-120 hypoxia inducible factor 1 subunit alpha Homo sapiens 59-68 32388677-4 2020 Mechanistically, in the GC cells under the 5-FU treatment, reactive oxygen species is accumulated and then induces the activation of HIF1alpha signaling to drive the expression of high-mobility group box 1, which leads to more macrophage"s infiltration into GC tumor. Fluorouracil 43-47 hypoxia inducible factor 1 subunit alpha Homo sapiens 133-142 32388677-6 2020 Blocking GDF15 using antibody or inhibiting FAO of tumor cells by etomoxir efficiently gave rise to the tumor cell sensitivity to 5-FU. Fluorouracil 130-134 growth differentiation factor 15 Rattus norvegicus 9-14 31938994-13 2020 CONCLUSIONS: Our data highlight that iASPP plays a crucial role in the inhibition of 5-Fu-induced apoptosis resistance by removing ROS accumulation in gastric adenocarcinoma, and that the removal of ROS induced by iASPP is Nrf2 signaling dependent. Fluorouracil 85-89 NFE2 like bZIP transcription factor 2 Homo sapiens 223-227 32652867-8 2020 Activation of the Wnt/beta-catenin pathway or overexpression of Chk1 abrogated the promoting effect of dbpA downregulation on 5-FU sensitivity of CRC cells. Fluorouracil 126-130 checkpoint kinase 1 Homo sapiens 64-68 32652867-10 2020 Our study indicated that knockdown of dbpA enhanced the sensitivity of colorectal cancer cells to 5-FU via Wnt/beta-catenin/Chk1 pathway, and DbpA may be a potential therapeutic target to sensitize drug resistance colorectal cancer to 5-FU and L-OHP. Fluorouracil 98-102 checkpoint kinase 1 Homo sapiens 124-128 32652867-10 2020 Our study indicated that knockdown of dbpA enhanced the sensitivity of colorectal cancer cells to 5-FU via Wnt/beta-catenin/Chk1 pathway, and DbpA may be a potential therapeutic target to sensitize drug resistance colorectal cancer to 5-FU and L-OHP. Fluorouracil 235-239 checkpoint kinase 1 Homo sapiens 124-128 33165366-14 2020 Overexpression of ATOH8 increases chemosensitivity to 5-FU, which is probably caused by inhibiting the phosphorylation of AKT (Ser473). Fluorouracil 54-58 thymoma viral proto-oncogene 1 Mus musculus 122-125 31938994-0 2020 iASPP-Mediated ROS Inhibition Drives 5-Fu Resistance Dependent on Nrf2 Antioxidative Signaling Pathway in Gastric Adenocarcinoma. Fluorouracil 37-41 protein phosphatase 1 regulatory subunit 13 like Homo sapiens 0-5 31938994-0 2020 iASPP-Mediated ROS Inhibition Drives 5-Fu Resistance Dependent on Nrf2 Antioxidative Signaling Pathway in Gastric Adenocarcinoma. Fluorouracil 37-41 NFE2 like bZIP transcription factor 2 Homo sapiens 66-70 31938994-1 2020 AIMS: Inhibitor for the apoptosis-stimulating protein of p53 (iASPP) has been reported to be correlated with 5-fluorouracil (5-Fu) resistance in renal cell carcinoma. Fluorouracil 109-123 tumor protein p53 Homo sapiens 57-60 31938994-1 2020 AIMS: Inhibitor for the apoptosis-stimulating protein of p53 (iASPP) has been reported to be correlated with 5-fluorouracil (5-Fu) resistance in renal cell carcinoma. Fluorouracil 109-123 protein phosphatase 1 regulatory subunit 13 like Homo sapiens 62-67 31938994-1 2020 AIMS: Inhibitor for the apoptosis-stimulating protein of p53 (iASPP) has been reported to be correlated with 5-fluorouracil (5-Fu) resistance in renal cell carcinoma. Fluorouracil 125-129 tumor protein p53 Homo sapiens 57-60 31938994-1 2020 AIMS: Inhibitor for the apoptosis-stimulating protein of p53 (iASPP) has been reported to be correlated with 5-fluorouracil (5-Fu) resistance in renal cell carcinoma. Fluorouracil 125-129 protein phosphatase 1 regulatory subunit 13 like Homo sapiens 62-67 31938994-2 2020 Here, we uncover mechanisms of iASPP-Nrf2-ROS regulation of 5-Fu resistance which are important for the development of alternative treatment strategies for gastric adenocarcinoma treatment. Fluorouracil 60-64 protein phosphatase 1 regulatory subunit 13 like Homo sapiens 31-36 31938994-2 2020 Here, we uncover mechanisms of iASPP-Nrf2-ROS regulation of 5-Fu resistance which are important for the development of alternative treatment strategies for gastric adenocarcinoma treatment. Fluorouracil 60-64 NFE2 like bZIP transcription factor 2 Homo sapiens 37-41 31938994-7 2020 RESULTS: We found that iASPP KD led to an apparent 5-Fu-induced ROS accumulation in MGC803 and SCG790 cells. Fluorouracil 51-55 protein phosphatase 1 regulatory subunit 13 like Homo sapiens 23-28 31938994-10 2020 Similarly, iASPP KD failed to enhance the Nrf2 KD-mediated ROS accumulation after 5-Fu treatment, suggesting that iASPP-induced antioxidative effects related to 5-Fu resistance are partially dependent on Nrf2. Fluorouracil 161-165 protein phosphatase 1 regulatory subunit 13 like Homo sapiens 114-119 31938994-13 2020 CONCLUSIONS: Our data highlight that iASPP plays a crucial role in the inhibition of 5-Fu-induced apoptosis resistance by removing ROS accumulation in gastric adenocarcinoma, and that the removal of ROS induced by iASPP is Nrf2 signaling dependent. Fluorouracil 85-89 protein phosphatase 1 regulatory subunit 13 like Homo sapiens 37-42 32945504-0 2020 Ginsenoside Rg3 enhances the anticancer effect of 5-FU in colon cancer cells via the PI3K/AKT pathway. Fluorouracil 50-54 AKT serine/threonine kinase 1 Homo sapiens 90-93 32945504-8 2020 In addition, the PI3K/AKT signaling pathway in colon cancer cells was suppressed by Rg3 and 5-FU. Fluorouracil 92-96 AKT serine/threonine kinase 1 Homo sapiens 22-25 32945504-7 2020 We also found that combined treatment of Rg3 and 5-FU significantly enhanced the apoptosis of colon cancer cells by activating the Apaf1/caspase 9/caspase 3 pathway and arrested the cell cycle of the colon cancer cells in G0/G1 by promoting the expression of Cyclin D1, CDK2 and CDK4. Fluorouracil 49-53 apoptotic peptidase activating factor 1 Homo sapiens 131-136 32945504-11 2020 Collectively, the present study demonstrated that ginsenoside Rg3 enhances the anticancer effect of 5-FU in colon cancer cells via the PI3K/AKT pathway. Fluorouracil 100-104 AKT serine/threonine kinase 1 Homo sapiens 140-143 32945504-7 2020 We also found that combined treatment of Rg3 and 5-FU significantly enhanced the apoptosis of colon cancer cells by activating the Apaf1/caspase 9/caspase 3 pathway and arrested the cell cycle of the colon cancer cells in G0/G1 by promoting the expression of Cyclin D1, CDK2 and CDK4. Fluorouracil 49-53 caspase 3 Homo sapiens 147-156 32957741-0 2020 Anti-Telomerase CD4+ Th1 Immunity and Monocytic-Myeloid-Derived-Suppressor Cells Are Associated with Long-Term Efficacy Achieved by Docetaxel, Cisplatin, and 5-Fluorouracil (DCF) in Advanced Anal Squamous Cell Carcinoma: Translational Study of Epitopes-HPV01 and 02 Trials. Fluorouracil 158-172 CD4 molecule Homo sapiens 16-19 32474153-0 2020 Cysteinyl leukotriene receptor 1 promotes 5-fluorouracil resistance and resistance-derived stemness in colon cancer cells. Fluorouracil 42-56 cysteinyl leukotriene receptor 1 Homo sapiens 0-32 32474153-5 2020 These 5-FU-R-cells expressed increased levels of CysLT1R and showed increased survival and migration compared to nonresistant cells. Fluorouracil 6-10 cysteinyl leukotriene receptor 1 Homo sapiens 49-56 32474153-7 2020 LTD4/CysLT1R signaling was further increased and abolished after CYSLTR1 CRISPR-Cas9-knockdown and reduced in CysLT1R-doxycycline-knockdown experiments and CysLT1R-antagonist montelukast/5-FU-treated cells. Fluorouracil 187-191 cysteinyl leukotriene receptor 1 Homo sapiens 5-12 32474153-10 2020 IL-4-mediated stemness in both HT-29-colonospheres and 5-FU-R-cell derived colonospheres was abolished by montelukast or montelukast + 5-FU-treatment. Fluorouracil 55-59 interleukin 4 Homo sapiens 0-4 32474153-10 2020 IL-4-mediated stemness in both HT-29-colonospheres and 5-FU-R-cell derived colonospheres was abolished by montelukast or montelukast + 5-FU-treatment. Fluorouracil 135-139 interleukin 4 Homo sapiens 0-4 33042471-8 2020 Additionally, CD44 knockdown overcame chemoresistance in response to fluorouracil and oxaliplatin with enhanced apoptosis and p27 upregulation, respectively. Fluorouracil 69-81 dynactin subunit 6 Homo sapiens 126-129 33005290-4 2020 Different mechanisms including microsatellite instability, increased expression level of key enzyme thymidylate synthase and its polymorphism, increased level of 5-FU-activating enzymes and mutation of TP53 are proposed as the main determinants of resistance to 5-FU in CRC cells. Fluorouracil 262-266 tumor protein p53 Homo sapiens 202-206 32895407-0 2020 Activated ROCK/Akt/eNOS and ET-1/ERK pathways in 5-fluorouracil-induced cardiotoxicity: modulation by simvastatin. Fluorouracil 49-63 endothelin 1 Rattus norvegicus 28-32 33041789-5 2020 Furthermore, compared with 5-FU treatment alone, the combination of Y14 and 5-FU significantly reduced the phosphorylation level of FGFR1, and enhanced the anti-cancer effect by inhibiting the viability and colony formation in two gastric cancer cell lines. Fluorouracil 27-31 RNA binding motif protein 8A Homo sapiens 68-71 33041789-5 2020 Furthermore, compared with 5-FU treatment alone, the combination of Y14 and 5-FU significantly reduced the phosphorylation level of FGFR1, and enhanced the anti-cancer effect by inhibiting the viability and colony formation in two gastric cancer cell lines. Fluorouracil 76-80 fibroblast growth factor receptor 1 Homo sapiens 132-137 32895407-0 2020 Activated ROCK/Akt/eNOS and ET-1/ERK pathways in 5-fluorouracil-induced cardiotoxicity: modulation by simvastatin. Fluorouracil 49-63 AKT serine/threonine kinase 1 Rattus norvegicus 15-18 32675286-0 2020 Inhibition of the ATR kinase enhances 5-FU sensitivity independently of non-homologous end-joining and homologous recombination repair pathways. Fluorouracil 38-42 ATR serine/threonine kinase Homo sapiens 18-21 32675286-3 2020 ATR Ser/Thr kinase (ATR) is a principal kinase in the DNA damage response and is activated in response to UV- and chemotherapeutic drug-induced DNA replication stress, but its role in cellular responses to 5-FU is unclear. Fluorouracil 206-210 ATR serine/threonine kinase Homo sapiens 0-3 32675286-3 2020 ATR Ser/Thr kinase (ATR) is a principal kinase in the DNA damage response and is activated in response to UV- and chemotherapeutic drug-induced DNA replication stress, but its role in cellular responses to 5-FU is unclear. Fluorouracil 206-210 ATR serine/threonine kinase Homo sapiens 20-23 32675286-4 2020 In this study, we examined the effect of ATR inhibition on 5-FU sensitivity of mammalian cells. Fluorouracil 59-63 ATR serine/threonine kinase Homo sapiens 41-44 32675286-5 2020 Using immunoblotting, we found that 5-FU treatment dose-dependently induced the phosphorylation of ATR at the autophosphorylation site Thr-1989 and thereby activated its kinase. Fluorouracil 36-40 ATR serine/threonine kinase Homo sapiens 99-102 32675286-6 2020 Administration of 5-FU with a specific ATR inhibitor (ATRi) remarkably decreased cell survival, compared with 5-FU treatment combined with other major DNA repair kinases inhibitors. Fluorouracil 18-22 ATR serine/threonine kinase Homo sapiens 39-42 32675286-7 2020 Of note, the ATR inhibition enhanced induction of DNA double-strand breaks and apoptosis in 5-FU-treated cells. Fluorouracil 92-96 ATR serine/threonine kinase Homo sapiens 13-16 32675286-10 2020 Moreover, the ATR inhibition enhanced the efficacy of the 5-FU treatment, independently of the non-homologous end-joining and homologous recombination repair pathways. Fluorouracil 58-62 ATR serine/threonine kinase Homo sapiens 14-17 32675286-11 2020 These findings suggest that ATR could be a potential therapeutic target in 5-FU-based chemotherapy. Fluorouracil 75-79 ATR serine/threonine kinase Homo sapiens 28-31 32895407-0 2020 Activated ROCK/Akt/eNOS and ET-1/ERK pathways in 5-fluorouracil-induced cardiotoxicity: modulation by simvastatin. Fluorouracil 49-63 Eph receptor B1 Rattus norvegicus 33-36 32895407-8 2020 Moreover, the cross-talk between ROCK/ NF-kappaB, ROS/COX-2/TXA2, Akt/eNOS and ET-1/ERK1/2 pathways contributes via different means to upsetting the vasoconstriction/vasodilatation equilibrium as well as endothelial cell function and finally leads to cardiomyocyte stress and death-the modulation of these trajectories offers simvastatin its potential cardio-protection against 5-FU. Fluorouracil 378-382 AKT serine/threonine kinase 1 Rattus norvegicus 66-69 32895407-8 2020 Moreover, the cross-talk between ROCK/ NF-kappaB, ROS/COX-2/TXA2, Akt/eNOS and ET-1/ERK1/2 pathways contributes via different means to upsetting the vasoconstriction/vasodilatation equilibrium as well as endothelial cell function and finally leads to cardiomyocyte stress and death-the modulation of these trajectories offers simvastatin its potential cardio-protection against 5-FU. Fluorouracil 378-382 endothelin 1 Rattus norvegicus 79-83 32829780-6 2020 Activation of 6PGD via gain-of-function approach promoted growth of normal kidney but not RCC cells, and alleviated the efficacy of chemotherapeutic (e.g., 5-FU) and immunotherapeutic (e.g., IFN-alpha) agents. Fluorouracil 156-160 phosphogluconate dehydrogenase Homo sapiens 14-18 32829780-7 2020 In contrast, 6PGD inhibition using siRNA knockdown and pharmacological inhibitor physcion augmented the inhibitory effects of 5-FU and IFN-alpha in RCC. Fluorouracil 126-130 phosphogluconate dehydrogenase Homo sapiens 13-17 32619557-0 2020 Synergistic therapy with tangeretin and 5-fluorouracil accelerates the ROS/JNK mediated apoptotic pathway in human colorectal cancer cell. Fluorouracil 40-54 mitogen-activated protein kinase 8 Homo sapiens 75-78 33193866-9 2020 Bcl-2 siRNA corona successfully entered the cytosol of Bel7402/5-FU MDR cells to downregulate Bcl-2 protein levels in vitro and in vivo. Fluorouracil 63-67 BCL2 apoptosis regulator Homo sapiens 0-5 33193866-9 2020 Bcl-2 siRNA corona successfully entered the cytosol of Bel7402/5-FU MDR cells to downregulate Bcl-2 protein levels in vitro and in vivo. Fluorouracil 63-67 BCL2 apoptosis regulator Homo sapiens 94-99 33193866-10 2020 Bcl-2 siRNA/Dox-TPGS-LPs showed superior to TPGS- (or siRNA-) linked Dox liposomes in cell apoptosis and cytotoxicity assay in Bel7402/5-FU MDR cells, and 7-fold greater effect than free Dox in tumor growth inhibition of Bel7402/5-FU xenograft nude mice. Fluorouracil 135-139 BCL2 apoptosis regulator Homo sapiens 0-5 33193866-10 2020 Bcl-2 siRNA/Dox-TPGS-LPs showed superior to TPGS- (or siRNA-) linked Dox liposomes in cell apoptosis and cytotoxicity assay in Bel7402/5-FU MDR cells, and 7-fold greater effect than free Dox in tumor growth inhibition of Bel7402/5-FU xenograft nude mice. Fluorouracil 229-233 BCL2 apoptosis regulator Homo sapiens 0-5 32559627-0 2020 Hydrazinocurcumin and 5-fluorouracil enhance apoptosis and restrain tumorigenicity of HepG2 cells via disrupting the PTEN-mediated PI3K/Akt signaling pathway. Fluorouracil 22-36 AKT serine/threonine kinase 1 Homo sapiens 136-139 32559627-6 2020 We found that HZC or 5-Fu induced apoptosis and repressed proliferation of HepG2 cells by upregulating the expression of PTEN and disrupting the PI3K/Akt signaling pathway activation. Fluorouracil 21-25 AKT serine/threonine kinase 1 Homo sapiens 150-153 32559627-9 2020 Inhibition of PTEN expression activated the PI3K/Akt signaling pathway and reversed the protective effects of HZC or 5-Fu. Fluorouracil 117-121 AKT serine/threonine kinase 1 Homo sapiens 49-52 32559627-10 2020 Thus, HZC and 5-Fu increase PTEN, which blocks the PI3K/Akt signaling pathway, ultimately inducing HepG2 cell apoptosis. Fluorouracil 14-18 AKT serine/threonine kinase 1 Homo sapiens 56-59 32619557-9 2020 Collectively, results indicate that combination of TAN and 5-FU significantly accelerates apoptosis via JNK mediated pathway. Fluorouracil 59-63 mitogen-activated protein kinase 8 Homo sapiens 104-107 32774071-2 2020 S-1, a composite preparation of a 5-fluorouracil prodrug, has proven to be a convenient oral chemotherapeutic agent with definite efficacy against advanced HCC. Fluorouracil 34-48 proteasome 26S subunit, non-ATPase 1 Homo sapiens 0-3 32592950-9 2020 In detail, the ACF inhibition phenotype detected in 5FU and WF groups could be explained through the expression changes detected in the apoptosis-related genes of Aurka, p53 and Cox2. Fluorouracil 52-55 cytochrome c oxidase subunit II Malus domestica 178-182 32888127-9 2020 However, mRNA expression of E-cadherin as an epithelial marker was significantly increased in 5-FU treatment combined with siRNA SEMA4D. Fluorouracil 94-98 cadherin 1 Homo sapiens 28-38 33463109-8 2020 It was also concluded that LPS in combination with 5-FU increased TLR-4 expression and down-regulated gene expression in NF-kappaB, ERK, and AKT pathways (p=0.001). Fluorouracil 51-55 AKT serine/threonine kinase 1 Homo sapiens 141-144 32867456-8 2020 In male, gastric cancer patients with stage III, intestinal type, diffuse type, simple surgical treatment and fluorouracil chemotherapy, the expression of KDM6A is related to the patient"s overall survival time (all P<0.05). Fluorouracil 110-122 lysine demethylase 6A Homo sapiens 155-160 32849774-8 2020 Lentiviral-induced FGD5-AS1 knockdown reduced cancer proliferation, 5-FU chemoresistance in vitro, and tumorigenicity in vivo. Fluorouracil 68-72 FGD5 antisense RNA 1 Homo sapiens 19-27 32849774-10 2020 Hsa-miR-153-3p inhibition or CITED2 upregulation reversed the tumor-suppressing effects of FGD5-AS1 downregulation on gastric cancer proliferation and 5-FU chemoresistance. Fluorouracil 151-155 Cbp/p300 interacting transactivator with Glu/Asp rich carboxy-terminal domain 2 Homo sapiens 29-35 32849774-10 2020 Hsa-miR-153-3p inhibition or CITED2 upregulation reversed the tumor-suppressing effects of FGD5-AS1 downregulation on gastric cancer proliferation and 5-FU chemoresistance. Fluorouracil 151-155 FGD5 antisense RNA 1 Homo sapiens 91-99 32502840-0 2020 Modulating effect of Coronarin D in 5-fluorouracil resistance human oral cancer cell lines induced apoptosis and cell cycle arrest through JNK1/2 signaling pathway. Fluorouracil 36-50 mitogen-activated protein kinase 8 Homo sapiens 139-145 32748110-0 2020 ABCB1 and ABCC2 genetic polymorphism as risk factors for neutropenia in esophageal cancer patients treated with docetaxel, cisplatin, and 5-fluorouracil chemotherapy. Fluorouracil 138-152 ATP binding cassette subfamily B member 1 Homo sapiens 0-5 32742376-5 2020 In HCT116 cells expressing wild-type (wt) TP53, SIRT inhibitors were found to act antagonistically with multiple chemotherapeutic agents (cisplatin, 5-fluorouracil, oxaliplatin, gefitinib, LY294002 and metformin), and decreased the anti-tumor effects of these agents. Fluorouracil 149-163 tumor protein p53 Homo sapiens 42-46 32755957-1 2020 Based on the enhancement of synergistic antitumour activity to treat cancer and the correlation between inflammation and carcinogenesis, the authors designed chitosan nanoparticles for co-delivery of 5-fluororacil (5-Fu: an as anti-cancer drug) and aspirin (a non-steroidal anti-inflammatory drug) and induced synergistic antitumour activity through the modulation of the nuclear factor kappa B (NF-kappaB)/cyclooxygenase-2 (COX-2) signalling pathways. Fluorouracil 215-219 nuclear factor kappa B subunit 1 Homo sapiens 372-394 32755957-1 2020 Based on the enhancement of synergistic antitumour activity to treat cancer and the correlation between inflammation and carcinogenesis, the authors designed chitosan nanoparticles for co-delivery of 5-fluororacil (5-Fu: an as anti-cancer drug) and aspirin (a non-steroidal anti-inflammatory drug) and induced synergistic antitumour activity through the modulation of the nuclear factor kappa B (NF-kappaB)/cyclooxygenase-2 (COX-2) signalling pathways. Fluorouracil 215-219 nuclear factor kappa B subunit 1 Homo sapiens 396-405 32755957-1 2020 Based on the enhancement of synergistic antitumour activity to treat cancer and the correlation between inflammation and carcinogenesis, the authors designed chitosan nanoparticles for co-delivery of 5-fluororacil (5-Fu: an as anti-cancer drug) and aspirin (a non-steroidal anti-inflammatory drug) and induced synergistic antitumour activity through the modulation of the nuclear factor kappa B (NF-kappaB)/cyclooxygenase-2 (COX-2) signalling pathways. Fluorouracil 215-219 prostaglandin-endoperoxide synthase 2 Homo sapiens 407-423 32755957-4 2020 Furthermore, the proposed results clearly indicated that the combination of 5-Fu and aspirin by chitosan nanoparticles enhanced the intracellular concentration of drugs and exerted synergistic growth inhibition and apoptosis induction on hepatocellular carcinoma cells by suppressing NF-kappaB activation and inhibition of expression of COX-2. Fluorouracil 76-80 nuclear factor kappa B subunit 1 Homo sapiens 284-293 32975155-3 2020 Results: Combination treatment with 5-FU and radiation had a stronger effect on decreasing Bcl-2 expression and increasing expression of Bax, cleaved caspase-9, cleaved caspase-3, cleaved PARP compared with each treatment alone. Fluorouracil 36-40 BCL2 apoptosis regulator Homo sapiens 91-96 32975155-3 2020 Results: Combination treatment with 5-FU and radiation had a stronger effect on decreasing Bcl-2 expression and increasing expression of Bax, cleaved caspase-9, cleaved caspase-3, cleaved PARP compared with each treatment alone. Fluorouracil 36-40 BCL2 associated X, apoptosis regulator Homo sapiens 137-140 32975155-3 2020 Results: Combination treatment with 5-FU and radiation had a stronger effect on decreasing Bcl-2 expression and increasing expression of Bax, cleaved caspase-9, cleaved caspase-3, cleaved PARP compared with each treatment alone. Fluorouracil 36-40 caspase 3 Homo sapiens 169-178 32760222-16 2020 Exogenous increase in miR-203 in the EC cell lines significantly inhibited Snail-1 mediated in vitro pro-metastatic function of invasion, wound-healing, and increased chemosensitivity to 5-FU. Fluorouracil 187-191 snail family transcriptional repressor 1 Homo sapiens 75-82 32689938-7 2020 Our results further showed that melatonin can downregulate the expression levels of 5-FU resistance-related genes, such as thymidylate synthase in GC and ATR, CHEK1, BAX and MYC in CRC. Fluorouracil 84-88 ATR serine/threonine kinase Homo sapiens 154-157 32689938-7 2020 Our results further showed that melatonin can downregulate the expression levels of 5-FU resistance-related genes, such as thymidylate synthase in GC and ATR, CHEK1, BAX and MYC in CRC. Fluorouracil 84-88 checkpoint kinase 1 Homo sapiens 159-164 32689938-7 2020 Our results further showed that melatonin can downregulate the expression levels of 5-FU resistance-related genes, such as thymidylate synthase in GC and ATR, CHEK1, BAX and MYC in CRC. Fluorouracil 84-88 BCL2 associated X, apoptosis regulator Homo sapiens 166-169 32689938-8 2020 The qRT-PCR results demonstrated that melatonin enhanced the sensitivity of CRC 5-FU resistant cells by decreasing the expression of ATR. Fluorouracil 80-84 ATR serine/threonine kinase Homo sapiens 133-136 32903312-6 2020 Additionally, RBFOX3 augmented the resistance of GC cells to 5-fluorouracil by repressing RBFOX3. Fluorouracil 61-75 RNA binding fox-1 homolog 3 Homo sapiens 90-96 32571958-5 2020 Moreover, blockade of P38 or CREB sensitizes HCC cells to 5FU. Fluorouracil 58-61 mitogen-activated protein kinase 14 Homo sapiens 22-25 32782527-0 2020 Konjac glucomannan reverses multi-drug resistance of HepG2/5-FU cells by suppressing AKT signaling and increasing p53 expression. Fluorouracil 59-63 AKT serine/threonine kinase 1 Homo sapiens 85-88 32782527-0 2020 Konjac glucomannan reverses multi-drug resistance of HepG2/5-FU cells by suppressing AKT signaling and increasing p53 expression. Fluorouracil 59-63 tumor protein p53 Homo sapiens 114-117 32782527-4 2020 Reverse transcription-quantitative PCR and western blotting were performed to determine the effects of 5-FU and KGM on the expression of MDR-associated genes including MDR1 and P-glycoprotein 1 (P-gp 1), and to analyze the effects of 5-FU and KGM on the levels of cell proliferation-related genes, including cyclin A, cyclin B1 and CDK2, and apoptosis-related genes, including caspase-3, Bax and BCL-2. Fluorouracil 103-107 ATP binding cassette subfamily B member 1 Homo sapiens 168-172 32782527-4 2020 Reverse transcription-quantitative PCR and western blotting were performed to determine the effects of 5-FU and KGM on the expression of MDR-associated genes including MDR1 and P-glycoprotein 1 (P-gp 1), and to analyze the effects of 5-FU and KGM on the levels of cell proliferation-related genes, including cyclin A, cyclin B1 and CDK2, and apoptosis-related genes, including caspase-3, Bax and BCL-2. Fluorouracil 103-107 ATP binding cassette subfamily B member 1 Homo sapiens 177-193 32782527-4 2020 Reverse transcription-quantitative PCR and western blotting were performed to determine the effects of 5-FU and KGM on the expression of MDR-associated genes including MDR1 and P-glycoprotein 1 (P-gp 1), and to analyze the effects of 5-FU and KGM on the levels of cell proliferation-related genes, including cyclin A, cyclin B1 and CDK2, and apoptosis-related genes, including caspase-3, Bax and BCL-2. Fluorouracil 103-107 ATP binding cassette subfamily B member 1 Homo sapiens 195-201 32768589-7 2020 5-FU significantly induced ABCB1 mRNA expression in HT29 cells; whereas with a 24 fold increase in HT29FU cells. Fluorouracil 0-4 ATP binding cassette subfamily B member 1 Homo sapiens 27-32 33463109-6 2020 The effects of LPS and 5-FU on cytotoxicity, apoptosis, and gene expression in NF-kappaB, ERK, and AKT signaling pathways were evaluated by MTT assay, Annexin V/propidium iodide (PI) apoptosis assay, and qRT-PCR, respectively. Fluorouracil 23-27 AKT serine/threonine kinase 1 Homo sapiens 99-102 32904684-0 2020 NHE1 Mediates 5-Fu Resistance in Gastric Cancer via STAT3 Signaling Pathway. Fluorouracil 14-18 solute carrier family 9 member A1 Homo sapiens 0-4 32904684-0 2020 NHE1 Mediates 5-Fu Resistance in Gastric Cancer via STAT3 Signaling Pathway. Fluorouracil 14-18 signal transducer and activator of transcription 3 Homo sapiens 52-57 32904684-2 2020 However, the role of NHE1 expression related to the 5-Fu resistance in gastric cancer has not been investigated. Fluorouracil 52-56 solute carrier family 9 member A1 Homo sapiens 21-25 32904684-3 2020 Methods: The expression of NHE1 was examined by qPCR in the SGC7901/5-FU cell line and its parental cell line. Fluorouracil 68-72 solute carrier family 9 member A1 Homo sapiens 27-31 32904684-4 2020 pcDNA3.1-NHE1 and NHE1-siRNA were transfected to SGC7901/5-FU resistance cells and cell apoptosis was detected via TUNEL assay. Fluorouracil 57-61 solute carrier family 9 member A1 Homo sapiens 18-22 32904684-5 2020 The upstream activators in NHE1 mediated 5-Fu resistant gastric cancer cells were detected by Western blot and immunofluorescent. Fluorouracil 41-45 solute carrier family 9 member A1 Homo sapiens 27-31 32904684-6 2020 Results: A significant increase of the expression of NHE1 was observed in SGC7901 5-FU resistance cells compared to the GES-1 and SGC7901 cell line. Fluorouracil 82-86 solute carrier family 9 member A1 Homo sapiens 53-57 32904684-7 2020 NHE1 can suppress the cell apoptosis of SGC7901 5-FU resistance cells and involved in cell cycle. Fluorouracil 48-52 solute carrier family 9 member A1 Homo sapiens 0-4 32904684-8 2020 Also, the migration and invasion of SGC7901 5-FU resistance cells were promoted by NHE1. Fluorouracil 44-48 solute carrier family 9 member A1 Homo sapiens 83-87 32904684-12 2020 Further investigations revealed that the constitutive activation of STAT3 may be induced by JAK1 and JAK2, and thus effect the 5-FU resistance by regulating NHE1. Fluorouracil 127-131 signal transducer and activator of transcription 3 Homo sapiens 68-73 32904684-12 2020 Further investigations revealed that the constitutive activation of STAT3 may be induced by JAK1 and JAK2, and thus effect the 5-FU resistance by regulating NHE1. Fluorouracil 127-131 Janus kinase 1 Homo sapiens 92-96 32904684-12 2020 Further investigations revealed that the constitutive activation of STAT3 may be induced by JAK1 and JAK2, and thus effect the 5-FU resistance by regulating NHE1. Fluorouracil 127-131 solute carrier family 9 member A1 Homo sapiens 157-161 32904684-13 2020 Discussion: In summary, our findings provided evidence that NHE1 contributed to 5-Fu resistance in gastric cancer cells by regulating the JAK/STAT3 pathway. Fluorouracil 80-84 solute carrier family 9 member A1 Homo sapiens 60-64 32904684-13 2020 Discussion: In summary, our findings provided evidence that NHE1 contributed to 5-Fu resistance in gastric cancer cells by regulating the JAK/STAT3 pathway. Fluorouracil 80-84 signal transducer and activator of transcription 3 Homo sapiens 142-147 32904684-14 2020 Therefore, NHE1 can be a useful marker for predicting and monitoring 5-Fu resistance. Fluorouracil 69-73 solute carrier family 9 member A1 Homo sapiens 11-15 32879665-2 2020 Treatment with fluorouracil (5-FU) might not achieve the expected inhibition of proliferation of malignant cells based on the fluorouracil-induced activation of the NF-kappaB pathway. Fluorouracil 126-138 nuclear factor kappa B subunit 1 Homo sapiens 165-174 32879665-8 2020 Treatment with 5-FU combined with IL-1RA could increase the chemosensitivity of the SW620 cell line, and decreased expression of the TAK1/NF-kappaB and MEK pathways resulted in limited proliferation in the SW620 cell line. Fluorouracil 15-19 nuclear factor kappa B subunit 1 Homo sapiens 138-147 32879665-8 2020 Treatment with 5-FU combined with IL-1RA could increase the chemosensitivity of the SW620 cell line, and decreased expression of the TAK1/NF-kappaB and MEK pathways resulted in limited proliferation in the SW620 cell line. Fluorouracil 15-19 mitogen-activated protein kinase kinase 7 Homo sapiens 152-155 32922964-10 2020 Polymorphisms of the glucocorticoid receptor and variants of CCL2, YAP1, miR-21-5p and NF-kappabeta might be responsible for different responses to treatments used in keloid scars such as 5-fluorouracil. Fluorouracil 188-202 nuclear receptor subfamily 3 group C member 1 Homo sapiens 21-44 32922964-10 2020 Polymorphisms of the glucocorticoid receptor and variants of CCL2, YAP1, miR-21-5p and NF-kappabeta might be responsible for different responses to treatments used in keloid scars such as 5-fluorouracil. Fluorouracil 188-202 nuclear factor kappa B subunit 1 Homo sapiens 87-99 32777949-4 2021 In this study, we investigated the effect of calcitriol (Vit-D) on inflammatory responses during 5-fluorouracil (5-FU) treatment. Fluorouracil 97-111 vitrin Homo sapiens 57-60 32777949-6 2021 The 5-FU group had higher AST, ALT, LDH, and CPK levels than those in the 5-FU + Vit-D group. Fluorouracil 4-8 solute carrier family 17 member 5 Homo sapiens 26-29 32777949-7 2021 The 5-FU + Vit-D group had a lower TNF-alpha value than the 5-FU. Fluorouracil 4-8 tumor necrosis factor Homo sapiens 35-44 32777949-8 2021 The IL-6 levels in the 5-FU + Vit-D group were also significantly lower than those in 5-FU. Fluorouracil 23-27 interleukin 6 Homo sapiens 4-8 32539222-9 2020 Importantly, the knockdown of GAPDH in colon cancer SW480 cells and xenograft models effectively enhances their sensitivity to the chemotherapeutic drug 5-FU. Fluorouracil 153-157 glyceraldehyde-3-phosphate dehydrogenase Homo sapiens 30-35 32658073-1 2020 OBJECTIVES: The objective of this study was to investigate the efficacy and tolerability of 5-fluorouracil-oxaliplatin (FOLFOX) in advanced gastroenteropancreatic neuroendocrine neoplasms (GEP-NENs). Fluorouracil 92-106 granulin precursor Homo sapiens 189-192 32903312-6 2020 Additionally, RBFOX3 augmented the resistance of GC cells to 5-fluorouracil by repressing RBFOX3. Fluorouracil 61-75 RNA binding fox-1 homolog 3 Homo sapiens 14-20 31560739-7 2020 Moreover, anchorage-independent growth of GC cells was decreased and the cells became more sensitive to 5-fluorouracil and etoposide treatment when CLIC4 was overexpressed. Fluorouracil 104-118 chloride intracellular channel 4 Homo sapiens 148-153 32653028-13 2020 CONCLUSION: Together, our study proposes that pharmacologic targeting of lncRNA HOTAIR sensitizes EC cells to 5-FU-based chemotherapy by attenuating the promoter hypermethylation of the MTHFR in EC. Fluorouracil 110-114 HOX transcript antisense RNA (non-protein coding) Mus musculus 80-86 32653028-13 2020 CONCLUSION: Together, our study proposes that pharmacologic targeting of lncRNA HOTAIR sensitizes EC cells to 5-FU-based chemotherapy by attenuating the promoter hypermethylation of the MTHFR in EC. Fluorouracil 110-114 methylenetetrahydrofolate reductase Mus musculus 186-191 32742490-0 2020 Combinational inhibition of EGFR and YAP reverses 5-Fu resistance in colorectal cancer. Fluorouracil 50-54 epidermal growth factor receptor Homo sapiens 28-32 32669857-0 2020 LncRNA NEAT1 Regulates 5-Fu Sensitivity, Apoptosis and Invasion in Colorectal Cancer Through the MiR-150-5p/CPSF4 Axis. Fluorouracil 23-27 nuclear paraspeckle assembly transcript 1 (non-protein coding) Mus musculus 7-12 32247004-12 2020 Besides, Andro markedly down-regulated the 5-Fu-induced protein expression of caspase8/3, Bax and the phosphorylation of p38. Fluorouracil 43-47 BCL2 associated X, apoptosis regulator Homo sapiens 90-93 32247004-12 2020 Besides, Andro markedly down-regulated the 5-Fu-induced protein expression of caspase8/3, Bax and the phosphorylation of p38. Fluorouracil 43-47 mitogen-activated protein kinase 14 Homo sapiens 121-124 32627138-7 2020 Expressions of tested ABC transporters (ABCA5, ABCB1, ABCB6, ABCC1, ABCC2, ABCC3, ABCC5, ABCC10 and ABCF2, and ABCG2) were also deregulated in 5-FU resistant Hep-2 cells. Fluorouracil 143-147 ATP binding cassette subfamily B member 1 Homo sapiens 47-52 32627138-7 2020 Expressions of tested ABC transporters (ABCA5, ABCB1, ABCB6, ABCC1, ABCC2, ABCC3, ABCC5, ABCC10 and ABCF2, and ABCG2) were also deregulated in 5-FU resistant Hep-2 cells. Fluorouracil 143-147 ATP binding cassette subfamily C member 1 Homo sapiens 61-66 32627138-7 2020 Expressions of tested ABC transporters (ABCA5, ABCB1, ABCB6, ABCC1, ABCC2, ABCC3, ABCC5, ABCC10 and ABCF2, and ABCG2) were also deregulated in 5-FU resistant Hep-2 cells. Fluorouracil 143-147 ATP binding cassette subfamily G member 2 (Junior blood group) Homo sapiens 111-116 32753880-12 2020 The Akt phosphorylation and expressions of glycolysis key enzymes, Hexokinase 2 and LDHA, were significantly upregulated in 5-Fu resistant gastric cancer cells. Fluorouracil 124-128 AKT serine/threonine kinase 1 Homo sapiens 4-7 32753880-12 2020 The Akt phosphorylation and expressions of glycolysis key enzymes, Hexokinase 2 and LDHA, were significantly upregulated in 5-Fu resistant gastric cancer cells. Fluorouracil 124-128 lactate dehydrogenase A Homo sapiens 84-88 32753880-13 2020 On the other way, inhibition of glycolysis or Akt pathway effectively overcame 5-Fu resistance from both in vitro and in vivo models. Fluorouracil 79-83 AKT serine/threonine kinase 1 Homo sapiens 46-49 32753880-14 2020 Finally, we report that the combination of Akt or glycolysis inhibitor with 5-Fu could synergistically enhance the cytotoxicity of 5-Fu to CagA-overexpressed gastric cancer cells. Fluorouracil 131-135 AKT serine/threonine kinase 1 Homo sapiens 43-46 32753880-15 2020 Discussion: In summary, our study demonstrated a CagA-Akt-glycolysis-5-Fu resistance axis, contributing to the development of new therapeutic agents against chemoresistant human gastric cancer. Fluorouracil 69-73 AKT serine/threonine kinase 1 Homo sapiens 54-57 32319648-8 2020 LS 174T cells with decreased expression levels of DYNC1LI1 were discovered to be more sensitive to 5-FU compared with LS 174T cells with endogenous DYNC1LI1 expression levels. Fluorouracil 99-103 dynein cytoplasmic 1 light intermediate chain 1 Homo sapiens 50-58 32319648-10 2020 Notably, the CRC cells with low MUC1 expression levels and high expression levels of the other MUCs (MUC2, MU4 and MUC5AC) were shown to benefit from 5-FU treatment. Fluorouracil 150-154 mucin 2, oligomeric mucus/gel-forming Homo sapiens 101-105 32669857-11 2020 Silencing of lnc-NEAT1 promoted the 5-Fu sensitivity, enhanced the apoptosis and suppressed the invasion of CRC cells. Fluorouracil 36-40 nuclear paraspeckle assembly transcript 1 (non-protein coding) Mus musculus 17-22 32669857-15 2020 In addition, interference of lnc-NEAT1 reduced tumor volume and improved the sensitivity of CRC to 5-Fu in vivo. Fluorouracil 99-103 nuclear paraspeckle assembly transcript 1 (non-protein coding) Mus musculus 33-38 32581212-0 2020 Enalapril overcomes chemoresistance and potentiates antitumor efficacy of 5-FU in colorectal cancer by suppressing proliferation, angiogenesis, and NF-kappaB/STAT3-regulated proteins. Fluorouracil 74-78 nuclear factor kappa B subunit 1 Homo sapiens 148-157 32647090-11 2020 A 5-FU resulted in severe ileal mucositis through TNF-alpha, NF-kappaB, MMP-9, and AQP-4 disturbances. Fluorouracil 2-6 tumor necrosis factor Rattus norvegicus 50-59 32665777-10 2020 Moreover, qPCR analyses showed that CASP3 and CASP9 mRNA levels significantly increased after pre-treatment with Pxd followed by 5-Fu and 1-OHP treatments, compared to 5-Fu with 1-OHP alone. Fluorouracil 129-133 caspase 3 Homo sapiens 36-41 32629871-0 2020 NRF2 Knockdown Resensitizes 5-Fluorouracil-Resistant Pancreatic Cancer Cells by Suppressing HO-1 and ABCG2 Expression. Fluorouracil 28-42 NFE2 like bZIP transcription factor 2 Homo sapiens 0-4 32665777-10 2020 Moreover, qPCR analyses showed that CASP3 and CASP9 mRNA levels significantly increased after pre-treatment with Pxd followed by 5-Fu and 1-OHP treatments, compared to 5-Fu with 1-OHP alone. Fluorouracil 168-172 caspase 3 Homo sapiens 36-41 32586901-4 2021 After 5-FU treatment, CAR cKO HSCs had lower levels of Notch1 expression and elevated protein level of Numb, a Notch antagonist. Fluorouracil 6-10 notch receptor 1 Homo sapiens 55-61 32581212-0 2020 Enalapril overcomes chemoresistance and potentiates antitumor efficacy of 5-FU in colorectal cancer by suppressing proliferation, angiogenesis, and NF-kappaB/STAT3-regulated proteins. Fluorouracil 74-78 signal transducer and activator of transcription 3 Homo sapiens 158-163 32580513-0 2020 MicroRNA-199b Downregulation Confers Resistance to 5-Fluorouracil Treatment and Predicts Poor Outcome and Response to Neoadjuvant Chemoradiotherapy in Locally Advanced Rectal Cancer Patients. Fluorouracil 51-65 microRNA 199b Homo sapiens 0-13 32606803-0 2020 Circ-PRKDC Contributes to 5-Fluorouracil Resistance of Colorectal Cancer Cells by Regulating miR-375/FOXM1 Axis and Wnt/beta-Catenin Pathway. Fluorouracil 26-40 protein kinase, DNA-activated, catalytic subunit Homo sapiens 5-10 32606803-0 2020 Circ-PRKDC Contributes to 5-Fluorouracil Resistance of Colorectal Cancer Cells by Regulating miR-375/FOXM1 Axis and Wnt/beta-Catenin Pathway. Fluorouracil 26-40 microRNA 375 Homo sapiens 93-100 32606803-9 2020 Results: Circ-PRKDC was upregulated in 5-FU-resistant CRC tissues and cells. Fluorouracil 39-43 protein kinase, DNA-activated, catalytic subunit Homo sapiens 14-19 32606803-11 2020 MiR-375 was a target of circ-PRKDC and miR-375 inhibition reversed the effects of circ-PRKDC silencing on 5-FU resistance, cell colony formation and invasion. Fluorouracil 106-110 microRNA 375 Homo sapiens 0-7 32606803-11 2020 MiR-375 was a target of circ-PRKDC and miR-375 inhibition reversed the effects of circ-PRKDC silencing on 5-FU resistance, cell colony formation and invasion. Fluorouracil 106-110 protein kinase, DNA-activated, catalytic subunit Homo sapiens 29-34 32606803-11 2020 MiR-375 was a target of circ-PRKDC and miR-375 inhibition reversed the effects of circ-PRKDC silencing on 5-FU resistance, cell colony formation and invasion. Fluorouracil 106-110 microRNA 375 Homo sapiens 39-46 32606803-11 2020 MiR-375 was a target of circ-PRKDC and miR-375 inhibition reversed the effects of circ-PRKDC silencing on 5-FU resistance, cell colony formation and invasion. Fluorouracil 106-110 protein kinase, DNA-activated, catalytic subunit Homo sapiens 87-92 32606803-13 2020 MiR-375 suppressed 5-FU resistance by targeting FOXM1. Fluorouracil 19-23 microRNA 375 Homo sapiens 0-7 32606803-16 2020 Conclusion: Circ-PRKDC enhanced 5-FU resistance in CRC by regulating FOXM1/miR-375 axis and wnt/beta-catenin pathway. Fluorouracil 32-36 protein kinase, DNA-activated, catalytic subunit Homo sapiens 17-22 32606803-16 2020 Conclusion: Circ-PRKDC enhanced 5-FU resistance in CRC by regulating FOXM1/miR-375 axis and wnt/beta-catenin pathway. Fluorouracil 32-36 microRNA 375 Homo sapiens 75-82 32629871-6 2020 NRF2 knockdown reversed 5-FU resistance of PDAC cells via suppression of ABCG2 and HO-1. Fluorouracil 24-28 NFE2 like bZIP transcription factor 2 Homo sapiens 0-4 32629871-6 2020 NRF2 knockdown reversed 5-FU resistance of PDAC cells via suppression of ABCG2 and HO-1. Fluorouracil 24-28 ATP binding cassette subfamily G member 2 (Junior blood group) Homo sapiens 73-78 32629871-7 2020 In summary, these data indicate that NRF2 is a potential target for resensitizing 5-FUR PDAC cells to 5-FU to improve treatment outcomes in patients with pancreatic cancer. Fluorouracil 82-86 NFE2 like bZIP transcription factor 2 Homo sapiens 37-41 32580513-3 2020 The tumor suppressor microRNA (miR)-199b directly targets the PP2A inhibitor SET, which has been involved in 5-FU resistance, and its downregulation has been found to correlate with poor outcome in metastatic colorectal cancer. Fluorouracil 109-113 microRNA 199b Homo sapiens 21-40 32580513-4 2020 Here, we studied the functional effects of miR-199b on 5-FU sensitivity after its ectopic modulation, and its expression was quantified by real-time-PCR in a cohort of 110 LARC patients to evaluate its potential clinical significance. Fluorouracil 55-59 microRNA 199b Homo sapiens 43-51 32580513-5 2020 Interestingly, our findings demonstrate that miR-199b enhances the sensitivity of colorectal cancer cells to 5-FU in a SET-dependent manner, and that both miR-199b overexpression and SET inhibition are able to overcome resistance to this drug using an acquired 5-FU-resistant model. Fluorouracil 109-113 microRNA 199b Homo sapiens 45-53 32580513-5 2020 Interestingly, our findings demonstrate that miR-199b enhances the sensitivity of colorectal cancer cells to 5-FU in a SET-dependent manner, and that both miR-199b overexpression and SET inhibition are able to overcome resistance to this drug using an acquired 5-FU-resistant model. Fluorouracil 261-265 microRNA 199b Homo sapiens 155-163 32580513-8 2020 In conclusion, our findings highlight the clinical impact of miR-199b downregulation predicting poor outcome and pathological response in LARC, and suggest the miR-199b/SET signaling axis as a novel molecular target to prevent the development of resistance to 5-FU treatment. Fluorouracil 260-264 microRNA 199b Homo sapiens 61-69 32580513-8 2020 In conclusion, our findings highlight the clinical impact of miR-199b downregulation predicting poor outcome and pathological response in LARC, and suggest the miR-199b/SET signaling axis as a novel molecular target to prevent the development of resistance to 5-FU treatment. Fluorouracil 260-264 microRNA 199b Homo sapiens 160-168 32606741-7 2020 ELE and 5-FU in combination regulated the PI3K/AKT pathway through p-AKT, P-85, p110r, p-PDK1, and p110a protein and RAF-MEK-ERK pathway inhibition through the p-c-raf and p-ERK downregulation. Fluorouracil 8-12 mitogen-activated protein kinase 1 Homo sapiens 174-177 32606741-0 2020 beta-Elemene Enhances the Chemotherapeutic Effect of 5-Fluorouracil in Triple-Negative Breast Cancer via PI3K/AKT, RAF-MEK-ErK, and NF-kappaB Signaling Pathways. Fluorouracil 53-67 AKT serine/threonine kinase 1 Homo sapiens 110-113 32606741-0 2020 beta-Elemene Enhances the Chemotherapeutic Effect of 5-Fluorouracil in Triple-Negative Breast Cancer via PI3K/AKT, RAF-MEK-ErK, and NF-kappaB Signaling Pathways. Fluorouracil 53-67 mitogen-activated protein kinase kinase 7 Homo sapiens 119-122 32606741-8 2020 The PI3K inhibitor LY294002 or RAF-MEK-ERK inhibitor U0126 in combination with ELE and 5-FU decreased cell viability in both cell lines significantly, thereby showing the involvement of these pathways in cell apoptosis. Fluorouracil 87-91 mitogen-activated protein kinase kinase 7 Homo sapiens 35-38 32606741-0 2020 beta-Elemene Enhances the Chemotherapeutic Effect of 5-Fluorouracil in Triple-Negative Breast Cancer via PI3K/AKT, RAF-MEK-ErK, and NF-kappaB Signaling Pathways. Fluorouracil 53-67 mitogen-activated protein kinase 1 Homo sapiens 123-126 32606741-6 2020 In molecular mechanisms, ELE and 5-FU in combination enhances apoptosis in both cell lines through Bl-2 family protein and caspase cascade modulation, thereby inhibiting NF-kB pathway through IKKbeta, IKKalpha, and p65 downregulation in the cytoplasm and p50 and p65 downregulation in the nucleus. Fluorouracil 33-37 nuclear factor kappa B subunit 1 Homo sapiens 255-258 32606741-8 2020 The PI3K inhibitor LY294002 or RAF-MEK-ERK inhibitor U0126 in combination with ELE and 5-FU decreased cell viability in both cell lines significantly, thereby showing the involvement of these pathways in cell apoptosis. Fluorouracil 87-91 mitogen-activated protein kinase 1 Homo sapiens 39-42 32606741-7 2020 ELE and 5-FU in combination regulated the PI3K/AKT pathway through p-AKT, P-85, p110r, p-PDK1, and p110a protein and RAF-MEK-ERK pathway inhibition through the p-c-raf and p-ERK downregulation. Fluorouracil 8-12 AKT serine/threonine kinase 1 Homo sapiens 47-50 32464550-0 2020 lncRNA HOTAIR Contributes to 5FU Resistance through Suppressing miR-218 and Activating NF-kappaB/TS Signaling in Colorectal Cancer. Fluorouracil 29-32 nuclear factor kappa B subunit 1 Homo sapiens 87-96 32606741-7 2020 ELE and 5-FU in combination regulated the PI3K/AKT pathway through p-AKT, P-85, p110r, p-PDK1, and p110a protein and RAF-MEK-ERK pathway inhibition through the p-c-raf and p-ERK downregulation. Fluorouracil 8-12 AKT serine/threonine kinase 1 Homo sapiens 69-72 32606741-7 2020 ELE and 5-FU in combination regulated the PI3K/AKT pathway through p-AKT, P-85, p110r, p-PDK1, and p110a protein and RAF-MEK-ERK pathway inhibition through the p-c-raf and p-ERK downregulation. Fluorouracil 8-12 phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha Homo sapiens 99-104 32606741-7 2020 ELE and 5-FU in combination regulated the PI3K/AKT pathway through p-AKT, P-85, p110r, p-PDK1, and p110a protein and RAF-MEK-ERK pathway inhibition through the p-c-raf and p-ERK downregulation. Fluorouracil 8-12 mitogen-activated protein kinase kinase 7 Homo sapiens 121-124 32606741-7 2020 ELE and 5-FU in combination regulated the PI3K/AKT pathway through p-AKT, P-85, p110r, p-PDK1, and p110a protein and RAF-MEK-ERK pathway inhibition through the p-c-raf and p-ERK downregulation. Fluorouracil 8-12 mitogen-activated protein kinase 1 Homo sapiens 125-128 32538746-2 2020 The purpose of this study is to investigate the efficacy of lobaplatin in combination with 5-fluorouracil (5-FU) and doxorubicin on AFP and treatment of primary carcinoma of the liver by transhepatic arterial chemotherapy and embolization (TACE). Fluorouracil 91-105 alpha fetoprotein Homo sapiens 132-135 32538746-2 2020 The purpose of this study is to investigate the efficacy of lobaplatin in combination with 5-fluorouracil (5-FU) and doxorubicin on AFP and treatment of primary carcinoma of the liver by transhepatic arterial chemotherapy and embolization (TACE). Fluorouracil 107-111 alpha fetoprotein Homo sapiens 132-135 32044957-0 2020 Overexpressing microRNA-34a overcomes ABCG2-mediated drug resistance to 5-FU in side population cells from colon cancer via suppressing DLL1. Fluorouracil 72-76 ATP binding cassette subfamily G member 2 (Junior blood group) Homo sapiens 38-43 32715733-8 2020 Experiments showed that downregulation of SPTBN1and LAMP1 proteins significantly enhanced the sensitivity of human gastric cancer cells SGC7901 to 5-FU and cisplatin. Fluorouracil 147-151 spectrin beta, non-erythrocytic 1 Homo sapiens 42-48 32078695-8 2020 Cisplatin, 5-fluorouracil and carboplatin induced dose-dependent apoptosis in primary lines of iNKT cells and inhibited CD1d-dependent interferon-gamma production and cytolytic degranulation by viable iNKT cells. Fluorouracil 11-25 interferon gamma Homo sapiens 135-151 32415349-10 2020 5-Fu decreased the levels of total protein and albumin in serum, and significantly increased the levels of IL-6 and TNF-alpha in muscle tissue. Fluorouracil 0-4 interleukin 6 Rattus norvegicus 107-111 32415349-10 2020 5-Fu decreased the levels of total protein and albumin in serum, and significantly increased the levels of IL-6 and TNF-alpha in muscle tissue. Fluorouracil 0-4 tumor necrosis factor Rattus norvegicus 116-125 32044957-8 2020 In addition, overexpressing miR-34a overcame ABCG2-mediated resistance to 5-FU via DLL1/Notch pathway in vitro, and suppressed tumor growth under 5-FU treatment in vivo. Fluorouracil 74-78 ATP binding cassette subfamily G member 2 (Junior blood group) Homo sapiens 45-50 32044957-8 2020 In addition, overexpressing miR-34a overcame ABCG2-mediated resistance to 5-FU via DLL1/Notch pathway in vitro, and suppressed tumor growth under 5-FU treatment in vivo. Fluorouracil 146-150 ATP binding cassette subfamily G member 2 (Junior blood group) Homo sapiens 45-50 32509181-0 2020 Emodin reverses 5-Fu resistance in human colorectal cancer via downregulation of PI3K/Akt signaling pathway. Fluorouracil 16-20 AKT serine/threonine kinase 1 Homo sapiens 86-89 32460371-6 2020 In a xenografted mouse model of cancer, HEP with 5-Fu significantly suppressed tumor growth, inhibited inflammatory markers such as interferon (IFN)-gamma, interleukin (IL)-1beta, IL-2, IL-6, tumor necrosis factor (TNF)-alpha, and lipopolysaccharide (LPS), and regulated the expression of Akt, CCDN1, CKD4, FOXM1, MMP7, MYC, PPAR-alpha, and PPAR-gamma. Fluorouracil 49-53 interferon gamma Mus musculus 132-154 32460371-6 2020 In a xenografted mouse model of cancer, HEP with 5-Fu significantly suppressed tumor growth, inhibited inflammatory markers such as interferon (IFN)-gamma, interleukin (IL)-1beta, IL-2, IL-6, tumor necrosis factor (TNF)-alpha, and lipopolysaccharide (LPS), and regulated the expression of Akt, CCDN1, CKD4, FOXM1, MMP7, MYC, PPAR-alpha, and PPAR-gamma. Fluorouracil 49-53 interleukin 6 Mus musculus 186-190 32460371-6 2020 In a xenografted mouse model of cancer, HEP with 5-Fu significantly suppressed tumor growth, inhibited inflammatory markers such as interferon (IFN)-gamma, interleukin (IL)-1beta, IL-2, IL-6, tumor necrosis factor (TNF)-alpha, and lipopolysaccharide (LPS), and regulated the expression of Akt, CCDN1, CKD4, FOXM1, MMP7, MYC, PPAR-alpha, and PPAR-gamma. Fluorouracil 49-53 tumor necrosis factor Mus musculus 192-225 32460371-6 2020 In a xenografted mouse model of cancer, HEP with 5-Fu significantly suppressed tumor growth, inhibited inflammatory markers such as interferon (IFN)-gamma, interleukin (IL)-1beta, IL-2, IL-6, tumor necrosis factor (TNF)-alpha, and lipopolysaccharide (LPS), and regulated the expression of Akt, CCDN1, CKD4, FOXM1, MMP7, MYC, PPAR-alpha, and PPAR-gamma. Fluorouracil 49-53 thymoma viral proto-oncogene 1 Mus musculus 289-292 32460371-6 2020 In a xenografted mouse model of cancer, HEP with 5-Fu significantly suppressed tumor growth, inhibited inflammatory markers such as interferon (IFN)-gamma, interleukin (IL)-1beta, IL-2, IL-6, tumor necrosis factor (TNF)-alpha, and lipopolysaccharide (LPS), and regulated the expression of Akt, CCDN1, CKD4, FOXM1, MMP7, MYC, PPAR-alpha, and PPAR-gamma. Fluorouracil 49-53 peroxisome proliferator activated receptor alpha Mus musculus 325-335 32509181-12 2020 In addition, the combination treatment (emodin plus 5-Fu) induced cell apoptosis via inhibiting Bcl-2 and activating cleaved caspase3 and Bax. Fluorouracil 52-56 BCL2 apoptosis regulator Homo sapiens 96-101 32509181-12 2020 In addition, the combination treatment (emodin plus 5-Fu) induced cell apoptosis via inhibiting Bcl-2 and activating cleaved caspase3 and Bax. Fluorouracil 52-56 caspase 3 Homo sapiens 125-133 32509181-12 2020 In addition, the combination treatment (emodin plus 5-Fu) induced cell apoptosis via inhibiting Bcl-2 and activating cleaved caspase3 and Bax. Fluorouracil 52-56 BCL2 associated X, apoptosis regulator Homo sapiens 138-141 32509181-13 2020 Moreover, emodin reduced 5-Fu resistant in CRC via downregulation of PI3K/Akt signaling. Fluorouracil 25-29 AKT serine/threonine kinase 1 Homo sapiens 74-77 32509181-15 2020 CONCLUSION: Our research revealed that emodin could reverse 5-Fu resistance in CRC through inactivating PI3K/Akt signaling pathway in vitro and in vivo. Fluorouracil 60-64 AKT serine/threonine kinase 1 Homo sapiens 109-112 32382150-0 2020 LncRNA SNORD3A specifically sensitizes breast cancer cells to 5-FU by sponging miR-185-5p to enhance UMPS expression. Fluorouracil 62-66 small nucleolar RNA, C/D box 3A Homo sapiens 7-14 32457882-0 2020 beta-Elemene Reverses the Resistance of p53-Deficient Colorectal Cancer Cells to 5-Fluorouracil by Inducing Pro-death Autophagy and Cyclin D3-Dependent Cycle Arrest. Fluorouracil 81-95 tumor protein p53 Homo sapiens 40-43 32457882-2 2020 5-fluorouracil remains a widely used chemotherapeutic drug in the treatment of advanced colorectal cancer, but chemotherapy drugs are prone to develop drug resistance, p53 deletion or mutation is an important reason for the resistance of colorectal cancer cells to 5-fluorouracil. Fluorouracil 0-14 tumor protein p53 Homo sapiens 168-171 32457882-2 2020 5-fluorouracil remains a widely used chemotherapeutic drug in the treatment of advanced colorectal cancer, but chemotherapy drugs are prone to develop drug resistance, p53 deletion or mutation is an important reason for the resistance of colorectal cancer cells to 5-fluorouracil. Fluorouracil 265-279 tumor protein p53 Homo sapiens 168-171 32457882-4 2020 This study aimed to investigate the effect of beta-elemene to 5-fluorouracil in drug-resistant p53-deficient colorectal cancer cells HCT116p53-/-, and determine the possible molecular mechanism of beta-elemene to reverse 5-fluorouracil resistance. Fluorouracil 62-76 tumor protein p53 Homo sapiens 95-98 32457882-9 2020 Determine the role of Cyclin-related protein Cyclin D3 in beta-elemene reversing the resistance of HCT116p53-/- to 5-fluorouracil was detected by overexpression of Cyclin D3. Fluorouracil 115-129 cyclin D3 Homo sapiens 45-54 32457882-9 2020 Determine the role of Cyclin-related protein Cyclin D3 in beta-elemene reversing the resistance of HCT116p53-/- to 5-fluorouracil was detected by overexpression of Cyclin D3. Fluorouracil 115-129 cyclin D3 Homo sapiens 164-173 32382150-5 2020 SNORD3A overexpression had no effect on cell proliferation but specifically sensitized breast cancer cells to 5-fluorouracil (5-FU) in vitro and in vivo. Fluorouracil 110-124 small nucleolar RNA, C/D box 3A Homo sapiens 0-7 32457882-12 2020 Conclusion: beta-elemene enhances the sensitivity of p53 wild-type cells to 5-fluorouracil, beta-elemene can reverse the resistance of HCT116p53-/- to 5-fluorouracil by inducing pro-death autophagy and Cyclin D3-dependent cycle arrest in p53-deficient colorectal cancer, which will provide a new method for the treatment of p53 deletion colorectal cancer patients. Fluorouracil 76-90 tumor protein p53 Homo sapiens 53-56 32382150-5 2020 SNORD3A overexpression had no effect on cell proliferation but specifically sensitized breast cancer cells to 5-fluorouracil (5-FU) in vitro and in vivo. Fluorouracil 126-130 small nucleolar RNA, C/D box 3A Homo sapiens 0-7 32382150-8 2020 miR-185-5p overexpression disrupted the effect of SNORD3A on chemosensitization to 5-FU in vitro and in vivo. Fluorouracil 83-87 small nucleolar RNA, C/D box 3A Homo sapiens 50-57 32382150-12 2020 Our findings indicate that Meis1-regulated SNORD3A specifically sensitizes breast cancer cells to 5-FU via enhancing UMPS expression. Fluorouracil 98-102 small nucleolar RNA, C/D box 3A Homo sapiens 43-50 32382150-13 2020 The SNORD3A-UMPS axis may serve as a potential biomarker and therapeutic target to improve the efficacy of 5-FU-based chemotherapy for breast cancer patients. Fluorouracil 107-111 small nucleolar RNA, C/D box 3A Homo sapiens 4-11 33489855-0 2021 Celecoxib induces apoptosis through Akt inhibition in 5-fluorouracil-resistant gastric cancer cells. Fluorouracil 54-68 AKT serine/threonine kinase 1 Homo sapiens 36-39 32462912-5 2020 We performed functional validation and observed that by targeting HNF4A, HCT116 cells were more sensitive toward both oxaliplatin and 5-fluorouracil significantly. Fluorouracil 134-148 hepatocyte nuclear factor 4 alpha Homo sapiens 66-71 32385145-0 2020 Heat shock and HSP70 regulate 5-FU-mediated caspase-1 activation in myeloid-derived suppressor cells and tumor growth in mice. Fluorouracil 30-34 heat shock protein 1B Mus musculus 15-20 32385145-11 2020 In contrast, in Hsp70-/- MDSCs, 5-FU-mediated caspase-1 activation is increased in vivo and in vitro without effect on 5-FU cytotoxicity. Fluorouracil 32-36 heat shock protein 1B Mus musculus 16-21 32385145-12 2020 In Hsp70-/- mice, the antitumor effect of 5-FU was impeded, with an increased Th17 and angiogenesis markers in tumors. Fluorouracil 42-46 heat shock protein 1B Mus musculus 3-8 32385145-14 2020 CONCLUSION: This study provides evidence on the role of HSP70 in tuning 5-FU antitumor effect and suggests that HS can be used to improve 5-FU anticancer effect. Fluorouracil 72-76 heat shock protein 1B Mus musculus 56-61 31826977-1 2020 LESSONS LEARNED: Trifluridine/tipiracil (FTD/TPI) shows promising antitumor activity in heavily pretreated patients with advanced biliary tract carcinoma, including patients with 5-fluorouracil refractory tumors.FTD/TPI has an acceptable safety profile and should be studied further in patients with advanced biliary tract carcinoma after progression on standard first-line therapy. Fluorouracil 179-193 triosephosphate isomerase 1 Homo sapiens 45-48 32061752-6 2020 We found that the anticancer drugs such as 5-fluorouracil (5-FU) activated the IRE1alpha-XBP1 pathway to induce the expression of ABCB1, ABCC1 and ABCG2 in colon cancer cells. Fluorouracil 43-57 ATP binding cassette subfamily B member 1 Homo sapiens 130-135 32061752-6 2020 We found that the anticancer drugs such as 5-fluorouracil (5-FU) activated the IRE1alpha-XBP1 pathway to induce the expression of ABCB1, ABCC1 and ABCG2 in colon cancer cells. Fluorouracil 43-57 ATP binding cassette subfamily C member 1 Homo sapiens 137-142 32061752-6 2020 We found that the anticancer drugs such as 5-fluorouracil (5-FU) activated the IRE1alpha-XBP1 pathway to induce the expression of ABCB1, ABCC1 and ABCG2 in colon cancer cells. Fluorouracil 43-57 ATP binding cassette subfamily G member 2 (Junior blood group) Homo sapiens 147-152 32061752-6 2020 We found that the anticancer drugs such as 5-fluorouracil (5-FU) activated the IRE1alpha-XBP1 pathway to induce the expression of ABCB1, ABCC1 and ABCG2 in colon cancer cells. Fluorouracil 59-63 ATP binding cassette subfamily B member 1 Homo sapiens 130-135 32061752-6 2020 We found that the anticancer drugs such as 5-fluorouracil (5-FU) activated the IRE1alpha-XBP1 pathway to induce the expression of ABCB1, ABCC1 and ABCG2 in colon cancer cells. Fluorouracil 59-63 ATP binding cassette subfamily C member 1 Homo sapiens 137-142 32061752-6 2020 We found that the anticancer drugs such as 5-fluorouracil (5-FU) activated the IRE1alpha-XBP1 pathway to induce the expression of ABCB1, ABCC1 and ABCG2 in colon cancer cells. Fluorouracil 59-63 ATP binding cassette subfamily G member 2 (Junior blood group) Homo sapiens 147-152 33489855-6 2021 These results suggest that COX-2 expression is associated with 5-FU resistance. Fluorouracil 63-67 mitochondrially encoded cytochrome c oxidase II Homo sapiens 27-32 33489855-7 2021 Unlike AGS FR cells, AGS cells showed increased levels of both cleaved caspase-3 and Bax following 5-FU treatment. Fluorouracil 99-103 caspase 3 Homo sapiens 71-80 33489855-7 2021 Unlike AGS FR cells, AGS cells showed increased levels of both cleaved caspase-3 and Bax following 5-FU treatment. Fluorouracil 99-103 BCL2 associated X, apoptosis regulator Homo sapiens 85-88 33489855-15 2021 Taken together, 5-FU-resistance in gastric cancer is correlated with COX-2 expression, and therefore the selective inhibition of COX-2 leads to suppression of cell proliferation of AGS FR cells. Fluorouracil 16-20 mitochondrially encoded cytochrome c oxidase II Homo sapiens 69-74 33489855-15 2021 Taken together, 5-FU-resistance in gastric cancer is correlated with COX-2 expression, and therefore the selective inhibition of COX-2 leads to suppression of cell proliferation of AGS FR cells. Fluorouracil 16-20 mitochondrially encoded cytochrome c oxidase II Homo sapiens 129-134 33489855-16 2021 Modulation of COX-2 expression and its catalytic activity may be a potential therapeutic strategy to overcome 5-FU-resistant gastric cancer. Fluorouracil 110-114 mitochondrially encoded cytochrome c oxidase II Homo sapiens 14-19 32425596-13 2020 Conclusion: circNRIP1 functioned as a miR-138-5p sponge to enhance hypoxia-induced resistance to 5-FU through modulation of HIF-1alpha-dependent glycolysis, which provides a novel potential approach to overcome hypoxia-induced 5-FU resistance in GC. Fluorouracil 97-101 hypoxia inducible factor 1 subunit alpha Homo sapiens 124-134 32213714-0 2020 Irreversible JNK1-JUN inhibition by JNK-IN-8 sensitizes pancreatic cancer to 5-FU/FOLFOX chemotherapy. Fluorouracil 77-81 mitogen-activated protein kinase 8 Homo sapiens 13-17 32425596-13 2020 Conclusion: circNRIP1 functioned as a miR-138-5p sponge to enhance hypoxia-induced resistance to 5-FU through modulation of HIF-1alpha-dependent glycolysis, which provides a novel potential approach to overcome hypoxia-induced 5-FU resistance in GC. Fluorouracil 227-231 hypoxia inducible factor 1 subunit alpha Homo sapiens 124-134 32004938-0 2020 Patchouli alcohol attenuates 5-fluorouracil-induced intestinal mucositis via TLR2/MyD88/NF-kB pathway and regulation of microbiota. Fluorouracil 29-43 toll-like receptor 2 Rattus norvegicus 77-81 32273521-0 2020 Comparative lipidomics of 5-Fluorouracil-sensitive and -resistant colorectal cancer cells reveals altered sphingomyelin and ceramide controlled by acid sphingomyelinase (SMPD1). Fluorouracil 26-40 sphingomyelin phosphodiesterase 1 Homo sapiens 147-168 32273521-0 2020 Comparative lipidomics of 5-Fluorouracil-sensitive and -resistant colorectal cancer cells reveals altered sphingomyelin and ceramide controlled by acid sphingomyelinase (SMPD1). Fluorouracil 26-40 sphingomyelin phosphodiesterase 1 Homo sapiens 170-175 32273521-7 2020 We found that 5-FU resistance in DLD-1/5-FU colorectal cancer cells was mainly associated with SM increase and Cer decrease, which are controlled by acid sphingomyelinase (SMPD1). Fluorouracil 14-18 sphingomyelin phosphodiesterase 1 Homo sapiens 149-170 32273521-7 2020 We found that 5-FU resistance in DLD-1/5-FU colorectal cancer cells was mainly associated with SM increase and Cer decrease, which are controlled by acid sphingomyelinase (SMPD1). Fluorouracil 14-18 sphingomyelin phosphodiesterase 1 Homo sapiens 172-177 32273521-9 2020 Furthermore, clinical colorectal cancer data set analysis showed that down-regulation of SMPD1 was associated with resistance to chemotherapy regimens that include 5-FU. Fluorouracil 164-168 sphingomyelin phosphodiesterase 1 Homo sapiens 89-94 32273521-10 2020 Thus, from our study, we propose that SM/Cer and SMPD1 are new potential target molecules for therapeutic strategies to overcome 5-FU resistance. Fluorouracil 129-133 sphingomyelin phosphodiesterase 1 Homo sapiens 49-54 32328199-0 2020 Synergistic Effects of Curcumin and 5-Fluorouracil on the Hepatocellular Carcinoma In vivo and vitro through regulating the expression of COX-2 and NF-kappaB. Fluorouracil 36-50 mitochondrially encoded cytochrome c oxidase II Homo sapiens 138-143 32328199-0 2020 Synergistic Effects of Curcumin and 5-Fluorouracil on the Hepatocellular Carcinoma In vivo and vitro through regulating the expression of COX-2 and NF-kappaB. Fluorouracil 36-50 nuclear factor kappa B subunit 1 Homo sapiens 148-157 30693808-0 2020 Cepharanthine combined with 5-fluorouracil inhibits the growth of p53-mutant human colorectal cancer cells. Fluorouracil 28-42 tumor protein p53 Homo sapiens 66-69 31102118-9 2020 Additionally, the combination of cardamonin and 5-FU might result in the apoptosis and cell cycle arrest of BGC-823/5-FU cells, accompanied by the downregulated expression levels of P-glycoprotein, beta-catenin and TCF4. Fluorouracil 48-52 ATP binding cassette subfamily B member 1 Homo sapiens 182-196 32100443-16 2020 Up-regulated BRD4 ultimately promoted cell proliferation and cell survival Down-regulated POU6F2-AS2 showed enhanced sensitivity of 5-FU. Fluorouracil 132-136 bromodomain containing 4 Homo sapiens 13-17 30693808-2 2020 The present study showed that cepharanthine alone or combined with 5-fluorouracil effectively controlled the growth of HT-29 human colorectal cancer cells harboring mutant p53 both in vitro and in vivo. Fluorouracil 67-81 tumor protein p53 Homo sapiens 172-175 32174438-7 2020 Furthermore, GL/f-CNOs hydrogels efficiently load the 5-fluorouracil (5-FU) and show a pH-responsive sustained drug release over 15 days. Fluorouracil 54-68 nitric oxide synthase 3 Homo sapiens 18-22 32174438-7 2020 Furthermore, GL/f-CNOs hydrogels efficiently load the 5-fluorouracil (5-FU) and show a pH-responsive sustained drug release over 15 days. Fluorouracil 70-74 nitric oxide synthase 3 Homo sapiens 18-22 32244885-6 2020 This reduction upgraded the effect of 5-FU by increasing both levels of apoptosis and markers of cell adhesion such as E-cadherin, whereas decreased epithelial-mesenchymal transition markers were associated with aggressive phenotypes and drug resistance, such as beta-catenin nuclear translocation and Zinc finger protein SNAI1 (SNAI1). Fluorouracil 38-42 cadherin 1 Homo sapiens 119-129 32235305-1 2020 Trastuzumab in combination with a platinum and fluorouracil is the treatment of choice for patients with advanced human epidermal growth factor receptor 2 (HER2) positive gastric cancer and gastroesophageal junction (GEJ) cancer. Fluorouracil 47-59 erb-b2 receptor tyrosine kinase 2 Homo sapiens 120-154 32235305-1 2020 Trastuzumab in combination with a platinum and fluorouracil is the treatment of choice for patients with advanced human epidermal growth factor receptor 2 (HER2) positive gastric cancer and gastroesophageal junction (GEJ) cancer. Fluorouracil 47-59 erb-b2 receptor tyrosine kinase 2 Homo sapiens 156-160 32244885-6 2020 This reduction upgraded the effect of 5-FU by increasing both levels of apoptosis and markers of cell adhesion such as E-cadherin, whereas decreased epithelial-mesenchymal transition markers were associated with aggressive phenotypes and drug resistance, such as beta-catenin nuclear translocation and Zinc finger protein SNAI1 (SNAI1). Fluorouracil 38-42 snail family transcriptional repressor 1 Homo sapiens 322-327 32244885-6 2020 This reduction upgraded the effect of 5-FU by increasing both levels of apoptosis and markers of cell adhesion such as E-cadherin, whereas decreased epithelial-mesenchymal transition markers were associated with aggressive phenotypes and drug resistance, such as beta-catenin nuclear translocation and Zinc finger protein SNAI1 (SNAI1). Fluorouracil 38-42 snail family transcriptional repressor 1 Homo sapiens 329-334 32044580-2 2020 Most sulfonamide derivatives efficiently inhibit the target CA IX (KIs in the range 0.47-44.7 nM) and CA XII (KIs in the range 2.9-83.1 nM), while the 5-FU coumarin derivatives showed a potent and totally selective inhibitory action against the target CA IX/XII over off-target CA I/II. Fluorouracil 151-155 carbonic anhydrase 3 Homo sapiens 278-285 32017310-2 2020 The most common drugs include capecitabine, pegylated liposomal doxorubicin and fluorouracil(PLD), tyrosine kinase inhibitor(TKI). Fluorouracil 80-92 glycosylphosphatidylinositol specific phospholipase D1 Homo sapiens 93-96 32122395-0 2020 New uracil analog U-332 is an inhibitor of NF-kappaB in 5-fluorouracil-resistant human leukemia HL-60 cell line. Fluorouracil 56-70 nuclear factor kappa B subunit 1 Homo sapiens 43-52 32122395-11 2020 RESULTS: In this report it was demonstrated, using RT-PCR and ELISA assay, that members of the NF-kappaB family c-Rel, RelA, RelB, NF-kappaB1, and NF-kappaB2 were all overexpressed in the 5-FU-resistant HL-60/5FU cells and that U-332 potently reduced the activity of c-Rel, RelA and NF-kappaB1 subunits in this cell line. Fluorouracil 188-192 nuclear factor kappa B subunit 1 Homo sapiens 95-104 32266094-0 2020 Endoplasmic reticulum stress confers 5-fluorouracil resistance in breast cancer cell via the GRP78/OCT4/lncRNA MIAT/AKT pathway. Fluorouracil 37-51 heat shock protein family A (Hsp70) member 5 Homo sapiens 93-98 32266094-0 2020 Endoplasmic reticulum stress confers 5-fluorouracil resistance in breast cancer cell via the GRP78/OCT4/lncRNA MIAT/AKT pathway. Fluorouracil 37-51 myocardial infarction associated transcript Homo sapiens 111-115 32266094-0 2020 Endoplasmic reticulum stress confers 5-fluorouracil resistance in breast cancer cell via the GRP78/OCT4/lncRNA MIAT/AKT pathway. Fluorouracil 37-51 AKT serine/threonine kinase 1 Homo sapiens 116-119 31788833-8 2020 It was also found that inhibition of TMEM45A increased the intracellular accumulation of Rhodamine-123 and down-regulated the expression of MDR1 in HCT-8/5-FU and SW480/5-FU cells. Fluorouracil 154-158 ATP binding cassette subfamily B member 1 Homo sapiens 140-144 31788833-8 2020 It was also found that inhibition of TMEM45A increased the intracellular accumulation of Rhodamine-123 and down-regulated the expression of MDR1 in HCT-8/5-FU and SW480/5-FU cells. Fluorouracil 169-173 ATP binding cassette subfamily B member 1 Homo sapiens 140-144 32109848-7 2020 RESULTS: We demonstrated that high intratumoral DC-SIGN+ macrophages infiltration predicted poor OS and inferior therapeutic responsiveness to fluorouracil-based ACT in patients with gastric cancer. Fluorouracil 143-155 CD209 molecule Homo sapiens 48-55 32109848-10 2020 CONCLUSIONS: DC-SIGN+ macrophages were associated with immunoinvasive TME and indicated poor prognosis and inferior therapeutic responsiveness to fluorouracil-based ACT. Fluorouracil 146-158 CD209 molecule Homo sapiens 13-20 32266127-12 2020 ESR1 expression was significantly correlated with 5-flurouracil (5-FU)-based adjuvant chemotherapy in training with an HR of 1.792 (95%CI: 1.100-2.921, p = 0.019). Fluorouracil 65-69 estrogen receptor 1 Homo sapiens 0-4 32266127-13 2020 Downregulation of ESR1 was related with enhanced chemosensitivity to 5-FU in CRC cell lines, while upregulation of ESR1 was correlated with decreased chemosensitivity. Fluorouracil 69-73 estrogen receptor 1 Homo sapiens 18-22 32266127-14 2020 Conclusions: The present study manifest clinical validity of ESR1 expression as a predictive biomarker on 5-FU-based adjuvant chemotherapy in stage II-III CRC. Fluorouracil 106-110 estrogen receptor 1 Homo sapiens 61-65 32266094-9 2020 5-FU induced ER stress increased the expression of GRP78 in MCF-7 cells. Fluorouracil 0-4 heat shock protein 5 Mus musculus 51-56 32266094-10 2020 GRP78 could positively regulate the expression of MIAT and AKT through upregulating OCT4, thereby contributing to 5-FU resistance in BC cells. Fluorouracil 114-118 heat shock protein family A (Hsp70) member 5 Homo sapiens 0-5 32266094-10 2020 GRP78 could positively regulate the expression of MIAT and AKT through upregulating OCT4, thereby contributing to 5-FU resistance in BC cells. Fluorouracil 114-118 myocardial infarction associated transcript Homo sapiens 50-54 32266094-10 2020 GRP78 could positively regulate the expression of MIAT and AKT through upregulating OCT4, thereby contributing to 5-FU resistance in BC cells. Fluorouracil 114-118 AKT serine/threonine kinase 1 Homo sapiens 59-62 32266094-12 2020 These data supported an important role of the ER stress-mediated GRP78/OCT4/lncRNA MIAT/AKT pathway in BC cell resistance to 5-FU, highlighting potential molecular targets for combating 5-FU resistance in BC. Fluorouracil 125-129 heat shock protein family A (Hsp70) member 5 Homo sapiens 65-70 32266094-12 2020 These data supported an important role of the ER stress-mediated GRP78/OCT4/lncRNA MIAT/AKT pathway in BC cell resistance to 5-FU, highlighting potential molecular targets for combating 5-FU resistance in BC. Fluorouracil 125-129 myocardial infarction associated transcript Homo sapiens 76-87 32266094-12 2020 These data supported an important role of the ER stress-mediated GRP78/OCT4/lncRNA MIAT/AKT pathway in BC cell resistance to 5-FU, highlighting potential molecular targets for combating 5-FU resistance in BC. Fluorouracil 125-129 AKT serine/threonine kinase 1 Homo sapiens 88-91 32266094-12 2020 These data supported an important role of the ER stress-mediated GRP78/OCT4/lncRNA MIAT/AKT pathway in BC cell resistance to 5-FU, highlighting potential molecular targets for combating 5-FU resistance in BC. Fluorouracil 186-190 heat shock protein family A (Hsp70) member 5 Homo sapiens 65-70 32266094-12 2020 These data supported an important role of the ER stress-mediated GRP78/OCT4/lncRNA MIAT/AKT pathway in BC cell resistance to 5-FU, highlighting potential molecular targets for combating 5-FU resistance in BC. Fluorouracil 186-190 AKT serine/threonine kinase 1 Homo sapiens 88-91 31960523-10 2020 Temsirolimus, an mTOR inhibitor, reduced the number of 5FU-tolerant persister cells. Fluorouracil 55-58 mechanistic target of rapamycin kinase Homo sapiens 17-21 32194724-5 2020 In vitro assays demonstrated that RPL11 knockdown in gastric cancer cell lines carrying the TP53 wild-type gene attenuated 5-FU-induced cell growth suppression and activation of the P53 pathway, but not in cells carrying mutated TP53, suggesting that 5-FU suppresses tumor progression via RPL11-mediated activation of the P53 pathway in gastric cancer. Fluorouracil 123-127 tumor protein p53 Homo sapiens 92-96 32133800-0 2020 Amyloid precursor protein regulates 5-fluorouracil resistance in human hepatocellular carcinoma cells by inhibiting the mitochondrial apoptotic pathway. Fluorouracil 36-50 amyloid beta precursor protein Homo sapiens 0-25 31923958-7 2020 Importantly, the cytotoxicity and cell apoptosis assays confirmed that co-delivery of 5-FU and p53 gene by the cross-linked MSN-g-PCAAMC-b-PDMAEMA@5-FU/p53 induced enhanced chemotherapeutic efficacy as compared to 5-FU delivery alone. Fluorouracil 86-90 tumor protein p53 Homo sapiens 152-155 31923958-7 2020 Importantly, the cytotoxicity and cell apoptosis assays confirmed that co-delivery of 5-FU and p53 gene by the cross-linked MSN-g-PCAAMC-b-PDMAEMA@5-FU/p53 induced enhanced chemotherapeutic efficacy as compared to 5-FU delivery alone. Fluorouracil 147-151 tumor protein p53 Homo sapiens 95-98 31923958-7 2020 Importantly, the cytotoxicity and cell apoptosis assays confirmed that co-delivery of 5-FU and p53 gene by the cross-linked MSN-g-PCAAMC-b-PDMAEMA@5-FU/p53 induced enhanced chemotherapeutic efficacy as compared to 5-FU delivery alone. Fluorouracil 147-151 tumor protein p53 Homo sapiens 95-98 32194724-5 2020 In vitro assays demonstrated that RPL11 knockdown in gastric cancer cell lines carrying the TP53 wild-type gene attenuated 5-FU-induced cell growth suppression and activation of the P53 pathway, but not in cells carrying mutated TP53, suggesting that 5-FU suppresses tumor progression via RPL11-mediated activation of the P53 pathway in gastric cancer. Fluorouracil 123-127 tumor protein p53 Homo sapiens 93-96 32194724-5 2020 In vitro assays demonstrated that RPL11 knockdown in gastric cancer cell lines carrying the TP53 wild-type gene attenuated 5-FU-induced cell growth suppression and activation of the P53 pathway, but not in cells carrying mutated TP53, suggesting that 5-FU suppresses tumor progression via RPL11-mediated activation of the P53 pathway in gastric cancer. Fluorouracil 123-127 tumor protein p53 Homo sapiens 182-185 32100959-9 2021 More importantly, the anti-oncogenic effect of HZC and 5-FU was implicated with activation of the p38 MAPK pathway. Fluorouracil 55-59 mitogen-activated protein kinase 14 Homo sapiens 98-101 32100959-10 2021 In vivo experimental results showed that HZC inhibited tumor growth more effectively than 5-FU through the p38 MAPK pathway. Fluorouracil 90-94 mitogen-activated protein kinase 14 Homo sapiens 107-110 32014926-2 2020 MATERIALS AND METHODS: Calcitriol and tacalcitol were used to increase the antiproliferative effect of 5-fluorouracil against the following human breast cancer cell lines: MCF-7, T47D, BT-474 (luminal); JIMT-1, SKBR-3 (HER2-enriched); MDA-MB-231 (triple-negative/basal-B), and non-malignant MCF-10A breast epithelial cells. Fluorouracil 103-117 erb-b2 receptor tyrosine kinase 2 Homo sapiens 219-223 31781926-2 2020 RESULTS: We successfully implemented a markerless deletion of upp in Pf-5 to obtain the 5-FU resistant strain Pf5139. Fluorouracil 88-92 upp Pseudomonas protegens Pf-5 62-65 31811910-8 2020 Taken together, our results suggest that FoxO3 could reverse 5-FU resistance in CRC via inhibiting the Nrf2/TR1 signaling pathway, and increasing the level of intracellular reactive oxygen species. Fluorouracil 61-65 forkhead box O3 Homo sapiens 41-46 31811910-8 2020 Taken together, our results suggest that FoxO3 could reverse 5-FU resistance in CRC via inhibiting the Nrf2/TR1 signaling pathway, and increasing the level of intracellular reactive oxygen species. Fluorouracil 61-65 NFE2 like bZIP transcription factor 2 Homo sapiens 103-107 31811910-9 2020 Chemotherapeutic agents targeting FoxO3 and/or TR1, including AUR, might be promising adjuvant sensitizers to reverse chemoresistance in 5-FU-resistant CRC. Fluorouracil 137-141 forkhead box O3 Homo sapiens 34-39 32098629-11 2020 Additionally, up-regulation of MUC5AC resulted in resistance to 5-fluorouracil (5-FU) and oxaliplatin, and its knockout increased sensitivity to these drugs. Fluorouracil 64-78 mucin 5, subtypes A and C, tracheobronchial/gastric Mus musculus 31-37 32098629-11 2020 Additionally, up-regulation of MUC5AC resulted in resistance to 5-fluorouracil (5-FU) and oxaliplatin, and its knockout increased sensitivity to these drugs. Fluorouracil 80-84 mucin 5, subtypes A and C, tracheobronchial/gastric Mus musculus 31-37 32098629-12 2020 Finally, we observed that up-regulation of MUC5AC conferred resistance to 5-FU through down-regulation of p53 and its target gene p21 and up-regulation of beta-catenin and its target genes CD44 and Lgr5. Fluorouracil 74-78 mucin 5, subtypes A and C, tracheobronchial/gastric Mus musculus 43-49 32190532-8 2020 VEGF silencing by the polyplex was found to augment the cytotoxic effects of the chemotherapeutic agent 5-fluorouracil. Fluorouracil 104-118 vascular endothelial growth factor A Homo sapiens 0-4 31959339-1 2020 BACKGROUND: Palliative chemotherapy of advanced oesophageal squamous cell cancer (ESCC) consists of cisplatin/5-fluorouracil (CF) to target epidermal growth factor receptor (EGFR) with panitumumab (P); chemotherapy enhanced overall survival (OS) in advanced colorectal or squamous cell head and neck cancers. Fluorouracil 110-124 epidermal growth factor receptor Homo sapiens 140-172 31959339-1 2020 BACKGROUND: Palliative chemotherapy of advanced oesophageal squamous cell cancer (ESCC) consists of cisplatin/5-fluorouracil (CF) to target epidermal growth factor receptor (EGFR) with panitumumab (P); chemotherapy enhanced overall survival (OS) in advanced colorectal or squamous cell head and neck cancers. Fluorouracil 110-124 Moloney sarcoma oncogene Mus musculus 242-244 31811910-0 2020 FoxO3 reverses 5-fluorouracil resistance in human colorectal cancer cells by inhibiting the Nrf2/TR1 signaling pathway. Fluorouracil 15-29 forkhead box O3 Homo sapiens 0-5 31811910-0 2020 FoxO3 reverses 5-fluorouracil resistance in human colorectal cancer cells by inhibiting the Nrf2/TR1 signaling pathway. Fluorouracil 15-29 NFE2 like bZIP transcription factor 2 Homo sapiens 92-96 31811910-2 2020 We found remarkably decreased expression of forkhead box 3 (FoxO3) protein, a tumor inhibitor, in 5-FU-resistant SW620 and HCT-8 (SW620/5-FU and HCT-8/5-FU) cells. Fluorouracil 98-102 forkhead box O3 Homo sapiens 60-65 31811910-2 2020 We found remarkably decreased expression of forkhead box 3 (FoxO3) protein, a tumor inhibitor, in 5-FU-resistant SW620 and HCT-8 (SW620/5-FU and HCT-8/5-FU) cells. Fluorouracil 136-140 forkhead box O3 Homo sapiens 60-65 31811910-2 2020 We found remarkably decreased expression of forkhead box 3 (FoxO3) protein, a tumor inhibitor, in 5-FU-resistant SW620 and HCT-8 (SW620/5-FU and HCT-8/5-FU) cells. Fluorouracil 136-140 forkhead box O3 Homo sapiens 60-65 31811910-3 2020 Moreover, FoxO3 overexpression sensitized SW620/5-FU and HCT-8/5-FU cells to 5-FU. Fluorouracil 48-52 forkhead box O3 Homo sapiens 10-15 31811910-3 2020 Moreover, FoxO3 overexpression sensitized SW620/5-FU and HCT-8/5-FU cells to 5-FU. Fluorouracil 63-67 forkhead box O3 Homo sapiens 10-15 31811910-3 2020 Moreover, FoxO3 overexpression sensitized SW620/5-FU and HCT-8/5-FU cells to 5-FU. Fluorouracil 63-67 forkhead box O3 Homo sapiens 10-15 31811910-5 2020 Thioredoxin reductase 1 (TR1), a pivotal target gene of Nrf2, was observed to promote 5-FU resistance by reducing intracellular ROS levels. Fluorouracil 86-90 NFE2 like bZIP transcription factor 2 Homo sapiens 56-60 31518438-0 2020 BTK inhibitors synergize with 5-FU to treat drug-resistant TP53-null colon cancers. Fluorouracil 30-34 tumor protein p53 Homo sapiens 59-63 31872284-7 2020 Collectively, these data indicated that NOD1 suppressed proliferation and enhanced response to sorafenib or 5-FU treatment through inhibiting SRC-MAPK axis in hepatocellular carcinoma. Fluorouracil 108-112 SRC proto-oncogene, non-receptor tyrosine kinase Homo sapiens 142-145 31760170-0 2020 LncRNA HAND2-AS1 inhibits 5-fluorouracil resistance by modulating miR-20a/PDCD4 axis in colorectal cancer. Fluorouracil 26-40 microRNA 20a Homo sapiens 66-73 31760170-12 2020 RESULTS: HAND2-AS1 and PDCD4 were downregulated and miR-20a was upregulated in 5-FU-resistant CRC tissues and cells. Fluorouracil 79-83 microRNA 20a Homo sapiens 52-59 31760170-13 2020 HAND2-AS1 suppressed 5-FU resistance, cell proliferation, migration and invasion and promoted cell apoptosis in 5-FU-resistant CRC cells. Fluorouracil 21-25 arylsulfatase B Mus musculus 6-9 31760170-13 2020 HAND2-AS1 suppressed 5-FU resistance, cell proliferation, migration and invasion and promoted cell apoptosis in 5-FU-resistant CRC cells. Fluorouracil 112-116 arylsulfatase B Mus musculus 6-9 31760170-15 2020 Moreover, HAND2-AS1 suppressed cell progression and 5-FU resistance by upregulating PDCD4 via sponging miR-20a in 5-FU-resistant CRC cells. Fluorouracil 52-56 arylsulfatase B Mus musculus 16-19 31760170-15 2020 Moreover, HAND2-AS1 suppressed cell progression and 5-FU resistance by upregulating PDCD4 via sponging miR-20a in 5-FU-resistant CRC cells. Fluorouracil 114-118 arylsulfatase B Mus musculus 16-19 31760170-15 2020 Moreover, HAND2-AS1 suppressed cell progression and 5-FU resistance by upregulating PDCD4 via sponging miR-20a in 5-FU-resistant CRC cells. Fluorouracil 114-118 microRNA 20a Homo sapiens 103-110 31760170-17 2020 CONCLUSION: HAND2-AS1/miR-20a/PDCD4 axis inhibited cell progression and 5-FU resistance in 5-FU-resistant CRC cells. Fluorouracil 72-76 arylsulfatase B Mus musculus 18-21 31760170-17 2020 CONCLUSION: HAND2-AS1/miR-20a/PDCD4 axis inhibited cell progression and 5-FU resistance in 5-FU-resistant CRC cells. Fluorouracil 72-76 microRNA 20a Homo sapiens 22-29 31760170-17 2020 CONCLUSION: HAND2-AS1/miR-20a/PDCD4 axis inhibited cell progression and 5-FU resistance in 5-FU-resistant CRC cells. Fluorouracil 91-95 arylsulfatase B Mus musculus 18-21 31760170-17 2020 CONCLUSION: HAND2-AS1/miR-20a/PDCD4 axis inhibited cell progression and 5-FU resistance in 5-FU-resistant CRC cells. Fluorouracil 91-95 microRNA 20a Homo sapiens 22-29 31746054-5 2020 Exposure to specific TLR2/6 or TLR5 ligands enhanced the expression of mesenchymal markers as well as the migratory activity of oxaliplatin- or 5-fluorouracil-resistant colon cancer cells. Fluorouracil 144-158 toll like receptor 2 Homo sapiens 21-27 31518438-4 2020 Using drug-resistant TP53-null colon cancer cells as a model we demonstrated that p65BTK silencing or chemical inhibition overcame the 5-fluorouracil resistance of CRC cell lines and patient-derived organoids and significantly reduced the growth of xenografted tumours. Fluorouracil 135-149 tumor protein p53 Homo sapiens 21-25 31518438-5 2020 Mechanistically, we show that blocking p65BTK in drug-resistant cells abolished a 5-FU-elicited TGFB1 protective response and triggered E2F-dependent apoptosis. Fluorouracil 82-86 transforming growth factor beta 1 Homo sapiens 96-101 31899315-0 2020 Modified Bu-zhong-yi-qi decoction synergies with 5 fluorouracile to inhibits gastric cancer progress via PD-1/PD- L1-dependent T cell immunization. Fluorouracil 51-64 CD274 molecule Sus scrofa 110-116 32043796-14 2020 IMPLICATIONS FOR PRACTICE: For RAS/RAF wild-type metastatic colorectal cancer, patients may receive 5-fluorouracil-based chemotherapy plus either bevacizumab or an anti-epidermal growth factor receptor (EGFR). Fluorouracil 100-114 epidermal growth factor receptor Homo sapiens 203-207 31837576-4 2020 Adding the epidermal growth factor receptor (EGFR) inhibitor cetuximab to a platinum/5-fluorouracil doublet (the so-called EXTREME regimen) produced a statistically but also clinically significant improvement of survival and became thus the standard first-line palliative treatment in adequately fit patients. Fluorouracil 85-99 epidermal growth factor receptor Homo sapiens 11-43 31708100-6 2020 In addition, the expression level of BRD4 was high in HCT116 cells exposed to 5-FU that showed lower apoptosis against the parental cells. Fluorouracil 78-82 bromodomain containing 4 Homo sapiens 37-41 31898732-8 2020 Moreover, SRPK2, Numb and p53 coimmunoprecipitated into a triple complex without or with the treatment of 5-fluorouracil in HCT116 cells, and p53 knockdown reversed the upregulation of wtp53 induced by SRPK2 silencing with chemical agent treatment. Fluorouracil 106-120 tumor protein p53 Homo sapiens 26-29 31864766-0 2020 Corrigendum to "5-Fluorouracil causes severe CNS demyelination by disruption of TCF7L2/HDAC1/HDAC2 complex in adolescent mice" [Toxicology 325 (2014) 144-150]. Fluorouracil 16-30 histone deacetylase 2 Mus musculus 93-98 31708100-7 2020 Moreover, the 5-FU-resistance was reversed significantly by BRD4 knockdown or inhibition. Fluorouracil 14-18 bromodomain containing 4 Homo sapiens 60-64 31947551-0 2020 Anti-EGFR-Coated Gold Nanoparticles In Vitro Carry 5-Fluorouracil to Colorectal Cancer Cells. Fluorouracil 51-65 epidermal growth factor receptor Homo sapiens 5-9 31961109-0 2020 Upregulation of RBM5 reverses 5-Fluorouracil resistance in human breast cancer cells. Fluorouracil 30-44 RNA binding motif protein 5 Homo sapiens 16-20 31947551-2 2020 5-FU was loaded on gold nanoparticles (AuNP) coated with anti-EGFR antibodies in order to target them towards colorectal cancer cells that overexpress epidermal growth factor receptors (EGFR). Fluorouracil 0-4 epidermal growth factor receptor Homo sapiens 62-66 31947551-2 2020 5-FU was loaded on gold nanoparticles (AuNP) coated with anti-EGFR antibodies in order to target them towards colorectal cancer cells that overexpress epidermal growth factor receptors (EGFR). Fluorouracil 0-4 epidermal growth factor receptor Homo sapiens 151-184 31947551-2 2020 5-FU was loaded on gold nanoparticles (AuNP) coated with anti-EGFR antibodies in order to target them towards colorectal cancer cells that overexpress epidermal growth factor receptors (EGFR). Fluorouracil 0-4 epidermal growth factor receptor Homo sapiens 186-190 31911756-0 2020 TSPAN9 suppresses the chemosensitivity of gastric cancer to 5-fluorouracil by promoting autophagy. Fluorouracil 60-74 tetraspanin 9 Homo sapiens 0-6 31371781-9 2020 In a tail vein injection pulmonary metastasis mouse model, intraperitoneal administration of garcinol (20 mg/kg) or 5-FU (20 mg/kg) significantly decreased the number of lung tumor nodules and the expression levels of Ki-67, p300, and p-Smad2/3 in lung tissues. Fluorouracil 116-120 SMAD family member 2 Mus musculus 237-244 31840981-2 2020 Here, a fusion protein was designed with both an antiepidermal growth factor receptor (EGFR) affibody and the prodrug enzyme cytosine deaminase, which can convert prodrug 5-fluorocytosine to the anticancer drug 5-fluorouracil. Fluorouracil 211-225 epidermal growth factor receptor Homo sapiens 87-91 31918721-4 2020 RESULTS: In this study, Engineered exosomes were exploited to simultaneously deliver an anticancer drug 5-FU and miR-21 inhibitor oligonucleotide (miR-21i) to Her2 expressing cancer cells. Fluorouracil 104-108 erb-b2 receptor tyrosine kinase 2 Homo sapiens 159-163 31896739-0 2020 Over-expression of EGFR regulated by RARA contributes to 5-FU resistance in colon cancer. Fluorouracil 57-61 epidermal growth factor receptor Homo sapiens 19-23 31896739-8 2020 The regulatory role of EGFR in 5-FU resistance was validated in colon cancer cells in vivo and in vitro. Fluorouracil 31-35 epidermal growth factor receptor Homo sapiens 23-27 31896739-9 2020 EGFR contributed to 5-FU resistance in colon cancer cells through autophagy induction, and EGFR overexpression in 5-FU resistant colon cancer was regulated by RARA. Fluorouracil 20-24 epidermal growth factor receptor Homo sapiens 0-4 31896739-9 2020 EGFR contributed to 5-FU resistance in colon cancer cells through autophagy induction, and EGFR overexpression in 5-FU resistant colon cancer was regulated by RARA. Fluorouracil 114-118 epidermal growth factor receptor Homo sapiens 91-95 32731241-5 2020 Intestinal-type adenocarcinoma carrying a functional p53 protein may be treated with preoperative cisplatin, 5-fluorouracil, and leucovorin. Fluorouracil 109-123 tumor protein p53 Homo sapiens 53-56 31911756-4 2020 Functional assays, such as the CCK-8 assay, were used to detect the proliferation of gastric cancer cells and the response of TSPAN9 to 5-fluorouracil (5-FU). Fluorouracil 136-150 tetraspanin 9 Homo sapiens 126-132 32999157-4 2020 Taking ADR data for fluorouracil as an example, we collected the three types of data and extracted their ADR information. Fluorouracil 20-32 aldo-keto reductase family 1 member B Homo sapiens 7-10 31911756-4 2020 Functional assays, such as the CCK-8 assay, were used to detect the proliferation of gastric cancer cells and the response of TSPAN9 to 5-fluorouracil (5-FU). Fluorouracil 152-156 tetraspanin 9 Homo sapiens 126-132 31911756-7 2020 Results: We demonstrated that TSPAN9 is overexpressed in 5-FU-resistant cells compared to parental cells. Fluorouracil 57-61 tetraspanin 9 Homo sapiens 30-36 31911756-8 2020 5-FU-mediated inhibition of cell proliferation can be significantly restored by increasing TSPAN9 expression, and inhibiting this expression in drug-resistant cells can restore the sensitivity of the cells to 5-FU. Fluorouracil 0-4 tetraspanin 9 Homo sapiens 91-97 31911756-12 2020 Conclusion: The current study reveals the important role of TSPAN9 in drug resistance to 5-FU in gastric cancer. Fluorouracil 89-93 tetraspanin 9 Homo sapiens 60-66 32865180-0 2020 Circ_0007031 enhances tumor progression and promotes 5-fluorouracil resistance in colorectal cancer through regulating miR-133b/ABCC5 axis. Fluorouracil 53-67 microRNA 133b Homo sapiens 119-127 31704613-0 2020 APC truncating mutations in Middle Eastern Population: Tankyrase inhibitor is an effective strategy to sensitize APC mutant CRC To 5-FU chemotherapy. Fluorouracil 131-135 tankyrase Homo sapiens 55-64 31704613-9 2020 Importantly, we were able to overcome the resistance to 5-FU seen in CRC cells carrying short APC by tankyrase inhibitor, XAV939, thereby inhibiting Wnt/beta-catenin signaling cascade. Fluorouracil 56-60 tankyrase Homo sapiens 101-110 31704613-11 2020 Furthermore, in vitro data showed that selective targeting of APC mutated CRC by tankyrase inhibitor can be an effective strategy to overcome 5-FU resistance in CRC cells. Fluorouracil 142-146 tankyrase Homo sapiens 81-90 32865180-17 2020 Our current work had led to the identification of circ_0007031 knockdown that repressed CRC cell malignant progression and enhanced 5-FU sensitivity via regulating ABCC5 expression by sponging miR-133b. Fluorouracil 132-136 microRNA 133b Homo sapiens 193-201 32865180-13 2020 Moreover, circ_0007031 knockdown regulated CRC cell progression and 5-FU sensitivity by miR-133b. Fluorouracil 68-72 microRNA 133b Homo sapiens 88-96 32865180-15 2020 Furthermore, miR-133b overexpression regulated CRC cell progression and sensitivity to 5-FU by down-regulating ABCC5. Fluorouracil 87-91 microRNA 133b Homo sapiens 13-21 31736281-5 2020 Of these genes, ABCG2, AHNAK2, BCL2, FZD1, and TP73 are associated with published evidence for resistance to 5-fluorouracil and cisplatin. Fluorouracil 109-123 ATP binding cassette subfamily G member 2 (Junior blood group) Homo sapiens 16-21 31774615-3 2020 CRC cells overexpressing Snail was illustrated to be more resistant to 5-fluorouracil (5-Fu). Fluorouracil 71-85 snail family transcriptional repressor 1 Homo sapiens 25-30 31774615-3 2020 CRC cells overexpressing Snail was illustrated to be more resistant to 5-fluorouracil (5-Fu). Fluorouracil 87-91 snail family transcriptional repressor 1 Homo sapiens 25-30 31774615-5 2020 Additionally, knockdown of ABCB1 significantly attenuated Snail-induced 5-Fu-resistance in CRC cells. Fluorouracil 72-76 ATP binding cassette subfamily B member 1 Homo sapiens 27-32 31774615-5 2020 Additionally, knockdown of ABCB1 significantly attenuated Snail-induced 5-Fu-resistance in CRC cells. Fluorouracil 72-76 snail family transcriptional repressor 1 Homo sapiens 58-63 31774615-7 2020 Snail and ABCB1 were upregulated in 5-Fu resistant HCT-8 (HCT-8/5-Fu) cells and inhibition of Snail decreased ABCB1 in HCT-8/5-Fu cells. Fluorouracil 36-40 snail family transcriptional repressor 1 Homo sapiens 0-5 31774615-7 2020 Snail and ABCB1 were upregulated in 5-Fu resistant HCT-8 (HCT-8/5-Fu) cells and inhibition of Snail decreased ABCB1 in HCT-8/5-Fu cells. Fluorouracil 36-40 ATP binding cassette subfamily B member 1 Homo sapiens 10-15 31774615-7 2020 Snail and ABCB1 were upregulated in 5-Fu resistant HCT-8 (HCT-8/5-Fu) cells and inhibition of Snail decreased ABCB1 in HCT-8/5-Fu cells. Fluorouracil 64-68 snail family transcriptional repressor 1 Homo sapiens 0-5 31774615-7 2020 Snail and ABCB1 were upregulated in 5-Fu resistant HCT-8 (HCT-8/5-Fu) cells and inhibition of Snail decreased ABCB1 in HCT-8/5-Fu cells. Fluorouracil 64-68 ATP binding cassette subfamily B member 1 Homo sapiens 10-15 31774615-7 2020 Snail and ABCB1 were upregulated in 5-Fu resistant HCT-8 (HCT-8/5-Fu) cells and inhibition of Snail decreased ABCB1 in HCT-8/5-Fu cells. Fluorouracil 64-68 snail family transcriptional repressor 1 Homo sapiens 94-99 31774615-7 2020 Snail and ABCB1 were upregulated in 5-Fu resistant HCT-8 (HCT-8/5-Fu) cells and inhibition of Snail decreased ABCB1 in HCT-8/5-Fu cells. Fluorouracil 64-68 snail family transcriptional repressor 1 Homo sapiens 0-5 31774615-7 2020 Snail and ABCB1 were upregulated in 5-Fu resistant HCT-8 (HCT-8/5-Fu) cells and inhibition of Snail decreased ABCB1 in HCT-8/5-Fu cells. Fluorouracil 64-68 ATP binding cassette subfamily B member 1 Homo sapiens 10-15 31774615-7 2020 Snail and ABCB1 were upregulated in 5-Fu resistant HCT-8 (HCT-8/5-Fu) cells and inhibition of Snail decreased ABCB1 in HCT-8/5-Fu cells. Fluorouracil 64-68 snail family transcriptional repressor 1 Homo sapiens 94-99 31401369-0 2020 Modulation of 5-fluorouracil activation of toll-like/MyD88/NF-kappaB/MAPK pathway by Saccharomyces boulardii CNCM I-745 probiotic. Fluorouracil 14-28 nuclear factor kappa B subunit 1 Homo sapiens 59-68 31736281-5 2020 Of these genes, ABCG2, AHNAK2, BCL2, FZD1, and TP73 are associated with published evidence for resistance to 5-fluorouracil and cisplatin. Fluorouracil 109-123 BCL2 apoptosis regulator Homo sapiens 31-35 31835085-13 2020 Serum IFN-gamma is significantly increased by LDN but decreased by 5-FU. Fluorouracil 67-71 interferon gamma Mus musculus 6-15 31835085-14 2020 Also, LDN and 5FU increased immunehistochemical staining of p21 while decreased immunostaining of Bcl2. Fluorouracil 14-17 B cell leukemia/lymphoma 2 Mus musculus 98-102 31835085-15 2020 In animals treated with a combination of LDN and 5FU a maximal downregulation of the antiapoptotic mediator BCL2 was observed. Fluorouracil 49-52 B cell leukemia/lymphoma 2 Mus musculus 108-112 31753399-6 2020 The expression of Caspase-3 and Caspase-9 apoptosis-related protein levels was slightly upregulated and Atg5 autophagy-related protein level was clearly downregulated according to control and 5-FU-treated cells after complex I and II treatment. Fluorouracil 192-196 caspase 3 Homo sapiens 18-27 32247577-7 2020 BOK, a BCL-2 family protein thought comparable to multidomain pro-apoptotic proteins BAX and BAK, has recently been identified as a key player in metabolism of and resistance to the commonly used chemotherapeutic 5-FU. Fluorouracil 213-217 BCL2 family apoptosis regulator BOK Homo sapiens 0-3 32247577-7 2020 BOK, a BCL-2 family protein thought comparable to multidomain pro-apoptotic proteins BAX and BAK, has recently been identified as a key player in metabolism of and resistance to the commonly used chemotherapeutic 5-FU. Fluorouracil 213-217 BCL2 apoptosis regulator Homo sapiens 7-12 32247577-7 2020 BOK, a BCL-2 family protein thought comparable to multidomain pro-apoptotic proteins BAX and BAK, has recently been identified as a key player in metabolism of and resistance to the commonly used chemotherapeutic 5-FU. Fluorouracil 213-217 BCL2 associated X, apoptosis regulator Homo sapiens 85-88 32247577-8 2020 As a result of such findings, which could see the potential use of BOK as a biomarker for 5-FU sensitivity or mimetic molecules as a resensitization strategy, new targets and mechanisms of pathology may arise from further investigation into the realm of alternate functions of BCL-2 family proteins. Fluorouracil 90-94 BCL2 family apoptosis regulator BOK Homo sapiens 67-70 31753399-6 2020 The expression of Caspase-3 and Caspase-9 apoptosis-related protein levels was slightly upregulated and Atg5 autophagy-related protein level was clearly downregulated according to control and 5-FU-treated cells after complex I and II treatment. Fluorouracil 192-196 autophagy related 5 Homo sapiens 104-108 31903119-9 2020 Further in vitro and in vivo models demonstrated that PiHL was crucial in maintaining cell proliferation and inducing 5-FU chemoresistance through a p53-dependent manner. Fluorouracil 118-122 tumor protein p53 Homo sapiens 149-152 31897166-0 2020 Oxymatrine reverses 5-fluorouracil resistance by inhibition of colon cancer cell epithelial-mesenchymal transition and NF-kappaB signaling in vitro. Fluorouracil 20-34 nuclear factor kappa B subunit 1 Homo sapiens 119-128 31897166-6 2020 The combination of oxymatrine and 5-FU reduced the protein expression of snail family transcriptional repressor 2 and vimentin, phosphorylated p65 and induced the expression of E-cadherin, by inhibiting the nuclear factor kappaB (NF-kappaB) signaling pathway. Fluorouracil 34-38 cadherin 1 Homo sapiens 177-187 31897166-6 2020 The combination of oxymatrine and 5-FU reduced the protein expression of snail family transcriptional repressor 2 and vimentin, phosphorylated p65 and induced the expression of E-cadherin, by inhibiting the nuclear factor kappaB (NF-kappaB) signaling pathway. Fluorouracil 34-38 nuclear factor kappa B subunit 1 Homo sapiens 222-228 31897166-6 2020 The combination of oxymatrine and 5-FU reduced the protein expression of snail family transcriptional repressor 2 and vimentin, phosphorylated p65 and induced the expression of E-cadherin, by inhibiting the nuclear factor kappaB (NF-kappaB) signaling pathway. Fluorouracil 34-38 nuclear factor kappa B subunit 1 Homo sapiens 230-239 31949471-7 2019 mRNA and protein expression of P-gp and ABCG2 was significantly higher in 5-FU/SW480 and L-OHP/SW480 cell lines, and ANXA1 expression decreased significantly (P < 0.05). Fluorouracil 74-78 ATP binding cassette subfamily G member 2 (Junior blood group) Homo sapiens 40-45 31969973-0 2020 Inhibition of protein FAK enhances 5-FU chemosensitivity to gastric carcinoma via p53 signaling pathways. Fluorouracil 35-39 tumor protein p53 Homo sapiens 82-85 31969973-9 2020 We further demonstrated that FAK silencing increased 5-FU-induced caspase-3 activity, and promoted p53 transcriptional activities. Fluorouracil 53-57 caspase 3 Homo sapiens 66-75 31858276-7 2019 Combination of 5-FU+ss-lap resulted in lower cell viability; most notably, 5-FU/ss-lap-loaded mesoporous silica nanoparticles (FNQ-MSN) exhibited significantly lower cell viability compared with that of any of the individual drug or physical combinations. Fluorouracil 15-19 moesin Homo sapiens 131-134 31881903-3 2019 To deeply investigate the MKK3 functions in cancer, taking advantage of a panel of authenticated colorectal cancer (CRC) lines and primary colonocytes, we found that MKK3 activates specifically p38delta MAPK protein, which signaling is further triggered by 5-fluorouracil (5-FU) treatments, a largely adopted chemotherapeutic drug in CRC clinical practice. Fluorouracil 257-271 mitogen-activated protein kinase 13 Homo sapiens 194-202 31881903-3 2019 To deeply investigate the MKK3 functions in cancer, taking advantage of a panel of authenticated colorectal cancer (CRC) lines and primary colonocytes, we found that MKK3 activates specifically p38delta MAPK protein, which signaling is further triggered by 5-fluorouracil (5-FU) treatments, a largely adopted chemotherapeutic drug in CRC clinical practice. Fluorouracil 273-277 mitogen-activated protein kinase 13 Homo sapiens 194-202 31881903-4 2019 The overall achieved results proposed the MKK3/p38delta MAPK as relevant molecular axis involved in abrogating efficacy to 5-FU treatments in CRC. Fluorouracil 123-127 mitogen-activated protein kinase 13 Homo sapiens 47-55 31858276-7 2019 Combination of 5-FU+ss-lap resulted in lower cell viability; most notably, 5-FU/ss-lap-loaded mesoporous silica nanoparticles (FNQ-MSN) exhibited significantly lower cell viability compared with that of any of the individual drug or physical combinations. Fluorouracil 75-79 moesin Homo sapiens 131-134 31858276-11 2019 These findings suggest the potential of NQO1 inhibitor in enhancing the chemotherapeutic potential of 5-FU in the treatment of HNSCC. Fluorouracil 102-106 NAD(P)H quinone dehydrogenase 1 Homo sapiens 40-44 31696188-0 2019 Bypassing pro-survival and resistance mechanisms of autophagy in EGFR-positive lung cancer cells by targeted delivery of 5FU using theranostic Ag2S quantum dots. Fluorouracil 121-124 epidermal growth factor receptor Homo sapiens 65-69 31696188-6 2019 Interestingly, while treatment of cells with free 5FU activated autophagy, a cellular mechanism conferring resistance to cell death, these EGFR targeting multimodal QDs significantly overcame drug resistance compared to 5FU treatment alone. Fluorouracil 50-53 epidermal growth factor receptor Homo sapiens 139-143 31696188-6 2019 Interestingly, while treatment of cells with free 5FU activated autophagy, a cellular mechanism conferring resistance to cell death, these EGFR targeting multimodal QDs significantly overcame drug resistance compared to 5FU treatment alone. Fluorouracil 220-223 epidermal growth factor receptor Homo sapiens 139-143 31796874-0 2019 Author Correction: Verbascoside: Identification, Quantification, and Potential Sensitization of Colorectal Cancer Cells to 5-FU by Targeting PI3K/AKT Pathway. Fluorouracil 123-127 AKT serine/threonine kinase 1 Homo sapiens 146-149 31835445-0 2019 Pharmacological Inhibition of TFF3 Enhances Sensitivity of CMS4 Colorectal Carcinoma to 5-Fluorouracil through Inhibition of p44/42 MAPK. Fluorouracil 88-102 trefoil factor 3, intestinal Mus musculus 30-34 31835445-8 2019 Furthermore, the forced expression of TFF3 decreased the sensitivity of CMS4 CRC cells to 5-fluorouracil (5-FU); while depleted TFF3 expression enhanced 5-FU sensitivity in CMS4 CRC cells. Fluorouracil 90-104 trefoil factor 3, intestinal Mus musculus 38-42 31835445-8 2019 Furthermore, the forced expression of TFF3 decreased the sensitivity of CMS4 CRC cells to 5-fluorouracil (5-FU); while depleted TFF3 expression enhanced 5-FU sensitivity in CMS4 CRC cells. Fluorouracil 106-110 trefoil factor 3, intestinal Mus musculus 38-42 31835445-8 2019 Furthermore, the forced expression of TFF3 decreased the sensitivity of CMS4 CRC cells to 5-fluorouracil (5-FU); while depleted TFF3 expression enhanced 5-FU sensitivity in CMS4 CRC cells. Fluorouracil 153-157 trefoil factor 3, intestinal Mus musculus 38-42 31835445-8 2019 Furthermore, the forced expression of TFF3 decreased the sensitivity of CMS4 CRC cells to 5-fluorouracil (5-FU); while depleted TFF3 expression enhanced 5-FU sensitivity in CMS4 CRC cells. Fluorouracil 153-157 trefoil factor 3, intestinal Mus musculus 128-132 31835445-9 2019 5-FU treatment induced TFF3 expression in CMS4 CRC cells. Fluorouracil 0-4 trefoil factor 3, intestinal Mus musculus 23-27 31911862-0 2019 RV-59 suppresses cytoplasmic Nrf2-mediated 5-fluorouracil resistance and tumor growth in colorectal cancer. Fluorouracil 43-57 NFE2 like bZIP transcription factor 2 Homo sapiens 29-33 31549215-5 2019 Further, expression levels of BATF2- and AP-1-related genes were confirmed in vincristine-resistant SGC7901/VCR cells treated with cisplatin or 5-fluorouracil. Fluorouracil 144-158 basic leucine zipper ATF-like transcription factor 2 Homo sapiens 30-35 31810922-6 2019 KIAA1199 knock down (KIAA1199-KD) suppressed proliferation, invasiveness, and sensitivity of GC cells to 5-fluorouracil (5-FU). Fluorouracil 105-119 cell migration inducing hyaluronidase 1 Homo sapiens 0-8 31810922-6 2019 KIAA1199 knock down (KIAA1199-KD) suppressed proliferation, invasiveness, and sensitivity of GC cells to 5-fluorouracil (5-FU). Fluorouracil 105-119 cell migration inducing hyaluronidase 1 Homo sapiens 21-29 31810922-6 2019 KIAA1199 knock down (KIAA1199-KD) suppressed proliferation, invasiveness, and sensitivity of GC cells to 5-fluorouracil (5-FU). Fluorouracil 121-125 cell migration inducing hyaluronidase 1 Homo sapiens 0-8 31810922-6 2019 KIAA1199 knock down (KIAA1199-KD) suppressed proliferation, invasiveness, and sensitivity of GC cells to 5-fluorouracil (5-FU). Fluorouracil 121-125 cell migration inducing hyaluronidase 1 Homo sapiens 21-29 31553932-4 2019 The investigation of preliminary molecular mechanism of 15d revealed that 15d could reverse drug resistance by inhibiting MDR1, ABCC1 and ABCG2 to increase the intracellular drug accumulation and induce apoptosis of Bel-7402/5-FU cells through mitochondria mediated pathway. Fluorouracil 225-229 ATP binding cassette subfamily B member 1 Homo sapiens 122-126 31553932-4 2019 The investigation of preliminary molecular mechanism of 15d revealed that 15d could reverse drug resistance by inhibiting MDR1, ABCC1 and ABCG2 to increase the intracellular drug accumulation and induce apoptosis of Bel-7402/5-FU cells through mitochondria mediated pathway. Fluorouracil 225-229 ATP binding cassette subfamily G member 2 (Junior blood group) Homo sapiens 138-143 31018249-0 2019 Fisetin and 5-fluorouracil: Effective combination for PIK3CA-mutant colorectal cancer. Fluorouracil 12-26 phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha Mus musculus 54-60 31525340-5 2019 Additionally, miR-133b overexpression reduces CRC stemness and overrides chemoresistance to 5-Fluorouracil (5-FU) and oxaliplatin (OXP), indicating a negative role of miR-133b in regulating CRC stemness and chemoresistance. Fluorouracil 92-106 microRNA 133b Homo sapiens 14-22 31525340-5 2019 Additionally, miR-133b overexpression reduces CRC stemness and overrides chemoresistance to 5-Fluorouracil (5-FU) and oxaliplatin (OXP), indicating a negative role of miR-133b in regulating CRC stemness and chemoresistance. Fluorouracil 108-112 microRNA 133b Homo sapiens 14-22 31018249-5 2019 Treatment of PIK3CA-mutant cells with fisetin and 5-FU reduced the expression of PI3K, phosphorylation of AKT, mTOR, its target proteins, constituents of mTOR signaling complex and this treatment increased the phosphorylation of AMPKalpha. Fluorouracil 50-54 phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha Mus musculus 13-19 31018249-5 2019 Treatment of PIK3CA-mutant cells with fisetin and 5-FU reduced the expression of PI3K, phosphorylation of AKT, mTOR, its target proteins, constituents of mTOR signaling complex and this treatment increased the phosphorylation of AMPKalpha. Fluorouracil 50-54 thymoma viral proto-oncogene 1 Mus musculus 106-109 31018249-9 2019 Fisetin could be used as a preventive agent plus an adjuvant with 5-FU for the treatment of PIK3CA-mutant colorectal cancer. Fluorouracil 66-70 phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha Mus musculus 92-98 31741260-9 2019 Taken together, the obtained data suggest that acquired 5-FU resistance in HL-60/5FU cells results from overexpression of ABCC1 and that targeting ABCC1 expression could be a potential approach to re-sensitize resistant leukemia cells to 5-FU. Fluorouracil 56-60 ATP binding cassette subfamily C member 1 Homo sapiens 122-127 31741260-9 2019 Taken together, the obtained data suggest that acquired 5-FU resistance in HL-60/5FU cells results from overexpression of ABCC1 and that targeting ABCC1 expression could be a potential approach to re-sensitize resistant leukemia cells to 5-FU. Fluorouracil 238-242 ATP binding cassette subfamily C member 1 Homo sapiens 122-127 31741260-9 2019 Taken together, the obtained data suggest that acquired 5-FU resistance in HL-60/5FU cells results from overexpression of ABCC1 and that targeting ABCC1 expression could be a potential approach to re-sensitize resistant leukemia cells to 5-FU. Fluorouracil 238-242 ATP binding cassette subfamily C member 1 Homo sapiens 147-152 30714842-0 2019 Conflicting alterations in hepatic expression of CYP3A and enzyme kinetics in rats exposed to 5-fluorouracil: relevance to pharmacokinetics of midazolam. Fluorouracil 94-108 cytochrome P450, family 3, subfamily a, polypeptide 62 Rattus norvegicus 49-54 31638265-5 2019 Although apoptosis-related protein expression levels were altered in each 5-FU-resistant colon cancer cell line variably, BH3 profiling indicated BCLXL dependence in 5-FU-resistant HT-29 cells only. Fluorouracil 166-170 BCL2 like 1 Homo sapiens 146-151 31638265-6 2019 Functional BCLXL inhibition in 5-FU-resistant HT-29 cells not only sensitized the cells to apoptosis but also overcame 5-FU resistance. Fluorouracil 31-35 BCL2 like 1 Homo sapiens 11-16 31638265-6 2019 Functional BCLXL inhibition in 5-FU-resistant HT-29 cells not only sensitized the cells to apoptosis but also overcame 5-FU resistance. Fluorouracil 119-123 BCL2 like 1 Homo sapiens 11-16 30714842-3 2019 In this study, we investigated the effects of 5-FU on the protein expression of hepatic CYP3A and their enzyme activity for metabolizing midazolam (MDZ), a typical substrate of CYP3A, in rat liver microsomes. Fluorouracil 46-50 cytochrome P450, family 3, subfamily a, polypeptide 62 Rattus norvegicus 88-93 30714842-7 2019 However, affinity of 5-FU-inducible CYP3A protein to MDZ for its 4- and 1"-hydroxylation was decreased. Fluorouracil 21-25 cytochrome P450, family 3, subfamily a, polypeptide 62 Rattus norvegicus 36-41 30714842-8 2019 Furthermore, the susceptibility of MDZ hydroxylation activity to a CYP3A inhibitor differed between the control and 5-FU groups. Fluorouracil 116-120 cytochrome P450, family 3, subfamily a, polypeptide 62 Rattus norvegicus 67-72 30714842-13 2019 Our findings provide novel information regarding the manifestation of inductive and interfering actions of 5-FU toward hepatic CYP3A to help in assessing the pharmacokinetics of CYP3A substrate drugs. Fluorouracil 107-111 cytochrome P450, family 3, subfamily a, polypeptide 62 Rattus norvegicus 127-132 30714842-13 2019 Our findings provide novel information regarding the manifestation of inductive and interfering actions of 5-FU toward hepatic CYP3A to help in assessing the pharmacokinetics of CYP3A substrate drugs. Fluorouracil 107-111 cytochrome P450, family 3, subfamily a, polypeptide 62 Rattus norvegicus 178-183 31815010-0 2019 PCDH17 increases the sensitivity of colorectal cancer to 5-fluorouracil treatment by inducing apoptosis and autophagic cell death. Fluorouracil 57-71 protocadherin 17 Homo sapiens 0-6 31582208-0 2019 H1, a derivative of tetrandrine, enhances the efficacy of 5-FU in Bel7402/5-FU cells via suppressing STAT3/MCL-1 and inducing PUMA. Fluorouracil 58-62 signal transducer and activator of transcription 3 Homo sapiens 101-106 31582208-8 2019 Finally, the combination of H1 and 5-FU results in an increase of cleaved PARP. Fluorouracil 35-39 poly(ADP-ribose) polymerase 1 Homo sapiens 74-78 31582208-9 2019 Taken together, H1 effectively improve the cytotoxic effect of 5-FU against Bel7402/5-FU cells via blocking STAT3/MCL-1 pathway and inducing PUMA. Fluorouracil 63-67 signal transducer and activator of transcription 3 Homo sapiens 108-113 31815010-3 2019 However, the relationship between PCDH17 and 5-FU resistance in CRC remains unclear. Fluorouracil 45-49 protocadherin 17 Homo sapiens 34-40 31695024-8 2019 Here, we demonstrate for the first time that in CRC the MKK3 specifically activates p38delta MAPK isoform to sustain prosurvival signaling and that such effect is exacerbated upon 5-FU challenge. Fluorouracil 180-184 mitogen-activated protein kinase 14 Homo sapiens 84-87 31815010-4 2019 Here, we revealed that PCDH17 was more highly expressed in 5-FU-sensitive CRC tissues than in 5-FU-resistant CRC tissues, and high expression of PCDH17 was correlated with high BECN1 expression. Fluorouracil 59-63 protocadherin 17 Homo sapiens 23-29 31815010-4 2019 Here, we revealed that PCDH17 was more highly expressed in 5-FU-sensitive CRC tissues than in 5-FU-resistant CRC tissues, and high expression of PCDH17 was correlated with high BECN1 expression. Fluorouracil 94-98 protocadherin 17 Homo sapiens 23-29 31815010-6 2019 Restoring PCDH17 expression augmented the 5-FU sensitivity of CRC in vitro and in vivo by promoting apoptosis and autophagic cell death. Fluorouracil 42-46 protocadherin 17 Homo sapiens 10-16 31815010-8 2019 PCDH17 inhibition by siRNA decreased the autophagy response and 5-FU sensitivity. Fluorouracil 64-68 protocadherin 17 Homo sapiens 0-6 31815010-10 2019 The compound SP600125, an inhibitor of JNK, suppressed autophagy and 5-FU-induced cell death in PCDH17-reexpressing CRC cells. Fluorouracil 69-73 mitogen-activated protein kinase 8 Homo sapiens 39-42 31815010-10 2019 The compound SP600125, an inhibitor of JNK, suppressed autophagy and 5-FU-induced cell death in PCDH17-reexpressing CRC cells. Fluorouracil 69-73 protocadherin 17 Homo sapiens 96-102 31815010-11 2019 Taken together, our findings suggest for the first time that PCDH17 increases the sensitivity of CRC to 5-FU treatment by inducing apoptosis and JNK-dependent autophagic cell death. Fluorouracil 104-108 protocadherin 17 Homo sapiens 61-67 31815010-11 2019 Taken together, our findings suggest for the first time that PCDH17 increases the sensitivity of CRC to 5-FU treatment by inducing apoptosis and JNK-dependent autophagic cell death. Fluorouracil 104-108 mitogen-activated protein kinase 8 Homo sapiens 145-148 31815010-12 2019 PCDH17 may be a potential prognostic marker for predicting 5-FU sensitivity in CRC patients. Fluorouracil 59-63 protocadherin 17 Homo sapiens 0-6 31729451-0 2019 Aspirin suppresses chemoresistance and enhances antitumor activity of 5-Fu in 5-Fu-resistant colorectal cancer by abolishing 5-Fu-induced NF-kappaB activation. Fluorouracil 70-74 nuclear factor kappa B subunit 1 Homo sapiens 138-147 31729451-0 2019 Aspirin suppresses chemoresistance and enhances antitumor activity of 5-Fu in 5-Fu-resistant colorectal cancer by abolishing 5-Fu-induced NF-kappaB activation. Fluorouracil 78-82 nuclear factor kappa B subunit 1 Homo sapiens 138-147 31729451-0 2019 Aspirin suppresses chemoresistance and enhances antitumor activity of 5-Fu in 5-Fu-resistant colorectal cancer by abolishing 5-Fu-induced NF-kappaB activation. Fluorouracil 78-82 nuclear factor kappa B subunit 1 Homo sapiens 138-147 31729451-8 2019 In vivo, aspirin markedly enhanced the antitumor activity of 5-Fu in suppressing tumor growth and metastasis, and down-regulating the expression of NF-kappaB-regulated genes in the 5-Fu-resistant cells. Fluorouracil 181-185 nuclear factor kappa B subunit 1 Homo sapiens 148-157 31729451-9 2019 Obviously, aspirin completely eradicated the 5-Fu-induced NF-kappaB activation, without inducing pronounced adverse effects. Fluorouracil 45-49 nuclear factor kappa B subunit 1 Homo sapiens 58-67 31719636-3 2019 The study aimed to elucidate the effects of insulin (INS), an inexpensive drug with a convincing safety profile, on the susceptibility of colon cancer to chemotherapeutic agents: 5-fluorouracil (FU), oxaliplatin (OXA), irinotecan (IRI), cyclophosphamide (CPA) and docetaxel (DOC). Fluorouracil 179-193 insulin Homo sapiens 44-51 31757048-7 2019 In parallel, the combination of ginkgetin and resveratrol synergistically relieved the 5-fluorouracil-induced inflammatory response by suppressing expressions of COX-2 and inflammatory cytokines. Fluorouracil 87-101 mitochondrially encoded cytochrome c oxidase II Homo sapiens 162-167 31729451-10 2019 Taken together, findings in this study suggest that aspirin can reverse chemoresistance and potentiate the antitumor effect of 5-Fu, which is achieved through abolishing the 5-Fu-induced NF-kappaB activation, suggesting that aspirin may be a promising adjuvant therapeutic agent for CRC. Fluorouracil 127-131 nuclear factor kappa B subunit 1 Homo sapiens 187-196 31729451-10 2019 Taken together, findings in this study suggest that aspirin can reverse chemoresistance and potentiate the antitumor effect of 5-Fu, which is achieved through abolishing the 5-Fu-induced NF-kappaB activation, suggesting that aspirin may be a promising adjuvant therapeutic agent for CRC. Fluorouracil 174-178 nuclear factor kappa B subunit 1 Homo sapiens 187-196 31521892-11 2019 Further study indicated that CP-25 could decrease P-gp expression and inhibit P-gp function in Bel7402/5-FU cells. Fluorouracil 103-107 ATP binding cassette subfamily B member 1 Homo sapiens 78-82 32104489-5 2019 Interestingly, due to high MCT1 affinity and good gastrointestinal stability, 5-FU-octanedioic acid monoester prodrug exhibited significant improvement in membrane permeability (13.1-fold) and oral bioavailability (4.1-fold) compared to 5-FU. Fluorouracil 78-82 solute carrier family 16 member 1 Homo sapiens 27-31 31521892-7 2019 Besides, P-gp high expression of human hepatoma cell line Bel7402/5-FU and Bel7402 were chose to study in MTX resistance and the function of P-gp was detected by Flow cytometry. Fluorouracil 66-70 ATP binding cassette subfamily B member 1 Homo sapiens 9-13 31498559-4 2019 Anti-CLDN4 extracellular domain antibody, previously established by us (4D3), inhibited the proliferation of MIA-PaCa-2 PDC cells and increased intracellular 5-fluorouracil (5-FU) concentration with lowering transepithelial electrical resistance. Fluorouracil 158-172 claudin 4 Homo sapiens 5-10 31760928-7 2019 Gemcitabine and 5-fluorouracil modulated expression of CSC markers, E-cadherin, and RXRbeta in Panc1 but not in Mia PaCa-2 cells. Fluorouracil 16-30 cadherin 1 Homo sapiens 68-78 31498559-4 2019 Anti-CLDN4 extracellular domain antibody, previously established by us (4D3), inhibited the proliferation of MIA-PaCa-2 PDC cells and increased intracellular 5-fluorouracil (5-FU) concentration with lowering transepithelial electrical resistance. Fluorouracil 174-178 claudin 4 Homo sapiens 5-10 30993729-6 2019 The results demonstrated that AlCl3 pretreatment attenuated 5-FU-induced apoptosis through Erk activation and reversed 5-FU-induced cell cycle arrest by downregulating p-Chk2Thr68 levels. Fluorouracil 60-64 mitogen-activated protein kinase 1 Homo sapiens 91-94 31689796-6 2019 Among patients with carcinoembryonic antigen (CEA) levels of <5 ng/mL at 1 month after LR, significant differences were noted only in those who underwent 5-FU/LV (HR = 0.58, P = .035) and oxaliplatin-based chemotherapy (HR = 0.38, P < .001). Fluorouracil 157-161 CEA cell adhesion molecule 3 Homo sapiens 46-49 31401143-13 2019 Incubation of Caco-2BBe monolayers with tumor necrosis factor caused occludin downregulation, which reduced CASP3 expression and prevented induction of apoptosis via the intrinsic pathway (stimulated by 5-fluorouracil) or extrinsic pathway (stimulated by tumor necrosis factor). Fluorouracil 203-217 occludin Mus musculus 69-77 31310349-1 2019 BACKGROUND: S-1 is an oral anticancer agent containing tegafur, a prodrug of 5-fluorouracil (5-FU). Fluorouracil 77-91 proteasome 26S subunit, non-ATPase 1 Homo sapiens 12-15 31310349-1 2019 BACKGROUND: S-1 is an oral anticancer agent containing tegafur, a prodrug of 5-fluorouracil (5-FU). Fluorouracil 93-97 proteasome 26S subunit, non-ATPase 1 Homo sapiens 12-15 31352611-0 2019 5-FU preferably induces apoptosis in BRAF V600E colorectal cancer cells via downregulation of Bcl-xL. Fluorouracil 0-4 B-Raf proto-oncogene, serine/threonine kinase Homo sapiens 37-41 31352611-0 2019 5-FU preferably induces apoptosis in BRAF V600E colorectal cancer cells via downregulation of Bcl-xL. Fluorouracil 0-4 BCL2 like 1 Homo sapiens 94-100 31664952-14 2019 Compared with the control group, mRNA expression of TNF-alpha was significantly up-regulated in the 5-FU group. Fluorouracil 100-104 tumor necrosis factor Mus musculus 52-61 31352611-3 2019 In this study, we demonstrated that BRAFV600E confers sensitivity to 5-FU in vitro and in vivo xenograft model, using the paired isogenic colorectal cancer cell lines RKO with either BRAF Wild Type (WT)(+/-) or mutant (Mut) (600E/-). Fluorouracil 69-73 B-Raf proto-oncogene, serine/threonine kinase Homo sapiens 36-40 31352611-4 2019 Our results revealed 5-FU preferably induces marked apoptosis in BRAF-mutant colorectal cancer cells, through attenuating expression of Bcl-xL and activation caspase-3/9 pathway, eventually conferring the anti-tumor efficacy of 5-FU in vitro and in vivo. Fluorouracil 21-25 B-Raf proto-oncogene, serine/threonine kinase Homo sapiens 65-69 31352611-4 2019 Our results revealed 5-FU preferably induces marked apoptosis in BRAF-mutant colorectal cancer cells, through attenuating expression of Bcl-xL and activation caspase-3/9 pathway, eventually conferring the anti-tumor efficacy of 5-FU in vitro and in vivo. Fluorouracil 21-25 BCL2 like 1 Homo sapiens 136-142 31352611-4 2019 Our results revealed 5-FU preferably induces marked apoptosis in BRAF-mutant colorectal cancer cells, through attenuating expression of Bcl-xL and activation caspase-3/9 pathway, eventually conferring the anti-tumor efficacy of 5-FU in vitro and in vivo. Fluorouracil 21-25 caspase 3 Homo sapiens 158-169 31352611-4 2019 Our results revealed 5-FU preferably induces marked apoptosis in BRAF-mutant colorectal cancer cells, through attenuating expression of Bcl-xL and activation caspase-3/9 pathway, eventually conferring the anti-tumor efficacy of 5-FU in vitro and in vivo. Fluorouracil 228-232 B-Raf proto-oncogene, serine/threonine kinase Homo sapiens 65-69 31352611-4 2019 Our results revealed 5-FU preferably induces marked apoptosis in BRAF-mutant colorectal cancer cells, through attenuating expression of Bcl-xL and activation caspase-3/9 pathway, eventually conferring the anti-tumor efficacy of 5-FU in vitro and in vivo. Fluorouracil 228-232 caspase 3 Homo sapiens 158-169 31352611-5 2019 Meanwhile, expression of Bcl-xL remained unchanged in BRAF WT group after treatment of 5-FU, although low extent of anti-tumor activity of 5-FU still being observed. Fluorouracil 87-91 BCL2 like 1 Homo sapiens 25-31 31352611-6 2019 In conclusion, these results provided a better understanding of clinical outcome of 5-FU between BRAF WT and mutant colorectal cancer patients, and suggested the inhibition of Bcl-xL might present an alternative strategy to enhance the therapeutic efficacy of 5-FU in colorectal cancer patients with BRAF mutation. Fluorouracil 84-88 B-Raf proto-oncogene, serine/threonine kinase Homo sapiens 97-101 31352611-6 2019 In conclusion, these results provided a better understanding of clinical outcome of 5-FU between BRAF WT and mutant colorectal cancer patients, and suggested the inhibition of Bcl-xL might present an alternative strategy to enhance the therapeutic efficacy of 5-FU in colorectal cancer patients with BRAF mutation. Fluorouracil 260-264 BCL2 like 1 Homo sapiens 176-182 31664952-15 2019 Moreover, mRNA expression of TNF-alpha in the DPP-4i + 5-FU group was down-regulated compared to the 5-FU group. Fluorouracil 55-59 tumor necrosis factor Mus musculus 29-38 31664952-15 2019 Moreover, mRNA expression of TNF-alpha in the DPP-4i + 5-FU group was down-regulated compared to the 5-FU group. Fluorouracil 101-105 tumor necrosis factor Mus musculus 29-38 31664952-16 2019 However, IL-6 in the 5-FU group was significantly down-regulated compared to the control, there was no significant difference in expression of IL-6 between the 5-FU and DPP4i + 5-FU group. Fluorouracil 21-25 interleukin 6 Mus musculus 9-13 31454556-9 2019 The knockdown of SRC, PKCdelta and PLCbeta3 increased the susceptibility of Bel/5-Fu cells to 5-Fu. Fluorouracil 80-84 SRC proto-oncogene, non-receptor tyrosine kinase Homo sapiens 17-20 31659152-8 2019 Moreover, tumor organoids derived from colon of the ApcminPpm1dT/+ mice were less sensitive to 5-fluorouracil when compared to ApcminPpm1d+/+and the sensitivity to 5-fluorouracil was restored by inhibition of PPM1D. Fluorouracil 164-178 protein phosphatase 1D magnesium-dependent, delta isoform Mus musculus 209-214 31325706-9 2019 Furthermore, QFG inhibited the cellular apoptosis in the jejunum tissue caused by 5-FU via the increasing Bcl-2 expression and decreasing Bax expression. Fluorouracil 82-86 B cell leukemia/lymphoma 2 Mus musculus 106-111 31476572-9 2019 Patterns of MBD4 sumoylation were altered, in a DNA damage-specific way, by the anti-metabolite 5-fluorouracil, the alkylating agent N-Methyl-N-nitrosourea and the crosslinking agent cisplatin. Fluorouracil 96-110 methyl-CpG binding domain 4, DNA glycosylase Homo sapiens 12-16 31569395-0 2019 N6-Isopentenyladenosine Inhibits Colorectal Cancer and Improves Sensitivity to 5-Fluorouracil-Targeting FBXW7 Tumor Suppressor. Fluorouracil 79-93 F-box and WD repeat domain containing 7 Homo sapiens 104-109 31569395-6 2019 Moreover, in FBXW7- and TP53-wild type cells, N6-isopentenyladenosine strongly synergizes with 5-Fluorouracil to inhibit colon cancer growth in vitro. Fluorouracil 95-109 F-box and WD repeat domain containing 7 Homo sapiens 13-18 31623083-4 2019 RESULTS: The results of this study indicate that 5-FU differentially affects superoxide production and caspase-3 activation when applied in cytotoxic concentrations against HeLa cells, while superoxide accumulation is in accordance with mitochondrial superoxide levels. Fluorouracil 49-53 caspase 3 Homo sapiens 103-112 31545250-3 2019 METHODS: We used immunohistochemistry to assess Notch1 expression in fresh HNSCC samples treated by PF (cisplatin+5- fluorouracil) and TPF (paclitaxel + cisplatin+5- fluorouracil). Fluorouracil 114-129 notch receptor 1 Homo sapiens 48-54 31324934-8 2019 There was 180-fold variation in the rate of 5-FU uptake into BMC (0.10-17.86 pmol min-1 105 viable cells-1) across the 34 subjects (healthy participants N = 24, cancer patients N = 10). Fluorouracil 44-48 CD59 molecule (CD59 blood group) Homo sapiens 82-87 31081972-9 2019 Then, the influence of ABCG2 on lidocaine + 5-Fu-caused cell viability loss, apoptosis, and inactivation of PI3K/AKT pathway were analyzed. Fluorouracil 44-48 ATP binding cassette subfamily G member 2 (Junior blood group) Homo sapiens 23-28 31081972-13 2019 Overexpression of ABCG2 reversed the synergistic effects of lidocaine + 5-Fu on JEG-3 and JAR cell viability and apoptosis, as well as PI3K/AKT pathway. Fluorouracil 72-76 ATP binding cassette subfamily G member 2 (Junior blood group) Homo sapiens 18-23 31454556-16 2019 Furthermore, knockdown of PLCbeta3, PKCdelta and SRC increased the susceptibility of Bel/5-Fu cells to 5-Fu. Fluorouracil 89-93 SRC proto-oncogene, non-receptor tyrosine kinase Homo sapiens 49-52 31454556-16 2019 Furthermore, knockdown of PLCbeta3, PKCdelta and SRC increased the susceptibility of Bel/5-Fu cells to 5-Fu. Fluorouracil 103-107 SRC proto-oncogene, non-receptor tyrosine kinase Homo sapiens 49-52 31569395-6 2019 Moreover, in FBXW7- and TP53-wild type cells, N6-isopentenyladenosine strongly synergizes with 5-Fluorouracil to inhibit colon cancer growth in vitro. Fluorouracil 95-109 tumor protein p53 Homo sapiens 24-28 31454556-9 2019 The knockdown of SRC, PKCdelta and PLCbeta3 increased the susceptibility of Bel/5-Fu cells to 5-Fu. Fluorouracil 94-98 SRC proto-oncogene, non-receptor tyrosine kinase Homo sapiens 17-20 31454556-15 2019 Our results showed that the phosphorylation levels of PLCbeta3 pS1105 and the protein levels of PLCbeta3, PKCdelta and SRC, which are major components of GnRH signaling pathway were higher in Bel/5-Fu cells than in Bel cells. Fluorouracil 196-200 SRC proto-oncogene, non-receptor tyrosine kinase Homo sapiens 119-122 31552174-7 2019 Our results also showed that ectopic expression of miR-375 suppressed CC cell proliferation, migration, invasion and angiogenesis, and increased the 5-fluorouracil-induced apoptosis and cell cycle arrest in vitro. Fluorouracil 149-163 microRNA 375 Homo sapiens 51-58 31543507-3 2019 In this study, we investigated the chemosensitivity of miR-375 to 5FU in CRC from biological and clinical aspects. Fluorouracil 66-69 microRNA 375 Homo sapiens 55-62 31543507-6 2019 Further mechanistic analysis demonstrated that miR-375 enhanced CRC cell sensitivity to 5FU by directly targeting YAP1 and SP1. Fluorouracil 88-91 microRNA 375 Homo sapiens 47-54 31546954-3 2019 Sensitization to 5-FU, oxaliplatin, and irinotecan by transfection with miR-195-5p and miR-497-5p mimics was studied using cell viability and clonogenic assays in cell lines HCT116, RKO, DLD-1, and SW480. Fluorouracil 17-21 microRNA 195 Homo sapiens 72-79 31519589-7 2019 Under the presence of the anti-cancer drug 5-fluorouracil (5FU), up-regulation of PGC-1alpha under hypoxia promoted resistance of CRC against 5FU-induced apoptosis. Fluorouracil 43-57 PPARG coactivator 1 alpha Homo sapiens 82-92 31488078-6 2019 Selectively, the effect of EGF receptor inhibition was augmented by a combination with 5-fluorouracil and oxaliplatin. Fluorouracil 87-101 epidermal growth factor receptor Homo sapiens 27-39 31491980-0 2019 Quinacrine-Mediated Inhibition of Nrf2 Reverses Hypoxia-Induced 5-Fluorouracil Resistance in Colorectal Cancer. Fluorouracil 64-78 nuclear factor, erythroid derived 2, like 2 Mus musculus 34-38 31491980-5 2019 Overexpression of Nrf2 effectively prevented the increase in the number of DNA double-strand breaks induced by QC alone or in combination with 5-FU. Fluorouracil 143-147 nuclear factor, erythroid derived 2, like 2 Mus musculus 18-22 31519589-7 2019 Under the presence of the anti-cancer drug 5-fluorouracil (5FU), up-regulation of PGC-1alpha under hypoxia promoted resistance of CRC against 5FU-induced apoptosis. Fluorouracil 59-62 PPARG coactivator 1 alpha Homo sapiens 82-92 31519589-7 2019 Under the presence of the anti-cancer drug 5-fluorouracil (5FU), up-regulation of PGC-1alpha under hypoxia promoted resistance of CRC against 5FU-induced apoptosis. Fluorouracil 142-145 PPARG coactivator 1 alpha Homo sapiens 82-92 31288002-7 2019 RESULTS: combined administration of luteolin and 5-FU in SEC model increased levels of p53, p21, caspase 3, DRAM and survivability while, tumor volume, weight, thioredoxin reductase one (TR1) activity and cyclin D1 expression showed the reverse with restoration of oxidant/antioxidant indices. Fluorouracil 49-53 DNA-damage regulated autophagy modulator 1 Mus musculus 108-112 31261026-0 2019 The long non-coding RNA HOTAIRM1 suppresses cell progression via sponging endogenous miR-17-5p/ B-cell translocation gene 3 (BTG3) axis in 5-fluorouracil resistant colorectal cancer cells. Fluorouracil 139-153 HOXA transcript antisense RNA, myeloid-specific 1 Homo sapiens 24-32 31261026-3 2019 This study intended to explore the possible role of long non-coding RNA HOTAIRM1 (HOTAIRM1) in the pathogenesis of 5-FU resistant CRC and its underlying mechanism. Fluorouracil 115-119 HOXA transcript antisense RNA, myeloid-specific 1 Homo sapiens 72-80 31261026-3 2019 This study intended to explore the possible role of long non-coding RNA HOTAIRM1 (HOTAIRM1) in the pathogenesis of 5-FU resistant CRC and its underlying mechanism. Fluorouracil 115-119 HOXA transcript antisense RNA, myeloid-specific 1 Homo sapiens 82-90 31261026-4 2019 Our data showed that HOTAIRM1 was downregulated in CRC tissues and cell lines (HCT116 and SW480), and even lower in 5-FU resistant CRC tissues and cell lines (HCT116/5-FU and SW480/5-FU). Fluorouracil 116-120 HOXA transcript antisense RNA, myeloid-specific 1 Homo sapiens 21-29 31544060-0 2019 Activation of p53 Gene Expression and Synergistic Antiproliferative Effects of 5-Fluorouracil and beta-escin on MCF7 Cells. Fluorouracil 79-93 tumor protein p53 Homo sapiens 14-17 31786874-17 2019 The miR-299 overexpression enhanced the chemosensitivity of the HK1 cells to 5-FU and also caused a decrease in their invasion ability. Fluorouracil 77-81 hexokinase 1 Homo sapiens 64-67 30796167-0 2019 Combination of 5-Fluorouracil with Epigenetic Modifiers Induces Radiosensitization, Somatostatin Receptor 2 Expression, and Radioligand Binding in Neuroendocrine Tumor Cells In Vitro. Fluorouracil 15-29 somatostatin receptor 2 Homo sapiens 84-107 30796167-7 2019 Results: Treatment with 5-fluorouracil alone or in combination with decitabine or tacedinaline reduced tumor cell viability and induced apoptosis, enhanced radiosensitivity in BON1 and QGP1 cells, induced SSTR2 expression, and resulted in increased radioligand binding of 68Ga-DOTATOC in NET cells. Fluorouracil 24-38 somatostatin receptor 2 Homo sapiens 205-210 30796167-8 2019 Conclusion: This preclinical study demonstrated that 5-fluorouracil alone or in combination with decitabine or tacedinaline caused radiosensitization of tumor cells, upregulation of SSTR2 expression in tumor cells, and increased radioligand binding of 68Ga-DOTATOC to these tumor cells. Fluorouracil 53-67 somatostatin receptor 2 Homo sapiens 182-187 31544060-5 2019 The cytotoxic effects, the number of colonies, apoptosis, p53 gene expression, and Bcl-2 signaling protein of the combined 5-FU and beta-escin on MCF7 cells were determined using 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide, clonogenic assay, flow cytometry, real-time quantitative polymerase chain reaction, and western blotting methods, respectively. Fluorouracil 123-127 BCL2 apoptosis regulator Homo sapiens 83-88 31544060-6 2019 Half-maximal inhibitory concentration values of beta-escin and 5-FU were 80 mug/ml and 2 muM, respectively. Fluorouracil 63-67 latexin Homo sapiens 89-92 31544060-8 2019 The expression of p53 and apoptosis increased in the combination of 5-FU and beta-escin on MCF7 cells compared to that of control group (P < 0.05). Fluorouracil 68-72 tumor protein p53 Homo sapiens 18-21 31544060-9 2019 In addition, the number of colonies and Bcl-2 signaling protein in combination of 5-FU and beta-escin decreased with respect to untreated control cells or single treatment of 5-FU and beta-escin. Fluorouracil 82-86 BCL2 apoptosis regulator Homo sapiens 40-45 31544060-9 2019 In addition, the number of colonies and Bcl-2 signaling protein in combination of 5-FU and beta-escin decreased with respect to untreated control cells or single treatment of 5-FU and beta-escin. Fluorouracil 175-179 BCL2 apoptosis regulator Homo sapiens 40-45 31544060-10 2019 The combination of 5-FU and beta-escin not only has synergistic effects by increasing cell apoptosis and p53 gene expression but also decreases Bcl-2 signaling protein in MCF7 cell lines. Fluorouracil 19-23 tumor protein p53 Homo sapiens 105-108 31544060-10 2019 The combination of 5-FU and beta-escin not only has synergistic effects by increasing cell apoptosis and p53 gene expression but also decreases Bcl-2 signaling protein in MCF7 cell lines. Fluorouracil 19-23 BCL2 apoptosis regulator Homo sapiens 144-149 31302002-5 2019 Furthermore, IKKalpha or BRAF inhibition synergistically enhances the therapeutic potential of 5-FU and irinotecan to eradicate chemotherapy-resistant metastatic human tumors in vivo. Fluorouracil 95-99 B-Raf proto-oncogene, serine/threonine kinase Homo sapiens 25-29 30993753-1 2019 We investigated the role of stattic as an adjuvant molecule to increase the cytotoxicity of 5-fluorouracil (5-FU) through specific inhibition of molecular targets, signal transducer and activator of transcription 3 (STAT3) and nuclear factor erythroid 2-related factor 2 (Nrf2) in HT-29 colon cancer cells. Fluorouracil 92-106 signal transducer and activator of transcription 3 Homo sapiens 216-221 31534970-6 2019 5-FU treatment increased the expressions of Oct3/4, Fbxw7, and p27 and increased the number of A549 cells at G0/G1. Fluorouracil 0-4 F-box and WD-40 domain protein 7 Mus musculus 52-57 31534970-8 2019 Release from 5-FU decreased the expressions of Oct3/4, Fbxw7 and p27; decreased the percentage of cells in the G0/G1 phase; increased the expressions of Skp2 and c-myc; and increased the proportion of cells in S phase. Fluorouracil 13-17 F-box and WD-40 domain protein 7 Mus musculus 55-60 31534970-9 2019 5-FU treatment led to high expressions of Oct3/4, c-myc, and p27, with low expressions of Fbxw7 and Skp2. Fluorouracil 0-4 F-box and WD-40 domain protein 7 Mus musculus 90-95 31534970-14 2019 Conclusion: 5-FU enriches the CSCs in lung adenocarcinoma cells via increasing Fbxw7 and decreasing Skp2 expression, followed by downregulation of c-myc and upregulation of p27, which switches cells to quiescence. Fluorouracil 12-16 F-box and WD-40 domain protein 7 Mus musculus 79-84 31695407-3 2019 Objective: We investigated the mechanisms for the HPV E6/E7 oncoprotein-mediated 5-fluorouracil (5-Fu) sensitivity. Fluorouracil 81-95 protein E6*;transforming protein E6 Human papillomavirus type 16 54-59 31695407-3 2019 Objective: We investigated the mechanisms for the HPV E6/E7 oncoprotein-mediated 5-fluorouracil (5-Fu) sensitivity. Fluorouracil 97-101 protein E6*;transforming protein E6 Human papillomavirus type 16 54-59 31695407-7 2019 Results: The HPV-16 E6/E7 oncoprotein induces 5-Fu resistance in cervical cancer cells. Fluorouracil 46-50 protein E6*;transforming protein E6 Human papillomavirus type 16 20-25 31695407-8 2019 Overexpression of E6/E7 renders CaSki and SiHa cells resistant to 5-Fu treatments. Fluorouracil 66-70 protein E6*;transforming protein E6 Human papillomavirus type 16 18-23 31695407-9 2019 We found E6/E7 expressions were significantly upregulated in 5-Fu-resistant cells compared with parental cells. Fluorouracil 61-65 protein E6*;transforming protein E6 Human papillomavirus type 16 9-14 31695407-12 2019 We report the E6/E7-mediated 5-Fu resistance was through upregulation of glycolysis pathway. Fluorouracil 29-33 protein E6*;transforming protein E6 Human papillomavirus type 16 14-19 31695407-13 2019 Importantly, inhibition of E6/E7 by shRNA effectively decreased cellular glycolysis and overcame 5-Fu resistance using in vitro and in vivo xenograft model. Fluorouracil 97-101 protein E6*;transforming protein E6 Human papillomavirus type 16 27-32 31695407-14 2019 Conclusion: Our study contributed to understanding the molecular mechanisms for HPV E6/E7-mediated 5-Fu resistance and development of new therapeutic strategies against cervical cancer. Fluorouracil 99-103 protein E6*;transforming protein E6 Human papillomavirus type 16 84-89 31395078-11 2019 FOXO1/CEBPB/NF-kappaB signaling was activated in CRC cells after 5-FU treatment and was required for CCL20 upregulation mediated by 5-FU. Fluorouracil 65-69 forkhead box O1 Homo sapiens 0-5 31395078-11 2019 FOXO1/CEBPB/NF-kappaB signaling was activated in CRC cells after 5-FU treatment and was required for CCL20 upregulation mediated by 5-FU. Fluorouracil 65-69 nuclear factor kappa B subunit 1 Homo sapiens 12-21 31395078-11 2019 FOXO1/CEBPB/NF-kappaB signaling was activated in CRC cells after 5-FU treatment and was required for CCL20 upregulation mediated by 5-FU. Fluorouracil 132-136 forkhead box O1 Homo sapiens 0-5 31395078-11 2019 FOXO1/CEBPB/NF-kappaB signaling was activated in CRC cells after 5-FU treatment and was required for CCL20 upregulation mediated by 5-FU. Fluorouracil 132-136 nuclear factor kappa B subunit 1 Homo sapiens 12-21 31592435-0 2019 Synergetic Impact of Combined 5-Fluorouracil and Rutin on Apoptosis in PC3 Cancer Cells through the Modulation of P53 Gene Expression. Fluorouracil 30-44 tumor protein p53 Homo sapiens 114-117 31592435-9 2019 Combination of 5-FU/rutin enhanced apoptosis and p53 gene expression in PC3 cells. Fluorouracil 15-19 tumor protein p53 Homo sapiens 49-52 31592435-10 2019 PC3 cell colony counts and Bcl-2 signaling protein were decreased by 5-FU/rutin combination. Fluorouracil 69-73 BCL2 apoptosis regulator Homo sapiens 27-32 31592435-11 2019 Conclusion: Synergistic effects of 5-FU/rutin combination on PC3 cells line enhanced apoptosis, p53 gene expression, and down-regulation of Bcl-2 protein, compared to control separate application. Fluorouracil 35-39 tumor protein p53 Homo sapiens 96-99 31592435-11 2019 Conclusion: Synergistic effects of 5-FU/rutin combination on PC3 cells line enhanced apoptosis, p53 gene expression, and down-regulation of Bcl-2 protein, compared to control separate application. Fluorouracil 35-39 BCL2 apoptosis regulator Homo sapiens 140-145 30973271-0 2019 Knockdown of REG Ialpha Enhances the Sensitivity to 5-Fluorouracil of Colorectal Cancer Cells via Cyclin D1/CDK4 Pathway and BAX/BCL-2 Pathways. Fluorouracil 52-66 regenerating family member 1 alpha Homo sapiens 13-16 30973271-10 2019 REG Ialpha knockdown promoted the cell apoptosis of HCT116 and LOVO under the 5-Fu treatment. Fluorouracil 78-82 regenerating family member 1 alpha Homo sapiens 0-3 30993753-6 2019 Our data from gene expression determined a substantial diminish in the mRNA levels of the Nrf2 and antiapoptotic gene Bcl-2 along with a noticeable increase in the level of the proapoptotic Bax in HT-29 colon cells that underwent cotreatment with 5-FU and stattic (P < 0.05). Fluorouracil 247-251 BCL2 apoptosis regulator Homo sapiens 118-123 30993753-6 2019 Our data from gene expression determined a substantial diminish in the mRNA levels of the Nrf2 and antiapoptotic gene Bcl-2 along with a noticeable increase in the level of the proapoptotic Bax in HT-29 colon cells that underwent cotreatment with 5-FU and stattic (P < 0.05). Fluorouracil 247-251 BCL2 associated X, apoptosis regulator Homo sapiens 190-193 30993753-8 2019 This therapeutic approach in colon cancer could mediate 5-FU chemoresistance via modulating therapeutic targets (ie, STAT3 and Nrf2 pathways) and decreased 5-FU-related adverse effects. Fluorouracil 56-60 signal transducer and activator of transcription 3 Homo sapiens 117-122 30993753-8 2019 This therapeutic approach in colon cancer could mediate 5-FU chemoresistance via modulating therapeutic targets (ie, STAT3 and Nrf2 pathways) and decreased 5-FU-related adverse effects. Fluorouracil 56-60 NFE2 like bZIP transcription factor 2 Homo sapiens 127-131 31423195-0 2019 SNHG20/miR-140-5p/NDRG3 axis contributes to 5-fluorouracil resistance in gastric cancer. Fluorouracil 44-58 small nucleolar RNA host gene 20 Homo sapiens 0-6 31189612-0 2019 Vorinostat Potentiates 5-Fluorouracil/Cisplatin Combination by Inhibiting Chemotherapy-Induced EGFR Nuclear Translocation and Increasing Cisplatin Uptake. Fluorouracil 23-37 epidermal growth factor receptor Homo sapiens 95-99 31189612-6 2019 Mechanistically, vorinostat reverted 5FU/CDDP-induced EGFR phosphorylation and nuclear translocation, leading to the impairment of nuclear EGFR noncanonical induction of genes such as thymidylate synthase and cyclin D1. Fluorouracil 37-40 epidermal growth factor receptor Homo sapiens 54-58 31423282-7 2019 The high expression of alpha-SMA, p-AKT and survivin in patients with aCRC were associated with oxaliplatin plus 5-FU resistance (P<0.001, P=0.023 and P=0.001, respectively). Fluorouracil 113-117 AKT serine/threonine kinase 1 Homo sapiens 36-39 31423195-10 2019 SNHG20 was revealed to be involved in mediating resistance to 5-FU in gastric cancer cell lines via NDRG3. Fluorouracil 62-66 small nucleolar RNA host gene 20 Homo sapiens 0-6 31423282-11 2019 In conclusion, the multifactorial predictive biomarker model of alpha-SMA, p-AKT, p-ERK and survivin expression for patients with aCRC to predict intrinsic resistance to oxaliplatin plus 5-FU regimens is of great efficiency and accuracy. Fluorouracil 187-191 AKT serine/threonine kinase 1 Homo sapiens 77-80 31423195-11 2019 In conclusion, the results of the present study suggest that the SNHG20/miR-140-5p/NDRG3 axis may be involved in mediating resistance to 5-FU in gastric cancer. Fluorouracil 137-141 small nucleolar RNA host gene 20 Homo sapiens 65-71 31311867-5 2019 Genetic deletion of Bok results in chemoresistance to 5-fluorouracil (5-FU) in different cell lines and in mice. Fluorouracil 54-68 BCL2-related ovarian killer Mus musculus 20-23 31418391-1 2019 OBJECTIVE: To explore the effect of bone morphogenetic protein 4(BMP4) on the cell cycle and apoptosis of hemaropoictic stem and progenitor cells (HSPC) in conditions of 5-fluorouracil (5-FU)-inducing bone marrow suppression and stress hemogenesis, and its possible mechanism. Fluorouracil 170-184 bone morphogenetic protein 4 Mus musculus 36-64 31418391-1 2019 OBJECTIVE: To explore the effect of bone morphogenetic protein 4(BMP4) on the cell cycle and apoptosis of hemaropoictic stem and progenitor cells (HSPC) in conditions of 5-fluorouracil (5-FU)-inducing bone marrow suppression and stress hemogenesis, and its possible mechanism. Fluorouracil 170-184 bone morphogenetic protein 4 Mus musculus 65-69 31418391-1 2019 OBJECTIVE: To explore the effect of bone morphogenetic protein 4(BMP4) on the cell cycle and apoptosis of hemaropoictic stem and progenitor cells (HSPC) in conditions of 5-fluorouracil (5-FU)-inducing bone marrow suppression and stress hemogenesis, and its possible mechanism. Fluorouracil 186-190 bone morphogenetic protein 4 Mus musculus 36-64 31418391-1 2019 OBJECTIVE: To explore the effect of bone morphogenetic protein 4(BMP4) on the cell cycle and apoptosis of hemaropoictic stem and progenitor cells (HSPC) in conditions of 5-fluorouracil (5-FU)-inducing bone marrow suppression and stress hemogenesis, and its possible mechanism. Fluorouracil 186-190 bone morphogenetic protein 4 Mus musculus 65-69 31028570-0 2019 Enhancement of chemosensitivity in 5-fluorouracil-resistant colon cancer cells with carcinoembryonic antigen-specific RNA aptamer. Fluorouracil 35-49 CEA cell adhesion molecule 3 Homo sapiens 84-108 31028570-4 2019 However, a major issue of 5-FU therapy is the occurrence of chemoresistance, and the fact that 5-FU induces CEA overexpression, which may induce the 5-FU resistance. Fluorouracil 95-99 CEA cell adhesion molecule 3 Homo sapiens 108-111 31028570-4 2019 However, a major issue of 5-FU therapy is the occurrence of chemoresistance, and the fact that 5-FU induces CEA overexpression, which may induce the 5-FU resistance. Fluorouracil 95-99 CEA cell adhesion molecule 3 Homo sapiens 108-111 31028570-6 2019 In the present study, we tested whether protecting CEA using the CEA aptamer could enhance 5-FU sensitivity in chemoresistant LS174T colon cancer cells. Fluorouracil 91-95 CEA cell adhesion molecule 3 Homo sapiens 51-54 31028570-6 2019 In the present study, we tested whether protecting CEA using the CEA aptamer could enhance 5-FU sensitivity in chemoresistant LS174T colon cancer cells. Fluorouracil 91-95 CEA cell adhesion molecule 3 Homo sapiens 65-68 31028570-7 2019 We observed that the CEA aptamer sensitized the 5-FU-resistant colon cancer cell line to 5-FU more than five-fold (IC50 ~ 5.995 muM), compared with cells treated with 5-FU alone (IC50 ~ 31.46 muM). Fluorouracil 48-52 CEA cell adhesion molecule 3 Homo sapiens 21-24 31028570-7 2019 We observed that the CEA aptamer sensitized the 5-FU-resistant colon cancer cell line to 5-FU more than five-fold (IC50 ~ 5.995 muM), compared with cells treated with 5-FU alone (IC50 ~ 31.46 muM). Fluorouracil 89-93 CEA cell adhesion molecule 3 Homo sapiens 21-24 31028570-7 2019 We observed that the CEA aptamer sensitized the 5-FU-resistant colon cancer cell line to 5-FU more than five-fold (IC50 ~ 5.995 muM), compared with cells treated with 5-FU alone (IC50 ~ 31.46 muM). Fluorouracil 89-93 CEA cell adhesion molecule 3 Homo sapiens 21-24 31028570-9 2019 Combinatorial treatment of 5-FU and CEA aptamer augmented caspase-8 activity in the 5-FU-resistant colon cancer cell line via aptamer-mediated disruption of CEA interaction with death receptor 5 and in mouse xenograft tumors. Fluorouracil 27-31 carcinoembryonic antigen gene family Mus musculus 157-160 31028570-9 2019 Combinatorial treatment of 5-FU and CEA aptamer augmented caspase-8 activity in the 5-FU-resistant colon cancer cell line via aptamer-mediated disruption of CEA interaction with death receptor 5 and in mouse xenograft tumors. Fluorouracil 84-88 carcinoembryonic antigen gene family Mus musculus 36-39 31028570-9 2019 Combinatorial treatment of 5-FU and CEA aptamer augmented caspase-8 activity in the 5-FU-resistant colon cancer cell line via aptamer-mediated disruption of CEA interaction with death receptor 5 and in mouse xenograft tumors. Fluorouracil 84-88 carcinoembryonic antigen gene family Mus musculus 157-160 31028570-10 2019 In conclusion, CEA-specific aptamer improved 5-FU sensitivity in chemoresistant colon cancer cells in vitro and in vivo, and thus represents a novel 5-FU adjuvant to overcome the chemoresistance in CRC patients. Fluorouracil 45-49 CEA cell adhesion molecule 3 Homo sapiens 15-18 31028570-10 2019 In conclusion, CEA-specific aptamer improved 5-FU sensitivity in chemoresistant colon cancer cells in vitro and in vivo, and thus represents a novel 5-FU adjuvant to overcome the chemoresistance in CRC patients. Fluorouracil 149-153 CEA cell adhesion molecule 3 Homo sapiens 15-18 31311867-5 2019 Genetic deletion of Bok results in chemoresistance to 5-fluorouracil (5-FU) in different cell lines and in mice. Fluorouracil 70-74 BCL2-related ovarian killer Mus musculus 20-23 31311867-6 2019 Conversely, cancer cells and primary tissues that acquire resistance to 5-FU down-regulate BOK expression. Fluorouracil 72-76 BCL2-related ovarian killer Mus musculus 91-94 31311867-8 2019 Our results have implications in developing BOK as a biomarker for 5-FU resistance and have the potential for the development of BOK-mimetics for sensitizing 5-FU-resistant cancers. Fluorouracil 67-71 BCL2-related ovarian killer Mus musculus 44-47 31311867-8 2019 Our results have implications in developing BOK as a biomarker for 5-FU resistance and have the potential for the development of BOK-mimetics for sensitizing 5-FU-resistant cancers. Fluorouracil 158-162 BCL2-related ovarian killer Mus musculus 44-47 31311867-8 2019 Our results have implications in developing BOK as a biomarker for 5-FU resistance and have the potential for the development of BOK-mimetics for sensitizing 5-FU-resistant cancers. Fluorouracil 158-162 BCL2-related ovarian killer Mus musculus 129-132 31346466-1 2019 Background: The epidermal growth factor receptor (EGFR) monoclonal IgG1 antibody cetuximab is approved for first-line treatment of recurrent and metastatic (R/M) HNSCC as a part of the standard of care EXTREME regimen (platinum/5-fluorouracil/cetuximab). Fluorouracil 228-242 epidermal growth factor receptor Homo sapiens 16-48 31366086-10 2019 Intriguingly, the combination of LA and anticancer drugs (doxorubicin, 5-fluorouracil) attenuated p53-mediated stabilization of p21 and resulted in synergistic killing in CRC cells in a p53-dependant manner. Fluorouracil 71-85 tumor protein p53 Homo sapiens 98-101 31366086-10 2019 Intriguingly, the combination of LA and anticancer drugs (doxorubicin, 5-fluorouracil) attenuated p53-mediated stabilization of p21 and resulted in synergistic killing in CRC cells in a p53-dependant manner. Fluorouracil 71-85 tumor protein p53 Homo sapiens 186-189 31324203-0 2019 Exosomal transfer of p-STAT3 promotes acquired 5-FU resistance in colorectal cancer cells. Fluorouracil 47-51 signal transducer and activator of transcription 3 Homo sapiens 23-28 31324203-9 2019 Xenograft models were established to determine whether exosomal p-STAT3 can induce 5-FU resistance in vivo. Fluorouracil 83-87 signal transducer and activator of transcription 3 Homo sapiens 66-71 31324203-12 2019 Inhibition of p-STAT3 re-sensitized RKO/P cells to 5-FU via caspase cascade. Fluorouracil 51-55 signal transducer and activator of transcription 3 Homo sapiens 16-21 31324203-13 2019 Furthermore, p-STAT3 packaged by exosomes from RKO/R cells increased resistance of tumor cells to 5-FU in vivo. Fluorouracil 98-102 signal transducer and activator of transcription 3 Homo sapiens 15-20 31324203-14 2019 CONCLUSIONS: Our results reveal a novel mechanism by which p-STAT3-containing exosomes contribute to acquired 5-FU resistance in CRC. Fluorouracil 110-114 signal transducer and activator of transcription 3 Homo sapiens 61-66 31341363-9 2019 Also, RA decreased protein expression of Wee1, while the combinational effect of RA and 5-Fu decreased protein expressions of cyclooxygenase-2, B cell lymphoma 2, and Wee1 but increased protein levels of Bax, cyclin D1, and cyclin E. CONCLUSION: Taken together, the results suggest that RA acts as an anti-cancer agent and enhancer of 5-Fu in bile duct cancer cells via regulating multiple cell cycle and apoptosis-related proteins. Fluorouracil 88-92 prostaglandin-endoperoxide synthase 2 Homo sapiens 126-161 31341363-9 2019 Also, RA decreased protein expression of Wee1, while the combinational effect of RA and 5-Fu decreased protein expressions of cyclooxygenase-2, B cell lymphoma 2, and Wee1 but increased protein levels of Bax, cyclin D1, and cyclin E. CONCLUSION: Taken together, the results suggest that RA acts as an anti-cancer agent and enhancer of 5-Fu in bile duct cancer cells via regulating multiple cell cycle and apoptosis-related proteins. Fluorouracil 88-92 BCL2 associated X, apoptosis regulator Homo sapiens 204-207 31346466-1 2019 Background: The epidermal growth factor receptor (EGFR) monoclonal IgG1 antibody cetuximab is approved for first-line treatment of recurrent and metastatic (R/M) HNSCC as a part of the standard of care EXTREME regimen (platinum/5-fluorouracil/cetuximab). Fluorouracil 228-242 epidermal growth factor receptor Homo sapiens 50-54 31295851-7 2019 In addition, we combined the therapeutic powers of miR-200b and 5-fluorourancil (5-FU) into a single compound (5-FU-miR-200b) to maximize the synergistic effects of these compounds. Fluorouracil 111-115 microRNA 200b Homo sapiens 116-124 31295851-8 2019 Chemically modified miR-200b (5-FU-miR-200b mimic) was more effective in inhibiting metastatic potentials of TNBC cells than unmodified miR-200b and does not require transfection reagents, implying its therapeutic potential in TNBC. Fluorouracil 30-34 microRNA 200b Homo sapiens 20-28 31295851-8 2019 Chemically modified miR-200b (5-FU-miR-200b mimic) was more effective in inhibiting metastatic potentials of TNBC cells than unmodified miR-200b and does not require transfection reagents, implying its therapeutic potential in TNBC. Fluorouracil 30-34 microRNA 200b Homo sapiens 35-43 31317696-8 2019 Finally, interference of FOXA1 or KRT7 increased the chemosensitivity of AGS and SGC-7901 cells to 5-fluorouracil (5-Fu) treatment by suppressing cell proliferation. Fluorouracil 99-113 keratin 7 Homo sapiens 34-38 31059014-7 2019 In vitro, lnc-PKD2-2-3 increased CD44, CD133 and OCT4 expression as well as the CD44+CD133+ cell proportion, raised the sphere formation efficiency and enhanced drug resistance to 5-FU in TFK-1 and Huh-28 cells. Fluorouracil 180-184 polycystin 2, transient receptor potential cation channel Homo sapiens 14-18 30797942-5 2019 Non-transplantation-related chemotherapies associated with increased risk for VOD/SOS include oxaliplatin and 5-fluorouracil chemotherapies. Fluorouracil 110-124 xylosyltransferase 2 Homo sapiens 82-85 31317696-8 2019 Finally, interference of FOXA1 or KRT7 increased the chemosensitivity of AGS and SGC-7901 cells to 5-fluorouracil (5-Fu) treatment by suppressing cell proliferation. Fluorouracil 115-119 keratin 7 Homo sapiens 34-38 31317696-9 2019 In conclusion, these data indicate that FOXA1 promoted proliferation, migration, invasion, and decreased chemosensitivity of GC cells to 5-Fu treatment through transcriptional activator KRT7. Fluorouracil 137-141 keratin 7 Homo sapiens 186-190 31004257-6 2019 Furthermore, we observed that both REV and 5-fluorouracil (5-Fu) significantly reduce LPA-induced YB-1 phosphorylation and subsequent breast cancer invasion. Fluorouracil 43-57 Y-box binding protein 1 Homo sapiens 98-102 30548625-11 2019 5FU increased the apoptosis of HepG2 cells with silenced Stat3 expression, but GCDA-induced chemoresistance was not reversed. Fluorouracil 0-3 signal transducer and activator of transcription 3 Homo sapiens 57-62 31180555-0 2019 Synergistic effect of kaempferol and 5-fluorouracil on the growth of colorectal cancer cells by regulating the PI3K/Akt signaling pathway. Fluorouracil 37-51 AKT serine/threonine kinase 1 Homo sapiens 116-119 31180555-11 2019 The present study demonstrated that kaempferol has a synergistic effect with 5-FU by inhibiting cell proliferation and inducing apoptosis in colorectal cancer cells via suppression of TS or attenuation of p-Akt activation. Fluorouracil 77-81 AKT serine/threonine kinase 1 Homo sapiens 207-210 31072625-0 2019 miR-145 Regulates the sensitivity of esophageal squamous cell carcinoma cells to 5-FU via targeting REV3L. Fluorouracil 81-85 REV3 like, DNA directed polymerase zeta catalytic subunit Homo sapiens 100-105 31072625-12 2019 Additionally, transfection of miR-145 mimic further altered expression of key genes involved in cell apoptosis (Bcl-2, Bax, Caspase3) in ESCC cells treated with 5-FU. Fluorouracil 161-165 BCL2 apoptosis regulator Homo sapiens 112-117 31072625-12 2019 Additionally, transfection of miR-145 mimic further altered expression of key genes involved in cell apoptosis (Bcl-2, Bax, Caspase3) in ESCC cells treated with 5-FU. Fluorouracil 161-165 BCL2 associated X, apoptosis regulator Homo sapiens 119-122 31072625-12 2019 Additionally, transfection of miR-145 mimic further altered expression of key genes involved in cell apoptosis (Bcl-2, Bax, Caspase3) in ESCC cells treated with 5-FU. Fluorouracil 161-165 caspase 3 Homo sapiens 124-132 31004726-14 2019 Besides, AP could significantly suppressed the 5-FU-mediated increases of the intestinal inflammatory cytokines (TNF-alpha, IFN-gamma, IL-6, IL-1beta and IL-17), while AMO or PGS only inhibited some of them after 5-FU chemotherapy. Fluorouracil 47-51 tumor necrosis factor Mus musculus 113-122 31004726-14 2019 Besides, AP could significantly suppressed the 5-FU-mediated increases of the intestinal inflammatory cytokines (TNF-alpha, IFN-gamma, IL-6, IL-1beta and IL-17), while AMO or PGS only inhibited some of them after 5-FU chemotherapy. Fluorouracil 47-51 interferon gamma Mus musculus 124-133 31004726-14 2019 Besides, AP could significantly suppressed the 5-FU-mediated increases of the intestinal inflammatory cytokines (TNF-alpha, IFN-gamma, IL-6, IL-1beta and IL-17), while AMO or PGS only inhibited some of them after 5-FU chemotherapy. Fluorouracil 47-51 interleukin 6 Mus musculus 135-139 31004726-14 2019 Besides, AP could significantly suppressed the 5-FU-mediated increases of the intestinal inflammatory cytokines (TNF-alpha, IFN-gamma, IL-6, IL-1beta and IL-17), while AMO or PGS only inhibited some of them after 5-FU chemotherapy. Fluorouracil 47-51 interleukin 1 beta Mus musculus 141-149 31243264-6 2019 We found that the interaction between GRP78 and SPARC increased during exposure to 5-FU, CPT-11, and tunicamycin, resulting in an attenuation of GRP78"s inhibition of apoptosis. Fluorouracil 83-87 heat shock protein family A (Hsp70) member 5 Homo sapiens 38-43 31243264-6 2019 We found that the interaction between GRP78 and SPARC increased during exposure to 5-FU, CPT-11, and tunicamycin, resulting in an attenuation of GRP78"s inhibition of apoptosis. Fluorouracil 83-87 heat shock protein family A (Hsp70) member 5 Homo sapiens 145-150 31243264-8 2019 In line with these findings, a lower expression of GRP78 relative to SPARC in CRC is associated with a lower IC50 for 5-FU in either sensitive or therapy-refractory CRC cells. Fluorouracil 118-122 heat shock protein family A (Hsp70) member 5 Homo sapiens 51-56 31000196-0 2019 Ribavirin sensitizes nasopharyngeal carcinoma to 5-fluorouracil through suppressing 5-fluorouracil-induced ERK-dependent-eIF4E activation. Fluorouracil 49-63 mitogen-activated protein kinase 1 Mus musculus 107-110 31000196-0 2019 Ribavirin sensitizes nasopharyngeal carcinoma to 5-fluorouracil through suppressing 5-fluorouracil-induced ERK-dependent-eIF4E activation. Fluorouracil 84-98 mitogen-activated protein kinase 1 Mus musculus 107-110 31000196-3 2019 Mechanism studies indicate that 5-FU treatment increases phosphorylation of eIF4E in NPC cells, and this is dependent on ERK activation. Fluorouracil 32-36 mitogen-activated protein kinase 1 Mus musculus 121-124 31217433-11 2019 Finally, we found a negative correlation between DHA content in plasma and the induction of caspase-1 activity in HLA-DR- CD33+ CD15+ MDSC of patients treated with 5-FU-based chemotherapy, strongly suggesting that our data are clinical relevant. Fluorouracil 164-168 caspase 1 Homo sapiens 92-101 31312359-6 2019 S100A11 inhibition increased the effects of 5-Fu on FaDu cells proliferation in vitro. Fluorouracil 44-48 S100 calcium binding protein A11 Homo sapiens 0-7 31293646-5 2019 Silencing of Nrf2 in laryngeal carcinoma cell line Hep-2 significantly reduced cell viability and enhanced apoptosis rates under cisplatin, 5-fluorouracil (5-FU) and phenethyl isothiocyanate (PEITC) exposure. Fluorouracil 140-154 NFE2 like bZIP transcription factor 2 Homo sapiens 13-17 31293646-5 2019 Silencing of Nrf2 in laryngeal carcinoma cell line Hep-2 significantly reduced cell viability and enhanced apoptosis rates under cisplatin, 5-fluorouracil (5-FU) and phenethyl isothiocyanate (PEITC) exposure. Fluorouracil 156-160 NFE2 like bZIP transcription factor 2 Homo sapiens 13-17 31004257-6 2019 Furthermore, we observed that both REV and 5-fluorouracil (5-Fu) significantly reduce LPA-induced YB-1 phosphorylation and subsequent breast cancer invasion. Fluorouracil 59-63 Y-box binding protein 1 Homo sapiens 98-102 31004257-8 2019 Therefore, our data demonstrate that the YB-1/EZH2 signaling axis mediates LPA-induced AREG expression and breast cancer cell invasion and its inhibition by REV and 5-Fu, providing potential therapeutic targets and inhibition of breast cancer. Fluorouracil 165-169 Y-box binding protein 1 Homo sapiens 41-45 31004257-8 2019 Therefore, our data demonstrate that the YB-1/EZH2 signaling axis mediates LPA-induced AREG expression and breast cancer cell invasion and its inhibition by REV and 5-Fu, providing potential therapeutic targets and inhibition of breast cancer. Fluorouracil 165-169 enhancer of zeste 2 polycomb repressive complex 2 subunit Homo sapiens 46-50 31011915-1 2019 BACKGROUND: S-1 is an oral anticancer drug composed of tegafur (FT), which is a prodrug of 5-FU, 5-chloro-2,4-dihydroxypyridine (CDHP), and potassium oxonate. Fluorouracil 91-95 proteasome 26S subunit, non-ATPase 1 Homo sapiens 12-15 30484020-11 2019 The mRNA levels of P-gp (0.28+-0.02) and HSP-27 (0.28+-0.09) in HCT-8/5-FU cells treated with combination drugs were lower than cells treated with 5-FU alone (P-gp, 0.48+-0.07, P=0.009; HSP-27, 0.57+-0.10, P=0.007). Fluorouracil 70-74 ATP binding cassette subfamily B member 1 Homo sapiens 19-23 30484020-11 2019 The mRNA levels of P-gp (0.28+-0.02) and HSP-27 (0.28+-0.09) in HCT-8/5-FU cells treated with combination drugs were lower than cells treated with 5-FU alone (P-gp, 0.48+-0.07, P=0.009; HSP-27, 0.57+-0.10, P=0.007). Fluorouracil 70-74 ATP binding cassette subfamily B member 1 Homo sapiens 159-163 30484020-12 2019 The protein levels of P-gp (0.25+-0.06) and HSP-27 (0.09+-0.02) in HCT-8/5-FU cells treated with combination drugs were decreased when compared to 5-FU alone (P-gp, 0.46+-0.02, P=0.005; HSP-27, 0.43+-0.01, P=0.000). Fluorouracil 73-77 ATP binding cassette subfamily B member 1 Homo sapiens 22-26 30484020-15 2019 Down-regulation of P-gp and HSP-27 may be the mechanism of curcumin reversing the drug resistance of HCT-8/5-FU to 5-FU. Fluorouracil 107-111 ATP binding cassette subfamily B member 1 Homo sapiens 19-23 30484020-15 2019 Down-regulation of P-gp and HSP-27 may be the mechanism of curcumin reversing the drug resistance of HCT-8/5-FU to 5-FU. Fluorouracil 115-119 ATP binding cassette subfamily B member 1 Homo sapiens 19-23 31011915-4 2019 The aim of this study was to investigate the correlation between tears and plasma concentrations of FT, 5-FU, and CDHP, which are components and active modulator of S-1. Fluorouracil 104-108 proteasome 26S subunit, non-ATPase 1 Homo sapiens 165-168 31042625-10 2019 Our data suggest that PCAF-mediated p53 acetylation is an essential regulatory mechanism for increasing the susceptibility of CRC to 5-FU. Fluorouracil 133-137 tumor protein p53 Homo sapiens 36-39 31081052-5 2019 The results revealed that TGF-beta1 treatment protected tumor cells from various apoptotic stresses, including 5-fluorouracil, etoposide and gamma-irradiation. Fluorouracil 111-125 transforming growth factor beta 1 Homo sapiens 26-35 30792218-8 2019 Moreover, knockdown of LGR5 resensitizes DAP3-depleted gastric cancer cells to 5-fluorouracil (5-FU) and oxaliplatin. Fluorouracil 79-93 death associated protein 3 Homo sapiens 41-45 30792218-8 2019 Moreover, knockdown of LGR5 resensitizes DAP3-depleted gastric cancer cells to 5-fluorouracil (5-FU) and oxaliplatin. Fluorouracil 95-99 death associated protein 3 Homo sapiens 41-45 31042625-8 2019 However, knockdown of p21 abolishes the beneficial effects of PCAF overexpression on increasing the sensitivity of HCT116/5-FU cells to 5-FU. Fluorouracil 122-126 cyclin dependent kinase inhibitor 1A Homo sapiens 22-25 31217730-9 2019 Knockdown Cx43 in B16F10 cells reduced the therapeutic effects of combination therapy (EPA plus 5-Fluorouracil). Fluorouracil 96-110 gap junction protein, alpha 1 Mus musculus 10-14 31042625-8 2019 However, knockdown of p21 abolishes the beneficial effects of PCAF overexpression on increasing the sensitivity of HCT116/5-FU cells to 5-FU. Fluorouracil 136-140 cyclin dependent kinase inhibitor 1A Homo sapiens 22-25 31120863-5 2019 We now demonstrate that simultaneous deletion of P110alpha and P110delta in double knockout (DKO) HSCs uncovers their redundant requirement in HSC cycling after 5-fluorouracil (5-FU) chemotherapy administration. Fluorouracil 161-175 phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha Homo sapiens 49-58 31120863-5 2019 We now demonstrate that simultaneous deletion of P110alpha and P110delta in double knockout (DKO) HSCs uncovers their redundant requirement in HSC cycling after 5-fluorouracil (5-FU) chemotherapy administration. Fluorouracil 177-181 phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha Homo sapiens 49-58 31120863-7 2019 We found that DKO HSCs and progenitors have impaired sensing of inflammatory signals ex vivo, and that levels of IL1-beta and MIG are higher in the bone marrow after LPS than after 5-FU administration. Fluorouracil 181-185 C-X-C motif chemokine ligand 9 Homo sapiens 126-129 30804456-6 2019 Of note, combined treatment with the conventional cytotoxic drug 5-FU together with Tubastatin A, a HDAC6-specific inhibitor, resulted in a significant in vivo synergistic inhibitory effect on tumor growth through suppression of CRC stemness. Fluorouracil 65-69 histone deacetylase 6 Homo sapiens 100-105 31115003-0 2019 MiR-195 reverses 5-FU resistance through targeting HMGA1 in gastric cancer cells. Fluorouracil 17-21 microRNA 195 Homo sapiens 0-7 31002510-5 2019 Compound 14 arrested the cell cycle at S and G2 phases and up-regulated thymidylate synthase and p53, consistent with the results of the combination, suggesting 14 adopted a collaborative mode of 5-FU and oxaliplatin to kill cancer cells. Fluorouracil 196-200 tumor protein p53 Homo sapiens 97-100 30825616-12 2019 GENERAL SIGNIFICANCE: The cytotoxic activity of Pd(II) complex and 5-FU on HeLa cells is mediated by EGFR inhibition and autophagy induction, leading to activation of mitochondrial apoptotic cell death. Fluorouracil 67-71 epidermal growth factor receptor Homo sapiens 101-105 30945479-6 2019 The therapeutic effects of LDDS-administered 5-FU on false-negative metastatic LNs were evaluated using bioluminescence imaging, high-frequency ultrasound (US), and histology in MHX10/Mo-lpr/lpr mice. Fluorouracil 45-49 Fas (TNF receptor superfamily member 6) Mus musculus 187-190 30945479-6 2019 The therapeutic effects of LDDS-administered 5-FU on false-negative metastatic LNs were evaluated using bioluminescence imaging, high-frequency ultrasound (US), and histology in MHX10/Mo-lpr/lpr mice. Fluorouracil 45-49 Fas (TNF receptor superfamily member 6) Mus musculus 191-194 30825616-3 2019 This study aimed to investigate whether EGFR inhibition by canertinib induces autophagy and this induction influence the effect of Palladium (Pd) (II) complex and 5-fluorouracil (5-FU) especially in nontoxic doses. Fluorouracil 163-177 epidermal growth factor receptor Homo sapiens 40-44 30825616-3 2019 This study aimed to investigate whether EGFR inhibition by canertinib induces autophagy and this induction influence the effect of Palladium (Pd) (II) complex and 5-fluorouracil (5-FU) especially in nontoxic doses. Fluorouracil 179-183 epidermal growth factor receptor Homo sapiens 40-44 30825616-7 2019 RESULTS: Blocking EGFR by the pan-ErbB tyrosine kinase inhibitor canertinib inhibited cell growth of HeLa cervical cancer cells in combination with Pd(II) complex and 5-FU. Fluorouracil 167-171 epidermal growth factor receptor Homo sapiens 18-22 31115003-1 2019 OBJECTIVE: To investigate the role of micro ribonucleic acid (miR)-195 in acquired resistance to 5-fluorouracil (5-FU) in gastric cancer and its potential mechanism. Fluorouracil 97-111 microRNA 195 Homo sapiens 38-70 31115003-1 2019 OBJECTIVE: To investigate the role of micro ribonucleic acid (miR)-195 in acquired resistance to 5-fluorouracil (5-FU) in gastric cancer and its potential mechanism. Fluorouracil 113-117 microRNA 195 Homo sapiens 38-70 31115003-6 2019 RESULTS: Both AGS/5-FU and SGC-7901/5-FU cells were significantly resistant to 5-FU compared with their parental cells, and miR-195 was down-regulated in AGS/5-FU and SGC-7901/5-FU cells, while HMGA1 was up-regulated in AGS and SGC-7901 cells. Fluorouracil 18-22 microRNA 195 Homo sapiens 124-131 31115003-10 2019 CONCLUSIONS: The down-regulation of miR-195 induces the resistance to 5-FU in gastric cancer through promoting the expression of HMGA1. Fluorouracil 70-74 microRNA 195 Homo sapiens 36-43 30879771-5 2019 Furthermore, an experiment using conoidinA, a Prx2 inhibitor, revealed that Prx2 inhibition can overcome 5-FU resistance in GC cells. Fluorouracil 105-109 peroxiredoxin 2 Homo sapiens 76-80 30683364-4 2019 Fluorescent properties of 5-FU were used with detection limit of 9 x 10-4 mg L-1 and a linear response up to 5 mg L-1 The drug loading and release procedures were optimized in sequential injection analysis (SIA) systems obtaining a huge economy regarding the time spent (4 min towards 2 h). Fluorouracil 26-30 immunoglobulin kappa variable 1-16 Homo sapiens 77-80 30683364-4 2019 Fluorescent properties of 5-FU were used with detection limit of 9 x 10-4 mg L-1 and a linear response up to 5 mg L-1 The drug loading and release procedures were optimized in sequential injection analysis (SIA) systems obtaining a huge economy regarding the time spent (4 min towards 2 h). Fluorouracil 26-30 immunoglobulin kappa variable 1-16 Homo sapiens 114-117 30742943-6 2019 SMURF2 is negatively regulated by USP47, and USP47 depletion sensitizes colon cancer cells to 5-FU treatment-induced apoptosis. Fluorouracil 94-98 SMAD specific E3 ubiquitin protein ligase 2 Mus musculus 0-6 31022917-7 2019 Inhibition of P-gp and MRP1 increased the 5-FU drug sensitivity in HCV infected Huh7.5.1 cells. Fluorouracil 42-46 ATP binding cassette subfamily C member 1 Homo sapiens 23-27 31010234-10 2019 Treatment with 5-fluorouracil (5-FU) significantly enhanced YB-1 phosphorylation in KRAS(G13D)-mutated HCT116 cells but not in KRAS wild-type SW48 cells. Fluorouracil 15-29 Y-box binding protein 1 Homo sapiens 60-64 31010234-10 2019 Treatment with 5-fluorouracil (5-FU) significantly enhanced YB-1 phosphorylation in KRAS(G13D)-mutated HCT116 cells but not in KRAS wild-type SW48 cells. Fluorouracil 31-35 Y-box binding protein 1 Homo sapiens 60-64 31010234-11 2019 Dual targeting of Akt and RSK sensitized HCT116 cells to 5-FU by stimulating 5-FU-induced apoptosis and inhibiting repair of 5-FU-induced DNA damage. Fluorouracil 57-61 AKT serine/threonine kinase 1 Homo sapiens 18-21 31010234-11 2019 Dual targeting of Akt and RSK sensitized HCT116 cells to 5-FU by stimulating 5-FU-induced apoptosis and inhibiting repair of 5-FU-induced DNA damage. Fluorouracil 57-61 ribosomal protein S6 kinase A2 Homo sapiens 26-29 31010234-11 2019 Dual targeting of Akt and RSK sensitized HCT116 cells to 5-FU by stimulating 5-FU-induced apoptosis and inhibiting repair of 5-FU-induced DNA damage. Fluorouracil 77-81 AKT serine/threonine kinase 1 Homo sapiens 18-21 31010234-11 2019 Dual targeting of Akt and RSK sensitized HCT116 cells to 5-FU by stimulating 5-FU-induced apoptosis and inhibiting repair of 5-FU-induced DNA damage. Fluorouracil 77-81 ribosomal protein S6 kinase A2 Homo sapiens 26-29 31010234-11 2019 Dual targeting of Akt and RSK sensitized HCT116 cells to 5-FU by stimulating 5-FU-induced apoptosis and inhibiting repair of 5-FU-induced DNA damage. Fluorouracil 77-81 AKT serine/threonine kinase 1 Homo sapiens 18-21 30914455-6 2019 Through performing loss-of-function assays, we demonstrated that knockdown of UBE2C expression obviously suppressed proliferation, migration, and invasion of HCC cells in vitro Moreover, HCC cells with UBE2C knockdown showed higher sensitivity for the treatment of chemotherapeutic drug, including adriamycin (ADR) and 5-fluorouracil (5-FU). Fluorouracil 319-333 ubiquitin conjugating enzyme E2 C Homo sapiens 78-83 31010234-11 2019 Dual targeting of Akt and RSK sensitized HCT116 cells to 5-FU by stimulating 5-FU-induced apoptosis and inhibiting repair of 5-FU-induced DNA damage. Fluorouracil 77-81 ribosomal protein S6 kinase A2 Homo sapiens 26-29 30914455-6 2019 Through performing loss-of-function assays, we demonstrated that knockdown of UBE2C expression obviously suppressed proliferation, migration, and invasion of HCC cells in vitro Moreover, HCC cells with UBE2C knockdown showed higher sensitivity for the treatment of chemotherapeutic drug, including adriamycin (ADR) and 5-fluorouracil (5-FU). Fluorouracil 319-333 ubiquitin conjugating enzyme E2 C Homo sapiens 202-207 30914455-6 2019 Through performing loss-of-function assays, we demonstrated that knockdown of UBE2C expression obviously suppressed proliferation, migration, and invasion of HCC cells in vitro Moreover, HCC cells with UBE2C knockdown showed higher sensitivity for the treatment of chemotherapeutic drug, including adriamycin (ADR) and 5-fluorouracil (5-FU). Fluorouracil 335-339 ubiquitin conjugating enzyme E2 C Homo sapiens 78-83 30914455-6 2019 Through performing loss-of-function assays, we demonstrated that knockdown of UBE2C expression obviously suppressed proliferation, migration, and invasion of HCC cells in vitro Moreover, HCC cells with UBE2C knockdown showed higher sensitivity for the treatment of chemotherapeutic drug, including adriamycin (ADR) and 5-fluorouracil (5-FU). Fluorouracil 335-339 ubiquitin conjugating enzyme E2 C Homo sapiens 202-207 31114248-6 2019 We further illuminated that M2 macrophages regulated 5-FU resistance of CRC cells through epithelial-mesenchymal transition (EMT) program, PI3K/AKT pathway, and caspase-mediated apoptosis. Fluorouracil 53-57 AKT serine/threonine kinase 1 Homo sapiens 144-147 31114248-9 2019 Conclusion: Our findings indicate that M2 macrophage regulated 5-FU-mediated CRC chemoresistance via the EMT program, PI3K/AKT pathway, and caspase-mediated apoptosis by releasing CCL22. Fluorouracil 63-67 AKT serine/threonine kinase 1 Homo sapiens 123-126 30737232-4 2019 Addition of a neutralizing antibody against the myeloid differentiation antigen GR-1 or gemcitabine/5-fluorouracil-depleted MDSCs alleviated MDSC-mediated immunosuppression and increased CD4+ and CD8+ T-cell tumor infiltration and GSK126 therapeutic efficacy. Fluorouracil 100-114 CD4 molecule Homo sapiens 187-190 31057299-1 2019 enhances the inhibitory effect of 5-fluorouracil on gastric cancer cells through the AKT-mTOR pathway. Fluorouracil 34-48 mechanistic target of rapamycin kinase Homo sapiens 89-93 31057299-21 2019 Extract plus 5-Fu further reduced the expression of the drug-resistance-related proteins p-AKT and mTOR after 48 h compared to 5-Fu alone. Fluorouracil 13-17 mechanistic target of rapamycin kinase Homo sapiens 99-103 31057299-21 2019 Extract plus 5-Fu further reduced the expression of the drug-resistance-related proteins p-AKT and mTOR after 48 h compared to 5-Fu alone. Fluorouracil 127-131 mechanistic target of rapamycin kinase Homo sapiens 99-103 31057299-22 2019 Compared to 5-Fu treatment alone, mTOR and p-AKT expression was significantly reduced by about 50% and 75%, respectively. Fluorouracil 12-16 mechanistic target of rapamycin kinase Homo sapiens 34-38 31057299-27 2019 effectively inhibited gastric cancer cell growth and enhanced the anti-cancer effect of 5-Fu through the AKT-mTOR pathway. Fluorouracil 88-92 mechanistic target of rapamycin kinase Homo sapiens 109-113 31105827-9 2019 We also demonstrated that increasing of miR-590-5p in 5-Fu resistant patients and liver cancer cells, and knockdown of miR-590-5p enhances chemosensitivity to 5-Fu in liver cancer. Fluorouracil 54-58 microRNA 590 Homo sapiens 40-47 31105827-9 2019 We also demonstrated that increasing of miR-590-5p in 5-Fu resistant patients and liver cancer cells, and knockdown of miR-590-5p enhances chemosensitivity to 5-Fu in liver cancer. Fluorouracil 159-163 microRNA 590 Homo sapiens 119-126 31011291-14 2019 Overexpression of LATS2 to further disrupt mitochondrial function via the JNK-MIEF1 signalling pathway might be a method to optimize 5-FU-based chemotherapy. Fluorouracil 133-137 mitogen-activated protein kinase 8 Homo sapiens 74-77 30979374-9 2019 Moreover, TRIM47 overexpression played a role in CRC chemoresistance in response to 5-FU therapy. Fluorouracil 84-88 tripartite motif containing 47 Homo sapiens 10-16 31011291-0 2019 Large tumor suppressor kinase 2 overexpression attenuates 5-FU-resistance in colorectal cancer via activating the JNK-MIEF1-mitochondrial division pathway. Fluorouracil 58-62 mitogen-activated protein kinase 8 Homo sapiens 114-117 31019975-0 2019 Pretreatment with Gemcitabine/5-Fluorouracil Enhances the Cytotoxicity of Trastuzumab to HER2-Negative Human Gallbladder Cancer Cells In Vitro and In Vivo. Fluorouracil 30-44 erb-b2 receptor tyrosine kinase 2 Homo sapiens 89-93 31011291-9 2019 Functional exploration showed that 5-FU treatment suppressed mitochondrial membrane potential, enhanced cyt-c release into the nucleus, induced an oxidative injury environment by promoting ROS production, and eventually upregulated Bax-related mitochondrial apoptosis. Fluorouracil 35-39 BCL2 associated X, apoptosis regulator Homo sapiens 232-235 31011291-11 2019 Mechanistically, LATS2 overexpression and 5-FU co-treatment amplified mitochondrial division by upregulating MIEF1 expression in a manner dependent on MAPK-JNK axis. Fluorouracil 42-46 mitogen-activated protein kinase 8 Homo sapiens 156-159 30959809-6 2019 The 5FU-resistant CRC cells displayed enhanced mitochondrial biogenesis, oxidative phosphorylation, and antioxidant enzyme activities against 5FU-induced reactive oxygen species, because of the increased expression of PGC-1alpha. Fluorouracil 4-7 PPARG coactivator 1 alpha Homo sapiens 218-228 30959809-7 2019 PGC-1alpha inhibited 5FU-induced endoplasmic reticulum (ER) stress in the 5FU-resistant CRC cells, resulting in the suppression of apoptosis. Fluorouracil 21-24 PPARG coactivator 1 alpha Homo sapiens 0-10 30952738-10 2019 In addition, among the patients with intense VEGFA expression (n=36), those who had positive cytoplasmic E-cadherin in their tumours had a lower response-rate to first-line therapy with irinotecan, fluorouracil and leucovorin regimen: 5 out of 36 (14%) were chemosensitive. Fluorouracil 198-210 vascular endothelial growth factor A Homo sapiens 45-50 30952738-10 2019 In addition, among the patients with intense VEGFA expression (n=36), those who had positive cytoplasmic E-cadherin in their tumours had a lower response-rate to first-line therapy with irinotecan, fluorouracil and leucovorin regimen: 5 out of 36 (14%) were chemosensitive. Fluorouracil 198-210 cadherin 1 Homo sapiens 105-115 31019975-9 2019 Western blot analysis showed that gemcitabine/5-fluorouracil increased the expressions of total and phosphorylated forms of HER2, thus enhancing the cytotoxicity of trastuzumab. Fluorouracil 46-60 erb-b2 receptor tyrosine kinase 2 Homo sapiens 124-128 31019975-12 2019 Our in vivo and in vitro data suggest that sequential therapy with gemcitabine/5-fluorouracil followed by trastuzumab represents a novel and promising therapeutic strategy against HER2-negative GBC. Fluorouracil 79-93 erb-b2 receptor tyrosine kinase 2 Homo sapiens 180-184 31019975-13 2019 The upregulation of phosphorylated HER2 and phosphorylated-AKT induced by gemcitabine/5-fluorouracil treatment shows that HER2/AKT pathway is triggered. Fluorouracil 86-100 erb-b2 receptor tyrosine kinase 2 Homo sapiens 35-39 31019975-13 2019 The upregulation of phosphorylated HER2 and phosphorylated-AKT induced by gemcitabine/5-fluorouracil treatment shows that HER2/AKT pathway is triggered. Fluorouracil 86-100 AKT serine/threonine kinase 1 Homo sapiens 59-62 31019975-13 2019 The upregulation of phosphorylated HER2 and phosphorylated-AKT induced by gemcitabine/5-fluorouracil treatment shows that HER2/AKT pathway is triggered. Fluorouracil 86-100 erb-b2 receptor tyrosine kinase 2 Homo sapiens 122-126 31019975-13 2019 The upregulation of phosphorylated HER2 and phosphorylated-AKT induced by gemcitabine/5-fluorouracil treatment shows that HER2/AKT pathway is triggered. Fluorouracil 86-100 AKT serine/threonine kinase 1 Homo sapiens 127-130 30810625-10 2019 In addition, 5-FU injection caused pronounced tissue injury accompanied by increased neutrophil accumulation, tumor necrosis factor-alpha (TNF-alpha), and interleukin-1 beta (IL-1beta) tissue levels, and positive immunostaining for TNF-alpha, IL-1beta, and inducible nitric oxide synthase (iNOS). Fluorouracil 13-17 interleukin 1 beta Homo sapiens 175-183 30842340-0 2019 Down-regulation of miR-543 expression increases the sensitivity of colorectal cancer cells to 5-Fluorouracil through the PTEN/PI3K/AKT pathway. Fluorouracil 94-108 AKT serine/threonine kinase 1 Homo sapiens 131-134 30842340-9 2019 These results indicate that miR-543 might be a target to increase the sensitivity of CRC cells to 5-FU through the PTEN/PI3K/AKT pathway. Fluorouracil 98-102 AKT serine/threonine kinase 1 Homo sapiens 125-128 31933924-10 2019 CONCLUSION: Our results suggest that SREBP1 protect the 5-FU treated CRC cells through caspase7 dependent PARP1 cleavage in apoptosis pathway and potentially provide a new target in the treatment of CRC. Fluorouracil 56-60 poly(ADP-ribose) polymerase 1 Homo sapiens 106-111 31127990-11 2019 Compared with administration of 5-FU or etoposide alone, TGF-Beta1 combined with 5-FU or etoposide significantly administration the viability of colon cancer HT-29 cells. Fluorouracil 32-36 transforming growth factor beta 1 Homo sapiens 57-66 31127996-16 2019 CONCLUSIONS: Combined treatment of bevacizumab and 5-fluorouracil can reduce the serum VEGF level of patients with metastatic colon cancer and prolong their PFS and OS. Fluorouracil 51-65 vascular endothelial growth factor A Homo sapiens 87-91 31205515-7 2019 Higher expression levels of both c-Myb and COX-2 were significantly associated with shorter overall survival for stage II and stage III patients with 5-Fu based chemotherapy. Fluorouracil 150-154 mitochondrially encoded cytochrome c oxidase II Homo sapiens 43-48 30915129-3 2019 In vitro, miR-214 could sensitize non-resistant colon cancer cells and 5-FU-resistant colon cancer cellsto 5-FU. Fluorouracil 71-75 microRNA 214 Homo sapiens 10-17 30915129-3 2019 In vitro, miR-214 could sensitize non-resistant colon cancer cells and 5-FU-resistant colon cancer cellsto 5-FU. Fluorouracil 107-111 microRNA 214 Homo sapiens 10-17 30915129-4 2019 Functionally, miR-214 inhibited cell clone formation and cell growth and enhanced 5-FU-inducing cell apoptosis and caspase-3 levels. Fluorouracil 82-86 microRNA 214 Homo sapiens 14-21 30915129-4 2019 Functionally, miR-214 inhibited cell clone formation and cell growth and enhanced 5-FU-inducing cell apoptosis and caspase-3 levels. Fluorouracil 82-86 caspase 3 Homo sapiens 115-124 30915129-7 2019 Overexpression of Hsp27 could block miR-214 with an effect on the sensitivity of colon cancer cells to 5-FU. Fluorouracil 103-107 microRNA 214 Homo sapiens 36-43 30915129-8 2019 In conclusion, miR-214 sensitizes colon cancer cells to 5-FU by targeting Hsp27, indicating a significant role for this miRNA in colon cancer chemotherapy. Fluorouracil 56-60 microRNA 214 Homo sapiens 15-22 30850009-0 2019 Cysteine-rich intestinal protein 1 suppresses apoptosis and chemosensitivity to 5-fluorouracil in colorectal cancer through ubiquitin-mediated Fas degradation. Fluorouracil 80-94 cysteine rich protein 1 Homo sapiens 0-34 30850009-4 2019 Functional assays, such as CCK8, TUNEL assay and in vivo tumor growth assay, were used to detect the proliferation, apoptosis and response to 5-FU of CRIP1. Fluorouracil 142-146 cysteine rich protein 1 Homo sapiens 150-155 30850009-8 2019 CRIP1 could dramatically recover the 5-Fluorouracil (5-FU) inhibited CRC cell proliferation in vitro and stimulate the tumor formation of CRC in vivo, probably through inhibiting CRC cell apoptosis. Fluorouracil 37-51 cysteine rich protein 1 Homo sapiens 0-5 30850009-8 2019 CRIP1 could dramatically recover the 5-Fluorouracil (5-FU) inhibited CRC cell proliferation in vitro and stimulate the tumor formation of CRC in vivo, probably through inhibiting CRC cell apoptosis. Fluorouracil 53-57 cysteine rich protein 1 Homo sapiens 0-5 30850009-9 2019 Moreover, CRIP1 also dramatically recovered the 5-Fluorouracil (5-FU) induced tumor cell apoptosis in vitro. Fluorouracil 48-62 cysteine rich protein 1 Homo sapiens 10-15 30850009-9 2019 Moreover, CRIP1 also dramatically recovered the 5-Fluorouracil (5-FU) induced tumor cell apoptosis in vitro. Fluorouracil 64-68 cysteine rich protein 1 Homo sapiens 10-15 30741544-0 2019 (-)-Epigallocatechin Gallate (EGCG) Enhances the Sensitivity of Colorectal Cancer Cells to 5-FU by Inhibiting GRP78/NF-kappaB/miR-155-5p/MDR1 Pathway. Fluorouracil 91-95 heat shock protein family A (Hsp70) member 5 Homo sapiens 110-115 30741544-0 2019 (-)-Epigallocatechin Gallate (EGCG) Enhances the Sensitivity of Colorectal Cancer Cells to 5-FU by Inhibiting GRP78/NF-kappaB/miR-155-5p/MDR1 Pathway. Fluorouracil 91-95 nuclear factor kappa B subunit 1 Homo sapiens 116-125 30741544-5 2019 Here, we report that EGCG reinforces the sensitivity of colon cancer cells to 5-FU, and the IC50 values of 5-FU is decreased from 40 +- 4.2 muM to 5 +- 0.36 muM in one human colon carcinoma cell line-HCT-116, and from 150 +- 6.4 muM to 11 +- 0.96 muM in the other human colon carcinoma cell line-DLD1 when these cells are cotreated with 50 muM EGCG. Fluorouracil 78-82 latexin Homo sapiens 157-160 30741544-5 2019 Here, we report that EGCG reinforces the sensitivity of colon cancer cells to 5-FU, and the IC50 values of 5-FU is decreased from 40 +- 4.2 muM to 5 +- 0.36 muM in one human colon carcinoma cell line-HCT-116, and from 150 +- 6.4 muM to 11 +- 0.96 muM in the other human colon carcinoma cell line-DLD1 when these cells are cotreated with 50 muM EGCG. Fluorouracil 78-82 latexin Homo sapiens 157-160 30741544-5 2019 Here, we report that EGCG reinforces the sensitivity of colon cancer cells to 5-FU, and the IC50 values of 5-FU is decreased from 40 +- 4.2 muM to 5 +- 0.36 muM in one human colon carcinoma cell line-HCT-116, and from 150 +- 6.4 muM to 11 +- 0.96 muM in the other human colon carcinoma cell line-DLD1 when these cells are cotreated with 50 muM EGCG. Fluorouracil 78-82 latexin Homo sapiens 157-160 30741544-5 2019 Here, we report that EGCG reinforces the sensitivity of colon cancer cells to 5-FU, and the IC50 values of 5-FU is decreased from 40 +- 4.2 muM to 5 +- 0.36 muM in one human colon carcinoma cell line-HCT-116, and from 150 +- 6.4 muM to 11 +- 0.96 muM in the other human colon carcinoma cell line-DLD1 when these cells are cotreated with 50 muM EGCG. Fluorouracil 78-82 latexin Homo sapiens 157-160 30741544-5 2019 Here, we report that EGCG reinforces the sensitivity of colon cancer cells to 5-FU, and the IC50 values of 5-FU is decreased from 40 +- 4.2 muM to 5 +- 0.36 muM in one human colon carcinoma cell line-HCT-116, and from 150 +- 6.4 muM to 11 +- 0.96 muM in the other human colon carcinoma cell line-DLD1 when these cells are cotreated with 50 muM EGCG. Fluorouracil 107-111 latexin Homo sapiens 140-143 30741544-5 2019 Here, we report that EGCG reinforces the sensitivity of colon cancer cells to 5-FU, and the IC50 values of 5-FU is decreased from 40 +- 4.2 muM to 5 +- 0.36 muM in one human colon carcinoma cell line-HCT-116, and from 150 +- 6.4 muM to 11 +- 0.96 muM in the other human colon carcinoma cell line-DLD1 when these cells are cotreated with 50 muM EGCG. Fluorouracil 107-111 latexin Homo sapiens 157-160 30741544-5 2019 Here, we report that EGCG reinforces the sensitivity of colon cancer cells to 5-FU, and the IC50 values of 5-FU is decreased from 40 +- 4.2 muM to 5 +- 0.36 muM in one human colon carcinoma cell line-HCT-116, and from 150 +- 6.4 muM to 11 +- 0.96 muM in the other human colon carcinoma cell line-DLD1 when these cells are cotreated with 50 muM EGCG. Fluorouracil 107-111 latexin Homo sapiens 157-160 30741544-5 2019 Here, we report that EGCG reinforces the sensitivity of colon cancer cells to 5-FU, and the IC50 values of 5-FU is decreased from 40 +- 4.2 muM to 5 +- 0.36 muM in one human colon carcinoma cell line-HCT-116, and from 150 +- 6.4 muM to 11 +- 0.96 muM in the other human colon carcinoma cell line-DLD1 when these cells are cotreated with 50 muM EGCG. Fluorouracil 107-111 latexin Homo sapiens 157-160 30741544-5 2019 Here, we report that EGCG reinforces the sensitivity of colon cancer cells to 5-FU, and the IC50 values of 5-FU is decreased from 40 +- 4.2 muM to 5 +- 0.36 muM in one human colon carcinoma cell line-HCT-116, and from 150 +- 6.4 muM to 11 +- 0.96 muM in the other human colon carcinoma cell line-DLD1 when these cells are cotreated with 50 muM EGCG. Fluorouracil 107-111 latexin Homo sapiens 157-160 30741544-8 2019 The elevated miR-155-5p strongly suppresses target gene MDR1 expression, which blocks the efflux of 5-FU. Fluorouracil 100-104 ATP binding cassette subfamily B member 1 Homo sapiens 56-60 30741544-9 2019 The accumulation of 5-FU resulted in caspase-3 and PARP activation, Bcl-2 reduction, and Bad increase, which ultimately lead to cancer cell apoptosis. Fluorouracil 20-24 caspase 3 Homo sapiens 37-46 30741544-9 2019 The accumulation of 5-FU resulted in caspase-3 and PARP activation, Bcl-2 reduction, and Bad increase, which ultimately lead to cancer cell apoptosis. Fluorouracil 20-24 BCL2 apoptosis regulator Homo sapiens 68-73 30741544-10 2019 Overall, our data show that EGCG may be act as a novel chemo-sensitizer, and the GRP78/NF-kappaB/miR-155-5p/MDR1 pathway plays a vital role in EGCG enhancing the sensitivity of colorectal cancer to 5-FU. Fluorouracil 198-202 heat shock protein family A (Hsp70) member 5 Homo sapiens 81-86 30741544-10 2019 Overall, our data show that EGCG may be act as a novel chemo-sensitizer, and the GRP78/NF-kappaB/miR-155-5p/MDR1 pathway plays a vital role in EGCG enhancing the sensitivity of colorectal cancer to 5-FU. Fluorouracil 198-202 nuclear factor kappa B subunit 1 Homo sapiens 87-96 30741544-10 2019 Overall, our data show that EGCG may be act as a novel chemo-sensitizer, and the GRP78/NF-kappaB/miR-155-5p/MDR1 pathway plays a vital role in EGCG enhancing the sensitivity of colorectal cancer to 5-FU. Fluorouracil 198-202 ATP binding cassette subfamily B member 1 Homo sapiens 108-112 30783438-0 2019 Downregulation of miR-183 inhibits the growth of PANC-1 pancreatic cancer cells in vitro and in vivo, and increases chemosensitivity to 5-fluorouracil and gemcitabine. Fluorouracil 136-150 microRNA 183 Homo sapiens 18-25 30783438-3 2019 The present study aimed to elucidate the role of miR-183 in the proliferation, apoptosis, and chemosensitivity to 5-fluorouracil and gemcitabine of human PC cells and the associated mechanisms. Fluorouracil 114-128 microRNA 183 Homo sapiens 49-56 30783438-12 2019 Knockdown of miR-183 was able to significantly increase the chemosensitivity of PANC-1 cells to 5-fluorouracil and gemcitabine. Fluorouracil 96-110 microRNA 183 Homo sapiens 13-20 30783438-13 2019 These results indicate that downregulation of miR-183 can inhibit the growth of PC cells in vitro and in vivo, and increase cell sensitivity to 5-fluorouracil and gemcitabine through regulating the PTEN/PI3K/Akt signaling pathway. Fluorouracil 144-158 microRNA 183 Homo sapiens 46-53 30899445-5 2019 Moreover, in vitro studies indicate that phospho-ERKs interfere with 5-fluorouracil-based chemotherapy. Fluorouracil 69-83 mitogen-activated protein kinase 3 Homo sapiens 49-53 30810625-10 2019 In addition, 5-FU injection caused pronounced tissue injury accompanied by increased neutrophil accumulation, tumor necrosis factor-alpha (TNF-alpha), and interleukin-1 beta (IL-1beta) tissue levels, and positive immunostaining for TNF-alpha, IL-1beta, and inducible nitric oxide synthase (iNOS). Fluorouracil 13-17 tumor necrosis factor Homo sapiens 110-137 30810625-10 2019 In addition, 5-FU injection caused pronounced tissue injury accompanied by increased neutrophil accumulation, tumor necrosis factor-alpha (TNF-alpha), and interleukin-1 beta (IL-1beta) tissue levels, and positive immunostaining for TNF-alpha, IL-1beta, and inducible nitric oxide synthase (iNOS). Fluorouracil 13-17 tumor necrosis factor Homo sapiens 139-148 30810625-10 2019 In addition, 5-FU injection caused pronounced tissue injury accompanied by increased neutrophil accumulation, tumor necrosis factor-alpha (TNF-alpha), and interleukin-1 beta (IL-1beta) tissue levels, and positive immunostaining for TNF-alpha, IL-1beta, and inducible nitric oxide synthase (iNOS). Fluorouracil 13-17 interleukin 1 beta Homo sapiens 155-173 30810625-10 2019 In addition, 5-FU injection caused pronounced tissue injury accompanied by increased neutrophil accumulation, tumor necrosis factor-alpha (TNF-alpha), and interleukin-1 beta (IL-1beta) tissue levels, and positive immunostaining for TNF-alpha, IL-1beta, and inducible nitric oxide synthase (iNOS). Fluorouracil 13-17 tumor necrosis factor Homo sapiens 232-241 30810625-10 2019 In addition, 5-FU injection caused pronounced tissue injury accompanied by increased neutrophil accumulation, tumor necrosis factor-alpha (TNF-alpha), and interleukin-1 beta (IL-1beta) tissue levels, and positive immunostaining for TNF-alpha, IL-1beta, and inducible nitric oxide synthase (iNOS). Fluorouracil 13-17 interleukin 1 beta Homo sapiens 243-251 30810625-10 2019 In addition, 5-FU injection caused pronounced tissue injury accompanied by increased neutrophil accumulation, tumor necrosis factor-alpha (TNF-alpha), and interleukin-1 beta (IL-1beta) tissue levels, and positive immunostaining for TNF-alpha, IL-1beta, and inducible nitric oxide synthase (iNOS). Fluorouracil 13-17 nitric oxide synthase 2 Homo sapiens 257-288 30810625-10 2019 In addition, 5-FU injection caused pronounced tissue injury accompanied by increased neutrophil accumulation, tumor necrosis factor-alpha (TNF-alpha), and interleukin-1 beta (IL-1beta) tissue levels, and positive immunostaining for TNF-alpha, IL-1beta, and inducible nitric oxide synthase (iNOS). Fluorouracil 13-17 nitric oxide synthase 2 Homo sapiens 290-294 30579838-0 2019 Schedule-dependent synergistic effects of 5-fluorouracil and selumetinib in KRAS or BRAF mutant colon cancer models. Fluorouracil 42-56 B-Raf proto-oncogene, serine/threonine kinase Homo sapiens 84-88 30728402-5 2019 ChIP and global ChIP-seq data also confirms that FOXM1 can also potentially regulate other 5-FU targets, such as TYMS, thymidine kinase 1 (TK-1) and thymidine phosphorylase (TYMP). Fluorouracil 91-95 thymidine kinase 1 Homo sapiens 119-137 30728402-5 2019 ChIP and global ChIP-seq data also confirms that FOXM1 can also potentially regulate other 5-FU targets, such as TYMS, thymidine kinase 1 (TK-1) and thymidine phosphorylase (TYMP). Fluorouracil 91-95 thymidine kinase 1 Homo sapiens 139-143 30770552-5 2019 After combination treatment of 5-FU and LEP-2a, Ras/Raf/MEK/ERK and PI3K/AKT/mTOR pathway were inactivated. Fluorouracil 31-35 mitogen-activated protein kinase kinase 7 Homo sapiens 56-59 30770552-5 2019 After combination treatment of 5-FU and LEP-2a, Ras/Raf/MEK/ERK and PI3K/AKT/mTOR pathway were inactivated. Fluorouracil 31-35 mitogen-activated protein kinase 1 Homo sapiens 60-63 30770552-5 2019 After combination treatment of 5-FU and LEP-2a, Ras/Raf/MEK/ERK and PI3K/AKT/mTOR pathway were inactivated. Fluorouracil 31-35 AKT serine/threonine kinase 1 Homo sapiens 73-76 30770552-5 2019 After combination treatment of 5-FU and LEP-2a, Ras/Raf/MEK/ERK and PI3K/AKT/mTOR pathway were inactivated. Fluorouracil 31-35 mechanistic target of rapamycin kinase Homo sapiens 77-81 30770552-7 2019 Furthermore, 5-FU combined with LEP-2a also resulted in p53 activation and NF-kappaB inhibition, and cell cycle arrest in the S phase as well as cell metastasis stagnation. Fluorouracil 13-17 tumor protein p53 Homo sapiens 56-59 30579838-7 2019 Induction of thymidine kinase 1, a rate-limiting enzyme in salvage pathway, by 5-FU was abrogated by subsequent treatment with selumetinib, and ERK reactivation after selumetinib was prohibited by pretreatment with 5-FU. Fluorouracil 79-83 thymidine kinase 1 Homo sapiens 13-31 30579838-7 2019 Induction of thymidine kinase 1, a rate-limiting enzyme in salvage pathway, by 5-FU was abrogated by subsequent treatment with selumetinib, and ERK reactivation after selumetinib was prohibited by pretreatment with 5-FU. Fluorouracil 215-219 thymidine kinase 1 Homo sapiens 13-31 30579838-7 2019 Induction of thymidine kinase 1, a rate-limiting enzyme in salvage pathway, by 5-FU was abrogated by subsequent treatment with selumetinib, and ERK reactivation after selumetinib was prohibited by pretreatment with 5-FU. Fluorouracil 215-219 mitogen-activated protein kinase 1 Homo sapiens 144-147 30579838-12 2019 Our results suggest that sequential administration of 5-FU plus selumetinib would be a promising strategy for patients having KRAS or BRAF mutant colon cancers. Fluorouracil 54-58 B-Raf proto-oncogene, serine/threonine kinase Homo sapiens 134-138 30488540-5 2019 In the present study, MDM4/MDM2 double knockdown with the siRNAs enhanced 5-fluorouracil (5-FU)-induced p53 activation, arrested the cell cycle at G1 phase, and potentiated the antitumor effect of 5-FU in wtTP53/highMDM4 human colon (HCT116 and LoVo) and gastric (SNU-1 and NUGC-4) cancer cells. Fluorouracil 74-88 tumor protein p53 Homo sapiens 104-107 30488540-5 2019 In the present study, MDM4/MDM2 double knockdown with the siRNAs enhanced 5-fluorouracil (5-FU)-induced p53 activation, arrested the cell cycle at G1 phase, and potentiated the antitumor effect of 5-FU in wtTP53/highMDM4 human colon (HCT116 and LoVo) and gastric (SNU-1 and NUGC-4) cancer cells. Fluorouracil 90-94 tumor protein p53 Homo sapiens 104-107 30488540-6 2019 Exposure to 5-FU alone induced MDM2 as well as p21 and PUMA by p53 activation. Fluorouracil 12-16 tumor protein p53 Homo sapiens 63-66 30488540-7 2019 As p53-MDM2 forms a negative feedback loop, enhancement of the antitumor effect of 5-FU by MDM4/MDM2 double knockdown could be attributed to blocking of the feedback mechanism in addition to direct suppression of these p53 antagonists. Fluorouracil 83-87 tumor protein p53 Homo sapiens 3-6 30488540-7 2019 As p53-MDM2 forms a negative feedback loop, enhancement of the antitumor effect of 5-FU by MDM4/MDM2 double knockdown could be attributed to blocking of the feedback mechanism in addition to direct suppression of these p53 antagonists. Fluorouracil 83-87 tumor protein p53 Homo sapiens 219-222 30666155-0 2019 ATR activated by EB virus facilitates chemotherapy resistance to cisplatin or 5-fluorouracil in human nasopharyngeal carcinoma. Fluorouracil 78-92 ATR serine/threonine kinase Homo sapiens 0-3 29948597-0 2019 Patrinia scabiosaefolia Inhibits Growth of 5-FU-Resistant Colorectal Carcinoma Cells via Induction of Apoptosis and Suppression of AKT Pathway. Fluorouracil 43-47 AKT serine/threonine kinase 1 Homo sapiens 131-134 30535504-0 2019 MEK inhibitor enhanced the antitumor effect of oxaliplatin and 5-fluorouracil in MEK1 Q56P-mutant colorectal cancer cells. Fluorouracil 63-77 mitogen-activated protein kinase kinase 7 Homo sapiens 0-3 30535504-5 2019 The results suggested that MEK inhibitors in combination with oxaliplatin/5-FU may offer an improved therapeutic effect in patients with MEK-mutant CRC. Fluorouracil 74-78 mitogen-activated protein kinase kinase 7 Homo sapiens 137-140 30640943-0 2019 Chemotherapeutic agent 5-fluorouracil increases survival of SOD1 mouse model of ALS. Fluorouracil 23-37 superoxide dismutase 1, soluble Mus musculus 60-64 30640943-3 2019 In the search for drug candidates for ALS, we studied the effect of known stem cell mobilizing agents (treatment) and antimetabolite 5-fluorouracil (5-FU) (anti-treatment) in SOD1G93A model of ALS. Fluorouracil 149-153 superoxide dismutase 1, soluble Mus musculus 175-179 30607648-0 2019 The pro-survival function of DLEC1 and its protection of cancer cells against 5-FU-induced apoptosis through up-regulation of BCL-XL. Fluorouracil 78-82 DLEC1 cilia and flagella associated protein Homo sapiens 29-34 30607648-0 2019 The pro-survival function of DLEC1 and its protection of cancer cells against 5-FU-induced apoptosis through up-regulation of BCL-XL. Fluorouracil 78-82 BCL2 like 1 Homo sapiens 126-132 30607648-4 2019 DLEC1 overexpression promoted cell survival and reduced cell death in cancer cells after 5-FU treatment, while DLEC1 down-regulation sensitized cancer cells to 5-FU. Fluorouracil 89-93 DLEC1 cilia and flagella associated protein Homo sapiens 0-5 30607648-6 2019 Our data also showed that BCL-XL was up-regulated by DLEC1 in stable clones after 5-FU treatment. Fluorouracil 82-86 BCL2 like 1 Homo sapiens 26-32 30607648-6 2019 Our data also showed that BCL-XL was up-regulated by DLEC1 in stable clones after 5-FU treatment. Fluorouracil 82-86 DLEC1 cilia and flagella associated protein Homo sapiens 53-58 30607648-7 2019 Altogether, these results indicated that DLEC1 protects cells against cell death induced by 5-FU through the attenuation of active proteins in caspase cascade and the up-regulation of BCL-XL. Fluorouracil 92-96 DLEC1 cilia and flagella associated protein Homo sapiens 41-46 30607648-7 2019 Altogether, these results indicated that DLEC1 protects cells against cell death induced by 5-FU through the attenuation of active proteins in caspase cascade and the up-regulation of BCL-XL. Fluorouracil 92-96 BCL2 like 1 Homo sapiens 184-190 30607648-8 2019 Therefore, DLEC1 can be a pro-survival protein under certain circumstances and a potential therapeutic target for increasing sensitivity of cancer cells to 5-FU. Fluorouracil 156-160 DLEC1 cilia and flagella associated protein Homo sapiens 11-16 30207796-0 2019 Serotonin 3 receptor signaling regulates 5-fluorouracil-mediated apoptosis indirectly via TNF-alpha production by enhancing serotonin release from enterochromaffin cells. Fluorouracil 41-55 tumor necrosis factor Mus musculus 90-99 30679569-0 2019 5-Fluorouracil Induces Enteric Neuron Death and Glial Activation During Intestinal Mucositis via a S100B-RAGE-NFkappaB-Dependent Pathway. Fluorouracil 0-14 S100 calcium binding protein B Homo sapiens 99-104 30679569-0 2019 5-Fluorouracil Induces Enteric Neuron Death and Glial Activation During Intestinal Mucositis via a S100B-RAGE-NFkappaB-Dependent Pathway. Fluorouracil 0-14 nuclear factor kappa B subunit 1 Homo sapiens 110-118 30679569-2 2019 In this report, we used an animal model to investigate the participation of the S100B/RAGE/NFkappaB pathway in intestinal mucositis and enteric neurotoxicity caused by 5-FU (450 mg/kg, IP, single dose). Fluorouracil 168-172 S100 calcium binding protein B Homo sapiens 80-85 30679569-2 2019 In this report, we used an animal model to investigate the participation of the S100B/RAGE/NFkappaB pathway in intestinal mucositis and enteric neurotoxicity caused by 5-FU (450 mg/kg, IP, single dose). Fluorouracil 168-172 nuclear factor kappa B subunit 1 Homo sapiens 91-99 30679569-3 2019 5-FU induced intestinal damage observed by shortened villi, loss of crypt architecture and intense inflammatory cell infiltrate as well as increased GFAP and S100B co-expression and decreased HuC/D protein expression in the small intestine. Fluorouracil 0-4 S100 calcium binding protein B Homo sapiens 158-163 30679569-4 2019 Furthermore, 5-FU increased RAGE and NFkappaB NLS immunostaining in enteric neurons, associated with a significant increase in the nitrite/nitrate, IL-6 and TNF-alpha levels, iNOS expression and MDA accumulation in the small intestine. Fluorouracil 13-17 nuclear factor kappa B subunit 1 Homo sapiens 37-45 30679569-4 2019 Furthermore, 5-FU increased RAGE and NFkappaB NLS immunostaining in enteric neurons, associated with a significant increase in the nitrite/nitrate, IL-6 and TNF-alpha levels, iNOS expression and MDA accumulation in the small intestine. Fluorouracil 13-17 interleukin 6 Homo sapiens 148-152 30679569-4 2019 Furthermore, 5-FU increased RAGE and NFkappaB NLS immunostaining in enteric neurons, associated with a significant increase in the nitrite/nitrate, IL-6 and TNF-alpha levels, iNOS expression and MDA accumulation in the small intestine. Fluorouracil 13-17 tumor necrosis factor Homo sapiens 157-166 30679569-4 2019 Furthermore, 5-FU increased RAGE and NFkappaB NLS immunostaining in enteric neurons, associated with a significant increase in the nitrite/nitrate, IL-6 and TNF-alpha levels, iNOS expression and MDA accumulation in the small intestine. Fluorouracil 13-17 nitric oxide synthase 2 Homo sapiens 175-179 30679569-5 2019 We provide evidence that 5-FU induces reactive gliosis and reduction of enteric neurons in a S100B/RAGE/NFkappaB-dependent manner, since pentamidine, a S100B inhibitor, prevented 5-FU-induced neuronal loss, enteric glia activation, intestinal inflammation, oxidative stress and histological injury. Fluorouracil 25-29 S100 calcium binding protein B Homo sapiens 93-98 30679569-5 2019 We provide evidence that 5-FU induces reactive gliosis and reduction of enteric neurons in a S100B/RAGE/NFkappaB-dependent manner, since pentamidine, a S100B inhibitor, prevented 5-FU-induced neuronal loss, enteric glia activation, intestinal inflammation, oxidative stress and histological injury. Fluorouracil 25-29 nuclear factor kappa B subunit 1 Homo sapiens 104-112 30679569-5 2019 We provide evidence that 5-FU induces reactive gliosis and reduction of enteric neurons in a S100B/RAGE/NFkappaB-dependent manner, since pentamidine, a S100B inhibitor, prevented 5-FU-induced neuronal loss, enteric glia activation, intestinal inflammation, oxidative stress and histological injury. Fluorouracil 25-29 S100 calcium binding protein B Homo sapiens 152-157 30679569-5 2019 We provide evidence that 5-FU induces reactive gliosis and reduction of enteric neurons in a S100B/RAGE/NFkappaB-dependent manner, since pentamidine, a S100B inhibitor, prevented 5-FU-induced neuronal loss, enteric glia activation, intestinal inflammation, oxidative stress and histological injury. Fluorouracil 179-183 S100 calcium binding protein B Homo sapiens 93-98 30679569-5 2019 We provide evidence that 5-FU induces reactive gliosis and reduction of enteric neurons in a S100B/RAGE/NFkappaB-dependent manner, since pentamidine, a S100B inhibitor, prevented 5-FU-induced neuronal loss, enteric glia activation, intestinal inflammation, oxidative stress and histological injury. Fluorouracil 179-183 nuclear factor kappa B subunit 1 Homo sapiens 104-112 30679569-5 2019 We provide evidence that 5-FU induces reactive gliosis and reduction of enteric neurons in a S100B/RAGE/NFkappaB-dependent manner, since pentamidine, a S100B inhibitor, prevented 5-FU-induced neuronal loss, enteric glia activation, intestinal inflammation, oxidative stress and histological injury. Fluorouracil 179-183 S100 calcium binding protein B Homo sapiens 152-157 30662270-0 2019 Complete response with fluorouracil and irinotecan with a BRAFV600E and EGFR inhibitor in BRAF-mutated metastatic colorectal cancer: a case report. Fluorouracil 23-35 epidermal growth factor receptor Homo sapiens 72-76 30662270-9 2019 Conclusion: The combination of fluorouracil and irinotecan with a BRAFV600E and EGFR inhibitor may have synergistic action, leading to recession of secondary metastases in patients with BRAFV600E-mutated colorectal cancer. Fluorouracil 31-43 epidermal growth factor receptor Homo sapiens 80-84 30723502-5 2019 The presence of R273H-P53 conferred the cancer cells with drug resistance not only against the widely used chemotherapeutic agents like cisplatin (CDDP) or 5-flurouracil (5-FU) but also against potent alternative modes of therapy like proteasomal inhibition. Fluorouracil 171-175 tumor protein p53 Homo sapiens 22-25 30666155-9 2019 Conclusion: Our data suggest that EBV activation of ATR-mediated DNA damage response might result in chemotherapy resistance to CDDP and 5-FU in NPC. Fluorouracil 137-141 ATR serine/threonine kinase Homo sapiens 52-55 30465515-10 2019 Furthermore, scFv significantly enhanced 5-FU-induced cell death, from 23.0+-1.0% to 28.4+-1.2% in MKN45 and 28.2+-0.7% to 36.6+-0.6% in AGS cells. Fluorouracil 41-45 immunglobulin heavy chain variable region Homo sapiens 13-17 30124494-1 2019 BACKGROUND: Combination therapy with fluorouracil, platinum, and trastuzumab (Tmab) is the first-line treatment for human epidermal growth factor receptor 2 (HER2)-positive gastric cancer, and there is currently no established second-line therapy. Fluorouracil 37-49 erb-b2 receptor tyrosine kinase 2 Homo sapiens 122-156 30124494-1 2019 BACKGROUND: Combination therapy with fluorouracil, platinum, and trastuzumab (Tmab) is the first-line treatment for human epidermal growth factor receptor 2 (HER2)-positive gastric cancer, and there is currently no established second-line therapy. Fluorouracil 37-49 erb-b2 receptor tyrosine kinase 2 Homo sapiens 158-162 30465515-12 2019 CONCLUSION: The single-chain antibody (scFv-Reg4) significantly inhibited gastric cancer cell proliferation and synergistically enhanced the lethal effect of 5-FU. Fluorouracil 158-162 immunglobulin heavy chain variable region Homo sapiens 39-43 30473361-9 2019 Using the BiFC and FRET systems, we demonstrated that the prototypical Nrf2-activiting compound tBHQ and the antitumor drug F-dUrd might interfere with the intracellular interaction between Keap1 and Nrf2 whereas the 5-Fu have little role in activating the protective response of Nrf2 pathway in cancer cells. Fluorouracil 217-221 NFE2 like bZIP transcription factor 2 Homo sapiens 71-75 30591459-0 2019 Therapeutic Effect of GGsTop, Selective Gamma-glutamyl Transpeptidase Inhibitor, on a Mouse Model of 5-Fluorouracil-induced Oral Mucositis. Fluorouracil 101-115 gamma-glutamyltransferase 1 Mus musculus 40-69 31582661-1 2019 The aim of this study was to clarify the relationship between chemotherapy-induced mucositis and endogenous glucagon-like peptide-2 (GLP-2) dynamics in the small intestine following treatment with either methotrexate or 5-fluorouracil. Fluorouracil 220-234 mast cell protease 10 Rattus norvegicus 108-131 31582661-1 2019 The aim of this study was to clarify the relationship between chemotherapy-induced mucositis and endogenous glucagon-like peptide-2 (GLP-2) dynamics in the small intestine following treatment with either methotrexate or 5-fluorouracil. Fluorouracil 220-234 mast cell protease 10 Rattus norvegicus 133-138 31582661-7 2019 In contrast, 5-fluorouracil significantly inhibited proglucagon, GLP-2 receptor, IGF-1, and TGF-beta2 mRNA expression as well as the number of anti-GLP-2 antibody-positive cells. Fluorouracil 13-27 mast cell protease 10 Rattus norvegicus 65-70 30307354-2 2019 CASE PRESENTATION: Here we present a KRAS/NRAS/BRAF wild-type mCRC patient who has been previously treated with FOLFIRI (fluorouracil, leucovorin, and irinotecan), XELOX (capecitabine and oxaliplatin), cetuximab and bevacizumab, and then received the next generation sequencing (NGS) and whose metastatic subcutaneous nodule was resected to generate patient-derived xenograft (PDX) models. Fluorouracil 121-133 B-Raf proto-oncogene, serine/threonine kinase Homo sapiens 47-51 30788349-0 2019 Histone deacetylase 6 selective inhibitor ACY1215 inhibits cell proliferation and enhances the chemotherapeutic effect of 5-fluorouracil in HCT116 cells. Fluorouracil 122-136 histone deacetylase 6 Homo sapiens 0-21 30473361-9 2019 Using the BiFC and FRET systems, we demonstrated that the prototypical Nrf2-activiting compound tBHQ and the antitumor drug F-dUrd might interfere with the intracellular interaction between Keap1 and Nrf2 whereas the 5-Fu have little role in activating the protective response of Nrf2 pathway in cancer cells. Fluorouracil 217-221 kelch like ECH associated protein 1 Homo sapiens 190-195 30473361-9 2019 Using the BiFC and FRET systems, we demonstrated that the prototypical Nrf2-activiting compound tBHQ and the antitumor drug F-dUrd might interfere with the intracellular interaction between Keap1 and Nrf2 whereas the 5-Fu have little role in activating the protective response of Nrf2 pathway in cancer cells. Fluorouracil 217-221 NFE2 like bZIP transcription factor 2 Homo sapiens 200-204 30473361-9 2019 Using the BiFC and FRET systems, we demonstrated that the prototypical Nrf2-activiting compound tBHQ and the antitumor drug F-dUrd might interfere with the intracellular interaction between Keap1 and Nrf2 whereas the 5-Fu have little role in activating the protective response of Nrf2 pathway in cancer cells. Fluorouracil 217-221 NFE2 like bZIP transcription factor 2 Homo sapiens 200-204 30468567-6 2018 In vitro and in vivo studies on the nanofibrous memembrane-coating demonstrate improved antitumor effects for the CUR/5-FU dual drug system which can be attributed to cell cycle arrest in the S phase in association with induced apoptosis in tumor cells by blocking signal transducer and activator of transcription3 (Stat3) and nuclear factor kappa beta (NF-kB) signaling pathways, suggesting potential in the treatment of CRC in the future. Fluorouracil 118-122 signal transducer and activator of transcription 3 Homo sapiens 316-321 31298161-0 2019 Role of Nuclear Factor Erythroid 2-Related Factor 2 (NRF-2) Mediated Antioxidant Response on the Synergistic Antitumor Effect of L-Arginine and 5-Fluro Uracil (5FU) in Breast Adenocarcinoma. Fluorouracil 160-163 NFE2 like bZIP transcription factor 2 Homo sapiens 8-51 31298161-0 2019 Role of Nuclear Factor Erythroid 2-Related Factor 2 (NRF-2) Mediated Antioxidant Response on the Synergistic Antitumor Effect of L-Arginine and 5-Fluro Uracil (5FU) in Breast Adenocarcinoma. Fluorouracil 160-163 NFE2 like bZIP transcription factor 2 Homo sapiens 53-58 31298161-10 2019 The present review summarizes the role of NRF-2 mediated antioxidant response on the synergistic antitumor effect of L-Arginine and 5-FU in BAC. Fluorouracil 132-136 NFE2 like bZIP transcription factor 2 Homo sapiens 42-47 30342137-4 2019 Additionally, a strength effect was also observed in regulating immune function of GP11 and 5-Fu simultaneous administration, such as enhancing serum interleukin-2 (IL-2) and tumor necrosis factor-alpha (TNF-alpha) secretion, and increasing immune organs weights. Fluorouracil 92-96 tumor necrosis factor Mus musculus 175-202 30342137-4 2019 Additionally, a strength effect was also observed in regulating immune function of GP11 and 5-Fu simultaneous administration, such as enhancing serum interleukin-2 (IL-2) and tumor necrosis factor-alpha (TNF-alpha) secretion, and increasing immune organs weights. Fluorouracil 92-96 tumor necrosis factor Mus musculus 204-213 30588031-7 2019 Furthermore, knockdown of CDC7 sensitized ESCC cells to Cis and 5-FU. Fluorouracil 64-68 cell division cycle 7 Homo sapiens 26-30 30468567-6 2018 In vitro and in vivo studies on the nanofibrous memembrane-coating demonstrate improved antitumor effects for the CUR/5-FU dual drug system which can be attributed to cell cycle arrest in the S phase in association with induced apoptosis in tumor cells by blocking signal transducer and activator of transcription3 (Stat3) and nuclear factor kappa beta (NF-kB) signaling pathways, suggesting potential in the treatment of CRC in the future. Fluorouracil 118-122 signal transducer and activator of transcription 3 Homo sapiens 265-314 30320939-9 2019 Our results showed that NFIB promoted cell proliferation and increased 5-FU resistance by activating the Akt pathway. Fluorouracil 71-75 AKT serine/threonine kinase 1 Homo sapiens 105-108 31372308-13 2019 Gene expression of casp-3, casp-4, and casp-10 were significantly inhibited in the DCLK1+ cells after 5-Fu treatment compared to the WT cells (p=7.616e-08, 1.575e-05 and 5.307e-08, respectively). Fluorouracil 102-106 caspase 3 Homo sapiens 19-25 31372308-13 2019 Gene expression of casp-3, casp-4, and casp-10 were significantly inhibited in the DCLK1+ cells after 5-Fu treatment compared to the WT cells (p=7.616e-08, 1.575e-05 and 5.307e-08, respectively). Fluorouracil 102-106 caspase 4 Homo sapiens 27-33 31372308-14 2019 Cleaved casp-3 amount and casp-3 positive cells were significantly decreased in the DCLK1+ cells after 5-Fu treatment compared to the WT cells (p=0.015). Fluorouracil 103-107 caspase 3 Homo sapiens 8-14 31372308-14 2019 Cleaved casp-3 amount and casp-3 positive cells were significantly decreased in the DCLK1+ cells after 5-Fu treatment compared to the WT cells (p=0.015). Fluorouracil 103-107 caspase 3 Homo sapiens 26-32 31372308-15 2019 Conclusions: In conclusion, our results demonstrated that DCLK1 overexpression enhanced the chemoresistance of CRC cells to 5-Fu treatment by suppressing gene expression of key caspases in the apoptosis pathway and activation of the apoptosis pathway. Fluorouracil 124-128 caspase 4 Homo sapiens 177-185 30429233-7 2018 At the present study, we found overexpression of miR-141 could inhibit proliferation, migration, tumor-forming and invasive potential of CRC cells in vitro and mitogen-activated protein kinase kinase kinase kinase 4 (MAP4K4) was verified as a directed target of miR-141 The combination treatment of miR-141 with 5-FU, directly targetting MAP4K4, could better inhibit invasion and metastasis of CRC cells colony than either one alone. Fluorouracil 312-316 microRNA 141 Homo sapiens 49-56 30429233-7 2018 At the present study, we found overexpression of miR-141 could inhibit proliferation, migration, tumor-forming and invasive potential of CRC cells in vitro and mitogen-activated protein kinase kinase kinase kinase 4 (MAP4K4) was verified as a directed target of miR-141 The combination treatment of miR-141 with 5-FU, directly targetting MAP4K4, could better inhibit invasion and metastasis of CRC cells colony than either one alone. Fluorouracil 312-316 mitogen-activated protein kinase kinase kinase kinase 4 Homo sapiens 160-215 30429233-7 2018 At the present study, we found overexpression of miR-141 could inhibit proliferation, migration, tumor-forming and invasive potential of CRC cells in vitro and mitogen-activated protein kinase kinase kinase kinase 4 (MAP4K4) was verified as a directed target of miR-141 The combination treatment of miR-141 with 5-FU, directly targetting MAP4K4, could better inhibit invasion and metastasis of CRC cells colony than either one alone. Fluorouracil 312-316 mitogen-activated protein kinase kinase kinase kinase 4 Homo sapiens 217-223 30429233-8 2018 Furthermore, overexpression of miR-141, targetting MAP4K4, enhanced the effected of 5-FU and suppressed the malignant biological behaviors, in vivo Our findings showed that 5-FU inhibited malignant behavior of human CRC cells in vitro and in vivo by enhancing the efficiency of miR-141 Our data suggested that targetting the miR-141/MAP4K4 signaling pathway could be a potential molecular target that may enhance chemotherapeutic efficacy in the treatment of CRC. Fluorouracil 84-88 microRNA 141 Homo sapiens 31-38 30429233-8 2018 Furthermore, overexpression of miR-141, targetting MAP4K4, enhanced the effected of 5-FU and suppressed the malignant biological behaviors, in vivo Our findings showed that 5-FU inhibited malignant behavior of human CRC cells in vitro and in vivo by enhancing the efficiency of miR-141 Our data suggested that targetting the miR-141/MAP4K4 signaling pathway could be a potential molecular target that may enhance chemotherapeutic efficacy in the treatment of CRC. Fluorouracil 84-88 mitogen-activated protein kinase kinase kinase kinase 4 Homo sapiens 51-57 30429233-8 2018 Furthermore, overexpression of miR-141, targetting MAP4K4, enhanced the effected of 5-FU and suppressed the malignant biological behaviors, in vivo Our findings showed that 5-FU inhibited malignant behavior of human CRC cells in vitro and in vivo by enhancing the efficiency of miR-141 Our data suggested that targetting the miR-141/MAP4K4 signaling pathway could be a potential molecular target that may enhance chemotherapeutic efficacy in the treatment of CRC. Fluorouracil 173-177 microRNA 141 Homo sapiens 31-38 30429233-8 2018 Furthermore, overexpression of miR-141, targetting MAP4K4, enhanced the effected of 5-FU and suppressed the malignant biological behaviors, in vivo Our findings showed that 5-FU inhibited malignant behavior of human CRC cells in vitro and in vivo by enhancing the efficiency of miR-141 Our data suggested that targetting the miR-141/MAP4K4 signaling pathway could be a potential molecular target that may enhance chemotherapeutic efficacy in the treatment of CRC. Fluorouracil 173-177 mitogen-activated protein kinase kinase kinase kinase 4 Homo sapiens 51-57 30429233-8 2018 Furthermore, overexpression of miR-141, targetting MAP4K4, enhanced the effected of 5-FU and suppressed the malignant biological behaviors, in vivo Our findings showed that 5-FU inhibited malignant behavior of human CRC cells in vitro and in vivo by enhancing the efficiency of miR-141 Our data suggested that targetting the miR-141/MAP4K4 signaling pathway could be a potential molecular target that may enhance chemotherapeutic efficacy in the treatment of CRC. Fluorouracil 173-177 microRNA 141 Homo sapiens 278-285 30429233-8 2018 Furthermore, overexpression of miR-141, targetting MAP4K4, enhanced the effected of 5-FU and suppressed the malignant biological behaviors, in vivo Our findings showed that 5-FU inhibited malignant behavior of human CRC cells in vitro and in vivo by enhancing the efficiency of miR-141 Our data suggested that targetting the miR-141/MAP4K4 signaling pathway could be a potential molecular target that may enhance chemotherapeutic efficacy in the treatment of CRC. Fluorouracil 173-177 microRNA 141 Homo sapiens 278-285 30429233-8 2018 Furthermore, overexpression of miR-141, targetting MAP4K4, enhanced the effected of 5-FU and suppressed the malignant biological behaviors, in vivo Our findings showed that 5-FU inhibited malignant behavior of human CRC cells in vitro and in vivo by enhancing the efficiency of miR-141 Our data suggested that targetting the miR-141/MAP4K4 signaling pathway could be a potential molecular target that may enhance chemotherapeutic efficacy in the treatment of CRC. Fluorouracil 173-177 mitogen-activated protein kinase kinase kinase kinase 4 Homo sapiens 333-339 30662725-2 2018 Herein, we developed 5-fluorouracil (5-FU)-loaded amino-functionalized mesoporous silica nanoparticle (MSN-NH2)-based galactosylated chitosans (GCs), which are galactose receptor-mediated materials for colon-specific drug delivery systems. Fluorouracil 21-35 moesin Homo sapiens 103-106 30662725-2 2018 Herein, we developed 5-fluorouracil (5-FU)-loaded amino-functionalized mesoporous silica nanoparticle (MSN-NH2)-based galactosylated chitosans (GCs), which are galactose receptor-mediated materials for colon-specific drug delivery systems. Fluorouracil 37-41 moesin Homo sapiens 103-106 30662725-5 2018 5-FU@MSN-NH2/GC showed high loading capacity and possessed much higher cytotoxicity on human colon cancer cells (SW620 cells) than 5-FU@MSN-NH2 and free 5-FU. Fluorouracil 0-4 moesin Homo sapiens 5-8 30662725-7 2018 Subsequently, 5-FU@MSN-NH2/GC anti-cancer activity on SW620 cells in vitro was confirmed by cell apoptosis. Fluorouracil 14-18 moesin Homo sapiens 19-22 30662808-0 2018 MiR-26b regulates 5-FU-resistance in human colorectal cancer via down-regulation of Pgp. Fluorouracil 18-22 ATP binding cassette subfamily B member 1 Homo sapiens 84-87 31949673-0 2018 Knockdown of PHGDH potentiates 5-FU cytotoxicity in gastric cancer cells via the Bcl-2/Bax/caspase-3 signaling pathway. Fluorouracil 31-35 BCL2 apoptosis regulator Homo sapiens 81-86 30205014-0 2018 Vitamin D potentiates anti-tumor activity of 5-fluorouracil via modulating caspase-3 and TGF-beta1 expression in hepatocellular carcinoma-induced in rats. Fluorouracil 45-59 transforming growth factor, beta 1 Rattus norvegicus 89-98 30205014-6 2018 Treatment with 5-FU + Vit D significantly decreased gene expression of nuclear factor erythroid 2-related factor 2 (NrF2) and transforming growth factor beta1 (TGF-beta1) at both the gene and protein level and serum AFP concentrations in comparison with their corresponding monotherapy. Fluorouracil 15-19 NFE2 like bZIP transcription factor 2 Rattus norvegicus 71-114 30205014-6 2018 Treatment with 5-FU + Vit D significantly decreased gene expression of nuclear factor erythroid 2-related factor 2 (NrF2) and transforming growth factor beta1 (TGF-beta1) at both the gene and protein level and serum AFP concentrations in comparison with their corresponding monotherapy. Fluorouracil 15-19 NFE2 like bZIP transcription factor 2 Rattus norvegicus 116-120 30205014-6 2018 Treatment with 5-FU + Vit D significantly decreased gene expression of nuclear factor erythroid 2-related factor 2 (NrF2) and transforming growth factor beta1 (TGF-beta1) at both the gene and protein level and serum AFP concentrations in comparison with their corresponding monotherapy. Fluorouracil 15-19 transforming growth factor, beta 1 Rattus norvegicus 126-158 30205014-6 2018 Treatment with 5-FU + Vit D significantly decreased gene expression of nuclear factor erythroid 2-related factor 2 (NrF2) and transforming growth factor beta1 (TGF-beta1) at both the gene and protein level and serum AFP concentrations in comparison with their corresponding monotherapy. Fluorouracil 15-19 transforming growth factor, beta 1 Rattus norvegicus 160-169 31949649-13 2018 Additionally, cell invasion was promoted by miR-106a-5p overexpression in the HT-29 cells and was inhibited by miR-106a-5p knockdown in the 5-FU resistant HT-29 cells; miR-106a-5p overexpression contributed to migration by increasing vimentin expression and by decreasing E-cadherin expression in the HT-29 cells; miR-106a-5p functioned by directly binding to TGFbetaR2. Fluorouracil 140-144 cadherin 1 Homo sapiens 272-282 31949673-0 2018 Knockdown of PHGDH potentiates 5-FU cytotoxicity in gastric cancer cells via the Bcl-2/Bax/caspase-3 signaling pathway. Fluorouracil 31-35 BCL2 associated X, apoptosis regulator Homo sapiens 87-90 31949673-0 2018 Knockdown of PHGDH potentiates 5-FU cytotoxicity in gastric cancer cells via the Bcl-2/Bax/caspase-3 signaling pathway. Fluorouracil 31-35 caspase 3 Homo sapiens 91-100 31949673-12 2018 Additionally, 5-FU treatment downregulated Bcl-2 expression and upregulated the expression of Bax and caspase-3, and this effect was remarkably enhanced by PHGDH knockdown. Fluorouracil 14-18 BCL2 apoptosis regulator Homo sapiens 43-48 31949673-12 2018 Additionally, 5-FU treatment downregulated Bcl-2 expression and upregulated the expression of Bax and caspase-3, and this effect was remarkably enhanced by PHGDH knockdown. Fluorouracil 14-18 BCL2 associated X, apoptosis regulator Homo sapiens 94-97 31949673-12 2018 Additionally, 5-FU treatment downregulated Bcl-2 expression and upregulated the expression of Bax and caspase-3, and this effect was remarkably enhanced by PHGDH knockdown. Fluorouracil 14-18 caspase 3 Homo sapiens 102-111 31949673-13 2018 In conclusion, knockdown of PHGDH potentiates 5-FU cytotoxicity in GC cells via the Bcl-2/Bax/caspase-3 signaling pathway. Fluorouracil 46-50 BCL2 apoptosis regulator Homo sapiens 84-89 31949673-13 2018 In conclusion, knockdown of PHGDH potentiates 5-FU cytotoxicity in GC cells via the Bcl-2/Bax/caspase-3 signaling pathway. Fluorouracil 46-50 BCL2 associated X, apoptosis regulator Homo sapiens 90-93 31949673-13 2018 In conclusion, knockdown of PHGDH potentiates 5-FU cytotoxicity in GC cells via the Bcl-2/Bax/caspase-3 signaling pathway. Fluorouracil 46-50 caspase 3 Homo sapiens 94-103 30539860-9 2018 Moreover, 3-MA inhibited while rapamycin facilitated 5-FU-induced p53 protein expression. Fluorouracil 53-57 tumor protein p53 Homo sapiens 66-69 29902094-0 2018 Suppression of NRF2/ARE by convallatoxin sensitises A549 cells to 5-FU-mediated apoptosis. Fluorouracil 66-70 NFE2 like bZIP transcription factor 2 Homo sapiens 15-19 30539860-11 2018 Especially, Beclin1 overexpression increased while Beclin1 knockdown decreased 5-FU-induced p53 expression. Fluorouracil 79-83 tumor protein p53 Homo sapiens 92-95 30142492-7 2018 Electrochemical measurements using differential pulse voltammetry showed a wide linear relationship between 5-FU concentration and peak height within the range 1.0-300.0 muM with a low detection limit (0.06 muM). Fluorouracil 108-112 latexin Homo sapiens 170-173 29761248-3 2018 The expression of BGN was bilaterally modulated in colon cancer cell lines HT-29 and SW-480 and the effect of treatments on the cell proliferation and resistance to 5-FU was assessed. Fluorouracil 165-169 biglycan Homo sapiens 18-21 29761248-6 2018 BGN knockdown increased HT-29 cells" sensitivity to 5-FU, represented by the lower colony number and higher apoptotic rate. Fluorouracil 52-56 biglycan Homo sapiens 0-3 29761248-7 2018 To the contrary, BGN overexpression promoted the resistance of SW-480 cells to 5-FU. Fluorouracil 79-83 biglycan Homo sapiens 17-20 30399198-2 2018 The aim of this study is to determine the interaction between BRAF mutation and microsatellite instability (MSI) status in determining survival benefit after adjuvant 5-FU based chemotherapy in stage III colon cancer. Fluorouracil 167-171 B-Raf proto-oncogene, serine/threonine kinase Homo sapiens 62-66 30565175-0 2018 Synergistic delivery of 5-fluorouracil and curcumin using human serum albumin-coated iron oxide nanoparticles by folic acid targeting. Fluorouracil 24-38 albumin Homo sapiens 70-77 30142492-7 2018 Electrochemical measurements using differential pulse voltammetry showed a wide linear relationship between 5-FU concentration and peak height within the range 1.0-300.0 muM with a low detection limit (0.06 muM). Fluorouracil 108-112 latexin Homo sapiens 207-210 30627095-9 2018 The success in these present cases indicates that FTD/TPI+Bmab as a second- or third-line treatment is a therapeutic option for elderly patients with mCRC who are not eligible for intensive chemotherapy, even after failure of treatment with 5-FU. Fluorouracil 241-245 triosephosphate isomerase 1 Homo sapiens 54-57 30486276-7 2018 Cell experiments showed that in SW620 cells with the galectin receptor, the LV@MSN-COOH/GC metabolized into methyl tetrahydrofolic acid (MTHF) and 5-fluorouracil (5-FU)@MSN-NH2/GC metabolized into FdUMP in vivo. Fluorouracil 147-161 moesin Homo sapiens 79-82 30486276-7 2018 Cell experiments showed that in SW620 cells with the galectin receptor, the LV@MSN-COOH/GC metabolized into methyl tetrahydrofolic acid (MTHF) and 5-fluorouracil (5-FU)@MSN-NH2/GC metabolized into FdUMP in vivo. Fluorouracil 147-161 moesin Homo sapiens 169-172 30486276-7 2018 Cell experiments showed that in SW620 cells with the galectin receptor, the LV@MSN-COOH/GC metabolized into methyl tetrahydrofolic acid (MTHF) and 5-fluorouracil (5-FU)@MSN-NH2/GC metabolized into FdUMP in vivo. Fluorouracil 163-167 moesin Homo sapiens 79-82 30486276-7 2018 Cell experiments showed that in SW620 cells with the galectin receptor, the LV@MSN-COOH/GC metabolized into methyl tetrahydrofolic acid (MTHF) and 5-fluorouracil (5-FU)@MSN-NH2/GC metabolized into FdUMP in vivo. Fluorouracil 163-167 moesin Homo sapiens 169-172 30464532-0 2018 EZH2 contributes to 5-FU resistance in gastric cancer by epigenetically suppressing FBXO32 expression. Fluorouracil 20-24 enhancer of zeste 2 polycomb repressive complex 2 subunit Homo sapiens 0-4 30451890-7 2018 Further, corresponding to CD44v6 knockdown cells, 5FU+ Silibinin treatment significantly decreased CD44v6, Nanog, CTNNB1 and CDKN2A expression whereas increased E-cadherin expression in HCT116 derived CD44+ cells. Fluorouracil 50-53 cyclin dependent kinase inhibitor 2A Homo sapiens 125-131 30451890-7 2018 Further, corresponding to CD44v6 knockdown cells, 5FU+ Silibinin treatment significantly decreased CD44v6, Nanog, CTNNB1 and CDKN2A expression whereas increased E-cadherin expression in HCT116 derived CD44+ cells. Fluorouracil 50-53 cadherin 1 Homo sapiens 161-171 30446678-0 2018 Verbascoside: Identification, Quantification, and Potential Sensitization of Colorectal Cancer Cells to 5-FU by Targeting PI3K/AKT Pathway. Fluorouracil 104-108 AKT serine/threonine kinase 1 Homo sapiens 127-130 30446678-10 2018 Additionally, 5-FU combined to VER was capable of significantly reducing PI3K and p-AKT/total AKT ratio. Fluorouracil 14-18 AKT serine/threonine kinase 1 Homo sapiens 84-87 30446678-10 2018 Additionally, 5-FU combined to VER was capable of significantly reducing PI3K and p-AKT/total AKT ratio. Fluorouracil 14-18 AKT serine/threonine kinase 1 Homo sapiens 94-97 30473630-17 2018 The RelB-silencing enhanced cytotoxic effect of 5-FU and induced cell accumulation in S-phase. Fluorouracil 48-52 RELB proto-oncogene, NF-kB subunit Homo sapiens 4-8 30473630-21 2018 Conclusion: Our studies here provided evidence that RelB plays an oncogenic role and conveys chemo-resistance to 5-FU. Fluorouracil 113-117 RELB proto-oncogene, NF-kB subunit Homo sapiens 52-56 30464532-3 2018 Materials and methods: In the present study, we investigated the functional role of EZH2 in 5-fluorouracil (5-FU) resistance of GC cells and discovered the underlying molecular mechanism. Fluorouracil 92-106 enhancer of zeste 2 polycomb repressive complex 2 subunit Homo sapiens 84-88 30464532-3 2018 Materials and methods: In the present study, we investigated the functional role of EZH2 in 5-fluorouracil (5-FU) resistance of GC cells and discovered the underlying molecular mechanism. Fluorouracil 108-112 enhancer of zeste 2 polycomb repressive complex 2 subunit Homo sapiens 84-88 30464532-4 2018 Results: Results revealed that EZH2 was upregulated in 5-FU-resistant GC tissues and cell lines. Fluorouracil 55-59 enhancer of zeste 2 polycomb repressive complex 2 subunit Homo sapiens 31-35 30464532-6 2018 EZH2 knockdown enhanced 5-FU sensitivity of AGS/5-FU and SGC-7901/5-FU cells. Fluorouracil 24-28 enhancer of zeste 2 polycomb repressive complex 2 subunit Homo sapiens 0-4 30464532-8 2018 FBXO32 overexpression could mimic the functional role of downregulated EZH2 in 5-FU resistance. Fluorouracil 79-83 enhancer of zeste 2 polycomb repressive complex 2 subunit Homo sapiens 71-75 30464532-9 2018 FBXO32 knockdown counteracted the inductive effect of EZH2 inhibition on 5-FU sensitivity of AGS/5-FU and SGC-7901/5-FU cells. Fluorouracil 73-77 enhancer of zeste 2 polycomb repressive complex 2 subunit Homo sapiens 54-58 30464532-9 2018 FBXO32 knockdown counteracted the inductive effect of EZH2 inhibition on 5-FU sensitivity of AGS/5-FU and SGC-7901/5-FU cells. Fluorouracil 97-101 enhancer of zeste 2 polycomb repressive complex 2 subunit Homo sapiens 54-58 30464532-10 2018 Furthermore, EZH2 knockdown facilitated 5-FU sensitivity of 5-FU-resistant GC cells in vivo. Fluorouracil 40-44 enhancer of zeste 2 polycomb repressive complex 2 subunit Homo sapiens 13-17 30464532-10 2018 Furthermore, EZH2 knockdown facilitated 5-FU sensitivity of 5-FU-resistant GC cells in vivo. Fluorouracil 60-64 enhancer of zeste 2 polycomb repressive complex 2 subunit Homo sapiens 13-17 30464532-11 2018 Conclusion: In summary, EZH2 depletion overcame 5-FU resistance in GC by epigenetically silencing FBXO32, providing a novel therapeutic target for GC chemoresistance. Fluorouracil 48-52 enhancer of zeste 2 polycomb repressive complex 2 subunit Homo sapiens 24-28 30011079-8 2018 Moreover, 5-FU-upregulated ERCC1 expression was regulated by extracellular signal-regulated kinase (ERK) 1/2 and p38 signaling through activating the transcription factor c-jun/activator protein (AP)-1. Fluorouracil 10-14 mitogen-activated protein kinase 3 Homo sapiens 61-108 30011079-8 2018 Moreover, 5-FU-upregulated ERCC1 expression was regulated by extracellular signal-regulated kinase (ERK) 1/2 and p38 signaling through activating the transcription factor c-jun/activator protein (AP)-1. Fluorouracil 10-14 mitogen-activated protein kinase 1 Homo sapiens 113-116 30055226-2 2018 We developed a dual-functionalized liposomal delivery system, conjugating cell penetrating peptide penetratin to transferrin-liposomes (Tf-Pen-conjugated liposomes) to enhance the transport of an anticancer chemotherapeutic drug, 5-fluorouracil (5-FU), across the blood-brain barrier into the tumor cells. Fluorouracil 230-244 proprotein convertase subtilisin/kexin type 1 inhibitor Mus musculus 139-142 30055226-2 2018 We developed a dual-functionalized liposomal delivery system, conjugating cell penetrating peptide penetratin to transferrin-liposomes (Tf-Pen-conjugated liposomes) to enhance the transport of an anticancer chemotherapeutic drug, 5-fluorouracil (5-FU), across the blood-brain barrier into the tumor cells. Fluorouracil 246-250 proprotein convertase subtilisin/kexin type 1 inhibitor Mus musculus 139-142 30333474-6 2018 The patient was started on a chemotherapy regimen of docetaxel, cisplatin, and 5-fluorouracil (TCF). Fluorouracil 79-93 hepatocyte nuclear factor 4 alpha Homo sapiens 95-98 30374014-10 2018 Transfection of wild-type p53 plasmid or treatments with cytotoxic reagents including irradiation and 5-FU all induced miR-492 overexpression. Fluorouracil 102-106 tumor protein p53 Homo sapiens 26-29 29737515-8 2018 Our data showed that phytosomal curcumin and its combination with 5-FU inhibited cell growth and invasive behavior of CRC cells through modulation of Wnt-pathway and E-cadherin. Fluorouracil 66-70 cadherin 1 Mus musculus 166-176 30328537-11 2018 Western blot analysis clearly showed that 5-FU and LY individually increased the expression of caspase-3 and PARP, while as expected FLNP induced a remarkable expression of these protein markers indicating the superior anticancer effect. Fluorouracil 42-46 caspase 3 Homo sapiens 95-104 30328537-11 2018 Western blot analysis clearly showed that 5-FU and LY individually increased the expression of caspase-3 and PARP, while as expected FLNP induced a remarkable expression of these protein markers indicating the superior anticancer effect. Fluorouracil 42-46 poly(ADP-ribose) polymerase 1 Homo sapiens 109-113 30151975-0 2018 Bevacizumab-enhanced antitumor effect of 5-fluorouracil via upregulation of thymidine phosphorylase through vascular endothelial growth factor A/vascular endothelial growth factor receptor 2-specificity protein 1 pathway. Fluorouracil 41-55 vascular endothelial growth factor A Homo sapiens 108-144 30151975-0 2018 Bevacizumab-enhanced antitumor effect of 5-fluorouracil via upregulation of thymidine phosphorylase through vascular endothelial growth factor A/vascular endothelial growth factor receptor 2-specificity protein 1 pathway. Fluorouracil 41-55 Sp1 transcription factor Homo sapiens 191-212 30379218-10 2018 TNF-a expression was lower in 5-FU/SIMV group (172.6+-18pg/ml) than in 5-FU/SAL (347.5+-63pg/ml). Fluorouracil 30-34 tumor necrosis factor Rattus norvegicus 0-5 30379218-10 2018 TNF-a expression was lower in 5-FU/SIMV group (172.6+-18pg/ml) than in 5-FU/SAL (347.5+-63pg/ml). Fluorouracil 71-75 tumor necrosis factor Rattus norvegicus 0-5 30379218-11 2018 Serum IL-1b was lower in 5-FU/SAL group (134.5+-23pg/ml) than in 5-FU/SIMV (48.3+-9pg/ml). Fluorouracil 25-29 interleukin 1 beta Rattus norvegicus 6-11 30379218-12 2018 Serum IL-6 was 61.8+-15pg/ml in 5-FU/SIMV and 129.4+-17pg/ml in 5-FU/SAL groups. Fluorouracil 32-36 interleukin 6 Rattus norvegicus 6-10 30379218-12 2018 Serum IL-6 was 61.8+-15pg/ml in 5-FU/SIMV and 129.4+-17pg/ml in 5-FU/SAL groups. Fluorouracil 64-68 interleukin 6 Rattus norvegicus 6-10 30059758-4 2018 Here, we show that in human wild-type (wt) p53 HCT-116 colon cancer cells treatment with oxaliplatin or 5-fluorouracil (5-FU) leads to a strong increase in ceramide synthase 5 (CerS5) expression and C16:0-ceramide levels, which was not shown in HCT-116 lacking p53 expression (HCT-116 p53-/-). Fluorouracil 104-118 tumor protein p53 Homo sapiens 43-46 30059758-4 2018 Here, we show that in human wild-type (wt) p53 HCT-116 colon cancer cells treatment with oxaliplatin or 5-fluorouracil (5-FU) leads to a strong increase in ceramide synthase 5 (CerS5) expression and C16:0-ceramide levels, which was not shown in HCT-116 lacking p53 expression (HCT-116 p53-/-). Fluorouracil 104-118 ceramide synthase 5 Homo sapiens 156-175 30059758-4 2018 Here, we show that in human wild-type (wt) p53 HCT-116 colon cancer cells treatment with oxaliplatin or 5-fluorouracil (5-FU) leads to a strong increase in ceramide synthase 5 (CerS5) expression and C16:0-ceramide levels, which was not shown in HCT-116 lacking p53 expression (HCT-116 p53-/-). Fluorouracil 104-118 ceramide synthase 5 Homo sapiens 177-182 30059758-4 2018 Here, we show that in human wild-type (wt) p53 HCT-116 colon cancer cells treatment with oxaliplatin or 5-fluorouracil (5-FU) leads to a strong increase in ceramide synthase 5 (CerS5) expression and C16:0-ceramide levels, which was not shown in HCT-116 lacking p53 expression (HCT-116 p53-/-). Fluorouracil 104-118 tumor protein p53 Homo sapiens 261-264 30059758-4 2018 Here, we show that in human wild-type (wt) p53 HCT-116 colon cancer cells treatment with oxaliplatin or 5-fluorouracil (5-FU) leads to a strong increase in ceramide synthase 5 (CerS5) expression and C16:0-ceramide levels, which was not shown in HCT-116 lacking p53 expression (HCT-116 p53-/-). Fluorouracil 104-118 tumor protein p53 Homo sapiens 261-264 30059758-4 2018 Here, we show that in human wild-type (wt) p53 HCT-116 colon cancer cells treatment with oxaliplatin or 5-fluorouracil (5-FU) leads to a strong increase in ceramide synthase 5 (CerS5) expression and C16:0-ceramide levels, which was not shown in HCT-116 lacking p53 expression (HCT-116 p53-/-). Fluorouracil 120-124 tumor protein p53 Homo sapiens 43-46 30059758-4 2018 Here, we show that in human wild-type (wt) p53 HCT-116 colon cancer cells treatment with oxaliplatin or 5-fluorouracil (5-FU) leads to a strong increase in ceramide synthase 5 (CerS5) expression and C16:0-ceramide levels, which was not shown in HCT-116 lacking p53 expression (HCT-116 p53-/-). Fluorouracil 120-124 ceramide synthase 5 Homo sapiens 156-175 30059758-4 2018 Here, we show that in human wild-type (wt) p53 HCT-116 colon cancer cells treatment with oxaliplatin or 5-fluorouracil (5-FU) leads to a strong increase in ceramide synthase 5 (CerS5) expression and C16:0-ceramide levels, which was not shown in HCT-116 lacking p53 expression (HCT-116 p53-/-). Fluorouracil 120-124 ceramide synthase 5 Homo sapiens 177-182 30059758-4 2018 Here, we show that in human wild-type (wt) p53 HCT-116 colon cancer cells treatment with oxaliplatin or 5-fluorouracil (5-FU) leads to a strong increase in ceramide synthase 5 (CerS5) expression and C16:0-ceramide levels, which was not shown in HCT-116 lacking p53 expression (HCT-116 p53-/-). Fluorouracil 120-124 tumor protein p53 Homo sapiens 261-264 30059758-4 2018 Here, we show that in human wild-type (wt) p53 HCT-116 colon cancer cells treatment with oxaliplatin or 5-fluorouracil (5-FU) leads to a strong increase in ceramide synthase 5 (CerS5) expression and C16:0-ceramide levels, which was not shown in HCT-116 lacking p53 expression (HCT-116 p53-/-). Fluorouracil 120-124 tumor protein p53 Homo sapiens 261-264 30059758-7 2018 Stable knockdown of CerS5 expression using CerS5-targeting shRNA led to an increased sensitivity of HCT-116 p53wt cells, but not of p53-/- cells, to oxaliplatin and 5-FU. Fluorouracil 165-169 ceramide synthase 5 Homo sapiens 20-25 30059758-7 2018 Stable knockdown of CerS5 expression using CerS5-targeting shRNA led to an increased sensitivity of HCT-116 p53wt cells, but not of p53-/- cells, to oxaliplatin and 5-FU. Fluorouracil 165-169 ceramide synthase 5 Homo sapiens 43-48 30059758-10 2018 In conclusion, in p53wt colon cancer cells chemosensitivity against oxaliplatin or 5-FU could be enhanced by downregulation of CerS5 expression leading to reduced autophagy and mitochondrial respiration. Fluorouracil 83-87 tumor protein p53 Homo sapiens 18-21 30059758-10 2018 In conclusion, in p53wt colon cancer cells chemosensitivity against oxaliplatin or 5-FU could be enhanced by downregulation of CerS5 expression leading to reduced autophagy and mitochondrial respiration. Fluorouracil 83-87 ceramide synthase 5 Homo sapiens 127-132 30056083-3 2018 Compared to 5-FU alone, MH synergistically enhanced the chemotherapeutic effects of 5-FU, by reducing cell proliferation through the suppression of EGFR, HER2, p-Akt and p-mTOR expression, and promoting apoptosis by the modulation pro-apoptotic (p53, Bax, Cyto c, FasL caspase-3, -8, -9 and cleave-PARP) and anti-apoptotic (Bcl-2) markers. Fluorouracil 84-88 epidermal growth factor receptor Homo sapiens 148-152 30056083-3 2018 Compared to 5-FU alone, MH synergistically enhanced the chemotherapeutic effects of 5-FU, by reducing cell proliferation through the suppression of EGFR, HER2, p-Akt and p-mTOR expression, and promoting apoptosis by the modulation pro-apoptotic (p53, Bax, Cyto c, FasL caspase-3, -8, -9 and cleave-PARP) and anti-apoptotic (Bcl-2) markers. Fluorouracil 84-88 erb-b2 receptor tyrosine kinase 2 Homo sapiens 154-158 30056083-3 2018 Compared to 5-FU alone, MH synergistically enhanced the chemotherapeutic effects of 5-FU, by reducing cell proliferation through the suppression of EGFR, HER2, p-Akt and p-mTOR expression, and promoting apoptosis by the modulation pro-apoptotic (p53, Bax, Cyto c, FasL caspase-3, -8, -9 and cleave-PARP) and anti-apoptotic (Bcl-2) markers. Fluorouracil 84-88 mechanistic target of rapamycin kinase Homo sapiens 172-176 30056083-3 2018 Compared to 5-FU alone, MH synergistically enhanced the chemotherapeutic effects of 5-FU, by reducing cell proliferation through the suppression of EGFR, HER2, p-Akt and p-mTOR expression, and promoting apoptosis by the modulation pro-apoptotic (p53, Bax, Cyto c, FasL caspase-3, -8, -9 and cleave-PARP) and anti-apoptotic (Bcl-2) markers. Fluorouracil 84-88 tumor protein p53 Homo sapiens 246-249 30056083-3 2018 Compared to 5-FU alone, MH synergistically enhanced the chemotherapeutic effects of 5-FU, by reducing cell proliferation through the suppression of EGFR, HER2, p-Akt and p-mTOR expression, and promoting apoptosis by the modulation pro-apoptotic (p53, Bax, Cyto c, FasL caspase-3, -8, -9 and cleave-PARP) and anti-apoptotic (Bcl-2) markers. Fluorouracil 84-88 BCL2 associated X, apoptosis regulator Homo sapiens 251-254 30056083-3 2018 Compared to 5-FU alone, MH synergistically enhanced the chemotherapeutic effects of 5-FU, by reducing cell proliferation through the suppression of EGFR, HER2, p-Akt and p-mTOR expression, and promoting apoptosis by the modulation pro-apoptotic (p53, Bax, Cyto c, FasL caspase-3, -8, -9 and cleave-PARP) and anti-apoptotic (Bcl-2) markers. Fluorouracil 84-88 BCL2 apoptosis regulator Homo sapiens 324-329 30056083-8 2018 MH also influenced the anti-metastasis effects of 5-FU by decreasing migration ability, suppressing the expression of MMP-2, MMP-9 and increasing N-cadherin and E-cadherin. Fluorouracil 50-54 cadherin 1 Homo sapiens 161-171 30250581-0 2018 MiR-1260b inhibitor enhances the chemosensitivity of colorectal cancer cells to fluorouracil by targeting PDCD4/IGF1. Fluorouracil 80-92 insulin like growth factor 1 Homo sapiens 112-116 29852230-5 2018 We established 5-FU-resistant SW620 and HT-29 cell lines and performed a variety of functional assays following exposure to miR-195-5p and anti-miR-195-5p. Fluorouracil 15-19 microRNA 195 Homo sapiens 144-151 29852230-6 2018 In 5-FU-resistant cells, expression of miR-195-5p, P-gp and ABCG2 was decreased. Fluorouracil 3-7 microRNA 195 Homo sapiens 39-46 29852230-6 2018 In 5-FU-resistant cells, expression of miR-195-5p, P-gp and ABCG2 was decreased. Fluorouracil 3-7 ATP binding cassette subfamily G member 2 (Junior blood group) Homo sapiens 60-65 29917268-7 2018 Furthermore, knocking out KAP1 remarkably increased the susceptibility of A549 cells to the anti-cancer drug 5-Fluorouracil, which correlated with increasing ERK phosphorylation. Fluorouracil 109-123 tripartite motif containing 28 Homo sapiens 26-30 29917268-7 2018 Furthermore, knocking out KAP1 remarkably increased the susceptibility of A549 cells to the anti-cancer drug 5-Fluorouracil, which correlated with increasing ERK phosphorylation. Fluorouracil 109-123 mitogen-activated protein kinase 1 Homo sapiens 158-161 29552688-7 2018 In addition, TNF-alpha and IL-1beta plasma levels were significantly lower in the control and 5-FU+melatonin groups than in the 5-FU group. Fluorouracil 94-98 tumor necrosis factor Rattus norvegicus 13-22 29552688-7 2018 In addition, TNF-alpha and IL-1beta plasma levels were significantly lower in the control and 5-FU+melatonin groups than in the 5-FU group. Fluorouracil 94-98 interleukin 1 beta Rattus norvegicus 27-35 29552688-7 2018 In addition, TNF-alpha and IL-1beta plasma levels were significantly lower in the control and 5-FU+melatonin groups than in the 5-FU group. Fluorouracil 128-132 tumor necrosis factor Rattus norvegicus 13-22 29552688-7 2018 In addition, TNF-alpha and IL-1beta plasma levels were significantly lower in the control and 5-FU+melatonin groups than in the 5-FU group. Fluorouracil 128-132 interleukin 1 beta Rattus norvegicus 27-35 30250224-7 2018 Importantly, we demonstrated that the mechanism of 5-fluorouracil resistance conferred to HCC cells by PGAM5 was via inhibiting BAX- and cytochrome C-mediated apoptotic signaling by interacting and stabilizing Bcl-xL. Fluorouracil 51-65 BCL2 associated X, apoptosis regulator Homo sapiens 128-131 29890207-8 2018 Of particular importance, HDAC1 inhibitor vorinostat restored ASPP2 transcription and produced a synergistic effect with 5-FU in elevating ASPP2, promoting apoptosis and inhibiting EMT in both in vitro and in vivo RCC models. Fluorouracil 121-125 histone deacetylase 1 Homo sapiens 26-31 32254979-8 2018 However, the nanocomplex loaded with {WGA + 5-FU} shows a ~1.5-fold decrease in cell viability in the case of specific cells (MCF-7 and MDA-MB-231) when compared to non-specific cells (HeLa and HEK). Fluorouracil 44-48 EPH receptor A3 Homo sapiens 194-197 30250224-7 2018 Importantly, we demonstrated that the mechanism of 5-fluorouracil resistance conferred to HCC cells by PGAM5 was via inhibiting BAX- and cytochrome C-mediated apoptotic signaling by interacting and stabilizing Bcl-xL. Fluorouracil 51-65 cytochrome c, somatic Homo sapiens 137-149 30250224-7 2018 Importantly, we demonstrated that the mechanism of 5-fluorouracil resistance conferred to HCC cells by PGAM5 was via inhibiting BAX- and cytochrome C-mediated apoptotic signaling by interacting and stabilizing Bcl-xL. Fluorouracil 51-65 BCL2 like 1 Homo sapiens 210-216 30345013-3 2018 In patients with pN1 and pT1-pT3 tumors, 3 months of treatment with 5-fluorouracil and oxaliplatin is comparable with respect to 3-year survival rate to 6 months of treatment. Fluorouracil 68-82 zinc finger protein 135 Homo sapiens 29-32 30257507-9 2018 RESULTS: IGF1-cultured colon cancer cells showed a significant increase in 5-FU resistance and enhanced stemness properties, including an increased percentage of ALDH1+, side-population cells, tumor sphere generation in vitro, and increased tumor initiation in vivo. Fluorouracil 75-79 insulin like growth factor 1 Homo sapiens 9-13 30257507-15 2018 CONCLUSION: We provided evidence of DB as a potential therapeutic agent for overcoming 5-FU resistance induced by IGF1, and suppressing cancer stem-like properties in association with miR-214 regulation. Fluorouracil 87-91 insulin like growth factor 1 Homo sapiens 114-118 30274314-8 2018 Buccal mucosa of 5-FU-injected rats showed increased Nuclear factor-kappa B (NF-kappaB) p50 and p65 in oral keratinocytes. Fluorouracil 17-21 synaptotagmin 1 Rattus norvegicus 96-99 30104401-8 2018 A specific correlation was found between the expression levels of APRT and cell sensitivity to the chemotherapeutic agent 5-fluorouracil (5-FU). Fluorouracil 122-136 adenine phosphoribosyltransferase Homo sapiens 66-70 30104401-8 2018 A specific correlation was found between the expression levels of APRT and cell sensitivity to the chemotherapeutic agent 5-fluorouracil (5-FU). Fluorouracil 138-142 adenine phosphoribosyltransferase Homo sapiens 66-70 30016638-7 2018 5-FU partially induced EMT and increased ABCB1 in colorectal HT-29 cells via TGF-beta signaling (an invasive tumor cell model). Fluorouracil 0-4 ATP binding cassette subfamily B member 1 Homo sapiens 41-46 30275715-0 2018 Dual inhibitor of PI3K and mTOR (NVP-BEZ235) augments the efficacy of fluorouracil on gastric cancer chemotherapy. Fluorouracil 70-82 mechanistic target of rapamycin kinase Homo sapiens 27-31 30271631-2 2018 The inhibitory effect of combined BVZ and 5-Fu in retinal pigment epithelial cells on vascular endothelial growth factor (VEGF) levels was demonstrated through in vitro experiments. Fluorouracil 42-46 vascular endothelial growth factor A Homo sapiens 86-120 30271631-2 2018 The inhibitory effect of combined BVZ and 5-Fu in retinal pigment epithelial cells on vascular endothelial growth factor (VEGF) levels was demonstrated through in vitro experiments. Fluorouracil 42-46 vascular endothelial growth factor A Homo sapiens 122-126 30250641-8 2018 We herein showed that resveratrol and 5-FU combination treatments caused the anti-cancer activities by simultaneously inhibiting STAT3 and Akt signaling pathways. Fluorouracil 38-42 signal transducer and activator of transcription 3 Homo sapiens 129-134 30126848-7 2018 Transfection with ZNF139-siRNA into SGC7901/ADR cells markedly increased expression of miR-185, and treating with chemotherapeutic drugs ADR, 5-FU, L-OHP, the survival rate of SGC7901/ADR cells obviously decreased after ZNF139-siRNA transfection. Fluorouracil 142-146 zinc finger with KRAB and SCAN domains 1 Homo sapiens 18-24 30126848-8 2018 On the other hand, transfection with pcDNA-ZNF139 in GC cell line SGC7901 resulted in an increased expression level of ZNF139 and a decline in the expression level of miR-185, meanwhile drug resistance of GC cells was clearly enhanced to ADR, 5-FU, L-OHP. Fluorouracil 243-247 zinc finger with KRAB and SCAN domains 1 Homo sapiens 43-49 30127974-11 2018 Combination itraconazole and 5-FU treatment showed a synergetic anticancer effect in SGC-7901 cells. Fluorouracil 29-33 sarcoglycan beta Homo sapiens 85-88 30214237-0 2018 Eukaryotic translation initiation factor 3 subunit G (EIF3G) resensitized HCT116/5-Fu to 5-fluorouracil (5-Fu) via inhibition of MRP and MDR1. Fluorouracil 81-85 eukaryotic translation initiation factor 3 subunit G Homo sapiens 0-52 30214237-0 2018 Eukaryotic translation initiation factor 3 subunit G (EIF3G) resensitized HCT116/5-Fu to 5-fluorouracil (5-Fu) via inhibition of MRP and MDR1. Fluorouracil 81-85 eukaryotic translation initiation factor 3 subunit G Homo sapiens 54-59 30214237-0 2018 Eukaryotic translation initiation factor 3 subunit G (EIF3G) resensitized HCT116/5-Fu to 5-fluorouracil (5-Fu) via inhibition of MRP and MDR1. Fluorouracil 89-103 eukaryotic translation initiation factor 3 subunit G Homo sapiens 0-52 30214237-0 2018 Eukaryotic translation initiation factor 3 subunit G (EIF3G) resensitized HCT116/5-Fu to 5-fluorouracil (5-Fu) via inhibition of MRP and MDR1. Fluorouracil 89-103 eukaryotic translation initiation factor 3 subunit G Homo sapiens 54-59 30250641-8 2018 We herein showed that resveratrol and 5-FU combination treatments caused the anti-cancer activities by simultaneously inhibiting STAT3 and Akt signaling pathways. Fluorouracil 38-42 AKT serine/threonine kinase 1 Homo sapiens 139-142 30214237-0 2018 Eukaryotic translation initiation factor 3 subunit G (EIF3G) resensitized HCT116/5-Fu to 5-fluorouracil (5-Fu) via inhibition of MRP and MDR1. Fluorouracil 105-109 eukaryotic translation initiation factor 3 subunit G Homo sapiens 0-52 30214237-0 2018 Eukaryotic translation initiation factor 3 subunit G (EIF3G) resensitized HCT116/5-Fu to 5-fluorouracil (5-Fu) via inhibition of MRP and MDR1. Fluorouracil 105-109 eukaryotic translation initiation factor 3 subunit G Homo sapiens 54-59 30214237-0 2018 Eukaryotic translation initiation factor 3 subunit G (EIF3G) resensitized HCT116/5-Fu to 5-fluorouracil (5-Fu) via inhibition of MRP and MDR1. Fluorouracil 105-109 ATP binding cassette subfamily B member 1 Homo sapiens 137-141 30214237-3 2018 The purpose of the present study was to investigate the underlying molecular mechanisms how eukaryotic translation initiation factor 3 subunit G (EIF3G) resensitized 5-Fu-resistant human CRC cells (HCT116/5-Fu) to 5-fluorouracil (5-Fu). Fluorouracil 166-170 eukaryotic translation initiation factor 3 subunit G Homo sapiens 92-144 30214237-3 2018 The purpose of the present study was to investigate the underlying molecular mechanisms how eukaryotic translation initiation factor 3 subunit G (EIF3G) resensitized 5-Fu-resistant human CRC cells (HCT116/5-Fu) to 5-fluorouracil (5-Fu). Fluorouracil 166-170 eukaryotic translation initiation factor 3 subunit G Homo sapiens 146-151 30214237-3 2018 The purpose of the present study was to investigate the underlying molecular mechanisms how eukaryotic translation initiation factor 3 subunit G (EIF3G) resensitized 5-Fu-resistant human CRC cells (HCT116/5-Fu) to 5-fluorouracil (5-Fu). Fluorouracil 214-228 eukaryotic translation initiation factor 3 subunit G Homo sapiens 92-144 30250641-12 2018 Resveratrol and 5-FU treatments inhibited STAT3 phosphorylation and its binding to the promoter region of human telomerase reverse transcriptase (hTERT). Fluorouracil 16-20 signal transducer and activator of transcription 3 Homo sapiens 42-47 30115914-0 2018 Correction: Long non-coding RNA LINC00152 promotes cell proliferation, metastasis, and confers 5-FU resistance in colorectal cancer by inhibiting miR-139-5p. Fluorouracil 95-99 cytoskeleton regulator RNA Homo sapiens 32-41 30214237-3 2018 The purpose of the present study was to investigate the underlying molecular mechanisms how eukaryotic translation initiation factor 3 subunit G (EIF3G) resensitized 5-Fu-resistant human CRC cells (HCT116/5-Fu) to 5-fluorouracil (5-Fu). Fluorouracil 214-228 eukaryotic translation initiation factor 3 subunit G Homo sapiens 146-151 30214237-3 2018 The purpose of the present study was to investigate the underlying molecular mechanisms how eukaryotic translation initiation factor 3 subunit G (EIF3G) resensitized 5-Fu-resistant human CRC cells (HCT116/5-Fu) to 5-fluorouracil (5-Fu). Fluorouracil 205-209 eukaryotic translation initiation factor 3 subunit G Homo sapiens 92-144 30214237-3 2018 The purpose of the present study was to investigate the underlying molecular mechanisms how eukaryotic translation initiation factor 3 subunit G (EIF3G) resensitized 5-Fu-resistant human CRC cells (HCT116/5-Fu) to 5-fluorouracil (5-Fu). Fluorouracil 205-209 eukaryotic translation initiation factor 3 subunit G Homo sapiens 146-151 30214237-6 2018 In addition, silencing EIF3G enhanced 5-Fu-induced apoptosis in HCT116/5-Fu cells. Fluorouracil 38-42 eukaryotic translation initiation factor 3 subunit G Homo sapiens 23-28 30214237-8 2018 Finally, the xenograft tumor model further confirmed that EIF3G resensitized HCT116/5-Fu tumors to 5-Fu. Fluorouracil 84-88 eukaryotic translation initiation factor 3 subunit G Homo sapiens 58-63 30214237-8 2018 Finally, the xenograft tumor model further confirmed that EIF3G resensitized HCT116/5-Fu tumors to 5-Fu. Fluorouracil 99-103 eukaryotic translation initiation factor 3 subunit G Homo sapiens 58-63 30214237-9 2018 We observed that EIF3G silencing followed by 5-Fu administration had a synergistic interaction effect on HCT116/5-Fu in vitro and in vivo. Fluorouracil 112-116 eukaryotic translation initiation factor 3 subunit G Homo sapiens 17-22 30214243-10 2018 Notably, the inhibitory effects of STARD13 on HCC cells stemness and 5-FU sensitivity were rescued by RhoA or YAP-5SA overexpression. Fluorouracil 69-73 ras homolog family member A Homo sapiens 102-106 29864476-0 2018 Skin cancer treatment effectiveness is improved by iontophoresis of EGFR-targeted liposomes containing 5-FU compared with subcutaneous injection. Fluorouracil 103-107 epidermal growth factor receptor Homo sapiens 68-72 30111797-5 2018 A microarray analysis revealed that the suppression of the checkpoint kinase 1 (CHK1) pathway explained the resistance to 5-FU, especially in p53 wild-type cancer cells such as HCT-8. Fluorouracil 122-126 checkpoint kinase 1 Homo sapiens 59-78 30111797-5 2018 A microarray analysis revealed that the suppression of the checkpoint kinase 1 (CHK1) pathway explained the resistance to 5-FU, especially in p53 wild-type cancer cells such as HCT-8. Fluorouracil 122-126 checkpoint kinase 1 Homo sapiens 80-84 30111797-5 2018 A microarray analysis revealed that the suppression of the checkpoint kinase 1 (CHK1) pathway explained the resistance to 5-FU, especially in p53 wild-type cancer cells such as HCT-8. Fluorouracil 122-126 tumor protein p53 Homo sapiens 142-145 30111797-6 2018 Our data also demonstrated that the CHK1 pathway is suppressed by the Wnt pathway in 5-FU-resistant cells. Fluorouracil 85-89 checkpoint kinase 1 Homo sapiens 36-40 30111797-7 2018 In summary, we have discovered a novel mechanism for 5-FU resistance mediated by histone deacetylation, which also revealed the crosstalk between the Wnt pathway and CHK1 pathway. Fluorouracil 53-57 checkpoint kinase 1 Homo sapiens 166-170 30119680-0 2018 lncRNA KRAL reverses 5-fluorouracil resistance in hepatocellular carcinoma cells by acting as a ceRNA against miR-141. Fluorouracil 21-35 microRNA 141 Homo sapiens 110-117 30119680-3 2018 Herein, our study is the first to demonstrate that lower expression of KRAL, a long non-coding RNA (lncRNA), mediates 5-FU resistance in HCC via the miR-141/Keap1 axis. Fluorouracil 118-122 microRNA 141 Homo sapiens 149-156 30119680-3 2018 Herein, our study is the first to demonstrate that lower expression of KRAL, a long non-coding RNA (lncRNA), mediates 5-FU resistance in HCC via the miR-141/Keap1 axis. Fluorouracil 118-122 kelch like ECH associated protein 1 Homo sapiens 157-162 30119680-5 2018 RESULTS: The quantitative analysis indicated that KRAL and Keap1 were significantly decreased and that Nrf2 was increased in HepG2/5-FU and SMMC-7721/5-FU cells compared with the corresponding expression levels in the respective parental cells. Fluorouracil 131-135 NFE2 like bZIP transcription factor 2 Homo sapiens 103-107 30119680-6 2018 Overexpression of KRAL increased Keap1 expression, and inactivating the Nrf2-dependent antioxidant pathway could reverse the resistance of HepG2/5-FU and SMMC-7721/5-FU cells to 5-FU. Fluorouracil 145-149 NFE2 like bZIP transcription factor 2 Homo sapiens 72-76 30119680-6 2018 Overexpression of KRAL increased Keap1 expression, and inactivating the Nrf2-dependent antioxidant pathway could reverse the resistance of HepG2/5-FU and SMMC-7721/5-FU cells to 5-FU. Fluorouracil 164-168 NFE2 like bZIP transcription factor 2 Homo sapiens 72-76 30119680-8 2018 These findings demonstrated that KRAL is an important regulator of Keap1; furthermore, the ceRNA network involving KRAL may serve as a treatment strategy against 5-FU resistance in hepatocellular carcinoma cells. Fluorouracil 162-166 kelch like ECH associated protein 1 Homo sapiens 67-72 30119680-9 2018 CONCLUSIONS: KRAL/miR-141/Keap1 axis mediates 5-fluorouracil resistance in HCC cell lines. Fluorouracil 46-60 microRNA 141 Homo sapiens 18-25 30119680-9 2018 CONCLUSIONS: KRAL/miR-141/Keap1 axis mediates 5-fluorouracil resistance in HCC cell lines. Fluorouracil 46-60 kelch like ECH associated protein 1 Homo sapiens 26-31 29864476-3 2018 In this work, an EGFR-targeted immunoliposome loaded with 5-fluorouracil (5- FU) was developed to allow co-administration of the antibody and the chemotherapeutic agent and selective delivery to SCC cells. Fluorouracil 58-72 epidermal growth factor receptor Homo sapiens 17-21 29864476-3 2018 In this work, an EGFR-targeted immunoliposome loaded with 5-fluorouracil (5- FU) was developed to allow co-administration of the antibody and the chemotherapeutic agent and selective delivery to SCC cells. Fluorouracil 74-79 epidermal growth factor receptor Homo sapiens 17-21 29980405-5 2018 Upon introduction of the WT-TP53 gene into the MIA-PaCa-2 pancreatic cancer cell line, the sensitivity to drugs used to treat pancreatic cancer cells such as: gemcitabine, fluorouracil (5FU), cisplatin, irinotecan, oxaliplatin, and paclitaxel increased significantly. Fluorouracil 172-184 tumor protein p53 Homo sapiens 28-32 30096914-11 2018 Administration with both AA and 5-FU in prevention and throughout was able to prevent decreases in Notch1 SOX2, nestin, DCX, and Nrf2 caused by 5-FU. Fluorouracil 144-148 NFE2 like bZIP transcription factor 2 Rattus norvegicus 129-133 30081850-13 2018 HCT-116 cells with high expression of BAG3 had higher cell viability and lower apoptosis rate than control cells after treatment with 5-FU, while the BAG3 knockout group demonstrated the opposite effects. Fluorouracil 134-138 BAG cochaperone 3 Homo sapiens 38-42 30081850-14 2018 So BAG3 expression level was associated with chemoresistance to 5-FU in HCT-116 cells. Fluorouracil 64-68 BAG cochaperone 3 Homo sapiens 3-7 30096914-9 2018 Treatment with 5-FU caused significant reductions in Notch1, sex determining region Y-box 2 (SOX2), nestin, doublecortin (DCX), and nuclear factor erythroid 2-related factor 2 (Nrf2) levels within the hippocampus. Fluorouracil 15-19 NFE2 like bZIP transcription factor 2 Rattus norvegicus 132-175 30096914-9 2018 Treatment with 5-FU caused significant reductions in Notch1, sex determining region Y-box 2 (SOX2), nestin, doublecortin (DCX), and nuclear factor erythroid 2-related factor 2 (Nrf2) levels within the hippocampus. Fluorouracil 15-19 NFE2 like bZIP transcription factor 2 Rattus norvegicus 177-181 30096914-11 2018 Administration with both AA and 5-FU in prevention and throughout was able to prevent decreases in Notch1 SOX2, nestin, DCX, and Nrf2 caused by 5-FU. Fluorouracil 32-36 NFE2 like bZIP transcription factor 2 Rattus norvegicus 129-133 29772441-0 2018 Six2 is negatively correlated with good prognosis and decreases 5-FU sensitivity via suppressing E-cadherin expression in hepatocellular carcinoma cells. Fluorouracil 64-68 cadherin 1 Homo sapiens 97-107 29772441-6 2018 And E-cadherin overexpression rescued six2-induced decrease of 5-FU sensitivity and promotion on HCC cells stemness. Fluorouracil 63-67 cadherin 1 Homo sapiens 4-14 29772441-7 2018 Therefore, our results suggest that Six2 is negatively correlated with good prognosis and decreases 5-FU sensitivity via suppressing E-cadherin expression in HCC cells. Fluorouracil 100-104 cadherin 1 Homo sapiens 133-143 29980405-5 2018 Upon introduction of the WT-TP53 gene into the MIA-PaCa-2 pancreatic cancer cell line, the sensitivity to drugs used to treat pancreatic cancer cells such as: gemcitabine, fluorouracil (5FU), cisplatin, irinotecan, oxaliplatin, and paclitaxel increased significantly. Fluorouracil 186-189 tumor protein p53 Homo sapiens 28-32 29762254-0 2018 Short article: Influence of regulatory NLRC5 variants on colorectal cancer survival and 5-fluorouracil-based chemotherapy. Fluorouracil 88-102 NLR family CARD domain containing 5 Homo sapiens 39-44 29762254-2 2018 OBJECTIVE: We aimed to evaluate the effect of potential regulatory variants in NLRC5 on overall survival and survival after 5-fluorouracil (5-FU)-based therapy of colorectal cancer (CRC) patients. Fluorouracil 124-138 NLR family CARD domain containing 5 Homo sapiens 79-84 29762254-2 2018 OBJECTIVE: We aimed to evaluate the effect of potential regulatory variants in NLRC5 on overall survival and survival after 5-fluorouracil (5-FU)-based therapy of colorectal cancer (CRC) patients. Fluorouracil 140-144 NLR family CARD domain containing 5 Homo sapiens 79-84 29737579-5 2018 Increased apoptosis following beta-elemene exposure was due to enhanced sensitivity to 5-FU through down-regulating miR-191. Fluorouracil 87-91 microRNA 191 Homo sapiens 116-123 29856982-0 2018 Activation of FOXO3a reverses 5-Fluorouracil resistance in human breast cancer cells. Fluorouracil 30-44 forkhead box O3 Homo sapiens 14-20 29737579-7 2018 Moreover, beta-elemene might improve resistance of colorectal carcinoma cells to 5-FU by down-regulating miR-191, thereby inhibiting the Wnt/beta-catenin pathway. Fluorouracil 81-85 microRNA 191 Homo sapiens 105-112 30068336-10 2018 Further studies where colorectal cancer (CRC) cells were subjected to 5-fluorouracil (5FU) treatment revealed a sharp increase in MASTL expression upon chemotherapy, along with increases in Bcl-xL and Survivin expression. Fluorouracil 70-84 BCL2 like 1 Homo sapiens 190-196 30068336-10 2018 Further studies where colorectal cancer (CRC) cells were subjected to 5-fluorouracil (5FU) treatment revealed a sharp increase in MASTL expression upon chemotherapy, along with increases in Bcl-xL and Survivin expression. Fluorouracil 86-89 BCL2 like 1 Homo sapiens 190-196 29931401-0 2018 Determination of 5-fluorouracil and tegafur in tear fluid of patients treated with oral fluoropyrimidine anticancer agent, S-1. Fluorouracil 17-31 proteasome 26S subunit, non-ATPase 1 Homo sapiens 123-126 30228942-1 2018 In preclinical models, IL-1beta inhibition could enhance the efficacy of fluorouracil (5-FU). Fluorouracil 73-85 interleukin 1 beta Homo sapiens 23-31 30228942-1 2018 In preclinical models, IL-1beta inhibition could enhance the efficacy of fluorouracil (5-FU). Fluorouracil 87-91 interleukin 1 beta Homo sapiens 23-31 29451302-1 2018 According to the Trastuzumab for Gastric Cancer (ToGA) study, trastuzumab plus cisplatin and capecitabine/5-fluorouracil (5-FU) is standard first-line treatment for human epidermal growth factor receptor 2 (HER2)-positive advanced oesophagogastric cancer. Fluorouracil 106-120 erb-b2 receptor tyrosine kinase 2 Homo sapiens 165-205 29451302-1 2018 According to the Trastuzumab for Gastric Cancer (ToGA) study, trastuzumab plus cisplatin and capecitabine/5-fluorouracil (5-FU) is standard first-line treatment for human epidermal growth factor receptor 2 (HER2)-positive advanced oesophagogastric cancer. Fluorouracil 106-120 erb-b2 receptor tyrosine kinase 2 Homo sapiens 207-211 29451302-1 2018 According to the Trastuzumab for Gastric Cancer (ToGA) study, trastuzumab plus cisplatin and capecitabine/5-fluorouracil (5-FU) is standard first-line treatment for human epidermal growth factor receptor 2 (HER2)-positive advanced oesophagogastric cancer. Fluorouracil 122-126 erb-b2 receptor tyrosine kinase 2 Homo sapiens 165-205 29451302-1 2018 According to the Trastuzumab for Gastric Cancer (ToGA) study, trastuzumab plus cisplatin and capecitabine/5-fluorouracil (5-FU) is standard first-line treatment for human epidermal growth factor receptor 2 (HER2)-positive advanced oesophagogastric cancer. Fluorouracil 122-126 erb-b2 receptor tyrosine kinase 2 Homo sapiens 207-211 29643149-5 2018 5-FU-mediated augmented lung metastasis was associated with increases in intrapulmonary neutrophil numbers and expression of neutrophilic chemokines, Cxcl1 and Cxcl2 in tumor cells, with few effects on intrapulmonary T-cell or macrophage numbers. Fluorouracil 0-4 chemokine (C-X-C motif) ligand 1 Mus musculus 150-155 29643149-5 2018 5-FU-mediated augmented lung metastasis was associated with increases in intrapulmonary neutrophil numbers and expression of neutrophilic chemokines, Cxcl1 and Cxcl2 in tumor cells, with few effects on intrapulmonary T-cell or macrophage numbers. Fluorouracil 0-4 chemokine (C-X-C motif) ligand 2 Mus musculus 160-165 29643149-6 2018 5-FU enhanced Cxcl1 and Cxcl2 expression in 4T1 cells in a NFkappaB-dependent manner. Fluorouracil 0-4 chemokine (C-X-C motif) ligand 1 Mus musculus 14-19 29643149-6 2018 5-FU enhanced Cxcl1 and Cxcl2 expression in 4T1 cells in a NFkappaB-dependent manner. Fluorouracil 0-4 chemokine (C-X-C motif) ligand 2 Mus musculus 24-29 29643149-10 2018 Collectively, 5-FU can enhance lung metastasis by inducing tumor cells to produce Cxcl1 and Cxcl2, which induced the migration of neutrophils expressing Prok2 with a capacity to enhance 4T1 cell proliferation. Fluorouracil 14-18 chemokine (C-X-C motif) ligand 1 Mus musculus 82-87 29643149-10 2018 Collectively, 5-FU can enhance lung metastasis by inducing tumor cells to produce Cxcl1 and Cxcl2, which induced the migration of neutrophils expressing Prok2 with a capacity to enhance 4T1 cell proliferation. Fluorouracil 14-18 chemokine (C-X-C motif) ligand 2 Mus musculus 92-97 29845287-5 2018 Western blot analysis further demonstrated that the phosphorylation of Akt was inhibited by lapatinib, and the results of the MTT assay revealed that the combination of lapatinib with either 5-FU or gemcitabine demonstrated synergistic antitumor effects, whereas a combinatory treatment of lapatinib with epirubicin, a typical anthracycline drug, exhibited antagonistic antitumor effects in HER2-positive breast cancer cells. Fluorouracil 191-195 AKT serine/threonine kinase 1 Homo sapiens 71-74 29845287-5 2018 Western blot analysis further demonstrated that the phosphorylation of Akt was inhibited by lapatinib, and the results of the MTT assay revealed that the combination of lapatinib with either 5-FU or gemcitabine demonstrated synergistic antitumor effects, whereas a combinatory treatment of lapatinib with epirubicin, a typical anthracycline drug, exhibited antagonistic antitumor effects in HER2-positive breast cancer cells. Fluorouracil 191-195 erb-b2 receptor tyrosine kinase 2 Homo sapiens 391-395 29767264-8 2018 It also inhibited the nuclear transition of p65 NF-kappaB, which is known to regulate inflammatory cytokine expression in keratinocytes suffering from 5-FU-induced dermatitis. Fluorouracil 151-155 nuclear factor kappa B subunit 1 Homo sapiens 48-57 29767264-10 2018 Moreover, ED attenuated 5-FU-induced transcriptional activation of NF-kappaB. Fluorouracil 24-28 nuclear factor kappa B subunit 1 Homo sapiens 67-76 29976570-1 2018 beta-Ureidopropionase (betaUP) catalyzes the third step of the reductive pyrimidine catabolic pathway responsible for breakdown of uracil-, thymine- and pyrimidine-based antimetabolites such as 5-fluorouracil. Fluorouracil 194-208 beta-ureidopropionase 1 Homo sapiens 0-21 29976570-1 2018 beta-Ureidopropionase (betaUP) catalyzes the third step of the reductive pyrimidine catabolic pathway responsible for breakdown of uracil-, thymine- and pyrimidine-based antimetabolites such as 5-fluorouracil. Fluorouracil 194-208 beta-ureidopropionase 1 Homo sapiens 23-29 29931401-1 2018 PURPOSE: To establish a method for the measurement of 5-fluorouracil (5-FU), and tegafur (FT) in tear samples from patients treated with oral fluoropyrimidine anticancer agent S-1. Fluorouracil 54-68 proteasome 26S subunit, non-ATPase 1 Homo sapiens 176-179 29931401-1 2018 PURPOSE: To establish a method for the measurement of 5-fluorouracil (5-FU), and tegafur (FT) in tear samples from patients treated with oral fluoropyrimidine anticancer agent S-1. Fluorouracil 70-74 proteasome 26S subunit, non-ATPase 1 Homo sapiens 176-179 29931401-9 2018 Decomposition from FT to 5-FU was suppressed when 50 mg/mL bovine serum albumin was added during extraction. Fluorouracil 25-29 albumin Homo sapiens 66-79 29931401-10 2018 The mean concentrations of 5-FU and FT in tears during S-1 treatment were 0.17 +- 0.11 and 1.94 +- 0.71 mug/mL, respectively. Fluorouracil 27-31 proteasome 26S subunit, non-ATPase 1 Homo sapiens 55-58 29702091-5 2018 Significantly, MALAT1 deletion sensitized HepG2 cells to 5-FU-induced cell cycle arrest in G1 phase, as evidenced by the significant reduction in Cyclin D1 and CDK4 and increase in p53, p21 and p27 protein levels. Fluorouracil 57-61 tumor protein p53 Homo sapiens 181-184 29715584-0 2018 DUOX2-mediated production of reactive oxygen species induces epithelial mesenchymal transition in 5-fluorouracil resistant human colon cancer cells. Fluorouracil 98-112 dual oxidase 2 Homo sapiens 0-5 29715584-4 2018 Here, we show that reactive oxygen species (ROS), produced by dual oxidase 2 (DUOX2), promote 5-FU-induced EMT. Fluorouracil 94-98 dual oxidase 2 Homo sapiens 62-76 29715584-4 2018 Here, we show that reactive oxygen species (ROS), produced by dual oxidase 2 (DUOX2), promote 5-FU-induced EMT. Fluorouracil 94-98 dual oxidase 2 Homo sapiens 78-83 29715584-5 2018 First, we showed that 5-FU-resistant SNUC5 colon cancer cells (SNUC5/FUR cells) undergo EMT by analyzing the expression of EMT markers such as N-cadherin, vimentin and E-cadherin. Fluorouracil 22-26 cadherin 1 Homo sapiens 168-178 29738772-5 2018 Interestingly, co-treatment with DHA could effectively restore the anticancer effect of 5-FU against HCT116 TP53-/- cells, which manifested as the inhibition of proliferation and induction of reactive oxygen species (ROS)-mediated apoptosis and was accompanied by the upregulation of B-cell lymphoma 2 (BCL-2) and downregulation of the BCL-2-associated X protein (BAX). Fluorouracil 88-92 tumor protein p53 Homo sapiens 108-112 29738772-5 2018 Interestingly, co-treatment with DHA could effectively restore the anticancer effect of 5-FU against HCT116 TP53-/- cells, which manifested as the inhibition of proliferation and induction of reactive oxygen species (ROS)-mediated apoptosis and was accompanied by the upregulation of B-cell lymphoma 2 (BCL-2) and downregulation of the BCL-2-associated X protein (BAX). Fluorouracil 88-92 BCL2 apoptosis regulator Homo sapiens 284-301 29738772-5 2018 Interestingly, co-treatment with DHA could effectively restore the anticancer effect of 5-FU against HCT116 TP53-/- cells, which manifested as the inhibition of proliferation and induction of reactive oxygen species (ROS)-mediated apoptosis and was accompanied by the upregulation of B-cell lymphoma 2 (BCL-2) and downregulation of the BCL-2-associated X protein (BAX). Fluorouracil 88-92 BCL2 apoptosis regulator Homo sapiens 303-308 29738772-5 2018 Interestingly, co-treatment with DHA could effectively restore the anticancer effect of 5-FU against HCT116 TP53-/- cells, which manifested as the inhibition of proliferation and induction of reactive oxygen species (ROS)-mediated apoptosis and was accompanied by the upregulation of B-cell lymphoma 2 (BCL-2) and downregulation of the BCL-2-associated X protein (BAX). Fluorouracil 88-92 BCL2 associated X, apoptosis regulator Homo sapiens 336-362 29738772-5 2018 Interestingly, co-treatment with DHA could effectively restore the anticancer effect of 5-FU against HCT116 TP53-/- cells, which manifested as the inhibition of proliferation and induction of reactive oxygen species (ROS)-mediated apoptosis and was accompanied by the upregulation of B-cell lymphoma 2 (BCL-2) and downregulation of the BCL-2-associated X protein (BAX). Fluorouracil 88-92 BCL2 associated X, apoptosis regulator Homo sapiens 364-367 29949874-6 2018 Knockout of GPRC5a reduced the proliferation and migration ability of PaCa cell lines and suppressed the chemotherapy drug resistance of gemcitabine, oxaliplatin, and fluorouracil in PaCa cells. Fluorouracil 167-179 G protein-coupled receptor class C group 5 member A Homo sapiens 12-18 29777330-0 2018 Down-regulating IL-6/GP130 targets improved the anti-tumor effects of 5-fluorouracil in colon cancer. Fluorouracil 70-84 interleukin 6 Homo sapiens 16-20 29945701-1 2018 BACKGROUND: There is no standard treatment for advanced non-small cell lung cancer (NSCLC) after the failure of two lines of chemotherapy, S-1 as the third generation of fluorouracil derivate with well safety and low toxicity, presented some efficacy in lung cancer treatment. Fluorouracil 170-182 proteasome 26S subunit, non-ATPase 1 Homo sapiens 139-142 29902974-10 2018 Subsequently the molecular inhibition of specific isoforms of ALDH by ALDH1A1 or ALDH1A3 siRNA led to sensitizing of cell lines HT-29/eGFP, HCT-116/eGFP to capecitabine and 5-FU. Fluorouracil 173-177 aldehyde dehydrogenase family 1, subfamily A3 Mus musculus 81-88 29914576-3 2018 The study aimed to investigate the inhibitory effect of beta-eudesmol on NQO1 enhanced chemotherapeutic effects of 5-fluorouracil (5-FU) and doxorubicin (DOX) in the high NQO1-expressing human CCA cell line, NQO1-KKU-100. Fluorouracil 115-129 NAD(P)H quinone dehydrogenase 1 Homo sapiens 73-77 29914576-3 2018 The study aimed to investigate the inhibitory effect of beta-eudesmol on NQO1 enhanced chemotherapeutic effects of 5-fluorouracil (5-FU) and doxorubicin (DOX) in the high NQO1-expressing human CCA cell line, NQO1-KKU-100. Fluorouracil 115-129 NAD(P)H quinone dehydrogenase 1 Homo sapiens 171-175 29914576-3 2018 The study aimed to investigate the inhibitory effect of beta-eudesmol on NQO1 enhanced chemotherapeutic effects of 5-fluorouracil (5-FU) and doxorubicin (DOX) in the high NQO1-expressing human CCA cell line, NQO1-KKU-100. Fluorouracil 131-135 NAD(P)H quinone dehydrogenase 1 Homo sapiens 73-77 29914576-3 2018 The study aimed to investigate the inhibitory effect of beta-eudesmol on NQO1 enhanced chemotherapeutic effects of 5-fluorouracil (5-FU) and doxorubicin (DOX) in the high NQO1-expressing human CCA cell line, NQO1-KKU-100. Fluorouracil 131-135 NAD(P)H quinone dehydrogenase 1 Homo sapiens 171-175 29914576-13 2018 In addition, it also potentiated the cytotoxic activities and inhibitory activities of 5-FU and DOX on cell migration through induction of cell apoptosis and activation of caspase 3/7. Fluorouracil 87-91 caspase 3 Homo sapiens 172-181 29847952-0 2018 An NAD(P)H:Quinone Oxidoreductase 1 Responsive and Self-Immolative Prodrug of 5-Fluorouracil for Safe and Effective Cancer Therapy. Fluorouracil 78-92 NAD(P)H quinone dehydrogenase 1 Homo sapiens 3-35 29847952-2 2018 Upon bioreductive activation by NQO1, 1 can release the parent drug 5-FU specifically in NQO1-overexpressing cancer cells. Fluorouracil 68-72 NAD(P)H quinone dehydrogenase 1 Homo sapiens 32-36 29847952-2 2018 Upon bioreductive activation by NQO1, 1 can release the parent drug 5-FU specifically in NQO1-overexpressing cancer cells. Fluorouracil 68-72 NAD(P)H quinone dehydrogenase 1 Homo sapiens 89-93 29777330-4 2018 Thus, we speculated that in colon cancer, the anti-tumor efficacy of 5-FU might be increased in combination with IL-6/GP130 inhibitors. Fluorouracil 69-73 interleukin 6 Homo sapiens 113-117 29777330-14 2018 Conversely, 5-FU activation is reduced following exogenous IL-6 treatment in cells. Fluorouracil 12-16 interleukin 6 Homo sapiens 59-63 29777330-15 2018 Further mechanistic studies determined that BZA treatment enhanced 5-FU anti-tumor activation by inhibiting the IL-6/GP130 signaling pathway and the phosphorylation status of the downstream effectors AKT, ERK and STAT3. Fluorouracil 67-71 interleukin 6 Homo sapiens 112-116 29777330-15 2018 Further mechanistic studies determined that BZA treatment enhanced 5-FU anti-tumor activation by inhibiting the IL-6/GP130 signaling pathway and the phosphorylation status of the downstream effectors AKT, ERK and STAT3. Fluorouracil 67-71 mitogen-activated protein kinase 1 Homo sapiens 205-208 29777330-15 2018 Further mechanistic studies determined that BZA treatment enhanced 5-FU anti-tumor activation by inhibiting the IL-6/GP130 signaling pathway and the phosphorylation status of the downstream effectors AKT, ERK and STAT3. Fluorouracil 67-71 signal transducer and activator of transcription 3 Homo sapiens 213-218 29777330-16 2018 In contrast, IL-6 can attenuate 5-FU function via activating IL-6R/GP130 signaling and the P-AKT, P-ERK and P-STAT3 levels. Fluorouracil 32-36 interleukin 6 Homo sapiens 13-17 29777330-16 2018 In contrast, IL-6 can attenuate 5-FU function via activating IL-6R/GP130 signaling and the P-AKT, P-ERK and P-STAT3 levels. Fluorouracil 32-36 interleukin 6 receptor Homo sapiens 61-66 29777330-16 2018 In contrast, IL-6 can attenuate 5-FU function via activating IL-6R/GP130 signaling and the P-AKT, P-ERK and P-STAT3 levels. Fluorouracil 32-36 AKT serine/threonine kinase 1 Homo sapiens 93-96 29510994-3 2018 Here, we report that elevated claudin-2 expression in stage II/III colorectal tumors is associated with poor recurrence-free survival following 5-fluorouracil-based chemotherapy, an outcome in which CSCs play an instrumental role. Fluorouracil 144-158 claudin 2 Homo sapiens 30-39 29859044-8 2018 Moreover, Slit3-repression induced chemoresistance to sorafenib, oxaliplatin and 5-FU through impairment of beta-catenin degradation and induction of cyclin D3 and survivin levels. Fluorouracil 81-85 slit guidance ligand 3 Homo sapiens 10-15 29859044-8 2018 Moreover, Slit3-repression induced chemoresistance to sorafenib, oxaliplatin and 5-FU through impairment of beta-catenin degradation and induction of cyclin D3 and survivin levels. Fluorouracil 81-85 cyclin D3 Homo sapiens 150-159 29233603-7 2018 RESULTS: Slices treated with 5-FU showed lower tumor cell fractions and dose-dependent alterations of proliferating tumor cells compared with controls (1 muM, Delta +3%; 10 muM, Delta -9%; 100 muM, Delta -15%). Fluorouracil 29-33 latexin Homo sapiens 154-157 29233603-7 2018 RESULTS: Slices treated with 5-FU showed lower tumor cell fractions and dose-dependent alterations of proliferating tumor cells compared with controls (1 muM, Delta +3%; 10 muM, Delta -9%; 100 muM, Delta -15%). Fluorouracil 29-33 latexin Homo sapiens 173-176 29233603-7 2018 RESULTS: Slices treated with 5-FU showed lower tumor cell fractions and dose-dependent alterations of proliferating tumor cells compared with controls (1 muM, Delta +3%; 10 muM, Delta -9%; 100 muM, Delta -15%). Fluorouracil 29-33 latexin Homo sapiens 173-176 29917191-11 2018 In addition, 5-fluorouracil and chloroquine both increased the expression of Notch1 in gastric CSCs. Fluorouracil 13-27 notch receptor 1 Homo sapiens 77-83 29554628-3 2018 The removal efficiency of 5-FU was higher (95%) when the concentration was 5 mg L-1 under the same conditions. Fluorouracil 26-30 immunoglobulin kappa variable 1-16 Homo sapiens 80-83 29554628-5 2018 System II, 77% of 5-FU degradation was achieved (50 mg L-1) after 6 h of electrolysis (kapp = 0.004 min-1). Fluorouracil 18-22 immunoglobulin kappa variable 1-16 Homo sapiens 55-58 29554628-6 2018 The degradation rate of 5-FU was complete when the concentration was 5 mg L-1 under the same conditions. Fluorouracil 24-28 immunoglobulin kappa variable 1-16 Homo sapiens 74-77 29772519-2 2018 The mechanisms underlying resistance to doxorubicin, cisplatin, and 5-fluorouracil involve p53 and P-glycoprotein (P-gp). Fluorouracil 68-82 tumor protein p53 Homo sapiens 91-94 29772519-2 2018 The mechanisms underlying resistance to doxorubicin, cisplatin, and 5-fluorouracil involve p53 and P-glycoprotein (P-gp). Fluorouracil 68-82 ATP binding cassette subfamily B member 1 Homo sapiens 99-113 29772519-2 2018 The mechanisms underlying resistance to doxorubicin, cisplatin, and 5-fluorouracil involve p53 and P-glycoprotein (P-gp). Fluorouracil 68-82 ATP binding cassette subfamily B member 1 Homo sapiens 115-119 28745083-0 2018 Elemental Diet Accelerates the Recovery From Oral Mucositis and Dermatitis Induced by 5-Fluorouracil Through the Induction of Fibroblast Growth Factor 2. Fluorouracil 86-100 fibroblast growth factor 2 Homo sapiens 126-152 29436749-0 2018 HOXA13 contributes to gastric carcinogenesis through DHRS2 interacting with MDM2 and confers 5-FU resistance by a p53-dependent pathway. Fluorouracil 93-97 tumor protein p53 Homo sapiens 114-117 29314782-6 2018 Although structural integrity of the model was preserved, 5-FU treatment resulted in a widening of epithelial intercellular spaces, characterized by E-cadherin dissolution from adherens junctions. Fluorouracil 58-62 cadherin 1 Homo sapiens 149-159 29620228-0 2018 beta-arrestin2 promotes 5-FU-induced apoptosis via the NF-kappaB pathway in colorectal cancer. Fluorouracil 24-28 arrestin beta 2 Homo sapiens 0-14 29620228-5 2018 In addition, the downregulation of beta-arrestin2 reduced 5-FU-induced apoptosis in the LoVo cells, while the overexpression of beta-arrestin2 increased the apoptosis of HCT116 cells in vitro. Fluorouracil 58-62 arrestin beta 2 Homo sapiens 35-49 29620228-6 2018 Furthermore, the downregulation of beta-arrestin2 reduced the expression of the pro-apoptotic proteins cleaved-caspase-3 and Bax, and increased the expression of the anti-apoptotic protein Bcl-2 after 5-FU treatment. Fluorouracil 201-205 arrestin beta 2 Homo sapiens 35-49 29620228-6 2018 Furthermore, the downregulation of beta-arrestin2 reduced the expression of the pro-apoptotic proteins cleaved-caspase-3 and Bax, and increased the expression of the anti-apoptotic protein Bcl-2 after 5-FU treatment. Fluorouracil 201-205 BCL2 apoptosis regulator Homo sapiens 189-194 29620228-9 2018 In conclusion, these results indicated that beta-arrestin2 promoted 5-FU-induced CRC cell apoptosis via the NF-kappaB pathway and may be used as a prognosis marker for CRC. Fluorouracil 68-72 arrestin beta 2 Homo sapiens 44-58 29436749-9 2018 Furthermore, HOXA13 conferred 5-FU resistance through MRP1 by a p53-dependent pathway. Fluorouracil 30-34 tumor protein p53 Homo sapiens 64-67 29899863-8 2018 The tumor burden induced by the NLS-mutated Nrf2-transfected shNrf2HCT116 clone was completely suppressed by treatment with 5-FU in combination with carfilzomib. Fluorouracil 124-128 NFE2 like bZIP transcription factor 2 Homo sapiens 44-48 29868263-8 2018 Exogenous expression of SNX1 inhibited the growth, migration, invasion and promoted the apoptosis and enhanced the sensitivity of GC cells to the chemotherapeutic drug 5-Fluorouracil (5-Fu) in vitro, while knockdown of SNX1 by short hairpin RNA (shRNA) significantly promoted the growth, migration, invasion and reduced the apoptosis and the sensitivity of GC cells to 5-Fu. Fluorouracil 168-182 sorting nexin 1 Homo sapiens 24-28 29795190-4 2018 Enforced miR-181a expression enhanced 5-FU-induced p53-dependent mitochondrial apoptosis, including declined Bcl-2/Bax ratio, loss of mitochondrial membrane potential, cytochrome c release, and caspase-9 and caspase-3 activation. Fluorouracil 38-42 tumor protein p53 Homo sapiens 51-54 29868263-8 2018 Exogenous expression of SNX1 inhibited the growth, migration, invasion and promoted the apoptosis and enhanced the sensitivity of GC cells to the chemotherapeutic drug 5-Fluorouracil (5-Fu) in vitro, while knockdown of SNX1 by short hairpin RNA (shRNA) significantly promoted the growth, migration, invasion and reduced the apoptosis and the sensitivity of GC cells to 5-Fu. Fluorouracil 184-188 sorting nexin 1 Homo sapiens 24-28 29868263-8 2018 Exogenous expression of SNX1 inhibited the growth, migration, invasion and promoted the apoptosis and enhanced the sensitivity of GC cells to the chemotherapeutic drug 5-Fluorouracil (5-Fu) in vitro, while knockdown of SNX1 by short hairpin RNA (shRNA) significantly promoted the growth, migration, invasion and reduced the apoptosis and the sensitivity of GC cells to 5-Fu. Fluorouracil 369-373 sorting nexin 1 Homo sapiens 24-28 29872316-7 2018 Apatinib combined with the aforementioned drugs, especially the combination of Apatinib and 5-FU, decreased the invasion and migration ability of the cells and increased the apoptosis ratio; expression of the anti-apoptotic protein Bcl-2 significantly decreased, and expression of the pro-apoptotic protein Bax increased. Fluorouracil 92-96 BCL2 apoptosis regulator Homo sapiens 232-237 29872316-7 2018 Apatinib combined with the aforementioned drugs, especially the combination of Apatinib and 5-FU, decreased the invasion and migration ability of the cells and increased the apoptosis ratio; expression of the anti-apoptotic protein Bcl-2 significantly decreased, and expression of the pro-apoptotic protein Bax increased. Fluorouracil 92-96 BCL2 associated X, apoptosis regulator Homo sapiens 307-310 29844931-0 2018 Dasatinib reduces 5-Fu-triggered apoptosis in colon carcinoma by directly modulating Src-dependent caspase-9 phosphorylation. Fluorouracil 18-22 SRC proto-oncogene, non-receptor tyrosine kinase Homo sapiens 85-88 29844931-6 2018 Dasatinib dramatically decreased 5-Fu triggered apoptosis in colon carcinoma via suppression of Src activation. Fluorouracil 33-37 SRC proto-oncogene, non-receptor tyrosine kinase Homo sapiens 96-99 29845757-10 2018 Adjusted pathway analyses showed significant associations for pyrimidine biosynthesis (P = 0.04) and fluorouracil drug metabolism (P < 0.01) with significant gene-chemotherapy interactions, including PON1 rs3917538. Fluorouracil 101-113 paraoxonase 1 Homo sapiens 203-207 29756138-8 2018 Our results showed that CMP in combination with 5-FU reversed intestinal shortening (p < 0.01) and alleviated 5-FU-induced colon injury (p < 0.001) via suppression of ROS production; increasing the levels of CAT, GSH-Px and GSH; decreasing expression of NF-kappaB, p-p38 and Bax; and elevating the levels of Nrf2 and Bcl-2. Fluorouracil 48-52 nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105 Mus musculus 260-269 29756138-8 2018 Our results showed that CMP in combination with 5-FU reversed intestinal shortening (p < 0.01) and alleviated 5-FU-induced colon injury (p < 0.001) via suppression of ROS production; increasing the levels of CAT, GSH-Px and GSH; decreasing expression of NF-kappaB, p-p38 and Bax; and elevating the levels of Nrf2 and Bcl-2. Fluorouracil 48-52 nuclear factor, erythroid derived 2, like 2 Mus musculus 314-318 29756138-8 2018 Our results showed that CMP in combination with 5-FU reversed intestinal shortening (p < 0.01) and alleviated 5-FU-induced colon injury (p < 0.001) via suppression of ROS production; increasing the levels of CAT, GSH-Px and GSH; decreasing expression of NF-kappaB, p-p38 and Bax; and elevating the levels of Nrf2 and Bcl-2. Fluorouracil 48-52 B cell leukemia/lymphoma 2 Mus musculus 323-328 29795190-4 2018 Enforced miR-181a expression enhanced 5-FU-induced p53-dependent mitochondrial apoptosis, including declined Bcl-2/Bax ratio, loss of mitochondrial membrane potential, cytochrome c release, and caspase-9 and caspase-3 activation. Fluorouracil 38-42 BCL2 apoptosis regulator Homo sapiens 109-114 29795190-4 2018 Enforced miR-181a expression enhanced 5-FU-induced p53-dependent mitochondrial apoptosis, including declined Bcl-2/Bax ratio, loss of mitochondrial membrane potential, cytochrome c release, and caspase-9 and caspase-3 activation. Fluorouracil 38-42 BCL2 associated X, apoptosis regulator Homo sapiens 115-118 29795190-4 2018 Enforced miR-181a expression enhanced 5-FU-induced p53-dependent mitochondrial apoptosis, including declined Bcl-2/Bax ratio, loss of mitochondrial membrane potential, cytochrome c release, and caspase-9 and caspase-3 activation. Fluorouracil 38-42 cytochrome c, somatic Homo sapiens 168-180 29795190-4 2018 Enforced miR-181a expression enhanced 5-FU-induced p53-dependent mitochondrial apoptosis, including declined Bcl-2/Bax ratio, loss of mitochondrial membrane potential, cytochrome c release, and caspase-9 and caspase-3 activation. Fluorouracil 38-42 caspase 3 Homo sapiens 208-217 29795190-5 2018 However, inhibition of miR-181a was associated with reduced p53-mediated mitochondrial apoptosis induced by 5-FU. Fluorouracil 108-112 tumor protein p53 Homo sapiens 60-63 29795190-9 2018 In conclusion, these results demonstrate that miR-181a increases p53 protein expression and transcriptional activity by targeting BIRC6 and promotes 5-FU-induced apoptosis in mesangial cells. Fluorouracil 149-153 tumor protein p53 Homo sapiens 65-68 29738539-6 2018 We found that HMS1, LOG1 (YJL055W), HAM1, and ATR1 confer resistance to both 5-FU and HAP, whereas ADE4, DUT1 and APT2 are specific for HAP resistance, and CPA1 and CPA2 specific for 5-FU resistance. Fluorouracil 77-81 borate transporter Saccharomyces cerevisiae S288C 46-50 29601890-9 2018 Only 5-Fu or the knockdown of RPA1 suppressed cell clone formation, induced cell cycle arrest at the G1 phase and promoted cell apoptosis by regulating the protein level of Caspase 3. Fluorouracil 5-9 caspase 3 Homo sapiens 173-182 29725400-6 2018 In 84 stage II and III patients who were administered 5-fluorouracil-based adjuvant chemotherapy, positive AQP1 expression was associated with an increased DFS rate compared with that of AQP1-negative patients (P=0.05). Fluorouracil 54-68 aquaporin 1 (Colton blood group) Homo sapiens 107-111 29695766-0 2018 Vinorelbine, cyclophosphamide and 5-FU effects on the circulating and intratumoural landscape of immune cells improve anti-PD-L1 efficacy in preclinical models of breast cancer and lymphoma. Fluorouracil 34-38 CD274 antigen Mus musculus 123-128 29695766-7 2018 Vinorelbine, cyclophosphamide and 5-FU reduced circulating APCs. Fluorouracil 34-38 amyloid P component, serum Mus musculus 59-63 29695766-15 2018 CONCLUSIONS: Vinorelbine, cyclophosphamide and 5-FU have significant preclinical effects on circulating and tumour-infiltrating immune cells and can be used to obtain synergy with anti-PD-L1. Fluorouracil 47-51 CD274 antigen Mus musculus 185-190 29210057-10 2018 Further functional assays demonstrated that TFF1 could increase the chemosensitivity of 5-FU by modulating NF-kappaB targeted genes. Fluorouracil 88-92 trefoil factor 1 Homo sapiens 44-48 29921390-9 2018 The percentage of cell apoptosis increased, and the Western blot showed that the expression of caspase-3, caspase-8, and c-myc, respectively, in the semi-combination group, the 5-Fluorouracil group, and the combination group increased successively and that the successive increasing of c-myc was the most significant. Fluorouracil 177-191 caspase 3 Homo sapiens 95-104 31938347-2 2018 In addition, susceptibility of HNSCC cells to 5-FU was compromised in the presence of cyclooxygenase 2 (COX2)-derived prostaglandin E2 (PGE2). Fluorouracil 46-50 prostaglandin-endoperoxide synthase 2 Homo sapiens 86-102 31938347-2 2018 In addition, susceptibility of HNSCC cells to 5-FU was compromised in the presence of cyclooxygenase 2 (COX2)-derived prostaglandin E2 (PGE2). Fluorouracil 46-50 prostaglandin-endoperoxide synthase 2 Homo sapiens 104-108 29512753-11 2018 Additionally, a Cell Counting Kit-8 assay demonstrated that specific inhibitors of NOS3 and BDNF/neurotrophic receptor tyrosine kinase, type 2 signaling reduced the IC50 of MCF-7/MDR cells in response to various anticancer drugs, including adriamycin, cisplatin and 5-fluorouracil. Fluorouracil 266-280 nitric oxide synthase 3 Homo sapiens 83-87 29725425-5 2018 In the present study, the role of Lin28B in the chemosensitivity of colon cancer cells to 5-fluorouracil (5-FU) was detected by establishing a Lin28B over-expressing HCT116 (EGFP-Lin28B-HCT116) cell line. Fluorouracil 90-104 lin-28 homolog B Homo sapiens 34-40 29725425-5 2018 In the present study, the role of Lin28B in the chemosensitivity of colon cancer cells to 5-fluorouracil (5-FU) was detected by establishing a Lin28B over-expressing HCT116 (EGFP-Lin28B-HCT116) cell line. Fluorouracil 90-104 lin-28 homolog B Homo sapiens 143-149 29725425-5 2018 In the present study, the role of Lin28B in the chemosensitivity of colon cancer cells to 5-fluorouracil (5-FU) was detected by establishing a Lin28B over-expressing HCT116 (EGFP-Lin28B-HCT116) cell line. Fluorouracil 90-104 lin-28 homolog B Homo sapiens 143-149 29725425-5 2018 In the present study, the role of Lin28B in the chemosensitivity of colon cancer cells to 5-fluorouracil (5-FU) was detected by establishing a Lin28B over-expressing HCT116 (EGFP-Lin28B-HCT116) cell line. Fluorouracil 106-110 lin-28 homolog B Homo sapiens 34-40 29725425-5 2018 In the present study, the role of Lin28B in the chemosensitivity of colon cancer cells to 5-fluorouracil (5-FU) was detected by establishing a Lin28B over-expressing HCT116 (EGFP-Lin28B-HCT116) cell line. Fluorouracil 106-110 lin-28 homolog B Homo sapiens 143-149 29725400-6 2018 In 84 stage II and III patients who were administered 5-fluorouracil-based adjuvant chemotherapy, positive AQP1 expression was associated with an increased DFS rate compared with that of AQP1-negative patients (P=0.05). Fluorouracil 54-68 aquaporin 1 (Colton blood group) Homo sapiens 187-191 29725425-5 2018 In the present study, the role of Lin28B in the chemosensitivity of colon cancer cells to 5-fluorouracil (5-FU) was detected by establishing a Lin28B over-expressing HCT116 (EGFP-Lin28B-HCT116) cell line. Fluorouracil 106-110 lin-28 homolog B Homo sapiens 143-149 29725425-8 2018 It was demonstrated that overexpression of Lin28B improved the chemotherapeutic sensitivity of colon cancer cells to 5-FU. Fluorouracil 117-121 lin-28 homolog B Homo sapiens 43-49 29725400-8 2018 This suggests that the expression of AQP1 may be a candidate biomarker predictive of response to 5-fluorouracil-based adjuvant chemotherapy following surgery in patients with stage II and III CRC. Fluorouracil 97-111 aquaporin 1 (Colton blood group) Homo sapiens 37-41 29725425-9 2018 Additional investigation revealed that Lin28B enhanced the chemosensitivity of colon cancer cells by promoting cell apoptosis induced by 5-FU; however, this effect was independent of Lin28B inhibiting the biogenesis of let-7, the well-known target of Lin28B. Fluorouracil 137-141 lin-28 homolog B Homo sapiens 39-45 29849804-8 2018 Additionally, bufalin combined with 5-FU reduced the expression levels of anti-apoptotic proteins, such as Mcl-1, XIAP and Bcl-2 and upregulated the levels of the pro-apoptotic proteins, Bax and Bad. Fluorouracil 36-40 BCL2 apoptosis regulator Homo sapiens 123-128 29849804-8 2018 Additionally, bufalin combined with 5-FU reduced the expression levels of anti-apoptotic proteins, such as Mcl-1, XIAP and Bcl-2 and upregulated the levels of the pro-apoptotic proteins, Bax and Bad. Fluorouracil 36-40 BCL2 associated X, apoptosis regulator Homo sapiens 187-190 29849804-10 2018 It was determined that the synergistic effect between 5-FU and bufalin was diminished following the silencing of Bax. Fluorouracil 54-58 BCL2 associated X, apoptosis regulator Homo sapiens 113-116 29713498-1 2018 Background: In the RAISE trial, ramucirumab+leucovorin/fluorouracil/irinotecan (FOLFIRI) improved the median overall survival (mOS) of patients with previously treated metastatic colorectal cancer versus patients treated with placebo+FOLFIRI but had a higher incidence of neutropaenia, leading to more chemotherapy dose modifications and discontinuations. Fluorouracil 55-67 Moloney sarcoma oncogene Mus musculus 127-130 29695684-9 2018 Moreover, 5-fluorouracil plus circularly permuted tumor necrosis factor-related apoptosis-inducing ligand increased apoptosis-related protein levels such as cleaved caspase-3, caspase-8, and poly-ADP-ribose polymerase and downregulated that of the survival protein B-cell lymphoma-extra-large. Fluorouracil 10-24 caspase 3 Homo sapiens 165-174 29695684-9 2018 Moreover, 5-fluorouracil plus circularly permuted tumor necrosis factor-related apoptosis-inducing ligand increased apoptosis-related protein levels such as cleaved caspase-3, caspase-8, and poly-ADP-ribose polymerase and downregulated that of the survival protein B-cell lymphoma-extra-large. Fluorouracil 10-24 poly(ADP-ribose) polymerase 1 Homo sapiens 191-217 29735329-0 2018 DNA methylation-mediated repression of miR-181a/135a/302c expression promotes the microsatellite-unstable colorectal cancer development and 5-FU resistance via targeting PLAG1. Fluorouracil 140-144 PLAG1 zinc finger Homo sapiens 170-175 30111992-1 2018 Background: 5-Fluorouracil (5-FU) is a pyrimidine analogue which selectively inhibits DNA synthesis, RNA synthesis, and VEGF antibodies. Fluorouracil 12-26 vascular endothelial growth factor A Homo sapiens 120-124 30111992-1 2018 Background: 5-Fluorouracil (5-FU) is a pyrimidine analogue which selectively inhibits DNA synthesis, RNA synthesis, and VEGF antibodies. Fluorouracil 28-32 vascular endothelial growth factor A Homo sapiens 120-124 29499490-2 2018 Among them, derivative 5h was more potent than the positive control 5-fluorouracil (5-Fu) on HepG-2, QGY-7703 and SMMC-7721 with IC50 values of 7.51, 3.06 and 4.08 muM, respectively. Fluorouracil 84-88 latexin Homo sapiens 164-167 29719589-4 2018 IFN expressed from OAd-hamIFN potentiated the cytotoxicity of radiation and chemotherapy (5-FU, Gemcitabine, and Cisplatin), and enhanced pancreatic cancer cell death in both in vitro and in vivo experimental settings. Fluorouracil 90-94 interferon alpha 1 Homo sapiens 0-3 29731993-0 2018 Over-activation of AKT signaling leading to 5-Fluorouracil resistance in SNU-C5/5-FU cells. Fluorouracil 44-58 AKT serine/threonine kinase 1 Homo sapiens 19-22 29731993-1 2018 Here, we investigated whether over-activation of AKT pathway is important in the resistance to 5-fluorouracil (5-FU) in SNU-C5/5-FU cells, 5-FU-resistant human colon cancer cells. Fluorouracil 95-109 AKT serine/threonine kinase 1 Homo sapiens 49-52 29731993-1 2018 Here, we investigated whether over-activation of AKT pathway is important in the resistance to 5-fluorouracil (5-FU) in SNU-C5/5-FU cells, 5-FU-resistant human colon cancer cells. Fluorouracil 111-115 AKT serine/threonine kinase 1 Homo sapiens 49-52 29731993-1 2018 Here, we investigated whether over-activation of AKT pathway is important in the resistance to 5-fluorouracil (5-FU) in SNU-C5/5-FU cells, 5-FU-resistant human colon cancer cells. Fluorouracil 127-131 AKT serine/threonine kinase 1 Homo sapiens 49-52 29731993-1 2018 Here, we investigated whether over-activation of AKT pathway is important in the resistance to 5-fluorouracil (5-FU) in SNU-C5/5-FU cells, 5-FU-resistant human colon cancer cells. Fluorouracil 127-131 AKT serine/threonine kinase 1 Homo sapiens 49-52 29731993-10 2018 These data suggest that inhibition of AKT activation may overcome 5-FU-resistance in SNU-C5/5-FU cells. Fluorouracil 66-70 AKT serine/threonine kinase 1 Homo sapiens 38-41 29731993-10 2018 These data suggest that inhibition of AKT activation may overcome 5-FU-resistance in SNU-C5/5-FU cells. Fluorouracil 92-96 AKT serine/threonine kinase 1 Homo sapiens 38-41 29719602-6 2018 In addition, leptin reduced the 5-FU effects on apoptosis by decreasing pro-apoptotic (Bax, Caspase-3 activation and PARP degradation) and increasing anti-apoptotic factors (RIP and Bcl-XL). Fluorouracil 32-36 BCL2 associated X, apoptosis regulator Homo sapiens 87-90 29719602-6 2018 In addition, leptin reduced the 5-FU effects on apoptosis by decreasing pro-apoptotic (Bax, Caspase-3 activation and PARP degradation) and increasing anti-apoptotic factors (RIP and Bcl-XL). Fluorouracil 32-36 caspase 3 Homo sapiens 92-101 29719602-6 2018 In addition, leptin reduced the 5-FU effects on apoptosis by decreasing pro-apoptotic (Bax, Caspase-3 activation and PARP degradation) and increasing anti-apoptotic factors (RIP and Bcl-XL). Fluorouracil 32-36 BCL2 like 1 Homo sapiens 182-188 29496692-6 2018 ILK inhibition increases sensitivity of resistant cells to 5-FU and oxaliplatin and reduces the levels of EMT and CSC markers in 5-FU resistant cells. Fluorouracil 59-63 integrin linked kinase Homo sapiens 0-3 29480364-4 2018 The effect of radiation, 5-fluorouracil (5-Fu), and gefitinib on the EGFR, AKT, and ERK1/2 activation in H1975 cells was determined by Western blot. Fluorouracil 25-39 mitogen-activated protein kinase 3 Homo sapiens 84-90 29480364-4 2018 The effect of radiation, 5-fluorouracil (5-Fu), and gefitinib on the EGFR, AKT, and ERK1/2 activation in H1975 cells was determined by Western blot. Fluorouracil 41-45 epidermal growth factor receptor Homo sapiens 69-73 29480364-4 2018 The effect of radiation, 5-fluorouracil (5-Fu), and gefitinib on the EGFR, AKT, and ERK1/2 activation in H1975 cells was determined by Western blot. Fluorouracil 41-45 mitogen-activated protein kinase 3 Homo sapiens 84-90 29484395-2 2018 We have previously demonstrated that ATP synthase-coupling factor 6, mitochondrial (ATP5J) is associated with CRC migration and 5-fluorouracil resistance; nevertheless, the exact molecular mechanism remains unclear. Fluorouracil 128-142 ATP synthase peripheral stalk subunit F6 Homo sapiens 84-89 29556386-5 2018 For example, miR-34a attenuates the chemoresistance of colon cancer to 5-FU by inhibiting E2F3 and SIRT1. Fluorouracil 71-75 E2F transcription factor 3 Homo sapiens 90-94 29514732-3 2018 Drug-induced PARP inhibition potentiates the activity of anticancer drugs such as 5-fluorouracil in enhancing DNA damage, whose repair involves PARP-1 activity. Fluorouracil 82-96 poly(ADP-ribose) polymerase 1 Homo sapiens 13-17 29514732-3 2018 Drug-induced PARP inhibition potentiates the activity of anticancer drugs such as 5-fluorouracil in enhancing DNA damage, whose repair involves PARP-1 activity. Fluorouracil 82-96 poly(ADP-ribose) polymerase 1 Homo sapiens 144-150 29514732-9 2018 Our results show that the novel PARP inhibitor HYDAMTIQ potently inhibits the growth of human tumor cells with defective DNA damage response pathways and exerts synergistic cytotoxicity in combination with 5-fluorouracil. Fluorouracil 206-220 poly(ADP-ribose) polymerase 1 Homo sapiens 32-36 29599307-11 2018 Cyclin D1 expression was decreased and E-cadherin expression was increased by irinotecan, 5-FU and all three doses of EEG. Fluorouracil 90-94 cadherin 1 Homo sapiens 39-49 29861605-8 2018 Results: 5-Fu/oxaliplatin exerted no significant effect on the expression of the stimulating phenotypes of DCs in vitro, while it could reduce the expression of programmed death ligand 1/2 (PD-L1/L2) and promote interleukin-12 (IL-12) secretion by DCs. Fluorouracil 9-13 CD274 antigen Mus musculus 190-195 29861605-10 2018 5-Fu/oxaliplatin further enhanced the stimulating phenotypic expression of DCs in tumor bearing mice, decreased PD-L1/L2 expression, and specifically activated the lymphocytes. Fluorouracil 0-4 CD274 antigen Mus musculus 112-117 29861605-12 2018 Conclusions: 5-Fu/oxaliplatin decreased the expression of the DC inhibitory phenotypes PD-L1/L2, promoted DC phenotypic maturation in tumor bearing mice, activated the lymphocytes of tumor bearing mice, and exerted synergistic effects with the CD1d-MC38/alpha-GC colon cancer tumor vaccine. Fluorouracil 13-17 CD274 antigen Mus musculus 87-92 29861605-12 2018 Conclusions: 5-Fu/oxaliplatin decreased the expression of the DC inhibitory phenotypes PD-L1/L2, promoted DC phenotypic maturation in tumor bearing mice, activated the lymphocytes of tumor bearing mice, and exerted synergistic effects with the CD1d-MC38/alpha-GC colon cancer tumor vaccine. Fluorouracil 13-17 CD1d1 antigen Mus musculus 244-248 29636622-0 2018 miR-206 regulates 5-FU resistance by targeting Bcl-2 in colon cancer cells. Fluorouracil 18-22 microRNA 206 Homo sapiens 0-7 29636622-0 2018 miR-206 regulates 5-FU resistance by targeting Bcl-2 in colon cancer cells. Fluorouracil 18-22 BCL2 apoptosis regulator Homo sapiens 47-52 29636622-3 2018 The current study aimed to explore the potential function of miR-206 in 5-FU resistance. Fluorouracil 72-76 microRNA 206 Homo sapiens 61-68 29636622-5 2018 miR-206 mimic was transfected to 5-FU-FR CRC, and the 5-FU sensitivity was detected by MTS and flow cytometry. Fluorouracil 33-37 microRNA 206 Homo sapiens 0-7 29636622-9 2018 We also identified miR-206 targeting Bcl-2 directly in CRC, which is required for miR-206 mediated-5-FU resistance. Fluorouracil 99-103 microRNA 206 Homo sapiens 19-26 29636622-9 2018 We also identified miR-206 targeting Bcl-2 directly in CRC, which is required for miR-206 mediated-5-FU resistance. Fluorouracil 99-103 BCL2 apoptosis regulator Homo sapiens 37-42 29636622-9 2018 We also identified miR-206 targeting Bcl-2 directly in CRC, which is required for miR-206 mediated-5-FU resistance. Fluorouracil 99-103 microRNA 206 Homo sapiens 82-89 29560281-4 2018 5-FU increased both the expression and secretion levels of TGF-beta1 in hepatoma cells, but not in normal hepatocytes. Fluorouracil 0-4 transforming growth factor beta 1 Homo sapiens 59-68 29560281-8 2018 Conversely, 5-FU stimulated the phosphorylation of extracellular signal-regulated kinase (ERK)1/2. Fluorouracil 12-16 mitogen-activated protein kinase 1 Homo sapiens 51-97 29560281-9 2018 Accordingly, the protein levels of E-cadherin and claudin-1 were reduced in 5-FU-treated cells. Fluorouracil 76-80 cadherin 1 Homo sapiens 35-45 29560281-10 2018 The combination of 5-FU and IFNalpha-2b, and the inhibition of ERK1/2 by a specific inhibitor neutralized the effects of 5-FU on TGF-beta-related signaling molecules and restored their protein levels to those observed in the control. Fluorouracil 121-125 mitogen-activated protein kinase 3 Homo sapiens 63-69 29560281-10 2018 The combination of 5-FU and IFNalpha-2b, and the inhibition of ERK1/2 by a specific inhibitor neutralized the effects of 5-FU on TGF-beta-related signaling molecules and restored their protein levels to those observed in the control. Fluorouracil 121-125 transforming growth factor beta 1 Homo sapiens 129-137 29560281-11 2018 Interestingly, the phosphorylated protein levels of SMAD2 and the total protein levels of E-cadherin and p15INK4b were increased in 5-FU-stimulated HuH-7 cells, but not in Hep G2 cells. Fluorouracil 132-136 cadherin 1 Homo sapiens 90-100 29560281-11 2018 Interestingly, the phosphorylated protein levels of SMAD2 and the total protein levels of E-cadherin and p15INK4b were increased in 5-FU-stimulated HuH-7 cells, but not in Hep G2 cells. Fluorouracil 132-136 cyclin dependent kinase inhibitor 2B Homo sapiens 105-113 29560281-12 2018 Our data suggest that the higher efficacy of the 5-FU and IFNalpha-2b combination therapy was associated with the regulation of TGF-beta expression, secretion, and the signals mediated by it. Fluorouracil 49-53 transforming growth factor beta 1 Homo sapiens 128-136 29061341-9 2018 5-FU-resistant cells exhibited decreased sensitivity to the CBS inhibitor aminooxyacetate (AOAA) in terms of suppression of cell viability, inhibition of cell proliferation and inhibition of oxidative phosphorylation. Fluorouracil 0-4 cystathionine beta-synthase Homo sapiens 60-63 29496692-6 2018 ILK inhibition increases sensitivity of resistant cells to 5-FU and oxaliplatin and reduces the levels of EMT and CSC markers in 5-FU resistant cells. Fluorouracil 129-133 integrin linked kinase Homo sapiens 0-3 29458395-0 2018 Herbal formula Huang Qin Ge Gen Tang enhances 5-fluorouracil antitumor activity through modulation of the E2F1/TS pathway. Fluorouracil 46-60 forkhead box G1 Homo sapiens 21-24 29203613-7 2018 Furthermore, Nfe2l1-KD cells were resistant to damage by the chemotherapeutic drugs STZ and 5-fluorouracil, which was linked to binding of hexokinase 1 with mitochondria, enhanced mitochondrial membrane potential and closed mitochondrial potential transition pore. Fluorouracil 92-106 nuclear factor, erythroid derived 2,-like 1 Mus musculus 13-19 29331856-0 2018 Schizandrin A enhances chemosensitivity of colon carcinoma cells to 5-fluorouracil through up-regulation of miR-195. Fluorouracil 68-82 microRNA 195 Homo sapiens 108-115 29331856-9 2018 Moreover, we explored that miR-195 was up-regulated by SchA; and overexpression of miR-195 reduced cell viability and sensitized 5-FU-resistant HCT116 and SW480 cells to 5-FU. Fluorouracil 129-133 microRNA 195 Homo sapiens 27-34 29331856-9 2018 Moreover, we explored that miR-195 was up-regulated by SchA; and overexpression of miR-195 reduced cell viability and sensitized 5-FU-resistant HCT116 and SW480 cells to 5-FU. Fluorouracil 129-133 microRNA 195 Homo sapiens 83-90 29331856-9 2018 Moreover, we explored that miR-195 was up-regulated by SchA; and overexpression of miR-195 reduced cell viability and sensitized 5-FU-resistant HCT116 and SW480 cells to 5-FU. Fluorouracil 170-174 microRNA 195 Homo sapiens 27-34 29331856-9 2018 Moreover, we explored that miR-195 was up-regulated by SchA; and overexpression of miR-195 reduced cell viability and sensitized 5-FU-resistant HCT116 and SW480 cells to 5-FU. Fluorouracil 170-174 microRNA 195 Homo sapiens 83-90 29331856-11 2018 Thus it was speculated that SchA might enhance cell chemosensitivity to 5-FU by up-regulating miR-195. Fluorouracil 72-76 microRNA 195 Homo sapiens 94-101 29331856-13 2018 Our results suggested that SchA sensitized 5-FU-resistant colon carcinoma cells to 5-FU by up-regulating miR-195. Fluorouracil 43-47 microRNA 195 Homo sapiens 105-112 29331856-13 2018 Our results suggested that SchA sensitized 5-FU-resistant colon carcinoma cells to 5-FU by up-regulating miR-195. Fluorouracil 83-87 microRNA 195 Homo sapiens 105-112 29467857-9 2018 miR-15 promoted apoptosis in colon cancer cells treated with 5-Fu and OX by inhibiting the expression of p50, which repressed the expression of B cell lymphoma-2 and B cell lymphoma-extra large; two direct target genes of nuclear factor-kappaB with anti-apoptotic functions. Fluorouracil 61-65 nuclear factor kappa B subunit 1 Homo sapiens 105-108 29155481-7 2018 The RGZ reduced leukocyte infiltration, preserved tissue structure, and dampened the 5-FU-induced expression of p53 and matrix metalloproteinase (Mmp)-2 after 5 days, and of Mmp-2 and interleukin (Il-1beta after 15 days. Fluorouracil 85-89 interleukin 1 beta Mus musculus 197-205 29155481-8 2018 The RGZ inhibited the 5-FU-induced increase of transforming growth factor-beta (TGF-beta) and nuclear factor-kappa B (NF-kappaB) proteins and restored collagen protein levels. Fluorouracil 22-26 nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105 Mus musculus 94-116 29155481-8 2018 The RGZ inhibited the 5-FU-induced increase of transforming growth factor-beta (TGF-beta) and nuclear factor-kappa B (NF-kappaB) proteins and restored collagen protein levels. Fluorouracil 22-26 nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105 Mus musculus 118-127 29330293-7 2018 The LIN28B-long isoform-expressing cells demonstrated increased drug resistance to 5-fluorouracil and cisplatin through the upregulation of ERCC1, a DNA repair gene, in a LET-7-dependent manner. Fluorouracil 83-97 lin-28 homolog B Homo sapiens 4-10 29434452-1 2018 AIM: To investigate the predictive value of PIK3CA and TP53 mutation status in colorectal cancer (CRC) patients treated with 5-fluorouracil-based chemotherapy. Fluorouracil 125-139 phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha Homo sapiens 44-50 29434452-12 2018 CONCLUSION: Double mutation of PIK3CA and TP53 is correlated with a shorter OS in stage II/III CRC patients treated with 5-fluorouracil-based therapy. Fluorouracil 121-135 phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha Homo sapiens 31-37 29434452-12 2018 CONCLUSION: Double mutation of PIK3CA and TP53 is correlated with a shorter OS in stage II/III CRC patients treated with 5-fluorouracil-based therapy. Fluorouracil 121-135 tumor protein p53 Homo sapiens 42-46 29434452-1 2018 AIM: To investigate the predictive value of PIK3CA and TP53 mutation status in colorectal cancer (CRC) patients treated with 5-fluorouracil-based chemotherapy. Fluorouracil 125-139 tumor protein p53 Homo sapiens 55-59 29042284-5 2018 Furthermore, Se-GP11 could enhance the immune functions during the tumor inhibition process of 5-Fu for increasing the cytokines secretion (IL-2 and TNF-alpha) and immune organs weights. Fluorouracil 95-99 tumor necrosis factor Mus musculus 149-158 29568368-3 2018 We evaluated the in vitro and in vivo efficacy and mechanisms of action of FTD and FTD/TPI against 5-fluorouracil (5-FU)-resistant MKN45/5FU, MKN74/5FU, and KATOIII/5FU human gastric cancer cells overexpressing thymidylate synthase (TS) and their respective parent cell lines. Fluorouracil 99-113 triosephosphate isomerase 1 Homo sapiens 87-90 29568368-3 2018 We evaluated the in vitro and in vivo efficacy and mechanisms of action of FTD and FTD/TPI against 5-fluorouracil (5-FU)-resistant MKN45/5FU, MKN74/5FU, and KATOIII/5FU human gastric cancer cells overexpressing thymidylate synthase (TS) and their respective parent cell lines. Fluorouracil 115-119 triosephosphate isomerase 1 Homo sapiens 87-90 29568368-10 2018 Thus, FTD/TPI is a promising chemotherapeutic agent against gastric cancers recurring following 5-FU therapy. Fluorouracil 96-100 triosephosphate isomerase 1 Homo sapiens 10-13 29175872-10 2018 Inhibition of the Notch pathway, using a gamma secretase inhibitor (GSI), enhanced the sensitivity of INS CSC-like cells to 5-FU. Fluorouracil 124-128 notch receptor 2 Homo sapiens 18-23 29175872-9 2018 Protein analysis showed an active NOTCH2-HES1 signalling in INS cell lines, especially in cells resistant to 5-FU. Fluorouracil 109-113 notch receptor 2 Homo sapiens 34-40 29305271-0 2018 Sulforaphane and 5-fluorouracil synergistically inducing autophagy in breast cancer: A possible role for the Nrf2-Keap1-ARE signaling? Fluorouracil 17-31 kelch like ECH associated protein 1 Homo sapiens 114-119 29434918-5 2018 Furthermore, knockdown of Arf6 was associated with elevated chemosensitivity of SGC-7901 cells to 5-fluorouracil through inactivation of the ERK1/2 signaling pathway. Fluorouracil 98-112 sarcoglycan beta Homo sapiens 80-83 29275107-0 2018 Transferrin targeted liposomal 5-fluorouracil induced apoptosis via mitochondria signaling pathway in cancer cells. Fluorouracil 31-45 transferrin Homo sapiens 0-11 29434918-5 2018 Furthermore, knockdown of Arf6 was associated with elevated chemosensitivity of SGC-7901 cells to 5-fluorouracil through inactivation of the ERK1/2 signaling pathway. Fluorouracil 98-112 mitogen-activated protein kinase 3 Homo sapiens 141-147 29141899-2 2018 Though distinct in their mechanisms of action, doxorubicin, paclitaxel, and 5-FU all induce rapid and robust upregulation of atypical G protein Gbeta5 in the myocardium correlating with oxidative stress, myocyte apoptosis, and the accumulation of proinflammatory and profibrotic cytokines. Fluorouracil 76-80 G protein subunit beta 5 Homo sapiens 144-150 29275107-1 2018 The purpose of this study was to prepare transferrin (Tf) targeted liposomal 5-Fluorouracil (5FU) to improve the safety and efficacy of the drug. Fluorouracil 77-91 transferrin Homo sapiens 41-52 28962868-7 2018 In addition, it avoided the release of cytochrome c from mitochondria to the cytoplasm in cells exposed to 5-FU, and restored their proliferative activity via Ki-67 expression. Fluorouracil 107-111 cytochrome c, somatic Homo sapiens 39-51 28962868-8 2018 Furthermore, FITOPROT regulated 5-FU-induced oxidative stress via Nrf2 involvement. Fluorouracil 32-36 NFE2 like bZIP transcription factor 2 Homo sapiens 66-70 29086459-11 2018 In humans, the expression of EGFR is increased in patients with colorectal cancer treated with 5-FU compared with cancer patients not on 5-FU. Fluorouracil 95-99 epidermal growth factor receptor Homo sapiens 29-33 29086459-11 2018 In humans, the expression of EGFR is increased in patients with colorectal cancer treated with 5-FU compared with cancer patients not on 5-FU. Fluorouracil 137-141 epidermal growth factor receptor Homo sapiens 29-33 29054700-0 2018 Rebamipide suppresses 5-fluorouracil-induced cell death via the activation of Akt/mTOR pathway and regulates the expression of Bcl-2 family proteins. Fluorouracil 22-36 AKT serine/threonine kinase 1 Homo sapiens 78-81 29054700-0 2018 Rebamipide suppresses 5-fluorouracil-induced cell death via the activation of Akt/mTOR pathway and regulates the expression of Bcl-2 family proteins. Fluorouracil 22-36 mechanistic target of rapamycin kinase Homo sapiens 82-86 29054700-8 2018 This is in contrast to 5-FU-induced suppression of Akt and mTOR activation, Bcl-2 and Bcl-xL expressions, and the enhanced expression of Bax and Bim. Fluorouracil 23-27 AKT serine/threonine kinase 1 Homo sapiens 51-54 29054700-8 2018 This is in contrast to 5-FU-induced suppression of Akt and mTOR activation, Bcl-2 and Bcl-xL expressions, and the enhanced expression of Bax and Bim. Fluorouracil 23-27 mechanistic target of rapamycin kinase Homo sapiens 59-63 29054700-8 2018 This is in contrast to 5-FU-induced suppression of Akt and mTOR activation, Bcl-2 and Bcl-xL expressions, and the enhanced expression of Bax and Bim. Fluorouracil 23-27 BCL2 apoptosis regulator Homo sapiens 76-81 29054700-8 2018 This is in contrast to 5-FU-induced suppression of Akt and mTOR activation, Bcl-2 and Bcl-xL expressions, and the enhanced expression of Bax and Bim. Fluorouracil 23-27 BCL2 like 1 Homo sapiens 86-92 29054700-8 2018 This is in contrast to 5-FU-induced suppression of Akt and mTOR activation, Bcl-2 and Bcl-xL expressions, and the enhanced expression of Bax and Bim. Fluorouracil 23-27 BCL2 associated X, apoptosis regulator Homo sapiens 137-140 29341150-10 2018 Akt activation was also confirmed in the radioresistant cell line SW480, and a 50 per cent improvement in sensitivity to CRT was observed in vitro and in vivo when SW480 cells were exposed to the Akt inhibitor MK2206 in combination with radiation and 5-fluorouracil. Fluorouracil 251-265 AKT serine/threonine kinase 1 Homo sapiens 0-3 29583038-0 2018 Dishevelled 1, a pivotal positive regulator of the Wnt signalling pathway, mediates 5-fluorouracil resistance in HepG2 cells. Fluorouracil 84-98 dishevelled segment polarity protein 1 Homo sapiens 0-13 29583038-6 2018 Silencing DVL1 using siDVL1 or other small molecular inhibitors in HepG2/5-FU cells could restore 5-FU responsiveness via reduced cell proliferation and migration, and increased apoptosis. Fluorouracil 73-77 dishevelled segment polarity protein 1 Homo sapiens 10-14 29583038-6 2018 Silencing DVL1 using siDVL1 or other small molecular inhibitors in HepG2/5-FU cells could restore 5-FU responsiveness via reduced cell proliferation and migration, and increased apoptosis. Fluorouracil 98-102 dishevelled segment polarity protein 1 Homo sapiens 10-14 29583038-8 2018 Collectively, our results provide the first clue towards understanding the contribution of DVL1-mediated acquired resistance to 5-FU in HepG2/5-FU cells, suggesting a promising therapeutic strategy for liver cancer resistant to 5-FU. Fluorouracil 128-132 dishevelled segment polarity protein 1 Homo sapiens 91-95 29583038-8 2018 Collectively, our results provide the first clue towards understanding the contribution of DVL1-mediated acquired resistance to 5-FU in HepG2/5-FU cells, suggesting a promising therapeutic strategy for liver cancer resistant to 5-FU. Fluorouracil 142-146 dishevelled segment polarity protein 1 Homo sapiens 91-95 29583038-8 2018 Collectively, our results provide the first clue towards understanding the contribution of DVL1-mediated acquired resistance to 5-FU in HepG2/5-FU cells, suggesting a promising therapeutic strategy for liver cancer resistant to 5-FU. Fluorouracil 142-146 dishevelled segment polarity protein 1 Homo sapiens 91-95 29183726-8 2018 Moreover, there were large bubbles blowing from the membrane of 5-FU-treated cells and the cleavage of GSDME but not GSDMD, which were blocked by the silence or specific inhibitor of caspase-3. Fluorouracil 64-68 caspase 3 Homo sapiens 183-192 29277783-6 2018 In addition, both chemical and genetic inhibition of HDAC1 reduced the activation of caspase-3 and cytotoxicity in 5-fluorouracil (5FU)-treated cancer cells. Fluorouracil 115-129 histone deacetylase 1 Homo sapiens 53-58 29277783-6 2018 In addition, both chemical and genetic inhibition of HDAC1 reduced the activation of caspase-3 and cytotoxicity in 5-fluorouracil (5FU)-treated cancer cells. Fluorouracil 115-129 caspase 3 Homo sapiens 85-94 29277783-6 2018 In addition, both chemical and genetic inhibition of HDAC1 reduced the activation of caspase-3 and cytotoxicity in 5-fluorouracil (5FU)-treated cancer cells. Fluorouracil 131-134 histone deacetylase 1 Homo sapiens 53-58 29277783-6 2018 In addition, both chemical and genetic inhibition of HDAC1 reduced the activation of caspase-3 and cytotoxicity in 5-fluorouracil (5FU)-treated cancer cells. Fluorouracil 131-134 caspase 3 Homo sapiens 85-94 29341150-10 2018 Akt activation was also confirmed in the radioresistant cell line SW480, and a 50 per cent improvement in sensitivity to CRT was observed in vitro and in vivo when SW480 cells were exposed to the Akt inhibitor MK2206 in combination with radiation and 5-fluorouracil. Fluorouracil 251-265 AKT serine/threonine kinase 1 Homo sapiens 196-199 29635244-8 2018 Further study showed a positive correlation between the expression level of MTDH and 5-FU resistance. Fluorouracil 85-89 metadherin Homo sapiens 76-80 29080751-9 2018 Downregulation of miR-195 sensitized HCT-116 cells after 5-FU treatment. Fluorouracil 57-61 microRNA 195 Homo sapiens 18-25 29080751-10 2018 Our results demonstrate that miR-195 can promote acquisition of drug resistance to 5-FU. Fluorouracil 83-87 microRNA 195 Homo sapiens 29-36 30613833-6 2018 Results: Significant resistance to 5-FU resulted from p53-loss or from gain-of-function (GOF) mutation (R248W) and was greatest when GOF mutation was coupled with loss of wild-type p53. Fluorouracil 35-39 tumor protein p53 Homo sapiens 54-57 30613833-6 2018 Results: Significant resistance to 5-FU resulted from p53-loss or from gain-of-function (GOF) mutation (R248W) and was greatest when GOF mutation was coupled with loss of wild-type p53. Fluorouracil 35-39 tumor protein p53 Homo sapiens 181-184 30613833-7 2018 F10 is much more potent than 5-FU (137-314-fold depending on TP53 mutational status). Fluorouracil 29-33 tumor protein p53 Homo sapiens 61-65 29635244-10 2018 The simultaneous inhibition of autophagy and overexpression of MTDH decreased the levels of P-gp and inhibited 5-FU resistance. Fluorouracil 111-115 metadherin Homo sapiens 63-67 29635244-13 2018 CONCLUSIONS: MTDH-stimulated cancer resistance to 5-FU may be mediated through autophagy activated by the AMPK/ATG5 pathway in GC. Fluorouracil 50-54 metadherin Homo sapiens 13-17 29635244-9 2018 MTDH overexpression in MKN45 cells increased the levels of P-glycoprotein (P-gp) and promoted 5-FU resistance, while inhibition of MTDH showed the opposite result. Fluorouracil 94-98 metadherin Homo sapiens 0-4 29635244-13 2018 CONCLUSIONS: MTDH-stimulated cancer resistance to 5-FU may be mediated through autophagy activated by the AMPK/ATG5 pathway in GC. Fluorouracil 50-54 autophagy related 5 Homo sapiens 111-115 29694984-0 2018 Camel Milk Ameliorates 5-Fluorouracil-Induced Renal Injury in Rats: Targeting MAPKs, NF-kappaB and PI3K/Akt/eNOS Pathways. Fluorouracil 23-37 AKT serine/threonine kinase 1 Rattus norvegicus 104-107 29364475-10 2018 Pretreatment with AKT inhibitor enhanced the drug-sensitivity of these cells to 5-Fu and MMC. Fluorouracil 80-84 AKT serine/threonine kinase 1 Homo sapiens 18-21 29689552-6 2018 We further elucidated that RBFOX3 knockdown synergized with 5-FU to inhibit the growth and invasion of HCC cells through PI3K/AKT and epithelial-mesenchymal transition (EMT) signaling, and promote apoptosis by activating the cytochrome-c/caspase signaling pathway. Fluorouracil 60-64 thymoma viral proto-oncogene 1 Mus musculus 126-129 28969563-5 2018 5-fluorouracil (5-FU) is extensively metabolized and at physiological concentrations, is found to be associated with Human Serum Albumin (HSA). Fluorouracil 0-14 albumin Homo sapiens 123-136 28969563-5 2018 5-fluorouracil (5-FU) is extensively metabolized and at physiological concentrations, is found to be associated with Human Serum Albumin (HSA). Fluorouracil 16-20 albumin Homo sapiens 123-136 29689552-0 2018 RBFOX3 Regulates the Chemosensitivity of Cancer Cells to 5-Fluorouracil via the PI3K/AKT, EMT and Cytochrome-C/Caspase Pathways. Fluorouracil 57-71 thymoma viral proto-oncogene 1 Mus musculus 85-88 28554183-1 2018 BACKGROUND/AIMS: This study documents the clinical efficacy and toxicity of S-1 and paclitaxel (S1/PTX) in patients with unresectable or postoperative recurrent esophageal squamous cell carcinoma (ESCC) who had been previously treated with fluorouracil (5FU), cisplatin, and docetaxel. Fluorouracil 240-252 proteasome 26S subunit, non-ATPase 1 Homo sapiens 76-94 28554183-1 2018 BACKGROUND/AIMS: This study documents the clinical efficacy and toxicity of S-1 and paclitaxel (S1/PTX) in patients with unresectable or postoperative recurrent esophageal squamous cell carcinoma (ESCC) who had been previously treated with fluorouracil (5FU), cisplatin, and docetaxel. Fluorouracil 254-257 proteasome 26S subunit, non-ATPase 1 Homo sapiens 76-94 28554183-9 2018 CONCLUSION: S1/PTX was found to have tolerable clinical efficacy in terms of the response rate, survival and toxicity in patients with unresectable or postoperative recurrent ESCC who had previously been treated with 5FU, cisplatin, and docetaxel. Fluorouracil 217-220 proteasome 26S subunit, non-ATPase 1 Homo sapiens 12-18 28722177-4 2018 We show that this is due to global alterations in nucleotide metabolism, including elevated expression of thymidylate synthase and thymidine kinase 1 (established 5-FU resistance mechanisms), which likely result in an increase in intracellular dTTP pools and a "dilution" of 5-FU anabolites. Fluorouracil 163-167 thymidine kinase 1 Homo sapiens 131-149 29362333-8 2018 DISCUSSION: It is known that S-1 not only achieves a high anticancer effect via dihydropyrimidine dehydrogenase(DPD)inhibition, which is a major metabolic pathway of 5-FU, but also increases the radiation susceptibility of malignancies. Fluorouracil 166-170 proteasome 26S subunit, non-ATPase 1 Homo sapiens 29-32 28722177-4 2018 We show that this is due to global alterations in nucleotide metabolism, including elevated expression of thymidylate synthase and thymidine kinase 1 (established 5-FU resistance mechanisms), which likely result in an increase in intracellular dTTP pools and a "dilution" of 5-FU anabolites. Fluorouracil 275-279 thymidine kinase 1 Homo sapiens 131-149 27871087-0 2018 The HDM2 (MDM2) Inhibitor NVP-CGM097 Inhibits Tumor Cell Proliferation and Shows Additive Effects with 5-Fluorouracil on the p53-p21-Rb-E2F1 Cascade in the p53wild type Neuroendocrine Tumor Cell Line GOT1. Fluorouracil 103-117 tumor protein p53 Homo sapiens 125-128 27871087-0 2018 The HDM2 (MDM2) Inhibitor NVP-CGM097 Inhibits Tumor Cell Proliferation and Shows Additive Effects with 5-Fluorouracil on the p53-p21-Rb-E2F1 Cascade in the p53wild type Neuroendocrine Tumor Cell Line GOT1. Fluorouracil 103-117 tumor protein p53 Homo sapiens 156-159 27871087-10 2018 NVP-CGM097 and 5-fluorouracil increased p53 and p21 expression in an additive manner. Fluorouracil 15-29 tumor protein p53 Homo sapiens 40-43 28226315-8 2018 Combined treatment with LEE011 and 5-fluorouracil or everolimus showed a significant enhancement in the inhibition of cell viability when compared to single-substance treatments due to PI3K-Akt-mTOR and Ras-Raf-MEK-ERK pathway downregulation and cooperative downregulation of cell cycle components. Fluorouracil 35-49 mitogen-activated protein kinase kinase 7 Homo sapiens 211-214 28226315-8 2018 Combined treatment with LEE011 and 5-fluorouracil or everolimus showed a significant enhancement in the inhibition of cell viability when compared to single-substance treatments due to PI3K-Akt-mTOR and Ras-Raf-MEK-ERK pathway downregulation and cooperative downregulation of cell cycle components. Fluorouracil 35-49 mitogen-activated protein kinase 1 Homo sapiens 215-218 29061672-9 2017 Further, they resensitized mutant p53-expressing cell lines resistant to 5-fluorouracil. Fluorouracil 73-87 tumor protein p53 Homo sapiens 34-37 29273065-0 2017 Curcumin synergizes with 5-fluorouracil by impairing AMPK/ULK1-dependent autophagy, AKT activity and enhancing apoptosis in colon cancer cells with tumor growth inhibition in xenograft mice. Fluorouracil 25-39 thymoma viral proto-oncogene 1 Mus musculus 84-87 29273065-14 2017 CONCLUSION: Pre-treatment with curcumin followed by 5-Fu may mediate autophagy turnover both in vitro and in vivo via AMPK/ULK1-dependent autophagy inhibition and AKT modulation, which may account for the increased susceptibility of the colon cancer cells/xenograft to the cytotoxicity of 5-Fu. Fluorouracil 52-56 AKT serine/threonine kinase 1 Homo sapiens 163-166 29115442-0 2018 GOLPH3 expression promotes the resistance of HT29 cells to 5-fluorouracil by activating multiple signaling pathways. Fluorouracil 59-73 golgi phosphoprotein 3 Homo sapiens 0-6 29115442-4 2018 In the present study, the association between the overexpression of the GOLPH3 gene and resistance of HT29 colonic cancer cells to 5-fluorouracil (5-FU) was investigated. Fluorouracil 131-145 golgi phosphoprotein 3 Homo sapiens 72-78 29115442-4 2018 In the present study, the association between the overexpression of the GOLPH3 gene and resistance of HT29 colonic cancer cells to 5-fluorouracil (5-FU) was investigated. Fluorouracil 147-151 golgi phosphoprotein 3 Homo sapiens 72-78 29115442-5 2018 Following confirmation of the effective silencing of the GOLPH3 gene, proliferation and apoptosis of colonic cancer cells were detected by MTT assay, colony formation assay and flow cytometry, and then the mechanism of GOLPH3-induced resistance to 5-FU chemotherapy in colonic cancer cells was investigated by western blotting. Fluorouracil 248-252 golgi phosphoprotein 3 Homo sapiens 57-63 29115442-5 2018 Following confirmation of the effective silencing of the GOLPH3 gene, proliferation and apoptosis of colonic cancer cells were detected by MTT assay, colony formation assay and flow cytometry, and then the mechanism of GOLPH3-induced resistance to 5-FU chemotherapy in colonic cancer cells was investigated by western blotting. Fluorouracil 248-252 golgi phosphoprotein 3 Homo sapiens 219-225 29115442-6 2018 The results demonstrated that the expression of phosphorylated (p)-glycoprotein and GOLPH3 was increased in HT29 cells following treatment with 5-FU, which resulted in the development of drug resistance. Fluorouracil 144-148 golgi phosphoprotein 3 Homo sapiens 84-90 29115442-7 2018 Silencing GOLPH3 increased the sensitivity of HT29 cells to 5-FU, reduced their tumorigenicity and partly reversed their resistance to 5-FU. Fluorouracil 60-64 golgi phosphoprotein 3 Homo sapiens 10-16 29115442-7 2018 Silencing GOLPH3 increased the sensitivity of HT29 cells to 5-FU, reduced their tumorigenicity and partly reversed their resistance to 5-FU. Fluorouracil 135-139 golgi phosphoprotein 3 Homo sapiens 10-16 29138869-3 2018 Mutated p53 in CRC was reported to be associated with resistance to commonly used chemotherapeutic agents including, 5-fluorouracil, oxaliplatin and irinotecan. Fluorouracil 117-131 tumor protein p53 Homo sapiens 8-11 28867645-7 2017 5-FU significantly reduced the pilocarpine-stimulated salivary flow rate on the 4th experimental day, associated with an increase in the SOD levels in saliva. Fluorouracil 0-4 superoxide dismutase 1 Homo sapiens 137-140 29383202-5 2017 Silencing Dishevelled1-3 resensitized HCT-8/VCR cells to multiple drugs including vincristine, 5-fluorouracil and oxaliplatin. Fluorouracil 95-109 dishevelled segment polarity protein 1 Homo sapiens 10-22 28058860-8 2017 Furthermore, 5-fluorouracil (5-FU) chemotherapy following siRNA-mediated knockdown lead to a significant enhancement of chemosensitivity with a higher rate of early apoptosis in Erk2 silencing relative to that of Erk1) + 9%, P < 0.01). Fluorouracil 13-27 mitogen-activated protein kinase 1 Homo sapiens 178-182 28058860-8 2017 Furthermore, 5-fluorouracil (5-FU) chemotherapy following siRNA-mediated knockdown lead to a significant enhancement of chemosensitivity with a higher rate of early apoptosis in Erk2 silencing relative to that of Erk1) + 9%, P < 0.01). Fluorouracil 13-27 mitogen-activated protein kinase 3 Homo sapiens 213-217 28058860-8 2017 Furthermore, 5-fluorouracil (5-FU) chemotherapy following siRNA-mediated knockdown lead to a significant enhancement of chemosensitivity with a higher rate of early apoptosis in Erk2 silencing relative to that of Erk1) + 9%, P < 0.01). Fluorouracil 29-33 mitogen-activated protein kinase 1 Homo sapiens 178-182 28058860-8 2017 Furthermore, 5-fluorouracil (5-FU) chemotherapy following siRNA-mediated knockdown lead to a significant enhancement of chemosensitivity with a higher rate of early apoptosis in Erk2 silencing relative to that of Erk1) + 9%, P < 0.01). Fluorouracil 29-33 mitogen-activated protein kinase 3 Homo sapiens 213-217 28058860-9 2017 5-FU treatment after dual knockdown of Erk1/2 showed higher rate of early apoptosis relative to single Erk1 silencing (+9.25%, P < 0.01) and also higher rate of late apoptosis compared to single Erk1 and Erk2 silencing (+4.96% and +4.66%, P < 0.01). Fluorouracil 0-4 mitogen-activated protein kinase 3 Homo sapiens 39-45 28058860-9 2017 5-FU treatment after dual knockdown of Erk1/2 showed higher rate of early apoptosis relative to single Erk1 silencing (+9.25%, P < 0.01) and also higher rate of late apoptosis compared to single Erk1 and Erk2 silencing (+4.96% and +4.66%, P < 0.01). Fluorouracil 0-4 mitogen-activated protein kinase 3 Homo sapiens 39-43 28058860-9 2017 5-FU treatment after dual knockdown of Erk1/2 showed higher rate of early apoptosis relative to single Erk1 silencing (+9.25%, P < 0.01) and also higher rate of late apoptosis compared to single Erk1 and Erk2 silencing (+4.96% and +4.66%, P < 0.01). Fluorouracil 0-4 mitogen-activated protein kinase 3 Homo sapiens 103-107 28058860-9 2017 5-FU treatment after dual knockdown of Erk1/2 showed higher rate of early apoptosis relative to single Erk1 silencing (+9.25%, P < 0.01) and also higher rate of late apoptosis compared to single Erk1 and Erk2 silencing (+4.96% and +4.66%, P < 0.01). Fluorouracil 0-4 mitogen-activated protein kinase 1 Homo sapiens 207-211 29163710-8 2017 In addition, high BRCA1 mRNA levels correlated with decreased median overall survival (mOS; P<0.001) and response rate (RR; P=0.002) in cisplatin-fluorouracil chemotherapy group and also correlated with increased mOS (P<0.001) and RR (P=0.023) in docetaxel-fluorouracil chemotherapy group. Fluorouracil 149-161 Moloney sarcoma oncogene Mus musculus 216-219 28767179-10 2017 Inhibition of the PI3K/AKT pathway enhanced the chemosensitivity to 5-FU in HCT-8/5-FU and LoVo/5-FU. Fluorouracil 68-72 AKT serine/threonine kinase 1 Homo sapiens 23-26 28767179-10 2017 Inhibition of the PI3K/AKT pathway enhanced the chemosensitivity to 5-FU in HCT-8/5-FU and LoVo/5-FU. Fluorouracil 82-86 AKT serine/threonine kinase 1 Homo sapiens 23-26 28767179-10 2017 Inhibition of the PI3K/AKT pathway enhanced the chemosensitivity to 5-FU in HCT-8/5-FU and LoVo/5-FU. Fluorouracil 82-86 AKT serine/threonine kinase 1 Homo sapiens 23-26 28767179-11 2017 Taken together, miR-135b and miR-182 may reverse the resistance to 5-FU in CRC cells by targeting ST6GALNAC2 via PI3K/AKT pathway, which render potential chemotherapy targets for the treatment of CRC. Fluorouracil 67-71 AKT serine/threonine kinase 1 Homo sapiens 118-121 29181845-20 2017 We would need to treat 10 adults with KGF in order to prevent one additional adult from developing this outcome (95% CI 5 to prevent the outcome to 14 to cause the outcome).There is probably a reduction in the risk of moderate to severe oral mucositis in adults receiving radiotherapy to the head and neck with cisplatin or fluorouracil (RR 0.91, 95% CI 0.83 to 1.00; 3 studies; 471 participants; moderate-quality evidence). Fluorouracil 324-336 fibroblast growth factor 7 Homo sapiens 38-41 29181845-28 2017 AUTHORS" CONCLUSIONS: We are confident that KGF is beneficial in the prevention of oral mucositis in adults who are receiving: a) radiotherapy to the head and neck with cisplatin or fluorouracil; or b) chemotherapy alone for mixed solid and haematological cancers. Fluorouracil 182-194 fibroblast growth factor 7 Homo sapiens 44-47 29180678-0 2017 Long non-coding RNA LINC00152 promotes cell proliferation, metastasis, and confers 5-FU resistance in colorectal cancer by inhibiting miR-139-5p. Fluorouracil 83-87 cytoskeleton regulator RNA Homo sapiens 20-29 29180678-6 2017 Furthermore, LINC00152 could increase the resistance of CRC cells to 5-fluorouracil (5-FU) by suppressing apoptosis. Fluorouracil 69-83 cytoskeleton regulator RNA Homo sapiens 13-22 29180678-6 2017 Furthermore, LINC00152 could increase the resistance of CRC cells to 5-fluorouracil (5-FU) by suppressing apoptosis. Fluorouracil 85-89 cytoskeleton regulator RNA Homo sapiens 13-22 29200829-0 2017 Andrographolide enhanced 5-fluorouracil-induced antitumor effect in colorectal cancer via inhibition of c-MET pathway. Fluorouracil 25-39 MET proto-oncogene, receptor tyrosine kinase Homo sapiens 104-109 29209153-7 2017 5-Fluorouracil and oxaliplatin treatment lead to an enhanced caspase 3-dependent apoptosis and produce an increase of autophagy. Fluorouracil 0-14 caspase 3 Homo sapiens 61-70 28928082-0 2017 miR-338-3p confers 5-fluorouracil resistance in p53 mutant colon cancer cells by targeting the mammalian target of rapamycin. Fluorouracil 19-33 tumor protein p53 Homo sapiens 48-51 28928082-0 2017 miR-338-3p confers 5-fluorouracil resistance in p53 mutant colon cancer cells by targeting the mammalian target of rapamycin. Fluorouracil 19-33 mechanistic target of rapamycin kinase Homo sapiens 95-124 28928082-1 2017 Evidence demonstrate that p53 mutations and microRNAs (miRs) are important components of 5-FU resistance in colorectal cancer (CRC). Fluorouracil 89-93 tumor protein p53 Homo sapiens 26-29 28928082-7 2017 Further experiments indicated that miR-338-3p mediated 5-FU resistance through down-regulation of mTOR expression. Fluorouracil 55-59 mechanistic target of rapamycin kinase Homo sapiens 98-102 28928082-8 2017 Moreover, inhibition of miR-338-3p in HT29 and HCT116 p53-/- cells increased their sensitivity to 5-FU treatment. Fluorouracil 98-102 tumor protein p53 Homo sapiens 54-57 28928082-10 2017 Our results reveal a critical and novel role of miR-338-3p in the correlation of 5-FU resistance with p53 status. Fluorouracil 81-85 tumor protein p53 Homo sapiens 102-105 28928082-11 2017 Moreover, the miR-338-3p inhibitor has the potential to overcome 5-FU resistance in p53 mutant colon cancer cells. Fluorouracil 65-69 tumor protein p53 Homo sapiens 84-87 29545913-2 2018 Although patients with advanced colorectal cancer (CRC) exhibiting a mismatch repair (MMR) deficiency reportedly do not benefit from 5-fluorouracil-based chemotherapy and we previously reported that truncated methyl-CpG binding domain protein 4 (MBD4) enhances 5-fluorouracil cytotoxicity in MMR-deficient CRC cells, little is known regarding the effect of MMR deficiency on trifluridine cytotoxicity in CRC. Fluorouracil 133-147 methyl-CpG binding domain 4, DNA glycosylase Homo sapiens 209-244 29545913-2 2018 Although patients with advanced colorectal cancer (CRC) exhibiting a mismatch repair (MMR) deficiency reportedly do not benefit from 5-fluorouracil-based chemotherapy and we previously reported that truncated methyl-CpG binding domain protein 4 (MBD4) enhances 5-fluorouracil cytotoxicity in MMR-deficient CRC cells, little is known regarding the effect of MMR deficiency on trifluridine cytotoxicity in CRC. Fluorouracil 133-147 methyl-CpG binding domain 4, DNA glycosylase Homo sapiens 246-250 29545913-2 2018 Although patients with advanced colorectal cancer (CRC) exhibiting a mismatch repair (MMR) deficiency reportedly do not benefit from 5-fluorouracil-based chemotherapy and we previously reported that truncated methyl-CpG binding domain protein 4 (MBD4) enhances 5-fluorouracil cytotoxicity in MMR-deficient CRC cells, little is known regarding the effect of MMR deficiency on trifluridine cytotoxicity in CRC. Fluorouracil 261-275 methyl-CpG binding domain 4, DNA glycosylase Homo sapiens 209-244 29545913-2 2018 Although patients with advanced colorectal cancer (CRC) exhibiting a mismatch repair (MMR) deficiency reportedly do not benefit from 5-fluorouracil-based chemotherapy and we previously reported that truncated methyl-CpG binding domain protein 4 (MBD4) enhances 5-fluorouracil cytotoxicity in MMR-deficient CRC cells, little is known regarding the effect of MMR deficiency on trifluridine cytotoxicity in CRC. Fluorouracil 261-275 methyl-CpG binding domain 4, DNA glycosylase Homo sapiens 246-250 29545913-8 2018 Moreover, MBD4tru cells were more sensitive than the control cells to trifluridine.Conclusions: Trifluridine induces cytotoxicity independently of the DNA MMR status as well as under 5-fluorouracil-refractory conditions, and the MBD4 frameshift mutation enhances trifluridine cytotoxicity. Fluorouracil 183-197 methyl-CpG binding domain 4, DNA glycosylase Homo sapiens 10-14 29117108-6 2017 It was shown that 5-FU increases the XRCC1 expression in HCT-116 cells and then affects the cell survival through CXCR4/Akt signaling. Fluorouracil 18-22 AKT serine/threonine kinase 1 Homo sapiens 120-123 29117108-7 2017 Moreover, 5-FU combined with AICAR further result in more survival inhibition in HCT-116 cells, accompanied with reduced CXCR4/Akt signaling activity and XRCC1 expression. Fluorouracil 10-14 AKT serine/threonine kinase 1 Homo sapiens 127-130 29116019-11 2017 RESULTS: Silencing CLDN6 increased the cytotoxicity of ADM, 5-FU, and DDP in MCF-7/MDR cells. Fluorouracil 60-64 claudin 6 Homo sapiens 19-24 28799948-12 2017 MTX, 5-FU, and cisplatin may offer particular promise through combined cytotoxicity and downregulation of Hedgehog pathway genes GLI1 and PTCH1. Fluorouracil 5-9 patched 1 Homo sapiens 138-143 29045553-2 2017 We evaluated the efficacy of oral 5-fluorouracil-based S-1 as second- or third-line therapy compared with standard docetaxel therapy in patients with advanced NSCLC. Fluorouracil 34-48 proteasome 26S subunit, non-ATPase 1 Homo sapiens 55-58 28642038-1 2017 Dihydropyrimidinase (DHP, EC 3.5.2.2), encoded by the gene DPYS, is the second enzyme in the catabolic pathway of pyrimidine and of fluoropyrimidine drugs such as 5-fluorouracil, which are commonly used in anticancer treatment; DHP catalyzes the hydrolytic ring opening of dihydrouracil and dihydro-5-fluorouracil. Fluorouracil 163-177 dihydropyrimidinase Homo sapiens 0-19 28429680-3 2017 Drug-induced PARP inhibition potentiates the activity of anticancer drugs such as 5-fluorouracil in enhancing DNA damage, whose repair involves PARP-1 activity. Fluorouracil 82-96 poly(ADP-ribose) polymerase 1 Homo sapiens 13-17 28429680-3 2017 Drug-induced PARP inhibition potentiates the activity of anticancer drugs such as 5-fluorouracil in enhancing DNA damage, whose repair involves PARP-1 activity. Fluorouracil 82-96 poly(ADP-ribose) polymerase 1 Homo sapiens 144-150 28429680-9 2017 Our results show that the novel PARP inhibitor HYDAMTIQ potently inhibits the growth of human tumor cells with defective DNA damage response pathways and exerts synergistic cytotoxicity in combination with 5-fluorouracil. Fluorouracil 206-220 poly(ADP-ribose) polymerase 1 Homo sapiens 32-36 28642038-1 2017 Dihydropyrimidinase (DHP, EC 3.5.2.2), encoded by the gene DPYS, is the second enzyme in the catabolic pathway of pyrimidine and of fluoropyrimidine drugs such as 5-fluorouracil, which are commonly used in anticancer treatment; DHP catalyzes the hydrolytic ring opening of dihydrouracil and dihydro-5-fluorouracil. Fluorouracil 163-177 dihydropyrimidinase Homo sapiens 21-24 28642038-1 2017 Dihydropyrimidinase (DHP, EC 3.5.2.2), encoded by the gene DPYS, is the second enzyme in the catabolic pathway of pyrimidine and of fluoropyrimidine drugs such as 5-fluorouracil, which are commonly used in anticancer treatment; DHP catalyzes the hydrolytic ring opening of dihydrouracil and dihydro-5-fluorouracil. Fluorouracil 163-177 dihydropyrimidinase Homo sapiens 59-63 28127745-1 2017 BACKGROUND AND PURPOSE: 5-fluorouracil (5FU) and its prodrug, capecitabine, can damage endothelial cells, whilst endothelial integrity is preserved by glucagon-like peptide 1 (GLP-1). Fluorouracil 24-38 glucagon Homo sapiens 176-181 28642038-1 2017 Dihydropyrimidinase (DHP, EC 3.5.2.2), encoded by the gene DPYS, is the second enzyme in the catabolic pathway of pyrimidine and of fluoropyrimidine drugs such as 5-fluorouracil, which are commonly used in anticancer treatment; DHP catalyzes the hydrolytic ring opening of dihydrouracil and dihydro-5-fluorouracil. Fluorouracil 163-177 dihydropyrimidinase Homo sapiens 228-231 28127745-6 2017 RT-PCR, western blotting, functional experiments with signalling inhibitors and ERK1/2 silencing were performed to characterize 5FU-induced phenotype and elucidate the pathways underlying 5FU and GLP-1 activity. Fluorouracil 128-131 glucagon Homo sapiens 196-201 28127745-9 2017 Furthermore, 5FU up-regulated VCAM1 and TYMP (encodes enzyme activating capecitabine and 5FU), and sVCAM-1 and CD146 concentrations were higher after than before capecitabine chemotherapy. Fluorouracil 13-16 vascular cell adhesion molecule 1 Homo sapiens 30-35 28127745-13 2017 5FU-triggered senescence was prevented by GLP-1, raising the possibility of using GLP-1 analogues and degradation inhibitors to treat 5FU and capecitabine vascular toxicity. Fluorouracil 0-3 glucagon Homo sapiens 42-47 28127745-13 2017 5FU-triggered senescence was prevented by GLP-1, raising the possibility of using GLP-1 analogues and degradation inhibitors to treat 5FU and capecitabine vascular toxicity. Fluorouracil 0-3 glucagon Homo sapiens 82-87 28774899-3 2017 We have evaluated the ability of the PET imaging agent, 89Zr-anti-gammaH2AX-TAT, to monitor DNA damage in response to fluorouracil (5-FU), gemcitabine, or capecitabine treatment in a mouse model of pancreatic cancer. Fluorouracil 118-130 H2A.X variant histone Mus musculus 66-75 28774899-3 2017 We have evaluated the ability of the PET imaging agent, 89Zr-anti-gammaH2AX-TAT, to monitor DNA damage in response to fluorouracil (5-FU), gemcitabine, or capecitabine treatment in a mouse model of pancreatic cancer. Fluorouracil 132-136 H2A.X variant histone Mus musculus 66-75 29262524-6 2017 Deletion of this MER61C element by a CRISPR/Cas9 approach, as well as siRNA-mediated knockdown of LINC01021 RNA significantly enhanced the sensitivity of the CRC cell line HCT116 towards the chemotherapeutic drugs doxorubicin and 5-FU, suggesting that LINC01021 is an integral part of the p53-mediated response to DNA damage. Fluorouracil 230-234 p53 upregulated regulator of p53 levels Homo sapiens 98-107 28818782-5 2017 5-FU can be effectively loaded into the meso-pores of MSN-P(OEGMA-co-RGD) (5-FU@MSN-RGD) with drug content ~7.5wt%. Fluorouracil 0-4 moesin Homo sapiens 54-57 28818782-5 2017 5-FU can be effectively loaded into the meso-pores of MSN-P(OEGMA-co-RGD) (5-FU@MSN-RGD) with drug content ~7.5wt%. Fluorouracil 75-79 moesin Homo sapiens 54-57 28818782-6 2017 And the dynamic diameter (Dh) and zeta potential (zeta) of 5-FU@MSN-RGD were determined to be 199.3+-5.4nm and -8.7+-0.5mV, respectively. Fluorouracil 59-63 moesin Homo sapiens 64-67 28818782-8 2017 In addition, compared with free 5-FU, 5-FU@MSN-RGD showed enhanced anticancer efficacy both in vitro and in vivo, implying promising clinical applications. Fluorouracil 38-42 moesin Homo sapiens 43-46 28970092-0 2017 A novel vascular-targeting peptide for gastric cancer delivers low-dose TNFalpha to normalize the blood vessels and improve the anti-cancer efficiency of 5-fluorouracil. Fluorouracil 154-168 tumor necrosis factor Mus musculus 72-80 29113268-0 2017 JAB1-STAT3 activation loop is associated with recurrence following 5-fluorouracil-based adjuvant chemotherapy in human colorectal cancer. Fluorouracil 67-81 signal transducer and activator of transcription 3 Homo sapiens 5-10 29113268-7 2017 In the present study, it was found that high JAB1 expression in primary colorectal cancer tissues is an independent predictor of recurrence following 5-fluorouracil (5-FU)-based adjuvant chemotherapy in colorectal cancer patients, and that high expression of both JAB1 and STAT3 in primary colorectal cancer tissues is associated with a lower recurrence-free survival rate following 5-FU-based adjuvant chemotherapy compared to high expression of only JAB1 or STAT3. Fluorouracil 166-170 signal transducer and activator of transcription 3 Homo sapiens 273-278 29113268-7 2017 In the present study, it was found that high JAB1 expression in primary colorectal cancer tissues is an independent predictor of recurrence following 5-fluorouracil (5-FU)-based adjuvant chemotherapy in colorectal cancer patients, and that high expression of both JAB1 and STAT3 in primary colorectal cancer tissues is associated with a lower recurrence-free survival rate following 5-FU-based adjuvant chemotherapy compared to high expression of only JAB1 or STAT3. Fluorouracil 166-170 signal transducer and activator of transcription 3 Homo sapiens 460-465 29113268-8 2017 Overall, these results suggest that JAB1 is a novel predictive marker of recurrence following 5-FU-based adjuvant chemotherapy in colorectal cancer patients, and that the JAB1-STAT3 activation loop may be a potential therapeutic target in recurrent colorectal cancer following 5-FU-based adjuvant chemotherapy. Fluorouracil 94-98 signal transducer and activator of transcription 3 Homo sapiens 176-181 29113268-8 2017 Overall, these results suggest that JAB1 is a novel predictive marker of recurrence following 5-FU-based adjuvant chemotherapy in colorectal cancer patients, and that the JAB1-STAT3 activation loop may be a potential therapeutic target in recurrent colorectal cancer following 5-FU-based adjuvant chemotherapy. Fluorouracil 277-281 signal transducer and activator of transcription 3 Homo sapiens 176-181 28970092-5 2017 A targeted therapy for improvement of the therapeutic efficacy of 5-FU and vascular function was performed through administration of TCP-1/TNFalpha fusion protein in this model. Fluorouracil 66-70 tumor necrosis factor Mus musculus 139-147 29124041-6 2017 While tight junction protein occludin was reduced, however, zonula occludens-1 (ZO-1) and junctional adhesion molecule-A (JAM-A) were increased in colonic tissues of 5-Fu treated mice. Fluorouracil 166-170 occludin Mus musculus 29-37 29442040-12 2017 Our results suggest that lidocaine sensitizes the cytotoxicity of 5-FU in melanoma cells via upregulation of miR-493, which might be involved in SOX4-mediated PI3K/AKT and Smad pathways. Fluorouracil 66-70 AKT serine/threonine kinase 1 Homo sapiens 164-167 29124041-6 2017 While tight junction protein occludin was reduced, however, zonula occludens-1 (ZO-1) and junctional adhesion molecule-A (JAM-A) were increased in colonic tissues of 5-Fu treated mice. Fluorouracil 166-170 tight junction protein 1 Mus musculus 60-78 29124041-6 2017 While tight junction protein occludin was reduced, however, zonula occludens-1 (ZO-1) and junctional adhesion molecule-A (JAM-A) were increased in colonic tissues of 5-Fu treated mice. Fluorouracil 166-170 tight junction protein 1 Mus musculus 80-84 29089858-11 2017 Overexpressed miR-1296-5p reduced its target protein level and mTORC1/S6 activation, inhibited the proliferation of ERBB2-positive breast cancer cells and sensitized these cells to cisplatin and 5-fluorouracil-induced apoptosis. Fluorouracil 195-209 microRNA 1296 Homo sapiens 14-22 28082170-6 2017 Notably, the hybrid CPT-Cap prodrug showed a synergistic effect and significantly enhanced potency against three esophageal adenocarcinoma cell lines compared with the two homo-prodrugs (dCPT-Sup35 and dCap-Sup35) as well as free parent drugs (CPT, 5-Fu and CPT/5-FU mixture (1:1)). Fluorouracil 249-253 CAP Drosophila melanogaster 24-27 29151957-0 2017 Curcumin Enhances the Anticancer Effect Of 5-fluorouracil against Gastric Cancer through Down-Regulation of COX-2 and NF- kappaB Signaling Pathways. Fluorouracil 43-57 mitochondrially encoded cytochrome c oxidase II Homo sapiens 108-113 29151957-11 2017 Furthermore, the protein expressions of COX-2 and NF-kappaB in MKN45 cells were decreased by 44.79% and 37.67%, 47.17% and 48.21%, 60.21% and 62.44%, respectively, after treatment of curcumin (25 mumol/l) and 5-FU (50 mumol/l) alone or in combination for 48 h. Curcumin also enhanced the anticancer activity of 5-FU without increasing toxicity in nude mice bearing MKN45 tumor xenografts in vivo. Fluorouracil 209-213 mitochondrially encoded cytochrome c oxidase II Homo sapiens 40-45 29151957-11 2017 Furthermore, the protein expressions of COX-2 and NF-kappaB in MKN45 cells were decreased by 44.79% and 37.67%, 47.17% and 48.21%, 60.21% and 62.44%, respectively, after treatment of curcumin (25 mumol/l) and 5-FU (50 mumol/l) alone or in combination for 48 h. Curcumin also enhanced the anticancer activity of 5-FU without increasing toxicity in nude mice bearing MKN45 tumor xenografts in vivo. Fluorouracil 209-213 nuclear factor kappa B subunit 1 Homo sapiens 50-59 29151957-11 2017 Furthermore, the protein expressions of COX-2 and NF-kappaB in MKN45 cells were decreased by 44.79% and 37.67%, 47.17% and 48.21%, 60.21% and 62.44%, respectively, after treatment of curcumin (25 mumol/l) and 5-FU (50 mumol/l) alone or in combination for 48 h. Curcumin also enhanced the anticancer activity of 5-FU without increasing toxicity in nude mice bearing MKN45 tumor xenografts in vivo. Fluorouracil 311-315 mitochondrially encoded cytochrome c oxidase II Homo sapiens 40-45 29151957-11 2017 Furthermore, the protein expressions of COX-2 and NF-kappaB in MKN45 cells were decreased by 44.79% and 37.67%, 47.17% and 48.21%, 60.21% and 62.44%, respectively, after treatment of curcumin (25 mumol/l) and 5-FU (50 mumol/l) alone or in combination for 48 h. Curcumin also enhanced the anticancer activity of 5-FU without increasing toxicity in nude mice bearing MKN45 tumor xenografts in vivo. Fluorouracil 311-315 nuclear factor kappa B subunit 1 Homo sapiens 50-59 29020632-3 2017 Here, we show that p53 activation by 5-fluorouracil or nutlin-3 synergizes with a reversible Cdk7as inhibitor to induce cell death. Fluorouracil 37-51 tumor protein p53 Homo sapiens 19-22 28082170-6 2017 Notably, the hybrid CPT-Cap prodrug showed a synergistic effect and significantly enhanced potency against three esophageal adenocarcinoma cell lines compared with the two homo-prodrugs (dCPT-Sup35 and dCap-Sup35) as well as free parent drugs (CPT, 5-Fu and CPT/5-FU mixture (1:1)). Fluorouracil 262-266 CAP Drosophila melanogaster 24-27 28857517-9 2017 Further investigation revealed that CISD2 enhanced sensitivity to 5-FU via an increase in apoptosis and inhibition of protective autophagy through the activation of the AKT/mTOR pathway. Fluorouracil 66-70 mechanistic target of rapamycin kinase Homo sapiens 173-177 28668765-9 2017 CONCLUSIONS: Topical application of ointment containing 0.5% green tea catechins could prevent tongue oxidative stress in 5-FU administered rats, via up-regulation of the Nrf2 signaling pathway. Fluorouracil 122-126 NFE2 like bZIP transcription factor 2 Rattus norvegicus 171-175 28708138-7 2017 Interestingly, treatment with macitentan, a dual ETAR and ETBR antagonist, able to interfere with tumor and microenvironment, disrupts the ET-1R/beta-arr1-beta-catenin interaction impairing pathways involved in cell survival, EMT, invasion, and enhancing sensitivity to oxaliplatin (OX) and 5-fluorouracil (5-FU). Fluorouracil 291-305 arrestin beta 1 Homo sapiens 145-154 28708138-7 2017 Interestingly, treatment with macitentan, a dual ETAR and ETBR antagonist, able to interfere with tumor and microenvironment, disrupts the ET-1R/beta-arr1-beta-catenin interaction impairing pathways involved in cell survival, EMT, invasion, and enhancing sensitivity to oxaliplatin (OX) and 5-fluorouracil (5-FU). Fluorouracil 307-311 arrestin beta 1 Homo sapiens 145-154 28857517-10 2017 In conclusion, CISD2 is down-regulated in gastric cancer, and its effects on the inhibition of cellular proliferation, metastatic ability, and increased chemotherapy sensitivity are mediated by antagonism to 5-FU-induced autophagy through the AKT/mTOR pathway. Fluorouracil 208-212 AKT serine/threonine kinase 1 Homo sapiens 243-246 28857517-10 2017 In conclusion, CISD2 is down-regulated in gastric cancer, and its effects on the inhibition of cellular proliferation, metastatic ability, and increased chemotherapy sensitivity are mediated by antagonism to 5-FU-induced autophagy through the AKT/mTOR pathway. Fluorouracil 208-212 mechanistic target of rapamycin kinase Homo sapiens 247-251 28656647-0 2017 Epigenetic silencing of ASPP1 confers 5-FU resistance in clear cell renal cell carcinoma by preventing p53 activation. Fluorouracil 38-42 protein phosphatase 1 regulatory subunit 13B Homo sapiens 24-29 29042944-0 2017 Pien Tze Huang induces apoptosis and inhibits proliferation of 5-fluorouracil-resistant colorectal carcinoma cells via increasing miR-22 expression. Fluorouracil 63-77 microRNA 22 Homo sapiens 130-136 28656647-7 2017 Further functional studies demonstrated that forced expression ASPP1 not only significantly inhibited the growth rate of ccRCC, but also promoted sensitivity of ccRCC to the conventional chemotherapeutic drug 5-fluorouracil (5-FU)-induced apoptosis. Fluorouracil 209-223 protein phosphatase 1 regulatory subunit 13B Homo sapiens 63-68 28656647-7 2017 Further functional studies demonstrated that forced expression ASPP1 not only significantly inhibited the growth rate of ccRCC, but also promoted sensitivity of ccRCC to the conventional chemotherapeutic drug 5-fluorouracil (5-FU)-induced apoptosis. Fluorouracil 225-229 protein phosphatase 1 regulatory subunit 13B Homo sapiens 63-68 28656647-9 2017 In contrast, ASPP1 knockdown promoted cell growth and prevent 5-FU-induced p53 activation and apoptosis. Fluorouracil 62-66 protein phosphatase 1 regulatory subunit 13B Homo sapiens 13-18 28656647-9 2017 In contrast, ASPP1 knockdown promoted cell growth and prevent 5-FU-induced p53 activation and apoptosis. Fluorouracil 62-66 tumor protein p53 Homo sapiens 75-78 28979703-13 2017 In conclusion, inhibition of miR-205-5p may reverse chemotherapeutic resistance to 5-Fu, and this may occur via the PTEN/JNK/ANXA3 pathway. Fluorouracil 83-87 mitogen-activated protein kinase 8 Homo sapiens 121-124 29158805-6 2017 Mechanistically, we showed that over-expression of SETDB1 significantly inhibited the apoptosis induced by 5-Fluorouracil in CRC cells, which was closely related to the inhibition of TP53 and BAX expression. Fluorouracil 107-121 SET domain bifurcated histone lysine methyltransferase 1 Homo sapiens 51-57 29137320-2 2017 We previously reported a phase I trial of CCRT using S-1, an oral 5-fluorouracil derivative, which yielded well safe and active outcomes. Fluorouracil 66-80 proteasome 26S subunit, non-ATPase 1 Homo sapiens 53-56 29137307-0 2017 Reversal of 5-fluorouracil resistance by EGCG is mediate by inactivation of TFAP2A/VEGF signaling pathway and down-regulation of MDR-1 and P-gp expression in gastric cancer. Fluorouracil 12-26 vascular endothelial growth factor A Homo sapiens 83-87 29137307-0 2017 Reversal of 5-fluorouracil resistance by EGCG is mediate by inactivation of TFAP2A/VEGF signaling pathway and down-regulation of MDR-1 and P-gp expression in gastric cancer. Fluorouracil 12-26 ATP binding cassette subfamily B member 1 Homo sapiens 129-134 28494379-4 2017 In this study, we analyzed the main intermolecular interactions between a drug used in the cancer treatment (5-fluorouracil) and HER2. Fluorouracil 109-123 erb-b2 receptor tyrosine kinase 2 Homo sapiens 129-133 28494379-6 2017 From the docking simulations it was possible to analyze the interactions that occur between some residues in the binding site of HER2 and 5-FU. Fluorouracil 138-142 erb-b2 receptor tyrosine kinase 2 Homo sapiens 129-133 28494379-11 2017 Therefore, this study allowed a careful evaluation on the main structural, spectroscopic and electronic properties involved in the interaction between 5-FU and HER2, an important biological complex related to the cancer treatment. Fluorouracil 151-155 erb-b2 receptor tyrosine kinase 2 Homo sapiens 160-164 28816773-5 2017 In our study, combined 3-BP and 5-FU treatment upregulated p53 and p21, whereas cyclin-dependent kinase CDK4 and CDK2 were downregulated, which led to G0/G1 phase arrest. Fluorouracil 32-36 tumor protein p53 Homo sapiens 59-62 28374966-8 2017 In cultured colonic epithelial cells, exposure to 5-FU also up-regulated TNF-alpha expression. Fluorouracil 50-54 tumor necrosis factor Mus musculus 73-82 28374966-10 2017 In particular, 5-FU appears to directly induce apoptosis via TNF-alpha and to suppress intestinal cell proliferation, thereby resulting in degradation of the epithelial barrier, as well as in secondary inflammation mediated by inflammatory cytokines. Fluorouracil 15-19 tumor necrosis factor Mus musculus 61-70 28665687-6 2017 Downregulation of ERCC6 conferred sensitivity to 5-fluorouracil (5-FU) in HCT116 and DLD1 cells. Fluorouracil 49-63 ERCC excision repair 6, chromatin remodeling factor Homo sapiens 18-23 28870916-0 2017 GRP78 Regulates Apoptosis, Cell Survival and Proliferation in 5-Fluorouracil-resistant SNUC5 Colon Cancer Cells. Fluorouracil 62-76 heat shock protein family A (Hsp70) member 5 Homo sapiens 0-5 28870916-3 2017 To address this problem, we investigated the expression of glucose-regulated protein (GRP78, 78 kDa) in 5-FU-resistant colorectal cancer (CRC) cells (SNUC5/5FUR). Fluorouracil 104-108 heat shock protein family A (Hsp70) member 5 Homo sapiens 86-91 28870916-5 2017 In the presence of 5-FU, GRP78 knockdown induced apoptosis via activation of caspase-3 and poly(ADP-ribose)-polymerase 1. Fluorouracil 19-23 heat shock protein family A (Hsp70) member 5 Homo sapiens 25-30 28870916-5 2017 In the presence of 5-FU, GRP78 knockdown induced apoptosis via activation of caspase-3 and poly(ADP-ribose)-polymerase 1. Fluorouracil 19-23 caspase 3 Homo sapiens 77-86 28870916-5 2017 In the presence of 5-FU, GRP78 knockdown induced apoptosis via activation of caspase-3 and poly(ADP-ribose)-polymerase 1. Fluorouracil 19-23 poly(ADP-ribose) polymerase 1 Homo sapiens 91-120 28870916-8 2017 These effects were blocked upon GRP78 knockdown, which indicates that GRP78 is involved in the development of 5-FU resistance in these CRC cells. Fluorouracil 110-114 heat shock protein family A (Hsp70) member 5 Homo sapiens 32-37 28870916-8 2017 These effects were blocked upon GRP78 knockdown, which indicates that GRP78 is involved in the development of 5-FU resistance in these CRC cells. Fluorouracil 110-114 heat shock protein family A (Hsp70) member 5 Homo sapiens 70-75 28870916-9 2017 Therefore, a combination of chemotherapy and GRP78-specific targeting may counteract 5-FU resistance in CRC cells. Fluorouracil 85-89 heat shock protein family A (Hsp70) member 5 Homo sapiens 45-50 28665687-0 2017 Elevated Expression of ERCC6 Confers Resistance to 5-Fluorouracil and Is Associated with Poor Patient Survival in Colorectal Cancer. Fluorouracil 51-65 ERCC excision repair 6, chromatin remodeling factor Homo sapiens 23-28 28665687-6 2017 Downregulation of ERCC6 conferred sensitivity to 5-fluorouracil (5-FU) in HCT116 and DLD1 cells. Fluorouracil 65-69 ERCC excision repair 6, chromatin remodeling factor Homo sapiens 18-23 28665687-7 2017 Stable knockdown of ERCC6 significantly enhanced antitumor activity of 5-FU in HCT116 xenograft mouse model. Fluorouracil 71-75 excision repair cross-complementing rodent repair deficiency, complementation group 6 Mus musculus 20-25 28665687-8 2017 ERCC6 was upregulated in CRC tissues compared to matched noncancerous adjacent tissues and was also upregulated in patients who were resistant to 5-FU treatment. Fluorouracil 146-150 ERCC excision repair 6, chromatin remodeling factor Homo sapiens 0-5 28665687-9 2017 In addition, high expression of ERCC6 was associated with poor overall survival in CRC patients with or without receiving 5-FU therapy. Fluorouracil 122-126 ERCC excision repair 6, chromatin remodeling factor Homo sapiens 32-37 28927061-2 2017 MKN45 and 5FU-resistant MKN45/F2R cells were treated with 5FU and fluoro-deoxyuridine (FdU) in combination with deoxyuridine (dU) and thymidine (dT). Fluorouracil 10-13 coagulation factor II thrombin receptor Homo sapiens 30-33 28713943-2 2017 In order to investigate whether the c-Jun N-terminal kinase (JNK) signaling pathway is involved in the mechanism underlying ASIV-induced downregulated the expression of mdr1, the present study used 5-fluorouracil-resistant Bel-7402/FU human hepatic cancer cells as target cells. Fluorouracil 198-212 mitogen-activated protein kinase 8 Homo sapiens 61-64 28927061-4 2017 MKN45/F2R cells exhibited 5FU resistance (56.2-fold relative to MKN45 cells), and demonstrated decreased orotate phosphoribosyltransferase (OPRT) and increased TS levels, requiring a higher concentration of 5FU to induce ternary complex formation than MKN45 cells. Fluorouracil 26-29 coagulation factor II thrombin receptor Homo sapiens 6-9 28927061-7 2017 The addition of dU and thymidine dT to 5FU promoted the formation of ternary complexes and reversed 5FU resistance in MKN45/F2R cells, although dT inhibited the efficacy of raltitrexed (another TS inhibitor). Fluorouracil 39-42 coagulation factor II thrombin receptor Homo sapiens 124-127 28851987-2 2017 Here we describe p53-dependent control of the rate-limiting enzyme in the pyrimidine catabolic pathway, dihydropyrimidine dehydrogenase (DPYD) and its effect on pharmacokinetics of and response to 5-fluorouracil (5-FU). Fluorouracil 197-211 tumor protein p53 Homo sapiens 17-20 28928817-6 2017 The proliferation of TE-1 cells was markedly inhibited at low concentrations of DCA and 5-FU treatment when subjected to Atg5 mRNA interference, indicating that autophagy performed a protective role in cell survival upon DCA treatment. Fluorouracil 88-92 autophagy related 5 Homo sapiens 121-125 28850174-23 2017 Testing all patients for HER-2 status may help to identify patients with HER-2-positive tumours, for whom, in the absence of contraindications, trastuzumab in combination with capecitabine or 5-FU in combination with cisplatin has been shown to be beneficial. Fluorouracil 192-196 erb-b2 receptor tyrosine kinase 2 Homo sapiens 25-30 28850174-23 2017 Testing all patients for HER-2 status may help to identify patients with HER-2-positive tumours, for whom, in the absence of contraindications, trastuzumab in combination with capecitabine or 5-FU in combination with cisplatin has been shown to be beneficial. Fluorouracil 192-196 erb-b2 receptor tyrosine kinase 2 Homo sapiens 73-78 28850174-24 2017 For HER-2 negative people, all different two-and three-drug combinations including irinotecan, docetaxel, oxaliplatin or oral 5-FU prodrugs are valid treatment options for advanced gastric cancer, and consideration of the side effects of each regimen is essential in the treatment decision. Fluorouracil 126-130 erb-b2 receptor tyrosine kinase 2 Homo sapiens 4-9 28851987-2 2017 Here we describe p53-dependent control of the rate-limiting enzyme in the pyrimidine catabolic pathway, dihydropyrimidine dehydrogenase (DPYD) and its effect on pharmacokinetics of and response to 5-fluorouracil (5-FU). Fluorouracil 213-217 tumor protein p53 Homo sapiens 17-20 28851987-3 2017 Using in silico/chromatin-immunoprecipitation (ChIP) analysis we identify a conserved p53 DNA-binding site (p53BS) downstream of the DPYD gene with increased p53 occupancy following 5-FU treatment of cells. Fluorouracil 182-186 tumor protein p53 Homo sapiens 86-89 28851987-3 2017 Using in silico/chromatin-immunoprecipitation (ChIP) analysis we identify a conserved p53 DNA-binding site (p53BS) downstream of the DPYD gene with increased p53 occupancy following 5-FU treatment of cells. Fluorouracil 182-186 tumor protein p53 Homo sapiens 108-111 28852196-12 2017 The results of this study suggest that specific ADAM12-L inhibition could optimize 5-FU-based chemotherapy of BC, thereby preventing BC recurrence in patients. Fluorouracil 83-87 ADAM metallopeptidase domain 12 Homo sapiens 48-54 28852196-0 2017 ADAM12-L confers acquired 5-fluorouracil resistance in breast cancer cells. Fluorouracil 26-40 ADAM metallopeptidase domain 12 Homo sapiens 0-6 28852196-5 2017 In this study, we observed that 5-FU induces expression of the ADAM12 isoform ADAM12-L but not ADAM12-S in BC cells and in recurrent BC tissues. Fluorouracil 32-36 ADAM metallopeptidase domain 12 Homo sapiens 63-69 28851987-6 2017 In-vivo, liver specific Tp53 loss increases the conversion of 5-FU to 5-FUH2 in plasma and elicits a diminished 5-FU therapeutic response in a syngeneic colorectal tumor model consistent with increased DPYD-activity. Fluorouracil 62-66 tumor protein p53 Homo sapiens 24-28 28852196-5 2017 In this study, we observed that 5-FU induces expression of the ADAM12 isoform ADAM12-L but not ADAM12-S in BC cells and in recurrent BC tissues. Fluorouracil 32-36 ADAM metallopeptidase domain 12 Homo sapiens 78-84 28852196-5 2017 In this study, we observed that 5-FU induces expression of the ADAM12 isoform ADAM12-L but not ADAM12-S in BC cells and in recurrent BC tissues. Fluorouracil 32-36 ADAM metallopeptidase domain 12 Homo sapiens 78-84 28852196-6 2017 The overexpression of ADAM12-L in BC cells following 5-FU treatment results in the acquisition of resistance to 5-FU. Fluorouracil 53-57 ADAM metallopeptidase domain 12 Homo sapiens 22-28 28852196-6 2017 The overexpression of ADAM12-L in BC cells following 5-FU treatment results in the acquisition of resistance to 5-FU. Fluorouracil 112-116 ADAM metallopeptidase domain 12 Homo sapiens 22-28 28852196-9 2017 Conversely, ADAM12 knockdown attenuated the levels of p-Akt and restored 5-FU sensitivity in 5-FU-resistant BC cells. Fluorouracil 73-77 ADAM metallopeptidase domain 12 Homo sapiens 12-18 28852196-9 2017 Conversely, ADAM12 knockdown attenuated the levels of p-Akt and restored 5-FU sensitivity in 5-FU-resistant BC cells. Fluorouracil 93-97 ADAM metallopeptidase domain 12 Homo sapiens 12-18 28851987-6 2017 In-vivo, liver specific Tp53 loss increases the conversion of 5-FU to 5-FUH2 in plasma and elicits a diminished 5-FU therapeutic response in a syngeneic colorectal tumor model consistent with increased DPYD-activity. Fluorouracil 70-74 tumor protein p53 Homo sapiens 24-28 28531805-11 2017 Our data indicated a novel therapeutic strategy to potentiate 5-FU-induced anti-tumor effect in gastric cancer cells with resistance to 5-FU by TXN through suppression of p-STAT3/NF-kappaB (p65 and p50) and Bcl-2. Fluorouracil 62-66 nuclear factor kappa B subunit 1 Homo sapiens 179-188 28852196-11 2017 These findings suggest that ADAM12-L mediates chemoresistance to 5-FU and 5-FU-induced recurrence of BC by enhancing PI3K/Akt signaling. Fluorouracil 65-69 ADAM metallopeptidase domain 12 Homo sapiens 28-34 28852196-11 2017 These findings suggest that ADAM12-L mediates chemoresistance to 5-FU and 5-FU-induced recurrence of BC by enhancing PI3K/Akt signaling. Fluorouracil 65-69 AKT serine/threonine kinase 1 Homo sapiens 122-125 28852196-11 2017 These findings suggest that ADAM12-L mediates chemoresistance to 5-FU and 5-FU-induced recurrence of BC by enhancing PI3K/Akt signaling. Fluorouracil 74-78 ADAM metallopeptidase domain 12 Homo sapiens 28-34 28852196-11 2017 These findings suggest that ADAM12-L mediates chemoresistance to 5-FU and 5-FU-induced recurrence of BC by enhancing PI3K/Akt signaling. Fluorouracil 74-78 AKT serine/threonine kinase 1 Homo sapiens 122-125 28531805-0 2017 Troxerutin (TXN) potentiated 5-Fluorouracil (5-Fu) treatment of human gastric cancer through suppressing STAT3/NF-kappaB and Bcl-2 signaling pathways. Fluorouracil 29-43 signal transducer and activator of transcription 3 Homo sapiens 105-110 28531805-11 2017 Our data indicated a novel therapeutic strategy to potentiate 5-FU-induced anti-tumor effect in gastric cancer cells with resistance to 5-FU by TXN through suppression of p-STAT3/NF-kappaB (p65 and p50) and Bcl-2. Fluorouracil 62-66 nuclear factor kappa B subunit 1 Homo sapiens 198-201 28531805-0 2017 Troxerutin (TXN) potentiated 5-Fluorouracil (5-Fu) treatment of human gastric cancer through suppressing STAT3/NF-kappaB and Bcl-2 signaling pathways. Fluorouracil 29-43 BCL2 apoptosis regulator Homo sapiens 125-130 28531805-11 2017 Our data indicated a novel therapeutic strategy to potentiate 5-FU-induced anti-tumor effect in gastric cancer cells with resistance to 5-FU by TXN through suppression of p-STAT3/NF-kappaB (p65 and p50) and Bcl-2. Fluorouracil 62-66 BCL2 apoptosis regulator Homo sapiens 207-212 28531805-11 2017 Our data indicated a novel therapeutic strategy to potentiate 5-FU-induced anti-tumor effect in gastric cancer cells with resistance to 5-FU by TXN through suppression of p-STAT3/NF-kappaB (p65 and p50) and Bcl-2. Fluorouracil 136-140 signal transducer and activator of transcription 3 Homo sapiens 173-178 28531805-0 2017 Troxerutin (TXN) potentiated 5-Fluorouracil (5-Fu) treatment of human gastric cancer through suppressing STAT3/NF-kappaB and Bcl-2 signaling pathways. Fluorouracil 45-49 signal transducer and activator of transcription 3 Homo sapiens 105-110 28531805-11 2017 Our data indicated a novel therapeutic strategy to potentiate 5-FU-induced anti-tumor effect in gastric cancer cells with resistance to 5-FU by TXN through suppression of p-STAT3/NF-kappaB (p65 and p50) and Bcl-2. Fluorouracil 136-140 nuclear factor kappa B subunit 1 Homo sapiens 179-188 28531805-0 2017 Troxerutin (TXN) potentiated 5-Fluorouracil (5-Fu) treatment of human gastric cancer through suppressing STAT3/NF-kappaB and Bcl-2 signaling pathways. Fluorouracil 45-49 nuclear factor kappa B subunit 1 Homo sapiens 111-120 28531805-11 2017 Our data indicated a novel therapeutic strategy to potentiate 5-FU-induced anti-tumor effect in gastric cancer cells with resistance to 5-FU by TXN through suppression of p-STAT3/NF-kappaB (p65 and p50) and Bcl-2. Fluorouracil 136-140 nuclear factor kappa B subunit 1 Homo sapiens 198-201 28531805-11 2017 Our data indicated a novel therapeutic strategy to potentiate 5-FU-induced anti-tumor effect in gastric cancer cells with resistance to 5-FU by TXN through suppression of p-STAT3/NF-kappaB (p65 and p50) and Bcl-2. Fluorouracil 136-140 BCL2 apoptosis regulator Homo sapiens 207-212 28531805-0 2017 Troxerutin (TXN) potentiated 5-Fluorouracil (5-Fu) treatment of human gastric cancer through suppressing STAT3/NF-kappaB and Bcl-2 signaling pathways. Fluorouracil 45-49 BCL2 apoptosis regulator Homo sapiens 125-130 28465257-0 2017 5-Fluorouracil targets histone acetyltransferases p300/CBP in the treatment of colorectal cancer. Fluorouracil 0-14 CREB binding protein Homo sapiens 55-58 28531805-7 2017 Decreasing of phosphorylated signal transducers and activation of transcription 3 (STAT3) was included in suppression of p65 by TXN with 5-FU in combination. Fluorouracil 137-141 signal transducer and activator of transcription 3 Homo sapiens 83-88 28531805-8 2017 Additionally, the presence of TXN sensitized gastric cancer cells resistant to 5-FU to 5-FU-induced apoptosis by suppressing Bcl-2. Fluorouracil 87-91 BCL2 apoptosis regulator Homo sapiens 125-130 28531805-11 2017 Our data indicated a novel therapeutic strategy to potentiate 5-FU-induced anti-tumor effect in gastric cancer cells with resistance to 5-FU by TXN through suppression of p-STAT3/NF-kappaB (p65 and p50) and Bcl-2. Fluorouracil 62-66 signal transducer and activator of transcription 3 Homo sapiens 173-178 28465257-4 2017 We identified that 5-FU reduces the binding ability of histone acetyltransferases p300 and CBP to chromatin, and induces their degradation through lysosome. Fluorouracil 19-23 CREB binding protein Homo sapiens 91-94 28465257-5 2017 Further work revealed that the degradation of p300/CBP induced by 5-FU was dependent on chaperone-mediated autophagy, mediated by heat-shock cognate protein 70 kDa (hsc70) and lysosomal-associated membrane protein 2A (LAMP2A). Fluorouracil 66-70 CREB binding protein Homo sapiens 51-54 28465257-6 2017 Moreover, the degradation of p300/CBP is relevant to cellular resistance to 5-FU, since blocking the degradation enhances 5-FU"s cytotoxicity in CRC cells. Fluorouracil 76-80 CREB binding protein Homo sapiens 34-37 28465257-6 2017 Moreover, the degradation of p300/CBP is relevant to cellular resistance to 5-FU, since blocking the degradation enhances 5-FU"s cytotoxicity in CRC cells. Fluorouracil 122-126 CREB binding protein Homo sapiens 34-37 28465257-7 2017 From clinical data, we demonstrated that low expression of p300/CBP in CRC tissue was closely associated with poor clinical response to 5-FU based-chemotherapy, based on the analysis of 262 colorectal samples from the patients receiving 5-FU treatment: compared to cases with high expression of p300/CBP, those with low expression had lower long-term disease-free survival rate and increased early-progression. Fluorouracil 136-140 CREB binding protein Homo sapiens 64-67 28465257-7 2017 From clinical data, we demonstrated that low expression of p300/CBP in CRC tissue was closely associated with poor clinical response to 5-FU based-chemotherapy, based on the analysis of 262 colorectal samples from the patients receiving 5-FU treatment: compared to cases with high expression of p300/CBP, those with low expression had lower long-term disease-free survival rate and increased early-progression. Fluorouracil 237-241 CREB binding protein Homo sapiens 64-67 28465257-8 2017 These results elucidate a novel pharmacological effect of 5-FU involving global histone de-acetylation by promoting the degradation of p300/CBP, and highlights p300 and CBP as promising predictors of chemo-sensitivity to 5-FU treatment. Fluorouracil 58-62 CREB binding protein Homo sapiens 140-143 28465257-8 2017 These results elucidate a novel pharmacological effect of 5-FU involving global histone de-acetylation by promoting the degradation of p300/CBP, and highlights p300 and CBP as promising predictors of chemo-sensitivity to 5-FU treatment. Fluorouracil 58-62 CREB binding protein Homo sapiens 169-172 28810654-9 2017 P38 and JNK-related protein phosphorylation are involved in apoptosis initiated by CCC combined 5-FU therapy. Fluorouracil 96-100 mitogen-activated protein kinase 14 Homo sapiens 0-3 28810654-9 2017 P38 and JNK-related protein phosphorylation are involved in apoptosis initiated by CCC combined 5-FU therapy. Fluorouracil 96-100 mitogen-activated protein kinase 8 Homo sapiens 8-11 29100318-7 2017 We found that in both lines, compared to Flt-1- CRC cells, Flt-1+ CRC cells generated significantly more tumor spheres in culture, appeared to be more resistant to fluorouracil-induced apoptosis, were more detectable in the circulation after subcutaneous transplantation, and had a higher chances to generate tumor after serial adoptive transplantation. Fluorouracil 164-176 fms related receptor tyrosine kinase 1 Homo sapiens 59-64 28823289-11 2017 After co-cultured with 5-fluorouracil-treated HS-5, the number of hUCB-MNC and the ratio of CD34+ cells were decreased. Fluorouracil 23-37 CD34 molecule Homo sapiens 92-96 28915668-0 2017 NSC30049 inhibits Chk1 pathway in 5-FU-resistant CRC bulk and stem cell populations. Fluorouracil 34-38 checkpoint kinase 1 Homo sapiens 18-22 28915668-12 2017 Thus, NSC49L as a single agent or combined with 5-FU can be developed as a therapeutic agent by targeting the Chk1 pathway in 5-FU-resistant CRC heterogeneous bulk and CRC stem cell populations. Fluorouracil 48-52 checkpoint kinase 1 Homo sapiens 110-114 28915668-12 2017 Thus, NSC49L as a single agent or combined with 5-FU can be developed as a therapeutic agent by targeting the Chk1 pathway in 5-FU-resistant CRC heterogeneous bulk and CRC stem cell populations. Fluorouracil 126-130 checkpoint kinase 1 Homo sapiens 110-114 28759561-0 2017 Regenerating Family Member 4 (Reg4) Enhances 5-Fluorouracil Resistance of Gastric Cancer Through Activating MAPK/Erk/Bim Signaling Pathway. Fluorouracil 45-59 mitogen-activated protein kinase 1 Homo sapiens 113-116 28591704-7 2017 Our results further demonstrate that miR-196b-5p promotes stemness and chemoresistance of CRC cells to 5-fluorouracil via targeting negative regulators SOCS1 and SOCS3 of STAT3 signaling pathway, giving rise to activation of STAT3 signaling. Fluorouracil 103-117 signal transducer and activator of transcription 3 Homo sapiens 171-176 28591704-7 2017 Our results further demonstrate that miR-196b-5p promotes stemness and chemoresistance of CRC cells to 5-fluorouracil via targeting negative regulators SOCS1 and SOCS3 of STAT3 signaling pathway, giving rise to activation of STAT3 signaling. Fluorouracil 103-117 signal transducer and activator of transcription 3 Homo sapiens 225-230 28696828-6 2017 And our results reveal that chemotherapeutics, Cisplatin (CDDP) and 5-Fluoracil (5-FU), result in the greater decrease of protein level of Bcl-2 and Mcl-1 in NPC cells than those in NPE cells. Fluorouracil 68-79 BCL2 apoptosis regulator Homo sapiens 139-144 28696828-6 2017 And our results reveal that chemotherapeutics, Cisplatin (CDDP) and 5-Fluoracil (5-FU), result in the greater decrease of protein level of Bcl-2 and Mcl-1 in NPC cells than those in NPE cells. Fluorouracil 81-85 BCL2 apoptosis regulator Homo sapiens 139-144 28668827-4 2017 Furthermore, anthracimycin had no effect on the enrichment of EpCAM-high liver cancer stem cells (CSCs), while fluorouracil dramatically enriched the CSCs with activation of the stemness-related genes EPCAM and SOX9 in HuH7 cells. Fluorouracil 111-123 epithelial cell adhesion molecule Homo sapiens 201-206 28697172-7 2017 Importantly, the RCC xenograft mouse model mice who received the combination treatment of 5-fluorouracil (5-FU) and anti-programmed cell death-ligand 1 (PD-L1) antibodies (Abs) had longer survival times compared to those who received 5-FU or anti-PD-L1 Abs alone. Fluorouracil 90-104 CD274 antigen Mus musculus 247-252 28697172-7 2017 Importantly, the RCC xenograft mouse model mice who received the combination treatment of 5-fluorouracil (5-FU) and anti-programmed cell death-ligand 1 (PD-L1) antibodies (Abs) had longer survival times compared to those who received 5-FU or anti-PD-L1 Abs alone. Fluorouracil 106-110 CD274 antigen Mus musculus 247-252 28697172-7 2017 Importantly, the RCC xenograft mouse model mice who received the combination treatment of 5-fluorouracil (5-FU) and anti-programmed cell death-ligand 1 (PD-L1) antibodies (Abs) had longer survival times compared to those who received 5-FU or anti-PD-L1 Abs alone. Fluorouracil 234-238 CD274 antigen Mus musculus 153-158 28697172-9 2017 CONCLUSIONS We conclude that 5-FU can sensitize RCC to anti-PD-L1 treatment by releasing the immune suppression in the tumor microenvironment. Fluorouracil 29-33 CD274 antigen Mus musculus 60-65 28662182-0 2017 Extreme low dose of 5-fluorouracil reverses MDR in cancer by sensitizing cancer associated fibroblasts and down-regulating P-gp. Fluorouracil 20-34 ATP binding cassette subfamily B member 1 Homo sapiens 123-127 28671577-0 2017 Silencing of NRF2 Reduces the Expression of ALDH1A1 and ALDH3A1 and Sensitizes to 5-FU in Pancreatic Cancer Cells. Fluorouracil 82-86 NFE2 like bZIP transcription factor 2 Homo sapiens 13-17 28671577-8 2017 Furthermore, this NRF2 depletion enhanced the antiproliferative effects of the chemotherapeutic agent, 5-fluorouracil (5-FU) in pancreatic cancer cells. Fluorouracil 103-117 NFE2 like bZIP transcription factor 2 Homo sapiens 18-22 28671577-8 2017 Furthermore, this NRF2 depletion enhanced the antiproliferative effects of the chemotherapeutic agent, 5-fluorouracil (5-FU) in pancreatic cancer cells. Fluorouracil 119-123 NFE2 like bZIP transcription factor 2 Homo sapiens 18-22 28289897-4 2017 The expression of E cadherin was studied after 5 fluorouracil (5FU) treatment and correlated to CRC relapse, chemo-resistance and survival. Fluorouracil 49-61 cadherin 1 Homo sapiens 18-28 28289897-4 2017 The expression of E cadherin was studied after 5 fluorouracil (5FU) treatment and correlated to CRC relapse, chemo-resistance and survival. Fluorouracil 63-66 cadherin 1 Homo sapiens 18-28 28436588-7 2017 This defect is in part due to increased apoptosis of HSPCs with reduced Erg dosage, a phenotype that becomes more drastic during 5-FU-induced stress hematopoiesis. Fluorouracil 129-133 ETS transcription factor ERG Homo sapiens 72-75 28665983-9 2017 Cisplatin, 5-FU and doxorubicin caused similar decreased of cell survival with the increase of let-7d level (p = 0.004, post-trend p = 0.046; p = 0.004, post trend p = 0.0005 and p<0.0001, post trend p = 0.0001, respectively). Fluorouracil 11-15 microRNA let-7d Homo sapiens 95-101 28662182-1 2017 We conducted a prospective, meaningful study of extreme low dose of 5-fluorouracil (5FU) as a metronomic agent targeting cancer associated fibroblasts (CAFs) to reverse Multidrug resistance (MDR) by sensitizing cancer associated fibroblasts and down-regulating P-glycoprotein (P-gp). Fluorouracil 68-82 ATP binding cassette subfamily B member 1 Homo sapiens 261-275 28662182-1 2017 We conducted a prospective, meaningful study of extreme low dose of 5-fluorouracil (5FU) as a metronomic agent targeting cancer associated fibroblasts (CAFs) to reverse Multidrug resistance (MDR) by sensitizing cancer associated fibroblasts and down-regulating P-glycoprotein (P-gp). Fluorouracil 68-82 ATP binding cassette subfamily B member 1 Homo sapiens 277-281 28662182-1 2017 We conducted a prospective, meaningful study of extreme low dose of 5-fluorouracil (5FU) as a metronomic agent targeting cancer associated fibroblasts (CAFs) to reverse Multidrug resistance (MDR) by sensitizing cancer associated fibroblasts and down-regulating P-glycoprotein (P-gp). Fluorouracil 84-87 ATP binding cassette subfamily B member 1 Homo sapiens 261-275 28662182-1 2017 We conducted a prospective, meaningful study of extreme low dose of 5-fluorouracil (5FU) as a metronomic agent targeting cancer associated fibroblasts (CAFs) to reverse Multidrug resistance (MDR) by sensitizing cancer associated fibroblasts and down-regulating P-glycoprotein (P-gp). Fluorouracil 84-87 ATP binding cassette subfamily B member 1 Homo sapiens 277-281 28640255-5 2017 Upregulation of AQP9 was associated with enhanced chemosensitivity to 5-fluorouracil (5-FU) both in vitro and in vivo. Fluorouracil 70-84 aquaporin 9 Homo sapiens 16-20 28640255-9 2017 Taken together, AQP9 enhances the cytotoxic response to 5-FU in CRC cells by simultaneously inducing S-phase arrest via activation of RAS signaling and facilitating drug uptake. Fluorouracil 56-60 aquaporin 9 Homo sapiens 16-20 28640255-10 2017 Our results suggest that AQP9 might be a novel predictor for the benefit of 5-FU-based chemotherapy in CRC. Fluorouracil 76-80 aquaporin 9 Homo sapiens 25-29 28640255-11 2017 The identification of AQP9-induced tumor sensitivity to 5-FU highlights the role of AQP9 in regulating chemosensitivity in CRC. Fluorouracil 56-60 aquaporin 9 Homo sapiens 22-26 28416637-8 2017 SJSA cells treated with 5-fluorouracil, which induces metabolic and genotoxic stress and activates p53, further implicated CDK19 in p53 target gene expression. Fluorouracil 24-38 tumor protein p53 Homo sapiens 99-102 28637493-6 2017 The correlation between 5-FU treatment and the expression and activation of NLRP3 inflammasome was further examined by evaluating NLRP3 and IL-1beta expression in OSCC cell lines without or with NLRP3 knocked down. Fluorouracil 24-28 interleukin 1 beta Mus musculus 140-148 28637493-11 2017 RESULTS: In the clinical analysis, expression and activation of NLRP3 inflammasome was clearly increased in OSCC tissues of patients who received 5-FU-based chemotherapy. Fluorouracil 146-150 NLR family pyrin domain containing 3 Homo sapiens 64-69 28637493-15 2017 Further investigation showed that intracellular ROS induced by 5-FU promoted the expression and activation of NLRP3 inflammasome and increased the production of interleukin (IL)-1beta, which then mediated the chemoresistance. Fluorouracil 63-67 interleukin 1 beta Mus musculus 161-183 28637493-18 2017 CONCLUSIONS: Our findings suggest that NLRP3 inflammasome promoted 5-FU resistance of OSCC both in vitro and in vivo, and targeting the ROS/NLRP3 inflammasome/IL-1beta signaling pathway may help 5-FU-based adjuvant chemotherapy of OSCC. Fluorouracil 67-71 interleukin 1 beta Mus musculus 159-167 28637493-18 2017 CONCLUSIONS: Our findings suggest that NLRP3 inflammasome promoted 5-FU resistance of OSCC both in vitro and in vivo, and targeting the ROS/NLRP3 inflammasome/IL-1beta signaling pathway may help 5-FU-based adjuvant chemotherapy of OSCC. Fluorouracil 195-199 interleukin 1 beta Mus musculus 159-167 27979915-2 2017 Toward this goal, we retrovirally transduced an immortalized, clonal NSC line to stably express cytosine deaminase (HB1.F3.CD.C21; CD-NSCs), which converts the prodrug 5-fluorocytosine (5-FC) to 5-fluorouracil (5-FU).Experimental Design: Recurrent high-grade glioma patients underwent intracranial administration of CD-NSCs during tumor resection or biopsy. Fluorouracil 195-209 histocompatibility minor HB-1 Homo sapiens 116-119 27979915-2 2017 Toward this goal, we retrovirally transduced an immortalized, clonal NSC line to stably express cytosine deaminase (HB1.F3.CD.C21; CD-NSCs), which converts the prodrug 5-fluorocytosine (5-FC) to 5-fluorouracil (5-FU).Experimental Design: Recurrent high-grade glioma patients underwent intracranial administration of CD-NSCs during tumor resection or biopsy. Fluorouracil 211-215 histocompatibility minor HB-1 Homo sapiens 116-119 28189472-4 2017 5-FU significantly elevated levels of blood urea nitrogen (BUN), creatinine, and uric acid; while it reduced activities of superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GSH-Px). Fluorouracil 0-4 catalase Rattus norvegicus 151-159 28189472-4 2017 5-FU significantly elevated levels of blood urea nitrogen (BUN), creatinine, and uric acid; while it reduced activities of superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GSH-Px). Fluorouracil 0-4 catalase Rattus norvegicus 161-164 28433634-5 2017 Here, we report that co-administration of 5-FU and SKI-II at low sub-toxic concentrations of 20 muM and 5 muM, respectively, synergistically inhibit cell proliferation, markedly reduce cell migration and the clonogenic survival, and increase apoptosis induction in HepG2 cells. Fluorouracil 42-46 latexin Homo sapiens 96-99 28433634-5 2017 Here, we report that co-administration of 5-FU and SKI-II at low sub-toxic concentrations of 20 muM and 5 muM, respectively, synergistically inhibit cell proliferation, markedly reduce cell migration and the clonogenic survival, and increase apoptosis induction in HepG2 cells. Fluorouracil 42-46 latexin Homo sapiens 106-109 28640255-5 2017 Upregulation of AQP9 was associated with enhanced chemosensitivity to 5-fluorouracil (5-FU) both in vitro and in vivo. Fluorouracil 86-90 aquaporin 9 Homo sapiens 16-20 28640255-6 2017 Overexpression of AQP9 resulted in an increased intracellular level of 5-FU in CRC cells, hence leading to a higher percentage of apoptosis after 5-FU treatment. Fluorouracil 71-75 aquaporin 9 Homo sapiens 18-22 28640255-6 2017 Overexpression of AQP9 resulted in an increased intracellular level of 5-FU in CRC cells, hence leading to a higher percentage of apoptosis after 5-FU treatment. Fluorouracil 146-150 aquaporin 9 Homo sapiens 18-22 28416637-8 2017 SJSA cells treated with 5-fluorouracil, which induces metabolic and genotoxic stress and activates p53, further implicated CDK19 in p53 target gene expression. Fluorouracil 24-38 tumor protein p53 Homo sapiens 132-135 29207609-0 2017 Reciprocal regulation of DGCR5 and miR-320a affects the cellular malignant phenotype and 5-FU response in pancreatic ductal adenocarcinoma. Fluorouracil 89-93 DiGeorge syndrome critical region gene 5 Homo sapiens 25-30 29207609-5 2017 Further experiments demonstrated that DGCR5 and miR-320a regulate each other in a reciprocal manner and that DGCR5 reverses the inhibition of PDCD4 by miR-320a, which is involved in the regulation of the PDAC cell phenotype and response to 5-FU. Fluorouracil 240-244 DiGeorge syndrome critical region gene 5 Homo sapiens 109-114 28551618-1 2017 BACKGROUND: Preclinical evidence demonstrates that mitogen-activated protein kinase kinase (MEK)/extracellular signal-regulated kinase (ERK) pathway inhibition increases sensitivity to 5-fluorouracil (5-FU) in colorectal cancer (CRC) cell lines and xenografts. Fluorouracil 185-199 mitogen-activated protein kinase kinase 7 Homo sapiens 51-90 28389232-10 2017 The mechanisms of AOG on enhancing the growth inhibitory effect of 5-FU may be through the influence of TLR-4/NF-kappaB pathway. Fluorouracil 67-71 nuclear factor kappa B subunit 1 Homo sapiens 110-119 28551635-0 2017 Enhanced Susceptibility to 5-Fluorouracil in Human Colon Cancer Cells by Silencing of GRP78. Fluorouracil 27-41 heat shock protein family A (Hsp70) member 5 Homo sapiens 86-91 28551635-6 2017 Because both anticancer drugs and down-regulation of GRP78 expression inhibit cancer progression and growth, we hypothesized that down-regulation of GRP78 expression might lead to enhanced susceptibility of cancer cells to cytotoxic action of 5-fluorouracil (5-FU). Fluorouracil 243-257 heat shock protein family A (Hsp70) member 5 Homo sapiens 53-58 28551635-6 2017 Because both anticancer drugs and down-regulation of GRP78 expression inhibit cancer progression and growth, we hypothesized that down-regulation of GRP78 expression might lead to enhanced susceptibility of cancer cells to cytotoxic action of 5-fluorouracil (5-FU). Fluorouracil 243-257 heat shock protein family A (Hsp70) member 5 Homo sapiens 149-154 28551635-6 2017 Because both anticancer drugs and down-regulation of GRP78 expression inhibit cancer progression and growth, we hypothesized that down-regulation of GRP78 expression might lead to enhanced susceptibility of cancer cells to cytotoxic action of 5-fluorouracil (5-FU). Fluorouracil 259-263 heat shock protein family A (Hsp70) member 5 Homo sapiens 149-154 28551618-1 2017 BACKGROUND: Preclinical evidence demonstrates that mitogen-activated protein kinase kinase (MEK)/extracellular signal-regulated kinase (ERK) pathway inhibition increases sensitivity to 5-fluorouracil (5-FU) in colorectal cancer (CRC) cell lines and xenografts. Fluorouracil 185-199 mitogen-activated protein kinase kinase 7 Homo sapiens 92-95 28551635-7 2017 MATERIALS AND METHODS: GRP78 expression was suppressed in LoVo colon cancer cells by utilizing small-interfering RNA (si-GRP78), and the cells were subsequently used to study the antiproliferative and anticancer effects of 5-FU treatment. Fluorouracil 223-227 heat shock protein family A (Hsp70) member 5 Homo sapiens 23-28 28551618-1 2017 BACKGROUND: Preclinical evidence demonstrates that mitogen-activated protein kinase kinase (MEK)/extracellular signal-regulated kinase (ERK) pathway inhibition increases sensitivity to 5-fluorouracil (5-FU) in colorectal cancer (CRC) cell lines and xenografts. Fluorouracil 201-205 mitogen-activated protein kinase kinase 7 Homo sapiens 51-90 28551635-8 2017 The signaling pathways responsible for the increase of LoVo cell susceptibility to 5-FU treatment after exposure to GRP78 siRNA were determined by western blot. Fluorouracil 83-87 heat shock protein family A (Hsp70) member 5 Homo sapiens 116-121 28551618-1 2017 BACKGROUND: Preclinical evidence demonstrates that mitogen-activated protein kinase kinase (MEK)/extracellular signal-regulated kinase (ERK) pathway inhibition increases sensitivity to 5-fluorouracil (5-FU) in colorectal cancer (CRC) cell lines and xenografts. Fluorouracil 201-205 mitogen-activated protein kinase kinase 7 Homo sapiens 92-95 28440463-11 2017 Consistent with this, Livin-knockdown cells showed greater expression of cleaved caspases-3 and -7 and poly(ADP-ribose)polymerase compared with that in control cells after cisplatin, 5-FU, or docetaxel treatment. Fluorouracil 183-187 caspase 3 Homo sapiens 81-98 28067150-0 2017 Low-dose 5-fluorouracil sensitizes HepG2 cells to TRAIL through TRAIL receptor DR5 and survivin-dependent mechanisms. Fluorouracil 9-23 TNF superfamily member 10 Homo sapiens 50-55 28067150-0 2017 Low-dose 5-fluorouracil sensitizes HepG2 cells to TRAIL through TRAIL receptor DR5 and survivin-dependent mechanisms. Fluorouracil 9-23 TNF superfamily member 10 Homo sapiens 64-69 28067150-3 2017 In the present study, we investigated the sensitizing effect of 5-fluorouracil (5-FU) on TRAIL-induced apoptosis in TRAIL-resistant HepG2 hepatocarcinoma cells. Fluorouracil 64-78 TNF superfamily member 10 Homo sapiens 89-94 28067150-3 2017 In the present study, we investigated the sensitizing effect of 5-fluorouracil (5-FU) on TRAIL-induced apoptosis in TRAIL-resistant HepG2 hepatocarcinoma cells. Fluorouracil 64-78 TNF superfamily member 10 Homo sapiens 116-121 28067150-3 2017 In the present study, we investigated the sensitizing effect of 5-fluorouracil (5-FU) on TRAIL-induced apoptosis in TRAIL-resistant HepG2 hepatocarcinoma cells. Fluorouracil 80-84 TNF superfamily member 10 Homo sapiens 89-94 28067150-3 2017 In the present study, we investigated the sensitizing effect of 5-fluorouracil (5-FU) on TRAIL-induced apoptosis in TRAIL-resistant HepG2 hepatocarcinoma cells. Fluorouracil 80-84 TNF superfamily member 10 Homo sapiens 116-121 28067150-4 2017 The results show that 5-FU pretreatment could sensitize HepG2 cells to TRAIL-mediated apoptosis. Fluorouracil 22-26 TNF superfamily member 10 Homo sapiens 71-76 28378512-4 2017 5-FU induced significant weight loss, shortened villi height, and increased histological severity, IL-1beta expression, and MPO activity compared to the normal control group. Fluorouracil 0-4 interleukin 1 beta Rattus norvegicus 99-107 28670496-6 2017 For example, resistance to 5-fluorouracil is mediated by alterations in miR-21, miR-27a/b, and miR-155; the sensitivity to Docetaxel is influenced by miR-98, miR-192, miR-194, miR-200b, miR-212, and miR-424; and the resistance to Cisplatin is mediated by miR-let-7, miR-15, miR-16 miR-21 and miR-214. Fluorouracil 27-41 microRNA 27a Homo sapiens 80-87 28266023-6 2017 In addition, Astragaloside II is capable of sensitizing cells to 5-fluorouracil-induced cell death via inhibition of pro-survival autophagy involvement of MAPK-mTOR pathway. Fluorouracil 65-79 mechanistic target of rapamycin kinase Homo sapiens 160-164 28497756-2 2017 We assessed the efficacy and safety of S-1, a chemotherapeutic agent based on fluorouracil, in patients with sorafenib-refractory advanced hepatocellular carcinoma. Fluorouracil 78-90 proteasome 26S subunit, non-ATPase 1 Homo sapiens 39-42 28631569-2 2017 Insulin-induced sensitivity of MCF-7 breast cancer cells to chemotherapeutic agents 5-fluorouracil and cyclophosphamide was evaluated. Fluorouracil 84-98 insulin Homo sapiens 0-7 28599477-9 2017 The combination of SM-1 and 5-FU treatment led to significantly increased caspase-3 activity compared with either compound alone. Fluorouracil 28-32 caspase 3 Homo sapiens 74-83 28599477-12 2017 5-FU and SM-1 treatment in combination increased tumor proliferation inhibition in HCT116 and LoVo xenograft mouse models of colorectal cancer, compared with SM-1 or 5-FU treatment alone. Fluorouracil 0-4 myosin, heavy polypeptide 11, smooth muscle Mus musculus 158-162 28599477-12 2017 5-FU and SM-1 treatment in combination increased tumor proliferation inhibition in HCT116 and LoVo xenograft mouse models of colorectal cancer, compared with SM-1 or 5-FU treatment alone. Fluorouracil 166-170 myosin, heavy polypeptide 11, smooth muscle Mus musculus 9-13 28631569-0 2017 Insulin-induced enhancement of MCF-7 breast cancer cell response to 5-fluorouracil and cyclophosphamide. Fluorouracil 68-82 insulin Homo sapiens 0-7 28653901-8 2017 Downregulation of gankyrin expression enhanced chemosensitivity to 5-fluorouracil and cisplatin by inducing cell apoptosis. Fluorouracil 67-81 proteasome 26S subunit, non-ATPase 10 Homo sapiens 18-26 28653901-11 2017 Gankyrin played an important role in gastric carcinogenesis and could be a potential effective therapeutic target for enhancing chemosensitivity to 5-fluorouracil and cisplatin. Fluorouracil 148-162 proteasome 26S subunit, non-ATPase 10 Homo sapiens 0-8 28074308-0 2017 Influence of TS and ABCB1 gene polymorphisms on survival outcomes of 5-FU-based chemotherapy in a Chinese population of advanced gastric cancer patients. Fluorouracil 69-73 ATP binding cassette subfamily B member 1 Homo sapiens 20-25 28432271-0 2017 Knockdown of PRDX2 sensitizes colon cancer cells to 5-FU by suppressing the PI3K/AKT signaling pathway. Fluorouracil 52-56 peroxiredoxin 2 Homo sapiens 13-18 28611669-0 2017 CD24 Expression Is Increased in 5-Fluorouracil-Treated Esophageal Adenocarcinoma Cells. Fluorouracil 32-46 CD24 molecule Homo sapiens 0-4 28611669-4 2017 OE19 and OE33 EAC cells surviving 5-FU exposure exhibited an increase in CSC markers CD24 and ABCG2 and also an increased resistance to apoptosis. Fluorouracil 34-38 CD24 molecule Homo sapiens 85-89 28611669-4 2017 OE19 and OE33 EAC cells surviving 5-FU exposure exhibited an increase in CSC markers CD24 and ABCG2 and also an increased resistance to apoptosis. Fluorouracil 34-38 ATP binding cassette subfamily G member 2 (Junior blood group) Homo sapiens 94-99 28611669-7 2017 Treatment with celecoxib alone or in combination with 5-FU also resulted in a reduction of CD24 expression. Fluorouracil 54-58 CD24 molecule Homo sapiens 91-95 28881790-6 2017 The FTD-resistant sublines were not cross-resistant to 5-fluorouracil (5-FU); 5-FU sensitivity was affected only slightly when let-7d-5p as overexpressed or knocked down. Fluorouracil 78-82 microRNA let-7d Homo sapiens 127-133 28432271-6 2017 Our data also suggested that the PI3K/AKT signaling pathway links PRDX2 with 5-FU-induced apoptosis in colon cancer. Fluorouracil 77-81 AKT serine/threonine kinase 1 Homo sapiens 38-41 28432271-6 2017 Our data also suggested that the PI3K/AKT signaling pathway links PRDX2 with 5-FU-induced apoptosis in colon cancer. Fluorouracil 77-81 peroxiredoxin 2 Homo sapiens 66-71 28432271-11 2017 Taken together, our study suggests that decreasing the expression of PRDX2 could be a promising strategy for increasing the sensitivity of colon cancer cells to 5-FU. Fluorouracil 161-165 peroxiredoxin 2 Homo sapiens 69-74 28432271-0 2017 Knockdown of PRDX2 sensitizes colon cancer cells to 5-FU by suppressing the PI3K/AKT signaling pathway. Fluorouracil 52-56 AKT serine/threonine kinase 1 Homo sapiens 81-84 28432271-3 2017 Peroxiredoxin-2 (PRDX2), is an important member of the ROS scavenging system, and may be a potential target that promotes chemosensitivity to 5-FU in colon cancer. Fluorouracil 142-146 peroxiredoxin 2 Homo sapiens 0-15 28432271-3 2017 Peroxiredoxin-2 (PRDX2), is an important member of the ROS scavenging system, and may be a potential target that promotes chemosensitivity to 5-FU in colon cancer. Fluorouracil 142-146 peroxiredoxin 2 Homo sapiens 17-22 28432271-4 2017 Here, we depleted PRDX2 by PRDX2-shRNA-LV transduction in two colon cancer cell lines and found that in vitro PRDX2 knockdown facilitates cell death, and apoptosis in 5-FU-treated colon cancer cells. Fluorouracil 167-171 peroxiredoxin 2 Homo sapiens 18-23 27878958-9 2017 Knockdown of Orai1 or pharmacological inhibition of SOCE enhanced 5-FU-induced inhibition of PI3K/AKT/mTOR pathway and potentiated 5-FU-activated autophagic cell death. Fluorouracil 66-70 AKT serine/threonine kinase 1 Homo sapiens 98-101 28481246-8 2017 Moreover, CMP in combination with 5-FU alleviated severe liver injury induced by 5-FU via reducing the levels of ROS, IL-1beta, and IL-6, decreasing expression of p-IkappaB-alpha, NF-kappaB, p-NF-kappaB, pp38 and Bax, and elevating levels of Nrf2, GCL, HO-1 and Bcl-2. Fluorouracil 34-38 interleukin 1 beta Mus musculus 118-126 28481246-8 2017 Moreover, CMP in combination with 5-FU alleviated severe liver injury induced by 5-FU via reducing the levels of ROS, IL-1beta, and IL-6, decreasing expression of p-IkappaB-alpha, NF-kappaB, p-NF-kappaB, pp38 and Bax, and elevating levels of Nrf2, GCL, HO-1 and Bcl-2. Fluorouracil 34-38 interleukin 6 Mus musculus 132-136 28481246-8 2017 Moreover, CMP in combination with 5-FU alleviated severe liver injury induced by 5-FU via reducing the levels of ROS, IL-1beta, and IL-6, decreasing expression of p-IkappaB-alpha, NF-kappaB, p-NF-kappaB, pp38 and Bax, and elevating levels of Nrf2, GCL, HO-1 and Bcl-2. Fluorouracil 34-38 nuclear factor, erythroid derived 2, like 2 Mus musculus 242-246 28481246-8 2017 Moreover, CMP in combination with 5-FU alleviated severe liver injury induced by 5-FU via reducing the levels of ROS, IL-1beta, and IL-6, decreasing expression of p-IkappaB-alpha, NF-kappaB, p-NF-kappaB, pp38 and Bax, and elevating levels of Nrf2, GCL, HO-1 and Bcl-2. Fluorouracil 34-38 germ cell-less, spermatogenesis associated 1 Mus musculus 248-251 28481246-8 2017 Moreover, CMP in combination with 5-FU alleviated severe liver injury induced by 5-FU via reducing the levels of ROS, IL-1beta, and IL-6, decreasing expression of p-IkappaB-alpha, NF-kappaB, p-NF-kappaB, pp38 and Bax, and elevating levels of Nrf2, GCL, HO-1 and Bcl-2. Fluorouracil 34-38 heme oxygenase 1 Mus musculus 253-257 28481246-8 2017 Moreover, CMP in combination with 5-FU alleviated severe liver injury induced by 5-FU via reducing the levels of ROS, IL-1beta, and IL-6, decreasing expression of p-IkappaB-alpha, NF-kappaB, p-NF-kappaB, pp38 and Bax, and elevating levels of Nrf2, GCL, HO-1 and Bcl-2. Fluorouracil 34-38 B cell leukemia/lymphoma 2 Mus musculus 262-267 27878958-6 2017 We found that 5-fluorouracil (5-FU) induced autophagic cell death in HepG2 hepatocarcinoma cells by inhibiting PI3K/AKT/mTOR pathway. Fluorouracil 14-28 AKT serine/threonine kinase 1 Homo sapiens 116-119 27878958-6 2017 We found that 5-fluorouracil (5-FU) induced autophagic cell death in HepG2 hepatocarcinoma cells by inhibiting PI3K/AKT/mTOR pathway. Fluorouracil 14-28 mechanistic target of rapamycin kinase Homo sapiens 120-124 27878958-9 2017 Knockdown of Orai1 or pharmacological inhibition of SOCE enhanced 5-FU-induced inhibition of PI3K/AKT/mTOR pathway and potentiated 5-FU-activated autophagic cell death. Fluorouracil 66-70 mechanistic target of rapamycin kinase Homo sapiens 102-106 27878958-6 2017 We found that 5-fluorouracil (5-FU) induced autophagic cell death in HepG2 hepatocarcinoma cells by inhibiting PI3K/AKT/mTOR pathway. Fluorouracil 30-34 AKT serine/threonine kinase 1 Homo sapiens 116-119 27878958-6 2017 We found that 5-fluorouracil (5-FU) induced autophagic cell death in HepG2 hepatocarcinoma cells by inhibiting PI3K/AKT/mTOR pathway. Fluorouracil 30-34 mechanistic target of rapamycin kinase Homo sapiens 120-124 28207045-6 2017 Treatment with miR-21 and miR-30d antagonists sensitized hypoxic CRC cells to 5-FU. Fluorouracil 78-82 microRNA 30d Homo sapiens 26-33 28159957-1 2017 Background: S-1 is a combination of tegafur [metabolized to 5-fluorouracil (5-FU)] with the modulators gimeracil (5-chloro-2,4-dihydroxypyridine) and oteracil potassium. Fluorouracil 60-74 proteasome 26S subunit, non-ATPase 1 Homo sapiens 12-15 28159957-1 2017 Background: S-1 is a combination of tegafur [metabolized to 5-fluorouracil (5-FU)] with the modulators gimeracil (5-chloro-2,4-dihydroxypyridine) and oteracil potassium. Fluorouracil 76-80 proteasome 26S subunit, non-ATPase 1 Homo sapiens 12-15 28159957-5 2017 Objective: We compared steady state pharmacokinetics of 5-FU for the initial S-1 dose and reduced doses in patients with head and neck cancer requiring dose reduction due to renal and non-renal toxicities. Fluorouracil 56-60 proteasome 26S subunit, non-ATPase 1 Homo sapiens 77-80 28529594-8 2017 Western blot analyses were then performed, and the results revealed an increase in tumor protein 53 and cleaved caspase 9, and a decrease in B-cell lymphoma 2 protein expressions in PsA and PsA + 5-FU treated colon cancer cells compared with the vehicle-treated (PBS) cells. Fluorouracil 196-200 tumor protein p53 Homo sapiens 83-99 28446688-3 2017 We show that the coadministration of G1T28 (trilaciclib), which is a small-molecule inhibitor of cyclin-dependent kinases 4 and 6 (CDK4/6), contemporaneously with cytotoxic chemotherapy protects murine hematopoietic stem cells (HSCs) from chemotherapy-induced exhaustion in a serial 5-fluorouracil treatment model. Fluorouracil 283-297 cyclin-dependent kinase 4 Mus musculus 97-129 28413604-7 2017 We demonstrated that knockdown of GLI1 or GLI2 sensitized LoVo-R cells to 5-FU treatment, reduced cell invasiveness. Fluorouracil 74-78 GLI family zinc finger 2 Homo sapiens 42-46 28353366-9 2017 Interleukin (IL)-1beta and tumor necrosis factor (TNF)-alpha mRNA expression were significantly lower in the 5-FU plus selenium group than in the 5-FU only group (IL-1beta, P < 0.01; TNF-alpha, P < 0.05). Fluorouracil 109-113 interleukin 1 beta Rattus norvegicus 0-22 28353366-9 2017 Interleukin (IL)-1beta and tumor necrosis factor (TNF)-alpha mRNA expression were significantly lower in the 5-FU plus selenium group than in the 5-FU only group (IL-1beta, P < 0.01; TNF-alpha, P < 0.05). Fluorouracil 109-113 tumor necrosis factor Rattus norvegicus 27-60 28353366-9 2017 Interleukin (IL)-1beta and tumor necrosis factor (TNF)-alpha mRNA expression were significantly lower in the 5-FU plus selenium group than in the 5-FU only group (IL-1beta, P < 0.01; TNF-alpha, P < 0.05). Fluorouracil 109-113 tumor necrosis factor Rattus norvegicus 186-195 28052346-7 2017 Complement became activated in mice receiving 5-FU, indicated by increased intestinal levels of C3a and C5a. Fluorouracil 46-50 hemolytic complement Mus musculus 104-107 28428709-9 2017 5-FU-induced expression of IL-13, IL-17A, TNF-alpha, and IFN-gamma in the ileum was Fn14 dependent. Fluorouracil 0-4 interleukin 13 Mus musculus 27-32 28428709-9 2017 5-FU-induced expression of IL-13, IL-17A, TNF-alpha, and IFN-gamma in the ileum was Fn14 dependent. Fluorouracil 0-4 tumor necrosis factor Mus musculus 42-51 28428709-9 2017 5-FU-induced expression of IL-13, IL-17A, TNF-alpha, and IFN-gamma in the ileum was Fn14 dependent. Fluorouracil 0-4 interferon gamma Mus musculus 57-66 28428709-10 2017 The severity of 5-FU-induced diarrhea was lower in IL-13Ralpha1 KO mice, indicating major role for IL-13 signaling via IL-13Ralpha1 in pathogenesis. Fluorouracil 16-20 interleukin 13 Mus musculus 51-56 29871302-8 2017 The combination of metformin and 5-fluorouracil produced an antagonism action in Hep-2 cells.Western blot assay showed that metformin, cisplatin, 5-fluorouracil could have caused the increase of expression level of AMPK-alpha, P21 and Cyclin D1 in Hep-2 cells while Paclitaxel could have cause the decrease of expression level of Cyclin D1. Fluorouracil 146-160 cyclin dependent kinase inhibitor 1A Homo sapiens 227-230 29871302-11 2017 Metformin has an antagonism on the anticancer effect to 5-fluorouracil in Hep-2 cells, and this antagonistic effect occurred partially through molecular signal pathways of AMPK-alpha, P21 and Cyclin D1 and it"s significantly related to the cell cycle arrest. Fluorouracil 56-70 cyclin dependent kinase inhibitor 1A Homo sapiens 184-187 28402255-7 2017 We found that 5-fluorouracil-based chemotherapy regimens significantly increased plasma levels of leptin and adiponectin and decreased plasma levels of resistin and visfatin in PR and SD patients, whereas the plasma levels of these molecules were not affected in PD patients. Fluorouracil 14-28 adiponectin, C1Q and collagen domain containing Homo sapiens 109-120 29871302-8 2017 The combination of metformin and 5-fluorouracil produced an antagonism action in Hep-2 cells.Western blot assay showed that metformin, cisplatin, 5-fluorouracil could have caused the increase of expression level of AMPK-alpha, P21 and Cyclin D1 in Hep-2 cells while Paclitaxel could have cause the decrease of expression level of Cyclin D1. Fluorouracil 33-47 cyclin dependent kinase inhibitor 1A Homo sapiens 227-230 28160563-8 2017 MiR-3622b-5p turned ERBB2-positive cancer cells more vulnerable to the apoptosis induced by cisplatin and 5-fluorouracil. Fluorouracil 106-120 erb-b2 receptor tyrosine kinase 2 Homo sapiens 20-25 28614773-3 2017 Cytosine arabinoside, 5-fluorouracil, and hydroxyurea showed strong cytotoxicity (IC50 < 10 muM), whereas indomethacin and dexamethasone had weaker cytotoxic effects. Fluorouracil 22-36 latexin Homo sapiens 95-98 28008607-7 2017 Combination therapy with 5-fluorouracil and miR-320a/miR-4496 suppressed gastric tumourigenesis and metastatic potential in an orthotopic mouse model, probably via suppression of CagA-induced CIC properties and chemoresistance. Fluorouracil 25-39 S100 calcium binding protein A8 (calgranulin A) Mus musculus 179-183 28454454-0 2017 Chemotherapy regimen based on sorafenib combined with 5-FU on HIF-1alpha and VEGF expression and survival in advanced gastric cancer patients. Fluorouracil 54-58 hypoxia inducible factor 1 subunit alpha Homo sapiens 62-72 27666139-11 2017 Cotreatment with celecoxib and 5-FU partially blocked AKT phosphorylation, although no significant changes in total AKT protein levels were detected. Fluorouracil 31-35 AKT serine/threonine kinase 1 Homo sapiens 54-57 28284059-0 2017 Reactivating p53 and Inducing Tumor Apoptosis (RITA) Enhances the Response of RITA-Sensitive Colorectal Cancer Cells to Chemotherapeutic Agents 5-Fluorouracil and Oxaliplatin. Fluorouracil 144-158 tumor protein p53 Homo sapiens 13-16 28454454-0 2017 Chemotherapy regimen based on sorafenib combined with 5-FU on HIF-1alpha and VEGF expression and survival in advanced gastric cancer patients. Fluorouracil 54-58 vascular endothelial growth factor A Homo sapiens 77-81 28454373-0 2017 Inhibition of CYFIP2 promotes gastric cancer cell proliferation and chemoresistance to 5-fluorouracil through activation of the Akt signaling pathway. Fluorouracil 87-101 AKT serine/threonine kinase 1 Homo sapiens 128-131 28222070-6 2017 Apoptosis and 5-FU effect were determined in PTBP3-silenced gastric cancer cells. Fluorouracil 14-18 polypyrimidine tract binding protein 3 Homo sapiens 45-50 28454373-8 2017 In SGC7901 cells, protein expression of active caspase-3 and cleaved poly (ADP-ribose) polymerase was increased following treatment with 5-FU, while phosphorylated Akt serine/threonine kinase 1 (Akt) levels were decreased. Fluorouracil 137-141 caspase 3 Homo sapiens 47-56 28454373-10 2017 In addition, inhibition of the Akt signaling pathway using the Akt inhibitor LY294002 restored CYFIP2-knockdown SGC7901 cell chemosensitivity to 5-FU. Fluorouracil 145-149 AKT serine/threonine kinase 1 Homo sapiens 31-34 28454373-10 2017 In addition, inhibition of the Akt signaling pathway using the Akt inhibitor LY294002 restored CYFIP2-knockdown SGC7901 cell chemosensitivity to 5-FU. Fluorouracil 145-149 AKT serine/threonine kinase 1 Homo sapiens 63-66 28454373-11 2017 The results of the present study demonstrate that decreased CYFIP2 expression is associated with increased gastric tumor growth in vitro and that CYFIP2 knockdown-induced activation of the Akt pro-survival signaling pathway confers resistance to 5-FU-based chemotherapy in gastric cancer cells. Fluorouracil 246-250 AKT serine/threonine kinase 1 Homo sapiens 189-192 28182993-3 2017 METHODS: The EpCAM+ cell lines HuH1 and HuH7 were treated with 5-fluorouracil (5-FU) or epirubicin in vitro. Fluorouracil 63-77 epithelial cell adhesion molecule Homo sapiens 13-18 28182993-3 2017 METHODS: The EpCAM+ cell lines HuH1 and HuH7 were treated with 5-fluorouracil (5-FU) or epirubicin in vitro. Fluorouracil 63-77 chloride intracellular channel 4 Homo sapiens 31-35 28182993-3 2017 METHODS: The EpCAM+ cell lines HuH1 and HuH7 were treated with 5-fluorouracil (5-FU) or epirubicin in vitro. Fluorouracil 79-83 epithelial cell adhesion molecule Homo sapiens 13-18 28182993-7 2017 RESULTS: 5-FU or epirubicin treatment resulted in the generation of CD90+ and CD105+ cells in vitro in HuH1 and HuH7 cells, which originally contain no CD90+ or CD105+ cells. Fluorouracil 9-13 chloride intracellular channel 4 Homo sapiens 103-107 28222070-10 2017 Further research found that inhibition of PTBP3 expression enhanced the chemosensitivity of gastric cancer cells towards 5-FU treatment. Fluorouracil 121-125 polypyrimidine tract binding protein 3 Homo sapiens 42-47 28222070-11 2017 This was mediated by reduced expression of histone deacetylase 6 (HDAC6), which further inhibited the phosphorylation of Akt and the expression of thymidylate synthase (TYMS), the critical determinant of 5-FU cytotoxicity. Fluorouracil 204-208 histone deacetylase 6 Homo sapiens 43-64 28222070-11 2017 This was mediated by reduced expression of histone deacetylase 6 (HDAC6), which further inhibited the phosphorylation of Akt and the expression of thymidylate synthase (TYMS), the critical determinant of 5-FU cytotoxicity. Fluorouracil 204-208 histone deacetylase 6 Homo sapiens 66-71 28222070-11 2017 This was mediated by reduced expression of histone deacetylase 6 (HDAC6), which further inhibited the phosphorylation of Akt and the expression of thymidylate synthase (TYMS), the critical determinant of 5-FU cytotoxicity. Fluorouracil 204-208 AKT serine/threonine kinase 1 Homo sapiens 121-124 28435473-6 2017 The present study also found that inhibition of mitochondrial COX-2 with resveratrol (RSV), a natural phytochemical, increased the sensitivity of NPC to 5-fluorouracil (5-FU), a classical chemotherapy drug for NPC. Fluorouracil 153-167 prostaglandin-endoperoxide synthase 2 Homo sapiens 62-67 28435473-6 2017 The present study also found that inhibition of mitochondrial COX-2 with resveratrol (RSV), a natural phytochemical, increased the sensitivity of NPC to 5-fluorouracil (5-FU), a classical chemotherapy drug for NPC. Fluorouracil 169-173 prostaglandin-endoperoxide synthase 2 Homo sapiens 62-67 28377359-5 2017 The effect of miR-206 on the sensitivity of ovarian cancer cells to 5-Fu was assessed. Fluorouracil 68-72 microRNA 206 Homo sapiens 14-21 28377359-10 2017 Transfection of SKOV3 cells with miR-206 significantly lowered the IC50 of 5-Fu to enhance the chemotherapy sensitivity of the cells to 5-Fu. Fluorouracil 75-79 microRNA 206 Homo sapiens 33-40 28377359-10 2017 Transfection of SKOV3 cells with miR-206 significantly lowered the IC50 of 5-Fu to enhance the chemotherapy sensitivity of the cells to 5-Fu. Fluorouracil 136-140 microRNA 206 Homo sapiens 33-40 28377359-11 2017 CONCLUSION: As a potential tumor suppressor, miR-206 directly targets CDK4 to suppress the cell growth and enhance the chemotherapy sensitivity to 5-Fu in ovarian cancer cells in vitro. Fluorouracil 147-151 microRNA 206 Homo sapiens 45-52 28000054-11 2017 Furthermore, 5-FU retains its ability to cause nuclear accumulation of p53 in the presence of irinotecan or topotecan. Fluorouracil 13-17 tumor protein p53 Homo sapiens 71-74 28178647-0 2017 Enhancement of TRAIL-induced apoptosis by 5-fluorouracil requires activating Bax and p53 pathways in TRAIL-resistant lung cancers. Fluorouracil 42-56 TNF superfamily member 10 Homo sapiens 15-20 28178647-0 2017 Enhancement of TRAIL-induced apoptosis by 5-fluorouracil requires activating Bax and p53 pathways in TRAIL-resistant lung cancers. Fluorouracil 42-56 BCL2 associated X, apoptosis regulator Homo sapiens 77-80 28178647-0 2017 Enhancement of TRAIL-induced apoptosis by 5-fluorouracil requires activating Bax and p53 pathways in TRAIL-resistant lung cancers. Fluorouracil 42-56 tumor protein p53 Homo sapiens 85-88 28178647-0 2017 Enhancement of TRAIL-induced apoptosis by 5-fluorouracil requires activating Bax and p53 pathways in TRAIL-resistant lung cancers. Fluorouracil 42-56 TNF superfamily member 10 Homo sapiens 101-106 28178647-4 2017 In the present study, we observed that 5-fluorouracil, which exerts anticancer effects by inhibiting tumor cell proliferation, enhanced TRAIL-induced apoptosis of TRAIL-resistant human adenocarcinoma A549 cells. Fluorouracil 39-53 TNF superfamily member 10 Homo sapiens 136-141 28178647-4 2017 In the present study, we observed that 5-fluorouracil, which exerts anticancer effects by inhibiting tumor cell proliferation, enhanced TRAIL-induced apoptosis of TRAIL-resistant human adenocarcinoma A549 cells. Fluorouracil 39-53 TNF superfamily member 10 Homo sapiens 163-168 28178647-5 2017 Interestingly, 5-fluorouracil treatment markedly increased Bax and p53 levels and 5-fluorouracil and TRAIL cotreatment increased Ac-cas3 and Ac-cas8 levels compared with those in control cells. Fluorouracil 15-29 BCL2 associated X, apoptosis regulator Homo sapiens 59-62 28178647-5 2017 Interestingly, 5-fluorouracil treatment markedly increased Bax and p53 levels and 5-fluorouracil and TRAIL cotreatment increased Ac-cas3 and Ac-cas8 levels compared with those in control cells. Fluorouracil 15-29 tumor protein p53 Homo sapiens 67-70 28178647-5 2017 Interestingly, 5-fluorouracil treatment markedly increased Bax and p53 levels and 5-fluorouracil and TRAIL cotreatment increased Ac-cas3 and Ac-cas8 levels compared with those in control cells. Fluorouracil 15-29 TNF superfamily member 10 Homo sapiens 101-106 28178647-6 2017 Taken together, the present study demonstrated that 5-fluorouracil enhances TRAIL-induced apoptosis in TRAIL-resistant lung adenocarcinoma cells by activating Bax and p53, and also suggest that TRAIL and 5-fluorouracil cotreatment can be used as an adequate therapeutic strategy for TRAIL-resistant human cancers. Fluorouracil 52-66 TNF superfamily member 10 Homo sapiens 76-81 28178647-6 2017 Taken together, the present study demonstrated that 5-fluorouracil enhances TRAIL-induced apoptosis in TRAIL-resistant lung adenocarcinoma cells by activating Bax and p53, and also suggest that TRAIL and 5-fluorouracil cotreatment can be used as an adequate therapeutic strategy for TRAIL-resistant human cancers. Fluorouracil 52-66 TNF superfamily member 10 Homo sapiens 103-108 28178647-6 2017 Taken together, the present study demonstrated that 5-fluorouracil enhances TRAIL-induced apoptosis in TRAIL-resistant lung adenocarcinoma cells by activating Bax and p53, and also suggest that TRAIL and 5-fluorouracil cotreatment can be used as an adequate therapeutic strategy for TRAIL-resistant human cancers. Fluorouracil 52-66 BCL2 associated X, apoptosis regulator Homo sapiens 159-162 28178647-6 2017 Taken together, the present study demonstrated that 5-fluorouracil enhances TRAIL-induced apoptosis in TRAIL-resistant lung adenocarcinoma cells by activating Bax and p53, and also suggest that TRAIL and 5-fluorouracil cotreatment can be used as an adequate therapeutic strategy for TRAIL-resistant human cancers. Fluorouracil 52-66 tumor protein p53 Homo sapiens 167-170 28178647-6 2017 Taken together, the present study demonstrated that 5-fluorouracil enhances TRAIL-induced apoptosis in TRAIL-resistant lung adenocarcinoma cells by activating Bax and p53, and also suggest that TRAIL and 5-fluorouracil cotreatment can be used as an adequate therapeutic strategy for TRAIL-resistant human cancers. Fluorouracil 52-66 TNF superfamily member 10 Homo sapiens 103-108 28178647-6 2017 Taken together, the present study demonstrated that 5-fluorouracil enhances TRAIL-induced apoptosis in TRAIL-resistant lung adenocarcinoma cells by activating Bax and p53, and also suggest that TRAIL and 5-fluorouracil cotreatment can be used as an adequate therapeutic strategy for TRAIL-resistant human cancers. Fluorouracil 52-66 TNF superfamily member 10 Homo sapiens 103-108 28178647-6 2017 Taken together, the present study demonstrated that 5-fluorouracil enhances TRAIL-induced apoptosis in TRAIL-resistant lung adenocarcinoma cells by activating Bax and p53, and also suggest that TRAIL and 5-fluorouracil cotreatment can be used as an adequate therapeutic strategy for TRAIL-resistant human cancers. Fluorouracil 204-218 TNF superfamily member 10 Homo sapiens 76-81 28178647-6 2017 Taken together, the present study demonstrated that 5-fluorouracil enhances TRAIL-induced apoptosis in TRAIL-resistant lung adenocarcinoma cells by activating Bax and p53, and also suggest that TRAIL and 5-fluorouracil cotreatment can be used as an adequate therapeutic strategy for TRAIL-resistant human cancers. Fluorouracil 204-218 TNF superfamily member 10 Homo sapiens 103-108 28178647-6 2017 Taken together, the present study demonstrated that 5-fluorouracil enhances TRAIL-induced apoptosis in TRAIL-resistant lung adenocarcinoma cells by activating Bax and p53, and also suggest that TRAIL and 5-fluorouracil cotreatment can be used as an adequate therapeutic strategy for TRAIL-resistant human cancers. Fluorouracil 204-218 TNF superfamily member 10 Homo sapiens 103-108 28178647-6 2017 Taken together, the present study demonstrated that 5-fluorouracil enhances TRAIL-induced apoptosis in TRAIL-resistant lung adenocarcinoma cells by activating Bax and p53, and also suggest that TRAIL and 5-fluorouracil cotreatment can be used as an adequate therapeutic strategy for TRAIL-resistant human cancers. Fluorouracil 204-218 TNF superfamily member 10 Homo sapiens 103-108 28011190-4 2017 Herein, we report a dendritic strategy that utilizes the two amine functionalities of lysine to create branch points that allow conjugation of the anticancer drug 5-fluorouracil (5-FU) to the tumor-targeting ligand substance P, along with an additional near-infrared (NIR) squaraine dye, to construct a theranostic dendritic agent, P-FU 4. Fluorouracil 163-177 tachykinin precursor 1 Homo sapiens 215-226 28011190-4 2017 Herein, we report a dendritic strategy that utilizes the two amine functionalities of lysine to create branch points that allow conjugation of the anticancer drug 5-fluorouracil (5-FU) to the tumor-targeting ligand substance P, along with an additional near-infrared (NIR) squaraine dye, to construct a theranostic dendritic agent, P-FU 4. Fluorouracil 179-183 tachykinin precursor 1 Homo sapiens 215-226 28591290-6 2017 (v) Primary topical 5-FU versus MMC versus interferon (IFN) showed similar rates of tumor recurrence, mild side effects for all drugs, and more severe side effects in the 5-FU arm, followed successively by MMC and IFN (level III, GR C). Fluorouracil 20-24 interferon alpha 1 Homo sapiens 55-58 28591290-6 2017 (v) Primary topical 5-FU versus MMC versus interferon (IFN) showed similar rates of tumor recurrence, mild side effects for all drugs, and more severe side effects in the 5-FU arm, followed successively by MMC and IFN (level III, GR C). Fluorouracil 20-24 interferon alpha 1 Homo sapiens 214-217 28591290-6 2017 (v) Primary topical 5-FU versus MMC versus interferon (IFN) showed similar rates of tumor recurrence, mild side effects for all drugs, and more severe side effects in the 5-FU arm, followed successively by MMC and IFN (level III, GR C). Fluorouracil 171-175 interferon alpha 1 Homo sapiens 55-58 27865009-0 2017 Melatonin synergizes the chemotherapeutic effect of 5-fluorouracil in colon cancer by suppressing PI3K/AKT and NF-kappaB/iNOS signaling pathways. Fluorouracil 52-66 thymoma viral proto-oncogene 1 Mus musculus 103-106 27838786-13 2017 In vivo, 53BP1 silencing accelerated tumor proliferation in nude mice and enhanced resistance to 5-FU. Fluorouracil 97-101 transformation related protein 53 binding protein 1 Mus musculus 9-14 27865009-6 2017 Further mechanism study demonstrated that melatonin synergized the antitumor effect of 5-FU by targeting the PI3K/AKT and NF-kappaB/inducible nitric oxide synthase (iNOS) signaling. Fluorouracil 87-91 nitric oxide synthase 2, inducible Mus musculus 165-169 27865009-7 2017 Melatonin in combination with 5-FU markedly suppressed the phosphorylation of PI3K, AKT, IKKalpha, IkappaBalpha, and p65 proteins, promoted the translocation of NF-kappaB p50/p65 from the nuclei to cytoplasm, abrogated their binding to the iNOS promoter, and thereby enhanced the inhibition of iNOS signaling. Fluorouracil 30-34 thymoma viral proto-oncogene 1 Mus musculus 84-87 27865009-0 2017 Melatonin synergizes the chemotherapeutic effect of 5-fluorouracil in colon cancer by suppressing PI3K/AKT and NF-kappaB/iNOS signaling pathways. Fluorouracil 52-66 nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105 Mus musculus 111-120 27865009-7 2017 Melatonin in combination with 5-FU markedly suppressed the phosphorylation of PI3K, AKT, IKKalpha, IkappaBalpha, and p65 proteins, promoted the translocation of NF-kappaB p50/p65 from the nuclei to cytoplasm, abrogated their binding to the iNOS promoter, and thereby enhanced the inhibition of iNOS signaling. Fluorouracil 30-34 nuclear factor of kappa light polypeptide gene enhancer in B cells inhibitor, alpha Mus musculus 99-111 27865009-0 2017 Melatonin synergizes the chemotherapeutic effect of 5-fluorouracil in colon cancer by suppressing PI3K/AKT and NF-kappaB/iNOS signaling pathways. Fluorouracil 52-66 nitric oxide synthase 2, inducible Mus musculus 121-125 27865009-7 2017 Melatonin in combination with 5-FU markedly suppressed the phosphorylation of PI3K, AKT, IKKalpha, IkappaBalpha, and p65 proteins, promoted the translocation of NF-kappaB p50/p65 from the nuclei to cytoplasm, abrogated their binding to the iNOS promoter, and thereby enhanced the inhibition of iNOS signaling. Fluorouracil 30-34 nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105 Mus musculus 161-174 27865009-7 2017 Melatonin in combination with 5-FU markedly suppressed the phosphorylation of PI3K, AKT, IKKalpha, IkappaBalpha, and p65 proteins, promoted the translocation of NF-kappaB p50/p65 from the nuclei to cytoplasm, abrogated their binding to the iNOS promoter, and thereby enhanced the inhibition of iNOS signaling. Fluorouracil 30-34 nitric oxide synthase 2, inducible Mus musculus 240-244 27865009-6 2017 Further mechanism study demonstrated that melatonin synergized the antitumor effect of 5-FU by targeting the PI3K/AKT and NF-kappaB/inducible nitric oxide synthase (iNOS) signaling. Fluorouracil 87-91 thymoma viral proto-oncogene 1 Mus musculus 114-117 27865009-7 2017 Melatonin in combination with 5-FU markedly suppressed the phosphorylation of PI3K, AKT, IKKalpha, IkappaBalpha, and p65 proteins, promoted the translocation of NF-kappaB p50/p65 from the nuclei to cytoplasm, abrogated their binding to the iNOS promoter, and thereby enhanced the inhibition of iNOS signaling. Fluorouracil 30-34 nitric oxide synthase 2, inducible Mus musculus 294-298 27865009-8 2017 In addition, pretreatment with a PI3K- or iNOS-specific inhibitor synergized the antitumor effects of 5-FU and melatonin. Fluorouracil 102-106 nitric oxide synthase 2, inducible Mus musculus 42-46 27865009-6 2017 Further mechanism study demonstrated that melatonin synergized the antitumor effect of 5-FU by targeting the PI3K/AKT and NF-kappaB/inducible nitric oxide synthase (iNOS) signaling. Fluorouracil 87-91 nitric oxide synthase 2, inducible Mus musculus 122-163 27865009-9 2017 Finally, we verified in a xenograft mouse model that melatonin and 5-FU exerted synergistic antitumor effect by inhibiting the AKT and iNOS signaling pathways. Fluorouracil 67-71 thymoma viral proto-oncogene 1 Mus musculus 127-130 28109867-5 2017 More importantly, the depletion of MDSC via the administration of anti-Gr-1 antibody or the blockade of IL-6 signaling sensitized 5-FU-resistant H22 hepatoma to chemotherapy in the immunocompetent C57BL/6N mice. Fluorouracil 130-134 interleukin 6 Homo sapiens 104-108 27865009-9 2017 Finally, we verified in a xenograft mouse model that melatonin and 5-FU exerted synergistic antitumor effect by inhibiting the AKT and iNOS signaling pathways. Fluorouracil 67-71 nitric oxide synthase 2, inducible Mus musculus 135-139 28055957-6 2017 Furthermore, 5-FU significantly induced c-Jun N-terminal kinase (JNK) activation and the expression of pro-inflammatory genes IL-8 and ICAM-1. Fluorouracil 13-17 mitogen-activated protein kinase 8 Homo sapiens 40-63 28055957-6 2017 Furthermore, 5-FU significantly induced c-Jun N-terminal kinase (JNK) activation and the expression of pro-inflammatory genes IL-8 and ICAM-1. Fluorouracil 13-17 mitogen-activated protein kinase 8 Homo sapiens 65-68 28055957-6 2017 Furthermore, 5-FU significantly induced c-Jun N-terminal kinase (JNK) activation and the expression of pro-inflammatory genes IL-8 and ICAM-1. Fluorouracil 13-17 C-X-C motif chemokine ligand 8 Homo sapiens 126-130 28055957-7 2017 Also in vivo, 5-FU significantly induced hepatic ACOX1 and HMOX1 expression as well as JNK-activation, pro-inflammatory gene expression and immune cell infiltration. Fluorouracil 14-18 mitogen-activated protein kinase 8 Homo sapiens 87-90 28349835-6 2017 Deglycosylation of epithelial cell adhesion molecule enhanced the cytotoxic effect of 5-fluorouracil, promoting apoptosis by downregulating the expression of the anti-apoptotic protein Bcl-2 and upregulating the expression of the pro-apoptotic proteins Bax and Caspase 3 via the extracellular-signal-regulated kinase 1/2 and c-Jun N-terminal kinase mitogen-activated protein kinase signaling pathways in MCF-7 and MDA-MB-231 cells. Fluorouracil 86-100 BCL2 associated X, apoptosis regulator Homo sapiens 253-256 28349835-6 2017 Deglycosylation of epithelial cell adhesion molecule enhanced the cytotoxic effect of 5-fluorouracil, promoting apoptosis by downregulating the expression of the anti-apoptotic protein Bcl-2 and upregulating the expression of the pro-apoptotic proteins Bax and Caspase 3 via the extracellular-signal-regulated kinase 1/2 and c-Jun N-terminal kinase mitogen-activated protein kinase signaling pathways in MCF-7 and MDA-MB-231 cells. Fluorouracil 86-100 caspase 3 Homo sapiens 261-270 28349835-6 2017 Deglycosylation of epithelial cell adhesion molecule enhanced the cytotoxic effect of 5-fluorouracil, promoting apoptosis by downregulating the expression of the anti-apoptotic protein Bcl-2 and upregulating the expression of the pro-apoptotic proteins Bax and Caspase 3 via the extracellular-signal-regulated kinase 1/2 and c-Jun N-terminal kinase mitogen-activated protein kinase signaling pathways in MCF-7 and MDA-MB-231 cells. Fluorouracil 86-100 mitogen-activated protein kinase 3 Homo sapiens 279-320 28179302-4 2017 CD24 inhibition reduced chemosensitivity to 5-FU, while STAT1 inhibition did not affect chemosensitivity to 5-FU in CD24 siRNA-transfected cells. Fluorouracil 44-48 CD24 molecule Homo sapiens 0-4 27776313-0 2017 Competitive binding of (-)-epigallocatechin-3-gallate and 5-fluorouracil to human serum albumin: A fluorescence and circular dichroism study. Fluorouracil 58-72 albumin Homo sapiens 82-95 28028695-9 2017 An increase in p53 levels was detected following 5-FU treatment; pifithrin-alpha, an inhibitor of p53 activation, reversed 5-FU-induced SESN2 expression. Fluorouracil 123-127 tumor protein p53 Homo sapiens 15-18 28028695-9 2017 An increase in p53 levels was detected following 5-FU treatment; pifithrin-alpha, an inhibitor of p53 activation, reversed 5-FU-induced SESN2 expression. Fluorouracil 49-53 tumor protein p53 Homo sapiens 15-18 28028695-9 2017 An increase in p53 levels was detected following 5-FU treatment; pifithrin-alpha, an inhibitor of p53 activation, reversed 5-FU-induced SESN2 expression. Fluorouracil 123-127 tumor protein p53 Homo sapiens 98-101 28028695-11 2017 Taken together, our results suggest that 5-FU increases SESN2 levels via a p53-dependent pathway, which contributes to inhibition of cancer cell migration in vitro. Fluorouracil 41-45 tumor protein p53 Homo sapiens 75-78 28352348-10 2017 5-FU+GA further decreased P53, survivin and TS mRNA and protein levels in the two CRC cell lines compared with single drugs, whereas increased P53 protein levels were observed in HCT116 cells. Fluorouracil 0-4 tumor protein p53 Homo sapiens 26-29 28352348-10 2017 5-FU+GA further decreased P53, survivin and TS mRNA and protein levels in the two CRC cell lines compared with single drugs, whereas increased P53 protein levels were observed in HCT116 cells. Fluorouracil 0-4 tumor protein p53 Homo sapiens 143-146 27637603-0 2017 The Presence of Serum p53 Antibody Predicts the Pathological Tumor Response to Neoadjuvant Chemotherapy with Docetaxel, Cisplatin and Fluorouracil (DCF) in Esophageal Squamous Cell Carcinoma. Fluorouracil 134-146 tumor protein p53 Homo sapiens 22-25 28051879-0 2017 WNT5A Promoter Methylation Is Associated with Better Responses and Longer Progression-Free Survival in Colorectal Cancer Patients Treated with 5-Fluorouracil-Based Chemotherapy. Fluorouracil 143-157 Wnt family member 5A Homo sapiens 0-5 28051879-9 2017 5-FU-induced tumor suppression (reduced cell viability) was reduced by WNT5A overexpression in hypermethylated HCT116 and SW620 cells and enhanced by WNT5A downregulation in unmethylated LoVo and SW480 cells. Fluorouracil 0-4 Wnt family member 5A Homo sapiens 71-76 28051879-9 2017 5-FU-induced tumor suppression (reduced cell viability) was reduced by WNT5A overexpression in hypermethylated HCT116 and SW620 cells and enhanced by WNT5A downregulation in unmethylated LoVo and SW480 cells. Fluorouracil 0-4 Wnt family member 5A Homo sapiens 150-155 28051879-10 2017 In 5-FU-treated CRC patients, WNT5A methylation status is associated with better drug response and longer progression-free survival, suggesting that 5-FU is more effective in CRC with WNT5A hypermethylation. Fluorouracil 3-7 Wnt family member 5A Homo sapiens 30-35 28051879-10 2017 In 5-FU-treated CRC patients, WNT5A methylation status is associated with better drug response and longer progression-free survival, suggesting that 5-FU is more effective in CRC with WNT5A hypermethylation. Fluorouracil 3-7 Wnt family member 5A Homo sapiens 184-189 28051879-10 2017 In 5-FU-treated CRC patients, WNT5A methylation status is associated with better drug response and longer progression-free survival, suggesting that 5-FU is more effective in CRC with WNT5A hypermethylation. Fluorouracil 149-153 Wnt family member 5A Homo sapiens 30-35 28051879-10 2017 In 5-FU-treated CRC patients, WNT5A methylation status is associated with better drug response and longer progression-free survival, suggesting that 5-FU is more effective in CRC with WNT5A hypermethylation. Fluorouracil 149-153 Wnt family member 5A Homo sapiens 184-189 28000878-4 2017 The upregulation of the Ca2+-permeable transient receptor potential channel 5 (TrpC5) activates the Wnt/beta-catenin signaling pathway in 5-fluorouracil (5-Fu)-resistant human colorectal cancer (CRC) HCT-8 (HCT-8/5-Fu) cells. Fluorouracil 138-152 transient receptor potential cation channel subfamily C member 5 Homo sapiens 39-77 28000878-4 2017 The upregulation of the Ca2+-permeable transient receptor potential channel 5 (TrpC5) activates the Wnt/beta-catenin signaling pathway in 5-fluorouracil (5-Fu)-resistant human colorectal cancer (CRC) HCT-8 (HCT-8/5-Fu) cells. Fluorouracil 138-152 transient receptor potential cation channel subfamily C member 5 Homo sapiens 79-84 28000878-4 2017 The upregulation of the Ca2+-permeable transient receptor potential channel 5 (TrpC5) activates the Wnt/beta-catenin signaling pathway in 5-fluorouracil (5-Fu)-resistant human colorectal cancer (CRC) HCT-8 (HCT-8/5-Fu) cells. Fluorouracil 154-158 transient receptor potential cation channel subfamily C member 5 Homo sapiens 39-77 28000878-4 2017 The upregulation of the Ca2+-permeable transient receptor potential channel 5 (TrpC5) activates the Wnt/beta-catenin signaling pathway in 5-fluorouracil (5-Fu)-resistant human colorectal cancer (CRC) HCT-8 (HCT-8/5-Fu) cells. Fluorouracil 154-158 transient receptor potential cation channel subfamily C member 5 Homo sapiens 79-84 26980771-0 2017 Usefulness of Heart-Type Fatty Acid-Binding Protein and Myocardial Performance Index for Early Detection of 5-Fluorouracil Cardiotoxicity. Fluorouracil 108-122 fatty acid binding protein 3 Homo sapiens 14-51 28344470-10 2017 Moreover, HT-29 cell viability after 250 muM 5-FU treatment in free or NPs forms was 55.45% and 34.01%, respectively. Fluorouracil 45-49 latexin Homo sapiens 41-44 28127258-10 2017 RESULTS: TNF-alpha strengthened the cytotoxicity of docetaxel, 5-FU and cisplatin against breast cancer cells both in vitro and in vivo. Fluorouracil 63-67 tumor necrosis factor Mus musculus 9-18 28114937-7 2017 Further function study demonstrated that overexpression of miR-939 suppressed GC cell growth, and enhanced 5-fluorouracil-induced chemosensitivity by compromising cellular growth and inducing apoptosis in vitro and in vivo. Fluorouracil 107-121 microRNA 939 Homo sapiens 59-66 27357544-9 2017 The most potent compounds 3d, 3e, and 3f possessing the greatest cytotoxicity activity with IC50 values slightly higher (15-33 muM) than that of 5-Fluorouracil (10-17 muM), indicating their potential to be antitumor agents. Fluorouracil 145-159 latexin Homo sapiens 167-170 28344470-7 2017 On HT-29, IC50 was only reached after 5 days of 5-FU treatment (11.25 muM). Fluorouracil 48-52 latexin Homo sapiens 70-73 28344470-8 2017 The HCT 116 viability following treatment with 100 muM 5-FU in free or NPs forms for 3 days was 38.8% and 18.6%, respectively. Fluorouracil 55-59 latexin Homo sapiens 51-54 28344470-9 2017 Similarly, when 250 muM was applied, HCT 116 viability was 17.03% and 14.6% after treatment with free and NPs forms of 5-FU, respectively. Fluorouracil 119-123 latexin Homo sapiens 20-23 27993681-11 2017 These results suggest that LPA signaling via LPA4 and LPA6 negatively regulates the cell motile activities of DLD1 and HCT116 cells as well as long-term 5-FU treated cells. Fluorouracil 153-157 lysophosphatidic acid receptor 4 Homo sapiens 45-49 28011480-6 2017 In contrast, treatment with CaLa (2.5 mM), alone and in combination with 5-FU, exerted antitumor activity against both anchored and unanchored CRC cells via calcium-mediated FAK proteolysis and inhibition of EMT markers, such as vimentin and SNAIL. Fluorouracil 73-77 snail family transcriptional repressor 1 Homo sapiens 242-247 26980771-1 2017 In the present study, we aimed to evaluate temporal changes in heart-type fatty acid-binding protein (h-FABP) and myocardial performance index (Tei index) following administration of 5-fluorouracil (5-FU), a chemotherapeutic agent associated with myocardial ischemia induced by coronary vasospasm. Fluorouracil 183-197 fatty acid binding protein 3 Homo sapiens 63-100 26980771-1 2017 In the present study, we aimed to evaluate temporal changes in heart-type fatty acid-binding protein (h-FABP) and myocardial performance index (Tei index) following administration of 5-fluorouracil (5-FU), a chemotherapeutic agent associated with myocardial ischemia induced by coronary vasospasm. Fluorouracil 183-197 fatty acid binding protein 3 Homo sapiens 102-108 26980771-1 2017 In the present study, we aimed to evaluate temporal changes in heart-type fatty acid-binding protein (h-FABP) and myocardial performance index (Tei index) following administration of 5-fluorouracil (5-FU), a chemotherapeutic agent associated with myocardial ischemia induced by coronary vasospasm. Fluorouracil 199-203 fatty acid binding protein 3 Homo sapiens 63-100 26980771-1 2017 In the present study, we aimed to evaluate temporal changes in heart-type fatty acid-binding protein (h-FABP) and myocardial performance index (Tei index) following administration of 5-fluorouracil (5-FU), a chemotherapeutic agent associated with myocardial ischemia induced by coronary vasospasm. Fluorouracil 199-203 fatty acid binding protein 3 Homo sapiens 102-108 27643822-0 2017 New Perspectives in the Treatment of Advanced Gastric Cancer: S-1 as a Novel Oral 5-FU Therapy in Combination with Cisplatin. Fluorouracil 82-86 proteasome 26S subunit, non-ATPase 1 Homo sapiens 62-65 29199237-0 2017 Active Ingredients of Hange-shashin-to, Baicalelin and 6-Gingerol, Inhibit 5-Fluorouracil-Induced Upregulation of CXCL1 in the Colon to Attenuate Diarrhea Development. Fluorouracil 75-89 chemokine (C-X-C motif) ligand 1 Mus musculus 114-119 29199237-2 2017 Recently we suggested that levels of chemokine (C-X-C motif) ligand 1 (CXCL1) and neutrophil recruitment in the colonic mucosa were drastically increased by the 5-FU administration in mice. Fluorouracil 161-165 chemokine (C-X-C motif) ligand 1 Mus musculus 37-69 29199237-2 2017 Recently we suggested that levels of chemokine (C-X-C motif) ligand 1 (CXCL1) and neutrophil recruitment in the colonic mucosa were drastically increased by the 5-FU administration in mice. Fluorouracil 161-165 chemokine (C-X-C motif) ligand 1 Mus musculus 71-76 29199237-4 2017 We therefore examined the effects of HST and its active ingredients on 5-FU-induced CXCL1 upregulation in cultured colon tissue, and also examined the effects of HST on 5-FU-induced diarrhea development in the mouse. Fluorouracil 71-75 chemokine (C-X-C motif) ligand 1 Mus musculus 84-89 29199237-11 2017 5-FU enhanced CXCL1 mRNA in the colon but the effect by 5-FU was markedly suppressed by application of HST and its active ingredients, baicalein and 6-gingerol. Fluorouracil 0-4 chemokine (C-X-C motif) ligand 1 Mus musculus 14-19 29199237-12 2017 Nuclear factor kappa B (NF-kappaB) was activated by 5-FU treatment in cultured colon tissue, which was also suppressed by HST and the combination of baicalein and 6-gingerol. Fluorouracil 52-56 nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105 Mus musculus 0-22 29199237-12 2017 Nuclear factor kappa B (NF-kappaB) was activated by 5-FU treatment in cultured colon tissue, which was also suppressed by HST and the combination of baicalein and 6-gingerol. Fluorouracil 52-56 nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105 Mus musculus 24-33 29199237-14 2017 Under such experimental condition, CXCL1 gene, protein levels of neutrophil elastase and myeloperoxidase upregulation induced by 5-FU in the colon was attenuated by HST. Fluorouracil 129-133 chemokine (C-X-C motif) ligand 1 Mus musculus 35-40 28296564-3 2017 AZD1775 significantly improved the cytotoxicity of 5-FU in a p53-mutated colorectal cancer cell line (HT29 cells), decreasing the IC50 from 9.3 muM to 3.5 muM. Fluorouracil 51-55 tumor protein p53 Homo sapiens 61-64 28296564-5 2017 Combination therapy also increased the amount of caspase-3 dependent apoptosis compared with 5-FU alone (4% vs. 13%). Fluorouracil 93-97 caspase 3 Homo sapiens 49-58 27643822-3 2017 S-1 (Teysuno ), an oral formulation containing the 5-fluorouracil (5-FU) prodrug tegafur and the two enzyme modulators gimeracil and oteracil, has not been available in non-Asia countries until recently. Fluorouracil 51-65 proteasome 26S subunit, non-ATPase 1 Homo sapiens 0-3 27643822-3 2017 S-1 (Teysuno ), an oral formulation containing the 5-fluorouracil (5-FU) prodrug tegafur and the two enzyme modulators gimeracil and oteracil, has not been available in non-Asia countries until recently. Fluorouracil 67-71 proteasome 26S subunit, non-ATPase 1 Homo sapiens 0-3 26715117-1 2017 BACKGROUND: Oral fluoropyrimidine S-1 contains tegafur, which is metabolized to 5-fluorouracil by cytochrome P450 2A6 (CYP2A6). Fluorouracil 80-94 proteasome 26S subunit, non-ATPase 1 Homo sapiens 34-37 28123745-1 2017 The purpose of this study was to evaluate the association between tumor necrosis factor (TNF)-alpha polymorphisms and oral mucositis (OM) from 5-fluorouracil (5-FU) plus cisplatin (CDDP) chemotherapy for esophageal cancer. Fluorouracil 143-157 tumor necrosis factor Homo sapiens 66-99 28123745-1 2017 The purpose of this study was to evaluate the association between tumor necrosis factor (TNF)-alpha polymorphisms and oral mucositis (OM) from 5-fluorouracil (5-FU) plus cisplatin (CDDP) chemotherapy for esophageal cancer. Fluorouracil 159-163 tumor necrosis factor Homo sapiens 66-99 27840964-0 2017 miR-503 inhibits proliferation making human hepatocellular carcinoma cells susceptible to 5-fluorouracil by targeting EIF4E. Fluorouracil 90-104 microRNA 503 Homo sapiens 0-7 28123586-0 2017 Downregulation of caveolin-1 increases the sensitivity of drug-resistant colorectal cancer HCT116 cells to 5-fluorouracil. Fluorouracil 107-121 caveolin 1 Homo sapiens 18-28 27878272-0 2017 miR-20b reduces 5-FU resistance by suppressing the ADAM9/EGFR signaling pathway in colon cancer. Fluorouracil 16-20 epidermal growth factor receptor Homo sapiens 57-61 27878272-12 2017 Our findings suggest that miR-20b reduces 5-FU resistance to induce apoptosis in vitro by suppressing ADAM9/EGFR in CC cells. Fluorouracil 42-46 epidermal growth factor receptor Homo sapiens 108-112 28123586-10 2017 MTT assay demonstrated that Cav-1 siRNA and MCD resensitized DRC to 5-FU. Fluorouracil 68-72 caveolin 1 Homo sapiens 28-33 27875297-1 2016 Uracil N-glycosylase 2 (UNG2), the nuclear isoform of UNG, catalyzes the removal of uracil or 5-fluorouracil lesions that accumulate in DNA following treatment with the anticancer agents 5-fluorouracil and 5-fluorodeoxyuridine (floxuridine), a 5-fluorouracil metabolite. Fluorouracil 94-108 uracil DNA glycosylase Homo sapiens 0-22 27875297-1 2016 Uracil N-glycosylase 2 (UNG2), the nuclear isoform of UNG, catalyzes the removal of uracil or 5-fluorouracil lesions that accumulate in DNA following treatment with the anticancer agents 5-fluorouracil and 5-fluorodeoxyuridine (floxuridine), a 5-fluorouracil metabolite. Fluorouracil 94-108 uracil DNA glycosylase Homo sapiens 24-28 27875297-1 2016 Uracil N-glycosylase 2 (UNG2), the nuclear isoform of UNG, catalyzes the removal of uracil or 5-fluorouracil lesions that accumulate in DNA following treatment with the anticancer agents 5-fluorouracil and 5-fluorodeoxyuridine (floxuridine), a 5-fluorouracil metabolite. Fluorouracil 94-108 uracil DNA glycosylase Homo sapiens 24-27 27875297-1 2016 Uracil N-glycosylase 2 (UNG2), the nuclear isoform of UNG, catalyzes the removal of uracil or 5-fluorouracil lesions that accumulate in DNA following treatment with the anticancer agents 5-fluorouracil and 5-fluorodeoxyuridine (floxuridine), a 5-fluorouracil metabolite. Fluorouracil 187-201 uracil DNA glycosylase Homo sapiens 0-22 27875297-1 2016 Uracil N-glycosylase 2 (UNG2), the nuclear isoform of UNG, catalyzes the removal of uracil or 5-fluorouracil lesions that accumulate in DNA following treatment with the anticancer agents 5-fluorouracil and 5-fluorodeoxyuridine (floxuridine), a 5-fluorouracil metabolite. Fluorouracil 187-201 uracil DNA glycosylase Homo sapiens 24-28 27875297-1 2016 Uracil N-glycosylase 2 (UNG2), the nuclear isoform of UNG, catalyzes the removal of uracil or 5-fluorouracil lesions that accumulate in DNA following treatment with the anticancer agents 5-fluorouracil and 5-fluorodeoxyuridine (floxuridine), a 5-fluorouracil metabolite. Fluorouracil 187-201 uracil DNA glycosylase Homo sapiens 24-27 27875297-1 2016 Uracil N-glycosylase 2 (UNG2), the nuclear isoform of UNG, catalyzes the removal of uracil or 5-fluorouracil lesions that accumulate in DNA following treatment with the anticancer agents 5-fluorouracil and 5-fluorodeoxyuridine (floxuridine), a 5-fluorouracil metabolite. Fluorouracil 187-201 uracil DNA glycosylase Homo sapiens 0-22 27875297-1 2016 Uracil N-glycosylase 2 (UNG2), the nuclear isoform of UNG, catalyzes the removal of uracil or 5-fluorouracil lesions that accumulate in DNA following treatment with the anticancer agents 5-fluorouracil and 5-fluorodeoxyuridine (floxuridine), a 5-fluorouracil metabolite. Fluorouracil 187-201 uracil DNA glycosylase Homo sapiens 24-28 27875297-1 2016 Uracil N-glycosylase 2 (UNG2), the nuclear isoform of UNG, catalyzes the removal of uracil or 5-fluorouracil lesions that accumulate in DNA following treatment with the anticancer agents 5-fluorouracil and 5-fluorodeoxyuridine (floxuridine), a 5-fluorouracil metabolite. Fluorouracil 187-201 uracil DNA glycosylase Homo sapiens 24-27 28060252-4 2016 In this protocol whole bone marrow cells from 5-flurouracil (5-FU) treated donor mice are transduced with a retrovirus encoding mutant CALR and transplanted into lethally irradiated syngeneic hosts. Fluorouracil 61-65 calreticulin Mus musculus 135-139 27924828-0 2016 rpL3 promotes the apoptosis of p53 mutated lung cancer cells by down-regulating CBS and NFkappaB upon 5-FU treatment. Fluorouracil 102-106 tumor protein p53 Homo sapiens 31-34 27894099-5 2016 We demonstrated that knockdown of Prdx2 reduced the self-renewal and sphere formation and resulted in increased 5-FU-induced apoptosis in human colon CSCs. Fluorouracil 112-116 peroxiredoxin 2 Homo sapiens 34-39 27591972-5 2016 The p53(del) cells was more sensitive to cisplatin (PDD) and 5-fluorouracil (5FU) than p53(wt) cells but there was not significant difference. Fluorouracil 61-75 tumor protein p53 Homo sapiens 4-7 27591972-5 2016 The p53(del) cells was more sensitive to cisplatin (PDD) and 5-fluorouracil (5FU) than p53(wt) cells but there was not significant difference. Fluorouracil 77-80 tumor protein p53 Homo sapiens 4-7 27924828-0 2016 rpL3 promotes the apoptosis of p53 mutated lung cancer cells by down-regulating CBS and NFkappaB upon 5-FU treatment. Fluorouracil 102-106 cystathionine beta-synthase Homo sapiens 80-83 27924828-2 2016 In the present study, we reporte that rpL3 induced by 5-FU treatment in Calu-6 cells represses CBS transcription and reduces CBS protein stability leading to a decrease of CBS protein levels. Fluorouracil 54-58 cystathionine beta-synthase Homo sapiens 95-98 27924828-2 2016 In the present study, we reporte that rpL3 induced by 5-FU treatment in Calu-6 cells represses CBS transcription and reduces CBS protein stability leading to a decrease of CBS protein levels. Fluorouracil 54-58 cystathionine beta-synthase Homo sapiens 125-128 27924828-2 2016 In the present study, we reporte that rpL3 induced by 5-FU treatment in Calu-6 cells represses CBS transcription and reduces CBS protein stability leading to a decrease of CBS protein levels. Fluorouracil 54-58 cystathionine beta-synthase Homo sapiens 125-128 27924828-4 2016 Furthermore, we demonstrate that rpL3 significantly enhances the apoptosis of 5-FU treated Calu-6 cells promoting the overexpression of the pro-apoptotic proteins Bax and the inhibition of the anti-apoptotic protein Bcl-2. Fluorouracil 78-82 BCL2 associated X, apoptosis regulator Homo sapiens 163-166 27924828-4 2016 Furthermore, we demonstrate that rpL3 significantly enhances the apoptosis of 5-FU treated Calu-6 cells promoting the overexpression of the pro-apoptotic proteins Bax and the inhibition of the anti-apoptotic protein Bcl-2. Fluorouracil 78-82 BCL2 apoptosis regulator Homo sapiens 216-221 27924828-6 2016 Our results suggest that combination of rpL3 and 5-FU is a promising strategy for chemotherapy of lung cancers lacking functional p53 that are resistant to 5-FU. Fluorouracil 49-53 tumor protein p53 Homo sapiens 130-133 27980427-0 2016 Curcumin sensitizes human gastric cancer cells to 5-fluorouracil through inhibition of the NFkappaB survival-signaling pathway. Fluorouracil 50-64 nuclear factor kappa B subunit 1 Homo sapiens 91-99 27833077-0 2016 Anti-EGFR antibody sensitizes colorectal cancer stem-like cells to Fluorouracil-induced apoptosis by affecting autophagy. Fluorouracil 67-79 epidermal growth factor receptor Homo sapiens 5-9 27833077-9 2016 Together, our data suggest that EGFR monoclonal antibody may sensitize CSC-like CRC cells to 5-FU-induced apoptosis by affecting autophagy. Fluorouracil 93-97 epidermal growth factor receptor Homo sapiens 32-36 27980427-3 2016 In this study, we found that the NFkappaB-signaling pathway can mediate 5-FU resistance in GC cells. Fluorouracil 72-76 nuclear factor kappa B subunit 1 Homo sapiens 33-41 27980427-4 2016 We developed a 5-FU-resistant GC cell line named SGCR/5-FU and found that the 5-FU-induced resistance increased cytosolic IkappaBalpha degradation and promoted NFkappaB nuclear translocation in GC cells. Fluorouracil 15-19 NFKB inhibitor alpha Homo sapiens 122-134 27980427-4 2016 We developed a 5-FU-resistant GC cell line named SGCR/5-FU and found that the 5-FU-induced resistance increased cytosolic IkappaBalpha degradation and promoted NFkappaB nuclear translocation in GC cells. Fluorouracil 15-19 nuclear factor kappa B subunit 1 Homo sapiens 160-168 27980427-4 2016 We developed a 5-FU-resistant GC cell line named SGCR/5-FU and found that the 5-FU-induced resistance increased cytosolic IkappaBalpha degradation and promoted NFkappaB nuclear translocation in GC cells. Fluorouracil 54-58 NFKB inhibitor alpha Homo sapiens 122-134 27980427-4 2016 We developed a 5-FU-resistant GC cell line named SGCR/5-FU and found that the 5-FU-induced resistance increased cytosolic IkappaBalpha degradation and promoted NFkappaB nuclear translocation in GC cells. Fluorouracil 54-58 nuclear factor kappa B subunit 1 Homo sapiens 160-168 27194111-0 2016 Curcumin Inhibits 5-Fluorouracil-induced Up-regulation of CXCL1 and CXCL2 of the Colon Associated with Attenuation of Diarrhoea Development. Fluorouracil 18-32 chemokine (C-X-C motif) ligand 1 Mus musculus 58-63 27693317-0 2016 Andrographolide reversed 5-FU resistance in human colorectal cancer by elevating BAX expression. Fluorouracil 25-29 BCL2 associated X, apoptosis regulator Homo sapiens 81-84 27693317-5 2016 Mechanism analysis showed that Andrographolide/5-FU co-treatment elevated apoptosis level of HCT116/5-FUR cells with highly increased level of BAX. Fluorouracil 47-51 BCL2 associated X, apoptosis regulator Homo sapiens 143-146 27693317-7 2016 Andrographolide-BAX interaction prevented BAX degradation, enhancing mitochondria-mediated apoptosis thus reversed 5-FU resistance while BAX silence diminished this effect. Fluorouracil 115-119 BCL2 associated X, apoptosis regulator Homo sapiens 16-19 27693317-8 2016 Further, by analyzing patient samples who received 5-FU involved chemotherapy, we found that expression level of BAX is correlated with PFS. Fluorouracil 51-55 BCL2 associated X, apoptosis regulator Homo sapiens 113-116 27693317-9 2016 Our results here provide a novel combination treatment strategy, especially for patients with 5-FU-resistant tumors expressing low level of BAX. Fluorouracil 94-98 BCL2 associated X, apoptosis regulator Homo sapiens 140-143 27693317-10 2016 Meanwhile, we also proposed that BAX expression may be a predicted and prognosis marker of 5-FU involved chemotherapy. Fluorouracil 91-95 BCL2 associated X, apoptosis regulator Homo sapiens 33-36 27627783-8 2016 Moreover, CITED2 caused chemoresistance to epirubicin and 5-fluorouracil, but not paclitaxel, in these cells, and it inhibited p53 accumulation after 5-fluorouracil treatment in MCF-7 cells. Fluorouracil 58-72 Cbp/p300 interacting transactivator with Glu/Asp rich carboxy-terminal domain 2 Homo sapiens 10-16 27627783-8 2016 Moreover, CITED2 caused chemoresistance to epirubicin and 5-fluorouracil, but not paclitaxel, in these cells, and it inhibited p53 accumulation after 5-fluorouracil treatment in MCF-7 cells. Fluorouracil 150-164 Cbp/p300 interacting transactivator with Glu/Asp rich carboxy-terminal domain 2 Homo sapiens 10-16 27194111-0 2016 Curcumin Inhibits 5-Fluorouracil-induced Up-regulation of CXCL1 and CXCL2 of the Colon Associated with Attenuation of Diarrhoea Development. Fluorouracil 18-32 chemokine (C-X-C motif) ligand 2 Mus musculus 68-73 27194111-2 2016 We recently reported that chemokine (C-X-C motif) ligand 1 (CXCL1) and neutrophils in the colonic mucosa were markedly increased by the administration of 5-FU in mice. Fluorouracil 154-158 chemokine (C-X-C motif) ligand 1 Mus musculus 26-58 27194111-2 2016 We recently reported that chemokine (C-X-C motif) ligand 1 (CXCL1) and neutrophils in the colonic mucosa were markedly increased by the administration of 5-FU in mice. Fluorouracil 154-158 chemokine (C-X-C motif) ligand 1 Mus musculus 60-65 27194111-12 2016 Under this condition, the CXCL1 and CXCL2 gene up-regulated by 5-FU administration was inhibited by curcumin. Fluorouracil 63-67 chemokine (C-X-C motif) ligand 1 Mus musculus 26-31 27194111-12 2016 Under this condition, the CXCL1 and CXCL2 gene up-regulated by 5-FU administration was inhibited by curcumin. Fluorouracil 63-67 chemokine (C-X-C motif) ligand 2 Mus musculus 36-41 27194111-13 2016 The gene expression of CXCL1 and CXCL2 was also enhanced by 5-FU application in vitro. Fluorouracil 60-64 chemokine (C-X-C motif) ligand 1 Mus musculus 23-28 27194111-13 2016 The gene expression of CXCL1 and CXCL2 was also enhanced by 5-FU application in vitro. Fluorouracil 60-64 chemokine (C-X-C motif) ligand 2 Mus musculus 33-38 27194111-14 2016 The 5-FU-induced up-regulated CXCL1 and CXCL2 gene expressions were inhibited by curcumin, Bay-117082 and bortezomib, nuclear factor kappa B (NF-kappaB) inhibitors, C646, a p300/cyclic adenosine monophosphate response element-binding protein-histone acetyltransferase (HAT) inhibitor. Fluorouracil 4-8 chemokine (C-X-C motif) ligand 1 Mus musculus 30-35 27194111-14 2016 The 5-FU-induced up-regulated CXCL1 and CXCL2 gene expressions were inhibited by curcumin, Bay-117082 and bortezomib, nuclear factor kappa B (NF-kappaB) inhibitors, C646, a p300/cyclic adenosine monophosphate response element-binding protein-histone acetyltransferase (HAT) inhibitor. Fluorouracil 4-8 chemokine (C-X-C motif) ligand 2 Mus musculus 40-45 27194111-14 2016 The 5-FU-induced up-regulated CXCL1 and CXCL2 gene expressions were inhibited by curcumin, Bay-117082 and bortezomib, nuclear factor kappa B (NF-kappaB) inhibitors, C646, a p300/cyclic adenosine monophosphate response element-binding protein-histone acetyltransferase (HAT) inhibitor. Fluorouracil 4-8 nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105 Mus musculus 118-140 27194111-14 2016 The 5-FU-induced up-regulated CXCL1 and CXCL2 gene expressions were inhibited by curcumin, Bay-117082 and bortezomib, nuclear factor kappa B (NF-kappaB) inhibitors, C646, a p300/cyclic adenosine monophosphate response element-binding protein-histone acetyltransferase (HAT) inhibitor. Fluorouracil 4-8 nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105 Mus musculus 142-151 27748935-6 2016 In this study, we found that when cells were treated with PPZ, the 5-fluorouracil (5-FU) chemosensitivity was upregulated, meanwhile the sphere formation ability and the relative expression levels of stem cell markers CD44, CD24, ABCG2, EpCAM and Lgr5 were significantly decreased. Fluorouracil 83-87 CD24 molecule Homo sapiens 224-228 28105142-8 2016 In the rAd/p53 + 5-Fu group, the tumor necrosis ratio, and Smad4 and Brca1 expression levels also significantly increased at various time points (P<0.05). Fluorouracil 17-21 tumor protein p53 Homo sapiens 11-14 27779692-5 2016 Upregulation of AMOT in LoVo cells markedly increased cell proliferation and apoptotic resistance to 5-fluorouracil. Fluorouracil 101-115 angiomotin Homo sapiens 16-20 28101205-11 2016 The results of the present study suggest that it is important to identify patients with CRC who may benefit from adjuvant chemotherapy with 5-FU or oxaliplatin, particularly CRC patients with MSS and mutated KRAS or BRAF, who have poorer overall survival rates than patients with microsatellite instability. Fluorouracil 140-144 B-Raf proto-oncogene, serine/threonine kinase Homo sapiens 216-220 27748935-6 2016 In this study, we found that when cells were treated with PPZ, the 5-fluorouracil (5-FU) chemosensitivity was upregulated, meanwhile the sphere formation ability and the relative expression levels of stem cell markers CD44, CD24, ABCG2, EpCAM and Lgr5 were significantly decreased. Fluorouracil 83-87 ATP binding cassette subfamily G member 2 (Junior blood group) Homo sapiens 230-235 27748935-6 2016 In this study, we found that when cells were treated with PPZ, the 5-fluorouracil (5-FU) chemosensitivity was upregulated, meanwhile the sphere formation ability and the relative expression levels of stem cell markers CD44, CD24, ABCG2, EpCAM and Lgr5 were significantly decreased. Fluorouracil 83-87 epithelial cell adhesion molecule Homo sapiens 237-242 28337106-8 2016 Exposure to hypoxia blunted sensitivity of HepG2 cells to Adriamycin, 5-fluorouracil and cis-platinum, as evidenced by modest alterations in cell viability and apoptosis rate, however the sensitivity was elevated with AEG-1 knockdown. Fluorouracil 70-84 metadherin Homo sapiens 218-223 27942222-0 2016 CTGF enhances resistance to 5-FU-mediating cell apoptosis through FAK/MEK/ERK signal pathway in colorectal cancer. Fluorouracil 28-32 mitogen-activated protein kinase kinase 7 Homo sapiens 70-73 27942222-0 2016 CTGF enhances resistance to 5-FU-mediating cell apoptosis through FAK/MEK/ERK signal pathway in colorectal cancer. Fluorouracil 28-32 mitogen-activated protein kinase 1 Homo sapiens 74-77 27942222-7 2016 We also found that CTGF facilitated resistance to 5-FU-induced apoptosis by increasing the expression of B-cell lymphoma-extra large (Bcl-xL) and survivin. Fluorouracil 50-54 BCL2 like 1 Homo sapiens 105-132 27942222-7 2016 We also found that CTGF facilitated resistance to 5-FU-induced apoptosis by increasing the expression of B-cell lymphoma-extra large (Bcl-xL) and survivin. Fluorouracil 50-54 BCL2 like 1 Homo sapiens 134-140 27942222-9 2016 Our current results indicate that the expression of phosphorylated forms of MEK/ERK increased in high CTGF expression cells and MEK inhibited increases in 5-FU-mediated apoptosis of resistant CRC cells. Fluorouracil 155-159 mitogen-activated protein kinase kinase 7 Homo sapiens 76-79 27942222-9 2016 Our current results indicate that the expression of phosphorylated forms of MEK/ERK increased in high CTGF expression cells and MEK inhibited increases in 5-FU-mediated apoptosis of resistant CRC cells. Fluorouracil 155-159 mitogen-activated protein kinase kinase 7 Homo sapiens 128-131 27942222-10 2016 Therefore, our data suggest that MEK/ERK signaling contributes to 5-FU resistance through upstream of CTGF, and supports CRC cell growth. Fluorouracil 66-70 mitogen-activated protein kinase kinase 7 Homo sapiens 33-36 27942222-10 2016 Therefore, our data suggest that MEK/ERK signaling contributes to 5-FU resistance through upstream of CTGF, and supports CRC cell growth. Fluorouracil 66-70 mitogen-activated protein kinase 1 Homo sapiens 37-40 27793037-9 2016 Overexpression of c-Myc reversed the inhibition of cyclinD1, CDK4, and CDK6, which accelerated the G1/S phase transition under hypoxia and enhanced sensitivity to 5-FU. Fluorouracil 163-167 cyclin dependent kinase 6 Homo sapiens 71-75 27835895-0 2016 Enhancement of 5-FU sensitivity by the proapoptotic rpL3 gene in p53 null colon cancer cells through combined polymer nanoparticles. Fluorouracil 15-19 tumor protein p53 Homo sapiens 65-68 27835895-8 2016 Furthermore, we show that the cancer-specific chemosensitizer effect of combined NPs may be dependent on L3 ability to affect 5-FU efflux by controlling P-gp (P-glycoprotein) expression. Fluorouracil 126-130 ATP binding cassette subfamily B member 1 Homo sapiens 153-157 27835895-8 2016 Furthermore, we show that the cancer-specific chemosensitizer effect of combined NPs may be dependent on L3 ability to affect 5-FU efflux by controlling P-gp (P-glycoprotein) expression. Fluorouracil 126-130 ATP binding cassette subfamily B member 1 Homo sapiens 159-173 27729614-9 2016 APC mutations were associated with poor prognosis in (5-fluorouracil treated) stage III colon cancers (p = 0.005; HR = 4.1), an effect that was further enhanced by mutations in MAPK pathway (KRAS, NRAS, BRAF) genes. Fluorouracil 54-68 B-Raf proto-oncogene, serine/threonine kinase Homo sapiens 203-207 27659530-0 2016 CD133+CD24lo defines a 5-Fluorouracil-resistant colon cancer stem cell-like phenotype. Fluorouracil 23-37 CD24 molecule Homo sapiens 6-10 27659530-9 2016 CD24 is one of the genes whose expression level is lower in the CD133+ and 5-FU-resistant colon cancer cells as compared to CD133+ and 5-FU-sensitive colon cancer cells. Fluorouracil 75-79 CD24 molecule Homo sapiens 0-4 27659530-9 2016 CD24 is one of the genes whose expression level is lower in the CD133+ and 5-FU-resistant colon cancer cells as compared to CD133+ and 5-FU-sensitive colon cancer cells. Fluorouracil 135-139 CD24 molecule Homo sapiens 0-4 27569869-4 2016 Capecitabine is activated to 5-FU by CES, CDA and TYMP, of which SNPs in CDA and CES2 were found to be associated with efficacy and toxicity. Fluorouracil 29-33 carboxylesterase 2 Homo sapiens 81-85 27586268-8 2016 Further studies demonstrated that the combined administration of 5-FU and beta-carotene significantly down-regulated the protein levels of Cav-1, p-AKT, p-NF-kappaB, p-mTOR and p-p70S6K in Eca109 cells more effectively than did 5-FU alone. Fluorouracil 65-69 caveolin 1 Homo sapiens 139-144 27586268-8 2016 Further studies demonstrated that the combined administration of 5-FU and beta-carotene significantly down-regulated the protein levels of Cav-1, p-AKT, p-NF-kappaB, p-mTOR and p-p70S6K in Eca109 cells more effectively than did 5-FU alone. Fluorouracil 228-232 caveolin 1 Homo sapiens 139-144 27578004-4 2016 Here, we report that H3K27 trimethylation (H3K27me3) at the DPYD promoter regulated by Ezh2 and UTX suppresses DPYD expression by inhibiting transcription factor PU.1 binding, leading to increased resistance to 5-FU. Fluorouracil 211-215 enhancer of zeste 2 polycomb repressive complex 2 subunit Homo sapiens 87-91 28133204-5 2016 Chemoradiotherapy(CRT) (5-FU and CDDP with 50 Gy of radiation)was administered. Fluorouracil 24-28 calcitonin receptor Homo sapiens 18-21 27578004-4 2016 Here, we report that H3K27 trimethylation (H3K27me3) at the DPYD promoter regulated by Ezh2 and UTX suppresses DPYD expression by inhibiting transcription factor PU.1 binding, leading to increased resistance to 5-FU. Fluorouracil 211-215 lysine demethylase 6A Homo sapiens 96-99 27578004-6 2016 Lastly, tumor expression data suggest that DPYD repression by Ezh2 predicts poor survival in 5-FU-treated cancers. Fluorouracil 93-97 enhancer of zeste 2 polycomb repressive complex 2 subunit Homo sapiens 62-66 27590709-7 2016 We observed that IL-1beta contributes to the apoptosis of enterocytes in mucositis induced by 5-FU. Fluorouracil 94-98 interleukin 1 beta Homo sapiens 17-25 27634156-5 2016 In addition, GRP78 knockdown enhanced the apoptosis induced by 5-fluorouracil (5-FU) in CRC cells. Fluorouracil 63-77 heat shock protein family A (Hsp70) member 5 Homo sapiens 13-18 27245475-10 2016 CONCLUSIONS: Because hENT1 and OAT2 are crucial for the uptake of gemcitabine and 5-fluorouracil, respectively, our results suggest that patients with AFP-producing GC could potentially benefit from gemcitabine/fluoropyrimidine combination chemotherapy. Fluorouracil 82-96 alpha fetoprotein Homo sapiens 151-154 27634156-5 2016 In addition, GRP78 knockdown enhanced the apoptosis induced by 5-fluorouracil (5-FU) in CRC cells. Fluorouracil 79-83 heat shock protein family A (Hsp70) member 5 Homo sapiens 13-18 27591637-6 2016 This new method could be used to evaluate the inhibition effect of 5-fluorouracil on UDG activity, and become a useful tool in biomedical research. Fluorouracil 67-81 uracil DNA glycosylase Homo sapiens 85-88 28053293-0 2016 Correction: 5-Fluorouracil-induced RNA stress engages a TRAIL-DISC-dependent apoptosis axis facilitated by p53. Fluorouracil 12-26 TNF superfamily member 10 Homo sapiens 56-61 28053293-0 2016 Correction: 5-Fluorouracil-induced RNA stress engages a TRAIL-DISC-dependent apoptosis axis facilitated by p53. Fluorouracil 12-26 tumor protein p53 Homo sapiens 107-110 27787516-0 2016 Melatonin enhances sensitivity to fluorouracil in oesophageal squamous cell carcinoma through inhibition of Erk and Akt pathway. Fluorouracil 34-46 mitogen-activated protein kinase 1 Mus musculus 108-111 27787516-0 2016 Melatonin enhances sensitivity to fluorouracil in oesophageal squamous cell carcinoma through inhibition of Erk and Akt pathway. Fluorouracil 34-46 thymoma viral proto-oncogene 1 Mus musculus 116-119 27787516-4 2016 In contrast, treatment of the conventional chemotherapeutic drug fluorouracil (5-Fu) resulted in activation of Erk and Akt, which could be reversed by co-treatment with melatonin. Fluorouracil 65-77 mitogen-activated protein kinase 1 Mus musculus 111-114 27787516-4 2016 In contrast, treatment of the conventional chemotherapeutic drug fluorouracil (5-Fu) resulted in activation of Erk and Akt, which could be reversed by co-treatment with melatonin. Fluorouracil 65-77 thymoma viral proto-oncogene 1 Mus musculus 119-122 27787516-4 2016 In contrast, treatment of the conventional chemotherapeutic drug fluorouracil (5-Fu) resulted in activation of Erk and Akt, which could be reversed by co-treatment with melatonin. Fluorouracil 79-83 mitogen-activated protein kinase 1 Mus musculus 111-114 27787516-4 2016 In contrast, treatment of the conventional chemotherapeutic drug fluorouracil (5-Fu) resulted in activation of Erk and Akt, which could be reversed by co-treatment with melatonin. Fluorouracil 79-83 thymoma viral proto-oncogene 1 Mus musculus 119-122 27787516-6 2016 Together, these results suggested that inhibition of Erk and Akt pathway by melatonin have an important role in sensitization of ESCC cells to 5-Fu. Fluorouracil 143-147 mitogen-activated protein kinase 1 Mus musculus 53-56 27787516-6 2016 Together, these results suggested that inhibition of Erk and Akt pathway by melatonin have an important role in sensitization of ESCC cells to 5-Fu. Fluorouracil 143-147 thymoma viral proto-oncogene 1 Mus musculus 61-64 27777774-7 2016 RESULTS: B7-H1 expression in human HCT 116 p53+/+ and HCT 116 p53-/- CRC cells lines, while low at baseline, can be induced by treatment with 5-FU. Fluorouracil 142-146 tumor protein p53 Homo sapiens 43-46 27612427-0 2016 DCTPP1 attenuates the sensitivity of human gastric cancer cells to 5-fluorouracil by up-regulating MDR1 expression epigenetically. Fluorouracil 67-81 ATP binding cassette subfamily B member 1 Homo sapiens 99-103 27612427-5 2016 Multidrug resistance 1 (MDR1) expression was unexpectedly down-regulated in DCTPP1-knockdown BGC-823 cells together with more intracellular 5-FU accumulation. Fluorouracil 140-144 ATP binding cassette subfamily B member 1 Homo sapiens 0-22 27612427-5 2016 Multidrug resistance 1 (MDR1) expression was unexpectedly down-regulated in DCTPP1-knockdown BGC-823 cells together with more intracellular 5-FU accumulation. Fluorouracil 140-144 ATP binding cassette subfamily B member 1 Homo sapiens 24-28 27777774-7 2016 RESULTS: B7-H1 expression in human HCT 116 p53+/+ and HCT 116 p53-/- CRC cells lines, while low at baseline, can be induced by treatment with 5-FU. Fluorouracil 142-146 tumor protein p53 Homo sapiens 62-65 27723829-6 2016 More importantly, BCL2A1 siRNA sensitized MDA-MB-231BR to 5-FU, whereas the overexpression of BCL2A1 conferred 5-FU-resistance on MDA-MB-231. Fluorouracil 58-62 BCL2 related protein A1 Homo sapiens 18-24 27428851-6 2016 The as-synthesized 5-FU@FACS-Mn:ZnS nanoparticle (NP) systemically induced higher level of apoptosis in breast cancer cells in vitro as compared to cells treated with free 5-FU drug following both cell cycle and annexin assays, respectively. Fluorouracil 19-23 annexin A11, opposite strand Mus musculus 212-219 27739418-7 2016 Then, we detected the effect of anti-TNF-alpha treatment and it synergistic function with 5-FU in an HCC xenograft mouse model and in HCC cell lines. Fluorouracil 90-94 tumor necrosis factor Mus musculus 37-46 27739418-9 2016 Anti-TNF-alpha treatment by infliximab synergizes with Fluorouracil (5-FU) by promoting apoptosis of HCC tumor cells through complement-dependent cytotoxicity (CDC) and antibody-dependent cellular cytotoxicity (ADCC) effects. Fluorouracil 55-67 tumor necrosis factor Homo sapiens 5-14 27739418-9 2016 Anti-TNF-alpha treatment by infliximab synergizes with Fluorouracil (5-FU) by promoting apoptosis of HCC tumor cells through complement-dependent cytotoxicity (CDC) and antibody-dependent cellular cytotoxicity (ADCC) effects. Fluorouracil 69-73 tumor necrosis factor Homo sapiens 5-14 27739418-10 2016 CONCLUSIONS Based on these data, we conclude that anti-TNF-alpha treatment could be a good way to increase the effect of classic chemotherapy of HCC patients, especially for the patients who have modest response to classic chemotherapy, such as 5-FU. Fluorouracil 245-249 tumor necrosis factor Homo sapiens 55-64 27723829-6 2016 More importantly, BCL2A1 siRNA sensitized MDA-MB-231BR to 5-FU, whereas the overexpression of BCL2A1 conferred 5-FU-resistance on MDA-MB-231. Fluorouracil 111-115 BCL2 related protein A1 Homo sapiens 94-100 27893202-0 2016 Role of GSTM1 Copy Number Variant in the Prognosis ofThai Colorectal Cancer Patients Treated with 5-FU-basedChemotherapy Background: Glutathione S-transferase M1 (GSTM1) is involved in the detoxification of carcinogenic agents.DNA copy number variants of GSTM1 may be associated with cancer progression and may result in reduced survivaltime of various cancers. Fluorouracil 98-102 glutathione S-transferase mu 1 Homo sapiens 8-13 27723829-7 2016 These results indicate that BCL2A1 is a key contributor to the intrinsic 5-FU-resistance in MDA-MB-231BR. Fluorouracil 73-77 BCL2 related protein A1 Homo sapiens 28-34 27893202-0 2016 Role of GSTM1 Copy Number Variant in the Prognosis ofThai Colorectal Cancer Patients Treated with 5-FU-basedChemotherapy Background: Glutathione S-transferase M1 (GSTM1) is involved in the detoxification of carcinogenic agents.DNA copy number variants of GSTM1 may be associated with cancer progression and may result in reduced survivaltime of various cancers. Fluorouracil 98-102 glutathione S-transferase mu 1 Homo sapiens 133-161 27893202-0 2016 Role of GSTM1 Copy Number Variant in the Prognosis ofThai Colorectal Cancer Patients Treated with 5-FU-basedChemotherapy Background: Glutathione S-transferase M1 (GSTM1) is involved in the detoxification of carcinogenic agents.DNA copy number variants of GSTM1 may be associated with cancer progression and may result in reduced survivaltime of various cancers. Fluorouracil 98-102 glutathione S-transferase mu 1 Homo sapiens 163-168 27893202-0 2016 Role of GSTM1 Copy Number Variant in the Prognosis ofThai Colorectal Cancer Patients Treated with 5-FU-basedChemotherapy Background: Glutathione S-transferase M1 (GSTM1) is involved in the detoxification of carcinogenic agents.DNA copy number variants of GSTM1 may be associated with cancer progression and may result in reduced survivaltime of various cancers. Fluorouracil 98-102 glutathione S-transferase mu 1 Homo sapiens 163-168 27893202-1 2016 Determination of DNA copy number variants was here used to assess the associationbetween GSTM1 copy number variant and pathological status and survival time of colorectal-cancer patients treatedwith 5-fluorouracil-based chemotherapy. Fluorouracil 199-213 glutathione S-transferase mu 1 Homo sapiens 89-94 27571921-9 2016 Moreover, FOXK1 suppression induced apoptosis and increased cell susceptibility to 5-fluorouracil (5-FU)-induced apoptosis. Fluorouracil 83-97 forkhead box K1 Homo sapiens 10-15 27554444-5 2016 Compounds 40 and 64 showed broad spectrum antitumor activity toward several tumor cell lines and proved to be 10 fold more active than 5-FU, with GI50 MG-MID values of 2.2 and 2.4muM, respectively. Fluorouracil 135-139 latexin Homo sapiens 179-182 27509880-0 2016 Combination of the histone deacetylase inhibitor depsipeptide and 5-fluorouracil upregulates major histocompatibility complex class II and p21 genes and activates caspase-3/7 in human colon cancer HCT-116 cells. Fluorouracil 66-80 caspase 3 Homo sapiens 163-174 27571921-9 2016 Moreover, FOXK1 suppression induced apoptosis and increased cell susceptibility to 5-fluorouracil (5-FU)-induced apoptosis. Fluorouracil 99-103 forkhead box K1 Homo sapiens 10-15 27509880-3 2016 Exposure to a combination of 5-FU (1.75 microM) and 1 nM depsipeptide for 24 and 48 h resulted in a 3- to 4-fold increase in activated caspase-3/7, while 5-FU alone failed to activate caspase-3/7. Fluorouracil 29-33 caspase 3 Homo sapiens 135-144 27571921-11 2016 A strong antitumorigenic effect of FOXK1-shRNA was enhanced when combined with 5-FU treatment. Fluorouracil 79-83 forkhead box K1 Homo sapiens 35-40 27509880-3 2016 Exposure to a combination of 5-FU (1.75 microM) and 1 nM depsipeptide for 24 and 48 h resulted in a 3- to 4-fold increase in activated caspase-3/7, while 5-FU alone failed to activate caspase-3/7. Fluorouracil 29-33 caspase 3 Homo sapiens 135-146 27509880-4 2016 Microarray and subsequent gene ontology analyses revealed that compared to 5-FU or depsipeptide alone, the combination treatment of 5-FU and depsipeptide upregulated genes related to cell death and the apoptotic process consistent with the inhibition of colony formation and caspase-3/7 activation. Fluorouracil 132-136 caspase 3 Homo sapiens 275-284 27571921-13 2016 FOXK1-shRNA may serve as a novel and potent therapeutic agent, alone or with 5-FU, against colon cancer. Fluorouracil 77-81 forkhead box K1 Homo sapiens 0-5 27671231-5 2016 Co-treatment of DY and 5-FU significantly elevated ROS levels, up-regulated Bax/Bcl-2 ratio and triggered mitochondrial dysfunction, followed by a release of cytochrome c and up-regulation of proteins such as cleaved-caspase-9/3 and cleaved-PARP. Fluorouracil 23-27 BCL2 associated X, apoptosis regulator Homo sapiens 76-79 27723906-0 2016 AFP-producing adenocarcinoma of the esophagogastric junction: report of a case with atypical immunohistochemical findings responding to palliative chemotherapy with 5-fluorouracil, leucovorin, oxaliplatin, and docetaxel (FLOT regime). Fluorouracil 165-179 alpha fetoprotein Homo sapiens 0-3 27671231-5 2016 Co-treatment of DY and 5-FU significantly elevated ROS levels, up-regulated Bax/Bcl-2 ratio and triggered mitochondrial dysfunction, followed by a release of cytochrome c and up-regulation of proteins such as cleaved-caspase-9/3 and cleaved-PARP. Fluorouracil 23-27 BCL2 apoptosis regulator Homo sapiens 80-85 27671231-5 2016 Co-treatment of DY and 5-FU significantly elevated ROS levels, up-regulated Bax/Bcl-2 ratio and triggered mitochondrial dysfunction, followed by a release of cytochrome c and up-regulation of proteins such as cleaved-caspase-9/3 and cleaved-PARP. Fluorouracil 23-27 cytochrome c, somatic Homo sapiens 158-170 27654003-0 2016 The Clinical Significance of MiR-429 as a Predictive Biomarker in Colorectal Cancer Patients Receiving 5-Fluorouracil Treatment. Fluorouracil 103-117 microRNA 429 Homo sapiens 29-36 27654003-9 2016 For patients receiving 5-FU-based treatment, miR-429 levels were significantly lower in responding group. Fluorouracil 23-27 microRNA 429 Homo sapiens 45-52 27654003-11 2016 Finally, Kaplan-Meier survival analysis showed that miR-429 is an independent prognostic indicator for chemo-response to 5-FU therapy among CRC patients. Fluorouracil 121-125 microRNA 429 Homo sapiens 52-59 27654003-13 2016 Furthermore, miR-429 could affect the chemo-sensitivity of CRC patients to 5-FU therapy and was associated with poor response to 5-FU-based chemotherapy in patients with CRC. Fluorouracil 75-79 microRNA 429 Homo sapiens 13-20 27654003-13 2016 Furthermore, miR-429 could affect the chemo-sensitivity of CRC patients to 5-FU therapy and was associated with poor response to 5-FU-based chemotherapy in patients with CRC. Fluorouracil 129-133 microRNA 429 Homo sapiens 13-20 27517750-2 2016 Uracil DNA glycosylase (UDG) is one of the main enzymes responsible for the removal of uracil and 5-FU. Fluorouracil 98-102 uracil DNA glycosylase Homo sapiens 0-22 27645787-12 2016 We found that mice treated with cytokine induced killer cells and PD-L1 monoclonal antibodies after one cycle of 5-FU had a better anti-tumor performance than those treated with chemotherapy or immunotherapy alone. Fluorouracil 113-117 CD274 antigen Mus musculus 66-71 27517750-2 2016 Uracil DNA glycosylase (UDG) is one of the main enzymes responsible for the removal of uracil and 5-FU. Fluorouracil 98-102 uracil DNA glycosylase Homo sapiens 24-27 27517750-3 2016 However, how exactly UDG mediates cellular sensitivity to 5-FdU, and if so whether it is through its ability to remove uracil and 5-FU have not been well characterized. Fluorouracil 130-134 uracil DNA glycosylase Homo sapiens 21-24 27517750-4 2016 In this study, we report that UDG depletion led to incorporation of uracil and 5-FU in DNA following 5-FdU treatment and significantly enhanced 5-FdU"s cytotoxicity in cancer cell lines. Fluorouracil 79-83 uracil DNA glycosylase Homo sapiens 30-33 27517750-5 2016 Co-treatment, but not post-treatment with thymidine prevented cell death of UDG depleted cells by 5-FdU, indicating that the enhanced cytotoxicity is due to the retention of uracil and 5-FU in genomic DNA in the absence of UDG. Fluorouracil 185-189 uracil DNA glycosylase Homo sapiens 76-79 27626067-5 2016 The patient was treated with trastuzumab combined with infusional 5-fluorouracil and leucovorin based on the presence of ERBB2 p.L755S kinase mutation in the tumor and based on the available evidence at the time when standard treatment options had been exhausted. Fluorouracil 66-80 erb-b2 receptor tyrosine kinase 2 Homo sapiens 121-126 27602148-6 2016 It was observed that RNAi-mediated downregulation of EGFR or MRP2 increased the sensitivity to 5-FU and cisplatin in OC2 cells. Fluorouracil 95-99 epidermal growth factor receptor Homo sapiens 53-57 27458056-0 2016 Suppression of TWIST1 enhances the sensitivity of colon cancer cells to 5-fluorouracil. Fluorouracil 72-86 twist family bHLH transcription factor 1 Homo sapiens 15-21 27458056-4 2016 The suppression of TWIST1 expression induced changes in the expression pattern of epithelial to mesenchymal transition markers, reduced the cells proliferation rate, increased their sensitivity to serum withdrawn, and increased the cytotoxic effect of 5FU. Fluorouracil 252-255 twist family bHLH transcription factor 1 Homo sapiens 19-25 27602148-7 2016 Downregulation of EGFR resulted in significant suppression of OC2 tumor growth following 5-FU administration. Fluorouracil 89-93 epidermal growth factor receptor Homo sapiens 18-22 27621580-0 2016 Synergistic anticancer effect of exogenous wild-type p53 gene combined with 5-FU in human colon cancer resistant to 5-FU in vivo. Fluorouracil 116-120 tumor protein p53 Homo sapiens 53-56 27527859-1 2016 Our aim was to decipher the role and clinical relevance of the YAP/TAZ transcriptional coactivators in the regulation of the proliferation/quiescence balance in human colon cancer cells (CCC) and survival after 5FU-based chemotherapy. Fluorouracil 211-214 tafazzin, phospholipid-lysophospholipid transacylase Homo sapiens 67-70 27621580-7 2016 Overexpression of PKC, P-gp and MRP1 was observed in the 5-FU and control groups. Fluorouracil 57-61 proline rich transmembrane protein 2 Homo sapiens 18-21 27566033-8 2016 RESULTS: IC50 values (muM) for OE-19 and OE-33 were 11.2 and 7.1 for tamoxifen, 19.6 and 4.7 for cisplatin, and 1.7 and 5.9 for 5-FU, respectively. Fluorouracil 128-132 latexin Homo sapiens 22-25 27621580-1 2016 AIM: To investigate the anticancer effect of a recombinant adenovirus-mediated p53 (rAd-p53) combined with 5-fluorouracil (5-FU) in human colon cancer resistant to 5-FU in vivo and the mechanism of rAd-p53 in reversal of 5-FU resistance. Fluorouracil 164-168 tumor protein p53 Homo sapiens 79-82 27621580-7 2016 Overexpression of PKC, P-gp and MRP1 was observed in the 5-FU and control groups. Fluorouracil 57-61 ATP binding cassette subfamily C member 1 Homo sapiens 32-36 27621580-8 2016 In the rAd/p53 + 5-FU group, the expression of P-gp and MRP1 was lower that of the control and 5-FU groups (P < 0.05), and the expression of PKC was lower than that of the control, 5-FU and rAd/p53 groups at more than 48 h (P < 0.05). Fluorouracil 17-21 tumor protein p53 Homo sapiens 11-14 27621580-1 2016 AIM: To investigate the anticancer effect of a recombinant adenovirus-mediated p53 (rAd-p53) combined with 5-fluorouracil (5-FU) in human colon cancer resistant to 5-FU in vivo and the mechanism of rAd-p53 in reversal of 5-FU resistance. Fluorouracil 164-168 tumor protein p53 Homo sapiens 88-91 27621580-8 2016 In the rAd/p53 + 5-FU group, the expression of P-gp and MRP1 was lower that of the control and 5-FU groups (P < 0.05), and the expression of PKC was lower than that of the control, 5-FU and rAd/p53 groups at more than 48 h (P < 0.05). Fluorouracil 17-21 ATP binding cassette subfamily C member 1 Homo sapiens 56-60 27621580-8 2016 In the rAd/p53 + 5-FU group, the expression of P-gp and MRP1 was lower that of the control and 5-FU groups (P < 0.05), and the expression of PKC was lower than that of the control, 5-FU and rAd/p53 groups at more than 48 h (P < 0.05). Fluorouracil 17-21 proline rich transmembrane protein 2 Homo sapiens 144-147 27621580-1 2016 AIM: To investigate the anticancer effect of a recombinant adenovirus-mediated p53 (rAd-p53) combined with 5-fluorouracil (5-FU) in human colon cancer resistant to 5-FU in vivo and the mechanism of rAd-p53 in reversal of 5-FU resistance. Fluorouracil 164-168 tumor protein p53 Homo sapiens 88-91 27621580-8 2016 In the rAd/p53 + 5-FU group, the expression of P-gp and MRP1 was lower that of the control and 5-FU groups (P < 0.05), and the expression of PKC was lower than that of the control, 5-FU and rAd/p53 groups at more than 48 h (P < 0.05). Fluorouracil 17-21 tumor protein p53 Homo sapiens 197-200 27621580-8 2016 In the rAd/p53 + 5-FU group, the expression of P-gp and MRP1 was lower that of the control and 5-FU groups (P < 0.05), and the expression of PKC was lower than that of the control, 5-FU and rAd/p53 groups at more than 48 h (P < 0.05). Fluorouracil 95-99 tumor protein p53 Homo sapiens 11-14 27621580-8 2016 In the rAd/p53 + 5-FU group, the expression of P-gp and MRP1 was lower that of the control and 5-FU groups (P < 0.05), and the expression of PKC was lower than that of the control, 5-FU and rAd/p53 groups at more than 48 h (P < 0.05). Fluorouracil 95-99 ATP binding cassette subfamily C member 1 Homo sapiens 56-60 27621580-8 2016 In the rAd/p53 + 5-FU group, the expression of P-gp and MRP1 was lower that of the control and 5-FU groups (P < 0.05), and the expression of PKC was lower than that of the control, 5-FU and rAd/p53 groups at more than 48 h (P < 0.05). Fluorouracil 95-99 tumor protein p53 Homo sapiens 11-14 27621580-8 2016 In the rAd/p53 + 5-FU group, the expression of P-gp and MRP1 was lower that of the control and 5-FU groups (P < 0.05), and the expression of PKC was lower than that of the control, 5-FU and rAd/p53 groups at more than 48 h (P < 0.05). Fluorouracil 95-99 ATP binding cassette subfamily C member 1 Homo sapiens 56-60 27621580-1 2016 AIM: To investigate the anticancer effect of a recombinant adenovirus-mediated p53 (rAd-p53) combined with 5-fluorouracil (5-FU) in human colon cancer resistant to 5-FU in vivo and the mechanism of rAd-p53 in reversal of 5-FU resistance. Fluorouracil 164-168 tumor protein p53 Homo sapiens 79-82 27621580-1 2016 AIM: To investigate the anticancer effect of a recombinant adenovirus-mediated p53 (rAd-p53) combined with 5-fluorouracil (5-FU) in human colon cancer resistant to 5-FU in vivo and the mechanism of rAd-p53 in reversal of 5-FU resistance. Fluorouracil 164-168 tumor protein p53 Homo sapiens 88-91 27621580-1 2016 AIM: To investigate the anticancer effect of a recombinant adenovirus-mediated p53 (rAd-p53) combined with 5-fluorouracil (5-FU) in human colon cancer resistant to 5-FU in vivo and the mechanism of rAd-p53 in reversal of 5-FU resistance. Fluorouracil 164-168 tumor protein p53 Homo sapiens 88-91 27621580-6 2016 The p53 expression was higher in the rAd/p53 and the rAd/p53 + 5-FU groups than that of the control and 5-FU groups (P < 0.05), and were higher in the rAd/p53 + 5-FU group than that of the rAd/p53 group (P < 0.05). Fluorouracil 63-67 tumor protein p53 Homo sapiens 4-7 27621580-9 2016 In the rAd/p53 group, the expression of P-gp and MRP1 was lower that of the control and 5-FU groups at more than 48 h (P < 0.05), and the expression of PKC was lower than that of the control and 5-FU groups at more than 120 h (P < 0.05). Fluorouracil 88-92 tumor protein p53 Homo sapiens 11-14 27621580-6 2016 The p53 expression was higher in the rAd/p53 and the rAd/p53 + 5-FU groups than that of the control and 5-FU groups (P < 0.05), and were higher in the rAd/p53 + 5-FU group than that of the rAd/p53 group (P < 0.05). Fluorouracil 104-108 tumor protein p53 Homo sapiens 4-7 27621580-9 2016 In the rAd/p53 group, the expression of P-gp and MRP1 was lower that of the control and 5-FU groups at more than 48 h (P < 0.05), and the expression of PKC was lower than that of the control and 5-FU groups at more than 120 h (P < 0.05). Fluorouracil 88-92 ATP binding cassette subfamily C member 1 Homo sapiens 49-53 27621580-9 2016 In the rAd/p53 group, the expression of P-gp and MRP1 was lower that of the control and 5-FU groups at more than 48 h (P < 0.05), and the expression of PKC was lower than that of the control and 5-FU groups at more than 120 h (P < 0.05). Fluorouracil 198-202 tumor protein p53 Homo sapiens 11-14 27621580-6 2016 The p53 expression was higher in the rAd/p53 and the rAd/p53 + 5-FU groups than that of the control and 5-FU groups (P < 0.05), and were higher in the rAd/p53 + 5-FU group than that of the rAd/p53 group (P < 0.05). Fluorouracil 104-108 tumor protein p53 Homo sapiens 4-7 27621580-10 2016 CONCLUSION: 5-FU combined with rAd-p53 has a synergistic anticancer effect in SW480/5-FU (5-FU resistance), which contributes to reversal of 5-FU resistance. Fluorouracil 84-88 tumor protein p53 Homo sapiens 35-38 27462786-2 2016 In the present study we aimed to investigate the clinical relevance of Plk3 expression and phosphorylation of caspase-8 at T273 in patients with anal squamous cell carcinoma (SSC) treated with 5-fluorouracil and mitomycin C-based chemoradiotherapy (CRT). Fluorouracil 193-207 polo like kinase 3 Homo sapiens 71-75 27621580-10 2016 CONCLUSION: 5-FU combined with rAd-p53 has a synergistic anticancer effect in SW480/5-FU (5-FU resistance), which contributes to reversal of 5-FU resistance. Fluorouracil 84-88 tumor protein p53 Homo sapiens 35-38 27621580-10 2016 CONCLUSION: 5-FU combined with rAd-p53 has a synergistic anticancer effect in SW480/5-FU (5-FU resistance), which contributes to reversal of 5-FU resistance. Fluorouracil 84-88 tumor protein p53 Homo sapiens 35-38 27527606-7 2016 RESULTS: Upon treatment with 5-fluorouracil (5-FU), apoptosis was increased in latently infected ACH2 cells encoding competent p53 compared with uninfected parent A3.01 cells, while the apoptosis of latently infected p53 null J1.1 cells was less than that of uninfected cells. Fluorouracil 29-43 tumor protein p53 Homo sapiens 127-130 27527606-7 2016 RESULTS: Upon treatment with 5-fluorouracil (5-FU), apoptosis was increased in latently infected ACH2 cells encoding competent p53 compared with uninfected parent A3.01 cells, while the apoptosis of latently infected p53 null J1.1 cells was less than that of uninfected cells. Fluorouracil 45-49 tumor protein p53 Homo sapiens 127-130 27527606-7 2016 RESULTS: Upon treatment with 5-fluorouracil (5-FU), apoptosis was increased in latently infected ACH2 cells encoding competent p53 compared with uninfected parent A3.01 cells, while the apoptosis of latently infected p53 null J1.1 cells was less than that of uninfected cells. Fluorouracil 29-43 tumor protein p53 Homo sapiens 217-220 27527606-7 2016 RESULTS: Upon treatment with 5-fluorouracil (5-FU), apoptosis was increased in latently infected ACH2 cells encoding competent p53 compared with uninfected parent A3.01 cells, while the apoptosis of latently infected p53 null J1.1 cells was less than that of uninfected cells. Fluorouracil 45-49 tumor protein p53 Homo sapiens 217-220 27527606-10 2016 Furthermore, the activation levels of p53 in both cells were further increased upon 5-FU treatment. Fluorouracil 84-88 tumor protein p53 Homo sapiens 38-41 26392056-7 2016 The observed synergistic interaction of both PBOX-15/Oxaliplatin and PBOX-15/5FU may involve activation of p38 MAPK and JNK pathway, which in turn significantly increased caspase-3 cleavage in DLD-1 cells, treated with PBOX-5/Oxaliplatin but not with PBOX-15/5FU. Fluorouracil 259-262 mitogen-activated protein kinase 14 Homo sapiens 107-110 27527606-12 2016 Inhibition of p53 in cells with latent HIV-1 infection diminished apoptosis upon 5-FU treatment. Fluorouracil 81-85 tumor protein p53 Homo sapiens 14-17 27330076-3 2016 Here we show that expression of pyruvate dehydrogenase kinase 4 (PDK4) is positively correlated with drug resistance of colon cancer cells and induced by 5-fluorouracil (5-FU) treatment in drug-resistant but not drug-sensitive cells. Fluorouracil 154-168 pyruvate dehydrogenase kinase 4 Homo sapiens 32-63 27330076-3 2016 Here we show that expression of pyruvate dehydrogenase kinase 4 (PDK4) is positively correlated with drug resistance of colon cancer cells and induced by 5-fluorouracil (5-FU) treatment in drug-resistant but not drug-sensitive cells. Fluorouracil 154-168 pyruvate dehydrogenase kinase 4 Homo sapiens 65-69 27330076-3 2016 Here we show that expression of pyruvate dehydrogenase kinase 4 (PDK4) is positively correlated with drug resistance of colon cancer cells and induced by 5-fluorouracil (5-FU) treatment in drug-resistant but not drug-sensitive cells. Fluorouracil 170-174 pyruvate dehydrogenase kinase 4 Homo sapiens 32-63 27330076-3 2016 Here we show that expression of pyruvate dehydrogenase kinase 4 (PDK4) is positively correlated with drug resistance of colon cancer cells and induced by 5-fluorouracil (5-FU) treatment in drug-resistant but not drug-sensitive cells. Fluorouracil 170-174 pyruvate dehydrogenase kinase 4 Homo sapiens 65-69 27330076-4 2016 Knockdown of PDK4 expression sensitizes colon cancer cells to 5-FU or oxaliplatin-induced apoptosis in vitro and increases the effectiveness of 5-FU in the inhibition of tumor growth in a mouse xenograft model in vivo In addition, we demonstrate for the first time that TGFbeta mediates drug resistance by regulating PDK4 expression and that 5-FU induces PDK4 expression in a TGFbeta signaling-dependent manner. Fluorouracil 62-66 pyruvate dehydrogenase kinase, isoenzyme 4 Mus musculus 13-17 27330076-4 2016 Knockdown of PDK4 expression sensitizes colon cancer cells to 5-FU or oxaliplatin-induced apoptosis in vitro and increases the effectiveness of 5-FU in the inhibition of tumor growth in a mouse xenograft model in vivo In addition, we demonstrate for the first time that TGFbeta mediates drug resistance by regulating PDK4 expression and that 5-FU induces PDK4 expression in a TGFbeta signaling-dependent manner. Fluorouracil 144-148 pyruvate dehydrogenase kinase, isoenzyme 4 Mus musculus 13-17 27330076-4 2016 Knockdown of PDK4 expression sensitizes colon cancer cells to 5-FU or oxaliplatin-induced apoptosis in vitro and increases the effectiveness of 5-FU in the inhibition of tumor growth in a mouse xenograft model in vivo In addition, we demonstrate for the first time that TGFbeta mediates drug resistance by regulating PDK4 expression and that 5-FU induces PDK4 expression in a TGFbeta signaling-dependent manner. Fluorouracil 144-148 pyruvate dehydrogenase kinase, isoenzyme 4 Mus musculus 13-17 27330076-5 2016 Mechanistically, knockdown or inhibition of PDK4 significantly increases the inhibitory effect of 5-FU on expression of the anti-apoptotic factors Bcl-2 and survivin. Fluorouracil 98-102 pyruvate dehydrogenase kinase 4 Homo sapiens 44-48 27330076-5 2016 Mechanistically, knockdown or inhibition of PDK4 significantly increases the inhibitory effect of 5-FU on expression of the anti-apoptotic factors Bcl-2 and survivin. Fluorouracil 98-102 BCL2 apoptosis regulator Homo sapiens 147-152 27507714-4 2016 Although Mef2c-deficient mice maintain relatively intact peripheral B-lymphoid cellularity during homeostasis, they exhibit poor B-lymphoid recovery after sub-lethal irradiation and 5-fluorouracil injection. Fluorouracil 182-196 myocyte enhancer factor 2C Mus musculus 9-14 26392056-7 2016 The observed synergistic interaction of both PBOX-15/Oxaliplatin and PBOX-15/5FU may involve activation of p38 MAPK and JNK pathway, which in turn significantly increased caspase-3 cleavage in DLD-1 cells, treated with PBOX-5/Oxaliplatin but not with PBOX-15/5FU. Fluorouracil 77-80 mitogen-activated protein kinase 14 Homo sapiens 107-110 26392056-7 2016 The observed synergistic interaction of both PBOX-15/Oxaliplatin and PBOX-15/5FU may involve activation of p38 MAPK and JNK pathway, which in turn significantly increased caspase-3 cleavage in DLD-1 cells, treated with PBOX-5/Oxaliplatin but not with PBOX-15/5FU. Fluorouracil 77-80 mitogen-activated protein kinase 8 Homo sapiens 120-123 26392056-7 2016 The observed synergistic interaction of both PBOX-15/Oxaliplatin and PBOX-15/5FU may involve activation of p38 MAPK and JNK pathway, which in turn significantly increased caspase-3 cleavage in DLD-1 cells, treated with PBOX-5/Oxaliplatin but not with PBOX-15/5FU. Fluorouracil 77-80 caspase 3 Homo sapiens 171-180 27128180-3 2016 The most promising compound 7w displayed a three-fold improvement compared with commercial anticancer drug fluorouracil in inhibiting HepG2 cell proliferation with IC50 value of 10.37 muM. Fluorouracil 107-119 latexin Homo sapiens 184-187 26392056-7 2016 The observed synergistic interaction of both PBOX-15/Oxaliplatin and PBOX-15/5FU may involve activation of p38 MAPK and JNK pathway, which in turn significantly increased caspase-3 cleavage in DLD-1 cells, treated with PBOX-5/Oxaliplatin but not with PBOX-15/5FU. Fluorouracil 259-262 mitogen-activated protein kinase 8 Homo sapiens 120-123 27648358-5 2016 Knockdown of PCDH20 expression increases Akt phosphorylation, which leads to elevated mTOR activity and enhanced 5-fluorouracil resistance; whereas rescue of PCDH20 expression in miR-122-expressing cells decreases Akt and mTOR phosphorylation, re-sensitizing hepatocellular carcinoma cell to 5-fluorouracil induced apoptosis. Fluorouracil 113-127 AKT serine/threonine kinase 1 Homo sapiens 41-44 27385218-0 2016 SEP enhanced the antitumor activity of 5-fluorouracil by up-regulating NKG2D/MICA and reversed immune suppression via inhibiting ROS and caspase-3 in mice. Fluorouracil 39-53 inhibitor of carbonic anhydrase Mus musculus 77-81 27385096-0 2016 5-FU targets rpL3 to induce mitochondrial apoptosis via cystathionine-beta-synthase in colon cancer cells lacking p53. Fluorouracil 0-4 cystathionine beta-synthase Homo sapiens 56-83 27385096-7 2016 It is noteworthy that silencing of CBS is associated to a strong increase of 5-FU-mediated inhibition of cell migration and proliferation. Fluorouracil 77-81 cystathionine beta-synthase Homo sapiens 35-38 27648358-6 2016 Moreover, a specific and potent Akt inhibitor reverses miR-122-conferred 5-fluorouracil resistance. Fluorouracil 73-87 AKT serine/threonine kinase 1 Homo sapiens 32-35 26392091-4 2016 The analysis of the changes in the expression of genes involved in the response to DNA damage (CDKN1A, GADD45A, MDM2), apoptosis (BAX, BCL2) and oncogenesis (MYC, JUN) showed that 5-FU, CDDP and ET upregulated the genes involved in DNA damage response, while the anti-apoptotic gene BCL2 and oncogene MYC were downregulated. Fluorouracil 180-184 cyclin dependent kinase inhibitor 1A Homo sapiens 95-101 27234614-0 2016 l-carnosine dipeptide overcomes acquired resistance to 5-fluorouracil in HT29 human colon cancer cells via downregulation of HIF1-alpha and induction of apoptosis. Fluorouracil 55-69 hypoxia inducible factor 1 subunit alpha Homo sapiens 125-135 27234614-2 2016 HIF-1alpha up-regulation decreases the effectiveness of several anticancer agents, including 5-fluorouracil (5-FU), because it induces the expression of drug efflux transporters, alters DNA repair mechanisms and modifies the balance between pro- and antiapoptotic factors. Fluorouracil 93-107 hypoxia inducible factor 1 subunit alpha Homo sapiens 0-10 27234614-2 2016 HIF-1alpha up-regulation decreases the effectiveness of several anticancer agents, including 5-fluorouracil (5-FU), because it induces the expression of drug efflux transporters, alters DNA repair mechanisms and modifies the balance between pro- and antiapoptotic factors. Fluorouracil 109-113 hypoxia inducible factor 1 subunit alpha Homo sapiens 0-10 27130783-0 2016 Role of peptide YY in 5-fluorouracil-induced reduction of dietary intake. Fluorouracil 22-36 peptide YY Mus musculus 8-18 26392091-4 2016 The analysis of the changes in the expression of genes involved in the response to DNA damage (CDKN1A, GADD45A, MDM2), apoptosis (BAX, BCL2) and oncogenesis (MYC, JUN) showed that 5-FU, CDDP and ET upregulated the genes involved in DNA damage response, while the anti-apoptotic gene BCL2 and oncogene MYC were downregulated. Fluorouracil 180-184 BCL2 apoptosis regulator Homo sapiens 135-139 26392091-4 2016 The analysis of the changes in the expression of genes involved in the response to DNA damage (CDKN1A, GADD45A, MDM2), apoptosis (BAX, BCL2) and oncogenesis (MYC, JUN) showed that 5-FU, CDDP and ET upregulated the genes involved in DNA damage response, while the anti-apoptotic gene BCL2 and oncogene MYC were downregulated. Fluorouracil 180-184 BCL2 apoptosis regulator Homo sapiens 283-287 27177453-7 2016 Cells combined treatment with allicin and 5-FU increased intracellular reactive oxygen species (ROS) level, reduced mitochondrial membrane potential (DeltaPsim), activated caspase-3 and PARP, and down-regulated Bcl-2 compared with DMSO, allicin and 5-FU treated alone. Fluorouracil 42-46 B cell leukemia/lymphoma 2 Mus musculus 211-216 26883251-7 2016 Under different concentrations of 5-FU and paclitaxel in MDA-MB231 cell, E-cadherin mRNA and protein expressions increased gradually with the increase of concentrations, and Vimentin and N-cadherin mRNA and protein expressions decreased gradually with the decrease of concentrations (all P < 0.05). Fluorouracil 34-38 cadherin 1 Homo sapiens 73-83 26728163-1 2016 PURPOSE: The purpose of this study was to characterize imaging biomarkers for the potential benefit of hypoxia-inducible factor-1 (HIF-1)alpha inhibition (by PX-12) during 5-fluorouracil (5-FU) chemotherapy in the treatment of colorectal cancer (CRC). Fluorouracil 172-186 hypoxia inducible factor 1 subunit alpha Homo sapiens 131-142 26728163-1 2016 PURPOSE: The purpose of this study was to characterize imaging biomarkers for the potential benefit of hypoxia-inducible factor-1 (HIF-1)alpha inhibition (by PX-12) during 5-fluorouracil (5-FU) chemotherapy in the treatment of colorectal cancer (CRC). Fluorouracil 188-192 hypoxia inducible factor 1 subunit alpha Homo sapiens 131-142 26728163-7 2016 CONCLUSION: Baseline [(18)F]FMISO muPET may predict the beneficial effect of HIF-1alpha inhibition during 5-FU chemotherapy in CRC. Fluorouracil 106-110 hypoxia inducible factor 1 subunit alpha Homo sapiens 77-87 27015836-6 2016 Also, knockdown of Nrf2 suppressed the replicative capability of those cells in colony-forming assay and enhanced their sensitivity to antiproliferative activity of Cis and 5-fluorouracil. Fluorouracil 173-187 NFE2 like bZIP transcription factor 2 Homo sapiens 19-23 27323852-0 2016 Nicotinamide N-methyltransferase enhances resistance to 5-fluorouracil in colorectal cancer cells through inhibition of the ASK1-p38 MAPK pathway. Fluorouracil 56-70 mitogen-activated protein kinase 14 Homo sapiens 129-132 27456431-10 2016 Our findings showed that the polymorphisms of MTRR 66 A > G and TS 5"-UTR 3R > 2R may be potential prognostic factors for GC patients receiving 5-FU. Fluorouracil 150-154 5-methyltetrahydrofolate-homocysteine methyltransferase reductase Homo sapiens 46-50 27323852-5 2016 The reduction in ROS leads to inactivation of the ASK1-p38 mitogen-activated protein kinase (MAPK) pathway, which reduces 5-FU-induced apoptosis. Fluorouracil 122-126 mitogen-activated protein kinase 14 Homo sapiens 55-58 27323852-7 2016 These observations suggest that NNMT and the 1-MNA it produces inhibit the ASK1-p38 MAPK pathway, resulting in increased CRC cell resistance to 5-FU. Fluorouracil 144-148 mitogen-activated protein kinase 14 Homo sapiens 80-83 27499633-0 2016 MK-2206 co-treatment with 5-fluorouracil or doxorubicin enhances chemosensitivity and apoptosis in gastric cancer by attenuation of Akt phosphorylation. Fluorouracil 26-40 AKT serine/threonine kinase 1 Homo sapiens 132-135 27508019-7 2016 Moreover, Enhancement of 5-FU-induced cytotoxicity and apoptosis are resulted from the transfection with miR-144 mimics in Bel-7402/5-FU cells. Fluorouracil 25-29 microRNA 144 Homo sapiens 105-112 27508019-7 2016 Moreover, Enhancement of 5-FU-induced cytotoxicity and apoptosis are resulted from the transfection with miR-144 mimics in Bel-7402/5-FU cells. Fluorouracil 132-136 microRNA 144 Homo sapiens 105-112 27499633-7 2016 Furthermore, a small dose (1 muM) of MK-2206 co-treatment with doxorubicin or 5-FU was sufficient for complete inhibition of chemotherapeutic alteration of phosphorylated Akt expression and significant enhancement of pro-apoptosis effect through the activation of caspase pathway. Fluorouracil 78-82 latexin Homo sapiens 29-32 27499633-7 2016 Furthermore, a small dose (1 muM) of MK-2206 co-treatment with doxorubicin or 5-FU was sufficient for complete inhibition of chemotherapeutic alteration of phosphorylated Akt expression and significant enhancement of pro-apoptosis effect through the activation of caspase pathway. Fluorouracil 78-82 AKT serine/threonine kinase 1 Homo sapiens 171-174 27210058-9 2016 Western blot analysis showed marked downregulation of HIF-1alpha and mTOR expression, and upregulation of AMPKalpha in cells treated with metformin and 5-FU combination treatment. Fluorouracil 152-156 hypoxia inducible factor 1 subunit alpha Homo sapiens 54-64 27283986-5 2016 Increased expression of HDAC2 correlated with drug resistance, and depletion by shRNA sensitised the multi-drug resistance cell line HT-29 to CRC chemotherapeutic drugs such as 5-fluorouracil (5-FU) and oxaliplatin (Oxa). Fluorouracil 177-191 histone deacetylase 2 Homo sapiens 24-29 27283986-5 2016 Increased expression of HDAC2 correlated with drug resistance, and depletion by shRNA sensitised the multi-drug resistance cell line HT-29 to CRC chemotherapeutic drugs such as 5-fluorouracil (5-FU) and oxaliplatin (Oxa). Fluorouracil 193-197 histone deacetylase 2 Homo sapiens 24-29 27283986-6 2016 Combined treatment with the HDACi suberoylanilide hydroxamic acid plus 5-FU or Oxa reduced the level of HDAC2 expression, modified chromatin structure and induced mitotic cell death in HT-29 cells. Fluorouracil 71-75 histone deacetylase 2 Homo sapiens 104-109 26831719-8 2016 Postoperative adjuvant chemotherapy was applied in 31 CEA band-positive cases with an oral 5-fluorouracil derivative HCFU (1-hexylcarbamoyl-5-fluorouracil) for 1 year, whereas chemotherapy was not administered to CEA band-negative group. Fluorouracil 91-105 CEA cell adhesion molecule 3 Homo sapiens 54-57 26831719-8 2016 Postoperative adjuvant chemotherapy was applied in 31 CEA band-positive cases with an oral 5-fluorouracil derivative HCFU (1-hexylcarbamoyl-5-fluorouracil) for 1 year, whereas chemotherapy was not administered to CEA band-negative group. Fluorouracil 91-105 CEA cell adhesion molecule 3 Homo sapiens 213-216 27468227-9 2016 Mechanistically, 5-FU and TQ remarkably cooperated to repress the expression of procancerous Wnt, beta-catenin, NF-kappaB, COX-2, iNOS, VEGF, and TBRAS and upregulate the expression of anti-tumorigenesis DKK-1, CDNK-1A, TGF-beta1, TGF-betaRII, Smad4, and GPx. Fluorouracil 17-21 nitric oxide synthase 2 Rattus norvegicus 130-134 27468227-9 2016 Mechanistically, 5-FU and TQ remarkably cooperated to repress the expression of procancerous Wnt, beta-catenin, NF-kappaB, COX-2, iNOS, VEGF, and TBRAS and upregulate the expression of anti-tumorigenesis DKK-1, CDNK-1A, TGF-beta1, TGF-betaRII, Smad4, and GPx. Fluorouracil 17-21 transforming growth factor, beta 1 Rattus norvegicus 220-229 27115207-0 2016 Production of truncated MBD4 protein by frameshift mutation in DNA mismatch repair-deficient cells enhances 5-fluorouracil sensitivity that is independent of hMLH1 status. Fluorouracil 108-122 methyl-CpG binding domain 4, DNA glycosylase Homo sapiens 24-28 27236157-9 2016 5-FU treatment at various concentrations induced the expressions of T?10 and ABC transporters (ABCB1, ABCG2 ABCA3) in two CCA cell lines, KKU-M055 and KKU-M214. Fluorouracil 0-4 ATP binding cassette subfamily B member 1 Homo sapiens 95-100 27236157-9 2016 5-FU treatment at various concentrations induced the expressions of T?10 and ABC transporters (ABCB1, ABCG2 ABCA3) in two CCA cell lines, KKU-M055 and KKU-M214. Fluorouracil 0-4 ATP binding cassette subfamily G member 2 (Junior blood group) Homo sapiens 102-107 27334757-8 2016 Furthermore, we implicated the involvement of NFBD1 in Rad51 and DNA-PKcs foci formation following CDDP or 5-FU chemotherapy. Fluorouracil 107-111 protein kinase, DNA-activated, catalytic subunit Homo sapiens 65-73 27129209-8 2016 We further explored that DNA damage-induced wild-type p53 leads to spindle assembly checkpoint arrest by repressing UBE2C, whereas mutant p53 causes premature anaphase exit by increasing UBE2C expression in the presence of 5-fluorouracil. Fluorouracil 223-237 tumor protein p53 Homo sapiens 138-141 27129209-8 2016 We further explored that DNA damage-induced wild-type p53 leads to spindle assembly checkpoint arrest by repressing UBE2C, whereas mutant p53 causes premature anaphase exit by increasing UBE2C expression in the presence of 5-fluorouracil. Fluorouracil 223-237 ubiquitin conjugating enzyme E2 C Homo sapiens 187-192 27221981-9 2016 Genetic depletion of Notch2 in HCC cells not only resulted in significantly inhibited proliferation, cell cycle progression and colony formation ability but also increased its sensitivity to 5-fluorouracil (5-FU) compared with controls. Fluorouracil 191-205 notch receptor 2 Homo sapiens 21-27 27221981-9 2016 Genetic depletion of Notch2 in HCC cells not only resulted in significantly inhibited proliferation, cell cycle progression and colony formation ability but also increased its sensitivity to 5-fluorouracil (5-FU) compared with controls. Fluorouracil 207-211 notch receptor 2 Homo sapiens 21-27 27221981-12 2016 Taken together, our findings indicate that Notch2 may confer stemness properties in HCC; downregulation of Notch2 inhibited the proliferation and tumor formation of HCC cells and increase their sensitivity to 5-FU, suggesting Notch2 as a potential therapeutic target for HCC. Fluorouracil 209-213 notch receptor 2 Homo sapiens 107-113 27221981-12 2016 Taken together, our findings indicate that Notch2 may confer stemness properties in HCC; downregulation of Notch2 inhibited the proliferation and tumor formation of HCC cells and increase their sensitivity to 5-FU, suggesting Notch2 as a potential therapeutic target for HCC. Fluorouracil 209-213 notch receptor 2 Homo sapiens 107-113 27340349-2 2016 In addition, the combined strategies of administering EGFR mAbs and traditional cytotoxic agents, such as 5-fluorouracil, oxaliplatin and irinotecan, have resulted in a more complicated management of CRC treatment-related side effects compared with EGFR mAb monotherapy. Fluorouracil 106-120 epidermal growth factor receptor Homo sapiens 54-58 27173050-0 2016 miR-139-5p sensitizes colorectal cancer cells to 5-fluorouracil by targeting NOTCH-1. Fluorouracil 49-63 notch receptor 1 Homo sapiens 77-84 27173050-7 2016 Furthermore, silencing NOTCH-1 expression promoted the chemotherapeutic effects of 5-FU, and up-regulation of NOTCH-1 abrogated miR-139-5p-mediated sensitization to 5-FU in LoVo and HCT-116 cells. Fluorouracil 83-87 notch receptor 1 Homo sapiens 23-30 27173050-7 2016 Furthermore, silencing NOTCH-1 expression promoted the chemotherapeutic effects of 5-FU, and up-regulation of NOTCH-1 abrogated miR-139-5p-mediated sensitization to 5-FU in LoVo and HCT-116 cells. Fluorouracil 165-169 notch receptor 1 Homo sapiens 23-30 27173050-7 2016 Furthermore, silencing NOTCH-1 expression promoted the chemotherapeutic effects of 5-FU, and up-regulation of NOTCH-1 abrogated miR-139-5p-mediated sensitization to 5-FU in LoVo and HCT-116 cells. Fluorouracil 165-169 notch receptor 1 Homo sapiens 110-117 27173050-8 2016 Taken together, our data indicate a new role of miR-139-5p/NOTCH-1 pathway in the drug resistance of CRC cells to 5-FU, which may be a promising therapeutic target for the anti-MDR treatment of CRC. Fluorouracil 114-118 notch receptor 1 Homo sapiens 59-66 26522725-0 2016 Inhibition of caspases primes colon cancer cells for 5-fluorouracil-induced TNF-alpha-dependent necroptosis driven by RIP1 kinase and NF-kappaB. Fluorouracil 53-67 tumor necrosis factor Homo sapiens 76-85 26522725-0 2016 Inhibition of caspases primes colon cancer cells for 5-fluorouracil-induced TNF-alpha-dependent necroptosis driven by RIP1 kinase and NF-kappaB. Fluorouracil 53-67 nuclear factor kappa B subunit 1 Homo sapiens 134-143 26522725-5 2016 We found that pan-caspase inhibitors facilitated 5-FU-induced necroptosis, which was mediated by autocrine secretion of tumor necrosis factor alpha (TNF-alpha). Fluorouracil 49-53 tumor necrosis factor Homo sapiens 120-147 26522725-5 2016 We found that pan-caspase inhibitors facilitated 5-FU-induced necroptosis, which was mediated by autocrine secretion of tumor necrosis factor alpha (TNF-alpha). Fluorouracil 49-53 tumor necrosis factor Homo sapiens 149-158 27259240-0 2016 Interaction of DNA demethylase and histone methyltransferase upregulates Nrf2 in 5-fluorouracil-resistant colon cancer cells. Fluorouracil 81-95 NFE2 like bZIP transcription factor 2 Homo sapiens 73-77 27259240-1 2016 We recently reported that DNA demethylase ten-eleven translocation 1 (TET1) upregulates nuclear factor erythroid 2-related factor 2 (Nrf2) in 5-fluorouracil-resistant colon cancer cells (SNUC5/5-FUR). Fluorouracil 142-156 NFE2 like bZIP transcription factor 2 Homo sapiens 88-131 27259240-1 2016 We recently reported that DNA demethylase ten-eleven translocation 1 (TET1) upregulates nuclear factor erythroid 2-related factor 2 (Nrf2) in 5-fluorouracil-resistant colon cancer cells (SNUC5/5-FUR). Fluorouracil 142-156 NFE2 like bZIP transcription factor 2 Homo sapiens 133-137 27259240-8 2016 These findings indicate that SNUC5/5-FUR cells are under oxidative stress, which induces expression of histone methylation-related proteins as well as DNA demethylase, leading to upregulation of Nrf2 and 5-FU resistance. Fluorouracil 35-39 NFE2 like bZIP transcription factor 2 Homo sapiens 195-199 27340349-2 2016 In addition, the combined strategies of administering EGFR mAbs and traditional cytotoxic agents, such as 5-fluorouracil, oxaliplatin and irinotecan, have resulted in a more complicated management of CRC treatment-related side effects compared with EGFR mAb monotherapy. Fluorouracil 106-120 epidermal growth factor receptor Homo sapiens 249-253 27144434-0 2016 MEK5/ERK5 signaling inhibition increases colon cancer cell sensitivity to 5-fluorouracil through a p53-dependent mechanism. Fluorouracil 74-88 mitogen-activated protein kinase kinase 5 Homo sapiens 0-4 27144434-2 2016 Here, we evaluated the impact of the MEK5/ERK5 cascade in colon cancer cell sensitivity to 5-fluorouracil (5-FU). Fluorouracil 107-111 mitogen-activated protein kinase kinase 5 Homo sapiens 37-41 27144434-0 2016 MEK5/ERK5 signaling inhibition increases colon cancer cell sensitivity to 5-fluorouracil through a p53-dependent mechanism. Fluorouracil 74-88 tumor protein p53 Homo sapiens 99-102 27144434-2 2016 Here, we evaluated the impact of the MEK5/ERK5 cascade in colon cancer cell sensitivity to 5-fluorouracil (5-FU). Fluorouracil 91-105 mitogen-activated protein kinase kinase 5 Homo sapiens 37-41 27145368-6 2016 Functional assays results indicated that the restoration of miR-199b considerably reduced cell invasion and migration in vitro and in vivo, and increased the sensitivity to 5-FU and oxaliplatin. Fluorouracil 173-177 microRNA 199b Homo sapiens 60-68 27144434-4 2016 In colon cancer cells, 5-FU exposure impaired endogenous KRAS/MEK5/ERK5 expression and/or activation. Fluorouracil 23-27 mitogen-activated protein kinase kinase 5 Homo sapiens 62-66 27268079-1 2016 BACKGROUND: It has been shown that epidermal growth factor receptor (EGFR) mutation status is associated with 5-fluorouracil (5-FU) sensitivity in non-small-cell lung cancer (NSCLC). Fluorouracil 110-124 epidermal growth factor receptor Homo sapiens 35-67 27144434-5 2016 In turn, MEK5 constitutive activation reduced 5-FU-induced cytotoxicity. Fluorouracil 46-50 mitogen-activated protein kinase kinase 5 Homo sapiens 9-13 27144434-6 2016 Using genetic and pharmacological approaches, we showed that ERK5 inhibition increased caspase-3/7 activity and apoptosis following 5-FU exposure. Fluorouracil 132-136 caspase 3 Homo sapiens 87-96 27268079-1 2016 BACKGROUND: It has been shown that epidermal growth factor receptor (EGFR) mutation status is associated with 5-fluorouracil (5-FU) sensitivity in non-small-cell lung cancer (NSCLC). Fluorouracil 110-124 epidermal growth factor receptor Homo sapiens 69-73 27268079-1 2016 BACKGROUND: It has been shown that epidermal growth factor receptor (EGFR) mutation status is associated with 5-fluorouracil (5-FU) sensitivity in non-small-cell lung cancer (NSCLC). Fluorouracil 126-130 epidermal growth factor receptor Homo sapiens 35-67 27268079-1 2016 BACKGROUND: It has been shown that epidermal growth factor receptor (EGFR) mutation status is associated with 5-fluorouracil (5-FU) sensitivity in non-small-cell lung cancer (NSCLC). Fluorouracil 126-130 epidermal growth factor receptor Homo sapiens 69-73 27284014-4 2016 We determined that our established PTX-resistant cancer cells display ABCB1/ABCC1-associated cross-resistance to chemically different drugs such as 5-fluorouracil, docetaxel, and cisplatin. Fluorouracil 148-162 ATP binding cassette subfamily B member 1 Homo sapiens 70-75 26687645-9 2016 Taken together, our findings indicated that OMT sensitizes HCC to 5-Fu treatment by the suppression of ERK activation through the overproduction of ROS, and combination treatment with OMT and 5-Fu would be a promising therapeutic strategy for HCC treatment. Fluorouracil 66-70 mitogen-activated protein kinase 1 Homo sapiens 103-106 27284014-4 2016 We determined that our established PTX-resistant cancer cells display ABCB1/ABCC1-associated cross-resistance to chemically different drugs such as 5-fluorouracil, docetaxel, and cisplatin. Fluorouracil 148-162 ATP binding cassette subfamily C member 1 Homo sapiens 76-81 27020656-9 2016 Mechanistically, paricalcitol and 5-FU had cooperated together to repress the expression of procancerous Wnt, beta-catenin, NF-kappaB, COX-2, iNOS, VEGF, and HSP-90 more, and to upregulate the expression of antitumorigenesis DKK-1 and CDNK-1A, compared with their monotherapies. Fluorouracil 34-38 nitric oxide synthase 2 Rattus norvegicus 142-146 27020656-9 2016 Mechanistically, paricalcitol and 5-FU had cooperated together to repress the expression of procancerous Wnt, beta-catenin, NF-kappaB, COX-2, iNOS, VEGF, and HSP-90 more, and to upregulate the expression of antitumorigenesis DKK-1 and CDNK-1A, compared with their monotherapies. Fluorouracil 34-38 heat shock protein 90 alpha family class A member 1 Rattus norvegicus 158-164 27035413-8 2016 Moreover, it enhanced 5-FU-induced cell cycle arrest by decreasing the expression of cyclins and cyclin-dependent kinases and inducing that of p21. Fluorouracil 22-26 cyclin dependent kinase inhibitor 1A Homo sapiens 143-146 27060169-9 2016 Finally, Hif-1alpha-deficient HSCs recover normally after hematopoietic injury induced by serial administration of 5-fluorouracil. Fluorouracil 115-129 hypoxia inducible factor 1 subunit alpha Homo sapiens 9-19 27163731-5 2016 SNUC5/FUR cells transfected with siRNA against GRP78, ATF6, ERK, or AKT were more sensitive to 5-FU than siControl RNA-transfected cells. Fluorouracil 95-99 heat shock protein family A (Hsp70) member 5 Homo sapiens 47-52 27163731-5 2016 SNUC5/FUR cells transfected with siRNA against GRP78, ATF6, ERK, or AKT were more sensitive to 5-FU than siControl RNA-transfected cells. Fluorouracil 95-99 mitogen-activated protein kinase 1 Homo sapiens 60-63 27284361-11 2016 Suppression of GEN1 in SKBR3 cells effectively increased the sensitivity to the chemotherapeutic drug 5-fluorouracil (5-FU), while MCF-7 cells showed no significant change in sensitivity following GEN1 suppression. Fluorouracil 102-116 GEN1 Holliday junction 5' flap endonuclease Homo sapiens 15-19 27284361-11 2016 Suppression of GEN1 in SKBR3 cells effectively increased the sensitivity to the chemotherapeutic drug 5-fluorouracil (5-FU), while MCF-7 cells showed no significant change in sensitivity following GEN1 suppression. Fluorouracil 118-122 GEN1 Holliday junction 5' flap endonuclease Homo sapiens 15-19 27284361-12 2016 However, when GEN1 was targeted in addition to Mus81, the MCF-7 cells also demonstrated a significantly increased sensitivity to 5-FU. Fluorouracil 129-133 GEN1 Holliday junction 5' flap endonuclease Homo sapiens 14-18 27284361-13 2016 In addition, when the level of Mus81 was low, GEN1 expression was increased under a low concentration of 5-FU. Fluorouracil 105-109 GEN1 Holliday junction 5' flap endonuclease Homo sapiens 46-50 27105527-3 2016 In the present work, we determined that high levels of activated Src kinase, measured as phospho-Src at the Tyr419 residue in CRC cell lines, can promote colorectal carcinoma cell resistance to oxaliplatin, but not to 5-fluorouracil (5FU), and that inhibition of this protein restores sensitivity to oxaliplatin. Fluorouracil 218-232 SRC proto-oncogene, non-receptor tyrosine kinase Homo sapiens 65-68 27105527-3 2016 In the present work, we determined that high levels of activated Src kinase, measured as phospho-Src at the Tyr419 residue in CRC cell lines, can promote colorectal carcinoma cell resistance to oxaliplatin, but not to 5-fluorouracil (5FU), and that inhibition of this protein restores sensitivity to oxaliplatin. Fluorouracil 218-232 SRC proto-oncogene, non-receptor tyrosine kinase Homo sapiens 97-100 27105527-3 2016 In the present work, we determined that high levels of activated Src kinase, measured as phospho-Src at the Tyr419 residue in CRC cell lines, can promote colorectal carcinoma cell resistance to oxaliplatin, but not to 5-fluorouracil (5FU), and that inhibition of this protein restores sensitivity to oxaliplatin. Fluorouracil 234-237 SRC proto-oncogene, non-receptor tyrosine kinase Homo sapiens 65-68 27105527-3 2016 In the present work, we determined that high levels of activated Src kinase, measured as phospho-Src at the Tyr419 residue in CRC cell lines, can promote colorectal carcinoma cell resistance to oxaliplatin, but not to 5-fluorouracil (5FU), and that inhibition of this protein restores sensitivity to oxaliplatin. Fluorouracil 234-237 SRC proto-oncogene, non-receptor tyrosine kinase Homo sapiens 97-100 26687759-0 2016 Lin28A enhances chemosensitivity of colon cancer cells to 5-FU by promoting apoptosis in a let-7 independent manner. Fluorouracil 58-62 lin-28 homolog A Homo sapiens 0-6 26687759-3 2016 In this study, we detected the expression of Lin28A in colon cancer patients and tested the effect of Lin28A on the chemotherapeutic sensitivity of colon cancer cells to 5-fluorouracil (5-FU). Fluorouracil 170-184 lin-28 homolog A Homo sapiens 102-108 26687759-5 2016 However, to our surprise, we found that oncogenic protein Lin28A-enforced expression in colon cancer cells enhanced the chemosensitivity of cancer cells to 5-FU via promoting the cell apoptosis. Fluorouracil 156-160 lin-28 homolog A Homo sapiens 58-64 27050375-10 2016 Moreover, STOX2 accelerated OSCC cell growth, invasion, suppressed apoptosis, and enhanced resistance to paclitaxel, cisplatin, and 5-FU. Fluorouracil 132-136 storkhead box 2 Homo sapiens 10-15 26845645-4 2016 Importantly, overexpression of miR-450b-5p in 5-FU-resistant HT-29 cells reduced cell viability, but elevated DNA fragmentation levels and caspase-3 activity were induced by treatment with 5-FU. Fluorouracil 46-50 caspase 3 Homo sapiens 139-148 27534737-0 2016 Correction: 5-Fluorouracil-induced RNA stress engages a TRAIL-DISC-dependent apoptosis axis facilitated by p53. Fluorouracil 12-26 TNF superfamily member 10 Homo sapiens 56-61 27534737-0 2016 Correction: 5-Fluorouracil-induced RNA stress engages a TRAIL-DISC-dependent apoptosis axis facilitated by p53. Fluorouracil 12-26 tumor protein p53 Homo sapiens 107-110 27009858-9 2016 P53 is strongly accumulated in response to 5-FU-induced dormant cells through the activation of ubiquitin ligase anaphase-promoting complex (APC/C) and TGF-beta/Smad signaling. Fluorouracil 43-47 tumor protein p53 Homo sapiens 0-3 26845645-4 2016 Importantly, overexpression of miR-450b-5p in 5-FU-resistant HT-29 cells reduced cell viability, but elevated DNA fragmentation levels and caspase-3 activity were induced by treatment with 5-FU. Fluorouracil 189-193 caspase 3 Homo sapiens 139-148 27212159-0 2016 Inhibition of mTOR suppresses human gallbladder carcinoma cell proliferation and enhances the cytotoxicity of 5-fluorouracil by downregulating MDR1 expression. Fluorouracil 110-124 mechanistic target of rapamycin kinase Homo sapiens 14-18 27212159-0 2016 Inhibition of mTOR suppresses human gallbladder carcinoma cell proliferation and enhances the cytotoxicity of 5-fluorouracil by downregulating MDR1 expression. Fluorouracil 110-124 ATP binding cassette subfamily B member 1 Homo sapiens 143-147 27249600-6 2016 Then, the effect of the miR-183-SOCS6 axis on IC50 of BEL-7402/5-FU cells to 5-FU were investigated by MTT assay. Fluorouracil 63-67 microRNA 183 Homo sapiens 24-31 27212159-8 2016 Upon 5-FU treatment, MDR1 expression was upregulated and OSI-027 could reverse 5-FU-induced MDR1 upregulation. Fluorouracil 5-9 ATP binding cassette subfamily B member 1 Homo sapiens 21-25 27249600-6 2016 Then, the effect of the miR-183-SOCS6 axis on IC50 of BEL-7402/5-FU cells to 5-FU were investigated by MTT assay. Fluorouracil 63-67 suppressor of cytokine signaling 6 Homo sapiens 32-37 27249600-6 2016 Then, the effect of the miR-183-SOCS6 axis on IC50 of BEL-7402/5-FU cells to 5-FU were investigated by MTT assay. Fluorouracil 77-81 microRNA 183 Homo sapiens 24-31 27249600-6 2016 Then, the effect of the miR-183-SOCS6 axis on IC50 of BEL-7402/5-FU cells to 5-FU were investigated by MTT assay. Fluorouracil 77-81 suppressor of cytokine signaling 6 Homo sapiens 32-37 27249600-10 2016 Both SOCS6 overexpression and miR-183 knockdown significantly increased the sensitivity of BEL-7402/5-FU cells to 5-FU. Fluorouracil 100-104 suppressor of cytokine signaling 6 Homo sapiens 5-10 27249600-10 2016 Both SOCS6 overexpression and miR-183 knockdown significantly increased the sensitivity of BEL-7402/5-FU cells to 5-FU. Fluorouracil 100-104 microRNA 183 Homo sapiens 30-37 27249600-10 2016 Both SOCS6 overexpression and miR-183 knockdown significantly increased the sensitivity of BEL-7402/5-FU cells to 5-FU. Fluorouracil 114-118 suppressor of cytokine signaling 6 Homo sapiens 5-10 27249600-10 2016 Both SOCS6 overexpression and miR-183 knockdown significantly increased the sensitivity of BEL-7402/5-FU cells to 5-FU. Fluorouracil 114-118 microRNA 183 Homo sapiens 30-37 27249600-11 2016 MiR-183 overexpression partly abrogated the effect of SOCS6 in enhancing 5-FU sensitivity. Fluorouracil 73-77 microRNA 183 Homo sapiens 0-7 27249600-11 2016 MiR-183 overexpression partly abrogated the effect of SOCS6 in enhancing 5-FU sensitivity. Fluorouracil 73-77 suppressor of cytokine signaling 6 Homo sapiens 54-59 27212159-8 2016 Upon 5-FU treatment, MDR1 expression was upregulated and OSI-027 could reverse 5-FU-induced MDR1 upregulation. Fluorouracil 5-9 ATP binding cassette subfamily B member 1 Homo sapiens 92-96 27212159-8 2016 Upon 5-FU treatment, MDR1 expression was upregulated and OSI-027 could reverse 5-FU-induced MDR1 upregulation. Fluorouracil 79-83 ATP binding cassette subfamily B member 1 Homo sapiens 92-96 27212159-9 2016 Moreover, MDR1 depletion sensitized gallbladder carcinoma cells to 5-FU stimulation and attenuated the synergistic effect of OSI-027 and 5-FU. Fluorouracil 67-71 ATP binding cassette subfamily B member 1 Homo sapiens 10-14 27212159-9 2016 Moreover, MDR1 depletion sensitized gallbladder carcinoma cells to 5-FU stimulation and attenuated the synergistic effect of OSI-027 and 5-FU. Fluorouracil 137-141 ATP binding cassette subfamily B member 1 Homo sapiens 10-14 26986234-8 2016 SIRT4 also increased the sensitivity of colorectal cancer cells to chemotherapeutic drug 5-fluorouracil by inhibiting the cell cycle. Fluorouracil 89-103 sirtuin 4 Homo sapiens 0-5 26892272-5 2016 Co-treatment with lupeol and 5-Fu induced apoptosis through up-regulating the expressions of Bax and p53 and down-regulating the expressions of survivin and Bcl-2. Fluorouracil 29-33 BCL2 associated X, apoptosis regulator Homo sapiens 93-96 26892272-5 2016 Co-treatment with lupeol and 5-Fu induced apoptosis through up-regulating the expressions of Bax and p53 and down-regulating the expressions of survivin and Bcl-2. Fluorouracil 29-33 tumor protein p53 Homo sapiens 101-104 26892272-5 2016 Co-treatment with lupeol and 5-Fu induced apoptosis through up-regulating the expressions of Bax and p53 and down-regulating the expressions of survivin and Bcl-2. Fluorouracil 29-33 BCL2 apoptosis regulator Homo sapiens 157-162 26662569-8 2016 The expression of PCNA and Bcl-XL is remarkably decreased, and the expression of Caspase-3 and cleaved Caspase-3 is obviously increased in GC cells treated with the single and combination of 5-Fu and PD. Fluorouracil 191-195 BCL2 like 1 Homo sapiens 27-33 26808144-0 2016 Distinct TRPV1- and TRPA1-based mechanisms underlying enhancement of oral ulcerative mucositis-induced pain by 5-fluorouracil. Fluorouracil 111-125 transient receptor potential cation channel, subfamily A, member 1 Rattus norvegicus 20-25 26808144-10 2016 These results suggest that 5-fluorouracil-associated leukopenia allows excessive oral bacterial infection in the oral ulcerative region, resulting in the enhancement of spontaneous pain through continuous TRPV1 activation and cyclooxygenase pathway, and mechanical allodynia through mechanical sensitization of TRPA1 caused by neuronal effects of bacterial toxins. Fluorouracil 27-41 transient receptor potential cation channel, subfamily A, member 1 Rattus norvegicus 311-316 26662569-8 2016 The expression of PCNA and Bcl-XL is remarkably decreased, and the expression of Caspase-3 and cleaved Caspase-3 is obviously increased in GC cells treated with the single and combination of 5-Fu and PD. Fluorouracil 191-195 caspase 3 Homo sapiens 81-112 27108536-5 2016 Flow cytometry analysis showed that NOTCH1 inhibition reduces CSCs frequency either alone or in combination with chemotherapeutic agents, namely, cisplatin, docetaxel, and 5-fluorouracil. Fluorouracil 172-186 notch receptor 1 Homo sapiens 36-42 26662313-7 2016 Interestingly, we found that the sensitivity of T-47D cells to some other chemotherapeutic agents (5-fluorouracil, doxorubicin, and tumor necrosis factor-related apoptosis-inducing ligand) was also regulated by miR-27a. Fluorouracil 99-113 microRNA 27a Homo sapiens 211-218 26643894-6 2016 Ectopic SNX1 expression repressed CRC cell growth and promoted tumor sensitivity to most commonly used chemotherapeutic drugs (oxaliplatin and 5-Fluorouracil). Fluorouracil 143-157 sorting nexin 1 Homo sapiens 8-12 27111450-5 2016 ESAM-KO mice experienced severe and prolonged anemia after 5-FU treatment compared to wild-type (WT) mice. Fluorouracil 59-63 endothelial cell-specific adhesion molecule Mus musculus 0-4 27111450-6 2016 Eight days after the 5-FU injection, compared to WT mice, ESAM-KO mice showed reduced numbers of erythroid progenitors in bone marrow (BM) and spleen, and reticulocytes in peripheral blood. Fluorouracil 21-25 endothelial cell-specific adhesion molecule Mus musculus 58-62 27111450-7 2016 Megakaryocyte-erythrocyte progenitors (MEPs) from the BM of 5-FU-treated ESAM-KO mice showed reduced burst forming unit-erythrocyte (BFU-E) capacities than those from WT mice. Fluorouracil 60-64 endothelial cell-specific adhesion molecule Mus musculus 73-77 27111450-8 2016 BM transplantation revealed that hematopoietic stem/progenitor cells from ESAM-KO donors were more sensitive to 5-FU treatment than that from WT donors in the WT host mice. Fluorouracil 112-116 endothelial cell-specific adhesion molecule Mus musculus 74-78 27111450-11 2016 We also found that 5-FU treatment induces the up-regulation of ESAM in primitive erythroid progenitors and macrophages that do not express ESAM under homeostatic conditions. Fluorouracil 19-23 endothelial cell-specific adhesion molecule Mus musculus 63-67 27111450-13 2016 Microarray analyses of primitive erythroid progenitors from 5-FU-treated WT and ESAM-KO mice revealed that various signaling pathways, including the GATA1 system, were impaired in ESAM-KO mice. Fluorouracil 60-64 endothelial cell-specific adhesion molecule Mus musculus 80-84 27111450-13 2016 Microarray analyses of primitive erythroid progenitors from 5-FU-treated WT and ESAM-KO mice revealed that various signaling pathways, including the GATA1 system, were impaired in ESAM-KO mice. Fluorouracil 60-64 endothelial cell-specific adhesion molecule Mus musculus 180-184 26956045-0 2016 The TGF-beta pathway is activated by 5-fluorouracil treatment in drug resistant colorectal carcinoma cells. Fluorouracil 37-51 transforming growth factor beta 1 Homo sapiens 4-12 26956045-4 2016 5-Fluorouracil (5FU) was able to stimulate the activation of SMAD3 and the transcription of specific genes such as ACVRL1, FN1 and TGFB1. Fluorouracil 0-14 fibronectin 1 Homo sapiens 123-126 26956045-4 2016 5-Fluorouracil (5FU) was able to stimulate the activation of SMAD3 and the transcription of specific genes such as ACVRL1, FN1 and TGFB1. Fluorouracil 0-14 transforming growth factor beta 1 Homo sapiens 131-136 26956045-4 2016 5-Fluorouracil (5FU) was able to stimulate the activation of SMAD3 and the transcription of specific genes such as ACVRL1, FN1 and TGFB1. Fluorouracil 16-19 fibronectin 1 Homo sapiens 123-126 26956045-4 2016 5-Fluorouracil (5FU) was able to stimulate the activation of SMAD3 and the transcription of specific genes such as ACVRL1, FN1 and TGFB1. Fluorouracil 16-19 transforming growth factor beta 1 Homo sapiens 131-136 26956045-6 2016 The role of the TGF-beta molecule in the chemoresistant colon carcinoma cells" response to 5FU was further demonstrated by conditioned medium (CM) experiments: CM from 5FU-treated chemoresistant cells was able to protect chemosensitive cells against the toxic action of 5FU. Fluorouracil 91-94 transforming growth factor beta 1 Homo sapiens 16-24 26956045-6 2016 The role of the TGF-beta molecule in the chemoresistant colon carcinoma cells" response to 5FU was further demonstrated by conditioned medium (CM) experiments: CM from 5FU-treated chemoresistant cells was able to protect chemosensitive cells against the toxic action of 5FU. Fluorouracil 168-171 transforming growth factor beta 1 Homo sapiens 16-24 26942699-5 2016 DDA1 overexpression in colon cancer lines promoted cell proliferation, facilitated cell cycle progression, inhibited 5-FU-induced apoptosis, enhanced invasion, and induced the epithelial-mesenchymal transition. Fluorouracil 117-121 DET1 and DDB1 associated 1 Homo sapiens 0-4 27091477-0 2016 Epidermal growth factor receptor inhibitor with fluorouracil, leucovorin, and irinotecan as an alternative treatment for advanced upper tract urothelial carcinoma: a case report. Fluorouracil 48-60 epidermal growth factor receptor Homo sapiens 0-32 27110583-11 2016 5-FU however, rescues the drug-resistance phenotype of fbxw7(DeltaG) through the induction of terminal differentiation. Fluorouracil 0-4 F-box and WD-40 domain protein 7 Mus musculus 55-60 27095304-2 2016 In this study, we observe that miR-3188 not only reduces cell-cycle transition and proliferation, but also significantly prolongs the survival time of tumour-bearing mice as well as sensitizes cells to 5-FU. Fluorouracil 202-206 microRNA 615 Mus musculus 31-34 26712905-0 2016 Preoperative versus postoperative docetaxel-cisplatin-fluorouracil (TCF) chemotherapy in locally advanced resectable gastric carcinoma: 10-year follow-up of the SAKK 43/99 phase III trial. Fluorouracil 54-66 hepatocyte nuclear factor 4 alpha Homo sapiens 68-71 27052330-4 2016 We established a 5-FU-resistant gastric cancer cell subline, and we evaluated its HCCR expression. Fluorouracil 17-21 LETM1 domain containing 1 Homo sapiens 82-86 27052330-5 2016 HCCR expression levels were high in gastric cancer lines, and expression was significantly increased in the 5-FU-resistant cancer cell subline. Fluorouracil 108-112 LETM1 domain containing 1 Homo sapiens 0-4 27052330-8 2016 In vivo and in vitro studies showed that HCCR plays an important role in the apoptosis induced by 5-FU. Fluorouracil 98-102 LETM1 domain containing 1 Homo sapiens 41-45 27052330-10 2016 In gastric cancer cells, HCCR confers a more aggressive phenotype and resistance to 5-FU-based chemotherapy. Fluorouracil 84-88 LETM1 domain containing 1 Homo sapiens 25-29 26919246-10 2016 Moreover, microRNA-200b synergized with 5-fluorouracil to induce apoptosis in vitro and suppressed tumorigenicity in vivo. Fluorouracil 40-54 microRNA 200b Homo sapiens 10-23 26494468-9 2016 Moreover, 5-fluorouracil-induced ephrin-B2 reverse signaling promotes tumorigenesis through the Src-ERK pathway, and drives EMT via the Src-FAK pathway. Fluorouracil 10-24 ephrin B2 Homo sapiens 33-42 27069140-0 2016 NFkappaB-Associated Pathways in Progression of Chemoresistance to 5-Fluorouracil in an In Vitro Model of Colonic Carcinoma. Fluorouracil 66-80 nuclear factor kappa B subunit 1 Homo sapiens 0-8 27069140-8 2016 The results suggest that chemoresistance to 5-FU in this colonic carcinoma model (cell lines SW480 and SW620) is strongly dependent on NFkappaB activation. Fluorouracil 44-48 nuclear factor kappa B subunit 1 Homo sapiens 135-143 26735343-8 2016 The RT-PCR assessment of caspase-3 expression revealed that there was a significant increase in caspase-3 expression in Hep-2 cell line treated with 5-fluorouracil nanoparticles or curcumin compared to non treated cancer cells. Fluorouracil 149-163 caspase 3 Homo sapiens 25-34 26735343-8 2016 The RT-PCR assessment of caspase-3 expression revealed that there was a significant increase in caspase-3 expression in Hep-2 cell line treated with 5-fluorouracil nanoparticles or curcumin compared to non treated cancer cells. Fluorouracil 149-163 caspase 3 Homo sapiens 96-105 26494468-9 2016 Moreover, 5-fluorouracil-induced ephrin-B2 reverse signaling promotes tumorigenesis through the Src-ERK pathway, and drives EMT via the Src-FAK pathway. Fluorouracil 10-24 SRC proto-oncogene, non-receptor tyrosine kinase Homo sapiens 96-99 26494468-9 2016 Moreover, 5-fluorouracil-induced ephrin-B2 reverse signaling promotes tumorigenesis through the Src-ERK pathway, and drives EMT via the Src-FAK pathway. Fluorouracil 10-24 mitogen-activated protein kinase 1 Homo sapiens 100-103 26494468-9 2016 Moreover, 5-fluorouracil-induced ephrin-B2 reverse signaling promotes tumorigenesis through the Src-ERK pathway, and drives EMT via the Src-FAK pathway. Fluorouracil 10-24 SRC proto-oncogene, non-receptor tyrosine kinase Homo sapiens 136-139 27478804-0 2016 Carcinoembryonic Antigen Expression and Resistance to Radiation and 5-Fluorouracil-Induced Apoptosis and Autophagy. Fluorouracil 68-82 CEA cell adhesion molecule 3 Homo sapiens 0-24 27044842-7 2016 In addition, IMP1338 markedly induced the phosphorylation of histone H2AX and Chk1 in both cell lines while the combination of 5-fluorouracil (5-FU) and radiation inhibited the viability of HCT116, HCT116 p53(-/-), and HT29 cells compared to 5-FU or radiation alone. Fluorouracil 127-141 tumor protein p53 Homo sapiens 205-208 27044842-7 2016 In addition, IMP1338 markedly induced the phosphorylation of histone H2AX and Chk1 in both cell lines while the combination of 5-fluorouracil (5-FU) and radiation inhibited the viability of HCT116, HCT116 p53(-/-), and HT29 cells compared to 5-FU or radiation alone. Fluorouracil 143-147 tumor protein p53 Homo sapiens 205-208 25917382-0 2016 Significance of mammalian target of rapamycin in patients with locally advanced stage IV head and neck squamous cell carcinoma receiving induction chemotherapy with docetaxel, cisplatin, and fluorouracil. Fluorouracil 191-203 mechanistic target of rapamycin kinase Homo sapiens 16-45 25917382-1 2016 BACKGROUND: This study evaluated the significance of mammalian target of rapamycin (mTOR) activation on the prognosis of patients with locally advanced head and neck squamous cell carcinoma (HNSCC) receiving induction chemotherapy with docetaxel, cisplatin, and fluorouracil (TPF). Fluorouracil 262-274 mechanistic target of rapamycin kinase Homo sapiens 53-82 25917382-1 2016 BACKGROUND: This study evaluated the significance of mammalian target of rapamycin (mTOR) activation on the prognosis of patients with locally advanced head and neck squamous cell carcinoma (HNSCC) receiving induction chemotherapy with docetaxel, cisplatin, and fluorouracil (TPF). Fluorouracil 262-274 mechanistic target of rapamycin kinase Homo sapiens 84-88 26842876-6 2016 Treatment of preexisting CSCs with a genotoxic drug combination (5-fluorouracil, doxorubicin, and cyclophosphamide) generated an NFkappaB-IL6-dependent inflammatory environment that imparted stemness to nonstem cancer cells, induced multidrug resistance, and enhanced the migration potential of CSCs. Fluorouracil 65-79 nuclear factor kappa B subunit 1 Homo sapiens 129-137 27478804-2 2016 In this study, we investigated the effect of carcinoembryonic antigen (CEA) overexpression on UV-and 5-fluorouracil (5-FU)-induced apoptosis and autophagy in colorectal cancer cells. Fluorouracil 101-115 CEA cell adhesion molecule 3 Homo sapiens 45-69 27478804-2 2016 In this study, we investigated the effect of carcinoembryonic antigen (CEA) overexpression on UV-and 5-fluorouracil (5-FU)-induced apoptosis and autophagy in colorectal cancer cells. Fluorouracil 101-115 CEA cell adhesion molecule 3 Homo sapiens 71-74 27478804-2 2016 In this study, we investigated the effect of carcinoembryonic antigen (CEA) overexpression on UV-and 5-fluorouracil (5-FU)-induced apoptosis and autophagy in colorectal cancer cells. Fluorouracil 117-121 CEA cell adhesion molecule 3 Homo sapiens 45-69 27478804-2 2016 In this study, we investigated the effect of carcinoembryonic antigen (CEA) overexpression on UV-and 5-fluorouracil (5-FU)-induced apoptosis and autophagy in colorectal cancer cells. Fluorouracil 117-121 CEA cell adhesion molecule 3 Homo sapiens 71-74 26785286-10 2016 CONCLUSION: These data reveal that 5-FU-induced cellular apoptosis in corneal epithelial cells may be mediated through caspase-8, caspase-9, and mitochondria-regulated pathways, as well as by upregulation of p21 and downregulation of Bcl-2-dependent signal transduction pathways. Fluorouracil 35-39 BCL2 apoptosis regulator Homo sapiens 234-239 26984381-10 2016 EpCAM expression was down-regulated by the 5-FU and cisplatin in HepG2 cells, however the EpCAM expression was up-regulated by 5-FU and cisplatin in Hep3B cell line. Fluorouracil 43-47 epithelial cell adhesion molecule Homo sapiens 0-5 26984381-10 2016 EpCAM expression was down-regulated by the 5-FU and cisplatin in HepG2 cells, however the EpCAM expression was up-regulated by 5-FU and cisplatin in Hep3B cell line. Fluorouracil 127-131 epithelial cell adhesion molecule Homo sapiens 90-95 26984381-11 2016 EpCAM expression was down-regulated by 5-FU, and up-regulated by cisplatin in Huh-7 cell line. Fluorouracil 39-43 epithelial cell adhesion molecule Homo sapiens 0-5 26977028-6 2016 RanBPM knockdown in gastric cancer cells reduced adhesion and promoted survival of gastric cancer cells after exposure to methotrexate and fluorouracil. Fluorouracil 139-151 RAN binding protein 9 Homo sapiens 0-6 27076940-2 2016 This phase I trial was designed to determine the maximum tolerated dose (MTD) and dose-limiting toxicity (DLT) of S-1, an oral 5-FU derivative, when given with radiotherapy in elderly patients. Fluorouracil 127-131 proteasome 26S subunit, non-ATPase 1 Homo sapiens 114-117 26976970-0 2016 Heterochromatin Protein 1 Binding Protein 3 Expression as a Candidate Marker of Intrinsic 5-Fluorouracil Resistance. Fluorouracil 90-104 heterochromatin protein 1 binding protein 3 Homo sapiens 0-43 26976970-8 2016 CONCLUSION: Using mouse models of human colorectal cancer, Hp1bp3 was identified as a candidate marker of intrinsic 5-FU resistance and may represent a potential biomarker for patient stratification or a target of clinical importance. Fluorouracil 116-120 heterochromatin protein 1 binding protein 3 Homo sapiens 59-65 26847386-4 2016 Effects on the severity of colitis were studied via histochemical and immunohistochemical staining, cytokine levels were determined by reverse transcriptoin-quantitative polymerase chain reaction and the effect of 5-FU on NF-kappaB was examined by western blotting. Fluorouracil 214-218 nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105 Mus musculus 222-231 26847386-7 2016 Tumor necrosis factor-alpha, interleukin-1beta and interferon gamma mRNA expression levels were significantly downregulated in the colon tissue of DSS mice treated with 5-FU compared with the untreated DSS mice (P<0.05). Fluorouracil 169-173 tumor necrosis factor Mus musculus 0-27 26847386-7 2016 Tumor necrosis factor-alpha, interleukin-1beta and interferon gamma mRNA expression levels were significantly downregulated in the colon tissue of DSS mice treated with 5-FU compared with the untreated DSS mice (P<0.05). Fluorouracil 169-173 interleukin 1 beta Mus musculus 29-46 26847386-7 2016 Tumor necrosis factor-alpha, interleukin-1beta and interferon gamma mRNA expression levels were significantly downregulated in the colon tissue of DSS mice treated with 5-FU compared with the untreated DSS mice (P<0.05). Fluorouracil 169-173 interferon gamma Mus musculus 51-67 26847386-9 2016 Furthermore, 5-FU treatment significantly reduced p-NF-kappaB-p56 protein expression levels in the colon tissue of DSS-treated mice (P<0.05). Fluorouracil 13-17 nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105 Mus musculus 52-61 26847386-11 2016 Thus, the modulating inflammatory response role of 5-FU may be partially associated with inhibiting NF-kappaB activation and 5-FU may be a novel therapeutic strategy for the treatment of inflammatory bowel disease. Fluorouracil 51-55 nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105 Mus musculus 100-109 26647806-0 2016 Smad4 sensitizes colorectal cancer to 5-fluorouracil through cell cycle arrest by inhibiting the PI3K/Akt/CDC2/survivin cascade. Fluorouracil 38-52 thymoma viral proto-oncogene 1 Mus musculus 102-105 26752104-7 2016 Downregulation of REV3L expression led to a decrease in cell proliferation and invasive capacity partly through suppression of cyclin D1 and survivin expression, and an increase in cellular sensitivity to 5-fluorouracil (5-FU) by induction of G1 phase arrest and apoptosis. Fluorouracil 205-219 REV3 like, DNA directed polymerase zeta catalytic subunit Homo sapiens 18-23 26752104-7 2016 Downregulation of REV3L expression led to a decrease in cell proliferation and invasive capacity partly through suppression of cyclin D1 and survivin expression, and an increase in cellular sensitivity to 5-fluorouracil (5-FU) by induction of G1 phase arrest and apoptosis. Fluorouracil 221-225 REV3 like, DNA directed polymerase zeta catalytic subunit Homo sapiens 18-23 26432329-8 2016 The single and combination of 5-Fu and BGJ398 decreased the expressions of PCNA, Bcl-xl, and FLIP while increased the expression of caspase-3 in GC cells, especially in shRNA groups. Fluorouracil 30-34 BCL2 like 1 Homo sapiens 81-87 26432329-8 2016 The single and combination of 5-Fu and BGJ398 decreased the expressions of PCNA, Bcl-xl, and FLIP while increased the expression of caspase-3 in GC cells, especially in shRNA groups. Fluorouracil 30-34 caspase 3 Homo sapiens 132-141 25961931-4 2016 In the present study we exposed a series of p53 wild-type human cancer cell lines to drugs such as actinomycin D (ActD), doxorubicin, 5-fluorouracil and CX-5461, which hinder ribosomal RNA (rRNA) synthesis. Fluorouracil 134-148 tumor protein p53 Homo sapiens 44-47 26840457-5 2016 In addition, NgBR suppresses p53 protein levels through activation of the PI3K/Akt/MDM2 pathway, which promotes p53 degradation via the ubiquitin proteasome pathway and thus increases the resistance of human hepatocellular cancer cells to 5-FU. Fluorouracil 239-243 tumor protein p53 Homo sapiens 29-32 26840027-2 2016 In this study, using gene expression profiles for a panel of cell lines with drug sensitivity data and two cohorts of patients, we extracted a signature consisting of two gene pairs (KCNE2 and API5, KCNE2 and PRPF3) whose within-sample relative expression orderings (REOs) could robustly predict prognoses of gastric cancer patients treated with 5-FU-based chemotherapy. Fluorouracil 346-350 apoptosis inhibitor 5 Homo sapiens 193-197 26840457-5 2016 In addition, NgBR suppresses p53 protein levels through activation of the PI3K/Akt/MDM2 pathway, which promotes p53 degradation via the ubiquitin proteasome pathway and thus increases the resistance of human hepatocellular cancer cells to 5-FU. Fluorouracil 239-243 AKT serine/threonine kinase 1 Homo sapiens 79-82 26840457-5 2016 In addition, NgBR suppresses p53 protein levels through activation of the PI3K/Akt/MDM2 pathway, which promotes p53 degradation via the ubiquitin proteasome pathway and thus increases the resistance of human hepatocellular cancer cells to 5-FU. Fluorouracil 239-243 tumor protein p53 Homo sapiens 112-115 26860465-8 2016 We also developed methods to determine the cytotoxic response of individual tumors to the chemotherapeutic treatment FAC (5-FU, Adriamycin [Doxorubicin] and Cyclophosphamide). Fluorouracil 122-126 FA complementation group C Homo sapiens 117-120 26482039-7 2016 Diffuse GA spheroid cells were resistant in a cytotoxicity assay to 5-fluorouracil and cisplatin chemotherapy, and this resistance could be reversed with RhoA pathway inhibition. Fluorouracil 68-82 ras homolog family member A Homo sapiens 154-158 26844701-0 2016 Low levels of Caspase-3 predict favourable response to 5FU-based chemotherapy in advanced colorectal cancer: Caspase-3 inhibition as a therapeutic approach. Fluorouracil 55-58 caspase 3 Homo sapiens 14-23 26844701-10 2016 Exposure of explant cultures to 5FU-based CT increased the percentage of cells positive for active Caspase-3 and Terminal Deoxynucleotidyl Transferase dUTP Nick end Labelling (TUNEL), but also the expression of regeneration and proliferation markers beta-Catenin and Ki-67, as well as cyclooxygenase-2 (COX-2). Fluorouracil 32-35 caspase 3 Homo sapiens 99-108 26844701-10 2016 Exposure of explant cultures to 5FU-based CT increased the percentage of cells positive for active Caspase-3 and Terminal Deoxynucleotidyl Transferase dUTP Nick end Labelling (TUNEL), but also the expression of regeneration and proliferation markers beta-Catenin and Ki-67, as well as cyclooxygenase-2 (COX-2). Fluorouracil 32-35 prostaglandin-endoperoxide synthase 2 Homo sapiens 285-301 26844701-10 2016 Exposure of explant cultures to 5FU-based CT increased the percentage of cells positive for active Caspase-3 and Terminal Deoxynucleotidyl Transferase dUTP Nick end Labelling (TUNEL), but also the expression of regeneration and proliferation markers beta-Catenin and Ki-67, as well as cyclooxygenase-2 (COX-2). Fluorouracil 32-35 prostaglandin-endoperoxide synthase 2 Homo sapiens 303-308 26691280-12 2016 Results indicated that 5-FU decreased H-ras, Rho-A, p53, Stat1 and increased Bax gene expression in Tumor2 and decreased Rac1, Rho-A, NF-kappaB and increased Bax and caspase-3 protein expression in Tumor2. Fluorouracil 23-27 ras homolog family member A Homo sapiens 45-50 26691280-12 2016 Results indicated that 5-FU decreased H-ras, Rho-A, p53, Stat1 and increased Bax gene expression in Tumor2 and decreased Rac1, Rho-A, NF-kappaB and increased Bax and caspase-3 protein expression in Tumor2. Fluorouracil 23-27 tumor protein p53 Homo sapiens 52-55 26691280-12 2016 Results indicated that 5-FU decreased H-ras, Rho-A, p53, Stat1 and increased Bax gene expression in Tumor2 and decreased Rac1, Rho-A, NF-kappaB and increased Bax and caspase-3 protein expression in Tumor2. Fluorouracil 23-27 BCL2 associated X, apoptosis regulator Homo sapiens 77-80 26691280-12 2016 Results indicated that 5-FU decreased H-ras, Rho-A, p53, Stat1 and increased Bax gene expression in Tumor2 and decreased Rac1, Rho-A, NF-kappaB and increased Bax and caspase-3 protein expression in Tumor2. Fluorouracil 23-27 ras homolog family member A Homo sapiens 127-132 26691280-12 2016 Results indicated that 5-FU decreased H-ras, Rho-A, p53, Stat1 and increased Bax gene expression in Tumor2 and decreased Rac1, Rho-A, NF-kappaB and increased Bax and caspase-3 protein expression in Tumor2. Fluorouracil 23-27 BCL2 associated X, apoptosis regulator Homo sapiens 158-161 26691280-12 2016 Results indicated that 5-FU decreased H-ras, Rho-A, p53, Stat1 and increased Bax gene expression in Tumor2 and decreased Rac1, Rho-A, NF-kappaB and increased Bax and caspase-3 protein expression in Tumor2. Fluorouracil 23-27 caspase 3 Homo sapiens 166-175 26691280-13 2016 5-FU decreased H-ras, Bcl-xL and NF-kappaB and increased Bax gene expression. Fluorouracil 0-4 BCL2 like 1 Homo sapiens 22-28 26691280-13 2016 5-FU decreased H-ras, Bcl-xL and NF-kappaB and increased Bax gene expression. Fluorouracil 0-4 BCL2 associated X, apoptosis regulator Homo sapiens 57-60 26691280-14 2016 5-FU decreased Rac1, Rho-A protein expression and increased Bax and caspase-3 protein expression in MDA-MB-231. Fluorouracil 0-4 ras homolog family member A Homo sapiens 21-26 26691280-14 2016 5-FU decreased Rac1, Rho-A protein expression and increased Bax and caspase-3 protein expression in MDA-MB-231. Fluorouracil 0-4 BCL2 associated X, apoptosis regulator Homo sapiens 60-63 26691280-14 2016 5-FU decreased Rac1, Rho-A protein expression and increased Bax and caspase-3 protein expression in MDA-MB-231. Fluorouracil 0-4 caspase 3 Homo sapiens 68-77 26691280-16 2016 It can be concluded that 5-FU may exert apoptotic activity in breast cancer cells transformed by low doses of ionizing alpha-particles in vitro regulating genes of Ras family and related to apoptosis such as Bax, Bcl-xL and NF-kappaB expression. Fluorouracil 25-29 BCL2 associated X, apoptosis regulator Homo sapiens 208-211 26691280-16 2016 It can be concluded that 5-FU may exert apoptotic activity in breast cancer cells transformed by low doses of ionizing alpha-particles in vitro regulating genes of Ras family and related to apoptosis such as Bax, Bcl-xL and NF-kappaB expression. Fluorouracil 25-29 BCL2 like 1 Homo sapiens 213-219 26893778-0 2016 Downregulation of Foxc2 enhances apoptosis induced by 5-fluorouracil through activation of MAPK and AKT pathways in colorectal cancer. Fluorouracil 54-68 AKT serine/threonine kinase 1 Homo sapiens 100-103 29874335-0 2016 S-1 monotherapy as second line chemotherapy in advanced gastric cancer patients previously treated with cisplatin/infusional fluorouracil [Retraction]. Fluorouracil 125-137 proteasome 26S subunit, non-ATPase 1 Homo sapiens 0-3 26893778-7 2016 Therefore, the downregulation of Foxc2, induced by 5-FU, may enhance apoptosis by the downregulation of apoptotic factors, including B cell lymphoma-2 and pro-caspase-3, in Foxc2-shRNA CRC cells. Fluorouracil 51-55 caspase 3 Homo sapiens 140-168 26893778-8 2016 Furthermore, the mitogen-activated protein kinase (MAPK) and phosphatidylinositide 3-kinases/protein kinase B (PI3K/AKT) pathways were essential for the sensitization effect of Foxc2 to 5-FU treatment. Fluorouracil 186-190 AKT serine/threonine kinase 1 Homo sapiens 116-119 26893778-9 2016 Overall, these findings reveal the mechanisms behind Foxc2 depletion and 5-FU treatment of CRC and suggest that Foxc2 enhances resistance to apoptosis, induced by 5-FU, through the activation of MAPK and P13K/AKT pathways, and may serve as a valuable clinical prognostic marker for CRC. Fluorouracil 163-167 AKT serine/threonine kinase 1 Homo sapiens 209-212 26546046-11 2016 A549 cells overexpressing TMPRSS4 conferred the opposite phenotype and were also more sensitive to the CSC-targeted drug salinomycin than control cells, but were more resistant to regular chemotherapeutic drugs (cisplatin, gemcitabine and 5-fluorouracil). Fluorouracil 239-253 transmembrane serine protease 4 Homo sapiens 26-33 26810644-6 2016 To assess the short-term cytotoxicity and examine the apoptotic effects upon addition of 5-FU in vitro, we performed LIVE/DEAD and caspase-3 activity assays. Fluorouracil 89-93 caspase 3 Homo sapiens 131-140 26573232-0 2016 A genome-wide association study identifies WT1 variant with better response to 5-fluorouracil, pirarubicin and cyclophosphamide neoadjuvant chemotherapy in breast cancer patients. Fluorouracil 79-93 WT1 transcription factor Homo sapiens 43-46 26810644-9 2016 RESULTS: Compared to PIT alone, the combination of HER2-targeted PIT and 5-FU rapidly induced significant cytotoxicity in both the short-term and long-term cytotoxicity assays. Fluorouracil 73-77 erb-b2 receptor tyrosine kinase 2 Homo sapiens 51-55 26810644-10 2016 While both 5-FU and/or trastuzumab-IR700 conjugate treatment induced an increase in caspase-3 activity, there was no additional increase in caspase-3 activity upon NIR light irradiation after incubation with 5-FU and/or trastuzumab-IR700. Fluorouracil 11-15 caspase 3 Homo sapiens 84-93 26810644-13 2016 CONCLUSIONS: PIT in combination with 5-FU resulted in enhanced antitumor effects compared to PIT alone for HER2-expressing human gastric cancer in vitro and in vivo. Fluorouracil 37-41 erb-b2 receptor tyrosine kinase 2 Homo sapiens 107-111 26673620-0 2016 MicroRNA-497 inhibits tumor growth and increases chemosensitivity to 5-fluorouracil treatment by targeting KSR1. Fluorouracil 69-83 kinase suppressor of ras 1 Homo sapiens 107-111 26463014-7 2016 The imaging-enabled BPLP-co-PLGA was fabricated into porous scaffolds whose degradation can be monitored through non-invasive imaging and nanoparticles that show theranostic potential demonstrated by fluorescent cellular labeling, imaging and sustained 5-fluorouracil delivery. Fluorouracil 253-267 opiorphin prepropeptide Homo sapiens 20-24 26505786-6 2016 Treatment with 5-FU or DOX in combination with curcumin induced apoptosis by inhibiting Bcl-2 and increasing Bax, caspase-3, and poly-ADP ribose polymerase (PARP) in NT8e cells. Fluorouracil 15-19 BCL2 apoptosis regulator Homo sapiens 88-93 26505786-6 2016 Treatment with 5-FU or DOX in combination with curcumin induced apoptosis by inhibiting Bcl-2 and increasing Bax, caspase-3, and poly-ADP ribose polymerase (PARP) in NT8e cells. Fluorouracil 15-19 BCL2 associated X, apoptosis regulator Homo sapiens 109-112 26505786-6 2016 Treatment with 5-FU or DOX in combination with curcumin induced apoptosis by inhibiting Bcl-2 and increasing Bax, caspase-3, and poly-ADP ribose polymerase (PARP) in NT8e cells. Fluorouracil 15-19 caspase 3 Homo sapiens 114-123 26505786-6 2016 Treatment with 5-FU or DOX in combination with curcumin induced apoptosis by inhibiting Bcl-2 and increasing Bax, caspase-3, and poly-ADP ribose polymerase (PARP) in NT8e cells. Fluorouracil 15-19 poly(ADP-ribose) polymerase 1 Homo sapiens 129-155 26505786-6 2016 Treatment with 5-FU or DOX in combination with curcumin induced apoptosis by inhibiting Bcl-2 and increasing Bax, caspase-3, and poly-ADP ribose polymerase (PARP) in NT8e cells. Fluorouracil 15-19 poly(ADP-ribose) polymerase 1 Homo sapiens 157-161 26505786-9 2016 In addition, curcumin exposure along with 5-FU or DOX inhibited cell proliferation through the downregulation of EGFR-ERK1/2 signaling molecules. Fluorouracil 42-46 epidermal growth factor receptor Homo sapiens 113-117 26505786-9 2016 In addition, curcumin exposure along with 5-FU or DOX inhibited cell proliferation through the downregulation of EGFR-ERK1/2 signaling molecules. Fluorouracil 42-46 mitogen-activated protein kinase 3 Homo sapiens 118-124 27109155-8 2016 It is known that the chemotherapeutic drug 5-FU can suppress the immune system, which can be identified by a reduced white blood cell count and decreased hematocrit, while the combination of AST and 5-FU can reverse the above hematologic toxicities. Fluorouracil 43-47 solute carrier family 17 member 5 Homo sapiens 191-194 26575609-7 2016 The Fat4-silenced cells which were treated with 5-FU, Cisplatin, Oxaliplatin and Paclitaxel individually demonstrated less sensitivities to these chemotherapy drugs compared with the control cells. Fluorouracil 48-52 FAT atypical cadherin 4 Homo sapiens 4-8 26811188-5 2016 CONCLUSIONS: The risk of febrile neutropenia, all-grade and high-grade neutropenia and leucopenia is less in S-1-based therapy than in non fluoropyrimidine regimens; yet comparable to the risk associated with infusional 5FU or capecitabine-based regimens. Fluorouracil 220-223 proteasome 26S subunit, non-ATPase 1 Homo sapiens 109-112 26462739-6 2016 Consistently, costimulation of HeLa cells with any chemotherapeutic agent in the presence of melatonin further increased caspase-3 activation, particularly in CIS- and 5-FU-challenged cells. Fluorouracil 168-172 caspase 3 Homo sapiens 121-130 27610130-12 2016 This analysis suggests a prognostic impact of both ERBB1 and MKi67 mRNA expression in LARC patients treated with capecitabine or fluorouracil-based chemoradiotherapy. Fluorouracil 129-141 epidermal growth factor receptor Homo sapiens 51-56 27610130-12 2016 This analysis suggests a prognostic impact of both ERBB1 and MKi67 mRNA expression in LARC patients treated with capecitabine or fluorouracil-based chemoradiotherapy. Fluorouracil 129-141 marker of proliferation Ki-67 Homo sapiens 61-66 26647656-6 2016 Regarding SAS, CD44v3+/CD24- cells also showed a higher drug resistance for CDDP, 5-FU and cetuximab and expressed higher mRNA levels of CSC property-related genes than the other cell fractions. Fluorouracil 82-86 CD24 molecule Homo sapiens 23-27 26774139-4 2016 In nude mice bearing human colon cancer LoVo cell xenografts, chidamide alone or in combination with 5-flurouracil (5-Fu) reduced the expression of HDAC1 and HDAC2, accompanied with increased acetylation of histone H3. Fluorouracil 116-120 histone deacetylase 1 Homo sapiens 148-153 26494862-0 2016 Genomically Incorporated 5-Fluorouracil that Escapes UNG-Initiated Base Excision Repair Blocks DNA Replication and Activates Homologous Recombination. Fluorouracil 25-39 uracil DNA glycosylase Homo sapiens 53-56 26774139-4 2016 In nude mice bearing human colon cancer LoVo cell xenografts, chidamide alone or in combination with 5-flurouracil (5-Fu) reduced the expression of HDAC1 and HDAC2, accompanied with increased acetylation of histone H3. Fluorouracil 116-120 histone deacetylase 2 Homo sapiens 158-163 26774139-9 2016 Chidamide alone or in combination with 5-Fu down regulated the expressions of p-AKT, p-mammalian target of rapamycin (mTOR), p-p70S6K, p-Raf, and p44/42 mitogen activated protein kinase (Erk1/2), indicating the blockage of these signaling pathways. Fluorouracil 39-43 mechanistic target of rapamycin kinase Homo sapiens 85-116 26774139-7 2016 Western blotting analysis showed that chidamide alone or in combination with 5-Fu upregulated the expressions of cleaved Caspase-3 and cleaved poly-ADP (adenosine diphosphate)-ribose polymerase (PARP). Fluorouracil 77-81 poly(ADP-ribose) polymerase 1 Homo sapiens 195-199 26774139-9 2016 Chidamide alone or in combination with 5-Fu down regulated the expressions of p-AKT, p-mammalian target of rapamycin (mTOR), p-p70S6K, p-Raf, and p44/42 mitogen activated protein kinase (Erk1/2), indicating the blockage of these signaling pathways. Fluorouracil 39-43 mechanistic target of rapamycin kinase Homo sapiens 118-122 26774139-8 2016 In addition, chidamide alone or in combination with 5-Fu increased the p53, phosphorylated-p53 (p-p53), p21 and gammaH2AX levels, but suppressed cyclin dependent kinase 4 (CDK4) expression in tumor cells. Fluorouracil 52-56 tumor protein p53 Homo sapiens 71-74 26774139-8 2016 In addition, chidamide alone or in combination with 5-Fu increased the p53, phosphorylated-p53 (p-p53), p21 and gammaH2AX levels, but suppressed cyclin dependent kinase 4 (CDK4) expression in tumor cells. Fluorouracil 52-56 tumor protein p53 Homo sapiens 91-94 26774139-9 2016 Chidamide alone or in combination with 5-Fu down regulated the expressions of p-AKT, p-mammalian target of rapamycin (mTOR), p-p70S6K, p-Raf, and p44/42 mitogen activated protein kinase (Erk1/2), indicating the blockage of these signaling pathways. Fluorouracil 39-43 mitogen-activated protein kinase 3 Homo sapiens 187-193 26774139-8 2016 In addition, chidamide alone or in combination with 5-Fu increased the p53, phosphorylated-p53 (p-p53), p21 and gammaH2AX levels, but suppressed cyclin dependent kinase 4 (CDK4) expression in tumor cells. Fluorouracil 52-56 tumor protein p53 Homo sapiens 91-94 26802647-10 2016 Furthermore, the mRNA level of ABCB1, a multidrug-resistant protein, was significantly decreased in the 5-fluorouracil combined with DHMEQ-treated cells. Fluorouracil 104-118 ATP binding cassette subfamily B member 1 Homo sapiens 31-36 26692822-13 2015 In addition, As2O3 in combination with 5-FU treatment caused up-regulation of DR5, caspase 3, caspase 8, and caspase 9, and down-regulation of BCL-2, but had no effect of DR4. Fluorouracil 39-43 caspase 3 Homo sapiens 83-92 26931435-7 2016 After HIF-1alpha-siRNA transfection, inhibition rates of 5-FU and L-OHP to tumor cells increased significantly. Fluorouracil 57-61 hypoxia inducible factor 1 subunit alpha Homo sapiens 6-16 26242265-3 2016 SGC-7901 gastric cancer cell line was treated with 5-fluorouracil (5-FU) or/and autophagy inhibitor bafilomycin A1. Fluorouracil 51-65 sarcoglycan beta Homo sapiens 0-3 26242265-3 2016 SGC-7901 gastric cancer cell line was treated with 5-fluorouracil (5-FU) or/and autophagy inhibitor bafilomycin A1. Fluorouracil 67-71 sarcoglycan beta Homo sapiens 0-3 26242265-8 2016 We observed that 5-FU induced autophagy in SGC-7901 cells. Fluorouracil 17-21 sarcoglycan beta Homo sapiens 43-46 26692822-13 2015 In addition, As2O3 in combination with 5-FU treatment caused up-regulation of DR5, caspase 3, caspase 8, and caspase 9, and down-regulation of BCL-2, but had no effect of DR4. Fluorouracil 39-43 BCL2 apoptosis regulator Homo sapiens 143-148 26556875-6 2015 Combining blockade of p-STAT3 with cytotoxic drugs cisplatin, docetaxel, 5-fluorouracil (TPF) enhanced the antitumor effect in vitro and in vivo with decreased tumor sphere formation and SP cells. Fluorouracil 73-87 signal transducer and activator of transcription 3 Mus musculus 22-29 26472927-5 2015 Further studies showed that treatment of tumor cells with almost all standard tumor therapeutics, including chemotherapy (cisplatin, 5-fluorouracil), radiation therapy, non-lethal heat shock, and cytokine therapy (TNF-alpha), could up-regulate the expression of B7-H6 in tumor cells and enhance tumor sensitivity to NK cell cytolysis. Fluorouracil 133-147 tumor necrosis factor Homo sapiens 214-223 26636340-0 2015 Overexpression of Lin28 Decreases the Chemosensitivity of Gastric Cancer Cells to Oxaliplatin, Paclitaxel, Doxorubicin, and Fluorouracil in Part via microRNA-107. Fluorouracil 124-136 lin-28 homolog A Homo sapiens 18-23 26636340-3 2015 In this study, we found that transfection of Lin28 into gastric cancer cells (MKN45 and MKN28) increased their resistance to the chemo-drugs oxaliplatin (OXA), paclitaxel (PTX), doxorubicin (ADM), and fluorouracil (5-Fu) compared with gastric cancer cells transfected with a control vector. Fluorouracil 201-213 lin-28 homolog A Homo sapiens 45-50 26636340-3 2015 In this study, we found that transfection of Lin28 into gastric cancer cells (MKN45 and MKN28) increased their resistance to the chemo-drugs oxaliplatin (OXA), paclitaxel (PTX), doxorubicin (ADM), and fluorouracil (5-Fu) compared with gastric cancer cells transfected with a control vector. Fluorouracil 215-219 lin-28 homolog A Homo sapiens 45-50 25404478-10 2015 Moreover, PRRX1 impaired resistance to 5-FU and radiation. Fluorouracil 39-43 paired related homeobox 1 Homo sapiens 10-15 27551256-4 2015 The decoy vascular endothelial growth factor receptor aflibercept has been approved in combination with 5-fluorouracil, leucovorin and irinotecan-based chemotherapy in metastatic colorectal cancer patients whose disease has progressed on a prior oxaliplatin-based chemotherapy regimen. Fluorouracil 104-118 vascular endothelial growth factor A Homo sapiens 10-44 25736303-8 2015 The combination of 5-FU and Res significantly increased the percentage of apoptotic cells and the level of activated caspase-3, cleaved PARP and p53 proteins as well as increased the Bax/Bcl-2 ratio. Fluorouracil 19-23 caspase 3 Homo sapiens 117-126 25736303-8 2015 The combination of 5-FU and Res significantly increased the percentage of apoptotic cells and the level of activated caspase-3, cleaved PARP and p53 proteins as well as increased the Bax/Bcl-2 ratio. Fluorouracil 19-23 tumor protein p53 Homo sapiens 145-148 25736303-8 2015 The combination of 5-FU and Res significantly increased the percentage of apoptotic cells and the level of activated caspase-3, cleaved PARP and p53 proteins as well as increased the Bax/Bcl-2 ratio. Fluorouracil 19-23 BCL2 associated X, apoptosis regulator Homo sapiens 183-186 25736303-8 2015 The combination of 5-FU and Res significantly increased the percentage of apoptotic cells and the level of activated caspase-3, cleaved PARP and p53 proteins as well as increased the Bax/Bcl-2 ratio. Fluorouracil 19-23 BCL2 apoptosis regulator Homo sapiens 187-192 26459801-0 2015 Targeting the 133p53 isoform can restore chemosensitivity in 5-fluorouracil-resistant cholangiocarcinoma cells. Fluorouracil 62-76 tumor protein p53 Homo sapiens 18-21 26459801-9 2015 Increased 133p53 was correlated with 5-FU in a dose-dependent manner. Fluorouracil 38-42 tumor protein p53 Homo sapiens 14-17 26460271-5 2015 Sorafenib and 5-FU treatment decreased growth rates in Huh7 and Huh-BAT cells; however, the treatments exerted different effects in SP cells and on the expression levels of JNK signaling molecules. Fluorouracil 14-18 mitogen-activated protein kinase 8 Homo sapiens 173-176 26460271-6 2015 Treatment with 5-FU increased the SP cell number and upregulated the expression of JNK signaling molecules. Fluorouracil 15-19 mitogen-activated protein kinase 8 Homo sapiens 83-86 26788191-8 2015 The mechanism through which TUSC4 overexpression enhances 5-FU sensitivity involves the downregulation of the function of the PI3K/Akt/mTOR network. Fluorouracil 58-62 AKT serine/threonine kinase 1 Homo sapiens 131-134 26788191-8 2015 The mechanism through which TUSC4 overexpression enhances 5-FU sensitivity involves the downregulation of the function of the PI3K/Akt/mTOR network. Fluorouracil 58-62 mechanistic target of rapamycin kinase Homo sapiens 135-139 26788191-9 2015 Furthermore, 5-FU upregulated caspase-3 and caspase-9, promoting apoptosis in TUSC4-overexpressing cells compared with cells that were transduced with TUSC4 or treated with 5-FU and NC cells. Fluorouracil 13-17 caspase 3 Homo sapiens 30-39 26136123-10 2015 We analyzed expression levels of survival and apoptosis-associated proteins (pAkt, Akt, Mcl-1, Bcl-2, Bad, and Bax) altered by 5-FU treatment. Fluorouracil 127-131 AKT serine/threonine kinase 1 Homo sapiens 78-81 26136123-10 2015 We analyzed expression levels of survival and apoptosis-associated proteins (pAkt, Akt, Mcl-1, Bcl-2, Bad, and Bax) altered by 5-FU treatment. Fluorouracil 127-131 BCL2 apoptosis regulator Homo sapiens 95-100 26136123-10 2015 We analyzed expression levels of survival and apoptosis-associated proteins (pAkt, Akt, Mcl-1, Bcl-2, Bad, and Bax) altered by 5-FU treatment. Fluorouracil 127-131 BCL2 associated X, apoptosis regulator Homo sapiens 111-114 26136123-11 2015 Survival and antiapoptosis signaling (pAkt, Akt, Mcl-1 and Bcl-2) was downregulated, and the proapoptotic proteins (Bad and Bax) were upregulated in 5-FU-treated control cells but expression levels of Bcl-2, Bad, and Bad were not altered in 5-FU-treated A7-nAChR-KD cells. Fluorouracil 149-153 BCL2 apoptosis regulator Homo sapiens 59-64 26136123-11 2015 Survival and antiapoptosis signaling (pAkt, Akt, Mcl-1 and Bcl-2) was downregulated, and the proapoptotic proteins (Bad and Bax) were upregulated in 5-FU-treated control cells but expression levels of Bcl-2, Bad, and Bad were not altered in 5-FU-treated A7-nAChR-KD cells. Fluorouracil 149-153 BCL2 associated X, apoptosis regulator Homo sapiens 124-127 26136123-11 2015 Survival and antiapoptosis signaling (pAkt, Akt, Mcl-1 and Bcl-2) was downregulated, and the proapoptotic proteins (Bad and Bax) were upregulated in 5-FU-treated control cells but expression levels of Bcl-2, Bad, and Bad were not altered in 5-FU-treated A7-nAChR-KD cells. Fluorouracil 149-153 BCL2 apoptosis regulator Homo sapiens 201-206 26807186-8 2015 After inhibiting Mcl-1, the cell migration and invasion decreased (P<0.05), the resistance to VCR, DDP and 5-Fu was reversed to different extents (P<0.05), TS mRNA expression increased significantly (P<0.05), MDR1 remained unchanged (P>0.05), but DPD and TOP2A decreased significantly (P<0.05). Fluorouracil 110-114 ATP binding cassette subfamily B member 1 Homo sapiens 218-222 26518892-6 2015 For example, overexpressing miR-34a, a master regulator of tumor suppression attenuates chemoresistance to 5-FU by downregulating silent information regulator 1 (SIRT1) and E2F3. Fluorouracil 107-111 E2F transcription factor 3 Homo sapiens 173-177 26310874-5 2015 Interestingly, resveratrol induced a transition from 5-FU-induced formation of microvilli to a planar cell surface, which was concomitant with up-regulation of desmosomes, gap- and tight junctions (claudin-2) and adhesion molecules (E-cadherin) expression in HCT116 and HCT116R cells. Fluorouracil 53-57 cadherin 1 Homo sapiens 233-243 26130327-0 2015 5-Fluorouracil preferentially sensitizes mutant KRAS non-small cell lung carcinoma cells to TRAIL-induced apoptosis. Fluorouracil 0-14 TNF superfamily member 10 Homo sapiens 92-97 28959548-10 2016 The formulation also modulated inflammatory response triggered by 5-FU through reduction of 68% of myeloperoxidase activity and a 4-fold increase in anti-inflammatory IL-10 levels. Fluorouracil 66-70 interleukin 10 Mus musculus 167-172 26378040-0 2015 GRP78 confers the resistance to 5-FU by activating the c-Src/LSF/TS axis in hepatocellular carcinoma. Fluorouracil 32-36 heat shock protein family A (Hsp70) member 5 Homo sapiens 0-5 26394773-8 2015 Aortic (18)F-FLT uptake was reduced when cell proliferation was suppressed with fluorouracil in apolipoprotein E knock out mice (P<0.05). Fluorouracil 80-92 fms related receptor tyrosine kinase 1 Homo sapiens 13-16 26378040-0 2015 GRP78 confers the resistance to 5-FU by activating the c-Src/LSF/TS axis in hepatocellular carcinoma. Fluorouracil 32-36 SRC proto-oncogene, non-receptor tyrosine kinase Homo sapiens 55-60 26378040-4 2015 Here, we report that over-expression of GRP78 contributes to acquired resistance to 5-FU in HCC by up-regulating the c-Src/LSF/TS axis. Fluorouracil 84-88 heat shock protein family A (Hsp70) member 5 Homo sapiens 40-45 26378040-5 2015 Moreover, we found that the resistance to 5-FU conferred by GRP78 is mediated by its ATPase domain. Fluorouracil 42-46 heat shock protein family A (Hsp70) member 5 Homo sapiens 60-65 26187504-11 2015 Importantly, APR-246 synergistically enhanced the inhibitory effects of cisplatin and 5-fluorouracil through p53 accumulation. Fluorouracil 86-100 phorbol-12-myristate-13-acetate-induced protein 1 Homo sapiens 13-16 26416450-0 2015 Acquired resistance to 5-fluorouracil via HSP90/Src-mediated increase in thymidylate synthase expression in colon cancer. Fluorouracil 23-37 SRC proto-oncogene, non-receptor tyrosine kinase Homo sapiens 48-51 26416450-3 2015 Here, we demonstrate that the enhanced HSP90 function and subsequent activation of Src induce expression of TYMS and acquired resistance to 5-FU in colon cancer. Fluorouracil 140-144 SRC proto-oncogene, non-receptor tyrosine kinase Homo sapiens 83-86 26416450-7 2015 Conversely, pharmacological blockade of HSP90 or Src in HCT116/R cells effectively suppressed the changes involved in 5-FU resistance in vitro and xenograft tumor growth, hematogenous spread, and metastatic tumor development in vivo. Fluorouracil 118-122 SRC proto-oncogene, non-receptor tyrosine kinase Homo sapiens 49-52 26416450-8 2015 This study suggests a novel function of HSP90-Src pathway in regulation of TYMS expression and acquisition of 5-FU resistance. Fluorouracil 110-114 SRC proto-oncogene, non-receptor tyrosine kinase Homo sapiens 46-49 25687871-8 2015 CONCLUSION: GRP78 expression is a predictive and prognostic factor for down staging, recurrence, and survival in rectal cancer patients treated with 5-fluorouracil and leucovorin neoadjuvant CRT. Fluorouracil 149-163 heat shock protein family A (Hsp70) member 5 Homo sapiens 12-17 26088456-10 2015 CONCLUSIONS: The choice of an anti-EGFR MoAb as first-line biologic is a valid option in RAS wild-type patients candidate to a doublet with infusional 5-FU. Fluorouracil 151-155 epidermal growth factor receptor Homo sapiens 35-39 26187504-11 2015 Importantly, APR-246 synergistically enhanced the inhibitory effects of cisplatin and 5-fluorouracil through p53 accumulation. Fluorouracil 86-100 tumor protein p53 Homo sapiens 109-112 26187504-12 2015 Finally, APR-246 demonstrated potent antitumour activity in CLX and PDX models, and restored chemosensitivity to a cisplatin/5-fluorouracil-resistant xenograft model. Fluorouracil 125-139 phorbol-12-myristate-13-acetate-induced protein 1 Homo sapiens 9-12 25652909-0 2015 Gastrointestinal toxicities of 5-fluorouracil increase the proportion of regulatory T cells in intestinal tract: advantages of alternate-day S-1 administration. Fluorouracil 31-45 eukaryotic translation elongation factor 1 alpha 2 Mus musculus 141-144 26811591-4 2015 S-1 is an oral prodrug of 5-FU, which has demonstrated high effectiveness for gastric cancer treatment and a favorable safety profile. Fluorouracil 26-30 proteasome 26S subunit, non-ATPase 1 Homo sapiens 0-3 26316041-9 2015 5-Fluorouracil activated p38, ERK1/2 and JNK1/2 in a time-dependent manner in HCT116 3D cultures. Fluorouracil 0-14 mitogen-activated protein kinase 1 Homo sapiens 25-28 26316041-6 2015 Knockdown of E-cadherin by lentiviral delivery of shRNA significantly reduced chemosensitivity to 5-fluorouracil and irinotecan, increased beta-catenin protein level in HCT116 3D cultures. Fluorouracil 98-112 cadherin 1 Homo sapiens 13-23 26316041-9 2015 5-Fluorouracil activated p38, ERK1/2 and JNK1/2 in a time-dependent manner in HCT116 3D cultures. Fluorouracil 0-14 mitogen-activated protein kinase 3 Homo sapiens 30-36 26316041-9 2015 5-Fluorouracil activated p38, ERK1/2 and JNK1/2 in a time-dependent manner in HCT116 3D cultures. Fluorouracil 0-14 mitogen-activated protein kinase 8 Homo sapiens 41-47 26151540-0 2015 MicroRNA-197 reverses the drug resistance of fluorouracil-induced SGC7901 cells by targeting mitogen-activated protein kinase 1. Fluorouracil 45-57 mitogen-activated protein kinase 1 Homo sapiens 93-127 26151540-9 2015 These results indicated that miR-197 may influence the sensitivity of 5-FU treatment in a gastric cancer cell line by targeting MAPK1. Fluorouracil 70-74 mitogen-activated protein kinase 1 Homo sapiens 128-133 26239225-0 2015 MicroRNA-133a and microRNA-326 co-contribute to hepatocellular carcinoma 5-fluorouracil and cisplatin sensitivity by directly targeting B-cell lymphoma-extra large. Fluorouracil 73-87 BCL2 like 1 Homo sapiens 136-163 26208523-11 2015 These data indicate that the DACH carrier ligand in oxaliplatin triggers signaling via the p53-miR-34a-E2F axis, leading to transcriptional regulation that ultimately results in accumulation of dUTP and reduced dTTP biosynthesis, potentially enhancing 5-FU cytotoxicity. Fluorouracil 252-256 tumor protein p53 Homo sapiens 91-94 26239225-8 2015 Combining miR-133a or miR-326 with 5-fluorouracil (5-FU) or cisplatin (DDP) resulted in increased cell death. Fluorouracil 51-55 microRNA 326 Homo sapiens 22-29 25707392-4 2015 This study evaluates the influence of common genetic variations within the VEGF pathway in the clinical outcomes of 172 metastatic colorectal cancer (mCRC) patients treated with first-line oxaliplatin/5-fluorouracil chemotherapy. Fluorouracil 201-215 vascular endothelial growth factor A Homo sapiens 75-79 25707392-9 2015 This study provides evidence that functional germline polymorphisms in the VEGF pathway may help to predict outcome in mCRC patients who undergo oxaliplatin/5-fluorouracil chemotherapy. Fluorouracil 157-171 vascular endothelial growth factor A Homo sapiens 75-79 26239225-9 2015 The results of the present study indicated that miR-133a, miR-326 and Bcl-xl acted protectively against the apoptosis, induced by 5-FU or DDP, in HepG2 cells. Fluorouracil 130-134 microRNA 326 Homo sapiens 58-65 26239225-9 2015 The results of the present study indicated that miR-133a, miR-326 and Bcl-xl acted protectively against the apoptosis, induced by 5-FU or DDP, in HepG2 cells. Fluorouracil 130-134 BCL2 like 1 Homo sapiens 70-76 26406888-10 2015 Those mice in 5-FU groups had significantly higher proinflammatory cytokine levels (TNF-alpha: 234.80 vs. 29.10, P<0.001, IL-6: 25.13 vs. 7.43, P<0.001, IFN-gamma: 22.07 vs. 17.06, P = 0.137). Fluorouracil 14-18 tumor necrosis factor Mus musculus 84-93 26410168-9 2015 Patients with Nrf2-positive expression had significantly lower survival rates compared to those in the negative group (p<0.01), with chemo-resistance against 5-fluorouracil (5-FU) (p<0.05). Fluorouracil 161-175 NFE2 like bZIP transcription factor 2 Homo sapiens 14-18 26410168-9 2015 Patients with Nrf2-positive expression had significantly lower survival rates compared to those in the negative group (p<0.01), with chemo-resistance against 5-fluorouracil (5-FU) (p<0.05). Fluorouracil 177-181 NFE2 like bZIP transcription factor 2 Homo sapiens 14-18 26406888-10 2015 Those mice in 5-FU groups had significantly higher proinflammatory cytokine levels (TNF-alpha: 234.80 vs. 29.10, P<0.001, IL-6: 25.13 vs. 7.43, P<0.001, IFN-gamma: 22.07 vs. 17.06, P = 0.137). Fluorouracil 14-18 interleukin 6 Mus musculus 125-129 26406888-10 2015 Those mice in 5-FU groups had significantly higher proinflammatory cytokine levels (TNF-alpha: 234.80 vs. 29.10, P<0.001, IL-6: 25.13 vs. 7.43, P<0.001, IFN-gamma: 22.07 vs. 17.06, P = 0.137). Fluorouracil 14-18 interferon gamma Mus musculus 159-168 26406888-12 2015 We also found TNF-alpha, IL-1beta and IL-6 mRNA expressions were up-regulated in intestinal mucositis tissues following 5-FU treatment (TNF-alpha: 4.35 vs. 1.18, IL-1beta: 2.29 vs. 1.07, IL-6: 1.49 vs. 1.02) and that probiotics treatment suppressed this up-regulation (P<0.05). Fluorouracil 120-124 tumor necrosis factor Mus musculus 14-23 26406888-12 2015 We also found TNF-alpha, IL-1beta and IL-6 mRNA expressions were up-regulated in intestinal mucositis tissues following 5-FU treatment (TNF-alpha: 4.35 vs. 1.18, IL-1beta: 2.29 vs. 1.07, IL-6: 1.49 vs. 1.02) and that probiotics treatment suppressed this up-regulation (P<0.05). Fluorouracil 120-124 interleukin 1 beta Mus musculus 25-33 26406888-12 2015 We also found TNF-alpha, IL-1beta and IL-6 mRNA expressions were up-regulated in intestinal mucositis tissues following 5-FU treatment (TNF-alpha: 4.35 vs. 1.18, IL-1beta: 2.29 vs. 1.07, IL-6: 1.49 vs. 1.02) and that probiotics treatment suppressed this up-regulation (P<0.05). Fluorouracil 120-124 interleukin 6 Mus musculus 38-42 26406888-12 2015 We also found TNF-alpha, IL-1beta and IL-6 mRNA expressions were up-regulated in intestinal mucositis tissues following 5-FU treatment (TNF-alpha: 4.35 vs. 1.18, IL-1beta: 2.29 vs. 1.07, IL-6: 1.49 vs. 1.02) and that probiotics treatment suppressed this up-regulation (P<0.05). Fluorouracil 120-124 tumor necrosis factor Mus musculus 136-148 26406888-12 2015 We also found TNF-alpha, IL-1beta and IL-6 mRNA expressions were up-regulated in intestinal mucositis tissues following 5-FU treatment (TNF-alpha: 4.35 vs. 1.18, IL-1beta: 2.29 vs. 1.07, IL-6: 1.49 vs. 1.02) and that probiotics treatment suppressed this up-regulation (P<0.05). Fluorouracil 120-124 interleukin 1 beta Mus musculus 162-170 26406888-12 2015 We also found TNF-alpha, IL-1beta and IL-6 mRNA expressions were up-regulated in intestinal mucositis tissues following 5-FU treatment (TNF-alpha: 4.35 vs. 1.18, IL-1beta: 2.29 vs. 1.07, IL-6: 1.49 vs. 1.02) and that probiotics treatment suppressed this up-regulation (P<0.05). Fluorouracil 120-124 interleukin 6 Mus musculus 187-191 26188124-8 2015 3) Finally, VTD or its modified analogs offer a valuable adjuvant chemotherapy strategy to improve the efficacy of 5-FU-based chemotherapy for colon cancer patients harboring WT-p53. Fluorouracil 115-119 tumor protein p53 Homo sapiens 178-181 26345461-1 2015 BACKGROUND: Neoadjuvant chemotherapy (NAC) with taxanes followed by fluorouracil, epirubicin, and cyclophosphamide (FEC), and concurrent trastuzumab is a potent regimen for HER2 over-expressing breast cancer. Fluorouracil 68-80 erb-b2 receptor tyrosine kinase 2 Homo sapiens 173-177 26368019-10 2015 Gyp was also found to up-regulate 5-Fu-caused phospho-p53 expression and thus augment 5-Fu-induced G0/G1 phase arrest. Fluorouracil 34-38 tumor protein p53 Homo sapiens 54-57 26368019-12 2015 Inhibition of ROS and p53 respectively reversed the cell death induced by 5-Fu + Gyp, suggesting the key roles of ROS and p53 in the process. Fluorouracil 74-78 tumor protein p53 Homo sapiens 22-25 26368019-12 2015 Inhibition of ROS and p53 respectively reversed the cell death induced by 5-Fu + Gyp, suggesting the key roles of ROS and p53 in the process. Fluorouracil 74-78 tumor protein p53 Homo sapiens 122-125 26208739-13 2015 All the observation was confirmed by silencing TS and inactivating the mTOR/p70S6K1 signaling pathway by rapamycin, both of which increased the chemo-sensitizing efficacy of 5-FU. Fluorouracil 174-178 mechanistic target of rapamycin kinase Homo sapiens 71-75 26051518-6 2015 Treatment with 5-Fluorouracil (5-FU), a frequently used but often clinically ineffective chemotherapy drug, induced apoptosis, down-regulation of anti-apoptotic genes (BCL-2, TRAF1, and c-FLIP) and decreased cell numbers in 2D, but only "nucleolar stress" in p3D and xenografts. Fluorouracil 15-29 BCL2 apoptosis regulator Homo sapiens 168-173 26051518-6 2015 Treatment with 5-Fluorouracil (5-FU), a frequently used but often clinically ineffective chemotherapy drug, induced apoptosis, down-regulation of anti-apoptotic genes (BCL-2, TRAF1, and c-FLIP) and decreased cell numbers in 2D, but only "nucleolar stress" in p3D and xenografts. Fluorouracil 15-29 TNF receptor associated factor 1 Homo sapiens 175-180 26051518-6 2015 Treatment with 5-Fluorouracil (5-FU), a frequently used but often clinically ineffective chemotherapy drug, induced apoptosis, down-regulation of anti-apoptotic genes (BCL-2, TRAF1, and c-FLIP) and decreased cell numbers in 2D, but only "nucleolar stress" in p3D and xenografts. Fluorouracil 15-29 CASP8 and FADD like apoptosis regulator Homo sapiens 186-192 26051518-6 2015 Treatment with 5-Fluorouracil (5-FU), a frequently used but often clinically ineffective chemotherapy drug, induced apoptosis, down-regulation of anti-apoptotic genes (BCL-2, TRAF1, and c-FLIP) and decreased cell numbers in 2D, but only "nucleolar stress" in p3D and xenografts. Fluorouracil 31-35 BCL2 apoptosis regulator Homo sapiens 168-173 26051518-6 2015 Treatment with 5-Fluorouracil (5-FU), a frequently used but often clinically ineffective chemotherapy drug, induced apoptosis, down-regulation of anti-apoptotic genes (BCL-2, TRAF1, and c-FLIP) and decreased cell numbers in 2D, but only "nucleolar stress" in p3D and xenografts. Fluorouracil 31-35 TNF receptor associated factor 1 Homo sapiens 175-180 26051518-6 2015 Treatment with 5-Fluorouracil (5-FU), a frequently used but often clinically ineffective chemotherapy drug, induced apoptosis, down-regulation of anti-apoptotic genes (BCL-2, TRAF1, and c-FLIP) and decreased cell numbers in 2D, but only "nucleolar stress" in p3D and xenografts. Fluorouracil 31-35 CASP8 and FADD like apoptosis regulator Homo sapiens 186-192 26220845-1 2015 PURPOSE: S-1, a novel oral prodrug of 5-fluorouracil (5-FU), and irinotecan with or without bevacizumab is known to be effective in metastatic colorectal cancer (mCRC). Fluorouracil 38-52 proteasome 26S subunit, non-ATPase 1 Homo sapiens 9-12 26220845-1 2015 PURPOSE: S-1, a novel oral prodrug of 5-fluorouracil (5-FU), and irinotecan with or without bevacizumab is known to be effective in metastatic colorectal cancer (mCRC). Fluorouracil 54-58 proteasome 26S subunit, non-ATPase 1 Homo sapiens 9-12 26208739-14 2015 CONCLUSIONS: These findings suggest that gossypol-mediated down-regulation of TS, cyclin D1, and the mTOR/p70S6K1 signaling pathways enhances the anti-tumor effect of 5-FU. Fluorouracil 167-171 mechanistic target of rapamycin kinase Homo sapiens 101-105 26623038-1 2015 In the treatment of human epidermal growth factor receptor 2 (HER2)-positive advanced gastric or gastroesophageal junction cancer, it has been reported that the combination of trastuzumab with capecitabine plus cisplatin, or with 5-fluorouracil (5-FU) plus cisplatin, significantly increased overall survival compared with chemotherapy alone (ToGA trial). Fluorouracil 230-244 erb-b2 receptor tyrosine kinase 2 Homo sapiens 26-60 26623038-1 2015 In the treatment of human epidermal growth factor receptor 2 (HER2)-positive advanced gastric or gastroesophageal junction cancer, it has been reported that the combination of trastuzumab with capecitabine plus cisplatin, or with 5-fluorouracil (5-FU) plus cisplatin, significantly increased overall survival compared with chemotherapy alone (ToGA trial). Fluorouracil 230-244 erb-b2 receptor tyrosine kinase 2 Homo sapiens 62-66 26623038-1 2015 In the treatment of human epidermal growth factor receptor 2 (HER2)-positive advanced gastric or gastroesophageal junction cancer, it has been reported that the combination of trastuzumab with capecitabine plus cisplatin, or with 5-fluorouracil (5-FU) plus cisplatin, significantly increased overall survival compared with chemotherapy alone (ToGA trial). Fluorouracil 246-250 erb-b2 receptor tyrosine kinase 2 Homo sapiens 62-66 26622665-4 2015 In the present study, it was hypothesized that the epigenetic modification of Nrf2 may be a potential target for 5-FU resistance in CRC treatment. Fluorouracil 113-117 NFE2 like bZIP transcription factor 2 Homo sapiens 78-82 26622665-9 2015 Furthermore, methylation analysis revealed Nrf2 promoter cytosine-phosphate-guanine island hypomethylation in 5-FU-treated cells. Fluorouracil 110-114 NFE2 like bZIP transcription factor 2 Homo sapiens 43-47 25976508-8 2015 5-Fu incorporation was achieved successfully (12.3mug 5Fu/mg CNP) and the maximum 5-Fu release took place at 2h. Fluorouracil 0-4 2',3'-cyclic nucleotide 3' phosphodiesterase Homo sapiens 61-64 26247730-5 2015 Knockdown of PPP2R1B expression increases AKT phosphorylation, which leads to elevated XIAP expression and enhanced 5-FU resistance; whereas rescue of PPP2R1B expression in miR-587-expressing cells decreases AKT phosphorylation/XIAP expression, re-sensitizing colon cancer cells to 5-FU-induced apoptosis. Fluorouracil 116-120 protein phosphatase 2 scaffold subunit Abeta Homo sapiens 13-20 26100106-0 2015 Corosolic acid enhances 5-fluorouracil-induced apoptosis against SNU-620 human gastric carcinoma cells by inhibition of mammalian target of rapamycin. Fluorouracil 24-38 mechanistic target of rapamycin kinase Homo sapiens 120-149 26100106-7 2015 Additionally, the mammalian target of rapamycin (mTOR) signaling pathway, which is highly activated in gastric cancer, was regulated by 5-FU and CRA, and additive mTOR/eukaryotic translation initiation factor 4E-binding protein 1 (4-EBP1) inhibition was observed with the combination treatment. Fluorouracil 136-140 mechanistic target of rapamycin kinase Homo sapiens 18-47 26100106-7 2015 Additionally, the mammalian target of rapamycin (mTOR) signaling pathway, which is highly activated in gastric cancer, was regulated by 5-FU and CRA, and additive mTOR/eukaryotic translation initiation factor 4E-binding protein 1 (4-EBP1) inhibition was observed with the combination treatment. Fluorouracil 136-140 mechanistic target of rapamycin kinase Homo sapiens 49-53 26100106-9 2015 Thus, these data indicate that CRA enhances the anticancer activities of 5-FU via mTOR inhibition in SNU-620 human gastric carcinoma cells. Fluorouracil 73-77 mechanistic target of rapamycin kinase Homo sapiens 82-86 25934339-1 2015 The purpose of this study is to evaluate the influence of germline polymorphisms of cytochrome P450 (CYP450) on objective response, progression-free survival (PFS) and overall suruvival (OS) in metastatic colorectal cancer (mCRC) receiving the combination chemotherapy of irinotecan, 5-fluorouracil, and leucovorin (FOLFIRI). Fluorouracil 284-298 cytochrome P450 family 4 subfamily F member 3 Homo sapiens 84-99 25934339-1 2015 The purpose of this study is to evaluate the influence of germline polymorphisms of cytochrome P450 (CYP450) on objective response, progression-free survival (PFS) and overall suruvival (OS) in metastatic colorectal cancer (mCRC) receiving the combination chemotherapy of irinotecan, 5-fluorouracil, and leucovorin (FOLFIRI). Fluorouracil 284-298 cytochrome P450 family 4 subfamily F member 3 Homo sapiens 101-107 26275292-12 2015 Further analyses of oxaliplatin+EGFR-I trials showed greater efficacy with infusional 5FU regimens (PFS HR 0.82, 95% CI 0.72-0.94) compared to capecitabine (HR 1.09; 95% CI 0.91-1.30) and bolus 5FU (HR 1.07; 95% CI 0.79-1.45); subgroup interaction was present with I2 = 72%, p = 0.03. Fluorouracil 86-89 epidermal growth factor receptor Homo sapiens 32-36 26247730-5 2015 Knockdown of PPP2R1B expression increases AKT phosphorylation, which leads to elevated XIAP expression and enhanced 5-FU resistance; whereas rescue of PPP2R1B expression in miR-587-expressing cells decreases AKT phosphorylation/XIAP expression, re-sensitizing colon cancer cells to 5-FU-induced apoptosis. Fluorouracil 116-120 AKT serine/threonine kinase 1 Homo sapiens 42-45 26247730-5 2015 Knockdown of PPP2R1B expression increases AKT phosphorylation, which leads to elevated XIAP expression and enhanced 5-FU resistance; whereas rescue of PPP2R1B expression in miR-587-expressing cells decreases AKT phosphorylation/XIAP expression, re-sensitizing colon cancer cells to 5-FU-induced apoptosis. Fluorouracil 282-286 protein phosphatase 2 scaffold subunit Abeta Homo sapiens 13-20 26247730-5 2015 Knockdown of PPP2R1B expression increases AKT phosphorylation, which leads to elevated XIAP expression and enhanced 5-FU resistance; whereas rescue of PPP2R1B expression in miR-587-expressing cells decreases AKT phosphorylation/XIAP expression, re-sensitizing colon cancer cells to 5-FU-induced apoptosis. Fluorouracil 282-286 AKT serine/threonine kinase 1 Homo sapiens 42-45 26247730-5 2015 Knockdown of PPP2R1B expression increases AKT phosphorylation, which leads to elevated XIAP expression and enhanced 5-FU resistance; whereas rescue of PPP2R1B expression in miR-587-expressing cells decreases AKT phosphorylation/XIAP expression, re-sensitizing colon cancer cells to 5-FU-induced apoptosis. Fluorouracil 282-286 AKT serine/threonine kinase 1 Homo sapiens 208-211 26247730-6 2015 Moreover, a specific and potent AKT inhibitor, MK2206, reverses miR-587-conferred 5-FU resistance. Fluorouracil 82-86 AKT serine/threonine kinase 1 Homo sapiens 32-35 25871911-10 2015 These surprising findings in a group of phenotypically similar patients with ER-positive, endocrine therapy-pretreated, HER2-negative metastases, are supported by preclinical data showing that sensitivity to 5-fluorouracil is enhanced by deficiencies in chromatin remodeling and homologous recombination genes. Fluorouracil 208-222 estrogen receptor 1 Homo sapiens 77-79 25871911-10 2015 These surprising findings in a group of phenotypically similar patients with ER-positive, endocrine therapy-pretreated, HER2-negative metastases, are supported by preclinical data showing that sensitivity to 5-fluorouracil is enhanced by deficiencies in chromatin remodeling and homologous recombination genes. Fluorouracil 208-222 erb-b2 receptor tyrosine kinase 2 Homo sapiens 120-124 25810324-1 2015 S-1 is an oral 5-fluorouracil agent containing tegafur, 5-chloro-2, 4-dihydroxypyridine (CDHP), and potassium oxonate. Fluorouracil 15-29 proteasome 26S subunit, non-ATPase 1 Homo sapiens 0-3 26189067-1 2015 BACKGROUND: Preoperative chemoradiotherapy with infusional fluorouracil, total mesorectal excision surgery, and postoperative chemotherapy with fluorouracil was established by the German CAO/ARO/AIO-94 trial as a standard combined modality treatment for locally advanced rectal cancer. Fluorouracil 144-156 cytochrome P450 family 19 subfamily A member 1 Homo sapiens 191-194 26189067-14 2015 INTERPRETATION: Adding oxaliplatin to fluorouracil-based neoadjuvant chemoradiotherapy and adjuvant chemotherapy (at the doses and intensities used in this trial) significantly improved disease-free survival of patients with clinically staged cT3-4 or cN1-2 rectal cancer compared with our former fluorouracil-based combined modality regimen (based on CAO/ARO/AIO-94). Fluorouracil 38-50 cytochrome P450 family 19 subfamily A member 1 Homo sapiens 356-359 26044651-6 2015 Furthermore, we showed that rAd/CEA-RPL23 synergized with classic chemotherapeutic agent 5-fluorouracil (5-FU) and enhanced its activity against LoVo cells in vivo and in vitro. Fluorouracil 89-103 CEA cell adhesion molecule 3 Homo sapiens 32-35 26093488-10 2015 OE33/DKK3 cells increased endothelial tube formation and were significantly more resistant to 5-fluorouracil and cisplatin, and DKK3 expression was significantly higher in chemoresistant esophageal adenocarcinomas (P < .005). Fluorouracil 94-108 dickkopf WNT signaling pathway inhibitor 3 Homo sapiens 5-9 26044651-6 2015 Furthermore, we showed that rAd/CEA-RPL23 synergized with classic chemotherapeutic agent 5-fluorouracil (5-FU) and enhanced its activity against LoVo cells in vivo and in vitro. Fluorouracil 105-109 CEA cell adhesion molecule 3 Homo sapiens 32-35 26002465-5 2015 5-FU treatment induced significantly increase of the mRNA expression of MDR1, ABCG2 and AKT1genes, but not protein level. Fluorouracil 0-4 ATP binding cassette subfamily B member 1 Homo sapiens 72-76 26002465-5 2015 5-FU treatment induced significantly increase of the mRNA expression of MDR1, ABCG2 and AKT1genes, but not protein level. Fluorouracil 0-4 ATP binding cassette subfamily G member 2 (Junior blood group) Homo sapiens 78-83 26002465-5 2015 5-FU treatment induced significantly increase of the mRNA expression of MDR1, ABCG2 and AKT1genes, but not protein level. Fluorouracil 0-4 AKT serine/threonine kinase 1 Homo sapiens 88-92 26003042-5 2015 In the combined therapy, the antitumor action of 5-fluorouracil (5-FU) was potentiated when the mice were pretreated with a low dose of TNFalpha (1ng/mouse) and to a greater extent by the same concentration of TCP-1/TNFalpha. Fluorouracil 49-63 tumor necrosis factor Mus musculus 136-144 26003042-5 2015 In the combined therapy, the antitumor action of 5-fluorouracil (5-FU) was potentiated when the mice were pretreated with a low dose of TNFalpha (1ng/mouse) and to a greater extent by the same concentration of TCP-1/TNFalpha. Fluorouracil 49-63 tumor necrosis factor Mus musculus 216-224 26003042-5 2015 In the combined therapy, the antitumor action of 5-fluorouracil (5-FU) was potentiated when the mice were pretreated with a low dose of TNFalpha (1ng/mouse) and to a greater extent by the same concentration of TCP-1/TNFalpha. Fluorouracil 65-69 tumor necrosis factor Mus musculus 136-144 26003042-5 2015 In the combined therapy, the antitumor action of 5-fluorouracil (5-FU) was potentiated when the mice were pretreated with a low dose of TNFalpha (1ng/mouse) and to a greater extent by the same concentration of TCP-1/TNFalpha. Fluorouracil 65-69 tumor necrosis factor Mus musculus 216-224 26003042-8 2015 At the same time, TCP-1/TNFalpha significantly improved 5-FU absorption into the tumor mass. Fluorouracil 56-60 tumor necrosis factor Mus musculus 24-32 25965911-4 2015 Our results show 5-FU induced cell apoptosis through p53/PUMA pathway, with aberrant Akt activation, which may well explain the mechanism of 5-FU resistance. Fluorouracil 17-21 tumor protein p53 Homo sapiens 53-56 26205949-11 2015 Mechanistically, vitamin D3/5-FU co-therapy significantly decreased the expression of Wnt, beta-catenin, iNOS, COX-2 and HSP-90 and significantly increased the expression of DKK-1, TGF-beta1, TGF-betaR2, smad4 (P < 0.05), in comparison with their corresponding monotherapy groups. Fluorouracil 28-32 nitric oxide synthase 2 Rattus norvegicus 105-109 26205949-11 2015 Mechanistically, vitamin D3/5-FU co-therapy significantly decreased the expression of Wnt, beta-catenin, iNOS, COX-2 and HSP-90 and significantly increased the expression of DKK-1, TGF-beta1, TGF-betaR2, smad4 (P < 0.05), in comparison with their corresponding monotherapy groups. Fluorouracil 28-32 heat shock protein 90 alpha family class A member 1 Rattus norvegicus 121-127 26205949-11 2015 Mechanistically, vitamin D3/5-FU co-therapy significantly decreased the expression of Wnt, beta-catenin, iNOS, COX-2 and HSP-90 and significantly increased the expression of DKK-1, TGF-beta1, TGF-betaR2, smad4 (P < 0.05), in comparison with their corresponding monotherapy groups. Fluorouracil 28-32 transforming growth factor, beta 1 Rattus norvegicus 181-190 26205949-12 2015 CONCLUSIONS: Vitamin D3 and 5-FU synergise together and exhibit better anticancer effects by modulating Wnt/beta-catenin pathway, TGF-beta1 signals, iNOS, COX-2 and HSP-90. Fluorouracil 28-32 transforming growth factor, beta 1 Rattus norvegicus 130-139 26205949-12 2015 CONCLUSIONS: Vitamin D3 and 5-FU synergise together and exhibit better anticancer effects by modulating Wnt/beta-catenin pathway, TGF-beta1 signals, iNOS, COX-2 and HSP-90. Fluorouracil 28-32 nitric oxide synthase 2 Rattus norvegicus 149-153 26205949-12 2015 CONCLUSIONS: Vitamin D3 and 5-FU synergise together and exhibit better anticancer effects by modulating Wnt/beta-catenin pathway, TGF-beta1 signals, iNOS, COX-2 and HSP-90. Fluorouracil 28-32 heat shock protein 90 alpha family class A member 1 Rattus norvegicus 165-171 26025485-3 2015 S-1, a novel oral fluorouracil, has showed very effective in metastatic gastric cancer and became the standard option for gastric cancer with D2 dissection. Fluorouracil 18-30 proteasome 26S subunit, non-ATPase 1 Homo sapiens 0-3 25677905-1 2015 The most important cytotoxic drug namely, cyclophosphamide used in breast cancer along with epirubicin and 5-fluorouracil, is transported by ABCC transporters and detoxified by glutathione S-transferases (GSTs). Fluorouracil 107-121 ATP binding cassette subfamily C member 1 Homo sapiens 141-145 26035698-11 2015 CONCLUSIONS: In two clinical trial cohorts, a systematic biomarker discovery and validation approach identified miR-320e to be a novel prognostic biomarker that is associated with adverse clinical outcome in stage III CRC patients treated with 5-FU-based adjuvant chemotherapy. Fluorouracil 244-248 microRNA 320e Homo sapiens 112-120 26084465-0 2015 The impact of insulin on chemotherapeutic sensitivity to 5-fluorouracil in gastric cancer cell lines SGC7901, MKN45 and MKN28. Fluorouracil 57-71 insulin Homo sapiens 14-21 26084465-2 2015 This study aimed to explore the impact of insulin on chemoresistance to 5-fluorouracil in gastric cancer and the possible mechanisms. Fluorouracil 72-86 insulin Homo sapiens 42-49 26084465-5 2015 The effect of insulin on chemotherapeutic sensitivity of the three gastric cancer cell lines to 5-fluorouracil was evaluated by pre-incubation with insulin before administration of 5-fluorouracil. Fluorouracil 96-110 insulin Homo sapiens 14-21 26084465-5 2015 The effect of insulin on chemotherapeutic sensitivity of the three gastric cancer cell lines to 5-fluorouracil was evaluated by pre-incubation with insulin before administration of 5-fluorouracil. Fluorouracil 96-110 insulin Homo sapiens 148-155 26084465-8 2015 Addition of 1 muM insulin remarkably promoted the proliferation of SGC7901, MKN45 and MKN28 cells and decreased the cytotoxicity of 5-fluorouracil. Fluorouracil 132-146 latexin Homo sapiens 14-17 26084465-8 2015 Addition of 1 muM insulin remarkably promoted the proliferation of SGC7901, MKN45 and MKN28 cells and decreased the cytotoxicity of 5-fluorouracil. Fluorouracil 132-146 insulin Homo sapiens 18-25 26084465-10 2015 CONCLUSION: Insulin improved the proliferation of gastric cancer cell lines and contributed to chemoresistance of gastric cancer cells to 5-fluorouracil which is likely to involve upregulation of P-glycoprotein. Fluorouracil 138-152 insulin Homo sapiens 12-19 26084465-10 2015 CONCLUSION: Insulin improved the proliferation of gastric cancer cell lines and contributed to chemoresistance of gastric cancer cells to 5-fluorouracil which is likely to involve upregulation of P-glycoprotein. Fluorouracil 138-152 ATP binding cassette subfamily B member 1 Homo sapiens 196-210 26425688-1 2015 We investigated the hypothesis that the varying treatment efficacy of adjuvant 5-fluorouracil (5FU) in stage III colon cancer is linked to the TP53 mutational status. Fluorouracil 79-93 tumor protein p53 Homo sapiens 143-147 26425688-1 2015 We investigated the hypothesis that the varying treatment efficacy of adjuvant 5-fluorouracil (5FU) in stage III colon cancer is linked to the TP53 mutational status. Fluorouracil 95-98 tumor protein p53 Homo sapiens 143-147 26425688-11 2015 The biomarker TP53 independently predicted effect of adjuvant 5FU in N1 colon cancer patients. Fluorouracil 62-65 tumor protein p53 Homo sapiens 14-18 25714249-6 2015 The combination of 5-FU and CGA led to a more prominent production of ROS and significantly inactivated ERK1/2, although CGA and 5-FU exerted no significant changes when used alone. Fluorouracil 19-23 mitogen-activated protein kinase 3 Homo sapiens 104-110 25714249-9 2015 This mediates the enhancement of 5-FU-induced inhibition of hepatocellular carcinoma cells" proliferation, that is, CGA sensitizes hepatocellular carcinoma cells to 5-FU treatment by the suppression of ERK activation through the overproduction of ROS. Fluorouracil 33-37 mitogen-activated protein kinase 1 Homo sapiens 202-205 25611452-3 2015 By analyzing the 10-year outcome data of the German CAO/ARO/AIO-94 phase 3 trial, the authors demonstrated that significantly fewer patients had poor prognostic features (eg, ypT3-4, ypN1-2) after preoperative 5-fluorouracil-based chemoradiotherapy. Fluorouracil 210-224 cytochrome P450 family 19 subfamily A member 1 Homo sapiens 56-59 25398650-10 2015 The expression levels of cxcl9 and cxcr3 were significantly up-regulated in intestinal mucosa after 5-FU injection. Fluorouracil 100-104 C-X-C motif chemokine ligand 9 Homo sapiens 25-30 25945744-15 2015 Altogether our findings suggest APOE-independent Ala-Gln regenerative effects after 5-FU challenge. Fluorouracil 84-88 apolipoprotein E Mus musculus 32-36 25815774-6 2015 Four SNPs are located in the MTRR gene, and another four SNPs showed significant association with 5-fluoro-uracil cytotoxicity in a recent in-vitro genome-wide association study. Fluorouracil 98-113 5-methyltetrahydrofolate-homocysteine methyltransferase reductase Homo sapiens 29-33 25707610-6 2015 Significantly, fewer patients treated with cisplatin/S-1 reported worsened physical well-being (PWB) scores (45.1 versus 51.7 %, p = 0.044) and experienced significantly longer time to worsening in PWB scores, with a median of 4.5 months (95 % confidence interval (CI), 3.1-5.1) compared to 3.0 months (2.8-4.6) with cisplatin/5-FU (CF) (p = 0.01). Fluorouracil 327-331 proteasome 26S subunit, non-ATPase 1 Homo sapiens 53-56 25708948-0 2015 Repression of Nrf2 enhances antitumor effect of 5-fluorouracil and gemcitabine on cholangiocarcinoma cells. Fluorouracil 48-62 NFE2 like bZIP transcription factor 2 Homo sapiens 14-18 25708948-8 2015 Knockdown of Nrf2 expression by siRNA suppressed protein expression of Nrf2-regulated genes and enhanced the sensitivity to 5-fluorouracil and gemcitabine of CCA cells in both high and low basal Nrf2 expression. Fluorouracil 124-138 NFE2 like bZIP transcription factor 2 Homo sapiens 13-17 26064061-0 2015 Hyperthermia combined with 5-fluorouracil promoted apoptosis and enhanced thermotolerance in human gastric cancer cell line SGC-7901. Fluorouracil 27-41 sarcoglycan beta Homo sapiens 124-127 26463141-5 2015 RESULTS: After combined treatment with TRAIL and DDP of the SGC7901/VCR cells, the IC50 of VCR, DDP, ADM, and 5-Fu treatment was significantly decreased compared with the control group or TRAIL-treated group (P < 0.05). Fluorouracil 110-114 TNF superfamily member 10 Homo sapiens 39-44 26463141-5 2015 RESULTS: After combined treatment with TRAIL and DDP of the SGC7901/VCR cells, the IC50 of VCR, DDP, ADM, and 5-Fu treatment was significantly decreased compared with the control group or TRAIL-treated group (P < 0.05). Fluorouracil 110-114 TNF superfamily member 10 Homo sapiens 188-193 26064061-2 2015 Human gastric cancer cell line SGC-7901 was cultivated with 5-fluorouracil at different temperatures. Fluorouracil 60-74 sarcoglycan beta Homo sapiens 31-34 26064061-6 2015 5-Fluorouracil induced apoptosis of SGC-7901 cells with a strong temperature dependence, which increased gradually with increase in temperature. Fluorouracil 0-14 sarcoglycan beta Homo sapiens 36-39 26064061-10 2015 These results suggested that hyperthermia combined with 5-fluorouracil had a synergistic effect in promoting apoptosis and enhancing thermotolerance in gastric cancer cell line SGC-7901. Fluorouracil 56-70 sarcoglycan beta Homo sapiens 177-180 25423960-0 2015 HPV Status Determines the Efficacy of Adjuvant Chemotherapy With S-1, an Oral Fluorouracil Prodrug, in Oropharyngeal Cancer. Fluorouracil 78-90 proteasome 26S subunit, non-ATPase 1 Homo sapiens 65-68 26269759-4 2015 The molecular mechanisms of Twist1 expression and its effects on chemosensitivity to 5-Fluorouracil and oxaliplatin were also explored by MTT assay, colony forming assay, flow cytometry assay. Fluorouracil 85-99 twist family bHLH transcription factor 1 Homo sapiens 28-34 25423960-2 2015 The object of this study is to evaluate the efficacy of adjuvant chemotherapy with S-1, an oral 5-fluorouracil prodrug, on survival of patients with OPC according to HPV status. Fluorouracil 96-110 proteasome 26S subunit, non-ATPase 1 Homo sapiens 83-86 26054673-3 2015 We found that tumorspheres generated from MCF-7 human breast cancer cells exhibited high proportions of quiescent cells and expressed MDR-1 at elevated levels, leading to resistance to 5-fluorouracil, paclitaxel, and doxorubicin. Fluorouracil 185-199 ATP binding cassette subfamily B member 1 Homo sapiens 134-139 25323586-0 2015 Bcl-2 stabilization by paxillin confers 5-fluorouracil resistance in colorectal cancer. Fluorouracil 40-54 BCL2 apoptosis regulator Homo sapiens 0-5 25323586-4 2015 We thus hypothesized that pPXN-Y31/Y118 may be required for Bcl-2 protein stability via PXN interacting with Bcl-2 to confer 5-FU resistance in colorectal cancer. Fluorouracil 125-129 BCL2 apoptosis regulator Homo sapiens 60-65 25323586-4 2015 We thus hypothesized that pPXN-Y31/Y118 may be required for Bcl-2 protein stability via PXN interacting with Bcl-2 to confer 5-FU resistance in colorectal cancer. Fluorouracil 125-129 BCL2 apoptosis regulator Homo sapiens 109-114 25323586-7 2015 An increase in Bcl-2 expression by PXN is responsible for resistance to 5-FU. Fluorouracil 72-76 BCL2 apoptosis regulator Homo sapiens 15-20 25323586-8 2015 The resistance to 5-FU can be abolished by inhibitor of Src and PAK1 or Bcl-2 antagonist in cell and animal models. Fluorouracil 18-22 SRC proto-oncogene, non-receptor tyrosine kinase Homo sapiens 56-59 25323586-8 2015 The resistance to 5-FU can be abolished by inhibitor of Src and PAK1 or Bcl-2 antagonist in cell and animal models. Fluorouracil 18-22 BCL2 apoptosis regulator Homo sapiens 72-77 25323586-10 2015 Patients with high PXN/high Bcl-2 or high pPXN-S272/high Bcl-2 tumors are commonly to have an unfavorable response to 5-FU-based chemotherapy, compared with patients who have high PXN, high pPXN-S272 or high Bcl-2 tumors alone. Fluorouracil 118-122 BCL2 apoptosis regulator Homo sapiens 28-33 25323586-10 2015 Patients with high PXN/high Bcl-2 or high pPXN-S272/high Bcl-2 tumors are commonly to have an unfavorable response to 5-FU-based chemotherapy, compared with patients who have high PXN, high pPXN-S272 or high Bcl-2 tumors alone. Fluorouracil 118-122 BCL2 apoptosis regulator Homo sapiens 57-62 25323586-10 2015 Patients with high PXN/high Bcl-2 or high pPXN-S272/high Bcl-2 tumors are commonly to have an unfavorable response to 5-FU-based chemotherapy, compared with patients who have high PXN, high pPXN-S272 or high Bcl-2 tumors alone. Fluorouracil 118-122 BCL2 apoptosis regulator Homo sapiens 57-62 25323586-11 2015 Therefore, we suggest that Src, PAK1 or Bcl-2 inhibitor may potentially overcome the resistance of 5-FU-based chemotherapy and consequently to improve outcomes in patients with PXN/Bcl-2 and pPXN-S272/Bcl-2-positive tumors. Fluorouracil 99-103 SRC proto-oncogene, non-receptor tyrosine kinase Homo sapiens 27-30 25323586-11 2015 Therefore, we suggest that Src, PAK1 or Bcl-2 inhibitor may potentially overcome the resistance of 5-FU-based chemotherapy and consequently to improve outcomes in patients with PXN/Bcl-2 and pPXN-S272/Bcl-2-positive tumors. Fluorouracil 99-103 BCL2 apoptosis regulator Homo sapiens 40-45 25521291-5 2015 Incubation of tongue cancer cells CAL 27 and SCC-25 in medium containing doxorubicin, 5-fluorouracil, trichostatin A, or etoposide significantly increased the expression of miR-375 and its primary transcript pri-miR-375. Fluorouracil 86-100 microRNA 375 Homo sapiens 173-180 25521291-5 2015 Incubation of tongue cancer cells CAL 27 and SCC-25 in medium containing doxorubicin, 5-fluorouracil, trichostatin A, or etoposide significantly increased the expression of miR-375 and its primary transcript pri-miR-375. Fluorouracil 86-100 microRNA 375 Homo sapiens 212-219 25544110-4 2015 In addition, following exposure to the chemotherapeutic drug 5-fluorouracil, a high survival rate was observed in the SP cells due to overexpression of the ABCG2 and B-cell lymphoma 2 proteins. Fluorouracil 61-75 ATP binding cassette subfamily G member 2 (Junior blood group) Homo sapiens 156-161 25612933-1 2015 The binding interaction of anticancer drug (using 5-fluorouracil (FU) as an example) with the model protein human serum albumin (HSA), and the FU-binding-induced microenvironment alterations in subdomain IIA of HSA molecule were studied by a combination of spectroscopic techniques and molecular docking method. Fluorouracil 50-64 albumin Homo sapiens 114-127 25612933-1 2015 The binding interaction of anticancer drug (using 5-fluorouracil (FU) as an example) with the model protein human serum albumin (HSA), and the FU-binding-induced microenvironment alterations in subdomain IIA of HSA molecule were studied by a combination of spectroscopic techniques and molecular docking method. Fluorouracil 50-64 albumin Homo sapiens 211-214 24171833-0 2015 Expression of vascular endothelial growth factor (VEGF) in macrophages, fibroblasts, and endothelial cells in pterygium treated with 5-Fluorouracil. Fluorouracil 133-147 vascular endothelial growth factor A Homo sapiens 14-48 25933112-8 2015 Moreover, the decrease in AKT and S6 phosphorylation induced by 5-FU was effectively reversed by capsaicin, indicating that capsaicin inhibits 5-FU-induced autophagy by activating the phosphoinositide 3-kinase (PI3K)/protein kinase B (AKT)/mammalian target of rapamycin (mTOR) pathway in CCA cells. Fluorouracil 64-68 AKT serine/threonine kinase 1 Homo sapiens 26-29 25933112-8 2015 Moreover, the decrease in AKT and S6 phosphorylation induced by 5-FU was effectively reversed by capsaicin, indicating that capsaicin inhibits 5-FU-induced autophagy by activating the phosphoinositide 3-kinase (PI3K)/protein kinase B (AKT)/mammalian target of rapamycin (mTOR) pathway in CCA cells. Fluorouracil 64-68 AKT serine/threonine kinase 1 Homo sapiens 235-238 25933112-8 2015 Moreover, the decrease in AKT and S6 phosphorylation induced by 5-FU was effectively reversed by capsaicin, indicating that capsaicin inhibits 5-FU-induced autophagy by activating the phosphoinositide 3-kinase (PI3K)/protein kinase B (AKT)/mammalian target of rapamycin (mTOR) pathway in CCA cells. Fluorouracil 64-68 mechanistic target of rapamycin kinase Homo sapiens 240-269 25933112-8 2015 Moreover, the decrease in AKT and S6 phosphorylation induced by 5-FU was effectively reversed by capsaicin, indicating that capsaicin inhibits 5-FU-induced autophagy by activating the phosphoinositide 3-kinase (PI3K)/protein kinase B (AKT)/mammalian target of rapamycin (mTOR) pathway in CCA cells. Fluorouracil 64-68 mechanistic target of rapamycin kinase Homo sapiens 271-275 25933112-8 2015 Moreover, the decrease in AKT and S6 phosphorylation induced by 5-FU was effectively reversed by capsaicin, indicating that capsaicin inhibits 5-FU-induced autophagy by activating the phosphoinositide 3-kinase (PI3K)/protein kinase B (AKT)/mammalian target of rapamycin (mTOR) pathway in CCA cells. Fluorouracil 143-147 AKT serine/threonine kinase 1 Homo sapiens 26-29 25933112-8 2015 Moreover, the decrease in AKT and S6 phosphorylation induced by 5-FU was effectively reversed by capsaicin, indicating that capsaicin inhibits 5-FU-induced autophagy by activating the phosphoinositide 3-kinase (PI3K)/protein kinase B (AKT)/mammalian target of rapamycin (mTOR) pathway in CCA cells. Fluorouracil 143-147 AKT serine/threonine kinase 1 Homo sapiens 235-238 25933112-8 2015 Moreover, the decrease in AKT and S6 phosphorylation induced by 5-FU was effectively reversed by capsaicin, indicating that capsaicin inhibits 5-FU-induced autophagy by activating the phosphoinositide 3-kinase (PI3K)/protein kinase B (AKT)/mammalian target of rapamycin (mTOR) pathway in CCA cells. Fluorouracil 143-147 mechanistic target of rapamycin kinase Homo sapiens 240-269 25933112-8 2015 Moreover, the decrease in AKT and S6 phosphorylation induced by 5-FU was effectively reversed by capsaicin, indicating that capsaicin inhibits 5-FU-induced autophagy by activating the phosphoinositide 3-kinase (PI3K)/protein kinase B (AKT)/mammalian target of rapamycin (mTOR) pathway in CCA cells. Fluorouracil 143-147 mechanistic target of rapamycin kinase Homo sapiens 271-275 24171833-0 2015 Expression of vascular endothelial growth factor (VEGF) in macrophages, fibroblasts, and endothelial cells in pterygium treated with 5-Fluorouracil. Fluorouracil 133-147 vascular endothelial growth factor A Homo sapiens 50-54 24171833-1 2015 PURPOSE: To evaluate the VEGF expression in macrophages, fibroblasts, and endothelial cells from pterygium before and after 5-fluorouracil (5-FU) exposure. Fluorouracil 124-138 vascular endothelial growth factor A Homo sapiens 25-29 24171833-1 2015 PURPOSE: To evaluate the VEGF expression in macrophages, fibroblasts, and endothelial cells from pterygium before and after 5-fluorouracil (5-FU) exposure. Fluorouracil 140-144 vascular endothelial growth factor A Homo sapiens 25-29 25995742-6 2015 RESULTS: It was noted that combined treatment of 5-FU + PUFAs on gastric carcinoma (MGC and SGC) cells produced a significant growth inhibitory action compared with either agent alone by inhibiting the production of TNF-alpha and VEGF and a simultaneous increase in the expression of LPL, PPAR-gamma, and C/EBP. Fluorouracil 49-53 CCAAT enhancer binding protein alpha Homo sapiens 305-310 25915935-1 2015 Dihydropyrimidinase (DHP) is the second enzyme in the catabolic pathway of uracil, thymine, and chemotherapeutic fluoropyrimidine agents such as 5-fluorouracil (5-FU). Fluorouracil 145-159 dihydropyrimidinase Homo sapiens 0-19 25915935-1 2015 Dihydropyrimidinase (DHP) is the second enzyme in the catabolic pathway of uracil, thymine, and chemotherapeutic fluoropyrimidine agents such as 5-fluorouracil (5-FU). Fluorouracil 145-159 dihydropyrimidinase Homo sapiens 21-24 25915935-1 2015 Dihydropyrimidinase (DHP) is the second enzyme in the catabolic pathway of uracil, thymine, and chemotherapeutic fluoropyrimidine agents such as 5-fluorouracil (5-FU). Fluorouracil 161-165 dihydropyrimidinase Homo sapiens 0-19 25915935-1 2015 Dihydropyrimidinase (DHP) is the second enzyme in the catabolic pathway of uracil, thymine, and chemotherapeutic fluoropyrimidine agents such as 5-fluorouracil (5-FU). Fluorouracil 161-165 dihydropyrimidinase Homo sapiens 21-24 25915935-9 2015 This is the first report of a DHP-deficient patient with DPYS compound heterozygous polymorphisms who was treated with a fluoropyrimidine, and our findings suggest that polymorphisms in the DPYS gene are pharmacogenomic markers associated with severe 5-FU toxicity in Japanese patients. Fluorouracil 251-255 dihydropyrimidinase Homo sapiens 57-61 25915935-9 2015 This is the first report of a DHP-deficient patient with DPYS compound heterozygous polymorphisms who was treated with a fluoropyrimidine, and our findings suggest that polymorphisms in the DPYS gene are pharmacogenomic markers associated with severe 5-FU toxicity in Japanese patients. Fluorouracil 251-255 dihydropyrimidinase Homo sapiens 190-194 25995742-0 2015 Polyunsaturated fatty acids augment tumoricidal action of 5-fluorouracil on gastric cancer cells by their action on vascular endothelial growth factor, tumor necrosis factor-alpha and lipid metabolism related factors. Fluorouracil 58-72 vascular endothelial growth factor A Homo sapiens 116-150 25995742-0 2015 Polyunsaturated fatty acids augment tumoricidal action of 5-fluorouracil on gastric cancer cells by their action on vascular endothelial growth factor, tumor necrosis factor-alpha and lipid metabolism related factors. Fluorouracil 58-72 tumor necrosis factor Homo sapiens 152-179 25995742-6 2015 RESULTS: It was noted that combined treatment of 5-FU + PUFAs on gastric carcinoma (MGC and SGC) cells produced a significant growth inhibitory action compared with either agent alone by inhibiting the production of TNF-alpha and VEGF and a simultaneous increase in the expression of LPL, PPAR-gamma, and C/EBP. Fluorouracil 49-53 tumor necrosis factor Homo sapiens 216-225 25995742-6 2015 RESULTS: It was noted that combined treatment of 5-FU + PUFAs on gastric carcinoma (MGC and SGC) cells produced a significant growth inhibitory action compared with either agent alone by inhibiting the production of TNF-alpha and VEGF and a simultaneous increase in the expression of LPL, PPAR-gamma, and C/EBP. Fluorouracil 49-53 vascular endothelial growth factor A Homo sapiens 230-234 25995742-6 2015 RESULTS: It was noted that combined treatment of 5-FU + PUFAs on gastric carcinoma (MGC and SGC) cells produced a significant growth inhibitory action compared with either agent alone by inhibiting the production of TNF-alpha and VEGF and a simultaneous increase in the expression of LPL, PPAR-gamma, and C/EBP. Fluorouracil 49-53 peroxisome proliferator activated receptor gamma Homo sapiens 289-299 25826088-1 2015 Stabilization of Bcl-2 protein by paxillin (PXN)-mediated ERK activation was recently reported to cause an unfavorable response to 5-Fluorouracil-based chemotherapy. Fluorouracil 131-145 BCL2 apoptosis regulator Homo sapiens 17-22 25906152-2 2015 We generated caspase-3 knockout (C3KO) and knockdown human colorectal cancer cells, and found that they are unexpectedly sensitized to DNA-damaging agents including 5-fluorouracil (5-FU), etoposide, and camptothecin. Fluorouracil 165-179 caspase 3 Homo sapiens 13-22 25906152-2 2015 We generated caspase-3 knockout (C3KO) and knockdown human colorectal cancer cells, and found that they are unexpectedly sensitized to DNA-damaging agents including 5-fluorouracil (5-FU), etoposide, and camptothecin. Fluorouracil 181-185 caspase 3 Homo sapiens 13-22 25906152-6 2015 5-FU treatment led to the formation of a z-VAD-resistant pro-caspase-8/RIP1/FADD complex, which was strongly stabilized by caspase-3 KO. Fluorouracil 0-4 caspase 3 Homo sapiens 123-132 25826088-1 2015 Stabilization of Bcl-2 protein by paxillin (PXN)-mediated ERK activation was recently reported to cause an unfavorable response to 5-Fluorouracil-based chemotherapy. Fluorouracil 131-145 mitogen-activated protein kinase 1 Homo sapiens 58-61 25840420-6 2015 MTRR 66 GA + GG genotypes decreased the risk of death (HR = 0.793, 95% CI = 0.651-0.967) in general, and in subgroups with more pronounced diffuse type, greater depth of invasion (T2/T3/T4), higher level lymph node metastasis (N1/N2/N3), advanced TNM stages (II/III level) and 5-Fu treatment. Fluorouracil 277-281 5-methyltetrahydrofolate-homocysteine methyltransferase reductase Homo sapiens 0-4 25901126-2 2015 Previously, using 2D electrophoresis-mass spectrometry, we identified RhoGDI2 as a contributor to 5-FU resistance in colon cancer cells, and also confer gastric cancer cells resistance to 5-FU. Fluorouracil 98-102 Rho GDP dissociation inhibitor beta Homo sapiens 70-77 25901126-2 2015 Previously, using 2D electrophoresis-mass spectrometry, we identified RhoGDI2 as a contributor to 5-FU resistance in colon cancer cells, and also confer gastric cancer cells resistance to 5-FU. Fluorouracil 188-192 Rho GDP dissociation inhibitor beta Homo sapiens 70-77 25855960-7 2015 PCAF was also found to sensitize HCC cells to 5-fluorouracil (5-FU) treatment by regulating GLI1/Bcl-2/BAX axis-dependent apoptosis. Fluorouracil 46-60 BCL2 apoptosis regulator Homo sapiens 97-102 25886460-9 2015 In contrast, 5-FU enhanced formation of PGE2, LTB4 and mPGES expression, but suppressed LXA4 synthesis and COX-2 expression. Fluorouracil 13-17 mitochondrially encoded cytochrome c oxidase II Homo sapiens 107-112 25855960-7 2015 PCAF was also found to sensitize HCC cells to 5-fluorouracil (5-FU) treatment by regulating GLI1/Bcl-2/BAX axis-dependent apoptosis. Fluorouracil 46-60 BCL2 associated X, apoptosis regulator Homo sapiens 103-106 25855960-7 2015 PCAF was also found to sensitize HCC cells to 5-fluorouracil (5-FU) treatment by regulating GLI1/Bcl-2/BAX axis-dependent apoptosis. Fluorouracil 62-66 BCL2 apoptosis regulator Homo sapiens 97-102 25855960-7 2015 PCAF was also found to sensitize HCC cells to 5-fluorouracil (5-FU) treatment by regulating GLI1/Bcl-2/BAX axis-dependent apoptosis. Fluorouracil 62-66 BCL2 associated X, apoptosis regulator Homo sapiens 103-106 25855960-10 2015 Together, these results show that PCAF can induce cell apoptosis by modulating a GLI1/Bcl-2/BAX axis that in turn suppresses HCC progression, and suggest that 5-FU may exert a stronger anti-tumor effect in patients with PCAF expression in HCC tumors. Fluorouracil 159-163 BCL2 apoptosis regulator Homo sapiens 86-91 25855960-10 2015 Together, these results show that PCAF can induce cell apoptosis by modulating a GLI1/Bcl-2/BAX axis that in turn suppresses HCC progression, and suggest that 5-FU may exert a stronger anti-tumor effect in patients with PCAF expression in HCC tumors. Fluorouracil 159-163 BCL2 associated X, apoptosis regulator Homo sapiens 92-95 24858038-5 2015 Here, we demonstrate cancer cells that overexpress Cks1 or Cks2 override the intra-S-phase checkpoint in the presence of replication stress-inducing chemotherapies such as 5-Fluorouracil (5-FU) and methotrexate (MTX) leading to enhanced sensitivity in vitro and in vivo. Fluorouracil 172-186 CDC28 protein kinase regulatory subunit 2 Homo sapiens 59-63 24858038-5 2015 Here, we demonstrate cancer cells that overexpress Cks1 or Cks2 override the intra-S-phase checkpoint in the presence of replication stress-inducing chemotherapies such as 5-Fluorouracil (5-FU) and methotrexate (MTX) leading to enhanced sensitivity in vitro and in vivo. Fluorouracil 188-192 CDC28 protein kinase regulatory subunit 2 Homo sapiens 59-63 25616574-7 2015 The recovery of platelet counts following a 5-fluorouracil challenge was delayed in Cdk2(fl/fl)Cdk4(-/-)vavCre mice revealing a critical role for Cdk2 and Cdk4 in stress hematopoiesis. Fluorouracil 44-58 cyclin-dependent kinase 4 Mus musculus 95-99 25860483-0 2015 Slug-dependent upregulation of L1CAM is responsible for the increased invasion potential of pancreatic cancer cells following long-term 5-FU treatment. Fluorouracil 136-140 L1 cell adhesion molecule Homo sapiens 31-36 25744576-1 2015 BACKGROUND: Trastuzumab with 5-fluorouracil (5-FU) and cisplatin offers prolonged survival in patients with HER2-overexpressing advanced gastric cancer (AGC) and advanced gastro-oesophageal junction cancer (AGOJ). Fluorouracil 29-43 erb-b2 receptor tyrosine kinase 2 Homo sapiens 108-112 25744576-1 2015 BACKGROUND: Trastuzumab with 5-fluorouracil (5-FU) and cisplatin offers prolonged survival in patients with HER2-overexpressing advanced gastric cancer (AGC) and advanced gastro-oesophageal junction cancer (AGOJ). Fluorouracil 45-49 erb-b2 receptor tyrosine kinase 2 Homo sapiens 108-112 25616574-7 2015 The recovery of platelet counts following a 5-fluorouracil challenge was delayed in Cdk2(fl/fl)Cdk4(-/-)vavCre mice revealing a critical role for Cdk2 and Cdk4 in stress hematopoiesis. Fluorouracil 44-58 cyclin-dependent kinase 4 Mus musculus 155-159 24476216-6 2015 We next established the cytotoxicity profile for 5-FU in MDA-MB-231 cells using a tetrazolium-based cell viability assay and obtained an LD50 value of 28 muM. Fluorouracil 49-53 latexin Homo sapiens 154-157 25625649-0 2015 gamma-Tocotrienol prevents 5-FU-induced reactive oxygen species production in human oral keratinocytes through the stabilization of 5-FU-induced activation of Nrf2. Fluorouracil 27-31 NFE2 like bZIP transcription factor 2 Homo sapiens 159-163 25625649-0 2015 gamma-Tocotrienol prevents 5-FU-induced reactive oxygen species production in human oral keratinocytes through the stabilization of 5-FU-induced activation of Nrf2. Fluorouracil 132-136 NFE2 like bZIP transcription factor 2 Homo sapiens 159-163 25625649-8 2015 Whereas 5-FU stimulated the expression of NF-E2-related factor 2 (Nrf2) protein in the nucleus up to 12 h after treatment of RT7 cells, gamma-tocotrienol had no obvious effect on the expression of nuclear Nrf2 protein. Fluorouracil 8-12 NFE2 like bZIP transcription factor 2 Homo sapiens 42-64 25625649-8 2015 Whereas 5-FU stimulated the expression of NF-E2-related factor 2 (Nrf2) protein in the nucleus up to 12 h after treatment of RT7 cells, gamma-tocotrienol had no obvious effect on the expression of nuclear Nrf2 protein. Fluorouracil 8-12 NFE2 like bZIP transcription factor 2 Homo sapiens 66-70 25625649-9 2015 Of note, the combined treatment with both agents stabilized the 5-FU-induced nuclear Nrf2 protein expression until 24 h after treatment. Fluorouracil 64-68 NFE2 like bZIP transcription factor 2 Homo sapiens 85-89 25625649-11 2015 These findings suggest that gamma-tocotrienol could prevent 5-FU-induced ROS generation by stabilizing Nrf2 activation, thereby leading to ROS detoxification and cell survival in human oral keratinocytes. Fluorouracil 60-64 NFE2 like bZIP transcription factor 2 Homo sapiens 103-107 25625841-8 2015 Treatment with an anti-human IL-6 receptor monoclonal antibody reduced spheroid formation, stem cell-related gene expression, and 5-fluorouracil (5-FU) resistance. Fluorouracil 130-144 interleukin 6 Homo sapiens 29-33 25625841-8 2015 Treatment with an anti-human IL-6 receptor monoclonal antibody reduced spheroid formation, stem cell-related gene expression, and 5-fluorouracil (5-FU) resistance. Fluorouracil 146-150 interleukin 6 Homo sapiens 29-33 25625841-9 2015 In addition, IL-6 treatment enhanced the levels of p-STAT3 (Tyr705), the expression of Oct-4, Klf4, Lgr5, and Notch 3, and chemoresistance to 5-FU. Fluorouracil 142-146 interleukin 6 Homo sapiens 13-17 25901146-4 2015 The 1F2-coupled 5-FU-loaded BSA nanoparticles interacted with nearly all HER2 receptors available on the surface of HER2-positive SKBR3 cells. Fluorouracil 16-20 erb-b2 receptor tyrosine kinase 2 Homo sapiens 73-77 25901146-4 2015 The 1F2-coupled 5-FU-loaded BSA nanoparticles interacted with nearly all HER2 receptors available on the surface of HER2-positive SKBR3 cells. Fluorouracil 16-20 erb-b2 receptor tyrosine kinase 2 Homo sapiens 116-120 25901146-9 2015 This novel system can efficiently be employed for targeted delivery of 5-FU to HER2-positive cancerous cells. Fluorouracil 71-75 erb-b2 receptor tyrosine kinase 2 Homo sapiens 79-83 24476216-7 2015 When 5-FU incubations were repeated with the addition of curcumin, the LD50 value increased to 200-300 muM, representing a 7-10-fold protection by curcumin against 5-FU cytotoxicity. Fluorouracil 5-9 latexin Homo sapiens 103-106 25789066-0 2015 A let-7b binding site SNP in the 3"-UTR of the Bcl-xL gene enhances resistance to 5-fluorouracil and doxorubicin in breast cancer cells. Fluorouracil 82-96 BCL2 like 1 Homo sapiens 47-53 25789066-4 2015 The data indicated that let-7b negatively regulates the expression of Bcl-xL and appears to sensitize MCF-7 cells to the chemotherapeutic agents 5-fluorouracil (5-FU) and doxorubicin. Fluorouracil 145-159 BCL2 like 1 Homo sapiens 70-76 25789066-4 2015 The data indicated that let-7b negatively regulates the expression of Bcl-xL and appears to sensitize MCF-7 cells to the chemotherapeutic agents 5-fluorouracil (5-FU) and doxorubicin. Fluorouracil 161-165 BCL2 like 1 Homo sapiens 70-76 25789066-5 2015 Furthermore, the SNP rs3208684 A>C was demonstrated to enhance Bcl-xL protein expression by disrupting the binding of let-7b to the 3"-UTR of Bcl-xL and, in MCF-7 cells, overexpression of let-7b in the presence of a mutant Bcl-xL 3"-UTR (C allele) significantly increased 5-FU and doxorubicin resistance. Fluorouracil 275-279 BCL2 like 1 Homo sapiens 66-72 25861418-11 2015 Radioimmunoassay showed that mice treated with AHCC plus 5-FU had the highest serum levels of IL-2 and TNFalpha compared with the vehicle group and 5-FU group. Fluorouracil 57-61 tumor necrosis factor Mus musculus 103-111 25789066-6 2015 Thus, the results of the present study demonstrate that the SNP rs3208684 A>C may upregulate Bcl-xL protein expression and enhance the resistance of the MCF-7 cells to 5-FU and doxorubicin by decreasing the binding of let-7b to the 3"-UTR of Bcl-xL. Fluorouracil 171-175 BCL2 like 1 Homo sapiens 96-102 25861418-13 2015 In addition, the combination of AHCC and 5-FU further up-regulated the expression of Bcl-2 associated X protein (Bax) (P < 0.01), while it down-regulated the expression of B cell lymphoma 2 (Bcl-2) (P < 0.01). Fluorouracil 41-45 B cell leukemia/lymphoma 2 Mus musculus 85-90 25861418-13 2015 In addition, the combination of AHCC and 5-FU further up-regulated the expression of Bcl-2 associated X protein (Bax) (P < 0.01), while it down-regulated the expression of B cell lymphoma 2 (Bcl-2) (P < 0.01). Fluorouracil 41-45 B cell leukemia/lymphoma 2 Mus musculus 175-192 25861418-13 2015 In addition, the combination of AHCC and 5-FU further up-regulated the expression of Bcl-2 associated X protein (Bax) (P < 0.01), while it down-regulated the expression of B cell lymphoma 2 (Bcl-2) (P < 0.01). Fluorouracil 41-45 B cell leukemia/lymphoma 2 Mus musculus 194-199 25789066-6 2015 Thus, the results of the present study demonstrate that the SNP rs3208684 A>C may upregulate Bcl-xL protein expression and enhance the resistance of the MCF-7 cells to 5-FU and doxorubicin by decreasing the binding of let-7b to the 3"-UTR of Bcl-xL. Fluorouracil 171-175 BCL2 like 1 Homo sapiens 245-251 25733851-3 2015 Our platform contains hydrogel embedded with dark-gold nanoparticles modified with 5-fluorouracil (5-FU)-intercalated nanobeacons that serve as an ON/OFF molecular nanoswitch triggered by the increased MRP1 expression within the tumor tissue microenvironment. Fluorouracil 83-97 ATP binding cassette subfamily B member 1 Homo sapiens 202-206 25756340-1 2015 PURPOSE: An oral antineoplastic drug, S-1, is known to be more effective with less toxicity and fewer gastrointestinal side effects than the conventional intravenous 5-fluorouracil. Fluorouracil 166-180 proteasome 26S subunit, non-ATPase 1 Homo sapiens 38-41 25733851-3 2015 Our platform contains hydrogel embedded with dark-gold nanoparticles modified with 5-fluorouracil (5-FU)-intercalated nanobeacons that serve as an ON/OFF molecular nanoswitch triggered by the increased MRP1 expression within the tumor tissue microenvironment. Fluorouracil 99-103 ATP binding cassette subfamily B member 1 Homo sapiens 202-206 28123791-10 2015 Identification of the precise mechanism through which DPYD is epigenetically regulated, and underlying reasons why exactly the break (FRA1E) happens, will consequently pave the way toward preventing severe toxicity to the antineoplastic drug 5-fluorouracil (5-FU) and development of the causative therapy for the dihydropyrimidine dehydrogenase deficiency. Fluorouracil 242-256 fragile site, aphidicolin type, common, fra(1)(p21.2) Homo sapiens 134-139 25616665-3 2015 Ectopic expression of miR-520g conferred resistance to 5-fluorouracil (5-FU)- or oxaliplatin-induced apoptosis in vitro and reduced the effectiveness of 5-FU in the inhibition of tumor growth in a mouse xenograft model in vivo. Fluorouracil 55-69 microRNA 520g Homo sapiens 22-30 25616665-3 2015 Ectopic expression of miR-520g conferred resistance to 5-fluorouracil (5-FU)- or oxaliplatin-induced apoptosis in vitro and reduced the effectiveness of 5-FU in the inhibition of tumor growth in a mouse xenograft model in vivo. Fluorouracil 71-75 microRNA 520g Homo sapiens 22-30 25616665-3 2015 Ectopic expression of miR-520g conferred resistance to 5-fluorouracil (5-FU)- or oxaliplatin-induced apoptosis in vitro and reduced the effectiveness of 5-FU in the inhibition of tumor growth in a mouse xenograft model in vivo. Fluorouracil 153-157 microRNA 520g Homo sapiens 22-30 25616665-6 2015 Inhibition of miR-520g in p53(-/-) cells increased their sensitivity to 5-FU treatment. Fluorouracil 72-76 microRNA 520g Homo sapiens 14-22 25616665-6 2015 Inhibition of miR-520g in p53(-/-) cells increased their sensitivity to 5-FU treatment. Fluorouracil 72-76 tumor protein p53 Homo sapiens 26-29 28123791-10 2015 Identification of the precise mechanism through which DPYD is epigenetically regulated, and underlying reasons why exactly the break (FRA1E) happens, will consequently pave the way toward preventing severe toxicity to the antineoplastic drug 5-fluorouracil (5-FU) and development of the causative therapy for the dihydropyrimidine dehydrogenase deficiency. Fluorouracil 258-262 fragile site, aphidicolin type, common, fra(1)(p21.2) Homo sapiens 134-139 25750344-5 2015 RESULTS: In patients with adenocarcinoma, tumors with EGFR gene mutations were significantly more sensitive to 5-fluorouracil (5-FU) than tumors without EGFR gene mutations (p<0.0149). Fluorouracil 111-125 epidermal growth factor receptor Homo sapiens 54-58 25750344-5 2015 RESULTS: In patients with adenocarcinoma, tumors with EGFR gene mutations were significantly more sensitive to 5-fluorouracil (5-FU) than tumors without EGFR gene mutations (p<0.0149). Fluorouracil 127-131 epidermal growth factor receptor Homo sapiens 54-58 25573239-9 2015 We propose that the EGFR dephosphorylation induced by VNR is related to cell growth inhibitory activity of VNR, and that this is one of the mechanisms of the synergistic effect of VNR + 5-FU in EGFR-mutated lung cancer cells. Fluorouracil 186-190 epidermal growth factor receptor Homo sapiens 20-24 25750344-6 2015 CONCLUSION: Our data suggest that patients with adenocarcinoma harboring EGFR gene mutations may be susceptible to 5-FU. Fluorouracil 115-119 epidermal growth factor receptor Homo sapiens 73-77 26222289-10 2015 Finally, gene expression studies suggested triggering of the p53 mediated caspase signalling gene cascade in 5-FU@DsAgNC treated cells. Fluorouracil 109-113 tumor protein p53 Homo sapiens 61-64 25461251-3 2015 Expression of Ryk on HSPCs in vivo is associated with a lower rate of proliferation, and, following treatment with fluorouracil (5-FU), the percentage of Ryk(+/high) HSPCs increased and the percentage of Ryk(-/low) HSPCs decreased. Fluorouracil 115-127 receptor-like tyrosine kinase Mus musculus 14-17 25461251-3 2015 Expression of Ryk on HSPCs in vivo is associated with a lower rate of proliferation, and, following treatment with fluorouracil (5-FU), the percentage of Ryk(+/high) HSPCs increased and the percentage of Ryk(-/low) HSPCs decreased. Fluorouracil 115-127 receptor-like tyrosine kinase Mus musculus 154-157 25461251-3 2015 Expression of Ryk on HSPCs in vivo is associated with a lower rate of proliferation, and, following treatment with fluorouracil (5-FU), the percentage of Ryk(+/high) HSPCs increased and the percentage of Ryk(-/low) HSPCs decreased. Fluorouracil 115-127 receptor-like tyrosine kinase Mus musculus 154-157 25461251-3 2015 Expression of Ryk on HSPCs in vivo is associated with a lower rate of proliferation, and, following treatment with fluorouracil (5-FU), the percentage of Ryk(+/high) HSPCs increased and the percentage of Ryk(-/low) HSPCs decreased. Fluorouracil 129-133 receptor-like tyrosine kinase Mus musculus 14-17 25461251-5 2015 We found that Ryk expression on HSPCs is associated with lower rates of apoptosis following 5-FU and radiation. Fluorouracil 92-96 receptor-like tyrosine kinase Mus musculus 14-17 25461251-7 2015 Furthermore, inhibition of Ryk signaling sensitized HSPCs to 5-FU treatment in association with increased levels of reactive oxygen species. Fluorouracil 61-65 receptor-like tyrosine kinase Mus musculus 27-30 25573239-9 2015 We propose that the EGFR dephosphorylation induced by VNR is related to cell growth inhibitory activity of VNR, and that this is one of the mechanisms of the synergistic effect of VNR + 5-FU in EGFR-mutated lung cancer cells. Fluorouracil 186-190 epidermal growth factor receptor Homo sapiens 194-198 25617735-11 2015 Inhibition of STAT3 decreased cyclinD1 expression to decrease the cell viability and increase rate of apoptosis when exposed to 5-FU treatment. Fluorouracil 128-132 signal transducer and activator of transcription 3 Homo sapiens 14-19 25784653-4 2015 Overexpression of miR-191 in colorectal cancer cell lines alters cell cycle progression and cell resistance to 5-Fu induced cell apoptosis. Fluorouracil 111-115 microRNA 191 Homo sapiens 18-25 26312918-8 2015 Five of them predicted histopathological response to fluorouracil-based chemotherapy regimens, of which the FAD binding protein NQO1 was subsequently validated by immunohistochemistry. Fluorouracil 53-65 NAD(P)H quinone dehydrogenase 1 Homo sapiens 128-132 25760541-1 2015 Genetic polymorphisms of the dihydropyrimidinase gene (DPYS) may be associated with the development of severe toxicity to 5-fluorouracil, a drug used to treat solid tumors. Fluorouracil 122-136 dihydropyrimidinase Homo sapiens 29-48 25932284-2 2015 S-1, an oral 5-FU derivative, has demonstrated a potential antitumor effect in patients with MBC. Fluorouracil 13-17 proteasome 26S subunit, non-ATPase 1 Homo sapiens 0-3 25544773-0 2015 Targeting the microRNA-21/AP1 axis by 5-fluorouracil and pirarubicin in human hepatocellular carcinoma. Fluorouracil 38-52 JunB proto-oncogene, AP-1 transcription factor subunit Homo sapiens 26-29 25502560-0 2015 Indirect modulation of sensitivity to 5-fluorouracil by microRNA-96 in human colorectal cancer cells. Fluorouracil 38-52 microRNA 96 Homo sapiens 56-67 25502560-5 2015 When the level of miR-96 increased, the expression of the anti-apoptotic regulator XIAP and p53 stability regulator UBE2N decreased, resulting in increased apoptosis and growth inhibition following 5-FU exposure. Fluorouracil 198-202 microRNA 96 Homo sapiens 18-24 25502560-5 2015 When the level of miR-96 increased, the expression of the anti-apoptotic regulator XIAP and p53 stability regulator UBE2N decreased, resulting in increased apoptosis and growth inhibition following 5-FU exposure. Fluorouracil 198-202 tumor protein p53 Homo sapiens 92-95 25502560-8 2015 In TSs, 5-FU resistance corresponded to a significantly lower level of miR-96, however only XIAP, not UBE2N, was up-regulated demonstrating partial agreement with the 2D condition regarding target expression. Fluorouracil 8-12 microRNA 96 Homo sapiens 71-77 25502560-9 2015 Overall, these results suggest that miR-96 may modulate 5-FU sensitivity in CRC cells by promoting apoptosis; however, differential expression of target genes in TSs warrants further studies on the 5-FU resistance mechanism under 3D conditions. Fluorouracil 56-60 microRNA 96 Homo sapiens 36-42 25760541-1 2015 Genetic polymorphisms of the dihydropyrimidinase gene (DPYS) may be associated with the development of severe toxicity to 5-fluorouracil, a drug used to treat solid tumors. Fluorouracil 122-136 dihydropyrimidinase Homo sapiens 55-59 25588809-13 2015 And, positive Nrf2 expression was significantly associated with resistance to 5FU-based adjuvant chemotherapy (p = 0.024). Fluorouracil 78-81 NFE2 like bZIP transcription factor 2 Homo sapiens 14-18 25351347-8 2015 mRNA and protein expression levels of HIF-2alpha, ABCG2 and Oct-4 were significantly lower in the celecoxib and 5-FU/celecoxib combination groups (P<0.01) compared with those of the hypoxia control and 5-FU groups. Fluorouracil 112-116 ATP binding cassette subfamily G member 2 (Junior blood group) Homo sapiens 50-55 25449431-0 2015 MiR-22 regulates 5-FU sensitivity by inhibiting autophagy and promoting apoptosis in colorectal cancer cells. Fluorouracil 17-21 microRNA 22 Homo sapiens 0-6 25449431-2 2015 Here, we showed that miR-22 inhibited autophagy and promoted apoptosis to increase the sensitivity of colorectal cancer (CRC) cells to 5-fluorouracil (5-FU) treatment both in vitro and in vivo. Fluorouracil 135-149 microRNA 22 Homo sapiens 21-27 25449431-2 2015 Here, we showed that miR-22 inhibited autophagy and promoted apoptosis to increase the sensitivity of colorectal cancer (CRC) cells to 5-fluorouracil (5-FU) treatment both in vitro and in vivo. Fluorouracil 151-155 microRNA 22 Homo sapiens 21-27 25449431-4 2015 Thus, miR-22 may function as an important switch between autophagy and apoptosis to regulate 5-FU sensitivity through post-transcriptional silencing of BTG1. Fluorouracil 93-97 microRNA 22 Homo sapiens 6-12 25449431-5 2015 Promisingly, miR-22 could be considered as both a predictor of 5-FU sensitivity for personalized treatment and a therapeutic target for colorectal cancer. Fluorouracil 63-67 microRNA 22 Homo sapiens 13-19 25404731-3 2015 In the present study, transient receptor potential channel TrpC5 was found to be overproduced at the mRNA and protein levels together with ABCB1 in 5-Fu-resistant human CRC HCT-8 (HCT-8/5-Fu) and LoVo (LoVo/5-Fu) cells. Fluorouracil 148-152 transient receptor potential cation channel subfamily C member 5 Homo sapiens 59-64 25850203-3 2015 Compound 17 was found to be the most potent against breast cancer cell lines with IC55 value 66.6 muM compared with the reference drug 5-fluorouracil with IC50 value 77.28 muM. Fluorouracil 135-149 latexin Homo sapiens 172-175 25404731-3 2015 In the present study, transient receptor potential channel TrpC5 was found to be overproduced at the mRNA and protein levels together with ABCB1 in 5-Fu-resistant human CRC HCT-8 (HCT-8/5-Fu) and LoVo (LoVo/5-Fu) cells. Fluorouracil 148-152 ATP binding cassette subfamily B member 1 Homo sapiens 139-144 25404731-5 2015 Suppressing TrpC5 expression with TrpC5-specific siRNA inhibited the canonical Wnt/beta-catenin signal pathway, reduced the induction of ABCB1, weakened the ABCB1 efflux pump, and caused a remarkable reversal of 5-Fu resistance in HCT-8/5-Fu and LoVo/5-Fu cells. Fluorouracil 212-216 transient receptor potential cation channel subfamily C member 5 Homo sapiens 12-17 25404731-5 2015 Suppressing TrpC5 expression with TrpC5-specific siRNA inhibited the canonical Wnt/beta-catenin signal pathway, reduced the induction of ABCB1, weakened the ABCB1 efflux pump, and caused a remarkable reversal of 5-Fu resistance in HCT-8/5-Fu and LoVo/5-Fu cells. Fluorouracil 212-216 transient receptor potential cation channel subfamily C member 5 Homo sapiens 34-39 25778705-7 2015 In the HER2+ cohort (n = 88), 50% of patients demonstrated possible benefit from a combination of trastuzumab with 5FU/capecitabine based on concurrent low TS, 53% with irinotecan (high TOPO1), 63% with cisplatin (low ERCC1) and 55% with gemcitabine (low RRM1). Fluorouracil 115-118 erb-b2 receptor tyrosine kinase 2 Homo sapiens 7-11 24889488-2 2015 The purpose of this study was to assess the prognostic impact of KRAS and BRAF mutation in patients treated with adjuvant 5-fluorouracil/leucovorin/oxaliplatin (FOLFOX). Fluorouracil 122-136 B-Raf proto-oncogene, serine/threonine kinase Homo sapiens 74-78 25648497-13 2015 In HT-29, HCT-116 and HCT-15 colorectal cancer lines, GHRH antagonist treatment caused cellular arrest in S-phase of cell cycle, potentiated inhibition of in vitro proliferation and in vivo growth produced by S-phase specific cytotoxic agents, 5-FU, irinotecan and cisplatin. Fluorouracil 244-248 growth hormone releasing hormone Homo sapiens 54-58 26479470-7 2015 Conversely, the anti-CXCL4 monoclonal antibody (CXCL4-mab) retarded tumor-regrowth after 5-FU treatment in immune-competent mice, but not nude mice. Fluorouracil 89-93 platelet factor 4 Mus musculus 21-26 26479470-7 2015 Conversely, the anti-CXCL4 monoclonal antibody (CXCL4-mab) retarded tumor-regrowth after 5-FU treatment in immune-competent mice, but not nude mice. Fluorouracil 89-93 platelet factor 4 Mus musculus 48-53 26479470-9 2015 Thus, the colon cancer cells in responding to the cytotoxic stress of 5-FU produce a high level of CXCL4, which suppresses antitumor immunity to confer the residual cancer cells an advantage for regrowth after chemotherapy. Fluorouracil 70-74 platelet factor 4 Mus musculus 99-104 25896253-0 2015 MiR-141 Activates Nrf2-Dependent Antioxidant Pathway via Down-Regulating the Expression of Keap1 Conferring the Resistance of Hepatocellular Carcinoma Cells to 5-Fluorouracil. Fluorouracil 160-174 microRNA 141 Homo sapiens 0-7 25896253-0 2015 MiR-141 Activates Nrf2-Dependent Antioxidant Pathway via Down-Regulating the Expression of Keap1 Conferring the Resistance of Hepatocellular Carcinoma Cells to 5-Fluorouracil. Fluorouracil 160-174 NFE2 like bZIP transcription factor 2 Homo sapiens 18-22 25896253-0 2015 MiR-141 Activates Nrf2-Dependent Antioxidant Pathway via Down-Regulating the Expression of Keap1 Conferring the Resistance of Hepatocellular Carcinoma Cells to 5-Fluorouracil. Fluorouracil 160-174 kelch like ECH associated protein 1 Homo sapiens 91-96 25896253-6 2015 Up-regulation of miR-141 expression resulted in a significant inhibition of 5-FU-mediated cytotoxicity and apoptosis in various hepatocellular carcinoma cells-lines. Fluorouracil 76-80 microRNA 141 Homo sapiens 17-24 25896253-8 2015 Treatment with miR-141 mimics in parental HepG2 cells, restored miR-141 expression and reduced Keap1 levels, thereby resulting in erythroid transcription factor NFE2-L2 (Nrf2) nuclear translocation, activation of Nrf2-dependent HO-1 gene transcription, and subsequent enhancement in 5-FU resistance. Fluorouracil 283-287 microRNA 141 Homo sapiens 15-22 25896253-9 2015 Conversely, restoring the expression of Keap1 partly recovered 5-FU sensitivity by counteracting miR-141-mediated 5-FU resistance. Fluorouracil 63-67 kelch like ECH associated protein 1 Homo sapiens 40-45 25896253-9 2015 Conversely, restoring the expression of Keap1 partly recovered 5-FU sensitivity by counteracting miR-141-mediated 5-FU resistance. Fluorouracil 63-67 microRNA 141 Homo sapiens 97-104 26513239-11 2015 Overexpression of miR-429 inhibited Bcl-2-mediated cell survival against apoptosis induced by Fluorouracil, while depletion of miR-429 augmented it. Fluorouracil 94-106 microRNA 429 Homo sapiens 18-25 26513239-11 2015 Overexpression of miR-429 inhibited Bcl-2-mediated cell survival against apoptosis induced by Fluorouracil, while depletion of miR-429 augmented it. Fluorouracil 94-106 BCL2 apoptosis regulator Homo sapiens 36-41 25896253-9 2015 Conversely, restoring the expression of Keap1 partly recovered 5-FU sensitivity by counteracting miR-141-mediated 5-FU resistance. Fluorouracil 114-118 kelch like ECH associated protein 1 Homo sapiens 40-45 25896253-9 2015 Conversely, restoring the expression of Keap1 partly recovered 5-FU sensitivity by counteracting miR-141-mediated 5-FU resistance. Fluorouracil 114-118 microRNA 141 Homo sapiens 97-104 25896253-10 2015 CONCLUSION: Our study showed that miR-141 plays a key role in 5-FU resistance by down-regulating Keap1 expression, thereby reactivating the Nrf2-dependent antioxidant pathway, which may serve as a potential target for overcoming 5-FU resistance in hepatocellular carcinoma cells. Fluorouracil 62-66 microRNA 141 Homo sapiens 34-41 25896253-10 2015 CONCLUSION: Our study showed that miR-141 plays a key role in 5-FU resistance by down-regulating Keap1 expression, thereby reactivating the Nrf2-dependent antioxidant pathway, which may serve as a potential target for overcoming 5-FU resistance in hepatocellular carcinoma cells. Fluorouracil 62-66 kelch like ECH associated protein 1 Homo sapiens 97-102 25896253-10 2015 CONCLUSION: Our study showed that miR-141 plays a key role in 5-FU resistance by down-regulating Keap1 expression, thereby reactivating the Nrf2-dependent antioxidant pathway, which may serve as a potential target for overcoming 5-FU resistance in hepatocellular carcinoma cells. Fluorouracil 62-66 NFE2 like bZIP transcription factor 2 Homo sapiens 140-144 25896253-10 2015 CONCLUSION: Our study showed that miR-141 plays a key role in 5-FU resistance by down-regulating Keap1 expression, thereby reactivating the Nrf2-dependent antioxidant pathway, which may serve as a potential target for overcoming 5-FU resistance in hepatocellular carcinoma cells. Fluorouracil 229-233 microRNA 141 Homo sapiens 34-41 25896253-10 2015 CONCLUSION: Our study showed that miR-141 plays a key role in 5-FU resistance by down-regulating Keap1 expression, thereby reactivating the Nrf2-dependent antioxidant pathway, which may serve as a potential target for overcoming 5-FU resistance in hepatocellular carcinoma cells. Fluorouracil 229-233 kelch like ECH associated protein 1 Homo sapiens 97-102 25896253-10 2015 CONCLUSION: Our study showed that miR-141 plays a key role in 5-FU resistance by down-regulating Keap1 expression, thereby reactivating the Nrf2-dependent antioxidant pathway, which may serve as a potential target for overcoming 5-FU resistance in hepatocellular carcinoma cells. Fluorouracil 229-233 NFE2 like bZIP transcription factor 2 Homo sapiens 140-144 25643258-0 2015 Dual Inhibition of Cdc7 and Cdk9 by PHA-767491 Suppresses Hepatocarcinoma Synergistically with 5-Fluorouracil. Fluorouracil 95-109 cell division cycle 7 Homo sapiens 19-23 25643258-0 2015 Dual Inhibition of Cdc7 and Cdk9 by PHA-767491 Suppresses Hepatocarcinoma Synergistically with 5-Fluorouracil. Fluorouracil 95-109 cyclin dependent kinase 9 Homo sapiens 28-32 25643258-1 2015 Activation of checkpoint kinase 1 (Chk1) is essential in chemoresistance of hepatocarcinoma (HCC) to 5-fluorouracil (5-FU) and other antimetabolite family of drugs. Fluorouracil 101-115 checkpoint kinase 1 Homo sapiens 14-33 25755712-7 2015 The Western blot results showed high concentration of cytochrome c in the cell cytosol after 24 h of 5-FU and BA combination treatment. Fluorouracil 101-105 cytochrome c, somatic Homo sapiens 54-66 25643258-1 2015 Activation of checkpoint kinase 1 (Chk1) is essential in chemoresistance of hepatocarcinoma (HCC) to 5-fluorouracil (5-FU) and other antimetabolite family of drugs. Fluorouracil 101-115 checkpoint kinase 1 Homo sapiens 35-39 25643258-1 2015 Activation of checkpoint kinase 1 (Chk1) is essential in chemoresistance of hepatocarcinoma (HCC) to 5-fluorouracil (5-FU) and other antimetabolite family of drugs. Fluorouracil 117-121 checkpoint kinase 1 Homo sapiens 14-33 25643258-1 2015 Activation of checkpoint kinase 1 (Chk1) is essential in chemoresistance of hepatocarcinoma (HCC) to 5-fluorouracil (5-FU) and other antimetabolite family of drugs. Fluorouracil 117-121 checkpoint kinase 1 Homo sapiens 35-39 25643258-2 2015 In this study, we demonstrated that PHA-767491, a dual inhibitor of two cell cycle checkpoint kinases, cell division cycle kinase 7 (Cdc7) and cyclin-dependent kinase 9 (Cdk9), has synergistic antitumor effect with 5-FU to suppress human HCC cells both in vitro and in vivo. Fluorouracil 215-219 cell division cycle 7 Homo sapiens 133-137 25643258-2 2015 In this study, we demonstrated that PHA-767491, a dual inhibitor of two cell cycle checkpoint kinases, cell division cycle kinase 7 (Cdc7) and cyclin-dependent kinase 9 (Cdk9), has synergistic antitumor effect with 5-FU to suppress human HCC cells both in vitro and in vivo. Fluorouracil 215-219 cyclin dependent kinase 9 Homo sapiens 170-174 25643258-3 2015 Compared with the sole use of each agent, PHA-767491 in combination with 5-FU exhibited much stronger cytotoxicity and induced significant apoptosis manifested by remarkably increased caspase 3 activation and poly(ADP-Ribose) polymerase fragmentation in HCC cells. Fluorouracil 73-77 caspase 3 Homo sapiens 184-193 25643258-3 2015 Compared with the sole use of each agent, PHA-767491 in combination with 5-FU exhibited much stronger cytotoxicity and induced significant apoptosis manifested by remarkably increased caspase 3 activation and poly(ADP-Ribose) polymerase fragmentation in HCC cells. Fluorouracil 73-77 poly(ADP-ribose) polymerase 1 Homo sapiens 209-236 25643258-4 2015 PHA-767491 directly counteracted the 5-FU-induced phosphorylation of Chk1, a substrate of Cdc7; and decreased the expression of the anti-apoptotic protein myeloid leukemia cell 1, a downstream target of Cdk9. Fluorouracil 37-41 checkpoint kinase 1 Homo sapiens 69-73 25643258-4 2015 PHA-767491 directly counteracted the 5-FU-induced phosphorylation of Chk1, a substrate of Cdc7; and decreased the expression of the anti-apoptotic protein myeloid leukemia cell 1, a downstream target of Cdk9. Fluorouracil 37-41 cell division cycle 7 Homo sapiens 90-94 25643258-4 2015 PHA-767491 directly counteracted the 5-FU-induced phosphorylation of Chk1, a substrate of Cdc7; and decreased the expression of the anti-apoptotic protein myeloid leukemia cell 1, a downstream target of Cdk9. Fluorouracil 37-41 cyclin dependent kinase 9 Homo sapiens 203-207 25643258-6 2015 Our study suggests that PHA- 767491 could enhance the efficacy of 5-FU by inhibiting Chk1 phosphorylation and down-regulating Mcl1 expression through inhibition of Cdc7 and Cdk9, thus combinational administration of PHA-767491 with 5-FU could be potentially beneficial to patients with advanced and resistant HCC. Fluorouracil 66-70 checkpoint kinase 1 Homo sapiens 85-89 25643258-6 2015 Our study suggests that PHA- 767491 could enhance the efficacy of 5-FU by inhibiting Chk1 phosphorylation and down-regulating Mcl1 expression through inhibition of Cdc7 and Cdk9, thus combinational administration of PHA-767491 with 5-FU could be potentially beneficial to patients with advanced and resistant HCC. Fluorouracil 66-70 cell division cycle 7 Homo sapiens 164-168 25643258-6 2015 Our study suggests that PHA- 767491 could enhance the efficacy of 5-FU by inhibiting Chk1 phosphorylation and down-regulating Mcl1 expression through inhibition of Cdc7 and Cdk9, thus combinational administration of PHA-767491 with 5-FU could be potentially beneficial to patients with advanced and resistant HCC. Fluorouracil 66-70 cyclin dependent kinase 9 Homo sapiens 173-177 25755712-8 2015 Treatment of BA-responsive RMS-13 cells with 5-FU and BA combination resulted in inhibition of GLI1, GLI2, PTCH1, and IGF2 genes. Fluorouracil 45-49 GLI family zinc finger 2 Homo sapiens 101-105 25755712-8 2015 Treatment of BA-responsive RMS-13 cells with 5-FU and BA combination resulted in inhibition of GLI1, GLI2, PTCH1, and IGF2 genes. Fluorouracil 45-49 patched 1 Homo sapiens 107-112 25310623-5 2015 5-FU treatment induced DNA damage and activation of ataxia telangiectasia mutated (ATM) and Chk1, leading to S-phase arrest, and Chk1 inhibition using SB218078 reduced S-phase arrest and increased apoptosis in the presence of 5-FU. Fluorouracil 0-4 checkpoint kinase 1 Homo sapiens 92-96 25310623-0 2015 5-FU resistance abrogates the amplified cytotoxic effects induced by inhibiting checkpoint kinase 1 in p53-mutated colon cancer cells. Fluorouracil 0-4 checkpoint kinase 1 Homo sapiens 80-99 25310623-5 2015 5-FU treatment induced DNA damage and activation of ataxia telangiectasia mutated (ATM) and Chk1, leading to S-phase arrest, and Chk1 inhibition using SB218078 reduced S-phase arrest and increased apoptosis in the presence of 5-FU. Fluorouracil 0-4 checkpoint kinase 1 Homo sapiens 129-133 25310623-0 2015 5-FU resistance abrogates the amplified cytotoxic effects induced by inhibiting checkpoint kinase 1 in p53-mutated colon cancer cells. Fluorouracil 0-4 tumor protein p53 Homo sapiens 103-106 25310623-6 2015 In contrast, in p53-deficient, 5-FU-resistant (5FUR) colon cancer cells that we developed, 5-FU enhanced DNA damage but did not induce Chk1/ATM activation or cell cycle arrest. Fluorouracil 31-35 tumor protein p53 Homo sapiens 16-19 25310623-6 2015 In contrast, in p53-deficient, 5-FU-resistant (5FUR) colon cancer cells that we developed, 5-FU enhanced DNA damage but did not induce Chk1/ATM activation or cell cycle arrest. Fluorouracil 91-95 tumor protein p53 Homo sapiens 16-19 25310623-8 2015 These results indicate that 5-FU-resistance abrogated the anticancer effect amplified by Chk1 inhibition, even in p53-deficient cancer cells. Fluorouracil 28-32 checkpoint kinase 1 Homo sapiens 89-93 25333644-8 2015 While silencing of PPARgamma significantly inhibit the cytotoxic effects of both gemcitabine and 5-fluorouracil in PC cells in vitro. Fluorouracil 97-111 peroxisome proliferator activated receptor gamma Homo sapiens 19-28 25333998-7 2015 Further, 5-FU attenuated SNX-2112-induced apoptosis by decreasing poly(ADP-ribose) polymerase (PARP) cleavage and inactivating caspase-3, -8 and -9. Fluorouracil 9-13 poly(ADP-ribose) polymerase 1 Homo sapiens 66-93 25333998-7 2015 Further, 5-FU attenuated SNX-2112-induced apoptosis by decreasing poly(ADP-ribose) polymerase (PARP) cleavage and inactivating caspase-3, -8 and -9. Fluorouracil 9-13 poly(ADP-ribose) polymerase 1 Homo sapiens 95-99 25333998-7 2015 Further, 5-FU attenuated SNX-2112-induced apoptosis by decreasing poly(ADP-ribose) polymerase (PARP) cleavage and inactivating caspase-3, -8 and -9. Fluorouracil 9-13 caspase 3 Homo sapiens 127-147 25333998-9 2015 Moreover, 5-FU partly recovered Hsp90 client proteins, including Akt, p-Akt, inhibitor of kappaB kinase (IKK)alpha, extracellular signal-regulated kinase (ERK)1/2, and glycogen synthase kinase (GSK)-3beta, which SNX-2112 had downregulated. Fluorouracil 10-14 AKT serine/threonine kinase 1 Homo sapiens 65-68 25333998-9 2015 Moreover, 5-FU partly recovered Hsp90 client proteins, including Akt, p-Akt, inhibitor of kappaB kinase (IKK)alpha, extracellular signal-regulated kinase (ERK)1/2, and glycogen synthase kinase (GSK)-3beta, which SNX-2112 had downregulated. Fluorouracil 10-14 AKT serine/threonine kinase 1 Homo sapiens 72-75 25333998-9 2015 Moreover, 5-FU partly recovered Hsp90 client proteins, including Akt, p-Akt, inhibitor of kappaB kinase (IKK)alpha, extracellular signal-regulated kinase (ERK)1/2, and glycogen synthase kinase (GSK)-3beta, which SNX-2112 had downregulated. Fluorouracil 10-14 mitogen-activated protein kinase 1 Homo sapiens 116-162 25444672-0 2015 Silencing of CD59 enhanced the sensitivity of HT29 cells to 5-Fluorouracil and Oxaliplatin. Fluorouracil 60-74 CD59 molecule (CD59 blood group) Homo sapiens 13-17 25901475-3 2015 Recently, TAS-102 (composed of FTD and tipiracil hydrochloride, TPI) was shown to prolong the survival of patients with colorectal cancer who received a median of 2 prior therapies, including 5-FU. Fluorouracil 192-196 triosephosphate isomerase 1 Homo sapiens 64-67 25444672-1 2015 Complement regulatory proteins (CD55 and CD59) were known to be expressed in many tumors and tumor cell lines including colorectal carcinoma, and were proposed as immunotherapy targets, however whether knocking down of CD55 and CD59 will affect the sensitivity of HT-29 cells to chemotherapy drugs for example, 5-Fluorouracil and Oxaliplatin and their possible mechanisms haven"t been studied. Fluorouracil 311-325 CD59 molecule (CD59 blood group) Homo sapiens 41-45 25444672-1 2015 Complement regulatory proteins (CD55 and CD59) were known to be expressed in many tumors and tumor cell lines including colorectal carcinoma, and were proposed as immunotherapy targets, however whether knocking down of CD55 and CD59 will affect the sensitivity of HT-29 cells to chemotherapy drugs for example, 5-Fluorouracil and Oxaliplatin and their possible mechanisms haven"t been studied. Fluorouracil 311-325 CD59 molecule (CD59 blood group) Homo sapiens 228-232 25444672-5 2015 We found that silencing CD59 in HT-29 cells could significantly enhance their sensitivity to 5-FU (P < 0.05) and Oxaliplatin (P < 0.05), and significantly reduced their IC50 concentration. Fluorouracil 93-97 CD59 molecule (CD59 blood group) Homo sapiens 24-28 25333573-0 2015 Inhibition of lactate dehydrogenase A by microRNA-34a resensitizes colon cancer cells to 5-fluorouracil. Fluorouracil 89-103 lactate dehydrogenase A Homo sapiens 14-37 25333573-6 2015 In addition, 5-FU-resistant colon cancer cells exhibited upregulation of lactate dehydrogenase A (LDHA) expression and activity compared with parental cells. Fluorouracil 13-17 lactate dehydrogenase A Homo sapiens 73-96 25333670-7 2015 Overexpression of the Bcl-xl mutated (C) allele in BEL-7402 HCC cells significantly decreased fluorouracil (5-FU) sensitivity, as compared with mock transfection and overexpression of the wild-type allele. Fluorouracil 94-106 BCL2 like 1 Homo sapiens 22-28 25333670-7 2015 Overexpression of the Bcl-xl mutated (C) allele in BEL-7402 HCC cells significantly decreased fluorouracil (5-FU) sensitivity, as compared with mock transfection and overexpression of the wild-type allele. Fluorouracil 108-112 BCL2 like 1 Homo sapiens 22-28 25333573-6 2015 In addition, 5-FU-resistant colon cancer cells exhibited upregulation of lactate dehydrogenase A (LDHA) expression and activity compared with parental cells. Fluorouracil 13-17 lactate dehydrogenase A Homo sapiens 98-102 25333670-8 2015 From this, it was concluded that let-7b increased 5-FU sensitivity by repressing Bcl-xl expression in HCC cells. Fluorouracil 50-54 BCL2 like 1 Homo sapiens 81-87 25333573-8 2015 Overexpression of miR-34a reduced the expression of LDHA, probably through binding to the 3" untranslated region, leading to the re-sensitization of 5-FU-resistant cancer cells to 5-FU. Fluorouracil 149-153 lactate dehydrogenase A Homo sapiens 52-56 25333573-9 2015 Additionally, overexpression of LDHA rendered colon cancer cells resistant to 5-FU, suggesting that the miR-34a-induced sensitization to 5-FU is mediated through the inhibition of LDHA. Fluorouracil 78-82 lactate dehydrogenase A Homo sapiens 32-36 25333573-9 2015 Additionally, overexpression of LDHA rendered colon cancer cells resistant to 5-FU, suggesting that the miR-34a-induced sensitization to 5-FU is mediated through the inhibition of LDHA. Fluorouracil 137-141 lactate dehydrogenase A Homo sapiens 32-36 25333573-10 2015 In conclusion, the current study showed that miR-34a is involved in sensitivity to 5-FU in part through its effects on LDHA expression. Fluorouracil 83-87 lactate dehydrogenase A Homo sapiens 119-123 25348361-0 2015 DNA-PKcs deficiency sensitizes the human hepatoma HepG2 cells to cisplatin and 5-fluorouracil through suppression of the PI3K/Akt/NF-kappaB pathway. Fluorouracil 79-93 protein kinase, DNA-activated, catalytic subunit Homo sapiens 0-8 25351906-6 2015 5-FU and paclitaxel treatment increased the number of SP cells and JNK phosphorylation, and decreased cell survival. Fluorouracil 0-4 mitogen-activated protein kinase 8 Homo sapiens 67-70 25348361-0 2015 DNA-PKcs deficiency sensitizes the human hepatoma HepG2 cells to cisplatin and 5-fluorouracil through suppression of the PI3K/Akt/NF-kappaB pathway. Fluorouracil 79-93 AKT serine/threonine kinase 1 Homo sapiens 126-129 25348361-0 2015 DNA-PKcs deficiency sensitizes the human hepatoma HepG2 cells to cisplatin and 5-fluorouracil through suppression of the PI3K/Akt/NF-kappaB pathway. Fluorouracil 79-93 nuclear factor kappa B subunit 1 Homo sapiens 130-139 25348361-1 2015 The aim of the present study was to investigate the effects of DNA-PKcs deficiency on the chemosensitivity of human hepatoma HepG2 cells to cisplatin (CDDP) and 5-fluorouracil (5-Fu), and to explore the underlying molecular mechanism. Fluorouracil 161-175 protein kinase, DNA-activated, catalytic subunit Homo sapiens 63-71 25348361-1 2015 The aim of the present study was to investigate the effects of DNA-PKcs deficiency on the chemosensitivity of human hepatoma HepG2 cells to cisplatin (CDDP) and 5-fluorouracil (5-Fu), and to explore the underlying molecular mechanism. Fluorouracil 177-181 protein kinase, DNA-activated, catalytic subunit Homo sapiens 63-71 25348361-6 2015 DNA-PKcs suppression further reduced the Akt phosphorylation level and Bcl-2 expression in HepG2 cells exposed to CDDP and 5-Fu, but enhanced the expression of pro-apoptotic proteins p53 and caspase-3. Fluorouracil 123-127 protein kinase, DNA-activated, catalytic subunit Homo sapiens 0-8 25348361-6 2015 DNA-PKcs suppression further reduced the Akt phosphorylation level and Bcl-2 expression in HepG2 cells exposed to CDDP and 5-Fu, but enhanced the expression of pro-apoptotic proteins p53 and caspase-3. Fluorouracil 123-127 AKT serine/threonine kinase 1 Homo sapiens 41-44 25348361-8 2015 The combined treatment with CDDP and 5-Fu resulted in significantly decrease of the transcriptional activity of NF-kappaB, which was further aggravated by DNA-PKcs siRNA treatment. Fluorouracil 37-41 nuclear factor kappa B subunit 1 Homo sapiens 112-121 25348361-8 2015 The combined treatment with CDDP and 5-Fu resulted in significantly decrease of the transcriptional activity of NF-kappaB, which was further aggravated by DNA-PKcs siRNA treatment. Fluorouracil 37-41 protein kinase, DNA-activated, catalytic subunit Homo sapiens 155-163 25348361-9 2015 In conclusion, DNA-PKcs suppression had complementary effects in combination with CDDP and 5-Fu treatment in HepG2 cells, which was associated with suppression of NF-kappaB signaling pathway cascade, activation of caspase-3 and p53, as well as down-regulation of Bcl-2 and GSH. Fluorouracil 91-95 protein kinase, DNA-activated, catalytic subunit Homo sapiens 15-23 25348361-9 2015 In conclusion, DNA-PKcs suppression had complementary effects in combination with CDDP and 5-Fu treatment in HepG2 cells, which was associated with suppression of NF-kappaB signaling pathway cascade, activation of caspase-3 and p53, as well as down-regulation of Bcl-2 and GSH. Fluorouracil 91-95 nuclear factor kappa B subunit 1 Homo sapiens 163-172 25348361-9 2015 In conclusion, DNA-PKcs suppression had complementary effects in combination with CDDP and 5-Fu treatment in HepG2 cells, which was associated with suppression of NF-kappaB signaling pathway cascade, activation of caspase-3 and p53, as well as down-regulation of Bcl-2 and GSH. Fluorouracil 91-95 caspase 3 Homo sapiens 214-223 25348361-9 2015 In conclusion, DNA-PKcs suppression had complementary effects in combination with CDDP and 5-Fu treatment in HepG2 cells, which was associated with suppression of NF-kappaB signaling pathway cascade, activation of caspase-3 and p53, as well as down-regulation of Bcl-2 and GSH. Fluorouracil 91-95 tumor protein p53 Homo sapiens 228-231 25348361-9 2015 In conclusion, DNA-PKcs suppression had complementary effects in combination with CDDP and 5-Fu treatment in HepG2 cells, which was associated with suppression of NF-kappaB signaling pathway cascade, activation of caspase-3 and p53, as well as down-regulation of Bcl-2 and GSH. Fluorouracil 91-95 BCL2 apoptosis regulator Homo sapiens 263-268 25426562-7 2015 In PAK6-knockdown cells treated with 5-FU, cell viability and phosphorylation of BAD decreased, and the number of apoptotic cells, levels of cleaved caspase 3 and PARP increased compared to control cells. Fluorouracil 37-41 poly(ADP-ribose) polymerase 1 Homo sapiens 163-167 26492225-7 2015 5-FU in combination with berberine or curcumin showed a synergistic inhibition of survivin and STAT3 level resulting in enhanced cell death in gastric cancer cells. Fluorouracil 0-4 signal transducer and activator of transcription 3 Homo sapiens 95-100 25473894-5 2015 Significantly, JNK inhibition promoted 5-FU- and GEM-induced increase in intracellular reactive oxygen species (ROS), and scavenging intracellular ROS by use of N-acetylcysteine impaired JNK inhibition-mediated promotion of the cytotoxicity of 5-FU and GEM. Fluorouracil 244-248 mitogen-activated protein kinase 8 Homo sapiens 15-18 25473894-3 2015 Here we show that JNK, which is upregulated in pancreatic CSCs and contributes to their maintenance, is critically involved in the resistance of pancreatic CSCs to 5-fluorouracil (5-FU) and gemcitabine (GEM). Fluorouracil 164-178 mitogen-activated protein kinase 8 Homo sapiens 18-21 25473894-5 2015 Significantly, JNK inhibition promoted 5-FU- and GEM-induced increase in intracellular reactive oxygen species (ROS), and scavenging intracellular ROS by use of N-acetylcysteine impaired JNK inhibition-mediated promotion of the cytotoxicity of 5-FU and GEM. Fluorouracil 244-248 mitogen-activated protein kinase 8 Homo sapiens 187-190 25473894-3 2015 Here we show that JNK, which is upregulated in pancreatic CSCs and contributes to their maintenance, is critically involved in the resistance of pancreatic CSCs to 5-fluorouracil (5-FU) and gemcitabine (GEM). Fluorouracil 180-184 mitogen-activated protein kinase 8 Homo sapiens 18-21 25473894-4 2015 We found that JNK inhibition effectively sensitizes otherwise chemoresistant pancreatic CSCs to 5-FU and GEM. Fluorouracil 96-100 mitogen-activated protein kinase 8 Homo sapiens 14-17 25473894-5 2015 Significantly, JNK inhibition promoted 5-FU- and GEM-induced increase in intracellular reactive oxygen species (ROS), and scavenging intracellular ROS by use of N-acetylcysteine impaired JNK inhibition-mediated promotion of the cytotoxicity of 5-FU and GEM. Fluorouracil 39-43 mitogen-activated protein kinase 8 Homo sapiens 15-18 25473894-5 2015 Significantly, JNK inhibition promoted 5-FU- and GEM-induced increase in intracellular reactive oxygen species (ROS), and scavenging intracellular ROS by use of N-acetylcysteine impaired JNK inhibition-mediated promotion of the cytotoxicity of 5-FU and GEM. Fluorouracil 39-43 mitogen-activated protein kinase 8 Homo sapiens 187-190 25327479-0 2015 Silencing of high-mobility group box 2 (HMGB2) modulates cisplatin and 5-fluorouracil sensitivity in head and neck squamous cell carcinoma. Fluorouracil 71-85 high mobility group box 2 Homo sapiens 13-38 25327479-0 2015 Silencing of high-mobility group box 2 (HMGB2) modulates cisplatin and 5-fluorouracil sensitivity in head and neck squamous cell carcinoma. Fluorouracil 71-85 high mobility group box 2 Homo sapiens 40-45 25327479-11 2015 We observed that siRNA-mediated silencing of HMGB2 increased the sensitivity of the HNSCC cell lines to cisplatin and 5-FU. Fluorouracil 118-122 high mobility group box 2 Homo sapiens 45-50 25553117-5 2015 The present study also demonstrated that in contrast to the classical chemotherapy drug 5-fluorouracil, which increased the proportion of side population cells and upregulated the expression of COX-2, parthenolide, a naturally occurring small molecule, preferentially targeted the side population cells of nasopharyngeal carcinoma cells and downregulated COX-2. Fluorouracil 88-102 prostaglandin-endoperoxide synthase 2 Homo sapiens 194-199 25553117-5 2015 The present study also demonstrated that in contrast to the classical chemotherapy drug 5-fluorouracil, which increased the proportion of side population cells and upregulated the expression of COX-2, parthenolide, a naturally occurring small molecule, preferentially targeted the side population cells of nasopharyngeal carcinoma cells and downregulated COX-2. Fluorouracil 88-102 prostaglandin-endoperoxide synthase 2 Homo sapiens 355-360 25431427-0 2014 RNA interference-mediated knockdown of astrocyte elevated gene-1 inhibits growth, induces apoptosis, and increases the chemosensitivity to 5-fluorouracil in renal cancer Caki-1 cells. Fluorouracil 139-153 metadherin Homo sapiens 39-64 25431427-8 2014 Finally, AEG-1 knockdown in Caki-1 cells remarkably suppressed cell proliferation and enhanced cell apoptosis in response to 5-fluorouracil (5-FU) treatment, suggesting that AEG-1 inhibition sensitizes Caki-1 cells to 5-FU. Fluorouracil 125-139 metadherin Homo sapiens 9-14 25431427-8 2014 Finally, AEG-1 knockdown in Caki-1 cells remarkably suppressed cell proliferation and enhanced cell apoptosis in response to 5-fluorouracil (5-FU) treatment, suggesting that AEG-1 inhibition sensitizes Caki-1 cells to 5-FU. Fluorouracil 125-139 metadherin Homo sapiens 174-179 25431427-8 2014 Finally, AEG-1 knockdown in Caki-1 cells remarkably suppressed cell proliferation and enhanced cell apoptosis in response to 5-fluorouracil (5-FU) treatment, suggesting that AEG-1 inhibition sensitizes Caki-1 cells to 5-FU. Fluorouracil 141-145 metadherin Homo sapiens 9-14 25431427-8 2014 Finally, AEG-1 knockdown in Caki-1 cells remarkably suppressed cell proliferation and enhanced cell apoptosis in response to 5-fluorouracil (5-FU) treatment, suggesting that AEG-1 inhibition sensitizes Caki-1 cells to 5-FU. Fluorouracil 141-145 metadherin Homo sapiens 174-179 25431427-8 2014 Finally, AEG-1 knockdown in Caki-1 cells remarkably suppressed cell proliferation and enhanced cell apoptosis in response to 5-fluorouracil (5-FU) treatment, suggesting that AEG-1 inhibition sensitizes Caki-1 cells to 5-FU. Fluorouracil 218-222 metadherin Homo sapiens 9-14 25431427-8 2014 Finally, AEG-1 knockdown in Caki-1 cells remarkably suppressed cell proliferation and enhanced cell apoptosis in response to 5-fluorouracil (5-FU) treatment, suggesting that AEG-1 inhibition sensitizes Caki-1 cells to 5-FU. Fluorouracil 218-222 metadherin Homo sapiens 174-179 25565817-5 2015 Herein, we report that NPs conjugated with antibody against GRP78 (mAb GRP78-NPs) inhibit the adhesion, invasion, and metastasis of hepatocellular carcinoma (HCC) and promote drug delivery of 5-fluorouracil into GRP78 high-expressed human hepatocellular carcinoma cells. Fluorouracil 192-206 heat shock protein family A (Hsp70) member 5 Homo sapiens 60-65 25565817-5 2015 Herein, we report that NPs conjugated with antibody against GRP78 (mAb GRP78-NPs) inhibit the adhesion, invasion, and metastasis of hepatocellular carcinoma (HCC) and promote drug delivery of 5-fluorouracil into GRP78 high-expressed human hepatocellular carcinoma cells. Fluorouracil 192-206 heat shock protein family A (Hsp70) member 5 Homo sapiens 71-80 25565817-5 2015 Herein, we report that NPs conjugated with antibody against GRP78 (mAb GRP78-NPs) inhibit the adhesion, invasion, and metastasis of hepatocellular carcinoma (HCC) and promote drug delivery of 5-fluorouracil into GRP78 high-expressed human hepatocellular carcinoma cells. Fluorouracil 192-206 heat shock protein family A (Hsp70) member 5 Homo sapiens 71-76 25401416-6 2014 A panel of genes was examined by qPCR coupled to p53 activation by Doxo, 5-Fluoruracil and Nutlin-3a, or to p53 or NFkappaB inhibition. Fluorouracil 73-86 tumor protein p53 Homo sapiens 49-52 25294903-0 2014 DNA methylation status of key cell-cycle regulators such as CDKNA2/p16 and CCNA1 correlates with treatment response to doxorubicin and 5-fluorouracil in locally advanced breast tumors. Fluorouracil 135-149 cyclin dependent kinase inhibitor 2A Homo sapiens 67-70 25430880-6 2014 Activity of SGC7901/ADR cells transfected with Vav3-siRNA combined with 5-fluorouracil/oxaliplatin was much lower than that of control groups, and MDR1/P-gp, GST-pi and Bcl-2, Bax genes were significantly downregulated in Vav3-siRNA transfection group. Fluorouracil 72-86 aldo-keto reductase family 1 member B Homo sapiens 20-23 25516776-7 2014 Rodel et al reported on the CAO/ARO/AIO-04 randomized phase III trial that compared standard treatment with 5-FU and radiation therapy, to oxaliplatin plus 5-FU in association with radiation therapy. Fluorouracil 108-112 cytochrome P450 family 19 subfamily A member 1 Homo sapiens 32-35 25516776-7 2014 Rodel et al reported on the CAO/ARO/AIO-04 randomized phase III trial that compared standard treatment with 5-FU and radiation therapy, to oxaliplatin plus 5-FU in association with radiation therapy. Fluorouracil 156-160 cytochrome P450 family 19 subfamily A member 1 Homo sapiens 32-35 25430880-6 2014 Activity of SGC7901/ADR cells transfected with Vav3-siRNA combined with 5-fluorouracil/oxaliplatin was much lower than that of control groups, and MDR1/P-gp, GST-pi and Bcl-2, Bax genes were significantly downregulated in Vav3-siRNA transfection group. Fluorouracil 72-86 vav guanine nucleotide exchange factor 3 Homo sapiens 47-51 25124805-6 2014 Whereas 5-FU was found to increase %MN-RET, no significant increases were observed for RBC(CD59-) or RET(CD59-) at any of the time points studied. Fluorouracil 8-12 RET Sus scrofa 39-42 25085076-1 2014 The aim of this study was to investigate the prognostic and predictive values of phospholipase C gamma 1 (PLCG1) expression in patients with locally advanced and resectable oral squamous cell carcinoma (OSCC), who were treated in a prospective, randomized, phase 3 trial evaluating standard treatment with surgery and postoperative radiation preceded or not by induction docetaxel, cisplatin, and 5-fluorouracil (TPF). Fluorouracil 397-411 phospholipase C gamma 1 Homo sapiens 81-104 25085076-1 2014 The aim of this study was to investigate the prognostic and predictive values of phospholipase C gamma 1 (PLCG1) expression in patients with locally advanced and resectable oral squamous cell carcinoma (OSCC), who were treated in a prospective, randomized, phase 3 trial evaluating standard treatment with surgery and postoperative radiation preceded or not by induction docetaxel, cisplatin, and 5-fluorouracil (TPF). Fluorouracil 397-411 phospholipase C gamma 1 Homo sapiens 106-111 25230779-12 2014 Notably, Akt inhibition by LY294002 restored the 5-FU cytotoxicity suppressed by CD133 overexpression, while Akt activation by epidermal growth factor reversed the 5-FU cytotoxicity enhanced by CD133 silencing. Fluorouracil 49-53 AKT serine/threonine kinase 1 Homo sapiens 9-12 25154726-5 2014 Further, patients in the MSS and BRAF-wild type group with stage IIIA CRC had favorable outcomes to 5-FU monotherapy, similar to those with stage II CRC. Fluorouracil 100-104 B-Raf proto-oncogene, serine/threonine kinase Homo sapiens 33-37 25230779-12 2014 Notably, Akt inhibition by LY294002 restored the 5-FU cytotoxicity suppressed by CD133 overexpression, while Akt activation by epidermal growth factor reversed the 5-FU cytotoxicity enhanced by CD133 silencing. Fluorouracil 164-168 AKT serine/threonine kinase 1 Homo sapiens 9-12 25230779-12 2014 Notably, Akt inhibition by LY294002 restored the 5-FU cytotoxicity suppressed by CD133 overexpression, while Akt activation by epidermal growth factor reversed the 5-FU cytotoxicity enhanced by CD133 silencing. Fluorouracil 164-168 AKT serine/threonine kinase 1 Homo sapiens 109-112 25230779-13 2014 Therefore, CD133 may inhibit 5-FU-induced apoptosis by regulating the expression of P-gp and Bcl-2 family mediated by phosphoinositide 3-kinase/Akt/p70S6K pathway in GC cells. Fluorouracil 29-33 ATP binding cassette subfamily B member 1 Homo sapiens 84-88 25364415-4 2014 Treatment with a selective inhibitor, p38 mitogen-activated protein kinase (MAPK; SB203580), caused the dose-dependent suppression of HSP27 phosphorylation, which was upregulated by 5-FU, reducing the half maximal inhibitory concentration values of 5-FU in the HCT116 and HCT15 cells. Fluorouracil 182-186 mitogen-activated protein kinase 14 Homo sapiens 38-74 25364415-4 2014 Treatment with a selective inhibitor, p38 mitogen-activated protein kinase (MAPK; SB203580), caused the dose-dependent suppression of HSP27 phosphorylation, which was upregulated by 5-FU, reducing the half maximal inhibitory concentration values of 5-FU in the HCT116 and HCT15 cells. Fluorouracil 249-253 mitogen-activated protein kinase 14 Homo sapiens 38-74 25230779-13 2014 Therefore, CD133 may inhibit 5-FU-induced apoptosis by regulating the expression of P-gp and Bcl-2 family mediated by phosphoinositide 3-kinase/Akt/p70S6K pathway in GC cells. Fluorouracil 29-33 BCL2 apoptosis regulator Homo sapiens 93-98 25230779-13 2014 Therefore, CD133 may inhibit 5-FU-induced apoptosis by regulating the expression of P-gp and Bcl-2 family mediated by phosphoinositide 3-kinase/Akt/p70S6K pathway in GC cells. Fluorouracil 29-33 AKT serine/threonine kinase 1 Homo sapiens 144-147 25344912-6 2014 Moreover, significantly higher expression level of p-AKT was observed in fluorouracil (5-FU)-resistant esophageal cancer cells. Fluorouracil 73-85 AKT serine/threonine kinase 1 Homo sapiens 53-56 25344912-6 2014 Moreover, significantly higher expression level of p-AKT was observed in fluorouracil (5-FU)-resistant esophageal cancer cells. Fluorouracil 87-91 AKT serine/threonine kinase 1 Homo sapiens 53-56 25427200-7 2014 Furthermore, c-Met knockdown enhanced the anti-proliferative effects of 5-FU and Taxol but not cisplatin, irinotecan or sorafenib. Fluorouracil 72-76 MET proto-oncogene, receptor tyrosine kinase Homo sapiens 13-18 25194504-4 2014 We demonstrated that transforming growth factor-beta1 (TGF-beta1)-induced EMT in the human cholangiocarcinoma (CCA) cell line, TFK-1, resulted in the acquisition of mesenchymal traits, as well as the expression of ALDH, which was accompanied by decreased sensitivity to the chemotherapeutic agent, 5-fluorouracil. Fluorouracil 298-312 transforming growth factor beta 1 Homo sapiens 21-53 25194504-4 2014 We demonstrated that transforming growth factor-beta1 (TGF-beta1)-induced EMT in the human cholangiocarcinoma (CCA) cell line, TFK-1, resulted in the acquisition of mesenchymal traits, as well as the expression of ALDH, which was accompanied by decreased sensitivity to the chemotherapeutic agent, 5-fluorouracil. Fluorouracil 298-312 transforming growth factor beta 1 Homo sapiens 55-64 25400452-5 2014 Intracellular signaling pathways are an integrated network, and nuclear factor kappa-light-chain-enhancer of activated B cells, AKT and extracellular signal-regulated kinases are signaling pathways that are particularly relevant to 5-FU resistance. Fluorouracil 232-236 AKT serine/threonine kinase 1 Homo sapiens 128-131 25389767-5 2014 Incubating the cells with 5-FU increased the expression of nucleotide-binding domain and leucine-rich repeat containing PYD-3 (NLRP3) and caspase-1. Fluorouracil 26-30 NLR family pyrin domain containing 3 Homo sapiens 127-132 25426963-4 2014 This HIF-1alpha-activated protein switch (Haps59) is designed to increase its ability to convert the prodrug 5-fluorocytosine into the chemotherapeutic 5-fluorouracil in a HIF-1alpha-dependent manner. Fluorouracil 152-166 hypoxia inducible factor 1 subunit alpha Homo sapiens 5-15 25426963-4 2014 This HIF-1alpha-activated protein switch (Haps59) is designed to increase its ability to convert the prodrug 5-fluorocytosine into the chemotherapeutic 5-fluorouracil in a HIF-1alpha-dependent manner. Fluorouracil 152-166 hypoxia inducible factor 1 subunit alpha Homo sapiens 172-182 25389767-5 2014 Incubating the cells with 5-FU increased the expression of nucleotide-binding domain and leucine-rich repeat containing PYD-3 (NLRP3) and caspase-1. Fluorouracil 26-30 caspase 1 Homo sapiens 138-147 25389767-6 2014 The cleavage of caspase-1 was observed in 5-FU-treated cells, which was followed by an increased secretion of interleukin (IL)-1beta. Fluorouracil 42-46 caspase 1 Homo sapiens 16-25 25389767-6 2014 The cleavage of caspase-1 was observed in 5-FU-treated cells, which was followed by an increased secretion of interleukin (IL)-1beta. Fluorouracil 42-46 interleukin 1 beta Homo sapiens 110-132 25389767-7 2014 The inhibition of the NLRP3 pathway slightly decreased the effects of 5-FU on cell viability and LDH release, suggesting that NLRP3 may be in part involved in 5-FU-induced cell death. Fluorouracil 70-74 NLR family pyrin domain containing 3 Homo sapiens 22-27 25389767-7 2014 The inhibition of the NLRP3 pathway slightly decreased the effects of 5-FU on cell viability and LDH release, suggesting that NLRP3 may be in part involved in 5-FU-induced cell death. Fluorouracil 70-74 NLR family pyrin domain containing 3 Homo sapiens 126-131 25389767-7 2014 The inhibition of the NLRP3 pathway slightly decreased the effects of 5-FU on cell viability and LDH release, suggesting that NLRP3 may be in part involved in 5-FU-induced cell death. Fluorouracil 159-163 NLR family pyrin domain containing 3 Homo sapiens 22-27 25389767-7 2014 The inhibition of the NLRP3 pathway slightly decreased the effects of 5-FU on cell viability and LDH release, suggesting that NLRP3 may be in part involved in 5-FU-induced cell death. Fluorouracil 159-163 NLR family pyrin domain containing 3 Homo sapiens 126-131 25386059-1 2014 S-1 is an oral 5-fluorouracil (5-FU) prodrug, which is designed to improve the antitumor activity of 5-FU by inhibiting dihydropyrimidine dehydrogenase, the key enzyme of 5-FU catabolism. Fluorouracil 15-29 proteasome 26S subunit, non-ATPase 1 Homo sapiens 0-3 25386059-1 2014 S-1 is an oral 5-fluorouracil (5-FU) prodrug, which is designed to improve the antitumor activity of 5-FU by inhibiting dihydropyrimidine dehydrogenase, the key enzyme of 5-FU catabolism. Fluorouracil 31-35 proteasome 26S subunit, non-ATPase 1 Homo sapiens 0-3 25386059-1 2014 S-1 is an oral 5-fluorouracil (5-FU) prodrug, which is designed to improve the antitumor activity of 5-FU by inhibiting dihydropyrimidine dehydrogenase, the key enzyme of 5-FU catabolism. Fluorouracil 101-105 proteasome 26S subunit, non-ATPase 1 Homo sapiens 0-3 25386059-1 2014 S-1 is an oral 5-fluorouracil (5-FU) prodrug, which is designed to improve the antitumor activity of 5-FU by inhibiting dihydropyrimidine dehydrogenase, the key enzyme of 5-FU catabolism. Fluorouracil 101-105 proteasome 26S subunit, non-ATPase 1 Homo sapiens 0-3 25178657-0 2014 5-Fluorouracil causes severe CNS demyelination by disruption of TCF7L2/HDAC1/HDAC2 complex in adolescent mice. Fluorouracil 0-14 histone deacetylase 2 Mus musculus 77-82 25375110-2 2014 TDG preferentially catalyzes the removal of thymine and uracil paired with guanine, and is also active on 5-fluorouracil (5-FU) paired with adenine or guanine. Fluorouracil 106-120 thymine DNA glycosylase Homo sapiens 0-3 25375110-2 2014 TDG preferentially catalyzes the removal of thymine and uracil paired with guanine, and is also active on 5-fluorouracil (5-FU) paired with adenine or guanine. Fluorouracil 122-126 thymine DNA glycosylase Homo sapiens 0-3 25699390-0 2014 Effects of hypoxia-inducible factor-1alpha silencing on drug resistance of human pancreatic cancer cell line Patu8988/5-Fu. Fluorouracil 118-122 hypoxia inducible factor 1 subunit alpha Homo sapiens 11-42 25178657-6 2014 Inhibition of crucial myelination-promoting factors by 5-FU is more significantly antagonized by co-transfection of TCF7L2, HDAC1 and HDAC2 than TCF7L2 alone. Fluorouracil 55-59 histone deacetylase 2 Mus musculus 134-139 25178657-7 2014 Our findings reveal that 5-FU could acutely induce the severe myelin degeneration in adolescence and disruption of TCF7L2/HDAC1/HDAC2 complex is at least partially involved in 5-FU-induced demyelination. Fluorouracil 176-180 histone deacetylase 2 Mus musculus 128-133 25141914-0 2014 Interaction of the 5-fluorouracil analog 5-fluoro-2"-deoxyuridine with "N" and "B" isoforms of human serum albumin: a spectroscopic and calorimetric study. Fluorouracil 19-33 albumin Homo sapiens 101-114 25135238-13 2014 CONCLUSIONS: The biomarker TP53 divides esophageal cancer patients into 2 categories with markedly different outcomes: patients with a normal TP53 marker status may experience notable benefits from neoadjuvant chemotherapy with cisplatin/fluorouracil, whereas those with a mutant TP53 marker status appear to be at risk for lack of response. Fluorouracil 238-250 tumor protein p53 Homo sapiens 27-31 25421769-9 2014 After treatment of 5-FU, cell proliferation was significantly inhibited, but cell apoptosis was significantly increased in DAPK over-expression group compared to FAM-siRNA group (P < 0.05). Fluorouracil 19-23 death associated protein kinase 1 Homo sapiens 123-127 25443274-5 2014 A second clinical trial was planned that will examine the relationship between expression of the DNA repair protein MRE11 and complete response in patients treated with concurrent 5-fluorouracil/mitomycin C plus radiation. Fluorouracil 180-194 MRE11 homolog, double strand break repair nuclease Homo sapiens 116-121 25149123-9 2014 Moreover, 5-fluorouracil (5-Fu) loaded FA-CM-beta-CD-BSA NPs down-regulate ATP levels and increase the expression of caspase-3. Fluorouracil 10-24 caspase 3 Homo sapiens 117-126 25301724-0 2014 Targeting the DNA replication checkpoint by pharmacologic inhibition of Chk1 kinase: a strategy to sensitize APC mutant colon cancer cells to 5-fluorouracil chemotherapy. Fluorouracil 142-156 checkpoint kinase 1 Homo sapiens 72-76 25301724-6 2014 Furthermore, we could increase sensitivity of APC truncated cells to 5-FU by inactivating the Chk1 kinase using drug treatment or siRNA-mediated knockdown. Fluorouracil 69-73 checkpoint kinase 1 Homo sapiens 94-98 25301724-7 2014 Our findings identify mutant APC as a potential tumor biomarker of resistance to 5-FU, and importantly we show that APC-mutant CRC cells can be made more sensitive to 5-FU by use of Chk1 inhibitors. Fluorouracil 167-171 checkpoint kinase 1 Homo sapiens 182-186 25419401-4 2014 Vascular endothelial growth factor and base fibroblast growth factor reduced obviously in SU6668+5-Fu group, SU6668 group and 5-Fu group compared with control group, and there were significant differences among SU6668+5-Fu group, SU6668 group and 5-Fu group (P<0.05). Fluorouracil 97-101 vascular endothelial growth factor A Homo sapiens 0-34 25419401-4 2014 Vascular endothelial growth factor and base fibroblast growth factor reduced obviously in SU6668+5-Fu group, SU6668 group and 5-Fu group compared with control group, and there were significant differences among SU6668+5-Fu group, SU6668 group and 5-Fu group (P<0.05). Fluorouracil 126-130 vascular endothelial growth factor A Homo sapiens 0-34 25419401-4 2014 Vascular endothelial growth factor and base fibroblast growth factor reduced obviously in SU6668+5-Fu group, SU6668 group and 5-Fu group compared with control group, and there were significant differences among SU6668+5-Fu group, SU6668 group and 5-Fu group (P<0.05). Fluorouracil 126-130 vascular endothelial growth factor A Homo sapiens 0-34 25149123-9 2014 Moreover, 5-fluorouracil (5-Fu) loaded FA-CM-beta-CD-BSA NPs down-regulate ATP levels and increase the expression of caspase-3. Fluorouracil 26-30 caspase 3 Homo sapiens 117-126 25419401-4 2014 Vascular endothelial growth factor and base fibroblast growth factor reduced obviously in SU6668+5-Fu group, SU6668 group and 5-Fu group compared with control group, and there were significant differences among SU6668+5-Fu group, SU6668 group and 5-Fu group (P<0.05). Fluorouracil 126-130 vascular endothelial growth factor A Homo sapiens 0-34 24583265-4 2014 We show that both ORAI1 and STIM1 play pro-survival anti-apoptotic role in pancreatic adenocarcinoma cell lines, as siRNA-mediated knockdown of ORAI1 and/or STIM1 increases apoptosis induced by chemotherapy drugs 5-fluorouracil (5-FU) or gemcitabine. Fluorouracil 213-227 stromal interaction molecule 1 Homo sapiens 28-33 25550779-8 2014 In cancer cells, transfection of lentivirus containing miR-137 mimic was able to markedly upregulate endogenous expression of miR-137, inhibited cancer cell invasion and increased sensitivities to chemotherapy reagent 5-FU. Fluorouracil 218-222 microRNA 137 Homo sapiens 55-62 24583265-4 2014 We show that both ORAI1 and STIM1 play pro-survival anti-apoptotic role in pancreatic adenocarcinoma cell lines, as siRNA-mediated knockdown of ORAI1 and/or STIM1 increases apoptosis induced by chemotherapy drugs 5-fluorouracil (5-FU) or gemcitabine. Fluorouracil 229-233 stromal interaction molecule 1 Homo sapiens 28-33 24583265-5 2014 We also demonstrate that both 5-FU and gemcitabine treatments increase SOCE in Panc1 pancreatic adenocarcinoma cell line via upregulation of ORAI1 and STIM1. Fluorouracil 30-34 stromal interaction molecule 1 Homo sapiens 151-156 25063444-5 2014 In CRC cells, IL-22 was able to attenuate the cytotoxic and apoptosis-inducing effects of 5-FU and OXA by activating the STAT3 pathway and subsequently increasing the expression of anti-apoptotic genes. Fluorouracil 90-94 signal transducer and activator of transcription 3 Homo sapiens 121-126 25063444-6 2014 In addition, IL-22 conferred resistance to 5-FU and OXA by inducing IL-8 autocrine expression through STAT3 activation. Fluorouracil 43-47 C-X-C motif chemokine ligand 8 Homo sapiens 68-72 25063444-6 2014 In addition, IL-22 conferred resistance to 5-FU and OXA by inducing IL-8 autocrine expression through STAT3 activation. Fluorouracil 43-47 signal transducer and activator of transcription 3 Homo sapiens 102-107 25050539-8 2014 Among these, collapsin response mediator protein 2 (CRMP-2), DNA replication complex GINS protein PSF2 (PSF-2) and selenium-binding protein 1 (SBP-1) were notable not only for their differential expression but also for decreased expression following 5-FU exposure, indicating their possible roles as novel biomarkers for sensitivity (CRMP-2, PSF-2) as well as resistance (SBP-1) to 5-FU. Fluorouracil 250-254 dihydropyrimidinase like 2 Homo sapiens 13-50 25050539-6 2014 Notably, the level of p-mTOR decreased upon 5-FU exposure in the monolayers, while its level was higher in the MCSs. Fluorouracil 44-48 mechanistic target of rapamycin kinase Homo sapiens 24-28 25050539-8 2014 Among these, collapsin response mediator protein 2 (CRMP-2), DNA replication complex GINS protein PSF2 (PSF-2) and selenium-binding protein 1 (SBP-1) were notable not only for their differential expression but also for decreased expression following 5-FU exposure, indicating their possible roles as novel biomarkers for sensitivity (CRMP-2, PSF-2) as well as resistance (SBP-1) to 5-FU. Fluorouracil 250-254 dihydropyrimidinase like 2 Homo sapiens 52-58 25050539-8 2014 Among these, collapsin response mediator protein 2 (CRMP-2), DNA replication complex GINS protein PSF2 (PSF-2) and selenium-binding protein 1 (SBP-1) were notable not only for their differential expression but also for decreased expression following 5-FU exposure, indicating their possible roles as novel biomarkers for sensitivity (CRMP-2, PSF-2) as well as resistance (SBP-1) to 5-FU. Fluorouracil 382-386 dihydropyrimidinase like 2 Homo sapiens 13-50 25050539-8 2014 Among these, collapsin response mediator protein 2 (CRMP-2), DNA replication complex GINS protein PSF2 (PSF-2) and selenium-binding protein 1 (SBP-1) were notable not only for their differential expression but also for decreased expression following 5-FU exposure, indicating their possible roles as novel biomarkers for sensitivity (CRMP-2, PSF-2) as well as resistance (SBP-1) to 5-FU. Fluorouracil 382-386 dihydropyrimidinase like 2 Homo sapiens 52-58 26279976-2 2014 5-Fluorouracil (5-FU)-encapsulated low density lipid nanoparticles (LDLN) were prepared by the emulsion congealing method which mimics the plasma-derived LDL by acquiring the apolipoprotein B-100 from the blood. Fluorouracil 0-14 apolipoprotein B Homo sapiens 175-195 24928731-3 2014 Compounds 4f and 4i were more potent than 5-Fu against T24 and MGC-803 cells with the IC50 values of 4.43 and 8.45 muM, respectively. Fluorouracil 42-46 latexin Homo sapiens 115-118 25233213-0 2014 tRNA modifying enzymes, NSUN2 and METTL1, determine sensitivity to 5-fluorouracil in HeLa cells. Fluorouracil 67-81 NOP2/Sun RNA methyltransferase 2 Homo sapiens 24-29 25233213-4 2014 Here, we show that combined knockdown of NSUN2 and METTL1 in HeLa cells drastically potentiate sensitivity of cells to 5-fluorouracil (5-FU) whereas heat stress of cells revealed no effects. Fluorouracil 119-133 NOP2/Sun RNA methyltransferase 2 Homo sapiens 41-46 25233213-4 2014 Here, we show that combined knockdown of NSUN2 and METTL1 in HeLa cells drastically potentiate sensitivity of cells to 5-fluorouracil (5-FU) whereas heat stress of cells revealed no effects. Fluorouracil 135-139 NOP2/Sun RNA methyltransferase 2 Homo sapiens 41-46 25016234-3 2014 Particularly, compound 28 showed a two-fold improvement compared to fluorouracil in inhibiting MDA-MB-231 and A549 cell proliferation with IC50 values of 7.46 and 12.78 muM, respectively. Fluorouracil 68-80 latexin Homo sapiens 169-172 24972040-10 2014 Under the present conditions, the expression levels of CXCL1, CXCL2, CXCL3, the neutrophil markers Elane and MPO, as well as Ly-6G-positive neutrophils, in the colon were significantly increased by 5-FU. Fluorouracil 198-202 chemokine (C-X-C motif) ligand 1 Mus musculus 55-60 26279976-2 2014 5-Fluorouracil (5-FU)-encapsulated low density lipid nanoparticles (LDLN) were prepared by the emulsion congealing method which mimics the plasma-derived LDL by acquiring the apolipoprotein B-100 from the blood. Fluorouracil 16-20 apolipoprotein B Homo sapiens 175-195 25134433-4 2014 METHODS: NF-kappaB reporter cells were established and treated with 5-fluorouracil (5-FU, DNA/RNA damaging), oxaliplatin (DNA damaging), camptothecin (CTP, topoisomerase inhibitor), phleomycin (radiomimetic), or erlotinib (EGFR inhibitor). Fluorouracil 68-82 nuclear factor kappa B subunit 1 Homo sapiens 9-18 25134433-4 2014 METHODS: NF-kappaB reporter cells were established and treated with 5-fluorouracil (5-FU, DNA/RNA damaging), oxaliplatin (DNA damaging), camptothecin (CTP, topoisomerase inhibitor), phleomycin (radiomimetic), or erlotinib (EGFR inhibitor). Fluorouracil 84-88 nuclear factor kappa B subunit 1 Homo sapiens 9-18 25140293-12 2014 We demonstrate that the combination of S-1 (5-FU) and eribulin exerts a synergistic effect for TNBC cell lines through MET-induction by eribulin. Fluorouracil 44-48 proteasome 26S subunit, non-ATPase 1 Homo sapiens 39-42 24962565-2 2014 TDG mediates the cytotoxicity of the anti-cancer chemotherapeutic drug 5-fluorouracil (5-FU) by prolonging S phase, generating DNA strand breaks, and inducing DNA damage signaling. Fluorouracil 71-85 thymine DNA glycosylase Homo sapiens 0-3 24962565-2 2014 TDG mediates the cytotoxicity of the anti-cancer chemotherapeutic drug 5-fluorouracil (5-FU) by prolonging S phase, generating DNA strand breaks, and inducing DNA damage signaling. Fluorouracil 87-91 thymine DNA glycosylase Homo sapiens 0-3 24962565-8 2014 Compared with forced expression of wild type TDG, CRL4(Cdt2)- resistant TDG (DeltaPIP) slows cell proliferation and slightly increases the toxicity of 5-FU. Fluorouracil 151-155 thymine DNA glycosylase Homo sapiens 72-75 25110412-3 2014 Resistance to cisplatin, irinotecan and 5-fluorouracil chemotherapy has been shown to involve mitogen-activated protein kinase (MAPK) signaling and recent studies identified p38alpha MAPK as a mediator of resistance to various agents in CRC patients. Fluorouracil 40-54 mitogen-activated protein kinase 14 Homo sapiens 174-182 24800927-11 2014 Taken together, activation of CXCL4 expression by 5-FU in mice participates in 5-FU-induced intestinal mucositis through upregulation of p53 via activation of p38-MAPK, and CXCL4mab is potentially beneficial in preventing CIM in the intestinal tract. Fluorouracil 50-54 platelet factor 4 Mus musculus 173-178 24712391-5 2014 The improvements in therapeutic response over either PTX-VE or 5-FU-TPGS therapy alone were demonstrated by the ability to effectively induce the apoptosis of tumor cells via up-regulation of tumor suppressor p53 and beta-tubulin and by the significant inhibition of cell cycle progression. Fluorouracil 63-67 tumor protein p53 Homo sapiens 209-212 24800927-0 2014 Activation of p38-MAPK by CXCL4/CXCR3 axis contributes to p53-dependent intestinal apoptosis initiated by 5-fluorouracil. Fluorouracil 106-120 platelet factor 4 Mus musculus 26-31 24800927-6 2014 CXCL4 and its receptor CXCR3 were confirmed at both the gene and protein levels to be homeostatically regulated during 5-FU-induced mucositis. Fluorouracil 119-123 platelet factor 4 Mus musculus 0-5 24800927-11 2014 Taken together, activation of CXCL4 expression by 5-FU in mice participates in 5-FU-induced intestinal mucositis through upregulation of p53 via activation of p38-MAPK, and CXCL4mab is potentially beneficial in preventing CIM in the intestinal tract. Fluorouracil 79-83 platelet factor 4 Mus musculus 30-35 24800927-8 2014 Mechanistically, CXCL4mab reduced the apoptosis of the crypt epithelia by suppression of the 5-FU-induced expression of p53 and Bax through its receptor CXCR3. Fluorouracil 93-97 platelet factor 4 Mus musculus 17-22 24801380-0 2014 Doxorubicin and 5-fluorouracil induced accumulation and transcriptional activity of p53 are independent of the phosphorylation at serine 15 in MCF-7 breast cancer cells. Fluorouracil 16-30 tumor protein p53 Homo sapiens 84-87 24800927-11 2014 Taken together, activation of CXCL4 expression by 5-FU in mice participates in 5-FU-induced intestinal mucositis through upregulation of p53 via activation of p38-MAPK, and CXCL4mab is potentially beneficial in preventing CIM in the intestinal tract. Fluorouracil 50-54 platelet factor 4 Mus musculus 30-35 24919507-9 2014 In in vitro studies, we observed increased expression of p21 and p-ERK1/2 diminution via use of both analogs as compared to use of 5-FU alone. Fluorouracil 131-135 mitogen-activated protein kinase 3 Homo sapiens 67-73 24859412-12 2014 Metformin inhibits EC cell growth and sensitizes EC cells to 5-FU cytotoxic effects by targeting CSCs and the components of mTOR. Fluorouracil 61-65 mechanistic target of rapamycin kinase Homo sapiens 124-128 24919507-12 2014 Our results suggest that the mechanism of potentiation of 5-FU antitumor action by both analogs is realized via increased p21 expression and decreased p-ERK1/2 level which may lead to diminution of thymidylate synthase expression. Fluorouracil 58-62 mitogen-activated protein kinase 3 Homo sapiens 153-159 25788859-11 2014 Decreased Survivin, Cyclin D, Bcl-2, and increased Caspase-3, P53 expression level were aslo confirmed by western blot in 5-fluorouracil combine with myricetin groups in vitro. Fluorouracil 122-136 caspase 3 Homo sapiens 51-60 24874475-8 2014 Isolation mediated by FACS revealed that the CD10-positive subpopulation was more refractory to cisplatin, fluorouracil and radiation than the CD10-negative subpopulation. Fluorouracil 107-119 membrane metalloendopeptidase Homo sapiens 45-49 25788859-11 2014 Decreased Survivin, Cyclin D, Bcl-2, and increased Caspase-3, P53 expression level were aslo confirmed by western blot in 5-fluorouracil combine with myricetin groups in vitro. Fluorouracil 122-136 tumor protein p53 Homo sapiens 62-65 25019346-0 2014 Knockdown of EpCAM enhances the chemosensitivity of breast cancer cells to 5-fluorouracil by downregulating the antiapoptotic factor Bcl-2. Fluorouracil 75-89 epithelial cell adhesion molecule Homo sapiens 13-18 25075187-12 2014 Our data indicate that the combination therapy of nanodelivered 5-FU with a PI3K/Akt inhibitor, BEZ-235, may promise a more effective approach for colon cancer treatment. Fluorouracil 64-68 AKT serine/threonine kinase 1 Homo sapiens 81-84 25019346-0 2014 Knockdown of EpCAM enhances the chemosensitivity of breast cancer cells to 5-fluorouracil by downregulating the antiapoptotic factor Bcl-2. Fluorouracil 75-89 BCL2 apoptosis regulator Homo sapiens 133-138 25019346-4 2014 Here, we investigated the effect of EpCAM gene knockdown on chemosensitivity to 5-fluorouracil (5-FU) in MCF-7 cells and explored the underlying mechanisms. Fluorouracil 80-94 epithelial cell adhesion molecule Homo sapiens 36-41 25019346-4 2014 Here, we investigated the effect of EpCAM gene knockdown on chemosensitivity to 5-fluorouracil (5-FU) in MCF-7 cells and explored the underlying mechanisms. Fluorouracil 96-100 epithelial cell adhesion molecule Homo sapiens 36-41 25019346-6 2014 EpCAM knockdown enhanced the cytotoxic effect of 5-FU, promoting apoptosis by downregulating the expression of the anti-apoptotic protein Bcl-2 and upregulating the expression of the pro-apoptotic proteins Bax, and caspase3 via the ERK1/2 and JNK MAPK signaling pathways in MCF-7 cells. Fluorouracil 49-53 epithelial cell adhesion molecule Homo sapiens 0-5 24435883-0 2014 Icariin-mediated inhibition of NF-kappaB activity enhances the in vitro and in vivo antitumour effect of 5-fluorouracil in colorectal cancer. Fluorouracil 105-119 nuclear factor kappa B subunit 1 Homo sapiens 31-40 24435883-10 2014 The antitumour activity of icariin and its potentiating effect on the antitumour activity of 5-FU implicated the suppression of NF-kappaB activity and consequent down-regulation of the gene products regulated by NF-kappaB. Fluorouracil 93-97 nuclear factor kappa B subunit 1 Homo sapiens 128-137 24435883-10 2014 The antitumour activity of icariin and its potentiating effect on the antitumour activity of 5-FU implicated the suppression of NF-kappaB activity and consequent down-regulation of the gene products regulated by NF-kappaB. Fluorouracil 93-97 nuclear factor kappa B subunit 1 Homo sapiens 212-221 24435883-11 2014 Our results showed that icariin, suppressed tumour growth and enhanced the antitumour activity of 5-FU in CRC by inhibiting NF-kappaB activity. Fluorouracil 98-102 nuclear factor kappa B subunit 1 Homo sapiens 124-133 24704391-4 2014 We have found that 5-FU induced 50% growth inhibition (IC:50) at 72 h with concentrations of 400 muM and 4 muM on H9c2 and HT-29, respectively. Fluorouracil 19-23 latexin Homo sapiens 97-100 25199288-10 2014 CONCLUSION: SJAMP and 5-FU can via decrease the expressions of PCNA protein, P53, Cyclin D1 and CDK4 proteins and mRNAs, increase the expressions of P21 proteins and mRNAs, to inhibit the growth of H22 tumor in mice. Fluorouracil 22-26 cyclin-dependent kinase 4 Mus musculus 96-100 24854862-7 2014 Especially, compounds 11 and 30 resulted in more potent cytotoxicity than the positive control, 5-fluorouracil (5-Fu), in SMMC-7721 cell line, with IC50 values of 15.85 and 12.06 muM, whereas compound 30 exhibited more potent cytotoxicity than 5-Fu in NCI-H460 cell line, with an IC50 value of 5.19 muM. Fluorouracil 112-116 latexin Homo sapiens 179-182 24704391-4 2014 We have found that 5-FU induced 50% growth inhibition (IC:50) at 72 h with concentrations of 400 muM and 4 muM on H9c2 and HT-29, respectively. Fluorouracil 19-23 latexin Homo sapiens 107-110 25120809-0 2014 S-1 monotherapy as second line chemotherapy in advanced gastric cancer patients previously treated with cisplatin/infusional fluorouracil. Fluorouracil 125-137 proteasome 26S subunit, non-ATPase 1 Homo sapiens 0-3 25120809-2 2014 To evaluate the efficacy and toxicity of S-1 monotherapy in patients with advanced gastric cancer after failure of first line cisplatin and fluorouracil combination (CF). Fluorouracil 140-152 proteasome 26S subunit, non-ATPase 1 Homo sapiens 41-44 25120809-13 2014 In conclusion, S-1 monotherapy provided a mild response rate and overall survival, and a favorable toxicity profile in the second line setting after the first line failure to cisplatin and fluorouracil combination. Fluorouracil 189-201 proteasome 26S subunit, non-ATPase 1 Homo sapiens 15-18 24515389-5 2014 It"s found the inhibition rate of 5-FU, L-OHP to well-differentiated GC tissues and cell line was lower than that in the poorly differentiated tissues and cell line; expressions of ZNF139 and MDR1/P-gp, MRP1 and Bcl-2 in well-differentiated GC tissues and cell line MKN28 were higher, while Bax expression was lower. Fluorouracil 34-38 zinc finger with KRAB and SCAN domains 1 Homo sapiens 181-187 24751000-4 2014 Concentrations of 10, 50, and 100 ng/mL of 5-FU chemotherapeutic were added separately in Hep-2 cell line for 24 hours at 37 C. Cell sensibility was evaluated with fluorescein isothiocyanate (FITC) label Bcl-2 by flow cytometry. Fluorouracil 43-47 BCL2 apoptosis regulator Homo sapiens 205-210 24992758-8 2014 Serum levels of TNF-alpha, IL-2, and IFN-gamma, frequencies of CD4 + and CD8+ T cells in the spleen, and splenic NK and CTL activities were also significantly increased in mice treated with 5-FU+PL or 5-FU+PTM compared with mice treated with 5-FU alone (P < 0.05). Fluorouracil 190-194 tumor necrosis factor Mus musculus 16-25 24992758-8 2014 Serum levels of TNF-alpha, IL-2, and IFN-gamma, frequencies of CD4 + and CD8+ T cells in the spleen, and splenic NK and CTL activities were also significantly increased in mice treated with 5-FU+PL or 5-FU+PTM compared with mice treated with 5-FU alone (P < 0.05). Fluorouracil 190-194 interferon gamma Mus musculus 37-46 24816738-0 2014 p16 Methylation is associated with chemosensitivity to fluorouracil in patients with advanced gastric cancer. Fluorouracil 55-67 cyclin dependent kinase inhibitor 2A Homo sapiens 0-3 24816738-6 2014 For all patients, a reverse correlation was only found between p16 methylation and clinical response (P = 0.017), which suggested that p16 methylation might be associated with chemosensitivity of fluorouracil in gastric cancer patients. Fluorouracil 196-208 cyclin dependent kinase inhibitor 2A Homo sapiens 63-66 24816738-6 2014 For all patients, a reverse correlation was only found between p16 methylation and clinical response (P = 0.017), which suggested that p16 methylation might be associated with chemosensitivity of fluorouracil in gastric cancer patients. Fluorouracil 196-208 cyclin dependent kinase inhibitor 2A Homo sapiens 135-138 24816738-7 2014 Results from in vitro experiments demonstrated that p16 methylation was closely correlated with the sensitivity of 5-fluorouracil in gastric cancer cells. Fluorouracil 115-129 cyclin dependent kinase inhibitor 2A Homo sapiens 52-55 24816738-9 2014 p16 Methylation might be used to predict chemosensitivity of fluorouracil for patients with AGC when validated in large samples in the future. Fluorouracil 61-73 cyclin dependent kinase inhibitor 2A Homo sapiens 0-3 24515389-5 2014 It"s found the inhibition rate of 5-FU, L-OHP to well-differentiated GC tissues and cell line was lower than that in the poorly differentiated tissues and cell line; expressions of ZNF139 and MDR1/P-gp, MRP1 and Bcl-2 in well-differentiated GC tissues and cell line MKN28 were higher, while Bax expression was lower. Fluorouracil 34-38 ATP binding cassette subfamily B member 1 Homo sapiens 192-196 24515389-5 2014 It"s found the inhibition rate of 5-FU, L-OHP to well-differentiated GC tissues and cell line was lower than that in the poorly differentiated tissues and cell line; expressions of ZNF139 and MDR1/P-gp, MRP1 and Bcl-2 in well-differentiated GC tissues and cell line MKN28 were higher, while Bax expression was lower. Fluorouracil 34-38 ATP binding cassette subfamily C member 1 Homo sapiens 203-207 24515389-5 2014 It"s found the inhibition rate of 5-FU, L-OHP to well-differentiated GC tissues and cell line was lower than that in the poorly differentiated tissues and cell line; expressions of ZNF139 and MDR1/P-gp, MRP1 and Bcl-2 in well-differentiated GC tissues and cell line MKN28 were higher, while Bax expression was lower. Fluorouracil 34-38 BCL2 apoptosis regulator Homo sapiens 212-217 24515389-5 2014 It"s found the inhibition rate of 5-FU, L-OHP to well-differentiated GC tissues and cell line was lower than that in the poorly differentiated tissues and cell line; expressions of ZNF139 and MDR1/P-gp, MRP1 and Bcl-2 in well-differentiated GC tissues and cell line MKN28 were higher, while Bax expression was lower. Fluorouracil 34-38 BCL2 associated X, apoptosis regulator Homo sapiens 291-294 24515389-6 2014 After ZNF139-siRNA was transfected into MKN28, ZNF139 expression in GC cells was inhibited by 90%; inhibition rate of 5-FU, L-OHP to tumor cells increased, and expressions of MDR1/P-gp, MRP1 and Bcl-2 were down-regulated, while Bax was up-regulated. Fluorouracil 118-122 zinc finger with KRAB and SCAN domains 1 Homo sapiens 6-12 24788596-5 2014 Furthermore, metformin sensitized ICC cells to certain chemotherapeutic agents, such as sorafenib, 5-fluorouracil and As2O3 by targeting the AMPK/mTOR/HIF-1alpha/MRP1 pathway and ERK. Fluorouracil 99-113 mechanistic target of rapamycin kinase Homo sapiens 146-150 24788596-5 2014 Furthermore, metformin sensitized ICC cells to certain chemotherapeutic agents, such as sorafenib, 5-fluorouracil and As2O3 by targeting the AMPK/mTOR/HIF-1alpha/MRP1 pathway and ERK. Fluorouracil 99-113 hypoxia inducible factor 1 subunit alpha Homo sapiens 151-161 24788596-5 2014 Furthermore, metformin sensitized ICC cells to certain chemotherapeutic agents, such as sorafenib, 5-fluorouracil and As2O3 by targeting the AMPK/mTOR/HIF-1alpha/MRP1 pathway and ERK. Fluorouracil 99-113 ATP binding cassette subfamily C member 1 Homo sapiens 162-166 24788596-5 2014 Furthermore, metformin sensitized ICC cells to certain chemotherapeutic agents, such as sorafenib, 5-fluorouracil and As2O3 by targeting the AMPK/mTOR/HIF-1alpha/MRP1 pathway and ERK. Fluorouracil 99-113 mitogen-activated protein kinase 1 Homo sapiens 179-182 24763265-4 2014 Compound 16 ranks as nearly 1.5-fold more potent (mean GI50 = 15.8 muM) compared to 5-FU (mean GI50 = 22.6 muM). Fluorouracil 84-88 latexin Homo sapiens 107-110 24700253-0 2014 Notch1 is overexpressed in human intrahepatic cholangiocarcinoma and is associated with its proliferation, invasiveness and sensitivity to 5-fluorouracil in vitro. Fluorouracil 139-153 notch receptor 1 Homo sapiens 0-6 24700253-9 2014 By silencing Notch1, the proliferation and invasiveness of ICC cells were inhibited and the inhibition rate of 5-FU was markedly increased. Fluorouracil 111-115 notch receptor 1 Homo sapiens 13-19 24700253-11 2014 Furthermore, Notch1 silencing clearly increased the percentage of apoptotic cells treated by 5-FU compared with the control. Fluorouracil 93-97 notch receptor 1 Homo sapiens 13-19 24700253-14 2014 Silencing Notch1 can inhibit the proliferation and invasiveness of ICC cells and increase their sensitivity to 5-FU in vitro. Fluorouracil 111-115 notch receptor 1 Homo sapiens 10-16 25031751-0 2014 S-1 monotherapy as second line chemotherapy in advanced gastric cancer patients previously treated with cisplatin/infusional fluorouracil. Fluorouracil 125-137 proteasome 26S subunit, non-ATPase 1 Homo sapiens 0-3 25031751-2 2014 To evaluate the efficacy and toxicity of S-1 monotherapy in patients with advanced gastric cancer after failure of first line cisplatin and fluorouracil combination (CF). Fluorouracil 140-152 proteasome 26S subunit, non-ATPase 1 Homo sapiens 41-44 25031751-13 2014 In conclusion, S-1 monotherapy provided a mild response rate and overall survival, and a favorable toxicity profile in the second line setting after the first line failure to cisplatin and fluorouracil combination. Fluorouracil 189-201 proteasome 26S subunit, non-ATPase 1 Homo sapiens 15-18 24851084-4 2014 RESULTS: Forced expression of S100A10 in COLO-320 CRC cells significantly increased the 50% inhibitory concentration (IC50) for L-OHP (P = 0.003), but did not change that for 5-FU, indicating that S100A10 is more specific to L-OHP than 5-FU. Fluorouracil 236-240 S100 calcium binding protein A10 Homo sapiens 30-37 24462821-0 2014 Inhibition of p53 increases chemosensitivity to 5-FU in nutrient-deprived hepatocarcinoma cells by suppressing autophagy. Fluorouracil 48-52 tumor protein p53 Homo sapiens 14-17 24462821-3 2014 In this study, we show that inhibition of p53 enhanced apoptosis and increased chemosensitivity to 5-fluorouracil (5-FU) in nutrient-deprived hepatocarcinoma cells (HCC). Fluorouracil 99-113 tumor protein p53 Homo sapiens 42-45 24462821-3 2014 In this study, we show that inhibition of p53 enhanced apoptosis and increased chemosensitivity to 5-fluorouracil (5-FU) in nutrient-deprived hepatocarcinoma cells (HCC). Fluorouracil 115-119 tumor protein p53 Homo sapiens 42-45 24462821-8 2014 Antioxidants reduced nutrient deprivation or 5-FU-induced cell death of HCC after p53 inhibition. Fluorouracil 45-49 tumor protein p53 Homo sapiens 82-85 24585249-8 2014 Enforced expression of SCGB2A1 in CRC-derived cell lines promoted proliferation (DLD1, SW480 and LoVo cells; p<0.05), decreased chemosensitivity to 5-fluorouracil and oxaliplatin (DLD1 and SW480 cell lines; p<0.05), and significantly increased the viability of irradiated cells (DLD1, SW480 and LoVo cell lines; p<0.05). Fluorouracil 151-165 secretoglobin family 2A member 1 Homo sapiens 23-30 24634414-2 2014 In this article, we show that overexpression of the MT1G isoform sensitizes colorectal cell lines to the chemotherapeutic agents oxaliplatin (OXA) and 5-fluorouracil (5-FU), in part through enhancing p53 and repressing NF-kappaB activity. Fluorouracil 151-165 tumor protein p53 Homo sapiens 200-203 24634414-2 2014 In this article, we show that overexpression of the MT1G isoform sensitizes colorectal cell lines to the chemotherapeutic agents oxaliplatin (OXA) and 5-fluorouracil (5-FU), in part through enhancing p53 and repressing NF-kappaB activity. Fluorouracil 151-165 nuclear factor kappa B subunit 1 Homo sapiens 219-228 24634414-6 2014 We show for the first time that OXA and 5-FU induce higher levels of intracellular labile zinc, as measured using the fluorescent probe FLUOZIN-3, and that such zinc contributes to the activation of p53 and repression of NF-kappaB. Fluorouracil 40-44 tumor protein p53 Homo sapiens 199-202 24634414-6 2014 We show for the first time that OXA and 5-FU induce higher levels of intracellular labile zinc, as measured using the fluorescent probe FLUOZIN-3, and that such zinc contributes to the activation of p53 and repression of NF-kappaB. Fluorouracil 40-44 nuclear factor kappa B subunit 1 Homo sapiens 221-230 24733045-0 2014 JNK confers 5-fluorouracil resistance in p53-deficient and mutant p53-expressing colon cancer cells by inducing survival autophagy. Fluorouracil 12-26 mitogen-activated protein kinase 8 Homo sapiens 0-3 24765178-5 2014 The present study aimed to investigate whether chemotherapy enriched the CSL-cells in the MEC cell line of MC3 using 5-fluorouracil (5-Fu). Fluorouracil 117-131 chorionic somatomammotropin hormone like 1 Homo sapiens 73-76 24765178-5 2014 The present study aimed to investigate whether chemotherapy enriched the CSL-cells in the MEC cell line of MC3 using 5-fluorouracil (5-Fu). Fluorouracil 133-137 chorionic somatomammotropin hormone like 1 Homo sapiens 73-76 24733045-0 2014 JNK confers 5-fluorouracil resistance in p53-deficient and mutant p53-expressing colon cancer cells by inducing survival autophagy. Fluorouracil 12-26 tumor protein p53 Homo sapiens 41-44 24733045-0 2014 JNK confers 5-fluorouracil resistance in p53-deficient and mutant p53-expressing colon cancer cells by inducing survival autophagy. Fluorouracil 12-26 tumor protein p53 Homo sapiens 66-69 24733045-3 2014 Here we report that 5-FU treatment causes aberrant autophagosome accumulation in HCT116 p53(-/-) and HT-29 cancer cells. Fluorouracil 20-24 tumor protein p53 Homo sapiens 88-91 24733045-5 2014 In further analysis, we show that JNK activation and phosphorylation of Bcl-2 are key determinants in 5-FU-induced autophagy. Fluorouracil 102-106 mitogen-activated protein kinase 8 Homo sapiens 34-37 24733045-5 2014 In further analysis, we show that JNK activation and phosphorylation of Bcl-2 are key determinants in 5-FU-induced autophagy. Fluorouracil 102-106 BCL2 apoptosis regulator Homo sapiens 72-77 24733045-6 2014 Inhibition of JNK by the compound SP600125 or JNK siRNA suppressed autophagy and phosphorylation of c-Jun and Bcl-2 but increased 5-FU-induced apoptosis in both HCT116 p53(-/-) and HT29 cells. Fluorouracil 130-134 mitogen-activated protein kinase 8 Homo sapiens 14-17 24733045-6 2014 Inhibition of JNK by the compound SP600125 or JNK siRNA suppressed autophagy and phosphorylation of c-Jun and Bcl-2 but increased 5-FU-induced apoptosis in both HCT116 p53(-/-) and HT29 cells. Fluorouracil 130-134 mitogen-activated protein kinase 8 Homo sapiens 46-49 24733045-6 2014 Inhibition of JNK by the compound SP600125 or JNK siRNA suppressed autophagy and phosphorylation of c-Jun and Bcl-2 but increased 5-FU-induced apoptosis in both HCT116 p53(-/-) and HT29 cells. Fluorouracil 130-134 tumor protein p53 Homo sapiens 168-171 24733045-7 2014 Taken together, our results suggest that JNK activation confers 5-FU resistance in HCT116 p53(-/-) and HT29 cells by promoting autophagy as a pro-survival effect, likely via inducing Bcl-2 phosphorylation. Fluorouracil 64-68 mitogen-activated protein kinase 8 Homo sapiens 41-44 24733045-7 2014 Taken together, our results suggest that JNK activation confers 5-FU resistance in HCT116 p53(-/-) and HT29 cells by promoting autophagy as a pro-survival effect, likely via inducing Bcl-2 phosphorylation. Fluorouracil 64-68 tumor protein p53 Homo sapiens 90-93 24733045-7 2014 Taken together, our results suggest that JNK activation confers 5-FU resistance in HCT116 p53(-/-) and HT29 cells by promoting autophagy as a pro-survival effect, likely via inducing Bcl-2 phosphorylation. Fluorouracil 64-68 BCL2 apoptosis regulator Homo sapiens 183-188 24733045-8 2014 These results provide a promising strategy to improve the efficacy of 5-FU-based chemotherapy for colorectal cancer patients harboring a p53 gene mutation. Fluorouracil 70-74 tumor protein p53 Homo sapiens 137-140 24486618-9 2014 The possible mechanism of 5-FU induced renal toxicity is the induction of oxidative stress; activation of apoptotic pathway by upregulation of p53, bax, caspase-3 and down regulating Bcl-2. Fluorouracil 26-30 BCL2, apoptosis regulator Rattus norvegicus 183-188 24743738-0 2014 Epigenetic modification of Nrf2 in 5-fluorouracil-resistant colon cancer cells: involvement of TET-dependent DNA demethylation. Fluorouracil 35-49 NFE2 like bZIP transcription factor 2 Homo sapiens 27-31 24743738-3 2014 Nuclear factor-erythroid 2-related factor 2 (Nrf2) is a transcriptional regulator and a possible target to overcome 5-FU resistance. Fluorouracil 116-120 NFE2 like bZIP transcription factor 2 Homo sapiens 0-43 24743738-3 2014 Nuclear factor-erythroid 2-related factor 2 (Nrf2) is a transcriptional regulator and a possible target to overcome 5-FU resistance. Fluorouracil 116-120 NFE2 like bZIP transcription factor 2 Homo sapiens 45-49 24743738-4 2014 The present study examined epigenetic changes associated with Nrf2 induction in a human CRC cell line (SNUC5) resistant to 5-FU (SNUC5/5-FUR). Fluorouracil 123-127 NFE2 like bZIP transcription factor 2 Homo sapiens 62-66 24743738-8 2014 The siRNA- or shRNA-mediated knockdown of Nrf2 or HO-1 significantly suppressed cancer cell viability and tumor growth in vitro and in vivo, resulting in enhanced 5-FU sensitivity. Fluorouracil 163-167 NFE2 like bZIP transcription factor 2 Homo sapiens 42-46 24743738-12 2014 These results suggested that the mechanism underlying the acquisition of 5-FU resistance in CRC involves the upregulation of Nrf2 and HO-1 expression via epigenetic modifications of DNA demethylation. Fluorouracil 73-77 NFE2 like bZIP transcription factor 2 Homo sapiens 125-129 24210071-6 2014 RESULTS: It was shown that in MCF-7 cells, the proliferation was inhibited, the apoptosis was promoted, the Bcl-2 expression was suppressed and the Bax expression was promoted by both 5-FU alone and morphine alone, while the superior effects were achieved in combination with the two drugs. Fluorouracil 184-188 BCL2 apoptosis regulator Homo sapiens 108-113 24210071-6 2014 RESULTS: It was shown that in MCF-7 cells, the proliferation was inhibited, the apoptosis was promoted, the Bcl-2 expression was suppressed and the Bax expression was promoted by both 5-FU alone and morphine alone, while the superior effects were achieved in combination with the two drugs. Fluorouracil 184-188 BCL2 associated X, apoptosis regulator Homo sapiens 148-151 24452447-0 2014 Overexpression of fibronectin confers cell adhesion-mediated drug resistance (CAM-DR) against 5-FU in oral squamous cell carcinoma cells. Fluorouracil 94-98 fibronectin 1 Homo sapiens 18-29 24608297-2 2014 OBJECTIVE: We report the clinical outcome of 5-fluorouracil/mitomycin C-based concurrent chemoradiotherapy for anal carcinoma in patients with HIV infection with an emphasis on the long-term course of CD4 counts and the HIV-related morbidity during follow-up. Fluorouracil 45-59 CD4 molecule Homo sapiens 201-204 24565962-3 2014 The two compounds exhibited stronger inhibitory activities than the positive control 5-fluorouracil (IC50=7.34, 11.50, 36.17, 18.83 muM) against the four tested cell lines. Fluorouracil 85-99 latexin Homo sapiens 132-135 24452447-3 2014 In the present study, we evaluated the ECM molecule fibronectin (FN) using DNA microarray data obtained from parental and 5-FU-resistant OSCC cell lines. Fluorouracil 122-126 fibronectin 1 Homo sapiens 52-63 24452447-3 2014 In the present study, we evaluated the ECM molecule fibronectin (FN) using DNA microarray data obtained from parental and 5-FU-resistant OSCC cell lines. Fluorouracil 122-126 fibronectin 1 Homo sapiens 65-67 24452447-8 2014 Cell adhesion to FN enhanced 5-FU resistance and activated integrin-mediated ILK/Akt/NF-kappaB survival signaling in the 5-FU-resistant OSCC cells. Fluorouracil 121-125 integrin linked kinase Homo sapiens 77-80 24452447-8 2014 Cell adhesion to FN enhanced 5-FU resistance and activated integrin-mediated ILK/Akt/NF-kappaB survival signaling in the 5-FU-resistant OSCC cells. Fluorouracil 121-125 AKT serine/threonine kinase 1 Homo sapiens 81-84 24452447-8 2014 Cell adhesion to FN enhanced 5-FU resistance and activated integrin-mediated ILK/Akt/NF-kappaB survival signaling in the 5-FU-resistant OSCC cells. Fluorouracil 121-125 nuclear factor kappa B subunit 1 Homo sapiens 85-94 24452447-9 2014 Furthermore, the inhibition of cell adhesion to FN by FNIII14 enhanced chemosensitivity to 5-FU and apoptosis by suppressing ILK/Akt/NF-kappaB signaling in the 5-FU-resistant cells. Fluorouracil 160-164 integrin linked kinase Homo sapiens 125-128 24452447-9 2014 Furthermore, the inhibition of cell adhesion to FN by FNIII14 enhanced chemosensitivity to 5-FU and apoptosis by suppressing ILK/Akt/NF-kappaB signaling in the 5-FU-resistant cells. Fluorouracil 160-164 AKT serine/threonine kinase 1 Homo sapiens 129-132 24452447-9 2014 Furthermore, the inhibition of cell adhesion to FN by FNIII14 enhanced chemosensitivity to 5-FU and apoptosis by suppressing ILK/Akt/NF-kappaB signaling in the 5-FU-resistant cells. Fluorouracil 160-164 nuclear factor kappa B subunit 1 Homo sapiens 133-142 24452447-10 2014 These novel findings demonstrate that FN is a potentially useful biomarker and therapeutic target for improving the treatment of OSCC, particularly in the setting of 5-FU resistance. Fluorouracil 166-170 fibronectin 1 Homo sapiens 38-40 24504010-7 2014 Genes with expression changed by drugs were related to GO term "extracellular region" and "p53 signaling pathway" in both 5-FU- and CDDP-treated cells. Fluorouracil 122-126 tumor protein p53 Homo sapiens 91-94 24249161-0 2014 MicroRNA-23a antisense enhances 5-fluorouracil chemosensitivity through APAF-1/caspase-9 apoptotic pathway in colorectal cancer cells. Fluorouracil 32-46 apoptotic peptidase activating factor 1 Homo sapiens 72-78 24249161-6 2014 The activity of caspases-3, -7, and -9 were also assessed in miR-23a antisense and 5-FU treated tumor cells. Fluorouracil 83-87 caspase 3 Homo sapiens 16-38 24249161-8 2014 We found that the expression of miR-23a was increased and the level of apoptosis-activating factor-1 (APAF-1) was decreased in 5-FU-treated colon cancer cells compared to untreated cells. Fluorouracil 127-131 apoptotic peptidase activating factor 1 Homo sapiens 71-100 24249161-8 2014 We found that the expression of miR-23a was increased and the level of apoptosis-activating factor-1 (APAF-1) was decreased in 5-FU-treated colon cancer cells compared to untreated cells. Fluorouracil 127-131 apoptotic peptidase activating factor 1 Homo sapiens 102-108 24249161-13 2014 This study shows that miR-23a antisense enhanced 5-FU-induced apoptosis in colorectal cancer cells through the APAF-1/caspase-9 apoptotic pathway. Fluorouracil 49-53 apoptotic peptidase activating factor 1 Homo sapiens 111-117 24549317-5 2014 We found knockdown of Rap1 by microRNA (miRNA) interference enhanced significantly apoptosis and 5-fluorouracil (5-FU) chemosensitivity in HepG2 cell line. Fluorouracil 97-111 TERF2 interacting protein Homo sapiens 22-26 24549317-5 2014 We found knockdown of Rap1 by microRNA (miRNA) interference enhanced significantly apoptosis and 5-fluorouracil (5-FU) chemosensitivity in HepG2 cell line. Fluorouracil 113-117 TERF2 interacting protein Homo sapiens 22-26 24549317-7 2014 In vivo, Rap1 miRNA combined with 5-FU treatment led to a significant reduction of tumor growth as compared with 5-FU alone. Fluorouracil 113-117 TERF2 interacting protein Homo sapiens 9-13 24549317-8 2014 The results indicate that Rap1 miRNA can effectively enhance sensitivity of HepG2 cell line to 5-FU chemotherapy in vitro and in vivo. Fluorouracil 95-99 TERF2 interacting protein Homo sapiens 26-30 24122668-0 2014 Down-regulation of BAX gene during carcinogenesis and acquisition of resistance to 5-FU in colorectal cancer. Fluorouracil 83-87 BCL2 associated X, apoptosis regulator Homo sapiens 19-22 24122668-10 2014 In conclusion, the results of our study suggest that BAX down-regulation could contribute as an important factor during both colorectal carcinogenesis and cell resistance to 5-FU. Fluorouracil 174-178 BCL2 associated X, apoptosis regulator Homo sapiens 53-56 24791593-7 2014 In addition, cyclin A was down-regulated in the let-7 g transfectants cells.The results showed that let-7 g microRNA contributed to an increase of 5-Fu-induced cell cycle inhibit in human hepatoma cell and sensitized cells to 5-Fu, leading to increased the effectiveness of the drug in treating hepatoma cancer. Fluorouracil 147-151 cyclin A2 Homo sapiens 13-21 24791593-7 2014 In addition, cyclin A was down-regulated in the let-7 g transfectants cells.The results showed that let-7 g microRNA contributed to an increase of 5-Fu-induced cell cycle inhibit in human hepatoma cell and sensitized cells to 5-Fu, leading to increased the effectiveness of the drug in treating hepatoma cancer. Fluorouracil 226-230 cyclin A2 Homo sapiens 13-21 24549317-0 2014 Downregulation of Rap1 promotes 5-fluorouracil-induced apoptosis in hepatocellular carcinoma cell line HepG2. Fluorouracil 32-46 TERF2 interacting protein Homo sapiens 18-22 24636413-5 2014 The method is applied to screening inhibitors and the results indicate that both of the 5-FU and cisplatin can inhibit UDG activity with the IC50 values of 6.1+-0.52 mM and 3.2+-0.24 mM, respectively. Fluorouracil 88-92 uracil DNA glycosylase Homo sapiens 119-122 24649094-6 2014 In response to glucose, 5-Fu-induced cell growth inhibition was attenuated in a dose-dependent manner, accompanied with activated p-Akt, while 2-DG enhanced 5-Fu-induced cell growth inhibition. Fluorouracil 24-28 AKT serine/threonine kinase 1 Homo sapiens 132-135 24637719-6 2014 Moreover, aberrant expression of p-ERK1/2 was associated with 5-fluorouracil resistance in breast cancer patients and BikDDA enhanced the therapeutic effects of 5-fluorouracil in vitro. Fluorouracil 62-76 mitogen-activated protein kinase 3 Homo sapiens 35-41 24637719-6 2014 Moreover, aberrant expression of p-ERK1/2 was associated with 5-fluorouracil resistance in breast cancer patients and BikDDA enhanced the therapeutic effects of 5-fluorouracil in vitro. Fluorouracil 161-175 mitogen-activated protein kinase 3 Homo sapiens 35-41 24649094-8 2014 In conclusion, high glucose weakens the antitumor effect of 5-Fu via PI3K/Akt signaling. Fluorouracil 60-64 AKT serine/threonine kinase 1 Homo sapiens 74-77 24405586-0 2014 High expression of dihydropyrimidine dehydrogenase in lung adenocarcinoma is associated with mutations in epidermal growth factor receptor: implications for the treatment of non--small-cell lung cancer using 5-fluorouracil. Fluorouracil 208-222 epidermal growth factor receptor Homo sapiens 106-138 24405586-1 2014 BACKGROUND: It has been shown that 5-fluorouracil (5-FU) sensitivity in patients with non-small-cell lung cancer (NSCLC) is associated with epidermal growth factor receptor (EGFR) mutation status. Fluorouracil 35-49 epidermal growth factor receptor Homo sapiens 140-172 24405586-1 2014 BACKGROUND: It has been shown that 5-fluorouracil (5-FU) sensitivity in patients with non-small-cell lung cancer (NSCLC) is associated with epidermal growth factor receptor (EGFR) mutation status. Fluorouracil 35-49 epidermal growth factor receptor Homo sapiens 174-178 24405586-1 2014 BACKGROUND: It has been shown that 5-fluorouracil (5-FU) sensitivity in patients with non-small-cell lung cancer (NSCLC) is associated with epidermal growth factor receptor (EGFR) mutation status. Fluorouracil 51-55 epidermal growth factor receptor Homo sapiens 140-172 24405586-1 2014 BACKGROUND: It has been shown that 5-fluorouracil (5-FU) sensitivity in patients with non-small-cell lung cancer (NSCLC) is associated with epidermal growth factor receptor (EGFR) mutation status. Fluorouracil 51-55 epidermal growth factor receptor Homo sapiens 174-178 24821671-0 2014 Kinetics and efficiency of a methyl-carboxylated 5-Fluorouracil-bovine serum albumin adduct for targeted delivery. Fluorouracil 49-63 albumin Homo sapiens 71-84 24821671-4 2014 Here, a 5-FU adduct, 5-fluorouracil acetate (FUAc) is synthesized and covalently coupled to bovine serum albumin (BSA) as model carrier molecule. Fluorouracil 8-12 albumin Homo sapiens 99-112 24323901-8 2014 Importantly, YES1 and YAP transcript levels were higher in liver metastases of patients with colon cancer after 5FU-based neoadjuvant chemotherapy. Fluorouracil 112-115 YES proto-oncogene 1, Src family tyrosine kinase Homo sapiens 13-17 24401318-6 2014 The IC50 of 5-FU for HCT116 cells overexpressing miR-27a or miR-27b was 4.4 mumol/L (both), significantly lower than that for cells expressing a nontargeting (scramble) control miRNA (14.3 mumol/L; P = 3.3 x 10(-5) and P = 1.5 x 10(-7), respectively). Fluorouracil 12-16 microRNA 27a Homo sapiens 49-56 24398626-11 2014 Consistently, 5-FU, a widely used chemotherapeutic agent, increased FOXO1 expression via inhibition of QKI. Fluorouracil 14-18 forkhead box O1 Homo sapiens 68-73 24587255-0 2014 A compensatory role of NF-kappaB to p53 in response to 5-FU-based chemotherapy for gastric cancer cell lines. Fluorouracil 55-59 nuclear factor kappa B subunit 1 Homo sapiens 23-32 24587255-0 2014 A compensatory role of NF-kappaB to p53 in response to 5-FU-based chemotherapy for gastric cancer cell lines. Fluorouracil 55-59 tumor protein p53 Homo sapiens 36-39 24587255-4 2014 To evaluate the biological significance of NF-kappaB in the context of 5-FU-based chemotherapy, we analyzed the NF-kappaB-dependent biological response upon 5-FU treatment in gastric cancer cell lines. Fluorouracil 157-161 nuclear factor kappa B subunit 1 Homo sapiens 112-121 24587255-5 2014 Seven genes induced by 5-FU treatment in an NF-kappaB-dependent manner were identified, five of which are known p53 targets. Fluorouracil 23-27 nuclear factor kappa B subunit 1 Homo sapiens 44-53 24587255-5 2014 Seven genes induced by 5-FU treatment in an NF-kappaB-dependent manner were identified, five of which are known p53 targets. Fluorouracil 23-27 tumor protein p53 Homo sapiens 112-115 24587255-8 2014 We also demonstrated that cell lines bearing Pro/Pro homozygosity in codon72 of p53 exon4, which is important for NF-kappaB binding to p53, are more resistant to 5-FU than those with Arg/Arg homozygosity. Fluorouracil 162-166 tumor protein p53 Homo sapiens 80-83 24587255-9 2014 We conclude that NF-kappaB plays an important role in the response to 5-FU treatment in gastric cancer cell lines, with a possible compensatory function of p53. Fluorouracil 70-74 nuclear factor kappa B subunit 1 Homo sapiens 17-26 24587255-9 2014 We conclude that NF-kappaB plays an important role in the response to 5-FU treatment in gastric cancer cell lines, with a possible compensatory function of p53. Fluorouracil 70-74 tumor protein p53 Homo sapiens 156-159 24587255-10 2014 These results suggest that NF-kappaB is a potential 5-FU-chemosensitivity prediction marker that may reflect 5-FU-induced stress-response pathways, including p53. Fluorouracil 52-56 nuclear factor kappa B subunit 1 Homo sapiens 27-36 24587255-10 2014 These results suggest that NF-kappaB is a potential 5-FU-chemosensitivity prediction marker that may reflect 5-FU-induced stress-response pathways, including p53. Fluorouracil 52-56 tumor protein p53 Homo sapiens 158-161 24587255-10 2014 These results suggest that NF-kappaB is a potential 5-FU-chemosensitivity prediction marker that may reflect 5-FU-induced stress-response pathways, including p53. Fluorouracil 109-113 nuclear factor kappa B subunit 1 Homo sapiens 27-36 24587255-10 2014 These results suggest that NF-kappaB is a potential 5-FU-chemosensitivity prediction marker that may reflect 5-FU-induced stress-response pathways, including p53. Fluorouracil 109-113 tumor protein p53 Homo sapiens 158-161 24591842-6 2014 Exposure to celecoxib (21.8 mumol/L) plus 5-fluorouracil (8.1 x 10(-3) g/L) or sorafenib (4.4 mumol/L) increased apoptosis but exerted no effect on COX2, phosphorylated epidermal growth-factor receptor (p-EGFR) and phosphorylated (p)-AKT expression. Fluorouracil 42-56 prostaglandin-endoperoxide synthase 2 Homo sapiens 148-152 24591842-6 2014 Exposure to celecoxib (21.8 mumol/L) plus 5-fluorouracil (8.1 x 10(-3) g/L) or sorafenib (4.4 mumol/L) increased apoptosis but exerted no effect on COX2, phosphorylated epidermal growth-factor receptor (p-EGFR) and phosphorylated (p)-AKT expression. Fluorouracil 42-56 epidermal growth factor receptor Homo sapiens 169-201 24384683-0 2014 Loss of Smad4 in colorectal cancer induces resistance to 5-fluorouracil through activating Akt pathway. Fluorouracil 57-71 AKT serine/threonine kinase 1 Homo sapiens 91-94 24384683-8 2014 Suppression of phosphatidylinositol-3-kinase (PI3K)/Akt pathway by LY294002 restored chemosensitivity of Smad4-deficient cells to 5-FU. Fluorouracil 130-134 AKT serine/threonine kinase 1 Homo sapiens 52-55 24384683-11 2014 CONCLUSION: Loss of Smad4 in CRC patients induces resistance to 5-FU-based therapy through activation of Akt pathway and inhibitors of this pathway may sensitise these patients to 5-FU. Fluorouracil 64-68 AKT serine/threonine kinase 1 Homo sapiens 105-108 23934972-2 2014 We have recently reported that STAT3 gene expression correlates with resistance of CRC cell lines to 5-fluorouracil (5-FU)-based chemoradiotherapy (CT/RT). Fluorouracil 101-115 signal transducer and activator of transcription 3 Homo sapiens 31-36 23934972-2 2014 We have recently reported that STAT3 gene expression correlates with resistance of CRC cell lines to 5-fluorouracil (5-FU)-based chemoradiotherapy (CT/RT). Fluorouracil 117-121 signal transducer and activator of transcription 3 Homo sapiens 31-36 24342832-4 2014 The expression levels of HIF-1alpha and PDK-1 were both elevated in the tumor tissues relative to the normal gastric tissues of most patients who showed recurrence after adjuvant 5-FU treatment. Fluorouracil 179-183 hypoxia inducible factor 1 subunit alpha Homo sapiens 25-35 24583651-4 2014 Entolimod-stimulated IL-6 production was essential for Entolimod"s ability to rescue mice from death caused by doses of 5-FU associated with hematopoietic failure. Fluorouracil 120-124 interleukin 6 Mus musculus 21-25 24371210-4 2014 However, following 5-fluorouracil treatment, Gadd45a(-/-) HSCs exhibited a faster recovery, associated with an increase in the proliferation rate. Fluorouracil 19-33 growth arrest and DNA-damage-inducible 45 alpha Mus musculus 45-52 24446491-7 2014 These functional differences between c-Kit(lo) and c-Kit(hi) HSCs persist even under conditions of stress hematopoiesis induced by 5-fluorouracil. Fluorouracil 131-145 KIT proto-oncogene, receptor tyrosine kinase Homo sapiens 37-42 24446491-7 2014 These functional differences between c-Kit(lo) and c-Kit(hi) HSCs persist even under conditions of stress hematopoiesis induced by 5-fluorouracil. Fluorouracil 131-145 KIT proto-oncogene, receptor tyrosine kinase Homo sapiens 51-56 24511010-1 2014 AIM: We aimed to investigate whether 3"-deoxy-3"-[(18)F]fluorothymidine ([(18)F]FLT) positron emission tomography (PET) can estimate thymidine kinase 1 (TK1) activity after thymidylate synthase (TS) inhibition by 5-fluorouracil (5-FU) in a mouse tumor model. Fluorouracil 213-227 fms related receptor tyrosine kinase 1 Homo sapiens 80-83 24383625-4 2014 Cytotoxicity study of the 5-FU-loaded nanoparticles (5-FU-NPs) in HepG2 and A549 cell lines demonstrated their greater potency in killing cancer cells with overexpressed asialoglycoprotein receptor (ASGPR) on the cell surface, compared to that of the free drug. Fluorouracil 26-30 asialoglycoprotein receptor 1 Homo sapiens 170-197 24383625-4 2014 Cytotoxicity study of the 5-FU-loaded nanoparticles (5-FU-NPs) in HepG2 and A549 cell lines demonstrated their greater potency in killing cancer cells with overexpressed asialoglycoprotein receptor (ASGPR) on the cell surface, compared to that of the free drug. Fluorouracil 26-30 asialoglycoprotein receptor 1 Homo sapiens 199-204 24383625-4 2014 Cytotoxicity study of the 5-FU-loaded nanoparticles (5-FU-NPs) in HepG2 and A549 cell lines demonstrated their greater potency in killing cancer cells with overexpressed asialoglycoprotein receptor (ASGPR) on the cell surface, compared to that of the free drug. Fluorouracil 53-57 asialoglycoprotein receptor 1 Homo sapiens 170-197 24383625-4 2014 Cytotoxicity study of the 5-FU-loaded nanoparticles (5-FU-NPs) in HepG2 and A549 cell lines demonstrated their greater potency in killing cancer cells with overexpressed asialoglycoprotein receptor (ASGPR) on the cell surface, compared to that of the free drug. Fluorouracil 53-57 asialoglycoprotein receptor 1 Homo sapiens 199-204 24511010-1 2014 AIM: We aimed to investigate whether 3"-deoxy-3"-[(18)F]fluorothymidine ([(18)F]FLT) positron emission tomography (PET) can estimate thymidine kinase 1 (TK1) activity after thymidylate synthase (TS) inhibition by 5-fluorouracil (5-FU) in a mouse tumor model. Fluorouracil 229-233 fms related receptor tyrosine kinase 1 Homo sapiens 80-83 24277474-0 2014 Thymidylate synthase expression and p21(WAF1)/p53 phenotype of colon cancers identify patients who may benefit from 5-fluorouracil based therapy. Fluorouracil 116-130 cyclin dependent kinase inhibitor 1A Homo sapiens 36-39 24277474-0 2014 Thymidylate synthase expression and p21(WAF1)/p53 phenotype of colon cancers identify patients who may benefit from 5-fluorouracil based therapy. Fluorouracil 116-130 cyclin dependent kinase inhibitor 1A Homo sapiens 40-44 24277474-0 2014 Thymidylate synthase expression and p21(WAF1)/p53 phenotype of colon cancers identify patients who may benefit from 5-fluorouracil based therapy. Fluorouracil 116-130 tumor protein p53 Homo sapiens 46-49 23852449-11 2014 In addition, treatment of indomethacin alone or combination of 5-FU and indomethacin decreased the expressions of PROM1 (CD133), CD44, PTGS2 (cyclooxygenase 2) and HES1, and increased PPARG expression. Fluorouracil 63-67 prostaglandin-endoperoxide synthase 2 Homo sapiens 135-140 23852449-11 2014 In addition, treatment of indomethacin alone or combination of 5-FU and indomethacin decreased the expressions of PROM1 (CD133), CD44, PTGS2 (cyclooxygenase 2) and HES1, and increased PPARG expression. Fluorouracil 63-67 prostaglandin-endoperoxide synthase 2 Homo sapiens 142-158 23852449-11 2014 In addition, treatment of indomethacin alone or combination of 5-FU and indomethacin decreased the expressions of PROM1 (CD133), CD44, PTGS2 (cyclooxygenase 2) and HES1, and increased PPARG expression. Fluorouracil 63-67 peroxisome proliferator activated receptor gamma Homo sapiens 184-189 23852449-12 2014 NSAIDs could selectively reduce the colon CSCs and suppress 5-FU-induced increase of CSCs via inhibiting PTGS2 (cyclooxygenase 2) and NOTCH/HES1, and activating PPARG. Fluorouracil 60-64 prostaglandin-endoperoxide synthase 2 Homo sapiens 105-110 23852449-12 2014 NSAIDs could selectively reduce the colon CSCs and suppress 5-FU-induced increase of CSCs via inhibiting PTGS2 (cyclooxygenase 2) and NOTCH/HES1, and activating PPARG. Fluorouracil 60-64 prostaglandin-endoperoxide synthase 2 Homo sapiens 112-128 23852449-12 2014 NSAIDs could selectively reduce the colon CSCs and suppress 5-FU-induced increase of CSCs via inhibiting PTGS2 (cyclooxygenase 2) and NOTCH/HES1, and activating PPARG. Fluorouracil 60-64 peroxisome proliferator activated receptor gamma Homo sapiens 161-166 24239278-3 2014 MATERIALS AND METHODS: The expression of EGFR, p53, Cyclin D1, p16, p21, p27, p-AKT, HIF-1alpha, Caspase 3 and BCL2 was analyzed by immunohistochemistry in 41 primary laryngeal/hypopharyngeal squamous cell carcinomas of patients that received induction chemotherapy (cisplatin and 5-fluorouracil) as part of their treatment. Fluorouracil 281-295 BCL2 apoptosis regulator Homo sapiens 111-115 24189396-4 2014 Moreover, a increased effect was also observed in boosting immunity functions when the Heps-bearing mice receiving SCPP11 combination with 5-Fu administration, including increased in thymus indexes and enhancing serum IL-2 and TNF-alpha secretion. Fluorouracil 139-143 tumor necrosis factor Mus musculus 227-236 24529061-6 2014 On phase II, trial patients with p16-negative hypoxic tumours had worse loco-regional control with cisplatin and 5FU compared with tirapazamine and cisplatin (P < 0.001) and worse failure-free survival (hazard ratio = 5.18; 95% confidence interval, 1.98-13.55; P = 0.001). Fluorouracil 113-116 cyclin dependent kinase inhibitor 2A Homo sapiens 33-36 24420907-6 2014 However, when Exo1(mut) HSCs were pushed into cell cycle in vivo with 5-fluorouracil or poly IC, the hematopoietic population became hypersensitive to IR, resulting in HSC defects and animal death. Fluorouracil 70-84 exonuclease 1 Mus musculus 14-18 24396484-3 2014 The present study revealed that the expression levels of the three antitumor miRNAs, miR-122a, miR-145 and miR-205, were significantly elevated in MDA-MB-453 LAR-type TNBC tumor cells treated with 5-fluorouracil together with ixabepilone. Fluorouracil 197-211 protein tyrosine phosphatase receptor type F Homo sapiens 158-161 24472145-5 2014 METHODS: We evaluated the expression of HER-2/neu protein in gastric cell lines by FACS and then comparing the cytotoxicity in chemotherapeutics (doxorubicin, cisplatin, paclitaxel, 5-FU) alone and in combination with Herceptin according to the expression of HER-2/neu protein by MTT assay. Fluorouracil 182-186 erb-b2 receptor tyrosine kinase 2 Homo sapiens 40-49 24444035-3 2014 METHODS: The expression of GOLPH3 was determined by qRT-PCR and immunohistochemistry in colorectal tissues from CRC patients treated with 5-FU based adjuvant chemotherapy after surgery. Fluorouracil 138-142 golgi phosphoprotein 3 Homo sapiens 27-33 24444035-0 2014 GOLPH3 predicts survival of colorectal cancer patients treated with 5-fluorouracil-based adjuvant chemotherapy. Fluorouracil 68-82 golgi phosphoprotein 3 Homo sapiens 0-6 24444035-5 2014 The effects of GOLPH3 on 5-FU sensitivity were examined in CRC cell lines. Fluorouracil 25-29 golgi phosphoprotein 3 Homo sapiens 15-21 24444035-7 2014 Kaplan-Meier survival curves indicated that high GOLPH3 expression was significantly associated with prolonged disease-free survival (DFS, P = 0.002) and overall survival (OS, P = 0.011) in patients who received 5-FU-based adjuvant chemotherapy. Fluorouracil 212-216 golgi phosphoprotein 3 Homo sapiens 49-55 24444035-8 2014 Moreover, multivariate analysis showed that GOLPH3 expression was an independent prognostic factor for DFS in CRC patients treated with 5-FU-based chemotherapy (HR, 0.468; 95%CI, 0.222-0.987; P = 0.046). Fluorouracil 136-140 golgi phosphoprotein 3 Homo sapiens 44-50 24444035-9 2014 In vitro, overexpression of GOLPH3 facilitated the 5-FU chemosensitivity in CRC cells; while siRNA-mediated knockdown of GOLPH3 reduced the sensitivity of CRC cells to 5-FU-induced apoptosis. Fluorouracil 51-55 golgi phosphoprotein 3 Homo sapiens 28-34 24444035-9 2014 In vitro, overexpression of GOLPH3 facilitated the 5-FU chemosensitivity in CRC cells; while siRNA-mediated knockdown of GOLPH3 reduced the sensitivity of CRC cells to 5-FU-induced apoptosis. Fluorouracil 168-172 golgi phosphoprotein 3 Homo sapiens 28-34 24444035-9 2014 In vitro, overexpression of GOLPH3 facilitated the 5-FU chemosensitivity in CRC cells; while siRNA-mediated knockdown of GOLPH3 reduced the sensitivity of CRC cells to 5-FU-induced apoptosis. Fluorouracil 168-172 golgi phosphoprotein 3 Homo sapiens 121-127 24444035-10 2014 CONCLUSIONS: Our results suggest that GOLPH3 is associated with prognosis in CRC patients treated with postoperative 5-FU-based adjuvant chemotherapy, and may serve as a potential indicator to predict 5-FU chemosensitivity. Fluorouracil 117-121 golgi phosphoprotein 3 Homo sapiens 38-44 24444035-10 2014 CONCLUSIONS: Our results suggest that GOLPH3 is associated with prognosis in CRC patients treated with postoperative 5-FU-based adjuvant chemotherapy, and may serve as a potential indicator to predict 5-FU chemosensitivity. Fluorouracil 201-205 golgi phosphoprotein 3 Homo sapiens 38-44 24052409-0 2014 Mahanine synergistically enhances cytotoxicity of 5-fluorouracil through ROS-mediated activation of PTEN and p53/p73 in colon carcinoma. Fluorouracil 50-64 tumor protein p53 Homo sapiens 109-112 24407236-0 2014 Antioxidants decrease the apoptotic effect of 5-Fu in colon cancer by regulating Src-dependent caspase-7 phosphorylation. Fluorouracil 46-50 SRC proto-oncogene, non-receptor tyrosine kinase Homo sapiens 81-84 24407236-6 2014 In this study, we show that 5-Fu can induce reactive oxygen species-dependent Src activation in colon cancer cells. Fluorouracil 28-32 SRC proto-oncogene, non-receptor tyrosine kinase Homo sapiens 78-81 24407236-10 2014 When using 5-Fu and antioxidants together, Src activation was blocked, resulting in decreased 5-Fu-induced apoptosis. Fluorouracil 11-15 SRC proto-oncogene, non-receptor tyrosine kinase Homo sapiens 43-46 24407236-10 2014 When using 5-Fu and antioxidants together, Src activation was blocked, resulting in decreased 5-Fu-induced apoptosis. Fluorouracil 94-98 SRC proto-oncogene, non-receptor tyrosine kinase Homo sapiens 43-46 24935593-5 2014 Effects of 5-FU+IL-2 on the expression and promoter activity of NKG2D ligands (MICA/MICB) in A549 cells in vitro were also assessed. Fluorouracil 11-15 inhibitor of carbonic anhydrase Mus musculus 79-83 24935593-10 2014 Combination treatment of 5-FU and IL-2 upregulated the expression and the promoter activity of MICA/MICB in A549 cells, which enhanced the recognition of A549 cells by NK cells. Fluorouracil 25-29 inhibitor of carbonic anhydrase Mus musculus 95-99 25087947-8 2014 Furthermore, combination treatment of GNA and 5-FU showed up-regulated of caspase-3, caspase-9, bax, RIP1, apoptosis-inducing factor (AIF), voltage-dependent anion channel (VDAC), cytochrome c and cyclophilin D and down-regulated bcl-2. Fluorouracil 46-50 caspase 3 Homo sapiens 74-83 25087947-8 2014 Furthermore, combination treatment of GNA and 5-FU showed up-regulated of caspase-3, caspase-9, bax, RIP1, apoptosis-inducing factor (AIF), voltage-dependent anion channel (VDAC), cytochrome c and cyclophilin D and down-regulated bcl-2. Fluorouracil 46-50 BCL2 associated X, apoptosis regulator Homo sapiens 96-99 25087947-8 2014 Furthermore, combination treatment of GNA and 5-FU showed up-regulated of caspase-3, caspase-9, bax, RIP1, apoptosis-inducing factor (AIF), voltage-dependent anion channel (VDAC), cytochrome c and cyclophilin D and down-regulated bcl-2. Fluorouracil 46-50 cytochrome c, somatic Homo sapiens 180-192 25087947-8 2014 Furthermore, combination treatment of GNA and 5-FU showed up-regulated of caspase-3, caspase-9, bax, RIP1, apoptosis-inducing factor (AIF), voltage-dependent anion channel (VDAC), cytochrome c and cyclophilin D and down-regulated bcl-2. Fluorouracil 46-50 peptidylprolyl isomerase F Homo sapiens 197-210 25087947-8 2014 Furthermore, combination treatment of GNA and 5-FU showed up-regulated of caspase-3, caspase-9, bax, RIP1, apoptosis-inducing factor (AIF), voltage-dependent anion channel (VDAC), cytochrome c and cyclophilin D and down-regulated bcl-2. Fluorouracil 46-50 BCL2 apoptosis regulator Homo sapiens 230-235 24434574-8 2014 Ad-mda-7 treatments upregulated Akt phosphorylation but suppressed IkappaB-alpha levels, whereas 5-FU treatments induced phosphorylation of p53 and extracellular signal-regulated protein kinases 1 and 2. Fluorouracil 97-101 tumor protein p53 Homo sapiens 140-143 24368879-2 2014 Ziv-aflibercept is a fusion protein which acts as a decoy receptor for vascular endothelial growth factor (VEGF)-A, VEGF-B, and placental growth factor (PlGF); it was approved in combination with 5-fluorouracil, leucovorin, and irinotecan (FOLFIRI) for the treatment of patients with metastatic colorectal cancer that is resistant to or has progressed after an oxaliplatin-containing fluoropyrimidine-based regimen. Fluorouracil 196-210 placental growth factor Homo sapiens 153-157 24434574-10 2014 These data collectively suggest that Ad-mda-7 induced apoptosis despite Akt activation and that the combinatory antitumor effects with 5-FU were produced partly by downregulating the Ad-mda-7-induced Akt activation. Fluorouracil 135-139 AKT serine/threonine kinase 1 Homo sapiens 200-203 24190362-9 2014 In addition, hTERTC27 overexpression evidently promoted the 5-FU-induced apoptosis by increasing the expression of activated caspase-3 and -9 and by downregulating the expression of B-cell lymphoma 2. Fluorouracil 60-64 caspase 3 Homo sapiens 125-141 24846461-9 2014 We here show that this temporal separation of pro- and anti-apoptotic signaling induced by inhibition of Dicer1 is synergistic and synthetic lethal to low-dose 5-FU chemotherapy in p53-mutated HACAT cells. Fluorouracil 160-164 tumor protein p53 Homo sapiens 181-184 24817302-7 2014 Stepwise regression analysis showed that the plasma concentration of fluorouracil was associated with myelosuppression, hand-foot syndrome, diarrhea, overall survival (OS) and DPD genotype. Fluorouracil 69-81 Moloney sarcoma oncogene Mus musculus 168-170 24293105-0 2014 Carcinoembryonic antigen expression level as a predictive factor for response to 5-fluorouracil in colorectal cancer. Fluorouracil 81-95 CEA cell adhesion molecule 3 Homo sapiens 0-24 24293105-9 2014 However, 5-FU treatment resulted in the selection of sub-populations of resistant cells that displayed increased CEA expression levels by increasing drug concentration. Fluorouracil 9-13 CEA cell adhesion molecule 3 Homo sapiens 113-116 24293105-12 2014 In comparison to the 3D spheroids of parental CHO, we observed a significantly elevated 5-FU resistance in 3D culture of the CEA-expressing CHO transfectants. Fluorouracil 88-92 CEA cell adhesion molecule 3 Homo sapiens 125-128 24293105-13 2014 Our findings suggest that the CEA level may be a suitable biomarker for predicting tumor response to 5-FU-based chemotherapy in CRC. Fluorouracil 101-105 CEA cell adhesion molecule 3 Homo sapiens 30-33 26629940-4 2014 It suggested that, compared to the control, body weight gain, the ratio of ovarian wet weight to body weight, primary follicle numbers, and the levels of AMH were significantly decreased, while the concentration of E2 and FSH was heavily increased following 5-FU administration. Fluorouracil 258-262 dihydrolipoamide S-succinyltransferase Rattus norvegicus 215-225 26629940-6 2014 Furthermore, at indicated times, 5-FU led to the reduced Bcl-2 and NF-kappaB expression and increased Bax expression while triptorelin plus 5-FU increased Bcl-2 and NF-kappaB expression and decreased Bax expression. Fluorouracil 140-144 BCL2, apoptosis regulator Rattus norvegicus 155-160 26629940-5 2014 In contrast, after coadministration of triptorelin with 5-FU, the ratio of ovarian wet weight to body weight and the levels of AMH were significantly increased, whereas the level of E2 and FSH was decreased significantly when compared with the 5-FU group. Fluorouracil 56-60 dihydrolipoamide S-succinyltransferase Rattus norvegicus 182-192 26629940-6 2014 Furthermore, at indicated times, 5-FU led to the reduced Bcl-2 and NF-kappaB expression and increased Bax expression while triptorelin plus 5-FU increased Bcl-2 and NF-kappaB expression and decreased Bax expression. Fluorouracil 33-37 BCL2, apoptosis regulator Rattus norvegicus 57-62 23428538-10 2014 We also showed that inhibiting Grp78 expression increased the cells" resistance to the cytotoxicity of the S-phase-specific anticancer drug 5-fluorouracil. Fluorouracil 140-154 heat shock protein family A (Hsp70) member 5 Homo sapiens 31-36 24141111-8 2014 The tumor inhibitory effect was greater with the HB1.F3.CD.IFN-beta cells, indicating an additional effect of IFN-beta to 5-FU. Fluorouracil 122-126 histocompatibility minor HB-1 Homo sapiens 49-52 24391839-8 2013 Notch-1 upregulation induced a possible epithelial-mesenchymal transition in U87-MCSF cells, which accounted for an increase in the proportion of CD24(high)/CD44(less) cancer stem cells in U87-MCSF cells after 5-FU treatment. Fluorouracil 210-214 notch receptor 1 Homo sapiens 0-7 24391839-9 2013 The elevated resistance of U87-MCSF cells towards 5-FU was due to the increase in the expressions (10.2 and 6 fold) of ABCB1 and mdm2, respectively. Fluorouracil 50-54 ATP binding cassette subfamily B member 1 Homo sapiens 119-124 24391839-10 2013 Furthermore, increase in expressions of ABCG1, mdm2 and CD24 was also observed in U87MG cells after prolonged incubation with 5-FU. Fluorouracil 126-130 ATP binding cassette subfamily G member 1 Homo sapiens 40-45 24391839-10 2013 Furthermore, increase in expressions of ABCG1, mdm2 and CD24 was also observed in U87MG cells after prolonged incubation with 5-FU. Fluorouracil 126-130 CD24 molecule Homo sapiens 56-60 24253812-3 2013 SMUG1 also processes radiation-induced oxidative base damage as well as 5-fluorouracil incorporated into DNA during chemotherapy. Fluorouracil 72-86 single-strand-selective monofunctional uracil-DNA glycosylase 1 Homo sapiens 0-5 24293316-3 2013 We show here that Doxorubicin, 5-Fluorouracil, Paclitaxel and Cisplatin treatments trigger, in various human cancer cell lines, an increase of netrin-1 expression which is accompanied by netrin-1 receptors increase. Fluorouracil 31-45 netrin 1 Mus musculus 187-195 24201083-3 2013 In this study we asked if the same chemotherapy regimens with GEM or 5-FU will enhance the antitumor effect of anti-CD40 and CpG. Fluorouracil 69-73 CD40 antigen Mus musculus 116-120 24349411-6 2013 The chemotherapeutic agent 5-fluorouracil (5-FU), which is used to treat LARC, synergized with AZD7762 and enhanced radiosensitization by AZD7762. Fluorouracil 27-41 C-C motif chemokine ligand 20 Homo sapiens 73-77 24349411-6 2013 The chemotherapeutic agent 5-fluorouracil (5-FU), which is used to treat LARC, synergized with AZD7762 and enhanced radiosensitization by AZD7762. Fluorouracil 43-47 C-C motif chemokine ligand 20 Homo sapiens 73-77 24324676-7 2013 In addition, in tumor-bearing mice, the relationship between the therapeutic effects of chemotherapy (5-FU) and the tumor accumulation of (99m)Tc-C3(BHam)2-annexin A5 just after the first treatment of 5-FU was evaluated. Fluorouracil 102-106 complement component 3 Mus musculus 146-155 24324676-13 2013 Accumulation of (99m)Tc-C3(BHam)2-annexin A5 in tumors significantly increased after 5-FU treatment. Fluorouracil 85-89 complement component 3 Mus musculus 24-33 24100731-0 2013 Lentivirus-mediated shRNA targeting of cyclin D1 enhances the chemosensitivity of human gastric cancer to 5-fluorouracil. Fluorouracil 106-120 cyclin D1 Homo sapiens 39-48 24131420-0 2013 Design of novel potent inhibitors of human uridine phosphorylase-1: synthesis, inhibition studies, thermodynamics, and in vitro influence on 5-fluorouracil cytotoxicity. Fluorouracil 141-155 uridine phosphorylase 1 Homo sapiens 43-66 24100731-6 2013 In this study, we investigated whether treatment of gastric cancer cells with shRNA targeting cyclin D1 (ShCCND1) or 5-FU, alone or in combination, influences the activation of phosphorylated AKT (pAKT) and pNFkappaB, which are markers that are increased in 5-FU chemoresistance. Fluorouracil 258-262 cyclin D1 Homo sapiens 94-103 24331695-10 2013 5-FU alone up-regulated cyclinD1 expression (1.45 +/- 0.12-fold change vs. untreated control group; P less than 0.01). Fluorouracil 0-4 cyclin D1 Homo sapiens 24-32 24331695-11 2013 Moreover, sorafenib alone significantly inhibited the RAF/MEK/ERK and STAT3 pathways, with the fold-changes of p-C-RAF, p-ERK1/2 and p-STAT3 being 0.56 +/- 0.05, 0.54 +/- 0.02 and 0.36 +/- 0.02, respectively (all P less than 0.01); 5-FU alone produced no significant effects on these pathways. Fluorouracil 232-236 zinc fingers and homeoboxes 2 Homo sapiens 54-57 24331695-14 2013 Sorafenib-inhibited RAF/MEK/ERK and STAT3 signaling and cyclinD1 expression may have induced the observed G1phase arrest and S phase reduction, thereby reducing the cells" sensitivity to 5-FU. Fluorouracil 187-191 zinc fingers and homeoboxes 2 Homo sapiens 20-23 24138824-3 2013 Our previous study showed that CRC patients with higher Lgr5 level are associated with poor response to 5-fluoracil-based treatment. Fluorouracil 104-115 leucine rich repeat containing G protein-coupled receptor 5 Homo sapiens 56-60 24278407-8 2013 Metformin enhanced the antiproliferative effects of 5-FU on CD133+ cscs in SW620 cells. Fluorouracil 52-56 prominin 1 Homo sapiens 60-65 24008552-8 2013 rAAV-FHL2-shRNA activated intrinsic and extrinsic apoptotic pathways and increased cell susceptibility to apoptotic stimuli by 5-FU. Fluorouracil 127-131 four and a half LIM domains 2 Homo sapiens 5-9 24008552-9 2013 Moreover, a xenograft model was established to explore rAAV-FHL2-shRNA with 5-FU mediated tumorigenesis in vivo. Fluorouracil 76-80 four and a half LIM domains 2 Homo sapiens 60-64 24138824-10 2013 Over-expression of Lgr5 also reduced the sensitivity of cultured CRC cells, including adherent and spheroids, towards 5-fluoracil and oxalipatin. Fluorouracil 118-129 leucine rich repeat containing G protein-coupled receptor 5 Homo sapiens 19-23 23108402-3 2013 Current knowledge states that in certain cell types, 5-FU-induced stress is signaling through a p53-dependent induction of tumor necrosis factor-receptor oligomerization required for death-inducing signaling complex formation and caspase-8 activation. Fluorouracil 53-57 caspase 8 Homo sapiens 230-239 24039897-0 2013 A Bmi1-miRNAs cross-talk modulates chemotherapy response to 5-fluorouracil in breast cancer cells. Fluorouracil 60-74 BMI1 proto-oncogene, polycomb ring finger Homo sapiens 2-6 24280569-5 2013 Increased expression of SLC29A1 in vitro has been described as a potential critical factor determining the sensitivity of pancreatic cancer cells to gemcitabine and 5-fluorouracil, the principal cytotoxic agents used in the treatment of pancreatic cancer. Fluorouracil 165-179 solute carrier family 29 member 1 (Augustine blood group) Homo sapiens 24-31 24228095-11 2013 The expression of Bax and Caspase-3 were dramatically increased after 5-FU treatment (p<0.01) and Curcumin treatment significantly reduced Bax expression (p<0.05) but had only a moderate effect on reducing caspase-3 expression (p>0.05). Fluorouracil 70-74 caspase 3 Rattus norvegicus 26-35 24228095-11 2013 The expression of Bax and Caspase-3 were dramatically increased after 5-FU treatment (p<0.01) and Curcumin treatment significantly reduced Bax expression (p<0.05) but had only a moderate effect on reducing caspase-3 expression (p>0.05). Fluorouracil 70-74 caspase 3 Rattus norvegicus 212-221 24039897-2 2013 Here, we found Bmi1 overexpression in 5-Fu (5-fluorouracil)-resistant MCF-7 cells (MCF-7/5-Fu) derived from MCF-7 breast cancer cells, MDA-MB-231 and MDA-MB-453 breast cancer cells compared to MCF-7 cells, was related with 5-Fu resistance and enrichment of CD44(+)/CD24(-) stem cell subpopulation. Fluorouracil 38-42 BMI1 proto-oncogene, polycomb ring finger Homo sapiens 15-19 24039897-2 2013 Here, we found Bmi1 overexpression in 5-Fu (5-fluorouracil)-resistant MCF-7 cells (MCF-7/5-Fu) derived from MCF-7 breast cancer cells, MDA-MB-231 and MDA-MB-453 breast cancer cells compared to MCF-7 cells, was related with 5-Fu resistance and enrichment of CD44(+)/CD24(-) stem cell subpopulation. Fluorouracil 44-58 BMI1 proto-oncogene, polycomb ring finger Homo sapiens 15-19 24039897-2 2013 Here, we found Bmi1 overexpression in 5-Fu (5-fluorouracil)-resistant MCF-7 cells (MCF-7/5-Fu) derived from MCF-7 breast cancer cells, MDA-MB-231 and MDA-MB-453 breast cancer cells compared to MCF-7 cells, was related with 5-Fu resistance and enrichment of CD44(+)/CD24(-) stem cell subpopulation. Fluorouracil 89-93 BMI1 proto-oncogene, polycomb ring finger Homo sapiens 15-19 24039897-3 2013 Bmi1 knockdown enhanced the sensitivity of breast cancer cells to 5-Fu and 5-Fu induced apoptosis via mitochondrial apoptotic pathway, and decreased the fraction of CD44(+)/CD24(-) subpopulation. Fluorouracil 66-70 BMI1 proto-oncogene, polycomb ring finger Homo sapiens 0-4 24039897-3 2013 Bmi1 knockdown enhanced the sensitivity of breast cancer cells to 5-Fu and 5-Fu induced apoptosis via mitochondrial apoptotic pathway, and decreased the fraction of CD44(+)/CD24(-) subpopulation. Fluorouracil 75-79 BMI1 proto-oncogene, polycomb ring finger Homo sapiens 0-4 24039897-5 2013 MiR-200c and miR-203 overexpression in breast cancer cells downregulated Bmi1 expression accompanied with reversion of resistance to 5-Fu mediated by Bmi1. Fluorouracil 133-137 microRNA 200c Homo sapiens 0-8 24039897-5 2013 MiR-200c and miR-203 overexpression in breast cancer cells downregulated Bmi1 expression accompanied with reversion of resistance to 5-Fu mediated by Bmi1. Fluorouracil 133-137 microRNA 203a Homo sapiens 13-20 24039897-5 2013 MiR-200c and miR-203 overexpression in breast cancer cells downregulated Bmi1 expression accompanied with reversion of resistance to 5-Fu mediated by Bmi1. Fluorouracil 133-137 BMI1 proto-oncogene, polycomb ring finger Homo sapiens 150-154 23900217-5 2013 In 5-fluorouracil (5-FU)-treated patients, the tumour overexpression of SOX9 correlated with markedly poorer survival (HR=8.72, P=0.034), but had no predictive effect in untreated patients (HR=0.70, P=0.29). Fluorouracil 3-17 SRY-box transcription factor 9 Homo sapiens 72-76 24124444-0 2013 A Ham1p-dependent mechanism and modulation of the pyrimidine biosynthetic pathway can both confer resistance to 5-fluorouracil in yeast. Fluorouracil 112-126 nucleoside triphosphate pyrophosphohydrolase HAM1 Saccharomyces cerevisiae S288C 2-7 24124444-8 2013 In contrast, HAM1 and YJL055W confer 5-FU resistance in a ura2 mutant, and selectively inhibit incorporation into RNA of 5-FU but not uracil. Fluorouracil 37-41 nucleoside triphosphate pyrophosphohydrolase HAM1 Saccharomyces cerevisiae S288C 13-17 24124444-8 2013 In contrast, HAM1 and YJL055W confer 5-FU resistance in a ura2 mutant, and selectively inhibit incorporation into RNA of 5-FU but not uracil. Fluorouracil 37-41 Log1p Saccharomyces cerevisiae S288C 22-29 24124444-8 2013 In contrast, HAM1 and YJL055W confer 5-FU resistance in a ura2 mutant, and selectively inhibit incorporation into RNA of 5-FU but not uracil. Fluorouracil 121-125 nucleoside triphosphate pyrophosphohydrolase HAM1 Saccharomyces cerevisiae S288C 13-17 24124444-8 2013 In contrast, HAM1 and YJL055W confer 5-FU resistance in a ura2 mutant, and selectively inhibit incorporation into RNA of 5-FU but not uracil. Fluorouracil 121-125 Log1p Saccharomyces cerevisiae S288C 22-29 24124444-10 2013 This suggests that HAM1 and YJL055W function together in mediating resistance to 5-FU. Fluorouracil 81-85 nucleoside triphosphate pyrophosphohydrolase HAM1 Saccharomyces cerevisiae S288C 19-23 24124444-10 2013 This suggests that HAM1 and YJL055W function together in mediating resistance to 5-FU. Fluorouracil 81-85 Log1p Saccharomyces cerevisiae S288C 28-35 23900217-5 2013 In 5-fluorouracil (5-FU)-treated patients, the tumour overexpression of SOX9 correlated with markedly poorer survival (HR=8.72, P=0.034), but had no predictive effect in untreated patients (HR=0.70, P=0.29). Fluorouracil 19-23 SRY-box transcription factor 9 Homo sapiens 72-76 23941782-10 2013 Cd plus 5-FU decreased cyclin D1 and increased cyclin A1 expression. Fluorouracil 8-12 cyclin D1 Homo sapiens 23-32 22643568-7 2013 TTP was significantly improved for patients who received irinotecan+5-FU+bevacizumab (median TTP, 13.73 +- 2.10 mo) when compared with irinotecan+5-FU (median TTP, 5.13 +- 0.70 mo). Fluorouracil 68-72 ZFP36 ring finger protein Homo sapiens 0-3 22643568-7 2013 TTP was significantly improved for patients who received irinotecan+5-FU+bevacizumab (median TTP, 13.73 +- 2.10 mo) when compared with irinotecan+5-FU (median TTP, 5.13 +- 0.70 mo). Fluorouracil 68-72 ZFP36 ring finger protein Homo sapiens 93-96 22643568-7 2013 TTP was significantly improved for patients who received irinotecan+5-FU+bevacizumab (median TTP, 13.73 +- 2.10 mo) when compared with irinotecan+5-FU (median TTP, 5.13 +- 0.70 mo). Fluorouracil 68-72 ZFP36 ring finger protein Homo sapiens 93-96 23729362-8 2013 Cell death of 5-fluorouracil (5FU)-treated p53-null GSK3B-silenced colon carcinoma cells occurred via PARP1-dependent and AIF-mediated but RIP1-independent necroptosis. Fluorouracil 14-28 glycogen synthase kinase 3 beta Homo sapiens 52-57 23861589-1 2013 PURPOSE: To determine whether 5-fluorouracil (5-FU) sensitivity is associated with the mRNA expressions of thymidylate synthase (TS), dihydropyrimidine dehydrogenase (DPD), and thymidine phosphorylase (TP) in patients with hepatocellular carcinoma (HCC) treated with 5-FU-based transarterial chemoembolization (TACE). Fluorouracil 30-44 thymidine phosphorylase Homo sapiens 202-204 23861589-1 2013 PURPOSE: To determine whether 5-fluorouracil (5-FU) sensitivity is associated with the mRNA expressions of thymidylate synthase (TS), dihydropyrimidine dehydrogenase (DPD), and thymidine phosphorylase (TP) in patients with hepatocellular carcinoma (HCC) treated with 5-FU-based transarterial chemoembolization (TACE). Fluorouracil 46-50 thymidine phosphorylase Homo sapiens 177-200 23861589-1 2013 PURPOSE: To determine whether 5-fluorouracil (5-FU) sensitivity is associated with the mRNA expressions of thymidylate synthase (TS), dihydropyrimidine dehydrogenase (DPD), and thymidine phosphorylase (TP) in patients with hepatocellular carcinoma (HCC) treated with 5-FU-based transarterial chemoembolization (TACE). Fluorouracil 46-50 thymidine phosphorylase Homo sapiens 202-204 23455382-5 2013 We used the chemotherapeutic agent 5-fluorouracil to induce apoptosis in HCC cell lines and found that hnRNP K was downregulated, independent of both p53 and caspases. Fluorouracil 35-49 heterogeneous nuclear ribonucleoprotein K Homo sapiens 103-110 23607451-5 2013 RESULTS: We show that HDP 5-FU administration does indeed radiosensitize both the highly radioresistant U87MG-VIII and HCT-116. Fluorouracil 26-30 cytochrome c oxidase subunit 8A Homo sapiens 110-114 23570661-0 2013 Stable gene-silence of Kif2a synergistic with 5-fluorouracil suppresses oral tongue squamous cell carcinoma growth in vitro and in vivo. Fluorouracil 46-60 kinesin family member 2A Homo sapiens 23-28 23570661-7 2013 pGPU6/GFP/Kif2a synergized the tumor suppression effect of 5-Fluorouracil (5-Fu) on Tca8113 cells. Fluorouracil 59-73 kinesin family member 2A Homo sapiens 10-15 23570661-7 2013 pGPU6/GFP/Kif2a synergized the tumor suppression effect of 5-Fluorouracil (5-Fu) on Tca8113 cells. Fluorouracil 75-79 kinesin family member 2A Homo sapiens 10-15 23727578-3 2013 p53 activation by 5-fluorouracil significantly increased hGBP1 expression in wild-type p53 cells, but not in p53-null cells. Fluorouracil 18-32 guanylate binding protein 1 Homo sapiens 57-62 23727578-4 2013 Knockdown of p53 expression remarkably impaired hGBP1 expression induced by 5-fluorouracil, type I interferon treatment, or influenza A virus infection. Fluorouracil 76-90 guanylate binding protein 1 Homo sapiens 48-53 23403306-2 2013 In this study, we introduced the human parental neural stem cells, HB1.F3, with the human interferon beta (IFN-beta) gene which is a typical cytokine gene that has an antitumor effect and the cytosine deaminase (CD) gene from Escherichia coli (E. coli) that could convert the non-toxic prodrug, 5-fluorocytosine (5-FC), to a toxic metabolite, 5-fluorouracil (5-FU). Fluorouracil 343-357 interferon beta 1 Homo sapiens 90-105 23528453-5 2013 Despite this, Shb knockout LT-HSCs responded promptly by entering the cell cycle in response to genotoxic stress by 5-fluorouracil treatment. Fluorouracil 116-130 src homology 2 domain-containing transforming protein B Mus musculus 14-17 23403306-2 2013 In this study, we introduced the human parental neural stem cells, HB1.F3, with the human interferon beta (IFN-beta) gene which is a typical cytokine gene that has an antitumor effect and the cytosine deaminase (CD) gene from Escherichia coli (E. coli) that could convert the non-toxic prodrug, 5-fluorocytosine (5-FC), to a toxic metabolite, 5-fluorouracil (5-FU). Fluorouracil 343-357 interferon beta 1 Homo sapiens 107-115 23403306-2 2013 In this study, we introduced the human parental neural stem cells, HB1.F3, with the human interferon beta (IFN-beta) gene which is a typical cytokine gene that has an antitumor effect and the cytosine deaminase (CD) gene from Escherichia coli (E. coli) that could convert the non-toxic prodrug, 5-fluorocytosine (5-FC), to a toxic metabolite, 5-fluorouracil (5-FU). Fluorouracil 359-363 interferon beta 1 Homo sapiens 90-105 23403306-2 2013 In this study, we introduced the human parental neural stem cells, HB1.F3, with the human interferon beta (IFN-beta) gene which is a typical cytokine gene that has an antitumor effect and the cytosine deaminase (CD) gene from Escherichia coli (E. coli) that could convert the non-toxic prodrug, 5-fluorocytosine (5-FC), to a toxic metabolite, 5-fluorouracil (5-FU). Fluorouracil 359-363 interferon beta 1 Homo sapiens 107-115 23403306-6 2013 In particular, HB1.F3.CD.IFN-beta cells showed the synergistic cytotoxic activity of 5-FU and IFN-beta. Fluorouracil 85-89 interferon beta 1 Homo sapiens 25-33 23646193-11 2013 Treatment of cells with 5-FU induced changes in cellular and nuclear morphology, a decrease in the number of stress fibers and a major decrease in the number of caveolin-3 positive cells. Fluorouracil 24-28 caveolin 3 Homo sapiens 161-171 23846927-5 2013 First, the predictive role of hENT1, which codes for a gemcitabine transporter into cells, was highlighted and might help us decide whether we benefit from gemcitabine or 5-fluorouracil in the adjuvant setting (Abstract #4006). Fluorouracil 171-185 solute carrier family 29 member 1 (Augustine blood group) Homo sapiens 30-35 23814492-8 2013 In addition, 5-FU and X-ray decreased the expression of mRNAs for suppressor of cytokine signaling 1 (SOCS1) and SOCS3. Fluorouracil 13-17 suppressor of cytokine signaling 3 Homo sapiens 113-118 23588527-3 2013 However, the means by which RRM-1 participates in the anticancer effects of 5-FU and cisplatin (CDDP) have not been well studied. Fluorouracil 76-80 ribonucleotide reductase catalytic subunit M1 Homo sapiens 28-33 23588527-4 2013 Here, we show that RRM-1 significantly contributes to the induction of DNA damage by 5-FU in esophageal cancer cell lines. Fluorouracil 85-89 ribonucleotide reductase catalytic subunit M1 Homo sapiens 19-24 23646193-12 2013 Our results suggest that the disorganization of the actin cytoskeleton and the reduction of caveolin-3 expression could explain the alterations in contractility observed in patients treated with 5-FU. Fluorouracil 195-199 caveolin 3 Homo sapiens 92-102 23588527-5 2013 An assay of gamma-H2AX focus formation, a marker of DNA damage, after 5-FU treatment revealed good correlation with the levels of RRM-1 protein expression. Fluorouracil 70-74 ribonucleotide reductase catalytic subunit M1 Homo sapiens 130-135 23588527-6 2013 Moreover, the increased sensitivity and RAD51 focus formation induced by the combination treatment of 5-FU and CDDP were significantly repressed by RRM-1 depletion. Fluorouracil 102-106 ribonucleotide reductase catalytic subunit M1 Homo sapiens 148-153 24250621-9 2013 5-FU also induced HMGB1 secretion, Cas3 and PARP activity and these effects were stronger in cells expressing WT TLR4 than the other cells. Fluorouracil 0-4 high mobility group box 1 Homo sapiens 18-23 23588527-7 2013 These results suggest that RRM-1 is involved not only in the induction of DNA damage by 5-FU but also in the synergistic cytotoxic effect in the combination therapy of 5-FU and CDDP. Fluorouracil 88-92 ribonucleotide reductase catalytic subunit M1 Homo sapiens 27-32 23588527-7 2013 These results suggest that RRM-1 is involved not only in the induction of DNA damage by 5-FU but also in the synergistic cytotoxic effect in the combination therapy of 5-FU and CDDP. Fluorouracil 168-172 ribonucleotide reductase catalytic subunit M1 Homo sapiens 27-32 23420099-9 2013 In conclusion, mRNA levels of SLC22A2, SLC23A2, ABCB1, ABCC2, Rad51, MSH2 and DPYD were confirmed to be strongly correlated with IC50 values for 5-FU, and mRNA levels of ABCC2, MSH2 and DPYD were confirmed to be strongly correlated with IC(50) values for CDDP. Fluorouracil 145-149 solute carrier family 23 member 2 Homo sapiens 39-46 23420099-9 2013 In conclusion, mRNA levels of SLC22A2, SLC23A2, ABCB1, ABCC2, Rad51, MSH2 and DPYD were confirmed to be strongly correlated with IC50 values for 5-FU, and mRNA levels of ABCC2, MSH2 and DPYD were confirmed to be strongly correlated with IC(50) values for CDDP. Fluorouracil 145-149 mutS homolog 2 Homo sapiens 69-73 23420099-9 2013 In conclusion, mRNA levels of SLC22A2, SLC23A2, ABCB1, ABCC2, Rad51, MSH2 and DPYD were confirmed to be strongly correlated with IC50 values for 5-FU, and mRNA levels of ABCC2, MSH2 and DPYD were confirmed to be strongly correlated with IC(50) values for CDDP. Fluorouracil 145-149 mutS homolog 2 Homo sapiens 177-181 23412092-6 2013 In both WT and Irf2(-/-) recipients, active type I IFN signaling greatly enhanced the sensitivity to 5-FU or low-dose irradiation of HSCs. Fluorouracil 101-105 interferon regulatory factor 2 Mus musculus 15-19 23202296-3 2013 Here we show that two clinically used chemotherapeutic agents, gemcitabine (Gem) and 5-fluorouracil (5FU), activate the NOD-like receptor family, pyrin domain containing-3 protein (Nlrp3)-dependent caspase-1 activation complex (termed the inflammasome) in myeloid-derived suppressor cells (MDSCs), leading to production of interleukin-1beta (IL-1beta), which curtails anticancer immunity. Fluorouracil 85-99 caspase 1 Mus musculus 198-207 23202296-3 2013 Here we show that two clinically used chemotherapeutic agents, gemcitabine (Gem) and 5-fluorouracil (5FU), activate the NOD-like receptor family, pyrin domain containing-3 protein (Nlrp3)-dependent caspase-1 activation complex (termed the inflammasome) in myeloid-derived suppressor cells (MDSCs), leading to production of interleukin-1beta (IL-1beta), which curtails anticancer immunity. Fluorouracil 101-104 caspase 1 Mus musculus 198-207 23202296-6 2013 Accordingly, Gem and 5FU exerted higher antitumor effects when tumors were established in Nlrp3(-/-) or Casp1(-/-) mice or wild-type mice treated with interleukin-1 receptor antagonist (IL-1Ra). Fluorouracil 21-24 caspase 1 Mus musculus 104-109 23451189-9 2013 Curcumin potentiated 5-FU-induced expression or cleavage of pro-apoptotic proteins (caspase-8, -9, -3, PARP and Bax), and down-regulated anti-apoptotic (Bcl-xL) and proliferative (cyclin D1) proteins. Fluorouracil 21-25 caspase 8 Homo sapiens 84-101 23271323-3 2013 This study investigated the role of nucleoside transporters, particularly human equilibrative nucleoside transporter 1 (hENT1), in predicting clinical treatment outcome with 5FU-based therapy. Fluorouracil 174-177 solute carrier family 29 member 1 (Augustine blood group) Homo sapiens 80-118 23271323-3 2013 This study investigated the role of nucleoside transporters, particularly human equilibrative nucleoside transporter 1 (hENT1), in predicting clinical treatment outcome with 5FU-based therapy. Fluorouracil 174-177 solute carrier family 29 member 1 (Augustine blood group) Homo sapiens 120-125 23451189-9 2013 Curcumin potentiated 5-FU-induced expression or cleavage of pro-apoptotic proteins (caspase-8, -9, -3, PARP and Bax), and down-regulated anti-apoptotic (Bcl-xL) and proliferative (cyclin D1) proteins. Fluorouracil 21-25 cyclin D1 Homo sapiens 180-189 23271323-5 2013 To provide mechanistic support for the role of hENT1 in 5FU resistance, cell viability of Caco-2 cells was measured, following incubation with varying concentrations of 5FU and a hENT1 inhibitor. Fluorouracil 56-59 solute carrier family 29 member 1 (Augustine blood group) Homo sapiens 47-52 22965880-0 2012 RHBDD2: a 5-fluorouracil responsive gene overexpressed in the advanced stages of colorectal cancer. Fluorouracil 10-24 rhomboid domain containing 2 Homo sapiens 0-6 23525727-10 2013 siRNA for p65 treatment significantly increased the apoptotic index in 5-FU-treated KYSE220 cells. Fluorouracil 71-75 RELA proto-oncogene, NF-kB subunit Homo sapiens 10-13 22965880-6 2012 In addition, we investigated RHBDD2 expression in response to the chemotherapy agent 5-fluorouracile (5FU). Fluorouracil 102-105 rhomboid domain containing 2 Homo sapiens 29-35 23108049-5 2012 Expression of shDUSP6 inhibited 5"-FU-induced cell death, whereas overexpression of DUSP6 increased susceptibility to 5"-FU. Fluorouracil 32-37 dual specificity phosphatase 6 Homo sapiens 16-21 23242307-0 2013 Bmi1 gene silencing inhibits the proliferation and invasiveness of human hepatocellular carcinoma cells and increases their sensitivity to 5-fluorouracil. Fluorouracil 151-165 BMI1 proto-oncogene, polycomb ring finger Homo sapiens 0-4 23108049-6 2012 5"-FU treatment dephosphorylated ERK in a DUSP6-dependent manner, resulting in destabilization of Bcl-2 and stabilization of Bad. Fluorouracil 0-5 dual specificity phosphatase 6 Homo sapiens 42-47 23242307-4 2013 The proliferation and migration of Bmi1-silenced tumor cells and their sensitivity to 5-FU treatment were determined by Cell Counting Kit-8 (CCK-8), transwell assays and 4",6-diamidino-2-phenylindole (DAPI) staining and flow cytometry, respectively. Fluorouracil 98-102 BMI1 proto-oncogene, polycomb ring finger Homo sapiens 35-39 23242307-7 2013 Moreover, Bmi1 gene silencing increased the percentage of apoptotic cells treated by 5-FU and decreased the IC50 values of 5-FU to a greater extent. Fluorouracil 97-101 BMI1 proto-oncogene, polycomb ring finger Homo sapiens 10-14 23099809-1 2012 BACKGROUND: The aim of this study was to investigate the value of the cyclin D1 isoforms D1a and D1b as prognostic factors and their relevance as predictors of response to adjuvant chemotherapy with 5-fluorouracil and levamisole (5-FU/LEV) in colorectal cancer (CRC). Fluorouracil 199-213 cyclin D1 Homo sapiens 70-79 23242307-7 2013 Moreover, Bmi1 gene silencing increased the percentage of apoptotic cells treated by 5-FU and decreased the IC50 values of 5-FU to a greater extent. Fluorouracil 135-139 BMI1 proto-oncogene, polycomb ring finger Homo sapiens 10-14 23242307-8 2013 Downregulation of the Bmi1 gene by RNAi can inhibit the proliferation and invasivesness of HCC cells and increase their sensitivity to 5-FU treatment. Fluorouracil 147-151 BMI1 proto-oncogene, polycomb ring finger Homo sapiens 22-26 23103836-5 2013 Knockdown of MGAT3 expression promoted MHCC97-L cells invasion and increased resistance to 5-fluorouracil in vitro. Fluorouracil 91-105 beta-1,4-mannosyl-glycoprotein 4-beta-N-acetylglucosaminyltransferase Homo sapiens 13-18 23229794-13 2013 5-FU mediated cell death in the EMT process induced by TGF-beta more effectively than HGF. Fluorouracil 0-4 transforming growth factor, beta 1 Mus musculus 55-63 22641337-0 2012 Water extract of Hedyotis Diffusa Willd suppresses proliferation of human HepG2 cells and potentiates the anticancer efficacy of low-dose 5-fluorouracil by inhibiting the CDK2-E2F1 pathway. Fluorouracil 150-164 cyclin dependent kinase 2 Homo sapiens 195-199 22641337-9 2012 In addition, HDW remarkably potentiated the anticancer effect of low-dose 5-FU in the absence of overt toxicity by downregulating the mRNA and protein levels of CDK2, cyclin E and E2F1. Fluorouracil 74-78 cyclin dependent kinase 2 Homo sapiens 185-189 21487682-2 2012 The aim of this study was to assess the effect of clusterin overexpression in CRC cells on sensitivity to 5-fluorouracil (5-FU), oxaliplatin and FOLFOX treatment under normoxic and graded hypoxic conditions. Fluorouracil 106-120 clusterin Homo sapiens 50-59 21487682-2 2012 The aim of this study was to assess the effect of clusterin overexpression in CRC cells on sensitivity to 5-fluorouracil (5-FU), oxaliplatin and FOLFOX treatment under normoxic and graded hypoxic conditions. Fluorouracil 122-126 clusterin Homo sapiens 50-59 21487682-5 2012 The response of parental and clusterin overexpressing cells to 5-FU, oxaliplatin and FOLFOX was examined using a crystal violet-based proliferation assay under normoxic conditions, 3% and 1% hypoxic conditions. Fluorouracil 63-67 clusterin Homo sapiens 29-38 22699078-9 2012 Axitinib, alone and in combination with 5-FU, reduced ABCG2 expression in the tumor tissue, and 5-FU has no such effect. Fluorouracil 40-44 ATP binding cassette subfamily G member 2 (Junior blood group) Mus musculus 54-59 22426744-5 2012 Cytosine deaminase (CD), one of the suicide genes, originating from bacterial (bCD) or yeast (yCD), which can convert the non-toxic prodrug, 5-fluorocytosine (5-FC), into 5-fluorouracil (5-FU), can inhibit cancer cell growth. Fluorouracil 195-209 cytosine deaminase Saccharomyces cerevisiae S288C 0-18 23390374-8 2013 Treatment of BALB/c mice that bear CT26/NY-ESO-1 tumors with 5-fluorouracil (5-FU) plus 12D7 was significantly more effective than chemotherapy alone. Fluorouracil 61-75 cancer/testis antigen 1A Homo sapiens 40-48 23390374-8 2013 Treatment of BALB/c mice that bear CT26/NY-ESO-1 tumors with 5-fluorouracil (5-FU) plus 12D7 was significantly more effective than chemotherapy alone. Fluorouracil 77-81 cancer/testis antigen 1A Homo sapiens 40-48 22426744-5 2012 Cytosine deaminase (CD), one of the suicide genes, originating from bacterial (bCD) or yeast (yCD), which can convert the non-toxic prodrug, 5-fluorocytosine (5-FC), into 5-fluorouracil (5-FU), can inhibit cancer cell growth. Fluorouracil 195-209 cytosine deaminase Saccharomyces cerevisiae S288C 20-22 22426744-5 2012 Cytosine deaminase (CD), one of the suicide genes, originating from bacterial (bCD) or yeast (yCD), which can convert the non-toxic prodrug, 5-fluorocytosine (5-FC), into 5-fluorouracil (5-FU), can inhibit cancer cell growth. Fluorouracil 211-215 cytosine deaminase Saccharomyces cerevisiae S288C 0-18 22426744-5 2012 Cytosine deaminase (CD), one of the suicide genes, originating from bacterial (bCD) or yeast (yCD), which can convert the non-toxic prodrug, 5-fluorocytosine (5-FC), into 5-fluorouracil (5-FU), can inhibit cancer cell growth. Fluorouracil 211-215 cytosine deaminase Saccharomyces cerevisiae S288C 20-22 22623418-7 2012 For example, the detoxification enzyme NQO1 was increased with treatment in both cell lines, while disparate members of the peroxiredoxin family, PRDX2 or PRDX5 and PRDX6, were elevated with 5-FU exposure in either SW480 or SW620, respectively. Fluorouracil 191-195 peroxiredoxin 6 Homo sapiens 165-170 22736137-8 2012 The 5-FU concentration in colorectal neoplasm was higher in the PEG-5-FU-MAMS group than that in the 5-FU-MAMS group(P<0.01), while the concentration was lower in the liver and the lung than that in the 5-FU-MAMS group(all P<0.01). Fluorouracil 4-8 neuronatin Mus musculus 64-69 22736137-10 2012 CONCLUSION: Both PEG-5-FU-MAMS and 5-FU-MAMS show significant magnetic targeting to the colorectal neoplasm, and passive target capacity of PEG-5-FU-MAMS to liver and the lung. Fluorouracil 21-25 neuronatin Mus musculus 140-145 21821547-0 2012 Recurrence risk score based on the specific activity of CDK1 and CDK2 predicts response to neoadjuvant paclitaxel followed by 5-fluorouracil, epirubicin and cyclophosphamide in breast cancers. Fluorouracil 126-140 cyclin dependent kinase 2 Homo sapiens 65-69 24191166-0 2013 A Type II Arabinogalactan from Anoectochilus formosanus for G-CSF Production in Macrophages and Leukopenia Improvement in CT26-Bearing Mice Treated with 5-Fluorouracil. Fluorouracil 153-167 colony stimulating factor 3 (granulocyte) Mus musculus 60-65 21523522-4 2012 RESULTS: After 5-FU treatment, only the CD71- fraction was significantly increased. Fluorouracil 15-19 transferrin receptor Homo sapiens 40-44 21523522-5 2012 Investigation of CD71 indicated that the CD71- cell fraction was present in the G1/G0 cell cycle phase and showed high resistance to the anticancer agent 5-FU. Fluorouracil 154-158 transferrin receptor Homo sapiens 17-21 21523522-5 2012 Investigation of CD71 indicated that the CD71- cell fraction was present in the G1/G0 cell cycle phase and showed high resistance to the anticancer agent 5-FU. Fluorouracil 154-158 transferrin receptor Homo sapiens 41-45 22161137-11 2012 In addition, AGS cells transfected with wild-type PDCD6 and treated with 5-FU showed synergistic inhibition of cell viability (P < 0.001). Fluorouracil 73-77 programmed cell death 6 Homo sapiens 50-55 23322993-21 2012 CONCLUSION: The combined effects of HHC with 5-FU exhibit a synergistic inhibition by decreasing ACF formation mediated by down-regulation of COX-2 expression. Fluorouracil 45-49 cytochrome c oxidase II, mitochondrial Rattus norvegicus 142-147 22188649-0 2012 ATR-Chk1 signaling pathway and homologous recombinational repair protect cells from 5-fluorouracil cytotoxicity. Fluorouracil 84-98 ATR serine/threonine kinase Gallus gallus 0-3 22188649-5 2012 5-FU induced gammaH2AX nuclear foci, which were colocalized with the key HRR factor Rad51, but not with DNA double-strand breaks (DSBs), in a dose-dependent manner as cells accumulated in the S phase. Fluorouracil 0-4 RAD51 recombinase Gallus gallus 84-89 22205688-2 2012 In colorectal cancer cells, HER3 blockade restricted cellular growth (G(2)-M arrest), survival, migration, and invasion, and potentiated the chemotherapeutic effect of 5-FU, supporting strategies that target HER3 in subsets of patients with colorectal cancer. Fluorouracil 168-172 erb-b2 receptor tyrosine kinase 3 Homo sapiens 28-32 22954703-4 2012 The CD133 (+) clonal SW620 cells displayed a differential gene expression profile, higher cellular reactive oxygen species (ROS), enhanced tumorigenesis and resistance to 5-fluorouracil. Fluorouracil 172-186 prominin 1 Homo sapiens 4-9 22416214-7 2012 The number of CD133(+) cells was also significantly increased by both 5-FU and MTX treatment in all of the cell lines tested. Fluorouracil 70-74 prominin 1 Homo sapiens 14-19 21713761-9 2012 In addition, FBI-1 could inhibit cell death induced by 5-fluorouracil or doxorubicin through suppressing the activation of p53. Fluorouracil 55-69 zinc finger and BTB domain containing 7A Homo sapiens 13-18 23549021-0 2012 Attachment of an anti-MUC1 monoclonal antibody to 5-FU loaded BSA nanoparticles for active targeting of breast cancer cells. Fluorouracil 50-54 mucin 1, cell surface associated Homo sapiens 22-26 22433290-0 2012 Plasma diamine oxidase activity is a useful biomarker for evaluating gastrointestinal tract toxicities during chemotherapy with oral fluorouracil anti-cancer drugs in patients with gastric cancer. Fluorouracil 133-145 amine oxidase copper containing 1 Homo sapiens 7-22 23063289-5 2012 Though FDXR has been reported to be differentially expressed upon treatment with 5-fluorouracil and its expression correlated to long term disease survival, to our knowledge this is a first study implicating a wide effect of anti-cancer drug treatment on FDXR expression. Fluorouracil 81-95 ferredoxin reductase Homo sapiens 7-11 22433290-8 2012 CONCLUSIONS: Plasma DAO activities may be useful for monitoring and evaluating gastrointestinal tract toxicities induced by adjuvant chemotherapy with oral fluorouracil in patients with gastric cancer. Fluorouracil 156-168 amine oxidase copper containing 1 Homo sapiens 20-23 23029137-3 2012 Our results show that, compared to beta-catenin knockdown, Tcf-4 knockdown more effectively inhibited colony formation, induced apoptosis, and increased 5-FU and oxaliplatin-mediated cytotoxicity in colon cancer cells. Fluorouracil 153-157 transcription factor 4 Homo sapiens 59-64 22675576-4 2012 Depletion of LSK cells by radiation or the cytotoxic chemical 5-fluorouracil results in an expansion of the LSK(-) population. Fluorouracil 62-76 lymphocyte protein tyrosine kinase Mus musculus 13-16 22675576-4 2012 Depletion of LSK cells by radiation or the cytotoxic chemical 5-fluorouracil results in an expansion of the LSK(-) population. Fluorouracil 62-76 lymphocyte protein tyrosine kinase Mus musculus 108-111 21910008-0 2011 The pro-apoptotic protein Prostate Apoptosis Response Protein-4 (Par-4) can be activated in colon cancer cells by treatment with Src inhibitor and 5-FU. Fluorouracil 147-151 pro-apoptotic WT1 regulator Homo sapiens 26-63 21910008-0 2011 The pro-apoptotic protein Prostate Apoptosis Response Protein-4 (Par-4) can be activated in colon cancer cells by treatment with Src inhibitor and 5-FU. Fluorouracil 147-151 pro-apoptotic WT1 regulator Homo sapiens 65-70 21910008-1 2011 The overexpression of the pro-apoptotic protein Prostate Apoptosis Response Protein-4 in colon cancer has been shown to increase response to the chemotherapeutic agent 5-fluorouracil (5-FU). Fluorouracil 168-182 pro-apoptotic WT1 regulator Homo sapiens 48-85 21910008-1 2011 The overexpression of the pro-apoptotic protein Prostate Apoptosis Response Protein-4 in colon cancer has been shown to increase response to the chemotherapeutic agent 5-fluorouracil (5-FU). Fluorouracil 184-188 pro-apoptotic WT1 regulator Homo sapiens 48-85 21910008-9 2011 Treating cells with PP2 and 5-FU resulted in reduced interaction of Par-4 with Akt1 and with the scaffolding protein 14-3-3sigma, and mobilization of Par-4 to the nucleus. Fluorouracil 28-32 pro-apoptotic WT1 regulator Homo sapiens 68-73 21910008-9 2011 Treating cells with PP2 and 5-FU resulted in reduced interaction of Par-4 with Akt1 and with the scaffolding protein 14-3-3sigma, and mobilization of Par-4 to the nucleus. Fluorouracil 28-32 pro-apoptotic WT1 regulator Homo sapiens 150-155 21910008-13 2011 The activation of the pro-apoptotic protein Par-4 as reported in this study is a novel mechanism by which apoptosis occurs with a Src kinase inhibitor and 5-FU. Fluorouracil 155-159 pro-apoptotic WT1 regulator Homo sapiens 44-49 21983179-3 2011 We recently reported overexpression of the Wnt transcription factor TCF4, also known as TCF7L2, in rectal cancers that were resistant to 5-fluorouracil-based chemoradiotherapy. Fluorouracil 137-151 transcription factor 4 Homo sapiens 68-72 21743967-0 2011 Overexpression of Nampt in gastric cancer and chemopotentiating effects of the Nampt inhibitor FK866 in combination with fluorouracil. Fluorouracil 121-133 nicotinamide phosphoribosyltransferase Homo sapiens 18-23 23205090-0 2012 Depletion of Bmi-1 enhances 5-fluorouracil-induced apoptosis and autophagy in hepatocellular carcinoma cells. Fluorouracil 28-42 BMI1 proto-oncogene, polycomb ring finger Homo sapiens 13-18 23205090-5 2012 The IC(50) values of 5-FU were significantly decreased to a greater extent in cells with Bmi-1 knockdown. Fluorouracil 21-25 BMI1 proto-oncogene, polycomb ring finger Homo sapiens 89-94 23205090-6 2012 Depletion of Bmi-1 increased sensitivity of the cells to 5-FU and increased apoptosis. Fluorouracil 57-61 BMI1 proto-oncogene, polycomb ring finger Homo sapiens 13-18 21806965-0 2011 Resistance of colorectal cancer cells to radiation and 5-FU is associated with MELK expression. Fluorouracil 55-59 maternal embryonic leucine zipper kinase Homo sapiens 79-83 22892453-4 2012 We designed a fusion protein termed L19CDy-His, consisting of the antibody single chain fragment L19 for targeting ED-B and yeast cytosine deaminase for the conversion of 5-fluorocytosine into cytotoxic 5-fluorouracil. Fluorouracil 203-217 cytosine deaminase Saccharomyces cerevisiae S288C 130-148 21806965-4 2011 In this study, SNU-503, which is a rectal cancer cell line, was treated with radiation or 5-fluorouracil (5-FU), and elevation of the MELK expression level was observed. Fluorouracil 90-104 maternal embryonic leucine zipper kinase Homo sapiens 134-138 21806965-4 2011 In this study, SNU-503, which is a rectal cancer cell line, was treated with radiation or 5-fluorouracil (5-FU), and elevation of the MELK expression level was observed. Fluorouracil 106-110 maternal embryonic leucine zipper kinase Homo sapiens 134-138 21806965-6 2011 We demonstrated that knockdown of MELK reduced the proliferation of cells with radiation or 5-FU treatment. Fluorouracil 92-96 maternal embryonic leucine zipper kinase Homo sapiens 34-38 21806965-8 2011 In conclusion, MELK could be associated with increased resistance of colorectal cancer cells against radiation and 5-FU. Fluorouracil 115-119 maternal embryonic leucine zipper kinase Homo sapiens 15-19 21652540-2 2011 Here we show that ATP-binding cassette member B5 (ABCB5) identifies therapy-refractory tumor cells in colorectal cancer patients following fluorouracil (5-FU)-based chemoradiation therapy and provide evidence for a functional role of ABCB5 in colorectal cancer 5-FU resistance. Fluorouracil 139-151 ATP binding cassette subfamily B member 5 Homo sapiens 18-48 22547150-3 2012 Previous publications have described a prototype based on an amphotropic murine leukemia virus (MLV), encoding yeast cytosine deaminase (CD) that converts the prodrug 5-fluorocytosine (5-FC) to the potent anticancer drug, 5-fluorouracil (5-FU) in an infected tumor. Fluorouracil 222-236 cytosine deaminase Saccharomyces cerevisiae S288C 117-135 22547150-3 2012 Previous publications have described a prototype based on an amphotropic murine leukemia virus (MLV), encoding yeast cytosine deaminase (CD) that converts the prodrug 5-fluorocytosine (5-FC) to the potent anticancer drug, 5-fluorouracil (5-FU) in an infected tumor. Fluorouracil 222-236 cytosine deaminase Saccharomyces cerevisiae S288C 137-139 22547150-3 2012 Previous publications have described a prototype based on an amphotropic murine leukemia virus (MLV), encoding yeast cytosine deaminase (CD) that converts the prodrug 5-fluorocytosine (5-FC) to the potent anticancer drug, 5-fluorouracil (5-FU) in an infected tumor. Fluorouracil 238-242 cytosine deaminase Saccharomyces cerevisiae S288C 117-135 22547150-3 2012 Previous publications have described a prototype based on an amphotropic murine leukemia virus (MLV), encoding yeast cytosine deaminase (CD) that converts the prodrug 5-fluorocytosine (5-FC) to the potent anticancer drug, 5-fluorouracil (5-FU) in an infected tumor. Fluorouracil 238-242 cytosine deaminase Saccharomyces cerevisiae S288C 137-139 22802336-5 2012 When treated with 5-fluorouracil (5FU), the Fgfr1 CKO mice showed defects in both proliferation and subsequent mobilization of HSPCs. Fluorouracil 18-32 fibroblast growth factor receptor 1 Mus musculus 44-49 22802336-5 2012 When treated with 5-fluorouracil (5FU), the Fgfr1 CKO mice showed defects in both proliferation and subsequent mobilization of HSPCs. Fluorouracil 34-37 fibroblast growth factor receptor 1 Mus musculus 44-49 22607196-6 2012 The synergistic effect of 5-FU induced by oroxylin A was also found in the suppression of Bcl-2 and in the activation of P53, Bax, PARP, and procaspase-3 proteins in HT-29 cells. Fluorouracil 26-30 collagen type XI alpha 2 chain Homo sapiens 131-135 22430613-8 2012 The sensitivity to other genotoxic agents such as carboplatin, cyclophosphamide and 5-fluorouracil was also increased by silencing the expression of elafin. Fluorouracil 84-98 peptidase inhibitor 3 Homo sapiens 149-155 22522606-14 2012 CONCLUSION: The present study suggested that BLTA in combination with 5-FU could enhance antitumor effect, with inhibiting TIM-3/TIM-3L pathway, cutting down immunosuppressive activity of CD4(+)CD25(+) T(reg) and enhancing cell-mediated immunity. Fluorouracil 70-74 hepatitis A virus cellular receptor 2 Mus musculus 123-128 22366766-0 2012 EBP50 gene transfection promotes 5-fluorouracil-induced apoptosis in gastric cancer cells through Bax- and Bcl-2-triggered mitochondrial pathways. Fluorouracil 33-47 SLC9A3 regulator 1 Homo sapiens 0-5 21652540-2 2011 Here we show that ATP-binding cassette member B5 (ABCB5) identifies therapy-refractory tumor cells in colorectal cancer patients following fluorouracil (5-FU)-based chemoradiation therapy and provide evidence for a functional role of ABCB5 in colorectal cancer 5-FU resistance. Fluorouracil 139-151 ATP binding cassette subfamily B member 5 Homo sapiens 50-55 22366766-3 2012 In the present study, using stable transfection of the ezrin-radixin-moesin-binding phosphoprotein 50 (EBP50) gene, we explored the genetic influences on 5-FU-induced apoptosis of human gastric cancer cells. Fluorouracil 154-158 SLC9A3 regulator 1 Homo sapiens 55-101 21652540-2 2011 Here we show that ATP-binding cassette member B5 (ABCB5) identifies therapy-refractory tumor cells in colorectal cancer patients following fluorouracil (5-FU)-based chemoradiation therapy and provide evidence for a functional role of ABCB5 in colorectal cancer 5-FU resistance. Fluorouracil 153-157 ATP binding cassette subfamily B member 5 Homo sapiens 18-48 22366766-3 2012 In the present study, using stable transfection of the ezrin-radixin-moesin-binding phosphoprotein 50 (EBP50) gene, we explored the genetic influences on 5-FU-induced apoptosis of human gastric cancer cells. Fluorouracil 154-158 SLC9A3 regulator 1 Homo sapiens 103-108 21652540-2 2011 Here we show that ATP-binding cassette member B5 (ABCB5) identifies therapy-refractory tumor cells in colorectal cancer patients following fluorouracil (5-FU)-based chemoradiation therapy and provide evidence for a functional role of ABCB5 in colorectal cancer 5-FU resistance. Fluorouracil 153-157 ATP binding cassette subfamily B member 5 Homo sapiens 50-55 21652540-2 2011 Here we show that ATP-binding cassette member B5 (ABCB5) identifies therapy-refractory tumor cells in colorectal cancer patients following fluorouracil (5-FU)-based chemoradiation therapy and provide evidence for a functional role of ABCB5 in colorectal cancer 5-FU resistance. Fluorouracil 153-157 ATP binding cassette subfamily B member 5 Homo sapiens 234-239 22366766-8 2012 Chemosensitivity and apoptosis rates of the BGC823/EBP50 cells were higher compared to the BGC823 and BGC823/neo cells following treatment with 5-FU. Fluorouracil 144-148 SLC9A3 regulator 1 Homo sapiens 51-56 22366766-9 2012 Stable overexpression of extrinsic EBP50 distinctly increases the 5-FU-induced apoptosis of gastric cancer cells, and is a novel strategy by which to improve the chemosensitivity of gastric cancer to 5-FU. Fluorouracil 66-70 SLC9A3 regulator 1 Homo sapiens 35-40 21652540-2 2011 Here we show that ATP-binding cassette member B5 (ABCB5) identifies therapy-refractory tumor cells in colorectal cancer patients following fluorouracil (5-FU)-based chemoradiation therapy and provide evidence for a functional role of ABCB5 in colorectal cancer 5-FU resistance. Fluorouracil 261-265 ATP binding cassette subfamily B member 5 Homo sapiens 18-48 22366766-9 2012 Stable overexpression of extrinsic EBP50 distinctly increases the 5-FU-induced apoptosis of gastric cancer cells, and is a novel strategy by which to improve the chemosensitivity of gastric cancer to 5-FU. Fluorouracil 200-204 SLC9A3 regulator 1 Homo sapiens 35-40 21652540-2 2011 Here we show that ATP-binding cassette member B5 (ABCB5) identifies therapy-refractory tumor cells in colorectal cancer patients following fluorouracil (5-FU)-based chemoradiation therapy and provide evidence for a functional role of ABCB5 in colorectal cancer 5-FU resistance. Fluorouracil 261-265 ATP binding cassette subfamily B member 5 Homo sapiens 50-55 22188649-7 2012 5-FU-induced Chk1 phosphorylation was significantly impaired in Rad9- or Rad17-deficient cells, and severe gammaH2AX nuclear foci and DSBs were formed, which was followed by apoptosis. Fluorouracil 0-4 RAD9 checkpoint clamp component A Gallus gallus 64-68 21652540-2 2011 Here we show that ATP-binding cassette member B5 (ABCB5) identifies therapy-refractory tumor cells in colorectal cancer patients following fluorouracil (5-FU)-based chemoradiation therapy and provide evidence for a functional role of ABCB5 in colorectal cancer 5-FU resistance. Fluorouracil 261-265 ATP binding cassette subfamily B member 5 Homo sapiens 234-239 22188649-9 2012 These results suggest that Rad9- and Rad17-independent activation of the ATR-Chk1 signaling pathway also significantly contributes to 5-FU tolerance. Fluorouracil 134-138 RAD9 checkpoint clamp component A Gallus gallus 27-31 22188649-9 2012 These results suggest that Rad9- and Rad17-independent activation of the ATR-Chk1 signaling pathway also significantly contributes to 5-FU tolerance. Fluorouracil 134-138 ATR serine/threonine kinase Gallus gallus 73-76 21652540-4 2011 Analysis of successive, patient-matched biopsy specimens obtained prior to and following neoadjuvant 5-FU-based chemoradiation therapy in a series of colorectal cancer patients revealed markedly enhanced abundance of ABCB5-positive tumor cells when residual disease was detected. Fluorouracil 101-105 ATP binding cassette subfamily B member 5 Homo sapiens 217-222 21652540-5 2011 Consistent with this finding, the ABCB5-expressing tumor cell population was also treatment refractory and exhibited resistance to 5-FU-induced apoptosis in a colorectal cancer xenograft model of 5-FU monotherapy. Fluorouracil 131-135 ATP binding cassette subfamily B member 5 Homo sapiens 34-39 21652540-5 2011 Consistent with this finding, the ABCB5-expressing tumor cell population was also treatment refractory and exhibited resistance to 5-FU-induced apoptosis in a colorectal cancer xenograft model of 5-FU monotherapy. Fluorouracil 196-200 ATP binding cassette subfamily B member 5 Homo sapiens 34-39 21652540-6 2011 Mechanistically, short hairpin RNA-mediated ABCB5 knockdown significantly inhibited tumorigenic xenograft growth and sensitized colorectal cancer cells to 5-FU-induced cell killing. Fluorouracil 155-159 ATP binding cassette subfamily B member 5 Homo sapiens 44-49 21068133-10 2011 Interestingly, CHD1L could inhibit apoptosis induced by 5-fluorourail (5-FU) but not doxorubicin. Fluorouracil 71-75 chromodomain helicase DNA binding protein 1 like Homo sapiens 15-20 22353519-1 2012 BACKGROUND/AIMS: We previously reported that combination therapy comprising hepatic arterial infusion chemotherapy (HAIC) with 3 drugs, namely, cisplatin (CDDP), 5-fluorouracil (5-FU) (low-dose FP) and isovorin and interferon (IFN)-alpha-2b was not beneficial for patients with advanced hepatocellular carcinoma (HCC). Fluorouracil 162-176 interferon alpha 2 Homo sapiens 215-240 22353519-1 2012 BACKGROUND/AIMS: We previously reported that combination therapy comprising hepatic arterial infusion chemotherapy (HAIC) with 3 drugs, namely, cisplatin (CDDP), 5-fluorouracil (5-FU) (low-dose FP) and isovorin and interferon (IFN)-alpha-2b was not beneficial for patients with advanced hepatocellular carcinoma (HCC). Fluorouracil 178-182 interferon alpha 2 Homo sapiens 215-240 21609932-9 2011 CONCLUSION: Our data demonstrate the importance of reduced SMAD4 expression in patients with mCRC receiving chemotherapy with oxaliplatin and 5-FU. Fluorouracil 142-146 SMAD family member 4 Homo sapiens 59-64 20630104-12 2010 The potentiation of the inhibitory effect of 5-FU by CQ was dependent on the increase of p21Cip1 and p27Kip1 and the decrease of CDK2. Fluorouracil 45-49 cyclin dependent kinase 2 Homo sapiens 129-133 20231086-6 2010 Inhibition of autophagy by 3-methyladenine (3-MA) or small interference RNA targeting Atg7 (Atg7 siRNA) significantly augmented 5-FU-induced apoptosis. Fluorouracil 128-132 autophagy related 7 Homo sapiens 86-90 20231086-6 2010 Inhibition of autophagy by 3-methyladenine (3-MA) or small interference RNA targeting Atg7 (Atg7 siRNA) significantly augmented 5-FU-induced apoptosis. Fluorouracil 128-132 autophagy related 7 Homo sapiens 92-96 20594292-10 2010 Notably, three out of four tumors harboring RB1 mutations displayed primary resistance to treatment with either 5-FU/mitomycin or doxorubicin while only 14 out of 64 tumors without mutations were resistant (p = 0.046). Fluorouracil 112-116 RB transcriptional corepressor 1 Homo sapiens 44-47 20514446-6 2010 5-FU (400 microM) induced apoptosis in MCF-7 cell monolayer as determined by HO/PI staining, PARP cleavage, p53 induction, Bax induction, and Bcl-2 down-regulation. Fluorouracil 0-4 collagen type XI alpha 2 chain Homo sapiens 93-97 20206682-5 2010 Finally, we demonstrate that RNAi-dependent repression of ung-1 gene, which encodes a uracil-DNA glycosylase, partially abolishes 5-FU effects on embryo hatching. Fluorouracil 130-134 Uracil-DNA glycosylase Caenorhabditis elegans 58-63 20206682-5 2010 Finally, we demonstrate that RNAi-dependent repression of ung-1 gene, which encodes a uracil-DNA glycosylase, partially abolishes 5-FU effects on embryo hatching. Fluorouracil 130-134 Uracil-DNA glycosylase Caenorhabditis elegans 86-108 20484035-0 2010 Oncostatin m renders epithelial cell adhesion molecule-positive liver cancer stem cells sensitive to 5-Fluorouracil by inducing hepatocytic differentiation. Fluorouracil 101-115 oncostatin M Homo sapiens 0-12 19727732-8 2010 Combination treatments of BENSpm with 5-FU or paclitaxel resulted in induction of SSAT mRNA and activity in both cell lines compared to either drug alone, while SMO mRNA and activity were increased only in MDA-MB-231 cells. Fluorouracil 38-42 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 82-86 19727732-10 2010 Further, RNAi studies demonstrated that both SSAT and SMO play a significant role in the response of MDA-MB-231 cells to treatment with BENSpm and 5-FU or paclitaxel. Fluorouracil 147-151 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 45-49 20408130-10 2010 After treatment with 5-FU, the expression of hnRNP K in LoVo decreased more significantly than in SW480, while PDI in SW480 increased more significantly than in LoVo cells. Fluorouracil 21-25 heterogeneous nuclear ribonucleoprotein K Homo sapiens 45-52 20408130-10 2010 After treatment with 5-FU, the expression of hnRNP K in LoVo decreased more significantly than in SW480, while PDI in SW480 increased more significantly than in LoVo cells. Fluorouracil 21-25 prolyl 4-hydroxylase subunit beta Homo sapiens 111-114 20031193-3 2010 Recent studies showed that the thymidylate synthase inhibitor 5-fluorouracil (5-FU) affects polyamine metabolism in colon carcinoma cells through the induction of the key catabolic enzyme spermidine/spermine N1-acetyltransferase (SSAT). Fluorouracil 62-76 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 188-228 20372780-5 2010 Treatment with CDDP and 5-FU led to phosphorylation of H2AX preferentially in S-phase cells, consistent with the induction of replication stress. Fluorouracil 24-28 H2A.X variant histone Homo sapiens 55-59 20085586-7 2010 Interestingly, RKO cells expressing mutant GPC5 showed enhanced cell death in response to 5-FU in cytotoxicity assays. Fluorouracil 90-94 glypican 5 Homo sapiens 43-47 22740971-6 2012 Following 2 cycles of combinative chemotherapy consisting of fluorouracil (5-FU) and dactinomycin (KSM), hCG concentrations decreased to normal levels. Fluorouracil 61-73 hypertrichosis 2 (generalised, congenital) Homo sapiens 105-108 22740971-6 2012 Following 2 cycles of combinative chemotherapy consisting of fluorouracil (5-FU) and dactinomycin (KSM), hCG concentrations decreased to normal levels. Fluorouracil 75-79 hypertrichosis 2 (generalised, congenital) Homo sapiens 105-108 22216841-12 2012 Epigenetic alterations of TFAP2E were independent of mutations in key regulatory cancer genes, microsatellite instability, and other genes that affect fluorouracil metabolism. Fluorouracil 151-163 transcription factor AP-2 epsilon Homo sapiens 26-32 22799343-5 2012 Compared to control vectors, overexpression of cyclin L2 inhibited the growth of BCG823 cells and enhance their chemosensitivity to fluorouracil, docetaxel and cisplatin. Fluorouracil 132-144 cyclin L2 Homo sapiens 47-56 20177669-10 2010 AFP was significantly elevated in TCA-intoxicated, but reversed in 5-FU-treated, groups. Fluorouracil 67-71 alpha-fetoprotein Rattus norvegicus 0-3 20081809-5 2010 Multivariate analysis revealed that positive expression for CD133 and Oct-4 was associated with significantly worse survival in patients treated by surgery alone (P=0.023 and P<0.001, respectively) and in patients treated with 5-fluorouracil-based chemotherapy (P=0.001 and P=0.021, respectively). Fluorouracil 230-244 prominin 1 Homo sapiens 60-65 21040359-6 2012 Hypermethylation of the DYPD gene (encodes the enzyme dihydropyrimidine dehydrogenase) and variation of the uridine diphosphate-glucuronosyltransferase 1A (UGT1A1) gene have predictive value for side effects and the efficacy of 5-fluoruracil and irinotecan, respectively. Fluorouracil 228-241 UDP glucuronosyltransferase family 1 member A1 Rattus norvegicus 156-162 20081809-6 2010 Stage III patients with negative CD133 expression showed an apparent survival benefit from 5-fluorouracil treatment (P=0.002), but not those with positive CD133 expression. Fluorouracil 91-105 prominin 1 Homo sapiens 33-38 20081809-9 2010 Our results show for the first time that CD133+ colorectal tumors are more resistant to 5-fluorouracil-based chemotherapy. Fluorouracil 88-102 prominin 1 Homo sapiens 41-46 20132554-9 2010 Data from our study also demonstrated that treatment with 5-FU caused a significant increase in unmethylated CASP8 and in CASP8 mRNA in all 3 cancer lines. Fluorouracil 58-62 caspase 8 Homo sapiens 109-114 20132554-9 2010 Data from our study also demonstrated that treatment with 5-FU caused a significant increase in unmethylated CASP8 and in CASP8 mRNA in all 3 cancer lines. Fluorouracil 58-62 caspase 8 Homo sapiens 122-127 19585117-10 2010 Western blotting assay revealed oroxylin A enhanced 5-FU-induced apoptosis in HepG2 cells by elevating the expressions of apoptotic-inducing proteins P53 and cleaved PARP and decreasing the expression of apoptotic-inhibitory proteins COX-2, Bcl-2, and pro-caspase3. Fluorouracil 52-56 collagen type XI alpha 2 chain Homo sapiens 166-170 19712668-6 2010 The results revealed an important role of BER, since BER-mutants (ntg1, ntg2, apn1, apn2) showed pronounced sensitivity to both 5-FU and FdUMP. Fluorouracil 128-132 bifunctional N-glycosylase/AP lyase NTG1 Saccharomyces cerevisiae S288C 66-70 19712668-6 2010 The results revealed an important role of BER, since BER-mutants (ntg1, ntg2, apn1, apn2) showed pronounced sensitivity to both 5-FU and FdUMP. Fluorouracil 128-132 bifunctional N-glycosylase/AP lyase NTG2 Saccharomyces cerevisiae S288C 72-76 20522971-2 2010 5-Fluorouracil (5FU) is a nucleoside analog and is used as an anti-tumor agent in patients whose plasma dCyd concentrations are increased. Fluorouracil 0-14 Cyd Drosophila melanogaster 104-108 20522971-2 2010 5-Fluorouracil (5FU) is a nucleoside analog and is used as an anti-tumor agent in patients whose plasma dCyd concentrations are increased. Fluorouracil 16-19 Cyd Drosophila melanogaster 104-108 20522971-3 2010 Because both dCyd and 5FU are pyrimidine analogues, it is possible that they have pharmacokinetic/ pharmacodynamic interaction, by which the anti-cancer efficacy of 5FU would be reduced. Fluorouracil 165-168 Cyd Drosophila melanogaster 13-17 20522971-4 2010 Here, we examined the effects of dCyd on the cytotoxicity of 5FU on mouse myeloma SP2/0-Ag14 (SP2/0) cells lacking hypoxanthine-guanine-phosphoribosyl transferase (HGPRT) and RH4 hybridomas with HGPRT under asynchronized conditions. Fluorouracil 61-64 Cyd Drosophila melanogaster 33-37 19879751-8 2010 IFN-lambda1 produced combinatory anti-tumour effects with chemotherapeutic agents, cisplatin (CDDP) and 5-fluorouracil (5-FU), in IFN-lambda1-sensitive oesophageal carcinoma cells but not in normal or Het-1A cells, while IFN-alpha achieved the combinatory suppressive effects to normal cells. Fluorouracil 120-124 interferon lambda 1 Homo sapiens 0-11 19879751-8 2010 IFN-lambda1 produced combinatory anti-tumour effects with chemotherapeutic agents, cisplatin (CDDP) and 5-fluorouracil (5-FU), in IFN-lambda1-sensitive oesophageal carcinoma cells but not in normal or Het-1A cells, while IFN-alpha achieved the combinatory suppressive effects to normal cells. Fluorouracil 120-124 interferon lambda 1 Homo sapiens 130-141 19760608-10 2009 Furthermore, restoration of KLK10 and OXGR1 expression reduced the ability of anchorage-independent growth, and sensitized HCC cells to doxorubicin- or 5-fluorouracil-induced cytotoxicity. Fluorouracil 152-166 kallikrein related peptidase 10 Homo sapiens 28-33 21971546-7 2011 Mechanistically, the synergistic effect of MPA on 5-FU in MDA-MB-231 cells can be recapitulated by inhibiting the RNA polymerase-I activity and requires the expression of nucleostemin. Fluorouracil 50-54 G protein nucleolar 3 Homo sapiens 171-183 21791367-1 2011 INTRODUCTION/BACKGROUND: Pyrimidine antimetabolites" target molecules thymidylate synthase (TS) and flopropyrimidine-metabolising enzymes such as dihydropyrimidine dehydrogenase (DPD), thymidine phosphorylase (TP) and orotate phosphoribosyltransferase (OPRT) are known as biomarkers of 5-fluorouracil (5-FU) treatment. Fluorouracil 286-300 thymidine phosphorylase Homo sapiens 185-208 21791367-1 2011 INTRODUCTION/BACKGROUND: Pyrimidine antimetabolites" target molecules thymidylate synthase (TS) and flopropyrimidine-metabolising enzymes such as dihydropyrimidine dehydrogenase (DPD), thymidine phosphorylase (TP) and orotate phosphoribosyltransferase (OPRT) are known as biomarkers of 5-fluorouracil (5-FU) treatment. Fluorouracil 286-300 thymidine phosphorylase Homo sapiens 210-212 21791367-1 2011 INTRODUCTION/BACKGROUND: Pyrimidine antimetabolites" target molecules thymidylate synthase (TS) and flopropyrimidine-metabolising enzymes such as dihydropyrimidine dehydrogenase (DPD), thymidine phosphorylase (TP) and orotate phosphoribosyltransferase (OPRT) are known as biomarkers of 5-fluorouracil (5-FU) treatment. Fluorouracil 302-306 thymidine phosphorylase Homo sapiens 185-208 21791367-1 2011 INTRODUCTION/BACKGROUND: Pyrimidine antimetabolites" target molecules thymidylate synthase (TS) and flopropyrimidine-metabolising enzymes such as dihydropyrimidine dehydrogenase (DPD), thymidine phosphorylase (TP) and orotate phosphoribosyltransferase (OPRT) are known as biomarkers of 5-fluorouracil (5-FU) treatment. Fluorouracil 302-306 thymidine phosphorylase Homo sapiens 210-212 19949674-4 2009 Estrogen receptor (ER)-negative tumors respond well to doxorubicin (P=0.038), and progesterone receptor (PR)-negative tumors to 5-FU (P=0.039), doxetaxel (P=0.038), doxorubicin (P=0.000), epirubicin (P=0.010), and paclitaxel (P=0.003). Fluorouracil 128-132 progesterone receptor Homo sapiens 82-103 21617862-9 2011 High expression of RRM1 (P=0.048) and TS x DPD (P=0.035) correlated significantly with sensitivity to GEM and 5-FU, respectively. Fluorouracil 110-114 ribonucleotide reductase catalytic subunit M1 Homo sapiens 19-23 21617862-12 2011 Quantitative analyses of RRM1, TP, DPD and TS mRNA levels in pancreatic cancer cells may be useful for predicting their sensitivity to GEM and 5-FU. Fluorouracil 143-147 ribonucleotide reductase catalytic subunit M1 Homo sapiens 25-29 19843160-4 2009 In addition, stable miR-143 overexpressing cells were selected with G418 and exposed to 5-fluorouracil. Fluorouracil 88-102 microRNA 143 Homo sapiens 20-27 19843160-5 2009 Increased stable expression of miR-143 was associated with decreased viability and increased cell death after exposure to 5-fluorouracil. Fluorouracil 122-136 microRNA 143 Homo sapiens 31-38 19843160-7 2009 In addition, extracellular-regulated protein kinase 5, nuclear factor-kappaB and Bcl-2 protein expression was down-regulated by miR-143, and further reduced by exposure to 5-fluorouracil. Fluorouracil 172-186 microRNA 143 Homo sapiens 128-135 19843160-9 2009 In addition, miR-143 increases the sensitivity of colon cancer cells to 5-fluorouracil, probably acting through extracellular-regulated protein kinase 5/nuclear factor-kappaB regulated pathways. Fluorouracil 72-86 microRNA 143 Homo sapiens 13-20 19921577-7 2009 Cyclin D1 positive cells showed more sensitive to 5-FU and HCPT than cyclin D1 negative cells. Fluorouracil 50-54 cyclin D1 Homo sapiens 0-9 19921578-10 2009 After intervention by 5-FU at IC(50), the expression of hnRNP K in Lovo decreased more as compared to SW480, while the expression of PDI in SW480 increased more as compared to Lovo. Fluorouracil 22-26 heterogeneous nuclear ribonucleoprotein K Homo sapiens 56-63 19921578-11 2009 CONCLUSION: There are significant differences in expression of hnRNP K and PDI proteins between Lovo and SW480 cell lines, and the proteins alter regularly after 5-FU intervention. Fluorouracil 162-166 heterogeneous nuclear ribonucleoprotein K Homo sapiens 63-70 19846930-5 2009 5-FU combined with TGF-beta3 and PGE(2) did not alter their inhibitory effects on IL-2-activated natural killer cell cytotoxicity, but substantially affected increased DNA synthesis of cells cultured in IL-2 and co-cultured with 10 ng/ml TGF-beta3 and 10 microM PGE(2). Fluorouracil 0-4 transforming growth factor beta 3 Homo sapiens 238-247 19846930-6 2009 CONCLUSION: Low 5-FU concentrations increase DNA synthesis in lymphocytes and exert a co-stimulatory activity on TGF-beta3 and PGE(2) modulation of IL-2-activated lymphocytes. Fluorouracil 16-20 transforming growth factor beta 3 Homo sapiens 113-122 19729995-0 2009 Delivery of PAR-4 plasmid in vivo via nanoliposomes sensitizes colon tumor cells subcutaneously implanted into nude mice to 5-FU. Fluorouracil 124-128 PRKC, apoptosis, WT1, regulator Mus musculus 12-17 19729995-4 2009 In these cells, overexpressed Par-4 led to increased apoptosis in the presence of 5-fluorouracil. Fluorouracil 82-96 PRKC, apoptosis, WT1, regulator Mus musculus 30-35 19729995-6 2009 Treating cells with the Par-4 nanoliposomes also increased susceptibility to 5-FU. Fluorouracil 77-81 PRKC, apoptosis, WT1, regulator Mus musculus 24-29 19729995-9 2009 Again, tumors in mice treated with the Par-4 nanoliposomes were more susceptible to 5-FU treatment. Fluorouracil 84-88 PRKC, apoptosis, WT1, regulator Mus musculus 39-44 19765320-0 2009 Transcriptional control of Flt3 ligand targeted by fluorouracil-induced Egr-1 promoter in hematopoietic damage. Fluorouracil 51-63 fms related receptor tyrosine kinase 3 ligand Homo sapiens 27-38 19765320-5 2009 The goal of this study was to explore the effect of Flt3 Ligand gene transcription regulated by fluorouracil-induced Egr-1 promoter on hematopoietic recovery. Fluorouracil 96-108 fms related receptor tyrosine kinase 3 ligand Homo sapiens 52-63 19765320-8 2009 Expression of FL by HFCL/EF cells after 5-FU treatment was determined with ELISA, western blot and RT-PCR assays. Fluorouracil 40-44 fms related receptor tyrosine kinase 3 ligand Homo sapiens 14-16 19765320-14 2009 RESULTS: 5-FU treatment increased EGFP levels and secreted FL levels in HFCL/EF cells. Fluorouracil 9-13 fms related receptor tyrosine kinase 3 ligand Homo sapiens 59-61 19714313-0 2009 Enhanced cytotoxicity of 5-FU by bFGF through up-regulation of uridine phosphorylase 1. Fluorouracil 25-29 uridine phosphorylase 1 Homo sapiens 63-86 19714313-3 2009 The biological factors that correlate with the response to 5-FU-based chemotherapy have been proposed to include uridine phosphorylase (UPP), thymidine phosphorylase (TPP), p53 and microsatellite instability. Fluorouracil 59-63 uridine phosphorylase 1 Homo sapiens 113-134 19714313-3 2009 The biological factors that correlate with the response to 5-FU-based chemotherapy have been proposed to include uridine phosphorylase (UPP), thymidine phosphorylase (TPP), p53 and microsatellite instability. Fluorouracil 59-63 uridine phosphorylase 1 Homo sapiens 136-139 19574900-7 2009 Clinical resolution of the neoplasm obtained using topical 5-FU was accompanied by a reduction in the expression of MMP-2, MMP-9, and TIMP-1 in tears and dysplastic conjunctival epithelium. Fluorouracil 59-63 matrix metallopeptidase 2 Homo sapiens 116-121 19698236-5 2009 It is concluded that cis-elements including T-Ag, PU.1, c-Ets, XPF-1, P2 alphaA, IL6-6RE and RAR may inhibit lrp16 expression and hormone or its inhibitor such as corticosteroid, tamoxifen, forskolin, phenylephrine, inflammatory factors such as IL6, IFNgamma and TNFalpha, and chemotherapeutics 5-fluorouracil may participate in the regulation of lrp16 gene expression in negative manner. Fluorouracil 295-309 mono-ADP ribosylhydrolase 1 Homo sapiens 109-114 19698236-5 2009 It is concluded that cis-elements including T-Ag, PU.1, c-Ets, XPF-1, P2 alphaA, IL6-6RE and RAR may inhibit lrp16 expression and hormone or its inhibitor such as corticosteroid, tamoxifen, forskolin, phenylephrine, inflammatory factors such as IL6, IFNgamma and TNFalpha, and chemotherapeutics 5-fluorouracil may participate in the regulation of lrp16 gene expression in negative manner. Fluorouracil 295-309 mono-ADP ribosylhydrolase 1 Homo sapiens 347-352 19567135-1 2009 BACKGROUND: Cytosine deaminase (CD) converts 5-fluorocytosine (5-FC) to 5-fluorouracil (5-FU) in CD/5-FC gene therapy, 5-FU will be mostly converted into nontoxic beta-alanine without uracil phosphoribosyltransferase (UPRT). Fluorouracil 72-86 uracil phosphoribosyltransferase homolog Rattus norvegicus 218-222 19567135-1 2009 BACKGROUND: Cytosine deaminase (CD) converts 5-fluorocytosine (5-FC) to 5-fluorouracil (5-FU) in CD/5-FC gene therapy, 5-FU will be mostly converted into nontoxic beta-alanine without uracil phosphoribosyltransferase (UPRT). Fluorouracil 88-92 uracil phosphoribosyltransferase homolog Rattus norvegicus 218-222 19567135-1 2009 BACKGROUND: Cytosine deaminase (CD) converts 5-fluorocytosine (5-FC) to 5-fluorouracil (5-FU) in CD/5-FC gene therapy, 5-FU will be mostly converted into nontoxic beta-alanine without uracil phosphoribosyltransferase (UPRT). Fluorouracil 119-123 uracil phosphoribosyltransferase homolog Rattus norvegicus 218-222 19567135-2 2009 UPRT catalyzes the conversion of 5-FU to 5-fluorouridine monophosphate, which directly kills CD::UPRT-expressing cells and surrounding cells via the bystander effect. Fluorouracil 33-37 uracil phosphoribosyltransferase homolog Rattus norvegicus 0-4 19567135-2 2009 UPRT catalyzes the conversion of 5-FU to 5-fluorouridine monophosphate, which directly kills CD::UPRT-expressing cells and surrounding cells via the bystander effect. Fluorouracil 33-37 uracil phosphoribosyltransferase homolog Rattus norvegicus 97-101 19567135-12 2009 RESULTS: (19)F-MRS on samples from C6-CD::UPRT cells cultured with 5-FC showed three broad resonance signals corresponding to 5-FC, 5-FU and fluorinated nucleotides (F-Nuctd). Fluorouracil 132-136 uracil phosphoribosyltransferase homolog Rattus norvegicus 42-46 19304841-4 2009 An isogenic mutant carrying a upp gene deletion was constructed and was resistant to 5-fluorouracil (5-FU), a toxic uracil analog that is also a substrate for UPRTase. Fluorouracil 85-99 uracil phosphoribosyltransferase Lactobacillus acidophilus NCFM 30-33 21566434-0 2011 [Diamine oxidase as blood biomarker in rats and humans to GI tract toxicity of fluorouracil anti-cancer drugs]. Fluorouracil 79-91 amine oxidase, copper containing 1 Rattus norvegicus 1-16 21566434-11 2011 Although DAO activity differs by the individual, it is a useful biomarker for estimating the degree of intestinal mucosal disorder, and possibly for estimating manifestations of diarrhea induced by 5-FU anti-cancer drug administration. Fluorouracil 198-202 amine oxidase copper containing 1 Homo sapiens 9-12 19304841-4 2009 An isogenic mutant carrying a upp gene deletion was constructed and was resistant to 5-fluorouracil (5-FU), a toxic uracil analog that is also a substrate for UPRTase. Fluorouracil 101-105 uracil phosphoribosyltransferase Lactobacillus acidophilus NCFM 30-33 19383845-8 2009 An increase in UMPK protein and mRNA levels following treatment with low-dose DAC was observed in cultured bolus 5-FU-resistant colorectal cancer cells (HCT-8) and in mice bearing these tumors. Fluorouracil 113-117 uridine-cytidine kinase 1 Mus musculus 15-19 21756828-0 2011 [Improved sensitivity of gastric carcinoma cells to fluorouracil-related drugs by transfection of thymidine phosphorylase gene]. Fluorouracil 52-64 thymidine phosphorylase Homo sapiens 98-121 21068133-12 2011 Furthermore, an adenoviral vector containing short hairpin RNAs against CHD1L (CHD1L-shRNAs) could suppress cell growth, clonogenicity and chemoresistance to 5-FU. Fluorouracil 158-162 chromodomain helicase DNA binding protein 1 like Homo sapiens 79-91 21449674-4 2011 RESULTS: Of the 24 genes analyzed, 13 produced significant changes on the phenotype of sensitivity to 5-FU (DHFR, DPYS, DTYMK, DUT, FPGS, GGH, NME1, NT5C, RRM1, TYMS, UCK2, UNG and UMPS). Fluorouracil 102-106 ribonucleotide reductase catalytic subunit M1 Homo sapiens 155-159 19383845-9 2009 We conclude that DAC-mediated restoration of sensitivity to bolus 5-FU is mediated at least in part by increased UMPK levels and clinical resistance to 5-FU due to decreased UMPK in colorectal cancer may be overcome by including methylation inhibitors such as DAC. Fluorouracil 66-70 uridine-cytidine kinase 1 Mus musculus 113-117 19426596-0 2009 [Effects of fluorouracil-induced Flt3 Ligand gene expression transcriptional regulated by Egr-1 promoter sequences]. Fluorouracil 12-24 fms related receptor tyrosine kinase 3 ligand Homo sapiens 33-44 20876774-9 2011 Mechanistic studies revealed that 5-FU-mediated suppression of c-FLIP results in increased TRAIL-induced recruitment and activation of caspase-8 at the death-inducing signalling complex (DISC), leading to caspase-3 activation and caspase-dependent cell death. Fluorouracil 34-38 caspase 8 Homo sapiens 135-144 20876774-9 2011 Mechanistic studies revealed that 5-FU-mediated suppression of c-FLIP results in increased TRAIL-induced recruitment and activation of caspase-8 at the death-inducing signalling complex (DISC), leading to caspase-3 activation and caspase-dependent cell death. Fluorouracil 34-38 caspase 8 Homo sapiens 135-142 21067862-1 2011 MiR-34a was identified as one of the down-regulated micro-RNAs (miRs) in human colorectal cancer 5-fluorouracil (5-FU)-resistant DLD-1 cells compared with those in the parental DLD-1 cells. Fluorouracil 97-111 microRNA 34a Homo sapiens 0-7 21067862-1 2011 MiR-34a was identified as one of the down-regulated micro-RNAs (miRs) in human colorectal cancer 5-fluorouracil (5-FU)-resistant DLD-1 cells compared with those in the parental DLD-1 cells. Fluorouracil 113-117 microRNA 34a Homo sapiens 0-7 21067862-3 2011 Furthermore, the expression of miR-34a in the 5-FU-resistant cells was sustained at a low-level, whereas it was up-regulated in the parental cells after the 5-FU treatment. Fluorouracil 46-50 microRNA 34a Homo sapiens 31-38 21067862-3 2011 Furthermore, the expression of miR-34a in the 5-FU-resistant cells was sustained at a low-level, whereas it was up-regulated in the parental cells after the 5-FU treatment. Fluorouracil 157-161 microRNA 34a Homo sapiens 31-38 21067862-4 2011 Sirt1, which is one of the target genes for miR-34a and related to drug-resistance, was strikingly up-regulated in the 5-FU-resistant cells. Fluorouracil 119-123 microRNA 34a Homo sapiens 44-51 21067862-5 2011 The ectopic expression of miR-34a in the 5-FU-resistant cells inhibited growth, as in the parental cells, and attenuated the resistance to 5-FU through the down-regulation of Sirt1 and E2F3. Fluorouracil 41-45 microRNA 34a Homo sapiens 26-33 21067862-5 2011 The ectopic expression of miR-34a in the 5-FU-resistant cells inhibited growth, as in the parental cells, and attenuated the resistance to 5-FU through the down-regulation of Sirt1 and E2F3. Fluorouracil 139-143 microRNA 34a Homo sapiens 26-33 21067862-7 2011 These findings suggest that miR-34a targeting the Sirt1 and E2F3 genes could negatively regulate, at least in part, the resistance to 5-FU in human colorectal cancer DLD-1 cells. Fluorouracil 134-138 microRNA 34a Homo sapiens 28-35 19302918-0 2009 Stem cells of GATA1-related leukemia undergo pernicious changes after 5-fluorouracil treatment. Fluorouracil 70-84 GATA binding protein 1 Mus musculus 14-19 21270338-8 2011 UROD down-regulation also radiosensitized several different models of human cancer, as well as sensitized tumors to chemotherapeutic agents, including 5-fluorouracil, cisplatin, and paclitaxel. Fluorouracil 151-165 uroporphyrinogen decarboxylase Homo sapiens 0-4 19291308-5 2009 In response to this limitation, specific inhibitors of UPP, such as 5-benzylacyclouridine (BAU), have been developed and investigated for their ability to modulate the cytotoxic side effects of 5-FU and its derivatives, so as to increase the therapeutic index of these agents. Fluorouracil 194-198 uridine phosphorylase 1 Homo sapiens 55-58 19143760-6 2009 RESULTS: Expression levels of Notch3, Jagged1, and Hey1 were increased in rat tracheal epithelial cells after treatment with 5-FU. Fluorouracil 125-129 hes-related family bHLH transcription factor with YRPW motif 1 Rattus norvegicus 51-55 19147571-3 2009 We then report that chemotherapy induces Notch-1, as oxaliplatin, 5-fluorouracil (5-FU), or SN-38 (the active metabolite of irinotecan) induced Notch-1 intracellular domain (NICD) protein and activated Hes-1. Fluorouracil 82-86 hes family bHLH transcription factor 1 Homo sapiens 202-207 19346744-6 2009 RESULTS: In comparison to untreated control, during cis + 5-FU therapy, significant down-regulation of leukocyte apoptosis was noted in mice pretreated with NLP or granulocyte colony stimulating factor (GCSF) during cis + 5-FU therapy. Fluorouracil 58-62 colony stimulating factor 3 (granulocyte) Mus musculus 164-201 19346744-6 2009 RESULTS: In comparison to untreated control, during cis + 5-FU therapy, significant down-regulation of leukocyte apoptosis was noted in mice pretreated with NLP or granulocyte colony stimulating factor (GCSF) during cis + 5-FU therapy. Fluorouracil 222-226 colony stimulating factor 3 (granulocyte) Mus musculus 164-201 19346744-6 2009 RESULTS: In comparison to untreated control, during cis + 5-FU therapy, significant down-regulation of leukocyte apoptosis was noted in mice pretreated with NLP or granulocyte colony stimulating factor (GCSF) during cis + 5-FU therapy. Fluorouracil 222-226 colony stimulating factor 3 (granulocyte) Mus musculus 203-207 20037211-0 2009 TPMT and DPD polymorphisms: Efficient screening method for Indian patients considering taking Thiopurine and 5-FU drugs. Fluorouracil 109-113 thiopurine S-methyltransferase Homo sapiens 0-4 22188667-6 2011 RESULTS: We found that the combined application of poly(I:C) and chemotherapeutics (cisPt, HU, 5-FU and MTX) has a stronger inhibitory effect on cell growth in tumor cells expressing functional TLR3 as compared with a single treatment. Fluorouracil 95-99 toll like receptor 3 Homo sapiens 194-198 19046630-0 2009 Mucin overexpression limits the effectiveness of 5-FU by reducing intracellular drug uptake and antineoplastic drug effects in pancreatic tumours. Fluorouracil 49-53 LOC100508689 Homo sapiens 0-5 20930123-6 2011 MRP5 mRNA expression in pancreatic adenocarcinoma cell lines correlated significantly with cellular sensitivity to 5-fluorouracil (5-FU) (r = 0.738, p < 0.05). Fluorouracil 115-129 ATP binding cassette subfamily C member 5 Homo sapiens 0-4 20930123-6 2011 MRP5 mRNA expression in pancreatic adenocarcinoma cell lines correlated significantly with cellular sensitivity to 5-fluorouracil (5-FU) (r = 0.738, p < 0.05). Fluorouracil 131-135 ATP binding cassette subfamily C member 5 Homo sapiens 0-4 20930123-7 2011 Long-term treatment with 5-FU increased expression of MRP5 by 2.4-fold and was associated with significant drug resistance [IC(50) values for control and 5-fluorouracil (5-FU)-resistant Patu-T cell lines were 11.3 +- 5.3 and 33.2 +- 6.9 muM, respectively (p < 0.05)]. Fluorouracil 25-29 ATP binding cassette subfamily C member 5 Homo sapiens 54-58 20930123-7 2011 Long-term treatment with 5-FU increased expression of MRP5 by 2.4-fold and was associated with significant drug resistance [IC(50) values for control and 5-fluorouracil (5-FU)-resistant Patu-T cell lines were 11.3 +- 5.3 and 33.2 +- 6.9 muM, respectively (p < 0.05)]. Fluorouracil 154-168 ATP binding cassette subfamily C member 5 Homo sapiens 54-58 20930123-7 2011 Long-term treatment with 5-FU increased expression of MRP5 by 2.4-fold and was associated with significant drug resistance [IC(50) values for control and 5-fluorouracil (5-FU)-resistant Patu-T cell lines were 11.3 +- 5.3 and 33.2 +- 6.9 muM, respectively (p < 0.05)]. Fluorouracil 170-174 ATP binding cassette subfamily C member 5 Homo sapiens 54-58 20930123-8 2011 Consequently, overexpression of MRP5 in Colo-357 cells resulted in significantly reduced accumulation of 5-FU related radioactivity and 5-FU cytotoxicity. Fluorouracil 105-109 ATP binding cassette subfamily C member 5 Homo sapiens 32-36 20930123-8 2011 Consequently, overexpression of MRP5 in Colo-357 cells resulted in significantly reduced accumulation of 5-FU related radioactivity and 5-FU cytotoxicity. Fluorouracil 136-140 ATP binding cassette subfamily C member 5 Homo sapiens 32-36 20930123-9 2011 Knockdown of MRP5 significantly increased cellular cytotoxicity of 5-FU to Patu-02 cells and enhanced accumulation of radioactivity related to 5-FU and its metabolites. Fluorouracil 67-71 ATP binding cassette subfamily C member 5 Homo sapiens 13-17 20930123-9 2011 Knockdown of MRP5 significantly increased cellular cytotoxicity of 5-FU to Patu-02 cells and enhanced accumulation of radioactivity related to 5-FU and its metabolites. Fluorouracil 143-147 ATP binding cassette subfamily C member 5 Homo sapiens 13-17 20930123-10 2011 Our results suggest that MRP5 is expressed and functionally active and contributes to variable sensitivities of pancreatic adenocarcinoma cell lines to 5-FU. Fluorouracil 152-156 ATP binding cassette subfamily C member 5 Homo sapiens 25-29 20930123-11 2011 Further investigations using models that resemble human pancreas tumors are necessary to prove a causative relation between expression and activity of MRP5 and tumor resistance to 5-FU. Fluorouracil 180-184 ATP binding cassette subfamily C member 5 Homo sapiens 151-155 22091436-4 2011 In addition, a factor that activates hENT1 is the inhibition of thymidylate synthase (TS), one of the 5-FU metabolic enzymes; TS inhibition mediates depleting intracellular nucleotide pools, resulting in the activation of the salvage pathway mediated through hENT1. Fluorouracil 102-106 solute carrier family 29 member 1 (Augustine blood group) Homo sapiens 37-42 21109972-4 2011 VK2 inhibited 5-FU-induced NF-kappaB activation and cyclin D1 expression. Fluorouracil 14-18 cyclin D1 Homo sapiens 52-61 21695264-0 2011 Matrix metalloproteinase-8 mediates the unfavorable systemic impact of local irradiation on pharmacokinetics of anti-cancer drug 5-Fluorouracil. Fluorouracil 129-143 matrix metallopeptidase 8 Rattus norvegicus 0-26 21695264-10 2011 Pretreatment with MMP-8 inhibitor reversed the effect of irradiation on AUC of 5-FU in plasma. Fluorouracil 79-83 matrix metallopeptidase 8 Rattus norvegicus 18-23 21695264-11 2011 Our findings first indicate that local irradiation modulate the systemic pharmacokinetics of 5-FU through stimulating the release of MMP-8. Fluorouracil 93-97 matrix metallopeptidase 8 Rattus norvegicus 133-138 19046630-2 2009 Studies suggest that mucin O-glycosylation limits the cytotoxic effect of fluorouracil (5-FU) against the growth of human pancreatic cancer cells in vitro. Fluorouracil 74-86 LOC100508689 Homo sapiens 21-26 19046630-2 2009 Studies suggest that mucin O-glycosylation limits the cytotoxic effect of fluorouracil (5-FU) against the growth of human pancreatic cancer cells in vitro. Fluorouracil 88-92 LOC100508689 Homo sapiens 21-26 19046630-3 2009 In the present study, we investigated the relationship between the levels of mucin O-glycosylation expressed in pancreatic tumours and the antitumour effect of 5-FU. Fluorouracil 160-164 LOC100508689 Homo sapiens 77-82 19015148-2 2009 METHODS: We investigated the 5-FU-related gene expression levels of thymidylate synthase (TS), DPD, thymidine phosphorylase (TP) and orotate phosphoribosyl transferase (OPRT) in resected tumor specimens from 51 patients with adenocarcinomas and 47 with squamous cell carcinomas using quantitative reverse transcription-PCR, and compared those levels between the two histological types. Fluorouracil 29-33 thymidine phosphorylase Homo sapiens 100-123 19439999-7 2009 In MKN-1 cells, an additive effect on growth inhibition was shown by the combined transfection with miR-143 and miR-145; further, higher sensitivity to 5-fluorouracil was also observed following the transfection with miR-143 or miR-145. Fluorouracil 152-166 microRNA 143 Homo sapiens 217-224 19077464-10 2009 Compared to parental Capan-1 cells, Capan-1 cells with acquired chemoresistance towards 5-fluorouracil showed an upregulated mRNA and protein expression of MRP3, MRP4, and MRP5. Fluorouracil 88-102 ATP binding cassette subfamily C member 3 Homo sapiens 156-160 19077464-10 2009 Compared to parental Capan-1 cells, Capan-1 cells with acquired chemoresistance towards 5-fluorouracil showed an upregulated mRNA and protein expression of MRP3, MRP4, and MRP5. Fluorouracil 88-102 ATP binding cassette subfamily C member 5 Homo sapiens 172-176 19077464-11 2009 In addition, silencing of MRP5 by RNA interference resulted in enhanced sensitivity of parental Capan-1 cells towards 5-fluorouracil cytotoxicity. Fluorouracil 118-132 ATP binding cassette subfamily C member 5 Homo sapiens 26-30 19077464-12 2009 CONCLUSION: MRP3, MRP4, and MRP5 are upregulated in 5-fluorouracil-resistant cells, and MRP5 contributes to 5-FU resistance in pancreatic carcinoma cells. Fluorouracil 52-66 ATP binding cassette subfamily C member 3 Homo sapiens 12-16 19077464-12 2009 CONCLUSION: MRP3, MRP4, and MRP5 are upregulated in 5-fluorouracil-resistant cells, and MRP5 contributes to 5-FU resistance in pancreatic carcinoma cells. Fluorouracil 52-66 ATP binding cassette subfamily C member 5 Homo sapiens 28-32 19077464-12 2009 CONCLUSION: MRP3, MRP4, and MRP5 are upregulated in 5-fluorouracil-resistant cells, and MRP5 contributes to 5-FU resistance in pancreatic carcinoma cells. Fluorouracil 108-112 ATP binding cassette subfamily C member 5 Homo sapiens 88-92 18794807-4 2008 As detected by MTT proliferation assay, propidium iodide and annexin V staining, a combination of 5-FU+Src kinase inhibitor PP2 (4-amino-5-(4-chlorophenyl)-7-(t-butyl)pyrazolo[3,4-d]pyrimidine) reflected the chemotherapeutic sensitivity and restored the 5-FU-induced apoptosis in 5-FU-resistant cells. Fluorouracil 254-258 neuropeptide Y receptor Y6 (pseudogene) Homo sapiens 124-127 18794807-4 2008 As detected by MTT proliferation assay, propidium iodide and annexin V staining, a combination of 5-FU+Src kinase inhibitor PP2 (4-amino-5-(4-chlorophenyl)-7-(t-butyl)pyrazolo[3,4-d]pyrimidine) reflected the chemotherapeutic sensitivity and restored the 5-FU-induced apoptosis in 5-FU-resistant cells. Fluorouracil 254-258 neuropeptide Y receptor Y6 (pseudogene) Homo sapiens 124-127 18794807-6 2008 Western blotting and RT-PCR analysis revealed that the expression of thymidylate synthase (TS) was higher in 5-FU-resistant cells, however, decreased significantly after pretreatment with PP2. Fluorouracil 109-113 neuropeptide Y receptor Y6 (pseudogene) Homo sapiens 188-191 18794807-7 2008 Furthermore, the combination of 5-FU+PP2 decreased the 5-FU-induced activation of epidermal growth factor receptor (EGFR)-AKT pathway. Fluorouracil 55-59 neuropeptide Y receptor Y6 (pseudogene) Homo sapiens 37-40 19157226-1 2008 OBJECTIVE: To observe the sensitivity of the PC-3 cell lines transfected with the PCI-NEO-SNCG plasmid to Cisplatin (DDP), 5-Fluorouracil (5-FU), Adriamycin (ADM), Vincristine (VCR) and Paclitaxel (TAX), and to explore the influence of the SNCG expression on the effectiveness of anti-tumor drugs. Fluorouracil 123-137 synuclein gamma Homo sapiens 90-94 24212609-6 2010 We have previously shown that 5-fluorouracil treatment affects the expression profile of relevant cellular transporters including multidrug resistance proteins (MRPs), and that MRP5 (ABCC5) influences chemoresistance of these tumor cells. Fluorouracil 30-44 ATP binding cassette subfamily C member 5 Homo sapiens 183-188 21078976-0 2010 MicroRNA-21 induces resistance to 5-fluorouracil by down-regulating human DNA MutS homolog 2 (hMSH2). Fluorouracil 34-48 mutS homolog 2 Homo sapiens 78-92 21078976-0 2010 MicroRNA-21 induces resistance to 5-fluorouracil by down-regulating human DNA MutS homolog 2 (hMSH2). Fluorouracil 34-48 mutS homolog 2 Homo sapiens 94-99 19009643-3 2008 Aim of the study was to determine whether the addition of the ghrelin agonist growth hormone releasing peptide 2 (GHRP-2) to cytotoxic therapy with 5-fluoruracil (5-FU) prevents the anorexia associated with chemotherapy in cancer cachectic mice. Fluorouracil 163-167 ghrelin Mus musculus 62-69 19189638-0 2008 Role of caspases in 5-FU and selenium-induced growth inhibition of colorectal cancer cells. Fluorouracil 20-24 caspase 8 Homo sapiens 8-16 18779317-5 2008 Activation of p53 by 5-fluorouracil increased the TLR3 mRNA in epithelial cell lines with wild-type p53 but not in cell lines harboring mutant p53. Fluorouracil 21-35 toll like receptor 3 Homo sapiens 50-54 18755584-4 2008 We analysed TRAIL-R 1, -2, -3 and -4 expression by immuno-histochemistry in CRC, using tissue micro arrays, and found that concomitant low/medium TRAIL-R1 and high TRAIL-R3 expression in primary CRC is significantly associated with a poor response to 5-FU-based first-line chemotherapy and with shorter progression-free survival. Fluorouracil 251-255 TNF receptor superfamily member 10a Homo sapiens 12-36 18755584-6 2008 Thus, the combination of TRAIL-R1 and TRAIL-R3 expression might represent a predictive and prognostic factor of the response to 5-FU-based first-line chemotherapy in patients with metastatic CRC. Fluorouracil 128-132 TNF receptor superfamily member 10a Homo sapiens 25-33 18064460-2 2008 PATIENTS AND METHODS: We investigated in patients with T2-T3 N0-3 ER, PgR <10% and HER2 negative breast cancers the activity both in terms of pathological (pCR) and objective responses of four courses of cisplatin containing chemotherapy (ECF, epirubicin, cisplatin, and fluorouracil as continuous infusion) followed by three courses of weekly paclitaxel. Fluorouracil 274-286 progesterone receptor Homo sapiens 70-73 18546291-2 2008 The role of nonhomologous end joining (NHEJ) genes (Ku70, Ku80 and DNA-PKcs) in double-strand break (DSB) repair, genomic instability and apoptosis suggest a possible impact on tumor response to radiotherapy, 5-fluorouracil or cisplatin, as these agents are direct or indirect inductors of DSBs. Fluorouracil 209-223 X-ray repair cross complementing 5 Homo sapiens 58-62 20930505-6 2010 Importantly, with knockdown of hMLH1 and hMSH2, we observed that decreased histone H3 expression by 5-FU was dependent on hMLH1. Fluorouracil 100-104 mutS homolog 2 Homo sapiens 41-46 17987291-2 2008 Since oxaliplatin and 5-fluorouracil (5FU) are used clinically in treatment of colorectal cancers, this study examines the effect of adding DENSPM to oxaliplatin/5FU combination on SSAT and spermine oxidase (SMO) in HCT-116 cells. Fluorouracil 162-165 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 181-185 17987291-6 2008 RESULTS: Oxaliplatin + 5FU + DENSPM produced significantly higher levels of SSAT and SMO mRNA, protein and activity than those seen with oxaliplatin+5FU with a significant depletion of cellular spermine and spermidine pools. Fluorouracil 23-26 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 76-80 17987291-6 2008 RESULTS: Oxaliplatin + 5FU + DENSPM produced significantly higher levels of SSAT and SMO mRNA, protein and activity than those seen with oxaliplatin+5FU with a significant depletion of cellular spermine and spermidine pools. Fluorouracil 23-26 spermine oxidase Homo sapiens 85-88 18344199-1 2008 In this study, we examined the age-associated defect of stromal cells, which support B cell development, treated with 5-fluorouracil (5-FU) to induce severe perturbation of hematopoiesis, including B lymphocyte development, using SAMP1 mice exhibiting senescence-mimicking stromal-cell impairment after 30 weeks of age. Fluorouracil 118-132 transmembrane protein 201 Mus musculus 230-235 20951595-6 2010 The resulting 4-(trifluoromethyl)-1-p-tolyl-[1,2,4]triazolo[4,3-a]quinoxaline (24), which interferes intracellularly with DHFR and TS reducing the protein levels like 5-FU, but without inducing TS ternary complex formation, was 2-times less toxic in vitro than cisplatin and 5-FU. Fluorouracil 167-171 dihydrofolate reductase Chlorocebus sabaeus 122-126 20951595-6 2010 The resulting 4-(trifluoromethyl)-1-p-tolyl-[1,2,4]triazolo[4,3-a]quinoxaline (24), which interferes intracellularly with DHFR and TS reducing the protein levels like 5-FU, but without inducing TS ternary complex formation, was 2-times less toxic in vitro than cisplatin and 5-FU. Fluorouracil 275-279 dihydrofolate reductase Chlorocebus sabaeus 122-126 18344199-1 2008 In this study, we examined the age-associated defect of stromal cells, which support B cell development, treated with 5-fluorouracil (5-FU) to induce severe perturbation of hematopoiesis, including B lymphocyte development, using SAMP1 mice exhibiting senescence-mimicking stromal-cell impairment after 30 weeks of age. Fluorouracil 134-138 transmembrane protein 201 Mus musculus 230-235 20920468-5 2010 However, when given in combination with the chemotherapeutic agent, 5-fluorouracil, the therapeutic tumor vaccine capable of Tim3 pathway inhibition had no additional anti-tumor effect. Fluorouracil 68-82 hepatitis A virus cellular receptor 2 Mus musculus 125-129 18618018-3 2008 We found that HSCs from Lnk-/- mice have an increased quiescent fraction, decelerated cell cycle kinetics, and enhanced resistance to repeat treatments with cytoablative 5-fluorouracil in vivo compared with WT HSCs. Fluorouracil 170-184 SH2B adaptor protein 3 Mus musculus 24-27 20940395-7 2010 Cyclin D1 deletion in fibroblasts or small interfering RNA-mediated reduction of endogenous cyclin D1 in colon cancer cells reduced the 5-fluorouracil-mediated DDR. Fluorouracil 136-150 cyclin D1 Homo sapiens 0-9 20940395-7 2010 Cyclin D1 deletion in fibroblasts or small interfering RNA-mediated reduction of endogenous cyclin D1 in colon cancer cells reduced the 5-fluorouracil-mediated DDR. Fluorouracil 136-150 cyclin D1 Homo sapiens 92-101 18452707-0 2008 Downregulation of BMI-1 enhances 5-fluorouracil-induced apoptosis in nasopharyngeal carcinoma cells. Fluorouracil 33-47 BMI1 proto-oncogene, polycomb ring finger Homo sapiens 18-23 21443122-2 2010 We explored the relationship between hENT1 expression and 5-fluorouracil (5-FU) response in pancreatic cancer cell line. Fluorouracil 58-72 solute carrier family 29 member 1 (Augustine blood group) Homo sapiens 37-42 21443122-2 2010 We explored the relationship between hENT1 expression and 5-fluorouracil (5-FU) response in pancreatic cancer cell line. Fluorouracil 74-78 solute carrier family 29 member 1 (Augustine blood group) Homo sapiens 37-42 21443122-8 2010 However, when the cells were treated with 5-FU, cells viability and IC50 value of 5-FU was significantly reduced in the transfected cells, and cell cycle of pSilence-hENT1-Panc-1 was arrest in G0/G1. Fluorouracil 42-46 solute carrier family 29 member 1 (Augustine blood group) Homo sapiens 166-171 21443122-8 2010 However, when the cells were treated with 5-FU, cells viability and IC50 value of 5-FU was significantly reduced in the transfected cells, and cell cycle of pSilence-hENT1-Panc-1 was arrest in G0/G1. Fluorouracil 82-86 solute carrier family 29 member 1 (Augustine blood group) Homo sapiens 166-171 20697686-8 2010 Cell viability assay revealed that F6-CD133+ cells were more sensitive to cisplatin while less to 5-fluorouracil. Fluorouracil 98-112 prominin 1 Homo sapiens 38-43 20446812-2 2010 With this assay, it was first determined that the 5-fluorouracil resistant cells capable of osseous tissue formation in vivo also migrated toward stromal derived factor-1 (SDF-1) in vitro. Fluorouracil 50-64 chemokine (C-X-C motif) ligand 12 Mus musculus 146-170 20446812-2 2010 With this assay, it was first determined that the 5-fluorouracil resistant cells capable of osseous tissue formation in vivo also migrated toward stromal derived factor-1 (SDF-1) in vitro. Fluorouracil 50-64 chemokine (C-X-C motif) ligand 12 Mus musculus 172-177 20856879-2 2010 Human UPP activity has been a focus of cancer research due to its role in activating fluoropyrimidine nucleoside chemotherapeutic agents such as 5-fluorouracil (5-FU) and capecitabine. Fluorouracil 145-159 uridine phosphorylase 1 Homo sapiens 6-9 20856879-2 2010 Human UPP activity has been a focus of cancer research due to its role in activating fluoropyrimidine nucleoside chemotherapeutic agents such as 5-fluorouracil (5-FU) and capecitabine. Fluorouracil 161-165 uridine phosphorylase 1 Homo sapiens 6-9 20856879-4 2010 Here we report the structure of hUPP1 bound to 5-FU at 2.3 A resolution. Fluorouracil 47-51 uridine phosphorylase 1 Homo sapiens 32-37 18452707-4 2008 In this study, 5-FU treatment could increase the percentage of apoptotic NPC cells among BMI-1/RNAi-transfected cells than that among cells transfected with the empty vector. Fluorouracil 15-19 BMI1 proto-oncogene, polycomb ring finger Homo sapiens 89-94 18452707-5 2008 The 50% inhibitory concentration (IC(50)) values of 5-FU were significantly decreased to a greater extent in the cells transfected with BMI-1/RNAi. Fluorouracil 52-56 BMI1 proto-oncogene, polycomb ring finger Homo sapiens 136-141 18751413-1 2008 This study was performed to assess the usefulness and safety of neoadjuvant chemotherapy utilizing the FAP regimen consisting of 5-fluorouracil, cisplatin and adriamycin for the treatment of highly advanced esophageal cancer. Fluorouracil 129-143 fibroblast activation protein alpha Homo sapiens 103-106 20800023-0 2010 5-Fluorouracil upregulates the activity of Wnt signaling pathway in CD133-positive colon cancer stem-like cells. Fluorouracil 0-14 prominin 1 Homo sapiens 68-73 20800023-1 2010 BACKGROUND AND OBJECTIVE: CD133-positive colon cancer stem like cells (CSLCs) are resistant to the conventional cytotoxic drug 5-fluorouracil (5-FU). Fluorouracil 127-141 prominin 1 Homo sapiens 26-31 20800023-1 2010 BACKGROUND AND OBJECTIVE: CD133-positive colon cancer stem like cells (CSLCs) are resistant to the conventional cytotoxic drug 5-fluorouracil (5-FU). Fluorouracil 143-147 prominin 1 Homo sapiens 26-31 20800023-3 2010 In the present study, we explored the impact of 5-FU on Wnt signaling pathway of CD133-positive colon CSLCs, and the relation between Wnt signaling pathway and drug resistance of CD133-positive colon CSLCs. Fluorouracil 48-52 prominin 1 Homo sapiens 81-86 20800023-9 2010 RESULTS: After the treatment with 5-FU, the cell proliferation rate of CD133-positive cells was higher than that of CD133-negative cells and the sensitivity of CD133-positive cells to 5-FU decreased. Fluorouracil 34-38 prominin 1 Homo sapiens 71-76 20800023-9 2010 RESULTS: After the treatment with 5-FU, the cell proliferation rate of CD133-positive cells was higher than that of CD133-negative cells and the sensitivity of CD133-positive cells to 5-FU decreased. Fluorouracil 34-38 prominin 1 Homo sapiens 116-121 20800023-9 2010 RESULTS: After the treatment with 5-FU, the cell proliferation rate of CD133-positive cells was higher than that of CD133-negative cells and the sensitivity of CD133-positive cells to 5-FU decreased. Fluorouracil 34-38 prominin 1 Homo sapiens 116-121 20800023-9 2010 RESULTS: After the treatment with 5-FU, the cell proliferation rate of CD133-positive cells was higher than that of CD133-negative cells and the sensitivity of CD133-positive cells to 5-FU decreased. Fluorouracil 184-188 prominin 1 Homo sapiens 71-76 20800023-11 2010 After the treatment with 1 mug/mL and 10 mug/mL of 5-FU, Wnt activity of CD133-positive cells was (90.1 +- 10.0)% (P = 0.012) and (52.9 +- 2.5)% (P = 0.047), respectively, whereas that of CD133-negative cells was (35.5 +- 3.3)% (P = 0.434) and (26.5 +- 0.4)% (P = 0.046), respectively. Fluorouracil 51-55 prominin 1 Homo sapiens 73-78 20800023-11 2010 After the treatment with 1 mug/mL and 10 mug/mL of 5-FU, Wnt activity of CD133-positive cells was (90.1 +- 10.0)% (P = 0.012) and (52.9 +- 2.5)% (P = 0.047), respectively, whereas that of CD133-negative cells was (35.5 +- 3.3)% (P = 0.434) and (26.5 +- 0.4)% (P = 0.046), respectively. Fluorouracil 51-55 prominin 1 Homo sapiens 188-193 20800023-14 2010 5-FU can upregulate Wnt activity of CD133-positive colon CSLCs. Fluorouracil 0-4 prominin 1 Homo sapiens 36-41 20800023-15 2010 Blocking Wnt activity may reverse drug sensitivity of CD133-positive cells to 5-FU. Fluorouracil 78-82 prominin 1 Homo sapiens 54-59 20837458-1 2010 BACKGROUND: Thymidylate synthase (TS), thymidine phosphorylase (TP), and dihydropyrimidine dehydrogenase (DPD) are key enzymes in the 5-fluorouracil (5-FU) pathway. Fluorouracil 134-148 thymidine phosphorylase Homo sapiens 39-62 20837458-1 2010 BACKGROUND: Thymidylate synthase (TS), thymidine phosphorylase (TP), and dihydropyrimidine dehydrogenase (DPD) are key enzymes in the 5-fluorouracil (5-FU) pathway. Fluorouracil 150-154 thymidine phosphorylase Homo sapiens 39-62 18490900-8 2008 In particular, expression levels of human equilibrative nucleoside transporter-1 and thymydilate synthase were significantly related to gemcitabine and 5-fluorouracil cytotoxicity. Fluorouracil 152-166 solute carrier family 29 member 1 (Augustine blood group) Homo sapiens 42-80 20458282-12 2010 Mz-Cyp1b1 cells were more sensitive to chemotherapeutic agents in vitro than mock-transfected cells, and Mz-Cyp1b1-induced tumors were more susceptible to 5-FU treatment. Fluorouracil 155-159 cytochrome P450 family 1 subfamily B member 1 Homo sapiens 108-114 18575723-9 2008 Our results suggest that hsp27, Prx 6 and hsp70 are potential 5-FU response proteins and they may represent potential targets for further evaluation in other 5-FU-sensitive and -resistant CRC cell lines. Fluorouracil 62-66 peroxiredoxin 6 Homo sapiens 32-37 18381962-6 2008 5-FU and methotrexate significantly reduced the growth rate of RB1-silenced but not of control MCF-7 and HCT-116 cells. Fluorouracil 0-4 RB transcriptional corepressor 1 Homo sapiens 63-66 20824050-2 2010 Our previous experimental chemotherapy studies have shown that treatment of human pancreatic carcinoma cells with 5-fluorouracil (5-FU) alters the cellular transporter expression profile and that modulation of the expression of multidrug resistance protein 5 (MRP5; ABCC5) influences the chemoresistance of these tumor cells. Fluorouracil 114-128 ATP binding cassette subfamily C member 5 Homo sapiens 228-258 20824050-2 2010 Our previous experimental chemotherapy studies have shown that treatment of human pancreatic carcinoma cells with 5-fluorouracil (5-FU) alters the cellular transporter expression profile and that modulation of the expression of multidrug resistance protein 5 (MRP5; ABCC5) influences the chemoresistance of these tumor cells. Fluorouracil 114-128 ATP binding cassette subfamily C member 5 Homo sapiens 260-264 20824050-2 2010 Our previous experimental chemotherapy studies have shown that treatment of human pancreatic carcinoma cells with 5-fluorouracil (5-FU) alters the cellular transporter expression profile and that modulation of the expression of multidrug resistance protein 5 (MRP5; ABCC5) influences the chemoresistance of these tumor cells. Fluorouracil 114-128 ATP binding cassette subfamily C member 5 Homo sapiens 266-271 20824050-2 2010 Our previous experimental chemotherapy studies have shown that treatment of human pancreatic carcinoma cells with 5-fluorouracil (5-FU) alters the cellular transporter expression profile and that modulation of the expression of multidrug resistance protein 5 (MRP5; ABCC5) influences the chemoresistance of these tumor cells. Fluorouracil 130-134 ATP binding cassette subfamily C member 5 Homo sapiens 228-258 20824050-2 2010 Our previous experimental chemotherapy studies have shown that treatment of human pancreatic carcinoma cells with 5-fluorouracil (5-FU) alters the cellular transporter expression profile and that modulation of the expression of multidrug resistance protein 5 (MRP5; ABCC5) influences the chemoresistance of these tumor cells. Fluorouracil 130-134 ATP binding cassette subfamily C member 5 Homo sapiens 260-264 20824050-2 2010 Our previous experimental chemotherapy studies have shown that treatment of human pancreatic carcinoma cells with 5-fluorouracil (5-FU) alters the cellular transporter expression profile and that modulation of the expression of multidrug resistance protein 5 (MRP5; ABCC5) influences the chemoresistance of these tumor cells. Fluorouracil 130-134 ATP binding cassette subfamily C member 5 Homo sapiens 266-271 20824050-7 2010 Combined treatment with 5-FU and gemcitabine caused a 5- to 40-fold increase in MRP5 and ENT1 expressions. Fluorouracil 24-28 ATP binding cassette subfamily C member 5 Homo sapiens 80-84 20824050-7 2010 Combined treatment with 5-FU and gemcitabine caused a 5- to 40-fold increase in MRP5 and ENT1 expressions. Fluorouracil 24-28 solute carrier family 29 member 1 (Augustine blood group) Homo sapiens 89-93 18381962-8 2008 CONCLUSIONS: The absence of pRB expression renders human breast cancer cells more sensitive to 5-FU and methotrexate and predicts a good clinical outcome for patients treated with adjuvant chemotherapy. Fluorouracil 95-99 RB transcriptional corepressor 1 Homo sapiens 28-31 17632733-6 2008 In vitro experiments with SW620 colorectal carcinoma cell line demonstrated that it was sensitive to ZD55-MnSOD, especially most sensitive to ZD55-MnSOD plus 5-FU treatment. Fluorouracil 158-162 superoxide dismutase 2 Homo sapiens 106-111 20628391-0 2010 UGT1A and TYMS genetic variants predict toxicity and response of colorectal cancer patients treated with first-line irinotecan and fluorouracil combination therapy. Fluorouracil 131-143 UDP glucuronosyltransferase family 1 member A complex locus Homo sapiens 0-5 20628391-9 2010 CONCLUSION: TYMS and UGT1A polymorphisms influence on tumour response and toxicities derived from irinotecan/5FU treatment in CRC patients. Fluorouracil 109-112 UDP glucuronosyltransferase family 1 member A complex locus Homo sapiens 21-26 19137262-1 2009 Comparative analysis of proteomes using 5-fluorouracil (5-FU)-resistant human colon cancer cell line revealed that decreased galectin-3 expression was significantly associated with retarded proliferation. Fluorouracil 40-54 galectin 3 Homo sapiens 125-135 19137262-1 2009 Comparative analysis of proteomes using 5-fluorouracil (5-FU)-resistant human colon cancer cell line revealed that decreased galectin-3 expression was significantly associated with retarded proliferation. Fluorouracil 56-60 galectin 3 Homo sapiens 125-135 19137262-2 2009 However, in the presence of 5-FU proliferation rate of cells with suppressed galectin-3 expression did not differ from that of cells with normal galectin-3 expression, even galectin-3 suppression augmented apoptosis. Fluorouracil 28-32 galectin 3 Homo sapiens 77-87 19137262-6 2009 The present study demonstrates that galectin-3 stabilizes hnRNP Q via complex formation, and reduction in the hnRNP Q level leads to slow proliferation and less susceptibility to 5-FU. Fluorouracil 179-183 galectin 3 Homo sapiens 36-46 19015929-0 2009 The effect of combination treatment with docosahexaenoic acid and 5-fluorouracil on the mRNA expression of apoptosis-related genes, including the novel gene BCL2L12, in gastric cancer cells. Fluorouracil 66-80 BCL2 like 12 Homo sapiens 157-164 19440006-0 2009 Treatment of gastric cancer cells with 5-fluorouracil/leucovorin and irinotecan induces distinct alterations in the mRNA expression of the apoptosis-related genes, including the novel gene BCL2L12. Fluorouracil 39-53 BCL2 like 12 Homo sapiens 189-196 19440006-3 2009 The aim of this study was to investigate the modulations in the BAX, BCL2 and BCL2L12 mRNA levels in gastric cancer cells, after their treatment with the anticancer drugs 5-fluorouracil and irinotecan as well as the antioxidant substance leucovorin. Fluorouracil 171-185 BCL2 like 12 Homo sapiens 78-85 19189638-6 2008 Conversely, RKO cells expressing wildtype p53, proteolytically activated caspase-8, -9, -7 and -3 and unmethylated caspase-8 were more responsive to 5-FU and selenous acid-induced apoptosis. Fluorouracil 149-153 caspase 8 Homo sapiens 73-97 19189638-6 2008 Conversely, RKO cells expressing wildtype p53, proteolytically activated caspase-8, -9, -7 and -3 and unmethylated caspase-8 were more responsive to 5-FU and selenous acid-induced apoptosis. Fluorouracil 149-153 caspase 8 Homo sapiens 73-82 18612238-0 2008 Thymidylate synthase and dihydropyrimidine dehydrogenase levels are associated with response to 5-fluorouracil in Caenorhabditis elegans. Fluorouracil 96-110 Thymidylate synthase Caenorhabditis elegans 0-20 18612238-2 2008 The targeted pyrimidine biosynthesis pathway includes dihydropyrimidine dehydrogenase (DPD), which converts 5-FU to an inactive metabolite, and thymidylate synthase (TS), which is a major target of 5-FU. Fluorouracil 108-112 Thymidylate synthase Caenorhabditis elegans 144-164 18612238-2 2008 The targeted pyrimidine biosynthesis pathway includes dihydropyrimidine dehydrogenase (DPD), which converts 5-FU to an inactive metabolite, and thymidylate synthase (TS), which is a major target of 5-FU. Fluorouracil 198-202 Thymidylate synthase Caenorhabditis elegans 144-164 18612238-2 2008 The targeted pyrimidine biosynthesis pathway includes dihydropyrimidine dehydrogenase (DPD), which converts 5-FU to an inactive metabolite, and thymidylate synthase (TS), which is a major target of 5-FU. Fluorouracil 198-202 Thymidylate synthase Caenorhabditis elegans 166-168 18783590-1 2008 BACKGROUND: The ability of cytosine deaminase (CD) to convert the antifungal agent 5-fluorocytosine (5-FC) into one of the most potent and largely used anticancer compound such as 5-fluorouracil (5-FU) raised considerable interest in this enzyme to model gene or antibody - directed enzyme-prodrug therapy (GDEPT/ADEPT) aiming to improve the therapeutic ratio (benefit versus toxic side-effects) of cancer chemotherapy. Fluorouracil 180-194 cytosine deaminase Saccharomyces cerevisiae S288C 27-45 18783590-1 2008 BACKGROUND: The ability of cytosine deaminase (CD) to convert the antifungal agent 5-fluorocytosine (5-FC) into one of the most potent and largely used anticancer compound such as 5-fluorouracil (5-FU) raised considerable interest in this enzyme to model gene or antibody - directed enzyme-prodrug therapy (GDEPT/ADEPT) aiming to improve the therapeutic ratio (benefit versus toxic side-effects) of cancer chemotherapy. Fluorouracil 180-194 cytosine deaminase Saccharomyces cerevisiae S288C 47-49 18783590-1 2008 BACKGROUND: The ability of cytosine deaminase (CD) to convert the antifungal agent 5-fluorocytosine (5-FC) into one of the most potent and largely used anticancer compound such as 5-fluorouracil (5-FU) raised considerable interest in this enzyme to model gene or antibody - directed enzyme-prodrug therapy (GDEPT/ADEPT) aiming to improve the therapeutic ratio (benefit versus toxic side-effects) of cancer chemotherapy. Fluorouracil 196-200 cytosine deaminase Saccharomyces cerevisiae S288C 27-45 18783590-1 2008 BACKGROUND: The ability of cytosine deaminase (CD) to convert the antifungal agent 5-fluorocytosine (5-FC) into one of the most potent and largely used anticancer compound such as 5-fluorouracil (5-FU) raised considerable interest in this enzyme to model gene or antibody - directed enzyme-prodrug therapy (GDEPT/ADEPT) aiming to improve the therapeutic ratio (benefit versus toxic side-effects) of cancer chemotherapy. Fluorouracil 196-200 cytosine deaminase Saccharomyces cerevisiae S288C 47-49 18270838-5 2008 RESULTS: After treatment with high-dose 5-FU, the intestinal mucosa suffered severe damage: the villi and crypts disappeared, the number of msi-1-positive cells increased greatly, the intestinal epithelial cells could be divided into two fractions by FACS, and the percentage of msi-1-positive cells was up to 67.75% in the fraction in which the value of FSC was higher. Fluorouracil 40-44 acyl-CoA synthetase long-chain family member 1 Mus musculus 251-255 18754885-5 2008 Anticancer drugs including doxorubicin, etoposide and 5-fluorouracil also induced cyclin G2 expression during induction of growth arrest of the MCF-7 cell at the G1 phase or G2/M phase. Fluorouracil 54-68 cyclin G2 Homo sapiens 82-91 18690847-3 2008 The aim of the study was to investigate the induction by celecoxib of some multidrug resistance proteins, MRP1, MRP2, MRP4 and MRP5, involved in the transport of irinotecan and 5-FU. Fluorouracil 177-181 ATP binding cassette subfamily C member 5 Homo sapiens 127-131 18537153-9 2008 CONCLUSIONS: Gene polymorphisms of DPYD and CDA predict survival of gastric cancer patients treated with 5-fluorouracil-based adjuvant chemotherapy. Fluorouracil 105-119 cytidine deaminase Homo sapiens 44-47 18523641-0 2008 Inhibition of p38 MAPK suppresses inflammatory cytokine induction by etoposide, 5-fluorouracil, and doxorubicin without affecting tumoricidal activity. Fluorouracil 80-94 mitogen-activated protein kinase 14 Mus musculus 14-22 18523641-9 2008 Study findings demonstrate that clinically relevant doses of etoposide, doxorubicin, and 5-FU activated p38 MAPK in both macrophages and LLC1 cells. Fluorouracil 89-93 mitogen-activated protein kinase 14 Mus musculus 104-112 18533195-2 2008 In this paper, the optimal controller represents the optimal drug dosage of CAF (Cyclophosphamide, Adriamycin and Fluorouracil) regimen in adjuvant chemotherapy after surgery for these patients. Fluorouracil 114-126 lysine acetyltransferase 2B Homo sapiens 76-79 18473752-1 2008 Capecitabine is a drug that requires the consecutive action of three enzymes: carboxylesterase 2 (CES 2), cytidine deaminase (CDD), and thymidine phosphorylase (TP) for transformation into 5-fluorouracil (5FU). Fluorouracil 189-203 cytidine deaminase Homo sapiens 106-124 18473752-1 2008 Capecitabine is a drug that requires the consecutive action of three enzymes: carboxylesterase 2 (CES 2), cytidine deaminase (CDD), and thymidine phosphorylase (TP) for transformation into 5-fluorouracil (5FU). Fluorouracil 189-203 cytidine deaminase Homo sapiens 126-129 17982488-6 2008 5-Fluorouracil treatment of colon carcinoma HCT116 cells expressing WT p53 results in a reduction of the cyclin B2 protein level suggesting that DNA damage may indeed cause repression of these genes. Fluorouracil 0-14 cyclin B2 Homo sapiens 105-114 17632733-7 2008 Treatment with both ZD55-MnSOD and 5-FU could induce more significant apoptosis in cancer cells compared with ZD55-MnSOD or 5-FU alone, respectively. Fluorouracil 35-39 superoxide dismutase 2 Homo sapiens 115-120 17632733-7 2008 Treatment with both ZD55-MnSOD and 5-FU could induce more significant apoptosis in cancer cells compared with ZD55-MnSOD or 5-FU alone, respectively. Fluorouracil 124-128 superoxide dismutase 2 Homo sapiens 25-30 17637740-2 2008 We found that the cytotoxic drugs methotrexate (MTX) and 5-fluorouracil (5-FU) were both able to sensitize resistant tumor cells for induction of apoptosis by p53-mediated upregulation of caspase-8. Fluorouracil 57-71 caspase 8 Homo sapiens 188-197 17982676-6 2007 Compared to 5-FU-treated TP53-proficient HCT116 cultures, 5-FU-treated TP53-depleted HCT116 cultures showed lack of CDKN1A induction, decreased apoptotic levels, decreased FAS and TNFRSF10B transcript levels and cleaved PARP protein levels, G1/S transition arrests, decreased CCND1 protein levels, and smaller intra-S phase arrests. Fluorouracil 58-62 collagen type XI alpha 2 chain Homo sapiens 220-224 17912239-0 2007 Mucin impedes cytotoxic effect of 5-FU against growth of human pancreatic cancer cells: overcoming cellular barriers for therapeutic gain. Fluorouracil 34-38 LOC100508689 Homo sapiens 0-5 18408432-3 2008 107) , M1 (liver), Stage IVb performed systemic chemotherapy by FAP (5-fluorouracil ( 5-FU)+doxorubicin (DXR)+cisplatin (CDDP) ) from March, 2004. Fluorouracil 69-83 fibroblast activation protein alpha Homo sapiens 64-67 18291415-3 2008 CD also converts 5-fluorocytosine (5FC) to 5-fluorouracil, an inhibitor of DNA synthesis and RNA function. Fluorouracil 43-57 cytosine deaminase Saccharomyces cerevisiae S288C 0-2 18082672-8 2008 In addition, the combination 5-FU plus scFv23/TNF induced apoptosis and this synergistic effect was dependent on activation of caspase-8 and caspase-3. Fluorouracil 29-33 caspase 8 Homo sapiens 127-136 17912239-5 2007 In this study we investigated the role of mucin in cytotoxic drug treatment to determine whether the extracellular domain of mucin impedes cytotoxic drug action of 5-FU. Fluorouracil 164-168 LOC100508689 Homo sapiens 125-130 17695509-5 2007 RESULTS: The expression levels of hENT1 mRNA significantly correlated with the IC50 value of 5-FU in all seven lines and also correlated with gemcitabine resistance in six lines (except AsPC1). Fluorouracil 93-97 solute carrier family 29 member 1 (Augustine blood group) Homo sapiens 34-39 17695509-7 2007 In the PSN1 cells, [3H] gemcitabine uptake via hENT1 was significantly inhibited by NBMPR, and 5-FU sensitivity was significantly increased when the cells were pretreated with NBMPR. Fluorouracil 95-99 5'-nucleotidase, cytosolic IIIA Homo sapiens 7-11 17695509-8 2007 CONCLUSION: Our results suggest that hENT1 plays an important role in 5-FU resistance and that hENT1 mRNA levels might be a useful marker to predict 5-FU sensitivity in pancreatic cancer. Fluorouracil 70-74 solute carrier family 29 member 1 (Augustine blood group) Homo sapiens 37-42 17695509-8 2007 CONCLUSION: Our results suggest that hENT1 plays an important role in 5-FU resistance and that hENT1 mRNA levels might be a useful marker to predict 5-FU sensitivity in pancreatic cancer. Fluorouracil 149-153 solute carrier family 29 member 1 (Augustine blood group) Homo sapiens 95-100 17552008-1 2007 AIM: To investigate the effects of granulocyte-colony stimulating factor (G-CSF) on peritoneal defense mechanisms and bacterial translocation after systemic 5-Fluorouracil (5-FU) administration. Fluorouracil 157-171 colony stimulating factor 3 Rattus norvegicus 74-79 17552008-1 2007 AIM: To investigate the effects of granulocyte-colony stimulating factor (G-CSF) on peritoneal defense mechanisms and bacterial translocation after systemic 5-Fluorouracil (5-FU) administration. Fluorouracil 173-177 colony stimulating factor 3 Rattus norvegicus 35-72 17552008-1 2007 AIM: To investigate the effects of granulocyte-colony stimulating factor (G-CSF) on peritoneal defense mechanisms and bacterial translocation after systemic 5-Fluorouracil (5-FU) administration. Fluorouracil 173-177 colony stimulating factor 3 Rattus norvegicus 74-79 17552008-12 2007 We conclude that intraperitoneal GCSF administration protects the effects of systemic 5-FU on peritoneal defense mechanisms. Fluorouracil 86-90 colony stimulating factor 3 Rattus norvegicus 33-37 18186026-0 2008 Control of 5-FOA and 5-FU resistance by Saccharomyces cerevisiae YJL055W. Fluorouracil 21-25 Log1p Saccharomyces cerevisiae S288C 65-72 18186026-4 2008 Overexpression of Yjl055Wp also suppressed the lethality induced by 5-FU, but deletion of YJL055W had no detectable effect on resistance to either 5-FOA or 5-FU. Fluorouracil 68-72 Log1p Saccharomyces cerevisiae S288C 18-26 17637740-2 2008 We found that the cytotoxic drugs methotrexate (MTX) and 5-fluorouracil (5-FU) were both able to sensitize resistant tumor cells for induction of apoptosis by p53-mediated upregulation of caspase-8. Fluorouracil 73-77 caspase 8 Homo sapiens 188-197 18383843-2 2008 The major mediator of cellular uptake of GEM is the human equilibrative nucleoside transporter 1 (hENT1) whose expression is up-regulated by thymidylate synthase inhibitors, such as 5-fluorouracil (5-FU). Fluorouracil 182-196 solute carrier family 29 member 1 (Augustine blood group) Homo sapiens 58-96 18383843-2 2008 The major mediator of cellular uptake of GEM is the human equilibrative nucleoside transporter 1 (hENT1) whose expression is up-regulated by thymidylate synthase inhibitors, such as 5-fluorouracil (5-FU). Fluorouracil 182-196 solute carrier family 29 member 1 (Augustine blood group) Homo sapiens 98-103 18383843-2 2008 The major mediator of cellular uptake of GEM is the human equilibrative nucleoside transporter 1 (hENT1) whose expression is up-regulated by thymidylate synthase inhibitors, such as 5-fluorouracil (5-FU). Fluorouracil 198-202 solute carrier family 29 member 1 (Augustine blood group) Homo sapiens 58-96 18383843-2 2008 The major mediator of cellular uptake of GEM is the human equilibrative nucleoside transporter 1 (hENT1) whose expression is up-regulated by thymidylate synthase inhibitors, such as 5-fluorouracil (5-FU). Fluorouracil 198-202 solute carrier family 29 member 1 (Augustine blood group) Homo sapiens 98-103 18772588-3 2008 The aim of this study was to investigate the effect and mechanisms of HK II on chemosensitivity of a colon cancer cell line (LoVo) to 5-fluorouracil (5-FU). Fluorouracil 134-148 hexokinase 2 Homo sapiens 70-75 18772588-3 2008 The aim of this study was to investigate the effect and mechanisms of HK II on chemosensitivity of a colon cancer cell line (LoVo) to 5-fluorouracil (5-FU). Fluorouracil 150-154 hexokinase 2 Homo sapiens 70-75 18772588-7 2008 RESULTS: In LoVo cells, HK II downregulation resulted in a decreased IC(50) value of 5-FU and increased apoptosis. Fluorouracil 85-89 hexokinase 2 Homo sapiens 24-29 18772588-9 2008 CONCLUSION: Our findings suggest that targeting HK II may be beneficial for patients with colon cancer treated with 5-FU. Fluorouracil 116-120 hexokinase 2 Homo sapiens 48-53 17951356-3 2008 Chemosensitivity experiments with 5-fluorouracil, cytosine arabinoside (araC), and mercaptopurine (MP) demonstrated that Hmgb1(-/-) mouse embryonic fibroblasts (MEFs) were 3 to 10 times more resistant to these drugs compared with Hmgb1(+)(/)(+) MEFs. Fluorouracil 34-48 high mobility group box 1 Mus musculus 121-126 17951356-7 2008 We have demonstrated for the first time that Hmgb1 is an essential activator of cellular response to genotoxic stress caused by chemotherapeutic agents (thiopurines, cytarabine, and 5-fluorouracil), which acts at early steps of antimetabolite-induced stress by stimulating phosphorylation of two DNA damage markers, p53 and H2AX. Fluorouracil 182-196 high mobility group box 1 Mus musculus 45-50 17283124-0 2007 5-Fluorouracil incorporated into DNA is excised by the Smug1 DNA glycosylase to reduce drug cytotoxicity. Fluorouracil 0-14 single-strand-selective monofunctional uracil-DNA glycosylase 1 Homo sapiens 55-60 16868766-8 2007 Similar to the case for other MRPs that possess only two membrane spanning domains (MRP4 and MRP5), MRP8 is a cyclic nucleotide efflux pump that is able to confer resistance to nucleoside-based agents, such as PMEA and 5FU. Fluorouracil 219-222 ATP binding cassette subfamily C member 5 Homo sapiens 93-97 19112505-0 2008 Reduction of Orc6 expression sensitizes human colon cancer cells to 5-fluorouracil and cisplatin. Fluorouracil 68-82 origin recognition complex subunit 6 Homo sapiens 13-17 19112505-1 2008 Previous studies from our group have shown that the expression levels of Orc6 were highly elevated in colorectal cancer patient specimens and the induction of Orc6 was associated with 5-fluorouracil (5-FU) treatment. Fluorouracil 184-198 origin recognition complex subunit 6 Homo sapiens 73-77 19112505-1 2008 Previous studies from our group have shown that the expression levels of Orc6 were highly elevated in colorectal cancer patient specimens and the induction of Orc6 was associated with 5-fluorouracil (5-FU) treatment. Fluorouracil 184-198 origin recognition complex subunit 6 Homo sapiens 159-163 19112505-1 2008 Previous studies from our group have shown that the expression levels of Orc6 were highly elevated in colorectal cancer patient specimens and the induction of Orc6 was associated with 5-fluorouracil (5-FU) treatment. Fluorouracil 200-204 origin recognition complex subunit 6 Homo sapiens 73-77 19112505-1 2008 Previous studies from our group have shown that the expression levels of Orc6 were highly elevated in colorectal cancer patient specimens and the induction of Orc6 was associated with 5-fluorouracil (5-FU) treatment. Fluorouracil 200-204 origin recognition complex subunit 6 Homo sapiens 159-163 19112505-4 2008 We demonstrated that the down regulation of Orc6 sensitizes colon cancer cells to both 5-FU and cisplatin (cis-pt) treatment. Fluorouracil 87-91 origin recognition complex subunit 6 Homo sapiens 44-48 17982676-6 2007 Compared to 5-FU-treated TP53-proficient HCT116 cultures, 5-FU-treated TP53-depleted HCT116 cultures showed lack of CDKN1A induction, decreased apoptotic levels, decreased FAS and TNFRSF10B transcript levels and cleaved PARP protein levels, G1/S transition arrests, decreased CCND1 protein levels, and smaller intra-S phase arrests. Fluorouracil 58-62 cyclin D1 Homo sapiens 276-281 17982676-7 2007 Alterations in gene expression in 5-FU-treated TP53-depleted HCT116 cultures confirmed previously-reported TP53 target genes and suggested potentially novel TP53 target genes (e.g. APOBEC3C, BIRC3, JMJD2B, LAMP3, MYO1E, PRRG1, SULF2, TACSTD2, TncRNA, ZFYVE20) that may play a role in mediating the 5-FU-induced DNA damage response in TP53-proficient cells. Fluorouracil 34-38 lysosomal associated membrane protein 3 Homo sapiens 206-211 17982676-7 2007 Alterations in gene expression in 5-FU-treated TP53-depleted HCT116 cultures confirmed previously-reported TP53 target genes and suggested potentially novel TP53 target genes (e.g. APOBEC3C, BIRC3, JMJD2B, LAMP3, MYO1E, PRRG1, SULF2, TACSTD2, TncRNA, ZFYVE20) that may play a role in mediating the 5-FU-induced DNA damage response in TP53-proficient cells. Fluorouracil 34-38 myosin IE Homo sapiens 213-218 18003156-5 2007 The effect of the hydrogels on the cytotoxicity of the chemotherapeutic agent 5-Fluoracil, an MRP substrate, was also assessed. Fluorouracil 78-89 ATP binding cassette subfamily C member 3 Homo sapiens 94-97 18086299-0 2007 CD40 signaling predicts response to preoperative trastuzumab and concomitant paclitaxel followed by 5-fluorouracil, epirubicin, and cyclophosphamide in HER-2-overexpressing breast cancer. Fluorouracil 100-114 CD40 molecule Homo sapiens 0-4 17361437-3 2007 Administration of Ad-mFlt3L can protect bone marrow injury caused by 5-Fu and stimulates proliferation and maturation of lymphocytes, APCs and NKs. Fluorouracil 69-73 FMS-like tyrosine kinase 3 ligand Mus musculus 21-27 17361437-5 2007 Adenovirus mediated Flt3L gene therapy synergies with chemotherapeutic drug, 5-Fu, in elicitation of long-lasting antitumor immunity. Fluorouracil 77-81 FMS-like tyrosine kinase 3 ligand Mus musculus 20-25 17032313-6 2006 ET(A)R blockade also resulted in sensitization to cisplatin and 5-fluorouracil-induced apoptosis. Fluorouracil 64-78 endothelin receptor type A Homo sapiens 0-6 17197759-2 2006 We report a case of HCC with liver cirrhosis and lung metastases who had been treated successfully by combination chemotherapy of 5-fluorouracil (5-FU) and interferon-alpha (IFN-alpha). Fluorouracil 130-144 HCC Homo sapiens 20-23 17197759-2 2006 We report a case of HCC with liver cirrhosis and lung metastases who had been treated successfully by combination chemotherapy of 5-fluorouracil (5-FU) and interferon-alpha (IFN-alpha). Fluorouracil 146-150 HCC Homo sapiens 20-23 16845689-3 2006 By applying a highly sensitive assay, a low-level but dose-dependent toxicity of 5-FC in fcy2 mutants was detected, whereas cells deficient in the cytosine deaminase (encoded by FCY1), which is essential for intracellular conversion of 5-FC to 5-fluorouracil, display strong dose-independent resistance. Fluorouracil 244-258 cytosine deaminase Saccharomyces cerevisiae S288C 178-182 17628013-2 2007 We found that specific c-Myc inhibition depleted cells of GSH by directly reducing the gene expression of both heavy and light subunits of the gamma-GCS enzyme and increased their susceptibility to antineoplastic drugs with different mechanisms of action, such as cisplatin (CDDP), staurosporine (STR), and 5-fluorouracil (5-FU). Fluorouracil 307-321 glutamate-cysteine ligase catalytic subunit Homo sapiens 143-152 17628013-2 2007 We found that specific c-Myc inhibition depleted cells of GSH by directly reducing the gene expression of both heavy and light subunits of the gamma-GCS enzyme and increased their susceptibility to antineoplastic drugs with different mechanisms of action, such as cisplatin (CDDP), staurosporine (STR), and 5-fluorouracil (5-FU). Fluorouracil 323-327 glutamate-cysteine ligase catalytic subunit Homo sapiens 143-152 17697537-13 2007 Both the positive rate and mean fluorescence intensity (MFI) of CD25 on CD4+ and CD8+ T cells were decreased after pretreatment of 5-FU. Fluorouracil 131-135 interleukin 2 receptor subunit alpha Homo sapiens 64-68 17611667-8 2007 Either trastuzumab or 5-FU concentration-dependently inhibited the growth of TRG cells. Fluorouracil 22-26 T cell receptor gamma locus Homo sapiens 77-80 17611667-9 2007 The combination of trastuzumab and 5-FU resulted in a significant inhibition of growth of TRG cells compared to either agent alone (P<0.001). Fluorouracil 35-39 T cell receptor gamma locus Homo sapiens 90-93 17537404-4 2007 However, tumor cells that adapt to oxidative stress by increasing manganese superoxide dismutase (MnSOD), Prx I, and Bcl-2 showed drug resistance to 5-FU. Fluorouracil 149-153 superoxide dismutase 2 Homo sapiens 66-96 17537404-4 2007 However, tumor cells that adapt to oxidative stress by increasing manganese superoxide dismutase (MnSOD), Prx I, and Bcl-2 showed drug resistance to 5-FU. Fluorouracil 149-153 superoxide dismutase 2 Homo sapiens 98-103 17695509-0 2007 Human equilibrative nucleoside transporter 1, as a predictor of 5-fluorouracil resistance in human pancreatic cancer. Fluorouracil 64-78 solute carrier family 29 member 1 (Augustine blood group) Homo sapiens 6-44 17545615-4 2007 Therefore, in the present study, we sought to test the therapeutic effect of an RCR vector (ACE-CD) carrying the yeast cytosine deaminase (CD) gene, which converts the nontoxic prodrug 5-fluorocytosine (5FC) into the chemotoxin 5-fluorouracil, after delivery by infusion into the locoregional circulation in a multifocal hepatic metastasis model of colon cancer. Fluorouracil 228-242 cytosine deaminase Saccharomyces cerevisiae S288C 119-137 16709241-5 2006 RESULTS: 5-FU treatment for 24 hours resulted in S phase arrests, p53 accumulation, up-regulation of p53-target genes on DNA damage response (ATF3, GADD34, GADD45A, PCNA), cell cycle-regulatory (CDKN1A), and apoptosis-regulatory pathways (FAS), and apoptosis induction in the parental and resistant cell lines. Fluorouracil 9-13 growth arrest and DNA damage inducible alpha Homo sapiens 156-163 16709241-11 2006 Differential expression in response to 5-FU treatment was demonstrated for genes involved in regulation of nucleotide binding/metabolism (ATAD2, GNL2, GNL3, MATR3), amino acid metabolism (AHCY, GSS, IVD, OAT), cytoskeleton organization (KRT7, KRT8, KRT19, MAST1), transport (MTCH1, NCBP1, SNAPAP, VPS52), and oxygen metabolism (COX5A, COX7C). Fluorouracil 39-43 G protein nucleolar 3 Homo sapiens 151-155 16709241-11 2006 Differential expression in response to 5-FU treatment was demonstrated for genes involved in regulation of nucleotide binding/metabolism (ATAD2, GNL2, GNL3, MATR3), amino acid metabolism (AHCY, GSS, IVD, OAT), cytoskeleton organization (KRT7, KRT8, KRT19, MAST1), transport (MTCH1, NCBP1, SNAPAP, VPS52), and oxygen metabolism (COX5A, COX7C). Fluorouracil 39-43 keratin 19 Homo sapiens 249-254 16709241-11 2006 Differential expression in response to 5-FU treatment was demonstrated for genes involved in regulation of nucleotide binding/metabolism (ATAD2, GNL2, GNL3, MATR3), amino acid metabolism (AHCY, GSS, IVD, OAT), cytoskeleton organization (KRT7, KRT8, KRT19, MAST1), transport (MTCH1, NCBP1, SNAPAP, VPS52), and oxygen metabolism (COX5A, COX7C). Fluorouracil 39-43 microtubule associated serine/threonine kinase 1 Homo sapiens 256-261 16709241-11 2006 Differential expression in response to 5-FU treatment was demonstrated for genes involved in regulation of nucleotide binding/metabolism (ATAD2, GNL2, GNL3, MATR3), amino acid metabolism (AHCY, GSS, IVD, OAT), cytoskeleton organization (KRT7, KRT8, KRT19, MAST1), transport (MTCH1, NCBP1, SNAPAP, VPS52), and oxygen metabolism (COX5A, COX7C). Fluorouracil 39-43 VPS52 subunit of GARP complex Homo sapiens 297-302 16709241-11 2006 Differential expression in response to 5-FU treatment was demonstrated for genes involved in regulation of nucleotide binding/metabolism (ATAD2, GNL2, GNL3, MATR3), amino acid metabolism (AHCY, GSS, IVD, OAT), cytoskeleton organization (KRT7, KRT8, KRT19, MAST1), transport (MTCH1, NCBP1, SNAPAP, VPS52), and oxygen metabolism (COX5A, COX7C). Fluorouracil 39-43 cytochrome c oxidase subunit 5A Homo sapiens 328-333 16337237-2 2006 Previously, it was demonstrated that DNA-damaging agents such as irradiation, cyclophosphamide or 5-fluorouracil increase the expression of SDF-1 by osteoblasts in murine marrow. Fluorouracil 98-112 chemokine (C-X-C motif) ligand 12 Mus musculus 140-145 16595493-3 2006 Glucose transporter-1 (Glut-1) and hexokinase II (HKII) proteins are highly expressed in many breast carcinomas, but their status while undergoing DOX or 5FU chemotherapy has not been systematically evaluated. Fluorouracil 154-157 hexokinase 2 Homo sapiens 35-48 17572015-8 2007 IFN-beta with 10 muM of 5-FU frequently induced synergistic antiproliferative effects. Fluorouracil 24-28 interferon beta 1 Homo sapiens 0-8 17394949-5 2007 During hypoxia, a hypoxia-responsive element regulates expression of the CD gene and facilitates the conversion of 5-FC to 5-fluorouracil, a highly toxic antimetabolite. Fluorouracil 123-137 cytosine deaminase Saccharomyces cerevisiae S288C 73-75 17443278-1 2007 BACKGROUND: Thymidine phosphorylase (TP), orotate phosphoribosyltransferase (OPRT), and dihydropyrimidine dehydrogenase (DPD) are important enzymes related to the metabolism of 5-fluorouracil and its derivatives. Fluorouracil 177-191 thymidine phosphorylase Homo sapiens 12-35 16797120-7 2007 Furthermore, we have found that reactive oxygen species (ROS) is an upstream signal of AMPK, and the combined treatment of EGCG and chemotherapeutic agents, 5-FU or Etoposide, exert a novel therapeutic effect on chemo-resistant colon cancer cells. Fluorouracil 157-161 protein kinase AMP-activated catalytic subunit alpha 2 Homo sapiens 87-91 16595493-3 2006 Glucose transporter-1 (Glut-1) and hexokinase II (HKII) proteins are highly expressed in many breast carcinomas, but their status while undergoing DOX or 5FU chemotherapy has not been systematically evaluated. Fluorouracil 154-157 hexokinase 2 Homo sapiens 50-54 16278042-0 2006 Diamine oxidase, a plasma biomarker in rats to GI tract toxicity of oral fluorouracil anti-cancer drugs. Fluorouracil 73-85 amine oxidase, copper containing 1 Rattus norvegicus 0-15 16282061-7 2005 The levels of CD3, CD4, CD4/CD8, IgG, IgM in 5-FU group were lower (P<0.05), while those in the three Shengmai Injection combined with 5-FU groups were higher than those in the control group (P<0.05). Fluorouracil 45-49 CD3 antigen, epsilon polypeptide Mus musculus 14-17 17364369-1 2007 CONCLUSION: The present study suggested that a high level of thymidine phosphorylase (TP) gene expression is significantly associated with favorable prognosis of patients treated with 5-fluorouracil (5-FU)-based chemotherapy. Fluorouracil 184-198 thymidine phosphorylase Homo sapiens 61-84 17364369-1 2007 CONCLUSION: The present study suggested that a high level of thymidine phosphorylase (TP) gene expression is significantly associated with favorable prognosis of patients treated with 5-fluorouracil (5-FU)-based chemotherapy. Fluorouracil 184-198 thymidine phosphorylase Homo sapiens 86-88 17364369-1 2007 CONCLUSION: The present study suggested that a high level of thymidine phosphorylase (TP) gene expression is significantly associated with favorable prognosis of patients treated with 5-fluorouracil (5-FU)-based chemotherapy. Fluorouracil 200-204 thymidine phosphorylase Homo sapiens 61-84 17364369-1 2007 CONCLUSION: The present study suggested that a high level of thymidine phosphorylase (TP) gene expression is significantly associated with favorable prognosis of patients treated with 5-fluorouracil (5-FU)-based chemotherapy. Fluorouracil 200-204 thymidine phosphorylase Homo sapiens 86-88 17237273-4 2007 It was also shown that SSAT mRNA was up-regulated in response to 5-FU or oxaliplatin in a panel of six colorectal cancer cell lines. Fluorouracil 65-69 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 23-27 17237273-7 2007 Western blot analyses showed that SSAT protein expression was dramatically enhanced when DENSpm was combined with oxaliplatin or 5-FU in HCT116 p53(+/+) cells. Fluorouracil 129-133 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 34-38 17607914-7 2007 Analysis of the expression of 5-fluorouracil (5-FU) (TS, DPD, TP)- and cisplatin (ERCC1, ERCC4, GADD45A, KU80)-related genes demonstrated an association of DPD expression with response and survival. Fluorouracil 30-44 growth arrest and DNA damage inducible alpha Homo sapiens 96-103 17607914-7 2007 Analysis of the expression of 5-fluorouracil (5-FU) (TS, DPD, TP)- and cisplatin (ERCC1, ERCC4, GADD45A, KU80)-related genes demonstrated an association of DPD expression with response and survival. Fluorouracil 30-44 X-ray repair cross complementing 5 Homo sapiens 105-109 17033231-1 2006 We performed a controlled study to compare the response to cyclophosphamide (CPA), adriamycin (ADM), and fluorouracil (5-FU) (CAF therapy) with that to uracil-tegafur (UFT) plus tamoxifen (TAM) (UFT+TAM therapy), when given as postoperative adjuvant therapy to women with breast cancer. Fluorouracil 105-117 lysine acetyltransferase 2B Homo sapiens 126-129 17033231-1 2006 We performed a controlled study to compare the response to cyclophosphamide (CPA), adriamycin (ADM), and fluorouracil (5-FU) (CAF therapy) with that to uracil-tegafur (UFT) plus tamoxifen (TAM) (UFT+TAM therapy), when given as postoperative adjuvant therapy to women with breast cancer. Fluorouracil 119-123 lysine acetyltransferase 2B Homo sapiens 126-129 16243820-4 2005 RNA expression levels of 5-FU metabolism-associated genes thymidylate synthase, thymidine phosphorylase, dihydropyrimidine dehydrogenase, methylenetetrahydrofolate reductase, MAP7, and ELF3, of platinum- and taxane-related genes caldesmon, ERCC1, ERCC4, HER-2/neu, and GADD45, and of multidrug resistance gene MRP1 were determined using real-time reverse transcriptase-PCR. Fluorouracil 25-29 growth arrest and DNA damage inducible alpha Homo sapiens 269-275 16243820-4 2005 RNA expression levels of 5-FU metabolism-associated genes thymidylate synthase, thymidine phosphorylase, dihydropyrimidine dehydrogenase, methylenetetrahydrofolate reductase, MAP7, and ELF3, of platinum- and taxane-related genes caldesmon, ERCC1, ERCC4, HER-2/neu, and GADD45, and of multidrug resistance gene MRP1 were determined using real-time reverse transcriptase-PCR. Fluorouracil 25-29 mutS homolog 3 Homo sapiens 310-314 16315867-6 2005 Radiation and 5-FU induce Th1-dominant state by inhibiting the OK-432-induced production of IL-10 and TGF-beta mediated by regulation of SOCS-1 and SOCS-3 expression, and are suggested to increase anti-cancer immunity. Fluorouracil 14-18 suppressor of cytokine signaling 3 Homo sapiens 148-154 16179862-9 2005 Treatment with antisense oligonucleotide plus 5-FU resulted in significantly decreased p125FAK expression in both C8161 and BL melanoma cell lines, demonstrated by Western blot analyses. Fluorouracil 46-50 protein tyrosine kinase 2 Homo sapiens 87-94 16115944-0 2005 Phase I/II combined chemoimmunotherapy with carcinoembryonic antigen-derived HLA-A2-restricted CAP-1 peptide and irinotecan, 5-fluorouracil, and leucovorin in patients with primary metastatic colorectal cancer. Fluorouracil 125-139 cyclase associated actin cytoskeleton regulatory protein 1 Homo sapiens 95-100 19956517-3 2005 The expression levels of thymidylate synthase (TS), thymidine phosphorylase (TP) and p53 have been known to be associated with the clinical response to 5-FU-based therapy as well as the prognosis, and that of vascular endothelial growth factor (VEGF) is associated with poor survival. Fluorouracil 152-156 thymidine phosphorylase Homo sapiens 52-75 19956517-3 2005 The expression levels of thymidylate synthase (TS), thymidine phosphorylase (TP) and p53 have been known to be associated with the clinical response to 5-FU-based therapy as well as the prognosis, and that of vascular endothelial growth factor (VEGF) is associated with poor survival. Fluorouracil 152-156 thymidine phosphorylase Homo sapiens 77-79 15870935-0 2005 A phase II and pharmacologic study of fluorouracil given by a 1-hour infusion daily for 5 days with leucovorin and interferon alpha-2a in adenocarcinoma of the large bowel. Fluorouracil 38-50 interferon alpha 2 Homo sapiens 115-134 15870935-1 2005 We have reported that increasing the length of infusion from 5 min to 1 h appeared to substantially reduce the toxicity associated with fluorouracil (5-FU) modulated by leucovorin (LV) and interferon alpha-2a (IFN-alpha). Fluorouracil 136-148 interferon alpha 2 Homo sapiens 189-208 15870935-1 2005 We have reported that increasing the length of infusion from 5 min to 1 h appeared to substantially reduce the toxicity associated with fluorouracil (5-FU) modulated by leucovorin (LV) and interferon alpha-2a (IFN-alpha). Fluorouracil 136-148 interferon alpha 2 Homo sapiens 210-219 15870935-1 2005 We have reported that increasing the length of infusion from 5 min to 1 h appeared to substantially reduce the toxicity associated with fluorouracil (5-FU) modulated by leucovorin (LV) and interferon alpha-2a (IFN-alpha). Fluorouracil 150-154 interferon alpha 2 Homo sapiens 189-208 15870935-1 2005 We have reported that increasing the length of infusion from 5 min to 1 h appeared to substantially reduce the toxicity associated with fluorouracil (5-FU) modulated by leucovorin (LV) and interferon alpha-2a (IFN-alpha). Fluorouracil 150-154 interferon alpha 2 Homo sapiens 210-219 15886469-5 2005 However, in HT-29 cells, the CPT-11/5-FU combination enhanced Mn-SOD activity when compared to cells treated with CPT-11 alone. Fluorouracil 36-40 superoxide dismutase 2 Homo sapiens 62-68 15886469-7 2005 CONCLUSION: Treatment with the CPT-11/5-FU combination may promote in HT-29 cell apoptosis by enhancing Mn-SOD activity. Fluorouracil 38-42 superoxide dismutase 2 Homo sapiens 104-110 16637064-2 2006 We recently reported that the combination of N(1), N(11)-diethylnorspermine (DENSPM) and 5-fluorouracil (5-FU) synergistically induces SSAT expression, depletes polyamine levels and causes apoptosis in colon cancer cells. Fluorouracil 89-103 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 135-139 15846298-5 2005 Treatment of cell lines in vitro with HGS-ETR1 enhanced the cytotoxicity of chemotherapeutic agents (camptothecin, cisplatin, carboplatin, or 5-fluorouracil) even in tumour cell lines that were not sensitive to HGS-ETR1 alone. Fluorouracil 142-156 CUGBP Elav-like family member 3 Homo sapiens 42-46 16637064-2 2006 We recently reported that the combination of N(1), N(11)-diethylnorspermine (DENSPM) and 5-fluorouracil (5-FU) synergistically induces SSAT expression, depletes polyamine levels and causes apoptosis in colon cancer cells. Fluorouracil 105-109 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 135-139 16868479-2 2006 Pretreatment of cancer cell lines with 5-fluorouracil (5-FU) leads to an increase in the expression of hENT1 and augments the effect of single-agent gemcitabine treatment in vitro. Fluorouracil 39-53 solute carrier family 29 member 1 (Augustine blood group) Homo sapiens 103-108 16868479-2 2006 Pretreatment of cancer cell lines with 5-fluorouracil (5-FU) leads to an increase in the expression of hENT1 and augments the effect of single-agent gemcitabine treatment in vitro. Fluorouracil 55-59 solute carrier family 29 member 1 (Augustine blood group) Homo sapiens 103-108 16868479-4 2006 METHODS: The expression level of hENT1 mRNA was examined using 6 types of human pancreatic cancer cell lines treated with 5-FU and MiaPaCa-2 xenograft tumors in BALB/c nu/nu mice treated with UFT. Fluorouracil 122-126 solute carrier family 29 member 1 (Augustine blood group) Homo sapiens 33-38 16868479-7 2006 RESULTS: MiaPaCa-2 cell line was one of the lines that showed the highest rate of 5-FU-induced increase in the hENT1 mRNA level. Fluorouracil 82-86 solute carrier family 29 member 1 (Augustine blood group) Homo sapiens 111-116 16898008-1 2006 We have reported a remarkably high anti-tumor efficacy using intra arterial 5-FU infusion chemotherapy combined with subcutaneous interferon-alpha injection to treat advanced hepatocellular carcinoma (HCC) with portal vein thrombus. Fluorouracil 76-80 HCC Homo sapiens 201-204 18221035-1 2006 Thymidine phosphorylase (TP), also known as platelet derived endothelial cell growth factor (PD-ECGF), is an enzyme involved in thymidine synthesis and degradation and exerts an angiogenic activity, whereas N4 pentyloxy-carbonyl- 5"-deoxy-5-fluorocytidine, commonly called capecitabine (CAP), is a TP-activated oral fluorpyrimidine, which generates 5-fluorouracil (5-FU) within tumours. Fluorouracil 349-363 thymidine phosphorylase Homo sapiens 44-91 18221035-1 2006 Thymidine phosphorylase (TP), also known as platelet derived endothelial cell growth factor (PD-ECGF), is an enzyme involved in thymidine synthesis and degradation and exerts an angiogenic activity, whereas N4 pentyloxy-carbonyl- 5"-deoxy-5-fluorocytidine, commonly called capecitabine (CAP), is a TP-activated oral fluorpyrimidine, which generates 5-fluorouracil (5-FU) within tumours. Fluorouracil 349-363 thymidine phosphorylase Homo sapiens 93-100 18221035-1 2006 Thymidine phosphorylase (TP), also known as platelet derived endothelial cell growth factor (PD-ECGF), is an enzyme involved in thymidine synthesis and degradation and exerts an angiogenic activity, whereas N4 pentyloxy-carbonyl- 5"-deoxy-5-fluorocytidine, commonly called capecitabine (CAP), is a TP-activated oral fluorpyrimidine, which generates 5-fluorouracil (5-FU) within tumours. Fluorouracil 365-369 thymidine phosphorylase Homo sapiens 44-91 18221035-1 2006 Thymidine phosphorylase (TP), also known as platelet derived endothelial cell growth factor (PD-ECGF), is an enzyme involved in thymidine synthesis and degradation and exerts an angiogenic activity, whereas N4 pentyloxy-carbonyl- 5"-deoxy-5-fluorocytidine, commonly called capecitabine (CAP), is a TP-activated oral fluorpyrimidine, which generates 5-fluorouracil (5-FU) within tumours. Fluorouracil 365-369 thymidine phosphorylase Homo sapiens 93-100 16631755-1 2006 Doxorubicin, cis-diamminedichloroplatinum (II) and 5-fluorouracil used in chemotherapy induce apoptosis in Hep3B cells in the absence of p53, p73, and functional Fas. Fluorouracil 51-65 tumor protein p73 Homo sapiens 142-145 15846298-7 2005 Combination of HGS-ETR1 with chemotherapeutic agents (topotecan, 5-fluorouracil, and irinotecan) in three independent colon cancer xenograft models resulted in an enhanced antitumour efficacy compared to either agent alone. Fluorouracil 65-79 CUGBP Elav-like family member 3 Homo sapiens 19-23 16015041-8 2005 Furthermore and most importantly, patients with Dnam-1 deletion who received adjuvant chemotherapy had a significantly lower risk of death compared to untreated patients with Dnam-1 deletion (hazard ratio = 0.51; p = 0.05), whereas those with Dnam-1 retention did not derive any benefit from 5-FU-based treatment (hazard ratio = 1.68; p = 0.16). Fluorouracil 292-296 CD226 molecule Homo sapiens 48-54 16586549-3 2006 5-FU, MTX, CDDP of different concentrations were given after transfecting cells with cyclin D1 ASODN for 24 h the dose-effect responses were observed and IC50s were calculated. Fluorouracil 0-4 cyclin D1 Homo sapiens 85-94 16586549-7 2006 Cyclin D1 ASODN could increase the chemosensitivity to 5-FU, MTX, CDDP in cells. Fluorouracil 55-59 cyclin D1 Homo sapiens 0-9 16278042-16 2006 In summary, DAO is a very sensitive plasma biomarker and will be useful for the quantitative evaluation of the small intestinal mucosal lesions induced by the anti-cancer drug, 5-FU, in rats. Fluorouracil 177-181 amine oxidase, copper containing 1 Rattus norvegicus 12-15 16015041-9 2005 CONCLUSIONS: Loss of Dnam-1 gene copy number and retention of Cadh-7 might be indicators of worse prognosis, and Dnam-1 deletion might predict for a beneficial response to adjuvant 5-FU-based chemotherapy in patients with CRC. Fluorouracil 181-185 CD226 molecule Homo sapiens 113-119 15999119-1 2005 The enzymes thymidylate synthase (TS), dihydropyrimidine dehydrogenase (DPD), thymidine phosphorylase (TP), and orotate phosphoribosyl transferase (OPRT) are involved in the metabolism of the anticancer drug 5-fluorouracil. Fluorouracil 208-222 thymidine phosphorylase Homo sapiens 78-101 15572680-6 2004 Consistent with this hypothesis, 5FU inhibits the growth of RRP6 mutants with defects in the degradation function of the enzyme and it interferes with the degradation of an rRNA precursor. Fluorouracil 33-36 exosome nuclease subunit RRP6 Saccharomyces cerevisiae S288C 60-64 15509509-2 2004 CD deaminates 5-fluorocytosine (5FC) to 5-fluorouracil (5FU), and UPRT subsequently converts 5FU to fluorouridine monophosphate, and both of these reactions can be monitored noninvasively in vitro and in vivo using 19F magnetic resonance spectroscopy (MRS). Fluorouracil 40-54 cytosine deaminase Saccharomyces cerevisiae S288C 0-2 16328315-1 2005 OBJECTIVE: The thymidylate synthase (TS) and dihydropyrimidine dehydrogenase (DPD) enzymes affect the outcome of 5-fluorouracil (5-FU)-based chemotherapy. Fluorouracil 113-127 LOW QUALITY PROTEIN: thymidylate synthase Meleagris gallopavo 15-35 16328315-1 2005 OBJECTIVE: The thymidylate synthase (TS) and dihydropyrimidine dehydrogenase (DPD) enzymes affect the outcome of 5-fluorouracil (5-FU)-based chemotherapy. Fluorouracil 129-133 LOW QUALITY PROTEIN: thymidylate synthase Meleagris gallopavo 15-35 16373718-7 2005 In addition, treatment of a 5-FU-resistant cell line with 5-FU down-regulated c-FLIP expression and sensitized the chemotherapy-resistant cell line to rTRAIL. Fluorouracil 28-32 TNF superfamily member 10 Rattus norvegicus 151-157 15509509-2 2004 CD deaminates 5-fluorocytosine (5FC) to 5-fluorouracil (5FU), and UPRT subsequently converts 5FU to fluorouridine monophosphate, and both of these reactions can be monitored noninvasively in vitro and in vivo using 19F magnetic resonance spectroscopy (MRS). Fluorouracil 56-59 cytosine deaminase Saccharomyces cerevisiae S288C 0-2 16373718-7 2005 In addition, treatment of a 5-FU-resistant cell line with 5-FU down-regulated c-FLIP expression and sensitized the chemotherapy-resistant cell line to rTRAIL. Fluorouracil 58-62 TNF superfamily member 10 Rattus norvegicus 151-157 15509509-2 2004 CD deaminates 5-fluorocytosine (5FC) to 5-fluorouracil (5FU), and UPRT subsequently converts 5FU to fluorouridine monophosphate, and both of these reactions can be monitored noninvasively in vitro and in vivo using 19F magnetic resonance spectroscopy (MRS). Fluorouracil 93-96 cytosine deaminase Saccharomyces cerevisiae S288C 0-2 16041207-2 2005 5-FU cytotoxicity can be modulated by folinic acid (FA) or interferon-alpha (INF-alpha). Fluorouracil 0-4 interferon alpha 17 Homo sapiens 77-86 15720808-2 2004 To this aim, we analyzed the serine threonine receptor-associated protein (STRAP), an inhibitor of TGF-beta signaling, with regard to prognosis and prediction of adjuvant 5-FU chemotherapy benefit. Fluorouracil 171-175 serine/threonine kinase receptor associated protein Homo sapiens 29-73 15720808-2 2004 To this aim, we analyzed the serine threonine receptor-associated protein (STRAP), an inhibitor of TGF-beta signaling, with regard to prognosis and prediction of adjuvant 5-FU chemotherapy benefit. Fluorouracil 171-175 serine/threonine kinase receptor associated protein Homo sapiens 75-80 15308648-0 2004 UPS1 and UPS2 from Arabidopsis mediate high affinity transport of uracil and 5-fluorouracil. Fluorouracil 77-91 ureide permease 1 Arabidopsis thaliana 0-4 15986457-5 2005 Phloretin, a glucose transporter 2 (GLUT2) inhibitor, completely abolished the absorption of 3-OMG in both control and 5-FU-treated mice, indicating the specific effect on the carrier-dependent process. Fluorouracil 119-123 solute carrier family 2 (facilitated glucose transporter), member 2 Mus musculus 36-41 15986457-6 2005 Protein and mRNA expressions of GLUT2 were significantly higher in 5-FU-treated mice compared to the control mice. Fluorouracil 67-71 solute carrier family 2 (facilitated glucose transporter), member 2 Mus musculus 32-37 15986457-9 2005 These results indicate that repeated oral administration of 5-FU did not hamper, but unexpectedly induced, SGLT1 and GLUT2 expression to enhance glucose absorption. Fluorouracil 60-64 solute carrier family 2 (facilitated glucose transporter), member 2 Mus musculus 117-122 15308648-7 2004 A detailed analysis of the substrate specificities of two members of the AtUPS family shows that AtUPS1 and AtUPS2 mediate high affinity uracil and 5-fluorouracil (a toxic uracil analogue) transport when expressed in yeast and Xenopus oocytes. Fluorouracil 148-162 ureide permease 1 Arabidopsis thaliana 97-103 15301717-0 2004 [Enhancement effect of interferon gamma on the sensitivity of RT4 bladder cancer cells to 5"-deoxy-5-fluorouridine,and 5-fluorouracil through up-regulation of PD-ECGF/TP]. Fluorouracil 119-133 thymidine phosphorylase Homo sapiens 159-166 15956974-7 2005 Chemosensitivity to gemcitabine or 5-fluorouracil (5-FU) was assessed by MTT assay in pancreatic cancer cells following NRP-1 overexpression or siRNA-induced downregulation of NRP-1. Fluorouracil 35-49 neuropilin 1 Homo sapiens 120-125 15301717-1 2004 BACKGROUND & OBJECTIVE: Platelet-derived endothelial cell growth factor/thymidine phosphorylase (PD-ECGF/TP) is an essential enzyme in converting 5"-deoxy-5-fluorouridine (5"-DFUR), and 5-fluorouracil (5-FU) to their active metabolites in vivo, and can be up-regulated by some cytokines such as interleukin-1, and interferon gamma (INFgamma). Fluorouracil 190-204 thymidine phosphorylase Homo sapiens 101-111 15956974-7 2005 Chemosensitivity to gemcitabine or 5-fluorouracil (5-FU) was assessed by MTT assay in pancreatic cancer cells following NRP-1 overexpression or siRNA-induced downregulation of NRP-1. Fluorouracil 51-55 neuropilin 1 Homo sapiens 120-125 15956974-10 2005 Neuropilin-1 overexpression in FG cells enhanced anoikis resistance and increased survival of cells by > 30% after exposure to clinically relevant levels of gemcitabine and 5-FU. Fluorouracil 176-180 neuropilin 1 Homo sapiens 0-12 15301717-1 2004 BACKGROUND & OBJECTIVE: Platelet-derived endothelial cell growth factor/thymidine phosphorylase (PD-ECGF/TP) is an essential enzyme in converting 5"-deoxy-5-fluorouridine (5"-DFUR), and 5-fluorouracil (5-FU) to their active metabolites in vivo, and can be up-regulated by some cytokines such as interleukin-1, and interferon gamma (INFgamma). Fluorouracil 206-210 thymidine phosphorylase Homo sapiens 101-111 15897250-0 2005 The multidrug resistance protein 5 (ABCC5) confers resistance to 5-fluorouracil and transports its monophosphorylated metabolites. Fluorouracil 65-79 ATP binding cassette subfamily C member 5 Homo sapiens 36-41 15897250-3 2005 The present study shows that the ATP-dependent multidrug resistance protein-5 (MRP5, ABCC5) confers resistance to 5-FU by transporting the monophosphate metabolites. Fluorouracil 114-118 ATP binding cassette subfamily C member 5 Homo sapiens 79-83 15301717-7 2004 CONCLUSIONS: INFgamma enhances cytotoxicity of 5"-DFUR, and 5-FU against RT4 cells through induction of PD-ECGF/TP. Fluorouracil 60-64 thymidine phosphorylase Homo sapiens 104-111 15897250-3 2005 The present study shows that the ATP-dependent multidrug resistance protein-5 (MRP5, ABCC5) confers resistance to 5-FU by transporting the monophosphate metabolites. Fluorouracil 114-118 ATP binding cassette subfamily C member 5 Homo sapiens 85-90 15897250-5 2005 In 3-day cytotoxicity assays, MRP5-transfected cells were approximately 9-fold resistant to 5-FU and 6-thioguanine. Fluorouracil 92-96 ATP binding cassette subfamily C member 5 Homo sapiens 30-34 15330188-3 2004 Because direct invasion of the thoracic aorta was suspected, FAP therapy (CDDP, 5-FU and ADM) was given as neoadjuvant chemotherapy. Fluorouracil 80-84 fibroblast activation protein alpha Homo sapiens 61-64 15897250-6 2005 Studies with inside-out membrane vesicles prepared from transfected cells showed that MRP5 mediates ATP-dependent transport of 5 micromol/L [(3)H]5-FdUMP, [(3)H]5-FUMP, [(3)H]dUMP, and not [(3)H]5-FUdR, or [(3)H]5-FU. Fluorouracil 161-165 ATP binding cassette subfamily C member 5 Homo sapiens 86-90 15897250-9 2005 Furthermore, the 5-FU drug sensitivity of HEK-MRP5 cells was partially modulated to that of the HEK-vector by the presence of 40 micromol/L 5-nitro-2-(3-phenylpropylamino)-benzoic acid but not by 2 mmol/L probenecid. Fluorouracil 17-21 ATP binding cassette subfamily C member 5 Homo sapiens 46-50 15150550-2 2004 This combination was based on an experimental hypothesis that taxane can increase tumour sensitivity to the effect of capecitabine through the upregulation of thymidine phosphorylase (TP), which is responsible for the metabolism of 5-fluorouracil (5-FU) and its derivatives, including capecitabine. Fluorouracil 232-246 thymidine phosphorylase Homo sapiens 159-182 15799730-2 2005 METHOD: Two different alkoxycarbonyl 5-FU prodrugs denoted C12 and C18 were synthesized and formulated as silicone oil suspensions. Fluorouracil 37-41 protegrin-4 Sus scrofa 59-62 15799730-6 2005 RESULTS: With the C12 prodrug silicone oil formulation, the concentration of free 5-FU in the vitreous water phase 1 hour after surgery was 3.30 +/- 1.62 microg/ml. Fluorouracil 82-86 protegrin-4 Sus scrofa 18-21 15150550-2 2004 This combination was based on an experimental hypothesis that taxane can increase tumour sensitivity to the effect of capecitabine through the upregulation of thymidine phosphorylase (TP), which is responsible for the metabolism of 5-fluorouracil (5-FU) and its derivatives, including capecitabine. Fluorouracil 232-246 thymidine phosphorylase Homo sapiens 184-186 15150550-2 2004 This combination was based on an experimental hypothesis that taxane can increase tumour sensitivity to the effect of capecitabine through the upregulation of thymidine phosphorylase (TP), which is responsible for the metabolism of 5-fluorouracil (5-FU) and its derivatives, including capecitabine. Fluorouracil 248-252 thymidine phosphorylase Homo sapiens 159-182 15150550-2 2004 This combination was based on an experimental hypothesis that taxane can increase tumour sensitivity to the effect of capecitabine through the upregulation of thymidine phosphorylase (TP), which is responsible for the metabolism of 5-fluorouracil (5-FU) and its derivatives, including capecitabine. Fluorouracil 248-252 thymidine phosphorylase Homo sapiens 184-186 15564287-4 2005 Treatment with 5-fluoro-2"-deoxyuridine (5-FdUrd) or 5-fluorouracil (5-FU) gives rise to a dose-dependent increase of uracil in Ung(-/-) MEFs (up to 1.5-fold) but not in wild-type cells. Fluorouracil 53-67 uracil DNA glycosylase Mus musculus 128-131 15150550-7 2004 Thymidine phosphorylase upregulation by several anticancer drugs implies the importance of individualised strategies for sensitisation of tumour tissues to 5-FU and its derivatives. Fluorouracil 156-160 thymidine phosphorylase Homo sapiens 0-23 15564287-4 2005 Treatment with 5-fluoro-2"-deoxyuridine (5-FdUrd) or 5-fluorouracil (5-FU) gives rise to a dose-dependent increase of uracil in Ung(-/-) MEFs (up to 1.5-fold) but not in wild-type cells. Fluorouracil 69-73 uracil DNA glycosylase Mus musculus 128-131 15319798-2 2004 Upon the availability of substrates, UPase can also catalyze the formation of nucleosides from uracil or 5-fluorouracil (5-FU) and ribose-1-phosphate (Rib-1-P). Fluorouracil 121-125 uridine phosphorylase 1 Homo sapiens 37-42 15952572-10 2005 CONCLUSION: The NPC patients with LRP and TS expression may be less sensitive to chemotherapy with DDP + 5-FU. Fluorouracil 105-109 major vault protein Homo sapiens 34-37 15546879-5 2005 By contrast, simultaneous combination of 5-FU with DFMO, an inhibitor of the polyamine biosynthetic enzyme ornithine decarboxylase, depleted putrescine but did not produce synergistic cell killing. Fluorouracil 41-45 ornithine decarboxylase 1 Homo sapiens 107-130 15319798-4 2004 UPase activity is usually elevated in various tumor tissues, and this induction appears to confer 5-FU therapeutic advantage to cancer patients. Fluorouracil 98-102 uridine phosphorylase 1 Homo sapiens 0-5 15050369-0 2004 Differential mucin expression in colon carcinoma HT-29 clones with variable resistance to 5-fluorouracil and methotrexate. Fluorouracil 90-104 LOC100508689 Homo sapiens 13-18 14614573-1 2004 PURPOSE: The aim of this study was to investigate the changes in two of the enzymes involved in fluorouracil metabolism, thymidine phosphorylase (TP) and dihydropyrimidine dehydrogenase (DPD), in uterine cervical squamous cell cancer tissue after radiotherapy. Fluorouracil 96-108 thymidine phosphorylase Homo sapiens 121-144 15655543-6 2005 Quantitative expression levels of drug pathway genes were determined using TaqMan RT-PCR (5-fluorouracil (5-FU): TYMS, DPYD, ECGF1; oxaliplatin: GSTP1 (glutathione S-transferase pi), ERCC1 and 2; irinotecan: ABCB1, ABCG2, CYP3A4, UGT1A1, CES2, TOP1). Fluorouracil 90-104 thymidine phosphorylase Homo sapiens 125-130 15611226-7 2005 Moreover, we demonstrate that chemotherapeutic agents that suppress protein synthesis and reverse the CD40-mediated dissociation of the translational repressor eukaryotic initiation factor 4E-binding protein from the initiation factor eukaryotic initiation factor 4E, such as 5-fluorouracil, etoposide, and quercetin, dramatically increase the susceptibility of cervical carcinoma cells to CD40L-induced apoptosis. Fluorouracil 276-290 CD40 molecule Homo sapiens 102-106 15611226-7 2005 Moreover, we demonstrate that chemotherapeutic agents that suppress protein synthesis and reverse the CD40-mediated dissociation of the translational repressor eukaryotic initiation factor 4E-binding protein from the initiation factor eukaryotic initiation factor 4E, such as 5-fluorouracil, etoposide, and quercetin, dramatically increase the susceptibility of cervical carcinoma cells to CD40L-induced apoptosis. Fluorouracil 276-290 eukaryotic translation initiation factor 4E Homo sapiens 160-191 15611226-7 2005 Moreover, we demonstrate that chemotherapeutic agents that suppress protein synthesis and reverse the CD40-mediated dissociation of the translational repressor eukaryotic initiation factor 4E-binding protein from the initiation factor eukaryotic initiation factor 4E, such as 5-fluorouracil, etoposide, and quercetin, dramatically increase the susceptibility of cervical carcinoma cells to CD40L-induced apoptosis. Fluorouracil 276-290 eukaryotic translation initiation factor 4E Homo sapiens 235-266 16491956-0 2005 Irinotecan/5-fluorouracil combination induces alterations in mitochondrial membrane potential and caspases on colon cancer cell lines. Fluorouracil 11-25 caspase 8 Homo sapiens 98-106 16491956-5 2005 In this study, we verified whether the collapse in mitochondrial membrane and the activation of caspases is responsible for increased apoptosis observed with CPT-11/5-FU treatment. Fluorouracil 165-169 caspase 8 Homo sapiens 96-104 16491956-12 2005 In spite of the differences among the cell lines, these results indicated that the increase in apoptosis in HT-29 cells observed with CPT-11 followed by 5-FU treatment could be explained by a disruption in mitochondria membrane potential that induced caspases activation. Fluorouracil 153-157 caspase 8 Homo sapiens 251-259 15585621-9 2004 Treatment of effector cells by IFNalpha and target HCC cells by 5-FU enhanced the cytotoxicity of CD14(+) monocytes and CD56(+) NK cells against HCC cells via a TRAIL-mediated pathway. Fluorouracil 64-68 CD14 molecule Homo sapiens 98-102 14614573-1 2004 PURPOSE: The aim of this study was to investigate the changes in two of the enzymes involved in fluorouracil metabolism, thymidine phosphorylase (TP) and dihydropyrimidine dehydrogenase (DPD), in uterine cervical squamous cell cancer tissue after radiotherapy. Fluorouracil 96-108 thymidine phosphorylase Homo sapiens 146-148 14654475-6 2003 As for IFN-alpha, synergistic effects were observed when combined with 5-FU and DOX on PLC/PRF/5 cells only, whereas IFN-beta showed synergistic effects with 5-FU and CDDP on HuH7 and PLC/PRF/5 cell lines. Fluorouracil 158-162 interferon beta 1 Homo sapiens 117-125 15547753-9 2004 Responses were observed as follows: first-line treatment 16.37%, after FAM 25%, following 5-FU-CDDP 26.83% and after 5-FU-LV-CPT-II, 30.61%. Fluorouracil 117-121 carnitine palmitoyltransferase 2 Homo sapiens 125-131 15364927-8 2004 Similarly, in HCT116 cells, Daxx conferred striking resistance to 5-fluorouracil-induced apoptosis. Fluorouracil 66-80 death domain associated protein Homo sapiens 28-32 15364927-9 2004 As p53 is required for 5-fluorouracil-induced cell death, our data show that Daxx can suppress cell death induced by p53 overexpression and p53-dependent stress response. Fluorouracil 23-37 death domain associated protein Homo sapiens 77-81 15585135-7 2004 Our experiments showed that 5-FU engaged the mitochondrial apoptotic pathway involving cytosolic cytochrome c release and subsequent activation of caspase-9 and caspase-3 as well as the membrane death receptor (DR)-mediated apoptotic pathway involving activation of caspase-8 with an Apo-1/CD95 (Fas)-dependent fashion. Fluorouracil 28-32 caspase 8 Homo sapiens 266-275 15585135-8 2004 In addition, we could observe reduction of HPV-18 E6/E7 gene expression and activation of p53, pRb, and p21waf1 proteins by 5-FU treatment in HeLa cervical carcinoma cells. Fluorouracil 124-128 RB transcriptional corepressor 1 Homo sapiens 95-98 15720808-3 2004 METHODS: The gene copy status of STRAP was determined using quantitative real-time polymerase chain reaction in 166 colorectal tumor biopsies, which had been collected from a randomized multicenter trial of 5-fluorouracil (5-FU)/mitomycin C (MMC) adjuvant chemotherapy of the Swiss Group for Clinical Cancer Research (SAKK). Fluorouracil 207-221 serine/threonine kinase receptor associated protein Homo sapiens 33-38 15720808-3 2004 METHODS: The gene copy status of STRAP was determined using quantitative real-time polymerase chain reaction in 166 colorectal tumor biopsies, which had been collected from a randomized multicenter trial of 5-fluorouracil (5-FU)/mitomycin C (MMC) adjuvant chemotherapy of the Swiss Group for Clinical Cancer Research (SAKK). Fluorouracil 223-227 serine/threonine kinase receptor associated protein Homo sapiens 33-38 15720808-7 2004 This suggests the amplification of STRAP as a strong predictor of an unfavorable effect of 5-FU-based adjuvant chemotherapy. Fluorouracil 91-95 serine/threonine kinase receptor associated protein Homo sapiens 35-40 15720808-8 2004 CONCLUSION: If confirmed, the STRAP gene copy status might provide a parameter to decide about the use of 5-FU-based adjuvant chemotherapy. Fluorouracil 106-110 serine/threonine kinase receptor associated protein Homo sapiens 30-35 15308648-9 2004 Arabidopsis ups2 insertion mutants and ups1 lines, in which transcript levels were reduced by post-transcriptional gene silencing, are more tolerant to 5-fluorouracil as compared with wild type plants. Fluorouracil 152-166 ureide permease 1 Arabidopsis thaliana 39-43 15374982-5 2004 Inducible silencing of KILLER/DR5 in vivo by exposure of mice to doxycycline led to accelerated growth of bioluminescent tumor xenografts and conferred resistance to the chemotherapeutic agent 5-fluorouracil. Fluorouracil 193-207 tumor necrosis factor receptor superfamily, member 10b Mus musculus 23-33 15342418-7 2004 P21Cip1, cdk1, cdk2, and cyclin E mRNA expression increased coincident with S-phase accumulation in HT29 cells treated with ZD9331 or 5fluorouracil/leucovorin, as demonstrated by cDNA microarray analyses. Fluorouracil 134-147 cyclin dependent kinase 2 Homo sapiens 15-19 15097041-8 2004 When growth hormone was also given with the dietary supplementation, the hypoproliferative effect of 5-FU was also prevented. Fluorouracil 101-105 gonadotropin releasing hormone receptor Rattus norvegicus 5-19 15097041-9 2004 CONCLUSION: Enriching the diet with DHA protects against intestinal lesions produced by the anti-tumoural drug 5-FU but requires the joint administration of supplementary protein and growth hormone to reduce the noxious effects of 5-FU. Fluorouracil 231-235 gonadotropin releasing hormone receptor Rattus norvegicus 183-197 14723346-1 2003 To enhance the liver targeting and reduce the side effects of 5-fluorouracil (5-Fu), it was acylated by stearyl chloride to obtain N1-stearyl-5-Fu (5-FuS). Fluorouracil 62-76 fused in sarcoma Mus musculus 150-153 15016739-12 2004 The 5-FU treatment revealed impaired intestinal barrier function of Id2-/- mice. Fluorouracil 4-8 inhibitor of DNA binding 2 Mus musculus 68-71 14961038-6 2004 When mouse bone marrow enriched for stem cells (5-fluorouracil-resistant, lineage negative) was transduced and cultured for two weeks, the Int-3-transduced population displayed a lower expression of differentiation markers and a three- to five-fold higher frequency of colony-forming cells (CFU-GM/BFU-E) than control cultures. Fluorouracil 48-62 notch 4 Mus musculus 139-144 14647415-4 2004 Furthermore, Ras suppresses basal as well as 5-fluorouracil (5-FU)-induced RhoB promoter activity and RhoB protein levels. Fluorouracil 45-59 ras homolog family member B Mus musculus 75-79 14647415-4 2004 Furthermore, Ras suppresses basal as well as 5-fluorouracil (5-FU)-induced RhoB promoter activity and RhoB protein levels. Fluorouracil 45-59 ras homolog family member B Mus musculus 102-106 14647415-4 2004 Furthermore, Ras suppresses basal as well as 5-fluorouracil (5-FU)-induced RhoB promoter activity and RhoB protein levels. Fluorouracil 61-65 ras homolog family member B Mus musculus 75-79 14647415-4 2004 Furthermore, Ras suppresses basal as well as 5-fluorouracil (5-FU)-induced RhoB promoter activity and RhoB protein levels. Fluorouracil 61-65 ras homolog family member B Mus musculus 102-106 14647415-7 2004 Finally, Ras-mediated resistance to 5-FU-induced apoptosis is reversed by RhoB. Fluorouracil 36-40 ras homolog family member B Mus musculus 74-78 14742277-7 2004 RG1503 blunted or abolished the following 5-FU-induced effects: increases in matrix metalloproteinase (MMP)-2, MMP-9, and plasmin, and decreases in tissue inhibitor of metalloproteinase (TIMP)-1 and TIMP-2. Fluorouracil 42-46 matrix metallopeptidase 2 Homo sapiens 77-109 14742277-7 2004 RG1503 blunted or abolished the following 5-FU-induced effects: increases in matrix metalloproteinase (MMP)-2, MMP-9, and plasmin, and decreases in tissue inhibitor of metalloproteinase (TIMP)-1 and TIMP-2. Fluorouracil 42-46 plasminogen Homo sapiens 122-129 14663369-2 2003 Encouraging results using the combination of cisplatin, cytarabine, caffeine, and continuous infusion (CI) 5-fluorouracil (5-FU) (PACE) for the treatment of advanced pancreatic carcinoma prompted a phase II study using PACE followed by external beam radiotherapy with CI of 5-FU (PACE-RT) for localized disease. Fluorouracil 107-121 furin, paired basic amino acid cleaving enzyme Homo sapiens 130-134 14663369-2 2003 Encouraging results using the combination of cisplatin, cytarabine, caffeine, and continuous infusion (CI) 5-fluorouracil (5-FU) (PACE) for the treatment of advanced pancreatic carcinoma prompted a phase II study using PACE followed by external beam radiotherapy with CI of 5-FU (PACE-RT) for localized disease. Fluorouracil 107-121 furin, paired basic amino acid cleaving enzyme Homo sapiens 219-223 14663369-2 2003 Encouraging results using the combination of cisplatin, cytarabine, caffeine, and continuous infusion (CI) 5-fluorouracil (5-FU) (PACE) for the treatment of advanced pancreatic carcinoma prompted a phase II study using PACE followed by external beam radiotherapy with CI of 5-FU (PACE-RT) for localized disease. Fluorouracil 107-121 furin, paired basic amino acid cleaving enzyme Homo sapiens 219-223 14663369-2 2003 Encouraging results using the combination of cisplatin, cytarabine, caffeine, and continuous infusion (CI) 5-fluorouracil (5-FU) (PACE) for the treatment of advanced pancreatic carcinoma prompted a phase II study using PACE followed by external beam radiotherapy with CI of 5-FU (PACE-RT) for localized disease. Fluorouracil 123-127 furin, paired basic amino acid cleaving enzyme Homo sapiens 130-134 14663369-2 2003 Encouraging results using the combination of cisplatin, cytarabine, caffeine, and continuous infusion (CI) 5-fluorouracil (5-FU) (PACE) for the treatment of advanced pancreatic carcinoma prompted a phase II study using PACE followed by external beam radiotherapy with CI of 5-FU (PACE-RT) for localized disease. Fluorouracil 123-127 furin, paired basic amino acid cleaving enzyme Homo sapiens 219-223 14663369-2 2003 Encouraging results using the combination of cisplatin, cytarabine, caffeine, and continuous infusion (CI) 5-fluorouracil (5-FU) (PACE) for the treatment of advanced pancreatic carcinoma prompted a phase II study using PACE followed by external beam radiotherapy with CI of 5-FU (PACE-RT) for localized disease. Fluorouracil 123-127 furin, paired basic amino acid cleaving enzyme Homo sapiens 219-223 14663369-2 2003 Encouraging results using the combination of cisplatin, cytarabine, caffeine, and continuous infusion (CI) 5-fluorouracil (5-FU) (PACE) for the treatment of advanced pancreatic carcinoma prompted a phase II study using PACE followed by external beam radiotherapy with CI of 5-FU (PACE-RT) for localized disease. Fluorouracil 274-278 furin, paired basic amino acid cleaving enzyme Homo sapiens 130-134 14559799-1 2003 Ferredoxin reductase (FDXR) is a putative contributor to TP53-mediated apoptosis from 5-fluorouracil chemotherapy through the generation of oxidative stress. Fluorouracil 86-100 ferredoxin reductase Homo sapiens 0-20 14559799-1 2003 Ferredoxin reductase (FDXR) is a putative contributor to TP53-mediated apoptosis from 5-fluorouracil chemotherapy through the generation of oxidative stress. Fluorouracil 86-100 ferredoxin reductase Homo sapiens 22-26 12904931-4 2003 METHODS: The inhibitory effect of 5-FU on CYP1A2, CYP2C9, CYP2C19, CYP2C8, CYP2E1, CYP2D6, and CYP3A4 activities was examined with specific probe drugs in human liver microsomes. Fluorouracil 34-38 cytochrome P450 family 2 subfamily C member 8 Homo sapiens 67-73 12915131-5 2003 These results indicate that Ras, Bcl-2, as well as Raf-1 and PI3K pathways play pivotal roles in 5-FU-induced apoptosis under Ha-ras-overexpressed condition. Fluorouracil 97-101 Raf-1 proto-oncogene, serine/threonine kinase Homo sapiens 51-56 12829029-8 2003 In contrast to in vivo homing, both in vitro migration toward stromal-derived factor (SDF)-1 and the average CXC chemokine receptor-4 (CXCR4) expression were lower in 5-FU-treated cells. Fluorouracil 167-171 chemokine (C-X-C motif) ligand 12 Mus musculus 62-92 12700011-5 2003 RESULTS: 5-FU cream induced significant micronuclei at doses of 37.5 mg (total weight of cream)/2 cm(2) and 75.0 mg/2 cm(2), as well as cytotoxic effects at doses of 150.0 and 300.0 mg/2 cm(2). Fluorouracil 9-13 cream Mus musculus 89-97 12637246-2 2003 The metabolic pathway(s) of OGT 719, a novel nucleoside analogue in which galactose is covalently attached to the N1 of 5-fluorouracil (FU), have been investigated with (19)F-NMR spectroscopy in (1) the isolated perfused rat liver (IPRL) model, (2) normal rats, (3) rats bearing the HSN LV10 sarcoma, (4) nude mice xenografted with the human hepatoma HepG2 and (5) urine from patients. Fluorouracil 120-134 O-linked N-acetylglucosamine (GlcNAc) transferase Rattus norvegicus 28-31 14723346-1 2003 To enhance the liver targeting and reduce the side effects of 5-fluorouracil (5-Fu), it was acylated by stearyl chloride to obtain N1-stearyl-5-Fu (5-FuS). Fluorouracil 78-82 fused in sarcoma Mus musculus 150-153 14723346-6 2003 Compared with 5-Fu injection, a study on the distribution of 5-FuS-SLN in mice showed that 5-FuS-SLN could double 5-Fu concentration in mice livers. Fluorouracil 14-18 fused in sarcoma Mus musculus 93-96 12879463-10 2003 Stratifying patients on the basis of the type of adjuvant therapy given, high syndecan-1 expression was associated with a higher risk of death only in patients treated with the cyclophosphamide-methotrexate-fluorouracil regimen (HR, 1.9; P = 0.09); at multivariate analysis for OS, this association proved to be of independent statistical significance (P = 0.03; HR, 2.15). Fluorouracil 207-219 syndecan 1 Homo sapiens 78-88 14607657-0 2003 Caspase-8 in apoptosis of hepatoma cell induced by 5-fluorouracil. Fluorouracil 51-65 caspase 8 Homo sapiens 0-9 14607657-1 2003 OBJECTIVE: To explore the relationship between the changes in the activity of caspase-8 and apoptosis of HepG2 cells induced by 5-fluorouracil (5-Fu). Fluorouracil 128-142 caspase 8 Homo sapiens 78-87 14607657-1 2003 OBJECTIVE: To explore the relationship between the changes in the activity of caspase-8 and apoptosis of HepG2 cells induced by 5-fluorouracil (5-Fu). Fluorouracil 144-148 caspase 8 Homo sapiens 78-87 14607657-5 2003 RESULTS: After the HepG2 cells were treated with 10(-2) mol/L 5-Fu, the caspase-8 activity increased gradually and reached the peak level (313.9+/-6.9) at 16 hours, then fell down. Fluorouracil 62-66 caspase 8 Homo sapiens 72-81 14607657-7 2003 With the increasing concentration of 5-Fu, the caspase-8 activity was also increased; the activity in high concentration 5-Fu was significantly higher than that in low concentration 5-Fu (370.5+/-4.7 vs 313.7+/-6.9; 225.7+/-5.4 vs 183.3+/-4.8; 183.3+/-4.8 vs 124.0+/-6.2, P<0.01). Fluorouracil 37-41 caspase 8 Homo sapiens 47-56 14607657-7 2003 With the increasing concentration of 5-Fu, the caspase-8 activity was also increased; the activity in high concentration 5-Fu was significantly higher than that in low concentration 5-Fu (370.5+/-4.7 vs 313.7+/-6.9; 225.7+/-5.4 vs 183.3+/-4.8; 183.3+/-4.8 vs 124.0+/-6.2, P<0.01). Fluorouracil 121-125 caspase 8 Homo sapiens 47-56 14607657-7 2003 With the increasing concentration of 5-Fu, the caspase-8 activity was also increased; the activity in high concentration 5-Fu was significantly higher than that in low concentration 5-Fu (370.5+/-4.7 vs 313.7+/-6.9; 225.7+/-5.4 vs 183.3+/-4.8; 183.3+/-4.8 vs 124.0+/-6.2, P<0.01). Fluorouracil 121-125 caspase 8 Homo sapiens 47-56 14607657-8 2003 The caspase-8 activity was the highest at 1X10(-1) mol/L 5-Fu (370.5+/-4.7). Fluorouracil 57-61 caspase 8 Homo sapiens 4-13 14607657-9 2003 The caspase-8 activity in low concentration 5-Fu was higher than in the blank control group and inhibitor group (124.0+/-6.2 vs 68.5+/-3.4; 124.0+/-6.2 vs 41.0+/-2.1, P<0.01). Fluorouracil 44-48 caspase 8 Homo sapiens 4-13 14607657-12 2003 CONCLUSIONS: 5-Fu can induce apoptosis of HepG2 cells via caspase-8 signal transduction pathway, which can be blocked by IETD-FMK. Fluorouracil 13-17 caspase 8 Homo sapiens 58-67 14607657-13 2003 5-Fu promotes the increase of caspase-8 activity in a time- or concentration-dependent manner. Fluorouracil 0-4 caspase 8 Homo sapiens 30-39 12507543-1 2003 OBJECTIVES: Thymidine phosphorylase (TdR-Pase) and dihydropyrimidine dehydrogenase (DPD) are thought to be key enzymes in the metabolic pathway of 5-fluorouracil (5-FU). Fluorouracil 147-161 thymidine phosphorylase Homo sapiens 37-45 12507543-1 2003 OBJECTIVES: Thymidine phosphorylase (TdR-Pase) and dihydropyrimidine dehydrogenase (DPD) are thought to be key enzymes in the metabolic pathway of 5-fluorouracil (5-FU). Fluorouracil 163-167 thymidine phosphorylase Homo sapiens 37-45 12507543-2 2003 Theoretically, cancer cells which have high TdR-Pase activity and/or low DPD activity should be sensitive to 5-FU. Fluorouracil 109-113 thymidine phosphorylase Homo sapiens 44-52 12507543-11 2003 There was a significant positive correlation between the TdR-Pase activity and 5-FU sensitivity. Fluorouracil 79-83 thymidine phosphorylase Homo sapiens 57-65 12507543-12 2003 In addition, a stronger positive correlation was found between TdR-Pase / DPD ratio and 5-FU sensitivity. Fluorouracil 88-92 thymidine phosphorylase Homo sapiens 63-71 12507543-15 2003 TdR-Pase appeared to be the enzyme regulating activation of 5-FU in RCC. Fluorouracil 60-64 thymidine phosphorylase Homo sapiens 0-8 12743424-2 2003 This report addressed the time-dependent dynamic alterations in the expression of three tumor-associated antigens: carcinoembryonic antigen (CEA), colon-specific antigen (CSAp) and mucin-1 (MUC-1) following chemotherapy with 5-fluorouracil (5-FU) or radioimmunotherapy (RAIT; (131)I-labeled anti-CEA IgG) in human colonic tumor xenografts. Fluorouracil 241-245 mucin 1, cell surface associated Homo sapiens 190-195 12743424-3 2003 Immunoassay results show that CEA and MUC-1 expression all increase rapidly after either 5-FU or RAIT. Fluorouracil 89-93 mucin 1, cell surface associated Homo sapiens 38-43 12773255-0 2003 [Role of caspase-8 and caspase-3 in hepatoma cells apoptosis induced by 5-fluorouracil]. Fluorouracil 72-86 caspase 8 Homo sapiens 9-18 12598341-1 2003 BACKGROUND: The aim of this study was to determine whether the efficacy of the combination of 5-fluorouracil (5-FU), leucovorin (LV) and radiation therapy (RT) could be improved by the addition of interferon-alpha2b (IFN-alpha) in patients who have had a "curative" resection, for rectal adenocarcinoma (Dukes" B2/C; T3 N0, T4 N0, N1-3). Fluorouracil 94-108 interferon alpha 2 Homo sapiens 197-215 12439919-15 2002 CONCLUSION: The continuous exposure of Bel(7402) cells to 5-FU led to overexpression of TS and MRP, as well as increased intracellular GSH content and total GST activity. Fluorouracil 58-62 ATP binding cassette subfamily C member 3 Homo sapiens 95-98 12414633-5 2002 We constructed replication-activated Ad vectors to express a secreted form of beta-glucuronidase and a cytosine deaminase/uracil phosphoribosyltransferase, which activate the prodrugs 9-aminocamptothecin glucuronide to 9-aminocamptothecin and 5-fluorocytosine to 5-fluorouracil (5-FU) and further to 5-fluoro-UMP, respectively. Fluorouracil 263-277 glucuronidase beta Homo sapiens 78-96 12414633-5 2002 We constructed replication-activated Ad vectors to express a secreted form of beta-glucuronidase and a cytosine deaminase/uracil phosphoribosyltransferase, which activate the prodrugs 9-aminocamptothecin glucuronide to 9-aminocamptothecin and 5-fluorocytosine to 5-fluorouracil (5-FU) and further to 5-fluoro-UMP, respectively. Fluorouracil 279-283 glucuronidase beta Homo sapiens 78-96 12465396-3 2002 The metastases partially responded to 10 cycles of CAF (cyclophosphamide, adriamycin, 5-fluorouracil). Fluorouracil 86-100 lysine acetyltransferase 2B Homo sapiens 51-54 12237773-0 2002 SMAD4 is a predictive marker for 5-fluorouracil-based chemotherapy in patients with colorectal cancer. Fluorouracil 33-47 SMAD family member 4 Homo sapiens 0-5 12237773-3 2002 Patients with normal SMAD4 diploidy turned out to have a three-fold higher benefit of 5-fluorouracil-based adjuvant chemotherapy with a border line significance (overall survival: 3.23, P=0.056; disease-free survival: 2.89, P=0.045). Fluorouracil 86-100 SMAD family member 4 Homo sapiens 21-26 12598341-1 2003 BACKGROUND: The aim of this study was to determine whether the efficacy of the combination of 5-fluorouracil (5-FU), leucovorin (LV) and radiation therapy (RT) could be improved by the addition of interferon-alpha2b (IFN-alpha) in patients who have had a "curative" resection, for rectal adenocarcinoma (Dukes" B2/C; T3 N0, T4 N0, N1-3). Fluorouracil 94-108 interferon alpha 2 Homo sapiens 217-226 12598341-1 2003 BACKGROUND: The aim of this study was to determine whether the efficacy of the combination of 5-fluorouracil (5-FU), leucovorin (LV) and radiation therapy (RT) could be improved by the addition of interferon-alpha2b (IFN-alpha) in patients who have had a "curative" resection, for rectal adenocarcinoma (Dukes" B2/C; T3 N0, T4 N0, N1-3). Fluorouracil 110-114 interferon alpha 2 Homo sapiens 197-215 12598341-1 2003 BACKGROUND: The aim of this study was to determine whether the efficacy of the combination of 5-fluorouracil (5-FU), leucovorin (LV) and radiation therapy (RT) could be improved by the addition of interferon-alpha2b (IFN-alpha) in patients who have had a "curative" resection, for rectal adenocarcinoma (Dukes" B2/C; T3 N0, T4 N0, N1-3). Fluorouracil 110-114 interferon alpha 2 Homo sapiens 217-226 12576456-10 2003 For lung resistance-related protein, this association was limited to 5-fluorouracil, Adriamycin/epirubicin, and cyclophosphamide. Fluorouracil 69-83 major vault protein Homo sapiens 4-35 12506476-0 2002 [Modified pharmacokinetic modulation chemotherapy (PMC) with medication of UFT and intraarterial infusion of 5-FU for advanced unresectable HCC]. Fluorouracil 109-113 HCC Homo sapiens 140-143 12552961-3 2002 Preclinical studies provided evidence of preferential conversion of inactive 5"-DFUR to active 5-FU in solid tumours due to the relative overexpression of the final anabolising enzyme, thymidine phosphorylase (TP), in neoplastic tissues more than in normal counterparts. Fluorouracil 95-99 thymidine phosphorylase Homo sapiens 185-208 12553027-5 2002 Thymidine phosphorylase (TP), the enzyme that converts 5"-DFUR into 5-FU and 5-FU into 5-fluoro-2"-deoxyuridine-5"-monophosphate (FdUMP), was estimated by ELISA. Fluorouracil 68-72 thymidine phosphorylase Homo sapiens 0-23 12553027-5 2002 Thymidine phosphorylase (TP), the enzyme that converts 5"-DFUR into 5-FU and 5-FU into 5-fluoro-2"-deoxyuridine-5"-monophosphate (FdUMP), was estimated by ELISA. Fluorouracil 68-72 thymidine phosphorylase Homo sapiens 25-27 12553027-5 2002 Thymidine phosphorylase (TP), the enzyme that converts 5"-DFUR into 5-FU and 5-FU into 5-fluoro-2"-deoxyuridine-5"-monophosphate (FdUMP), was estimated by ELISA. Fluorouracil 77-81 thymidine phosphorylase Homo sapiens 0-23 12553027-5 2002 Thymidine phosphorylase (TP), the enzyme that converts 5"-DFUR into 5-FU and 5-FU into 5-fluoro-2"-deoxyuridine-5"-monophosphate (FdUMP), was estimated by ELISA. Fluorouracil 77-81 thymidine phosphorylase Homo sapiens 25-27 12553027-6 2002 As a result, a significant correlation between TP expression and sensitivity to 5-FU and 5"-DFUR was found in all 4 RCC cell lines. Fluorouracil 80-84 thymidine phosphorylase Homo sapiens 47-49 12553027-9 2002 These results suggested that TP may be useful as a predictive factor in combination therapy with IFN gamma and 5-FU or 5"-DFUF, which may be a promising treatment for advanced RCC. Fluorouracil 111-115 thymidine phosphorylase Homo sapiens 29-31 12402042-6 2002 In addition, BID-null mouse embryonic fibroblasts are more resistant than are wild-type fibroblasts to the DNA damaging agent adriamycin and the nucleotide analogue 5-fluorouracil, both of which stabilize endogenous p53. Fluorouracil 165-179 BH3 interacting domain death agonist Mus musculus 13-16 12378627-1 2002 AIM: Our previous studies showed increased sensitivity to 5-FU in colon cancer cell lines with microsatellite instability, and considered that mutations of TGFbeta-R II, IGF IIR, RIZ gene might enhance the potentials of cell growth and proliferation, which increased the sensitivity to 5-FU. Fluorouracil 58-62 transforming growth factor beta receptor 2 Homo sapiens 156-168 12378627-1 2002 AIM: Our previous studies showed increased sensitivity to 5-FU in colon cancer cell lines with microsatellite instability, and considered that mutations of TGFbeta-R II, IGF IIR, RIZ gene might enhance the potentials of cell growth and proliferation, which increased the sensitivity to 5-FU. Fluorouracil 286-290 transforming growth factor beta receptor 2 Homo sapiens 156-168 12529971-0 2002 IFN gamma-induced up-regulation of PD-ECGF/TP enhances the cytotoxicity of 5-fluorouracil and 5"-deoxy-5-fluorouridine in bladder cancer cells. Fluorouracil 75-89 thymidine phosphorylase Homo sapiens 35-42 12118326-8 2002 These results suggested that pRb and E2F-1 play important roles in the acquisition of 5-FU resistance by cancer cells and that cancer therapy targeting transcription factor E2F might be effective. Fluorouracil 86-90 RB transcriptional corepressor 1 Homo sapiens 29-32 11934891-2 2002 We found that overproduction of SDT1 caused hyposensitivity to not only 6-azauracil but also 5-fluorouracil and 5-fluorocytosine. Fluorouracil 93-107 nucleotidase Saccharomyces cerevisiae S288C 32-36 11881914-10 2002 Extreme drug resistance to 5-FU was associated with negative ER and PR status. Fluorouracil 27-31 progesterone receptor Homo sapiens 68-70 12016389-1 2002 BACKGROUND: Thymidine phosphorylase (TP) has diverse functions within cells, including increasing the sensitivity of cancer cells to cytotoxic drugs including 5-fluorouracil (5-FU) and methotrexate. Fluorouracil 159-173 thymidine phosphorylase Homo sapiens 12-35 12016389-1 2002 BACKGROUND: Thymidine phosphorylase (TP) has diverse functions within cells, including increasing the sensitivity of cancer cells to cytotoxic drugs including 5-fluorouracil (5-FU) and methotrexate. Fluorouracil 159-173 thymidine phosphorylase Homo sapiens 37-39 12016389-1 2002 BACKGROUND: Thymidine phosphorylase (TP) has diverse functions within cells, including increasing the sensitivity of cancer cells to cytotoxic drugs including 5-fluorouracil (5-FU) and methotrexate. Fluorouracil 175-179 thymidine phosphorylase Homo sapiens 12-35 12016389-1 2002 BACKGROUND: Thymidine phosphorylase (TP) has diverse functions within cells, including increasing the sensitivity of cancer cells to cytotoxic drugs including 5-fluorouracil (5-FU) and methotrexate. Fluorouracil 175-179 thymidine phosphorylase Homo sapiens 37-39 12467230-0 2001 Combination of thymidine phosphorylase gene transfer and deoxyinosine treatment greatly enhances 5-fluorouracil antitumor activity in vitro and in vivo. Fluorouracil 97-111 thymidine phosphorylase Homo sapiens 15-38 12467230-1 2001 We reported previously that 5-fluorouracil (FUra) efficacy could be enhanced by increasing tumoral thymidine phosphorylase (TP) activity. Fluorouracil 28-42 thymidine phosphorylase Homo sapiens 99-122 12467230-1 2001 We reported previously that 5-fluorouracil (FUra) efficacy could be enhanced by increasing tumoral thymidine phosphorylase (TP) activity. Fluorouracil 28-42 thymidine phosphorylase Homo sapiens 124-126 12467230-1 2001 We reported previously that 5-fluorouracil (FUra) efficacy could be enhanced by increasing tumoral thymidine phosphorylase (TP) activity. Fluorouracil 44-48 thymidine phosphorylase Homo sapiens 99-122 12467230-1 2001 We reported previously that 5-fluorouracil (FUra) efficacy could be enhanced by increasing tumoral thymidine phosphorylase (TP) activity. Fluorouracil 44-48 thymidine phosphorylase Homo sapiens 124-126 12467230-6 2001 The purpose of the present work was to study the effects of a combined modulation (TP gene transfer + use of d-Ino) on the sensitivity to FUra of the LS174T human colorectal cell line. Fluorouracil 138-142 thymidine phosphorylase Homo sapiens 83-85 12467230-11 2001 Results showed that whereas FUra alone was completely ineffective on wild-type tumor growth, the size of TP-transfected tumors in animals treated with the FUra/d-Ino combination was reduced by 80% (P < 0.05). Fluorouracil 155-160 thymidine phosphorylase Homo sapiens 105-107 12467230-12 2001 Our results suggest that FUra exhibits stronger antiproliferative activity when activated via TP through the DNA pathway and that high tumoral TP activity therefore leads to enhanced sensitivity to fluoropyrimidines. Fluorouracil 25-29 thymidine phosphorylase Homo sapiens 94-96 12467230-12 2001 Our results suggest that FUra exhibits stronger antiproliferative activity when activated via TP through the DNA pathway and that high tumoral TP activity therefore leads to enhanced sensitivity to fluoropyrimidines. Fluorouracil 25-29 thymidine phosphorylase Homo sapiens 143-145 11590433-0 2001 Ferredoxin reductase affects p53-dependent, 5-fluorouracil-induced apoptosis in colorectal cancer cells. Fluorouracil 44-58 ferredoxin reductase Homo sapiens 0-20 11590433-3 2001 The gene encoding mitochondrial ferredoxin reductase (protein, FR; gene, FDXR) was one of the few genes significantly induced by p53 after 5-FU treatment. Fluorouracil 139-143 ferredoxin reductase Homo sapiens 32-52 11590433-3 2001 The gene encoding mitochondrial ferredoxin reductase (protein, FR; gene, FDXR) was one of the few genes significantly induced by p53 after 5-FU treatment. Fluorouracil 139-143 ferredoxin reductase Homo sapiens 73-77 11590433-5 2001 Targeted disruption of the FDXR gene in human colon cancer cells showed that it was essential for viability, and partial disruption of the gene resulted in decreased sensitivity to 5-FU-induced apoptosis. Fluorouracil 181-185 ferredoxin reductase Homo sapiens 27-31 11848487-6 2001 When the esophageal cancer cells were treated with 5-fluorouracil (5-FU) in the presence of a low concentration of hIFN-beta, the effectiveness of 5-FU was markedly enhanced. Fluorouracil 51-65 interferon beta 1 Homo sapiens 115-124 11848487-6 2001 When the esophageal cancer cells were treated with 5-fluorouracil (5-FU) in the presence of a low concentration of hIFN-beta, the effectiveness of 5-FU was markedly enhanced. Fluorouracil 67-71 interferon beta 1 Homo sapiens 115-124 11848487-6 2001 When the esophageal cancer cells were treated with 5-fluorouracil (5-FU) in the presence of a low concentration of hIFN-beta, the effectiveness of 5-FU was markedly enhanced. Fluorouracil 147-151 interferon beta 1 Homo sapiens 115-124 11491013-3 2001 The PKC beta inhibitor 317615.2HCl was not very cytotoxic toward HS746T or Hep3B cells in culture and was, in the main, additive in cytotoxicity with cisplatin, 5-fluorouracil and gemcitabine when cell in monolayer were exposed to these agents in combination with 317615.2HCl. Fluorouracil 161-175 protein kinase C beta Homo sapiens 4-12 12173327-10 2002 CONCLUSIONS: The addition of gemcitabine and 5-FU to subcutaneous IL2 and IFNA results in a similar response rate to what was observed in previous studies of IL2-based therapy. Fluorouracil 45-49 interferon alpha 2 Homo sapiens 74-78 11986258-2 2002 We found that mice rendered deficient in CD8 alpha molecules by homologous recombination were susceptible to 5-fluorouracil (5-FU)-induced lethality accompanied by translocation of members of the enterobacteria. Fluorouracil 125-129 CD8 antigen, alpha chain Mus musculus 41-50 11564055-8 2001 The cytotoxic activities of mercaptopurine and fluorouracil are regulated by thiopurine methyltransferase (TPMT) and dihydropyrimidine dehydrogenase (DPD), respectively. Fluorouracil 47-59 thiopurine S-methyltransferase Homo sapiens 77-105 11564055-8 2001 The cytotoxic activities of mercaptopurine and fluorouracil are regulated by thiopurine methyltransferase (TPMT) and dihydropyrimidine dehydrogenase (DPD), respectively. Fluorouracil 47-59 thiopurine S-methyltransferase Homo sapiens 107-111 11196169-3 2001 We have shown previously that 5-fluorouracil (5-FU) induces apoptosis in vitro via the activation of the CD95/CD95L system. Fluorouracil 30-44 Fas ligand (TNF superfamily, member 6) Mus musculus 110-115 11196169-3 2001 We have shown previously that 5-fluorouracil (5-FU) induces apoptosis in vitro via the activation of the CD95/CD95L system. Fluorouracil 46-50 Fas ligand (TNF superfamily, member 6) Mus musculus 110-115 11196169-10 2001 Furthermore, in the thymi of 5-FU-treated animals, CD95L was strongly up-regulated. Fluorouracil 29-33 Fas ligand (TNF superfamily, member 6) Mus musculus 51-56 11196169-13 2001 Thus, a significant portion of apoptosis of thymocytes in vivo on treatment with 5-FU is mediated via the CD95/CD95L pathway. Fluorouracil 81-85 Fas ligand (TNF superfamily, member 6) Mus musculus 111-116 11104786-4 2000 Conditioning with DNA-damaging agents (ionizing irradiation, cyclophosphamide, and 5-fluorouracil) caused an increase in SDF-1 expression and in CXCR4-dependent homing and repopulation by human stem cells transplanted into NOD/SCID mice. Fluorouracil 83-97 C-X-C motif chemokine ligand 12 Homo sapiens 121-126 11104786-4 2000 Conditioning with DNA-damaging agents (ionizing irradiation, cyclophosphamide, and 5-fluorouracil) caused an increase in SDF-1 expression and in CXCR4-dependent homing and repopulation by human stem cells transplanted into NOD/SCID mice. Fluorouracil 83-97 atrophin 1 Homo sapiens 223-226 11071927-4 2000 We show that upon treatment of HepG2 cells with 5-fluorouracil or methotrexate, p53 levels increase while concentrations of cyclin B2 mRNA, measured by RT-PCR with the LightCycler system, are reduced. Fluorouracil 48-62 cyclin B2 Homo sapiens 124-133 10779637-0 2000 Morphological change, loss of deltapsi(m) and activation of caspases upon apoptosis of colorectal adenocarcinoma induced by 5-FU. Fluorouracil 124-128 caspase 8 Homo sapiens 60-68 10722720-1 2000 We found that antitumor drugs such as cytotrienin A, camptothecin, taxol, and 5-fluorouracil induced the activation of a 36-kDa protein kinase (p36 myelin basic protein (MBP) kinase) during apoptosis in human promyelocytic leukemia HL-60 cells. Fluorouracil 78-92 myelin basic protein Homo sapiens 170-173 10648600-8 2000 Forced coexpression of ICSBP inhibited the Bcr-Abl-induced colony formation of BM cells from 5-FU-treated mice in vitro and Bcr-Abl-induced CML-like disease in vivo. Fluorouracil 93-97 interferon regulatory factor 8 Mus musculus 23-28 10648600-10 2000 Overexpression of ICSBP consistently promotes rather than inhibits Bcr-Abl-induced B lymphoproliferation in a murine model where BM cells from non-5-FU-treated donors were used, indicating that ICSBP has a specific antitumor activity toward myeloid neoplasms. Fluorouracil 147-151 interferon regulatory factor 8 Mus musculus 18-23 11986258-3 2002 The number of i-IEL was greatly reduced on day 6 after 5-FU administration in both CD8 alpha(+/-) mice and CD8 alpha(-/-) mice, whereas the recovery of the level of i-IEL thereafter was significantly impaired in CD8 alpha(-/-) mice compared with that in CD8 alpha(+/-) mice. Fluorouracil 55-59 CD8 antigen, alpha chain Mus musculus 83-92 11986258-3 2002 The number of i-IEL was greatly reduced on day 6 after 5-FU administration in both CD8 alpha(+/-) mice and CD8 alpha(-/-) mice, whereas the recovery of the level of i-IEL thereafter was significantly impaired in CD8 alpha(-/-) mice compared with that in CD8 alpha(+/-) mice. Fluorouracil 55-59 CD8 antigen, alpha chain Mus musculus 107-116 11986258-3 2002 The number of i-IEL was greatly reduced on day 6 after 5-FU administration in both CD8 alpha(+/-) mice and CD8 alpha(-/-) mice, whereas the recovery of the level of i-IEL thereafter was significantly impaired in CD8 alpha(-/-) mice compared with that in CD8 alpha(+/-) mice. Fluorouracil 55-59 CD8 antigen, alpha chain Mus musculus 107-116 11986258-3 2002 The number of i-IEL was greatly reduced on day 6 after 5-FU administration in both CD8 alpha(+/-) mice and CD8 alpha(-/-) mice, whereas the recovery of the level of i-IEL thereafter was significantly impaired in CD8 alpha(-/-) mice compared with that in CD8 alpha(+/-) mice. Fluorouracil 55-59 CD8 antigen, alpha chain Mus musculus 107-116 11127938-10 2000 The AUC0-6h of 5-FU ranged from 120 to 325 (ng/ml)h. Uracil had a t 1/2alpha of 0.2-0.5 h and the level quickly returned to the endogenous level. Fluorouracil 15-19 interleukin 1 receptor like 1 Homo sapiens 66-69 11986258-5 2002 Transfer of CD8(+) i-IEL conferred significant protection against 5-FU-induced lethality in CD8 alpha(-/-) mice. Fluorouracil 66-70 CD8 antigen, alpha chain Mus musculus 92-101 12019408-1 2002 BACKGROUND: Thymidine phosphorylase (TP) is an essential enzyme for activation of 5-fluorouracil and its derivatives and identical to platelet-derived endothelial cell growth factor. Fluorouracil 82-96 thymidine phosphorylase Homo sapiens 12-35 12019408-1 2002 BACKGROUND: Thymidine phosphorylase (TP) is an essential enzyme for activation of 5-fluorouracil and its derivatives and identical to platelet-derived endothelial cell growth factor. Fluorouracil 82-96 thymidine phosphorylase Homo sapiens 37-39 26680854-12 2002 Furthermore, 5-FU increased the enzymatic activity of caspase-3 protease with PARP digestion in HepG2 cells. Fluorouracil 13-17 collagen type XI alpha 2 chain Homo sapiens 78-82 11862430-9 2002 With regard to biochemical parameters, serum alanine aminotransferase and cholesterol levels were correlated with 5-fluorouracil clearance. Fluorouracil 114-128 glutamic--pyruvic transaminase Homo sapiens 45-69 12704877-26 2002 IFNa-modulation of 5-FU (plus LEV) adds toxicity and high treatment costs without therapeutic benefit. Fluorouracil 19-23 interferon alpha 2 Homo sapiens 0-4 11730652-9 2001 Failure of the initial 5-FU revision correlated significantly with preneedling IOP > 30 mm Hg (P =.0003), lack of MMC use during the previous filtration surgery (P =.013), and IOP >10 mm Hg immediately following needling revision (P =.0012) according to Cox"s proportional hazards regression analysis. Fluorouracil 23-27 cytochrome c oxidase subunit 8A Homo sapiens 260-263 11562746-1 2001 Thymidine phosphorylase (TP) is an enzyme which converts doxifluridine (5"-DFUR) to 5-fluorouracil (5-FU). Fluorouracil 84-98 thymidine phosphorylase Homo sapiens 0-23 10595916-7 1999 In addition, numbers of apoptotic cells were significantly higher in control tumors as compared to Bcl-x(L)-expressing tumors in animals treated with methotrexate or 5-fluorouracil. Fluorouracil 166-180 BCL2-like 1 Mus musculus 99-104 10568827-0 1999 Apoptosis of colorectal adenocarcinoma induced by 5-FU and/or IFN-gamma through caspase 3 and caspase 8. Fluorouracil 50-54 caspase 8 Homo sapiens 94-103 10568827-2 1999 We examined the role of caspases on the apoptosis induction of 5-FU and IFN-gamma using a colorectal adenocarcinoma cell line. Fluorouracil 63-67 caspase 8 Homo sapiens 24-32 10568827-3 1999 The activities of caspase 3 and caspase 8 increased when apoptosis was induced by 5-FU and/or IFN-gamma. Fluorouracil 82-86 caspase 8 Homo sapiens 32-41 10568827-6 1999 Thus, caspase 3 and caspase 8 play crucial roles in apoptosis induced by 5-FU and/or IFN-gamma, regardless of the Fas-Fas ligand system. Fluorouracil 73-77 caspase 8 Homo sapiens 20-29 10697613-0 1999 Thymidine phosphorylase expression in invasive carcinoma: correlations with clinicopathologic variables and in vitro chemosensitivity to 5-fluorouracil. Fluorouracil 137-151 thymidine phosphorylase Homo sapiens 0-23 10697613-6 1999 CONCLUSION: The present results suggest that TP is important for remodeling the existing vasculature early in tumor development and intraductal extension, expressions of TP and Bcl-2 are tightly linked and TP status can not generally predict chemotherapeutic sensitivity for 5-FU as a single molecular marker. Fluorouracil 275-279 thymidine phosphorylase Homo sapiens 45-47 10697613-6 1999 CONCLUSION: The present results suggest that TP is important for remodeling the existing vasculature early in tumor development and intraductal extension, expressions of TP and Bcl-2 are tightly linked and TP status can not generally predict chemotherapeutic sensitivity for 5-FU as a single molecular marker. Fluorouracil 275-279 thymidine phosphorylase Homo sapiens 170-172 10697613-6 1999 CONCLUSION: The present results suggest that TP is important for remodeling the existing vasculature early in tumor development and intraductal extension, expressions of TP and Bcl-2 are tightly linked and TP status can not generally predict chemotherapeutic sensitivity for 5-FU as a single molecular marker. Fluorouracil 275-279 thymidine phosphorylase Homo sapiens 170-172 10517490-10 1999 COX-2 induction is likely a central event in the accelerated hematopoiesis following myelotoxic injury, because recovery from 5-FU-induced myeloablation is markedly impaired in Cox-2-/- mice but is normal after phenylhydrazine induction of anemia. Fluorouracil 126-130 cytochrome c oxidase II, mitochondrial Mus musculus 0-5 10517490-10 1999 COX-2 induction is likely a central event in the accelerated hematopoiesis following myelotoxic injury, because recovery from 5-FU-induced myeloablation is markedly impaired in Cox-2-/- mice but is normal after phenylhydrazine induction of anemia. Fluorouracil 126-130 cytochrome c oxidase II, mitochondrial Mus musculus 177-182 10499641-6 1999 However, the increasing actions of CDDP and 5-FU on GSTpi, DPD, MRP, and TS expression varied according to the exposure time, concentration, and schedule. Fluorouracil 44-48 ATP binding cassette subfamily C member 3 Homo sapiens 64-67 10499641-7 1999 A low concentration of CDDP (1 microg/ml, 30 min) followed by 5-FU (0.5 microg/ml, 72 h) was found to cause a less increased expression of DPD, MRP, GSTpi, and TS than either drug alone, thus resulting in synergistic cytotoxicity in 5-FU-resistant COLO201 and CDDP-resistant HCC-48 cells. Fluorouracil 62-66 ATP binding cassette subfamily C member 3 Homo sapiens 144-147 11562746-1 2001 Thymidine phosphorylase (TP) is an enzyme which converts doxifluridine (5"-DFUR) to 5-fluorouracil (5-FU). Fluorouracil 84-98 thymidine phosphorylase Homo sapiens 25-27 11562746-1 2001 Thymidine phosphorylase (TP) is an enzyme which converts doxifluridine (5"-DFUR) to 5-fluorouracil (5-FU). Fluorouracil 100-104 thymidine phosphorylase Homo sapiens 0-23 10466633-1 1999 The use of cytosine deaminase (CD) in conjunction with 5-fluorocytosine (5-FC) has been studied for cancer gene therapy as a means of achieving tumor-specific generation of the toxic metabolite 5-fluorouracil (5-FU). Fluorouracil 194-208 cytosine deaminase Saccharomyces cerevisiae S288C 11-29 11562746-1 2001 Thymidine phosphorylase (TP) is an enzyme which converts doxifluridine (5"-DFUR) to 5-fluorouracil (5-FU). Fluorouracil 100-104 thymidine phosphorylase Homo sapiens 25-27 10466633-1 1999 The use of cytosine deaminase (CD) in conjunction with 5-fluorocytosine (5-FC) has been studied for cancer gene therapy as a means of achieving tumor-specific generation of the toxic metabolite 5-fluorouracil (5-FU). Fluorouracil 210-214 cytosine deaminase Saccharomyces cerevisiae S288C 11-29 11562746-5 2001 When we compared prognosis in two chemotherapy groups with high TP expression, better survival was observed in 5"-DFUR than in 5-FU group (p=0.0413). Fluorouracil 127-131 thymidine phosphorylase Homo sapiens 64-66 11504493-5 1999 The influence of tumor TP on fluoropyrimidine toxicity is variable, but capecitabine is a prodrug of fluorouracil that requires activation by TP and hence may have a higher therapeutic index than other fluoropyrimidines. Fluorouracil 101-113 thymidine phosphorylase Homo sapiens 142-144 10397721-1 1999 We have recently isolated a cDNA encoding a novel human receptor-type tyrosine phosphatase, termed PTP-RO (for a protein tyrosine phosphatase receptor omicron), from 5-fluorouracil-treated murine bone marrow cells. Fluorouracil 166-180 protein tyrosine phosphatase receptor type U Homo sapiens 99-105 10397721-1 1999 We have recently isolated a cDNA encoding a novel human receptor-type tyrosine phosphatase, termed PTP-RO (for a protein tyrosine phosphatase receptor omicron), from 5-fluorouracil-treated murine bone marrow cells. Fluorouracil 166-180 protein tyrosine phosphatase receptor type U Homo sapiens 113-158 11562746-6 2001 Especially in stage III, patients with high TP had better survival in 5"-DFUR than in 5-FU group. Fluorouracil 86-90 thymidine phosphorylase Homo sapiens 44-46 11389879-3 2001 In this study, a Chinese hamster ovary cell line expressing human cytochrome P450 CYP1B1 was used to evaluate the cytotoxic profile of several anticancer drugs (docetaxel, paclitaxel, cyclophosphamide, doxorubicin, 5-fluorouracil, cisplatin, and carboplatin) commonly used clinically in the treatment of cancer. Fluorouracil 215-229 cytochrome P450 family 1 subfamily B member 1 Homo sapiens 82-88 10391096-3 1999 The Mn-SOD activity was increased by treatments with 5-fluorouracil (5-FU), peplomycin and 137Cs, reaching plateau levels at 12 h after treatment and then decreasing gradually. Fluorouracil 53-67 superoxide dismutase 2 Homo sapiens 4-10 10391096-3 1999 The Mn-SOD activity was increased by treatments with 5-fluorouracil (5-FU), peplomycin and 137Cs, reaching plateau levels at 12 h after treatment and then decreasing gradually. Fluorouracil 69-73 superoxide dismutase 2 Homo sapiens 4-10 11264006-8 2001 The expression of Fas-associated death domain-like interleukin 1-converting enzyme-inhibitory protein (FLIP), which acts as an inhibitor of an initiator caspase (caspase-8), was down-regulated by 5-FU treatment in cl-1 cells. Fluorouracil 196-200 caspase 8 Homo sapiens 162-171 11504311-4 2001 Patients whose tumors were overexpressing cyclin D1 showed complete or partial response to neoadjuvant chemotherapy with cisplatin/5-FU. Fluorouracil 131-135 cyclin D1 Homo sapiens 42-51 10199464-1 1999 The case described here illustrates the antitumor activity of a four-drug systemic combination chemobiotherapy with platinol, recombinant interferon alpha 2b, doxorubicin (Adriamycin), and 5-fluorouracil (5-FU) (PIAF) in a patient with diffuse hepatocellular carcinoma involving the liver and lungs. Fluorouracil 205-209 interferon alpha 2 Homo sapiens 138-157 10089915-2 1999 Studies were performed to determine whether the in vivo administration of Flk-2/Flt-3 ligand (FL) is also capable of sensitizing progenitors to 5-FU. Fluorouracil 144-148 FMS-like tyrosine kinase 3 ligand Mus musculus 80-92 10024690-0 1999 Dihydropyrimidine dehydrogenase, multidrug resistance-associated protein, and thymidylate synthase gene expression levels can predict 5-fluorouracil resistance in human gastrointestinal cancer cells. Fluorouracil 134-148 ATP binding cassette subfamily C member 3 Homo sapiens 33-72 10024690-1 1999 Gene expression of dihydropyrimidine dehydrogenase (DPD) and newly multidrug resistance-associated protein (MRP) was found to correlate well with primary 5-FU resistance in 7 human gastrointestinal cancer cell lines. Fluorouracil 154-158 ATP binding cassette subfamily C member 3 Homo sapiens 67-106 10024690-1 1999 Gene expression of dihydropyrimidine dehydrogenase (DPD) and newly multidrug resistance-associated protein (MRP) was found to correlate well with primary 5-FU resistance in 7 human gastrointestinal cancer cell lines. Fluorouracil 154-158 ATP binding cassette subfamily C member 3 Homo sapiens 108-111 10024690-4 1999 DPD and MRP expression levels can predict primary 5-FU resistance, and TS may be a potent predictor of cellular 5-FU resistance after 5-FU treatment. Fluorouracil 50-54 ATP binding cassette subfamily C member 3 Homo sapiens 8-11 10412941-0 1999 Biomodulation of 5-fluorouracil by interferon-alpha in human renal carcinoma cells: relationship to the expression of thymidine phosphorylase. Fluorouracil 17-31 thymidine phosphorylase Homo sapiens 118-141 10412941-7 1999 The relative IFN-alpha-induced increase in sensitivity to 5-FU correlated with the relative IFN-alpha-induced increase in TP expression (P < 0.05). Fluorouracil 58-62 thymidine phosphorylase Homo sapiens 122-124 10412941-8 1999 In addition, two of three RCC cell lines with more than a twofold increase in sensitivity to 5-FU induced by IFN-alpha showed a higher TP expression without IFN-alpha stimulation. Fluorouracil 93-97 thymidine phosphorylase Homo sapiens 135-137 10412941-9 1999 CONCLUSIONS: These results suggest that IFN-alpha upregulates TP expression and modulates 5-FU anabolism thus enhancing 5-FU cytotoxicity in a dose- and schedule-dependent manner in some RCC cells. Fluorouracil 120-124 thymidine phosphorylase Homo sapiens 62-64 10412941-10 1999 The results imply that TP expression measurement in RCC could identify subgroups of metastatic RCC that may respond to IFN-alpha/5-FU combination therapy, and sequential administration of IFN-alpha followed by 5-FU may be beneficial in such cases. Fluorouracil 129-133 thymidine phosphorylase Homo sapiens 23-25 10211086-3 1999 They received tamoxifen 30 mg daily orally and by randomisation either 400 mg/m2, cyclophosphamide, 25 mg/m2 doxorubicin and 500 mg/m2 5-fluorouracil (CAF) or 40 mg/m2 methotrexate instead of Dox (CMF) intravenously (i.v.) Fluorouracil 135-149 lysine acetyltransferase 2B Homo sapiens 151-154 10081495-5 1998 EGF and TGF-alpha up-regulated thymidine phosphorylase (dThdPase) expression of tumor cells and consequently enhanced the antiproliferative action of 5"-dFUrd, which is converted to 5-fluorouracil by dThdPase. Fluorouracil 182-196 transforming growth factor alpha Homo sapiens 8-17 9796967-0 1998 High basal level gene expression of thymidine phosphorylase (platelet-derived endothelial cell growth factor) in colorectal tumors is associated with nonresponse to 5-fluorouracil. Fluorouracil 165-179 thymidine phosphorylase Homo sapiens 36-59 9796967-1 1998 The gene expression levels of the nucleoside cleavage enzyme/angiogenic factor thymidine phosphorylase (TP), also known as platelet-derived endothelial cell growth factor, were measured by quantitative reverse transcription-PCR in 38 pretreatment biopsies of colorectal tumors from patients who were subsequently treated with 5-fluorouracil (5-FUra) and leucovorin (LV). Fluorouracil 326-340 thymidine phosphorylase Homo sapiens 79-102 9796967-1 1998 The gene expression levels of the nucleoside cleavage enzyme/angiogenic factor thymidine phosphorylase (TP), also known as platelet-derived endothelial cell growth factor, were measured by quantitative reverse transcription-PCR in 38 pretreatment biopsies of colorectal tumors from patients who were subsequently treated with 5-fluorouracil (5-FUra) and leucovorin (LV). Fluorouracil 326-340 thymidine phosphorylase Homo sapiens 104-106 9796967-1 1998 The gene expression levels of the nucleoside cleavage enzyme/angiogenic factor thymidine phosphorylase (TP), also known as platelet-derived endothelial cell growth factor, were measured by quantitative reverse transcription-PCR in 38 pretreatment biopsies of colorectal tumors from patients who were subsequently treated with 5-fluorouracil (5-FUra) and leucovorin (LV). Fluorouracil 342-348 thymidine phosphorylase Homo sapiens 79-102 9796967-1 1998 The gene expression levels of the nucleoside cleavage enzyme/angiogenic factor thymidine phosphorylase (TP), also known as platelet-derived endothelial cell growth factor, were measured by quantitative reverse transcription-PCR in 38 pretreatment biopsies of colorectal tumors from patients who were subsequently treated with 5-fluorouracil (5-FUra) and leucovorin (LV). Fluorouracil 342-348 thymidine phosphorylase Homo sapiens 104-106 9786315-1 1998 In six published phase II trials, irinotecan (CPT-II; Camptosar; Pharmacia & Upjohn Co, Kalamazoo, MI) has demonstrated consistent activity with response rates of approximately 13% to 27% in patients with advanced colorectal cancer (CRC) refractory to 5-fluorouracil (5-FU) therapy. Fluorouracil 256-270 carnitine palmitoyltransferase 2 Homo sapiens 46-52 9786315-1 1998 In six published phase II trials, irinotecan (CPT-II; Camptosar; Pharmacia & Upjohn Co, Kalamazoo, MI) has demonstrated consistent activity with response rates of approximately 13% to 27% in patients with advanced colorectal cancer (CRC) refractory to 5-fluorouracil (5-FU) therapy. Fluorouracil 272-276 carnitine palmitoyltransferase 2 Homo sapiens 46-52 11702857-0 2001 Combination of drugs elevating extracellular adenosine with granulocyte colony-stimulating factor promotes granulopoietic recovery in the murine bone marrow after 5-fluorouracil treatment. Fluorouracil 163-177 colony stimulating factor 3 (granulocyte) Mus musculus 60-97 9815298-1 1998 BACKGROUND: Preclinical and early clinical trials suggested that the biologic agent interferon beta ser (IFN beta ser) may augment the anticancer activity of 5-fluorouracil (5-FU). Fluorouracil 158-172 interferon beta 1 Homo sapiens 84-99 9815298-1 1998 BACKGROUND: Preclinical and early clinical trials suggested that the biologic agent interferon beta ser (IFN beta ser) may augment the anticancer activity of 5-fluorouracil (5-FU). Fluorouracil 158-172 interferon beta 1 Homo sapiens 105-113 9815298-1 1998 BACKGROUND: Preclinical and early clinical trials suggested that the biologic agent interferon beta ser (IFN beta ser) may augment the anticancer activity of 5-fluorouracil (5-FU). Fluorouracil 174-178 interferon beta 1 Homo sapiens 84-99 9815298-1 1998 BACKGROUND: Preclinical and early clinical trials suggested that the biologic agent interferon beta ser (IFN beta ser) may augment the anticancer activity of 5-fluorouracil (5-FU). Fluorouracil 174-178 interferon beta 1 Homo sapiens 105-113 9676830-9 1998 The susceptibility to 5-FU cytotoxicity in the extremely high PD-ECGF expression groups (>70% of PD-ECGF score) was significantly higher than that in the low group, whereas there was no difference in their sensitivity to cisplatin. Fluorouracil 22-26 thymidine phosphorylase Homo sapiens 62-69 9676830-9 1998 The susceptibility to 5-FU cytotoxicity in the extremely high PD-ECGF expression groups (>70% of PD-ECGF score) was significantly higher than that in the low group, whereas there was no difference in their sensitivity to cisplatin. Fluorouracil 22-26 thymidine phosphorylase Homo sapiens 100-107 9676830-10 1998 These results showed that carcinoma cells with high PD-ECGF expression were sensitive to 5-FU in spite of poor prognosis. Fluorouracil 89-93 thymidine phosphorylase Homo sapiens 52-59 11702857-1 2001 Combined administration of drugs elevating extracellular adenosine, namely dipyridamole and adenosine monophosphate, together with granulocyte colony-stimulating factor was shown to enhance granulopoietic recovery in the bone marrow of mice treated with 5-fluorouracil. Fluorouracil 254-268 colony stimulating factor 3 (granulocyte) Mus musculus 131-168 11095583-0 2000 Roles of cytochromes P450 1A2, 2A6, and 2C8 in 5-fluorouracil formation from tegafur, an anticancer prodrug, in human liver microsomes. Fluorouracil 47-61 cytochrome P450 family 2 subfamily B member 6 Homo sapiens 21-25 11095583-1 2000 Tegafur, an anticancer prodrug, is bioactivated to 5-fluorouracil (5-FU) mainly by cytochrome P450 (P450) enzymes. Fluorouracil 51-65 cytochrome P450 family 2 subfamily B member 6 Homo sapiens 94-98 11095583-1 2000 Tegafur, an anticancer prodrug, is bioactivated to 5-fluorouracil (5-FU) mainly by cytochrome P450 (P450) enzymes. Fluorouracil 51-65 cytochrome P450 family 2 subfamily B member 6 Homo sapiens 100-104 11095583-1 2000 Tegafur, an anticancer prodrug, is bioactivated to 5-fluorouracil (5-FU) mainly by cytochrome P450 (P450) enzymes. Fluorouracil 67-71 cytochrome P450 family 2 subfamily B member 6 Homo sapiens 94-98 11095583-1 2000 Tegafur, an anticancer prodrug, is bioactivated to 5-fluorouracil (5-FU) mainly by cytochrome P450 (P450) enzymes. Fluorouracil 67-71 cytochrome P450 family 2 subfamily B member 6 Homo sapiens 100-104 11095583-2 2000 The conversion from tegafur into 5-FU catalyzed by human liver microsomal P450 enzymes was investigated. Fluorouracil 33-37 cytochrome P450 family 2 subfamily B member 6 Homo sapiens 74-78 11095583-3 2000 In fourteen cDNA-expressed human P450 enzymes having measurable activities, CYP1A2, CYP2A6, CYP2E1, and CYP3A5 were highly active in catalyzing 5-FU formation at a tegafur concentration of 100 microM. Fluorouracil 144-148 cytochrome P450 family 2 subfamily B member 6 Homo sapiens 33-37 11095583-9 2000 Polyclonal anti-CYP1A2 antibody, monoclonal anti-CYP2A6, and anti-CYP2C8 antibodies inhibited 5-FU formation activities to different extents in those two microsomal samples. Fluorouracil 94-98 cytochrome P450 family 2 subfamily C member 8 Homo sapiens 66-72 11095583-10 2000 These results suggest that CYP1A2, CYP2A6, and CYP2C8 have important roles in human liver microsomal 5-FU formation and that the involvement of these three P450 forms differs among individual humans. Fluorouracil 101-105 cytochrome P450 family 2 subfamily C member 8 Homo sapiens 47-53 11095583-10 2000 These results suggest that CYP1A2, CYP2A6, and CYP2C8 have important roles in human liver microsomal 5-FU formation and that the involvement of these three P450 forms differs among individual humans. Fluorouracil 101-105 cytochrome P450 family 2 subfamily B member 6 Homo sapiens 156-160 11142168-0 2000 [A case of breast cancer with multiple organ metastases responding remarkably to combination therapy of CAF (cyclophosphamide, adriamycin and 5-FU), 5"-DFUR and MPA (medroxyprogesterone acetate)]. Fluorouracil 142-146 lysine acetyltransferase 2B Homo sapiens 104-107 11205264-1 2000 BACKGROUND: Thymidine phosphorylase (TdR-Pase) is an essential enzyme for the metabolism of fluorouracil-related drugs and it is also recognized as a potent angiogenic factor. Fluorouracil 92-104 thymidine phosphorylase Homo sapiens 37-45 11205264-3 2000 Furthermore, we investigated the relationship between TdR-Pase activity and chemosensitivity to fluorouracil-related drugs. Fluorouracil 96-108 thymidine phosphorylase Homo sapiens 54-62 11073333-13 2000 PD-ECGF is thymidine phosphorylase, a key enzyme in the activation of fluoropyrimidines, including 5-fluorouracil. Fluorouracil 99-113 thymidine phosphorylase Homo sapiens 0-7 9548989-1 1998 The main purpose of this study was to evaluate the inhibitory effects of 5-fluorouracil antineoplastics, cephem antibiotics containing the methyltetrazolylthiol (MTT) group and antidiabetics on aldehyde dehydrogenase (ALDH) activity in vivo and in vitro. Fluorouracil 73-87 aldehyde dehydrogenase 3 family, member A1 Rattus norvegicus 194-216 11016005-3 2000 After three courses of CAF therapy (cyclophosphamide, doxorubicin (DXR), 5-FU), the primary tumor was decreased by 56% and the liver metastases had disappeared. Fluorouracil 73-77 lysine acetyltransferase 2B Homo sapiens 23-26 9469365-1 1998 PURPOSE: We have previously demonstrated high locoregional control rates in patients with poor-prognosis head and neck cancer using fluorouracil (5-FU), hydroxyurea (HU), and concomitant radiotherapy (RT) (FHX). Fluorouracil 132-144 forkhead box J2 Homo sapiens 206-209 9469365-1 1998 PURPOSE: We have previously demonstrated high locoregional control rates in patients with poor-prognosis head and neck cancer using fluorouracil (5-FU), hydroxyurea (HU), and concomitant radiotherapy (RT) (FHX). Fluorouracil 146-150 forkhead box J2 Homo sapiens 206-209 9619762-10 1998 CONCLUSION: This study demonstrates that CDA, ARA-C, CDDP, and 5FU possess concentration-dependent apoptosis-inducing potential in the cell lines studied. Fluorouracil 63-66 cytidine deaminase Homo sapiens 41-44 10958597-2 2000 Interferon alpha 2b is known to have antiproliferative effects on several cell lines and has well documented in vitro evidence of synergism with 5-FU. Fluorouracil 145-149 interferon alpha 2 Homo sapiens 0-19 10965024-9 2000 Moreover, AS1 ODNs coupled with 5-FU decreased viable colon cancer cells 40% more than did 5-FU alone (P < 0.05). Fluorouracil 32-36 prostaglandin D2 receptor Homo sapiens 10-13 10965024-9 2000 Moreover, AS1 ODNs coupled with 5-FU decreased viable colon cancer cells 40% more than did 5-FU alone (P < 0.05). Fluorouracil 91-95 prostaglandin D2 receptor Homo sapiens 10-13 10960921-3 2000 These tumors, when becoming necrotic, are rich enough in beta-glucuronidase to allow (19)F magnetic resonance spectroscopy monitoring, at the tumor level, of both prodrug elimination and 5-FU liberation without preliminary treatment by a specifically targeted enzyme conjugate. Fluorouracil 187-191 glucuronidase beta Homo sapiens 57-75 10887111-8 2000 In addition, these Cx43-reintroduced stromal cells showed an increased support ability (3.7-fold) for CAFC-week 1 in normal mouse BM and 5-fold higher supportive ability for CAFC-week 4 in 5-fluorouracil-treated BM cells as compared with Cx43-deficient FL stromal cells. Fluorouracil 189-203 gap junction protein, alpha 3 Mus musculus 19-23 10887111-8 2000 In addition, these Cx43-reintroduced stromal cells showed an increased support ability (3.7-fold) for CAFC-week 1 in normal mouse BM and 5-fold higher supportive ability for CAFC-week 4 in 5-fluorouracil-treated BM cells as compared with Cx43-deficient FL stromal cells. Fluorouracil 189-203 gap junction protein, alpha 3 Mus musculus 238-242 10530779-1 1999 5"-Deoxy-5-fluorouridine (5"-dFUrd) is a prodrug of 5-fluorouracil (5-FUra) activated by pyrimidine nucleoside phosphorylase (PyN Pase), mainly by uridine phosphorylase (Urd Pase) in rodents and by thymidine phosphorylase (TdR Pase) in humans, which is preferentially located in tumor tissues compared to normal tissues. Fluorouracil 52-66 thymidine phosphorylase Homo sapiens 223-231 10530779-1 1999 5"-Deoxy-5-fluorouridine (5"-dFUrd) is a prodrug of 5-fluorouracil (5-FUra) activated by pyrimidine nucleoside phosphorylase (PyN Pase), mainly by uridine phosphorylase (Urd Pase) in rodents and by thymidine phosphorylase (TdR Pase) in humans, which is preferentially located in tumor tissues compared to normal tissues. Fluorouracil 68-74 thymidine phosphorylase Homo sapiens 223-231 10517490-0 1999 Cyclooxygenase-2 is essential for normal recovery from 5-fluorouracil-induced myelotoxicity in mice. Fluorouracil 55-69 prostaglandin-endoperoxide synthase 2 Mus musculus 0-16 9554039-9 1998 On the other hand, the shortening of the rhG-CSF treatment from eight to four days caused a rapid granulopoietic recovery comparable to animals receiving eight days of G-CSF with no significant delay in megakaryocytic recovery when compared with mice treated with 5-FU alone; however, with four days of rhG-CSF, the mobilization of CFU into the peripheral blood was significantly less effective. Fluorouracil 264-268 colony stimulating factor 3 (granulocyte) Mus musculus 43-48 9242554-4 1997 In addition, Bcl-XL provided significantly greater cell viability than Bcl-2 against methotrexate, fluorouracil, and hydroxyurea, three S-phase specific agents. Fluorouracil 99-111 BCL2-like 1 Mus musculus 13-19 11091585-1 1997 Thirty-two patients with advanced breast cancer refractory to combination chemotherapy with cyclophosphamide (CPA), doxorubicin (ADR) and 5-fluorouracil (5-EU) (CAF) were treated with the combination of mitomycin C, etoposide, doxifluridine and medroxyprogesterone acetate as second line therapy. Fluorouracil 138-152 lysine acetyltransferase 2B Homo sapiens 161-164 21590142-2 1997 PyNPase is an enzyme which converts 5"-DFUR to 5-FU in tumor tissue and has been reported to be identical to the platelet-derived endothelial cell growth factor (PD-ECGF) that has angiogenic activity. Fluorouracil 47-51 thymidine phosphorylase Homo sapiens 113-160 9066692-3 1997 This present communication describes the testing of a glycan, PS1, obtained from the Tice substrain of BCG against the hormonal dependent human breast cancer cell line MCF-7 and the hormonally independent BT-20 line, using 5-fluorouracil (5-FU) as a positive control. Fluorouracil 223-237 presenilin 1 Homo sapiens 62-65 9066692-3 1997 This present communication describes the testing of a glycan, PS1, obtained from the Tice substrain of BCG against the hormonal dependent human breast cancer cell line MCF-7 and the hormonally independent BT-20 line, using 5-fluorouracil (5-FU) as a positive control. Fluorouracil 239-243 presenilin 1 Homo sapiens 62-65 10517490-4 1999 We hypothesized that COX-2 induction plays a role in the recovery phase of 5-fluorouracil (5-FU) induced bone marrow injury, because significant macrophage-driven phagocytic removal of necrotic debris and stromal cell reorganization of repopulating marrow occur after 5-FU induction of bone marrow necrosis. Fluorouracil 75-89 cytochrome c oxidase II, mitochondrial Mus musculus 21-26 10517490-4 1999 We hypothesized that COX-2 induction plays a role in the recovery phase of 5-fluorouracil (5-FU) induced bone marrow injury, because significant macrophage-driven phagocytic removal of necrotic debris and stromal cell reorganization of repopulating marrow occur after 5-FU induction of bone marrow necrosis. Fluorouracil 91-95 cytochrome c oxidase II, mitochondrial Mus musculus 21-26 10517490-4 1999 We hypothesized that COX-2 induction plays a role in the recovery phase of 5-fluorouracil (5-FU) induced bone marrow injury, because significant macrophage-driven phagocytic removal of necrotic debris and stromal cell reorganization of repopulating marrow occur after 5-FU induction of bone marrow necrosis. Fluorouracil 268-272 cytochrome c oxidase II, mitochondrial Mus musculus 21-26 10517490-6 1999 Mild anemia was present in 5-FU-treated Cox-2-/- and Cox-2+/- mice on days 8 and 12, which was more severe in Cox-2-/- mice. Fluorouracil 27-31 cytochrome c oxidase II, mitochondrial Mus musculus 40-45 10517490-7 1999 Cox-2-/- mice had markedly decreased bone marrow cell counts per femur and reduced numbers of erythroid and myeloid colony-forming cells compared to heterozygote mice on days 8 and 12 post 5-FU. Fluorouracil 189-193 cytochrome c oxidase II, mitochondrial Mus musculus 0-5 10517490-8 1999 Histologic examination of 5-FU-treated Cox-2-/- mice revealed a failure to repopulate the intact marrow stroma with hematopoietic cells. Fluorouracil 26-30 cytochrome c oxidase II, mitochondrial Mus musculus 39-44 10416617-5 1999 The suppression of cyclin D1 expression after the stable transfection of a cyclin D1 antisense construct in PANC-1 and COLO-357 human pancreatic cancer cells resulted in a significant increase in sensitivity to the fluoropyrimidines 5-fluorouracil and 5-fluoro-2"-deoxyuridine and to mitoxantrone. Fluorouracil 233-247 cyclin D1 Homo sapiens 19-28 9012684-5 1997 Furthermore, four Tg mice showed impaired myeloid differentiation in response to the treatment by 5-FU on granulocyte-colony stimulating factor (G-CSF), although they exhibited apparently normal myelopoiesis in the untreated state. Fluorouracil 98-102 colony stimulating factor 3 (granulocyte) Mus musculus 106-143 9012684-5 1997 Furthermore, four Tg mice showed impaired myeloid differentiation in response to the treatment by 5-FU on granulocyte-colony stimulating factor (G-CSF), although they exhibited apparently normal myelopoiesis in the untreated state. Fluorouracil 98-102 colony stimulating factor 3 (granulocyte) Mus musculus 145-150 9310231-6 1997 In addition, dThdPase activity (by inference PD-ECGF) has been found to be a major determinant of the toxicity of 5-fluorouracil and its prodrugs, which are extensively studied clinically as anti-cancer agents. Fluorouracil 114-128 thymidine phosphorylase Homo sapiens 45-52 9192553-0 1997 Transforming growth factor-beta 3 mediated modulation of cell cycling and attenuation of 5-fluorouracil induced oral mucositis. Fluorouracil 89-103 transforming growth factor beta 3 Homo sapiens 0-33 9192553-5 1997 Administration of topical TGF-beta 3 prior to chemotherapy with 5-fluorouracil (5-FU) significantly reduced the severity of mucositis with respect to time, reduced chemotherapy-associated weight loss and increased survival. Fluorouracil 64-78 transforming growth factor beta 3 Homo sapiens 26-36 9192553-5 1997 Administration of topical TGF-beta 3 prior to chemotherapy with 5-fluorouracil (5-FU) significantly reduced the severity of mucositis with respect to time, reduced chemotherapy-associated weight loss and increased survival. Fluorouracil 80-84 transforming growth factor beta 3 Homo sapiens 26-36 8969073-6 1996 In the human tumor transplantation to nude mice, the BCM of the antitumor effect of 5-FU by LV was demonstrated in MC-1 and MPC-2. Fluorouracil 84-88 mitochondrial pyruvate carrier 2 Mus musculus 124-129 10416617-5 1999 The suppression of cyclin D1 expression after the stable transfection of a cyclin D1 antisense construct in PANC-1 and COLO-357 human pancreatic cancer cells resulted in a significant increase in sensitivity to the fluoropyrimidines 5-fluorouracil and 5-fluoro-2"-deoxyuridine and to mitoxantrone. Fluorouracil 233-247 cyclin D1 Homo sapiens 75-84 10885898-1 1999 A clinical trial regimen modulating 5-fluorouracil (5-FU) with both folinic acid (FA) and recombinant alpha-2a-interferon (ralpha-2a-IFN) was noted to have a response rate of 54% and median survival of 16.3 months (Grem et al., J Clin Oncol 1993, 11: 1737-45). Fluorouracil 36-50 interferon alpha 2 Homo sapiens 102-121 10851542-0 1996 Alpha interferon-2b, leucovorin, and 5-fluorouracil (ALF) in non-small cell lung cancer. Fluorouracil 37-51 afamin Homo sapiens 53-56 10885898-1 1999 A clinical trial regimen modulating 5-fluorouracil (5-FU) with both folinic acid (FA) and recombinant alpha-2a-interferon (ralpha-2a-IFN) was noted to have a response rate of 54% and median survival of 16.3 months (Grem et al., J Clin Oncol 1993, 11: 1737-45). Fluorouracil 52-56 interferon alpha 2 Homo sapiens 102-121 10190647-8 1999 The cytotoxic activities of mercaptopurine and fluorouracil are regulated by thiopurine methyltransferase (TPMT) and dihydropyrimidine dehydrogenase (DPD), respectively. Fluorouracil 47-59 thiopurine S-methyltransferase Homo sapiens 77-105 8708718-2 1996 PURPOSE: To determine the effects of interferon alpha-2a (IFN alpha) on the efficacy and toxicity of fluorouracil (FUra) and leucovorin (LV) in patients with advanced colorectal cancer. Fluorouracil 101-113 interferon alpha 2 Homo sapiens 37-56 8708718-2 1996 PURPOSE: To determine the effects of interferon alpha-2a (IFN alpha) on the efficacy and toxicity of fluorouracil (FUra) and leucovorin (LV) in patients with advanced colorectal cancer. Fluorouracil 101-113 interferon alpha 2 Homo sapiens 58-67 8708718-2 1996 PURPOSE: To determine the effects of interferon alpha-2a (IFN alpha) on the efficacy and toxicity of fluorouracil (FUra) and leucovorin (LV) in patients with advanced colorectal cancer. Fluorouracil 115-119 interferon alpha 2 Homo sapiens 37-56 8708718-2 1996 PURPOSE: To determine the effects of interferon alpha-2a (IFN alpha) on the efficacy and toxicity of fluorouracil (FUra) and leucovorin (LV) in patients with advanced colorectal cancer. Fluorouracil 115-119 interferon alpha 2 Homo sapiens 58-67 8638535-0 1996 Phase I-II trial of recombinant interferon alpha-2b with cisplatin and 5-fluorouracil in recurrent and/or metastatic carcinoma of head and neck. Fluorouracil 71-85 interferon alpha 2 Homo sapiens 32-51 8619029-5 1996 Pretreatment with a single dose of IL-1 resulted in the death of mice treated with 5-FU provided IL-1 was given 18 h, but not 4 or 48 h, prior to administration of sublethal doses of 5-FU. Fluorouracil 83-87 interleukin 1 complex Mus musculus 35-39 8619029-5 1996 Pretreatment with a single dose of IL-1 resulted in the death of mice treated with 5-FU provided IL-1 was given 18 h, but not 4 or 48 h, prior to administration of sublethal doses of 5-FU. Fluorouracil 83-87 interleukin 1 complex Mus musculus 97-101 8619029-5 1996 Pretreatment with a single dose of IL-1 resulted in the death of mice treated with 5-FU provided IL-1 was given 18 h, but not 4 or 48 h, prior to administration of sublethal doses of 5-FU. Fluorouracil 183-187 interleukin 1 complex Mus musculus 35-39 8619029-7 1996 Similarly, the toxicity of 5-FU to progenitor cells was reduced when two injections of IL-1 were administered 48 h apart. Fluorouracil 27-31 interleukin 1 complex Mus musculus 87-91 8697140-1 1996 Studies were carried out to determine whether the combination of IL-1 + M-CSF, similar to the effect of these cytokines on neutropenia, was able to reduce the duration of thrombocytopenia in the 5-fluorouracil (5-FU)-myelosuppressed mouse. Fluorouracil 195-209 interleukin 1 complex Mus musculus 65-69 8697140-1 1996 Studies were carried out to determine whether the combination of IL-1 + M-CSF, similar to the effect of these cytokines on neutropenia, was able to reduce the duration of thrombocytopenia in the 5-fluorouracil (5-FU)-myelosuppressed mouse. Fluorouracil 211-215 interleukin 1 complex Mus musculus 65-69 8697140-8 1996 Furthermore, the data presented are consistent with the hypothesis that IL-1 + M-CSF initially acts on a multilineage, 5-FU-resistant target cell and that IL-6 (and possibly IL-3 and GM-CSF) serves as a secondary cytokine further to enhance platelet production during rebound thrombopoiesis in the 5-FU-treated mouse. Fluorouracil 119-123 interleukin 1 complex Mus musculus 72-76 10387998-3 1996 Methenyltetrahydrofolate synthetase (MTHFS) catalyzes the transformation of 5-formyltetrahydrofolate to methenylH(4)folate, which is the obligatory initial metabolic step prior to the intracellular conversion of 5-formylH(4)folate to other reduced folates and the increase in intracellular folate pools required for 5-FU potentiation. Fluorouracil 316-320 methenyltetrahydrofolate synthetase Homo sapiens 0-35 10387998-3 1996 Methenyltetrahydrofolate synthetase (MTHFS) catalyzes the transformation of 5-formyltetrahydrofolate to methenylH(4)folate, which is the obligatory initial metabolic step prior to the intracellular conversion of 5-formylH(4)folate to other reduced folates and the increase in intracellular folate pools required for 5-FU potentiation. Fluorouracil 316-320 methenyltetrahydrofolate synthetase Homo sapiens 37-42 21594349-0 1996 Effect of 5-fluorouracil treatment on IL-2R gene expression in gastric carcinoma patients. Fluorouracil 10-24 interleukin 2 receptor subunit alpha Homo sapiens 38-43 8731973-1 1995 We have previously shown that platelet factor 4 (PF 4) is a potent inhibitor of megakaryocytopoiesis and that it may protect stem cells from 5-fluorouracil (5-FU) cytotoxicity. Fluorouracil 141-155 platelet factor 4 Homo sapiens 49-53 8731973-1 1995 We have previously shown that platelet factor 4 (PF 4) is a potent inhibitor of megakaryocytopoiesis and that it may protect stem cells from 5-fluorouracil (5-FU) cytotoxicity. Fluorouracil 157-161 platelet factor 4 Homo sapiens 49-53 8731973-6 1995 Moreover, incubation of CD34+ cells with PF 4 in liquid culture caused an increase in the number of both stem cell factor (SCF)-binding cells and CD34 antigen-bearing cells, and exhibited greater capacity to form MK colonies than control after the treatment of 5-FU. Fluorouracil 261-265 platelet factor 4 Homo sapiens 41-45 10190647-8 1999 The cytotoxic activities of mercaptopurine and fluorouracil are regulated by thiopurine methyltransferase (TPMT) and dihydropyrimidine dehydrogenase (DPD), respectively. Fluorouracil 47-59 thiopurine S-methyltransferase Homo sapiens 107-111 9796967-2 1998 The range of TP gene expression (relative mRNA levels) in those tumors nonresponsive to 5-FUra was much broader than that of the responding tumors. Fluorouracil 88-94 thymidine phosphorylase Homo sapiens 13-15 9796967-7 1998 TP and TS expressions were found to be independent variables in these tumors, so that low expression levels of both TS and TP in tumors predicted a very high response rate (11 of 14) to 5-FUra/LV as well as a significantly longer survival, whereas none (0 of 24) of the patients with high expression of either TP or TS were responders. Fluorouracil 186-192 thymidine phosphorylase Homo sapiens 0-2 9796967-7 1998 TP and TS expressions were found to be independent variables in these tumors, so that low expression levels of both TS and TP in tumors predicted a very high response rate (11 of 14) to 5-FUra/LV as well as a significantly longer survival, whereas none (0 of 24) of the patients with high expression of either TP or TS were responders. Fluorouracil 186-192 thymidine phosphorylase Homo sapiens 123-125 9796967-7 1998 TP and TS expressions were found to be independent variables in these tumors, so that low expression levels of both TS and TP in tumors predicted a very high response rate (11 of 14) to 5-FUra/LV as well as a significantly longer survival, whereas none (0 of 24) of the patients with high expression of either TP or TS were responders. Fluorouracil 186-192 thymidine phosphorylase Homo sapiens 123-125 9797804-6 1998 Overexpression of Thymidine Phosphorylase has been found to be associated with chemo-sensitivity to prodrug of 5-FU. Fluorouracil 111-115 thymidine phosphorylase Homo sapiens 18-41 9757455-5 1998 Thymidine phosphorylase (TPase) and thymidine kinase (TK), key enzymes for metabolism of 5-FU derivatives, were measured in cerebrospinal fluid (CSF). Fluorouracil 89-93 thymidine phosphorylase Homo sapiens 0-23 9815929-8 1995 When the prolonged infusion of IFN-beta followed a 1-h exposure to FUra, the observed TS inhibition and recovery, at each time point, were very similar to the expected values, indicating that the interactions between these drugs at the level of TS are not the determinant of the synergism. Fluorouracil 67-71 interferon beta 1 Homo sapiens 31-39 9815929-10 1995 During the continuous exposure to IFN-beta, a significant accumulation of HCT-8 cells in S-phase was observed at 24, 48, and 72 h compared to untreated controls (P = 0.003); however, under the same experimental conditions producing synergy in the clonogenic assay, no significant cell cycle perturbations were produced by the combination of FUra followed by IFN-beta compared to those caused by each agent alone. Fluorouracil 341-345 interferon beta 1 Homo sapiens 34-42 9815929-15 1995 These results suggest that the mechanism of this synergism may be related to the ability of IFN-beta to promote the incorporation of intracellular FUra metabolites into nucleic acids and/or to inhibit the cleavage of FUra nucleotides from RNA/DNA. Fluorouracil 147-151 interferon beta 1 Homo sapiens 92-100 9726437-3 1998 pretreatment with interferon (IFN)-alpha2b in patients with advanced colorectal carcinoma refractory to previous therapy with 5-FU modulated by methotrexate (MTX) or leucovorin (LV) or both. Fluorouracil 126-130 interferon alpha 2 Homo sapiens 18-42 9563485-0 1998 Interleukin 15 protects against toxicity and potentiates antitumor activity of 5-fluorouracil alone and in combination with leucovorin in rats bearing colorectal cancer. Fluorouracil 79-93 interleukin 15 Rattus norvegicus 0-14 9563485-5 1998 IL-15 induced a dramatic decrease in chemotherapy-induced gastrointestinal toxicities, significant potentiation of antitumor activity, and an increased therapeutic index of FUra administered on single dose, daily x 5 and weekly x 4 schedules. Fluorouracil 173-177 interleukin 15 Rattus norvegicus 0-5 9563485-8 1998 Taken together, the results clearly demonstrated the ability of IL-15, but not IL-2, to provide significant improvement of the therapeutic index of FUra alone and in combination with LV. Fluorouracil 148-152 interleukin 15 Rattus norvegicus 64-69 9537263-1 1998 The enzyme/cytokine thymidine phosphorylase/platelet-derived endothelial cell growth factor (TP/PD-ECGF) has diverse functions within cells, including the regulation of steady-state thymidine levels, the conversion of cancer chemotherapeutic agent 5-fluorouracil to an active metabolite, and the mediation of angiogenesis in normal and malignant cells. Fluorouracil 248-262 thymidine phosphorylase Homo sapiens 96-103 7589288-2 1995 In mice, exogenous G-CSF reduces neutrophil recovery after 5-fluorouracil (5-FU) treatment from 14 to 8 days. Fluorouracil 59-73 colony stimulating factor 3 (granulocyte) Mus musculus 19-24 7589288-2 1995 In mice, exogenous G-CSF reduces neutrophil recovery after 5-fluorouracil (5-FU) treatment from 14 to 8 days. Fluorouracil 75-79 colony stimulating factor 3 (granulocyte) Mus musculus 19-24 9524089-9 1998 Several studies have indicated that FdUrd is rapidly converted to 5-FU in the presence of thymidine phosphorylase, so that a high dose of FdUrd must be administered to obtain good efficacy. Fluorouracil 66-70 thymidine phosphorylase Homo sapiens 90-113 8566832-6 1995 In the presence of 5-FU, a high degree of polymegathism and delay in actin and vinculin redistribution to the cell borders after wound closure was observed. Fluorouracil 19-23 actin epsilon 1 Bos taurus 69-74 9492821-7 1998 Patients with rapidly progressing and/or endocrine-resistant tumor should be treated with anthracycline containing regimen such as CAF (cyclophosphamide, adriamycin, 5-fluorouracil). Fluorouracil 166-180 lysine acetyltransferase 2B Homo sapiens 131-134 9434160-15 1997 Expression of PTPRO was also observed in human CD34+ bone marrow cells and 5-FU-treated murine primitive stem cells. Fluorouracil 75-79 protein tyrosine phosphatase receptor type U Homo sapiens 14-19 9464625-3 1997 (Proc ASCO 1992; 11: 347) raised the possibility of the known interaction between 5-fluorouracil and interferon-alpha2a improving response rates in melanoma. Fluorouracil 82-96 interferon alpha 2 Homo sapiens 101-119 9362454-4 1997 In FL5.12 cells expressing Bcl-XL and Bak wt or Bak deltaBH3, both Bak wt or Bak deltaBH3 were able to antagonize the protective effect of Bcl-XL when treated with etoposide or fluorouracil. Fluorouracil 177-189 BCL2-like 1 Mus musculus 27-33 9362454-4 1997 In FL5.12 cells expressing Bcl-XL and Bak wt or Bak deltaBH3, both Bak wt or Bak deltaBH3 were able to antagonize the protective effect of Bcl-XL when treated with etoposide or fluorouracil. Fluorouracil 177-189 BCL2-like 1 Mus musculus 139-145 9815767-1 1997 The enzyme/cytokine thymidine phosphorylase/platelet-derived endothelial cell growth factor (TP/PD-ECGF) has diverse functions within cells, including the regulation of steady-state thymidine levels, the conversion of the cancer chemotherapeutic agent 5-fluorouracil (FUra) to an active metabolite, and the mediation of angiogenesis in normal and malignant cells. Fluorouracil 252-266 thymidine phosphorylase Homo sapiens 96-103 9815767-1 1997 The enzyme/cytokine thymidine phosphorylase/platelet-derived endothelial cell growth factor (TP/PD-ECGF) has diverse functions within cells, including the regulation of steady-state thymidine levels, the conversion of the cancer chemotherapeutic agent 5-fluorouracil (FUra) to an active metabolite, and the mediation of angiogenesis in normal and malignant cells. Fluorouracil 268-272 thymidine phosphorylase Homo sapiens 96-103 9175720-2 1997 Previously, TGF-beta3 was shown to protect epithelial cells and hematopoietic cells from cytotoxic damage in vitro and in vivo, and to reduce the severity and duration of oral mucositis induced by 5-fluorouracil (5-FU) in vivo. Fluorouracil 197-211 transforming growth factor beta 3 Homo sapiens 12-21 9175720-2 1997 Previously, TGF-beta3 was shown to protect epithelial cells and hematopoietic cells from cytotoxic damage in vitro and in vivo, and to reduce the severity and duration of oral mucositis induced by 5-fluorouracil (5-FU) in vivo. Fluorouracil 213-217 transforming growth factor beta 3 Homo sapiens 12-21 9175720-4 1997 We report that preincubation of cells with TGF-beta3 for 24 hr resulted in enhanced clonogenicity following exposure to vinblastine, vincristine, etoposide, taxol, ara-C, methotrexate, or 5-FU. Fluorouracil 188-192 transforming growth factor beta 3 Homo sapiens 43-52 9127172-9 1997 Therefore, biochemical modulation of 5-FU with FA and IFN-alpha shows some positive effects in the treatment of pancreatic cancer with moderate toxicity. Fluorouracil 37-41 interferon alpha 2 Homo sapiens 54-63 9066609-3 1997 Furthermore, the antitumor activity of 5-FU on C-1 cells was augmented by IFN alpha or beta. Fluorouracil 39-43 interferon alpha 2 Homo sapiens 74-83 7474606-3 1995 Experimental data suggest that PC-3, a human hormone refractory prostate cancer cell line, showed a 2-fold increase in 5-Fluorouracil (5FU) sensitivity in the presence of alpha-2a Interferon (IFN alpha 2a) at 100 IU/ml, compared to that without IFN alpha 2a. Fluorouracil 135-138 interferon alpha 2 Homo sapiens 192-203 7474606-3 1995 Experimental data suggest that PC-3, a human hormone refractory prostate cancer cell line, showed a 2-fold increase in 5-Fluorouracil (5FU) sensitivity in the presence of alpha-2a Interferon (IFN alpha 2a) at 100 IU/ml, compared to that without IFN alpha 2a. Fluorouracil 135-138 interferon alpha 2 Homo sapiens 245-256 7565905-4 1995 CBP-7 and CBP-6 clones exhibited cross-resistance to cisplatin (cis-DDP), CBP-7 clone became markedly more sensitive and CBP-3 slightly more sensitive to 5-fluorouracil (5-FU), CBP-6 became sensitive to etoposide (Et), CBP-6 became sensitive and CBP-7 resistant to vinblastine (VBL). Fluorouracil 154-168 ubiquinol-cytochrome c reductase complex assembly factor 1 Homo sapiens 121-126 7565905-4 1995 CBP-7 and CBP-6 clones exhibited cross-resistance to cisplatin (cis-DDP), CBP-7 clone became markedly more sensitive and CBP-3 slightly more sensitive to 5-fluorouracil (5-FU), CBP-6 became sensitive to etoposide (Et), CBP-6 became sensitive and CBP-7 resistant to vinblastine (VBL). Fluorouracil 170-174 ubiquinol-cytochrome c reductase complex assembly factor 1 Homo sapiens 121-126 1498068-0 1992 Double biochemical modulation of 5-fluorouracil by leucovorin and cyclic low dose interferon alpha 2b in advanced colorectal cancer patients. Fluorouracil 33-47 interferon alpha 2 Homo sapiens 82-101 1587307-2 1992 Murine bone marrow (BM) harvested 24 h after 5-fluorouracil (5-FU) administration (d1 5-FU BM) was stimulated with IL-1 and IL-3 to expand its progenitor pool during 7 days of suspension culture (delta-culture), and this in vitro expanded BM was compared to fresh d1 5-FU BM in its ability to reconstitute lethally irradiated or high-dose 5-FU-treated hosts. Fluorouracil 61-65 interleukin 1 complex Mus musculus 115-119 1587307-2 1992 Murine bone marrow (BM) harvested 24 h after 5-fluorouracil (5-FU) administration (d1 5-FU BM) was stimulated with IL-1 and IL-3 to expand its progenitor pool during 7 days of suspension culture (delta-culture), and this in vitro expanded BM was compared to fresh d1 5-FU BM in its ability to reconstitute lethally irradiated or high-dose 5-FU-treated hosts. Fluorouracil 86-90 interleukin 1 complex Mus musculus 115-119 1587307-2 1992 Murine bone marrow (BM) harvested 24 h after 5-fluorouracil (5-FU) administration (d1 5-FU BM) was stimulated with IL-1 and IL-3 to expand its progenitor pool during 7 days of suspension culture (delta-culture), and this in vitro expanded BM was compared to fresh d1 5-FU BM in its ability to reconstitute lethally irradiated or high-dose 5-FU-treated hosts. Fluorouracil 86-90 interleukin 1 complex Mus musculus 115-119 1587307-2 1992 Murine bone marrow (BM) harvested 24 h after 5-fluorouracil (5-FU) administration (d1 5-FU BM) was stimulated with IL-1 and IL-3 to expand its progenitor pool during 7 days of suspension culture (delta-culture), and this in vitro expanded BM was compared to fresh d1 5-FU BM in its ability to reconstitute lethally irradiated or high-dose 5-FU-treated hosts. Fluorouracil 86-90 interleukin 1 complex Mus musculus 115-119 1587307-7 1992 In conjunction with G-CSF post-transplantation cytokine therapy, high-dose 5-FU-treated mice transplanted with delta-cultured BM also demonstrated improved recovery kinetics of neutrophils and erythrocytes. Fluorouracil 75-79 colony stimulating factor 3 (granulocyte) Mus musculus 20-25 1553576-1 1992 Preclinical data suggest that folinic acid as well as interferon alpha-2b may enhance the antitumor activity of 5-fluorouracil (5-FU). Fluorouracil 112-126 interferon alpha 2 Homo sapiens 54-73 1553576-1 1992 Preclinical data suggest that folinic acid as well as interferon alpha-2b may enhance the antitumor activity of 5-fluorouracil (5-FU). Fluorouracil 128-132 interferon alpha 2 Homo sapiens 54-73 1553576-2 1992 In a phase I trial, we recently showed that interferon alpha-2b (IFN), folinic acid and 5-FU can be safely administered with a 4-hour infusion of 5-FU. Fluorouracil 146-150 interferon alpha 2 Homo sapiens 44-63 1373685-3 1992 Furthermore, IL-1, IL-6, and KL, alone or in combination, synergized with the colony-stimulating factors (CSFs) granulocyte CSF (G-CSF), macrophage CSF (M-CSF), granulocyte-macrophage CSF (GM-CSF), or interleukin 3 (IL-3) in clonal and liquid cultures of 5-FU-purged bone marrow. Fluorouracil 255-259 interleukin 1 complex Mus musculus 13-17 1534247-3 1992 The toxicity of 5-FU was enhanced by IFN-alpha in only one line (SW-480). Fluorouracil 16-20 interferon alpha 2 Homo sapiens 37-46 7541666-7 1995 In canine and murine models, serum levels of MGDF activity peak during the thrombocytopenic periods after irradiation, 5-fluorouracil, or antiplatelet antisera injections. Fluorouracil 119-133 C-MPL ligand Canis lupus familiaris 45-49 21224110-0 1995 A phase I study of FAP (5-Fluorouracil, alpha-interferon and cisplatin) combined with methotrexate for the treatment of advanced urothelial malignancies. Fluorouracil 24-38 fibroblast activation protein alpha Homo sapiens 19-22 21224110-3 1995 Our goal was to identify the starting dose of FAP (5-fluorouracil-alpha-interferon-cisplatin) that will permit delivery of methotrexate in patients with advanced chemotherapy-refractory urothelial cancers. Fluorouracil 51-65 fibroblast activation protein alpha Homo sapiens 46-49 7601293-5 1995 This strong inhibitory effect of 5-fluorouracil on metastasis was almost completely suppressed when mice were treated with CSA concomitantly. Fluorouracil 33-47 excision repaiross-complementing rodent repair deficiency, complementation group 8 Mus musculus 123-126 8542247-1 1995 The purpose of this study was to evaluate a potential pharmacokinetic (PK) interaction between fluorouracil (5-FU) and the biomodulating agent interferon alpha (IFN-alpha) in patients with metastatic colorectal carcinoma. Fluorouracil 95-107 interferon alpha 2 Homo sapiens 161-170 1534247-7 1992 Potentiation of 5"-dFUrd effect by IFN-alpha may thus be explained by an enhancement of its conversion to 5-FU through stimulation of pyrimidine phosphorylase activity. Fluorouracil 106-110 interferon alpha 2 Homo sapiens 35-44 1374741-5 1992 Proliferative responses of bone marrow cells to granulocyte/macrophage colony stimulating factor (GM-CSF) or granulocyte colony stimulating factor (G-CSF) were suppressed by 5-FU treatment and their recoveries were enhanced by SPR-901. Fluorouracil 174-178 colony stimulating factor 3 (granulocyte) Mus musculus 109-146 1374741-5 1992 Proliferative responses of bone marrow cells to granulocyte/macrophage colony stimulating factor (GM-CSF) or granulocyte colony stimulating factor (G-CSF) were suppressed by 5-FU treatment and their recoveries were enhanced by SPR-901. Fluorouracil 174-178 colony stimulating factor 3 (granulocyte) Mus musculus 148-153 1940339-0 1991 Effects of recombinant transforming growth factor-beta 1 on hematologic recovery after treatment of mice with 5-fluorouracil. Fluorouracil 110-124 transforming growth factor, beta 1 Mus musculus 23-56 7733626-0 1995 Recombinant human interferon alpha-2a increases the antitumor activity of 5-fluorouracil on human colon carcinoma xenograft Co-4 without any change in 5-FU pharmacokinetics. Fluorouracil 74-88 interferon alpha 2 Homo sapiens 18-37 7733626-1 1995 We investigated the modulating effect of recombinant human interferon alpha-2a (IFN-alpha) on the antitumor activity of 5-fluorouracil (5-FU) against a human colon carcinoma xenograft (Co-4) in nude mice with reference to changes in the pharmacokinetic pattern of 5-FU. Fluorouracil 120-134 interferon alpha 2 Homo sapiens 59-78 7733626-1 1995 We investigated the modulating effect of recombinant human interferon alpha-2a (IFN-alpha) on the antitumor activity of 5-fluorouracil (5-FU) against a human colon carcinoma xenograft (Co-4) in nude mice with reference to changes in the pharmacokinetic pattern of 5-FU. Fluorouracil 120-134 interferon alpha 2 Homo sapiens 80-89 7733626-1 1995 We investigated the modulating effect of recombinant human interferon alpha-2a (IFN-alpha) on the antitumor activity of 5-fluorouracil (5-FU) against a human colon carcinoma xenograft (Co-4) in nude mice with reference to changes in the pharmacokinetic pattern of 5-FU. Fluorouracil 136-140 interferon alpha 2 Homo sapiens 59-78 7733626-1 1995 We investigated the modulating effect of recombinant human interferon alpha-2a (IFN-alpha) on the antitumor activity of 5-fluorouracil (5-FU) against a human colon carcinoma xenograft (Co-4) in nude mice with reference to changes in the pharmacokinetic pattern of 5-FU. Fluorouracil 136-140 interferon alpha 2 Homo sapiens 80-89 7733626-4 1995 This result suggests that the modulating effect of IFN-alpha on 5-FU does not involve augmentation of 5-FU pharmacokinetic parameters. Fluorouracil 64-68 interferon alpha 2 Homo sapiens 51-60 7989127-8 1994 The higher SOD2 and lower G6PD activity observed in FUra-resistant cell in comparison with parental cells at all times after sub-culture could be characteristic both of differentiative and of differentiated cells. Fluorouracil 52-56 superoxide dismutase 2 Homo sapiens 11-15 7525886-1 1994 PURPOSE: We previously demonstrated high locoregional control rates in patients with poor-prognosis head and neck cancer using fluorouracil (5-FU), hydroxyurea (HU), and concomitant radiotherapy (FHX). Fluorouracil 141-145 forkhead box J2 Homo sapiens 196-199 7917927-0 1994 Double modulation of 5-fluorouracil with interferon alpha 2a and high-dose leucovorin: a phase I and II study. Fluorouracil 21-35 interferon alpha 2 Homo sapiens 41-60 7917928-14 1994 These results, while not inconsistent with previous reports of a reduced rate of FUra elimination at higher IFN-alpha doses, suggest that any clinical effect of this moderate dose of IFN-alpha on FUra toxicity or activity is due to modulation at target cells, not to pharmacokinetic interaction. Fluorouracil 81-85 interferon alpha 2 Homo sapiens 183-192 7917928-14 1994 These results, while not inconsistent with previous reports of a reduced rate of FUra elimination at higher IFN-alpha doses, suggest that any clinical effect of this moderate dose of IFN-alpha on FUra toxicity or activity is due to modulation at target cells, not to pharmacokinetic interaction. Fluorouracil 196-200 interferon alpha 2 Homo sapiens 183-192 8064224-0 1994 Recombinant transforming growth factor beta 1 and beta 2 protect mice from acutely lethal doses of 5-fluorouracil and doxorubicin. Fluorouracil 99-113 transforming growth factor, beta 1 Mus musculus 12-45 8064224-5 1994 Further studies showed that the administration of TGF-beta protected up to 90% of these mice undergoing hematologic recovery from a rechallenge in vivo with high dose 5-FU, while survival in mice not given TGF-beta was < 40%. Fluorouracil 167-171 transforming growth factor, beta 1 Mus musculus 50-58 8064224-7 1994 These results demonstrate that TGF-beta can protect mice from both the lethal hematopoietic toxicity of 5-FU, as well as the nonhematopoietic toxicity of DXR. Fluorouracil 104-108 transforming growth factor, beta 1 Mus musculus 31-39 8074466-0 1994 Recombinant human interferon alpha-2a increases 5-fluorouracil efficacy by elevating fluorouridine concentration in tumor tissue. Fluorouracil 48-62 interferon alpha 2 Homo sapiens 18-37 8074466-3 1994 The in vitro antitumor activity of 5-FU was enhanced by the addition of IFN-alpha, but IFN-alpha did not increase the effect of FUR or FUdR. Fluorouracil 35-39 interferon alpha 2 Homo sapiens 72-81 8074466-7 1994 The intratumoral concentration of FUR was significantly increased by the addition of IFN-alpha in Co-4 tumor tissue treated with 5-FU. Fluorouracil 129-133 interferon alpha 2 Homo sapiens 85-94 8137250-0 1994 Potentiation of the antitumor activity of 5-fluorouracil in colon carcinoma cells by the combination of interferon and deoxyribonucleosides results from complementary effects on thymidine phosphorylase. Fluorouracil 42-56 thymidine phosphorylase Homo sapiens 178-201 1940339-2 1991 These data suggest that TGF-beta might either protect, or further depress, progenitor cell levels in mice exposed to a cell cycle-active drug such as 5-fluorouracil (5FU). Fluorouracil 150-164 transforming growth factor, beta 1 Mus musculus 24-32 1940339-2 1991 These data suggest that TGF-beta might either protect, or further depress, progenitor cell levels in mice exposed to a cell cycle-active drug such as 5-fluorouracil (5FU). Fluorouracil 166-169 transforming growth factor, beta 1 Mus musculus 24-32 1811238-0 1991 Influence of interferon-alpha-2b on the blood-plasma levels of intraarterial administered fluorouracil. Fluorouracil 90-102 interferon alpha 2 Homo sapiens 13-32 7880618-1 1994 Interferon-alpha (IFN-alpha) enhances the activity of the 5-fluorouracil (5-FU) prodrug 5"-deoxy-5-fluorouridine (5"-dFUrd) in colorectal cancer cells in vitro by upregulating the enzyme pyrimidine nucleoside phosphorylase (PNPase), which is responsible for converting 5"-dFUrd to 5-FU. Fluorouracil 58-72 polyribonucleotide nucleotidyltransferase 1 Mus musculus 187-222 7880618-1 1994 Interferon-alpha (IFN-alpha) enhances the activity of the 5-fluorouracil (5-FU) prodrug 5"-deoxy-5-fluorouridine (5"-dFUrd) in colorectal cancer cells in vitro by upregulating the enzyme pyrimidine nucleoside phosphorylase (PNPase), which is responsible for converting 5"-dFUrd to 5-FU. Fluorouracil 58-72 polyribonucleotide nucleotidyltransferase 1 Mus musculus 224-230 7880618-1 1994 Interferon-alpha (IFN-alpha) enhances the activity of the 5-fluorouracil (5-FU) prodrug 5"-deoxy-5-fluorouridine (5"-dFUrd) in colorectal cancer cells in vitro by upregulating the enzyme pyrimidine nucleoside phosphorylase (PNPase), which is responsible for converting 5"-dFUrd to 5-FU. Fluorouracil 74-78 polyribonucleotide nucleotidyltransferase 1 Mus musculus 187-222 7880618-1 1994 Interferon-alpha (IFN-alpha) enhances the activity of the 5-fluorouracil (5-FU) prodrug 5"-deoxy-5-fluorouridine (5"-dFUrd) in colorectal cancer cells in vitro by upregulating the enzyme pyrimidine nucleoside phosphorylase (PNPase), which is responsible for converting 5"-dFUrd to 5-FU. Fluorouracil 74-78 polyribonucleotide nucleotidyltransferase 1 Mus musculus 224-230 1831268-6 1991 Bone marrow progenitors obtained from mice 3 days after treatment with 5-fluorouracil responded to a combination of GM-CSF and TGF-beta 1, whereas either factor alone had no effect. Fluorouracil 71-85 transforming growth factor, beta 1 Mus musculus 127-137 7915575-1 1994 To test if the incorporation of 5-fluorouracil (5-FU) and leucovorin in a modified etoposide, doxorubicin, cisplatin (EAP) regimen could diminish its toxicity and improve its efficacy, 18 patients with far-advanced, unresectable gastric cancer, diagnosed at National Taiwan University Hospital between January 1991 and December 1992, were treated with a FAPEL combination chemotherapy. Fluorouracil 32-46 glutamyl aminopeptidase Homo sapiens 118-121 8407987-0 1993 Effects of 5-fluorouracil substitution on the RNA conformation and in vitro translation of thymidylate synthase messenger RNA. Fluorouracil 11-25 thymidylate synthase Oryctolagus cuniculus 91-111 8407987-1 1993 In vitro transcribed thymidylate synthase (TS) mRNA which is 100% substituted with 5-fluorouracil (FUra) was analyzed for changes in mRNA secondary structure, for alterations in translational efficiency, and for evidence of translational miscoding in vitro. Fluorouracil 83-97 thymidylate synthase Oryctolagus cuniculus 43-45 8407987-2 1993 FUra substitution in TS mRNA results in an altered migration pattern in non-denaturing RNA gels and in decreased hyperchromicity in RNA melting temperature studies, consistent with a change in mRNA secondary structure. Fluorouracil 0-4 thymidylate synthase Oryctolagus cuniculus 21-23 8407987-4 1993 Analysis of the in vitro translation product of FUra-substituted TS mRNA by Western immunoblotting, isoelectric focusing, 5-fluoro-2"-deoxyuridine 5"-monophosphate binding, and TS catalytic activity experiments shows no difference compared to control TS mRNA. Fluorouracil 48-52 thymidylate synthase Oryctolagus cuniculus 65-67 8407987-4 1993 Analysis of the in vitro translation product of FUra-substituted TS mRNA by Western immunoblotting, isoelectric focusing, 5-fluoro-2"-deoxyuridine 5"-monophosphate binding, and TS catalytic activity experiments shows no difference compared to control TS mRNA. Fluorouracil 48-52 thymidylate synthase Oryctolagus cuniculus 177-179 8407987-4 1993 Analysis of the in vitro translation product of FUra-substituted TS mRNA by Western immunoblotting, isoelectric focusing, 5-fluoro-2"-deoxyuridine 5"-monophosphate binding, and TS catalytic activity experiments shows no difference compared to control TS mRNA. Fluorouracil 48-52 thymidylate synthase Oryctolagus cuniculus 177-179 8407987-5 1993 We conclude that the in vitro translation products of FUra-substituted and control TS mRNA are identical. Fluorouracil 54-58 thymidylate synthase Oryctolagus cuniculus 83-85 8364921-0 1993 Locus of the interaction among 5-fluorouracil, leucovorin, and interferon-alpha 2a in colon carcinoma cells. Fluorouracil 31-45 interferon alpha 2 Homo sapiens 63-82 8149941-0 1993 Influence of different doses of interferon-alpha-2b on the blood plasma levels of 5-fluorouracil. Fluorouracil 82-96 interferon alpha 2 Homo sapiens 32-51 8514539-3 1993 METHODS AND MATERIALS: IL-1 was administered to C3H/Km mice in combination with fractionated irradiation, or with cyclophosphamide, cisplatin, or 5-fluorouracil (5FU) followed by irradiation. Fluorouracil 146-160 interleukin 1 complex Mus musculus 23-27 8514539-3 1993 METHODS AND MATERIALS: IL-1 was administered to C3H/Km mice in combination with fractionated irradiation, or with cyclophosphamide, cisplatin, or 5-fluorouracil (5FU) followed by irradiation. Fluorouracil 162-165 interleukin 1 complex Mus musculus 23-27 1991681-1 1991 The RIF-1 tumor line contains cells that are resistant to various anti-neoplastic drugs, including 5-fluorouracil (5FU), methotrexate (MTX), adriamycin (ADR), and etoposide (VP16). Fluorouracil 99-113 replication timing regulatory factor 1 Homo sapiens 4-9 1991681-1 1991 The RIF-1 tumor line contains cells that are resistant to various anti-neoplastic drugs, including 5-fluorouracil (5FU), methotrexate (MTX), adriamycin (ADR), and etoposide (VP16). Fluorouracil 115-118 replication timing regulatory factor 1 Homo sapiens 4-9 2011506-0 1991 Direct selection of stabilised yeast URA3 transformants with 5-fluorouracil. Fluorouracil 61-75 orotidine-5'-phosphate decarboxylase Saccharomyces cerevisiae S288C 37-41 1989891-0 1991 Compensatory mechanisms in platelet production: the response of Sl/Sld mice to 5-fluorouracil. Fluorouracil 79-93 mucin 19 Mus musculus 67-70 1989891-3 1991 The platelet recovery in Sl/Sld mice after 5-FU administration contrasted that found in their normal littermates. Fluorouracil 43-47 mucin 19 Mus musculus 28-31 1989891-6 1991 A significant increase in marrow megakaryocyte number and size was observed at days 8 and 11 in both +/+ and Sl/Sld mice after 5-FU administration. Fluorouracil 127-131 mucin 19 Mus musculus 112-115 1989891-8 1991 It is concluded that the already compromised marrow of Sl/Sld mice is able to respond to the damage invoked by 5-FU to produce larger than normal megakaryocytes. Fluorouracil 111-115 mucin 19 Mus musculus 58-61 33946823-7 2021 Application of anti-PrPC antibody with 5-fluorouracil significantly suppressed the CRC progression in a murine xenograft model. Fluorouracil 39-53 prion protein Mus musculus 20-24 33822896-0 2021 Andrographis overcomes 5-fluorouracil associated chemoresistance through inhibition of DKK1 in colorectal cancer. Fluorouracil 23-37 dickkopf WNT signaling pathway inhibitor 1 Homo sapiens 87-91 33822896-7 2021 Among a panel of differentially expressed genes, DKK1 overexpression was a critical event for 5FU resistance. Fluorouracil 94-97 dickkopf WNT signaling pathway inhibitor 1 Homo sapiens 49-53 33822896-8 2021 Moreover, andrographis significantly downregulated 5FU-induced DKK1 overexpression, accompanied with enhanced anti-tumor effects by abrogating downstream Akt-phosphorylation. Fluorouracil 51-54 dickkopf WNT signaling pathway inhibitor 1 Homo sapiens 63-67 33766090-9 2021 RESULTS: IRF8 expression can precisely predict the complete pathological response to monoclonal antibody therapy or to select combinations of chemotherapy such as FAC (fluorouracil, adriamycin, and cytoxan) in ER-negative BC subtypes. Fluorouracil 168-180 epiregulin Homo sapiens 210-212 23307041-10 2013 Moreover, the patients with high FAK only or combined with low JWA had significant benefit from adjuvant fluorouracil-leucovorin-oxaliplatin (FLO) therapy compared with those with surgery alone (P = 0.003); however, the cases with adjuvant fluorouracil-leucovorin-cisplatin (FLP) therapy did not show these effects. Fluorouracil 105-117 protein tyrosine kinase 2 Homo sapiens 33-36 34821902-5 2021 In addition, GA not only ameliorated the damage to hippocampal neurons and mitochondrial structure, but also significantly improved abnormal protein expression of mitochondrial biogenesis related marker PGC-1alpha, and mitochondrial dynamics related markers MFN2, DRP1 and FIS1 in the hippocampi of 5-FU-treated mice. Fluorouracil 299-303 peroxisome proliferative activated receptor, gamma, coactivator 1 alpha Mus musculus 203-213 34821902-5 2021 In addition, GA not only ameliorated the damage to hippocampal neurons and mitochondrial structure, but also significantly improved abnormal protein expression of mitochondrial biogenesis related marker PGC-1alpha, and mitochondrial dynamics related markers MFN2, DRP1 and FIS1 in the hippocampi of 5-FU-treated mice. Fluorouracil 299-303 mitofusin 2 Mus musculus 258-262 34821902-5 2021 In addition, GA not only ameliorated the damage to hippocampal neurons and mitochondrial structure, but also significantly improved abnormal protein expression of mitochondrial biogenesis related marker PGC-1alpha, and mitochondrial dynamics related markers MFN2, DRP1 and FIS1 in the hippocampi of 5-FU-treated mice. Fluorouracil 299-303 fission, mitochondrial 1 Mus musculus 273-277 34821902-6 2021 Moreover, GA could up-regulate the expression of neuronal survival and growth-related proteins, such as BDNF, p-ERK, p-CREB, p-Akt, p-GSK3beta, Nrf2, p-mTOR, and p-S6, in the hippocampi of 5-FU-treated mice. Fluorouracil 189-193 glycogen synthase kinase 3 alpha Mus musculus 134-142 34844630-0 2021 Long noncoding RNA CRART16 confers 5-FU resistance in colorectal cancer cells by sponging miR-193b-5p. Fluorouracil 35-39 microRNA 193b Homo sapiens 90-98 34844630-14 2021 In addition, CRART16 promoted 5-FU resistance by suppressing the expression of miR-193b-5p. Fluorouracil 30-34 microRNA 193b Homo sapiens 79-87 34844630-16 2021 CONCLUSIONS: CRART16 confers 5-FU resistance in CRC cells through the CRART16/miR-193b-5p/HMGA2/MAPK pathway. Fluorouracil 29-33 microRNA 193b Homo sapiens 78-86 34843983-0 2022 Vesicular IFN-gamma as a cooperative attacker to enhance anti-cancer effect of 5-fluorouracil via thymidine phosphorylase upregulation and tumor microenvironment normalization. Fluorouracil 79-93 thymidine phosphorylase Homo sapiens 98-121 34843983-1 2022 On the basis of immuno-modulating effect and upregulating the activity of thymidine phosphorylase (TP), interferon-gamma (IFN-gamma) as a cooperative attacker was explored to enhance the anticancer activity of 5-FU. Fluorouracil 210-214 thymidine phosphorylase Homo sapiens 74-97 34843983-1 2022 On the basis of immuno-modulating effect and upregulating the activity of thymidine phosphorylase (TP), interferon-gamma (IFN-gamma) as a cooperative attacker was explored to enhance the anticancer activity of 5-FU. Fluorouracil 210-214 thymidine phosphorylase Homo sapiens 99-101 34843983-3 2022 The IFN-gamma-EDP vesicles allowed IFN-gamma to accumulate at the tumor site and be taken up by tumor cells, resulting in significantly upregulated expression level of TP, distinct inhibition of cell growth, more cellular apoptosis and more serious cell cycle arrest when administrated combined with 5-FU. Fluorouracil 300-304 thymidine phosphorylase Homo sapiens 168-170 34596215-9 2021 These findings showed that JNK/ERK signaling pathway is involved in miR-20b-5p/SDC2 axis-mediated 5-FU resistance in SW480/5-FU cells, indicating that the miR-20b-5p/SDC2 axis is a potential target for reversing 5-FU resistance in CRC. Fluorouracil 98-102 microRNA 20b Homo sapiens 68-75 34596215-9 2021 These findings showed that JNK/ERK signaling pathway is involved in miR-20b-5p/SDC2 axis-mediated 5-FU resistance in SW480/5-FU cells, indicating that the miR-20b-5p/SDC2 axis is a potential target for reversing 5-FU resistance in CRC. Fluorouracil 98-102 microRNA 20b Homo sapiens 155-162 34596215-9 2021 These findings showed that JNK/ERK signaling pathway is involved in miR-20b-5p/SDC2 axis-mediated 5-FU resistance in SW480/5-FU cells, indicating that the miR-20b-5p/SDC2 axis is a potential target for reversing 5-FU resistance in CRC. Fluorouracil 123-127 microRNA 20b Homo sapiens 68-75 34596215-9 2021 These findings showed that JNK/ERK signaling pathway is involved in miR-20b-5p/SDC2 axis-mediated 5-FU resistance in SW480/5-FU cells, indicating that the miR-20b-5p/SDC2 axis is a potential target for reversing 5-FU resistance in CRC. Fluorouracil 123-127 microRNA 20b Homo sapiens 155-162 34596215-9 2021 These findings showed that JNK/ERK signaling pathway is involved in miR-20b-5p/SDC2 axis-mediated 5-FU resistance in SW480/5-FU cells, indicating that the miR-20b-5p/SDC2 axis is a potential target for reversing 5-FU resistance in CRC. Fluorouracil 212-216 microRNA 20b Homo sapiens 68-75 34596215-9 2021 These findings showed that JNK/ERK signaling pathway is involved in miR-20b-5p/SDC2 axis-mediated 5-FU resistance in SW480/5-FU cells, indicating that the miR-20b-5p/SDC2 axis is a potential target for reversing 5-FU resistance in CRC. Fluorouracil 212-216 microRNA 20b Homo sapiens 155-162 34605863-0 2021 Exosomal lncRNA FOXD3-AS1 upregulates ELAVL1 expression and activates PI3K/Akt pathway to enhance lung cancer cell proliferation, invasion, and 5-fluorouracil resistance. Fluorouracil 144-158 prostaglandin D2 receptor Homo sapiens 22-25 34605863-1 2021 Long non-coding RNA (lncRNA) FOXD3-AS1 expression is upregulated in lung cancer; however, its effect and mechanism on 5-fluorouracil (5-FU) resistance remain unclear. Fluorouracil 118-132 prostaglandin D2 receptor Homo sapiens 35-38 34605863-1 2021 Long non-coding RNA (lncRNA) FOXD3-AS1 expression is upregulated in lung cancer; however, its effect and mechanism on 5-fluorouracil (5-FU) resistance remain unclear. Fluorouracil 134-138 prostaglandin D2 receptor Homo sapiens 35-38 34718327-9 2021 Referring to the data from GEO dataset we verified GPER activation restored ERK1/2 activity in CIM and 5-fluorouracil-treated IEC-6 cells. Fluorouracil 103-117 mitogen activated protein kinase 3 Rattus norvegicus 76-82 34414684-10 2021 Single-cell analysis showed that cell clusters with low expression of CK8/18 and ITGB4 were more sensitive to 5FU and radiotherapy (RT). Fluorouracil 110-113 integrin subunit beta 4 Homo sapiens 81-86 34261152-7 2021 We showed that WNT5A, MDR1, and DKK1 mRNA expression levels were down-regulated in the allicin- and allicin/5-FU-treated cells. Fluorouracil 108-112 dickkopf WNT signaling pathway inhibitor 1 Homo sapiens 32-36 34391754-5 2021 In tumor tissues of groups that received 5-FU and andrographolide sulfonate, CD4+ and CD8+ T cell infiltration was increased, and the expression of IFN-gamma and Granzyme B detected by immunohistochemistry and qPCR was upregulated, reflecting improved antitumor immunity. Fluorouracil 41-45 granzyme B Mus musculus 162-172 34533177-5 2021 Herein, theranostic Ag2S quantum dots (AS-2MPA) optically trackable in near-infrared (NIR), conjugated with endothelial growth factor receptor (EGFR) targeting Cetuximab (Cet) and loaded with ALA for PDT monotherapy or ALA/5-fluorouracil (5FU) for the combination therapy are proposed for enhanced treatment of EGFR(+) CRC. Fluorouracil 223-237 angiotensin II receptor type 1 Homo sapiens 20-24 34533177-5 2021 Herein, theranostic Ag2S quantum dots (AS-2MPA) optically trackable in near-infrared (NIR), conjugated with endothelial growth factor receptor (EGFR) targeting Cetuximab (Cet) and loaded with ALA for PDT monotherapy or ALA/5-fluorouracil (5FU) for the combination therapy are proposed for enhanced treatment of EGFR(+) CRC. Fluorouracil 239-242 angiotensin II receptor type 1 Homo sapiens 20-24 34659884-14 2021 These results indicated that leptin mediated 5-FU resistance through YAP-dependent AXL overexpression in CRC. Fluorouracil 45-49 Yes1 associated transcriptional regulator Homo sapiens 69-72 2616741-1 1989 The RIF-1 tumor cell line contains a small number of cells (1-20 per 10(6) cells) that are resistant to various single antineoplastic drugs, including 5-fluorouracil (5FU), methotrexate (MTX), and adriamycin (ADR). Fluorouracil 151-165 replication timing regulatory factor 1 Homo sapiens 4-9 8317894-5 1993 Moreover, when TAT was used in combination with 5-FU, the accumulative effect was significantly increased. Fluorouracil 48-52 tyrosine aminotransferase Homo sapiens 15-18 2616741-1 1989 The RIF-1 tumor cell line contains a small number of cells (1-20 per 10(6) cells) that are resistant to various single antineoplastic drugs, including 5-fluorouracil (5FU), methotrexate (MTX), and adriamycin (ADR). Fluorouracil 167-170 replication timing regulatory factor 1 Homo sapiens 4-9 2587004-0 1989 Phase II trial of combination chemotherapy with fluorouracil (F), doxorubicin (A), and cisplatin (P) (Fap) in hormonally resistant metastatic prostatic adenocarcinoma. Fluorouracil 48-60 fibroblast activation protein alpha Homo sapiens 102-105 3167226-3 1988 To determine whether they are clonal, we examined the phosphoglycerate kinase-1 (PGK-1) isozyme type of colonies originally grown from spleen cells of 5-FU-treated mice which had PGK-1 isozyme mosaicism. Fluorouracil 151-155 phosphoglycerate kinase 1 Mus musculus 81-86 3167226-3 1988 To determine whether they are clonal, we examined the phosphoglycerate kinase-1 (PGK-1) isozyme type of colonies originally grown from spleen cells of 5-FU-treated mice which had PGK-1 isozyme mosaicism. Fluorouracil 151-155 phosphoglycerate kinase 1 Mus musculus 179-184 2944475-5 1986 Effectiveness of chemotherapy with L-PAM was antagonized by treatment in combination with 5-FU. Fluorouracil 90-94 peptidylglycine alpha-amidating monooxygenase Mus musculus 37-40 2418161-1 1985 Mouse interferon, or human hybrid recombinant interferon alpha A/D, administered during the 2 day period following the administration of a toxic dose of 5-fluorouracil (FUra), yielded significant protection from body weight loss, leukopenia, and mortality in Balb/c X DBA/8 F1 mice. Fluorouracil 153-167 interferon alpha 2 Homo sapiens 46-66 2418161-1 1985 Mouse interferon, or human hybrid recombinant interferon alpha A/D, administered during the 2 day period following the administration of a toxic dose of 5-fluorouracil (FUra), yielded significant protection from body weight loss, leukopenia, and mortality in Balb/c X DBA/8 F1 mice. Fluorouracil 169-173 interferon alpha 2 Homo sapiens 46-66 7419607-2 1980 Uracil and 5-fluorouracil shared a saturable transport system (Km = 5 to 15 mM) capable of rapid equilibration of these substrates across the cell membrane (t 1/2 at 25 degrees in first-order range of concentration = 25 to 58 sec). Fluorouracil 11-25 interleukin 1 receptor like 1 Homo sapiens 157-168 33907844-0 2021 Vanillin downregulates NNMT and attenuates NNMT-related resistance to 5-fluorouracil via ROS-induced cell apoptosis in colorectal cancer cells. Fluorouracil 70-84 nicotinamide N-methyltransferase Homo sapiens 43-47 33907844-3 2021 It has been reported that NNMT inhibits apoptosis and enhances resistance to 5-fluorouracil (5-Fu) via inhibition of the apoptosis signal regulating kinase 1 (ASK1)-p38 MAPK pathway in CRC cells. Fluorouracil 77-91 nicotinamide N-methyltransferase Homo sapiens 26-30 33907844-3 2021 It has been reported that NNMT inhibits apoptosis and enhances resistance to 5-fluorouracil (5-Fu) via inhibition of the apoptosis signal regulating kinase 1 (ASK1)-p38 MAPK pathway in CRC cells. Fluorouracil 93-97 nicotinamide N-methyltransferase Homo sapiens 26-30 33907844-5 2021 The aim of the present study was to explore the effect of vanillin on promoting apoptosis and attenuating NNMT-induced resistance to 5-Fu in CRC. Fluorouracil 133-137 nicotinamide N-methyltransferase Homo sapiens 106-110 33907844-9 2021 Vanillin was able to reverse NNMT-induced increased cell proliferation, decreased cell apoptosis and resistance to 5-Fu by inhibiting NNMT expression. Fluorouracil 115-119 nicotinamide N-methyltransferase Homo sapiens 29-33 33907844-9 2021 Vanillin was able to reverse NNMT-induced increased cell proliferation, decreased cell apoptosis and resistance to 5-Fu by inhibiting NNMT expression. Fluorouracil 115-119 nicotinamide N-methyltransferase Homo sapiens 134-138 33907844-13 2021 Considering that vanillin is an important flavor and aromatic component used in foods worldwide, vanillin is deemed to be a promising anticancer candidate by inhibiting NNMT and may attenuate NNMT-induced resistance to 5-Fu in human CRC therapy with few side effects. Fluorouracil 219-223 nicotinamide N-methyltransferase Homo sapiens 192-196 33727040-0 2021 Yes associated protein 1 promotes resistance to 5-fluorouracil in gastric cancer by regulating GLUT3-dependent glycometabolism reprogramming of tumor-associated macrophages. Fluorouracil 48-62 Yes1 associated transcriptional regulator Homo sapiens 0-24 33727040-6 2021 Meanwhile, polarized M2 macrophages enhance 5-FU resistance in tumor cells by secreting CCL8 and activating phosphorylation of JAK1/STAT3 signaling pathway. Fluorouracil 44-48 C-C motif chemokine ligand 8 Homo sapiens 88-92 33526512-9 2021 Both loss of PSAT1 and removal of serine from the diet were necessary to suppress CRC xenograft growth and enhance the anti-tumor activity of 5-fluorouracil (5-FU). Fluorouracil 142-156 phosphoserine aminotransferase 1 Homo sapiens 13-18 33907880-9 2021 SELENBP1 knockdown enhances resistance of OSCC cells to 5-FU and cisplatin, while SENENBP1 overexpression displays the opposite effects. Fluorouracil 56-60 selenium binding protein 1 Homo sapiens 0-8 33954114-4 2021 Modulation of expression levels of microRNAs or long non-coding RNAs may be a suitable approach to sensitize tumor cells to 5-FU treatment via modulating multiple biological signaling pathways such as Hippo/YAP, Wnt/beta-catenin, Hedgehog, NF-kB, and Notch cascades. Fluorouracil 124-128 Yes1 associated transcriptional regulator Homo sapiens 207-210 33874986-5 2021 5"-deoxy-5-fluorocytidine (5"-DFCR) is a cytidine analogue (metabolite of capecitabine), which is converted by CDA and subsequently by TYMP into 5-fluorouracil, a chemotherapeutic agent frequently used to treat solid tumors. Fluorouracil 145-159 cytidine deaminase Homo sapiens 111-114 33874986-5 2021 5"-deoxy-5-fluorocytidine (5"-DFCR) is a cytidine analogue (metabolite of capecitabine), which is converted by CDA and subsequently by TYMP into 5-fluorouracil, a chemotherapeutic agent frequently used to treat solid tumors. Fluorouracil 145-159 thymidine phosphorylase Homo sapiens 135-139 32189577-2 2021 Among these compounds A2, A4, A11 and A14 possessed high inhibition activity against A-549 cell lines with IC50 values at 4.91, 3.22, 27.43 and 18.14 muM, respectively, better than that of 5-fluorouracil (IC50=59.27 muM). Fluorouracil 189-203 immunoglobulin kappa variable 6D-41 (non-functional) Homo sapiens 38-41 8517649-0 1993 Interferon beta increases antitumor activity of 5-fluorouracil against human colon carcinoma cells in vitro and in vivo. Fluorouracil 48-62 interferon beta 1 Homo sapiens 0-15 8517649-1 1993 The modulating effect of human fibroblast-derived interferon beta (IFN-beta) on the antitumor effect of 5-fluorouracil (5-FU) against human colon carcinoma cells in vitro and in vivo was investigated. Fluorouracil 104-118 interferon beta 1 Homo sapiens 50-65 8517649-1 1993 The modulating effect of human fibroblast-derived interferon beta (IFN-beta) on the antitumor effect of 5-fluorouracil (5-FU) against human colon carcinoma cells in vitro and in vivo was investigated. Fluorouracil 104-118 interferon beta 1 Homo sapiens 67-75 8517649-1 1993 The modulating effect of human fibroblast-derived interferon beta (IFN-beta) on the antitumor effect of 5-fluorouracil (5-FU) against human colon carcinoma cells in vitro and in vivo was investigated. Fluorouracil 120-124 interferon beta 1 Homo sapiens 50-65 8517649-1 1993 The modulating effect of human fibroblast-derived interferon beta (IFN-beta) on the antitumor effect of 5-fluorouracil (5-FU) against human colon carcinoma cells in vitro and in vivo was investigated. Fluorouracil 120-124 interferon beta 1 Homo sapiens 67-75 33883985-5 2021 Tranilast alone or in combination with 5-FU inhibited tumor growth and was associated with a reduction of TGF-beta expression and CD31 positive endothelial cells. Fluorouracil 39-43 transforming growth factor alpha Homo sapiens 106-114 8395907-0 1993 Temporal changes in ACTH, cortisol and IAP in rats under immunochemotherapy with 5-FU and Krestine. Fluorouracil 81-85 Cd47 molecule Rattus norvegicus 39-42 8395907-4 1993 Our results indicated that 1) in the non-cancer-bearing rats, 5-FU administration led to an increase in serum cortisol and IAP, however, PSK concurrent administration clearly lowered the levels of cortisol and IAP; 2) in the cancer-bearing rats, the levels of ACTH, cortisol and IAP increased as the cancer progressed, but in the immunothemotherapy administration groups these levels were lower; 3) the immunothemotherapy administration group had greater effects on both tumor growth and liver metastasis. Fluorouracil 62-66 Cd47 molecule Rattus norvegicus 123-126 8427959-5 1993 Similarly, in vitro treatment with IL-1 of bone marrow cells isolated from 5-fluorouracil-treated mice results in elevated levels of MnSOD RNA. Fluorouracil 75-89 interleukin 1 complex Mus musculus 35-39 33883985-5 2021 Tranilast alone or in combination with 5-FU inhibited tumor growth and was associated with a reduction of TGF-beta expression and CD31 positive endothelial cells. Fluorouracil 39-43 platelet and endothelial cell adhesion molecule 1 Homo sapiens 130-134 33423358-4 2021 We first clarified the relationship between KHDRBS3 and 5-FU resistance. Fluorouracil 56-60 KH RNA binding domain containing, signal transduction associated 3 Homo sapiens 44-51 33662636-10 2021 In addition, ZFX expression was negatively correlated with the sensitivity of fresh ESCC tissues to chemotherapeutic drugs, including cisplatin, docetaxel, fluorouracil, and irinotecan. Fluorouracil 156-168 zinc finger protein X-linked Homo sapiens 13-16 8179244-7 1993 In carcinoid syndromes whether treated priorly or not with a 5-fluoro-uracil-streptozoticin combination, INF-alpha leads to an objective response in two-thirds of the patients. Fluorouracil 61-76 interferon alpha 17 Homo sapiens 105-114 8398300-2 1993 5-Fluorouracil (5-FU) activity has been improved by the use of leucovorin (LV) or alpha-2a interferon (alpha-IF). Fluorouracil 0-14 interferon alpha 2 Homo sapiens 82-101 8398300-2 1993 5-Fluorouracil (5-FU) activity has been improved by the use of leucovorin (LV) or alpha-2a interferon (alpha-IF). Fluorouracil 0-14 interferon alpha 2 Homo sapiens 103-111 8398300-2 1993 5-Fluorouracil (5-FU) activity has been improved by the use of leucovorin (LV) or alpha-2a interferon (alpha-IF). Fluorouracil 16-20 interferon alpha 2 Homo sapiens 82-101 8398300-2 1993 5-Fluorouracil (5-FU) activity has been improved by the use of leucovorin (LV) or alpha-2a interferon (alpha-IF). Fluorouracil 16-20 interferon alpha 2 Homo sapiens 103-111 1433371-0 1992 Decreased catabolism of fluorouracil in peripheral blood mononuclear cells during combination therapy with fluorouracil, leucovorin, and interferon alpha-2a. Fluorouracil 24-36 interferon alpha 2 Homo sapiens 137-156 1433371-1 1992 BACKGROUND: We previously reported that recombinant interferon alpha-2a (IFN alpha-2a) therapy was associated with a dose-dependent decrease in fluorouracil (5-FU) clearance. Fluorouracil 144-156 interferon alpha 2 Homo sapiens 52-71 1433371-1 1992 BACKGROUND: We previously reported that recombinant interferon alpha-2a (IFN alpha-2a) therapy was associated with a dose-dependent decrease in fluorouracil (5-FU) clearance. Fluorouracil 158-162 interferon alpha 2 Homo sapiens 52-71 33452458-12 2021 GC cells treated with siNOTCH3, siPHLDB2, miR-491-5p, miR-875-5p, were more sensitive to Cisplatin and 5-FU. Fluorouracil 103-107 microRNA 491 Homo sapiens 42-49 33599179-0 2021 JAK2/STAT3 inhibitor reduced 5-FU resistance and autophagy through ATF6-mediated ER stress. Fluorouracil 29-33 Janus kinase 2 Homo sapiens 0-4 33599179-3 2021 The mechanisms of action of JAK2/STAT3 pathway were investigated in AGS cells with drug resistance of 5-fluorouracil (5-FU) by corresponding inhibitors. Fluorouracil 102-116 Janus kinase 2 Homo sapiens 28-32 33599179-3 2021 The mechanisms of action of JAK2/STAT3 pathway were investigated in AGS cells with drug resistance of 5-fluorouracil (5-FU) by corresponding inhibitors. Fluorouracil 118-122 Janus kinase 2 Homo sapiens 28-32 33599179-11 2021 These findings indicated that the involvement of JAK2/STAT3 pathway in regulating ER stress affected the 5-FU resistance of AGS cells and autophagy, which was mediated by ATF6. Fluorouracil 105-109 Janus kinase 2 Homo sapiens 49-53 33599179-12 2021 Targeting JAK2/STAT3 pathway could be a potential approach to decrease the 5-FU resistance of gastric cancer and enhance the sensitivity of gastric cancer to 5-FU. Fluorouracil 75-79 Janus kinase 2 Homo sapiens 10-14 33599179-12 2021 Targeting JAK2/STAT3 pathway could be a potential approach to decrease the 5-FU resistance of gastric cancer and enhance the sensitivity of gastric cancer to 5-FU. Fluorouracil 158-162 Janus kinase 2 Homo sapiens 10-14 33408861-6 2021 Overexpression of CEA and PDGF was noted in the carcinogenic group, while expression of CEA and PDGF in the prophylactic, vitamin D and indomethacin and 5-FU groups were markedly reduced. Fluorouracil 153-157 CEA cell adhesion molecule 20 Rattus norvegicus 88-91 33486902-12 2021 Signal transduction pathway analysis showed that after Bel-7402 cells acquired resistance to 5-Fu, CCND1, MCM2, and MCM3 gene expression was upregulated in the G1 to S cell cycle control signal transduction pathway, CDKN1C and CCNG2 gene expression was downregulated, and MCM2 and MCM3 gene expression was upregulated in the DNA replication signal transduction pathway. Fluorouracil 93-97 cyclin D1 Homo sapiens 99-104 33486902-12 2021 Signal transduction pathway analysis showed that after Bel-7402 cells acquired resistance to 5-Fu, CCND1, MCM2, and MCM3 gene expression was upregulated in the G1 to S cell cycle control signal transduction pathway, CDKN1C and CCNG2 gene expression was downregulated, and MCM2 and MCM3 gene expression was upregulated in the DNA replication signal transduction pathway. Fluorouracil 93-97 minichromosome maintenance complex component 3 Homo sapiens 116-120 33486902-12 2021 Signal transduction pathway analysis showed that after Bel-7402 cells acquired resistance to 5-Fu, CCND1, MCM2, and MCM3 gene expression was upregulated in the G1 to S cell cycle control signal transduction pathway, CDKN1C and CCNG2 gene expression was downregulated, and MCM2 and MCM3 gene expression was upregulated in the DNA replication signal transduction pathway. Fluorouracil 93-97 cyclin G2 Homo sapiens 227-232 33486902-12 2021 Signal transduction pathway analysis showed that after Bel-7402 cells acquired resistance to 5-Fu, CCND1, MCM2, and MCM3 gene expression was upregulated in the G1 to S cell cycle control signal transduction pathway, CDKN1C and CCNG2 gene expression was downregulated, and MCM2 and MCM3 gene expression was upregulated in the DNA replication signal transduction pathway. Fluorouracil 93-97 minichromosome maintenance complex component 3 Homo sapiens 281-285 33039558-6 2021 STAG3 knockdown inhibited cell migration and increased drug sensitivity to oxaliplatin, 5-fluorouracil, irinotecan hydrochloride hydrate, and BRAF inhibitor in CRC cell lines. Fluorouracil 88-102 stromal antigen 3 Homo sapiens 0-5 33536745-0 2021 CircNRIP1 Modulates the miR-515-5p/IL-25 Axis to Control 5-Fu and Cisplatin Resistance in Nasopharyngeal Carcinoma. Fluorouracil 57-61 nuclear receptor interacting protein 1 Homo sapiens 0-9 33536745-8 2021 We further found that 5-Fu and CDDP IC50 values in NPC cells in which circNRIP1 had been knocked down were restored following miR-515-5p inhibitor transfection. Fluorouracil 22-26 nuclear receptor interacting protein 1 Homo sapiens 70-79 33500399-5 2021 Moreover, 4DPG boosts the tumor-suppressor protein, checkpoint kinase 2 (Chk2) via phosphorylation at Thr68 in a dose-dependent manner in 5-FU-R cells. Fluorouracil 138-142 checkpoint kinase 2 Homo sapiens 52-71 33500399-5 2021 Moreover, 4DPG boosts the tumor-suppressor protein, checkpoint kinase 2 (Chk2) via phosphorylation at Thr68 in a dose-dependent manner in 5-FU-R cells. Fluorouracil 138-142 checkpoint kinase 2 Homo sapiens 73-77 33420580-0 2021 Babao Dan () Alleviates 5-Fluorouracil-Induced Intestinal Damage via Wnt/beta-Catenin Pathway. Fluorouracil 24-38 wingless-type MMTV integration site family, member 3 Mus musculus 69-72 33420580-15 2021 CONCLUSIONS: BBD attenuates the adverse effects induced by 5-FU via Wnt/beta-catenin pathway, suggesting it may act as a potential agent against chemotherapy-induced intestinal mucositis. Fluorouracil 59-63 wingless-type MMTV integration site family, member 3 Mus musculus 68-71 33419031-8 2021 Furthermore, ALDH1B1-overexpressing HT29 cells exhibited enhanced resistance against doxorubicin, fluorouracil (5-FU) and etoposide. Fluorouracil 98-110 aldehyde dehydrogenase 1 family member B1 Homo sapiens 13-20 33419031-8 2021 Furthermore, ALDH1B1-overexpressing HT29 cells exhibited enhanced resistance against doxorubicin, fluorouracil (5-FU) and etoposide. Fluorouracil 112-116 aldehyde dehydrogenase 1 family member B1 Homo sapiens 13-20 33500737-11 2021 Notably, targeted therapy via the co-delivery of 5-FU and miR-34a(m) by TCP1-CD-QD nanocarriers significantly inhibited the growth of PDX tumors. Fluorouracil 49-53 t-complex 1 Homo sapiens 72-76 33349222-11 2021 The optimized formulation (5-FU-PLGA-PEG-NP) was lyophilized using 4% trehalose (cryoprotectants) & conjugated with Anti-EGFR mAb on its surface to produce Anti-EGFR-5-FU-PLGA-PEG-NP; the final formulation, which increases target specificity and drug delivery system of nanoparticles. Fluorouracil 27-31 C-type lectin domain containing 14A Homo sapiens 161-167 33311453-0 2020 Inhibition of EZH2 enhances the therapeutic effect of 5-FU via PUMA upregulation in colorectal cancer. Fluorouracil 54-58 BCL2 binding component 3 Homo sapiens 63-67 33335403-6 2020 The expression of some apoptotic and autophagy-related genes such as Bax, Bcl2, Beclin1 and ATG7 was significantly induced by carbon-ion beam irradiation alone and was further enhanced when the beam was combined with 5-FU. Fluorouracil 217-221 autophagy related 7 Homo sapiens 92-96 33335403-7 2020 The spheroid forming capacity of CD133+ cell subpopulations was significantly inhibited by carbon-ion beam in combination with 5-FU. Fluorouracil 127-131 prominin 1 Homo sapiens 33-38 33109719-5 2020 Meanwhile, treatment with 5-fluorouracil (5-FU) could increase PD-1 expression by inhibiting the transcription of KLHL22. Fluorouracil 26-40 kelch like family member 22 Homo sapiens 114-120 33109719-5 2020 Meanwhile, treatment with 5-fluorouracil (5-FU) could increase PD-1 expression by inhibiting the transcription of KLHL22. Fluorouracil 42-46 kelch like family member 22 Homo sapiens 114-120 33109719-6 2020 These findings reveal that KLHL22 plays a crucial role in preventing excessive T cell suppression by maintaining PD-1 expression homeostasis and suggest the therapeutic potential of 5-FU in combination with anti-PD-1 in colorectal cancer patients. Fluorouracil 182-186 kelch like family member 22 Homo sapiens 27-33 32388677-4 2020 Mechanistically, in the GC cells under the 5-FU treatment, reactive oxygen species is accumulated and then induces the activation of HIF1alpha signaling to drive the expression of high-mobility group box 1, which leads to more macrophage"s infiltration into GC tumor. Fluorouracil 43-47 high mobility group box 1 Homo sapiens 180-205 32669374-4 2020 Patients and Methods We performed a single-arm, open-label, phase I/II study of the PARP inhibitor, veliparib, with 5-fluorouracil (no 5FU bolus) and oxaliplatin (FOLFOX) for patients with metastatic PDAC. Fluorouracil 116-130 collagen type XI alpha 2 chain Homo sapiens 84-88 33165366-14 2020 Overexpression of ATOH8 increases chemosensitivity to 5-FU, which is probably caused by inhibiting the phosphorylation of AKT (Ser473). Fluorouracil 54-58 atonal bHLH transcription factor 8 Mus musculus 18-23 33165433-6 2020 Further, the FAK RNAi cells became more sensitive to chemotherapeutic drugs such as 5-FU and docetaxel and therefore the rate of cell survival is declined. Fluorouracil 84-88 protein tyrosine kinase 2 Homo sapiens 13-16 32945504-7 2020 We also found that combined treatment of Rg3 and 5-FU significantly enhanced the apoptosis of colon cancer cells by activating the Apaf1/caspase 9/caspase 3 pathway and arrested the cell cycle of the colon cancer cells in G0/G1 by promoting the expression of Cyclin D1, CDK2 and CDK4. Fluorouracil 49-53 cyclin D1 Homo sapiens 259-268 32895407-8 2020 Moreover, the cross-talk between ROCK/ NF-kappaB, ROS/COX-2/TXA2, Akt/eNOS and ET-1/ERK1/2 pathways contributes via different means to upsetting the vasoconstriction/vasodilatation equilibrium as well as endothelial cell function and finally leads to cardiomyocyte stress and death-the modulation of these trajectories offers simvastatin its potential cardio-protection against 5-FU. Fluorouracil 378-382 cytochrome c oxidase II, mitochondrial Rattus norvegicus 54-59 32895407-8 2020 Moreover, the cross-talk between ROCK/ NF-kappaB, ROS/COX-2/TXA2, Akt/eNOS and ET-1/ERK1/2 pathways contributes via different means to upsetting the vasoconstriction/vasodilatation equilibrium as well as endothelial cell function and finally leads to cardiomyocyte stress and death-the modulation of these trajectories offers simvastatin its potential cardio-protection against 5-FU. Fluorouracil 378-382 mitogen activated protein kinase 3 Rattus norvegicus 84-90 32996748-4 2020 RESULTS: Serum levels of miR-205 and -375 are associated with the response of luminal A tumors and miR-205 and -21 with the response of luminal B tumors to neoadjuvant polychemotherapy in fluorouracil + doxorubicin + cyclophosphamide and doxorubicin + cyclophosphamide regimens. Fluorouracil 188-200 microRNA 205 Homo sapiens 99-106 32872257-0 2020 Synergistic Interactions of 5-Fluorouracil with Inhibitors of Protein Kinase CK2 Correlate with p38 MAPK Activation and FAK Inhibition in the Triple-Negative Breast Cancer Cell Line. Fluorouracil 28-42 protein tyrosine kinase 2 Homo sapiens 120-123 32872257-7 2020 We conclude that the synergistic interactions (CI < 1) observed for both the combinations of 5-FU and 14B or CX-4945 in MDA-MB-231 correlated with an activation of p38 MAPK, inhibition of FAK, increased expression of apoptogenic markers, prolongation of S-phase of cell cycle, and destabilization of actin network. Fluorouracil 93-97 protein tyrosine kinase 2 Homo sapiens 188-191 32833164-10 2021 Experiments using mouse ACTH-producing pituitary tumor AtT20 cells demonstrated that treatment with 5-fluorouracil in combination with temozolomide had an additive effect in reducing cell viability and ACTH production in the culture medium. Fluorouracil 100-114 pro-opiomelanocortin-alpha Mus musculus 24-28 32833164-10 2021 Experiments using mouse ACTH-producing pituitary tumor AtT20 cells demonstrated that treatment with 5-fluorouracil in combination with temozolomide had an additive effect in reducing cell viability and ACTH production in the culture medium. Fluorouracil 100-114 pro-opiomelanocortin-alpha Mus musculus 202-206 32367570-12 2020 Moreover, when glycolysis was inhibited by 2-deoxyglucose, the roles of NNMT on 5-FU sensitivity was weakened. Fluorouracil 80-84 nicotinamide N-methyltransferase Homo sapiens 72-76 32367570-13 2020 In vivo experiments showed that NNMT knockdown significantly increased the sensitivity of xenografts to 5-FU and suppressed the Warburg effect. Fluorouracil 104-108 nicotinamide N-methyltransferase Homo sapiens 32-36 32367570-14 2020 Overall, these results demonstrated that NNMT decreases 5-FU sensitivity in human ESCC cells through promoting the Warburg effect, suggesting that NNMT may contribute to predict the treatment effects of the clinical chemotherapy in ESCC. Fluorouracil 56-60 nicotinamide N-methyltransferase Homo sapiens 41-45 32367570-14 2020 Overall, these results demonstrated that NNMT decreases 5-FU sensitivity in human ESCC cells through promoting the Warburg effect, suggesting that NNMT may contribute to predict the treatment effects of the clinical chemotherapy in ESCC. Fluorouracil 56-60 nicotinamide N-methyltransferase Homo sapiens 147-151 32801774-0 2020 lncRNA UCA1 Contributes to 5-Fluorouracil Resistance of Colorectal Cancer Cells Through miR-23b-3p/ZNF281 Axis. Fluorouracil 27-41 urothelial cancer associated 1 Homo sapiens 7-11 32801774-8 2020 Murine xenograft model was established to verify the role of UCA1 on the 5-FU resistance of CRC in vivo. Fluorouracil 73-77 urothelial cancer associated 1 Homo sapiens 61-65 32801774-9 2020 Results: The 5-FU resistance of CRC was positively related to the level of UCA1 and autophagy. Fluorouracil 13-17 urothelial cancer associated 1 Homo sapiens 75-79 32801774-10 2020 UCA1 accelerated the 5-FU resistance of CRC cells through facilitating autophagy and suppressing apoptosis. Fluorouracil 21-25 urothelial cancer associated 1 Homo sapiens 0-4 32801774-12 2020 The knockdown of miR-23b-3p reversed the inhibitory effects of UCA1 interference on the 5-FU resistance and autophagy and the promoting impact on the apoptosis of CRC cells. Fluorouracil 88-92 urothelial cancer associated 1 Homo sapiens 63-67 32801774-15 2020 UCA1 interference enhanced the 5-FU sensitivity of CRC through miR-23b-3p/ZNF281 axis in vivo. Fluorouracil 31-35 urothelial cancer associated 1 Homo sapiens 0-4 32801774-16 2020 Conclusion: UCA1 mediated 5-FU resistance of CRC cells through facilitating autophagy and inhibiting apoptosis via miR-23b-3p/ZNF281 axis in vivo and in vitro. Fluorouracil 26-30 urothelial cancer associated 1 Homo sapiens 12-16 32546724-0 2020 SphK2 confers 5-fluorouracil resistance to colorectal cancer via upregulating H3K56ac-mediated DPD expression. Fluorouracil 14-28 sphingosine kinase 2 Mus musculus 0-5 1417007-1 1992 Potentiation of cytotoxic effects of 5-fluorouracil (5-FU) were investigated by simultaneous or sequential combination of l-leucovorin (LV) against human esophageal cancer cell line (TE-1, TE-2) and 23 human clinical cancer samples in vitro. Fluorouracil 37-51 N-alpha-acetyltransferase 10, NatA catalytic subunit Homo sapiens 189-193 1511393-5 1992 Recent efforts in the management of patients with advanced disease have been directed at optimizing the activity of 5-FU by (1) enhancing the inhibition of DNA synthesis through the concomitant administration of folinic acid; (2) increasing drug incorporation into RNA through pretreatment with methotrexate or phosphonacetyl-L-aspartate; and (3) improving the drug"s activity through the synergistic action of alpha-2a-interferon. Fluorouracil 116-120 interferon alpha 2 Homo sapiens 411-430 1703493-9 1991 When sorted WGA+Lin- spleen cells of the 5-FU-treated mice were cultured in vitro in the presence of recombinant interleukin 3 (IL-3), interleukin 6 (IL-6), and granulocyte colony-stimulating factor (G-CSF), colony formation was observed only in wells with IL-3, whereas unfractionated spleen cells formed colonies in the presence of IL-3, IL-6, or G-CSF. Fluorouracil 41-45 colony stimulating factor 3 (granulocyte) Mus musculus 161-198 1703493-9 1991 When sorted WGA+Lin- spleen cells of the 5-FU-treated mice were cultured in vitro in the presence of recombinant interleukin 3 (IL-3), interleukin 6 (IL-6), and granulocyte colony-stimulating factor (G-CSF), colony formation was observed only in wells with IL-3, whereas unfractionated spleen cells formed colonies in the presence of IL-3, IL-6, or G-CSF. Fluorouracil 41-45 colony stimulating factor 3 (granulocyte) Mus musculus 200-205 1703493-9 1991 When sorted WGA+Lin- spleen cells of the 5-FU-treated mice were cultured in vitro in the presence of recombinant interleukin 3 (IL-3), interleukin 6 (IL-6), and granulocyte colony-stimulating factor (G-CSF), colony formation was observed only in wells with IL-3, whereas unfractionated spleen cells formed colonies in the presence of IL-3, IL-6, or G-CSF. Fluorouracil 41-45 colony stimulating factor 3 (granulocyte) Mus musculus 349-354 34633539-9 2022 Groups with EP and treated with 5-FU or CIS showed high immunolabelling pattern of RANKL, TNF-alpha, and IL-1beta, moderate of BAX, and low of HIF-1alpha. Fluorouracil 32-36 TNF superfamily member 11 Rattus norvegicus 83-88 34592338-15 2022 AFE also efficiently regressed CT26-derived solid tumor in Balb/c mice acting alone or in synergy with 5FU through inducing autophagy as a major mechanism of action as indicated by upregulation of Beclin 1 and phospho-AMPK, and inhibition of phosphor-S6K1 levels in the tumor tissue lysates. Fluorouracil 103-106 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 218-222 34800596-7 2022 Our data revealed that 5-FU could induce cardiotoxicity which was detected as significant increases of troponin I, lactate dehydrogenase (LDH), creatine kinase- MB (CK-MB), endothelin receptors, malondialdehyde (MDA), toll like receptor4 (TLR4), myeloid differentiation primary response 88 (MyD88), nuclear factor kappa B (NFkappaB), and caspase 3 levels. Fluorouracil 23-27 caspase 3 Rattus norvegicus 338-347 34546854-0 2021 Exosomal-mediated transfer of APCDD1L-AS1 induces 5-fluorouracil resistance in oral squamous cell carcinoma via miR-1224-5p/nuclear receptor binding SET domain protein 2 (NSD2) axis. Fluorouracil 50-64 prostaglandin D2 receptor Homo sapiens 38-41 34546854-3 2021 However, the role of APCDD1L-AS1 in 5-fluorouracil (5-FU) resistance regulation within OSCC is still obscure. Fluorouracil 52-56 prostaglandin D2 receptor Homo sapiens 29-32 34546854-9 2021 APCDD1L-AS1 knockdown impaired 5-FU resistance in 5-FU-resistant OSCC cells by reducing IC50 value, suppressing cell viability, and accelerating cell apoptosis. Fluorouracil 31-35 prostaglandin D2 receptor Homo sapiens 8-11 34546854-9 2021 APCDD1L-AS1 knockdown impaired 5-FU resistance in 5-FU-resistant OSCC cells by reducing IC50 value, suppressing cell viability, and accelerating cell apoptosis. Fluorouracil 50-54 prostaglandin D2 receptor Homo sapiens 8-11 34758839-0 2021 Lactate induces aberration in the miR-30a-DBF4 axis to promote the development of gastric cancer and weakens the sensitivity to 5-Fu. Fluorouracil 128-132 microRNA 30a Homo sapiens 34-41 34758839-10 2021 Furthermore, rescue experiments revealed that the miR-30a-DBF4 axis regulated the GC cell proliferation, migration and the sensitivity to 5-Fu. Fluorouracil 138-142 microRNA 30a Homo sapiens 50-57 34758839-13 2021 Furthermore, our study identified the lactate-miR-30a-DBF4 axis as a crucial regulator of tumor progression and the tumor sensitivity to 5-Fu, which maybe serve useful for the development of novel therapeutic targets. Fluorouracil 137-141 microRNA 30a Homo sapiens 46-53 34474344-0 2021 LEF1 silencing sensitizes colorectal cancer cells to oxaliplatin, 5-FU, and irinotecan. Fluorouracil 66-70 lymphoid enhancer binding factor 1 Homo sapiens 0-4 34474344-10 2021 In summary, we showed the role of LEF1 in chemo-resistance of colorectal cancer cells to Oxaliplatin, Irinotecan and 5-FU. Fluorouracil 117-121 lymphoid enhancer binding factor 1 Homo sapiens 34-38 34790665-14 2021 Moreover, knockdown of FEZF1-AS1 inhibited tumor growth and increased 5-FU sensitivity in GC cells in vivo. Fluorouracil 70-74 FEZ family zinc finger 1 Homo sapiens 23-28 34790665-14 2021 Moreover, knockdown of FEZF1-AS1 inhibited tumor growth and increased 5-FU sensitivity in GC cells in vivo. Fluorouracil 70-74 prostaglandin D2 receptor Homo sapiens 29-32 34827096-3 2021 This study was designed to evaluate the capacity of using first-line chemotherapies including cisplatin, 5-fluorouracil (5-FU) and vinorelbine to act as a chemo-sensitizer on CD133+ (prominin-1 positive) CSCs derived from NSCLC cell lines (A549, H460 and H2170) for the purpose of MSC-TRAIL-induced inhibition. Fluorouracil 105-119 prominin 1 Homo sapiens 175-180 34827096-3 2021 This study was designed to evaluate the capacity of using first-line chemotherapies including cisplatin, 5-fluorouracil (5-FU) and vinorelbine to act as a chemo-sensitizer on CD133+ (prominin-1 positive) CSCs derived from NSCLC cell lines (A549, H460 and H2170) for the purpose of MSC-TRAIL-induced inhibition. Fluorouracil 105-119 prominin 1 Homo sapiens 183-193 34827096-3 2021 This study was designed to evaluate the capacity of using first-line chemotherapies including cisplatin, 5-fluorouracil (5-FU) and vinorelbine to act as a chemo-sensitizer on CD133+ (prominin-1 positive) CSCs derived from NSCLC cell lines (A549, H460 and H2170) for the purpose of MSC-TRAIL-induced inhibition. Fluorouracil 121-125 prominin 1 Homo sapiens 175-180 34685438-7 2021 Overall, the present study elucidated the role of adipocyte-containing microenvironment in 5-FU resistance development of CRC through controlling the SREBP-1 level and further enhanced the concept of clinical application of 6-shogaol and AMPK signaling in CRC therapy. Fluorouracil 91-95 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 238-242 34261152-9 2021 CONCLUSION: Our findings indicate that the combination of allicin with 5-FU could reverse multidrug resistance in the GC cells by reducing the expression of WNT5A, DKK1, MDR1, P-gp, and CD44 levels. Fluorouracil 71-75 dickkopf WNT signaling pathway inhibitor 1 Homo sapiens 164-168 34504596-0 2021 Decreased expression of miR-3135b reduces sensitivity to 5-fluorouracil in colorectal cancer by direct repression of PIM1. Fluorouracil 57-71 microRNA 3135b Homo sapiens 24-33 34504596-5 2021 Microarray data analysis indicated that the level of miR-3135b expression was decreased in patients with recurrent CRC that were treated with 5-FU when compared with non-recurrent cases. Fluorouracil 142-146 microRNA 3135b Homo sapiens 53-62 34504596-6 2021 Overexpression of miR-3135b increased the sensitivity of CRC cells to 5-FU treatment. Fluorouracil 70-74 microRNA 3135b Homo sapiens 18-27 34504596-11 2021 Therefore, the present study identified miR-3135b as a novel regulator of 5-FU sensitivity in CRC. Fluorouracil 74-78 microRNA 3135b Homo sapiens 40-49 34670669-0 2021 (Curcumin combined with 5-FU promotes autophagy and down-regulates the expression of Yes-associated protein (YAP) in hepatocellular carcinoma cells). Fluorouracil 24-28 Yes1 associated transcriptional regulator Homo sapiens 85-107 34670669-0 2021 (Curcumin combined with 5-FU promotes autophagy and down-regulates the expression of Yes-associated protein (YAP) in hepatocellular carcinoma cells). Fluorouracil 24-28 Yes1 associated transcriptional regulator Homo sapiens 109-112 34670669-1 2021 Objective To investigate the effect of curcumin combined with 5-FU on autophagy and Yes-associated protein (YAP) expression in hepatocellular carcinoma cells. Fluorouracil 62-66 Yes1 associated transcriptional regulator Homo sapiens 84-106 34670669-1 2021 Objective To investigate the effect of curcumin combined with 5-FU on autophagy and Yes-associated protein (YAP) expression in hepatocellular carcinoma cells. Fluorouracil 62-66 Yes1 associated transcriptional regulator Homo sapiens 108-111 34670669-6 2021 Compared with the control group, group with curcumin, group with 5-FU, and combination group could increase the expression level of LC3II protein and decrease that of YAP in HepG2 cells, HepG2 cells with stable YAP overexpression, and HepG2 cells with stable YAP knockdown. Fluorouracil 65-69 Yes1 associated transcriptional regulator Homo sapiens 167-170 34670669-6 2021 Compared with the control group, group with curcumin, group with 5-FU, and combination group could increase the expression level of LC3II protein and decrease that of YAP in HepG2 cells, HepG2 cells with stable YAP overexpression, and HepG2 cells with stable YAP knockdown. Fluorouracil 65-69 Yes1 associated transcriptional regulator Homo sapiens 211-214 34670669-6 2021 Compared with the control group, group with curcumin, group with 5-FU, and combination group could increase the expression level of LC3II protein and decrease that of YAP in HepG2 cells, HepG2 cells with stable YAP overexpression, and HepG2 cells with stable YAP knockdown. Fluorouracil 65-69 Yes1 associated transcriptional regulator Homo sapiens 259-262 34670669-7 2021 Conclusion The combination of curcumin and 5-FU induces autophagy and down-regulates the expression of YAP in hepatocellular carcinoma cells. Fluorouracil 43-47 Yes1 associated transcriptional regulator Homo sapiens 103-106 34589618-0 2021 miR-30a attenuates drug sensitivity to 5-FU by modulating cell proliferation possibly by downregulating cyclin E2 in oral squamous cell carcinoma. Fluorouracil 39-43 microRNA 30a Homo sapiens 0-7 34589618-0 2021 miR-30a attenuates drug sensitivity to 5-FU by modulating cell proliferation possibly by downregulating cyclin E2 in oral squamous cell carcinoma. Fluorouracil 39-43 cyclin E2 Homo sapiens 104-113 34589618-3 2021 Therefore, we investigated the effects and molecular mechanism of miR-30a on 5-FU sensitivity. Fluorouracil 77-81 microRNA 30a Homo sapiens 66-73 34589618-4 2021 Stable overexpression of miR-30a in parental OSCC cells decreased cell proliferation and attenuated drug sensitivity to 5-FU. Fluorouracil 120-124 microRNA 30a Homo sapiens 25-32 34589618-9 2021 CCNE2 knockdown with siRNA in OSCC cells yielded decreased drug sensitivity to 5-FU, similar to miR-30a overexpressing cells. Fluorouracil 79-83 cyclin E2 Homo sapiens 0-5 34575229-0 2021 Ribophorin II Overexpression Is Associated with Poor Response to Induction Chemotherapy with Docetaxel, Cisplatin, and Fluorouracil in P16-Negative Locally Advanced Head and Neck Squamous Cell Carcinoma. Fluorouracil 119-131 ribophorin II Homo sapiens 0-13 34575229-1 2021 This study aims to evaluate the relationship between human ribophorin II (RPN2) and the effect of treatment using induction therapy with docetaxel, cisplatin, and fluorouracil (TPF) for p-16 negative locally advanced head and neck squamous cell carcinoma (HNSCC). Fluorouracil 163-175 ribophorin II Homo sapiens 59-72 34575229-1 2021 This study aims to evaluate the relationship between human ribophorin II (RPN2) and the effect of treatment using induction therapy with docetaxel, cisplatin, and fluorouracil (TPF) for p-16 negative locally advanced head and neck squamous cell carcinoma (HNSCC). Fluorouracil 163-175 ribophorin II Homo sapiens 74-78 34540836-7 2021 Dysfunction of MOF in hepatocellular carcinoma cells also results in chemoresistance to trichostatin A, sorafenib and 5-fluorouracil via HIF-1alpha. Fluorouracil 118-132 lysine acetyltransferase 8 Homo sapiens 15-18 34097885-10 2021 CONCLUSION: Tumor-specific targeted delivery of 5FU using EGFR-aptamers as carrier achieved high target specificity, overcame 5FU resistance, proved to be effective in a syngeneic orthotopic transplantation model, in KPC mice, in a CDX model as well as PDOs and therefore represents a promising backbone for pancreatic cancer chemotherapy in patients. Fluorouracil 48-51 caudal type homeobox 1 Mus musculus 232-235 34389694-3 2021 We found that elevated expression of cIAP1 and cIAP2 (but not XIAP) significantly correlated with poor prognosis in patients with microsatellite stable (MSS) stage III colorectal cancer treated with 5-fluorouracil (5FU)-based adjuvant chemotherapy, suggesting their involvement in promoting chemoresistance. Fluorouracil 199-213 baculoviral IAP repeat containing 2 Homo sapiens 37-42 34389694-3 2021 We found that elevated expression of cIAP1 and cIAP2 (but not XIAP) significantly correlated with poor prognosis in patients with microsatellite stable (MSS) stage III colorectal cancer treated with 5-fluorouracil (5FU)-based adjuvant chemotherapy, suggesting their involvement in promoting chemoresistance. Fluorouracil 215-218 baculoviral IAP repeat containing 2 Homo sapiens 37-42 34572508-1 2021 Nicotinamide N-methyltransferase (NNMT) plays multiple roles in improving the aggressiveness of colorectal cancer (CRC) and enhancing resistance to 5-Fluorouracil (5-FU), making it an attractive therapeutic target. Fluorouracil 148-162 nicotinamide N-methyltransferase Homo sapiens 0-32 34572508-1 2021 Nicotinamide N-methyltransferase (NNMT) plays multiple roles in improving the aggressiveness of colorectal cancer (CRC) and enhancing resistance to 5-Fluorouracil (5-FU), making it an attractive therapeutic target. Fluorouracil 148-162 nicotinamide N-methyltransferase Homo sapiens 34-38 34572508-1 2021 Nicotinamide N-methyltransferase (NNMT) plays multiple roles in improving the aggressiveness of colorectal cancer (CRC) and enhancing resistance to 5-Fluorouracil (5-FU), making it an attractive therapeutic target. Fluorouracil 164-168 nicotinamide N-methyltransferase Homo sapiens 0-32 34572508-1 2021 Nicotinamide N-methyltransferase (NNMT) plays multiple roles in improving the aggressiveness of colorectal cancer (CRC) and enhancing resistance to 5-Fluorouracil (5-FU), making it an attractive therapeutic target. Fluorouracil 164-168 nicotinamide N-methyltransferase Homo sapiens 34-38 34572508-3 2021 The aim of the present study is to explore the effect of Cur on attenuating NNMT-induced resistance to 5-FU in CRC. Fluorouracil 103-107 nicotinamide N-methyltransferase Homo sapiens 76-80 34572508-8 2021 In summary, it is proposed that Cur can reverse NNMT-induced cell proliferation and 5-FU resistance through ROS generation and cell cycle arrest. Fluorouracil 84-88 nicotinamide N-methyltransferase Homo sapiens 48-52 34572508-9 2021 Given that Cur has long been used, we suppose that Cur is a promising anticancer drug candidate with minimal side effects for human CRC therapy and can attenuate NNMT-induced resistance to 5-FU. Fluorouracil 189-193 nicotinamide N-methyltransferase Homo sapiens 162-166 34416072-12 2022 The improvement in vitiligo patients by microneedling and 5-fluorouracil could be due to upregulation of MMP2 in affected vitiligo specimens. Fluorouracil 58-72 matrix metallopeptidase 2 Homo sapiens 105-109 34214844-0 2021 Retinoblastoma tumor suppressor gene 1 enhances 5-Fluorouracil chemosensitivity through SDF-1/CXCR4 axis by regulating autophagy in gastric cancer. Fluorouracil 48-62 C-X-C motif chemokine ligand 12 Homo sapiens 88-93 34214844-10 2021 The results showed that RB1 expressions were downregulated in GC cell lines and had significant differences between 5-FU resistance cell lines (SNU-620/5-FU and NUGC-3/5-FU) and non-resistance cell lines (SNU-620 and NUGC-3). Fluorouracil 116-120 RB transcriptional corepressor 1 Homo sapiens 24-27 34214844-10 2021 The results showed that RB1 expressions were downregulated in GC cell lines and had significant differences between 5-FU resistance cell lines (SNU-620/5-FU and NUGC-3/5-FU) and non-resistance cell lines (SNU-620 and NUGC-3). Fluorouracil 152-156 RB transcriptional corepressor 1 Homo sapiens 24-27 32546724-2 2020 Herein we revealed a previously unrecognized mechanism of 5-fluorouracil (5-FU) resistance contributed by high SphK2-upregulated dihydropyrimidine dehydrogenase (DPD) in colorectal cancer (CRC), which is evidenced from human CRC specimens, animal models, and cancer cell lines. Fluorouracil 58-72 sphingosine kinase 2 Homo sapiens 111-116 32546724-2 2020 Herein we revealed a previously unrecognized mechanism of 5-fluorouracil (5-FU) resistance contributed by high SphK2-upregulated dihydropyrimidine dehydrogenase (DPD) in colorectal cancer (CRC), which is evidenced from human CRC specimens, animal models, and cancer cell lines. Fluorouracil 74-78 sphingosine kinase 2 Homo sapiens 111-116 32546724-5 2020 Assays of ChIP-Seq and luciferase reporter gene demonstrated that high SphK2 upregulated DPD through promoting the HDAC1-mediated H3K56ac, leading to the degradation of intracellular 5-FU into inactive alpha-fluoro-beta-alanine (FBAL). Fluorouracil 183-187 sphingosine kinase 2 Mus musculus 71-76 32546724-6 2020 Lastly, inhibition of SphK2 by SLR080811 exhibited excellent inhibition on DPD expression and potently reversed 5-FU resistance in colorectal tumors of villin-SphK2 Tg mice. Fluorouracil 112-116 sphingosine kinase 2 Mus musculus 22-27 32546724-7 2020 Overall, this study manifests that SphK2high conferred 5-FU resistance through upregulating tumoral DPD, which highlights the strategies of blocking SphK2 to overcome 5-FU resistance in CRC. Fluorouracil 55-59 sphingosine kinase 2 Mus musculus 35-40 32546724-7 2020 Overall, this study manifests that SphK2high conferred 5-FU resistance through upregulating tumoral DPD, which highlights the strategies of blocking SphK2 to overcome 5-FU resistance in CRC. Fluorouracil 167-171 sphingosine kinase 2 Mus musculus 35-40 32546724-7 2020 Overall, this study manifests that SphK2high conferred 5-FU resistance through upregulating tumoral DPD, which highlights the strategies of blocking SphK2 to overcome 5-FU resistance in CRC. Fluorouracil 167-171 sphingosine kinase 2 Mus musculus 149-154 32601379-6 2020 In agreement, ectopic transfection of miR-3135b in HCT-15 cancer cells significantly inhibited cell proliferation, sensitized cells to 5-fluoruracil (5-FU), and promoted late apoptosis and necrosis. Fluorouracil 135-148 microRNA 3135b Homo sapiens 38-47 32601379-6 2020 In agreement, ectopic transfection of miR-3135b in HCT-15 cancer cells significantly inhibited cell proliferation, sensitized cells to 5-fluoruracil (5-FU), and promoted late apoptosis and necrosis. Fluorouracil 150-154 microRNA 3135b Homo sapiens 38-47 32527012-5 2020 Moreover, following 5-fluorouracil (5-FU) treatment, STRAP is mobilized from the cytoplasm to the nucleus and promotes STRAP acetylation. Fluorouracil 20-34 serine/threonine kinase receptor associated protein Homo sapiens 53-58 32527012-5 2020 Moreover, following 5-fluorouracil (5-FU) treatment, STRAP is mobilized from the cytoplasm to the nucleus and promotes STRAP acetylation. Fluorouracil 20-34 serine/threonine kinase receptor associated protein Homo sapiens 119-124 32527012-5 2020 Moreover, following 5-fluorouracil (5-FU) treatment, STRAP is mobilized from the cytoplasm to the nucleus and promotes STRAP acetylation. Fluorouracil 36-40 serine/threonine kinase receptor associated protein Homo sapiens 53-58 32527012-5 2020 Moreover, following 5-fluorouracil (5-FU) treatment, STRAP is mobilized from the cytoplasm to the nucleus and promotes STRAP acetylation. Fluorouracil 36-40 serine/threonine kinase receptor associated protein Homo sapiens 119-124 32606741-8 2020 The PI3K inhibitor LY294002 or RAF-MEK-ERK inhibitor U0126 in combination with ELE and 5-FU decreased cell viability in both cell lines significantly, thereby showing the involvement of these pathways in cell apoptosis. Fluorouracil 87-91 zinc fingers and homeoboxes 2 Homo sapiens 31-34 32005747-8 2020 Furthermore, we identified 38 single genes that were significantly associated with capecitabine benefit and these were dominated by immune response pathway and enzymes involved in activating capecitabine to fluorouracil, including TYMP However, these results were not significant when adjusted for multiple testing. Fluorouracil 207-219 thymidine phosphorylase Homo sapiens 231-235 34360807-8 2021 Moreover, LMWF enhanced the suppressive effects of 5-FU on tumor cell migration through the c-MET/matrix metalloproteinase (MMP)-2 signaling pathway in both HCT116 and Caco-2 cells. Fluorouracil 51-55 matrix metallopeptidase 2 Homo sapiens 92-130 32044957-6 2020 We found that miR-34a was significantly downregulated in SP cells, and that overexpressing miR-34a overcame drug resistance to 5-FU. Fluorouracil 127-131 microRNA 34a Homo sapiens 91-98 32044957-8 2020 In addition, overexpressing miR-34a overcame ABCG2-mediated resistance to 5-FU via DLL1/Notch pathway in vitro, and suppressed tumor growth under 5-FU treatment in vivo. Fluorouracil 74-78 microRNA 34a Homo sapiens 28-35 32044957-8 2020 In addition, overexpressing miR-34a overcame ABCG2-mediated resistance to 5-FU via DLL1/Notch pathway in vitro, and suppressed tumor growth under 5-FU treatment in vivo. Fluorouracil 146-150 microRNA 34a Homo sapiens 28-35 32044957-9 2020 In conclusion, our findings suggest that miR-34a acts as a tumor suppressor via enhancing chemosensitivity to 5-FU in SP cells, which provides a novel therapeutic target in chemotherapy-resistant colon cancer. Fluorouracil 110-114 microRNA 34a Homo sapiens 41-48 32357935-12 2020 Furthermore, depletion of TRAF4 impaired CHK1 activity and sensitized CRC cells to fluorouracil and other chemotherapeutic agents in vitro and in vivo. Fluorouracil 83-95 TNF receptor associated factor 4 Homo sapiens 26-31 32260072-7 2020 Expression of TIE2 also increased the resistance to the chemotherapeutic 5-Fluorouracil. Fluorouracil 73-87 TEK receptor tyrosine kinase Homo sapiens 14-18 34299320-7 2021 We identified the upregulation of thymidine phosphorylase (TYMP), which is one of the most commonly reported mutated genes leading to 5-fluorouracil resistance, as the cause of such enhanced vasculogenic ability. Fluorouracil 134-148 thymidine phosphorylase Homo sapiens 34-57 34299320-7 2021 We identified the upregulation of thymidine phosphorylase (TYMP), which is one of the most commonly reported mutated genes leading to 5-fluorouracil resistance, as the cause of such enhanced vasculogenic ability. Fluorouracil 134-148 thymidine phosphorylase Homo sapiens 59-63 31587155-11 2020 The SIRT1 inhibitor EX-527 dramatically inhibited the expression of Cyclin B1 and resistance-associated protein 3 (MRP3) to reduce 5-FU drug resistance in vivo. Fluorouracil 131-135 ATP binding cassette subfamily C member 3 Homo sapiens 115-119 34335757-0 2021 All-Trans Retinoic Acid Enhances Chemosensitivity to 5-FU by Targeting miR-378c/E2F7 Axis in Colorectal Cancer. Fluorouracil 53-57 microRNA 378c Homo sapiens 71-79 34335757-0 2021 All-Trans Retinoic Acid Enhances Chemosensitivity to 5-FU by Targeting miR-378c/E2F7 Axis in Colorectal Cancer. Fluorouracil 53-57 E2F transcription factor 7 Homo sapiens 80-84 34335757-7 2021 Additionally, treatment of 5-FU combined with ATRA could increase miR-378c expression, whereas it decreased the expression of E2F7. Fluorouracil 27-31 microRNA 378c Homo sapiens 66-74 34335757-7 2021 Additionally, treatment of 5-FU combined with ATRA could increase miR-378c expression, whereas it decreased the expression of E2F7. Fluorouracil 27-31 E2F transcription factor 7 Homo sapiens 126-130 34335757-9 2021 Furthermore, miR-378c inhibitor or vector with E2F7 partially counteracted the effects of 5-FU combined with ATRA on viability, migration, invasion, and apoptosis of HCT116 cells. Fluorouracil 90-94 microRNA 378c Homo sapiens 13-21 34335757-9 2021 Furthermore, miR-378c inhibitor or vector with E2F7 partially counteracted the effects of 5-FU combined with ATRA on viability, migration, invasion, and apoptosis of HCT116 cells. Fluorouracil 90-94 E2F transcription factor 7 Homo sapiens 47-51 32044580-0 2020 Inclusion of a 5-fluorouracil moiety in nitrogenous bases derivatives as human carbonic anhydrase IX and XII inhibitors produced a targeted action against MDA-MB-231 and T47D breast cancer cells. Fluorouracil 15-29 carbonic anhydrase 9 Homo sapiens 79-100 34589581-0 2021 Targeting EGFR sensitizes 5-Fu-resistant colon cancer cells through modification of the lncRNA-FGD5-AS1-miR-330-3p-Hexokinase 2 axis. Fluorouracil 26-30 prostaglandin D2 receptor Homo sapiens 100-103 32044580-2 2020 Most sulfonamide derivatives efficiently inhibit the target CA IX (KIs in the range 0.47-44.7 nM) and CA XII (KIs in the range 2.9-83.1 nM), while the 5-FU coumarin derivatives showed a potent and totally selective inhibitory action against the target CA IX/XII over off-target CA I/II. Fluorouracil 151-155 carbonic anhydrase 9 Homo sapiens 252-257 34589581-0 2021 Targeting EGFR sensitizes 5-Fu-resistant colon cancer cells through modification of the lncRNA-FGD5-AS1-miR-330-3p-Hexokinase 2 axis. Fluorouracil 26-30 hexokinase 2 Homo sapiens 115-127 34589581-4 2021 Here we report that EGFR and lncRNA-FGD5-AS1 promoted 5-Fu resistance of CRC. Fluorouracil 54-58 prostaglandin D2 receptor Homo sapiens 41-44 31846800-9 2020 We demonstrated enhanced inhibition of PDAC cell proliferation by 5-FU-miR-15a compared to native miR-15a. Fluorouracil 66-70 microRNA 15a Homo sapiens 71-78 34589581-5 2021 By establishing the 5-Fu-resistant CRC cell line, we detected that EGFR, FGD5-AS1, and glucose metabolism were significantly elevated in 5-Fu-resistant CRC cells. Fluorouracil 20-24 FYVE, RhoGEF and PH domain containing 5 Homo sapiens 73-77 34589581-5 2021 By establishing the 5-Fu-resistant CRC cell line, we detected that EGFR, FGD5-AS1, and glucose metabolism were significantly elevated in 5-Fu-resistant CRC cells. Fluorouracil 20-24 prostaglandin D2 receptor Homo sapiens 78-81 34589581-5 2021 By establishing the 5-Fu-resistant CRC cell line, we detected that EGFR, FGD5-AS1, and glucose metabolism were significantly elevated in 5-Fu-resistant CRC cells. Fluorouracil 137-141 FYVE, RhoGEF and PH domain containing 5 Homo sapiens 73-77 34589581-5 2021 By establishing the 5-Fu-resistant CRC cell line, we detected that EGFR, FGD5-AS1, and glucose metabolism were significantly elevated in 5-Fu-resistant CRC cells. Fluorouracil 137-141 prostaglandin D2 receptor Homo sapiens 78-81 34589581-9 2021 Rescue experiments demonstrated that FGD5-AS1 promotes glycolysis through modulating the miR-330-3p-HK2 axis, leading to 5-Fu resistance of CRC cancer cells. Fluorouracil 121-125 hexokinase 2 Homo sapiens 100-103 34279763-3 2021 Here we examined the SIRT5 (Resveratrol and Suramin) and p53 (Nutlin3a) modulators alone or in combination with 5-FU on the proliferation of colon cancer cells and effect of 5-FU on the SIRT5 and FOXO3a protein expressions whether p53 dependent or independent manner. Fluorouracil 174-178 sirtuin 5 Homo sapiens 186-191 34279763-4 2021 METHODS AND RESULTS: According to our MTT assay results, Resveratrol (RSV), Nutlin3a and Suramin was found to be more effective in HCT-116 p53+/+ cells and these differences were evaluated together with the effect of 5-FU on the SIRT5, FOXO3a and Bim protein expressions in HCT-116 p53 +/+ and HCT-116 p53 -/- cells. Fluorouracil 217-221 sirtuin 5 Homo sapiens 229-234 34279763-6 2021 Our western blot experiment results showed that while Suramin decreased SIRT5 and RSV decreased FOXO3a protein expressions significantly in HCT-116 p53 -/- cells, 5-FU decreased significantly SIRT5 and FOXO3a protein expressions in a p53 independent manner. Fluorouracil 163-167 sirtuin 5 Homo sapiens 192-197 34279763-7 2021 CONCLUSIONS: In this study, the effect of 5-FU on SIRT5 and FOXO 3a proteins was determined for the first time in HCT-116 p53 +/+ and HCT-116 p53 -/- cells. Fluorouracil 42-46 sirtuin 5 Homo sapiens 50-55 31846800-10 2020 In vivo we showed the therapeutic power of 5-FU-miR-15a alone or in combination with gemcitabine with near complete elimination of PDAC lung metastatic tumor growth. Fluorouracil 43-47 microRNA 15a Homo sapiens 48-55 31846800-11 2020 These results support the future development of 5-FU-miR-15a as a novel therapeutic agent as well as a prognostic biomarker in the clinical management of PDAC. Fluorouracil 48-52 microRNA 15a Homo sapiens 53-60 32132038-6 2020 During exposure to 5FU, viability, CDK4 activity, cell-cycle progression, invasion, and sphere formation were enhanced, while apoptosis was decreased in 5FU-resistant CRC cells. Fluorouracil 19-22 cyclin dependent kinase 4 Homo sapiens 35-39 34257696-0 2021 Erteng-Sanjie Capsule Enhances Chemosensitivity of 5-Fluorouracil in Tumor-Bearing Nude Mice with Gastric Cancer by Inhibiting Notch1/Hes1 Signaling Pathway. Fluorouracil 51-65 hes family bHLH transcription factor 1 Mus musculus 134-138 31313286-11 2020 Taken together, our data indicated that modification of ERRFI1 by KHSRP occurs through miR-501-5p, an essential mechanism driving CRC proliferation and 5-FU resistance. Fluorouracil 152-156 ERBB receptor feedback inhibitor 1 Homo sapiens 56-62 32021372-0 2020 Effect of Topical 5-Fluorouracil Alone versus Its Combination with Erbium:YAG (2940 nm) Laser in Treatment of Vitiligo. Fluorouracil 18-32 VAMAS6 Homo sapiens 110-118 34168463-7 2021 Results: Both 5-Fu and CDDP result in the apoptosis of A549 and NCI-H226 cells and improve the expressions of has-miR-134 and has-miR-296. Fluorouracil 14-18 microRNA 134 Homo sapiens 114-121 34306337-10 2021 miR-192-5p mediated the improvement of urethral scar by triamcinolone acetonide combined with 5-FU by directly targeting ATG7, which is marker gene of autophagy. Fluorouracil 94-98 autophagy related 7 Homo sapiens 121-125 34067869-6 2021 Adjuvant BGP-15 treatment did, however, prevent the 5FU-induced phosphorylation of p38 MAPK and p65 NF-B subunit, signalling pathways involved in cell stress and inflammatory signalling, respectively. Fluorouracil 52-55 mitogen-activated protein kinase 14 Mus musculus 83-91 34068442-8 2021 Treatment of gastric cancer cells with CML-HMGB1 enhanced cell proliferation and invasion, sphere formation, and protection from thapsigargin-induced apoptosis, and decreased 5-FU sensitivity in comparison to HMGB1. Fluorouracil 175-179 high mobility group box 1 Homo sapiens 43-48 34602411-6 2021 In vitro, the protein and mRNA expressions of FAK, PI3K, AKT and mTOR in beta-carboline alkaloids groups were significantly lower than those in control and fluorouracil groups (P<0.05). Fluorouracil 156-168 protein tyrosine kinase 2 Homo sapiens 46-49 34602411-9 2021 FAK, PI3K, AKT and mTOR proteins in tumor tissues of beta-carboline alkaloids and fluorouracil groups were significantly lower than control group (P<0.05). Fluorouracil 82-94 protein tyrosine kinase 2 Homo sapiens 0-3 34981469-9 2021 The expression levels of all tested genes were altered in all treatment groups compared to the control, with that of WNT1, CTNNB1, TCF, MTOR, AKT1, BIRC5, and CCND1 showing the most robust changes in the combined curcumin/berberine/5-FU treatment. Fluorouracil 232-236 cyclin D1 Homo sapiens 159-164 35490372-8 2022 The chemoresistant subline of HCT116 cells derived by OxaPt differs from the subline derived by 5-FU treatment - it responds to OxaPt by upregulating ATG7 protein level and autophagic flux, in contrast to downregulation in cells derived by 5-FU. Fluorouracil 96-100 autophagy related 7 Homo sapiens 150-154 35490372-9 2022 Moreover, 5-FU and OxaPt treatments significantly modulate protein levels of core-autophagy proteins ATG7 and ATG12. Fluorouracil 10-14 autophagy related 7 Homo sapiens 101-105 35624466-16 2022 AP4-deficiency also sensitized CRC cells to 5-FU treatment, whereas ectopic AP4 conferred resistance to 5-FU in a miR-22-3p and MDC1-dependent manner. Fluorouracil 104-108 microRNA 223 Mus musculus 114-123 35624466-17 2022 CONCLUSIONS: In summary, AP4, miR-22-3p and MDC1 form a conserved and coherent, regulatory feed-forward loop to promote DNA repair, which suppresses DNA damage, senescence and CIN, and contributes to 5-FU resistance. Fluorouracil 200-204 microRNA 223 Mus musculus 30-39 32021372-11 2020 Conclusion: The combination of Er:YAG with 5-FU is safe and effective in treating and improving outcome in vitiligo especially of non-resistant areas. Fluorouracil 43-47 VAMAS6 Homo sapiens 107-115 35608750-10 2022 5-fluorouracil induces the phosphorylation of KAP1, a target of the checkpoint kinase ataxia-telangiectasia mutated (ATM), stronger in HDAC2-negative cells than in their HDAC2-positive counterparts. Fluorouracil 0-14 tripartite motif-containing 28 Mus musculus 46-50 32865180-0 2020 Circ_0007031 enhances tumor progression and promotes 5-fluorouracil resistance in colorectal cancer through regulating miR-133b/ABCC5 axis. Fluorouracil 53-67 ATP binding cassette subfamily C member 5 Homo sapiens 128-133 35608750-10 2022 5-fluorouracil induces the phosphorylation of KAP1, a target of the checkpoint kinase ataxia-telangiectasia mutated (ATM), stronger in HDAC2-negative cells than in their HDAC2-positive counterparts. Fluorouracil 0-14 ataxia telangiectasia mutated Mus musculus 117-120 31736281-5 2020 Of these genes, ABCG2, AHNAK2, BCL2, FZD1, and TP73 are associated with published evidence for resistance to 5-fluorouracil and cisplatin. Fluorouracil 109-123 frizzled class receptor 1 Homo sapiens 37-41 31736281-5 2020 Of these genes, ABCG2, AHNAK2, BCL2, FZD1, and TP73 are associated with published evidence for resistance to 5-fluorouracil and cisplatin. Fluorouracil 109-123 tumor protein p73 Homo sapiens 47-51 31696188-0 2019 Bypassing pro-survival and resistance mechanisms of autophagy in EGFR-positive lung cancer cells by targeted delivery of 5FU using theranostic Ag2S quantum dots. Fluorouracil 121-124 angiotensin II receptor type 1 Homo sapiens 143-147 31696188-3 2019 Here, we have developed PEGylated Ag2S QDs functionalized with Cetuximab (Cet) antibody and loaded with an anticancer drug, 5-fluorouracil (5FU). Fluorouracil 124-138 angiotensin II receptor type 1 Homo sapiens 34-38 31696188-3 2019 Here, we have developed PEGylated Ag2S QDs functionalized with Cetuximab (Cet) antibody and loaded with an anticancer drug, 5-fluorouracil (5FU). Fluorouracil 140-143 angiotensin II receptor type 1 Homo sapiens 34-38 31696188-7 2019 The improved therapeutic outcome of 5FU delivered to A549 cells by Cet conjugated Ag2S QDs is suggested as the synergistic outcome of enhanced receptor mediated uptake of nanoparticles, and hence the drug, coupled with suppressed autophagy even in the absence of addition of an autophagy suppressor. Fluorouracil 36-39 angiotensin II receptor type 1 Homo sapiens 82-86 30582964-6 2019 Interestingly, HCT116RFK866 cells, which are resistant to other class NAMPT inhibitors, were more sensitive to the anticancer 5-fluorouracil and cisplatin and gamma-ray irradiation compared to parental HCT116 cells. Fluorouracil 126-140 nicotinamide phosphoribosyltransferase Homo sapiens 70-75 35367196-3 2022 Since the sensitivity of 5-Fu is negatively correlated with oxytocin receptor (OXTR) expression in MSS CRC cell lines, our current study aimed to investigate the synergistic antitumor activity of 5-Fu combined with atosiban, an antagonist of OXTR. Fluorouracil 25-29 oxytocin receptor Homo sapiens 60-77 35367196-3 2022 Since the sensitivity of 5-Fu is negatively correlated with oxytocin receptor (OXTR) expression in MSS CRC cell lines, our current study aimed to investigate the synergistic antitumor activity of 5-Fu combined with atosiban, an antagonist of OXTR. Fluorouracil 25-29 oxytocin receptor Homo sapiens 79-83 35484333-10 2022 Both in vivo and in vitro experiments revealed that combination chemotherapy with GAA and 5-fluorouracil (5FU) yielded improved treatment outcomes. Fluorouracil 106-109 alpha glucosidase Homo sapiens 82-85 35194905-7 2022 In contrast, DC2, which features two different cage cavities, was found to interact with two different guests, 5-FU and cisplatin, selectively. Fluorouracil 111-115 monoacylglycerol O-acyltransferase 1 Homo sapiens 13-16 35411625-6 2022 5-FU resulted in significant cardiotoxicity, represented by an increase in the serum levels of cardiac enzymes and malondialdehyde, as well as cyclooxygenase-2 (COX-2) and tumor necrosis factor-alpha (TNF-alpha) expression, and histopathological degeneration. Fluorouracil 0-4 prostaglandin-endoperoxide synthase 2 Rattus norvegicus 143-159 35411625-6 2022 5-FU resulted in significant cardiotoxicity, represented by an increase in the serum levels of cardiac enzymes and malondialdehyde, as well as cyclooxygenase-2 (COX-2) and tumor necrosis factor-alpha (TNF-alpha) expression, and histopathological degeneration. Fluorouracil 0-4 prostaglandin-endoperoxide synthase 2 Rattus norvegicus 161-166 35462906-11 2022 Conclusion: Dormant CRC is associated with high glutamine metabolism and synergizes with CAFs in 5-FU resistance, and the key effectors are LMOD1, MAB21L2, and ASPN. Fluorouracil 97-101 leiomodin 1 Homo sapiens 140-145 35191521-6 2022 In vitro, the AZD6738/5-FU combination increased the number of mitotic cells according to flow cytometry, decreased the checkpoint kinase 1 phosphorylation levels and increased cleaved caspase-3 and phosphorylated form of H2A.X variant histone levels according to western blotting, and decreased the proliferation rate of four colon cancer cell lines according to cell viability experiments. Fluorouracil 22-26 H2A.X variant histone Homo sapiens 222-227 31741260-0 2019 New uracil analogs as downregulators of ABC transporters in 5-fluorouracil-resistant human leukemia HL-60 cell line. Fluorouracil 60-74 ATP binding cassette subfamily B member 6 (Langereis blood group) Homo sapiens 40-43 31799650-16 2019 Besides, miR-335 overexpression increased cell sensitivity to 5-Fluoracil (Fu) treatment and decreased the expression levels of ATP-binding cassette transporter B1 (ABCB1) and ATP-binding cassette G2 (ABCG2) in GBC-SD and SGC-996 cells. Fluorouracil 62-73 microRNA 335 Homo sapiens 9-16 31496029-7 2019 Western blot assay was achieved to determine the UPP1 expression correlates with the function of 5-FU regulate epithelial-mesenchymal transition. Fluorouracil 97-101 uridine phosphorylase 1 Homo sapiens 49-53 31496029-11 2019 Western blot assay proves the effect of UPP1 expression on 5-FU regulates epithelial-mesenchymal transition pathway. Fluorouracil 59-63 uridine phosphorylase 1 Homo sapiens 40-44 31377317-7 2019 In GC cells, CHAF1A knockdown significantly decreased the IC50 of 5-FU. Fluorouracil 66-70 chromatin assembly factor 1 subunit A Homo sapiens 13-19 31579069-4 2019 Overexpression of miR-361 enhanced the 5-FU susceptibility of parental and resistant HCT116 and HT29 cells in vitro. Fluorouracil 39-43 microRNA 361 Homo sapiens 18-25 34978498-1 2022 Objective: Targeted deep sequencing was used to characterize the mutational spectrum of APC in Chinese colorectal tumors in comparison to that in Caucasians from The Cancer Genome Atlas (TCGA) and to investigate whether APC mutations can predict overall survival in CRC patients receiving adjuvant chemotherapy.Methods: A total of 315 Chinese CRC patients including 241 stage II/III patients receiving fluorouracil-based adjuvant chemotherapy were included in this study. Fluorouracil 402-414 APC regulator of WNT signaling pathway Homo sapiens 88-91 34978498-5 2022 Among stage II/III patients receiving fluorouracil-based adjuvant chemotherapy, APC mutations showed a significant association with worse survival (HR = 1.69; 95% CI, 1.10-2.62; p = .0179). Fluorouracil 38-50 APC regulator of WNT signaling pathway Homo sapiens 80-83 34978498-7 2022 Among individual mutation sites, Arg232Ter, the most frequent mutation in Chinese CRC, exhibited the strongest negative impact on survival (HR = 2.65; 95% CI, 1.16-6.03; p =.0202).Conclusion: APC overall mutation was an independent predictor for overall survival of stage II/III CRC patients receiving fluorouracil-based chemotherapy. Fluorouracil 302-314 APC regulator of WNT signaling pathway Homo sapiens 192-195 35448163-7 2022 Furthermore, a few lncRNAs, such as AFAP1-AS1 and LINC01014, block the efficiency of chemotherapeutic drugs, including cisplatin, 5-fluorouracil, paclitaxel, and gefitinib, used for ESCC treatment. Fluorouracil 130-144 prostaglandin D2 receptor Homo sapiens 42-45 35408903-9 2022 Taken together, our data suggest that kaempferol may play an important role in overcoming resistance to 5-Fu therapy by regulating the miR-326-hnRNPA1/A2/PTBP1-PKM2 axis. Fluorouracil 104-108 heterogeneous nuclear ribonucleoprotein A1 Homo sapiens 143-153 35112408-11 2022 In conclusion, the current study presents the first preclinical evidence for the potential merit of 5-FU/Bio-A combination for the treatment of ER+ breast cancer. Fluorouracil 100-104 epiregulin Homo sapiens 144-146 35101590-17 2022 Both in vivo and in vitro experiments indicated that 5-FU increased the expression of ferroptosis, mainly by reducing the expression of glutathione peroxidase 4 (GPX4) and ferritin heavy chain 1 (FTH1), but enhancing the expression of transferrin receptor 1 (TfR1). Fluorouracil 53-57 glutathione peroxidase 4 Rattus norvegicus 136-160 35101590-17 2022 Both in vivo and in vitro experiments indicated that 5-FU increased the expression of ferroptosis, mainly by reducing the expression of glutathione peroxidase 4 (GPX4) and ferritin heavy chain 1 (FTH1), but enhancing the expression of transferrin receptor 1 (TfR1). Fluorouracil 53-57 glutathione peroxidase 4 Rattus norvegicus 162-166 35101590-17 2022 Both in vivo and in vitro experiments indicated that 5-FU increased the expression of ferroptosis, mainly by reducing the expression of glutathione peroxidase 4 (GPX4) and ferritin heavy chain 1 (FTH1), but enhancing the expression of transferrin receptor 1 (TfR1). Fluorouracil 53-57 transferrin receptor Rattus norvegicus 235-257 35101590-17 2022 Both in vivo and in vitro experiments indicated that 5-FU increased the expression of ferroptosis, mainly by reducing the expression of glutathione peroxidase 4 (GPX4) and ferritin heavy chain 1 (FTH1), but enhancing the expression of transferrin receptor 1 (TfR1). Fluorouracil 53-57 transferrin receptor Rattus norvegicus 259-263 35180871-0 2022 MeCP2 confers 5-fluorouracil resistance in gastric cancer via upregulating the NOX4/PKM2 pathway. Fluorouracil 14-28 NADPH oxidase 4 Homo sapiens 79-83 35180871-9 2022 Silencing NOX4 rescued the inductive effect of MeCP2 overexpression on 5-FU sensitivity of GC cells and reduced the expression of NOX4 and PKM2 in MeCP2 overexpressed 5-FU-resistant GC cells. Fluorouracil 71-75 NADPH oxidase 4 Homo sapiens 10-14 35180871-9 2022 Silencing NOX4 rescued the inductive effect of MeCP2 overexpression on 5-FU sensitivity of GC cells and reduced the expression of NOX4 and PKM2 in MeCP2 overexpressed 5-FU-resistant GC cells. Fluorouracil 167-171 NADPH oxidase 4 Homo sapiens 10-14 35180871-9 2022 Silencing NOX4 rescued the inductive effect of MeCP2 overexpression on 5-FU sensitivity of GC cells and reduced the expression of NOX4 and PKM2 in MeCP2 overexpressed 5-FU-resistant GC cells. Fluorouracil 167-171 NADPH oxidase 4 Homo sapiens 130-134 35180871-11 2022 CONCLUSION: MeCP2 confers 5-FU resistance in GC cells via upregulating the NOX4/PKM2 pathway, which may lead to a promising therapeutic strategy for GC. Fluorouracil 26-30 NADPH oxidase 4 Homo sapiens 75-79 35198633-9 2022 Results: 5-FU resulted in a significant cardiotoxicity represented by an increase in cardiac enzymes, MDA (malondialdehyde) levels, COX-2 (cyclooxygenase-2) expression, and histopathological degenerations. Fluorouracil 9-13 prostaglandin-endoperoxide synthase 2 Rattus norvegicus 132-137 35198633-9 2022 Results: 5-FU resulted in a significant cardiotoxicity represented by an increase in cardiac enzymes, MDA (malondialdehyde) levels, COX-2 (cyclooxygenase-2) expression, and histopathological degenerations. Fluorouracil 9-13 prostaglandin-endoperoxide synthase 2 Rattus norvegicus 139-155 31454556-7 2019 The western blotting results confirmed that the expression levels of PLCbeta3 and PLCbeta3 pS1105 in Bel/5-Fu cells were increased as compared to Bel cells. Fluorouracil 105-109 phospholipase C beta 3 Homo sapiens 69-77 31454556-7 2019 The western blotting results confirmed that the expression levels of PLCbeta3 and PLCbeta3 pS1105 in Bel/5-Fu cells were increased as compared to Bel cells. Fluorouracil 105-109 phospholipase C beta 3 Homo sapiens 82-90 31454556-9 2019 The knockdown of SRC, PKCdelta and PLCbeta3 increased the susceptibility of Bel/5-Fu cells to 5-Fu. Fluorouracil 80-84 protein kinase C delta Homo sapiens 22-30 31454556-9 2019 The knockdown of SRC, PKCdelta and PLCbeta3 increased the susceptibility of Bel/5-Fu cells to 5-Fu. Fluorouracil 80-84 phospholipase C beta 3 Homo sapiens 35-43 31454556-9 2019 The knockdown of SRC, PKCdelta and PLCbeta3 increased the susceptibility of Bel/5-Fu cells to 5-Fu. Fluorouracil 94-98 protein kinase C delta Homo sapiens 22-30 31454556-9 2019 The knockdown of SRC, PKCdelta and PLCbeta3 increased the susceptibility of Bel/5-Fu cells to 5-Fu. Fluorouracil 94-98 phospholipase C beta 3 Homo sapiens 35-43 31454556-15 2019 Our results showed that the phosphorylation levels of PLCbeta3 pS1105 and the protein levels of PLCbeta3, PKCdelta and SRC, which are major components of GnRH signaling pathway were higher in Bel/5-Fu cells than in Bel cells. Fluorouracil 196-200 phospholipase C beta 3 Homo sapiens 54-62 31454556-15 2019 Our results showed that the phosphorylation levels of PLCbeta3 pS1105 and the protein levels of PLCbeta3, PKCdelta and SRC, which are major components of GnRH signaling pathway were higher in Bel/5-Fu cells than in Bel cells. Fluorouracil 196-200 phospholipase C beta 3 Homo sapiens 96-104 31454556-15 2019 Our results showed that the phosphorylation levels of PLCbeta3 pS1105 and the protein levels of PLCbeta3, PKCdelta and SRC, which are major components of GnRH signaling pathway were higher in Bel/5-Fu cells than in Bel cells. Fluorouracil 196-200 protein kinase C delta Homo sapiens 106-114 31454556-15 2019 Our results showed that the phosphorylation levels of PLCbeta3 pS1105 and the protein levels of PLCbeta3, PKCdelta and SRC, which are major components of GnRH signaling pathway were higher in Bel/5-Fu cells than in Bel cells. Fluorouracil 196-200 gonadotropin releasing hormone 1 Homo sapiens 154-158 30902718-6 2019 Further, the results showed that MBP-FMBP-2 significantly reversed the 5-Fu resistance in human colorectal cancer HCT-8/Fu cell through inhibiting cell proliferation, promoting cell apoptosis and increasing the intracellular accumulation of 5-Fu. Fluorouracil 71-75 myelin basic protein Homo sapiens 33-36 30902718-6 2019 Further, the results showed that MBP-FMBP-2 significantly reversed the 5-Fu resistance in human colorectal cancer HCT-8/Fu cell through inhibiting cell proliferation, promoting cell apoptosis and increasing the intracellular accumulation of 5-Fu. Fluorouracil 241-245 myelin basic protein Homo sapiens 33-36 31115533-0 2019 TFAP2E methylation promotes 5-fluorouracil resistance via exosomal miR-106a-5p and miR-421 in gastric cancer MGC-803 cells. Fluorouracil 28-42 transcription factor AP-2 epsilon Homo sapiens 0-6 31115533-1 2019 Hypermethylation of transcription factor activating enhancer-binding protein 2e (TFAP2E) has been reported to be associated with chemoresistance to 5-fluorouracil (5-FU) in gastric cancer (GC). Fluorouracil 148-162 transcription factor AP-2 epsilon Homo sapiens 81-87 31115533-1 2019 Hypermethylation of transcription factor activating enhancer-binding protein 2e (TFAP2E) has been reported to be associated with chemoresistance to 5-fluorouracil (5-FU) in gastric cancer (GC). Fluorouracil 164-168 transcription factor AP-2 epsilon Homo sapiens 81-87 31115533-10 2019 Collectively, our data support an important role of exosomes and exosomal miRNAs in TFAP2E methylation-induced chemoresistance to 5-FU in GC. Fluorouracil 130-134 transcription factor AP-2 epsilon Homo sapiens 84-90 31042625-8 2019 However, knockdown of p21 abolishes the beneficial effects of PCAF overexpression on increasing the sensitivity of HCT116/5-FU cells to 5-FU. Fluorouracil 136-140 lysine acetyltransferase 2B Homo sapiens 62-66 31042625-10 2019 Our data suggest that PCAF-mediated p53 acetylation is an essential regulatory mechanism for increasing the susceptibility of CRC to 5-FU. Fluorouracil 133-137 lysine acetyltransferase 2B Homo sapiens 22-26 31178935-10 2019 Further research is required to explore the cardioprotective effect of agents such as coenzyme complex, GLP-1 analogues and degradation inhibitors on 5-FU-induced coronary artery vasospasm. Fluorouracil 150-154 glucagon like peptide 1 receptor Homo sapiens 104-109 35122829-7 2022 Moreover, 5-FU could gradually release from chitosan at a more acidic pH (tumor tissues) environment. Fluorouracil 10-14 phenylalanine hydroxylase Homo sapiens 70-72 35122829-8 2022 These results revealed the underlying atomic interaction mechanism between 5-FU and chitosan at various pH levels, and may be helpful in the design of chitosan-based drug delivery systems. Fluorouracil 75-79 phenylalanine hydroxylase Homo sapiens 104-106 35070952-9 2021 After treatment with 5-FU, HSC3-miR-155-5p tumor-bearing nude mice presented growing tumors, while HSC3-TP53INP1 group possessed shrinking tumors. Fluorouracil 21-25 microRNA 155 Mus musculus 32-39 35070952-10 2021 In conclusion, these results lead to the proposal that miR-155-5p enhances 5-FU resistance by decreasing TP53INP1 expression in OSCC. Fluorouracil 75-79 microRNA 155 Mus musculus 55-62 30716387-6 2019 Furthermore, MALAT1 silencing downregulated the expression of ATP-binding cassette transporters (ABC), breast cancer resistance protein (BCRP), and multi-drug resistance proteins including MDR1 and MRP1, resulting in decreased resistance of cancer cells to 5-FU. Fluorouracil 257-261 metastasis associated lung adenocarcinoma transcript 1 (non-coding RNA) Mus musculus 13-19 34974791-8 2022 CircPTK2 knockdown constrained cell proliferation, migration, invasion, resistance to 5-FU and oxaliplatin, and the Wnt/beta-catenin signaling. Fluorouracil 86-90 protein tyrosine kinase 2 Homo sapiens 0-8 34974791-14 2022 In conclusion, circPTK2 interference suppressed CRC proliferation, migration, invasion and chemoresistance via regulating miR-136-5p and YTHDF1.Abbreviations: circRNAs: circular RNAs; CRC: colorectal cancer; circPTK2: circRNA protein tyrosine kinase 2; miR: microRNA; YTHDF1: YTH domain family protein 1; CCK-8: cell counting kit-8; 5-FU: 5-fluorouracil; RIP: RNA immunoprecipitation. Fluorouracil 333-337 protein tyrosine kinase 2 Homo sapiens 15-23 34974791-14 2022 In conclusion, circPTK2 interference suppressed CRC proliferation, migration, invasion and chemoresistance via regulating miR-136-5p and YTHDF1.Abbreviations: circRNAs: circular RNAs; CRC: colorectal cancer; circPTK2: circRNA protein tyrosine kinase 2; miR: microRNA; YTHDF1: YTH domain family protein 1; CCK-8: cell counting kit-8; 5-FU: 5-fluorouracil; RIP: RNA immunoprecipitation. Fluorouracil 339-353 protein tyrosine kinase 2 Homo sapiens 15-23 35103981-11 2022 5-FU suppressed the stemness maintenance of CSCs in PANC-1 cells, as demonstrated by the inhibition of tumorsphere formation, the decrease in CD44+CD133+ cells" fraction, and downregulation of OCT4, Nanog, and SOX2 expression. Fluorouracil 0-4 prominin 1 Homo sapiens 147-152 2476639-3 1989 The suppressive effects of TGF beta were more profound on colony formation from cells of 5-fluorouracil (5-FU)-treated mice than those of normal mice. Fluorouracil 89-103 transforming growth factor, beta 1 Mus musculus 27-35 2476639-3 1989 The suppressive effects of TGF beta were more profound on colony formation from cells of 5-fluorouracil (5-FU)-treated mice than those of normal mice. Fluorouracil 105-109 transforming growth factor, beta 1 Mus musculus 27-35 2476639-4 1989 Addition of IL-6 or granulocyte colony-stimulating factor (G-CSF), which act synergistically with IL-3 on dormant progenitors, partially neutralized the inhibition by TGF beta of colony formation from cells of 5-FU-treated mice. Fluorouracil 210-214 colony stimulating factor 3 (granulocyte) Mus musculus 20-57 30716387-6 2019 Furthermore, MALAT1 silencing downregulated the expression of ATP-binding cassette transporters (ABC), breast cancer resistance protein (BCRP), and multi-drug resistance proteins including MDR1 and MRP1, resulting in decreased resistance of cancer cells to 5-FU. Fluorouracil 257-261 ATP binding cassette subfamily B member 6 (Langereis blood group) Homo sapiens 62-95 2476639-4 1989 Addition of IL-6 or granulocyte colony-stimulating factor (G-CSF), which act synergistically with IL-3 on dormant progenitors, partially neutralized the inhibition by TGF beta of colony formation from cells of 5-FU-treated mice. Fluorouracil 210-214 colony stimulating factor 3 (granulocyte) Mus musculus 59-64 2476639-4 1989 Addition of IL-6 or granulocyte colony-stimulating factor (G-CSF), which act synergistically with IL-3 on dormant progenitors, partially neutralized the inhibition by TGF beta of colony formation from cells of 5-FU-treated mice. Fluorouracil 210-214 transforming growth factor, beta 1 Mus musculus 167-175 31022917-0 2019 Hepatitis C Virus-Induced FUT8 Causes 5-FU Drug Resistance in Human Hepatoma Huh7.5.1 Cells. Fluorouracil 38-42 fucosyltransferase 8 Homo sapiens 26-30 31022917-5 2019 Results: We found that FUT8 not only promoted Huh7.5.1 proliferation by activating PI3K-AKT-NF-kappaB signaling, but also stimulated the expression of the drug-resistant proteins P-glycoprotein (P-gp) and multidrug resistance related protein 1 (MRP1) and enhanced the 5-fluorouracil (5-FU) chemo-resistance of Huh7.5.1 cells. Fluorouracil 268-282 fucosyltransferase 8 Homo sapiens 23-27 31022917-5 2019 Results: We found that FUT8 not only promoted Huh7.5.1 proliferation by activating PI3K-AKT-NF-kappaB signaling, but also stimulated the expression of the drug-resistant proteins P-glycoprotein (P-gp) and multidrug resistance related protein 1 (MRP1) and enhanced the 5-fluorouracil (5-FU) chemo-resistance of Huh7.5.1 cells. Fluorouracil 284-288 fucosyltransferase 8 Homo sapiens 23-27 2846312-8 1988 The effects of a 24 h in vitro exposure of KS-1 cells to a range of concentrations of 5-fluorouracil, adriamycin, mitomycin C or cisplatin have been quantitated by clonogenic assay and these values have been compared with those reported using a range of other human tumour cell lines, under comparable experimental conditions. Fluorouracil 86-100 zinc finger protein 382 Homo sapiens 43-47 31022917-6 2019 Silencing of FUT8 reduced the cell proliferation and increased the 5-FU sensitivity of HCV-infected Huh7.5.1 cells. Fluorouracil 67-71 fucosyltransferase 8 Homo sapiens 13-17 3281726-8 1988 Growth of mixed erythroid colonies from 5-FU-treated marrow is thus stimulated by adherent marrow cell-derived factors that appear distinct not only from the known CSFs including IL 3, but also from IL 1. Fluorouracil 40-44 interleukin 1 complex Mus musculus 199-203 31022917-8 2019 HCV-induced FUT8 promotes proliferation and 5-FU resistance of Huh7.5.1 cells. Fluorouracil 44-48 fucosyltransferase 8 Homo sapiens 12-16 31114248-4 2019 Results: M2 macrophages decreased the inhibitory effect of 5-FU on CRC cells migration and invasion by secreting CCL22, and declined the apoptosis induced by 5-FU. Fluorouracil 59-63 C-C motif chemokine ligand 22 Homo sapiens 113-118 31114248-9 2019 Conclusion: Our findings indicate that M2 macrophage regulated 5-FU-mediated CRC chemoresistance via the EMT program, PI3K/AKT pathway, and caspase-mediated apoptosis by releasing CCL22. Fluorouracil 63-67 C-C motif chemokine ligand 22 Homo sapiens 180-185 31019568-0 2019 Overexpression of long noncoding RNA LINC01419 in esophageal squamous cell carcinoma and its relation to the sensitivity to 5-fluorouracil by mediating GSTP1 methylation. Fluorouracil 124-138 long intergenic non-protein coding RNA 1419 Homo sapiens 37-46 3263749-4 1988 The 5-FU resistant BM progenitor is asialoGM1-, Thy.1+, Lyt.1- and Lyt.2-. Fluorouracil 4-8 CD8 antigen, alpha chain Mus musculus 67-72 31019568-2 2019 Herein, this study elucidates the role and mechanism by which LINC01419 regulates the DNA methylation of glutathione S-transferase pi 1 (GSTP1) in relation to ESCC progression and the sensitivity of ESCC cells to 5-fluorouracil (5-FU). Fluorouracil 213-227 long intergenic non-protein coding RNA 1419 Homo sapiens 62-71 31019568-2 2019 Herein, this study elucidates the role and mechanism by which LINC01419 regulates the DNA methylation of glutathione S-transferase pi 1 (GSTP1) in relation to ESCC progression and the sensitivity of ESCC cells to 5-fluorouracil (5-FU). Fluorouracil 229-233 long intergenic non-protein coding RNA 1419 Homo sapiens 62-71 31019568-6 2019 The silencing of LINC01419 led to decreased proliferation, increased apoptosis, and enhanced sensitivity to 5-FU in ESCC cells. Fluorouracil 108-112 long intergenic non-protein coding RNA 1419 Homo sapiens 17-26 3258352-1 1988 Blast colonies were developed by rIL-3 from the spleen cells of mice pretreated with 5-fluorouracil (5-FU) in the methylcellulose cultures. Fluorouracil 85-99 interleukin 3 Rattus norvegicus 33-38 31019568-7 2019 Notably, LINC01419 could bind to the promoter region of the GSTP1 gene, resulting in elevated GSTP1 methylation and reduced GSTP1 levels via the recruitment of DNA methyltransferase among ESCC cells, whereby ESCC progression was stimulated accompanied by reduced ESCC cell sensitivity to 5-FU. Fluorouracil 288-292 long intergenic non-protein coding RNA 1419 Homo sapiens 9-18 3257232-7 1988 IL-1 which synergistically interacts with various CSF species to confer a clonogenic response by primitive stem cells present in 5-fluorouracil-treated marrow also failed to stimulate eosinophil production. Fluorouracil 129-143 interleukin 1 complex Mus musculus 0-4 3257232-9 1988 Furthermore, pre-culture of 5-fluorouracil-treated marrow cells with a combination of IL-1 and IL-3 resulted in a more than 260-fold increase of CFU-eo over input numbers. Fluorouracil 28-42 interleukin 1 complex Mus musculus 86-90 31019568-8 2019 GSTP1 demethylation by 5-Aza-CdR was observed to reverse the effects of LINC01419 overexpression in ESCC cells and the response to 5-FU. Fluorouracil 131-135 long intergenic non-protein coding RNA 1419 Homo sapiens 72-81 31019568-9 2019 Conclusion: Highly expressed LINC01419 in ESCC promotes GSTP1 methylation, which ultimately acts to promote the event of ESCC and diminish the sensitivity of ESCC cells to 5-FU, highlighting a novel potential strategy to improve 5-FU-based chemotherapy in ESCC. Fluorouracil 172-176 long intergenic non-protein coding RNA 1419 Homo sapiens 29-38 31019568-9 2019 Conclusion: Highly expressed LINC01419 in ESCC promotes GSTP1 methylation, which ultimately acts to promote the event of ESCC and diminish the sensitivity of ESCC cells to 5-FU, highlighting a novel potential strategy to improve 5-FU-based chemotherapy in ESCC. Fluorouracil 229-233 long intergenic non-protein coding RNA 1419 Homo sapiens 29-38 31037126-7 2019 The potential of systemic miR-29c oligonucleotide-based therapy in overcoming 5-FU chemoresistance was evaluated in tumor xenograft model. Fluorouracil 78-82 microRNA 29c Homo sapiens 26-33 31037126-10 2019 Systemically administered miR-29c dramatically improved response of 5-FU chemoresistant ESCC xenografts in vivo. Fluorouracil 68-72 microRNA 29c Homo sapiens 26-33 30782177-10 2019 Knockdown of KRT16 enhanced chemosensitivity of OSCC towards 5-fluorouracil (5-FU). Fluorouracil 61-75 keratin 16 Homo sapiens 13-18 30782177-10 2019 Knockdown of KRT16 enhanced chemosensitivity of OSCC towards 5-fluorouracil (5-FU). Fluorouracil 77-81 keratin 16 Homo sapiens 13-18 30531622-8 2019 Through this analysis, the authors found a set of genes, including YAP1 and CCL-2, whose expression changes predict 5-fluorouracil therapy status and include genes that have not previously been associated with keloid biology and are of unknown function. Fluorouracil 116-130 Yes1 associated transcriptional regulator Homo sapiens 67-71 3120645-7 1987 Values of the skin reaction after dosing were significantly (p less than 0.05) high compared to those before dosing in groups A and C. Concentrations of Tegafur and 5-FU in serum reached to the peak 2 hr later and were maintained high enough to expect clinical responses even at 4 hr after administration in groups A and B. Fluorouracil 165-169 PEAK1 related, kinase-activating pseudokinase 1 Homo sapiens 194-200 29957058-5 2019 Both coinjection of debris and systemic treatment with 5-FU increased plasma OPN levels in tumor-bearing mice. Fluorouracil 55-59 secreted phosphoprotein 1 Mus musculus 77-80 3897094-5 1985 The dose effect factor (DEF) was 9.11 for 5-FU and in the range 1.25-1.59 for the other drugs. Fluorouracil 42-46 UTP25 small subunit processome component Mus musculus 24-27 3974248-5 1985 The author discovered for the first time that oral administration of 5-Fu could improve the liver function as manifested by a marked decrease of serum GPT level in advanced gastric cancer. Fluorouracil 69-73 glutamic--pyruvic transaminase Homo sapiens 151-154 6329908-2 1984 Selection depends on the 5-fluorouracil + 5" AMP resistance of upp- ush - [ pLA7ush ::cloned DNA] cells, whereas upp- ush - [ pLA7ush +] cells are sensitive under the same conditions. Fluorouracil 25-39 uridine phosphorylase 1 Homo sapiens 63-66 29495973-0 2018 MicroRNA-623 Targets Cyclin D1 to Inhibit Cell Proliferation and Enhance the Chemosensitivity of Cells to 5-Fluorouracil in Gastric Cancer. Fluorouracil 106-120 cyclin D1 Homo sapiens 21-30 30692503-7 2018 Interestingly, the panel also revealed that he had mismatch-repair(MMR)deficiency with MSH2 mutation, which is reported as a possible cause of resistance to 5-fluorouracil in colorectal cancer. Fluorouracil 157-171 mutS homolog 2 Homo sapiens 87-91 6451639-0 1981 5-Fluorouracil as an aid in management of acne and melasma. Fluorouracil 0-14 activation induced cytidine deaminase Homo sapiens 21-24 31949673-0 2018 Knockdown of PHGDH potentiates 5-FU cytotoxicity in gastric cancer cells via the Bcl-2/Bax/caspase-3 signaling pathway. Fluorouracil 31-35 phosphoglycerate dehydrogenase Homo sapiens 13-18 6966969-0 1980 Association of host immunity with 5-fluorouracil-initiated cure of plasmacytoma LPC-1 in BALB/c mice. Fluorouracil 34-48 annexin A1 Mus musculus 80-85 31949673-3 2018 Phosphoglycerate dehydrogenase (PHGDH) has been reported to play a vital role in the development of 5-FU resistance in cancer cells. Fluorouracil 100-104 phosphoglycerate dehydrogenase Homo sapiens 0-30 31949673-3 2018 Phosphoglycerate dehydrogenase (PHGDH) has been reported to play a vital role in the development of 5-FU resistance in cancer cells. Fluorouracil 100-104 phosphoglycerate dehydrogenase Homo sapiens 32-37 31949673-5 2018 In this study, PHGDH expression was much higher in the GC tissues of 5-FU-resistant patients than that in the GC tissues of 5-FU-sensitive patients. Fluorouracil 69-73 phosphoglycerate dehydrogenase Homo sapiens 15-20 31949673-5 2018 In this study, PHGDH expression was much higher in the GC tissues of 5-FU-resistant patients than that in the GC tissues of 5-FU-sensitive patients. Fluorouracil 124-128 phosphoglycerate dehydrogenase Homo sapiens 15-20 1257062-0 1976 [5-fluorouracil effectiveness and toxicity in the treatment of digestive trac.t neoplasms as a function of the mode of administration]. Fluorouracil 1-15 T cell receptor alpha constant Homo sapiens 73-77 31949673-6 2018 Moreover, the expression of PHGDH was obviously increased in BGC823/5-FU cells compared with that in BGC823 cells. Fluorouracil 68-72 phosphoglycerate dehydrogenase Homo sapiens 28-33 165496-3 1975 In 5-fluorouracil and 5-chlorouracil, however, the halogen is evidently abstracted by the Na to form NaF or NaC1 and the neutral uracil radical. Fluorouracil 3-17 nucleus accumbens associated 1 Homo sapiens 108-112 31949673-9 2018 The knockdown of PHGDH made possible the inhibitory effect of 5-FU on the proliferation of BGC823/5-FU cells. Fluorouracil 62-66 phosphoglycerate dehydrogenase Homo sapiens 17-22 34042519-8 2021 Results: PD increased 5-FU-induced ICD in CRC cells, as demonstrated by the extracellular levels of adenosine triphosphate (ATP) and high-mobility group box 1 (HMGB1), and the surface levels of calreticulin (CRT). Fluorouracil 22-26 high mobility group box 1 Mus musculus 133-158 31949673-9 2018 The knockdown of PHGDH made possible the inhibitory effect of 5-FU on the proliferation of BGC823/5-FU cells. Fluorouracil 98-102 phosphoglycerate dehydrogenase Homo sapiens 17-22 34042519-8 2021 Results: PD increased 5-FU-induced ICD in CRC cells, as demonstrated by the extracellular levels of adenosine triphosphate (ATP) and high-mobility group box 1 (HMGB1), and the surface levels of calreticulin (CRT). Fluorouracil 22-26 high mobility group box 1 Mus musculus 160-165 31949673-11 2018 Notably, the promoting effect of 5-FU on the apoptosis of BGC823/5-FU cells was markedly enhanced by PHGDH knockdown. Fluorouracil 33-37 phosphoglycerate dehydrogenase Homo sapiens 101-106 31949673-11 2018 Notably, the promoting effect of 5-FU on the apoptosis of BGC823/5-FU cells was markedly enhanced by PHGDH knockdown. Fluorouracil 65-69 phosphoglycerate dehydrogenase Homo sapiens 101-106 31949673-12 2018 Additionally, 5-FU treatment downregulated Bcl-2 expression and upregulated the expression of Bax and caspase-3, and this effect was remarkably enhanced by PHGDH knockdown. Fluorouracil 14-18 phosphoglycerate dehydrogenase Homo sapiens 156-161 31949673-13 2018 In conclusion, knockdown of PHGDH potentiates 5-FU cytotoxicity in GC cells via the Bcl-2/Bax/caspase-3 signaling pathway. Fluorouracil 46-50 phosphoglycerate dehydrogenase Homo sapiens 28-33 30539860-8 2018 Consistently, 3-MA inhibited, while rapamycin facilitated 5-FU-induced expressions of Beclin1 and LC3B. Fluorouracil 58-62 microtubule associated protein 1 light chain 3 beta Homo sapiens 98-102 33855690-1 2021 INTRODUCTION: The phase III KEYNOTE-048 trial showed that the programmed death receptor 1 (PD-1) inhibitor pembrolizumab, in the combined positive score (CPS) >= 1 population and combined with platinum + 5-fluorouracil in the total population, improves survival over cetuximab + platinum + 5-fluorouracil in recurrent or metastatic (R/M) head and neck squamous cell carcinoma (HNSCC). Fluorouracil 204-218 programmed cell death 1 Homo sapiens 91-95 33855690-1 2021 INTRODUCTION: The phase III KEYNOTE-048 trial showed that the programmed death receptor 1 (PD-1) inhibitor pembrolizumab, in the combined positive score (CPS) >= 1 population and combined with platinum + 5-fluorouracil in the total population, improves survival over cetuximab + platinum + 5-fluorouracil in recurrent or metastatic (R/M) head and neck squamous cell carcinoma (HNSCC). Fluorouracil 290-304 programmed cell death 1 Homo sapiens 62-89 33855690-1 2021 INTRODUCTION: The phase III KEYNOTE-048 trial showed that the programmed death receptor 1 (PD-1) inhibitor pembrolizumab, in the combined positive score (CPS) >= 1 population and combined with platinum + 5-fluorouracil in the total population, improves survival over cetuximab + platinum + 5-fluorouracil in recurrent or metastatic (R/M) head and neck squamous cell carcinoma (HNSCC). Fluorouracil 290-304 programmed cell death 1 Homo sapiens 91-95 30250581-9 2018 Notably, miR-1260b inhibitor could significantly enhanced the chemoresponse of HCT116 cells to 5-FU via reduced proliferation, increased apoptosis, and downregulation of PDCD4, p-Akt and p-ERK protein expression. Fluorouracil 95-99 programmed cell death 4 Homo sapiens 170-175 33059056-5 2021 In HCC cell lines of Huh7 and Hep3B, LINC01189 was upregulated to investigate its effects on cancer cell proliferation and 5-FU chemoresistance. Fluorouracil 123-127 long intergenic non-protein coding RNA 1189 Homo sapiens 37-46 29890207-5 2018 Further studies revealed that ASPP2 downregulation promoted EMT and increased resistance to 5-Fluorouracil (5-FU)-induced apoptosis. Fluorouracil 92-106 tumor protein p53 binding protein 2 Homo sapiens 30-35 33059056-9 2021 LINC01189 overexpression inhibited HCC cancer cell proliferation and 5-FU chemoresistance. Fluorouracil 69-73 long intergenic non-protein coding RNA 1189 Homo sapiens 0-9 33059056-11 2021 Upregulating hsa-miR-155-5p reversed the LINC01189-mediated inhibition on HCC proliferation and 5-FU chemoresistance. Fluorouracil 96-100 long intergenic non-protein coding RNA 1189 Homo sapiens 41-50 33938344-0 2021 LncRNA ENSG00000254615 Modulates Proliferation and 5-FU Resistance by Regulating p21 and Cyclin D1 in Colorectal Cancer. Fluorouracil 51-55 cyclin D1 Homo sapiens 89-98 29890207-5 2018 Further studies revealed that ASPP2 downregulation promoted EMT and increased resistance to 5-Fluorouracil (5-FU)-induced apoptosis. Fluorouracil 108-112 tumor protein p53 binding protein 2 Homo sapiens 30-35 30174840-0 2018 Genetic and pharmacological inhibition of eIF4E effectively targets esophageal cancer cells and augments 5-FU"s efficacy. Fluorouracil 105-109 eukaryotic translation initiation factor 4E Homo sapiens 42-47 33986804-5 2021 The effect of E2F1 on gastric cancer cell sensitivity of 5-Fu was evaluated using cell viability assay and TdT-mediated dUTP Nick-End Labeling staining. Fluorouracil 57-61 E2F transcription factor 1 L homeolog Xenopus laevis 14-18 29702091-5 2018 Significantly, MALAT1 deletion sensitized HepG2 cells to 5-FU-induced cell cycle arrest in G1 phase, as evidenced by the significant reduction in Cyclin D1 and CDK4 and increase in p53, p21 and p27 protein levels. Fluorouracil 57-61 cyclin D1 Homo sapiens 146-155 33731881-7 2021 The median expression of 5-FU-related genes TYMS, TYMP, and DYPD was significantly higher in mucinous CRC compared to non-mucinous CRC (p < 0.001, p = 0.003, p < 0.001, respectively). Fluorouracil 25-29 thymidine phosphorylase Homo sapiens 50-54 29702091-5 2018 Significantly, MALAT1 deletion sensitized HepG2 cells to 5-FU-induced cell cycle arrest in G1 phase, as evidenced by the significant reduction in Cyclin D1 and CDK4 and increase in p53, p21 and p27 protein levels. Fluorouracil 57-61 cyclin dependent kinase 4 Homo sapiens 160-164 29702091-9 2018 The nude mice transplantation model also confirmed the promoted sensitivity of MALAT1-silenced HepG2 cells to 5-FU by blocking tumor cell proliferation and inducing apoptosis. Fluorouracil 110-114 metastasis associated lung adenocarcinoma transcript 1 (non-coding RNA) Mus musculus 79-85 33645623-0 2021 Inhibition of lncRNA-NEAT1 sensitizes 5-Fu resistant cervical cancer cells through de-repressing the microRNA-34a/LDHA axis. Fluorouracil 38-42 microRNA 34a Homo sapiens 101-113 33645623-9 2021 Overexpression of miR-34a significantly sensitized 5-Fu resistant cells. Fluorouracil 51-55 microRNA 34a Homo sapiens 18-25 29535127-1 2018 Purpose: A recent study reported that 5-fluorouracil (5-FU)-based chemotherapy is less effective in treating patients with advanced colorectal cancer demonstrating hypermethylation of the TFAP2E gene. Fluorouracil 38-52 transcription factor AP-2 epsilon Homo sapiens 188-194 33645623-15 2021 Finally, we demonstrated inhibition of NEAT1 significantly sensitized cervical cancer cells to 5-Fu through the miR-34a/LDHA pathway. Fluorouracil 95-99 microRNA 34a Homo sapiens 112-119 29535127-1 2018 Purpose: A recent study reported that 5-fluorouracil (5-FU)-based chemotherapy is less effective in treating patients with advanced colorectal cancer demonstrating hypermethylation of the TFAP2E gene. Fluorouracil 54-58 transcription factor AP-2 epsilon Homo sapiens 188-194 29738539-2 2018 In the yeast Saccharomyces cerevisiae, overexpression of the HAM1 gene encoding inosine triphosphate pyrophosphatase confers resistance to both the purine analogue 6-N-hydroxylaminopurine (HAP) and the pyrimidine analogue 5-fluorouracil (5-FU) (Carlsson et al., 2013, PLoS One 8, e52094). Fluorouracil 222-236 nucleoside triphosphate pyrophosphohydrolase HAM1 Saccharomyces cerevisiae S288C 61-65 29738539-2 2018 In the yeast Saccharomyces cerevisiae, overexpression of the HAM1 gene encoding inosine triphosphate pyrophosphatase confers resistance to both the purine analogue 6-N-hydroxylaminopurine (HAP) and the pyrimidine analogue 5-fluorouracil (5-FU) (Carlsson et al., 2013, PLoS One 8, e52094). Fluorouracil 238-242 nucleoside triphosphate pyrophosphohydrolase HAM1 Saccharomyces cerevisiae S288C 61-65 29738539-6 2018 We found that HMS1, LOG1 (YJL055W), HAM1, and ATR1 confer resistance to both 5-FU and HAP, whereas ADE4, DUT1 and APT2 are specific for HAP resistance, and CPA1 and CPA2 specific for 5-FU resistance. Fluorouracil 77-81 nucleoside triphosphate pyrophosphohydrolase HAM1 Saccharomyces cerevisiae S288C 36-40 29635904-2 2018 The purpose of this study is to determine whether the gene glycerophosphodiester phosphodiesterase domain containing 5 (GDPD5) contributes to CRC cell metastasis and 5-Fu resistance. Fluorouracil 166-170 glycerophosphodiester phosphodiesterase domain containing 5 Homo sapiens 59-118 33499874-12 2021 LINC00680 overexpression significantly enhanced HCC cell stemness and decreased in vitro and in vivo chemosensitivity to 5-fluorouracil (5-Fu), whereas LINC00680 knockdown led to opposite results. Fluorouracil 121-135 long intergenic non-protein coding RNA 680 Homo sapiens 0-9 29635904-2 2018 The purpose of this study is to determine whether the gene glycerophosphodiester phosphodiesterase domain containing 5 (GDPD5) contributes to CRC cell metastasis and 5-Fu resistance. Fluorouracil 166-170 glycerophosphodiester phosphodiesterase domain containing 5 Homo sapiens 120-125 33499874-12 2021 LINC00680 overexpression significantly enhanced HCC cell stemness and decreased in vitro and in vivo chemosensitivity to 5-fluorouracil (5-Fu), whereas LINC00680 knockdown led to opposite results. Fluorouracil 137-141 long intergenic non-protein coding RNA 680 Homo sapiens 0-9 29635904-7 2018 Transwell Matrigel invasion assays were performed to explore whether GDPD5 affects the invasion capabilities of 5-Fu resistant CRC cells. Fluorouracil 112-116 glycerophosphodiester phosphodiesterase domain containing 5 Homo sapiens 69-74 31938367-7 2018 In addition, our results showed that overall survival among Zhuang NPC patients with low expression of MTA2 increased significantly owing to "carboplatin + fluorouracil" chemotherapy. Fluorouracil 156-168 metastasis associated 1 family member 2 Homo sapiens 103-107 29512733-9 2018 The present study quantified changes in sirtuin (SIRT1, SIRT3, SIRT5, and SIRT6) expression following 5-FU treatment and using a specific inhibitor, sirtinol, the present study investigated their involvement in 5-FU-mediated autophagy. Fluorouracil 102-106 sirtuin 6 Homo sapiens 74-79 29352327-11 2018 In addition, immunofluorescence analysis showed increased expression of active cofilin, LIMK1, LIMK2, and SSH1 in HT29 colon cancer cells resistant to 5-fluorouracil compared to parental HT29 cells. Fluorouracil 151-165 cofilin 1 Homo sapiens 79-86 29352327-11 2018 In addition, immunofluorescence analysis showed increased expression of active cofilin, LIMK1, LIMK2, and SSH1 in HT29 colon cancer cells resistant to 5-fluorouracil compared to parental HT29 cells. Fluorouracil 151-165 LIM domain kinase 1 Homo sapiens 88-93 28722334-0 2018 Potential emerging treatment in vitiligo using Er:YAG in combination with 5FU and clobetasol. Fluorouracil 74-77 VAMAS6 Homo sapiens 32-40 28884413-5 2018 The results showed that knockdown of PCAT-1 in CRC cells suppressed cell motility and invasiveness, and sensitized the cells to 5-fluorouracil, as evidenced by the reduced viability and induced apoptosis in PCAT-1-silenced cells compared to the parental cells in response to 5-fluorouracil treatment. Fluorouracil 128-142 prostate cancer associated transcript 1 Homo sapiens 37-43 28884413-5 2018 The results showed that knockdown of PCAT-1 in CRC cells suppressed cell motility and invasiveness, and sensitized the cells to 5-fluorouracil, as evidenced by the reduced viability and induced apoptosis in PCAT-1-silenced cells compared to the parental cells in response to 5-fluorouracil treatment. Fluorouracil 128-142 prostate cancer associated transcript 1 Homo sapiens 207-213 28884413-5 2018 The results showed that knockdown of PCAT-1 in CRC cells suppressed cell motility and invasiveness, and sensitized the cells to 5-fluorouracil, as evidenced by the reduced viability and induced apoptosis in PCAT-1-silenced cells compared to the parental cells in response to 5-fluorouracil treatment. Fluorouracil 275-289 prostate cancer associated transcript 1 Homo sapiens 37-43 29543785-14 2018 Inhibition of TUG1 reduced the growth of tumors in vivo and improved the chemosensitivity of A375 cells to cisplatin and 5-FU. Fluorouracil 121-125 taurine up-regulated 1 Homo sapiens 14-18 29872564-9 2018 To conclude, CCL22 was identified as an independent adverse prognostic immunobiomarker for patients with gastric cancer after surgery, which is associated with tumor-infiltrating immunocytes and could be incorporated into TNM staging system to redefine a high-risk subgroup who were more likely to benefit from 5-fluorouracil based adjuvant chemotherapy. Fluorouracil 311-325 C-C motif chemokine ligand 22 Homo sapiens 13-18 33564301-10 2021 A tremendous rise of the CD3+/CD8+ count and a significant decrease of CD3+CD4+/CD3+CD8+ ratios were found in the 5-FU group and were both reversed by Lcr35. Fluorouracil 114-118 CD3 antigen, epsilon polypeptide Mus musculus 25-28 33564301-10 2021 A tremendous rise of the CD3+/CD8+ count and a significant decrease of CD3+CD4+/CD3+CD8+ ratios were found in the 5-FU group and were both reversed by Lcr35. Fluorouracil 114-118 CD3 antigen, epsilon polypeptide Mus musculus 71-74 33564301-10 2021 A tremendous rise of the CD3+/CD8+ count and a significant decrease of CD3+CD4+/CD3+CD8+ ratios were found in the 5-FU group and were both reversed by Lcr35. Fluorouracil 114-118 CD3 antigen, epsilon polypeptide Mus musculus 71-74 33569416-0 2021 Repressing PDCD4 activates JNK/ABCG2 pathway to induce chemoresistance to fluorouracil in colorectal cancer cells. Fluorouracil 74-86 programmed cell death 4 Homo sapiens 11-16 33569416-12 2021 Overexpression of PDCD4 inhibited phosphorylation of c-Jun and ABCG2 expression, and recovered sensitivity to 5-FU in HCT116/FUR cells. Fluorouracil 110-114 programmed cell death 4 Homo sapiens 18-23 33569416-16 2021 Conclusions: Our results demonstrated that 5-FU treatment upregulated miR-21, which directly repressed PDCD4, and subsequently activated the JNK pathway, leading to the upregulation of ABCG2 in CRC cells. Fluorouracil 43-47 programmed cell death 4 Homo sapiens 103-108 33276189-1 2021 Three new fluorescent molecular rotors were synthesized with the aim of using them as sensors to dose thymidine phosphorylase, one of the target enzymes of 5-fluorouracil, a potent chemotherapic drug largely used in the treatment of many solid tumors, that acts by hindering the metabolism of pyrimidines. Fluorouracil 156-170 thymidine phosphorylase Homo sapiens 102-125 31846964-4 2021 METHODS: Small intestinal mucositis was induced in wild-type, NLRP3-/-, and caspase-1-/- mice by intraperitoneal injection of 5-FU. Fluorouracil 126-130 caspase 1 Mus musculus 76-85 33240411-0 2021 Overexpression of microRNA-124-5p sensitizes non-small cell lung cancer cells to treatment with 5-fluorouracil via AEG-1 regulation. Fluorouracil 96-110 microRNA 1245a Homo sapiens 18-33 33240411-5 2021 Transfection with a miR-124-5p mimic enhanced inhibition of cell viability induced by 5-FU in A549/5-FU cells, whereas miR-124-5p inhibitor transfection partially reversed 5-FU-induced cell viability inhibition in A549 and H1299 cells. Fluorouracil 86-90 microRNA 1245a Homo sapiens 20-30 33240411-5 2021 Transfection with a miR-124-5p mimic enhanced inhibition of cell viability induced by 5-FU in A549/5-FU cells, whereas miR-124-5p inhibitor transfection partially reversed 5-FU-induced cell viability inhibition in A549 and H1299 cells. Fluorouracil 99-103 microRNA 1245a Homo sapiens 20-30 33240411-5 2021 Transfection with a miR-124-5p mimic enhanced inhibition of cell viability induced by 5-FU in A549/5-FU cells, whereas miR-124-5p inhibitor transfection partially reversed 5-FU-induced cell viability inhibition in A549 and H1299 cells. Fluorouracil 99-103 microRNA 1245a Homo sapiens 20-30 33240411-6 2021 A decrease in miR-124-5p expression level was observed in A549/5-FU cells compared with the parental A549 cells. Fluorouracil 63-67 microRNA 1245a Homo sapiens 14-24 33240411-7 2021 Furthermore, AEG-1 was predicted as a target gene of miR-124-5p, and its expression was increased in A549/5-FU cells compared with A549 cells. Fluorouracil 106-110 microRNA 1245a Homo sapiens 53-63 33240411-8 2021 Additionally, the upregulation of miR-124-5p was associated with lower expression levels of AEG-1 in A549/5-FU cells, compared with parental A549 cells. Fluorouracil 106-110 microRNA 1245a Homo sapiens 34-44 33240411-10 2021 Notably, the overexpression of AEG-1 reversed the ability of the miR-124-5p mimic to increase the sensitivity of A549/5-FU cells to 5-FU treatment. Fluorouracil 118-122 microRNA 1245a Homo sapiens 65-75 33240411-10 2021 Notably, the overexpression of AEG-1 reversed the ability of the miR-124-5p mimic to increase the sensitivity of A549/5-FU cells to 5-FU treatment. Fluorouracil 132-136 microRNA 1245a Homo sapiens 65-75 33935122-9 2021 CXCR2 was significantly over expressed in HeLa cells treated with 5FU (8.66-fold) and AgNPs-F (1.12-fold) but under expressed in cells treated with AgNPs-L (0.76-fold). Fluorouracil 66-69 C-X-C motif chemokine receptor 2 Homo sapiens 0-5 29053388-7 2018 The cells treated with 5-FU or IRINO exhibited several hallmarks of SIPS: growth arrest, increased size and granularity, polyploidization, augmented activity of the SA-beta-galactosidase, accumulation of P21 and CYCLIN D1 proteins, and the senescence-associated secretory phenotype. Fluorouracil 23-27 galactosidase beta 1 Homo sapiens 168-186 29053388-7 2018 The cells treated with 5-FU or IRINO exhibited several hallmarks of SIPS: growth arrest, increased size and granularity, polyploidization, augmented activity of the SA-beta-galactosidase, accumulation of P21 and CYCLIN D1 proteins, and the senescence-associated secretory phenotype. Fluorouracil 23-27 cyclin D1 Homo sapiens 212-221 29202398-1 2018 Previously a novel ubenimex-fluorouracil (5-FU) conjugate, BC-01 was identified and validated as a potent CD13 inhibitor with marked in vitro and in vivo antitumor potency. Fluorouracil 42-46 alanyl aminopeptidase, membrane Homo sapiens 106-110 32338281-5 2020 In vitro, TUSC3 promotes the formation of stemness and induces the drug resistance to 5-fluorouracil (5-FU) and cis-Dichlorodiammineplatinum(II) (DDP) in CRC cells. Fluorouracil 86-100 tumor suppressor candidate 3 Homo sapiens 10-15 32338281-5 2020 In vitro, TUSC3 promotes the formation of stemness and induces the drug resistance to 5-fluorouracil (5-FU) and cis-Dichlorodiammineplatinum(II) (DDP) in CRC cells. Fluorouracil 102-106 tumor suppressor candidate 3 Homo sapiens 10-15 33354409-6 2020 Results indicated that gastric cancer patients with high IL-9 expression showed improved overall survival and gained more benefit from 5-fluorouracil-based adjuvant chemotherapy (ACT). Fluorouracil 135-149 interleukin 9 Homo sapiens 57-61 33051247-5 2020 Further studies showed that protein levels of multidrug resistance-associated protein 5 (MRP5/ABCC5), a 5-FU efflux transporter, were reduced around 50% by let-7c in HCC cells. Fluorouracil 104-108 ATP binding cassette subfamily C member 5 Homo sapiens 46-87 33051247-5 2020 Further studies showed that protein levels of multidrug resistance-associated protein 5 (MRP5/ABCC5), a 5-FU efflux transporter, were reduced around 50% by let-7c in HCC cells. Fluorouracil 104-108 ATP binding cassette subfamily C member 5 Homo sapiens 89-93 33051247-5 2020 Further studies showed that protein levels of multidrug resistance-associated protein 5 (MRP5/ABCC5), a 5-FU efflux transporter, were reduced around 50% by let-7c in HCC cells. Fluorouracil 104-108 ATP binding cassette subfamily C member 5 Homo sapiens 94-99 33051247-12 2020 In particular, let-7c enhances 5-FU exposure (via suppressing ABCC5/MRP5 expression) and co-targets thymidylate synthase with 5-FU (let-7c reduces protein expression while 5-FU irreversibly inactivates enzyme). Fluorouracil 31-35 ATP binding cassette subfamily C member 5 Homo sapiens 62-67 33051247-12 2020 In particular, let-7c enhances 5-FU exposure (via suppressing ABCC5/MRP5 expression) and co-targets thymidylate synthase with 5-FU (let-7c reduces protein expression while 5-FU irreversibly inactivates enzyme). Fluorouracil 31-35 ATP binding cassette subfamily C member 5 Homo sapiens 68-72 33051247-12 2020 In particular, let-7c enhances 5-FU exposure (via suppressing ABCC5/MRP5 expression) and co-targets thymidylate synthase with 5-FU (let-7c reduces protein expression while 5-FU irreversibly inactivates enzyme). Fluorouracil 126-130 ATP binding cassette subfamily C member 5 Homo sapiens 62-67 33051247-12 2020 In particular, let-7c enhances 5-FU exposure (via suppressing ABCC5/MRP5 expression) and co-targets thymidylate synthase with 5-FU (let-7c reduces protein expression while 5-FU irreversibly inactivates enzyme). Fluorouracil 126-130 ATP binding cassette subfamily C member 5 Homo sapiens 68-72 33299895-0 2020 M2 Macrophages Mediate the Resistance of Gastric Adenocarcinoma Cells to 5-Fluorouracil through the Expression of Integrin beta3, Focal Adhesion Kinase, and Cofilin. Fluorouracil 73-87 cofilin 1 Homo sapiens 157-164 33299895-8 2020 These results reveal that integrin beta3, focal adhesion protein (FAK), and cofilin proteins are potential targets for the improvement of fluorouracil efficacy in gastric cancer treatment. Fluorouracil 138-150 protein tyrosine kinase 2 Homo sapiens 66-69 33299895-8 2020 These results reveal that integrin beta3, focal adhesion protein (FAK), and cofilin proteins are potential targets for the improvement of fluorouracil efficacy in gastric cancer treatment. Fluorouracil 138-150 cofilin 1 Homo sapiens 76-83 33177877-8 2020 Results: We found that CDK1 was highly expressed in tumor tissues, especially in fluorouracil-resistant tissues. Fluorouracil 81-93 cyclin-dependent kinase 1 Mus musculus 23-27 33177877-10 2020 CDK1 promoted migration, invasion and inhibited apoptosis in 5-Fu-resistant CRC cells. Fluorouracil 61-65 cyclin-dependent kinase 1 Mus musculus 0-4 33177877-11 2020 Down-regulation of CDK1 inhibited fluorouracil-resistant CRC cell proliferation and tumorigenesis in vivo. Fluorouracil 34-46 cyclin-dependent kinase 1 Mus musculus 19-23 28226315-8 2018 Combined treatment with LEE011 and 5-fluorouracil or everolimus showed a significant enhancement in the inhibition of cell viability when compared to single-substance treatments due to PI3K-Akt-mTOR and Ras-Raf-MEK-ERK pathway downregulation and cooperative downregulation of cell cycle components. Fluorouracil 35-49 zinc fingers and homeoboxes 2 Homo sapiens 207-210 33177877-12 2020 Conclusion: High expression of CDK1 may lead to poor clinical prognosis, and inhibition of CDK1 enhances 5-Fu sensitivity in CRC. Fluorouracil 105-109 cyclin-dependent kinase 1 Mus musculus 91-95 28226315-10 2018 CONCLUSIONS: Our data demonstrate that the CDK 4/6 inhibitor LEE011 exhibits promising anti-tumoral properties alone and in combination treatment approaches with 5-fluorouracil or everolimus in human neuroendocrine tumor cell lines. Fluorouracil 162-176 cyclin dependent kinase 4 Homo sapiens 43-50 30285552-1 2018 The enzyme thymidine phosphorylase (TP) is important for activation of capecitabine and 5-fluorouracil. Fluorouracil 88-102 thymidine phosphorylase Homo sapiens 11-34 33195236-4 2020 Expression of ATF3 was significantly down-regulated in long-term HSCs (LT-HSCs) after exposure to stresses such as 5-fluorouracil challenge or irradiation. Fluorouracil 115-129 activating transcription factor 3 Mus musculus 14-18 32904684-12 2020 Further investigations revealed that the constitutive activation of STAT3 may be induced by JAK1 and JAK2, and thus effect the 5-FU resistance by regulating NHE1. Fluorouracil 127-131 Janus kinase 2 Homo sapiens 101-105 32922964-10 2020 Polymorphisms of the glucocorticoid receptor and variants of CCL2, YAP1, miR-21-5p and NF-kappabeta might be responsible for different responses to treatments used in keloid scars such as 5-fluorouracil. Fluorouracil 188-202 Yes1 associated transcriptional regulator Homo sapiens 67-71 30285552-1 2018 The enzyme thymidine phosphorylase (TP) is important for activation of capecitabine and 5-fluorouracil. Fluorouracil 88-102 thymidine phosphorylase Homo sapiens 36-38 32777949-6 2021 The 5-FU group had higher AST, ALT, LDH, and CPK levels than those in the 5-FU + Vit-D group. Fluorouracil 4-8 phosphatidylinositol-4-phosphate 3-kinase catalytic subunit type 2 alpha Homo sapiens 45-48 29487697-1 2018 Our study addresses the issue of the clinical reliability of three candidate DPYD and one UGT single nucleotide polymorphisms in predicting 5-fluorouracil- and irinotecan-related adverse events. Fluorouracil 140-154 UDP glucuronosyltransferase family 1 member A complex locus Homo sapiens 90-93 32367570-8 2020 Therefore, the function of NNMT on 5-FU sensitivity was analyzed in vitro and in vivo. Fluorouracil 35-39 nicotinamide N-methyltransferase Homo sapiens 27-31 32367570-9 2020 NNMT downregulation significantly increased 5-FU sensitivity in TE1 cells. Fluorouracil 44-48 nicotinamide N-methyltransferase Homo sapiens 0-4 31922572-0 2020 Expression quantitative trait loci in ABC transporters are associated with survival in 5-FU treated colorectal cancer patients. Fluorouracil 87-91 ATP binding cassette subfamily B member 6 (Langereis blood group) Homo sapiens 38-41 32418739-0 2020 CCND1 silencing suppresses liver cancer stem cell differentiation and overcomes 5-Fluorouracil resistance in hepatocellular carcinoma. Fluorouracil 80-94 cyclin D1 Homo sapiens 0-5 32418739-5 2020 Herein, this study was designed to explore the role of CCND1 in regulating LCSCs differentiation and 5-Fu resistance in HCC cells. Fluorouracil 101-105 cyclin D1 Homo sapiens 55-60 32418739-10 2020 Furthermore, CCND1 silencing significantly increased protein level of gamma-H2AX and decreased that of RAD51 under 5-Fu exposure. Fluorouracil 115-119 cyclin D1 Homo sapiens 13-18 32418739-11 2020 Moreover, CCND1 silencing enhanced the sensitivity of HepG2 and SMMC-7721 cells to 5-Fu, which was effectively abrogated by RAD51 upregulation. Fluorouracil 83-87 cyclin D1 Homo sapiens 10-15 32418739-12 2020 CONCLUSION: Collectively, CCND1 silencing suppresses LCSCs differentiation and overcomes 5-Fu resistance in HCC. Fluorouracil 89-93 cyclin D1 Homo sapiens 26-31 32319648-10 2020 Notably, the CRC cells with low MUC1 expression levels and high expression levels of the other MUCs (MUC2, MU4 and MUC5AC) were shown to benefit from 5-FU treatment. Fluorouracil 150-154 mucin 1, cell surface associated Homo sapiens 32-36 29416778-7 2018 Additionally, by replacing uracil in miR-15a with 5-fluorouracil, we created a novel miR-15a mimic with enhanced therapeutic potential. Fluorouracil 50-64 microRNA 15a Homo sapiens 85-92 32560278-10 2020 These results suggest that the COX-2 pathway is one of the underlying protective mechanisms of RUT against 5-FU-induced intestinal mucositis. Fluorouracil 107-111 prostaglandin-endoperoxide synthase 2 Mus musculus 31-36 32606741-0 2020 beta-Elemene Enhances the Chemotherapeutic Effect of 5-Fluorouracil in Triple-Negative Breast Cancer via PI3K/AKT, RAF-MEK-ErK, and NF-kappaB Signaling Pathways. Fluorouracil 53-67 zinc fingers and homeoboxes 2 Homo sapiens 115-118 32606741-6 2020 In molecular mechanisms, ELE and 5-FU in combination enhances apoptosis in both cell lines through Bl-2 family protein and caspase cascade modulation, thereby inhibiting NF-kB pathway through IKKbeta, IKKalpha, and p65 downregulation in the cytoplasm and p50 and p65 downregulation in the nucleus. Fluorouracil 33-37 RELA proto-oncogene, NF-kB subunit Homo sapiens 215-218 32606741-6 2020 In molecular mechanisms, ELE and 5-FU in combination enhances apoptosis in both cell lines through Bl-2 family protein and caspase cascade modulation, thereby inhibiting NF-kB pathway through IKKbeta, IKKalpha, and p65 downregulation in the cytoplasm and p50 and p65 downregulation in the nucleus. Fluorouracil 33-37 RELA proto-oncogene, NF-kB subunit Homo sapiens 263-266 32606741-7 2020 ELE and 5-FU in combination regulated the PI3K/AKT pathway through p-AKT, P-85, p110r, p-PDK1, and p110a protein and RAF-MEK-ERK pathway inhibition through the p-c-raf and p-ERK downregulation. Fluorouracil 8-12 zinc fingers and homeoboxes 2 Homo sapiens 117-120 32606741-7 2020 ELE and 5-FU in combination regulated the PI3K/AKT pathway through p-AKT, P-85, p110r, p-PDK1, and p110a protein and RAF-MEK-ERK pathway inhibition through the p-c-raf and p-ERK downregulation. Fluorouracil 8-12 Raf-1 proto-oncogene, serine/threonine kinase Homo sapiens 162-167 32715733-8 2020 Experiments showed that downregulation of SPTBN1and LAMP1 proteins significantly enhanced the sensitivity of human gastric cancer cells SGC7901 to 5-FU and cisplatin. Fluorouracil 147-151 lysosomal associated membrane protein 1 Homo sapiens 52-57 29371922-8 2017 This inhibitory effect of etoposide-induced apoptosis conferred by CagA was also demonstrated in SCM1 and MKN45 gastric cancer cell lines, with two additional chemotherapeutics, 5-FU and cisplatin. Fluorouracil 178-182 S100 calcium binding protein A8 Homo sapiens 67-71 32460371-4 2020 In this study, we assessed the auxiliary antitumor effects of immunomodulatory fungal proteins from Hericium erinaceus (HEP) administered with the chemotherapy drug 5-Fluorouracil (5-Fu), and we attempted to identify new potential prebiotic bacteria for auxiliary antitumor treatment. Fluorouracil 165-179 histocompatibility 51 Mus musculus 120-123 32198070-3 2020 In this study, we analyzed the methylproteomes of both 5-fluorouracil (5-Fu) resistant Bel/5-Fu cell line and its parental Bel cell line by employing SPE-SCX based label-free quantitative proteomics. Fluorouracil 71-75 scleraxis bHLH transcription factor Homo sapiens 154-157 29039459-7 2017 In addition, cell proliferation was effectively suppressed when exposed to 5-FU plus CD13-neutralizing antibody (CD13 Ab) compared with 5-FU alone. Fluorouracil 75-79 alanyl aminopeptidase, membrane Homo sapiens 113-117 32173531-0 2020 Inhibition of NOTCH signaling pathway chemosensitizes HCC CD133+ cells to vincristine and 5-fluorouracil through upregulation of BBC3. Fluorouracil 90-104 BCL2 binding component 3 Homo sapiens 129-133 32173531-9 2020 Importantly, DAPT enhanced the apoptosis rate of VIN- and 5-FU-treated CD133+ cells for 3- and 2-fold, which was correlated with the enhanced expression of pro-apoptotic BBC3 (BCL-2-binding component 3) and decreased expression of HES1 that was reported to regulate BBC3 negatively. Fluorouracil 58-62 BCL2 binding component 3 Homo sapiens 170-174 32173531-9 2020 Importantly, DAPT enhanced the apoptosis rate of VIN- and 5-FU-treated CD133+ cells for 3- and 2-fold, which was correlated with the enhanced expression of pro-apoptotic BBC3 (BCL-2-binding component 3) and decreased expression of HES1 that was reported to regulate BBC3 negatively. Fluorouracil 58-62 BCL2 binding component 3 Homo sapiens 176-201 29039459-7 2017 In addition, cell proliferation was effectively suppressed when exposed to 5-FU plus CD13-neutralizing antibody (CD13 Ab) compared with 5-FU alone. Fluorouracil 136-140 alanyl aminopeptidase, membrane Homo sapiens 85-89 32173531-9 2020 Importantly, DAPT enhanced the apoptosis rate of VIN- and 5-FU-treated CD133+ cells for 3- and 2-fold, which was correlated with the enhanced expression of pro-apoptotic BBC3 (BCL-2-binding component 3) and decreased expression of HES1 that was reported to regulate BBC3 negatively. Fluorouracil 58-62 hes family bHLH transcription factor 1 Homo sapiens 231-235 32173531-9 2020 Importantly, DAPT enhanced the apoptosis rate of VIN- and 5-FU-treated CD133+ cells for 3- and 2-fold, which was correlated with the enhanced expression of pro-apoptotic BBC3 (BCL-2-binding component 3) and decreased expression of HES1 that was reported to regulate BBC3 negatively. Fluorouracil 58-62 BCL2 binding component 3 Homo sapiens 266-270 29039459-7 2017 In addition, cell proliferation was effectively suppressed when exposed to 5-FU plus CD13-neutralizing antibody (CD13 Ab) compared with 5-FU alone. Fluorouracil 136-140 alanyl aminopeptidase, membrane Homo sapiens 113-117 32173531-11 2020 The results highlighted the role of NOTCH/HES1/BBC3 axis in resistance of CD133+ cells to VIN and 5-FU. Fluorouracil 98-102 hes family bHLH transcription factor 1 Homo sapiens 42-46 28886238-7 2017 This results in the accumulation or activation of CRL4 substrates including LATS1 and p73, which contribute to cell apoptosis induced by actinomycin D and 5-fluorouracil. Fluorouracil 155-169 tumor protein p73 Homo sapiens 86-89 32173531-11 2020 The results highlighted the role of NOTCH/HES1/BBC3 axis in resistance of CD133+ cells to VIN and 5-FU. Fluorouracil 98-102 BCL2 binding component 3 Homo sapiens 47-51 32385145-0 2020 Heat shock and HSP70 regulate 5-FU-mediated caspase-1 activation in myeloid-derived suppressor cells and tumor growth in mice. Fluorouracil 30-34 caspase 1 Mus musculus 44-53 32385145-1 2020 BACKGROUND: We have previously shown that 5-fluorouracil (5-FU) selectively kills myeloid-derived suppressor cells (MDSCs) and activates NLRP3 (NOD-leucine rich repeat and pyrin containing protein 3) inflammasome. Fluorouracil 42-56 Mediterranean fever Mus musculus 172-177 32385145-1 2020 BACKGROUND: We have previously shown that 5-fluorouracil (5-FU) selectively kills myeloid-derived suppressor cells (MDSCs) and activates NLRP3 (NOD-leucine rich repeat and pyrin containing protein 3) inflammasome. Fluorouracil 58-62 Mediterranean fever Mus musculus 172-177 32385145-7 2020 RESULTS: HS inhibits 5-FU-mediated caspase-1 activation in vitro and in vivo without affecting its cytotoxicity on MDSCs. Fluorouracil 21-25 caspase 1 Mus musculus 35-44 32385145-11 2020 In contrast, in Hsp70-/- MDSCs, 5-FU-mediated caspase-1 activation is increased in vivo and in vitro without effect on 5-FU cytotoxicity. Fluorouracil 32-36 caspase 1 Mus musculus 46-55 32061752-6 2020 We found that the anticancer drugs such as 5-fluorouracil (5-FU) activated the IRE1alpha-XBP1 pathway to induce the expression of ABCB1, ABCC1 and ABCG2 in colon cancer cells. Fluorouracil 43-57 endoplasmic reticulum to nucleus signaling 1 Homo sapiens 79-88 32061752-6 2020 We found that the anticancer drugs such as 5-fluorouracil (5-FU) activated the IRE1alpha-XBP1 pathway to induce the expression of ABCB1, ABCC1 and ABCG2 in colon cancer cells. Fluorouracil 59-63 endoplasmic reticulum to nucleus signaling 1 Homo sapiens 79-88 32061752-7 2020 Inhibition of IRE1alpha RNase activity with small molecule 4mu8c suppressed the drug-induced expression of these ABC transporters and sensitized 5-FU-resistant colon cancer cells to drug treatment. Fluorouracil 145-149 endoplasmic reticulum to nucleus signaling 1 Homo sapiens 14-23 28117030-0 2017 Three Combined Treatments, a Novel HDAC Inhibitor OBP-801/YM753, 5-Fluorouracil, and Paclitaxel, Induce G2 Phase Arrest Through the p38 Pathway in Human Ovarian Cancer Cells. Fluorouracil 65-79 odorant binding protein 2A Homo sapiens 50-53 32426369-10 2020 But, XRCC1 knockdown could significantly improve the sensitivity of CD133+GBC-SD cells to 5-Fluorouracil via promoting cell necrosis and apoptosis. Fluorouracil 90-104 prominin 1 Homo sapiens 68-73 32234878-5 2020 RESULTS: Following APEX1 knockdown, the MTT assay revealed that the IC50 of cisplatin and 5-FU in AGS cells was decreased approximately 7% and 15%, respectively, however, their decrease in chemoresistant KATO-III cells was decreased by approximately 21% and 67% for cisplatin and 5-FU, respectively. Fluorouracil 90-94 apurinic/apyrimidinic endodeoxyribonuclease 1 Homo sapiens 19-24 32234878-5 2020 RESULTS: Following APEX1 knockdown, the MTT assay revealed that the IC50 of cisplatin and 5-FU in AGS cells was decreased approximately 7% and 15%, respectively, however, their decrease in chemoresistant KATO-III cells was decreased by approximately 21% and 67% for cisplatin and 5-FU, respectively. Fluorouracil 280-284 apurinic/apyrimidinic endodeoxyribonuclease 1 Homo sapiens 19-24 28979703-7 2017 In addition, miR-205-5p expression was upregulated by 5-fluorouracil (5-Fu) treatment in Bel-7402 (Bel) cells. Fluorouracil 54-68 microRNA 205 Homo sapiens 13-20 28979703-7 2017 In addition, miR-205-5p expression was upregulated by 5-fluorouracil (5-Fu) treatment in Bel-7402 (Bel) cells. Fluorouracil 70-74 microRNA 205 Homo sapiens 13-20 28979703-9 2017 We next demonstrated that sensitivity to 5-Fu was increased in Bel/Fu cells after treatment with a miR-205-5p inhibitor. Fluorouracil 41-45 microRNA 205 Homo sapiens 99-106 28979703-10 2017 Similarly, increased resistance to 5-Fu was observed in Bel cells after transfection with a miR-205-5p mimic. Fluorouracil 35-39 microRNA 205 Homo sapiens 92-99 28979703-11 2017 We injected nude mice with Bel/5-Fu cells to promote tumor growth, and found that co-treatment with a miR-205-5p antagomir and 5-Fu slowed tumor growth more than either treatment alone. Fluorouracil 31-35 microRNA 205 Mus musculus 102-109 28979703-13 2017 In conclusion, inhibition of miR-205-5p may reverse chemotherapeutic resistance to 5-Fu, and this may occur via the PTEN/JNK/ANXA3 pathway. Fluorouracil 83-87 microRNA 205 Homo sapiens 29-36 28791524-4 2017 The 5-FU@FACS-Mn:ZnS quantum dots (QDs) based on the histological assessment conducted in the 4T1 challenged mice showed an improved tumor remission in the liver, spleen and lungs. Fluorouracil 4-8 acyl-CoA synthetase long-chain family member 1 Mus musculus 9-13 32056006-14 2020 Inhibition of MARCKS phosphorylation via bosutinib rendered cells more sensitive to the chemotherapeutics doxorubicin and 5-FU. Fluorouracil 122-126 myristoylated alanine rich protein kinase C substrate Homo sapiens 14-20 32100443-16 2020 Up-regulated BRD4 ultimately promoted cell proliferation and cell survival Down-regulated POU6F2-AS2 showed enhanced sensitivity of 5-FU. Fluorouracil 132-136 POU6F2 antisense RNA 2 Homo sapiens 90-100 31846800-8 2020 To investigate the therapeutic potential of miR-15a, we used a modified miR-15a (5-FU-miR-15a) with uracil (U) residues in the guide strand replaced with 5-fluorouracil (5-FU). Fluorouracil 81-85 microRNA 15a Homo sapiens 44-51 32122395-11 2020 RESULTS: In this report it was demonstrated, using RT-PCR and ELISA assay, that members of the NF-kappaB family c-Rel, RelA, RelB, NF-kappaB1, and NF-kappaB2 were all overexpressed in the 5-FU-resistant HL-60/5FU cells and that U-332 potently reduced the activity of c-Rel, RelA and NF-kappaB1 subunits in this cell line. Fluorouracil 188-192 RELA proto-oncogene, NF-kB subunit Homo sapiens 119-123 32122395-12 2020 CONCLUSIONS: This finding indicates that c-Rel, RelA and NF-kappaB1 subunits are responsible for the resistance of HL-60/5FU cells to 5-FU and that U-332 is able to reverse this resistance. Fluorouracil 134-138 RELA proto-oncogene, NF-kB subunit Homo sapiens 48-52 28791524-5 2017 The 5-FU@FACS-Mn:ZnS composite induced anti-proliferative properties in these organs as compared to the free 5-FU drug. Fluorouracil 4-8 acyl-CoA synthetase long-chain family member 1 Mus musculus 9-13 28791524-5 2017 The 5-FU@FACS-Mn:ZnS composite induced anti-proliferative properties in these organs as compared to the free 5-FU drug. Fluorouracil 109-113 acyl-CoA synthetase long-chain family member 1 Mus musculus 9-13 28739692-0 2017 WNT/beta-Catenin Signaling Inhibitor IC-2 Suppresses Sphere Formation and Sensitizes Colorectal Cancer Cells to 5-Fluorouracil. Fluorouracil 112-126 dynein cytoplasmic 1 intermediate chain 2 Homo sapiens 37-41 31932471-2 2020 Loss of function mutations of SMAD4 in colon cancer is associated with metastatic progression and resistance to 5-fluorouracil (5-FU), the most extensively used drug of almost all chemotherapy combinations used in the treatment of metastatic colon cancer. Fluorouracil 112-126 SMAD family member 4 Homo sapiens 30-35 31932471-2 2020 Loss of function mutations of SMAD4 in colon cancer is associated with metastatic progression and resistance to 5-fluorouracil (5-FU), the most extensively used drug of almost all chemotherapy combinations used in the treatment of metastatic colon cancer. Fluorouracil 128-132 SMAD family member 4 Homo sapiens 30-35 28739692-8 2017 In addition, IC-2 increasesd cytotoxicity of 5-fluorouracil (5-FU) in DLD-1 cells. Fluorouracil 45-59 dynein cytoplasmic 1 intermediate chain 2 Homo sapiens 13-17 28739692-8 2017 In addition, IC-2 increasesd cytotoxicity of 5-fluorouracil (5-FU) in DLD-1 cells. Fluorouracil 61-65 dynein cytoplasmic 1 intermediate chain 2 Homo sapiens 13-17 28531805-11 2017 Our data indicated a novel therapeutic strategy to potentiate 5-FU-induced anti-tumor effect in gastric cancer cells with resistance to 5-FU by TXN through suppression of p-STAT3/NF-kappaB (p65 and p50) and Bcl-2. Fluorouracil 62-66 RELA proto-oncogene, NF-kB subunit Homo sapiens 190-193 28465257-0 2017 5-Fluorouracil targets histone acetyltransferases p300/CBP in the treatment of colorectal cancer. Fluorouracil 0-14 E1A binding protein p300 Homo sapiens 50-54 28465257-4 2017 We identified that 5-FU reduces the binding ability of histone acetyltransferases p300 and CBP to chromatin, and induces their degradation through lysosome. Fluorouracil 19-23 E1A binding protein p300 Homo sapiens 82-86 28465257-5 2017 Further work revealed that the degradation of p300/CBP induced by 5-FU was dependent on chaperone-mediated autophagy, mediated by heat-shock cognate protein 70 kDa (hsc70) and lysosomal-associated membrane protein 2A (LAMP2A). Fluorouracil 66-70 E1A binding protein p300 Homo sapiens 46-50 28465257-6 2017 Moreover, the degradation of p300/CBP is relevant to cellular resistance to 5-FU, since blocking the degradation enhances 5-FU"s cytotoxicity in CRC cells. Fluorouracil 76-80 E1A binding protein p300 Homo sapiens 29-33 28465257-6 2017 Moreover, the degradation of p300/CBP is relevant to cellular resistance to 5-FU, since blocking the degradation enhances 5-FU"s cytotoxicity in CRC cells. Fluorouracil 122-126 E1A binding protein p300 Homo sapiens 29-33 28465257-7 2017 From clinical data, we demonstrated that low expression of p300/CBP in CRC tissue was closely associated with poor clinical response to 5-FU based-chemotherapy, based on the analysis of 262 colorectal samples from the patients receiving 5-FU treatment: compared to cases with high expression of p300/CBP, those with low expression had lower long-term disease-free survival rate and increased early-progression. Fluorouracil 136-140 E1A binding protein p300 Homo sapiens 59-63 28465257-7 2017 From clinical data, we demonstrated that low expression of p300/CBP in CRC tissue was closely associated with poor clinical response to 5-FU based-chemotherapy, based on the analysis of 262 colorectal samples from the patients receiving 5-FU treatment: compared to cases with high expression of p300/CBP, those with low expression had lower long-term disease-free survival rate and increased early-progression. Fluorouracil 237-241 E1A binding protein p300 Homo sapiens 59-63 28465257-8 2017 These results elucidate a novel pharmacological effect of 5-FU involving global histone de-acetylation by promoting the degradation of p300/CBP, and highlights p300 and CBP as promising predictors of chemo-sensitivity to 5-FU treatment. Fluorouracil 58-62 E1A binding protein p300 Homo sapiens 135-139 28465257-8 2017 These results elucidate a novel pharmacological effect of 5-FU involving global histone de-acetylation by promoting the degradation of p300/CBP, and highlights p300 and CBP as promising predictors of chemo-sensitivity to 5-FU treatment. Fluorouracil 58-62 E1A binding protein p300 Homo sapiens 160-164 28668827-4 2017 Furthermore, anthracimycin had no effect on the enrichment of EpCAM-high liver cancer stem cells (CSCs), while fluorouracil dramatically enriched the CSCs with activation of the stemness-related genes EPCAM and SOX9 in HuH7 cells. Fluorouracil 111-123 SRY-box transcription factor 9 Homo sapiens 211-215 28387831-3 2017 Cytosine deaminase in infected tumor cells converts the antifungal prodrug 5-fluorocytosine into the anticancer drug 5-fluorouracil, mediating local tumor destruction without significant systemic adverse effects. Fluorouracil 117-131 cytosine deaminase Saccharomyces cerevisiae S288C 0-18 28166203-3 2017 In this study, we for the first time demonstrated that treatment with antitumor reagents such as oxaliplatin, 5-fluorouracil and pirarubicin (THP) dramatically induced HULC expression and protective autophagy. Fluorouracil 110-124 hepatocellular carcinoma up-regulated long non-coding RNA Homo sapiens 168-172 31802650-11 2020 Inhibition of miR-34a or overexpression of HMGB1 could effectively reverse elevated 5-FU sensitivity upon NEAT1 knockdown. Fluorouracil 84-88 microRNA 34a Homo sapiens 14-21 31802650-11 2020 Inhibition of miR-34a or overexpression of HMGB1 could effectively reverse elevated 5-FU sensitivity upon NEAT1 knockdown. Fluorouracil 84-88 high mobility group box 1 Homo sapiens 43-48 31802650-13 2020 CONCLUSION: These findings indicate that LncRNA NEAT1 could target miR-34a and promote autophagy to facilitate 5-FU chemoresistance in CRC. Fluorouracil 111-115 microRNA 34a Homo sapiens 67-74 31313286-0 2020 Inhibition of KHSRP sensitizes colorectal cancer to 5-fluoruracil through miR-501-5p-mediated ERRFI1 mRNA degradation. Fluorouracil 52-65 ERBB receptor feedback inhibitor 1 Homo sapiens 94-100 31313286-7 2020 Sensitivity to 5-FU mediated by KHSRP knockdown was reversed by ERRFI1 knockdown. Fluorouracil 15-19 ERBB receptor feedback inhibitor 1 Homo sapiens 64-70 31648589-6 2020 5-FU loaded NPs were characterized by SEM, DSC, TGA and FT-IR. Fluorouracil 0-4 desmocollin 3 Homo sapiens 43-46 31648589-6 2020 5-FU loaded NPs were characterized by SEM, DSC, TGA and FT-IR. Fluorouracil 0-4 T-box transcription factor 1 Homo sapiens 48-51 31648589-7 2020 SEM image implied that NPs were spherical in shape and the results of DSC, TGA and FT-IR suggest that 5-FU was encapsulated into NPs. Fluorouracil 102-106 desmocollin 3 Homo sapiens 70-73 31648589-7 2020 SEM image implied that NPs were spherical in shape and the results of DSC, TGA and FT-IR suggest that 5-FU was encapsulated into NPs. Fluorouracil 102-106 T-box transcription factor 1 Homo sapiens 75-78 31992359-7 2020 Knocking down TRIM6 expression suppressed CRC cell proliferation, induced cell cycle arrested at G2/M phase and increased sensitivity to 5-fluorouracil and oxaliplatin. Fluorouracil 137-151 tripartite motif containing 6 Homo sapiens 14-19 32865180-15 2020 Furthermore, miR-133b overexpression regulated CRC cell progression and sensitivity to 5-FU by down-regulating ABCC5. Fluorouracil 87-91 ATP binding cassette subfamily C member 5 Homo sapiens 111-116 32865180-17 2020 Our current work had led to the identification of circ_0007031 knockdown that repressed CRC cell malignant progression and enhanced 5-FU sensitivity via regulating ABCC5 expression by sponging miR-133b. Fluorouracil 132-136 ATP binding cassette subfamily C member 5 Homo sapiens 164-169 32314722-6 2020 The biological characteristics of Lgr5+ CSCs were assessed by the colony formation assay and 5-FU chemotherapy sensitivity assay. Fluorouracil 93-97 leucine rich repeat containing G protein-coupled receptor 5 Homo sapiens 34-38 31969973-0 2020 Inhibition of protein FAK enhances 5-FU chemosensitivity to gastric carcinoma via p53 signaling pathways. Fluorouracil 35-39 protein tyrosine kinase 2 Homo sapiens 22-25 31969973-5 2020 CCK-8 assay, colony formation assay, flow cytometry, dual-luciferase reporter assays, and western blot assays were conducted to determine the underlying mechanisms of FAK in 5-FU chemosensitivity in GC. Fluorouracil 174-178 protein tyrosine kinase 2 Homo sapiens 167-170 31969973-8 2020 Importantly, FAK silencing enhanced the therapeutic efficacy of 5-FU, leading to reduced tumor growth in vivo. Fluorouracil 64-68 protein tyrosine kinase 2 Homo sapiens 13-16 31969973-9 2020 We further demonstrated that FAK silencing increased 5-FU-induced caspase-3 activity, and promoted p53 transcriptional activities. Fluorouracil 53-57 protein tyrosine kinase 2 Homo sapiens 29-32 31969973-11 2020 These findings indicate that FAK plays a critical role in 5-FU chemosensitivity in GC, and the use of FAK inhibitors as an adjunct to 5-FU might be an effective strategy for patients who undergo chemotherapy. Fluorouracil 58-62 protein tyrosine kinase 2 Homo sapiens 29-32 31542354-0 2019 Inhibition of hydrogen sulfide synthesis reverses acquired resistance to 5-FU through miR-215-5p-EREG/TYMS axis in colon cancer cells. Fluorouracil 73-77 epiregulin Homo sapiens 97-101 28416637-8 2017 SJSA cells treated with 5-fluorouracil, which induces metabolic and genotoxic stress and activates p53, further implicated CDK19 in p53 target gene expression. Fluorouracil 24-38 cyclin dependent kinase 19 Homo sapiens 123-128 29207609-0 2017 Reciprocal regulation of DGCR5 and miR-320a affects the cellular malignant phenotype and 5-FU response in pancreatic ductal adenocarcinoma. Fluorouracil 89-93 microRNA 320a Homo sapiens 35-43 29207609-5 2017 Further experiments demonstrated that DGCR5 and miR-320a regulate each other in a reciprocal manner and that DGCR5 reverses the inhibition of PDCD4 by miR-320a, which is involved in the regulation of the PDAC cell phenotype and response to 5-FU. Fluorouracil 240-244 programmed cell death 4 Homo sapiens 142-147 28388363-8 2017 Combined treatments of OATP1A2 substrates 5-fluorouracil, paclitaxel and methotrexate with 0.5 Gy irradiation resulted in greater cytotoxicity toward MCF7 cells than with the treatment of antineoplastic agents and higher doses. Fluorouracil 42-56 solute carrier organic anion transporter family member 1A2 Homo sapiens 23-30 28526879-6 2017 In addition, Musashi-1 formed SGs when CRC cell lines were treated with 5-fluorouracil. Fluorouracil 72-86 musashi RNA binding protein 1 Homo sapiens 13-22 31638183-0 2019 In vitro and in vivo studies on the association of long non-coding RNAs H19 and urothelial cancer associated 1 with the susceptibility to 5-fluorouracil in rectal cancer. Fluorouracil 138-152 urothelial cancer associated 1 Homo sapiens 80-110 31638183-4 2019 Bioinformatic analysis identified H19 and urothelial cancer associated 1 (UCA1) as candidate biomarkers for 5FU susceptibility. Fluorouracil 108-111 urothelial cancer associated 1 Homo sapiens 42-72 31638183-4 2019 Bioinformatic analysis identified H19 and urothelial cancer associated 1 (UCA1) as candidate biomarkers for 5FU susceptibility. Fluorouracil 108-111 urothelial cancer associated 1 Homo sapiens 74-78 31638183-6 2019 The ratios of changes of H19 and UCA1 expression in response to 5FU were low in cells resistant to 5FU, whereas ratios were high in cells susceptible to 5FU. Fluorouracil 64-67 urothelial cancer associated 1 Homo sapiens 33-37 31638183-6 2019 The ratios of changes of H19 and UCA1 expression in response to 5FU were low in cells resistant to 5FU, whereas ratios were high in cells susceptible to 5FU. Fluorouracil 99-102 urothelial cancer associated 1 Homo sapiens 33-37 31638183-6 2019 The ratios of changes of H19 and UCA1 expression in response to 5FU were low in cells resistant to 5FU, whereas ratios were high in cells susceptible to 5FU. Fluorouracil 99-102 urothelial cancer associated 1 Homo sapiens 33-37 31638183-11 2019 The increase in H19 and UCA1 expression may represent the response to impaired cell cycle in cells susceptible to 5FU. Fluorouracil 114-117 urothelial cancer associated 1 Homo sapiens 24-28 31638183-12 2019 Our results indicate that changes in H19 and UCA1 expression may be considered for predicting the susceptibility to 5FU-based NAC in rectal cancer. Fluorouracil 116-119 urothelial cancer associated 1 Homo sapiens 45-49 31760928-7 2019 Gemcitabine and 5-fluorouracil modulated expression of CSC markers, E-cadherin, and RXRbeta in Panc1 but not in Mia PaCa-2 cells. Fluorouracil 16-30 retinoid X receptor beta Homo sapiens 84-91 31659102-0 2019 Regulation of REG4 Expression and Prediction of 5-Fluorouracil Sensitivity by CDX2 in Ovarian Mucinous Carcinoma. Fluorouracil 48-62 cdx2 None 78-82 31659102-8 2019 OMC-3 cells with ectopically overexpressed CDX2 showed enhanced apoptosis and sensitivity to 5-FU. Fluorouracil 93-97 cdx2 None 43-47 31659102-9 2019 CONCLUSION: CDX2 promotes resistance to paclitaxel and sensitivity to 5-FU. Fluorouracil 70-74 cdx2 None 12-16 31659102-10 2019 Novel 5-FU-based chemotherapy based on CDX2 may be used in ovarian mucinous carcinoma. Fluorouracil 6-10 cdx2 None 39-43 28432271-5 2017 In addition, we found that PRDX2 depletion in mice treated with 5-FU resulted in, inhibition of tumor growth, compared with mice treated with 5-FU alone. Fluorouracil 64-68 peroxiredoxin 2 Mus musculus 27-32 28432271-5 2017 In addition, we found that PRDX2 depletion in mice treated with 5-FU resulted in, inhibition of tumor growth, compared with mice treated with 5-FU alone. Fluorouracil 142-146 peroxiredoxin 2 Mus musculus 27-32 28393252-9 2017 In vitro assays revealed that ATOH8 knockdown in colon cancer cells inhibited cell proliferation, induced cell cycle arrest at the S phase, and increased the percentage of apoptotic cells and sensitivity to 5-fluorouracil (5-FU). Fluorouracil 207-221 atonal bHLH transcription factor 8 Homo sapiens 30-35 28393252-9 2017 In vitro assays revealed that ATOH8 knockdown in colon cancer cells inhibited cell proliferation, induced cell cycle arrest at the S phase, and increased the percentage of apoptotic cells and sensitivity to 5-fluorouracil (5-FU). Fluorouracil 223-227 atonal bHLH transcription factor 8 Homo sapiens 30-35 28431245-5 2017 Also, disturbances in bacterial deoxynucleotide pools amplify 5-FU-induced autophagy and cell death in host cells, an effect regulated by the nucleoside diphosphate kinase ndk-1. Fluorouracil 62-66 Nucleoside diphosphate kinase Caenorhabditis elegans 172-177 28445968-0 2017 USP22 knockdown enhanced chemosensitivity of hepatocellular carcinoma cells to 5-Fu by up-regulation of Smad4 and suppression of Akt. Fluorouracil 79-83 SMAD family member 4 Homo sapiens 104-109 31619711-4 2019 The sphere-forming activity of each population and the anti-sphere-forming effects of FTD and fluorouracil (5-FU) on CD44+CD133+ cells were then measured. Fluorouracil 94-106 prominin 1 Homo sapiens 122-127 31619711-4 2019 The sphere-forming activity of each population and the anti-sphere-forming effects of FTD and fluorouracil (5-FU) on CD44+CD133+ cells were then measured. Fluorouracil 108-112 prominin 1 Homo sapiens 122-127 31404537-0 2019 Six1 is negatively correlated with poor prognosis and reduces 5-fluorouracil sensitivity via attenuating the stemness of hepatocellular carcinoma cells. Fluorouracil 62-76 SIX homeobox 1 Homo sapiens 0-4 31404537-5 2019 Functional experiments revealed that six1 knockdown enhanced 5-fluorouracil (5-FU) sensitivity and reduced the stemness of HCC cells. Fluorouracil 61-75 SIX homeobox 1 Homo sapiens 37-41 31404537-5 2019 Functional experiments revealed that six1 knockdown enhanced 5-fluorouracil (5-FU) sensitivity and reduced the stemness of HCC cells. Fluorouracil 77-81 SIX homeobox 1 Homo sapiens 37-41 31404537-6 2019 Additionally, six1 knockdown partially reversed 5-FU resistance and attenuated the stemness in 5-FU-resistant HCC cells. Fluorouracil 48-52 SIX homeobox 1 Homo sapiens 14-18 31404537-6 2019 Additionally, six1 knockdown partially reversed 5-FU resistance and attenuated the stemness in 5-FU-resistant HCC cells. Fluorouracil 95-99 SIX homeobox 1 Homo sapiens 14-18 31404537-8 2019 Overexpression of sox2 rescued the inhibitory effects of six1 knockdown on the stemness and 5-FU sensitivity of HCC cells. Fluorouracil 92-96 SIX homeobox 1 Homo sapiens 57-61 27834032-9 2017 CD107a+/ROSlow cells were enriched in HT29 and DLD1 cultures after treatments with oxaliplatin, 5-fluorouracil, and the irinotecan metabolite SN38. Fluorouracil 96-110 lysosomal associated membrane protein 1 Homo sapiens 0-6 28196676-4 2017 Similarly, brequinar sodium is another DHODH inhibitor that showed anti-tumour effect in MC38 colon carcinoma cells when used in combination with fluorouracil. Fluorouracil 146-158 dihydroorotate dehydrogenase Mus musculus 39-44 31581233-0 2019 RPL22L1 induction in colorectal cancer is associated with poor prognosis and 5-FU resistance. Fluorouracil 77-81 ribosomal protein L22 like 1 Homo sapiens 0-7 31581233-5 2019 Interestingly, the association of high RPL22L1 expression with poor prognosis appears to be linked to resistance to 5-Fluorouracil, which is a core component of most CRC therapeutic regimens. Fluorouracil 116-130 ribosomal protein L22 like 1 Homo sapiens 39-46 28089833-7 2017 Silencing of Rufy3 by siRNA reversed EMT and greatly diminished the invasion of 5-FU-treated cells. Fluorouracil 80-84 RUN and FYVE domain containing 3 Homo sapiens 13-18 28052346-0 2017 Properdin deficiency protects from 5-fluorouracil-induced small intestinal mucositis in a complement activation-independent, interleukin-10-dependent mechanism. Fluorouracil 35-49 complement factor properdin Mus musculus 0-9 28377359-11 2017 CONCLUSION: As a potential tumor suppressor, miR-206 directly targets CDK4 to suppress the cell growth and enhance the chemotherapy sensitivity to 5-Fu in ovarian cancer cells in vitro. Fluorouracil 147-151 cyclin dependent kinase 4 Homo sapiens 70-74 28367243-7 2017 Our results indicated that knock-down Six1 could decrease colony formation number and rendered cells sensitive to 5- Fluorouracil drug treatment. Fluorouracil 114-129 SIX homeobox 1 Homo sapiens 38-42 28382142-4 2017 Methods: PRC1 was transfected into HCC cells to detect its effects of chemoresistance to 5-fluorouracil in vitro and in vivo. Fluorouracil 89-103 protein regulator of cytokinesis 1 Homo sapiens 9-13 28382142-5 2017 This study also investigated the impact of PRC1 on 5-FU-induced G2/M phase arrest and the potential molecular mechanism. Fluorouracil 51-55 protein regulator of cytokinesis 1 Homo sapiens 43-47 28382142-7 2017 Results: Ectopic expression of PRC1 significantly increased the chemoresistance, promoted the tumor growth and abrogated 5-FU-induced G2/M phase arrest via p21/p27-pRBs pathway. Fluorouracil 121-125 protein regulator of cytokinesis 1 Homo sapiens 31-35 28382142-10 2017 Conclusion: High PRC1 expression in HCC cells increased chemoresistance, attenuated 5-FU-induced apoptosis, abrogated 5-FU-induced G2/M phase arrest, and predicts an unfavorable survival, especially for the patients who received chemotherapy. Fluorouracil 84-88 protein regulator of cytokinesis 1 Homo sapiens 17-21 28382142-10 2017 Conclusion: High PRC1 expression in HCC cells increased chemoresistance, attenuated 5-FU-induced apoptosis, abrogated 5-FU-induced G2/M phase arrest, and predicts an unfavorable survival, especially for the patients who received chemotherapy. Fluorouracil 118-122 protein regulator of cytokinesis 1 Homo sapiens 17-21 31581233-7 2019 This link between RPL22L1 induction and 5-Fluorouracil resistance appears to be causal, because ectopic expression or knockdown of RPL22L1 in cell lines increases and decreases 5-Fluorouracil resistance, respectively, and this is associated with changes in expression of the DNA-repair genes, MGMT and MLH1. Fluorouracil 40-54 ribosomal protein L22 like 1 Homo sapiens 18-25 28076332-8 2017 Furthermore, ACP2-knockdown CRC cells showed an increase in chemoresistance to 5-FU treatment and increased proliferation marker in the ACP2 knockdown clone.Taken together, our results suggested that ACP2 is an unfavorable prognostic factor for stage II CRC and may serve as a potential chemotherapy-sensitive marker to help identify a subset of stage II and III CRC patients for whom chemotherapy would improve survival.Highlights1. Fluorouracil 79-83 acid phosphatase 2, lysosomal Homo sapiens 13-17 31581233-7 2019 This link between RPL22L1 induction and 5-Fluorouracil resistance appears to be causal, because ectopic expression or knockdown of RPL22L1 in cell lines increases and decreases 5-Fluorouracil resistance, respectively, and this is associated with changes in expression of the DNA-repair genes, MGMT and MLH1. Fluorouracil 40-54 ribosomal protein L22 like 1 Homo sapiens 131-138 31581233-7 2019 This link between RPL22L1 induction and 5-Fluorouracil resistance appears to be causal, because ectopic expression or knockdown of RPL22L1 in cell lines increases and decreases 5-Fluorouracil resistance, respectively, and this is associated with changes in expression of the DNA-repair genes, MGMT and MLH1. Fluorouracil 177-191 ribosomal protein L22 like 1 Homo sapiens 18-25 31581233-7 2019 This link between RPL22L1 induction and 5-Fluorouracil resistance appears to be causal, because ectopic expression or knockdown of RPL22L1 in cell lines increases and decreases 5-Fluorouracil resistance, respectively, and this is associated with changes in expression of the DNA-repair genes, MGMT and MLH1. Fluorouracil 177-191 ribosomal protein L22 like 1 Homo sapiens 131-138 31581233-8 2019 In summary, our data suggest that RPL22L1 might be a prognostic marker in CRC and predict 5-FU responsiveness. Fluorouracil 90-94 ribosomal protein L22 like 1 Homo sapiens 34-41 31543507-6 2019 Further mechanistic analysis demonstrated that miR-375 enhanced CRC cell sensitivity to 5FU by directly targeting YAP1 and SP1. Fluorouracil 88-91 Yes1 associated transcriptional regulator Homo sapiens 114-118 31261026-0 2019 The long non-coding RNA HOTAIRM1 suppresses cell progression via sponging endogenous miR-17-5p/ B-cell translocation gene 3 (BTG3) axis in 5-fluorouracil resistant colorectal cancer cells. Fluorouracil 139-153 microRNA 17 Homo sapiens 85-94 31534970-7 2019 5-FU treatment triggered nuclear translocation of beta-catenin, decreased the expression levels of c-myc and Skp2, and decreased the number of A549 cells at S phase. Fluorouracil 0-4 S-phase kinase-associated protein 2 Mus musculus 109-113 31534970-8 2019 Release from 5-FU decreased the expressions of Oct3/4, Fbxw7 and p27; decreased the percentage of cells in the G0/G1 phase; increased the expressions of Skp2 and c-myc; and increased the proportion of cells in S phase. Fluorouracil 13-17 S-phase kinase-associated protein 2 Mus musculus 153-157 31534970-9 2019 5-FU treatment led to high expressions of Oct3/4, c-myc, and p27, with low expressions of Fbxw7 and Skp2. Fluorouracil 0-4 S-phase kinase-associated protein 2 Mus musculus 100-104 31534970-14 2019 Conclusion: 5-FU enriches the CSCs in lung adenocarcinoma cells via increasing Fbxw7 and decreasing Skp2 expression, followed by downregulation of c-myc and upregulation of p27, which switches cells to quiescence. Fluorouracil 12-16 S-phase kinase-associated protein 2 Mus musculus 100-104 28028695-9 2017 An increase in p53 levels was detected following 5-FU treatment; pifithrin-alpha, an inhibitor of p53 activation, reversed 5-FU-induced SESN2 expression. Fluorouracil 49-53 sestrin 2 Homo sapiens 136-141 28028695-9 2017 An increase in p53 levels was detected following 5-FU treatment; pifithrin-alpha, an inhibitor of p53 activation, reversed 5-FU-induced SESN2 expression. Fluorouracil 123-127 sestrin 2 Homo sapiens 136-141 28028695-10 2017 5-FU prevented serum-induced in vitro cell migration, but knockdown of SESN2 or treatment with pifithrin-alpha reversed a 5-FU-mediated decrease in cell migration. Fluorouracil 122-126 sestrin 2 Homo sapiens 71-76 28028695-11 2017 Taken together, our results suggest that 5-FU increases SESN2 levels via a p53-dependent pathway, which contributes to inhibition of cancer cell migration in vitro. Fluorouracil 41-45 sestrin 2 Homo sapiens 56-61 31327733-7 2019 In addition, Cables1-/- mice displayed increased sensitivity to the chemotherapeutic agent 5-fluorouracil due to an abnormal microenvironment. Fluorouracil 91-105 CDK5 and Abl enzyme substrate 1 Mus musculus 13-20 28012398-12 2017 For serum SDF-1 the level was further lower in model mice treated with combination therapy of JPBS and 5-FU. Fluorouracil 103-107 chemokine (C-X-C motif) ligand 12 Mus musculus 10-15 31528224-0 2019 Long non-coding RNA TUG1 mediates 5-fluorouracil resistance by acting as a ceRNA of miR-197-3p in colorectal cancer. Fluorouracil 34-48 taurine up-regulated 1 Homo sapiens 20-24 28025107-7 2017 RESULTS: 5-FU and/or apigenin caused significant increase in tissue levels of Beclin-1, caspases 3, 9 and JNK activities, MDA with significant decrease in tumor volume, Mcl-1expression, tissue glutathione peroxidase and total antioxidant capacity and alleviated the histopathological changes with significant decrease of Ki-67 proliferation index compared to vehicle treated SEC control group. Fluorouracil 9-13 myeloid cell leukemia sequence 1 Mus musculus 169-174 31087138-0 2019 MicroRNA-552 deficiency mediates 5-fluorouracil resistance by targeting SMAD2 signaling in DNA-mismatch-repair-deficient colorectal cancer. Fluorouracil 33-47 microRNA 552 Homo sapiens 0-12 31087138-0 2019 MicroRNA-552 deficiency mediates 5-fluorouracil resistance by targeting SMAD2 signaling in DNA-mismatch-repair-deficient colorectal cancer. Fluorouracil 33-47 SMAD family member 2 Homo sapiens 72-77 31087138-2 2019 This study is designed to elucidate whether changes in miR-552 expression levels correlate to 5-FU-based chemoresistance in CRC, and to further identify the putative targets of miR-552 using multiple approaches. Fluorouracil 94-98 microRNA 552 Homo sapiens 55-62 31087138-3 2019 METHODS: miR-552 expression was assessed in 5-FU-resistant CRC tissues and cells using real-time PCR. Fluorouracil 44-48 microRNA 552 Homo sapiens 9-16 28977800-0 2017 XRCC2-Deficient Cells are Highly Sensitive to 5-Fluorouracil in Colorectal Cancer. Fluorouracil 46-60 X-ray repair cross complementing 2 Homo sapiens 0-5 31087138-4 2019 Effects of miR-552 dysregulation on 5-FU resistance in CRC cells were determined by measuring cell viability, apoptosis and in vivo oncogenic capacity. Fluorouracil 36-40 microRNA 552 Homo sapiens 11-18 31087138-6 2019 RESULTS: Expression of miR-552 was significantly downregulated in 5-FU-resistant CRC tissues and cells, and this downregulation, regulated by dMMR, was associated with poor postchemotherapy prognosis. Fluorouracil 66-70 microRNA 552 Homo sapiens 23-30 31087138-7 2019 Functionally, forced expression of miR-552 exhibited a proapoptotic effect and attenuated 5-FU resistance, whereas inhibition of miR-552 expression potentiated 5-FU resistance in CRC cells. Fluorouracil 90-94 microRNA 552 Homo sapiens 35-42 31087138-7 2019 Functionally, forced expression of miR-552 exhibited a proapoptotic effect and attenuated 5-FU resistance, whereas inhibition of miR-552 expression potentiated 5-FU resistance in CRC cells. Fluorouracil 160-164 microRNA 552 Homo sapiens 129-136 31087138-8 2019 Mechanically, miR-552 directly targeted the 3"-UTR of SMAD2, and stable ablation of SMAD2 neutralized the promoting effects of miR-552 deficiency-induced 5-FU resistance. Fluorouracil 154-158 SMAD family member 2 Homo sapiens 84-89 31087138-8 2019 Mechanically, miR-552 directly targeted the 3"-UTR of SMAD2, and stable ablation of SMAD2 neutralized the promoting effects of miR-552 deficiency-induced 5-FU resistance. Fluorouracil 154-158 microRNA 552 Homo sapiens 127-134 31087138-9 2019 CONCLUSIONS: Overall, our findings have revealed a critical role of miR-552/SMAD2 cascade in modulating cellular response to 5-FU chemotherapy. Fluorouracil 125-129 microRNA 552 Homo sapiens 68-75 31087138-9 2019 CONCLUSIONS: Overall, our findings have revealed a critical role of miR-552/SMAD2 cascade in modulating cellular response to 5-FU chemotherapy. Fluorouracil 125-129 SMAD family member 2 Homo sapiens 76-81 31087138-10 2019 miR-552 may act as an efficient mechanistic link synchronizing dMMR and 5-FU resistance in CRC. Fluorouracil 72-76 microRNA 552 Homo sapiens 0-7 31028570-9 2019 Combinatorial treatment of 5-FU and CEA aptamer augmented caspase-8 activity in the 5-FU-resistant colon cancer cell line via aptamer-mediated disruption of CEA interaction with death receptor 5 and in mouse xenograft tumors. Fluorouracil 27-31 tumor necrosis factor receptor superfamily, member 10b Mus musculus 178-194 31028570-9 2019 Combinatorial treatment of 5-FU and CEA aptamer augmented caspase-8 activity in the 5-FU-resistant colon cancer cell line via aptamer-mediated disruption of CEA interaction with death receptor 5 and in mouse xenograft tumors. Fluorouracil 84-88 tumor necrosis factor receptor superfamily, member 10b Mus musculus 178-194 30951773-2 2019 For this aim, anticancer 5-fluorouracil (5-FU) drug was loaded into chitosan/polyacrylic acid/Fe3O4 magnetic nanocomposite hydrogel (CS/PAA/Fe3O4) through immersing in the drug solution. Fluorouracil 25-39 citrate synthase Homo sapiens 133-135 30951773-2 2019 For this aim, anticancer 5-fluorouracil (5-FU) drug was loaded into chitosan/polyacrylic acid/Fe3O4 magnetic nanocomposite hydrogel (CS/PAA/Fe3O4) through immersing in the drug solution. Fluorouracil 41-45 citrate synthase Homo sapiens 133-135 30792218-8 2019 Moreover, knockdown of LGR5 resensitizes DAP3-depleted gastric cancer cells to 5-fluorouracil (5-FU) and oxaliplatin. Fluorouracil 79-93 leucine rich repeat containing G protein-coupled receptor 5 Homo sapiens 23-27 30792218-8 2019 Moreover, knockdown of LGR5 resensitizes DAP3-depleted gastric cancer cells to 5-fluorouracil (5-FU) and oxaliplatin. Fluorouracil 95-99 leucine rich repeat containing G protein-coupled receptor 5 Homo sapiens 23-27 30792218-9 2019 We also observed that ectopic expression of LGR5 reduces apoptosis in gastric cancer cells on treatment with 5-FU and oxaliplatin, which is accompanied by prevention of caspase-3 cleavage. Fluorouracil 109-113 leucine rich repeat containing G protein-coupled receptor 5 Homo sapiens 44-48 30938104-0 2019 Long non-coding RNA PCAT6 targets miR-204 to modulate the chemoresistance of colorectal cancer cells to 5-fluorouracil-based treatment through HMGA2 signaling. Fluorouracil 104-118 prostate cancer associated transcript 6 Homo sapiens 20-25 30938104-7 2019 Furthermore, we revealed that PCAT6 knockdown attenuated CRC chemoresistance to 5-FU through miR-204/HMGA2/PI3K; miR-204 inhibition could partially reverse the effect of PCAT6 knockdown. Fluorouracil 80-84 prostate cancer associated transcript 6 Homo sapiens 30-35 30938104-7 2019 Furthermore, we revealed that PCAT6 knockdown attenuated CRC chemoresistance to 5-FU through miR-204/HMGA2/PI3K; miR-204 inhibition could partially reverse the effect of PCAT6 knockdown. Fluorouracil 80-84 prostate cancer associated transcript 6 Homo sapiens 170-175 28977800-3 2017 However, the role of XRCC2 in the chemoresistance of colorectal cancer (CRC) treated with 5-FU remains unclear. Fluorouracil 90-94 X-ray repair cross complementing 2 Homo sapiens 21-26 28977800-9 2017 Patients with negative XRCC2 expression exhibit greater sensitivity to treatment with 5-FU-based chemotherapy than those with positive XRCC2 expression. Fluorouracil 86-90 X-ray repair cross complementing 2 Homo sapiens 23-28 28977800-10 2017 Moreover, our observations revealed that the knockdown of XRCC2 in CRC cells increased the sensitivities to 5-FU in terms of cell proliferation, apoptosis and cell cycle arrest. Fluorouracil 108-112 X-ray repair cross complementing 2 Homo sapiens 58-63 27989099-2 2017 We recently reported that CD133+ colon cancer cells showed chemoresistance to 5-fluorouracil through increased survivin expression and proposed the survivin inhibitor YM155 as an effective therapy for colon cancer in an in vitro study. Fluorouracil 78-92 prominin 1 Homo sapiens 26-31 27840964-0 2017 miR-503 inhibits proliferation making human hepatocellular carcinoma cells susceptible to 5-fluorouracil by targeting EIF4E. Fluorouracil 90-104 eukaryotic translation initiation factor 4E Homo sapiens 118-123 27974852-9 2016 In the HT126 cells study, cell growth assay showed miR-130a sponge inhibited colon cancer cells growth and sensitized the anti-cancer drug effect of 5-FU to blocked cancer cell growth. Fluorouracil 149-153 microRNA 130a Homo sapiens 51-59 30802150-4 2019 HMMR was found to be substantially up-regulated in 5-fluorouracil (5-Fu)-resistant GC biopsies and cell lines. Fluorouracil 51-65 hyaluronan mediated motility receptor Homo sapiens 0-4 30802150-4 2019 HMMR was found to be substantially up-regulated in 5-fluorouracil (5-Fu)-resistant GC biopsies and cell lines. Fluorouracil 67-71 hyaluronan mediated motility receptor Homo sapiens 0-4 30802150-7 2019 Importantly, silencing of HMMR effectively increased the susceptibility to 5-Fu therapy both in vitro and in vivo. Fluorouracil 75-79 hyaluronan mediated motility receptor Homo sapiens 26-30 30762286-9 2019 Furthermore, SSRP1 induced apoptosis and SSRP1 knockdown augmented the sensitivity of CRC cells to 5-fluorouracil and cisplatin. Fluorouracil 99-113 structure specific recognition protein 1 Homo sapiens 13-18 30762286-9 2019 Furthermore, SSRP1 induced apoptosis and SSRP1 knockdown augmented the sensitivity of CRC cells to 5-fluorouracil and cisplatin. Fluorouracil 99-113 structure specific recognition protein 1 Homo sapiens 41-46 31023384-7 2019 The cytotoxicity of T cells induced by CD3-HAC towards PD-L1-positive cells was detected in vitro and in vivo in combination with 5-FU. Fluorouracil 130-134 CD3 antigen, epsilon polypeptide Mus musculus 39-42 31114248-0 2019 M2 macrophages confer resistance to 5-fluorouracil in colorectal cancer through the activation of CCL22/PI3K/AKT signaling. Fluorouracil 36-50 C-C motif chemokine ligand 22 Homo sapiens 98-103 31097925-3 2019 This study aims to investigate whether the combination of CFL and 5-fluorouracil could reduce FAK protein level and iCa2+ and enhance p21 level. Fluorouracil 66-80 protein tyrosine kinase 2 Homo sapiens 94-97 31097925-9 2019 Combination of CFL and 5-fluorouracil significantly decreased FAK expression (p<0.05), iCa2+ (p<0.05), and increased p21 expression (p<0.05) in HT-29 cells. Fluorouracil 23-37 protein tyrosine kinase 2 Homo sapiens 62-65 31057736-1 2019 In the present investigation folate peptide (FA-Pep) conjugated 5-fluorouracil (5-FU) loaded nanoparticles were synthesized and their tumor targeting potentiality was monitored by different in vitro and in vivo techniques. Fluorouracil 64-78 prolyl endopeptidase Mus musculus 48-51 31057736-1 2019 In the present investigation folate peptide (FA-Pep) conjugated 5-fluorouracil (5-FU) loaded nanoparticles were synthesized and their tumor targeting potentiality was monitored by different in vitro and in vivo techniques. Fluorouracil 80-84 prolyl endopeptidase Mus musculus 48-51 30741544-9 2019 The accumulation of 5-FU resulted in caspase-3 and PARP activation, Bcl-2 reduction, and Bad increase, which ultimately lead to cancer cell apoptosis. Fluorouracil 20-24 collagen type XI alpha 2 chain Homo sapiens 51-55 27974852-10 2016 We developed a prognostic 4-microRNA expression signature for colon cancer patient survival, and validated miR-130a sponge could sensitized 5-FU anti-cancer effect. Fluorouracil 140-144 microRNA 130a Homo sapiens 107-115 28051262-10 2016 MiR-379 overexpression sensitized Huh7 and HepG2 cells to 5-FU, PTX and DOX and also enhanced DOX-induced cell apoptosis. Fluorouracil 58-62 microRNA 379 Homo sapiens 0-7 27748935-6 2016 In this study, we found that when cells were treated with PPZ, the 5-fluorouracil (5-FU) chemosensitivity was upregulated, meanwhile the sphere formation ability and the relative expression levels of stem cell markers CD44, CD24, ABCG2, EpCAM and Lgr5 were significantly decreased. Fluorouracil 83-87 leucine rich repeat containing G protein-coupled receptor 5 Homo sapiens 247-251 27569869-4 2016 Capecitabine is activated to 5-FU by CES, CDA and TYMP, of which SNPs in CDA and CES2 were found to be associated with efficacy and toxicity. Fluorouracil 29-33 thymidine phosphorylase Homo sapiens 50-54 27798882-0 2016 The Significant Role of Cyclin D1 in the Synergistic Growth-inhibitory Effect of Combined Therapy of Vandetanib with 5-Fluorouracil for Gastric Cancer. Fluorouracil 117-131 cyclin D1 Homo sapiens 24-33 27798882-13 2016 CONCLUSION: The synergistic effect of vandetanib with 5-FU is related to vandetanib-induced reduction of TYMS via down-regulation of cyclin D1. Fluorouracil 54-58 cyclin D1 Homo sapiens 133-142 27383136-6 2016 Moreover, interference with endogenous HMGB1 sensitized the effects of chemotherapeutic drugs, including 5-Fu, DDP, and OXA. Fluorouracil 105-109 high mobility group box 1 Homo sapiens 39-44 30649964-1 2019 INTRODUCTION: Capecitabine is an oral prodrug of 5-fluorouracil (5-FU) which is converted to 5FU by a series of reactions catalyzed by different enzymes, the last of the enzymes being thymidine phosphorylase (TP). Fluorouracil 49-63 thymidine phosphorylase Homo sapiens 184-207 27760942-2 2016 Pathological findings showed invasive ductal carcinoma that was ER and PgR positive and HER2 negative.5 -FU and tamoxifen were administered for 2 years as adjuvant therapy.Bone metastasis was found in 2002, and endocrine therapy was started, using anastrozole, exemestane, letrozole, medroxyprogesterone acetate, and fulvestrant.However, liver, lung, pleural, penetiral, and lymph-node metastases were observed, and the following chemotherapy regimen was administered: CAF, capecitabine, paclitaxel, vinorelbine, gemcitabine, methotrexate plus mitomycin C, and eribulin.Then, estrogen therapy with ethinylestradiol( EE2)was started in December 2013.T he pleural effusion disappeared and the liver metastases were reduced.After 11 months of progression-free survival(PFS), regrowth of the liver metastases was seen.Thus, everolimus plus exemestane was administered, and approximately 8 months of PFS was obtained.Therefore, both EE2 and everolimus are effective therapy even for heavily pretreated metastatic breast cancer. Fluorouracil 102-107 lysine acetyltransferase 2B Homo sapiens 469-472 30649964-1 2019 INTRODUCTION: Capecitabine is an oral prodrug of 5-fluorouracil (5-FU) which is converted to 5FU by a series of reactions catalyzed by different enzymes, the last of the enzymes being thymidine phosphorylase (TP). Fluorouracil 49-63 thymidine phosphorylase Homo sapiens 209-211 30649964-1 2019 INTRODUCTION: Capecitabine is an oral prodrug of 5-fluorouracil (5-FU) which is converted to 5FU by a series of reactions catalyzed by different enzymes, the last of the enzymes being thymidine phosphorylase (TP). Fluorouracil 65-69 thymidine phosphorylase Homo sapiens 184-207 30649964-1 2019 INTRODUCTION: Capecitabine is an oral prodrug of 5-fluorouracil (5-FU) which is converted to 5FU by a series of reactions catalyzed by different enzymes, the last of the enzymes being thymidine phosphorylase (TP). Fluorouracil 65-69 thymidine phosphorylase Homo sapiens 209-211 30649964-1 2019 INTRODUCTION: Capecitabine is an oral prodrug of 5-fluorouracil (5-FU) which is converted to 5FU by a series of reactions catalyzed by different enzymes, the last of the enzymes being thymidine phosphorylase (TP). Fluorouracil 93-96 thymidine phosphorylase Homo sapiens 184-207 30649964-1 2019 INTRODUCTION: Capecitabine is an oral prodrug of 5-fluorouracil (5-FU) which is converted to 5FU by a series of reactions catalyzed by different enzymes, the last of the enzymes being thymidine phosphorylase (TP). Fluorouracil 93-96 thymidine phosphorylase Homo sapiens 209-211 27671231-5 2016 Co-treatment of DY and 5-FU significantly elevated ROS levels, up-regulated Bax/Bcl-2 ratio and triggered mitochondrial dysfunction, followed by a release of cytochrome c and up-regulation of proteins such as cleaved-caspase-9/3 and cleaved-PARP. Fluorouracil 23-27 collagen type XI alpha 2 chain Homo sapiens 241-245 27549330-10 2016 Multivariate analyses demonstrated that EIF5A2 was an independent prognostic marker of poor overall survival (OS) (P = 0.041), failure-free survival (FFS) (P = 0.029), and distant failure-free survival (D-FFS) (P = 0.043) in patients with locoregionally advanced NPC patients treated with cisplatin + 5-Fu chemoradiotherapy. Fluorouracil 301-305 eukaryotic translation initiation factor 5A2 Homo sapiens 40-46 30649964-2 2019 TP is found to be elevated in tumor cells in comparison to normal cells, which consequently tumor-localizes the production of 5-FU, thereby limiting its systemic toxicity. Fluorouracil 126-130 thymidine phosphorylase Homo sapiens 0-2 30728402-5 2019 ChIP and global ChIP-seq data also confirms that FOXM1 can also potentially regulate other 5-FU targets, such as TYMS, thymidine kinase 1 (TK-1) and thymidine phosphorylase (TYMP). Fluorouracil 91-95 thymidine phosphorylase Homo sapiens 174-178 30207796-5 2019 In serotonin 3A receptor (5-HT3AR) null (HTR3A-/-) mice, the number of apoptotic cells induced by 5-FU was decreased compared with that in wild-type (WT) mice. Fluorouracil 98-102 5-hydroxytryptamine (serotonin) receptor 3A Mus musculus 41-46 30675240-1 2019 Oncostatin M (OSM) induces the differentiation of liver cancer stem cells (LCSCs) and increases sensitivity to the chemotherapeutic agent 5-fluorouracil, whereas salinomycin (Sal) induces apoptosis in cancer stem cells and inhibits the proliferation of liver cancer cells. Fluorouracil 138-152 oncostatin M Homo sapiens 0-12 30106136-0 2018 ZBTB7 evokes 5-fluorouracil resistance in colorectal cancer through the NF-kappaB signaling pathway. Fluorouracil 13-27 zinc finger and BTB domain containing 7A Homo sapiens 0-5 30106136-3 2018 However, the function of ZBTB7 to 5-fluorouracil (5-FU) resistance has not yet been studied. Fluorouracil 34-48 zinc finger and BTB domain containing 7A Homo sapiens 25-30 30106136-3 2018 However, the function of ZBTB7 to 5-fluorouracil (5-FU) resistance has not yet been studied. Fluorouracil 50-54 zinc finger and BTB domain containing 7A Homo sapiens 25-30 30106136-8 2018 5-FU administration decreased viability to a greater extent in the ZBTB7-shRNA group compared with the control, which was dose- and time-dependent. Fluorouracil 0-4 zinc finger and BTB domain containing 7A Homo sapiens 67-72 30106136-9 2018 Analysis of gene expression omnibus data demonstrated that ZBTB7 mediated 5-FU resistance, potentially through nuclear factor (NF)-kappaB signaling. Fluorouracil 74-78 zinc finger and BTB domain containing 7A Homo sapiens 59-64 30106136-11 2018 Collectively, the findings demonstrated that ZBTB7 mediated 5-FU resistance in CRC cells through NF-kappaB signaling. Fluorouracil 60-64 zinc finger and BTB domain containing 7A Homo sapiens 45-50 30106136-12 2018 Thus, targeting ZBTB7 and NF-kappaB signaling may be an effective strategy to reverse 5-FU resistance in CRC. Fluorouracil 86-90 zinc finger and BTB domain containing 7A Homo sapiens 16-21 30074279-7 2018 We demonstrated that knockdown of YAP1 sensitized LoVo-R cells to 5-FU treatment in cultured cells and in mice. Fluorouracil 66-70 yes-associated protein 1 Mus musculus 34-38 30074279-8 2018 The relevance of our studies to colorectal cancer patients is reflected by our discovery that high expression of YAP target genes in the tumor was associated with an increased risk of cancer relapse and poor survival in a larger cohort of colorectal cancer patients who underwent 5-FU-related chemotherapy. Fluorouracil 280-284 Yes1 associated transcriptional regulator Homo sapiens 113-116 30056083-3 2018 Compared to 5-FU alone, MH synergistically enhanced the chemotherapeutic effects of 5-FU, by reducing cell proliferation through the suppression of EGFR, HER2, p-Akt and p-mTOR expression, and promoting apoptosis by the modulation pro-apoptotic (p53, Bax, Cyto c, FasL caspase-3, -8, -9 and cleave-PARP) and anti-apoptotic (Bcl-2) markers. Fluorouracil 84-88 collagen type XI alpha 2 chain Homo sapiens 298-302 30056083-8 2018 MH also influenced the anti-metastasis effects of 5-FU by decreasing migration ability, suppressing the expression of MMP-2, MMP-9 and increasing N-cadherin and E-cadherin. Fluorouracil 50-54 matrix metallopeptidase 2 Homo sapiens 118-123 31949552-10 2018 CONCLUSION: We conclude that integrin beta1 mediated 5FU chemo resistance in colorectal cancer could be translationally regulated by eIF4E. Fluorouracil 53-56 eukaryotic translation initiation factor 4E Homo sapiens 133-138 27549330-13 2016 Our results also demonstrated that EIF5A2 overexpression induced chemoresistance of NPC cells to 5-Fu. Fluorouracil 97-101 eukaryotic translation initiation factor 5A2 Homo sapiens 35-41 27549330-14 2016 CONCLUSIONS: Our findings suggested that EIF5A2 expression, as examined by immunohistochemistry, could function as an independent prognostic factor of outcomes in NPC patients with cisplatin + 5-Fu chemoradiotherapy. Fluorouracil 193-197 eukaryotic translation initiation factor 5A2 Homo sapiens 41-47 27462786-2 2016 In the present study we aimed to investigate the clinical relevance of Plk3 expression and phosphorylation of caspase-8 at T273 in patients with anal squamous cell carcinoma (SSC) treated with 5-fluorouracil and mitomycin C-based chemoradiotherapy (CRT). Fluorouracil 193-207 caspase 8 Homo sapiens 110-119 30042169-9 2018 Notably, overexpression of miR-629-5p also conferred 5-fluorouracil sensitivity, which was partly abrogated by coexpression of CXXC4. Fluorouracil 53-67 microRNA 629 Homo sapiens 27-34 30042169-10 2018 Overall, the results presented here suggest that miR-629-5p functions as a tumor promoter by improving proliferation and migration and repressing apoptosis and 5-FU sensitivity in colorectal cancer progression by directly down-regulating CXXC4. Fluorouracil 160-164 microRNA 629 Homo sapiens 49-56 27648358-0 2016 Targeting PCDH20 gene by microRNA-122 confers 5-FU resistance in hepatic carcinoma. Fluorouracil 46-50 protocadherin 20 Homo sapiens 10-16 29643149-0 2018 Involvement of Prokineticin 2-expressing Neutrophil Infiltration in 5-Fluorouracil-induced Aggravation of Breast Cancer Metastasis to Lung. Fluorouracil 68-82 prokineticin 2 Mus musculus 15-29 29643149-4 2018 Only 5-FU markedly increased the numbers and sizes of lung metastasis foci, with enhanced tumor cell proliferation and angiogenesis as evidenced by increases in Ki67-positive cell numbers and CD31-positive areas, respectively. Fluorouracil 5-9 platelet/endothelial cell adhesion molecule 1 Mus musculus 192-196 27648358-5 2016 Knockdown of PCDH20 expression increases Akt phosphorylation, which leads to elevated mTOR activity and enhanced 5-fluorouracil resistance; whereas rescue of PCDH20 expression in miR-122-expressing cells decreases Akt and mTOR phosphorylation, re-sensitizing hepatocellular carcinoma cell to 5-fluorouracil induced apoptosis. Fluorouracil 113-127 protocadherin 20 Homo sapiens 13-19 29643149-10 2018 Collectively, 5-FU can enhance lung metastasis by inducing tumor cells to produce Cxcl1 and Cxcl2, which induced the migration of neutrophils expressing Prok2 with a capacity to enhance 4T1 cell proliferation. Fluorouracil 14-18 prokineticin 2 Mus musculus 153-158 27648358-5 2016 Knockdown of PCDH20 expression increases Akt phosphorylation, which leads to elevated mTOR activity and enhanced 5-fluorouracil resistance; whereas rescue of PCDH20 expression in miR-122-expressing cells decreases Akt and mTOR phosphorylation, re-sensitizing hepatocellular carcinoma cell to 5-fluorouracil induced apoptosis. Fluorouracil 292-306 protocadherin 20 Homo sapiens 13-19 29902974-10 2018 Subsequently the molecular inhibition of specific isoforms of ALDH by ALDH1A1 or ALDH1A3 siRNA led to sensitizing of cell lines HT-29/eGFP, HCT-116/eGFP to capecitabine and 5-FU. Fluorouracil 173-177 aldehyde dehydrogenase family 1, subfamily A1 Mus musculus 70-77 26392091-4 2016 The analysis of the changes in the expression of genes involved in the response to DNA damage (CDKN1A, GADD45A, MDM2), apoptosis (BAX, BCL2) and oncogenesis (MYC, JUN) showed that 5-FU, CDDP and ET upregulated the genes involved in DNA damage response, while the anti-apoptotic gene BCL2 and oncogene MYC were downregulated. Fluorouracil 180-184 growth arrest and DNA damage inducible alpha Homo sapiens 103-110 27350037-9 2016 In an in vitro experiment, 5-fluorouracil (5-FU), an active metabolite of capecitabine, inhibited galectin-3 production by HT-29 cells. Fluorouracil 27-41 galectin 3 Homo sapiens 98-108 29463559-10 2018 Finally, RB1 knockdown in a cell line established from a capecitabine-responder PDX decreased sensitivity to 5-FU treatment.Conclusions: We identified capecitabine as efficient chemotherapy in TNBC PDX models established from residual disease and resistant to anthracyclines, taxanes, and platins. Fluorouracil 109-113 RB transcriptional corepressor 1 Homo sapiens 9-12 27350037-9 2016 In an in vitro experiment, 5-fluorouracil (5-FU), an active metabolite of capecitabine, inhibited galectin-3 production by HT-29 cells. Fluorouracil 43-47 galectin 3 Homo sapiens 98-108 29720580-0 2018 Targeting mTORC1/2 Complexes Inhibit Tumorigenesis and Enhance Sensitivity to 5-Flourouracil (5-FU) in Hepatocellular Carcinoma: A Preclinical Study of mTORC1/2-Targeted Therapy in Hepatocellular Carcinoma (HCC). Fluorouracil 94-98 CREB regulated transcription coactivator 2 Mus musculus 10-18 26883251-9 2016 Compared with vector cell, overexpressed linc-ROR cell presented decreased sensibility of 5-FU and paclitaxel with decreased E-cadherin expression, increased Vimentin, N-cadherin expression, and invasion ability (all P < 0.05). Fluorouracil 90-94 long intergenic non-protein coding RNA, regulator of reprogramming Homo sapiens 41-49 29720580-0 2018 Targeting mTORC1/2 Complexes Inhibit Tumorigenesis and Enhance Sensitivity to 5-Flourouracil (5-FU) in Hepatocellular Carcinoma: A Preclinical Study of mTORC1/2-Targeted Therapy in Hepatocellular Carcinoma (HCC). Fluorouracil 94-98 CREB regulated transcription coactivator 1 Mus musculus 10-16 27323827-0 2016 Metformin mediates resensitivity to 5-fluorouracil in hepatocellular carcinoma via the suppression of YAP. Fluorouracil 36-50 Yes1 associated transcriptional regulator Homo sapiens 102-105 27323852-0 2016 Nicotinamide N-methyltransferase enhances resistance to 5-fluorouracil in colorectal cancer cells through inhibition of the ASK1-p38 MAPK pathway. Fluorouracil 56-70 nicotinamide N-methyltransferase Homo sapiens 0-32 29893327-12 2018 Conclusion: We determined that uPAR and CAIX levels were higher in the fluorouracil, epirubicin, and cyclophosphamide (FEC) chemotherapy group than in the control group, but there was no difference between the FEC and epirubicin/adriamycin chemotherapy groups in terms of basal and postchemotherapy uPAR, CAIX levels. Fluorouracil 71-83 carbonic anhydrase 9 Homo sapiens 40-44 27323852-2 2016 In this study, we investigated the effect of NNMT on 5-fluorouracil (5-FU) sensitivity of colorectal cancer (CRC) cells, and the underlying mechanisms. Fluorouracil 53-67 nicotinamide N-methyltransferase Homo sapiens 45-49 29556386-5 2018 For example, miR-34a attenuates the chemoresistance of colon cancer to 5-FU by inhibiting E2F3 and SIRT1. Fluorouracil 71-75 microRNA 34a Homo sapiens 13-20 27323852-2 2016 In this study, we investigated the effect of NNMT on 5-fluorouracil (5-FU) sensitivity of colorectal cancer (CRC) cells, and the underlying mechanisms. Fluorouracil 69-73 nicotinamide N-methyltransferase Homo sapiens 45-49 27323852-3 2016 Our results show that down-regulation of NNMT in CRC HT-29 cells diminishes 5-FU resistance, while over expression of NNMT in SW480 cells enhances it. Fluorouracil 76-80 nicotinamide N-methyltransferase Homo sapiens 41-45 27323852-4 2016 NNMT reduces reactive oxygen species (ROS) production induced by 5-FU by increasing 1-MNA in CRC cells. Fluorouracil 65-69 nicotinamide N-methyltransferase Homo sapiens 0-4 27175567-0 2016 B7-H3 upregulates BRCC3 expression, antagonizing DNA damage caused by 5-Fu. Fluorouracil 70-74 CD276 molecule Homo sapiens 0-5 29533973-8 2018 Recent studies indicate that induction of polyamine catabolic enzymes SSAT and spermine oxidase (SMO) play key roles in the anti-proliferative and apoptotic effects of polyamine analogues and their combinations with chemotherapeutic agents such as 5-fluorouracil (5-FU) and paclitaxel. Fluorouracil 248-262 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 70-74 29533973-8 2018 Recent studies indicate that induction of polyamine catabolic enzymes SSAT and spermine oxidase (SMO) play key roles in the anti-proliferative and apoptotic effects of polyamine analogues and their combinations with chemotherapeutic agents such as 5-fluorouracil (5-FU) and paclitaxel. Fluorouracil 264-268 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 70-74 27183638-6 2016 In addition, Dok1/Dok2 deficiency induces resistance to 5-FU-induced hematopoietic stem cell exhaustion. Fluorouracil 56-60 docking protein 1 Mus musculus 13-17 29155481-0 2018 Peroxisome proliferator activated receptor-gamma stimulation for prevention of 5-fluorouracil-induced oral mucositis in mice. Fluorouracil 79-93 peroxisome proliferator activated receptor gamma Mus musculus 0-48 27142386-15 2016 Smaller tumor size and negative lymph node status were both associated with a higher treatment efficacy to anthracycline treatment combined with 5-FU (cT1/2 vs cT3/4, p = 0.035, cN+ vs cN-, p < 0.05). Fluorouracil 145-149 MAGE family member A2B Homo sapiens 151-156 29218654-0 2018 miR-200c as a Predictive Biomarker for 5-Fluorouracil Chemosensitivity in Colorectal Cancer. Fluorouracil 39-53 microRNA 200c Homo sapiens 0-8 26985715-10 2016 Importantly, loss of RUNX3 expression contributed to 5-FU and CDDP resistance by inducing MRP expression. Fluorouracil 53-57 ATP binding cassette subfamily C member 3 Homo sapiens 90-93 26662569-0 2016 The over-expression of FGFR4 could influence the features of gastric cancer cells and inhibit the efficacy of PD173074 and 5-fluorouracil towards gastric cancer. Fluorouracil 123-137 fibroblast growth factor receptor 4 Homo sapiens 23-28 27046651-0 2016 LncRNA-UCA1 enhances cell proliferation and 5-fluorouracil resistance in colorectal cancer by inhibiting miR-204-5p. Fluorouracil 44-58 urothelial cancer associated 1 Homo sapiens 7-11 27046651-5 2016 Functional assays revealed the in vitro and in vivo growth-promoting function of UCA1 and revealed that UCA1 can decrease the sensitivity of CRC cells to 5-FU by attenuating apoptosis. Fluorouracil 154-158 urothelial cancer associated 1 Homo sapiens 104-108 26494468-9 2016 Moreover, 5-fluorouracil-induced ephrin-B2 reverse signaling promotes tumorigenesis through the Src-ERK pathway, and drives EMT via the Src-FAK pathway. Fluorouracil 10-24 protein tyrosine kinase 2 Homo sapiens 140-143 26864640-0 2016 MicroRNA-21 induces 5-fluorouracil resistance in human pancreatic cancer cells by regulating PTEN and PDCD4. Fluorouracil 20-34 programmed cell death 4 Homo sapiens 102-107 29511598-0 2018 miR-34a increases the sensitivity of colorectal cancer cells to 5-fluorouracil in vitro and in vivo. Fluorouracil 64-78 microRNA 34a Homo sapiens 0-7 29511598-1 2018 This study was designed to investigate the significance of the effect of miR-34a on 5-fluorouracil (5-FU) sensitivity in vitro and in vivo. Fluorouracil 84-98 microRNA 34a Homo sapiens 73-80 29511598-1 2018 This study was designed to investigate the significance of the effect of miR-34a on 5-fluorouracil (5-FU) sensitivity in vitro and in vivo. Fluorouracil 100-104 microRNA 34a Homo sapiens 73-80 29511598-5 2018 Patients with high levels of miR-34a expression were found to benefit more from 5-FU-based chemotherapy than patients with low levels of miR-34a expression, regardless of disease stage. Fluorouracil 80-84 microRNA 34a Homo sapiens 29-36 29511598-9 2018 CONCLUSION: miR-34a might function as a predictor of fluorouracil chemosensitivity in CRC, and a combination strategy of miR-34a with fluorouracil was expected to be more beneficial for CRC patients. Fluorouracil 53-65 microRNA 34a Homo sapiens 12-19 29175872-9 2018 Protein analysis showed an active NOTCH2-HES1 signalling in INS cell lines, especially in cells resistant to 5-FU. Fluorouracil 109-113 hes family bHLH transcription factor 1 Homo sapiens 41-45 26864640-7 2016 Overexpression of PTEN and PDCD4 antagonized miR-21-induced resistance to 5-FU and migration activity. Fluorouracil 74-78 programmed cell death 4 Homo sapiens 27-32 26864640-8 2016 Our work demonstrates that miR-21 can confer drug resistance to 5-FU in pancreatic cancer cells by regulating the expression of tumor suppressor genes, as the target genes of miR-21, PTEN and PDCD4 can rescue 5-FU sensitivity and the phenotypic characteristics disrupted by miR-21. Fluorouracil 64-68 programmed cell death 4 Homo sapiens 192-197 26864640-8 2016 Our work demonstrates that miR-21 can confer drug resistance to 5-FU in pancreatic cancer cells by regulating the expression of tumor suppressor genes, as the target genes of miR-21, PTEN and PDCD4 can rescue 5-FU sensitivity and the phenotypic characteristics disrupted by miR-21. Fluorouracil 209-213 programmed cell death 4 Homo sapiens 192-197 26785286-10 2016 CONCLUSION: These data reveal that 5-FU-induced cellular apoptosis in corneal epithelial cells may be mediated through caspase-8, caspase-9, and mitochondria-regulated pathways, as well as by upregulation of p21 and downregulation of Bcl-2-dependent signal transduction pathways. Fluorouracil 35-39 caspase 8 Homo sapiens 119-128 25810491-10 2016 Hypermethylation of TFAP2E was associated with lack of response to fluorouracil-based chemotherapy, indicating that it might be a potential predictor of treatment response in patients with GC. Fluorouracil 67-79 transcription factor AP-2 epsilon Homo sapiens 20-26 27112471-7 2016 CONCLUSIONS: Operating time>=280 minutes and intraperitoneal chemotherapy with 5-FU sustained release are independent risk factors for perineal incision complications after APE for rectal cancer. Fluorouracil 82-86 apurinic/apyrimidinic endodeoxyribonuclease 1 Homo sapiens 176-179 29343747-1 2018 We investigated the relationship between methylomic [5-methylation on deoxycytosine to form 5-methylcytosine (5mC)] and transcriptomic information in response to chemotherapeutic 5-fluorouracil (5-FU) exposure and cisplatin (CDDP) administration using the ornithine decarboxylase (ODC) degron-positive cancer stem cell model of gastrointestinal tumour. Fluorouracil 179-193 ornithine decarboxylase 1 Homo sapiens 256-279 29343747-1 2018 We investigated the relationship between methylomic [5-methylation on deoxycytosine to form 5-methylcytosine (5mC)] and transcriptomic information in response to chemotherapeutic 5-fluorouracil (5-FU) exposure and cisplatin (CDDP) administration using the ornithine decarboxylase (ODC) degron-positive cancer stem cell model of gastrointestinal tumour. Fluorouracil 179-193 ornithine decarboxylase 1 Homo sapiens 281-284 29066414-9 2018 Our results demonstrate that Z-505 ameliorates cisplatin- and 5-FU-induced anorexia through the activation of the ghrelin receptor, GHSR1a, suggesting its usefulness in the preventive treatment of anorexia during chemotherapy. Fluorouracil 62-66 growth hormone secretagogue receptor Rattus norvegicus 114-130 29689552-0 2018 RBFOX3 Regulates the Chemosensitivity of Cancer Cells to 5-Fluorouracil via the PI3K/AKT, EMT and Cytochrome-C/Caspase Pathways. Fluorouracil 57-71 RNA binding protein, fox-1 homolog (C. elegans) 3 Mus musculus 0-6 29689552-1 2018 BACKGROUND/AIMS: RBFOX3, an RNA-binding fox protein, plays an important role in the differentiation of neuronal development, but its role in the chemosensitivity of hepatocellular carcinoma (HCC) to 5-FU is unknown. Fluorouracil 199-203 RNA binding protein, fox-1 homolog (C. elegans) 3 Mus musculus 17-23 29689552-2 2018 METHODS: In this study, we examined the biological functions of RBFOX3 and its effect on the chemosensitivity of HCC cells to 5-FU in vitro and in a mouse xenograft model. Fluorouracil 126-130 RNA binding protein, fox-1 homolog (C. elegans) 3 Mus musculus 64-70 29689552-4 2018 Moreover, knockdown of RBFOX3 improved the inhibitory effect of 5-fluorouracil (5-FU) on cell proliferation, migration and invasion, and enhanced the apoptosis induced by 5-FU. Fluorouracil 64-78 RNA binding protein, fox-1 homolog (C. elegans) 3 Mus musculus 23-29 27112471-8 2016 For patients receiving APE procedure, intraperitoneal chemotherapy with 5-FU sustained release should be used with caution, and the operative time should be reduced when possible. Fluorouracil 72-76 apurinic/apyrimidinic endodeoxyribonuclease 1 Homo sapiens 23-26 26908448-3 2016 Here, ANXA11 acted as a suppressor for the tumorigenicity, LNM and 5-FU resistance of Hca-P via c-Jun. Fluorouracil 67-71 jun proto-oncogene Mus musculus 96-101 26908448-11 2016 Interestingly, compared with scramble-Hca-P cells, the levels of c-Jun and c-Jun (pSer73) in shRNA-Anxa11-Hca-P cells were upregulated in the presences of 0.1 and 1.0 mg/L 5-FU. Fluorouracil 172-176 jun proto-oncogene Mus musculus 65-70 26908448-11 2016 Interestingly, compared with scramble-Hca-P cells, the levels of c-Jun and c-Jun (pSer73) in shRNA-Anxa11-Hca-P cells were upregulated in the presences of 0.1 and 1.0 mg/L 5-FU. Fluorouracil 172-176 jun proto-oncogene Mus musculus 75-80 26908448-12 2016 The levels changes from c-Jun and c-Jun (pSer73) in Hca-P cells showed a more obvious tendency with the combination of ANXA11 knockdown and 5-FU treatment. Fluorouracil 140-144 jun proto-oncogene Mus musculus 24-29 26908448-12 2016 The levels changes from c-Jun and c-Jun (pSer73) in Hca-P cells showed a more obvious tendency with the combination of ANXA11 knockdown and 5-FU treatment. Fluorouracil 140-144 jun proto-oncogene Mus musculus 34-39 26475334-2 2016 We found that fluorouracil (5-FU)-resistant esophageal squamous cell carcinoma cell lines, established through exposure to increasing concentrations of 5-FU, showed upregulation of Id1, IGF2, and E2F1. Fluorouracil 14-26 inhibitor of DNA binding 1, HLH protein Homo sapiens 181-184 26475334-2 2016 We found that fluorouracil (5-FU)-resistant esophageal squamous cell carcinoma cell lines, established through exposure to increasing concentrations of 5-FU, showed upregulation of Id1, IGF2, and E2F1. Fluorouracil 28-32 inhibitor of DNA binding 1, HLH protein Homo sapiens 181-184 26475334-2 2016 We found that fluorouracil (5-FU)-resistant esophageal squamous cell carcinoma cell lines, established through exposure to increasing concentrations of 5-FU, showed upregulation of Id1, IGF2, and E2F1. Fluorouracil 152-156 inhibitor of DNA binding 1, HLH protein Homo sapiens 181-184 26847386-9 2016 Furthermore, 5-FU treatment significantly reduced p-NF-kappaB-p56 protein expression levels in the colon tissue of DSS-treated mice (P<0.05). Fluorouracil 13-17 interferon-induced protein with tetratricopeptide repeats 1 Mus musculus 62-65 26647806-0 2016 Smad4 sensitizes colorectal cancer to 5-fluorouracil through cell cycle arrest by inhibiting the PI3K/Akt/CDC2/survivin cascade. Fluorouracil 38-52 cyclin-dependent kinase 1 Mus musculus 106-110 26647806-0 2016 Smad4 sensitizes colorectal cancer to 5-fluorouracil through cell cycle arrest by inhibiting the PI3K/Akt/CDC2/survivin cascade. Fluorouracil 38-52 baculoviral IAP repeat-containing 5 Mus musculus 111-119 26878873-8 2016 Colony formation assays showed that overexpression of miR-193b significantly impedes the ability of KYSE450 cells to recover following 5-fluorouracil (5-FU) treatment. Fluorouracil 135-149 microRNA 193b Homo sapiens 54-62 30321081-6 2018 SND1 affected the 5-Fu-induced apoptosis levels of HCC cells by modulating the expression of UCA1 (urothelial cancer associated 1), which is a lncRNA (long non-coding RNA). Fluorouracil 18-22 urothelial cancer associated 1 Homo sapiens 93-97 30321081-6 2018 SND1 affected the 5-Fu-induced apoptosis levels of HCC cells by modulating the expression of UCA1 (urothelial cancer associated 1), which is a lncRNA (long non-coding RNA). Fluorouracil 18-22 urothelial cancer associated 1 Homo sapiens 99-129 29273065-0 2017 Curcumin synergizes with 5-fluorouracil by impairing AMPK/ULK1-dependent autophagy, AKT activity and enhancing apoptosis in colon cancer cells with tumor growth inhibition in xenograft mice. Fluorouracil 25-39 unc-51 like kinase 1 Mus musculus 58-62 29273065-14 2017 CONCLUSION: Pre-treatment with curcumin followed by 5-Fu may mediate autophagy turnover both in vitro and in vivo via AMPK/ULK1-dependent autophagy inhibition and AKT modulation, which may account for the increased susceptibility of the colon cancer cells/xenograft to the cytotoxicity of 5-Fu. Fluorouracil 52-56 unc-51 like autophagy activating kinase 1 Homo sapiens 123-127 29344142-7 2017 Following treatment with fluorouracil or gemcitabine, cells in the CD133+ group exhibited a decreased sensitivity to these drugs. Fluorouracil 25-37 prominin 1 Homo sapiens 67-72 29344244-6 2017 Furthermore, PSAT1 overexpression was associated with response to irinotecan, 5-fluorouracil and leucovorin chemotherapy, and with shorter survival time, and retained significance as an independent prognostic factor for CRC when subjected to the multivariate analysis with a Cox"s proportional hazards model. Fluorouracil 78-92 phosphoserine aminotransferase 1 Homo sapiens 13-18 26878873-8 2016 Colony formation assays showed that overexpression of miR-193b significantly impedes the ability of KYSE450 cells to recover following 5-fluorouracil (5-FU) treatment. Fluorouracil 151-155 microRNA 193b Homo sapiens 54-62 26864651-5 2016 Interestingly, the content of CD133 + CXCR4+ cells in HCT116 cancer cells and RKO cells treated by 5-Fu/P85 copolymer micelles was decreased. Fluorouracil 99-103 prominin 1 Homo sapiens 30-35 28911246-6 2017 With 5-fluorouracil-loaded LC-PLGA NPs, we were able to demonstrate significant increases in the uptake efficiency and cytotoxicity in colon cancer cells that were positive for OCTN2 and ATB0,+. Fluorouracil 5-19 solute carrier family 22 member 5 Homo sapiens 177-182 28109077-6 2017 In contrast, the sequential combination of both folinate salts and 5-FU was antagonistic at 24 and 72 h. The simultaneous combination of 5-FU and NaLV or CaLV inhibited TYMS gene expression at 24 h, whereas the sequential combination reduced SLC19A1 gene expression. Fluorouracil 67-71 solute carrier family 19 member 1 Homo sapiens 242-249 28109077-6 2017 In contrast, the sequential combination of both folinate salts and 5-FU was antagonistic at 24 and 72 h. The simultaneous combination of 5-FU and NaLV or CaLV inhibited TYMS gene expression at 24 h, whereas the sequential combination reduced SLC19A1 gene expression. Fluorouracil 137-141 solute carrier family 19 member 1 Homo sapiens 242-249 28531805-7 2017 Decreasing of phosphorylated signal transducers and activation of transcription 3 (STAT3) was included in suppression of p65 by TXN with 5-FU in combination. Fluorouracil 137-141 RELA proto-oncogene, NF-kB subunit Homo sapiens 121-124 26864651-6 2016 Importantly, the epithelial-mesenchymal transition (EMT) of CD133 + CXCR4+ cells, which was strongly associated with liver metastasis of colon cancer, was also suppressed by giving 5-Fu/P85 copolymer micelles. Fluorouracil 181-185 prominin 1 Homo sapiens 60-65 26864651-7 2016 The results indicated that 5-Fu/P85 copolymer micelles could inhibit the growth and metastasis of colon cancer, which could be attributed to the decrease of the content of CD133 + CXCR4+ cells and suppression of EMT of CD133 + CXCR4+ cells. Fluorouracil 27-31 prominin 1 Homo sapiens 172-177 26864651-7 2016 The results indicated that 5-Fu/P85 copolymer micelles could inhibit the growth and metastasis of colon cancer, which could be attributed to the decrease of the content of CD133 + CXCR4+ cells and suppression of EMT of CD133 + CXCR4+ cells. Fluorouracil 27-31 prominin 1 Homo sapiens 219-224 26754678-12 2016 CONCLUSIONS: Hepatic arterial infusion chemoembolization therapy with cisplatin suspension in lipiodol combined with 5-fluorouracil is effective treatment for unresectable HCC with portal vein tumor thrombosis. Fluorouracil 117-131 HCC Homo sapiens 172-175 26334617-8 2016 Cell lines with G648C mutation in polbeta gene were more sensitive to treatment with 5-fluorouracil and cisplatin than those with wild-type polbeta. Fluorouracil 85-99 DNA polymerase beta Homo sapiens 34-41 29021025-2 2016 Therefore, we investigated whether the novel HDAC inhibitor OBP-801/YM753 could enhance the effects of 5-FU with radiation on esophageal squamous carcinoma KYSE170 cells. Fluorouracil 103-107 odorant binding protein 2A Homo sapiens 60-63 29021025-3 2016 The inhibition of the cell growth was significantly stronger with the combination of OBP-801/YM753 with 5-FU than with the 5-FU treatment only. Fluorouracil 104-108 odorant binding protein 2A Homo sapiens 85-88 29021025-5 2016 Western blot analysis showed that OBP-801/YM753 suppressed the expression of thymidylate synthase induced by 5-FU. Fluorouracil 109-113 odorant binding protein 2A Homo sapiens 34-37 26673620-0 2016 MicroRNA-497 inhibits tumor growth and increases chemosensitivity to 5-fluorouracil treatment by targeting KSR1. Fluorouracil 69-83 microRNA 497 Homo sapiens 0-12 26673620-6 2016 Overexpression of miR-497 inhibited cell proliferation, migration, invasion and increased chemosensitivity to 5-fluorouracil treatment, whereas forced expression of KSR1 had the opposite effect. Fluorouracil 110-124 microRNA 497 Homo sapiens 18-25 26774139-8 2016 In addition, chidamide alone or in combination with 5-Fu increased the p53, phosphorylated-p53 (p-p53), p21 and gammaH2AX levels, but suppressed cyclin dependent kinase 4 (CDK4) expression in tumor cells. Fluorouracil 52-56 cyclin dependent kinase 4 Homo sapiens 145-170 26774139-8 2016 In addition, chidamide alone or in combination with 5-Fu increased the p53, phosphorylated-p53 (p-p53), p21 and gammaH2AX levels, but suppressed cyclin dependent kinase 4 (CDK4) expression in tumor cells. Fluorouracil 52-56 cyclin dependent kinase 4 Homo sapiens 172-176 26318481-12 2015 The data of MTT assay revealed that infection with Cx43 adenovirus, cell proliferation ability decreased and sensitivity to chemotherapy drugs (including doxorubicin, fluorouracil, oxaliplatin) increased. Fluorouracil 167-179 gap junction protein alpha 1 Homo sapiens 51-55 26692822-13 2015 In addition, As2O3 in combination with 5-FU treatment caused up-regulation of DR5, caspase 3, caspase 8, and caspase 9, and down-regulation of BCL-2, but had no effect of DR4. Fluorouracil 39-43 caspase 8 Homo sapiens 94-103 25736303-8 2015 The combination of 5-FU and Res significantly increased the percentage of apoptotic cells and the level of activated caspase-3, cleaved PARP and p53 proteins as well as increased the Bax/Bcl-2 ratio. Fluorouracil 19-23 collagen type XI alpha 2 chain Homo sapiens 136-140 26571380-6 2015 5-Fluoracil showed a slight inhibitory effect on cell proliferation that was more significant in mixed- than mucin-IHCCA primary cultures and, induced apoptosis only in mucin-IHCCA. Fluorouracil 0-11 LOC100508689 Homo sapiens 109-114 26571380-6 2015 5-Fluoracil showed a slight inhibitory effect on cell proliferation that was more significant in mixed- than mucin-IHCCA primary cultures and, induced apoptosis only in mucin-IHCCA. Fluorouracil 0-11 LOC100508689 Homo sapiens 169-174 26805208-4 2015 She was treated with systemic chemotherapy consisting of FAP (5-fluorouracil [5-FU], doxorubicin [DXR] and cisplatin[CDDP]), which resulted in significant tumor shrinkage. Fluorouracil 62-76 fibroblast activation protein alpha Homo sapiens 57-60 26805208-4 2015 She was treated with systemic chemotherapy consisting of FAP (5-fluorouracil [5-FU], doxorubicin [DXR] and cisplatin[CDDP]), which resulted in significant tumor shrinkage. Fluorouracil 78-82 fibroblast activation protein alpha Homo sapiens 57-60 26518892-6 2015 For example, overexpressing miR-34a, a master regulator of tumor suppression attenuates chemoresistance to 5-FU by downregulating silent information regulator 1 (SIRT1) and E2F3. Fluorouracil 107-111 microRNA 34a Homo sapiens 28-35 26378040-0 2015 GRP78 confers the resistance to 5-FU by activating the c-Src/LSF/TS axis in hepatocellular carcinoma. Fluorouracil 32-36 transcription factor CP2 Homo sapiens 61-64 26196680-10 2015 SW480 cells that naturally express Lgr5 were slightly more sensitive to 5-fluorouracil than non-Lgr5-expressing cells (0.0002<P<0.0344). Fluorouracil 72-86 leucine rich repeat containing G protein-coupled receptor 5 Homo sapiens 35-39 26408730-6 2015 In elderly patients treatment with 5-FU plus FA decreased the risk for an event by 1.5-fold compared to 5-FU (HR=0.657, 95%CI=0.495-0.870, p=0.004) and 5-FU plus INFa (HR=0.685, 95%CI=0.515-0.912, p=0.009). Fluorouracil 35-39 interferon alpha 17 Homo sapiens 162-166 26418978-6 2015 CONCLUSION MiR-21 can mediate the drug resistance to 5-FU by inhibiting its target PDCD4, which can regulate the expression of ABCC5 and CD44 genes. Fluorouracil 53-57 programmed cell death 4 Homo sapiens 83-88 26418978-6 2015 CONCLUSION MiR-21 can mediate the drug resistance to 5-FU by inhibiting its target PDCD4, which can regulate the expression of ABCC5 and CD44 genes. Fluorouracil 53-57 ATP binding cassette subfamily C member 5 Homo sapiens 127-132 25956534-4 2015 In this study, in vitro 5-FU not only directly blocked both stromal cell- and RANKL-induced osteoclastogenesis through NF-kappaB pathway, but also indirectly inhibited osteoclast formation and angiogenesis by suppressing the expression of osteoclast-activating factors including IL-1beta, MCP-1 and tumor angiogenesis factor VEGF in stromal cells. Fluorouracil 24-28 vascular endothelial growth factor A Gallus gallus 325-329 28461325-6 2017 Gastric adenocarcinoma spheroid cells were resistant to 5-fluorouracil and cisplatin chemotherapy, and this chemotherapy resistance could be reversed with Rac1 shRNA or NSC23766. Fluorouracil 56-70 Rac family small GTPase 1 Mus musculus 155-159 28724889-0 2017 Aptamer-mediated survivin RNAi enables 5-fluorouracil to eliminate colorectal cancer stem cells. Fluorouracil 39-53 baculoviral IAP repeat-containing 5 Mus musculus 17-25 28724889-4 2017 When combined with the conventional chemotherapeutic agents, the aptamer-guided survivin RNAi was able to enhance the sensitivity towards 5-FU or oxaliplatin in colorectal cancer stem cells, increase apoptosis, inhibit tumour growth and improve the overall survival of mice bearing xenograft colorectal cancer. Fluorouracil 138-142 baculoviral IAP repeat-containing 5 Mus musculus 80-88 28698581-8 2017 Additionally, GTSE1 modulated the sensitivity of HCC to 5-fluorouracil therapy. Fluorouracil 56-70 G2 and S-phase expressed 1 Homo sapiens 14-19 28624221-0 2017 miR-1290 Is a Biomarker in DNA-Mismatch-Repair-Deficient Colon Cancer and Promotes Resistance to 5-Fluorouracil by Directly Targeting hMSH2. Fluorouracil 97-111 mutS homolog 2 Homo sapiens 134-139 28624221-8 2017 Furthermore, we demonstrated that inhibition of the expression of miR-1290 enhanced sensitivity to 5-FU treatment in vitro and in tumor xenografts in vivo by direct targeting hMSH2. Fluorouracil 99-103 mutS homolog 2 Homo sapiens 175-180 27836590-3 2017 The surface of as-prepared Ag2S QDs was modified with polyethylenimine, followed by combination with the aptamer/5-Fu complex to form Ag2S QDs/aptamer/5-Fu hybrids. Fluorouracil 151-155 angiotensin II receptor type 1 Homo sapiens 134-138 27836590-4 2017 During the combination of Ag2S QDs with aptamer/5-Fu complex, near-infrared (NIR) photoluminescence (PL) of QDs (peaked at 850nm) was markedly reduced under excitation at 625nm, attributed to photo-induced electron transfer from QDs to 5-Fu. Fluorouracil 48-52 angiotensin II receptor type 1 Homo sapiens 26-30 27836590-4 2017 During the combination of Ag2S QDs with aptamer/5-Fu complex, near-infrared (NIR) photoluminescence (PL) of QDs (peaked at 850nm) was markedly reduced under excitation at 625nm, attributed to photo-induced electron transfer from QDs to 5-Fu. Fluorouracil 236-240 angiotensin II receptor type 1 Homo sapiens 26-30 28428709-0 2017 Disruption of the TWEAK/Fn14 pathway prevents 5-fluorouracil-induced diarrhea in mice. Fluorouracil 46-60 tumor necrosis factor (ligand) superfamily, member 12 Mus musculus 18-23 28428709-0 2017 Disruption of the TWEAK/Fn14 pathway prevents 5-fluorouracil-induced diarrhea in mice. Fluorouracil 46-60 tumor necrosis factor receptor superfamily, member 12a Mus musculus 24-28 28428709-1 2017 AIM: To clarify the roles of TWEAK and its receptor Fn14 in 5-fluorouracil (5-FU)-induced diarrhea. Fluorouracil 60-74 tumor necrosis factor (ligand) superfamily, member 12 Mus musculus 29-34 28428709-1 2017 AIM: To clarify the roles of TWEAK and its receptor Fn14 in 5-fluorouracil (5-FU)-induced diarrhea. Fluorouracil 60-74 tumor necrosis factor receptor superfamily, member 12a Mus musculus 52-56 28428709-1 2017 AIM: To clarify the roles of TWEAK and its receptor Fn14 in 5-fluorouracil (5-FU)-induced diarrhea. Fluorouracil 76-80 tumor necrosis factor (ligand) superfamily, member 12 Mus musculus 29-34 28428709-1 2017 AIM: To clarify the roles of TWEAK and its receptor Fn14 in 5-fluorouracil (5-FU)-induced diarrhea. Fluorouracil 76-80 tumor necrosis factor receptor superfamily, member 12a Mus musculus 52-56 28428709-6 2017 RESULTS: 5-FU induced high Fn14 expression in epithelial cells. Fluorouracil 9-13 tumor necrosis factor receptor superfamily, member 12a Mus musculus 27-31 28428709-7 2017 The severity of 5-FU-induced diarrhea was lower in Fn14 KO mice compared with WT mice. Fluorouracil 16-20 tumor necrosis factor receptor superfamily, member 12a Mus musculus 51-55 28428709-8 2017 Administration of anti-TWEAK antibody reduced 5-FU-induced diarrhea without affecting the antitumor effects of 5-FU in vivo. Fluorouracil 46-50 tumor necrosis factor (ligand) superfamily, member 12 Mus musculus 23-28 28428709-9 2017 5-FU-induced expression of IL-13, IL-17A, TNF-alpha, and IFN-gamma in the ileum was Fn14 dependent. Fluorouracil 0-4 tumor necrosis factor receptor superfamily, member 12a Mus musculus 84-88 28428709-12 2017 IL-13Ralpha2 was upregulated in the ileum of 5-FU-treated Fn14 KO mice. Fluorouracil 45-49 tumor necrosis factor receptor superfamily, member 12a Mus musculus 58-62 28428709-14 2017 CONCLUSION: Disruption of the TWEAK/Fn14 pathway affects several interconnected pathways, including those associated with IL-13, IL-33, and IL-13Ralpha2, to attenuate 5-FU-induced intestinal side effects. Fluorouracil 167-171 tumor necrosis factor (ligand) superfamily, member 12 Mus musculus 30-35 28428709-14 2017 CONCLUSION: Disruption of the TWEAK/Fn14 pathway affects several interconnected pathways, including those associated with IL-13, IL-33, and IL-13Ralpha2, to attenuate 5-FU-induced intestinal side effects. Fluorouracil 167-171 tumor necrosis factor receptor superfamily, member 12a Mus musculus 36-40 29871302-8 2017 The combination of metformin and 5-fluorouracil produced an antagonism action in Hep-2 cells.Western blot assay showed that metformin, cisplatin, 5-fluorouracil could have caused the increase of expression level of AMPK-alpha, P21 and Cyclin D1 in Hep-2 cells while Paclitaxel could have cause the decrease of expression level of Cyclin D1. Fluorouracil 146-160 cyclin D1 Homo sapiens 235-244 29871302-8 2017 The combination of metformin and 5-fluorouracil produced an antagonism action in Hep-2 cells.Western blot assay showed that metformin, cisplatin, 5-fluorouracil could have caused the increase of expression level of AMPK-alpha, P21 and Cyclin D1 in Hep-2 cells while Paclitaxel could have cause the decrease of expression level of Cyclin D1. Fluorouracil 146-160 cyclin D1 Homo sapiens 330-339 29871302-11 2017 Metformin has an antagonism on the anticancer effect to 5-fluorouracil in Hep-2 cells, and this antagonistic effect occurred partially through molecular signal pathways of AMPK-alpha, P21 and Cyclin D1 and it"s significantly related to the cell cycle arrest. Fluorouracil 56-70 cyclin D1 Homo sapiens 192-201 28284059-0 2017 Reactivating p53 and Inducing Tumor Apoptosis (RITA) Enhances the Response of RITA-Sensitive Colorectal Cancer Cells to Chemotherapeutic Agents 5-Fluorouracil and Oxaliplatin. Fluorouracil 144-158 RBPJ interacting and tubulin associated 1 Homo sapiens 47-51 28284059-0 2017 Reactivating p53 and Inducing Tumor Apoptosis (RITA) Enhances the Response of RITA-Sensitive Colorectal Cancer Cells to Chemotherapeutic Agents 5-Fluorouracil and Oxaliplatin. Fluorouracil 144-158 RBPJ interacting and tubulin associated 1 Homo sapiens 78-82 28284059-10 2017 Sensitivity to RITA appeared independent of p53 status and was associated with an increase in antiproliferative response to 5FU and oxaliplatin, a transcriptional increase of p53 targets p21 and NOXA, and a decrease in MYC mRNA. Fluorouracil 124-127 RBPJ interacting and tubulin associated 1 Homo sapiens 15-19 28284059-13 2017 We found a substantial number of RITA-sensitive CRC cells within both panels of established CRC cell lines and primary patient-derived CRC cell lines (6/14) that provide a rationale for combining RITA with 5FU or oxaliplatin to enhance the antiproliferative response to both chemotherapeutic agents. Fluorouracil 206-209 RBPJ interacting and tubulin associated 1 Homo sapiens 33-37 26208739-14 2015 CONCLUSIONS: These findings suggest that gossypol-mediated down-regulation of TS, cyclin D1, and the mTOR/p70S6K1 signaling pathways enhances the anti-tumor effect of 5-FU. Fluorouracil 167-171 cyclin D1 Homo sapiens 82-91 26133391-0 2015 Suppression of KLF8 induces cell differentiation and sensitizes colorectal cancer to 5-fluorouracil. Fluorouracil 85-99 Kruppel-like factor 8 Mus musculus 15-19 26133391-9 2015 Moreover, KLF8 silencing induced apoptosis and sensitized cancer cells to 5-fluorouracil (5-FU). Fluorouracil 74-88 Kruppel-like factor 8 Mus musculus 10-14 26133391-9 2015 Moreover, KLF8 silencing induced apoptosis and sensitized cancer cells to 5-fluorouracil (5-FU). Fluorouracil 90-94 Kruppel-like factor 8 Mus musculus 10-14 26133391-10 2015 A strong antitumorigenic effect by lenti-KLF8-shRNA, which was enhanced when combined with 5-FU treatment, was exerted in nude mice. Fluorouracil 91-95 Kruppel-like factor 8 Mus musculus 41-45 26022890-4 2015 Possible interactions of 5-FU with PCH were pointed out using different characterization methods like spectroscopic techniques (FT-IR, UV-vis, XPS), thermogravimetrical and BET analysis. Fluorouracil 25-29 delta/notch like EGF repeat containing Homo sapiens 173-176 26189067-14 2015 INTERPRETATION: Adding oxaliplatin to fluorouracil-based neoadjuvant chemoradiotherapy and adjuvant chemotherapy (at the doses and intensities used in this trial) significantly improved disease-free survival of patients with clinically staged cT3-4 or cN1-2 rectal cancer compared with our former fluorouracil-based combined modality regimen (based on CAO/ARO/AIO-94). Fluorouracil 38-50 5'-nucleotidase, cytosolic IA Homo sapiens 252-255 25936796-3 2015 Co-treatment using resveratrol and 5-FU inhibited cell proliferation more efficiently compared with use of either drug alone and the antiproliferative effect coincided with changes in the expression levels of AMP-activated protein kinase (AMPK), cyclooxygenase-2, vasodilator-stimulated phosphoprotein (VASP) and vascular endothelial growth factor (VEGF). Fluorouracil 35-39 prostaglandin-endoperoxide synthase 2 Mus musculus 246-262 28381187-7 2017 Short hairpin RNA-mediated knockdown of tripartite motif-containing protein 28 in breast cancer cells revealed a decreased expression of epithelial-to-mesenchymal transition markers and increased expression of epithelial markers, decreased migration and invasion, and increased chemosensitivity to doxorubicin, 5-fluorouracil, and methotrexate. Fluorouracil 311-325 tripartite motif-containing 28 Mus musculus 40-78 27582048-1 2017 The anticancer drug 5-fluorouracil (5-FU) and its metabolite 5-fluoro-2"-deoxyuridine (FUdR) inhibit thymidylate synthase and induce uracil bases in DNA. Fluorouracil 20-34 Thymidylate synthase Caenorhabditis elegans 101-121 27582048-1 2017 The anticancer drug 5-fluorouracil (5-FU) and its metabolite 5-fluoro-2"-deoxyuridine (FUdR) inhibit thymidylate synthase and induce uracil bases in DNA. Fluorouracil 36-40 Thymidylate synthase Caenorhabditis elegans 101-121 28176874-0 2017 CXCL12/CXCR4 axis induced miR-125b promotes invasion and confers 5-fluorouracil resistance through enhancing autophagy in colorectal cancer. Fluorouracil 65-79 C-X-C motif chemokine ligand 12 Homo sapiens 0-6 25936796-3 2015 Co-treatment using resveratrol and 5-FU inhibited cell proliferation more efficiently compared with use of either drug alone and the antiproliferative effect coincided with changes in the expression levels of AMP-activated protein kinase (AMPK), cyclooxygenase-2, vasodilator-stimulated phosphoprotein (VASP) and vascular endothelial growth factor (VEGF). Fluorouracil 35-39 vasodilator-stimulated phosphoprotein Mus musculus 264-301 25936796-3 2015 Co-treatment using resveratrol and 5-FU inhibited cell proliferation more efficiently compared with use of either drug alone and the antiproliferative effect coincided with changes in the expression levels of AMP-activated protein kinase (AMPK), cyclooxygenase-2, vasodilator-stimulated phosphoprotein (VASP) and vascular endothelial growth factor (VEGF). Fluorouracil 35-39 vasodilator-stimulated phosphoprotein Mus musculus 303-307 25936796-4 2015 Furthermore, co-treatment with resveratrol and 5-FU reduced tumor growth compared with that in the control group and this growth-inhibitory effect was associated with changes in the expression levels of AMPK, VASP and VEGF. Fluorouracil 47-51 vasodilator-stimulated phosphoprotein Mus musculus 209-213 26044651-6 2015 Furthermore, we showed that rAd/CEA-RPL23 synergized with classic chemotherapeutic agent 5-fluorouracil (5-FU) and enhanced its activity against LoVo cells in vivo and in vitro. Fluorouracil 89-103 ribosomal protein L23 Homo sapiens 36-41 26044651-6 2015 Furthermore, we showed that rAd/CEA-RPL23 synergized with classic chemotherapeutic agent 5-fluorouracil (5-FU) and enhanced its activity against LoVo cells in vivo and in vitro. Fluorouracil 105-109 ribosomal protein L23 Homo sapiens 36-41 26002465-2 2015 However, this claim has been challenged recently and we previously reported that patients with CD133(+) colon cancer have benefit from 5-fluorouracil (5-FU) chemotherapy incontrast to no benefit in patients with CD133(-) cancer. Fluorouracil 135-149 prominin 1 Homo sapiens 95-100 26002465-2 2015 However, this claim has been challenged recently and we previously reported that patients with CD133(+) colon cancer have benefit from 5-fluorouracil (5-FU) chemotherapy incontrast to no benefit in patients with CD133(-) cancer. Fluorouracil 151-155 prominin 1 Homo sapiens 95-100 26002465-4 2015 We comparatively analyzed the sequential changes of MDR1, ABCG2, AKT1 and survivin expression and the result of proliferation assay (WST-1 assay) with 5-FU treatment in CD133(+) and siRNA-induced CD133(-) cells, derived from Caco-2 colon cancer cell line. Fluorouracil 151-155 prominin 1 Homo sapiens 169-174 26002465-4 2015 We comparatively analyzed the sequential changes of MDR1, ABCG2, AKT1 and survivin expression and the result of proliferation assay (WST-1 assay) with 5-FU treatment in CD133(+) and siRNA-induced CD133(-) cells, derived from Caco-2 colon cancer cell line. Fluorouracil 151-155 prominin 1 Homo sapiens 196-201 26002465-8 2015 The cytotoxicity assay demonstrated notable increase of chemoresistance to 5-FU treatment (10 muM) in CD133(+) cells at 96 h after siRNA transfection. Fluorouracil 75-79 prominin 1 Homo sapiens 102-107 26002465-9 2015 From this study, we conclude that CD133(+) cells may have chemoresistance to 5-FU through the mechanism which is related with survivin expression, instead of MDR1, ABCG2 and AKT1 expression. Fluorouracil 77-81 prominin 1 Homo sapiens 34-39 26003042-5 2015 In the combined therapy, the antitumor action of 5-fluorouracil (5-FU) was potentiated when the mice were pretreated with a low dose of TNFalpha (1ng/mouse) and to a greater extent by the same concentration of TCP-1/TNFalpha. Fluorouracil 49-63 t-complex protein 1 Mus musculus 210-215 26003042-5 2015 In the combined therapy, the antitumor action of 5-fluorouracil (5-FU) was potentiated when the mice were pretreated with a low dose of TNFalpha (1ng/mouse) and to a greater extent by the same concentration of TCP-1/TNFalpha. Fluorouracil 65-69 t-complex protein 1 Mus musculus 210-215 26003042-8 2015 At the same time, TCP-1/TNFalpha significantly improved 5-FU absorption into the tumor mass. Fluorouracil 56-60 t-complex protein 1 Mus musculus 18-23 26211574-0 2015 Decreased expression of PinX1 protein predicts poor prognosis of colorectal cancer patients receiving 5-FU adjuvant chemotherapy. Fluorouracil 102-106 PIN2 (TERF1) interacting telomerase inhibitor 1 Homo sapiens 24-29 26211574-8 2015 In conclusion, PinX1 protein expression is decreased in CRC, which may be a new promising tumor marker for CRC prognosis and 5-FU chemosensitivity. Fluorouracil 125-129 PIN2 (TERF1) interacting telomerase inhibitor 1 Homo sapiens 15-20 25820415-8 2015 K19(+) cells displayed high proliferation capacity and 5-fluorouracil resistance in vitro. Fluorouracil 55-69 keratin 19 Homo sapiens 0-3 28176874-9 2017 MiR-125b functions as an important downstream mediator upon the activation of CXCL12/CXCR4 axis that involved in EMT, invasion and 5-FU resistance of CRC. Fluorouracil 131-135 C-X-C motif chemokine ligand 12 Homo sapiens 78-84 25689483-0 2015 The c-MYC-ABCB5 axis plays a pivotal role in 5-fluorouracil resistance in human colon cancer cells. Fluorouracil 45-59 ATP binding cassette subfamily B member 5 Homo sapiens 10-15 27981483-3 2017 According to the results, SSL/[Fe(C2Omicron4)3]3-/Eta2Omicron2 process was the most efficient, since faster degradation of 5-FU and higher mineralization percentages were achieved. Fluorouracil 123-127 DNA polymerase iota Homo sapiens 50-62 27935870-7 2017 Our data indicate that Oct3/4, Sox2, and Nanog are transiently expressed in response to 5-FU-induced injury, and then they are gradually silenced as the cells differentiate. Fluorouracil 88-92 Nanog homeobox Rattus norvegicus 41-46 27935870-9 2017 Treatment with 5-FU reversed the methylation of the Oct3/4, Nanog, and Sox2 promoters, which corresponded to increases in Oct3/4, Nanog, and Sox2 mRNA and protein. Fluorouracil 15-19 Nanog homeobox Rattus norvegicus 60-65 27935870-9 2017 Treatment with 5-FU reversed the methylation of the Oct3/4, Nanog, and Sox2 promoters, which corresponded to increases in Oct3/4, Nanog, and Sox2 mRNA and protein. Fluorouracil 15-19 Nanog homeobox Rattus norvegicus 130-135 25689483-5 2015 Furthermore, c-MYC knockdown decreased the expression level of ABCB5, which is involved in 5-FU resistance. Fluorouracil 91-95 ATP binding cassette subfamily B member 5 Homo sapiens 63-68 25689483-8 2015 ABCB5 knockdown decreased the survival rate following 5-FU treatment as expected, and the ABCB5 expression level was increased in 5-FU-resistant human colon cancer cells. Fluorouracil 54-58 ATP binding cassette subfamily B member 5 Homo sapiens 0-5 25689483-8 2015 ABCB5 knockdown decreased the survival rate following 5-FU treatment as expected, and the ABCB5 expression level was increased in 5-FU-resistant human colon cancer cells. Fluorouracil 130-134 ATP binding cassette subfamily B member 5 Homo sapiens 0-5 25689483-8 2015 ABCB5 knockdown decreased the survival rate following 5-FU treatment as expected, and the ABCB5 expression level was increased in 5-FU-resistant human colon cancer cells. Fluorouracil 130-134 ATP binding cassette subfamily B member 5 Homo sapiens 90-95 25689483-11 2015 In contrast, 5-FU treatment alone increased the ABCB5 expression level. Fluorouracil 13-17 ATP binding cassette subfamily B member 5 Homo sapiens 48-53 25689483-12 2015 Taken together, these results suggest that c-MYC confers resistance to 5-FU through regulating ABCB5 expression in human colon cancer cells. Fluorouracil 71-75 ATP binding cassette subfamily B member 5 Homo sapiens 95-100 25739674-10 2015 Most importantly, exogenous induction of YAP1 induces resistance to 5-fluorouracil and docetaxcel, whereas knockdown of YAP1 sensitizes esophageal cancer cells to these cytotoxics. Fluorouracil 68-82 Yes1 associated transcriptional regulator Homo sapiens 41-45 25398650-10 2015 The expression levels of cxcl9 and cxcr3 were significantly up-regulated in intestinal mucosa after 5-FU injection. Fluorouracil 100-104 C-X-C motif chemokine receptor 3 Homo sapiens 35-40 25938772-6 2015 In addition, fibroblast-derived conditioned medium (CM) promoted percentage, clonogenicity and tumor growth of CSCs (i.e., CD133+ and TOP-GFP+) upon treatment with 5-fluorouracil (5-Fu) or oxaliplatin (OXA). Fluorouracil 164-178 prominin 1 Homo sapiens 123-128 27869649-11 2017 Importantly, calcipotriol plus 5-FU treatment induced TSLP, HLA class II, and natural killer cell group 2D (NKG2D) ligand expression in the lesional keratinocytes associated with a marked CD4+ T cell infiltration, which peaked on days 10-11 after treatment, without pain, crusting, or ulceration. Fluorouracil 31-35 killer cell lectin like receptor K1 Homo sapiens 78-106 27869649-11 2017 Importantly, calcipotriol plus 5-FU treatment induced TSLP, HLA class II, and natural killer cell group 2D (NKG2D) ligand expression in the lesional keratinocytes associated with a marked CD4+ T cell infiltration, which peaked on days 10-11 after treatment, without pain, crusting, or ulceration. Fluorouracil 31-35 killer cell lectin like receptor K1 Homo sapiens 108-113 28011480-6 2017 In contrast, treatment with CaLa (2.5 mM), alone and in combination with 5-FU, exerted antitumor activity against both anchored and unanchored CRC cells via calcium-mediated FAK proteolysis and inhibition of EMT markers, such as vimentin and SNAIL. Fluorouracil 73-77 protein tyrosine kinase 2 Homo sapiens 174-177 25323586-8 2015 The resistance to 5-FU can be abolished by inhibitor of Src and PAK1 or Bcl-2 antagonist in cell and animal models. Fluorouracil 18-22 p21 (RAC1) activated kinase 1 Homo sapiens 64-68 25323586-11 2015 Therefore, we suggest that Src, PAK1 or Bcl-2 inhibitor may potentially overcome the resistance of 5-FU-based chemotherapy and consequently to improve outcomes in patients with PXN/Bcl-2 and pPXN-S272/Bcl-2-positive tumors. Fluorouracil 99-103 p21 (RAC1) activated kinase 1 Homo sapiens 32-36 25885470-9 2015 CD13(+)/CD166(-) cells showed high ALDH activity, spheroid forming ability and resistance to 5-fluorouracil. Fluorouracil 93-107 alanyl aminopeptidase, membrane Homo sapiens 0-4 25885470-9 2015 CD13(+)/CD166(-) cells showed high ALDH activity, spheroid forming ability and resistance to 5-fluorouracil. Fluorouracil 93-107 activated leukocyte cell adhesion molecule Homo sapiens 8-13 25855960-7 2015 PCAF was also found to sensitize HCC cells to 5-fluorouracil (5-FU) treatment by regulating GLI1/Bcl-2/BAX axis-dependent apoptosis. Fluorouracil 46-60 lysine acetyltransferase 2B Homo sapiens 0-4 25855960-7 2015 PCAF was also found to sensitize HCC cells to 5-fluorouracil (5-FU) treatment by regulating GLI1/Bcl-2/BAX axis-dependent apoptosis. Fluorouracil 62-66 lysine acetyltransferase 2B Homo sapiens 0-4 25855960-8 2015 In vivo experiments also confirmed the regulatory effect of PCAF on the GLI1/Bcl-2/BAX axis and its synergistic antitumor effects with 5-FU. Fluorouracil 135-139 lysine acetyltransferase 2B Homo sapiens 60-64 25855960-10 2015 Together, these results show that PCAF can induce cell apoptosis by modulating a GLI1/Bcl-2/BAX axis that in turn suppresses HCC progression, and suggest that 5-FU may exert a stronger anti-tumor effect in patients with PCAF expression in HCC tumors. Fluorouracil 159-163 lysine acetyltransferase 2B Homo sapiens 34-38 25855960-10 2015 Together, these results show that PCAF can induce cell apoptosis by modulating a GLI1/Bcl-2/BAX axis that in turn suppresses HCC progression, and suggest that 5-FU may exert a stronger anti-tumor effect in patients with PCAF expression in HCC tumors. Fluorouracil 159-163 lysine acetyltransferase 2B Homo sapiens 220-224 25963703-6 2015 We administered chemotherapy for colon cancer using 5-fluorouracil plus Leucovorin(5-FU/LV), after which the CPK levels gradually decreased. Fluorouracil 52-66 phosphatidylinositol-4-phosphate 3-kinase catalytic subunit type 2 alpha Homo sapiens 109-112 25963703-6 2015 We administered chemotherapy for colon cancer using 5-fluorouracil plus Leucovorin(5-FU/LV), after which the CPK levels gradually decreased. Fluorouracil 83-87 phosphatidylinositol-4-phosphate 3-kinase catalytic subunit type 2 alpha Homo sapiens 109-112 25634668-0 2015 Blockage of PTPRJ promotes cell growth and resistance to 5-FU through activation of JAK1/STAT3 in the cervical carcinoma cell line C33A. Fluorouracil 57-61 protein tyrosine phosphatase receptor type J Homo sapiens 12-17 25634668-8 2015 Our further study indicated that PTPRJ levels were highly correlated with cell survival when the C33A cells were treated with 5-fluorouracil (5-FU), an important chemotherapeutic agent for cervical cancer. Fluorouracil 126-140 protein tyrosine phosphatase receptor type J Homo sapiens 33-38 25634668-8 2015 Our further study indicated that PTPRJ levels were highly correlated with cell survival when the C33A cells were treated with 5-fluorouracil (5-FU), an important chemotherapeutic agent for cervical cancer. Fluorouracil 142-146 protein tyrosine phosphatase receptor type J Homo sapiens 33-38 24747973-7 2015 Finally, by treating zebrafish harboring ERBB2-driven gliomas with an appropriate cytotoxic chemotherapy (5-fluorouracil) or tyrosine kinase inhibitor (erlotinib), we show that these models can effectively assess drug efficacy. Fluorouracil 106-120 erb-b2 receptor tyrosine kinase 2 Danio rerio 41-46 25098891-0 2015 5-Fluorouracil causes leukocytes attraction in the peritoneal cavity by activating autophagy and HMGB1 release in colon carcinoma cells. Fluorouracil 0-14 high mobility group box 1 Mus musculus 97-102 25098891-7 2015 Our results identify autophagy induction and HMGB1 release in colon carcinoma cells as key events responsible for 5-FU elicited leukocyte attraction and define a novel rate-limiting target for combinatorial therapies. Fluorouracil 114-118 high mobility group box 1 Mus musculus 45-50 25747889-17 2015 Compared to NS group, mRNA and proteins expression of Foxp3 and TIM-3 down regulated in BLTA and 5-FU group (P<0.01). Fluorouracil 97-101 hepatitis A virus cellular receptor 2 Mus musculus 64-69 26011332-2 2015 METHODS: A total of 102 patients who underwent postoperative fluorouracil (5-FU)-based radio-chemotherapy in our institution between 2004 and 2010 for stage IB-IV (AJCC 6th Edn.) Fluorouracil 61-73 ribonuclease A family member 2 Homo sapiens 173-176 27458977-9 2017 miR-34a injection significantly inhibited the tumor growth of PDAC tumors and sensitized the anticancer effects of 5-fluorouracil (5-FU). Fluorouracil 115-129 microRNA 34a Homo sapiens 0-7 27458977-9 2017 miR-34a injection significantly inhibited the tumor growth of PDAC tumors and sensitized the anticancer effects of 5-fluorouracil (5-FU). Fluorouracil 131-135 microRNA 34a Homo sapiens 0-7 27458977-12 2017 miR-34a, but not miR-150, significantly sensitized the anticancer effect of 5-FU in BxPC-3 cells in vitro. Fluorouracil 76-80 microRNA 34a Homo sapiens 0-7 26011332-2 2015 METHODS: A total of 102 patients who underwent postoperative fluorouracil (5-FU)-based radio-chemotherapy in our institution between 2004 and 2010 for stage IB-IV (AJCC 6th Edn.) Fluorouracil 75-79 ribonuclease A family member 2 Homo sapiens 173-176 25617735-8 2015 Inhibition of cyclinD1 decreased the cell viability assessed by MTT and increased rate of apoptosis when exposed to 5-FU treatment while overexpression of cyclinD1 showed the reverse effect. Fluorouracil 116-120 cyclin D1 Homo sapiens 14-22 25617735-11 2015 Inhibition of STAT3 decreased cyclinD1 expression to decrease the cell viability and increase rate of apoptosis when exposed to 5-FU treatment. Fluorouracil 128-132 cyclin D1 Homo sapiens 30-38 25482885-0 2015 miR-203 enhances chemosensitivity to 5-fluorouracil by targeting thymidylate synthase in colorectal cancer. Fluorouracil 37-51 microRNA 203a Homo sapiens 0-7 25482885-2 2015 However, the molecular mechanism as to how miR-203 modulates the chemosensitivity to 5-fluorouracil (5-FU) in colorectal cancer is poorly known. Fluorouracil 85-99 microRNA 203a Homo sapiens 43-50 25482885-2 2015 However, the molecular mechanism as to how miR-203 modulates the chemosensitivity to 5-fluorouracil (5-FU) in colorectal cancer is poorly known. Fluorouracil 101-105 microRNA 203a Homo sapiens 43-50 25482885-3 2015 In the present study, we found that miR-203 was downregulated in the 5-FU-resistant cell line LoVo/5-Fu, and was inversely correlated with the extent of 5-FU chemoresistance. Fluorouracil 69-73 microRNA 203a Homo sapiens 36-43 25482885-3 2015 In the present study, we found that miR-203 was downregulated in the 5-FU-resistant cell line LoVo/5-Fu, and was inversely correlated with the extent of 5-FU chemoresistance. Fluorouracil 99-103 microRNA 203a Homo sapiens 36-43 25482885-3 2015 In the present study, we found that miR-203 was downregulated in the 5-FU-resistant cell line LoVo/5-Fu, and was inversely correlated with the extent of 5-FU chemoresistance. Fluorouracil 153-157 microRNA 203a Homo sapiens 36-43 25482885-7 2015 Finally, we discovered that miR-203 increased the inhibitory effects of 5-FU on tumor growth in vivo. Fluorouracil 72-76 microRNA 203a Homo sapiens 28-35 25482885-8 2015 Overall, our data indicate that miR-203 enhances 5-FU chemosensitivity via the downregulation of TYMS in colorectal cancer and provide important insight into the mechanism of 5-FU resistance in colorectal cancer patients. Fluorouracil 49-53 microRNA 203a Homo sapiens 32-39 25482885-8 2015 Overall, our data indicate that miR-203 enhances 5-FU chemosensitivity via the downregulation of TYMS in colorectal cancer and provide important insight into the mechanism of 5-FU resistance in colorectal cancer patients. Fluorouracil 175-179 microRNA 203a Homo sapiens 32-39 25482885-9 2015 More important, the present study suggests that miR-203 has the potential as a therapeutic strategy for 5-FU-resistant colorectal cancer. Fluorouracil 104-108 microRNA 203a Homo sapiens 48-55 25497015-0 2015 Osteopontin-integrin alpha(v)beta(3) axis is crucial for 5-fluorouracil resistance in oral squamous cell carcinoma. Fluorouracil 57-71 secreted phosphoprotein 1 Mus musculus 0-11 28008906-5 2016 Knockdown of PHLDB3 more efficiently inhibits the growth of mouse xenograft tumours derived from human colon cancer HCT116 cells that contain wild type p53 compared with p53-deficient HCT116 cells, and also sensitizes tumour cells to doxorubicin and 5-Fluorouracil. Fluorouracil 250-264 pleckstrin homology like domain, family B, member 3 Mus musculus 13-19 28101205-8 2016 Cytoplasmic KRAS levels decreased whereas nuclear MutS protein homolog 2 (MSH2) levels increased slightly in CRC HCT116 cells that were microsatellite instable, following treatment with 76.9 microM 5-FU for 2 days. Fluorouracil 198-202 mutS homolog 2 Homo sapiens 50-72 28101205-8 2016 Cytoplasmic KRAS levels decreased whereas nuclear MutS protein homolog 2 (MSH2) levels increased slightly in CRC HCT116 cells that were microsatellite instable, following treatment with 76.9 microM 5-FU for 2 days. Fluorouracil 198-202 mutS homolog 2 Homo sapiens 74-78 27659530-0 2016 CD133+CD24lo defines a 5-Fluorouracil-resistant colon cancer stem cell-like phenotype. Fluorouracil 23-37 prominin 1 Homo sapiens 0-5 27659530-5 2016 We report here that 5-FU treatment selectively enriches a subset of CD133+ colon cancer cells in vitro. Fluorouracil 20-24 prominin 1 Homo sapiens 68-73 27659530-6 2016 5-FU chemotherapy also increases CD133+ tumor cells in human colon cancer patients. Fluorouracil 0-4 prominin 1 Homo sapiens 33-38 27748862-0 2016 Gap junction composed of connexin43 modulates 5-fluorouracil, oxaliplatin and irinotecan resistance on colorectal cancers. Fluorouracil 46-60 gap junction protein alpha 1 Homo sapiens 25-35 27748862-4 2016 The current study investigated the effects of connexin43 (Cx43) gap junctions on 5-fluorouracil (5-FU), oxaliplatin and irinotecan in colon cancer cells. Fluorouracil 81-95 gap junction protein alpha 1 Homo sapiens 46-56 27748862-4 2016 The current study investigated the effects of connexin43 (Cx43) gap junctions on 5-fluorouracil (5-FU), oxaliplatin and irinotecan in colon cancer cells. Fluorouracil 81-95 gap junction protein alpha 1 Homo sapiens 58-62 27748862-4 2016 The current study investigated the effects of connexin43 (Cx43) gap junctions on 5-fluorouracil (5-FU), oxaliplatin and irinotecan in colon cancer cells. Fluorouracil 97-101 gap junction protein alpha 1 Homo sapiens 46-56 27748862-4 2016 The current study investigated the effects of connexin43 (Cx43) gap junctions on 5-fluorouracil (5-FU), oxaliplatin and irinotecan in colon cancer cells. Fluorouracil 97-101 gap junction protein alpha 1 Homo sapiens 58-62 27748862-7 2016 Downregulation of Cx43 gap junction functioning attenuated 5-FU, oxaliplatin and irinotecan toxicity in colon cancer cells, which was increased in cells treated with a Cx43 gap junction function enhancer. Fluorouracil 59-63 gap junction protein alpha 1 Homo sapiens 18-22 27748862-7 2016 Downregulation of Cx43 gap junction functioning attenuated 5-FU, oxaliplatin and irinotecan toxicity in colon cancer cells, which was increased in cells treated with a Cx43 gap junction function enhancer. Fluorouracil 59-63 gap junction protein alpha 1 Homo sapiens 168-172 25497015-3 2015 Here we found increased osteopontin (OPN) gene expression in OSCC tissues with resistance to 5-FU-based chemoradiotherapy. Fluorouracil 93-97 secreted phosphoprotein 1 Mus musculus 24-35 25497015-3 2015 Here we found increased osteopontin (OPN) gene expression in OSCC tissues with resistance to 5-FU-based chemoradiotherapy. Fluorouracil 93-97 secreted phosphoprotein 1 Mus musculus 37-40 25497015-4 2015 OPN overexpression in OSCC cells led to 5-FU resistance and abrogated the prosurvival effect of the drug in a mouse xenograft model. Fluorouracil 40-44 secreted phosphoprotein 1 Mus musculus 0-3 25497015-5 2015 OPN-induced 5-FU resistance required integrin alphavbeta3. Fluorouracil 12-16 secreted phosphoprotein 1 Mus musculus 0-3 25497015-7 2015 Our data suggest that the OPN-integrin alphavbeta3 axis is crucial for 5-FU resistance in OSCC. Fluorouracil 71-75 secreted phosphoprotein 1 Mus musculus 26-29 25452783-12 2015 The expression levels of HIF-2, ABCG2 and Oct-4 mRNA and protein were high in the blank control group, and were further increased in the 5-Fu group. Fluorouracil 137-141 ATP binding cassette subfamily G member 2 (Junior blood group) Mus musculus 32-37 27830015-3 2016 This study aims to evaluate the function of miR-134 in gastric cancer and investigate its effect on the sensitivity of gastric cancer cells to 5-FU. Fluorouracil 143-147 microRNA 134 Homo sapiens 44-51 27830015-6 2016 Finally, the up-regulation of miR-134 enhanced the sensitivity of gastric cancer cells to 5-FU. Fluorouracil 90-94 microRNA 134 Homo sapiens 30-37 27830015-7 2016 In conclusion, miR-134 suppresses tumor development in gastric cancer by targeting KRAS and enhances cell sensitivity to 5-FU. Fluorouracil 121-125 microRNA 134 Homo sapiens 15-22 27726102-0 2016 MiRNA-221-3p desensitizes pancreatic cancer cells to 5-fluorouracil by targeting RB1. Fluorouracil 53-67 RB transcriptional corepressor 1 Homo sapiens 81-84 27775798-5 2016 We also examined the effects of ZNRF2 on cell growth and cell survival in the presence of fluorouracil. Fluorouracil 90-102 zinc and ring finger 2 Homo sapiens 32-37 27775798-9 2016 In vitro, overexpression of ZNRF2 increased NSCLC cell growth and suppressed apoptotic cell death in the presence of Fluorouracil, while depletion of ZNRF2 decreased NSCLC cell growth and increased apoptotic cell death in the presence of fluorouracil. Fluorouracil 117-129 zinc and ring finger 2 Homo sapiens 28-33 27775798-9 2016 In vitro, overexpression of ZNRF2 increased NSCLC cell growth and suppressed apoptotic cell death in the presence of Fluorouracil, while depletion of ZNRF2 decreased NSCLC cell growth and increased apoptotic cell death in the presence of fluorouracil. Fluorouracil 238-250 zinc and ring finger 2 Homo sapiens 28-33 25561897-13 2015 Furthermore, cell lines with T889C mutation in POLB gene were more resistant to the treatment of 5-fluorouracil, cisplatin and epirubicin than those with wild type POLB. Fluorouracil 97-111 DNA polymerase beta Homo sapiens 47-51 25333998-9 2015 Moreover, 5-FU partly recovered Hsp90 client proteins, including Akt, p-Akt, inhibitor of kappaB kinase (IKK)alpha, extracellular signal-regulated kinase (ERK)1/2, and glycogen synthase kinase (GSK)-3beta, which SNX-2112 had downregulated. Fluorouracil 10-14 glycogen synthase kinase 3 beta Homo sapiens 168-204 27698820-3 2016 Increased cell motility and epithelial-mesenchymal transition were observed by migration assay in human hepatoblastoma PLC/RAF/5 cells following 5-Fu treatment, as well as a significant enhancement in their sphere-forming abilities. Fluorouracil 145-149 zinc fingers and homeoboxes 2 Homo sapiens 123-126 25333573-0 2015 Inhibition of lactate dehydrogenase A by microRNA-34a resensitizes colon cancer cells to 5-fluorouracil. Fluorouracil 89-103 microRNA 34a Homo sapiens 41-53 27698820-6 2016 These findings indicate that low-dose 5-Fu treatment may efficiently enrich the CSC-like cell population in PLC/RAF/5 cells. Fluorouracil 38-42 zinc fingers and homeoboxes 2 Homo sapiens 112-115 25333573-8 2015 Overexpression of miR-34a reduced the expression of LDHA, probably through binding to the 3" untranslated region, leading to the re-sensitization of 5-FU-resistant cancer cells to 5-FU. Fluorouracil 149-153 microRNA 34a Homo sapiens 18-25 25333573-9 2015 Additionally, overexpression of LDHA rendered colon cancer cells resistant to 5-FU, suggesting that the miR-34a-induced sensitization to 5-FU is mediated through the inhibition of LDHA. Fluorouracil 78-82 microRNA 34a Homo sapiens 104-111 25333573-9 2015 Additionally, overexpression of LDHA rendered colon cancer cells resistant to 5-FU, suggesting that the miR-34a-induced sensitization to 5-FU is mediated through the inhibition of LDHA. Fluorouracil 137-141 microRNA 34a Homo sapiens 104-111 25333573-10 2015 In conclusion, the current study showed that miR-34a is involved in sensitivity to 5-FU in part through its effects on LDHA expression. Fluorouracil 83-87 microRNA 34a Homo sapiens 45-52 25034007-8 2015 Mitochondrial dysfunction subsequently initiates downstream events that trigger caspase-3 activation, and our results showed that 5-FU and capecitabine activated caspase-3 which leads to apoptosis or necrosis. Fluorouracil 130-134 caspase 3 Rattus norvegicus 80-89 25034007-8 2015 Mitochondrial dysfunction subsequently initiates downstream events that trigger caspase-3 activation, and our results showed that 5-FU and capecitabine activated caspase-3 which leads to apoptosis or necrosis. Fluorouracil 130-134 caspase 3 Rattus norvegicus 162-171 25230779-0 2014 Overexpression of CD133 enhances chemoresistance to 5-fluorouracil by activating the PI3K/Akt/p70S6K pathway in gastric cancer cells. Fluorouracil 52-66 prominin 1 Homo sapiens 18-23 25230779-3 2014 Hence, the present study investigated the function of CD133 in 5-FU resistance in human GC cells. Fluorouracil 63-67 prominin 1 Homo sapiens 54-59 25230779-10 2014 Furthermore, CD133 silencing enhanced 5-FU cytotoxicity and apoptotic characteristics, whereas CD133 overexpression increased 5-FU resistance. Fluorouracil 38-42 prominin 1 Homo sapiens 13-18 25230779-10 2014 Furthermore, CD133 silencing enhanced 5-FU cytotoxicity and apoptotic characteristics, whereas CD133 overexpression increased 5-FU resistance. Fluorouracil 126-130 prominin 1 Homo sapiens 95-100 25230779-12 2014 Notably, Akt inhibition by LY294002 restored the 5-FU cytotoxicity suppressed by CD133 overexpression, while Akt activation by epidermal growth factor reversed the 5-FU cytotoxicity enhanced by CD133 silencing. Fluorouracil 49-53 prominin 1 Homo sapiens 81-86 25230779-13 2014 Therefore, CD133 may inhibit 5-FU-induced apoptosis by regulating the expression of P-gp and Bcl-2 family mediated by phosphoinositide 3-kinase/Akt/p70S6K pathway in GC cells. Fluorouracil 29-33 prominin 1 Homo sapiens 11-16 25178657-0 2014 5-Fluorouracil causes severe CNS demyelination by disruption of TCF7L2/HDAC1/HDAC2 complex in adolescent mice. Fluorouracil 0-14 transcription factor 7 like 2, T cell specific, HMG box Mus musculus 64-70 25178657-4 2014 Gene-chip microarray transcriptome analysis identifies that oligodendrocyte-specific factor TCF7L2 may be a toxic target of 5-FU-impaired myelination. Fluorouracil 124-128 transcription factor 7 like 2, T cell specific, HMG box Mus musculus 92-98 25178657-5 2014 5-FU-decreased TCF7L2 results in disruption of the interaction between TCF7L2 and HDAC1/2. Fluorouracil 0-4 transcription factor 7 like 2, T cell specific, HMG box Mus musculus 15-21 25178657-5 2014 5-FU-decreased TCF7L2 results in disruption of the interaction between TCF7L2 and HDAC1/2. Fluorouracil 0-4 transcription factor 7 like 2, T cell specific, HMG box Mus musculus 71-77 25178657-6 2014 Inhibition of crucial myelination-promoting factors by 5-FU is more significantly antagonized by co-transfection of TCF7L2, HDAC1 and HDAC2 than TCF7L2 alone. Fluorouracil 55-59 transcription factor 7 like 2, T cell specific, HMG box Mus musculus 116-122 25178657-6 2014 Inhibition of crucial myelination-promoting factors by 5-FU is more significantly antagonized by co-transfection of TCF7L2, HDAC1 and HDAC2 than TCF7L2 alone. Fluorouracil 55-59 transcription factor 7 like 2, T cell specific, HMG box Mus musculus 145-151 25178657-7 2014 Our findings reveal that 5-FU could acutely induce the severe myelin degeneration in adolescence and disruption of TCF7L2/HDAC1/HDAC2 complex is at least partially involved in 5-FU-induced demyelination. Fluorouracil 176-180 transcription factor 7 like 2, T cell specific, HMG box Mus musculus 115-121 25088576-8 2014 MRP3 down-regulation significantly increased 5-fluorouracil or irradiation-induced cell apoptosis and attenuated tumor growth following irradiation in animal models. Fluorouracil 45-59 ATP binding cassette subfamily C member 3 Homo sapiens 0-4 27300755-6 2016 Moreover, ALN-treated mice exhibited an enhanced resistance of HSCs in response to the genotoxic stress of 5-fluorouracil, as determined by mitochondrial ROS generation, SA-beta-gal activity, and p16INK4a expression in subsets of LSK and CD150+ CD48- LSK cells as well as competitive assay. Fluorouracil 107-121 lymphocyte protein tyrosine kinase Mus musculus 230-233 25157181-6 2014 Unexpectedly, Cdk6 R31C impairs the potential of hematopoietic progenitors to repopulate upon adoptive transfer or after 5-fluorouracil-induced damage. Fluorouracil 121-135 cyclin-dependent kinase 6 Mus musculus 14-18 25272957-6 2014 The benefit on DFS in AREG-/EREG- patients was even stronger in the group that received 5-FU/FA/irinotecan as adjuvant treatment (p=0.002). Fluorouracil 88-92 epiregulin Homo sapiens 28-32 27708551-12 2016 Concordantly, lentiviral-mediated re-expression of BMP2 inhibited HCT116 CRC growth, sphere formation, clonogenic potential, cell migration, and sensitized CRC cells to 5-fluorouracil (5-FU) in vitro. Fluorouracil 169-183 bone morphogenetic protein 2 Homo sapiens 51-55 27708551-12 2016 Concordantly, lentiviral-mediated re-expression of BMP2 inhibited HCT116 CRC growth, sphere formation, clonogenic potential, cell migration, and sensitized CRC cells to 5-fluorouracil (5-FU) in vitro. Fluorouracil 185-189 bone morphogenetic protein 2 Homo sapiens 51-55 27260988-0 2016 Up-regulation of stem cell markers by P21-activated kinase 1 contributes to 5-fluorouracil resistance of colorectal cancer. Fluorouracil 76-90 p21 (RAC1) activated kinase 1 Homo sapiens 38-60 27260988-7 2016 Furthermore PAK overexpression partially overcame the inhibition of CRC growth by 5-FU, and PAK inhibition was synergistic with 5-FU treatment. Fluorouracil 82-86 p21 (RAC1) activated kinase 1 Homo sapiens 12-15 27385218-0 2016 SEP enhanced the antitumor activity of 5-fluorouracil by up-regulating NKG2D/MICA and reversed immune suppression via inhibiting ROS and caspase-3 in mice. Fluorouracil 39-53 killer cell lectin-like receptor subfamily K, member 1 Mus musculus 71-76 27385218-5 2016 The results obtained indicated that SEP alone stimulated NK-92 cytotoxicity and coordinated with 5-FU to augment the cytotoxicity of NK-92 cells against HepG-2 or A549 cells in vitro. Fluorouracil 97-101 membrane metalloendopeptidase like 1 Homo sapiens 36-39 27385218-7 2016 Additionally, 5-FU could increase MICA expression on HepG-2 or A549 cells and prevent membrane MICA from shedding as soluble MICA, which were abrogated in the tumor cells transfected with ADAM 10 overexpression plasmid. Fluorouracil 14-18 MHC class I polypeptide-related sequence A Homo sapiens 34-38 27385218-7 2016 Additionally, 5-FU could increase MICA expression on HepG-2 or A549 cells and prevent membrane MICA from shedding as soluble MICA, which were abrogated in the tumor cells transfected with ADAM 10 overexpression plasmid. Fluorouracil 14-18 MHC class I polypeptide-related sequence A Homo sapiens 95-99 27385218-7 2016 Additionally, 5-FU could increase MICA expression on HepG-2 or A549 cells and prevent membrane MICA from shedding as soluble MICA, which were abrogated in the tumor cells transfected with ADAM 10 overexpression plasmid. Fluorouracil 14-18 MHC class I polypeptide-related sequence A Homo sapiens 95-99 27385218-7 2016 Additionally, 5-FU could increase MICA expression on HepG-2 or A549 cells and prevent membrane MICA from shedding as soluble MICA, which were abrogated in the tumor cells transfected with ADAM 10 overexpression plasmid. Fluorouracil 14-18 ADAM metallopeptidase domain 10 Homo sapiens 188-195 26939902-5 2016 In this study, we used the HepG2 cell line and found that metformin/AICAR downregulated NANOG expression with decreased cell viability and enhanced chemosensitivity to 5-fluorouracil (5-FU). Fluorouracil 168-182 5-aminoimidazole-4-carboxamide ribonucleotide formyltransferase/IMP cyclohydrolase Homo sapiens 68-73 26939902-5 2016 In this study, we used the HepG2 cell line and found that metformin/AICAR downregulated NANOG expression with decreased cell viability and enhanced chemosensitivity to 5-fluorouracil (5-FU). Fluorouracil 184-188 5-aminoimidazole-4-carboxamide ribonucleotide formyltransferase/IMP cyclohydrolase Homo sapiens 68-73 27369741-10 2016 Calnexin gene-silencing significantly reduced cell survival and increased cancer cell susceptibility to 5FU chemotherapy. Fluorouracil 104-107 calnexin Homo sapiens 0-8 27144434-9 2016 Finally, ERK5 inhibition using XMD8-92 was shown to increase the antitumor effects of 5-FU in a murine subcutaneous xenograft model, enhancing apoptosis while markedly reducing tumor growth. Fluorouracil 86-90 mitogen-activated protein kinase 7 Mus musculus 9-13 27020656-9 2016 Mechanistically, paricalcitol and 5-FU had cooperated together to repress the expression of procancerous Wnt, beta-catenin, NF-kappaB, COX-2, iNOS, VEGF, and HSP-90 more, and to upregulate the expression of antitumorigenesis DKK-1 and CDNK-1A, compared with their monotherapies. Fluorouracil 34-38 cytochrome c oxidase II, mitochondrial Rattus norvegicus 135-140 27020656-9 2016 Mechanistically, paricalcitol and 5-FU had cooperated together to repress the expression of procancerous Wnt, beta-catenin, NF-kappaB, COX-2, iNOS, VEGF, and HSP-90 more, and to upregulate the expression of antitumorigenesis DKK-1 and CDNK-1A, compared with their monotherapies. Fluorouracil 34-38 dickkopf WNT signaling pathway inhibitor 1 Rattus norvegicus 225-230 25050539-8 2014 Among these, collapsin response mediator protein 2 (CRMP-2), DNA replication complex GINS protein PSF2 (PSF-2) and selenium-binding protein 1 (SBP-1) were notable not only for their differential expression but also for decreased expression following 5-FU exposure, indicating their possible roles as novel biomarkers for sensitivity (CRMP-2, PSF-2) as well as resistance (SBP-1) to 5-FU. Fluorouracil 250-254 selenium binding protein 1 Homo sapiens 115-141 25050539-8 2014 Among these, collapsin response mediator protein 2 (CRMP-2), DNA replication complex GINS protein PSF2 (PSF-2) and selenium-binding protein 1 (SBP-1) were notable not only for their differential expression but also for decreased expression following 5-FU exposure, indicating their possible roles as novel biomarkers for sensitivity (CRMP-2, PSF-2) as well as resistance (SBP-1) to 5-FU. Fluorouracil 250-254 selenium binding protein 1 Homo sapiens 143-148 25050539-8 2014 Among these, collapsin response mediator protein 2 (CRMP-2), DNA replication complex GINS protein PSF2 (PSF-2) and selenium-binding protein 1 (SBP-1) were notable not only for their differential expression but also for decreased expression following 5-FU exposure, indicating their possible roles as novel biomarkers for sensitivity (CRMP-2, PSF-2) as well as resistance (SBP-1) to 5-FU. Fluorouracil 382-386 selenium binding protein 1 Homo sapiens 115-141 25050539-8 2014 Among these, collapsin response mediator protein 2 (CRMP-2), DNA replication complex GINS protein PSF2 (PSF-2) and selenium-binding protein 1 (SBP-1) were notable not only for their differential expression but also for decreased expression following 5-FU exposure, indicating their possible roles as novel biomarkers for sensitivity (CRMP-2, PSF-2) as well as resistance (SBP-1) to 5-FU. Fluorouracil 382-386 selenium binding protein 1 Homo sapiens 143-148 25202056-0 2014 Expression of ABCB6 is related to resistance to 5-FU, SN-38 and vincristine. Fluorouracil 48-52 ATP binding cassette subfamily B member 6 (Langereis blood group) Homo sapiens 14-19 26843428-2 2016 Herein we report that exposure to DNA-damaging agents that generate replicative stress such as camptothecin (CPT), 5-fluoro-uracil (5FU) and ultraviolet radiation (UVC) causes downregulation of Stau2 in HCT116 colorectal cancer cells. Fluorouracil 115-130 staufen double-stranded RNA binding protein 2 Homo sapiens 194-199 26843428-2 2016 Herein we report that exposure to DNA-damaging agents that generate replicative stress such as camptothecin (CPT), 5-fluoro-uracil (5FU) and ultraviolet radiation (UVC) causes downregulation of Stau2 in HCT116 colorectal cancer cells. Fluorouracil 132-135 staufen double-stranded RNA binding protein 2 Homo sapiens 194-199 26808144-10 2016 These results suggest that 5-fluorouracil-associated leukopenia allows excessive oral bacterial infection in the oral ulcerative region, resulting in the enhancement of spontaneous pain through continuous TRPV1 activation and cyclooxygenase pathway, and mechanical allodynia through mechanical sensitization of TRPA1 caused by neuronal effects of bacterial toxins. Fluorouracil 27-41 transient receptor potential cation channel, subfamily V, member 1 Rattus norvegicus 205-210 25202056-5 2014 ABCB6 expression enhanced resistance to 5-fluorouracil (5-FU), SN-38 and vincristine (Vcr) but not to arsenite. Fluorouracil 40-54 ATP binding cassette subfamily B member 6 (Langereis blood group) Homo sapiens 0-5 25202056-5 2014 ABCB6 expression enhanced resistance to 5-fluorouracil (5-FU), SN-38 and vincristine (Vcr) but not to arsenite. Fluorouracil 56-60 ATP binding cassette subfamily B member 6 (Langereis blood group) Homo sapiens 0-5 25202056-6 2014 Conversely, down-regulation of ABCB6 in KAS cells increased the sensitivity of KAS cells to 5-FU, SN-38 and Vcr, but not to arsenite. Fluorouracil 92-96 ATP binding cassette subfamily B member 6 (Langereis blood group) Homo sapiens 31-36 25202056-7 2014 Our findings suggest that ABCB6 is involved in 5-FU, SN-38 and Vcr resistance. Fluorouracil 47-51 ATP binding cassette subfamily B member 6 (Langereis blood group) Homo sapiens 26-31 25071013-7 2014 Additionally, we found that ablation of EIF5A2 enhanced the chemosensitivity of HCC cells to 5-Fluorouracil (5-FU). Fluorouracil 93-107 eukaryotic translation initiation factor 5A2 Homo sapiens 40-46 25071013-7 2014 Additionally, we found that ablation of EIF5A2 enhanced the chemosensitivity of HCC cells to 5-Fluorouracil (5-FU). Fluorouracil 109-113 eukaryotic translation initiation factor 5A2 Homo sapiens 40-46 24800927-11 2014 Taken together, activation of CXCL4 expression by 5-FU in mice participates in 5-FU-induced intestinal mucositis through upregulation of p53 via activation of p38-MAPK, and CXCL4mab is potentially beneficial in preventing CIM in the intestinal tract. Fluorouracil 50-54 mitogen-activated protein kinase 14 Mus musculus 159-167 24800927-11 2014 Taken together, activation of CXCL4 expression by 5-FU in mice participates in 5-FU-induced intestinal mucositis through upregulation of p53 via activation of p38-MAPK, and CXCL4mab is potentially beneficial in preventing CIM in the intestinal tract. Fluorouracil 79-83 mitogen-activated protein kinase 14 Mus musculus 159-167 24890748-7 2014 The aim of the present study was to investigate the expression pattern of MMP-14 and MMP-2 in human papilloma virus (HPV)-negative and p16-positive SCC and to evaluate the chemosensitivity of the tumour cells to the chemotherapeutic agents, imatinib and 5-fluorouracil (5-FU). Fluorouracil 254-268 matrix metallopeptidase 14 Homo sapiens 74-80 24890748-7 2014 The aim of the present study was to investigate the expression pattern of MMP-14 and MMP-2 in human papilloma virus (HPV)-negative and p16-positive SCC and to evaluate the chemosensitivity of the tumour cells to the chemotherapeutic agents, imatinib and 5-fluorouracil (5-FU). Fluorouracil 270-274 matrix metallopeptidase 14 Homo sapiens 74-80 24837597-9 2014 The mean administered dose for cisplatin was 93.6 mg/m2 in Arm 1 and 97.2 mg/m2 in Arm 2, and 3732.6 and 3880 mg/m2 in Arm 1 and Arm 2, respectively, for 5-fluorouracil. Fluorouracil 154-168 Jupiter microtubule associated homolog 1 Homo sapiens 129-134 24936150-2 2014 The enzyme thymidine phosphorylase (TP) catalyzes the conversion of 5-FU to its active metabolite, 5-fluoro-2"-deoxyuridine. Fluorouracil 68-72 thymidine phosphorylase Homo sapiens 11-34 24936150-2 2014 The enzyme thymidine phosphorylase (TP) catalyzes the conversion of 5-FU to its active metabolite, 5-fluoro-2"-deoxyuridine. Fluorouracil 68-72 thymidine phosphorylase Homo sapiens 36-38 24005798-2 2014 This study in rats investigated whether a decreased level of plasma DAO could reflect the severity of mucosal injury due to intravenous 5-fluorouracil (5-FU) treatment. Fluorouracil 136-150 amine oxidase, copper containing 1 Rattus norvegicus 68-71 26799587-8 2016 In addition, BDH2 or lncRNA TP73-AS1 knockdown enhanced the chemosensitivity of esophageal cancer cells to 5-FU and cisplatin. Fluorouracil 107-111 tumor protein p73 Homo sapiens 28-32 26799587-8 2016 In addition, BDH2 or lncRNA TP73-AS1 knockdown enhanced the chemosensitivity of esophageal cancer cells to 5-FU and cisplatin. Fluorouracil 107-111 prostaglandin D2 receptor Homo sapiens 33-36 25810491-3 2016 Hypermethylation of transcription factor activating enhancer-binding protein 2 (TFAP2E) has been implicated in chemotherapy resistance to fluorouracil-based chemotherapy in patients with colorectal cancer, but its role in GC is still unknown. Fluorouracil 139-151 transcription factor AP-2 epsilon Homo sapiens 81-87 25810491-8 2016 Hypermethylation of TFAP2E occurred more frequently in tumors with lower differentiation grades (P < .001) and was significantly associated with nonresponse to fluorouracil-based chemotherapy (P = .010). Fluorouracil 163-175 transcription factor AP-2 epsilon Homo sapiens 20-26 27462446-5 2016 During stress hematopoiesis, Trib2 (-/-) developing thymocytes undergo accelerated proliferation and demonstrate hypersensitivity to 5-fluorouracil (5-FU)-induced cell death. Fluorouracil 133-147 tribbles pseudokinase 2 Mus musculus 29-34 27462446-5 2016 During stress hematopoiesis, Trib2 (-/-) developing thymocytes undergo accelerated proliferation and demonstrate hypersensitivity to 5-fluorouracil (5-FU)-induced cell death. Fluorouracil 149-153 tribbles pseudokinase 2 Mus musculus 29-34 26985934-8 2016 A dosage of 20 mug/mL 5-FU resulted in a significant decrease in the proliferation and apoptosis of HCT116 cells and significantly decreased expression levels of LGR4. Fluorouracil 22-26 leucine rich repeat containing G protein-coupled receptor 4 Homo sapiens 162-166 26985934-10 2016 5-FU induces apoptosis of colorectal cancer cells and inhibits proliferation by suppressing LGR4 proteins. Fluorouracil 0-4 leucine rich repeat containing G protein-coupled receptor 4 Homo sapiens 92-96 24005798-2 2014 This study in rats investigated whether a decreased level of plasma DAO could reflect the severity of mucosal injury due to intravenous 5-fluorouracil (5-FU) treatment. Fluorouracil 152-156 amine oxidase, copper containing 1 Rattus norvegicus 68-71 24005798-5 2014 After 5-FU treatment, the majority of rats developed moderate to severe diarrhea, and levels of plasma DAO activity significantly decreased compared to those of control group (P < 0.05). Fluorouracil 6-10 amine oxidase, copper containing 1 Rattus norvegicus 103-106 24005798-8 2014 In conclusion, plasma DAO activity decreases in response to severe intestinal mucosal injury after 5-FU treatment, and SDF supplementation might be a practical and useful treatment for reducing the intestinal toxicity of 5-FU. Fluorouracil 99-103 amine oxidase, copper containing 1 Rattus norvegicus 22-25 26998056-10 2016 miRNA levels increased with cancer progression, and lapatinib and 5-fluorouracil (5-FU; the active form of capecitabine) treatment increased the miRNA levels (specifically miR-210 and miR-221) in the treatment-resistant pancreatic cancer PANC-1 and MIA PaCa-2 cell lines. Fluorouracil 66-80 microRNA 210 Homo sapiens 172-179 26998056-10 2016 miRNA levels increased with cancer progression, and lapatinib and 5-fluorouracil (5-FU; the active form of capecitabine) treatment increased the miRNA levels (specifically miR-210 and miR-221) in the treatment-resistant pancreatic cancer PANC-1 and MIA PaCa-2 cell lines. Fluorouracil 82-86 microRNA 210 Homo sapiens 172-179 26840027-2 2016 In this study, using gene expression profiles for a panel of cell lines with drug sensitivity data and two cohorts of patients, we extracted a signature consisting of two gene pairs (KCNE2 and API5, KCNE2 and PRPF3) whose within-sample relative expression orderings (REOs) could robustly predict prognoses of gastric cancer patients treated with 5-FU-based chemotherapy. Fluorouracil 346-350 potassium voltage-gated channel subfamily E regulatory subunit 2 Homo sapiens 183-188 26840027-2 2016 In this study, using gene expression profiles for a panel of cell lines with drug sensitivity data and two cohorts of patients, we extracted a signature consisting of two gene pairs (KCNE2 and API5, KCNE2 and PRPF3) whose within-sample relative expression orderings (REOs) could robustly predict prognoses of gastric cancer patients treated with 5-FU-based chemotherapy. Fluorouracil 346-350 potassium voltage-gated channel subfamily E regulatory subunit 2 Homo sapiens 199-204 24849329-0 2014 Use of metformin alone is not associated with survival outcomes of colorectal cancer cell but AMPK activator AICAR sensitizes anticancer effect of 5-fluorouracil through AMPK activation. Fluorouracil 147-161 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 94-98 26716512-6 2016 Treatment of breast cancer cells with 5-fluorouracil (5-FU) increased the expression of pro-apoptotic and anti-proliferative factor, BAX and p21 protein through phosphorylation of p53 and p38. Fluorouracil 38-52 mitogen-activated protein kinase 14 Mus musculus 188-191 26716512-6 2016 Treatment of breast cancer cells with 5-fluorouracil (5-FU) increased the expression of pro-apoptotic and anti-proliferative factor, BAX and p21 protein through phosphorylation of p53 and p38. Fluorouracil 54-58 mitogen-activated protein kinase 14 Mus musculus 188-191 26801910-9 2016 Systematic experiments demonstrated that the CNGRC-yCD protein retained both the APN-binding affinity of NGR and the enzyme activity of yCD to convert 5-FC into 5-FU. Fluorouracil 161-165 alanyl aminopeptidase, membrane Homo sapiens 81-84 26497305-0 2016 AMPK activator AICAR promotes 5-FU-induced apoptosis in gastric cancer cells. Fluorouracil 30-34 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 0-4 26497305-0 2016 AMPK activator AICAR promotes 5-FU-induced apoptosis in gastric cancer cells. Fluorouracil 30-34 5-aminoimidazole-4-carboxamide ribonucleotide formyltransferase/IMP cyclohydrolase Homo sapiens 15-20 26497305-7 2016 Importantly, AICAR enhanced the sensitivity to 5-FU-induced reduction of cellular viability and increased apoptosis in SGC-7901 cells. Fluorouracil 47-51 5-aminoimidazole-4-carboxamide ribonucleotide formyltransferase/IMP cyclohydrolase Homo sapiens 13-18 26497305-9 2016 Finally, p-AMPK levels were reduced in 5-FU-resistant gastric cancer cells compared to human immortalized gastric epithelial cell line and 5-FU-sensitive gastric cancer cells. Fluorouracil 39-43 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 11-15 26497305-9 2016 Finally, p-AMPK levels were reduced in 5-FU-resistant gastric cancer cells compared to human immortalized gastric epithelial cell line and 5-FU-sensitive gastric cancer cells. Fluorouracil 139-143 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 11-15 26497305-10 2016 AICAR not only induces apoptosis alone but also enhances pro-apoptotic effect of 5-FU in SGC-7901 cells, which lays an experimental foundation to develop AICAR as a chemotherapeutic sensitizer against gastric cancer. Fluorouracil 81-85 5-aminoimidazole-4-carboxamide ribonucleotide formyltransferase/IMP cyclohydrolase Homo sapiens 0-5 26497305-10 2016 AICAR not only induces apoptosis alone but also enhances pro-apoptotic effect of 5-FU in SGC-7901 cells, which lays an experimental foundation to develop AICAR as a chemotherapeutic sensitizer against gastric cancer. Fluorouracil 81-85 5-aminoimidazole-4-carboxamide ribonucleotide formyltransferase/IMP cyclohydrolase Homo sapiens 154-159 26640619-10 2016 PAN-811 did not inhibit MTX-induced death of H460 cells but, interestingly, demonstrated a synergistic effect with 5-FU or CDDP in reducing cancer cell viability. Fluorouracil 115-119 adenosine deaminase 2 Homo sapiens 0-3 26472927-5 2015 Further studies showed that treatment of tumor cells with almost all standard tumor therapeutics, including chemotherapy (cisplatin, 5-fluorouracil), radiation therapy, non-lethal heat shock, and cytokine therapy (TNF-alpha), could up-regulate the expression of B7-H6 in tumor cells and enhance tumor sensitivity to NK cell cytolysis. Fluorouracil 133-147 natural killer cell cytotoxicity receptor 3 ligand 1 Homo sapiens 262-267 24849329-0 2014 Use of metformin alone is not associated with survival outcomes of colorectal cancer cell but AMPK activator AICAR sensitizes anticancer effect of 5-fluorouracil through AMPK activation. Fluorouracil 147-161 5-aminoimidazole-4-carboxamide ribonucleotide formyltransferase/IMP cyclohydrolase Homo sapiens 109-114 24884501-0 2014 FCGR2A and FCGR3A polymorphisms and clinical outcome in metastatic colorectal cancer patients treated with first-line 5-fluorouracil/folinic acid and oxaliplatin +/- cetuximab. Fluorouracil 118-132 Fc gamma receptor IIa Homo sapiens 0-6 26653552-0 2015 Aminopeptidase N inhibitor 4cc synergizes antitumor effects of 5-fluorouracil on human liver cancer cells through ROS-dependent CD13 inhibition. Fluorouracil 63-77 alanyl aminopeptidase, membrane Homo sapiens 0-16 26653552-0 2015 Aminopeptidase N inhibitor 4cc synergizes antitumor effects of 5-fluorouracil on human liver cancer cells through ROS-dependent CD13 inhibition. Fluorouracil 63-77 alanyl aminopeptidase, membrane Homo sapiens 128-132 26653552-2 2015 Here, we report the effect of an APN inhibitor 4cc in enhancing sensitivity of hepatocellular carcinoma (HCC) cell lines and xenograft model in response to 5-fluorouracil (5-FU) in vivo and in vitro. Fluorouracil 156-170 alanyl aminopeptidase, membrane Homo sapiens 33-36 26653552-2 2015 Here, we report the effect of an APN inhibitor 4cc in enhancing sensitivity of hepatocellular carcinoma (HCC) cell lines and xenograft model in response to 5-fluorouracil (5-FU) in vivo and in vitro. Fluorouracil 172-176 alanyl aminopeptidase, membrane Homo sapiens 33-36 26653552-6 2015 These results showed that the APN inhibitor 4cc synergizes antitumor effects of 5-FU on human liver cancer cells via ROS-mediated drug resistance inhibition and concurrent activation of the mitochondrial pathways of apoptosis. Fluorouracil 80-84 alanyl aminopeptidase, membrane Homo sapiens 30-33 24486618-9 2014 The possible mechanism of 5-FU induced renal toxicity is the induction of oxidative stress; activation of apoptotic pathway by upregulation of p53, bax, caspase-3 and down regulating Bcl-2. Fluorouracil 26-30 caspase 3 Rattus norvegicus 153-162 23958557-11 2014 Functionally, K19/KRT19 knockdown results in reduced invasion, loss of invadopodia formation and decreased resistance to doxorubicin, 5-fluorouracil and sorafenib. Fluorouracil 134-148 keratin 19 Homo sapiens 14-17 26420216-7 2015 Continuous treatment with 5-fluorouracil also induced YAP expression and promoted tumor formation in vivo. Fluorouracil 26-40 Yes1 associated transcriptional regulator Homo sapiens 54-57 26544726-9 2015 These results suggest that SMA is a possible candidate as an effective anti-cancer agent alone or in combination with cytotoxic chemotherapeutic drugs, such as 5-FU and cisplatin, and that the mode of action for SMA involves stabilization of the beta-catenin destruction complex through inhibition of tankyrase and the PI3K/Akt signaling pathway. Fluorouracil 160-164 survival of motor neuron 1, telomeric Homo sapiens 27-30 26099525-21 2015 Alternatively, expression of ATOH8 in PLC8024 and Huh7 cells significantly reduced the numbers of cells expressing CD133, and increased the chemo-sensitivity of Huh7 cells to 5-fluorouracil (5-FU) and cisplatin, in vitro and in mice. Fluorouracil 175-189 atonal bHLH transcription factor 8 Homo sapiens 29-34 26099525-21 2015 Alternatively, expression of ATOH8 in PLC8024 and Huh7 cells significantly reduced the numbers of cells expressing CD133, and increased the chemo-sensitivity of Huh7 cells to 5-fluorouracil (5-FU) and cisplatin, in vitro and in mice. Fluorouracil 191-195 atonal bHLH transcription factor 8 Homo sapiens 29-34 23958557-11 2014 Functionally, K19/KRT19 knockdown results in reduced invasion, loss of invadopodia formation and decreased resistance to doxorubicin, 5-fluorouracil and sorafenib. Fluorouracil 134-148 keratin 19 Homo sapiens 18-23 24362470-4 2014 Here, we found that colorectal cancer (CRC) cells treated with oxaliplatin (OXA) and/or 5-fluorouracil (5-Fu) released high levels of high-mobility group box 1 (HMGB1) and heat shock protein 70 (HSP70). Fluorouracil 104-108 high mobility group box 1 Homo sapiens 134-159 24362470-4 2014 Here, we found that colorectal cancer (CRC) cells treated with oxaliplatin (OXA) and/or 5-fluorouracil (5-Fu) released high levels of high-mobility group box 1 (HMGB1) and heat shock protein 70 (HSP70). Fluorouracil 104-108 high mobility group box 1 Homo sapiens 161-166 24362470-5 2014 After OXA/5-Fu therapy, the sera of CRC patients also exhibited increased levels of HMGB1 and HSP70, both of which are well-known DAMPs. Fluorouracil 10-14 high mobility group box 1 Homo sapiens 84-89 24821671-8 2014 Proliferation inhibition of membrane albumin-binding protein (mABP)-expressing T-47D cells by FUAc-BSA is similar to that of 5-FU and only moderate for MDA-MB-231 cells that lack such expression. Fluorouracil 125-129 sex hormone binding globulin Mus musculus 62-66 24073856-0 2014 In vivo 5FU-exposed human medullary thyroid carcinoma cells contain a chemoresistant CD133+ tumor-initiating cell subset. Fluorouracil 8-11 prominin 1 Homo sapiens 85-90 24073856-7 2014 However, when MTC xenotransplants were treated with the chemotherapeutic drug 5-fluorouracil (5FU) in vivo, CD133 expression increased in MTC cells. Fluorouracil 78-92 prominin 1 Homo sapiens 108-113 24073856-7 2014 However, when MTC xenotransplants were treated with the chemotherapeutic drug 5-fluorouracil (5FU) in vivo, CD133 expression increased in MTC cells. Fluorouracil 94-97 prominin 1 Homo sapiens 108-113 24323901-8 2014 Importantly, YES1 and YAP transcript levels were higher in liver metastases of patients with colon cancer after 5FU-based neoadjuvant chemotherapy. Fluorouracil 112-115 Yes1 associated transcriptional regulator Homo sapiens 22-25 24578608-0 2014 Genetic polymorphisms in SLC23A2 as predictive biomarkers of severe acute toxicities after treatment with a definitive 5-fluorouracil/cisplatin-based chemoradiotherapy in Japanese patients with esophageal squamous cell carcinoma. Fluorouracil 119-133 solute carrier family 23 member 2 Homo sapiens 25-32 24578608-2 2014 In the present study, single nucleotide polymorphisms (SNPs) in SLC23A2 gene were retrospectively evaluated in 49 Japanese patients with ESCC who were treated with a definitive 5-FU/CDDP-based CRT, and the predictive values for the clinical response, severe acute toxicities, and long-term survival were assessed. Fluorouracil 177-181 solute carrier family 23 member 2 Homo sapiens 64-71 23852449-6 2014 In Caco-2 and SW620 cells, compared to controls, PROM1 (CD133)(+) CD44(+) cells were significantly decreased by indomethacin treatment, and increased by 5-fluorouracil (5-FU) treatment. Fluorouracil 153-167 prominin 1 Homo sapiens 49-54 23852449-6 2014 In Caco-2 and SW620 cells, compared to controls, PROM1 (CD133)(+) CD44(+) cells were significantly decreased by indomethacin treatment, and increased by 5-fluorouracil (5-FU) treatment. Fluorouracil 153-167 prominin 1 Homo sapiens 56-61 23852449-6 2014 In Caco-2 and SW620 cells, compared to controls, PROM1 (CD133)(+) CD44(+) cells were significantly decreased by indomethacin treatment, and increased by 5-fluorouracil (5-FU) treatment. Fluorouracil 169-173 prominin 1 Homo sapiens 49-54 23852449-6 2014 In Caco-2 and SW620 cells, compared to controls, PROM1 (CD133)(+) CD44(+) cells were significantly decreased by indomethacin treatment, and increased by 5-fluorouracil (5-FU) treatment. Fluorouracil 169-173 prominin 1 Homo sapiens 56-61 23852449-7 2014 This 5-FU-induced increase of PROM1 (CD133)(+) CD44(+) cells was significantly attenuated by combination with indomethacin. Fluorouracil 5-9 prominin 1 Homo sapiens 30-35 23852449-7 2014 This 5-FU-induced increase of PROM1 (CD133)(+) CD44(+) cells was significantly attenuated by combination with indomethacin. Fluorouracil 5-9 prominin 1 Homo sapiens 37-42 23852449-11 2014 In addition, treatment of indomethacin alone or combination of 5-FU and indomethacin decreased the expressions of PROM1 (CD133), CD44, PTGS2 (cyclooxygenase 2) and HES1, and increased PPARG expression. Fluorouracil 63-67 prominin 1 Homo sapiens 114-119 23852449-11 2014 In addition, treatment of indomethacin alone or combination of 5-FU and indomethacin decreased the expressions of PROM1 (CD133), CD44, PTGS2 (cyclooxygenase 2) and HES1, and increased PPARG expression. Fluorouracil 63-67 prominin 1 Homo sapiens 121-126 23852449-11 2014 In addition, treatment of indomethacin alone or combination of 5-FU and indomethacin decreased the expressions of PROM1 (CD133), CD44, PTGS2 (cyclooxygenase 2) and HES1, and increased PPARG expression. Fluorouracil 63-67 hes family bHLH transcription factor 1 Homo sapiens 164-168 23852449-12 2014 NSAIDs could selectively reduce the colon CSCs and suppress 5-FU-induced increase of CSCs via inhibiting PTGS2 (cyclooxygenase 2) and NOTCH/HES1, and activating PPARG. Fluorouracil 60-64 hes family bHLH transcription factor 1 Homo sapiens 140-144 24337061-0 2014 TWEAK/Fn14 signaling mediates gastric cancer cell resistance to 5-fluorouracil via NF-kappaB activation. Fluorouracil 64-78 TNF receptor superfamily member 12A Homo sapiens 6-10 24337061-2 2014 In the present study, we show that Fn14 promotes resistance to 5-fluorouracil (5-FU) in gastric cancer (GC). Fluorouracil 63-77 TNF receptor superfamily member 12A Homo sapiens 35-39 24337061-2 2014 In the present study, we show that Fn14 promotes resistance to 5-fluorouracil (5-FU) in gastric cancer (GC). Fluorouracil 79-83 TNF receptor superfamily member 12A Homo sapiens 35-39 24337061-3 2014 We found that 5-FU treatment upregulated Fn14 expression in various cancer cell lines, including GC cell lines, and that knockdown of Fn14 using shRNA accelerated 5-FU sensitivity. Fluorouracil 14-18 TNF receptor superfamily member 12A Homo sapiens 41-45 24337061-3 2014 We found that 5-FU treatment upregulated Fn14 expression in various cancer cell lines, including GC cell lines, and that knockdown of Fn14 using shRNA accelerated 5-FU sensitivity. Fluorouracil 163-167 TNF receptor superfamily member 12A Homo sapiens 134-138 24337061-4 2014 In contrast, Fn14 overexpression or TWEAK treatment promoted resistance to 5-FU. Fluorouracil 75-79 TNF receptor superfamily member 12A Homo sapiens 13-17 24337061-6 2014 We first revealed that 5-FU-mediated upregulation of Fn14 occurred as a result of NF-kappaB activation, indicating that 5-FU-mediated NF-kappaB activation was the principal event underlying Fn14 upregulation and 5-FU resistance in GC. Fluorouracil 23-27 TNF receptor superfamily member 12A Homo sapiens 53-57 24337061-6 2014 We first revealed that 5-FU-mediated upregulation of Fn14 occurred as a result of NF-kappaB activation, indicating that 5-FU-mediated NF-kappaB activation was the principal event underlying Fn14 upregulation and 5-FU resistance in GC. Fluorouracil 23-27 TNF receptor superfamily member 12A Homo sapiens 190-194 24337061-6 2014 We first revealed that 5-FU-mediated upregulation of Fn14 occurred as a result of NF-kappaB activation, indicating that 5-FU-mediated NF-kappaB activation was the principal event underlying Fn14 upregulation and 5-FU resistance in GC. Fluorouracil 120-124 TNF receptor superfamily member 12A Homo sapiens 53-57 24337061-6 2014 We first revealed that 5-FU-mediated upregulation of Fn14 occurred as a result of NF-kappaB activation, indicating that 5-FU-mediated NF-kappaB activation was the principal event underlying Fn14 upregulation and 5-FU resistance in GC. Fluorouracil 120-124 TNF receptor superfamily member 12A Homo sapiens 190-194 24337061-6 2014 We first revealed that 5-FU-mediated upregulation of Fn14 occurred as a result of NF-kappaB activation, indicating that 5-FU-mediated NF-kappaB activation was the principal event underlying Fn14 upregulation and 5-FU resistance in GC. Fluorouracil 120-124 TNF receptor superfamily member 12A Homo sapiens 53-57 24337061-6 2014 We first revealed that 5-FU-mediated upregulation of Fn14 occurred as a result of NF-kappaB activation, indicating that 5-FU-mediated NF-kappaB activation was the principal event underlying Fn14 upregulation and 5-FU resistance in GC. Fluorouracil 120-124 TNF receptor superfamily member 12A Homo sapiens 190-194 24337061-7 2014 Taken together, our results suggest that Fn14 is a novel therapeutic target and that inhibition of Fn14 combined with 5-FU treatment may be an effective molecular therapeutic strategy to treat 5-FU-resistant gastric cancers. Fluorouracil 193-197 TNF receptor superfamily member 12A Homo sapiens 99-103 24447928-7 2014 The exposure of both cell lines to 5-FU significantly increased the intracellular levels of miR-145 and miR-34a in the 5-FU-sensitive DLD-1 cells, whereas the level of neither miR was elevated in the DLD-1/5FU cells. Fluorouracil 35-39 microRNA 34a Homo sapiens 104-111 24447928-7 2014 The exposure of both cell lines to 5-FU significantly increased the intracellular levels of miR-145 and miR-34a in the 5-FU-sensitive DLD-1 cells, whereas the level of neither miR was elevated in the DLD-1/5FU cells. Fluorouracil 119-123 microRNA 34a Homo sapiens 104-111 24447928-10 2014 As to the miR-34a secreted into MVs, the increase in the level in DLD-1/5FU cells was greater than that in the parental DLD-1 cells after the treatment with 5-FU. Fluorouracil 157-161 microRNA 34a Homo sapiens 10-17 24052409-0 2014 Mahanine synergistically enhances cytotoxicity of 5-fluorouracil through ROS-mediated activation of PTEN and p53/p73 in colon carcinoma. Fluorouracil 50-64 tumor protein p73 Homo sapiens 113-116 24403450-3 2014 MATERIALS AND METHODS: Firstly, half-maximal (50%) inhibitory concentration (IC50) values for cisplatin or 5-FU were calculated in cervical adenocarcinoma, HCA-1, and TCO-2 cell lines by 3-(4,5-di-methylthiazol-2-yl)-2,5-diphenyltetrazolium bromide, yellow tetrazole (MTT) assay. Fluorouracil 107-111 HCA1 Homo sapiens 156-161 24403450-7 2014 RESULTS: HCA-1 and TCO-2 cells exhibited similar sensitivity to cisplatin, and 5-FU, and comparable expression of ERCC1 mRNA and protein levels. Fluorouracil 79-83 HCA1 Homo sapiens 9-14 24403450-9 2014 ERCC1 expression was significantly elevated by cisplatin treatment, which was reduced by co-administration of 5-FU in HCA-1, TCO-2 and HCA-1R cells. Fluorouracil 110-114 HCA1 Homo sapiens 118-123 24935593-0 2014 5-Fluorouracil and interleukin-2 immunochemotherapy enhances immunogenicity of non-small cell lung cancer A549 cells through upregulation of NKG2D ligands. Fluorouracil 0-14 killer cell lectin-like receptor subfamily K, member 1 Mus musculus 141-146 24935593-5 2014 Effects of 5-FU+IL-2 on the expression and promoter activity of NKG2D ligands (MICA/MICB) in A549 cells in vitro were also assessed. Fluorouracil 11-15 killer cell lectin-like receptor subfamily K, member 1 Mus musculus 64-69 24935593-10 2014 Combination treatment of 5-FU and IL-2 upregulated the expression and the promoter activity of MICA/MICB in A549 cells, which enhanced the recognition of A549 cells by NK cells. Fluorouracil 25-29 MHC I like leukocyte 2 Mus musculus 100-104 26004085-6 2015 In an exploratory cohort of 69 patients selected from two prospective studies treated with either doxorubicin monotherapy or 5-FU and mitomycin for locally advanced breast cancers, we found defects in the pRB-pathway to be associated with therapy resistance (p-values ranging from 0.001 to 0.094, depending on the cut-off value applied to p27 expression levels). Fluorouracil 125-129 RB transcriptional corepressor 1 Homo sapiens 205-208 23530500-6 2014 Furthermore, down-regulation of PRDX6 and PSMB7 enhanced SMMC-7721/5-FU cells to 5-FU sensitivity. Fluorouracil 67-71 peroxiredoxin 6 Homo sapiens 32-37 26208523-11 2015 These data indicate that the DACH carrier ligand in oxaliplatin triggers signaling via the p53-miR-34a-E2F axis, leading to transcriptional regulation that ultimately results in accumulation of dUTP and reduced dTTP biosynthesis, potentially enhancing 5-FU cytotoxicity. Fluorouracil 252-256 microRNA 34a Homo sapiens 95-102 23530500-7 2014 CONCLUSIONS: Our study suggests that targeting drug resistant genes such as PRDX6 and PSMB7 could be a novel approach to overcome 5-FU resistance in HCC cells. Fluorouracil 130-134 peroxiredoxin 6 Homo sapiens 76-81 24697169-0 2014 Targeting liver cancer via ASGP receptor using 5-FU-loaded surface-modified PLGA nanoparticles. Fluorouracil 47-51 mucin 4, cell surface associated Homo sapiens 27-31 25665511-0 2015 LGR5 rs17109924 is a predictive genetic biomarker for time to recurrence in patients with colon cancer treated with 5-fluorouracil-based adjuvant chemotherapy. Fluorouracil 116-130 leucine rich repeat containing G protein-coupled receptor 5 Homo sapiens 0-4 25665511-1 2015 We recently found variants in cancer stem cell genes (CD44, ALCAM and LGR5) significantly associated with increased time to recurrence (TTR) in patients with stage III and high-risk stage II colon cancer treated with 5-fluorouracil (5-FU)-based chemotherapy. Fluorouracil 217-231 activated leukocyte cell adhesion molecule Homo sapiens 60-65 25665511-1 2015 We recently found variants in cancer stem cell genes (CD44, ALCAM and LGR5) significantly associated with increased time to recurrence (TTR) in patients with stage III and high-risk stage II colon cancer treated with 5-fluorouracil (5-FU)-based chemotherapy. Fluorouracil 217-231 leucine rich repeat containing G protein-coupled receptor 5 Homo sapiens 70-74 25665511-1 2015 We recently found variants in cancer stem cell genes (CD44, ALCAM and LGR5) significantly associated with increased time to recurrence (TTR) in patients with stage III and high-risk stage II colon cancer treated with 5-fluorouracil (5-FU)-based chemotherapy. Fluorouracil 233-237 activated leukocyte cell adhesion molecule Homo sapiens 60-65 25665511-1 2015 We recently found variants in cancer stem cell genes (CD44, ALCAM and LGR5) significantly associated with increased time to recurrence (TTR) in patients with stage III and high-risk stage II colon cancer treated with 5-fluorouracil (5-FU)-based chemotherapy. Fluorouracil 233-237 leucine rich repeat containing G protein-coupled receptor 5 Homo sapiens 70-74 25665511-3 2015 Patients who received 5-FU-based adjuvant chemotherapy (n=391) carrying at least one C allele in LGR5 rs17109924 had a significantly increased TTR compared with patients carrying the homozygous T/T variant (HR 0.38, 95%CI 0.19-0.79; P=0.006). Fluorouracil 22-26 leucine rich repeat containing G protein-coupled receptor 5 Homo sapiens 97-101 25665511-6 2015 We confirmed in a large and independent study cohort that LGR5 rs17109924 is a predictive genetic biomarker for TTR in patients with colon cancer treated with 5-FU-based adjuvant chemotherapy. Fluorouracil 159-163 leucine rich repeat containing G protein-coupled receptor 5 Homo sapiens 58-62 26210742-10 2015 Lastly, treatment with ISG15 suppressed apoptosis in HT29 cells, in the presence and absence of 5-fluorouracil (5FU). Fluorouracil 96-110 ISG15 ubiquitin like modifier Homo sapiens 23-28 26623038-6 2015 In this model, treatment with trastuzumab alone or trastuzumab plus oxaliplatin enhanced the expression of thymidine phosphorylase (TP), a key enzyme in the generation of 5-FU from capecitabine in tumor tissues. Fluorouracil 171-175 thymidine phosphorylase Homo sapiens 107-130 26623038-6 2015 In this model, treatment with trastuzumab alone or trastuzumab plus oxaliplatin enhanced the expression of thymidine phosphorylase (TP), a key enzyme in the generation of 5-FU from capecitabine in tumor tissues. Fluorouracil 171-175 thymidine phosphorylase Homo sapiens 132-134 24244031-0 2014 Differential clinical benefits of 5-fluorouracil-based adjuvant chemotherapy for patients with stage III colorectal cancer according to CD133 expression status. Fluorouracil 34-48 prominin 1 Homo sapiens 136-141 24244031-9 2014 CONCLUSIONS: CD133-positive patients showed resistance to 5-FU-based chemotherapy, while CD133-negative patients experienced significant survival benefits from adjuvant chemotherapy not shared by CD133-positive patients. Fluorouracil 58-62 prominin 1 Homo sapiens 13-18 24854104-0 2014 The novel HDAC inhibitor OBP-801/YM753 enhances the effects of 5-fluorouracil with radiation on esophageal squamous carcinoma cells. Fluorouracil 63-77 odorant binding protein 2A Homo sapiens 25-28 24239965-0 2014 A complex interplay between PGC-1 co-activators and mTORC1 regulates hematopoietic recovery following 5-fluorouracil treatment. Fluorouracil 102-116 CREB regulated transcription coactivator 1 Mus musculus 52-58 25979230-6 2015 Addition of curcumin to oxaliplatin/5-FU enhanced anti-proliferative and pro-apoptotic effects in a proportion of patient-derived explants, whilst reducing expression of stem cell-associated markers ALDH and CD133. Fluorouracil 36-40 prominin 1 Homo sapiens 208-213 26017781-8 2015 Atoh1 protein also enriched cancer stem cells with upregulated Lgr5 expression and cells in G0/G1 cell cycle phase, resulting in both the chemoresistance to 5-fluorouracil and oxaliplatin and the promotion of cell migration. Fluorouracil 157-171 leucine rich repeat containing G protein-coupled receptor 5 Homo sapiens 63-67 26256086-8 2015 The effects of chemotherapeutic agents (5-FU and pirarubicin) on GP73 expression were tested in three HCC cell lines (HepG2, HCCLM3 and MHCC97H). Fluorouracil 40-44 golgi membrane protein 1 Homo sapiens 65-69 25982998-10 2015 More importantly, after treated with eIF4E siRNA, cellular migratory capacity on fibronectin of HT-29 and beta6-transfected SW480 as well as their survival to 5-FU was decreased distinctly. Fluorouracil 159-163 eukaryotic translation initiation factor 4E Homo sapiens 37-42 26205949-11 2015 Mechanistically, vitamin D3/5-FU co-therapy significantly decreased the expression of Wnt, beta-catenin, iNOS, COX-2 and HSP-90 and significantly increased the expression of DKK-1, TGF-beta1, TGF-betaR2, smad4 (P < 0.05), in comparison with their corresponding monotherapy groups. Fluorouracil 28-32 prostaglandin-endoperoxide synthase 2 Rattus norvegicus 111-116 26205949-11 2015 Mechanistically, vitamin D3/5-FU co-therapy significantly decreased the expression of Wnt, beta-catenin, iNOS, COX-2 and HSP-90 and significantly increased the expression of DKK-1, TGF-beta1, TGF-betaR2, smad4 (P < 0.05), in comparison with their corresponding monotherapy groups. Fluorouracil 28-32 dickkopf WNT signaling pathway inhibitor 1 Rattus norvegicus 174-179 26205949-12 2015 CONCLUSIONS: Vitamin D3 and 5-FU synergise together and exhibit better anticancer effects by modulating Wnt/beta-catenin pathway, TGF-beta1 signals, iNOS, COX-2 and HSP-90. Fluorouracil 28-32 prostaglandin-endoperoxide synthase 2 Rattus norvegicus 155-160 26193446-8 2015 We conclude that SLC46A1/PCFT and SLC19A1/RFC-1 are associated with DFS of patients with colorectal cancer and hypothesize that poor response to 5-fluorouracil plus leucovorin therapy in some patients may be linked to low expression of these genes. Fluorouracil 145-159 solute carrier family 19 member 1 Homo sapiens 34-41 26062749-9 2015 Additionally, miR-126-3p was correlated with basal-like breast cancer, and miR-374b-5p modified the therapeutic effects of 5-Fluorouracil and Cyclophosphamide treatments in basal-like breast cancer patients. Fluorouracil 123-137 microRNA 374b Homo sapiens 75-83 25963746-12 2015 5-FU increased the IFN-beta/receptor 2 (IFNAR2) and BXA levels, indicating that 5-FU increased sensitivity of endometrial cancer cells to IFN-beta, leading to apoptosis of cancer cells. Fluorouracil 0-4 interferon beta 1 Homo sapiens 19-27 25963746-12 2015 5-FU increased the IFN-beta/receptor 2 (IFNAR2) and BXA levels, indicating that 5-FU increased sensitivity of endometrial cancer cells to IFN-beta, leading to apoptosis of cancer cells. Fluorouracil 80-84 interferon beta 1 Homo sapiens 19-27 25519757-7 2015 RESULTS: In the 5-FU/EP and 5-FU/EP/SRP groups, there was less PBF, greater breakdown of periodontal tissues and increased immunostaining for RANKL compared with the EP and EP/SRP groups. Fluorouracil 16-20 TNF superfamily member 11 Rattus norvegicus 142-147 25519757-7 2015 RESULTS: In the 5-FU/EP and 5-FU/EP/SRP groups, there was less PBF, greater breakdown of periodontal tissues and increased immunostaining for RANKL compared with the EP and EP/SRP groups. Fluorouracil 28-32 TNF superfamily member 11 Rattus norvegicus 142-147 26090311-3 2015 The codA gene of Escherichia coli encodes cytosine deaminase that hydrolyzes 5-fluorocytosine (5-FC) into the cytotoxic compound 5 fluorouracil. Fluorouracil 131-143 plasmid maintenance protein CcdA Escherichia coli 4-8 24239965-3 2014 Current findings show that mTORC1 is activated in HSPCs following 5-fluorouracil treatment and that mTORC1 activation is dependent on mitochondrial ETC capacity of HSPCs. Fluorouracil 66-80 CREB regulated transcription coactivator 1 Mus musculus 27-33 24351824-0 2013 Cbl-b enhances sensitivity to 5-fluorouracil via EGFR- and mitochondria-mediated pathways in gastric cancer cells. Fluorouracil 30-44 Cbl proto-oncogene B Homo sapiens 0-5 25996601-2 2015 We have previously shown in vitro that recognition of 5-fluorouracil (5-FU) within DNA and subsequent cytotoxicity was most effective when both hMutSalpha (hMSH2-hMSH6 heterodimer) and hMutSbeta (hMSH2-hMSH3 heterodimer) MMR complexes were present, compared to hMutSalpha > hMutSbeta alone. Fluorouracil 54-68 mutS homolog 2 Homo sapiens 156-194 25996601-2 2015 We have previously shown in vitro that recognition of 5-fluorouracil (5-FU) within DNA and subsequent cytotoxicity was most effective when both hMutSalpha (hMSH2-hMSH6 heterodimer) and hMutSbeta (hMSH2-hMSH3 heterodimer) MMR complexes were present, compared to hMutSalpha > hMutSbeta alone. Fluorouracil 54-68 mutS homolog 2 Homo sapiens 156-161 25996601-2 2015 We have previously shown in vitro that recognition of 5-fluorouracil (5-FU) within DNA and subsequent cytotoxicity was most effective when both hMutSalpha (hMSH2-hMSH6 heterodimer) and hMutSbeta (hMSH2-hMSH3 heterodimer) MMR complexes were present, compared to hMutSalpha > hMutSbeta alone. Fluorouracil 54-68 mutS homolog 3 Homo sapiens 202-207 25996601-2 2015 We have previously shown in vitro that recognition of 5-fluorouracil (5-FU) within DNA and subsequent cytotoxicity was most effective when both hMutSalpha (hMSH2-hMSH6 heterodimer) and hMutSbeta (hMSH2-hMSH3 heterodimer) MMR complexes were present, compared to hMutSalpha > hMutSbeta alone. Fluorouracil 70-74 mutS homolog 2 Homo sapiens 156-194 25996601-2 2015 We have previously shown in vitro that recognition of 5-fluorouracil (5-FU) within DNA and subsequent cytotoxicity was most effective when both hMutSalpha (hMSH2-hMSH6 heterodimer) and hMutSbeta (hMSH2-hMSH3 heterodimer) MMR complexes were present, compared to hMutSalpha > hMutSbeta alone. Fluorouracil 70-74 mutS homolog 2 Homo sapiens 156-161 25996601-2 2015 We have previously shown in vitro that recognition of 5-fluorouracil (5-FU) within DNA and subsequent cytotoxicity was most effective when both hMutSalpha (hMSH2-hMSH6 heterodimer) and hMutSbeta (hMSH2-hMSH3 heterodimer) MMR complexes were present, compared to hMutSalpha > hMutSbeta alone. Fluorouracil 70-74 mutS homolog 3 Homo sapiens 202-207 25996601-12 2015 The loss of contribution of hMSH3 for 5-FU cytotoxicity may not adversely affect patient outcome, contrasting patients whose tumors completely lack DNA MMR function (MSI-H). Fluorouracil 38-42 mutS homolog 3 Homo sapiens 28-33 25659689-0 2015 Aptamer decorated hyaluronan/chitosan nanoparticles for targeted delivery of 5-fluorouracil to MUC1 overexpressing adenocarcinomas. Fluorouracil 77-91 mucin 1, cell surface associated Homo sapiens 95-99 25659689-1 2015 An aptamer (Apt) conjugated hyaluronan/chitosan nanoparticles (HACSNPs) were prepared as carrier for targeted delivery of 5-fluorouracil (5FU) to mucin1 (MUC1) overexpressing colorectal adenocarcinomas. Fluorouracil 122-136 mucin 1, cell surface associated Homo sapiens 146-152 25659689-1 2015 An aptamer (Apt) conjugated hyaluronan/chitosan nanoparticles (HACSNPs) were prepared as carrier for targeted delivery of 5-fluorouracil (5FU) to mucin1 (MUC1) overexpressing colorectal adenocarcinomas. Fluorouracil 122-136 mucin 1, cell surface associated Homo sapiens 154-158 25681512-0 2015 Smad4 inactivation predicts for worse prognosis and response to fluorouracil-based treatment in colorectal cancer. Fluorouracil 64-76 SMAD family member 4 Homo sapiens 0-5 25585539-5 2015 Combining miR-34a transfection with 5-fluorouracil (5-FU) treatment further enhanced the inhibition in SW480 cell migration and invasion (both, p<0.05) compared to 5-FU treatment alone. Fluorouracil 52-56 microRNA 34a Homo sapiens 10-17 25906152-6 2015 5-FU treatment led to the formation of a z-VAD-resistant pro-caspase-8/RIP1/FADD complex, which was strongly stabilized by caspase-3 KO. Fluorouracil 0-4 caspase 8 Homo sapiens 61-70 25238407-0 2015 Ubiquitin D is an independent prognostic marker for survival in stage IIB-IIC colon cancer patients treated with 5-fluoruracil-based adjuvant chemotherapy. Fluorouracil 113-126 ubiquitin D Homo sapiens 0-11 25238407-3 2015 We previously showed that ubiquitin D (UBD) can predict the prognosis of colon cancer; however, there are limited data on whether UBD is an independent prognostic factor for stage II patients treated with 5-FU-based adjuvant chemotherapy. Fluorouracil 205-209 ubiquitin D Homo sapiens 130-133 25238407-10 2015 CONCLUSION: UBD may help to identify recurrent risk in stage IIB-IIC colon cancer patients and further predict which patients benefit from postoperative 5-FU-based adjuvant chemotherapy. Fluorouracil 153-157 ubiquitin D Homo sapiens 12-15 25861418-10 2015 Compared to mice treated with 5-FU, mice treated with AHCC plus 5-FU had higher thymus index, percentages of CD3(+), CD4(+), and NK cells (P < 0.01), and ratio of CD4(+)/CD8(+) (P < 0.01) in peripheral blood. Fluorouracil 64-68 CD3 antigen, epsilon polypeptide Mus musculus 109-112 25782664-4 2015 Overexpressed DHX32 promoted SW480 cancer cells proliferation, migration, and invasion, as well as decreased the susceptibility to chemotherapy agent 5-Fluorouracil. Fluorouracil 150-164 DEAH-box helicase 32 (putative) Homo sapiens 14-19 25169655-0 2015 Elevation in 5-FU-induced apoptosis in head and neck cancer stem cells by a combination of CDHP and GSK3beta inhibitors. Fluorouracil 13-17 glycogen synthase kinase 3 beta Homo sapiens 100-108 25169655-11 2015 Combination of both CDHP and GSK3beta inhibitors markedly enhanced 5-FU-induced apoptosis of CD44(high) /ESA(low) cells. Fluorouracil 67-71 glycogen synthase kinase 3 beta Homo sapiens 29-37 25572969-6 2015 In addition, we found that ABCC4 knockdown in 5-fluorouracil (5-FU)-resistant cancer cells restored 5-FU sensitivity, resulting in the inhibition of cell proliferation and tumour growth in nude mice. Fluorouracil 46-60 ATP-binding cassette, sub-family C (CFTR/MRP), member 4 Mus musculus 27-32 25572969-6 2015 In addition, we found that ABCC4 knockdown in 5-fluorouracil (5-FU)-resistant cancer cells restored 5-FU sensitivity, resulting in the inhibition of cell proliferation and tumour growth in nude mice. Fluorouracil 62-66 ATP-binding cassette, sub-family C (CFTR/MRP), member 4 Mus musculus 27-32 25572969-6 2015 In addition, we found that ABCC4 knockdown in 5-fluorouracil (5-FU)-resistant cancer cells restored 5-FU sensitivity, resulting in the inhibition of cell proliferation and tumour growth in nude mice. Fluorouracil 100-104 ATP-binding cassette, sub-family C (CFTR/MRP), member 4 Mus musculus 27-32 25901207-0 2015 SOD2 rs4880 CT/CC genotype predicts poor survival for Chinese gastric cancer patients received platinum and fluorouracil based adjuvant chemotherapy. Fluorouracil 108-120 superoxide dismutase 2 Homo sapiens 0-4 25678847-6 2015 B lymphoma Mo-MLV insertion region 1 (BMI1), a putative CSC protein, was analyzed by immunohistochemical staining and subjected to pairwise comparison in GC tissues treated with or without neoadjuvant 5Fu-based chemotherapy. Fluorouracil 201-204 BMI1 proto-oncogene, polycomb ring finger Homo sapiens 38-42 25678847-7 2015 The correlation between BMI1 expression and recurrence-free survival in GC patients who received 5Fu-based neoadjuvant chemotherapy was then examined. Fluorouracil 97-100 BMI1 proto-oncogene, polycomb ring finger Homo sapiens 24-28 25678847-12 2015 The BMI1 protein was highly expressed consistently in the remaining GC tissues after 5Fu-based neoadjuvant chemotherapy, and BMI1 levels were correlated positively with recurrence-free survival in GC patients who received 5Fu-based neoadjuvant chemotherapy. Fluorouracil 85-88 BMI1 proto-oncogene, polycomb ring finger Homo sapiens 4-8 25678847-12 2015 The BMI1 protein was highly expressed consistently in the remaining GC tissues after 5Fu-based neoadjuvant chemotherapy, and BMI1 levels were correlated positively with recurrence-free survival in GC patients who received 5Fu-based neoadjuvant chemotherapy. Fluorouracil 222-225 BMI1 proto-oncogene, polycomb ring finger Homo sapiens 4-8 25678847-12 2015 The BMI1 protein was highly expressed consistently in the remaining GC tissues after 5Fu-based neoadjuvant chemotherapy, and BMI1 levels were correlated positively with recurrence-free survival in GC patients who received 5Fu-based neoadjuvant chemotherapy. Fluorouracil 222-225 BMI1 proto-oncogene, polycomb ring finger Homo sapiens 125-129 25511698-5 2015 Moreover, lack of MUC1 in these cells profoundly altered their sensitivity to gemcitabine and 5-Fluorouracil chemotherapeutic drugs. Fluorouracil 94-108 mucin 1, transmembrane Mus musculus 18-22 26037388-3 2015 CCK-8 assay indicated that microRNA-210 upregulation by microRNA-210 mimics reduced the chemotherapeutic 5-FU-induced osteoblast cell death, and colony formation assay demonstrated that microRNA-210 mimics promoted osteoblast cells growth. Fluorouracil 105-109 microRNA 210 Homo sapiens 27-39 26037388-3 2015 CCK-8 assay indicated that microRNA-210 upregulation by microRNA-210 mimics reduced the chemotherapeutic 5-FU-induced osteoblast cell death, and colony formation assay demonstrated that microRNA-210 mimics promoted osteoblast cells growth. Fluorouracil 105-109 microRNA 210 Homo sapiens 56-68 26037388-3 2015 CCK-8 assay indicated that microRNA-210 upregulation by microRNA-210 mimics reduced the chemotherapeutic 5-FU-induced osteoblast cell death, and colony formation assay demonstrated that microRNA-210 mimics promoted osteoblast cells growth. Fluorouracil 105-109 microRNA 210 Homo sapiens 56-68 24512327-9 2015 The results demonstrated that 5-FU treatment significantly inhibited G-CSF, GM-CSF, and M-CSF expression in all three sites at all timepoints from 6-72 h post 5-FU. Fluorouracil 30-34 peripheral blood stem cell response to granulocyte colony stimulating factor 1 Mus musculus 69-74 25034007-13 2015 Our findings showed that the cytotoxic action of 5-FU and capecitabine on cardiomyocytes are mediated by oxidative stress and subsequent mitochondrial dysfunction which causes caspase-3 activation and cell death. Fluorouracil 49-53 caspase 3 Rattus norvegicus 176-185 25877313-1 2015 OBJECTIVE: To explore the changes of anticancer efficiency of 5"-deoxy-5-fluorouridine (5"-DFUR) and 5-fluorouracil (5-Fu) in colorectal cancer cell line HT29 and LS174T cells after transfection of thymidine phosphorylase (TP) cDNA with a lentiviral vector. Fluorouracil 117-121 thymidine phosphorylase Homo sapiens 198-221 25877313-1 2015 OBJECTIVE: To explore the changes of anticancer efficiency of 5"-deoxy-5-fluorouridine (5"-DFUR) and 5-fluorouracil (5-Fu) in colorectal cancer cell line HT29 and LS174T cells after transfection of thymidine phosphorylase (TP) cDNA with a lentiviral vector. Fluorouracil 117-121 thymidine phosphorylase Homo sapiens 223-225 25877313-5 2015 Finally, the concentration of converted 5-Fu was detected by high performance liquid chromatography (HPLC) either in the medium containing a series of concentrations of 5"-DFUR, in which HT29/HT29-TP or LS174T/LS174T-TP cells were cultured, or in the cell culture lysates. Fluorouracil 40-44 thymidine phosphorylase Homo sapiens 197-199 25877313-5 2015 Finally, the concentration of converted 5-Fu was detected by high performance liquid chromatography (HPLC) either in the medium containing a series of concentrations of 5"-DFUR, in which HT29/HT29-TP or LS174T/LS174T-TP cells were cultured, or in the cell culture lysates. Fluorouracil 40-44 thymidine phosphorylase Homo sapiens 217-219 25877313-11 2015 The IC50 values of 5-Fu of HT29-TP cells and its parents cells were (5.42 +- 0.75) micromol/L and (14.19 +- 0.97) micromol/L, respectively (P < 0.05), while (4.41 +- 0.96)micromol/L in LS174T-TP cells and (16.42 +- 2.12)micromol/L in its parents cells, respectively (P < 0.05). Fluorouracil 19-23 thymidine phosphorylase Homo sapiens 32-34 25877313-11 2015 The IC50 values of 5-Fu of HT29-TP cells and its parents cells were (5.42 +- 0.75) micromol/L and (14.19 +- 0.97) micromol/L, respectively (P < 0.05), while (4.41 +- 0.96)micromol/L in LS174T-TP cells and (16.42 +- 2.12)micromol/L in its parents cells, respectively (P < 0.05). Fluorouracil 19-23 thymidine phosphorylase Homo sapiens 195-197 25877313-12 2015 The HPLC results showed that the 5-Fu concentration detected from media contained a series of concentrations of 5"-DFUR for culturing HT29-TP and LS174T-TP cells were 12.2 to 28.7-folds and 13.1 to 23.6-folds, respectively, higher than that in their parents cells, (P < 0.01 for all). Fluorouracil 33-37 thymidine phosphorylase Homo sapiens 139-141 25877313-12 2015 The HPLC results showed that the 5-Fu concentration detected from media contained a series of concentrations of 5"-DFUR for culturing HT29-TP and LS174T-TP cells were 12.2 to 28.7-folds and 13.1 to 23.6-folds, respectively, higher than that in their parents cells, (P < 0.01 for all). Fluorouracil 33-37 thymidine phosphorylase Homo sapiens 153-155 25877313-13 2015 Otherwise, just a little of 5-Fu was detected in the two TP-transfected cells lysate, about 0.9% to 4.2% of 5-Fu detected in the media of the same cultured cells, whereas no 5-Fu was detected in the two parent cell lysates. Fluorouracil 28-32 thymidine phosphorylase Homo sapiens 57-59 25877313-14 2015 CONCLUSIONS: Transfection of TP cDNA into colorectal cancer cell lines HT29 and LS174T with lentiviral vector can improve the expression of both TP mRNA and TP protein levels in passaged cells, enhance the conversion of 5-Fu from 5"-DFUR in the medium, and result in an enhanced anticancer effect on these two cell lines. Fluorouracil 220-224 thymidine phosphorylase Homo sapiens 29-31 25877313-14 2015 CONCLUSIONS: Transfection of TP cDNA into colorectal cancer cell lines HT29 and LS174T with lentiviral vector can improve the expression of both TP mRNA and TP protein levels in passaged cells, enhance the conversion of 5-Fu from 5"-DFUR in the medium, and result in an enhanced anticancer effect on these two cell lines. Fluorouracil 220-224 thymidine phosphorylase Homo sapiens 145-147 25877313-14 2015 CONCLUSIONS: Transfection of TP cDNA into colorectal cancer cell lines HT29 and LS174T with lentiviral vector can improve the expression of both TP mRNA and TP protein levels in passaged cells, enhance the conversion of 5-Fu from 5"-DFUR in the medium, and result in an enhanced anticancer effect on these two cell lines. Fluorouracil 220-224 thymidine phosphorylase Homo sapiens 145-147 25378405-7 2014 Sesn2 deletion or knockdown sensitizes squamous cell carcinoma (SCC) cells to 5-fluorouracil-induced apoptosis and melanoma cells to UVB- and vemurafenib-induced apoptosis. Fluorouracil 78-92 sestrin 2 Homo sapiens 0-5 25537222-0 2014 The influence of 5-fluorouracil on activity of thymidine phosphorylase in gastric adenocarcinoma and normal adjacent tissue. Fluorouracil 17-31 thymidine phosphorylase Homo sapiens 47-70 25537222-1 2014 UNLABELLED: The aim of the present study was to evaluate the change of thymidine phosphorylase (TP) activity in gastric adenocarcinoma and adjacent tissue upon the intraarterial administration of 5-fluorouracil (5-FU). Fluorouracil 196-210 thymidine phosphorylase Homo sapiens 71-94 25537222-1 2014 UNLABELLED: The aim of the present study was to evaluate the change of thymidine phosphorylase (TP) activity in gastric adenocarcinoma and adjacent tissue upon the intraarterial administration of 5-fluorouracil (5-FU). Fluorouracil 196-210 thymidine phosphorylase Homo sapiens 96-98 25537222-1 2014 UNLABELLED: The aim of the present study was to evaluate the change of thymidine phosphorylase (TP) activity in gastric adenocarcinoma and adjacent tissue upon the intraarterial administration of 5-fluorouracil (5-FU). Fluorouracil 212-216 thymidine phosphorylase Homo sapiens 71-94 25537222-1 2014 UNLABELLED: The aim of the present study was to evaluate the change of thymidine phosphorylase (TP) activity in gastric adenocarcinoma and adjacent tissue upon the intraarterial administration of 5-fluorouracil (5-FU). Fluorouracil 212-216 thymidine phosphorylase Homo sapiens 96-98 25537222-6 2014 The activity of TP was decreased with the course of the time after 5-FU administration in tumor and normal adjacent tissue. Fluorouracil 67-71 thymidine phosphorylase Homo sapiens 16-18 25537222-7 2014 There were statistically significant differences in the TP activity in both tissues between 2-20 min and 40-60 min after 5-FU injection (p < 0.05). Fluorouracil 121-125 thymidine phosphorylase Homo sapiens 56-58 25537222-8 2014 CONCLUSION: 5-FU administration results in the decrease of TP activity in tumor and normal adjacent tissues that might have importance for chemotherapy with fluoropyrimidines. Fluorouracil 12-16 thymidine phosphorylase Homo sapiens 59-61 25052233-0 2014 Human uridine phosphorylase-1 inhibitors: a new approach to ameliorate 5-fluorouracil-induced intestinal mucositis. Fluorouracil 71-85 uridine phosphorylase 1 Homo sapiens 6-29 25052233-9 2014 CONCLUSION: Our results bring support to the hUP1 inhibitor strategy as a novel possibility of prevention and treatment of mucositis during the 5-FU chemotherapy, based on the approach of uridine accumulation in plasma and tissues. Fluorouracil 144-148 heterogeneous nuclear ribonucleoprotein A1 Homo sapiens 45-49 25364408-3 2014 The 5-FU metabolizing enzymes studied were thymidylate synthase, dihydropyrimidine dehydrogenase and thymidine phosphorylase (TP). Fluorouracil 4-8 thymidine phosphorylase Homo sapiens 101-124 25364408-3 2014 The 5-FU metabolizing enzymes studied were thymidylate synthase, dihydropyrimidine dehydrogenase and thymidine phosphorylase (TP). Fluorouracil 4-8 thymidine phosphorylase Homo sapiens 126-128 25364408-10 2014 These results indicate that the mRNA expression of TP, a metabolizing enzyme of 5-FU, is a significant predictor of response to post-operative chemotherapy with S-1 in patients with stage III colorectal cancer. Fluorouracil 80-84 thymidine phosphorylase Homo sapiens 51-53 24351824-5 2013 The present study showed that Cbl-b knockdown caused higher proliferation concomitant with the decrease of apoptosis induced by 5-FU treatment in gastric cancer cell. Fluorouracil 128-132 Cbl proto-oncogene B Homo sapiens 30-35 24351824-7 2013 These results suggest that Cbl-b enhances sensitivity to 5-FU via EGFR- and mitochondria-mediated pathways in gastric cancer cells. Fluorouracil 57-61 Cbl proto-oncogene B Homo sapiens 27-32 23941814-9 2013 Simvastatin alone or plus 5-FU significantly suppressed E2F-1 and TS expressions in EGI-1 and MZ-ChA-1. Fluorouracil 26-30 E2F transcription factor 1 Homo sapiens 56-61 23941814-9 2013 Simvastatin alone or plus 5-FU significantly suppressed E2F-1 and TS expressions in EGI-1 and MZ-ChA-1. Fluorouracil 26-30 thymidylate synthetase Homo sapiens 66-68 24047797-8 2013 MPO activity was significantly increased in jejunum (days 8 and 9) and ileum (day 8) following 5-FU injection, compared to normal controls (P < 0.05). Fluorouracil 95-99 myeloperoxidase Rattus norvegicus 0-3 23968134-0 2013 Thymidylate synthase gene polymorphism and survival of colorectal cancer patients receiving adjuvant 5-fluorouracil. Fluorouracil 101-115 thymidylate synthetase Homo sapiens 0-20 23968134-1 2013 Limited studies indicate a possible association of 5"-UTR thymidylate synthase enhancer region polymorphism and treatment outcome in patients medicated with 5-fluorouracil (5-FU). Fluorouracil 157-171 thymidylate synthetase Homo sapiens 58-78 23968134-1 2013 Limited studies indicate a possible association of 5"-UTR thymidylate synthase enhancer region polymorphism and treatment outcome in patients medicated with 5-fluorouracil (5-FU). Fluorouracil 173-177 thymidylate synthetase Homo sapiens 58-78 23846337-9 2013 Interestingly, it was found that GKN1 exerted a synergistic anti-cancerous effect with 5-fluorouracil on tumor cell growth, which suggests a possible therapeutic intervention method for gastric cancer. Fluorouracil 87-101 gastrokine 1 Homo sapiens 33-37 23941782-10 2013 Cd plus 5-FU decreased cyclin D1 and increased cyclin A1 expression. Fluorouracil 8-12 cyclin A1 Homo sapiens 47-56 23681919-9 2013 In response to 5-fluorouracil treatment, elevated numbers of dividing Lin(-) Sca(+) cells were found in the Kit(V558Delta;T669I/+) BM compared to wild type. Fluorouracil 15-29 KIT proto-oncogene receptor tyrosine kinase Mus musculus 108-111 25321193-5 2014 Patients with high preoperative Sdc-1 serum levels were less responsive to 5-Fluorouracil, Oxaliplatin, Irintecan, Cisplatin or Paclitaxel chemotherapy. Fluorouracil 75-89 syndecan 1 Homo sapiens 32-37 23564482-4 2013 By enhancing expression of SGO1, sensitivity of SGC7901 cells to vincristine (VCR), adriamycin, 5-fluorouracil (5-FU), and cisplatin (CDDP) was significantly diminished. Fluorouracil 96-110 shugoshin 1 Homo sapiens 27-31 23564482-4 2013 By enhancing expression of SGO1, sensitivity of SGC7901 cells to vincristine (VCR), adriamycin, 5-fluorouracil (5-FU), and cisplatin (CDDP) was significantly diminished. Fluorouracil 112-116 shugoshin 1 Homo sapiens 27-31 23894404-8 2013 CONCLUSION: The XPD and XRCC1 allelic variants may be prognostic markers for CRC patients receiving 5-FU based chemotherapy. Fluorouracil 100-104 ERCC excision repair 2, TFIIH core complex helicase subunit Homo sapiens 16-19 23729362-8 2013 Cell death of 5-fluorouracil (5FU)-treated p53-null GSK3B-silenced colon carcinoma cells occurred via PARP1-dependent and AIF-mediated but RIP1-independent necroptosis. Fluorouracil 14-28 receptor interacting serine/threonine kinase 1 Homo sapiens 139-143 23861589-1 2013 PURPOSE: To determine whether 5-fluorouracil (5-FU) sensitivity is associated with the mRNA expressions of thymidylate synthase (TS), dihydropyrimidine dehydrogenase (DPD), and thymidine phosphorylase (TP) in patients with hepatocellular carcinoma (HCC) treated with 5-FU-based transarterial chemoembolization (TACE). Fluorouracil 46-50 thymidylate synthetase Homo sapiens 107-127 23861589-1 2013 PURPOSE: To determine whether 5-fluorouracil (5-FU) sensitivity is associated with the mRNA expressions of thymidylate synthase (TS), dihydropyrimidine dehydrogenase (DPD), and thymidine phosphorylase (TP) in patients with hepatocellular carcinoma (HCC) treated with 5-FU-based transarterial chemoembolization (TACE). Fluorouracil 46-50 thymidylate synthetase Homo sapiens 129-131 23645036-1 2013 Thymidylate synthetase is the major target of 5-fluorouracil (5-FU), which is widely used for the treatment of gastric cancer (GC) and colorectal cancer (CRC). Fluorouracil 46-60 thymidylate synthetase Homo sapiens 0-22 25368235-7 2014 Gemcitabine, 5-FU and IFN-gamma induced up-regulation of mucin-1. Fluorouracil 13-17 mucin 1, cell surface associated Homo sapiens 57-64 23645036-1 2013 Thymidylate synthetase is the major target of 5-fluorouracil (5-FU), which is widely used for the treatment of gastric cancer (GC) and colorectal cancer (CRC). Fluorouracil 62-66 thymidylate synthetase Homo sapiens 0-22 23749896-0 2013 Unexpected alteration of beta-catenin and c-KIT expression by 5-FU and docetaxel in p16-positive squamous cell carcinoma compared to HPV-negative HNSCC cells in vitro. Fluorouracil 62-66 catenin beta 1 Homo sapiens 25-37 23749896-8 2013 At best, 5-FU had a slight influence on the alteration of the expression of beta-catenin. Fluorouracil 9-13 catenin beta 1 Homo sapiens 76-88 23749899-8 2013 Under treatment with low concentrations of 5-fluorouracil and cisplatin, all examined cell lines showed an increasing secretion of the cytokines IL-6 and G-CSF. Fluorouracil 43-57 colony stimulating factor 3 Homo sapiens 154-159 23749899-10 2013 Regarding GM-CSF and TNF-alpha, we demonstrated an increase in secretion by the primary tumors under low doses of 5-fluorouracil and cisplatin, whereas the metastases showed a sharp drop of GM-CSF and TNF-alpha secretion. Fluorouracil 114-128 colony stimulating factor 2 Homo sapiens 10-16 23438367-3 2013 Thymidylate synthase (TS) is a direct target of 5-FU, and the low TS level has been generally supposed to sensitize 5-FU"s efficacy. Fluorouracil 48-52 thymidylate synthetase Homo sapiens 0-20 23438367-3 2013 Thymidylate synthase (TS) is a direct target of 5-FU, and the low TS level has been generally supposed to sensitize 5-FU"s efficacy. Fluorouracil 48-52 thymidylate synthetase Homo sapiens 22-24 23438367-3 2013 Thymidylate synthase (TS) is a direct target of 5-FU, and the low TS level has been generally supposed to sensitize 5-FU"s efficacy. Fluorouracil 116-120 thymidylate synthetase Homo sapiens 0-20 23438367-3 2013 Thymidylate synthase (TS) is a direct target of 5-FU, and the low TS level has been generally supposed to sensitize 5-FU"s efficacy. Fluorouracil 116-120 thymidylate synthetase Homo sapiens 22-24 24649191-0 2013 Predictive value of orotate phosphoribosyltransferase in colorectal cancer patients receiving 5-FU-based chemotherapy. Fluorouracil 94-98 uridine monophosphate synthetase Homo sapiens 20-53 25070488-7 2014 Furthermore, we find that SIRT5 knockdown makes lung cancer cells more sensitive to drug (cis-diamminedichloroplatinum [CDDP], 5-fluorouracil [5-FU] or bleomycin) treatment in vitro and in vivo. Fluorouracil 127-141 sirtuin 5 Homo sapiens 26-31 25070488-7 2014 Furthermore, we find that SIRT5 knockdown makes lung cancer cells more sensitive to drug (cis-diamminedichloroplatinum [CDDP], 5-fluorouracil [5-FU] or bleomycin) treatment in vitro and in vivo. Fluorouracil 143-147 sirtuin 5 Homo sapiens 26-31 24649191-3 2013 Surgically obtained specimens from 106 patients treated for CRC were immunohistochemically assessed to investigate the correlation between the protein expression of the 5-FU metabolic enzymes orotate phosphoribosyltransferase (OPRT), thymidylate synthase (TS) and dihydropyrimidine dehydrogenase (DPD), and clinicopathological characteristics as well as the correlation between the protein expression and outcomes of 5-FU-based chemotherapy. Fluorouracil 169-173 uridine monophosphate synthetase Homo sapiens 192-225 24649191-4 2013 A correlation was detected between the high expression of the 5-FU metabolic enzyme OPRT and negative lymph node metastasis (P=0.0496), as well as between DPD and advanced Tumor-Node-Metastasis (TNM) grade cases (IIIA-IVB) and positive lymph node metastases (P=0.0414, respectively). Fluorouracil 62-66 uridine monophosphate synthetase Homo sapiens 84-88 24649191-5 2013 In all 106 patients and in 79 patients undergoing 5-FU-based chemotherapy, survival was improved in those patients with a positive OPRT expression (P=0.0144 and 0.0167, respectively). Fluorouracil 50-54 uridine monophosphate synthetase Homo sapiens 131-135 24649191-6 2013 OPRT expression was higher in the 79 patients with no recurrence (P=0.0179) as well as in patients treated with R0 surgery and 5-FU-based chemotherapy without side-effects (P=0.0126). Fluorouracil 127-131 uridine monophosphate synthetase Homo sapiens 0-4 23554123-6 2013 siRNA-mediated silencing of CD147 gene expression restored the sensitivity of CSC-like cells to 5-fluorouracil (5-FU), along with decreasing the expression of thymidylate synthase, p-AKT, and beta-catenin, while increasing the expression of p-glycogen synthase kinase (GSK)3beta. Fluorouracil 96-110 basigin (Ok blood group) Homo sapiens 28-33 25688504-0 2014 Extracellular chaperonin 10 augments apoptotic cell death induced by 5-fluorouracil in human colon cancer cells. Fluorouracil 69-83 heat shock protein family E (Hsp10) member 1 Homo sapiens 14-27 25688504-5 2014 RESULTS: Chaperonin 10 (cpn10) was secreted at a lower level by 5-FU-resistant cells compared to the non-resistant parent cell line. Fluorouracil 64-68 heat shock protein family E (Hsp10) member 1 Homo sapiens 9-22 25688504-5 2014 RESULTS: Chaperonin 10 (cpn10) was secreted at a lower level by 5-FU-resistant cells compared to the non-resistant parent cell line. Fluorouracil 64-68 heat shock protein family E (Hsp10) member 1 Homo sapiens 24-29 25688504-6 2014 The proliferation of both the parent and 5-FU-resistant cell lines increased slightly when extracellular cpn10 alone was added. Fluorouracil 41-45 heat shock protein family E (Hsp10) member 1 Homo sapiens 105-110 25688504-7 2014 However, in the presence of 5-FU, cpn10 augmented 5-FU-induced apoptotic death in both cell lines. Fluorouracil 28-32 heat shock protein family E (Hsp10) member 1 Homo sapiens 34-39 25688504-7 2014 However, in the presence of 5-FU, cpn10 augmented 5-FU-induced apoptotic death in both cell lines. Fluorouracil 50-54 heat shock protein family E (Hsp10) member 1 Homo sapiens 34-39 25688504-9 2014 CONCLUSIONS: Our findings indicate that concurrent treatment with cpn10 and 5-FU warrants further investigation in an effort to overcome 5-FU resistance and enhance the efficacy of 5-FU therapy for colon cancer. Fluorouracil 137-141 heat shock protein family E (Hsp10) member 1 Homo sapiens 66-71 25688504-9 2014 CONCLUSIONS: Our findings indicate that concurrent treatment with cpn10 and 5-FU warrants further investigation in an effort to overcome 5-FU resistance and enhance the efficacy of 5-FU therapy for colon cancer. Fluorouracil 137-141 heat shock protein family E (Hsp10) member 1 Homo sapiens 66-71 25233213-0 2014 tRNA modifying enzymes, NSUN2 and METTL1, determine sensitivity to 5-fluorouracil in HeLa cells. Fluorouracil 67-81 methyltransferase 1, tRNA methylguanosine Homo sapiens 34-40 25233213-4 2014 Here, we show that combined knockdown of NSUN2 and METTL1 in HeLa cells drastically potentiate sensitivity of cells to 5-fluorouracil (5-FU) whereas heat stress of cells revealed no effects. Fluorouracil 119-133 methyltransferase 1, tRNA methylguanosine Homo sapiens 51-57 25233213-4 2014 Here, we show that combined knockdown of NSUN2 and METTL1 in HeLa cells drastically potentiate sensitivity of cells to 5-fluorouracil (5-FU) whereas heat stress of cells revealed no effects. Fluorouracil 135-139 methyltransferase 1, tRNA methylguanosine Homo sapiens 51-57 25202075-0 2014 Matrix metalloproteinase-2 and -14 in p16-positive and -negative HNSCC after exposure To 5-FU and docetaxel In Vitro. Fluorouracil 89-93 matrix metallopeptidase 2 Homo sapiens 0-34 24972040-10 2014 Under the present conditions, the expression levels of CXCL1, CXCL2, CXCL3, the neutrophil markers Elane and MPO, as well as Ly-6G-positive neutrophils, in the colon were significantly increased by 5-FU. Fluorouracil 198-202 lymphocyte antigen 6 complex, locus G Mus musculus 125-130 24962565-8 2014 Compared with forced expression of wild type TDG, CRL4(Cdt2)- resistant TDG (DeltaPIP) slows cell proliferation and slightly increases the toxicity of 5-FU. Fluorouracil 151-155 denticleless E3 ubiquitin protein ligase homolog Homo sapiens 55-59 24800927-0 2014 Activation of p38-MAPK by CXCL4/CXCR3 axis contributes to p53-dependent intestinal apoptosis initiated by 5-fluorouracil. Fluorouracil 106-120 mitogen-activated protein kinase 14 Mus musculus 14-17 23554123-6 2013 siRNA-mediated silencing of CD147 gene expression restored the sensitivity of CSC-like cells to 5-fluorouracil (5-FU), along with decreasing the expression of thymidylate synthase, p-AKT, and beta-catenin, while increasing the expression of p-glycogen synthase kinase (GSK)3beta. Fluorouracil 112-116 basigin (Ok blood group) Homo sapiens 28-33 24250621-0 2013 5-Fluorouracil Induce the Expression of TLR4 on HCT116 Colorectal Cancer Cell Line Expressing Different Variants of TLR4. Fluorouracil 0-14 toll like receptor 4 Homo sapiens 40-44 24250621-0 2013 5-Fluorouracil Induce the Expression of TLR4 on HCT116 Colorectal Cancer Cell Line Expressing Different Variants of TLR4. Fluorouracil 0-14 toll like receptor 4 Homo sapiens 116-120 24250621-3 2013 The present study examined the impact of two common polymorphisms of the TLR4 genes on the response of the HCT116 colorectal cancer cells to 5-FU. Fluorouracil 141-145 toll like receptor 4 Homo sapiens 73-77 24250621-6 2013 FACS analysis was performed to show the effect of 5-FU and LPS on the expression of different variants of TLR4. Fluorouracil 50-54 toll like receptor 4 Homo sapiens 106-110 24250621-8 2013 5-FU significantly induced the expression of TLR4 protein in the presence and absence of LPS. Fluorouracil 0-4 toll like receptor 4 Homo sapiens 45-49 24250621-9 2013 5-FU also induced HMGB1 secretion, Cas3 and PARP activity and these effects were stronger in cells expressing WT TLR4 than the other cells. Fluorouracil 0-4 embryonal Fyn-associated substrate Homo sapiens 35-39 24250621-9 2013 5-FU also induced HMGB1 secretion, Cas3 and PARP activity and these effects were stronger in cells expressing WT TLR4 than the other cells. Fluorouracil 0-4 toll like receptor 4 Homo sapiens 113-117 24250621-10 2013 In conclusion, 5-FU-induced TLR4 expression and LPS had synergistic effect with 5-FU to induced apoptosis in colorectal cancer cells. Fluorouracil 15-19 toll like receptor 4 Homo sapiens 28-32 23232983-10 2013 After 5-FU treatment, PRODH mRNA expression was upregulated 2-fold and production of superoxide was increased by a factor of 3. Fluorouracil 6-10 proline dehydrogenase 1 Homo sapiens 22-27 23432846-6 2013 Compared to normal gastric mucosa tissues, hTERT mRNA expression was significantly increased in GC (P<0.05), which was related with a worse differentiation and drug-resistance to 5-fluorouracil or adriamycin in GC. Fluorouracil 182-196 telomerase reverse transcriptase Homo sapiens 43-48 24755241-9 2014 Knockdown of TRAF6 sensitizes the cells to treatment of the conventional anti-cancer drugs 5-fluorouracil and etoposide. Fluorouracil 91-105 LOC222344 Homo sapiens 13-18 25013487-2 2014 Involvement of protein kinase C (PKC) was assessed by evaluating the extent of their activation in CRC, following treatment with 5-FU, using biochemical inhibitors and western blot analysis. Fluorouracil 129-133 protein kinase C delta Homo sapiens 33-36 25013487-6 2014 The treatment of HCT116 cells with 5-FU increased the expression, phosphorylation and cleavage of PKCdelta. Fluorouracil 35-39 protein kinase C delta Homo sapiens 98-106 25013487-7 2014 The inhibition of PKCdelta was found to significantly inhibit 5-FU-induced apoptosis. Fluorouracil 62-66 protein kinase C delta Homo sapiens 18-26 23108452-11 2013 The activities of AST and LDH were prone to be increased by more than 300 muM of CCl(4,) but not affected by all doses of 5-FU except for 800 nM of 5-FU in AST activities. Fluorouracil 148-152 solute carrier family 17 (anion/sugar transporter), member 5 Mus musculus 156-159 25013487-8 2014 These results indicated that 5-FU induces apoptosis in CRC by the activation of PKCdelta and caspase-9. Fluorouracil 29-33 protein kinase C delta Homo sapiens 80-88 25013487-9 2014 In addition, the levels of PKCdelta activation may determine the sensitivity of CRC to 5-FU. Fluorouracil 87-91 protein kinase C delta Homo sapiens 27-35 23010741-0 2013 Enhanced RegIV expression predicts the intrinsic 5-fluorouracil (5-FU) resistance in advanced gastric cancer. Fluorouracil 49-63 regenerating family member 4 Homo sapiens 9-14 25046749-6 2014 Further, our results showed that co-treatment with a low concentration cordycepin could remarkably enhance the chemosensitivity of GBC-SD cells to gemcitabine and 5-fluorouracil (5-FU), and the mechanism may be attributed to AMPK activation and MDR degradation. Fluorouracil 163-177 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 225-229 25046749-6 2014 Further, our results showed that co-treatment with a low concentration cordycepin could remarkably enhance the chemosensitivity of GBC-SD cells to gemcitabine and 5-fluorouracil (5-FU), and the mechanism may be attributed to AMPK activation and MDR degradation. Fluorouracil 179-183 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 225-229 23010741-0 2013 Enhanced RegIV expression predicts the intrinsic 5-fluorouracil (5-FU) resistance in advanced gastric cancer. Fluorouracil 65-69 regenerating family member 4 Homo sapiens 9-14 24833352-5 2014 Here we demonstrate that SPARC-deficient mice display higher resistance to serial treatment with the chemotherapeutic agent 5-fluorouracil (5-FU). Fluorouracil 124-138 secreted acidic cysteine rich glycoprotein Mus musculus 25-30 23010741-1 2013 AIM: RegIV, a member of the Regenerating (REG) gene family, may be a marker for the prediction of resistance to 5-fluorouracil (5-FU)-based chemotherapy. Fluorouracil 112-126 regenerating family member 4 Homo sapiens 5-10 24833352-5 2014 Here we demonstrate that SPARC-deficient mice display higher resistance to serial treatment with the chemotherapeutic agent 5-fluorouracil (5-FU). Fluorouracil 140-144 secreted acidic cysteine rich glycoprotein Mus musculus 25-30 23010741-1 2013 AIM: RegIV, a member of the Regenerating (REG) gene family, may be a marker for the prediction of resistance to 5-fluorouracil (5-FU)-based chemotherapy. Fluorouracil 128-132 regenerating family member 4 Homo sapiens 5-10 24751000-3 2014 METHODS: To elucidate the mechanisms of variations to 5-FU outcome, the authors investigated MTHFR, DHFR, TYMS and SLC19A1 folate genes expression for 5-FU response in laryngeal cancer cell line (Hep-2). Fluorouracil 151-155 solute carrier family 19 member 1 Homo sapiens 115-122 23010741-2 2013 However, the relationship between the intrinsic drug resistance of gastric cancer (GC) cells to 5-FU used alone (single FU) or in multidrug therapeutic regimens (5-FU combinations) and RegIV expression has not been investigated. Fluorouracil 96-100 regenerating family member 4 Homo sapiens 185-190 23010741-6 2013 RegIV expression was evaluated as a novel predictive biomarker for the intrinsic drug resistance of primary GC cells to single 5-FU or 5-FU combinations. Fluorouracil 127-131 regenerating family member 4 Homo sapiens 0-5 23010741-6 2013 RegIV expression was evaluated as a novel predictive biomarker for the intrinsic drug resistance of primary GC cells to single 5-FU or 5-FU combinations. Fluorouracil 135-139 regenerating family member 4 Homo sapiens 0-5 23010741-7 2013 RESULTS: Upregulation of RegIV mRNA transcripts was observed in 36 of the 45 tumor specimens and was positively correlated with the invasive depth of the tumor cells (p = 0.000), the clinical stages (p = 0.000) and the in vitro intrinsic drug resistance of primary GC cells to 5-FU (p = 0.000) or 5-FU combinations. Fluorouracil 277-281 regenerating family member 4 Homo sapiens 25-30 23010741-7 2013 RESULTS: Upregulation of RegIV mRNA transcripts was observed in 36 of the 45 tumor specimens and was positively correlated with the invasive depth of the tumor cells (p = 0.000), the clinical stages (p = 0.000) and the in vitro intrinsic drug resistance of primary GC cells to 5-FU (p = 0.000) or 5-FU combinations. Fluorouracil 297-301 regenerating family member 4 Homo sapiens 25-30 23010741-8 2013 CONCLUSION: RegIV mRNA transcript level was strongly associated with the intrinsic resistance of GC cells to single 5-FU or 5-FU combinations, suggesting that RegIV may play an important role in the intrinsic resistance of GC cells to 5-FU and that targeted therapy against the RegIV gene could be applied to overcome 5-FU resistance in the treatment of GC. Fluorouracil 116-120 regenerating family member 4 Homo sapiens 12-17 23010741-8 2013 CONCLUSION: RegIV mRNA transcript level was strongly associated with the intrinsic resistance of GC cells to single 5-FU or 5-FU combinations, suggesting that RegIV may play an important role in the intrinsic resistance of GC cells to 5-FU and that targeted therapy against the RegIV gene could be applied to overcome 5-FU resistance in the treatment of GC. Fluorouracil 116-120 regenerating family member 4 Homo sapiens 159-164 23010741-8 2013 CONCLUSION: RegIV mRNA transcript level was strongly associated with the intrinsic resistance of GC cells to single 5-FU or 5-FU combinations, suggesting that RegIV may play an important role in the intrinsic resistance of GC cells to 5-FU and that targeted therapy against the RegIV gene could be applied to overcome 5-FU resistance in the treatment of GC. Fluorouracil 116-120 regenerating family member 4 Homo sapiens 159-164 23010741-8 2013 CONCLUSION: RegIV mRNA transcript level was strongly associated with the intrinsic resistance of GC cells to single 5-FU or 5-FU combinations, suggesting that RegIV may play an important role in the intrinsic resistance of GC cells to 5-FU and that targeted therapy against the RegIV gene could be applied to overcome 5-FU resistance in the treatment of GC. Fluorouracil 124-128 regenerating family member 4 Homo sapiens 12-17 23010741-8 2013 CONCLUSION: RegIV mRNA transcript level was strongly associated with the intrinsic resistance of GC cells to single 5-FU or 5-FU combinations, suggesting that RegIV may play an important role in the intrinsic resistance of GC cells to 5-FU and that targeted therapy against the RegIV gene could be applied to overcome 5-FU resistance in the treatment of GC. Fluorouracil 124-128 regenerating family member 4 Homo sapiens 159-164 23010741-8 2013 CONCLUSION: RegIV mRNA transcript level was strongly associated with the intrinsic resistance of GC cells to single 5-FU or 5-FU combinations, suggesting that RegIV may play an important role in the intrinsic resistance of GC cells to 5-FU and that targeted therapy against the RegIV gene could be applied to overcome 5-FU resistance in the treatment of GC. Fluorouracil 124-128 regenerating family member 4 Homo sapiens 159-164 23010741-8 2013 CONCLUSION: RegIV mRNA transcript level was strongly associated with the intrinsic resistance of GC cells to single 5-FU or 5-FU combinations, suggesting that RegIV may play an important role in the intrinsic resistance of GC cells to 5-FU and that targeted therapy against the RegIV gene could be applied to overcome 5-FU resistance in the treatment of GC. Fluorouracil 124-128 regenerating family member 4 Homo sapiens 12-17 23010741-8 2013 CONCLUSION: RegIV mRNA transcript level was strongly associated with the intrinsic resistance of GC cells to single 5-FU or 5-FU combinations, suggesting that RegIV may play an important role in the intrinsic resistance of GC cells to 5-FU and that targeted therapy against the RegIV gene could be applied to overcome 5-FU resistance in the treatment of GC. Fluorouracil 124-128 regenerating family member 4 Homo sapiens 159-164 23010741-8 2013 CONCLUSION: RegIV mRNA transcript level was strongly associated with the intrinsic resistance of GC cells to single 5-FU or 5-FU combinations, suggesting that RegIV may play an important role in the intrinsic resistance of GC cells to 5-FU and that targeted therapy against the RegIV gene could be applied to overcome 5-FU resistance in the treatment of GC. Fluorouracil 124-128 regenerating family member 4 Homo sapiens 159-164 23010741-8 2013 CONCLUSION: RegIV mRNA transcript level was strongly associated with the intrinsic resistance of GC cells to single 5-FU or 5-FU combinations, suggesting that RegIV may play an important role in the intrinsic resistance of GC cells to 5-FU and that targeted therapy against the RegIV gene could be applied to overcome 5-FU resistance in the treatment of GC. Fluorouracil 124-128 regenerating family member 4 Homo sapiens 12-17 23010741-8 2013 CONCLUSION: RegIV mRNA transcript level was strongly associated with the intrinsic resistance of GC cells to single 5-FU or 5-FU combinations, suggesting that RegIV may play an important role in the intrinsic resistance of GC cells to 5-FU and that targeted therapy against the RegIV gene could be applied to overcome 5-FU resistance in the treatment of GC. Fluorouracil 124-128 regenerating family member 4 Homo sapiens 159-164 23010741-8 2013 CONCLUSION: RegIV mRNA transcript level was strongly associated with the intrinsic resistance of GC cells to single 5-FU or 5-FU combinations, suggesting that RegIV may play an important role in the intrinsic resistance of GC cells to 5-FU and that targeted therapy against the RegIV gene could be applied to overcome 5-FU resistance in the treatment of GC. Fluorouracil 124-128 regenerating family member 4 Homo sapiens 159-164 23420099-9 2013 In conclusion, mRNA levels of SLC22A2, SLC23A2, ABCB1, ABCC2, Rad51, MSH2 and DPYD were confirmed to be strongly correlated with IC50 values for 5-FU, and mRNA levels of ABCC2, MSH2 and DPYD were confirmed to be strongly correlated with IC(50) values for CDDP. Fluorouracil 145-149 solute carrier family 22 member 2 Homo sapiens 30-37 22527182-11 2013 These Mcl-1-expressing cell lines were relatively resistant to chemotherapeutic agents such as 5-fluorouracil (5-FU) and cisplatin (CDDP). Fluorouracil 95-109 MCL1 apoptosis regulator, BCL2 family member Homo sapiens 6-11 24755081-7 2014 Overexpression of KIN enhanced, while silencing KIN impaired, chemoresistance to oxaliplatin (Ox) or 5-fluorouracil (5-FU) in CRC cell lines. Fluorouracil 101-115 Kin17 DNA and RNA binding protein Homo sapiens 18-21 24755081-7 2014 Overexpression of KIN enhanced, while silencing KIN impaired, chemoresistance to oxaliplatin (Ox) or 5-fluorouracil (5-FU) in CRC cell lines. Fluorouracil 117-121 Kin17 DNA and RNA binding protein Homo sapiens 18-21 24849329-0 2014 Use of metformin alone is not associated with survival outcomes of colorectal cancer cell but AMPK activator AICAR sensitizes anticancer effect of 5-fluorouracil through AMPK activation. Fluorouracil 147-161 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 170-174 24849329-5 2014 Different from metformin, AICAR emerged antitumor activity and sensitized anticancer effect of 5-FU on CRC cells in vitro and in vivo. Fluorouracil 95-99 5-aminoimidazole-4-carboxamide ribonucleotide formyltransferase/IMP cyclohydrolase Homo sapiens 26-31 24849329-7 2014 Taken together, our results suggest that metformin has not antineoplastic activity for CRC cells as a single agent but AMPK activator AICAR can induce apoptosis and enhance the cytotoxic effect of 5-FU through AMPK activation. Fluorouracil 197-201 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 119-123 24849329-7 2014 Taken together, our results suggest that metformin has not antineoplastic activity for CRC cells as a single agent but AMPK activator AICAR can induce apoptosis and enhance the cytotoxic effect of 5-FU through AMPK activation. Fluorouracil 197-201 5-aminoimidazole-4-carboxamide ribonucleotide formyltransferase/IMP cyclohydrolase Homo sapiens 134-139 24849329-7 2014 Taken together, our results suggest that metformin has not antineoplastic activity for CRC cells as a single agent but AMPK activator AICAR can induce apoptosis and enhance the cytotoxic effect of 5-FU through AMPK activation. Fluorouracil 197-201 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 210-214 24816638-5 2014 Sal reversed the 5-FU-induced increase in CD133(+) EPCAM(+) cells, epithelial-mesenchymal transition and activation of the Wnt/beta-catenin signaling pathway. Fluorouracil 17-21 prominin 1 Homo sapiens 42-47 24801886-5 2014 Among the proteins identified under both serum-depleted and 5-fluorouracil-treated conditions, Rab1A was identified as an essential molecule for cancer cell survival. Fluorouracil 60-74 RAB1A, member RAS oncogene family Homo sapiens 95-100 24752302-7 2014 Moreover, treatment with the chemotherapeutic agent 5-fluorouracil (5-FU) also induces GzmB production in HSCs. Fluorouracil 52-66 granzyme B Mus musculus 87-91 24752302-7 2014 Moreover, treatment with the chemotherapeutic agent 5-fluorouracil (5-FU) also induces GzmB production in HSCs. Fluorouracil 68-72 granzyme B Mus musculus 87-91 22527182-11 2013 These Mcl-1-expressing cell lines were relatively resistant to chemotherapeutic agents such as 5-fluorouracil (5-FU) and cisplatin (CDDP). Fluorouracil 111-115 MCL1 apoptosis regulator, BCL2 family member Homo sapiens 6-11 23202296-3 2013 Here we show that two clinically used chemotherapeutic agents, gemcitabine (Gem) and 5-fluorouracil (5FU), activate the NOD-like receptor family, pyrin domain containing-3 protein (Nlrp3)-dependent caspase-1 activation complex (termed the inflammasome) in myeloid-derived suppressor cells (MDSCs), leading to production of interleukin-1beta (IL-1beta), which curtails anticancer immunity. Fluorouracil 85-99 NLR family, pyrin domain containing 3 Mus musculus 181-186 23202296-3 2013 Here we show that two clinically used chemotherapeutic agents, gemcitabine (Gem) and 5-fluorouracil (5FU), activate the NOD-like receptor family, pyrin domain containing-3 protein (Nlrp3)-dependent caspase-1 activation complex (termed the inflammasome) in myeloid-derived suppressor cells (MDSCs), leading to production of interleukin-1beta (IL-1beta), which curtails anticancer immunity. Fluorouracil 101-104 NLR family, pyrin domain containing 3 Mus musculus 181-186 23202296-6 2013 Accordingly, Gem and 5FU exerted higher antitumor effects when tumors were established in Nlrp3(-/-) or Casp1(-/-) mice or wild-type mice treated with interleukin-1 receptor antagonist (IL-1Ra). Fluorouracil 21-24 NLR family, pyrin domain containing 3 Mus musculus 90-95 23554900-12 2013 In the MCF7 breast cancer cell line, leptin could induce cell proliferation and reduced the efficacy of all breast cancer therapies (tamoxifen, 5-fluorouracil, taxol and vinblastin). Fluorouracil 144-158 leptin Homo sapiens 37-43 23152059-8 2012 miR-204 targeted Bcl-2 messenger RNA and increased responsiveness of GC cells to 5-fluorouracil and oxaliplatin treatment. Fluorouracil 81-95 microRNA 204 Homo sapiens 0-7 23152059-9 2012 Ectopic expression of Bcl-2 protein counteracted miR-204 pro-apoptotic activity in response to 5-fluorouracil. Fluorouracil 95-109 microRNA 204 Homo sapiens 49-56 22633450-6 2012 Expression of thymidylate synthase (TS) has been associated with improved outcome following 5-FU based adjuvant treatment in gastrointestinal cancer. Fluorouracil 92-96 thymidylate synthetase Homo sapiens 14-34 24885567-11 2014 RESULTS: MELK mRNA and protein expression were both elevated in human gastric cancer, and this was associated with chemoresistance to 5-fluorouracil (5-FU). Fluorouracil 134-148 maternal embryonic leucine zipper kinase Homo sapiens 9-13 24885567-11 2014 RESULTS: MELK mRNA and protein expression were both elevated in human gastric cancer, and this was associated with chemoresistance to 5-fluorouracil (5-FU). Fluorouracil 150-154 maternal embryonic leucine zipper kinase Homo sapiens 9-13 22633450-6 2012 Expression of thymidylate synthase (TS) has been associated with improved outcome following 5-FU based adjuvant treatment in gastrointestinal cancer. Fluorouracil 92-96 thymidylate synthetase Homo sapiens 36-38 22526901-0 2012 FANCJ expression predicts the response to 5-fluorouracil-based chemotherapy in MLH1-proficient colorectal cancer. Fluorouracil 42-56 BRCA1 interacting helicase 1 Homo sapiens 0-5 22526901-0 2012 FANCJ expression predicts the response to 5-fluorouracil-based chemotherapy in MLH1-proficient colorectal cancer. Fluorouracil 42-56 mutL homolog 1 Homo sapiens 79-83 22526901-8 2012 Among patients with stage II/III tumors who received 5-FU, patients with tumors exhibiting high FANCJ expression had significantly worse RFS than did patients with tumors exhibiting low FANCJ expression (P < 0.01). Fluorouracil 53-57 BRCA1 interacting helicase 1 Homo sapiens 96-101 22526901-10 2012 High FANCJ expression was correlated with 5-FU resistance in tumors with normal MLH1 expression (P < 0.05) but not in tumors not expressing MLH1 (P = 0.9). Fluorouracil 42-46 BRCA1 interacting helicase 1 Homo sapiens 5-10 22526901-10 2012 High FANCJ expression was correlated with 5-FU resistance in tumors with normal MLH1 expression (P < 0.05) but not in tumors not expressing MLH1 (P = 0.9). Fluorouracil 42-46 mutL homolog 1 Homo sapiens 80-84 22526901-11 2012 In vitro, FANCJ overexpression was correlated with 5-FU resistance in MLH1-proficient HCT116 3-6 cells but not in MLH1-deficient HCT116 cells. Fluorouracil 51-55 BRCA1 interacting helicase 1 Homo sapiens 10-15 22526901-11 2012 In vitro, FANCJ overexpression was correlated with 5-FU resistance in MLH1-proficient HCT116 3-6 cells but not in MLH1-deficient HCT116 cells. Fluorouracil 51-55 mutL homolog 1 Homo sapiens 70-74 22526901-12 2012 CONCLUSIONS: FANCJ could be a useful biomarker to predict the response to 5-FU and prognosis of CRC, particularly in tumors with normal MLH1 expression. Fluorouracil 74-78 BRCA1 interacting helicase 1 Homo sapiens 13-18 22560972-4 2012 We examined whether the effects of one TS inhibitor, 5-fluorouracil (5FU), on FLT uptake require proliferating cells and whether the effects are limited to increasing TK1 activity. Fluorouracil 53-67 thymidylate synthetase Homo sapiens 39-41 22560972-4 2012 We examined whether the effects of one TS inhibitor, 5-fluorouracil (5FU), on FLT uptake require proliferating cells and whether the effects are limited to increasing TK1 activity. Fluorouracil 69-72 thymidylate synthetase Homo sapiens 39-41 22993328-7 2012 RESULTS: The frequency of cells that were capable of initiating spheres was higher in 5-FU-pre treated cells, which also overexpressed stem cell marker genes, OCT4 and NANOG. Fluorouracil 86-90 POU class 5 homeobox 1 Homo sapiens 159-163 22947087-5 2012 Combinational therapy of overexpressed hTERTC27 driven by the 5-FU-activated Egr-1 promoter and 5-FU synergistically inhibited cell proliferation and promoted apoptosis of C666-1 cells for about 4.75-fold and 1.76-fold in comparison with a sole therapy of hTERTC27 or 5-FU in vitro. Fluorouracil 62-66 early growth response 1 Homo sapiens 77-82 24671766-5 2014 Additionally, we developed a copper-inducible reporter, with which we demonstrate that 5-fluorouracil mimics the mRNA decay phenotype of cells lacking the 3"-5" exonuclease Rrp6p. Fluorouracil 87-101 exosome nuclease subunit RRP6 Saccharomyces cerevisiae S288C 173-178 24781822-3 2014 SLC6A6 knockdown (KD) attenuated cell survival and was accompanied by enhanced drug sensitivity to 5-fluorouracil (5-FU), doxycycline (DOX) and SN-38. Fluorouracil 99-113 solute carrier family 6 member 6 Homo sapiens 0-6 24781822-3 2014 SLC6A6 knockdown (KD) attenuated cell survival and was accompanied by enhanced drug sensitivity to 5-fluorouracil (5-FU), doxycycline (DOX) and SN-38. Fluorouracil 115-119 solute carrier family 6 member 6 Homo sapiens 0-6 24708484-0 2014 P21 and CD166 as predictive markers of poor response and outcome after fluorouracil-based chemoradiotherapy for the patients with rectal cancer. Fluorouracil 71-83 activated leukocyte cell adhesion molecule Homo sapiens 8-13 24708484-9 2014 CONCLUSION: These show high p21 and CD166 expression at the pretreatment biopsy were associated with tumor regression and poor prognosis in patients treated with 5-FU based CRT. Fluorouracil 162-166 activated leukocyte cell adhesion molecule Homo sapiens 36-41 24370904-7 2014 Although 5-FU did not affect the sphere-forming ability and increased the populations expressing other stem/progenitor markers CD133 and CD13 (p < 0.05), VB4-845 strongly suppressed the sphere-formation and decreased the population expressing CD133 and CD13 (p < 0.0005, <0.01, respectively). Fluorouracil 9-13 prominin 1 Homo sapiens 127-132 24370904-7 2014 Although 5-FU did not affect the sphere-forming ability and increased the populations expressing other stem/progenitor markers CD133 and CD13 (p < 0.05), VB4-845 strongly suppressed the sphere-formation and decreased the population expressing CD133 and CD13 (p < 0.0005, <0.01, respectively). Fluorouracil 9-13 alanyl aminopeptidase, membrane Homo sapiens 127-131 24370904-7 2014 Although 5-FU did not affect the sphere-forming ability and increased the populations expressing other stem/progenitor markers CD133 and CD13 (p < 0.05), VB4-845 strongly suppressed the sphere-formation and decreased the population expressing CD133 and CD13 (p < 0.0005, <0.01, respectively). Fluorouracil 9-13 alanyl aminopeptidase, membrane Homo sapiens 137-141 22947087-6 2012 In vivo experiments showed that overexpressed hTERTC27 driven by 5-FU-activated Egr-1 promoter and 5-FU synergistically reduced tumor volume, tumor weight, and local infiltration, which may be relative to tumor cell apoptosis. Fluorouracil 65-69 early growth response 1 Homo sapiens 80-85 22947087-7 2012 These results suggest that combinational therapy of overexpressed hTERTC27, which is driven by the 5-FU-activated Egr-1 promoter, and 5-FU may provide a novel approach to treat nasopharyngeal cancer. Fluorouracil 99-103 early growth response 1 Homo sapiens 114-119 22819905-1 2012 BACKGROUND/AIMS: Thymidylate synthase (TS) is an enzyme for DNA-synthesis and the target for 5-fluorouracil whereas cyclin-D1 plays a critical role in the progression of cells through the G1 phase of the cell-cycle. Fluorouracil 93-107 thymidylate synthetase Homo sapiens 17-37 22819905-1 2012 BACKGROUND/AIMS: Thymidylate synthase (TS) is an enzyme for DNA-synthesis and the target for 5-fluorouracil whereas cyclin-D1 plays a critical role in the progression of cells through the G1 phase of the cell-cycle. Fluorouracil 93-107 thymidylate synthetase Homo sapiens 39-41 22614071-0 2012 Inhibition of the mTOR/S6K signal is necessary to enhance fluorouracil-induced apoptosis in gastric cancer cells with HER2 amplification. Fluorouracil 58-70 ribosomal protein S6 kinase B1 Homo sapiens 23-26 22614071-8 2012 In summary, inhibition of the mTOR/S6K signal may be a key molecular event in enhancing fluorouracil-induced apoptosis specifically in gastric cancer cells with HER2 amplification. Fluorouracil 88-100 ribosomal protein S6 kinase B1 Homo sapiens 35-38 21898388-7 2012 In gastric cancer patients with stage II and III, 5-FU-based adjuvant chemotherapy showed better disease-free survival in the MSS/MSI-L group, but showed no benefits in the MSI-H group. Fluorouracil 50-54 RB binding protein 4, chromatin remodeling factor Homo sapiens 130-133 22532570-3 2012 This interaction is increased by 5-fluorouracil or doxorubicin treatment and is responsible for Ser(15) phosphorylation of p53. Fluorouracil 33-47 transformation related protein 53, pseudogene Mus musculus 123-126 24535229-8 2014 The experiments showed that T.Tn and TE2 proliferation was strongly inhibited by the combination of 5-FU/radiation and the COX-2 inhibitor. Fluorouracil 100-104 N-alpha-acetyltransferase 10, NatA catalytic subunit Homo sapiens 37-40 22641663-1 2012 AIM: The activity of the widely used anticancer drug 5-fluorouracil (5-FU) is determined by the presence of several enzymes, including dihydropyrimidine dehydrogenase (DPD), orotate phosphoribosyl transferase (OPRT), and thymidylate synthase (TS). Fluorouracil 53-67 uridine monophosphate synthetase Homo sapiens 174-208 23567490-0 2014 The cyclin D1 (CCND1) rs9344 G>A polymorphism predicts clinical outcome in colon cancer patients treated with adjuvant 5-FU-based chemotherapy. Fluorouracil 122-126 cyclin D1 Homo sapiens 4-13 23567490-0 2014 The cyclin D1 (CCND1) rs9344 G>A polymorphism predicts clinical outcome in colon cancer patients treated with adjuvant 5-FU-based chemotherapy. Fluorouracil 122-126 cyclin D1 Homo sapiens 15-20 23567490-4 2014 Patients treated with 5-fluorouracil-based chemotherapy, carrying the CCND1 rs9344 A/A genotype had significantly decreased time-to-tumor recurrence (TTR) in univariate analysis and multivariate analysis (hazard ratio (HR) 2.47; 95% confidence interval (CI) 1.16-5.29; P=0.019). Fluorouracil 22-36 cyclin D1 Homo sapiens 70-75 23752739-0 2014 Gender-specific profiling in SCN1A polymorphisms and time-to-recurrence in patients with stage II/III colorectal cancer treated with adjuvant 5-fluoruracil chemotherapy. Fluorouracil 142-155 sodium voltage-gated channel alpha subunit 1 Homo sapiens 29-34 23752739-1 2014 This study was designed to analyze the gender-related association between SCN1A polymorphisms (voltage-gated sodium channels; alpha-subunit) and time-to-recurrence (TTR) in patients with colorectal cancer (CRC) treated with 5-fluoruracil (5-FU)-based adjuvant chemotherapy. Fluorouracil 224-237 sodium voltage-gated channel alpha subunit 1 Homo sapiens 74-79 23752739-1 2014 This study was designed to analyze the gender-related association between SCN1A polymorphisms (voltage-gated sodium channels; alpha-subunit) and time-to-recurrence (TTR) in patients with colorectal cancer (CRC) treated with 5-fluoruracil (5-FU)-based adjuvant chemotherapy. Fluorouracil 239-243 sodium voltage-gated channel alpha subunit 1 Homo sapiens 74-79 23752739-7 2014 The study validated gender-dependent association between genomic SCN1A rs3812718 polymorphism and TTR in CRC patients treated with adjuvant 5-FU-based chemotherapy. Fluorouracil 140-144 sodium voltage-gated channel alpha subunit 1 Homo sapiens 65-70 24362470-4 2014 Here, we found that colorectal cancer (CRC) cells treated with oxaliplatin (OXA) and/or 5-fluorouracil (5-Fu) released high levels of high-mobility group box 1 (HMGB1) and heat shock protein 70 (HSP70). Fluorouracil 88-102 high mobility group box 1 Homo sapiens 134-159 24362470-4 2014 Here, we found that colorectal cancer (CRC) cells treated with oxaliplatin (OXA) and/or 5-fluorouracil (5-Fu) released high levels of high-mobility group box 1 (HMGB1) and heat shock protein 70 (HSP70). Fluorouracil 88-102 high mobility group box 1 Homo sapiens 161-166 24401318-6 2014 The IC50 of 5-FU for HCT116 cells overexpressing miR-27a or miR-27b was 4.4 mumol/L (both), significantly lower than that for cells expressing a nontargeting (scramble) control miRNA (14.3 mumol/L; P = 3.3 x 10(-5) and P = 1.5 x 10(-7), respectively). Fluorouracil 12-16 microRNA 27b Homo sapiens 60-67 24398626-11 2014 Consistently, 5-FU, a widely used chemotherapeutic agent, increased FOXO1 expression via inhibition of QKI. Fluorouracil 14-18 QKI, KH domain containing RNA binding Homo sapiens 103-106 24384683-0 2014 Loss of Smad4 in colorectal cancer induces resistance to 5-fluorouracil through activating Akt pathway. Fluorouracil 57-71 SMAD family member 4 Homo sapiens 8-13 24384683-3 2014 METHODS: We evaluated how the loss of Smad4 in CRC enhanced chemoresistance to 5-fluorouracil (5-FU) using two CRC cell lines in vitro and in vivo. Fluorouracil 79-93 SMAD family member 4 Homo sapiens 38-43 24384683-3 2014 METHODS: We evaluated how the loss of Smad4 in CRC enhanced chemoresistance to 5-fluorouracil (5-FU) using two CRC cell lines in vitro and in vivo. Fluorouracil 95-99 SMAD family member 4 Homo sapiens 38-43 24384683-5 2014 RESULTS: Knockdown or loss of Smad4 induced tumorigenicity, migration, invasion, angiogenesis, metastasis, and 5-FU resistance. Fluorouracil 111-115 SMAD family member 4 Homo sapiens 30-35 24384683-8 2014 Suppression of phosphatidylinositol-3-kinase (PI3K)/Akt pathway by LY294002 restored chemosensitivity of Smad4-deficient cells to 5-FU. Fluorouracil 130-134 SMAD family member 4 Homo sapiens 105-110 24384683-11 2014 CONCLUSION: Loss of Smad4 in CRC patients induces resistance to 5-FU-based therapy through activation of Akt pathway and inhibitors of this pathway may sensitise these patients to 5-FU. Fluorouracil 64-68 SMAD family member 4 Homo sapiens 20-25 24384683-11 2014 CONCLUSION: Loss of Smad4 in CRC patients induces resistance to 5-FU-based therapy through activation of Akt pathway and inhibitors of this pathway may sensitise these patients to 5-FU. Fluorouracil 180-184 SMAD family member 4 Homo sapiens 20-25 22641663-1 2012 AIM: The activity of the widely used anticancer drug 5-fluorouracil (5-FU) is determined by the presence of several enzymes, including dihydropyrimidine dehydrogenase (DPD), orotate phosphoribosyl transferase (OPRT), and thymidylate synthase (TS). Fluorouracil 53-67 uridine monophosphate synthetase Homo sapiens 210-214 22641663-1 2012 AIM: The activity of the widely used anticancer drug 5-fluorouracil (5-FU) is determined by the presence of several enzymes, including dihydropyrimidine dehydrogenase (DPD), orotate phosphoribosyl transferase (OPRT), and thymidylate synthase (TS). Fluorouracil 53-67 thymidylate synthetase Homo sapiens 221-241 22641663-1 2012 AIM: The activity of the widely used anticancer drug 5-fluorouracil (5-FU) is determined by the presence of several enzymes, including dihydropyrimidine dehydrogenase (DPD), orotate phosphoribosyl transferase (OPRT), and thymidylate synthase (TS). Fluorouracil 53-67 thymidylate synthetase Homo sapiens 243-245 22641663-1 2012 AIM: The activity of the widely used anticancer drug 5-fluorouracil (5-FU) is determined by the presence of several enzymes, including dihydropyrimidine dehydrogenase (DPD), orotate phosphoribosyl transferase (OPRT), and thymidylate synthase (TS). Fluorouracil 69-73 uridine monophosphate synthetase Homo sapiens 174-208 22641663-1 2012 AIM: The activity of the widely used anticancer drug 5-fluorouracil (5-FU) is determined by the presence of several enzymes, including dihydropyrimidine dehydrogenase (DPD), orotate phosphoribosyl transferase (OPRT), and thymidylate synthase (TS). Fluorouracil 69-73 uridine monophosphate synthetase Homo sapiens 210-214 22641663-1 2012 AIM: The activity of the widely used anticancer drug 5-fluorouracil (5-FU) is determined by the presence of several enzymes, including dihydropyrimidine dehydrogenase (DPD), orotate phosphoribosyl transferase (OPRT), and thymidylate synthase (TS). Fluorouracil 69-73 thymidylate synthetase Homo sapiens 221-241 22641663-1 2012 AIM: The activity of the widely used anticancer drug 5-fluorouracil (5-FU) is determined by the presence of several enzymes, including dihydropyrimidine dehydrogenase (DPD), orotate phosphoribosyl transferase (OPRT), and thymidylate synthase (TS). Fluorouracil 69-73 thymidylate synthetase Homo sapiens 243-245 22970005-0 2012 Prognostic value of nuclear maspin expression for adjuvant 5-fluorouracil-based chemotherapy in advanced gastric cancer. Fluorouracil 59-73 serpin family B member 5 Homo sapiens 28-34 24503538-9 2014 A similar phenotype and downstream pathway changes were observed following FGFR4 silencing in cell lines resistant to 5-FU, oxaliplatin and SN38 and upon exposure of parental cells to the FGFR small-molecule inhibitor BGJ398. Fluorouracil 118-122 fibroblast growth factor receptor 4 Homo sapiens 75-80 22970005-7 2012 Among the nuclear maspin-expressing patients, those who were treated with 5-FU-based adjuvant chemotherapy showed significantly longer OS than those without chemotherapy (p=0.0004). Fluorouracil 74-78 serpin family B member 5 Homo sapiens 18-24 22970005-9 2012 Patients with positive nuclear maspin expression may be more responsive to adjuvant 5-FU chemotherapy. Fluorouracil 84-88 serpin family B member 5 Homo sapiens 31-37 22048868-1 2012 BACKGROUND: The combination chemotherapy regimen of streptozocin and 5-fluorouracil (FU/STZ) has been used for the treatment of metastatic neuroendocrine tumours. Fluorouracil 69-83 ST3 beta-galactoside alpha-2,3-sialyltransferase 4 Homo sapiens 88-91 22623418-7 2012 For example, the detoxification enzyme NQO1 was increased with treatment in both cell lines, while disparate members of the peroxiredoxin family, PRDX2 or PRDX5 and PRDX6, were elevated with 5-FU exposure in either SW480 or SW620, respectively. Fluorouracil 191-195 peroxiredoxin 5 Homo sapiens 155-160 22623418-8 2012 Cell adhesion-associated proteins CTNNB1 and RhoA showed decreased expression with 5-FU treatment in both cell lines. Fluorouracil 83-87 catenin beta 1 Homo sapiens 34-40 22322462-0 2012 MicroRNA-21-mediated regulation of Sprouty2 protein expression enhances the cytotoxic effect of 5-fluorouracil and metformin in colon cancer cells. Fluorouracil 96-110 microRNA 21 Homo sapiens 0-11 21821547-0 2012 Recurrence risk score based on the specific activity of CDK1 and CDK2 predicts response to neoadjuvant paclitaxel followed by 5-fluorouracil, epirubicin and cyclophosphamide in breast cancers. Fluorouracil 126-140 cyclin dependent kinase 1 Homo sapiens 56-60 22139443-0 2012 Differentiation-inducing factor-1 enhances 5-fluorouracil action on oral cancer cells inhibiting E2F1 and thymidylate synthase mRNAs accumulation. Fluorouracil 43-57 E2F transcription factor 1 Homo sapiens 97-101 22139443-0 2012 Differentiation-inducing factor-1 enhances 5-fluorouracil action on oral cancer cells inhibiting E2F1 and thymidylate synthase mRNAs accumulation. Fluorouracil 43-57 thymidylate synthetase Homo sapiens 106-126 22543147-1 2012 OBJECTIVE: To investigate the effect of 1,25-dihydroxyvitamin D(3) and 5-fluorouracil, either alone or in combination, on the expression of IGFBP-3 in human esophageal carcinoma 109 cell xenograft in nude mice. Fluorouracil 71-85 insulin like growth factor binding protein 3 Homo sapiens 140-147 22284030-0 2012 In regard to "Thymidylate synthase gene polymorphism affects the response to preoperative 5-fluorouracil chemoradiation therapy in patients with rectal cancer" (Int J Radiat Oncol Biol Phys 2011;81:669-676). Fluorouracil 90-104 thymidylate synthetase Homo sapiens 14-34 24189196-3 2014 5-FU/Meg-fib-graft-PNIPAAm NGs showed particle size of 165-195 nm size. Fluorouracil 0-4 protein tyrosine phosphatase non-receptor type 4 Homo sapiens 5-8 24189196-4 2014 The drug loading efficiency with 5-FU was 60% and 70% for Meg. Fluorouracil 33-37 protein tyrosine phosphatase non-receptor type 4 Homo sapiens 58-61 22291191-5 2012 Administration of these 5-FU-resistant CD11b(-)CD45(-) MSCs 6 d after myelin oligodendrocyte glycoprotein (MOG) immunization completely remitted MOG-induced experimental autoimmune encephalomyelitis after initial development of mild disease. Fluorouracil 24-28 myelin oligodendrocyte glycoprotein Mus musculus 70-105 22291191-5 2012 Administration of these 5-FU-resistant CD11b(-)CD45(-) MSCs 6 d after myelin oligodendrocyte glycoprotein (MOG) immunization completely remitted MOG-induced experimental autoimmune encephalomyelitis after initial development of mild disease. Fluorouracil 24-28 myelin oligodendrocyte glycoprotein Mus musculus 107-110 22291191-5 2012 Administration of these 5-FU-resistant CD11b(-)CD45(-) MSCs 6 d after myelin oligodendrocyte glycoprotein (MOG) immunization completely remitted MOG-induced experimental autoimmune encephalomyelitis after initial development of mild disease. Fluorouracil 24-28 myelin oligodendrocyte glycoprotein Mus musculus 145-148 22192357-0 2012 14-3-3sigma regulation by p53 mediates a chemotherapy response to 5-fluorouracil in MCF-7 breast cancer cells via Akt inactivation. Fluorouracil 66-80 stratifin Homo sapiens 0-11 22192357-1 2012 We previously demonstrated that 14-3-3sigma was downregulated in 5-fluorouracil (5-Fu)-resistant MCF-7 breast cancer cells (MCF-7/5-Fu). Fluorouracil 65-79 stratifin Homo sapiens 32-43 22192357-1 2012 We previously demonstrated that 14-3-3sigma was downregulated in 5-fluorouracil (5-Fu)-resistant MCF-7 breast cancer cells (MCF-7/5-Fu). Fluorouracil 81-85 stratifin Homo sapiens 32-43 22192357-2 2012 Here, we found that stably enhanced 14-3-3sigma expression strengthened the effects of 5-Fu, Mitoxantrone and cDDP. Fluorouracil 87-91 stratifin Homo sapiens 36-47 22192357-5 2012 Meanwhile, initial treatments with high concentrations of 5-Fu clearly induced 14-3-3sigma and p53 expression in a time-dependent manner. Fluorouracil 58-62 stratifin Homo sapiens 79-90 23317245-1 2012 We conducted this study to detect associations between XRCC1 Arg399Gln and XPD Lys751Gln genotypes and survival of colorectal cancer patients treated with 5-FU/oxalipatin chemotherapy. Fluorouracil 155-159 ERCC excision repair 2, TFIIH core complex helicase subunit Homo sapiens 75-78 23317245-8 2012 In conclusion, it is suggested that the XRCC1 Arg399Gln and XPD Lys751Gln polymorphisms should be routinely assessed to determine colorectal patients who are more likely to benefit from 5-FU/oxalipatin chemotherapy. Fluorouracil 186-190 ERCC excision repair 2, TFIIH core complex helicase subunit Homo sapiens 60-63 22324043-8 2012 TS mRNA levels in RRC1 were significantly reversely correlated with 5-FU concentrations on day 2 (correlation coefficient = -0.867, P = 0.015). Fluorouracil 68-72 thymidylate synthetase Homo sapiens 0-2 24339132-0 2014 CD133 and CD133-regulated nucleophosmin linked to 5-fluorouracil susceptibility in human colon cancer cell line SW620. Fluorouracil 50-64 prominin 1 Homo sapiens 0-5 24339132-0 2014 CD133 and CD133-regulated nucleophosmin linked to 5-fluorouracil susceptibility in human colon cancer cell line SW620. Fluorouracil 50-64 prominin 1 Homo sapiens 10-15 24339132-0 2014 CD133 and CD133-regulated nucleophosmin linked to 5-fluorouracil susceptibility in human colon cancer cell line SW620. Fluorouracil 50-64 nucleophosmin 1 Homo sapiens 26-39 24339132-10 2014 The CD133+ subpopulation percentage or its value normalized against CD133 protein level was only linked to intrinsic susceptibility of human colon cancer cells to 5-fluorouracil (5-FU). Fluorouracil 163-177 prominin 1 Homo sapiens 4-9 24339132-10 2014 The CD133+ subpopulation percentage or its value normalized against CD133 protein level was only linked to intrinsic susceptibility of human colon cancer cells to 5-fluorouracil (5-FU). Fluorouracil 163-177 prominin 1 Homo sapiens 68-73 24339132-10 2014 The CD133+ subpopulation percentage or its value normalized against CD133 protein level was only linked to intrinsic susceptibility of human colon cancer cells to 5-fluorouracil (5-FU). Fluorouracil 179-183 prominin 1 Homo sapiens 4-9 24339132-10 2014 The CD133+ subpopulation percentage or its value normalized against CD133 protein level was only linked to intrinsic susceptibility of human colon cancer cells to 5-fluorouracil (5-FU). Fluorouracil 179-183 prominin 1 Homo sapiens 68-73 24396484-3 2014 The present study revealed that the expression levels of the three antitumor miRNAs, miR-122a, miR-145 and miR-205, were significantly elevated in MDA-MB-453 LAR-type TNBC tumor cells treated with 5-fluorouracil together with ixabepilone. Fluorouracil 197-211 microRNA 205 Homo sapiens 107-114 22545049-2 2012 In the anabolic pathway of 5-FU, the first step in activation of the drug is phosphorylation of 5-FU by orotate phosphoribosyltransferase (OPRT), which directly metabolizes 5-FU to 5-fluorouridine monophosphate (FUMP) in the presence of 5-phosphoribosyl-1-pyrophosphate. Fluorouracil 27-31 uridine monophosphate synthetase Homo sapiens 104-137 22545049-2 2012 In the anabolic pathway of 5-FU, the first step in activation of the drug is phosphorylation of 5-FU by orotate phosphoribosyltransferase (OPRT), which directly metabolizes 5-FU to 5-fluorouridine monophosphate (FUMP) in the presence of 5-phosphoribosyl-1-pyrophosphate. Fluorouracil 27-31 uridine monophosphate synthetase Homo sapiens 139-143 22545049-2 2012 In the anabolic pathway of 5-FU, the first step in activation of the drug is phosphorylation of 5-FU by orotate phosphoribosyltransferase (OPRT), which directly metabolizes 5-FU to 5-fluorouridine monophosphate (FUMP) in the presence of 5-phosphoribosyl-1-pyrophosphate. Fluorouracil 96-100 uridine monophosphate synthetase Homo sapiens 104-137 22545049-2 2012 In the anabolic pathway of 5-FU, the first step in activation of the drug is phosphorylation of 5-FU by orotate phosphoribosyltransferase (OPRT), which directly metabolizes 5-FU to 5-fluorouridine monophosphate (FUMP) in the presence of 5-phosphoribosyl-1-pyrophosphate. Fluorouracil 96-100 uridine monophosphate synthetase Homo sapiens 139-143 22545049-2 2012 In the anabolic pathway of 5-FU, the first step in activation of the drug is phosphorylation of 5-FU by orotate phosphoribosyltransferase (OPRT), which directly metabolizes 5-FU to 5-fluorouridine monophosphate (FUMP) in the presence of 5-phosphoribosyl-1-pyrophosphate. Fluorouracil 96-100 uridine monophosphate synthetase Homo sapiens 104-137 22545049-2 2012 In the anabolic pathway of 5-FU, the first step in activation of the drug is phosphorylation of 5-FU by orotate phosphoribosyltransferase (OPRT), which directly metabolizes 5-FU to 5-fluorouridine monophosphate (FUMP) in the presence of 5-phosphoribosyl-1-pyrophosphate. Fluorouracil 96-100 uridine monophosphate synthetase Homo sapiens 139-143 22545049-3 2012 To date, OPRT expression in the tumors has been related to the clinical response or survival of cancer patients receiving 5-FU-based chemotherapy. Fluorouracil 122-126 uridine monophosphate synthetase Homo sapiens 9-13 22545049-4 2012 In this study, we examined whether OPRT expression correlates with the chemosensitivity to 5-FU and cell proliferation in HNSCC. Fluorouracil 91-95 uridine monophosphate synthetase Homo sapiens 35-39 22545049-7 2012 OPRT transfection increases the cytotoxicity of 5-FU without affecting cell proliferation of HNSCC cells in vitro. Fluorouracil 48-52 uridine monophosphate synthetase Homo sapiens 0-4 22545049-8 2012 These results indicate that OPRT expression plays an important role in the sensitivity of HNSCC to 5-FU chemotherapy. Fluorouracil 99-103 uridine monophosphate synthetase Homo sapiens 28-32 21910008-9 2011 Treating cells with PP2 and 5-FU resulted in reduced interaction of Par-4 with Akt1 and with the scaffolding protein 14-3-3sigma, and mobilization of Par-4 to the nucleus. Fluorouracil 28-32 stratifin Homo sapiens 117-128 21983179-3 2011 We recently reported overexpression of the Wnt transcription factor TCF4, also known as TCF7L2, in rectal cancers that were resistant to 5-fluorouracil-based chemoradiotherapy. Fluorouracil 137-151 transcription factor 7 like 2 Homo sapiens 88-94 21550686-11 2011 A positive expression of TS, DPD and OPRT might be an important factor in predicting the effectiveness of 5-FU based chemotherapy in this disease. Fluorouracil 106-110 thymidylate synthetase Homo sapiens 25-27 21550686-11 2011 A positive expression of TS, DPD and OPRT might be an important factor in predicting the effectiveness of 5-FU based chemotherapy in this disease. Fluorouracil 106-110 uridine monophosphate synthetase Homo sapiens 37-41 21903770-4 2011 Direct sequencing of the TP53 gene and Western blot analysis for the p53 protein after induction with 5-fluorouracil was conducted. Fluorouracil 102-116 transformation related protein 53 Mus musculus 69-72 22202337-1 2011 It has been reported that thymidylate synthase (TS), dihydropyrimidine dehydrogenase (DPD), thymidine phosphorylase (TP), and excision repair cross-complementing-1 (ERCC-1) were useful markers to predict the efficacy of anti cancer agents including 5-fluorouracil (5-FU) and oxaliplatin for unresectable advanced colorectal cancer. Fluorouracil 249-263 thymidylate synthetase Homo sapiens 26-46 24577774-1 2014 OBJECTIVE: To explore the relationship between CD133(+) subsets cells in human gastric cancer (GC) and molecules of drug resistance and their sensitivity to 5-FU. Fluorouracil 157-161 prominin 1 Homo sapiens 47-52 24577774-10 2014 CCK-8 detection showed that CD133(-) subgroup of MKN45 GC cell line was more sensitive than CD133(+) cells to 5-FU (P<0.05). Fluorouracil 110-114 prominin 1 Homo sapiens 28-33 24577774-10 2014 CCK-8 detection showed that CD133(-) subgroup of MKN45 GC cell line was more sensitive than CD133(+) cells to 5-FU (P<0.05). Fluorouracil 110-114 prominin 1 Homo sapiens 92-97 22202337-1 2011 It has been reported that thymidylate synthase (TS), dihydropyrimidine dehydrogenase (DPD), thymidine phosphorylase (TP), and excision repair cross-complementing-1 (ERCC-1) were useful markers to predict the efficacy of anti cancer agents including 5-fluorouracil (5-FU) and oxaliplatin for unresectable advanced colorectal cancer. Fluorouracil 249-263 ERCC excision repair 1, endonuclease non-catalytic subunit Homo sapiens 165-171 22202337-1 2011 It has been reported that thymidylate synthase (TS), dihydropyrimidine dehydrogenase (DPD), thymidine phosphorylase (TP), and excision repair cross-complementing-1 (ERCC-1) were useful markers to predict the efficacy of anti cancer agents including 5-fluorouracil (5-FU) and oxaliplatin for unresectable advanced colorectal cancer. Fluorouracil 265-269 thymidylate synthetase Homo sapiens 26-46 22202337-1 2011 It has been reported that thymidylate synthase (TS), dihydropyrimidine dehydrogenase (DPD), thymidine phosphorylase (TP), and excision repair cross-complementing-1 (ERCC-1) were useful markers to predict the efficacy of anti cancer agents including 5-fluorouracil (5-FU) and oxaliplatin for unresectable advanced colorectal cancer. Fluorouracil 265-269 ERCC excision repair 1, endonuclease non-catalytic subunit Homo sapiens 165-171 22202378-10 2011 There was negative findings of immunostaining with thymidylate synthetase (TS), which was target enzyme for 5-FU at a biopsy sample of the primary gastric tumor before chemotherapy of S-1. Fluorouracil 108-112 thymidylate synthetase Homo sapiens 51-73 22011696-5 2011 DISCUSSION: The drug interaction between warfarin and S-1 presumably leads to elevated PT-INR because the 5-fluorouracil (5-FU), which is metabolite of FT in S-1, inhibits the metabolic processing of S-warfarin by cytochrome P450 (CYP) 2C9. Fluorouracil 106-120 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 214-239 24007863-8 2014 Mechanistically, compared with 5-FU alone, the combination more noticeably downregulated EGFR phosphorylation and Akt phosphorylation as well as the expression of the apoptotic protector Bcl-xL and the cell cycle regulator cyclin D1. Fluorouracil 31-35 cyclin D1 Homo sapiens 223-232 23430338-6 2014 Expression of MAGE-A11 was significantly associated with a poorer response to treatment with DDP, 5-FU, docetaxel, and paclitaxel. Fluorouracil 98-102 MAGE family member A11 Homo sapiens 14-22 24705750-9 2014 Serum diamine oxidase activity in 5-FU+glutamine group were significantly superior to that in 5-FU group (p=0.028). Fluorouracil 34-38 amine oxidase, copper containing 1 Rattus norvegicus 6-21 22011696-5 2011 DISCUSSION: The drug interaction between warfarin and S-1 presumably leads to elevated PT-INR because the 5-fluorouracil (5-FU), which is metabolite of FT in S-1, inhibits the metabolic processing of S-warfarin by cytochrome P450 (CYP) 2C9. Fluorouracil 122-126 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 214-239 24270644-10 2014 Loss of DAP1 in colorectal cancer cells resulted in a gain in cellular migration and loss of their sensitivity of apoptosis to chemotherapeutic agent, 5-FU. Fluorouracil 151-155 death associated protein Homo sapiens 8-12 21952624-0 2011 Overexpression of cIAP2 contributes to 5-FU resistance and a poor prognosis in oral squamous cell carcinoma. Fluorouracil 39-43 baculoviral IAP repeat containing 3 Homo sapiens 18-23 24854104-2 2014 Therefore, we investigated whether the novel HDAC inhibitor OBP-801/YM753 could enhance the effects of 5-FU with radiation on esophageal squamous carcinoma KYSE170 cells. Fluorouracil 103-107 odorant binding protein 2A Homo sapiens 60-63 24854104-3 2014 The inhibition of the cell growth was significantly stronger with the combination of OBP-801/YM753 with 5-FU than with the 5-FU treatment only. Fluorouracil 104-108 odorant binding protein 2A Homo sapiens 85-88 24854104-5 2014 Western blot analysis showed that OBP-801/YM753 suppressed the expression of thymidylate synthase induced by 5-FU. Fluorouracil 109-113 odorant binding protein 2A Homo sapiens 34-37 24141111-8 2014 The tumor inhibitory effect was greater with the HB1.F3.CD.IFN-beta cells, indicating an additional effect of IFN-beta to 5-FU. Fluorouracil 122-126 interferon beta 1 Homo sapiens 59-67 21952624-3 2011 METHODS: We focussed on the cellular inhibitor of apoptosis protein 2 (cIAP2) on the basis of a DNA microarray data using parental and 5-FU-resistant OSCC cell lines. Fluorouracil 135-139 baculoviral IAP repeat containing 3 Homo sapiens 28-69 21952624-3 2011 METHODS: We focussed on the cellular inhibitor of apoptosis protein 2 (cIAP2) on the basis of a DNA microarray data using parental and 5-FU-resistant OSCC cell lines. Fluorouracil 135-139 baculoviral IAP repeat containing 3 Homo sapiens 71-76 21952624-4 2011 The effects of cIAP2 downregulation on 5-FU sensitivity and apoptosis were evaluated. Fluorouracil 39-43 baculoviral IAP repeat containing 3 Homo sapiens 15-20 21952624-5 2011 An immunohistochemical analysis of cIAP2 and related proteins, cIAP1 and X-linked IAP, was performed in 54 OSCC patients who were treated with 5-FU-based chemoradiotherapy and surgery. Fluorouracil 143-147 baculoviral IAP repeat containing 3 Homo sapiens 35-40 21952624-6 2011 RESULTS: The downregulation of cIAP2 significantly enhanced the sensitivity of the 5-FU-resistant cells to 5-FU, with a significant increase in apoptosis. Fluorouracil 83-87 baculoviral IAP repeat containing 3 Homo sapiens 31-36 21952624-6 2011 RESULTS: The downregulation of cIAP2 significantly enhanced the sensitivity of the 5-FU-resistant cells to 5-FU, with a significant increase in apoptosis. Fluorouracil 107-111 baculoviral IAP repeat containing 3 Homo sapiens 31-36 21952624-9 2011 CONCLUSION: These novel findings demonstrate that cIAP2 may represent a potentially useful therapeutic target for improving the treatment and survival of OSCC patients, particularly in the setting of 5-FU resistance. Fluorouracil 200-204 baculoviral IAP repeat containing 3 Homo sapiens 50-55 21811101-1 2011 The DNA replicative gene, thymidylate synthase (TYMS), is inhibited upon treatment with the anticancer drug 5-fluorouracil (5FU). Fluorouracil 108-122 thymidylate synthetase Homo sapiens 26-46 21811101-1 2011 The DNA replicative gene, thymidylate synthase (TYMS), is inhibited upon treatment with the anticancer drug 5-fluorouracil (5FU). Fluorouracil 108-122 thymidylate synthetase Homo sapiens 48-52 21811101-1 2011 The DNA replicative gene, thymidylate synthase (TYMS), is inhibited upon treatment with the anticancer drug 5-fluorouracil (5FU). Fluorouracil 124-127 thymidylate synthetase Homo sapiens 26-46 21811101-1 2011 The DNA replicative gene, thymidylate synthase (TYMS), is inhibited upon treatment with the anticancer drug 5-fluorouracil (5FU). Fluorouracil 124-127 thymidylate synthetase Homo sapiens 48-52 21807902-8 2011 Interestingly, treatment of cells with the ribosomal stress-inducing agent actinomycin D or 5-fluorouracil significantly decreased the c-myc mRNA levels in an L11- and Ago2-dependent manner. Fluorouracil 92-106 MYC proto-oncogene, bHLH transcription factor Homo sapiens 135-140 21868518-2 2011 The aim of this study was to evaluate the prognostic significance of molecular biomarkers including TS expression, after pulmonary metastasectomy followed by 5-fluorouracil-based adjuvant chemotherapy. Fluorouracil 158-172 thymidylate synthetase Homo sapiens 100-102 21868518-7 2011 CONCLUSION: Expression level of TS, OPRT, ERCC1, BRCA1 and MVD in resected colorectal lung metastases may play an important role for predicting outcome after 5-fluorouracil-based adjuvant therapy. Fluorouracil 158-172 thymidylate synthetase Homo sapiens 32-34 21868518-7 2011 CONCLUSION: Expression level of TS, OPRT, ERCC1, BRCA1 and MVD in resected colorectal lung metastases may play an important role for predicting outcome after 5-fluorouracil-based adjuvant therapy. Fluorouracil 158-172 uridine monophosphate synthetase Homo sapiens 36-40 21868518-7 2011 CONCLUSION: Expression level of TS, OPRT, ERCC1, BRCA1 and MVD in resected colorectal lung metastases may play an important role for predicting outcome after 5-fluorouracil-based adjuvant therapy. Fluorouracil 158-172 ERCC excision repair 1, endonuclease non-catalytic subunit Homo sapiens 42-47 21710497-7 2011 Finally, treatments with the UPRT-expressing Ad-FZ33 with antibodies against EpCAM or EGFR, followed by 5-FU administration, significantly suppressed the growth of biliary cancer xenografts in nude mice. Fluorouracil 104-108 uracil phosphoribosyltransferase Mus musculus 29-33 21570764-0 2011 PGE2 targets squamous cell carcinoma cell with the activated epidermal growth factor receptor family for survival against 5-fluorouracil through NR4A2 induction. Fluorouracil 122-136 epidermal growth factor receptor Mus musculus 61-93 21353513-2 2011 Furthermore, the gender-dependence of this effect and the possible involvement of combined effect of propolis and 5-Fluorouracil (5FU) on dihydropyrimidine dehydrogenase (DPD) transcriptional and translational level, were determined. Fluorouracil 114-128 dihydropyrimidine dehydrogenase Mus musculus 171-174 21353513-2 2011 Furthermore, the gender-dependence of this effect and the possible involvement of combined effect of propolis and 5-Fluorouracil (5FU) on dihydropyrimidine dehydrogenase (DPD) transcriptional and translational level, were determined. Fluorouracil 130-133 dihydropyrimidine dehydrogenase Mus musculus 138-169 21353513-2 2011 Furthermore, the gender-dependence of this effect and the possible involvement of combined effect of propolis and 5-Fluorouracil (5FU) on dihydropyrimidine dehydrogenase (DPD) transcriptional and translational level, were determined. Fluorouracil 130-133 dihydropyrimidine dehydrogenase Mus musculus 171-174 21035287-0 2011 Thymidylate synthase expression as a predictor of clinical response to 5-fluorouracil-based chemoradiotherapy in patients with maxillary sinus squamous cell carcinoma. Fluorouracil 71-85 thymidylate synthetase Homo sapiens 0-20 21471424-9 2011 CONCLUSIONS: Our results indicate that MTHFR activity and a specific combination of the MTHFR 1298A>C and TYMS 3"-UTR ins/del polymorphisms are possible predictors of 5-FU treatment-related toxicity. Fluorouracil 170-174 thymidylate synthetase Homo sapiens 109-113 21246413-6 2011 MiR-148a upregulation significantly increased sensitivity to chemotherapy in seven out of ten cell lines, represented by a decrease in cell viability of 22.6 +- 7.9% to 50.5 +- 10.6% after cisplatin (p <= 0.014) and 6.0 +- 0.8% to 15.0 +- 4.1% after 5-FU treatment (p <= 0.012). Fluorouracil 253-257 microRNA 148a Homo sapiens 0-8 21190322-1 2011 The prodrug 5-fluorouracil (5-FU), after activation into 5-F-dUMP, is an extensively used anticancer agent that inhibits thymidylate synthase and leads to increases in dUTP and 5-F-dUTP levels in cells. Fluorouracil 12-26 thymidylate synthetase Homo sapiens 121-141 21190322-1 2011 The prodrug 5-fluorouracil (5-FU), after activation into 5-F-dUMP, is an extensively used anticancer agent that inhibits thymidylate synthase and leads to increases in dUTP and 5-F-dUTP levels in cells. Fluorouracil 28-32 thymidylate synthetase Homo sapiens 121-141 20811948-0 2011 Tyrosine kinase inhibitor PTK/ZK enhances the antitumor effects of interferon-alpha/5-fluorouracil therapy for hepatocellular carcinoma cells. Fluorouracil 84-98 protein tyrosine kinase 2 beta Homo sapiens 26-32 20811948-6 2011 PTK/ZK enhanced the IFN/5-FU induced apoptosis, based on increased proteins levels of Bax and reduced Bcl-xL and Bcl-2. Fluorouracil 24-28 protein tyrosine kinase 2 beta Homo sapiens 0-6 21082354-5 2011 We also found that ectopic expression of survivin or treatment with IGF-1 inhibits the release of Smac/DIABLO and caspases activation after 5-Fu treatment. Fluorouracil 140-144 diablo IAP-binding mitochondrial protein Homo sapiens 98-102 21082354-5 2011 We also found that ectopic expression of survivin or treatment with IGF-1 inhibits the release of Smac/DIABLO and caspases activation after 5-Fu treatment. Fluorouracil 140-144 diablo IAP-binding mitochondrial protein Homo sapiens 103-109 21082354-6 2011 Our results strongly suggest that IGF-1 inhibits 5-Fu induced apoptosis through increasing survivin levels, which prevents Smac/DIABLO release and blocks the activation of caspases. Fluorouracil 49-53 diablo IAP-binding mitochondrial protein Homo sapiens 123-127 21082354-6 2011 Our results strongly suggest that IGF-1 inhibits 5-Fu induced apoptosis through increasing survivin levels, which prevents Smac/DIABLO release and blocks the activation of caspases. Fluorouracil 49-53 diablo IAP-binding mitochondrial protein Homo sapiens 128-134 20500514-7 2010 COLM-5 cells showed expression pattern of 5-FU metabolizing enzymes such as high dihydropyrimidine dehydrogenase (DPD) and low thymidylate synthase (TS)/orotate phosphoribosyltransferase (OPRT) both in vitro and in vivo. Fluorouracil 42-46 thymidylate synthetase Homo sapiens 127-147 20500514-7 2010 COLM-5 cells showed expression pattern of 5-FU metabolizing enzymes such as high dihydropyrimidine dehydrogenase (DPD) and low thymidylate synthase (TS)/orotate phosphoribosyltransferase (OPRT) both in vitro and in vivo. Fluorouracil 42-46 uridine monophosphate synthetase Homo sapiens 153-186 20500514-7 2010 COLM-5 cells showed expression pattern of 5-FU metabolizing enzymes such as high dihydropyrimidine dehydrogenase (DPD) and low thymidylate synthase (TS)/orotate phosphoribosyltransferase (OPRT) both in vitro and in vivo. Fluorouracil 42-46 uridine monophosphate synthetase Homo sapiens 188-192 20630104-12 2010 The potentiation of the inhibitory effect of 5-FU by CQ was dependent on the increase of p21Cip1 and p27Kip1 and the decrease of CDK2. Fluorouracil 45-49 cyclin dependent kinase inhibitor 1B Homo sapiens 101-108 20623626-6 2010 A test of drug resistance in MCF-7-Chk cells revealed that these cells had an increased resistance to 5-fluorouracil and higher expression of thymidylate synthase compared to control MCF-7 cells. Fluorouracil 102-116 choline kinase alpha Homo sapiens 35-38 21029695-0 2010 [Association between genetic polymorphisms of ERCC1, XRCC1, GSTP1 and survival of advanced gastric cancer patients treated with oxaliplatin/5-Fu-based chemotherapy]. Fluorouracil 140-144 ERCC excision repair 1, endonuclease non-catalytic subunit Homo sapiens 46-51 21029695-0 2010 [Association between genetic polymorphisms of ERCC1, XRCC1, GSTP1 and survival of advanced gastric cancer patients treated with oxaliplatin/5-Fu-based chemotherapy]. Fluorouracil 140-144 glutathione S-transferase pi 1 Homo sapiens 60-65 21029695-10 2010 CONCLUSION: Genetic polymorphisms of ERCC1-118, XRCC1-399 and GSTP1-105 are associated with TTP and OS of advanced gastric cancer patients treated with oxaliplatin/5-Fu-based combination chemotherapy as the first-line chemotherapy. Fluorouracil 164-168 ERCC excision repair 1, endonuclease non-catalytic subunit Homo sapiens 37-42 21029695-10 2010 CONCLUSION: Genetic polymorphisms of ERCC1-118, XRCC1-399 and GSTP1-105 are associated with TTP and OS of advanced gastric cancer patients treated with oxaliplatin/5-Fu-based combination chemotherapy as the first-line chemotherapy. Fluorouracil 164-168 glutathione S-transferase pi 1 Homo sapiens 62-67 20384633-6 2010 Both the mRNA and protein expression levels of thymidylate synthase (TS), dihydropyrimidine dehydrogenase (DPD), and orotate phosphoribosyltransferase (OPRT), which are associated with 5-FU sensitivity/response, were analyzed in the cells undergoing treatment. Fluorouracil 185-189 thymidylate synthetase Homo sapiens 47-67 20384633-6 2010 Both the mRNA and protein expression levels of thymidylate synthase (TS), dihydropyrimidine dehydrogenase (DPD), and orotate phosphoribosyltransferase (OPRT), which are associated with 5-FU sensitivity/response, were analyzed in the cells undergoing treatment. Fluorouracil 185-189 uridine monophosphate synthetase Homo sapiens 117-150 20384633-6 2010 Both the mRNA and protein expression levels of thymidylate synthase (TS), dihydropyrimidine dehydrogenase (DPD), and orotate phosphoribosyltransferase (OPRT), which are associated with 5-FU sensitivity/response, were analyzed in the cells undergoing treatment. Fluorouracil 185-189 uridine monophosphate synthetase Homo sapiens 152-156 20384633-7 2010 5-Fluorouracil-resistant lung cancer cells displayed high expression of TS mRNA and protein. Fluorouracil 0-14 thymidylate synthetase Homo sapiens 72-74 20384633-10 2010 We conclude that combination therapy with SAHA and S-1 in lung cancer may be promising due to its potential to overcome S-1 resistance via modulation of 5-FU/S-1 sensitivity-associated biomarker (TS) by HDAC inhibitor. Fluorouracil 153-157 thymidylate synthetase Homo sapiens 196-198 20567103-1 2010 Thymidylate synthase(TS), dihydropyrimidine dehydrogenase(DPD), and orotate phosphoribosyl transferase(OPRT)are initial key enzymes in the 5-fluorouracil(5-FU)metabolic pathway. Fluorouracil 139-153 thymidylate synthetase Homo sapiens 0-20 20567103-1 2010 Thymidylate synthase(TS), dihydropyrimidine dehydrogenase(DPD), and orotate phosphoribosyl transferase(OPRT)are initial key enzymes in the 5-fluorouracil(5-FU)metabolic pathway. Fluorouracil 139-153 uridine monophosphate synthetase Homo sapiens 103-107 20567103-1 2010 Thymidylate synthase(TS), dihydropyrimidine dehydrogenase(DPD), and orotate phosphoribosyl transferase(OPRT)are initial key enzymes in the 5-fluorouracil(5-FU)metabolic pathway. Fluorouracil 154-158 thymidylate synthetase Homo sapiens 0-20 20567103-1 2010 Thymidylate synthase(TS), dihydropyrimidine dehydrogenase(DPD), and orotate phosphoribosyl transferase(OPRT)are initial key enzymes in the 5-fluorouracil(5-FU)metabolic pathway. Fluorouracil 154-158 uridine monophosphate synthetase Homo sapiens 103-107 19830689-10 2010 Furthermore, SPARC overexpression was found to reduce HCC cell viability in response to 5-FU-based chemotherapy in vitro, partially through induction of apoptosis. Fluorouracil 88-92 secreted protein acidic and cysteine rich Homo sapiens 13-18 20514304-0 2010 Genetic polymorphism of GSTP1: prediction of clinical outcome to oxaliplatin/5-FU-based chemotherapy in advanced gastric cancer. Fluorouracil 77-81 glutathione S-transferase pi 1 Homo sapiens 24-29 20514304-1 2010 The aim of this study was to evaluate the predictive value of the polymorphism Glutathione S-transferase P1 (GSTP1) Ile(105)Val on oxaliplatin/5-FU-based chemotherapy in advanced gastric cancer. Fluorouracil 143-147 glutathione S-transferase pi 1 Homo sapiens 79-107 20514304-1 2010 The aim of this study was to evaluate the predictive value of the polymorphism Glutathione S-transferase P1 (GSTP1) Ile(105)Val on oxaliplatin/5-FU-based chemotherapy in advanced gastric cancer. Fluorouracil 143-147 glutathione S-transferase pi 1 Homo sapiens 109-114 19727732-10 2010 Further, RNAi studies demonstrated that both SSAT and SMO play a significant role in the response of MDA-MB-231 cells to treatment with BENSpm and 5-FU or paclitaxel. Fluorouracil 147-151 smoothened, frizzled class receptor Homo sapiens 54-57 20372793-0 2010 The role of thymidine phosphorylase in the induction of early growth response protein-1 and thrombospondin-1 by 5-fluorouracil in human cancer carcinoma cells. Fluorouracil 112-126 early growth response 1 Homo sapiens 56-87 20372793-6 2010 5-Formyl-tetrahydrofolate (leucovorin; LV) stabilized the complex of thymidylate synthase (TS) and 5-fluoro-deoxyuridine-monophosphate (FdUMP), increased the sensitivity to 5-FU of TP expressing AZ521 cells, but not of the parental cells. Fluorouracil 173-177 thymidylate synthetase Homo sapiens 69-89 20372793-8 2010 5-FU increased the expression of early growth response protein-1 (Egr-1) and an angiogenesis inhibitor, thrombospondin-1 (TSP-1), in KB/TP cells but only slightly in KB/CV cells, if any. Fluorouracil 0-4 early growth response 1 Homo sapiens 33-64 20372793-8 2010 5-FU increased the expression of early growth response protein-1 (Egr-1) and an angiogenesis inhibitor, thrombospondin-1 (TSP-1), in KB/TP cells but only slightly in KB/CV cells, if any. Fluorouracil 0-4 early growth response 1 Homo sapiens 66-71 20819423-0 2010 Variants in the dihydropyrimidine dehydrogenase, methylenetetrahydrofolate reductase and thymidylate synthase genes predict early toxicity of 5-fluorouracil in colorectal cancer patients. Fluorouracil 142-156 thymidylate synthetase Homo sapiens 89-109 20819423-1 2010 Adverse drug reactions to 5-fluorouracil (5-FU)-based chemotherapy have been reported to be due, in part, to genetic variants of the genes for the drug-related enzymes thymidylate synthase (TS; TYMS gene), methylenetetrahydrofolate reductase (MTHFR gene) and dihydropyrimidine dehydrogenase (DPD; DPYD gene). Fluorouracil 26-40 thymidylate synthetase Homo sapiens 168-188 20819423-1 2010 Adverse drug reactions to 5-fluorouracil (5-FU)-based chemotherapy have been reported to be due, in part, to genetic variants of the genes for the drug-related enzymes thymidylate synthase (TS; TYMS gene), methylenetetrahydrofolate reductase (MTHFR gene) and dihydropyrimidine dehydrogenase (DPD; DPYD gene). Fluorouracil 26-40 thymidylate synthetase Homo sapiens 190-192 20819423-1 2010 Adverse drug reactions to 5-fluorouracil (5-FU)-based chemotherapy have been reported to be due, in part, to genetic variants of the genes for the drug-related enzymes thymidylate synthase (TS; TYMS gene), methylenetetrahydrofolate reductase (MTHFR gene) and dihydropyrimidine dehydrogenase (DPD; DPYD gene). Fluorouracil 26-40 thymidylate synthetase Homo sapiens 194-198 20819423-1 2010 Adverse drug reactions to 5-fluorouracil (5-FU)-based chemotherapy have been reported to be due, in part, to genetic variants of the genes for the drug-related enzymes thymidylate synthase (TS; TYMS gene), methylenetetrahydrofolate reductase (MTHFR gene) and dihydropyrimidine dehydrogenase (DPD; DPYD gene). Fluorouracil 42-46 thymidylate synthetase Homo sapiens 168-188 20819423-1 2010 Adverse drug reactions to 5-fluorouracil (5-FU)-based chemotherapy have been reported to be due, in part, to genetic variants of the genes for the drug-related enzymes thymidylate synthase (TS; TYMS gene), methylenetetrahydrofolate reductase (MTHFR gene) and dihydropyrimidine dehydrogenase (DPD; DPYD gene). Fluorouracil 42-46 thymidylate synthetase Homo sapiens 190-192 20819423-1 2010 Adverse drug reactions to 5-fluorouracil (5-FU)-based chemotherapy have been reported to be due, in part, to genetic variants of the genes for the drug-related enzymes thymidylate synthase (TS; TYMS gene), methylenetetrahydrofolate reductase (MTHFR gene) and dihydropyrimidine dehydrogenase (DPD; DPYD gene). Fluorouracil 42-46 thymidylate synthetase Homo sapiens 194-198 20530421-6 2010 A metabolite of 5-FU irreversibly binds thymidylate synthase (TS) thus inhibiting its activity. Fluorouracil 16-20 thymidylate synthetase Homo sapiens 40-60 23787902-8 2013 Ectopic expression of DACH1 enhanced chemosensitivity to 5-fluorouracil (5-FU) by inducing p21 expression in HCC cells. Fluorouracil 57-71 dachshund family transcription factor 1 Homo sapiens 22-27 23787902-8 2013 Ectopic expression of DACH1 enhanced chemosensitivity to 5-fluorouracil (5-FU) by inducing p21 expression in HCC cells. Fluorouracil 57-71 H3 histone pseudogene 16 Homo sapiens 91-94 23787902-8 2013 Ectopic expression of DACH1 enhanced chemosensitivity to 5-fluorouracil (5-FU) by inducing p21 expression in HCC cells. Fluorouracil 73-77 dachshund family transcription factor 1 Homo sapiens 22-27 20530422-0 2010 Arsenic trioxide suppresses thymidylate synthase in 5-FU-resistant colorectal cancer cell line HT29 In Vitro re-sensitizing cells to 5-FU. Fluorouracil 52-56 thymidylate synthetase Homo sapiens 28-48 23787902-8 2013 Ectopic expression of DACH1 enhanced chemosensitivity to 5-fluorouracil (5-FU) by inducing p21 expression in HCC cells. Fluorouracil 73-77 H3 histone pseudogene 16 Homo sapiens 91-94 20530432-2 2010 MATERIALS AND METHODS: We evaluated the influence of hepatocyte growth factor, vascular endothelial growth factor and epidermal growth factor on the effect of 5-fluorouracil, oxaliplatin and SN-38 (the active metabolite of irinotecan) on WiDr cells. Fluorouracil 159-173 epidermal growth factor Homo sapiens 118-141 20056608-0 2010 Arabidopsis uracil DNA glycosylase (UNG) is required for base excision repair of uracil and increases plant sensitivity to 5-fluorouracil. Fluorouracil 123-137 uracil-DNA glycosylase Arabidopsis thaliana 12-34 23787902-10 2013 Down-regulation of DACH1 is a novel mechanism for gaining resistance to the antiproliferative signaling of TGF-beta1 and 5-FU resistance. Fluorouracil 121-125 dachshund family transcription factor 1 Homo sapiens 19-24 24394004-1 2013 Microsatellite instability( MSI) in colorectal carcinoma is reportedly associated with resistance to 5-fluorouracil-based chemotherapy. Fluorouracil 101-115 RB binding protein 4, chromatin remodeling factor Homo sapiens 28-31 20515563-9 2010 A larger case series investigating the role of TS gene polymorphisms as predictors of sensitivity to 5-fluorouracil-based chemotherapy is required. Fluorouracil 101-115 thymidylate synthetase Homo sapiens 47-49 24394041-12 2013 Here, we report a rare case of esophageal carcinoma, which was curatively resected after complete response was achieved following treatment with 5-FU/CDDP as NAC. Fluorouracil 145-149 synuclein alpha Homo sapiens 158-161 20012317-0 2010 Expression of thymidylate synthase determines the response of gastric cancer patients undergoing gastrectomy to 5-fluorouracil-based adjuvant chemotherapy. Fluorouracil 112-126 thymidylate synthetase Homo sapiens 14-34 20012317-1 2010 PURPOSE: We investigated whether the intensity of thymidylate synthase (TS) staining in tissue samples obtained from gastric cancer (GC) patients undergoing gastrectomy could predict response to 5-FU-based adjuvant chemotherapy after gastrectomy. Fluorouracil 195-199 thymidylate synthetase Homo sapiens 50-70 20012317-1 2010 PURPOSE: We investigated whether the intensity of thymidylate synthase (TS) staining in tissue samples obtained from gastric cancer (GC) patients undergoing gastrectomy could predict response to 5-FU-based adjuvant chemotherapy after gastrectomy. Fluorouracil 195-199 thymidylate synthetase Homo sapiens 72-74 20012317-6 2010 However, multivariate forward stepwise logistic regression analysis revealed that low TS expression was independently associated with females and responders to 5-FU-based adjuvant chemotherapy. Fluorouracil 160-164 thymidylate synthetase Homo sapiens 86-88 24192114-0 2013 Role of cyclin polymorphisms in predicting outcome of 5-fluorouracil-based chemotherapy in colorectal cancer: one piece in a complex puzzle. Fluorouracil 54-68 proliferating cell nuclear antigen Homo sapiens 8-14 20012317-9 2010 CONCLUSIONS: Low TS expression is significantly associated with female GC patients and responders to 5-FU-based adjuvant chemotherapy. Fluorouracil 101-105 thymidylate synthetase Homo sapiens 17-19 20012317-11 2010 The results suggest that prospective assessment of TS staining intensity in tissue samples obtained from GC patients undergoing gastrectomy would be useful to predict the patients who would be benefited from 5-FU-based adjuvant chemotherapy after gastrectomy. Fluorouracil 208-212 thymidylate synthetase Homo sapiens 51-53 20081809-5 2010 Multivariate analysis revealed that positive expression for CD133 and Oct-4 was associated with significantly worse survival in patients treated by surgery alone (P=0.023 and P<0.001, respectively) and in patients treated with 5-fluorouracil-based chemotherapy (P=0.001 and P=0.021, respectively). Fluorouracil 230-244 POU class 5 homeobox 1 Homo sapiens 70-75 20572591-2 2010 In the present study we investigated the role of the second mitochondria-derived activator of caspase (Smac/DIABLO) in the action of cisplatin (DDP), 5-fluorouracil (5-FU), and the combination of both in Hep-2 cells. Fluorouracil 150-164 diablo IAP-binding mitochondrial protein Homo sapiens 53-101 20572591-2 2010 In the present study we investigated the role of the second mitochondria-derived activator of caspase (Smac/DIABLO) in the action of cisplatin (DDP), 5-fluorouracil (5-FU), and the combination of both in Hep-2 cells. Fluorouracil 150-164 diablo IAP-binding mitochondrial protein Homo sapiens 103-107 20572591-2 2010 In the present study we investigated the role of the second mitochondria-derived activator of caspase (Smac/DIABLO) in the action of cisplatin (DDP), 5-fluorouracil (5-FU), and the combination of both in Hep-2 cells. Fluorouracil 150-164 diablo IAP-binding mitochondrial protein Homo sapiens 108-114 20572591-2 2010 In the present study we investigated the role of the second mitochondria-derived activator of caspase (Smac/DIABLO) in the action of cisplatin (DDP), 5-fluorouracil (5-FU), and the combination of both in Hep-2 cells. Fluorouracil 166-170 diablo IAP-binding mitochondrial protein Homo sapiens 53-101 20572591-2 2010 In the present study we investigated the role of the second mitochondria-derived activator of caspase (Smac/DIABLO) in the action of cisplatin (DDP), 5-fluorouracil (5-FU), and the combination of both in Hep-2 cells. Fluorouracil 166-170 diablo IAP-binding mitochondrial protein Homo sapiens 103-107 20572591-2 2010 In the present study we investigated the role of the second mitochondria-derived activator of caspase (Smac/DIABLO) in the action of cisplatin (DDP), 5-fluorouracil (5-FU), and the combination of both in Hep-2 cells. Fluorouracil 166-170 diablo IAP-binding mitochondrial protein Homo sapiens 108-114 19621385-12 2010 The combination of Ki23057 and 5-FU decreased DPD expression and increased apoptosis rates and p21 expression level of SGC cells. Fluorouracil 31-35 H3 histone pseudogene 16 Homo sapiens 95-98 20725619-0 2010 Analysis of the thymidylate synthase gene structure in colorectal cancer patients and its possible relation with the 5-Fluorouracil drug response. Fluorouracil 117-131 thymidylate synthetase Homo sapiens 16-36 24045662-0 2013 gamma-Glutamyl hydrolase modulation and folate influence chemosensitivity of cancer cells to 5-fluorouracil and methotrexate. Fluorouracil 93-107 gamma-glutamyl hydrolase Homo sapiens 0-24 23553437-6 2013 We show that specific blocking of IL-4 and IL-13-mediated STAT6 activation by either an IL-4-binding fusion protein APG598 or an IL-4R antagonist APG201 (R121D/Y124D) renders HL cells more prone to apoptotic killing by chemotherapeutic drugs such as Mitomycin C, 5-Fluorouracil, Etopside, Doxorubicin and Paclitaxel. Fluorouracil 263-277 signal transducer and activator of transcription 6 Homo sapiens 58-63 24228095-11 2013 The expression of Bax and Caspase-3 were dramatically increased after 5-FU treatment (p<0.01) and Curcumin treatment significantly reduced Bax expression (p<0.05) but had only a moderate effect on reducing caspase-3 expression (p>0.05). Fluorouracil 70-74 BCL2 associated X, apoptosis regulator Rattus norvegicus 18-21 24124444-6 2013 Our results suggest that CPA1, CPA2, and HMS1 confer 5-FU resistance by stimulating pyrimidine biosynthesis. Fluorouracil 53-57 carbamoyl-phosphate synthase (glutamine-hydrolyzing) CPA1 Saccharomyces cerevisiae S288C 25-29 24124444-6 2013 Our results suggest that CPA1, CPA2, and HMS1 confer 5-FU resistance by stimulating pyrimidine biosynthesis. Fluorouracil 53-57 carbamoyl-phosphate synthase (glutamine-hydrolyzing) CPA2 Saccharomyces cerevisiae S288C 31-35 20725619-1 2010 Thymidylate synthase (TS) catalyzes methylation of dUMP to dTMP and it is the target for the 5-Fluorouracil (5-FU) activity. Fluorouracil 93-107 thymidylate synthetase Homo sapiens 0-20 20725619-1 2010 Thymidylate synthase (TS) catalyzes methylation of dUMP to dTMP and it is the target for the 5-Fluorouracil (5-FU) activity. Fluorouracil 109-113 thymidylate synthetase Homo sapiens 0-20 19712668-6 2010 The results revealed an important role of BER, since BER-mutants (ntg1, ntg2, apn1, apn2) showed pronounced sensitivity to both 5-FU and FdUMP. Fluorouracil 128-132 DNA-(apurinic or apyrimidinic site) lyase APN1 Saccharomyces cerevisiae S288C 78-82 19712668-6 2010 The results revealed an important role of BER, since BER-mutants (ntg1, ntg2, apn1, apn2) showed pronounced sensitivity to both 5-FU and FdUMP. Fluorouracil 128-132 DNA-(apurinic or apyrimidinic site) lyase APN2 Saccharomyces cerevisiae S288C 84-88 19712668-9 2010 Interestingly, deficiencies in HR (rad52) and PPR (rad6, rad18) were associated with increased sensitivity to 5-FU, but not to FdUMP. Fluorouracil 110-114 recombinase RAD52 Saccharomyces cerevisiae S288C 35-40 19712668-9 2010 Interestingly, deficiencies in HR (rad52) and PPR (rad6, rad18) were associated with increased sensitivity to 5-FU, but not to FdUMP. Fluorouracil 110-114 E2 ubiquitin-conjugating protein RAD6 Saccharomyces cerevisiae S288C 51-55 19455332-9 2010 Estrogen depletion down-regulated the level of expression of one of the molecules related to 5-FU resistance, thymidylate synthase, as observed with 4-OH-TAM in our previous study. Fluorouracil 93-97 thymidylate synthetase Homo sapiens 110-130 20571234-0 2010 Thymidylate synthase gene polymorphisms effecting 5-FU response in breast cancer patients. Fluorouracil 50-54 thymidylate synthetase Homo sapiens 0-20 20571234-2 2010 The target enzyme for 5- Fluorouracil is thymidylate synthase (TYMS) this enzyme is also involved in folate metabolism. Fluorouracil 22-37 thymidylate synthetase Homo sapiens 41-61 20571234-2 2010 The target enzyme for 5- Fluorouracil is thymidylate synthase (TYMS) this enzyme is also involved in folate metabolism. Fluorouracil 22-37 thymidylate synthetase Homo sapiens 63-67 20407238-1 2010 BACKGROUND: Expression levels of thymidylate synthase (TS), dihydropyrimidine dehydrogenase (DPD), and orotate phosphoribosyltransferase (OPRT) have been reported to be associated with tumor response to 5-fluorouracil (5-FU). Fluorouracil 203-217 thymidylate synthetase Homo sapiens 33-53 20407238-1 2010 BACKGROUND: Expression levels of thymidylate synthase (TS), dihydropyrimidine dehydrogenase (DPD), and orotate phosphoribosyltransferase (OPRT) have been reported to be associated with tumor response to 5-fluorouracil (5-FU). Fluorouracil 203-217 uridine monophosphate synthetase Homo sapiens 103-136 20407238-1 2010 BACKGROUND: Expression levels of thymidylate synthase (TS), dihydropyrimidine dehydrogenase (DPD), and orotate phosphoribosyltransferase (OPRT) have been reported to be associated with tumor response to 5-fluorouracil (5-FU). Fluorouracil 203-217 uridine monophosphate synthetase Homo sapiens 138-142 20407238-1 2010 BACKGROUND: Expression levels of thymidylate synthase (TS), dihydropyrimidine dehydrogenase (DPD), and orotate phosphoribosyltransferase (OPRT) have been reported to be associated with tumor response to 5-fluorouracil (5-FU). Fluorouracil 219-223 thymidylate synthetase Homo sapiens 33-53 20407238-1 2010 BACKGROUND: Expression levels of thymidylate synthase (TS), dihydropyrimidine dehydrogenase (DPD), and orotate phosphoribosyltransferase (OPRT) have been reported to be associated with tumor response to 5-fluorouracil (5-FU). Fluorouracil 219-223 uridine monophosphate synthetase Homo sapiens 103-136 20407238-1 2010 BACKGROUND: Expression levels of thymidylate synthase (TS), dihydropyrimidine dehydrogenase (DPD), and orotate phosphoribosyltransferase (OPRT) have been reported to be associated with tumor response to 5-fluorouracil (5-FU). Fluorouracil 219-223 uridine monophosphate synthetase Homo sapiens 138-142 23801079-0 2013 Recombinant GnRH-p53 protein sensitizes breast cancer cells to 5-fluorouracil-induced apoptosis in vitro and in vivo. Fluorouracil 63-77 transformation related protein 53, pseudogene Mus musculus 17-20 20407238-8 2010 CONCLUSION: DPD and OPRT protein levels in CRC suggest that female gender and colonic tumors are positive prognostic factors in patients who receive chemotherapy with 5-FU. Fluorouracil 167-171 uridine monophosphate synthetase Homo sapiens 20-24 23801079-5 2013 Treatments of cells from breast cancer cell-lines MDA-MB-231, T47D, or SKBR-3 with GnRH-p53 in combination with 5-FU significantly enhanced p53-activated apoptosis signals, including PUMA expression, BAX translocation to mitochondria, and activated caspase-3. Fluorouracil 112-116 transformation related protein 53, pseudogene Mus musculus 140-143 23801079-7 2013 Systemic treatment of the tumor-bearing mice via tail vein injection of GnRH-p53 markedly augmented the anticancer efficacy of 5-FU. Fluorouracil 127-131 transformation related protein 53, pseudogene Mus musculus 77-80 20178687-4 2010 In this study, the poly(amidoamine) (PAMAM) dendrimer was employed as a carrier to co-deliver antisense-miR-21 oligonucleotide (as-miR-21) and 5-fluorouracil (5-FU) to achieve delivery of as-miR-21 to human glioblastoma cells and enhance the cytotoxicity of 5-FU antisense therapy. Fluorouracil 159-163 microRNA 21 Homo sapiens 104-110 23822562-8 2013 Extraction of Siamese Crocodile 3 (ESC-3) bile enhanced the drug sensitivity of QBC939/5-FU cells to 5-FU, paralleled with downregulation of beta-catenin and P-gp. Fluorouracil 87-91 catenin beta 1 Homo sapiens 141-153 20178687-4 2010 In this study, the poly(amidoamine) (PAMAM) dendrimer was employed as a carrier to co-deliver antisense-miR-21 oligonucleotide (as-miR-21) and 5-fluorouracil (5-FU) to achieve delivery of as-miR-21 to human glioblastoma cells and enhance the cytotoxicity of 5-FU antisense therapy. Fluorouracil 258-262 microRNA 21 Homo sapiens 104-110 20178687-8 2010 The co-delivery of as-miR-21 significantly improved the cytotoxicity of 5-FU and dramatically increased the apoptosis of U251 cells, while the migration ability of the tumor cells was decreased. Fluorouracil 72-76 microRNA 21 Homo sapiens 22-28 20047135-0 2009 Genetic polymorphisms of GSTP1 related to response to 5-FU-oxaliplatin-based chemotherapy and clinical outcome in advanced colorectal cancer patients. Fluorouracil 54-58 glutathione S-transferase pi 1 Homo sapiens 25-30 20047135-8 2009 CONCLUSION: The GSTP1 105Val/105Val genotype is associated with a higher clinical response rate to oxaliplatin-based chemotherapy and with increased survival of patients with advanced colo-rectal cancer, receiving 5-FU/oxaliplatin chemotherapy. Fluorouracil 214-218 glutathione S-transferase pi 1 Homo sapiens 16-21 20026854-7 2009 Fluorouracil use produced the following clearance rates: 90% for superficial BCC and 27% to 85% for SCC in situ. Fluorouracil 0-12 serpin family B member 3 Homo sapiens 100-103 20026854-10 2009 CONCLUSIONS: Evidence supports the use of topical imiquimod as monotherapy for superficial BCC and topical fluorouracil as monotherapy for superficial BCC and SCC in situ. Fluorouracil 107-119 serpin family B member 3 Homo sapiens 159-162 19760608-10 2009 Furthermore, restoration of KLK10 and OXGR1 expression reduced the ability of anchorage-independent growth, and sensitized HCC cells to doxorubicin- or 5-fluorouracil-induced cytotoxicity. Fluorouracil 152-166 oxoglutarate receptor 1 Homo sapiens 38-43 19694534-1 2009 Thymidylate synthase (TS) inhibitors, such as 5-fluorouracil (5-FU) and 5-fluorodeoxyuridine (5-FUdR), are amongst the most frequently used chemotherapeutic drugs available, although their efficacy is often limited by myelotoxicity. Fluorouracil 46-60 thymidylate synthetase Homo sapiens 0-20 19694534-1 2009 Thymidylate synthase (TS) inhibitors, such as 5-fluorouracil (5-FU) and 5-fluorodeoxyuridine (5-FUdR), are amongst the most frequently used chemotherapeutic drugs available, although their efficacy is often limited by myelotoxicity. Fluorouracil 46-60 thymidylate synthetase Homo sapiens 22-24 19694534-1 2009 Thymidylate synthase (TS) inhibitors, such as 5-fluorouracil (5-FU) and 5-fluorodeoxyuridine (5-FUdR), are amongst the most frequently used chemotherapeutic drugs available, although their efficacy is often limited by myelotoxicity. Fluorouracil 62-66 thymidylate synthetase Homo sapiens 0-20 19694534-1 2009 Thymidylate synthase (TS) inhibitors, such as 5-fluorouracil (5-FU) and 5-fluorodeoxyuridine (5-FUdR), are amongst the most frequently used chemotherapeutic drugs available, although their efficacy is often limited by myelotoxicity. Fluorouracil 62-66 thymidylate synthetase Homo sapiens 22-24 19765544-5 2009 In vitro experiments showed that minocycline suppressed the upregulation of PARP-1 activity in enterocyte IEC-6 cells treated with 5-FU. Fluorouracil 131-135 poly (ADP-ribose) polymerase 1 Rattus norvegicus 76-82 19793002-6 2009 The downregulation of cIAP2 efficiently enhances apoptosis through the activation of caspase 3/7 and 5-fluorouracil (5-FU) sensitivity in colorectal cancer cells exposed to 5-FU. Fluorouracil 101-115 baculoviral IAP repeat containing 3 Homo sapiens 22-27 19793002-6 2009 The downregulation of cIAP2 efficiently enhances apoptosis through the activation of caspase 3/7 and 5-fluorouracil (5-FU) sensitivity in colorectal cancer cells exposed to 5-FU. Fluorouracil 117-121 baculoviral IAP repeat containing 3 Homo sapiens 22-27 19793002-6 2009 The downregulation of cIAP2 efficiently enhances apoptosis through the activation of caspase 3/7 and 5-fluorouracil (5-FU) sensitivity in colorectal cancer cells exposed to 5-FU. Fluorouracil 173-177 baculoviral IAP repeat containing 3 Homo sapiens 22-27 19210287-3 2009 By using gene-deficient mice, we found that plasmin and its activators tPA and uPA play a role in the haematopoietic recovery upon delivery of the cytotoxic agent 5-fluoro-uracil (5-FU). Fluorouracil 163-178 proline-rich acidic protein 1 Mus musculus 79-82 19210287-3 2009 By using gene-deficient mice, we found that plasmin and its activators tPA and uPA play a role in the haematopoietic recovery upon delivery of the cytotoxic agent 5-fluoro-uracil (5-FU). Fluorouracil 180-184 proline-rich acidic protein 1 Mus musculus 79-82 19921578-10 2009 After intervention by 5-FU at IC(50), the expression of hnRNP K in Lovo decreased more as compared to SW480, while the expression of PDI in SW480 increased more as compared to Lovo. Fluorouracil 22-26 peptidyl arginine deiminase 1 Homo sapiens 133-136 19921578-11 2009 CONCLUSION: There are significant differences in expression of hnRNP K and PDI proteins between Lovo and SW480 cell lines, and the proteins alter regularly after 5-FU intervention. Fluorouracil 162-166 peptidyl arginine deiminase 1 Homo sapiens 75-78 19724848-10 2009 Western blot analysis revealed that treatment with 5-FU and CDHP suppressed expression of integrins alphav, alpha3, alpha6, beta1, beta3, beta4, beta5, and beta6. Fluorouracil 51-55 basic helix-loop-helix family, member e23 Mus musculus 138-143 19362768-7 2009 With the changes in caspase-6 and cell cycle, ZBP-89 greatly enhanced the killing effectiveness of 5-fluorouracil or staurosporine in HCC cells. Fluorouracil 99-113 caspase 6 Homo sapiens 20-29 19765320-0 2009 Transcriptional control of Flt3 ligand targeted by fluorouracil-induced Egr-1 promoter in hematopoietic damage. Fluorouracil 51-63 early growth response 1 Homo sapiens 72-77 19765320-5 2009 The goal of this study was to explore the effect of Flt3 Ligand gene transcription regulated by fluorouracil-induced Egr-1 promoter on hematopoietic recovery. Fluorouracil 96-108 early growth response 1 Homo sapiens 117-122 19684609-10 2009 Since distribution of PTEN in HCC tissues is significantly decreased compared with the paracancerous tissue, over-expression of PTEN by rosiglitazone enhances 5-FU-inhibited cell growth of HCC. Fluorouracil 159-163 phosphatase and tensin homolog Homo sapiens 128-132 19500106-3 2009 In the current study, we investigated the role of focal adhesion kinase (FAK) in 5-fluorouracil (5-FU) chemoresistance in colon carcinoma MCS culture cells. Fluorouracil 81-95 PTK2 protein tyrosine kinase 2 Mus musculus 50-71 19500106-3 2009 In the current study, we investigated the role of focal adhesion kinase (FAK) in 5-fluorouracil (5-FU) chemoresistance in colon carcinoma MCS culture cells. Fluorouracil 81-95 PTK2 protein tyrosine kinase 2 Mus musculus 73-76 19500106-3 2009 In the current study, we investigated the role of focal adhesion kinase (FAK) in 5-fluorouracil (5-FU) chemoresistance in colon carcinoma MCS culture cells. Fluorouracil 97-101 PTK2 protein tyrosine kinase 2 Mus musculus 50-71 19500106-3 2009 In the current study, we investigated the role of focal adhesion kinase (FAK) in 5-fluorouracil (5-FU) chemoresistance in colon carcinoma MCS culture cells. Fluorouracil 97-101 PTK2 protein tyrosine kinase 2 Mus musculus 73-76 19500106-6 2009 However, silencing of FAK combined with 5-FU treatment significantly decreased the 50% inhibitory concentration (IC(50)) of 5-FU and markedly increased the population of apoptosis cells, which was associated with the reduction of the levels of Akt and nuclear factor-kappa B (NF-kappaB). Fluorouracil 124-128 PTK2 protein tyrosine kinase 2 Mus musculus 22-25 19500106-7 2009 Moreover, knockdown of FAK could inhibit tumor growth and increase the sensitivity of the tumor to 5-FU in the nude mouse xenograft. Fluorouracil 99-103 PTK2 protein tyrosine kinase 2 Mus musculus 23-26 19500106-8 2009 These results indicate that while not affecting cellular proliferation in the absence of 5-FU, RNA interference targeting FAK potentiated 5-FU-induced cytotoxicity in vitro and in vivo, and partially reversed multicellular resistance, which may contribute to its chemosensitizing effect through efficiently suppressing Akt/NF-kappaB activity. Fluorouracil 138-142 PTK2 protein tyrosine kinase 2 Mus musculus 122-125 19723892-2 2009 A clear p53-dependent expression pattern of PDF was shown in a panel of colorectal cancer cell lines following acute exposure to oxaliplatin, 5-fluorouracil, and SN38. Fluorouracil 142-156 peptide deformylase, mitochondrial Homo sapiens 44-47 19622726-4 2009 In addition, AEG-1 enhances the expression of dihydropyrimidine dehydrogenase (DPYD) that catalyzes the initial and rate-limiting step in the catabolism of 5-FU. Fluorouracil 156-160 dihydropyrimidine dehydrogenase Mus musculus 46-77 19622726-4 2009 In addition, AEG-1 enhances the expression of dihydropyrimidine dehydrogenase (DPYD) that catalyzes the initial and rate-limiting step in the catabolism of 5-FU. Fluorouracil 156-160 dihydropyrimidine dehydrogenase Mus musculus 79-83 19622726-5 2009 siRNA-mediated inhibition of AEG-1, LSF, or DPYD significantly increased the sensitivity of HCC cells to 5-FU in vitro and a lentivirus delivering AEG-1 siRNA in combination with 5-FU markedly inhibited growth of HCC cells xenotransplanted in athymic nude mice when compared to either agent alone. Fluorouracil 105-109 dihydropyrimidine dehydrogenase Mus musculus 44-48 19698236-5 2009 It is concluded that cis-elements including T-Ag, PU.1, c-Ets, XPF-1, P2 alphaA, IL6-6RE and RAR may inhibit lrp16 expression and hormone or its inhibitor such as corticosteroid, tamoxifen, forskolin, phenylephrine, inflammatory factors such as IL6, IFNgamma and TNFalpha, and chemotherapeutics 5-fluorouracil may participate in the regulation of lrp16 gene expression in negative manner. Fluorouracil 295-309 retinoic acid receptor alpha Homo sapiens 93-96 24037930-7 2013 Field therapy for areas of severe actinic damage with photodynamic therapy, imiquimod, 5-fluorouracil, ingenol mebutate, or diclofenac sodium may theoretically decrease the risk of SCC through treatment of precancerous changes. Fluorouracil 87-101 serpin family B member 3 Homo sapiens 181-184 19432884-2 2009 We analyzed the influence of codon 751 Lys-->Gln polymorphism of XPD on its protein expression levels, clinico-pathological features, and outcome of 188 Chinese patients with metastatic colorectal carcinoma (CRC) that had been treated with first-line Oxaliplatin + Leucovorin + 5-Fluorouracil (FOLFOX-4) chemotherapy. Fluorouracil 281-295 ERCC excision repair 2, TFIIH core complex helicase subunit Homo sapiens 68-71 19595187-0 2009 [Effect of Fluorouracil-inducible GM-CSF gene therapy regulated by Egr-1 promoter on chemotherapeutic hematopoietic damage of tumor-bearing mice]. Fluorouracil 11-23 early growth response 1 Mus musculus 67-72 19595187-1 2009 OBJECTIVE: In order to explore the regulating effects of Egr-1 promoter sequences in transcriptional targeting by 5-fluorouracil (5-Fu) on the expression of hematopoietic growth factor genes. Fluorouracil 114-128 early growth response 1 Mus musculus 57-62 19595187-1 2009 OBJECTIVE: In order to explore the regulating effects of Egr-1 promoter sequences in transcriptional targeting by 5-fluorouracil (5-Fu) on the expression of hematopoietic growth factor genes. Fluorouracil 130-134 early growth response 1 Mus musculus 57-62 19302291-0 2009 Down-regulation of cIAP2 enhances 5-FU sensitivity through the apoptotic pathway in human colon cancer cells. Fluorouracil 34-38 baculoviral IAP repeat containing 3 Homo sapiens 19-24 19302291-5 2009 Next, the role of the cellular inhibitor of apoptosis 2 (cIAP2) gene, which was up-regulated in DLD-1/FU, was investigated for 5-FU resistance using RNA interference. Fluorouracil 127-131 baculoviral IAP repeat containing 3 Homo sapiens 22-55 19302291-5 2009 Next, the role of the cellular inhibitor of apoptosis 2 (cIAP2) gene, which was up-regulated in DLD-1/FU, was investigated for 5-FU resistance using RNA interference. Fluorouracil 127-131 baculoviral IAP repeat containing 3 Homo sapiens 57-62 19302291-6 2009 The down-regulation of cIAP2 efficiently enhanced 5-FU sensitivity, the activation of caspase 3/7 and apoptosis under exposure to 5-FU. Fluorouracil 50-54 baculoviral IAP repeat containing 3 Homo sapiens 23-28 19302291-6 2009 The down-regulation of cIAP2 efficiently enhanced 5-FU sensitivity, the activation of caspase 3/7 and apoptosis under exposure to 5-FU. Fluorouracil 130-134 baculoviral IAP repeat containing 3 Homo sapiens 23-28 19302291-7 2009 The immunohistochemistry of cIAP2 in cancer and corresponding normal tissues from colorectal cancer patients in stage III revealed that cIAP2 was more frequently expressed in cancer tissues than in normal tissues, and cIAP2-positive patients had a trend toward early recurrence after fluorouracil-based chemotherapy. Fluorouracil 284-296 baculoviral IAP repeat containing 3 Homo sapiens 136-141 19302291-7 2009 The immunohistochemistry of cIAP2 in cancer and corresponding normal tissues from colorectal cancer patients in stage III revealed that cIAP2 was more frequently expressed in cancer tissues than in normal tissues, and cIAP2-positive patients had a trend toward early recurrence after fluorouracil-based chemotherapy. Fluorouracil 284-296 baculoviral IAP repeat containing 3 Homo sapiens 136-141 19339911-0 2009 Association of thymidylate synthase variants with 5-fluorouracil cytotoxicity. Fluorouracil 50-64 thymidylate synthetase Homo sapiens 15-35 19339911-3 2009 One of the known targets of 5-fluorouracil (5-FU) treatment is thymidylate synthase (TYMS). Fluorouracil 28-42 thymidylate synthetase Homo sapiens 63-83 19339911-3 2009 One of the known targets of 5-fluorouracil (5-FU) treatment is thymidylate synthase (TYMS). Fluorouracil 28-42 thymidylate synthetase Homo sapiens 85-89 19339911-3 2009 One of the known targets of 5-fluorouracil (5-FU) treatment is thymidylate synthase (TYMS). Fluorouracil 44-48 thymidylate synthetase Homo sapiens 63-83 19339911-3 2009 One of the known targets of 5-fluorouracil (5-FU) treatment is thymidylate synthase (TYMS). Fluorouracil 44-48 thymidylate synthetase Homo sapiens 85-89 19339911-4 2009 We hypothesized that genetic variants in TYMS would alter cytotoxicity because of 5-FU treatment using a LCL model system. Fluorouracil 82-86 thymidylate synthetase Homo sapiens 41-45 19339911-9 2009 Two intronic SNPs in TYMS (rs2847153 and rs2853533) were significantly associated (P<0.01) with 5-FU cytotoxicity in the HapMap subset using the mixed models approach. Fluorouracil 99-103 thymidylate synthetase Homo sapiens 21-25 19339911-11 2009 These results highlight the importance of the TYMS gene variants in response to 5-FU treatment. Fluorouracil 80-84 thymidylate synthetase Homo sapiens 46-50 19426596-0 2009 [Effects of fluorouracil-induced Flt3 Ligand gene expression transcriptional regulated by Egr-1 promoter sequences]. Fluorouracil 12-24 early growth response 1 Homo sapiens 90-95 19426596-1 2009 AIM: To explore the regulatory effects of Egr-1 promoter sequences in transcriptional targeting by 5-fluorouracil(5-Fu) on the expression of hematopoietic growth factor genes. Fluorouracil 99-113 early growth response 1 Homo sapiens 42-47 19426596-1 2009 AIM: To explore the regulatory effects of Egr-1 promoter sequences in transcriptional targeting by 5-fluorouracil(5-Fu) on the expression of hematopoietic growth factor genes. Fluorouracil 114-118 early growth response 1 Homo sapiens 42-47 18704422-0 2009 The polymorphisms of TS and MTHFR predict survival of gastric cancer patients treated with fluorouracil-based adjuvant chemotherapy in Chinese population. Fluorouracil 91-103 thymidylate synthetase Homo sapiens 21-23 18704422-1 2009 PURPOSE: The aim of this study was to investigate the association of the thymidylate synthase (TS) and methylenetetrahydrofolate reductase (MTHFR) polymorphisms with the clinical outcomes of gastric cancer patients treated with 5-FU-based adjuvant chemotherapy. Fluorouracil 228-232 thymidylate synthetase Homo sapiens 73-93 18704422-8 2009 CONCLUSION: The polymorphisms of TS 3"-UTR ins6/del6 and MTHFR C677T appear to be potential prognostic factors in gastric cancer patients treated with 5-FU-based adjuvant chemotherapy, which may allow identification of gastric cancer patients who will benefit from 5-FU chemotherapy. Fluorouracil 151-155 thymidylate synthetase Homo sapiens 33-35 18704422-8 2009 CONCLUSION: The polymorphisms of TS 3"-UTR ins6/del6 and MTHFR C677T appear to be potential prognostic factors in gastric cancer patients treated with 5-FU-based adjuvant chemotherapy, which may allow identification of gastric cancer patients who will benefit from 5-FU chemotherapy. Fluorouracil 265-269 thymidylate synthetase Homo sapiens 33-35 19288006-1 2009 The enzymes thymidylate synthase (TS), dihydropyrimidine dehydrogenase (DPD) and orotate phosphoribosyl transferase (OPRT) are involved in the metabolism of the anticancer drug 5-fluorouracil (FU). Fluorouracil 177-191 thymidylate synthetase Homo sapiens 12-32 19288006-1 2009 The enzymes thymidylate synthase (TS), dihydropyrimidine dehydrogenase (DPD) and orotate phosphoribosyl transferase (OPRT) are involved in the metabolism of the anticancer drug 5-fluorouracil (FU). Fluorouracil 177-191 thymidylate synthetase Homo sapiens 34-36 19288006-1 2009 The enzymes thymidylate synthase (TS), dihydropyrimidine dehydrogenase (DPD) and orotate phosphoribosyl transferase (OPRT) are involved in the metabolism of the anticancer drug 5-fluorouracil (FU). Fluorouracil 177-191 uridine monophosphate synthetase Homo sapiens 81-115 19288006-1 2009 The enzymes thymidylate synthase (TS), dihydropyrimidine dehydrogenase (DPD) and orotate phosphoribosyl transferase (OPRT) are involved in the metabolism of the anticancer drug 5-fluorouracil (FU). Fluorouracil 177-191 uridine monophosphate synthetase Homo sapiens 117-121 19288006-2 2009 Expression of TS, DPD and OPRT in cancer tissue has been reported to be associated with sensitivity and/or resistance to 5-FU therapy. Fluorouracil 121-125 thymidylate synthetase Homo sapiens 14-16 19288006-2 2009 Expression of TS, DPD and OPRT in cancer tissue has been reported to be associated with sensitivity and/or resistance to 5-FU therapy. Fluorouracil 121-125 uridine monophosphate synthetase Homo sapiens 26-30 19374805-2 2009 TS is the target enzyme of 5-fluorouracil (5-FU) and involved in folate metabolism. Fluorouracil 27-41 thymidylate synthetase Homo sapiens 0-2 23842854-10 2013 In conclusion, the GSTP1 expression is a good predictor of prognosis, and it may be closely related to the chemotherapeutic efficacy of 5-FU plus cisplatin in ESCC patients. Fluorouracil 136-140 glutathione S-transferase pi 1 Homo sapiens 19-24 23444104-3 2013 We have previously reported on the efficacy of AxE1CAUP, an oncolytic adenovirus (OAd) expressing uracil phosphoribosyltransferase (UPRT), an enzyme that markedly enhanced the toxicity of 5-fluorouracil (5-FU), in immunodeficient, Ad-nonpermissive nude mice. Fluorouracil 188-202 uracil phosphoribosyltransferase Mus musculus 132-136 23444104-3 2013 We have previously reported on the efficacy of AxE1CAUP, an oncolytic adenovirus (OAd) expressing uracil phosphoribosyltransferase (UPRT), an enzyme that markedly enhanced the toxicity of 5-fluorouracil (5-FU), in immunodeficient, Ad-nonpermissive nude mice. Fluorouracil 204-208 uracil phosphoribosyltransferase Mus musculus 98-130 23444104-3 2013 We have previously reported on the efficacy of AxE1CAUP, an oncolytic adenovirus (OAd) expressing uracil phosphoribosyltransferase (UPRT), an enzyme that markedly enhanced the toxicity of 5-fluorouracil (5-FU), in immunodeficient, Ad-nonpermissive nude mice. Fluorouracil 204-208 uracil phosphoribosyltransferase Mus musculus 132-136 23941782-9 2013 C-myc expression was increased by all treatments involving Cd, especially 5-FU plus Cd at the half time of treatment. Fluorouracil 74-78 MYC proto-oncogene, bHLH transcription factor Homo sapiens 0-5 19374805-2 2009 TS is the target enzyme of 5-fluorouracil (5-FU) and involved in folate metabolism. Fluorouracil 43-47 thymidylate synthetase Homo sapiens 0-2 19374805-3 2009 TS gene polymorphisms play an important role in the efficiency of fluorouracil activity in vivo. Fluorouracil 66-78 thymidylate synthetase Homo sapiens 0-2 19374805-4 2009 This study investigated the allelic frequencies and distribution characters of single-nucleotide polymorphisms within the coding region (cSNPs) of TS gene in Chinese children with acute leukemia (AL) and normal control children in order to explore the possible relationship between the cSNP in human TS gene and chemotherapeutic effects of 5-fluorouracils. Fluorouracil 340-355 thymidylate synthetase Homo sapiens 147-149 18618519-0 2009 Calcium and calcium sensing receptor modulates the expression of thymidylate synthase, NAD(P)H:quinone oxidoreductase 1 and survivin in human colon carcinoma cells: promotion of cytotoxic response to mitomycin C and fluorouracil. Fluorouracil 216-228 thymidylate synthetase Homo sapiens 65-85 19194123-0 2009 Prognostic value of ERCC1, thymidylate synthase, and glutathione S-transferase pi for 5-FU/oxaliplatin chemotherapy in advanced colorectal cancer. Fluorouracil 86-90 ERCC excision repair 1, endonuclease non-catalytic subunit Homo sapiens 20-25 19194123-1 2009 BACKGROUND: The aim of this study was to determine whether the expression of the excision repair cross-complementing 1 (ERCC1), thymidylate synthase (TS) and glutathione S-transferase pi (GSTpi) predict clinical outcome in patients with advanced colorectal cancer treated with fluorouracil (5-FU)/oxaliplatin chemotherapy. Fluorouracil 277-289 ERCC excision repair 1, endonuclease non-catalytic subunit Homo sapiens 81-118 19194123-1 2009 BACKGROUND: The aim of this study was to determine whether the expression of the excision repair cross-complementing 1 (ERCC1), thymidylate synthase (TS) and glutathione S-transferase pi (GSTpi) predict clinical outcome in patients with advanced colorectal cancer treated with fluorouracil (5-FU)/oxaliplatin chemotherapy. Fluorouracil 277-289 ERCC excision repair 1, endonuclease non-catalytic subunit Homo sapiens 120-125 19194123-1 2009 BACKGROUND: The aim of this study was to determine whether the expression of the excision repair cross-complementing 1 (ERCC1), thymidylate synthase (TS) and glutathione S-transferase pi (GSTpi) predict clinical outcome in patients with advanced colorectal cancer treated with fluorouracil (5-FU)/oxaliplatin chemotherapy. Fluorouracil 277-289 thymidylate synthetase Homo sapiens 128-148 19143760-1 2009 OBJECTIVES: This study is to explore the role of Notch signalling during the regeneration of rat tracheal epithelium after injury induced by 5-fluorouracil (5-FU). Fluorouracil 141-155 notch receptor 3 Rattus norvegicus 49-54 19143760-1 2009 OBJECTIVES: This study is to explore the role of Notch signalling during the regeneration of rat tracheal epithelium after injury induced by 5-fluorouracil (5-FU). Fluorouracil 157-161 notch receptor 3 Rattus norvegicus 49-54 19143760-6 2009 RESULTS: Expression levels of Notch3, Jagged1, and Hey1 were increased in rat tracheal epithelial cells after treatment with 5-FU. Fluorouracil 125-129 notch receptor 3 Rattus norvegicus 30-36 18932044-0 2009 Low-dose continuous 5-fluorouracil infusion stimulates VEGF-A-mediated angiogenesis. Fluorouracil 20-34 vascular endothelial growth factor A Rattus norvegicus 55-61 19082493-0 2009 Combination of polymorphisms within 5" and 3" untranslated regions of thymidylate synthase gene modulates survival in 5 fluorouracil-treated colorectal cancer patients. Fluorouracil 120-132 thymidylate synthetase Homo sapiens 70-90 23915286-0 2013 MicroRNA-433 negatively regulates the expression of thymidylate synthase (TYMS) responsible for 5-fluorouracil sensitivity in HeLa cells. Fluorouracil 96-110 thymidylate synthetase Homo sapiens 52-72 23915286-0 2013 MicroRNA-433 negatively regulates the expression of thymidylate synthase (TYMS) responsible for 5-fluorouracil sensitivity in HeLa cells. Fluorouracil 96-110 thymidylate synthetase Homo sapiens 74-78 23915286-2 2013 High TYMS expression levels in tumors are generally associated with resistance to 5-fluorouracil (5-FU). Fluorouracil 82-96 thymidylate synthetase Homo sapiens 5-9 23915286-2 2013 High TYMS expression levels in tumors are generally associated with resistance to 5-fluorouracil (5-FU). Fluorouracil 98-102 thymidylate synthetase Homo sapiens 5-9 23915286-4 2013 The purpose of this study is to identify novel microRNAs (miRNAs) which regulate the expression of TYMS and to determine whether miRNAs binding to the 3"-untranslated region (UTR) of TYMS mRNA affect the proliferation of HeLa cells treated with 5-FU. Fluorouracil 245-249 thymidylate synthetase Homo sapiens 183-187 23915286-11 2013 Furthermore, miR-433 increased inhibition of cell proliferation in HeLa cells treated with 5-FU at over 2.0 muM. Fluorouracil 91-95 microRNA 433 Homo sapiens 13-20 23915286-12 2013 CONCLUSION: The results indicate that miR-433 post-transcriptionally regulates the expression of TYMS mRNA and protein, and increases sensitivity to 5-FU in HeLa cells. Fluorouracil 149-153 microRNA 433 Homo sapiens 38-45 23915286-13 2013 This is the first report showing that a miRNA regulating TYMS expression has a significant impact on sensitivity to 5-FU treatment. Fluorouracil 116-120 thymidylate synthetase Homo sapiens 57-61 23760813-3 2013 Although several reports have shown the detrimental effect of some dihydropyrimidine dehydrogenase (DPYD) and thymidylate synthase (TYMS) gene polymorphisms in patients undergoing 5-FU-based treatment, they account for only a minority of toxicities. Fluorouracil 180-184 thymidylate synthetase Homo sapiens 110-130 23760813-3 2013 Although several reports have shown the detrimental effect of some dihydropyrimidine dehydrogenase (DPYD) and thymidylate synthase (TYMS) gene polymorphisms in patients undergoing 5-FU-based treatment, they account for only a minority of toxicities. Fluorouracil 180-184 thymidylate synthetase Homo sapiens 132-136 23816136-0 2013 miR-381, a novel intrinsic WEE1 inhibitor, sensitizes renal cancer cells to 5-FU by up-regulation of Cdc2 activities in 786-O. Fluorouracil 76-80 microRNA 381 Homo sapiens 0-7 23816136-0 2013 miR-381, a novel intrinsic WEE1 inhibitor, sensitizes renal cancer cells to 5-FU by up-regulation of Cdc2 activities in 786-O. Fluorouracil 76-80 cyclin dependent kinase 1 Homo sapiens 101-105 23816136-2 2013 We aim to investigate exact role of miR-381 in chemotherapy sensitivity of 5-fluorouracil (5-FU) in renal cancer cells. Fluorouracil 75-89 microRNA 381 Homo sapiens 36-43 23816136-2 2013 We aim to investigate exact role of miR-381 in chemotherapy sensitivity of 5-fluorouracil (5-FU) in renal cancer cells. Fluorouracil 91-95 microRNA 381 Homo sapiens 36-43 23816136-6 2013 RESULTS: We showed that miR-381 combined with 5-FU inhibited proliferation and potentiated the anti-tumour efficacies of 5-FU at tolerated concentration in vitro. Fluorouracil 121-125 microRNA 381 Homo sapiens 24-31 23816136-7 2013 miR-381 combined with 5-FU led to Cdc2 activation, mitotic catastrophe, and cell apoptosis through inhibitory WEE1. Fluorouracil 22-26 cyclin dependent kinase 1 Homo sapiens 34-38 23816136-9 2013 IC50 of 5-FU decreased significantly in the presence of miR-381. Fluorouracil 8-12 microRNA 381 Homo sapiens 56-63 23816136-10 2013 CONCLUSION: miR-381 increases sensitivity of 786-O cells to 5-FU by inhibitory WEE1 and increase of Cdc2 activity. Fluorouracil 60-64 microRNA 381 Homo sapiens 12-19 23481023-9 2013 Moreover, expression of PEA-15 resulted in significant protection from cell death induced by cytotoxic drugs (5-FU, cisplatin), by the death ligand TRAIL, or by serum withdrawal. Fluorouracil 110-114 proliferation and apoptosis adaptor protein 15 Homo sapiens 24-30 23507557-5 2013 The results demonstrated that combination of PT and 5-FU induced apoptosis which was determined using MTT, cell cycle analysis, annexin-V assay, and Hoechst 33258 staining. Fluorouracil 52-56 annexin A5 Homo sapiens 128-137 19015148-2 2009 METHODS: We investigated the 5-FU-related gene expression levels of thymidylate synthase (TS), DPD, thymidine phosphorylase (TP) and orotate phosphoribosyl transferase (OPRT) in resected tumor specimens from 51 patients with adenocarcinomas and 47 with squamous cell carcinomas using quantitative reverse transcription-PCR, and compared those levels between the two histological types. Fluorouracil 29-33 thymidylate synthetase Homo sapiens 68-88 19015148-2 2009 METHODS: We investigated the 5-FU-related gene expression levels of thymidylate synthase (TS), DPD, thymidine phosphorylase (TP) and orotate phosphoribosyl transferase (OPRT) in resected tumor specimens from 51 patients with adenocarcinomas and 47 with squamous cell carcinomas using quantitative reverse transcription-PCR, and compared those levels between the two histological types. Fluorouracil 29-33 uridine monophosphate synthetase Homo sapiens 133-167 19015148-2 2009 METHODS: We investigated the 5-FU-related gene expression levels of thymidylate synthase (TS), DPD, thymidine phosphorylase (TP) and orotate phosphoribosyl transferase (OPRT) in resected tumor specimens from 51 patients with adenocarcinomas and 47 with squamous cell carcinomas using quantitative reverse transcription-PCR, and compared those levels between the two histological types. Fluorouracil 29-33 uridine monophosphate synthetase Homo sapiens 169-173 19082440-10 2009 Furthermore, the OPRT/DPD expression ratio, a powerful predictive factor to evaluate 5-FU sensitivity, in the HRPC group was significantly higher than that in the low grade HSPC group. Fluorouracil 85-89 uridine monophosphate synthetase Homo sapiens 17-21 23216104-11 2013 In this study, we have shown that 5-FU treatment enriched the population of cells expressing the putative embryonic markers Oct3/4 and Sox2 and exhibiting nuclear accumulation of beta-catenin. Fluorouracil 34-38 POU class 5 homeobox 1 Homo sapiens 124-130 23216104-11 2013 In this study, we have shown that 5-FU treatment enriched the population of cells expressing the putative embryonic markers Oct3/4 and Sox2 and exhibiting nuclear accumulation of beta-catenin. Fluorouracil 34-38 catenin beta 1 Homo sapiens 179-191 19439999-7 2009 In MKN-1 cells, an additive effect on growth inhibition was shown by the combined transfection with miR-143 and miR-145; further, higher sensitivity to 5-fluorouracil was also observed following the transfection with miR-143 or miR-145. Fluorouracil 152-166 microRNA 145 Homo sapiens 228-235 19145509-5 2009 RESULTS: The combined use of EGF and 5-fluorouracil significantly inhibited the growth of colorectal cancer xenografts in nude mice with the inhibitory rate of 57.05% which was higher than 5-fluorouracil did (40.97%)(P<0.05). Fluorouracil 189-203 epidermal growth factor Homo sapiens 29-32 19145509-8 2009 CONCLUSION: Epidermal growth factor, which may recruit colorectal cancer cells into activated phases of the cell cycle, can enhance the sensitivity of colorectal cancer cell Caco-2 to 5-fluorouracil. Fluorouracil 184-198 epidermal growth factor Homo sapiens 12-35 18854306-8 2008 In short term transplant experiments, DYRK3-/- progenitors also supported enhanced erythroblast formation, and erythropoietic advantages due to DYRK3-deficiency also were observed in 5-fluorouracil-treated mice expressing a compromised erythropoietin receptor EPOR-HM allele. Fluorouracil 183-197 erythropoietin Mus musculus 236-250 18854306-8 2008 In short term transplant experiments, DYRK3-/- progenitors also supported enhanced erythroblast formation, and erythropoietic advantages due to DYRK3-deficiency also were observed in 5-fluorouracil-treated mice expressing a compromised erythropoietin receptor EPOR-HM allele. Fluorouracil 183-197 erythropoietin receptor Mus musculus 260-264 18794807-6 2008 Western blotting and RT-PCR analysis revealed that the expression of thymidylate synthase (TS) was higher in 5-FU-resistant cells, however, decreased significantly after pretreatment with PP2. Fluorouracil 109-113 thymidylate synthetase Homo sapiens 69-89 18324404-6 2008 RESULTS: On the third day of treatment, 5-FU induced a significant villi shortening, an increase in crypt depth and intestinal MPO activity and a decrease in villus/crypt ratio and GSH concentration. Fluorouracil 40-44 myeloperoxidase Rattus norvegicus 127-130 19020759-2 2008 The expression levels of thymidylate synthase (TS) and excision repair cross-complementing factor 1 (ERCC1) have been reported to be prognostic markers for patients with 5-FU/oxaliplatin chemotherapy. Fluorouracil 170-174 thymidylate synthetase Homo sapiens 25-45 19020759-2 2008 The expression levels of thymidylate synthase (TS) and excision repair cross-complementing factor 1 (ERCC1) have been reported to be prognostic markers for patients with 5-FU/oxaliplatin chemotherapy. Fluorouracil 170-174 ERCC excision repair 1, endonuclease non-catalytic subunit Homo sapiens 55-99 19020759-2 2008 The expression levels of thymidylate synthase (TS) and excision repair cross-complementing factor 1 (ERCC1) have been reported to be prognostic markers for patients with 5-FU/oxaliplatin chemotherapy. Fluorouracil 170-174 ERCC excision repair 1, endonuclease non-catalytic subunit Homo sapiens 101-106 19020767-1 2008 It has been reported that the expression of thymidylate synthase (TS), dihydropyrimidine dehydrogenase (DPD) and orotate phosphoribosyltransferase (OPRT) may predict the clinical efficacy of 5-fluorouracil (5-FU)-based therapy in cancer patients. Fluorouracil 191-205 thymidylate synthetase Homo sapiens 44-64 19020740-0 2008 Decreased orotate phosphoribosyltransferase activity produces 5-fluorouracil resistance in a human gastric cancer cell line. Fluorouracil 62-76 uridine monophosphate synthetase Homo sapiens 10-43 19020740-5 2008 Although protein expression and activity of thymidylate synthase and dihydropyrimidine dehydrogenase did not change, orotate phosphoribosyl-transferase (OPRT) protein expression and activity significantly decreased in the 5-FU resistant MKN45/F2R cells. Fluorouracil 222-226 uridine monophosphate synthetase Homo sapiens 117-151 19020740-5 2008 Although protein expression and activity of thymidylate synthase and dihydropyrimidine dehydrogenase did not change, orotate phosphoribosyl-transferase (OPRT) protein expression and activity significantly decreased in the 5-FU resistant MKN45/F2R cells. Fluorouracil 222-226 uridine monophosphate synthetase Homo sapiens 153-157 19020740-7 2008 OPRT-knockout MKN45 parent cells using small interfering RNA demonstrated 15.8-fold increased resistance to 5-FU compared to the control cells. Fluorouracil 108-112 uridine monophosphate synthetase Homo sapiens 0-4 18816083-8 2008 In addition, pretreatment of KB/V cells with a CyPA-binding immunosuppressive drug, cyclosporine A (CsA), enhanced their chemosensitivity to VCR and 5-Fu. Fluorouracil 149-153 peptidylprolyl isomerase A Homo sapiens 47-51 23643670-9 2013 We conclude that an acidic tumor microenvironment triggers downregulation of hMLH1, potentially removing the execution component of MMR for 5FU cytotoxicity, whereas other mechanisms remain stable to implement overall 5FU sensitivity. Fluorouracil 140-143 mutL homolog 1 Homo sapiens 77-82 23814492-8 2013 In addition, 5-FU and X-ray decreased the expression of mRNAs for suppressor of cytokine signaling 1 (SOCS1) and SOCS3. Fluorouracil 13-17 suppressor of cytokine signaling 1 Homo sapiens 66-100 23814492-8 2013 In addition, 5-FU and X-ray decreased the expression of mRNAs for suppressor of cytokine signaling 1 (SOCS1) and SOCS3. Fluorouracil 13-17 suppressor of cytokine signaling 1 Homo sapiens 102-107 23619566-0 2013 NK4 regulates 5-fluorouracil sensitivity in cholangiocarcinoma cells by modulating the intrinsic apoptosis pathway. Fluorouracil 14-28 interleukin 32 Homo sapiens 0-3 18949417-0 2008 Heat shock protein 27, a novel regulator of 5-fluorouracil resistance in colon cancer. Fluorouracil 44-58 heat shock protein family B (small) member 1 Homo sapiens 0-21 23619566-1 2013 The aim of the present study was to investigate the role of NK4, an antagonist for hepatocyte growth factor (HGF) and the Met receptor, in regulating the response of cholangiocarcinoma (CCA) cells to 5-fluorouracil (5-FU). Fluorouracil 200-214 interleukin 32 Homo sapiens 60-63 18949417-2 2008 Heat shock protein 27 (HSP27) mRNA expression has recently been shown to be correlated with 5-FU resistance in 5-FU-resistant cell lines. Fluorouracil 92-96 heat shock protein family B (small) member 1 Homo sapiens 0-21 23619566-1 2013 The aim of the present study was to investigate the role of NK4, an antagonist for hepatocyte growth factor (HGF) and the Met receptor, in regulating the response of cholangiocarcinoma (CCA) cells to 5-fluorouracil (5-FU). Fluorouracil 216-220 interleukin 32 Homo sapiens 60-63 23619566-6 2013 However, 5-FU-induced apoptosis was significantly increased in the Hu-NK4 cells when compared to that in the Hu-Em cells. Fluorouracil 9-13 interleukin 32 Homo sapiens 70-73 18949417-2 2008 Heat shock protein 27 (HSP27) mRNA expression has recently been shown to be correlated with 5-FU resistance in 5-FU-resistant cell lines. Fluorouracil 92-96 heat shock protein family B (small) member 1 Homo sapiens 23-28 23619566-7 2013 Further investigation revealed that NK4 gene expression enhanced 5-FU-induced caspase-3 and caspase-9 activation, and that the apoptosis of cells was associated with modulation of expression of the Bcl-2 family members. Fluorouracil 65-69 interleukin 32 Homo sapiens 36-39 23619566-7 2013 Further investigation revealed that NK4 gene expression enhanced 5-FU-induced caspase-3 and caspase-9 activation, and that the apoptosis of cells was associated with modulation of expression of the Bcl-2 family members. Fluorouracil 65-69 caspase 9 Homo sapiens 92-101 23619566-9 2013 Collectively, these results suggest that following 5-FU treatment in CCA cell lines, NK4 was involved in apoptosis induction through the intrinsic mitochondrial pathway. Fluorouracil 51-55 interleukin 32 Homo sapiens 85-88 23619566-10 2013 This indicates that NK4 may be an important mediator of 5-FU-induced cell death. Fluorouracil 56-60 interleukin 32 Homo sapiens 20-23 23619566-11 2013 Moreover, downregulation of NK4 in response to 5-FU may represent an intrinsic mechanism of resistance to this anticancer drug. Fluorouracil 47-51 interleukin 32 Homo sapiens 28-31 18949417-2 2008 Heat shock protein 27 (HSP27) mRNA expression has recently been shown to be correlated with 5-FU resistance in 5-FU-resistant cell lines. Fluorouracil 111-115 heat shock protein family B (small) member 1 Homo sapiens 0-21 18949417-2 2008 Heat shock protein 27 (HSP27) mRNA expression has recently been shown to be correlated with 5-FU resistance in 5-FU-resistant cell lines. Fluorouracil 111-115 heat shock protein family B (small) member 1 Homo sapiens 23-28 23438367-3 2013 Thymidylate synthase (TS) is a direct target of 5-FU, and the low TS level has been generally supposed to sensitize 5-FU"s efficacy. Fluorouracil 116-120 thymidylate synthetase Homo sapiens 66-68 18949417-3 2008 In this study, we attempted to elucidate the functional mechanism of HSP27 in 5-FU resistance in colon cancer. Fluorouracil 78-82 heat shock protein family B (small) member 1 Homo sapiens 69-74 23438367-4 2013 We therefore hypothesized that RB-reactivating agents could enhance the efficacy of 5-FU, because the RB-reactivating agents could suppress the function of transcription factor E2F of TS gene promoter. Fluorouracil 84-88 thymidylate synthetase Homo sapiens 184-186 18949417-12 2008 These data indicated that HSP27 is closely connected with 5-FU resistance in colon cancer and suggested that HSP27 levels predicted 5-FU resistance. Fluorouracil 58-62 heat shock protein family B (small) member 1 Homo sapiens 26-31 18949417-12 2008 These data indicated that HSP27 is closely connected with 5-FU resistance in colon cancer and suggested that HSP27 levels predicted 5-FU resistance. Fluorouracil 132-136 heat shock protein family B (small) member 1 Homo sapiens 109-114 18949417-13 2008 HSP27 down-regulation overcame 5-FU resistance and HSP27 may be a clinical target in patients with 5-FU-resistant colon cancer. Fluorouracil 31-35 heat shock protein family B (small) member 1 Homo sapiens 0-5 18949417-13 2008 HSP27 down-regulation overcame 5-FU resistance and HSP27 may be a clinical target in patients with 5-FU-resistant colon cancer. Fluorouracil 99-103 heat shock protein family B (small) member 1 Homo sapiens 0-5 18949417-13 2008 HSP27 down-regulation overcame 5-FU resistance and HSP27 may be a clinical target in patients with 5-FU-resistant colon cancer. Fluorouracil 99-103 heat shock protein family B (small) member 1 Homo sapiens 51-56 18583030-2 2008 We have previously demonstrated that Egr-1 induced by 5-FU enhanced TSP-1 expression in human colon cancer KM12C cells. Fluorouracil 54-58 early growth response 1 Homo sapiens 37-42 18583030-7 2008 Meanwhile, 5-FU dose-dependently decreased the expression of miR-17-92 cluster. Fluorouracil 11-15 miR-17-92a-1 cluster host gene Homo sapiens 61-70 18583030-8 2008 These findings suggest that 5-FU decreased the expression of c-Myc and consequently miR-17-92 cluster and increased the expression of TSP-1 mRNA. Fluorouracil 28-32 MYC proto-oncogene, bHLH transcription factor Homo sapiens 61-66 23718853-11 2013 The in vivo experiment also confirmed that the Huh7-HBx group was much more resistant to ADM or 5-FU than the control. Fluorouracil 96-100 X protein Hepatitis B virus 52-55 18583030-8 2008 These findings suggest that 5-FU decreased the expression of c-Myc and consequently miR-17-92 cluster and increased the expression of TSP-1 mRNA. Fluorouracil 28-32 miR-17-92a-1 cluster host gene Homo sapiens 84-93 18834353-8 2008 When cells were treated with 20 microM 5-fluorouracil and 200 microg/ml Bupleuri Radix simultaneously, Bax protein increased in HepG2 cells at 24 hr; however, p21 and p53 proteins were up-regulated in normal human lymphocytes. Fluorouracil 39-53 H3 histone pseudogene 16 Homo sapiens 159-162 18776995-0 2008 Down-regulation of Sonic hedgehog signaling pathway activity is involved in 5-fluorouracil-induced apoptosis and motility inhibition in Hep3B cells. Fluorouracil 76-90 sonic hedgehog signaling molecule Homo sapiens 19-33 23737952-13 2013 Compared to untreated mouse blood, a 2-fold increase in the percentage of proplatelets was detected following exposure to 1800 s(-1) on VWF of samples from mice treated with 5-FU. Fluorouracil 174-178 Von Willebrand factor Mus musculus 136-139 18776995-1 2008 The Sonic hedgehog (SHh) pathway plays a critical role in normal embryogenesis and carcinogenesis, but its function in cancer cells treated with 5-fluorouracil (5-FU) remains unknown. Fluorouracil 145-159 sonic hedgehog signaling molecule Homo sapiens 4-18 18776995-1 2008 The Sonic hedgehog (SHh) pathway plays a critical role in normal embryogenesis and carcinogenesis, but its function in cancer cells treated with 5-fluorouracil (5-FU) remains unknown. Fluorouracil 145-159 sonic hedgehog signaling molecule Homo sapiens 20-23 18776995-1 2008 The Sonic hedgehog (SHh) pathway plays a critical role in normal embryogenesis and carcinogenesis, but its function in cancer cells treated with 5-fluorouracil (5-FU) remains unknown. Fluorouracil 161-165 sonic hedgehog signaling molecule Homo sapiens 4-18 18776995-1 2008 The Sonic hedgehog (SHh) pathway plays a critical role in normal embryogenesis and carcinogenesis, but its function in cancer cells treated with 5-fluorouracil (5-FU) remains unknown. Fluorouracil 161-165 sonic hedgehog signaling molecule Homo sapiens 20-23 18776995-2 2008 We examined the expression of a subset of SHh signaling pathway genes, including SHh, SMO, PTC1, Su(Fu) and HIP in human hepatocellular carcinoma (HCC) cell lines, Hep3B and HepG2, treated with 5-FU by reverse transcription-polymerase chain reaction. Fluorouracil 194-198 sonic hedgehog signaling molecule Homo sapiens 42-45 32260953-3 2013 This hybrid nanostructure possesses a superior capability of binding the anticancer drug 5-fluorouracil (5-FU) with a high loading capacity of up to 0.27 mg mg-1 with a 5-FU concentration of 0.5 mg mL-1, and also possesses a pH-activated release profile. Fluorouracil 89-103 L1 cell adhesion molecule Mus musculus 198-202 18757417-9 2008 Blockade of the p38 MAPK pathway by SB203580 remarkably inhibited the phosphorylation of HSP27 induced by 5-FU and decreased the induction of Egr-1 and TSP-1 by 5-FU in KM12C cells. Fluorouracil 106-110 heat shock protein family B (small) member 1 Homo sapiens 89-94 32260953-3 2013 This hybrid nanostructure possesses a superior capability of binding the anticancer drug 5-fluorouracil (5-FU) with a high loading capacity of up to 0.27 mg mg-1 with a 5-FU concentration of 0.5 mg mL-1, and also possesses a pH-activated release profile. Fluorouracil 105-109 L1 cell adhesion molecule Mus musculus 198-202 18757417-9 2008 Blockade of the p38 MAPK pathway by SB203580 remarkably inhibited the phosphorylation of HSP27 induced by 5-FU and decreased the induction of Egr-1 and TSP-1 by 5-FU in KM12C cells. Fluorouracil 161-165 heat shock protein family B (small) member 1 Homo sapiens 89-94 32260953-5 2013 In vitro cytotoxicity tests suggest that the obtained GN-CNT-Fe3O4 hybrid is nontoxic for Chang liver cells, even at the high concentration of 80 mug mL-1, however, the 5-FU-loaded GN-CNT-Fe3O4 hybrid showed significant cytotoxic effects in HepG2 cells. Fluorouracil 169-173 L1 cell adhesion molecule Mus musculus 150-154 18757417-9 2008 Blockade of the p38 MAPK pathway by SB203580 remarkably inhibited the phosphorylation of HSP27 induced by 5-FU and decreased the induction of Egr-1 and TSP-1 by 5-FU in KM12C cells. Fluorouracil 161-165 early growth response 1 Homo sapiens 142-147 18757417-10 2008 These findings suggest that the p38 MAPK pathway plays a crucial role in the induction of Egr-1 by 5-FU and that induced Egr-1 augments TSP-1 promoter activity, with the subsequent production of TSP-1 mRNA and protein. Fluorouracil 99-103 early growth response 1 Homo sapiens 90-95 18756484-5 2008 This synergistic interaction was augmented by the addition of a subtumoricidal dose (0.5 microg/mL) of 5-fluorouracil (5-FU), which enhanced p53 expression and facilitated the release of virions from tumor cells. Fluorouracil 103-117 transformation related protein 53, pseudogene Mus musculus 141-144 23290343-9 2013 In addition, the inclusion of patients with N2 or N3 disease will help to determine whether the addition of docetaxel, cisplatin and 5-fluorouracil to CRT reduces the incidence of distant relapse in advanced laryngeal SCC. Fluorouracil 133-147 serpin family B member 3 Homo sapiens 218-221 23429289-6 2013 Consequently, when we generated MSCs that secreted TRAIL-R2-specific variants of soluble TRAIL (sTRAIL), we found that such engineered MSCs, labeled MSC.sTRAIL(DR5), had enhanced antitumor activity in combination with 5-FU when compared with MSC.sTRAIL. Fluorouracil 218-222 TNF receptor superfamily member 10b Homo sapiens 51-59 23429289-6 2013 Consequently, when we generated MSCs that secreted TRAIL-R2-specific variants of soluble TRAIL (sTRAIL), we found that such engineered MSCs, labeled MSC.sTRAIL(DR5), had enhanced antitumor activity in combination with 5-FU when compared with MSC.sTRAIL. Fluorouracil 218-222 TNF receptor superfamily member 10b Homo sapiens 160-163 23429291-1 2013 5-Fluorouracil (5-FU) is the first rationally designed antimetabolite, which achieves its therapeutic efficacy through inhibition of the enzyme thymidylate synthase (TS), which is essential for the synthesis and repair of DNA. Fluorouracil 0-14 thymidylate synthetase Homo sapiens 144-164 23429291-1 2013 5-Fluorouracil (5-FU) is the first rationally designed antimetabolite, which achieves its therapeutic efficacy through inhibition of the enzyme thymidylate synthase (TS), which is essential for the synthesis and repair of DNA. Fluorouracil 16-20 thymidylate synthetase Homo sapiens 144-164 23229803-7 2013 The antitumor activity of capecitabine and 5"-DFUR correlated significantly with the mRNA levels of TP and with the TP/DPD ratio, whereas the activity of 5-FU correlated significantly with OPRT, TMPK, UMPK and CD. Fluorouracil 178-182 uridine monophosphate synthetase Homo sapiens 213-217 24324958-6 2013 Our results showed that there were significant synergistic effects of low dose 5-Fu and TRAIL on TRAIL-resistant AGS cells, and this effect was supposed to be mediated by decreasing DcR2 expression and increasing DR5 expression. Fluorouracil 79-83 TNF receptor superfamily member 10b Homo sapiens 213-216 23107827-0 2013 Inflammatory intestinal damage induced by 5-fluorouracil requires IL-4. Fluorouracil 42-56 interleukin 4 Mus musculus 66-70 23107827-4 2013 This study aimed to evaluate the role of IL-4 in 5-FU-induced intestinal mucositis. Fluorouracil 49-53 interleukin 4 Mus musculus 41-45 23107827-7 2013 RESULTS: 5-FU induced significant damage in the intestinal epithelium of IL-4+/+ mice (reduction in the villus/crypt ratio: control=3.31+-0.21 mum, 5-FU=0.99+-0.10 mum). Fluorouracil 9-13 interleukin 4 Mus musculus 73-77 23107827-9 2013 5-FU-induced epithelial damage increased the MPO activity (neutrophil number) and the level of pro-inflammatory cytokines (IL-4, TNF-alpha, IL-1beta and CXCL-8) in the duodenum. Fluorouracil 0-4 interleukin 4 Mus musculus 123-127 23107827-11 2013 CONCLUSION: Our data suggest that IL-4 participates as a pro-inflammatory cytokine in a 5-FU-induced intestinal damage model and suggests that IL-4 antagonists may be novel therapeutics for this condition. Fluorouracil 88-92 interleukin 4 Mus musculus 34-38 23107827-11 2013 CONCLUSION: Our data suggest that IL-4 participates as a pro-inflammatory cytokine in a 5-FU-induced intestinal damage model and suggests that IL-4 antagonists may be novel therapeutics for this condition. Fluorouracil 88-92 interleukin 4 Mus musculus 143-147 23169295-10 2012 In validation study, ERCC1 and DPD but not TOP1 expressions in cancer cells were significantly higher in FOLFOX (oxaliplatin, folinic acid, and 5-FU)-treated patients (N=24) than nontreated patients (N=21). Fluorouracil 144-148 ERCC excision repair 1, endonuclease non-catalytic subunit Homo sapiens 21-26 23085230-6 2012 Here, we adopted a prodrug system that uses 5-fluorocytosine (5-FC) and human EGF (hEGF) fused with yeast cytosine deaminase (Fcy) to target EGFR-overexpressing cancer cells and to convert 5-FC to a significantly more toxic chemotherapeutic, 5-fluorouracil (5-FU). Fluorouracil 242-256 epidermal growth factor Homo sapiens 78-81 23085230-6 2012 Here, we adopted a prodrug system that uses 5-fluorocytosine (5-FC) and human EGF (hEGF) fused with yeast cytosine deaminase (Fcy) to target EGFR-overexpressing cancer cells and to convert 5-FC to a significantly more toxic chemotherapeutic, 5-fluorouracil (5-FU). Fluorouracil 242-256 epidermal growth factor Homo sapiens 83-87 23085230-6 2012 Here, we adopted a prodrug system that uses 5-fluorocytosine (5-FC) and human EGF (hEGF) fused with yeast cytosine deaminase (Fcy) to target EGFR-overexpressing cancer cells and to convert 5-FC to a significantly more toxic chemotherapeutic, 5-fluorouracil (5-FU). Fluorouracil 258-262 epidermal growth factor Homo sapiens 78-81 23085230-6 2012 Here, we adopted a prodrug system that uses 5-fluorocytosine (5-FC) and human EGF (hEGF) fused with yeast cytosine deaminase (Fcy) to target EGFR-overexpressing cancer cells and to convert 5-FC to a significantly more toxic chemotherapeutic, 5-fluorouracil (5-FU). Fluorouracil 258-262 epidermal growth factor Homo sapiens 83-87 22172707-5 2012 Following treatment with 5-FU, JAK1 and STAT5 immunoreactivities were decreased in MCF-7 cells in comparison with both gemcitabine-treated and non-treated groups. Fluorouracil 25-29 signal transducer and activator of transcription 5A Homo sapiens 40-45 23265074-3 2012 Thymidylate synthase (TS) is one of the initial key enzymes in the 5-fluouracil (5-FU) metabolic pathway. Fluorouracil 81-85 thymidylate synthetase Homo sapiens 0-20 23265074-3 2012 Thymidylate synthase (TS) is one of the initial key enzymes in the 5-fluouracil (5-FU) metabolic pathway. Fluorouracil 81-85 thymidylate synthetase Homo sapiens 22-24 23265074-4 2012 Clinical studies showed that intratumoural TS level was related to the response to 5-FU-based chemotherapy in patients with several types of cancer such as gastroenterological and head and neck cancers. Fluorouracil 83-87 thymidylate synthetase Homo sapiens 43-45 18756484-5 2008 This synergistic interaction was augmented by the addition of a subtumoricidal dose (0.5 microg/mL) of 5-fluorouracil (5-FU), which enhanced p53 expression and facilitated the release of virions from tumor cells. Fluorouracil 119-123 transformation related protein 53, pseudogene Mus musculus 141-144 18698031-9 2008 More importantly, an increased 5-FU antitumor activity was found in tumors with the double Chk1 and p53 silencing. Fluorouracil 31-35 transformation related protein 53, pseudogene Mus musculus 100-103 18497562-2 2008 In this study, the role of caspase-6 activation in 5-fluorouracil (5-FU)-elicited apoptosis as well as the combination effects between RSV and 5-FU on their apoptosis induction was further investigated in the same colon cancer cell model. Fluorouracil 51-65 caspase 6 Homo sapiens 27-36 18497562-2 2008 In this study, the role of caspase-6 activation in 5-fluorouracil (5-FU)-elicited apoptosis as well as the combination effects between RSV and 5-FU on their apoptosis induction was further investigated in the same colon cancer cell model. Fluorouracil 67-71 caspase 6 Homo sapiens 27-36 18497562-4 2008 We found that 5-FU triggered apoptosis and caspase-6 activation in the cancer cells, which were entirely abrogated by caspase-6 inhibitors. Fluorouracil 14-18 caspase 6 Homo sapiens 43-52 18497562-4 2008 We found that 5-FU triggered apoptosis and caspase-6 activation in the cancer cells, which were entirely abrogated by caspase-6 inhibitors. Fluorouracil 14-18 caspase 6 Homo sapiens 118-127 18497562-10 2008 In conclusion, our results suggest that, like RSV, 5-FU triggers the cancer cell apoptosis by activating caspase-6. Fluorouracil 51-55 caspase 6 Homo sapiens 105-114 18687176-14 2008 The level of IL-10 in 5-FU group was also lower than that in severe sepsis group, but higher than that in control group (both P<0.01). Fluorouracil 22-26 interleukin 10 Rattus norvegicus 13-18 18687176-15 2008 CONCLUSION: 5-FU may lower simultaneously the level of proinflammatory IL-6 and anti-inflammatory IL-10, alleviate lung edema and inflammation. Fluorouracil 12-16 interleukin 10 Rattus norvegicus 98-103 18443433-0 2008 Evaluating the drug-target relationship between thymidylate synthase expression and tumor response to 5-fluorouracil. Fluorouracil 102-116 thymidylate synthetase Homo sapiens 48-68 18443433-2 2008 Thymidylate synthase is a target of 5-fluoruracil, a pyrimidine analog used to treat gastrointestinal and other cancers. Fluorouracil 36-49 thymidylate synthetase Homo sapiens 0-20 18443433-3 2008 The 5-fluorouracil metabolite, fluoro-deoxyuridine monophosphate, forms a ternary complex with thymidylate synthase and 5,10-methylene tetrahydrofolate. Fluorouracil 4-18 thymidylate synthetase Homo sapiens 95-115 18443433-4 2008 The purpose of this study was to evaluate the time-honored connection between thymidylate synthase and 5-fluorouracil. Fluorouracil 103-117 thymidylate synthetase Homo sapiens 78-98 18443433-7 2008 The relationship between thymidylate synthase expression and 5-fluorouracil response was analyzed for the overall group, as well as for subsets. Fluorouracil 61-75 thymidylate synthetase Homo sapiens 25-45 18443433-8 2008 Overall, the literature supported an approximately 2-fold inverse relationship between thymidylate synthase expression and response to 5-fluoruracil. Fluorouracil 135-148 thymidylate synthetase Homo sapiens 87-107 18443433-12 2008 In sum, the connection between thymidylate synthase expression and patient response to 5-fluorouracil does not satisfy expectations for an effective drug-target relationship; and thus, studies of the thymidylate synthase tandem repeat status might only be clinically valuable in regards to patient toxicity. Fluorouracil 87-101 thymidylate synthetase Homo sapiens 31-51 18575723-9 2008 Our results suggest that hsp27, Prx 6 and hsp70 are potential 5-FU response proteins and they may represent potential targets for further evaluation in other 5-FU-sensitive and -resistant CRC cell lines. Fluorouracil 62-66 heat shock protein family B (small) member 1 Homo sapiens 25-30 18575723-9 2008 Our results suggest that hsp27, Prx 6 and hsp70 are potential 5-FU response proteins and they may represent potential targets for further evaluation in other 5-FU-sensitive and -resistant CRC cell lines. Fluorouracil 158-162 heat shock protein family B (small) member 1 Homo sapiens 25-30 18442042-2 2008 TS messenger RNA and protein levels are predictive of response to 5-fluorouracil-containing therapy for patients with colorectal cancer and gastric cancer. Fluorouracil 66-80 thymidylate synthetase Homo sapiens 0-2 23084747-6 2012 Conversely, platelets and myeloid cells from miR-150 null marrow recovered faster after 5-fluorouracil treatment. Fluorouracil 88-102 microRNA 150 Mus musculus 45-52 22899557-5 2012 We established mda-7/IL-24 overexpressing BEL-7402/5-fluorouracil (5-FU) cell lines and their drug sensitivity to 5-FU and doxorubicin (DOX) which were investigated by MTT. Fluorouracil 51-65 interleukin 24 Homo sapiens 15-20 22899557-5 2012 We established mda-7/IL-24 overexpressing BEL-7402/5-fluorouracil (5-FU) cell lines and their drug sensitivity to 5-FU and doxorubicin (DOX) which were investigated by MTT. Fluorouracil 51-65 interleukin 24 Homo sapiens 21-26 22899557-5 2012 We established mda-7/IL-24 overexpressing BEL-7402/5-fluorouracil (5-FU) cell lines and their drug sensitivity to 5-FU and doxorubicin (DOX) which were investigated by MTT. Fluorouracil 67-71 interleukin 24 Homo sapiens 15-20 22899557-5 2012 We established mda-7/IL-24 overexpressing BEL-7402/5-fluorouracil (5-FU) cell lines and their drug sensitivity to 5-FU and doxorubicin (DOX) which were investigated by MTT. Fluorouracil 67-71 interleukin 24 Homo sapiens 21-26 22899557-5 2012 We established mda-7/IL-24 overexpressing BEL-7402/5-fluorouracil (5-FU) cell lines and their drug sensitivity to 5-FU and doxorubicin (DOX) which were investigated by MTT. Fluorouracil 114-118 interleukin 24 Homo sapiens 21-26 22842517-0 2012 Suppression of heat shock protein 27 expression promotes 5-fluorouracil sensitivity in colon cancer cells in a xenograft model. Fluorouracil 57-71 heat shock protein family B (small) member 1 Homo sapiens 15-36 22842517-1 2012 The present study investigates whether the expression levels of heat shock protein 27 (HSP27) in colon cancer cells are associated with 5-fluorouracil (5-FU) sensitivity in a xenograft model, as well as the mechanism responsible for regulating 5-FU sensitivity. Fluorouracil 148-162 heat shock protein family B (small) member 1 Homo sapiens 99-104 22842517-1 2012 The present study investigates whether the expression levels of heat shock protein 27 (HSP27) in colon cancer cells are associated with 5-fluorouracil (5-FU) sensitivity in a xenograft model, as well as the mechanism responsible for regulating 5-FU sensitivity. Fluorouracil 164-168 heat shock protein family B (small) member 1 Homo sapiens 99-104 22842517-1 2012 The present study investigates whether the expression levels of heat shock protein 27 (HSP27) in colon cancer cells are associated with 5-fluorouracil (5-FU) sensitivity in a xenograft model, as well as the mechanism responsible for regulating 5-FU sensitivity. Fluorouracil 280-284 heat shock protein family B (small) member 1 Homo sapiens 99-104 22842517-5 2012 The suppression of HSP27 protein expression led to enhanced 5-FU sensitivity. Fluorouracil 72-76 heat shock protein family B (small) member 1 Homo sapiens 31-36 22842517-6 2012 The mRNA expression levels of dihydropyrimidine dehydrogenase and orotate phosphoribosyltransferase, but not those of thymidylate synthase, and the number of apoptotic cells increased in the transfected cells after 5-FU exposure. Fluorouracil 251-255 uridine monophosphate synthetase Homo sapiens 78-111 22842517-7 2012 In conclusion, the suppression of HSP27 expression in colon cancer cells may promote 5-FU sensitivity by inducing apoptosis, despite the acceleration in 5-FU metabolism. Fluorouracil 97-101 heat shock protein family B (small) member 1 Homo sapiens 46-51 22842517-7 2012 In conclusion, the suppression of HSP27 expression in colon cancer cells may promote 5-FU sensitivity by inducing apoptosis, despite the acceleration in 5-FU metabolism. Fluorouracil 177-181 heat shock protein family B (small) member 1 Homo sapiens 46-51 23020798-9 2012 CONCLUSION: Polymorphisms of ERCC1, GSTs, TS and MTHFR were closely associated with clinical outcomes of GC patients treated with platinum/5-Fu-based chemotherapy. Fluorouracil 139-143 ERCC excision repair 1, endonuclease non-catalytic subunit Homo sapiens 29-34 23017148-6 2012 Short incubations with 5-fluorouracil (5-FU) also induced AQP3 expression and increased cell volume, and the inhibition of AQP3 expression significantly blocked growth inhibition triggered by this drug. Fluorouracil 23-37 aquaporin 3 (Gill blood group) Homo sapiens 58-62 23017148-6 2012 Short incubations with 5-fluorouracil (5-FU) also induced AQP3 expression and increased cell volume, and the inhibition of AQP3 expression significantly blocked growth inhibition triggered by this drug. Fluorouracil 39-43 aquaporin 3 (Gill blood group) Homo sapiens 58-62 23017148-7 2012 To further establish whether AQP3 induction is related to cell cycle arrest and apoptosis, cells were exposed to long incubations with escalating doses of 5-FU. Fluorouracil 155-159 aquaporin 3 (Gill blood group) Homo sapiens 29-33 22998564-2 2012 High levels of thymidylate synthase (TS), the target enzyme of 5-FU and DPD which degrades the majority of 5-FU, are associated with poor prognosis in some cancers. Fluorouracil 63-67 thymidylate synthetase Homo sapiens 15-35 22998564-2 2012 High levels of thymidylate synthase (TS), the target enzyme of 5-FU and DPD which degrades the majority of 5-FU, are associated with poor prognosis in some cancers. Fluorouracil 63-67 thymidylate synthetase Homo sapiens 37-39 22912546-10 2012 When the relationship between TP, OPRT, TS and DPD mRNA expression levels and the sensitivity of CCA tissues to 5-FU was examined, only OPRT mRNA expression was significantly correlated with the response to 5-FU. Fluorouracil 207-211 uridine monophosphate synthetase Homo sapiens 136-140 22912546-13 2012 Whether OPRT mRNA could be used to predict the success of 5-FU chemotherapy in CCA patients requires confirmation in patients. Fluorouracil 58-62 uridine monophosphate synthetase Homo sapiens 8-12 18458674-8 2008 We also demonstrate that SPARC repression in CRC cell lines could be reversed following exposure to 5-Aza, which resulted in increased SPARC expression, leading to a significant reduction in cell viability (by an additional 39% in RKO cells) and greater apoptosis (an additional 18% in RKO cells), when combined with 5-FU in vitro (in comparison to 5-FU alone). Fluorouracil 317-321 secreted protein acidic and cysteine rich Homo sapiens 25-30 22931617-6 2012 CONCLUSION: OPRT expression in colorectal carcinoma tissues is not correlated with the toxicities of 5-FU-based regimen, but OPRT expression in the normal tissues can help predict the toxicities associated with 5-FU. Fluorouracil 211-215 uridine monophosphate synthetase Homo sapiens 125-129 22315133-2 2012 The aim of this study was to investigate whether 14-3-3sigma expression is also associated with resistance to neoadjuvant chemotherapy consisting of paclitaxel followed by 5-FU/epirubicin/cyclophosphamide (P-FEC) in human breast cancer patients. Fluorouracil 172-176 stratifin Homo sapiens 49-60 24750599-4 2012 BRP alone or combined with 5-FU could significantly inhibit Sarcoma-180 (S180) tumor growth and increase the spleen index in a dose-dependent manner. Fluorouracil 27-31 growth differentiation factor 5 Mus musculus 0-3 24750599-5 2012 Meanwhile a synergistic effect was observed in boosting various immunity functions when the tumor bearing mice receiving BRP plus 5-FU administration, such as stimulating lymphocytes proliferation, increasing NK cell cytotoxicity, enhancing serum interleukin-2 (IL-2) and interferon-gamma (TNF-gamma) secretion, as well as augmenting CD4+ and CD8+ spleen T lymphocytes subsets. Fluorouracil 130-134 interleukin 2 Mus musculus 247-260 24750599-5 2012 Meanwhile a synergistic effect was observed in boosting various immunity functions when the tumor bearing mice receiving BRP plus 5-FU administration, such as stimulating lymphocytes proliferation, increasing NK cell cytotoxicity, enhancing serum interleukin-2 (IL-2) and interferon-gamma (TNF-gamma) secretion, as well as augmenting CD4+ and CD8+ spleen T lymphocytes subsets. Fluorouracil 130-134 interleukin 2 Mus musculus 262-266 24750599-7 2012 In conclusion, the combination of BRP may boost the suppressed immunity in tumor bearing mice subject to 5-FU chemotherapy, and could serve as a new, promising approach for cancer treatment. Fluorouracil 105-109 growth differentiation factor 5 Mus musculus 34-37 18458674-8 2008 We also demonstrate that SPARC repression in CRC cell lines could be reversed following exposure to 5-Aza, which resulted in increased SPARC expression, leading to a significant reduction in cell viability (by an additional 39% in RKO cells) and greater apoptosis (an additional 18% in RKO cells), when combined with 5-FU in vitro (in comparison to 5-FU alone). Fluorouracil 317-321 secreted protein acidic and cysteine rich Homo sapiens 135-140 18458674-8 2008 We also demonstrate that SPARC repression in CRC cell lines could be reversed following exposure to 5-Aza, which resulted in increased SPARC expression, leading to a significant reduction in cell viability (by an additional 39% in RKO cells) and greater apoptosis (an additional 18% in RKO cells), when combined with 5-FU in vitro (in comparison to 5-FU alone). Fluorouracil 349-353 secreted protein acidic and cysteine rich Homo sapiens 25-30 18458674-8 2008 We also demonstrate that SPARC repression in CRC cell lines could be reversed following exposure to 5-Aza, which resulted in increased SPARC expression, leading to a significant reduction in cell viability (by an additional 39% in RKO cells) and greater apoptosis (an additional 18% in RKO cells), when combined with 5-FU in vitro (in comparison to 5-FU alone). Fluorouracil 349-353 secreted protein acidic and cysteine rich Homo sapiens 135-140 18553230-5 2008 The low level of dihydropyrimidine denhydrogenase (DPD), thymidylate synthase (TS) activities, and a high level of orotate phosphoribosyl-transferase (OPRT) activity enhance the antitumor effect of 5-FU and S-1. Fluorouracil 198-202 uridine monophosphate synthetase Homo sapiens 115-149 18553230-5 2008 The low level of dihydropyrimidine denhydrogenase (DPD), thymidylate synthase (TS) activities, and a high level of orotate phosphoribosyl-transferase (OPRT) activity enhance the antitumor effect of 5-FU and S-1. Fluorouracil 198-202 uridine monophosphate synthetase Homo sapiens 151-155 18497992-6 2008 5-FU-induced activation of EGFR followed by radiation in SW480 cells resulted in up-regulation of ERCC1. Fluorouracil 0-4 ERCC excision repair 1, endonuclease non-catalytic subunit Homo sapiens 98-103 18497992-7 2008 In contrast, 5-FU-induced degradation of EGFR followed by radiation in the other radiosensitive cell lines resulted in down-regulation of ERCC1. Fluorouracil 13-17 ERCC excision repair 1, endonuclease non-catalytic subunit Homo sapiens 138-143 18497992-9 2008 Interaction of EGFR and ERCC1 might correlate with radiation-induced DNA damage when p53 mutant colon cancer cell lines are exposed to 5-FU followed by radiation. Fluorouracil 135-139 ERCC excision repair 1, endonuclease non-catalytic subunit Homo sapiens 24-29 18600533-1 2008 Fluorouracil (5FU) acts by RNA-incorporation and inhibition of thymidylate synthase; the first action is counteracted by uridine, and the second is enhanced by leucovorin (LV). Fluorouracil 0-12 thymidylate synthetase Homo sapiens 63-83 22267605-6 2012 Furthermore, Gata3 mutant hematopoietic progenitor cells fail to be recruited into an increased cycling state after 5-fluorouracil-induced myelosuppression. Fluorouracil 116-130 GATA binding protein 3 Mus musculus 13-18 22188649-6 2012 Inhibition of Chk1 kinase by UCN-01 increased 5-FU-induced gammaH2AX and enhanced 5-FU cytotoxicity not only in wild-type cells but also in Rad54- or BRCA2-deficient cells, suggesting that HRR and Chk1 kinase have non-overlapping roles in 5-FU tolerance. Fluorouracil 46-50 BRCA2, DNA repair associated Gallus gallus 150-155 22206670-5 2012 Moreover, we found that TQ enhanced the 5-FU-induced killing of gastric cancer cells by mediating the downregulation of the anti-apoptotic protein bcl-2, the upregulation of the pro-apoptotic protein bax, and the activation of both caspase-3 and caspase-9. Fluorouracil 40-44 caspase 9 Homo sapiens 246-255 22206670-7 2012 These data suggest that the TQ/5-FU combined treatment induces apoptosis by enhancing the activation of both caspase-3 and caspase-9 in gastric cancer cells. Fluorouracil 31-35 caspase 9 Homo sapiens 123-132 22216841-9 2012 Colorectal-cancer cell lines overexpressing DKK4 showed increased chemoresistance to fluorouracil but not irinotecan or oxaliplatin. Fluorouracil 85-97 dickkopf WNT signaling pathway inhibitor 4 Homo sapiens 44-48 21989268-0 2012 Identification of phosphorylated serine-15 and -82 residues of HSPB1 in 5-fluorouracil-resistant colorectal cancer cells by proteomics. Fluorouracil 72-86 heat shock protein family B (small) member 1 Homo sapiens 63-68 21989268-5 2012 Short interfering RNA knockdown of endogenous HSPB1 in DLD-1/5-FU cells restored the sensitivity to 5-FU. Fluorouracil 61-65 heat shock protein family B (small) member 1 Homo sapiens 46-51 21989268-7 2012 The current findings indicate that phosphorylated HSPB1 may play an important role in 5-FU resistance. Fluorouracil 86-90 heat shock protein family B (small) member 1 Homo sapiens 50-55 21359954-4 2012 In MDA-MB-453 cells, DNMT3b KD reduces the IC(50) for DOX from 0.086 to 0.048 muM (44% reduction), for PAX from 0.497 to 0.376 nM (24%), and for 5-FU from 0.817 to 0.145 mM (82%). Fluorouracil 145-149 DNA methyltransferase 3 beta Homo sapiens 21-27 21359954-6 2012 5-aza treatment of DNMT3b KD cells reduced the IC(50) for DOX to 0.036 muM (59%), for PAX to 0.313 nM (37%) and for 5-FU to 0.067 (92%). Fluorouracil 116-120 DNA methyltransferase 3 beta Homo sapiens 19-25 21359954-8 2012 The effectiveness of DOX, PAX, and 5-FU is enhanced through targeted and/or pharmacological inhibition of DNMT3b, strongly suggesting that combined epigenetic and cytotoxic treatment will improve the efficacy of breast cancer chemotherapy. Fluorouracil 35-39 DNA methyltransferase 3 beta Homo sapiens 106-112 21940361-0 2012 Predictive value of expression of ERCC 1 and GST-p for 5-fluorouracil/oxaliplatin chemotherapy in advanced colorectal cancer. Fluorouracil 55-69 ERCC excision repair 1, endonuclease non-catalytic subunit Homo sapiens 34-40 21940361-0 2012 Predictive value of expression of ERCC 1 and GST-p for 5-fluorouracil/oxaliplatin chemotherapy in advanced colorectal cancer. Fluorouracil 55-69 glutathione S-transferase pi 1 Homo sapiens 45-50 21940361-9 2012 CONCLUSIONS: Immunohistochemical studies for ERCC-1 and GST-p may be useful in prediction of the response to 5-fluorouracil/oxaliplatin chemotherapy in advanced colorectal cancer patients. Fluorouracil 109-123 ERCC excision repair 1, endonuclease non-catalytic subunit Homo sapiens 45-51 21940361-9 2012 CONCLUSIONS: Immunohistochemical studies for ERCC-1 and GST-p may be useful in prediction of the response to 5-fluorouracil/oxaliplatin chemotherapy in advanced colorectal cancer patients. Fluorouracil 109-123 glutathione S-transferase pi 1 Homo sapiens 56-61 22567180-10 2012 CONCLUSIONS: ERCC1 C118T may be a predictive marker of treatment response to 5-FU/platinum chemotherapy for CRC. Fluorouracil 77-81 ERCC excision repair 1, endonuclease non-catalytic subunit Homo sapiens 13-18 22205615-8 2012 5-FU treatment greatly inhibited the expression of the major stemness-associated genes NANOG, OCT4, and SOX2. Fluorouracil 0-4 POU class 5 homeobox 1 Homo sapiens 94-98 22740861-1 2012 Irinotecan hydrochloride (CPT-11) is reported to be involved in the downregulation of thymidylate synthase (TS), a target molecule of 5-fluorouracil (5-FU) and oral fluoropyrimidine S-1. Fluorouracil 134-148 thymidylate synthetase Homo sapiens 86-106 22740861-1 2012 Irinotecan hydrochloride (CPT-11) is reported to be involved in the downregulation of thymidylate synthase (TS), a target molecule of 5-fluorouracil (5-FU) and oral fluoropyrimidine S-1. Fluorouracil 150-154 thymidylate synthetase Homo sapiens 86-106 23056627-0 2012 Transcriptional activation and cell cycle block are the keys for 5-fluorouracil induced up-regulation of human thymidylate synthase expression. Fluorouracil 65-79 thymidylate synthetase Homo sapiens 111-131 23056627-1 2012 BACKGROUND: 5-fluorouracil, a commonly used chemotherapeutic agent, up-regulates expression of human thymidylate synthase (hTS). Fluorouracil 12-26 thymidylate synthetase Homo sapiens 101-121 23056627-8 2012 CONCLUSIONS/SIGNIFICANCE: Altogether, our data indicate that constitutive TYMS mRNA transcription, cell cycle-induced hTS regulation and hTS enzyme stability are the three key mechanisms responsible for 5-fluorouracil induced up-regulation of human thymidylate synthase expression in the two ovarian cancer cell lines studied. Fluorouracil 203-217 thymidylate synthetase Homo sapiens 74-78 23056627-8 2012 CONCLUSIONS/SIGNIFICANCE: Altogether, our data indicate that constitutive TYMS mRNA transcription, cell cycle-induced hTS regulation and hTS enzyme stability are the three key mechanisms responsible for 5-fluorouracil induced up-regulation of human thymidylate synthase expression in the two ovarian cancer cell lines studied. Fluorouracil 203-217 thymidylate synthetase Homo sapiens 249-269 18600533-1 2008 Fluorouracil (5FU) acts by RNA-incorporation and inhibition of thymidylate synthase; the first action is counteracted by uridine, and the second is enhanced by leucovorin (LV). Fluorouracil 14-17 thymidylate synthetase Homo sapiens 63-83 18600534-0 2008 Functional inactivity and mutations of p53 differentially affect sensitivity to 5-fluorouracil and antifolate inhibitors of thymidylate synthase (TS) by altering TS levels in colorectal cancer cells. Fluorouracil 80-94 thymidylate synthetase Homo sapiens 162-164 18245778-1 2008 BACKGROUND: Low tumour expression levels of thymidylate synthase (TS), dihydropyrimidine dehydrogenase (DPD) and thymidine phosphorylase (TP) have been linked with improved outcome for colorectal cancer (CRC) patients treated with 5-fluorouracil (5-FU). Fluorouracil 231-245 thymidylate synthetase Homo sapiens 44-64 22496803-1 2012 5-Fluorouracil (5FU), a widely used chemotherapeutic drug, inhibits the DNA replicative enzyme, thymidylate synthase (Tyms). Fluorouracil 0-14 thymidylate synthetase Homo sapiens 96-116 22496803-1 2012 5-Fluorouracil (5FU), a widely used chemotherapeutic drug, inhibits the DNA replicative enzyme, thymidylate synthase (Tyms). Fluorouracil 0-14 thymidylate synthetase Homo sapiens 118-122 22496803-1 2012 5-Fluorouracil (5FU), a widely used chemotherapeutic drug, inhibits the DNA replicative enzyme, thymidylate synthase (Tyms). Fluorouracil 16-19 thymidylate synthetase Homo sapiens 96-116 22496803-1 2012 5-Fluorouracil (5FU), a widely used chemotherapeutic drug, inhibits the DNA replicative enzyme, thymidylate synthase (Tyms). Fluorouracil 16-19 thymidylate synthetase Homo sapiens 118-122 22496803-3 2012 Clinical associations between 5FU-related toxicity and the TYMS VNTR were reported, however, results were inconsistent, suggesting that additional genetic variation in the TYMS gene might influence Tyms expression. Fluorouracil 30-33 thymidylate synthetase Homo sapiens 59-63 18245778-1 2008 BACKGROUND: Low tumour expression levels of thymidylate synthase (TS), dihydropyrimidine dehydrogenase (DPD) and thymidine phosphorylase (TP) have been linked with improved outcome for colorectal cancer (CRC) patients treated with 5-fluorouracil (5-FU). Fluorouracil 247-251 thymidylate synthetase Homo sapiens 44-64 18473752-2 2008 The metabolism of 5FU requires the activity of thymidylate synthase (TS) and dihydropyrimidine dehydrogenase (DPD) among other enzymes. Fluorouracil 18-21 thymidylate synthetase Homo sapiens 47-67 22039255-8 2011 Dmtf1(-/-) BM cells showed hyper proliferation after 5-fluorouracil-induced myeloablation. Fluorouracil 53-67 cyclin D binding myb like transcription factor 1 Mus musculus 0-5 21723890-9 2011 Furthermore, a treatment combining Ad-miR-145 with 5-FU significantly showed anti-tumor effects, compared to treating alone. Fluorouracil 51-55 microRNA 145 Homo sapiens 38-45 18473752-2 2008 The metabolism of 5FU requires the activity of thymidylate synthase (TS) and dihydropyrimidine dehydrogenase (DPD) among other enzymes. Fluorouracil 18-21 thymidylate synthetase Homo sapiens 69-71 19110579-3 2008 Under conditions of 5-fluorouracil treatment, the effect of the adrenergic system was aimed at the formation of granulocytic and fibroblast-type cell complexes, activation of the production of colony-forming activity by microenvironmental cells, and acceleration of maturation of neutrophilic granulocytes associated with the system of granulocytic CSF and peripheral alpha-adrenergic structures. Fluorouracil 20-34 colony stimulating factor 2 Homo sapiens 349-352 21858274-5 2011 From the RLS assay, the sequence of five anticancer drugs activities was as follows: CTX < MTX < Pt < MMC < 5-Fu. Fluorouracil 120-124 cytochrome P450 family 27 subfamily A member 1 Homo sapiens 85-88 21791367-1 2011 INTRODUCTION/BACKGROUND: Pyrimidine antimetabolites" target molecules thymidylate synthase (TS) and flopropyrimidine-metabolising enzymes such as dihydropyrimidine dehydrogenase (DPD), thymidine phosphorylase (TP) and orotate phosphoribosyltransferase (OPRT) are known as biomarkers of 5-fluorouracil (5-FU) treatment. Fluorouracil 286-300 thymidylate synthetase Homo sapiens 70-90 17520254-0 2008 Expression level of thymidylate synthase mRNA reflects 5-fluorouracil sensitivity with low dose and long duration in primary colorectal cancer. Fluorouracil 55-69 thymidylate synthetase Homo sapiens 20-40 21791367-1 2011 INTRODUCTION/BACKGROUND: Pyrimidine antimetabolites" target molecules thymidylate synthase (TS) and flopropyrimidine-metabolising enzymes such as dihydropyrimidine dehydrogenase (DPD), thymidine phosphorylase (TP) and orotate phosphoribosyltransferase (OPRT) are known as biomarkers of 5-fluorouracil (5-FU) treatment. Fluorouracil 286-300 uridine monophosphate synthetase Homo sapiens 218-251 21791367-1 2011 INTRODUCTION/BACKGROUND: Pyrimidine antimetabolites" target molecules thymidylate synthase (TS) and flopropyrimidine-metabolising enzymes such as dihydropyrimidine dehydrogenase (DPD), thymidine phosphorylase (TP) and orotate phosphoribosyltransferase (OPRT) are known as biomarkers of 5-fluorouracil (5-FU) treatment. Fluorouracil 286-300 uridine monophosphate synthetase Homo sapiens 253-257 21791367-1 2011 INTRODUCTION/BACKGROUND: Pyrimidine antimetabolites" target molecules thymidylate synthase (TS) and flopropyrimidine-metabolising enzymes such as dihydropyrimidine dehydrogenase (DPD), thymidine phosphorylase (TP) and orotate phosphoribosyltransferase (OPRT) are known as biomarkers of 5-fluorouracil (5-FU) treatment. Fluorouracil 302-306 thymidylate synthetase Homo sapiens 70-90 21791367-1 2011 INTRODUCTION/BACKGROUND: Pyrimidine antimetabolites" target molecules thymidylate synthase (TS) and flopropyrimidine-metabolising enzymes such as dihydropyrimidine dehydrogenase (DPD), thymidine phosphorylase (TP) and orotate phosphoribosyltransferase (OPRT) are known as biomarkers of 5-fluorouracil (5-FU) treatment. Fluorouracil 302-306 uridine monophosphate synthetase Homo sapiens 218-251 18239605-0 2008 Oncolytic adenovirus-mediated shRNA against Apollon inhibits tumor cell growth and enhances antitumor effect of 5-fluorouracil. Fluorouracil 112-126 baculoviral IAP repeat containing 6 Homo sapiens 44-51 21791367-1 2011 INTRODUCTION/BACKGROUND: Pyrimidine antimetabolites" target molecules thymidylate synthase (TS) and flopropyrimidine-metabolising enzymes such as dihydropyrimidine dehydrogenase (DPD), thymidine phosphorylase (TP) and orotate phosphoribosyltransferase (OPRT) are known as biomarkers of 5-fluorouracil (5-FU) treatment. Fluorouracil 302-306 uridine monophosphate synthetase Homo sapiens 253-257 18357380-9 2008 The effects of 5-FU and SN-38 on thymidylate synthase (TS) protein expression, an important determinant of 5-FU sensitivity, were assessed by Western blot analysis in H69 cells. Fluorouracil 15-19 thymidylate synthetase Homo sapiens 33-53 21536130-1 2011 BACKGROUND AND OBJECTIVES: Thymidylate synthase (TS) expression levels appear to be related to response to 5-fluorouracil-(5-FU)-based chemotherapy in colorectal cancer (CRC) patients. Fluorouracil 107-121 thymidylate synthetase Homo sapiens 27-47 21536130-1 2011 BACKGROUND AND OBJECTIVES: Thymidylate synthase (TS) expression levels appear to be related to response to 5-fluorouracil-(5-FU)-based chemotherapy in colorectal cancer (CRC) patients. Fluorouracil 107-121 thymidylate synthetase Homo sapiens 49-51 21536130-1 2011 BACKGROUND AND OBJECTIVES: Thymidylate synthase (TS) expression levels appear to be related to response to 5-fluorouracil-(5-FU)-based chemotherapy in colorectal cancer (CRC) patients. Fluorouracil 123-127 thymidylate synthetase Homo sapiens 27-47 21536130-1 2011 BACKGROUND AND OBJECTIVES: Thymidylate synthase (TS) expression levels appear to be related to response to 5-fluorouracil-(5-FU)-based chemotherapy in colorectal cancer (CRC) patients. Fluorouracil 123-127 thymidylate synthetase Homo sapiens 49-51 21536130-3 2011 To evaluate the influence of TS expression and polymorphisms on clinical outcome of 5-FU-treated patients we performed a comprehensive genetic analysis on 63 CRC patients. Fluorouracil 84-88 thymidylate synthetase Homo sapiens 29-31 18357380-9 2008 The effects of 5-FU and SN-38 on thymidylate synthase (TS) protein expression, an important determinant of 5-FU sensitivity, were assessed by Western blot analysis in H69 cells. Fluorouracil 15-19 thymidylate synthetase Homo sapiens 55-57 18357380-9 2008 The effects of 5-FU and SN-38 on thymidylate synthase (TS) protein expression, an important determinant of 5-FU sensitivity, were assessed by Western blot analysis in H69 cells. Fluorouracil 107-111 thymidylate synthetase Homo sapiens 33-53 18357380-9 2008 The effects of 5-FU and SN-38 on thymidylate synthase (TS) protein expression, an important determinant of 5-FU sensitivity, were assessed by Western blot analysis in H69 cells. Fluorouracil 107-111 thymidylate synthetase Homo sapiens 55-57 21919605-8 2011 Specific combinations of functional polymorphisms in DPYD and TYMS were demonstrated to be associated with DFS and overall survival in patients receiving adjuvant 5-FU-based treatment. Fluorouracil 163-167 thymidylate synthetase Homo sapiens 62-66 18357380-10 2008 Treatment with SN-38 for 24 h suppressed TS protein expression and this low level of TS was maintained for at least 72 h. Pretreatment with SN-38 inhibited the 5-FU-induced increase of TS protein. Fluorouracil 160-164 thymidylate synthetase Homo sapiens 41-43 18357380-10 2008 Treatment with SN-38 for 24 h suppressed TS protein expression and this low level of TS was maintained for at least 72 h. Pretreatment with SN-38 inhibited the 5-FU-induced increase of TS protein. Fluorouracil 160-164 thymidylate synthetase Homo sapiens 85-87 18357380-10 2008 Treatment with SN-38 for 24 h suppressed TS protein expression and this low level of TS was maintained for at least 72 h. Pretreatment with SN-38 inhibited the 5-FU-induced increase of TS protein. Fluorouracil 160-164 thymidylate synthetase Homo sapiens 85-87 18357380-11 2008 The synergistic effect induced by the combination of SN-38 and 5-FU may be attributable to the SN-38-induced suppression of TS protein. Fluorouracil 63-67 thymidylate synthetase Homo sapiens 124-126 18377724-4 2008 Our results showed that CAS overexpression enhanced apoptosis induced by doxorubicin, 5-fluorouracil, cisplatin, and tamoxifen, but inhibited paclitaxel-induced apoptosis of cancer cells. Fluorouracil 86-100 chromosome segregation 1 like Homo sapiens 24-27 18377724-6 2008 CAS overexpression enhanced p53 accumulation induced by doxorubicin, 5-fluorouracil, cisplatin, tamoxifen, and etoposide. Fluorouracil 69-83 chromosome segregation 1 like Homo sapiens 0-3 18507058-5 2008 TS mRNA levels in the supernatants were inversely correlated with the in vitro sensitivity of cancer cells to 5-FU in the gastrointestinal group (p = 0.002). Fluorouracil 110-114 thymidylate synthetase Homo sapiens 0-2 21630057-2 2011 With this study, we aimed to elucidate the role of TS gene polymorphisms genotyping in therapy response in stage III colon carcinoma patients treated with 5-FU adjuvant chemotherapy. Fluorouracil 155-159 thymidylate synthetase Homo sapiens 51-53 21804305-1 2011 Capecitabine is an oral anticancer prodrug which is converted to 5-fluorouracil (5-FU) via 3 enzymatic steps, these being 5"-deoxy-5-fluorocytidine (5"-DFCR), 5"-deoxy-5-fluorouridine (5"-DFUR), and finally 5-FU by carboxylesterase (CES), cytidine deaminase (CDA), and thymidine phosphorylase (TP), respectively. Fluorouracil 65-79 cytidine deaminase Mus musculus 239-257 21804305-1 2011 Capecitabine is an oral anticancer prodrug which is converted to 5-fluorouracil (5-FU) via 3 enzymatic steps, these being 5"-deoxy-5-fluorocytidine (5"-DFCR), 5"-deoxy-5-fluorouridine (5"-DFUR), and finally 5-FU by carboxylesterase (CES), cytidine deaminase (CDA), and thymidine phosphorylase (TP), respectively. Fluorouracil 65-79 cytidine deaminase Mus musculus 259-262 21804305-1 2011 Capecitabine is an oral anticancer prodrug which is converted to 5-fluorouracil (5-FU) via 3 enzymatic steps, these being 5"-deoxy-5-fluorocytidine (5"-DFCR), 5"-deoxy-5-fluorouridine (5"-DFUR), and finally 5-FU by carboxylesterase (CES), cytidine deaminase (CDA), and thymidine phosphorylase (TP), respectively. Fluorouracil 81-85 cytidine deaminase Mus musculus 239-257 21804305-1 2011 Capecitabine is an oral anticancer prodrug which is converted to 5-fluorouracil (5-FU) via 3 enzymatic steps, these being 5"-deoxy-5-fluorocytidine (5"-DFCR), 5"-deoxy-5-fluorouridine (5"-DFUR), and finally 5-FU by carboxylesterase (CES), cytidine deaminase (CDA), and thymidine phosphorylase (TP), respectively. Fluorouracil 81-85 cytidine deaminase Mus musculus 259-262 18507058-6 2008 CONCLUSION: The cell-free mRNA transcripts in malignant effusions were highly detectable and cell-free TS mRNA in gastrointestinal cancer patients were strongly associated with the sensitivity of primary cancer cells to 5-FU in vitro. Fluorouracil 220-224 thymidylate synthetase Homo sapiens 103-105 18281538-1 2008 PURPOSE: The predictive role of the quantification of thymidylate synthase (TS) in tumors treated with antifolate drugs, such as 5-fluorouracil (5-FU), has been extensively reported in a variety of human tumors. Fluorouracil 129-143 thymidylate synthetase Homo sapiens 54-74 18281538-1 2008 PURPOSE: The predictive role of the quantification of thymidylate synthase (TS) in tumors treated with antifolate drugs, such as 5-fluorouracil (5-FU), has been extensively reported in a variety of human tumors. Fluorouracil 129-143 thymidylate synthetase Homo sapiens 76-78 18281538-1 2008 PURPOSE: The predictive role of the quantification of thymidylate synthase (TS) in tumors treated with antifolate drugs, such as 5-fluorouracil (5-FU), has been extensively reported in a variety of human tumors. Fluorouracil 145-149 thymidylate synthetase Homo sapiens 54-74 18281538-1 2008 PURPOSE: The predictive role of the quantification of thymidylate synthase (TS) in tumors treated with antifolate drugs, such as 5-fluorouracil (5-FU), has been extensively reported in a variety of human tumors. Fluorouracil 145-149 thymidylate synthetase Homo sapiens 76-78 18281538-9 2008 In patients with WD-NEC treated with 5-FU, high TS mRNA levels were associated with shorter time to progression (P = 0.002) and overall survival (P = 0.04). Fluorouracil 37-41 thymidylate synthetase Homo sapiens 48-50 18281538-12 2008 CONCLUSIONS: This study, for the first time, (a) reports the differential TS expression in the spectrum of NETs and (b) indicates TS as a possible predictive marker of treatment efficacy in WD-NEC patients treated with 5-FU. Fluorouracil 219-223 thymidylate synthetase Homo sapiens 74-76 18281538-12 2008 CONCLUSIONS: This study, for the first time, (a) reports the differential TS expression in the spectrum of NETs and (b) indicates TS as a possible predictive marker of treatment efficacy in WD-NEC patients treated with 5-FU. Fluorouracil 219-223 thymidylate synthetase Homo sapiens 130-132 18059190-5 2008 Myeloperoxidase activity in the proximal and mid small intestine were significantly lower in 5-FU+OO-treated rats compared to 5-FU+vehicle-treated controls (p < 0.05). Fluorouracil 93-97 myeloperoxidase Rattus norvegicus 0-15 22010341-13 2011 C-myc siRNA combination with 5-Fu could obviously increase cell apoptosis, even in the low concentration of 5-Fu (P < 0.05). Fluorouracil 29-33 MYC proto-oncogene, bHLH transcription factor Homo sapiens 0-5 22010341-13 2011 C-myc siRNA combination with 5-Fu could obviously increase cell apoptosis, even in the low concentration of 5-Fu (P < 0.05). Fluorouracil 108-112 MYC proto-oncogene, bHLH transcription factor Homo sapiens 0-5 22010341-15 2011 C-myc siRNA can effectively inhibit the expression of c-myc and has anti-proliferation effects, increasing the sensitivity of Hep-2 cells to 5-Fu. Fluorouracil 141-145 MYC proto-oncogene, bHLH transcription factor Homo sapiens 0-5 21610170-5 2011 Specifically, Endo possesses tumor antiangiogenesis activity that targets tumor endothelial cells, followed by CD, which converts the nontoxic prodrug 5-fluorocytosine (5-FC) to the cytotoxic antitumor drug 5-fluorouracil (5-FU) in the local tumor area. Fluorouracil 207-221 collagen type XVIII alpha 1 chain Homo sapiens 14-18 21610170-5 2011 Specifically, Endo possesses tumor antiangiogenesis activity that targets tumor endothelial cells, followed by CD, which converts the nontoxic prodrug 5-fluorocytosine (5-FC) to the cytotoxic antitumor drug 5-fluorouracil (5-FU) in the local tumor area. Fluorouracil 223-227 collagen type XVIII alpha 1 chain Homo sapiens 14-18 21613406-2 2011 These agents cause imbalances in deoxynucleotide triphosphate levels and the accumulation of uracil and 5-FU in the genome, events that activate the ATR- and ATM-dependent checkpoint signaling pathways and the base excision repair (BER) pathway. Fluorouracil 104-108 ATM serine/threonine kinase Homo sapiens 158-161 20665103-6 2011 CK5+ cells had lower proliferative indices than CK5- cells, were less sensitive to 5-fluorouracil and docetaxel, and cultures became enriched for CK5+ cells after treatments. Fluorouracil 83-97 keratin 5 Homo sapiens 0-3 21444628-2 2011 5-Fluorouracil (5-FU) belongs to antimetabolite chemotherapeutics, and its mechanism of cytotoxicity is involved in the inhibition of thymidylate synthase (TS). Fluorouracil 0-14 thymidylate synthetase Homo sapiens 134-154 21444628-2 2011 5-Fluorouracil (5-FU) belongs to antimetabolite chemotherapeutics, and its mechanism of cytotoxicity is involved in the inhibition of thymidylate synthase (TS). Fluorouracil 16-20 thymidylate synthetase Homo sapiens 134-154 18059190-5 2008 Myeloperoxidase activity in the proximal and mid small intestine were significantly lower in 5-FU+OO-treated rats compared to 5-FU+vehicle-treated controls (p < 0.05). Fluorouracil 126-130 myeloperoxidase Rattus norvegicus 0-15 17942376-1 2008 Thymidylate synthase (TS) is an important target of several chemotherapeutic agents, including 5-FU and raltitrexed (Tomudex). Fluorouracil 95-99 thymidylate synthetase Homo sapiens 0-20 21677839-9 2011 Periostin-silenced gastric cancer cells exhibited reduced cell proliferation, elevated sensitivity to chemotherapy with 5-fluorouracil, and decreased cell invasion and Snail expression (P < 0.05). Fluorouracil 120-134 periostin Homo sapiens 0-9 18035049-0 2008 Folylpolyglutamate synthase and gamma-glutamyl hydrolase regulate leucovorin-enhanced 5-fluorouracil anticancer activity. Fluorouracil 86-100 folylpolyglutamate synthase Homo sapiens 0-27 18035049-0 2008 Folylpolyglutamate synthase and gamma-glutamyl hydrolase regulate leucovorin-enhanced 5-fluorouracil anticancer activity. Fluorouracil 86-100 gamma-glutamyl hydrolase Homo sapiens 32-56 18035049-6 2008 These results suggest that FPGS and GGH expression levels in tumors are determinants of the efficacy of LV in enhancing the antitumor activity of 5-FU. Fluorouracil 146-150 folylpolyglutamate synthase Homo sapiens 27-31 18035049-6 2008 These results suggest that FPGS and GGH expression levels in tumors are determinants of the efficacy of LV in enhancing the antitumor activity of 5-FU. Fluorouracil 146-150 gamma-glutamyl hydrolase Homo sapiens 36-39 17943475-7 2008 TS-MMR expression was significantly (p=0.029 for whole series; p=0.004 for the 5-FU treated cases) related to response to treatment; tumours with low levels of both TS and MMR responded better (n=14/27, 51.8%) than those with high TS and MMR (n=3/18, 16.6%). Fluorouracil 79-83 thymidylate synthetase Homo sapiens 0-2 17943475-9 2008 CONCLUSIONS: The present data suggest that MSI patients with low TS and deficient MMR demonstrate a significantly shorter DFS and longer WMS than patients with high expression of both markers, and they are also more likely to obtain the greatest benefit from 5-FU based chemotherapy. Fluorouracil 259-263 thymidylate synthetase Homo sapiens 65-67 18607850-2 2008 This study aimed to assess the range of gene copies per nucleus of thymidylate synthase (TYMS), thymidine phosphorylase (TP) and dihydrofolate reductase (DHFR) in colorectal cancer, and to evaluate its prognostic significance following adjuvant chemotherapy, since these enzymes are closely related to efficacy of 5-fluorouracil (5FU). Fluorouracil 314-328 thymidylate synthetase Homo sapiens 67-87 18607850-2 2008 This study aimed to assess the range of gene copies per nucleus of thymidylate synthase (TYMS), thymidine phosphorylase (TP) and dihydrofolate reductase (DHFR) in colorectal cancer, and to evaluate its prognostic significance following adjuvant chemotherapy, since these enzymes are closely related to efficacy of 5-fluorouracil (5FU). Fluorouracil 314-328 thymidylate synthetase Homo sapiens 89-93 18607850-2 2008 This study aimed to assess the range of gene copies per nucleus of thymidylate synthase (TYMS), thymidine phosphorylase (TP) and dihydrofolate reductase (DHFR) in colorectal cancer, and to evaluate its prognostic significance following adjuvant chemotherapy, since these enzymes are closely related to efficacy of 5-fluorouracil (5FU). Fluorouracil 314-328 dihydrofolate reductase Homo sapiens 154-158 18607850-2 2008 This study aimed to assess the range of gene copies per nucleus of thymidylate synthase (TYMS), thymidine phosphorylase (TP) and dihydrofolate reductase (DHFR) in colorectal cancer, and to evaluate its prognostic significance following adjuvant chemotherapy, since these enzymes are closely related to efficacy of 5-fluorouracil (5FU). Fluorouracil 330-333 thymidylate synthetase Homo sapiens 67-87 18607850-2 2008 This study aimed to assess the range of gene copies per nucleus of thymidylate synthase (TYMS), thymidine phosphorylase (TP) and dihydrofolate reductase (DHFR) in colorectal cancer, and to evaluate its prognostic significance following adjuvant chemotherapy, since these enzymes are closely related to efficacy of 5-fluorouracil (5FU). Fluorouracil 330-333 thymidylate synthetase Homo sapiens 89-93 21892263-7 2008 The main purpose of our study was to look for a correlation between the levels of expression of the genes for sensitivity to 5-FU (TS, TP, DPD) within the tumor and the clinical response observed after three courses of chemotherapy combining 5-FU/platinum salt in patients presenting with advanced cancer of the pharyngo-larynx. Fluorouracil 125-129 thymidylate synthetase Homo sapiens 131-133 21892263-7 2008 The main purpose of our study was to look for a correlation between the levels of expression of the genes for sensitivity to 5-FU (TS, TP, DPD) within the tumor and the clinical response observed after three courses of chemotherapy combining 5-FU/platinum salt in patients presenting with advanced cancer of the pharyngo-larynx. Fluorouracil 242-246 thymidylate synthetase Homo sapiens 131-133 18197934-2 2008 Gene expression of 5-FU metabolic enzymes such as thymidylate synthase (TS), thymidine phosphorylase (TP), dihydropyrimidine dehydrogenase (DPD) and orotate phosphoribosyl transferase (OPRT), has recently been investigated in order to predict the 5-FU sensitivity of several cancers. Fluorouracil 19-23 thymidylate synthetase Homo sapiens 50-70 21609450-11 2011 Furthermore, HRH4 stimulation promoted the 5-Fu-induced cell apoptosis in HRH4-positive colorectal cells. Fluorouracil 43-47 histamine receptor H4 Homo sapiens 13-17 21609450-11 2011 Furthermore, HRH4 stimulation promoted the 5-Fu-induced cell apoptosis in HRH4-positive colorectal cells. Fluorouracil 43-47 histamine receptor H4 Homo sapiens 74-78 18197934-2 2008 Gene expression of 5-FU metabolic enzymes such as thymidylate synthase (TS), thymidine phosphorylase (TP), dihydropyrimidine dehydrogenase (DPD) and orotate phosphoribosyl transferase (OPRT), has recently been investigated in order to predict the 5-FU sensitivity of several cancers. Fluorouracil 19-23 thymidylate synthetase Homo sapiens 72-74 18197934-2 2008 Gene expression of 5-FU metabolic enzymes such as thymidylate synthase (TS), thymidine phosphorylase (TP), dihydropyrimidine dehydrogenase (DPD) and orotate phosphoribosyl transferase (OPRT), has recently been investigated in order to predict the 5-FU sensitivity of several cancers. Fluorouracil 19-23 uridine monophosphate synthetase Homo sapiens 149-183 18197934-2 2008 Gene expression of 5-FU metabolic enzymes such as thymidylate synthase (TS), thymidine phosphorylase (TP), dihydropyrimidine dehydrogenase (DPD) and orotate phosphoribosyl transferase (OPRT), has recently been investigated in order to predict the 5-FU sensitivity of several cancers. Fluorouracil 19-23 uridine monophosphate synthetase Homo sapiens 185-189 18197934-9 2008 TS and DPD mRNA expression levels may be useful indicators in predicting the anti-tumor activity of 5-FU in ESCC. Fluorouracil 100-104 thymidylate synthetase Homo sapiens 0-2 17640667-0 2008 Effect of IGF-I on healing of colonic anastomoses in rats under 5-FU treatment. Fluorouracil 64-68 insulin-like growth factor 1 Rattus norvegicus 10-15 21307648-7 2011 Myeloperoxidase levels in the jejunum of 5-FU treated rats were increased in vehicle and BR11 SN treatments compared to untreated controls, whereas no significant increase was observed after EcN SN treatment. Fluorouracil 41-45 myeloperoxidase Rattus norvegicus 0-15 17640667-1 2008 BACKGROUND: The aim of this experimental study was to investigate whether insulin-like growth factor I (IGF-I) can protect the colonic healing from the adverse effects of intraperitoneal administration of 5-fluorouracil (5-FU). Fluorouracil 205-219 insulin-like growth factor 1 Rattus norvegicus 74-102 17640667-1 2008 BACKGROUND: The aim of this experimental study was to investigate whether insulin-like growth factor I (IGF-I) can protect the colonic healing from the adverse effects of intraperitoneal administration of 5-fluorouracil (5-FU). Fluorouracil 205-219 insulin-like growth factor 1 Rattus norvegicus 104-109 17640667-1 2008 BACKGROUND: The aim of this experimental study was to investigate whether insulin-like growth factor I (IGF-I) can protect the colonic healing from the adverse effects of intraperitoneal administration of 5-fluorouracil (5-FU). Fluorouracil 221-225 insulin-like growth factor 1 Rattus norvegicus 74-102 17640667-1 2008 BACKGROUND: The aim of this experimental study was to investigate whether insulin-like growth factor I (IGF-I) can protect the colonic healing from the adverse effects of intraperitoneal administration of 5-fluorouracil (5-FU). Fluorouracil 221-225 insulin-like growth factor 1 Rattus norvegicus 104-109 17640667-9 2008 The administration of IGF-I resulted in a significant rise of bursting pressure in the IGF-I +5-FU group compared with the 5-FU group (P < 0.001). Fluorouracil 94-98 insulin-like growth factor 1 Rattus norvegicus 22-27 17640667-9 2008 The administration of IGF-I resulted in a significant rise of bursting pressure in the IGF-I +5-FU group compared with the 5-FU group (P < 0.001). Fluorouracil 94-98 insulin-like growth factor 1 Rattus norvegicus 87-92 17640667-9 2008 The administration of IGF-I resulted in a significant rise of bursting pressure in the IGF-I +5-FU group compared with the 5-FU group (P < 0.001). Fluorouracil 123-127 insulin-like growth factor 1 Rattus norvegicus 22-27 20020938-4 2008 Our studies showed that CAS over-expression increased p53 accumulation and apoptosis induced by 5-fluorouracil, doxorubicin, cisplatin, and tamoxifen in HT-29 cancer cells. Fluorouracil 96-110 chromosome segregation 1 like Homo sapiens 24-27 21298326-7 2011 Furthermore, the CD26 effect was enhanced when apigenin was paired with chemotherapeutic agents utilized in the treatment of advanced colorectal cancer including irinotecan, 5-fluorouracil and oxaliplatin. Fluorouracil 174-188 dipeptidyl peptidase 4 Homo sapiens 17-21 17971768-0 2007 Combination therapy with PEG-IFN-alpha and 5-FU inhibits HepG2 tumour cell growth in nude mice by apoptosis of p53. Fluorouracil 43-47 transformation related protein 53, pseudogene Mus musculus 111-114 21068133-13 2011 An in vivo study found that CHD1L-shRNAs could inhibit xenograft tumour growth and increase the sensitivity of tumour cells to 5-FU in nude mice. Fluorouracil 127-131 chromodomain helicase DNA binding protein 1-like Mus musculus 28-33 18056454-0 2007 Choline kinase down-regulation increases the effect of 5-fluorouracil in breast cancer cells. Fluorouracil 55-69 choline kinase alpha Homo sapiens 0-14 21480341-8 2011 In mouse xenograft models, combination of a CD13 inhibitor and the genotoxic chemotherapeutic fluorouracil (5-FU) drastically reduced tumor volume compared with either agent alone. Fluorouracil 108-112 alanyl (membrane) aminopeptidase Mus musculus 44-48 21480341-9 2011 5-FU inhibited CD90+ proliferating CSCs, some of which produce CD13+ semiquiescent CSCs, while CD13 inhibition suppressed the self-renewing and tumor-initiating ability of dormant CSCs. Fluorouracil 0-4 alanyl (membrane) aminopeptidase Mus musculus 63-67 21468552-7 2011 A similar reaction has also been observed in patients with the XRCC1 Arg399Gln polymorphism, while patients with the GSTP1 Ile105Val polymorphism have an improved response to oxaliplatin/5FU therapy. Fluorouracil 187-190 glutathione S-transferase pi 1 Homo sapiens 117-122 17982676-6 2007 Compared to 5-FU-treated TP53-proficient HCT116 cultures, 5-FU-treated TP53-depleted HCT116 cultures showed lack of CDKN1A induction, decreased apoptotic levels, decreased FAS and TNFRSF10B transcript levels and cleaved PARP protein levels, G1/S transition arrests, decreased CCND1 protein levels, and smaller intra-S phase arrests. Fluorouracil 58-62 TNF receptor superfamily member 10b Homo sapiens 180-189 21449674-4 2011 RESULTS: Of the 24 genes analyzed, 13 produced significant changes on the phenotype of sensitivity to 5-FU (DHFR, DPYS, DTYMK, DUT, FPGS, GGH, NME1, NT5C, RRM1, TYMS, UCK2, UNG and UMPS). Fluorouracil 102-106 dihydrofolate reductase Homo sapiens 108-112 21449674-4 2011 RESULTS: Of the 24 genes analyzed, 13 produced significant changes on the phenotype of sensitivity to 5-FU (DHFR, DPYS, DTYMK, DUT, FPGS, GGH, NME1, NT5C, RRM1, TYMS, UCK2, UNG and UMPS). Fluorouracil 102-106 folylpolyglutamate synthase Homo sapiens 132-136 17996122-8 2007 The 5-Fu treatment nearly abolishes transcription of hTERT (the major component of telomerase) mRNA. Fluorouracil 4-8 telomerase reverse transcriptase Homo sapiens 53-58 21449674-4 2011 RESULTS: Of the 24 genes analyzed, 13 produced significant changes on the phenotype of sensitivity to 5-FU (DHFR, DPYS, DTYMK, DUT, FPGS, GGH, NME1, NT5C, RRM1, TYMS, UCK2, UNG and UMPS). Fluorouracil 102-106 gamma-glutamyl hydrolase Homo sapiens 138-141 21449674-4 2011 RESULTS: Of the 24 genes analyzed, 13 produced significant changes on the phenotype of sensitivity to 5-FU (DHFR, DPYS, DTYMK, DUT, FPGS, GGH, NME1, NT5C, RRM1, TYMS, UCK2, UNG and UMPS). Fluorouracil 102-106 5', 3'-nucleotidase, cytosolic Homo sapiens 149-153 21449674-4 2011 RESULTS: Of the 24 genes analyzed, 13 produced significant changes on the phenotype of sensitivity to 5-FU (DHFR, DPYS, DTYMK, DUT, FPGS, GGH, NME1, NT5C, RRM1, TYMS, UCK2, UNG and UMPS). Fluorouracil 102-106 thymidylate synthetase Homo sapiens 161-165 17711513-6 2007 The overexpression of Gadd45beta in HCC cell lines also induces drug resistance against 5-FU. Fluorouracil 88-92 growth arrest and DNA damage inducible beta Homo sapiens 22-32 21449674-4 2011 RESULTS: Of the 24 genes analyzed, 13 produced significant changes on the phenotype of sensitivity to 5-FU (DHFR, DPYS, DTYMK, DUT, FPGS, GGH, NME1, NT5C, RRM1, TYMS, UCK2, UNG and UMPS). Fluorouracil 102-106 uridine monophosphate synthetase Homo sapiens 181-185 21222484-0 2011 Effect of the thymidylate synthase inhibitors on dUTP and TTP pool levels and the activities of DNA repair glycosylases on uracil and 5-fluorouracil in DNA. Fluorouracil 134-148 thymidylate synthetase Homo sapiens 14-34 21222484-1 2011 5-Fluorouracil (5-FU), 5-fluorodeoxyuridine (5-dUrd), and raltitrixed (RTX) are anticancer agents that target thymidylate synthase (TS), thereby blocking the conversion of dUMP into dTMP. Fluorouracil 0-14 thymidylate synthetase Homo sapiens 110-130 21222484-1 2011 5-Fluorouracil (5-FU), 5-fluorodeoxyuridine (5-dUrd), and raltitrixed (RTX) are anticancer agents that target thymidylate synthase (TS), thereby blocking the conversion of dUMP into dTMP. Fluorouracil 16-20 thymidylate synthetase Homo sapiens 110-130 17914563-0 2007 Decreased expression of hMLH1 correlates with reduced 5-fluorouracil-mediated apoptosis in colon cancer cells. Fluorouracil 54-68 mutL homolog 1 Homo sapiens 24-29 20647221-1 2011 BACKGROUND: To assess the predictive value of polymorphism in nine genes, primarily thymidylate synthase (TS) and orotate phosphoribosyltransferase (OPRT), which relates to 5-fluorouracil (5-FU) metabolism, for toxicity in patients treated with oral uracil/tegafur (UFT) plus leucovorin (LV). Fluorouracil 173-187 thymidylate synthetase Homo sapiens 84-104 20647221-1 2011 BACKGROUND: To assess the predictive value of polymorphism in nine genes, primarily thymidylate synthase (TS) and orotate phosphoribosyltransferase (OPRT), which relates to 5-fluorouracil (5-FU) metabolism, for toxicity in patients treated with oral uracil/tegafur (UFT) plus leucovorin (LV). Fluorouracil 173-187 uridine monophosphate synthetase Homo sapiens 114-147 20647221-1 2011 BACKGROUND: To assess the predictive value of polymorphism in nine genes, primarily thymidylate synthase (TS) and orotate phosphoribosyltransferase (OPRT), which relates to 5-fluorouracil (5-FU) metabolism, for toxicity in patients treated with oral uracil/tegafur (UFT) plus leucovorin (LV). Fluorouracil 173-187 uridine monophosphate synthetase Homo sapiens 149-153 20647221-1 2011 BACKGROUND: To assess the predictive value of polymorphism in nine genes, primarily thymidylate synthase (TS) and orotate phosphoribosyltransferase (OPRT), which relates to 5-fluorouracil (5-FU) metabolism, for toxicity in patients treated with oral uracil/tegafur (UFT) plus leucovorin (LV). Fluorouracil 189-193 thymidylate synthetase Homo sapiens 84-104 20647221-1 2011 BACKGROUND: To assess the predictive value of polymorphism in nine genes, primarily thymidylate synthase (TS) and orotate phosphoribosyltransferase (OPRT), which relates to 5-fluorouracil (5-FU) metabolism, for toxicity in patients treated with oral uracil/tegafur (UFT) plus leucovorin (LV). Fluorouracil 189-193 uridine monophosphate synthetase Homo sapiens 114-147 20647221-1 2011 BACKGROUND: To assess the predictive value of polymorphism in nine genes, primarily thymidylate synthase (TS) and orotate phosphoribosyltransferase (OPRT), which relates to 5-fluorouracil (5-FU) metabolism, for toxicity in patients treated with oral uracil/tegafur (UFT) plus leucovorin (LV). Fluorouracil 189-193 uridine monophosphate synthetase Homo sapiens 149-153 17914563-2 2007 However, the effect of hMLH1 on the cytotoxicity induced by 5-FU has not yet been sufficiently confirmed. Fluorouracil 60-64 mutL homolog 1 Homo sapiens 23-28 17914563-3 2007 In this study, we assessed the effect of hMLH1 on cytotoxicity and apoptosis induced by 5-FU using newly developed cell lines. Fluorouracil 88-92 mutL homolog 1 Homo sapiens 41-46 17914563-7 2007 In both of our two cell lines, hMLH1-deficient cells exhibited approximately 2.4-fold clonal surviving fraction compared to hMLH1-proficient cells for 10 days after the administration of 5-FU. Fluorouracil 187-191 mutL homolog 1 Homo sapiens 31-36 17914563-8 2007 Additionally, hMLH1-deficient cells treated with 5-FU exhibited 34-45% less apoptosis than hMLH1-proficient cells according to the results of DAPI staining and Annexin-V assay. Fluorouracil 49-53 mutL homolog 1 Homo sapiens 14-19 17914563-8 2007 Additionally, hMLH1-deficient cells treated with 5-FU exhibited 34-45% less apoptosis than hMLH1-proficient cells according to the results of DAPI staining and Annexin-V assay. Fluorouracil 49-53 mutL homolog 1 Homo sapiens 91-96 17914563-8 2007 Additionally, hMLH1-deficient cells treated with 5-FU exhibited 34-45% less apoptosis than hMLH1-proficient cells according to the results of DAPI staining and Annexin-V assay. Fluorouracil 49-53 annexin A5 Homo sapiens 160-169 17914563-9 2007 Furthermore, hMLH1-deficient cells treated with 5-FU exhibited an approximately 2-fold greater incorporation of 5-FU into DNA than control cells, suggesting that the recognition of 5-FU-incorporated DNA is impaired in hMLH1-deficient cells, resulting in reduced apoptosis. Fluorouracil 48-52 mutL homolog 1 Homo sapiens 13-18 17914563-9 2007 Furthermore, hMLH1-deficient cells treated with 5-FU exhibited an approximately 2-fold greater incorporation of 5-FU into DNA than control cells, suggesting that the recognition of 5-FU-incorporated DNA is impaired in hMLH1-deficient cells, resulting in reduced apoptosis. Fluorouracil 48-52 mutL homolog 1 Homo sapiens 218-223 17914563-9 2007 Furthermore, hMLH1-deficient cells treated with 5-FU exhibited an approximately 2-fold greater incorporation of 5-FU into DNA than control cells, suggesting that the recognition of 5-FU-incorporated DNA is impaired in hMLH1-deficient cells, resulting in reduced apoptosis. Fluorouracil 112-116 mutL homolog 1 Homo sapiens 13-18 17914563-9 2007 Furthermore, hMLH1-deficient cells treated with 5-FU exhibited an approximately 2-fold greater incorporation of 5-FU into DNA than control cells, suggesting that the recognition of 5-FU-incorporated DNA is impaired in hMLH1-deficient cells, resulting in reduced apoptosis. Fluorouracil 112-116 mutL homolog 1 Homo sapiens 218-223 17914563-9 2007 Furthermore, hMLH1-deficient cells treated with 5-FU exhibited an approximately 2-fold greater incorporation of 5-FU into DNA than control cells, suggesting that the recognition of 5-FU-incorporated DNA is impaired in hMLH1-deficient cells, resulting in reduced apoptosis. Fluorouracil 112-116 mutL homolog 1 Homo sapiens 13-18 17914563-9 2007 Furthermore, hMLH1-deficient cells treated with 5-FU exhibited an approximately 2-fold greater incorporation of 5-FU into DNA than control cells, suggesting that the recognition of 5-FU-incorporated DNA is impaired in hMLH1-deficient cells, resulting in reduced apoptosis. Fluorouracil 112-116 mutL homolog 1 Homo sapiens 218-223 17914563-10 2007 Our conclusions were that decreased expression of hMLH1 in colon cancer cells reduced the apoptosis induced by 5-FU, suggesting that hMLH1 is a key determinant of 5-FU chemosensitivity. Fluorouracil 111-115 mutL homolog 1 Homo sapiens 50-55 17914563-10 2007 Our conclusions were that decreased expression of hMLH1 in colon cancer cells reduced the apoptosis induced by 5-FU, suggesting that hMLH1 is a key determinant of 5-FU chemosensitivity. Fluorouracil 111-115 mutL homolog 1 Homo sapiens 133-138 17914563-10 2007 Our conclusions were that decreased expression of hMLH1 in colon cancer cells reduced the apoptosis induced by 5-FU, suggesting that hMLH1 is a key determinant of 5-FU chemosensitivity. Fluorouracil 163-167 mutL homolog 1 Homo sapiens 50-55 17914563-10 2007 Our conclusions were that decreased expression of hMLH1 in colon cancer cells reduced the apoptosis induced by 5-FU, suggesting that hMLH1 is a key determinant of 5-FU chemosensitivity. Fluorouracil 163-167 mutL homolog 1 Homo sapiens 133-138 18396642-6 2007 The positive rate of hTERT mRNA expression was 90.0% (54/60) and positive cells showed resistance to 5-Fu and ADM. Fluorouracil 101-105 telomerase reverse transcriptase Homo sapiens 21-26 17854149-0 2007 Thymidylate synthase and thymidine phosphorylase gene expression as predictive parameters for the efficacy of 5-fluorouracil-based adjuvant chemotherapy for gastric cancer. Fluorouracil 110-124 thymidylate synthetase Homo sapiens 0-20 17854149-1 2007 AIM: To investigate the prognostic role of thymidylate synthase (TS) and thymidine phosphorylase (TP) mRNA levels in T3 or T4 gastric cancer treated with 5-fluorouracil-based adjuvant chemotherapy. Fluorouracil 154-168 thymidylate synthetase Homo sapiens 43-63 17854149-1 2007 AIM: To investigate the prognostic role of thymidylate synthase (TS) and thymidine phosphorylase (TP) mRNA levels in T3 or T4 gastric cancer treated with 5-fluorouracil-based adjuvant chemotherapy. Fluorouracil 154-168 thymidylate synthetase Homo sapiens 65-67 17854149-8 2007 CONCLUSION: Expression of TS and TP mRNA is a useful predictive parameter for the survival of postoperative gastric cancer patients after 5-fluorouracil-based adjuvant chemotherapy. Fluorouracil 138-152 thymidylate synthetase Homo sapiens 26-28 17845510-8 2007 The combination of BetA with IRT or OXT was effective against SNU-C5/5FU-R cells, and the combination of BetA with 5-fluorouracil, IRT or OXT was effective against SNU-C5/OXT-R cells. Fluorouracil 115-129 complement C5 Homo sapiens 168-176 17786329-3 2007 We designed a recombinant fusion construct of a phage display-generated anti-gpA33 single chain fragment, A33scFv, with cytosine deaminase from yeast (CDy), which converts 5-fluorocytosine (5-FC) into 5-fluorouracil (5-FU). Fluorouracil 201-215 glycoprotein A33 Homo sapiens 77-82 17786329-3 2007 We designed a recombinant fusion construct of a phage display-generated anti-gpA33 single chain fragment, A33scFv, with cytosine deaminase from yeast (CDy), which converts 5-fluorocytosine (5-FC) into 5-fluorouracil (5-FU). Fluorouracil 217-221 glycoprotein A33 Homo sapiens 77-82 17503221-7 2007 Bim isoforms were differentially regulated after chemotherapeutic drug 5-Fluorouracil (5-FU) treatment. Fluorouracil 71-85 BCL2 like 11 Homo sapiens 0-3 21133646-1 2011 The objective of this study was to determine whether the expressions of the excision cross-complementing (ERCC1), thymidylate synthase (TS) and glutathione S-transferase P1 (GSTP1) are predictive of clinical outcomes in advanced gastric cancer (AGC) patients receiving treatment with adjuvant 5-fluorouracil (5-FU) and cisplatin (FP) chemotherapy. Fluorouracil 293-307 glutathione S-transferase pi 1 Homo sapiens 174-179 21133646-1 2011 The objective of this study was to determine whether the expressions of the excision cross-complementing (ERCC1), thymidylate synthase (TS) and glutathione S-transferase P1 (GSTP1) are predictive of clinical outcomes in advanced gastric cancer (AGC) patients receiving treatment with adjuvant 5-fluorouracil (5-FU) and cisplatin (FP) chemotherapy. Fluorouracil 309-313 glutathione S-transferase pi 1 Homo sapiens 174-179 17503221-7 2007 Bim isoforms were differentially regulated after chemotherapeutic drug 5-Fluorouracil (5-FU) treatment. Fluorouracil 87-91 BCL2 like 11 Homo sapiens 0-3 18019677-1 2007 BACKGROUND/AIMS: 5-fluorouracil (5-FU)-related metabolic enzymes, including dihydropyrimidine dehydrogenase (DPD), thymidylate synthase (TS), thymidylate phosphorylase (TP), and orotate phosphoribosyl transferase (OPRT) are initial, rate-limiting enzymes in the metabolism of 5-FU. Fluorouracil 276-280 thymidylate synthetase Homo sapiens 137-139 21043999-6 2011 SCDSF and 5-Fu alone exerted opposite effects on Bax and Bcl-xL proteins, meanwhile SCDSF+5-Fu induced an almost complete suppression of Bcl-xL release and a dramatic increase in the Bax/Bcl-xL ratio. Fluorouracil 10-14 BCL2 associated X, apoptosis regulator a Danio rerio 49-52 21043999-6 2011 SCDSF and 5-Fu alone exerted opposite effects on Bax and Bcl-xL proteins, meanwhile SCDSF+5-Fu induced an almost complete suppression of Bcl-xL release and a dramatic increase in the Bax/Bcl-xL ratio. Fluorouracil 90-94 BCL2 associated X, apoptosis regulator a Danio rerio 183-186 17923759-0 2007 Change of the expression of human telomerase reverse transcriptase mRNA and human telomerase RNA after cisplatin and 5-fluorouracil exposure in head and neck squamous cell carcinoma cell lines. Fluorouracil 117-131 telomerase reverse transcriptase Homo sapiens 34-66 17923759-5 2007 Cell cytotoxicity, the change of telomerase activity, and hTERT mRNA and hTR expression by 5-FU and cisplatin exposure were assessed by MTT assay, TRAP assay, and real-time RT-PCR, respectively. Fluorouracil 91-95 telomerase reverse transcriptase Homo sapiens 58-63 17096160-3 2007 In this study, we report the results of hyperfractionation (Hfx) RTx with concurrent docetaxel, cisplatin and 5-fluorouracil (TPF) chemotherapy (CTx) in patients with locally advanced SCCHN and compare Hfx and Cfx RTx with concurrent TPF CTx. Fluorouracil 110-124 cytochrome P450 family 27 subfamily A member 1 Homo sapiens 145-148 21194879-5 2011 The chemosensitivity of cell lines with various expression levels of PTEN was evaluated using 5-flurouracil (5-FU), oxaliplatin and irinotecan (CPT), and clinical significance was evaluated by immunohistochemical analysis of 133 CRC specimens. Fluorouracil 109-113 phosphatase and tensin homolog Homo sapiens 69-73 21194879-7 2011 HT-29 and LoVo PTEN expression was suppressed by a low concentration of 5-FU and oxaliplatin; however, SW480 was insensitive to these chemotherapeutic agents. Fluorouracil 72-76 phosphatase and tensin homolog Homo sapiens 15-19 21194879-10 2011 CONCLUSION: Cell lines with a high expression of PTEN are sensitive to chemotherapy with 5-FU and oxaliplatin. Fluorouracil 89-93 phosphatase and tensin homolog Homo sapiens 49-53 21174056-0 2011 Combined therapy with a thymidylate synthase-inhibiting vector and S-1 has effective antitumor activity against 5-FU-resistant tumors. Fluorouracil 112-116 thymidylate synthetase Homo sapiens 24-44 21174056-1 2011 High levels of intratumoral thymidylate synthase (TS) expression are associated with resistance to 5-fluorourcil (5-FU). Fluorouracil 114-118 thymidylate synthetase Homo sapiens 28-48 21174056-1 2011 High levels of intratumoral thymidylate synthase (TS) expression are associated with resistance to 5-fluorourcil (5-FU). Fluorouracil 114-118 thymidylate synthetase Homo sapiens 50-52 20387074-2 2011 Several studies have evaluated in patients with colon cancer, either the role of genes involved in the 5-FU pathway, such as thymidylate synthase (TS), thymidine phosphorylase (TP) and dihydropyrimidine dehydrogenase (DPD) or the role of microsatellite instability (MSI) as prognostic or predictive markers for adjuvant chemotherapy efficacy, with discordant results. Fluorouracil 103-107 thymidylate synthetase Homo sapiens 125-145 20387074-2 2011 Several studies have evaluated in patients with colon cancer, either the role of genes involved in the 5-FU pathway, such as thymidylate synthase (TS), thymidine phosphorylase (TP) and dihydropyrimidine dehydrogenase (DPD) or the role of microsatellite instability (MSI) as prognostic or predictive markers for adjuvant chemotherapy efficacy, with discordant results. Fluorouracil 103-107 thymidylate synthetase Homo sapiens 147-149 20387074-8 2011 CONCLUSIONS: This retrospective investigation suggests that TS gene expression at mRNA level can be a useful marker of better survival in patients (especially of those with cancers of stage II) receiving 5-FU adjuvant chemotherapy, independently of the MSI status. Fluorouracil 204-208 thymidylate synthetase Homo sapiens 60-62 20425122-4 2011 RESULTS: In the urothelial bladder cancer cell lines RT4 and T24, 5-FU-induced TS inhibition proved to be associated with cell type-dependent (a) sensitivity to the drug, (b) Caspase-mediated apoptosis, (c) p53 stabilization and activation, as well as Rb phosphorylation and E2F1 expression and (d) transcriptional regulation of p53 target genes and their cognate proteins, while an E2F-dependent transcriptional network did not seem to be critically engaged in such type of responses. Fluorouracil 66-70 E2F transcription factor 1 Homo sapiens 275-279 17699714-7 2007 Bevacizumab/5-FU-induced growth suppression was associated with reduction in microvessel density, inhibition of cell proliferation; up-regulation of phosphatase and tensin homologue, p21(Cip1/Waf1), p16(INK4a), and p27(Kip1); hypophosphorylation of retinoblastoma protein; and inhibition of Akt/mammalian target of rapamycin pathway. Fluorouracil 12-16 interferon alpha inducible protein 27 Homo sapiens 215-218 17699714-7 2007 Bevacizumab/5-FU-induced growth suppression was associated with reduction in microvessel density, inhibition of cell proliferation; up-regulation of phosphatase and tensin homologue, p21(Cip1/Waf1), p16(INK4a), and p27(Kip1); hypophosphorylation of retinoblastoma protein; and inhibition of Akt/mammalian target of rapamycin pathway. Fluorouracil 12-16 cyclin dependent kinase inhibitor 1B Homo sapiens 219-223 17716232-1 2007 Several studies indicate that low thymidylate synthase (TS) protein levels in tumor and normal tissues of colorectal cancer patients are associated with better clinical response to fluorouracil-based chemotherapy and higher risk of toxicity. Fluorouracil 181-193 thymidylate synthetase Homo sapiens 34-54 17716232-1 2007 Several studies indicate that low thymidylate synthase (TS) protein levels in tumor and normal tissues of colorectal cancer patients are associated with better clinical response to fluorouracil-based chemotherapy and higher risk of toxicity. Fluorouracil 181-193 thymidylate synthetase Homo sapiens 56-58 17549346-1 2007 The enzyme orotate phosphoribosyl transferase (OPRT) is involved in the metabolism of the anticancer drug 5-fluorouracil (5-FU), and is a key enzyme for conversion of 5-FU to its active form in tumor tissue. Fluorouracil 106-120 uridine monophosphate synthetase Homo sapiens 47-51 20177420-4 2011 5-FU targets folate metabolism through inhibition of thymidylate synthase (TYMS). Fluorouracil 0-4 thymidylate synthetase Homo sapiens 53-73 20177420-4 2011 5-FU targets folate metabolism through inhibition of thymidylate synthase (TYMS). Fluorouracil 0-4 thymidylate synthetase Homo sapiens 75-79 17549346-1 2007 The enzyme orotate phosphoribosyl transferase (OPRT) is involved in the metabolism of the anticancer drug 5-fluorouracil (5-FU), and is a key enzyme for conversion of 5-FU to its active form in tumor tissue. Fluorouracil 122-126 uridine monophosphate synthetase Homo sapiens 47-51 17549346-1 2007 The enzyme orotate phosphoribosyl transferase (OPRT) is involved in the metabolism of the anticancer drug 5-fluorouracil (5-FU), and is a key enzyme for conversion of 5-FU to its active form in tumor tissue. Fluorouracil 167-171 uridine monophosphate synthetase Homo sapiens 47-51 17237819-4 2007 Forced expression of Reg IV inhibited 5-FU-induced apoptosis. Fluorouracil 38-42 regenerating family member 4 Homo sapiens 21-27 17237819-6 2007 Among 36 GC patients treated with a combination chemotherapy of low-dose 5-FU and cisplatin, all 14 Reg IV-positive patients showed no change or disease progression. Fluorouracil 73-77 regenerating family member 4 Homo sapiens 100-106 17237819-10 2007 These results indicate that expression of Reg IV is a marker for prediction of resistance to 5-FU-based chemotherapy in patients with GC. Fluorouracil 93-97 regenerating family member 4 Homo sapiens 42-48 17330233-0 2007 Thymidylate synthase and dihydropyrimidine dehydrogenase mRNA expression after administration of 5-fluorouracil to patients with colorectal cancer. Fluorouracil 97-111 thymidylate synthetase Homo sapiens 0-20 17330233-1 2007 This study explores the effect of 5-fluorouracil (5FU) exposure on mRNA levels of its target enzyme thymidylate synthase (TS) and the rate-limiting catabolic enzyme dihydropyrimidine dehydrogenase (DPD) in tumors of colorectal cancer patients. Fluorouracil 34-48 thymidylate synthetase Homo sapiens 100-120 17330233-1 2007 This study explores the effect of 5-fluorouracil (5FU) exposure on mRNA levels of its target enzyme thymidylate synthase (TS) and the rate-limiting catabolic enzyme dihydropyrimidine dehydrogenase (DPD) in tumors of colorectal cancer patients. Fluorouracil 34-48 thymidylate synthetase Homo sapiens 122-124 17330233-1 2007 This study explores the effect of 5-fluorouracil (5FU) exposure on mRNA levels of its target enzyme thymidylate synthase (TS) and the rate-limiting catabolic enzyme dihydropyrimidine dehydrogenase (DPD) in tumors of colorectal cancer patients. Fluorouracil 50-53 thymidylate synthetase Homo sapiens 100-120 17330233-1 2007 This study explores the effect of 5-fluorouracil (5FU) exposure on mRNA levels of its target enzyme thymidylate synthase (TS) and the rate-limiting catabolic enzyme dihydropyrimidine dehydrogenase (DPD) in tumors of colorectal cancer patients. Fluorouracil 50-53 thymidylate synthetase Homo sapiens 122-124 17570219-10 2007 XAF1 expression suppressed tumor cell growth and enhanced cellular response to various apoptotic stimuli, such as 5-fluorouracil, etoposide, H(2)O(2), gamma-irradiation, ultraviolet, and tumor necrosis factor-alpha, whereas knockdown of its expression protected cells from the stresses. Fluorouracil 114-128 XIAP associated factor 1 Homo sapiens 0-4 21542283-13 2011 It can be concluded that ASODN targeting apollon can suppress the expression of apollon mRNA, and inhibit the proliferation, induce apoptosis, arrest cell cycle at S phase of colorectal cancer Lovo cells in vitro and enhance the chemo-sensitivity to 5-FU, DDP and EPI. Fluorouracil 250-254 baculoviral IAP repeat containing 6 Homo sapiens 41-48 21542283-13 2011 It can be concluded that ASODN targeting apollon can suppress the expression of apollon mRNA, and inhibit the proliferation, induce apoptosis, arrest cell cycle at S phase of colorectal cancer Lovo cells in vitro and enhance the chemo-sensitivity to 5-FU, DDP and EPI. Fluorouracil 250-254 baculoviral IAP repeat containing 6 Homo sapiens 80-87 21067862-2 2011 Exposure to 5-FU at 30 muM activated phosphoinositide 3-kinase (PI3K)/Akt signaling markedly from 12h up to 48 h in the 5-FU-resistant cells compared with that in the parental cells and resulted in an overt difference in growth at those times. Fluorouracil 12-16 phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit delta Homo sapiens 37-62 21067862-2 2011 Exposure to 5-FU at 30 muM activated phosphoinositide 3-kinase (PI3K)/Akt signaling markedly from 12h up to 48 h in the 5-FU-resistant cells compared with that in the parental cells and resulted in an overt difference in growth at those times. Fluorouracil 120-124 phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit delta Homo sapiens 37-62 21255398-11 2011 Knockdown of RAD21 in the MDA-MB-231 breast cancer cell line significantly enhanced sensitivity to cyclophosphamide, 5-fluorouracil and etoposide. Fluorouracil 117-131 RAD21 cohesin complex component Homo sapiens 13-18 17311258-6 2007 We also looked for correlations between the expression of IAPs and resistance to paclitaxel, doxorubicin, CDDP and 5-fluorouracil, and found that resistance to these drugs correlates most significantly with expression of cIAP-2. Fluorouracil 115-129 baculoviral IAP repeat containing 3 Homo sapiens 221-227 17311258-7 2007 Using RNAi to downregulate these proteins we further confirmed that the levels of cIAP-2 and XIAP influence the response to the anti-cancer drugs, although only marginally for 5-FU. Fluorouracil 176-180 baculoviral IAP repeat containing 3 Homo sapiens 82-88 17119966-0 2007 Mechanisms of acquired chemoresistance to 5-fluorouracil and tomudex: thymidylate synthase dependent and independent networks. Fluorouracil 42-56 thymidylate synthetase Homo sapiens 70-90 17119966-1 2007 PURPOSE: Thymidylate synthase (TS) over-expression is widely accepted as a major molecular mechanism responsible for 5-fluorouracil (5-FU) and tomudex (TDX) resistance. Fluorouracil 117-131 thymidylate synthetase Homo sapiens 9-29 17119966-1 2007 PURPOSE: Thymidylate synthase (TS) over-expression is widely accepted as a major molecular mechanism responsible for 5-fluorouracil (5-FU) and tomudex (TDX) resistance. Fluorouracil 133-137 thymidylate synthetase Homo sapiens 9-29 17465714-3 2007 The most recent update regarding gastric cancer pharmacogenetics highlights a prominent role of genetic polymorphisms of thymidylate synthase and glutathione S-transferase in the pharmacological treatment with commonly used drugs, such as 5-fluorouracil and platinum derivatives. Fluorouracil 239-253 thymidylate synthetase Homo sapiens 121-141 17482957-2 2007 5-Fluorouracil (5-FU), an anticancer agent used clinically against various cancers, including prostate cancer, inhibits DNA synthesis by binding TS. Fluorouracil 0-14 thymidylate synthetase Homo sapiens 145-147 21468918-3 2011 More improved suppression of NIK, followed by the improved antiproliferative effect on Hep3B cells, was achieved when 5-FU was co-treated with siRNA. Fluorouracil 118-122 mitogen-activated protein kinase kinase kinase 14 Homo sapiens 29-32 21963492-6 2011 After 5-FU treatment, SCF mRNA levels in the BM markedly increased, approaching TGF-beta mRNA levels, whereas SCF levels in the spleen showed limited oscillations whose increases paralleled those in TGF-beta levels. Fluorouracil 6-10 kit ligand Mus musculus 22-25 21963492-6 2011 After 5-FU treatment, SCF mRNA levels in the BM markedly increased, approaching TGF-beta mRNA levels, whereas SCF levels in the spleen showed limited oscillations whose increases paralleled those in TGF-beta levels. Fluorouracil 6-10 kit ligand Mus musculus 110-113 17482957-2 2007 5-Fluorouracil (5-FU), an anticancer agent used clinically against various cancers, including prostate cancer, inhibits DNA synthesis by binding TS. Fluorouracil 16-20 thymidylate synthetase Homo sapiens 145-147 17417073-0 2007 Thymidylate synthase (TYMS) and dihydropyrimidine dehydrogenase (DPYD) polymorphisms in the Korean population for prediction of 5-fluorouracil-associated toxicity. Fluorouracil 128-142 thymidylate synthetase Homo sapiens 0-20 17417073-0 2007 Thymidylate synthase (TYMS) and dihydropyrimidine dehydrogenase (DPYD) polymorphisms in the Korean population for prediction of 5-fluorouracil-associated toxicity. Fluorouracil 128-142 thymidylate synthetase Homo sapiens 22-26 17417073-1 2007 The important cellular proteins for 5-fluorouracil (5-FU) metabolism are the major target enzymes, thymidylate synthase, and the rate-limiting enzyme in the degradation pathway, dihydropyrimidine dehydrogenase. Fluorouracil 36-50 thymidylate synthetase Homo sapiens 99-119 17417073-1 2007 The important cellular proteins for 5-fluorouracil (5-FU) metabolism are the major target enzymes, thymidylate synthase, and the rate-limiting enzyme in the degradation pathway, dihydropyrimidine dehydrogenase. Fluorouracil 52-56 thymidylate synthetase Homo sapiens 99-119 17417073-2 2007 Adverse drug reactions to 5-FU-based chemotherapy have been reported to be in part the result of polymorphisms in the thymidylate synthase (TYMS) and dihydropyrimidine dehydrogenase (DPYD) genes. Fluorouracil 26-30 thymidylate synthetase Homo sapiens 118-138 17417073-2 2007 Adverse drug reactions to 5-FU-based chemotherapy have been reported to be in part the result of polymorphisms in the thymidylate synthase (TYMS) and dihydropyrimidine dehydrogenase (DPYD) genes. Fluorouracil 26-30 thymidylate synthetase Homo sapiens 140-144 17265526-10 2007 CONCLUSIONS: The GSTP1*C variant conferred a possible protective effect against pancreatic cancer in older individuals and a significant survival advantage in patients who received 5-florouracil. Fluorouracil 181-194 glutathione S-transferase pi 1 Homo sapiens 17-22 17237997-8 2007 5-FU caused an 83% reduction in sucrase and a 510% increase in MPO activity. Fluorouracil 0-4 myeloperoxidase Rattus norvegicus 63-66 16724208-2 2007 Conflicting data exists about the relevance of MSI in predicting the prognosis and benefit of 5-fluorouracil (5-FU) based chemotherapy in patients with CRC. Fluorouracil 94-108 RB binding protein 4, chromatin remodeling factor Homo sapiens 47-50 20737575-8 2011 Furthermore, the authors demonstrated that miR-145 inhibited cell proliferation and sensitized LS174T cells to 5-fluorouracil-induced apoptosis. Fluorouracil 111-125 microRNA 145 Homo sapiens 43-50 16724208-3 2007 We investigated the usefulness of MSI as a predictor of distinct clinical attributes influencing recurrence rate and disease-free survival (DFS) subject to the use of adjuvant or palliative chemotherapy with 5-FU in stage II- stage IV CRC. Fluorouracil 208-212 RB binding protein 4, chromatin remodeling factor Homo sapiens 34-37 17096352-0 2007 The prognostic significance of thymidylate synthase and dihydropyrimidine dehydrogenase in colorectal cancer of 303 patients adjuvantly treated with 5-fluorouracil. Fluorouracil 149-163 thymidylate synthetase Homo sapiens 31-51 21362378-0 2011 Associations between gene polymorphisms of thymidylate synthase with its protein expression and chemosensitivity to 5-fluorouracil in pancreatic carcinoma cells. Fluorouracil 116-130 thymidylate synthetase Homo sapiens 43-63 21362378-3 2011 In this study, we investigated the associations between polymorphisms of the TS gene and its protein expression, and the implications on the efficacy of 5-fluorouracil (5-FU) in pancreatic cancer cells. Fluorouracil 153-167 thymidylate synthetase Homo sapiens 77-79 17096352-1 2007 Cytotoxic effect of 5-fluorouracil 5-FU is mediated through inhibition of thymidylate synthase (TS), and 5-FU is catabolised by dihydropyrimidine dehydrogenase (DPD). Fluorouracil 20-34 thymidylate synthetase Homo sapiens 74-94 21362378-3 2011 In this study, we investigated the associations between polymorphisms of the TS gene and its protein expression, and the implications on the efficacy of 5-fluorouracil (5-FU) in pancreatic cancer cells. Fluorouracil 169-173 thymidylate synthetase Homo sapiens 77-79 17096352-1 2007 Cytotoxic effect of 5-fluorouracil 5-FU is mediated through inhibition of thymidylate synthase (TS), and 5-FU is catabolised by dihydropyrimidine dehydrogenase (DPD). Fluorouracil 20-34 thymidylate synthetase Homo sapiens 96-98 21362378-12 2011 Cells with the 2R/2R and 2R/3R genotypes of TS were hypersensitive to 5-FU in vitro as compared with those with the 3R/3R cells. Fluorouracil 70-74 thymidylate synthetase Homo sapiens 44-46 21362378-13 2011 CONCLUSIONS: Polymorphisms in the TS gene influenced its protein expression and affected sensitivity of 5-FU in seven pancreatic cancer cell lines. Fluorouracil 104-108 thymidylate synthetase Homo sapiens 34-36 17096352-1 2007 Cytotoxic effect of 5-fluorouracil 5-FU is mediated through inhibition of thymidylate synthase (TS), and 5-FU is catabolised by dihydropyrimidine dehydrogenase (DPD). Fluorouracil 35-39 thymidylate synthetase Homo sapiens 74-94 21362378-15 2011 Cells of the 3R/3R genotype with high TS protein expression were shown lower 5-FU sensitivity than cells with the 2R/2R or 2R/3R genotypes. Fluorouracil 77-81 thymidylate synthetase Homo sapiens 38-40 17096352-1 2007 Cytotoxic effect of 5-fluorouracil 5-FU is mediated through inhibition of thymidylate synthase (TS), and 5-FU is catabolised by dihydropyrimidine dehydrogenase (DPD). Fluorouracil 35-39 thymidylate synthetase Homo sapiens 96-98 21362378-16 2011 These data warrant large-scale clinical studies to assess the role of polymorphisms in the TS gene on its protein expression and chemosensitivity to 5-FU in pancreatic cancer. Fluorouracil 149-153 thymidylate synthetase Homo sapiens 91-93 17096352-2 2007 Efficacy of 5-FU may therefore depend on the TS and DPD activity of colorectal cancer. Fluorouracil 12-16 thymidylate synthetase Homo sapiens 45-47 17203168-6 2007 Results show that TS genotype analysis clearly differentiates patients with a worst response to a 5-fluorouracil based chemotherapy. Fluorouracil 98-112 thymidylate synthetase Homo sapiens 18-20 21196216-1 2011 5-Fluorouracil (5-FU) interferes with tumor-cell proliferation by inhibiting thymidylate synthase (TS). Fluorouracil 0-14 thymidylate synthetase Homo sapiens 77-97 21196216-1 2011 5-Fluorouracil (5-FU) interferes with tumor-cell proliferation by inhibiting thymidylate synthase (TS). Fluorouracil 0-14 thymidylate synthetase Homo sapiens 99-101 21196216-1 2011 5-Fluorouracil (5-FU) interferes with tumor-cell proliferation by inhibiting thymidylate synthase (TS). Fluorouracil 16-20 thymidylate synthetase Homo sapiens 77-97 21196216-1 2011 5-Fluorouracil (5-FU) interferes with tumor-cell proliferation by inhibiting thymidylate synthase (TS). Fluorouracil 16-20 thymidylate synthetase Homo sapiens 99-101 21196216-3 2011 TS-TR variations were analyzed in 57 stage II-IV ESCC patients undergoing chemoradiotherapy combined with 5-FU and cisplatinum (CDDP), and in 106 controls. Fluorouracil 106-110 thymidylate synthetase Homo sapiens 0-2 17327702-7 2007 Furthermore, MDMX overexpression promotes resistance to the chemotherapeutic agent 5-FU, which at low concentrations activates p53 by inhibiting RNA metabolism. Fluorouracil 83-87 MDM4 regulator of p53 Homo sapiens 13-17 17192711-6 2007 CONCLUSION: The results suggest that OPRT is a main enzyme participating in the phosphorylation of 5-fluorouracil and has an important role in tumor growth. Fluorouracil 99-113 uridine monophosphate synthetase Homo sapiens 37-41 18095079-8 2007 CONCLUSION: These results suggest that the OPRT level is significantly higher in gastric carcinoma tissue than in normal gastric mucosa and that the OPRT level in gastric carcinoma is a novel variable that is independent of the levels of other previously known enzymes related to 5-fluorouracil (FU) metabolism. Fluorouracil 280-294 uridine monophosphate synthetase Homo sapiens 149-153 16538493-1 2007 BACKGROUND AND AIMS: Thymidylate synthase (TS) is an important enzyme for DNA synthesis and the target for 5-fluorouracil (5-FU). Fluorouracil 107-121 thymidylate synthetase Homo sapiens 21-41 16538493-1 2007 BACKGROUND AND AIMS: Thymidylate synthase (TS) is an important enzyme for DNA synthesis and the target for 5-fluorouracil (5-FU). Fluorouracil 107-121 thymidylate synthetase Homo sapiens 43-45 16538493-1 2007 BACKGROUND AND AIMS: Thymidylate synthase (TS) is an important enzyme for DNA synthesis and the target for 5-fluorouracil (5-FU). Fluorouracil 123-127 thymidylate synthetase Homo sapiens 21-41 16538493-1 2007 BACKGROUND AND AIMS: Thymidylate synthase (TS) is an important enzyme for DNA synthesis and the target for 5-fluorouracil (5-FU). Fluorouracil 123-127 thymidylate synthetase Homo sapiens 43-45 17045692-0 2007 Role of the Fas/FasL pathway in combination therapy with interferon-alpha and fluorouracil against hepatocellular carcinoma in vitro. Fluorouracil 78-90 Fas ligand Homo sapiens 16-20 17660867-1 2007 The cytotoxic effect of 5-fluorouracil (5-FU) is mediated by the inhibition of thymidylate synthase (TS), however, at the same time 5-FU is catabolized by dihydropyrimidine dehydrogenase (DPD). Fluorouracil 24-38 thymidylate synthetase Homo sapiens 79-99 17660867-1 2007 The cytotoxic effect of 5-fluorouracil (5-FU) is mediated by the inhibition of thymidylate synthase (TS), however, at the same time 5-FU is catabolized by dihydropyrimidine dehydrogenase (DPD). Fluorouracil 40-44 thymidylate synthetase Homo sapiens 79-99 16929515-1 2006 We evaluated DNA polymorphisms in the thymidylate synthase (TS) and 5,10-methylene-tetrahydrofolate reductase (MTHFR) genes for an association with response and survival in locally advanced gastric cancer treated with 5-FU based preoperative chemotherapy (CTx). Fluorouracil 218-222 thymidylate synthetase Homo sapiens 38-58 21368461-2 2011 Orotate phosphoribosyltransferase (OPRT) and thymidine phosphorylase (TP) are essential enzymes for activation of 5-FU. Fluorouracil 114-118 uridine monophosphate synthetase Homo sapiens 0-33 21368461-2 2011 Orotate phosphoribosyltransferase (OPRT) and thymidine phosphorylase (TP) are essential enzymes for activation of 5-FU. Fluorouracil 114-118 uridine monophosphate synthetase Homo sapiens 35-39 16929515-1 2006 We evaluated DNA polymorphisms in the thymidylate synthase (TS) and 5,10-methylene-tetrahydrofolate reductase (MTHFR) genes for an association with response and survival in locally advanced gastric cancer treated with 5-FU based preoperative chemotherapy (CTx). Fluorouracil 218-222 thymidylate synthetase Homo sapiens 60-62 17172428-7 2006 Interestingly, exposure of cells infected with an anti-stathmin adenovirus to Taxol or etoposide resulted in a complete loss of proliferation and clonogenicity, whereas exposure of the same cells to 5-FU or Adriamycin potentiated the growth-inhibitory effects of the anti-stathmin ribozyme, but the cells continued to proliferate. Fluorouracil 199-203 stathmin 1 Homo sapiens 55-63 17172428-7 2006 Interestingly, exposure of cells infected with an anti-stathmin adenovirus to Taxol or etoposide resulted in a complete loss of proliferation and clonogenicity, whereas exposure of the same cells to 5-FU or Adriamycin potentiated the growth-inhibitory effects of the anti-stathmin ribozyme, but the cells continued to proliferate. Fluorouracil 199-203 stathmin 1 Homo sapiens 272-280 17172428-9 2006 In contrast, cells infected with the anti-stathmin adenovirus showed a marked increase in apoptosis on exposure to Taxol or etoposide and a modest increase on exposure to 5-FU or Adriamycin. Fluorouracil 171-175 stathmin 1 Homo sapiens 42-50 17016601-0 2006 Genotype of thymidylate synthase likely to affect efficacy of adjuvant 5-FU based chemotherapy in colon cancer. Fluorouracil 71-75 thymidylate synthetase Homo sapiens 12-32 17016601-1 2006 Thymidylate synthase [TS, (EC 2.1.1.45)] is the target enzyme in 5-fluorouracil treatment. Fluorouracil 65-79 thymidylate synthetase Homo sapiens 0-20 17016601-1 2006 Thymidylate synthase [TS, (EC 2.1.1.45)] is the target enzyme in 5-fluorouracil treatment. Fluorouracil 65-79 thymidylate synthetase Homo sapiens 22-24 17016601-8 2006 In this prospective examination on a randomized controlled trial, the patients with colon cancer of the 2R/2R TS genotype may be good responders to 5-FU-based adjuvant chemotherapy. Fluorouracil 148-152 thymidylate synthetase Homo sapiens 110-112 17016601-9 2006 Furthermore, differences in the proportions of the TS genotypes can account for the interracial differences in the adverse effects of 5-FU-based chemotherapy. Fluorouracil 134-138 thymidylate synthetase Homo sapiens 51-53 17018589-1 2006 Thymidylate synthase (TS) is an important target for 5-fluorouracil (5FU)-based therapy. Fluorouracil 53-67 thymidylate synthetase Homo sapiens 0-20 20880064-1 2011 AIMS: Dihydropyrimidine dehydrogenase (DPD) and thymidylate synthase (TS) are key enzymes in the metabolism of 5-fluorouracil and have been implicated as possible prognostic markers for cancer patients. Fluorouracil 113-127 thymidylate synthetase Homo sapiens 50-70 17018589-1 2006 Thymidylate synthase (TS) is an important target for 5-fluorouracil (5FU)-based therapy. Fluorouracil 53-67 thymidylate synthetase Homo sapiens 22-24 17018589-1 2006 Thymidylate synthase (TS) is an important target for 5-fluorouracil (5FU)-based therapy. Fluorouracil 69-72 thymidylate synthetase Homo sapiens 0-20 20951162-6 2011 The cytotoxicity studies showed 5-FU-FNPs were toxic to MCF7, PC3 and KB cells while they are comparatively non toxic to L929 cells. Fluorouracil 32-36 chromobox 8 Homo sapiens 62-65 17018589-1 2006 Thymidylate synthase (TS) is an important target for 5-fluorouracil (5FU)-based therapy. Fluorouracil 69-72 thymidylate synthetase Homo sapiens 22-24 22091436-4 2011 In addition, a factor that activates hENT1 is the inhibition of thymidylate synthase (TS), one of the 5-FU metabolic enzymes; TS inhibition mediates depleting intracellular nucleotide pools, resulting in the activation of the salvage pathway mediated through hENT1. Fluorouracil 102-106 thymidylate synthetase Homo sapiens 64-84 16957513-6 2006 When treated with 5-FU, Fas expression rates in SW480 increased, but FasL remained unchanged. Fluorouracil 18-22 Fas ligand Homo sapiens 69-73 22091436-4 2011 In addition, a factor that activates hENT1 is the inhibition of thymidylate synthase (TS), one of the 5-FU metabolic enzymes; TS inhibition mediates depleting intracellular nucleotide pools, resulting in the activation of the salvage pathway mediated through hENT1. Fluorouracil 102-106 thymidylate synthetase Homo sapiens 86-88 22091436-4 2011 In addition, a factor that activates hENT1 is the inhibition of thymidylate synthase (TS), one of the 5-FU metabolic enzymes; TS inhibition mediates depleting intracellular nucleotide pools, resulting in the activation of the salvage pathway mediated through hENT1. Fluorouracil 102-106 thymidylate synthetase Homo sapiens 126-128 21761314-1 2011 Orotate phosphoribosyl transferase (OPRT) is the initial enzyme of 5-FU activation, in which 5-FU is converted to 5-fluorouridinemonophosphate. Fluorouracil 67-71 uridine monophosphate synthetase Homo sapiens 0-34 21761314-1 2011 Orotate phosphoribosyl transferase (OPRT) is the initial enzyme of 5-FU activation, in which 5-FU is converted to 5-fluorouridinemonophosphate. Fluorouracil 67-71 uridine monophosphate synthetase Homo sapiens 36-40 21761314-1 2011 Orotate phosphoribosyl transferase (OPRT) is the initial enzyme of 5-FU activation, in which 5-FU is converted to 5-fluorouridinemonophosphate. Fluorouracil 93-97 uridine monophosphate synthetase Homo sapiens 0-34 21761314-1 2011 Orotate phosphoribosyl transferase (OPRT) is the initial enzyme of 5-FU activation, in which 5-FU is converted to 5-fluorouridinemonophosphate. Fluorouracil 93-97 uridine monophosphate synthetase Homo sapiens 36-40 16880781-1 2006 The sensitivity to 5-fluorouracil (5-FU) has been reported to be associated with target molecule thymidylate synthase (TS), fluoropyrimidine-metabolising enzymes such as orotate phosphoribosyltransferase (OPRT), and dihydropyrimidine dehydrogenase (DPD). Fluorouracil 19-33 thymidylate synthetase Homo sapiens 97-117 16880781-1 2006 The sensitivity to 5-fluorouracil (5-FU) has been reported to be associated with target molecule thymidylate synthase (TS), fluoropyrimidine-metabolising enzymes such as orotate phosphoribosyltransferase (OPRT), and dihydropyrimidine dehydrogenase (DPD). Fluorouracil 19-33 thymidylate synthetase Homo sapiens 119-121 16880781-1 2006 The sensitivity to 5-fluorouracil (5-FU) has been reported to be associated with target molecule thymidylate synthase (TS), fluoropyrimidine-metabolising enzymes such as orotate phosphoribosyltransferase (OPRT), and dihydropyrimidine dehydrogenase (DPD). Fluorouracil 19-33 uridine monophosphate synthetase Homo sapiens 170-203 16880781-1 2006 The sensitivity to 5-fluorouracil (5-FU) has been reported to be associated with target molecule thymidylate synthase (TS), fluoropyrimidine-metabolising enzymes such as orotate phosphoribosyltransferase (OPRT), and dihydropyrimidine dehydrogenase (DPD). Fluorouracil 19-33 uridine monophosphate synthetase Homo sapiens 205-209 21761314-9 2011 Furthermore, the OPRT/ DPD expression ratio, a powerful predictive factor to evaluate 5-FU sensitivity, in the HRPC group was significantly higher than that in the low-grade HSPC group. Fluorouracil 86-90 uridine monophosphate synthetase Homo sapiens 17-21 22194930-4 2011 These studies demonstrate that both FdUrd and 5-FU activate the ATR and ATM checkpoint signaling pathways, indicating that they cause genotoxic damage. Fluorouracil 46-50 ATM serine/threonine kinase Homo sapiens 72-75 22194930-7 2011 Consistent with a role for the BER pathway, we show that small molecule poly(ADP-ribose) polymerase 1/2 (PARP) inhibitors, AZD2281 and ABT-888, remarkably sensitized both mismatch repair (MMR)-proficient and -deficient colon cancer cell lines to FdUrd but not to 5-FU. Fluorouracil 263-267 poly(ADP-ribose) polymerase family member 12 Homo sapiens 72-103 22194930-7 2011 Consistent with a role for the BER pathway, we show that small molecule poly(ADP-ribose) polymerase 1/2 (PARP) inhibitors, AZD2281 and ABT-888, remarkably sensitized both mismatch repair (MMR)-proficient and -deficient colon cancer cell lines to FdUrd but not to 5-FU. Fluorouracil 263-267 poly(ADP-ribose) polymerase family member 12 Homo sapiens 105-109 16880781-1 2006 The sensitivity to 5-fluorouracil (5-FU) has been reported to be associated with target molecule thymidylate synthase (TS), fluoropyrimidine-metabolising enzymes such as orotate phosphoribosyltransferase (OPRT), and dihydropyrimidine dehydrogenase (DPD). Fluorouracil 35-39 thymidylate synthetase Homo sapiens 97-117 21887339-0 2011 The chemotherapeutic drug 5-fluorouracil promotes PKR-mediated apoptosis in a p53-independent manner in colon and breast cancer cells. Fluorouracil 26-40 eukaryotic translation initiation factor 2 alpha kinase 2 Homo sapiens 50-53 16880781-1 2006 The sensitivity to 5-fluorouracil (5-FU) has been reported to be associated with target molecule thymidylate synthase (TS), fluoropyrimidine-metabolising enzymes such as orotate phosphoribosyltransferase (OPRT), and dihydropyrimidine dehydrogenase (DPD). Fluorouracil 35-39 thymidylate synthetase Homo sapiens 119-121 21887339-3 2011 We have identified the ds-RNA-dependent protein kinase (PKR) as a key molecular target of 5-FU involved in apoptosis induction in human colon and breast cancer cell lines. Fluorouracil 90-94 eukaryotic translation initiation factor 2 alpha kinase 2 Homo sapiens 56-59 16880781-1 2006 The sensitivity to 5-fluorouracil (5-FU) has been reported to be associated with target molecule thymidylate synthase (TS), fluoropyrimidine-metabolising enzymes such as orotate phosphoribosyltransferase (OPRT), and dihydropyrimidine dehydrogenase (DPD). Fluorouracil 35-39 uridine monophosphate synthetase Homo sapiens 170-203 21887339-5 2011 PKR protein was activated by 5-FU treatment in a p53-independent manner, inducing phosphorylation of the protein synthesis translation initiation factor eIF-2alpha and cell death by apoptosis. Fluorouracil 29-33 eukaryotic translation initiation factor 2 alpha kinase 2 Homo sapiens 0-3 16880781-1 2006 The sensitivity to 5-fluorouracil (5-FU) has been reported to be associated with target molecule thymidylate synthase (TS), fluoropyrimidine-metabolising enzymes such as orotate phosphoribosyltransferase (OPRT), and dihydropyrimidine dehydrogenase (DPD). Fluorouracil 35-39 uridine monophosphate synthetase Homo sapiens 205-209 21887339-6 2011 Furthermore, PKR interference promoted a decreased response to 5-FU treatment and those cells were not affected by the synergistic antitumor activity of 5-FU/IFNalpha combination. Fluorouracil 63-67 eukaryotic translation initiation factor 2 alpha kinase 2 Homo sapiens 13-16 21887339-7 2011 These results, taken together, provide evidence that PKR is a key molecular target of 5-FU with potential relevance in the clinical use of this drug. Fluorouracil 86-90 eukaryotic translation initiation factor 2 alpha kinase 2 Homo sapiens 53-56 16943523-0 2006 Lymph node status and TS gene expression are prognostic markers in stage II/III rectal cancer after neoadjuvant fluorouracil-based chemoradiotherapy. Fluorouracil 112-124 thymidylate synthetase Homo sapiens 22-24 21629658-5 2011 Furthermore, CALB2 silencing decreased 5-FU-induced cytochrome c and smac release from the mitochondria and also decreased 5-FU-induced activation of caspases 9 and 3/7. Fluorouracil 39-43 diablo IAP-binding mitochondrial protein Homo sapiens 69-73 21629658-5 2011 Furthermore, CALB2 silencing decreased 5-FU-induced cytochrome c and smac release from the mitochondria and also decreased 5-FU-induced activation of caspases 9 and 3/7. Fluorouracil 123-127 caspase 9 Homo sapiens 150-166 16584912-5 2006 Furthermore, we measured the activity of the 5-FU metabolizing enzymes (thymidylate synthetase (TS), dihydrouracil dehydrogenase (DPD), orotate phosphoribosyl transferase (OPRT), and thymidine phosphorylase (TP)) in each cell line. Fluorouracil 45-49 thymidylate synthetase Homo sapiens 72-94 20727673-0 2010 RAD001 shows activity against gastric cancer cells and overcomes 5-FU resistance by downregulating thymidylate synthase. Fluorouracil 65-69 thymidylate synthetase Homo sapiens 99-119 20727673-5 2010 Furthermore, RAD001 conferred sensitivity to 5-FU-resistant cell lines by downregulating thymidylate synthase (TS). Fluorouracil 45-49 thymidylate synthetase Homo sapiens 89-109 16584912-14 2006 5-FU is phosphorylated by OPRT and TP and detoxified by DPD. Fluorouracil 0-4 uridine monophosphate synthetase Homo sapiens 26-30 21078976-0 2010 MicroRNA-21 induces resistance to 5-fluorouracil by down-regulating human DNA MutS homolog 2 (hMSH2). Fluorouracil 34-48 microRNA 21 Homo sapiens 0-11 17078208-1 2006 The major mechanism of action of 5-fluorouracil (5FU)-based therapies is thought to be inhibition of thymidylate synthase (TS). Fluorouracil 33-47 thymidylate synthetase Homo sapiens 101-121 21078976-4 2010 Cells that overproduce miR-21 exhibit significantly reduced 5-fluorouracil (5-FU)-induced G2/M damage arrest and apoptosis that is characteristic of defects in the core MMR component. Fluorouracil 60-74 microRNA 21 Homo sapiens 23-29 21078976-4 2010 Cells that overproduce miR-21 exhibit significantly reduced 5-fluorouracil (5-FU)-induced G2/M damage arrest and apoptosis that is characteristic of defects in the core MMR component. Fluorouracil 76-80 microRNA 21 Homo sapiens 23-29 21078976-5 2010 Moreover, xenograft studies demonstrate that miR-21 overexpression dramatically reduces the therapeutic efficacy of 5-FU. Fluorouracil 116-120 microRNA 21 Homo sapiens 45-51 20633010-6 2010 5-FU induced p53 and p21 accumulation together with a decrease in cyclin B1 and Bcl-2 levels in treated keloid fibroblasts. Fluorouracil 0-4 H3 histone pseudogene 16 Homo sapiens 21-24 20633010-6 2010 5-FU induced p53 and p21 accumulation together with a decrease in cyclin B1 and Bcl-2 levels in treated keloid fibroblasts. Fluorouracil 0-4 cyclin B1 Homo sapiens 66-75 17078208-1 2006 The major mechanism of action of 5-fluorouracil (5FU)-based therapies is thought to be inhibition of thymidylate synthase (TS). Fluorouracil 33-47 thymidylate synthetase Homo sapiens 123-125 20930505-4 2010 Analysis revealed 43 pathways differentially affected by 5-FU compared to control (P 1.4-fold) and downregulated cdc25C, cyclins B1 and B2, histone H2A, H2B, and H3 (< -1.4-fold) over control. Fluorouracil 57-61 cell division cycle 25C Homo sapiens 113-138 20930505-6 2010 Importantly, with knockdown of hMLH1 and hMSH2, we observed that decreased histone H3 expression by 5-FU was dependent on hMLH1. Fluorouracil 100-104 mutL homolog 1 Homo sapiens 31-36 17078208-1 2006 The major mechanism of action of 5-fluorouracil (5FU)-based therapies is thought to be inhibition of thymidylate synthase (TS). Fluorouracil 49-52 thymidylate synthetase Homo sapiens 101-121 20930505-6 2010 Importantly, with knockdown of hMLH1 and hMSH2, we observed that decreased histone H3 expression by 5-FU was dependent on hMLH1. Fluorouracil 100-104 mutL homolog 1 Homo sapiens 122-127 20930505-8 2010 Our data suggest that 5-FU induces a G1/S arrest by regulating cyclin E and cdc25C expression, and MMR recognition of 5-FU in DNA may modulate cyclin E to affect the cell cycle. Fluorouracil 22-26 cell division cycle 25C Homo sapiens 76-82 17078208-1 2006 The major mechanism of action of 5-fluorouracil (5FU)-based therapies is thought to be inhibition of thymidylate synthase (TS). Fluorouracil 49-52 thymidylate synthetase Homo sapiens 123-125 16734727-2 2006 Among these, orotate phosphoribosyltransferase (OPRT EC 2.4.2.10) is a key enzyme related to the first-step activation process of 5-FU and has been shown to be an important enzyme that helps to predict sensitivity to 5-FU and its related derivatives. Fluorouracil 130-134 uridine monophosphate synthetase Homo sapiens 13-46 20727737-0 2010 Amplification of thymidylate synthetase in metastatic colorectal cancer patients pretreated with 5-fluorouracil-based chemotherapy. Fluorouracil 97-111 thymidylate synthetase Homo sapiens 17-39 20727737-5 2010 Gain of TYMS DNA copy number was observed in 18% of the 5-FU exposed metastases, while only 4% of the unexposed metastases exhibited TYMS copy gain (p = 0.036). Fluorouracil 56-60 thymidylate synthetase Homo sapiens 8-12 20727737-7 2010 Median survival time was similar in 5-FU-exposed patients with metastases containing TYMS amplification and those with no amplification. Fluorouracil 36-40 thymidylate synthetase Homo sapiens 85-89 16734727-2 2006 Among these, orotate phosphoribosyltransferase (OPRT EC 2.4.2.10) is a key enzyme related to the first-step activation process of 5-FU and has been shown to be an important enzyme that helps to predict sensitivity to 5-FU and its related derivatives. Fluorouracil 130-134 uridine monophosphate synthetase Homo sapiens 48-52 20727737-9 2010 These results suggest amplification of TYMS amplification as a putative mechanism for clinical resistance to 5-FU-based chemotherapy and may have important ramifications for the post-resection chemotherapy choices for metastatic colorectal cancer. Fluorouracil 109-113 thymidylate synthetase Homo sapiens 39-43 16734727-2 2006 Among these, orotate phosphoribosyltransferase (OPRT EC 2.4.2.10) is a key enzyme related to the first-step activation process of 5-FU and has been shown to be an important enzyme that helps to predict sensitivity to 5-FU and its related derivatives. Fluorouracil 217-221 uridine monophosphate synthetase Homo sapiens 13-46 16734727-2 2006 Among these, orotate phosphoribosyltransferase (OPRT EC 2.4.2.10) is a key enzyme related to the first-step activation process of 5-FU and has been shown to be an important enzyme that helps to predict sensitivity to 5-FU and its related derivatives. Fluorouracil 217-221 uridine monophosphate synthetase Homo sapiens 48-52 16734727-5 2006 OPRT levels were measured in eight human cancer xenografts and in 75 gastric cancer tissues using both a newly established ELISA and a conventional enzyme assay, using radiolabeled 5-FU as a substrate. Fluorouracil 181-185 uridine monophosphate synthetase Homo sapiens 0-4 16734727-7 2006 The ELISA system for OPRT requires a minimal amount of carcinoma tissue, making it an easy-to-use assay system to predict sensitivity to 5-FU and its derivatives in gastric carcinoma. Fluorouracil 137-141 uridine monophosphate synthetase Homo sapiens 21-25 16897968-6 2006 As one of the reasonable mechanism of antitumor synergism by the combination, CPT-11 and taxanes were found to reduce the expression of TS in human tumor resistant to 5-FU with high expression TS levels. Fluorouracil 167-171 thymidylate synthetase Homo sapiens 136-138 16709241-5 2006 RESULTS: 5-FU treatment for 24 hours resulted in S phase arrests, p53 accumulation, up-regulation of p53-target genes on DNA damage response (ATF3, GADD34, GADD45A, PCNA), cell cycle-regulatory (CDKN1A), and apoptosis-regulatory pathways (FAS), and apoptosis induction in the parental and resistant cell lines. Fluorouracil 9-13 activating transcription factor 3 Homo sapiens 142-146 16709241-5 2006 RESULTS: 5-FU treatment for 24 hours resulted in S phase arrests, p53 accumulation, up-regulation of p53-target genes on DNA damage response (ATF3, GADD34, GADD45A, PCNA), cell cycle-regulatory (CDKN1A), and apoptosis-regulatory pathways (FAS), and apoptosis induction in the parental and resistant cell lines. Fluorouracil 9-13 proliferating cell nuclear antigen Homo sapiens 165-169 16709241-11 2006 Differential expression in response to 5-FU treatment was demonstrated for genes involved in regulation of nucleotide binding/metabolism (ATAD2, GNL2, GNL3, MATR3), amino acid metabolism (AHCY, GSS, IVD, OAT), cytoskeleton organization (KRT7, KRT8, KRT19, MAST1), transport (MTCH1, NCBP1, SNAPAP, VPS52), and oxygen metabolism (COX5A, COX7C). Fluorouracil 39-43 adenosylhomocysteinase Homo sapiens 188-192 16709241-11 2006 Differential expression in response to 5-FU treatment was demonstrated for genes involved in regulation of nucleotide binding/metabolism (ATAD2, GNL2, GNL3, MATR3), amino acid metabolism (AHCY, GSS, IVD, OAT), cytoskeleton organization (KRT7, KRT8, KRT19, MAST1), transport (MTCH1, NCBP1, SNAPAP, VPS52), and oxygen metabolism (COX5A, COX7C). Fluorouracil 39-43 SNAP associated protein Homo sapiens 289-295 16827120-5 2006 MATERIALS AND METHODS: The sequence-dependent interaction among MTX, 5-FU and RAL on the proliferation and viability of human bone marrow HS-5 cells was determined by the MTT assay and the Trypan blue dye exclusion assay by exposing the cells to MTX, 5-FU and RAL alone, RAL 24 h prior to 5-FU followed 2 h later by MTX, and 5-FU 2 h prior to MTX followed 24 h later by RAL. Fluorouracil 251-255 metaxin 1 Homo sapiens 64-67 20958072-6 2010 siRNA targeting of choline kinase-alpha (Chk-alpha), an enzyme significantly up-regulated in aggressive breast cancer cells, was combined with the prodrug enzyme bacterial cytosine deaminase (bCD) that converts the nontoxic prodrug 5-fluorocytosine (5-FC) to cytotoxic 5-fluorouracil (5-FU). Fluorouracil 269-283 choline kinase alpha Homo sapiens 19-39 20958072-6 2010 siRNA targeting of choline kinase-alpha (Chk-alpha), an enzyme significantly up-regulated in aggressive breast cancer cells, was combined with the prodrug enzyme bacterial cytosine deaminase (bCD) that converts the nontoxic prodrug 5-fluorocytosine (5-FC) to cytotoxic 5-fluorouracil (5-FU). Fluorouracil 269-283 choline kinase alpha Homo sapiens 41-50 20958072-6 2010 siRNA targeting of choline kinase-alpha (Chk-alpha), an enzyme significantly up-regulated in aggressive breast cancer cells, was combined with the prodrug enzyme bacterial cytosine deaminase (bCD) that converts the nontoxic prodrug 5-fluorocytosine (5-FC) to cytotoxic 5-fluorouracil (5-FU). Fluorouracil 285-289 choline kinase alpha Homo sapiens 19-39 20958072-6 2010 siRNA targeting of choline kinase-alpha (Chk-alpha), an enzyme significantly up-regulated in aggressive breast cancer cells, was combined with the prodrug enzyme bacterial cytosine deaminase (bCD) that converts the nontoxic prodrug 5-fluorocytosine (5-FC) to cytotoxic 5-fluorouracil (5-FU). Fluorouracil 285-289 choline kinase alpha Homo sapiens 41-50 20978511-9 2010 miR-21 expression in clinical HCC specimens was significantly associated with the clinical response to the IFN-alpha/5-FU combination therapy and survival rate. Fluorouracil 117-121 microRNA 21 Homo sapiens 0-6 20978511-10 2010 CONCLUSIONS: The miR-21 in HCC cell lines and clinical HCC samples is a significant modulator of the anti-tumour effect of IFN-alpha and 5-FU. Fluorouracil 137-141 microRNA 21 Homo sapiens 17-23 20978511-11 2010 This suggests that miR-21 is a potentially suitable marker for the prediction of the clinical response to the IFN-alpha/5-FU combination therapy. Fluorouracil 120-124 microRNA 21 Homo sapiens 19-25 21062447-0 2010 Suppression of microRNA-31 increases sensitivity to 5-FU at an early stage, and affects cell migration and invasion in HCT-116 colon cancer cells. Fluorouracil 52-56 microRNA 31 Homo sapiens 15-26 16675565-2 2006 Given that thymidylate synthase (TS) is inhibited by 5-FU, we studied the relationship between MSI and TS expression, and the prognostic effect of these and other markers (i.e., p53 and 17p allelic imbalance). Fluorouracil 53-57 thymidylate synthetase Homo sapiens 11-31 21062447-8 2010 However, when combined with 5-FU, anti-miR-31 inhibited the proliferation of the two cell lines as early as 24 h after exposure to 5-FU (p = 0.038 and 0.044). Fluorouracil 131-135 microRNA 31 Homo sapiens 39-45 21062447-12 2010 CONCLUSIONS: Suppression of miR-31 increases sensitivity to 5-FU at an early stage, and affects cell migration and invasion in HCT-116 colon cancer cells. Fluorouracil 60-64 microRNA 31 Homo sapiens 28-34 20876284-6 2010 Here, we provide genetic evidence that ATM kinase activity is required to trigger 5-FU- and neocarzinostatin-dependent cFLIP(L) and cFLIP(S) down-regulation, which in turn sensitize hepatocellular carcinoma (HCC) cell lines to TRAIL. Fluorouracil 82-86 ATM serine/threonine kinase Homo sapiens 39-42 16675565-2 2006 Given that thymidylate synthase (TS) is inhibited by 5-FU, we studied the relationship between MSI and TS expression, and the prognostic effect of these and other markers (i.e., p53 and 17p allelic imbalance). Fluorouracil 53-57 thymidylate synthetase Homo sapiens 33-35 16596200-5 2006 As a result, we identified four genes (Bcl-2, Bcl-XL, cIAP2, and CFLAR) whose expression was four or more times higher in HCT116/ hRFI cells than in HCT116/LacZ cells, and found that Bcl-2 and the ratio of Bcl-2/Bax or Bcl-2/Bak were upregulated when HCT116/hRFI cells were treated with 5-FU. Fluorouracil 287-291 baculoviral IAP repeat containing 3 Homo sapiens 54-59 16809149-0 2006 Thymidylate synthase and dihydropyrimidine dehydrogenase are related to histological effects of 5-fluorouracil and cisplatin neoadjuvant chemotherapy for primary gastric cancer patients. Fluorouracil 96-110 thymidylate synthetase Homo sapiens 0-20 16809149-1 2006 UNLABELLED: Thymidylate synthase (TS), dihydropyrimidine dehydrogenase (DPD), and vascular endothelial growth factor (VEGF) are associated with the effect of 5-fluorouracil (5-FU) based adjuvant chemotherapy. Fluorouracil 158-172 thymidylate synthetase Homo sapiens 12-32 16809149-1 2006 UNLABELLED: Thymidylate synthase (TS), dihydropyrimidine dehydrogenase (DPD), and vascular endothelial growth factor (VEGF) are associated with the effect of 5-fluorouracil (5-FU) based adjuvant chemotherapy. Fluorouracil 158-172 thymidylate synthetase Homo sapiens 34-36 16809149-1 2006 UNLABELLED: Thymidylate synthase (TS), dihydropyrimidine dehydrogenase (DPD), and vascular endothelial growth factor (VEGF) are associated with the effect of 5-fluorouracil (5-FU) based adjuvant chemotherapy. Fluorouracil 174-178 thymidylate synthetase Homo sapiens 12-32 16612158-6 2006 Enzyme activities of OPRT were also determined using a conventional enzyme assay using radiolabeled 5-fluorouracil as a substrate. Fluorouracil 100-114 uridine monophosphate synthetase Homo sapiens 21-25 16575011-0 2006 Tumor thymidylate synthase 1494del6 genotype as a prognostic factor in colorectal cancer patients receiving fluorouracil-based adjuvant treatment. Fluorouracil 108-120 thymidylate synthetase Homo sapiens 6-26 16619549-2 2006 Thymidylate synthase (TS) and dihydropyrimidine dehydrogenase (DPD) are the major determinants of individual sensitivity to 5-FU, and the impact of TS and DPD expression on prognosis and 5-FU efficacy has been studied in gastrointestinal carcinomas. Fluorouracil 124-128 thymidylate synthetase Homo sapiens 0-20 16619549-2 2006 Thymidylate synthase (TS) and dihydropyrimidine dehydrogenase (DPD) are the major determinants of individual sensitivity to 5-FU, and the impact of TS and DPD expression on prognosis and 5-FU efficacy has been studied in gastrointestinal carcinomas. Fluorouracil 124-128 thymidylate synthetase Homo sapiens 22-24 16619549-2 2006 Thymidylate synthase (TS) and dihydropyrimidine dehydrogenase (DPD) are the major determinants of individual sensitivity to 5-FU, and the impact of TS and DPD expression on prognosis and 5-FU efficacy has been studied in gastrointestinal carcinomas. Fluorouracil 187-191 thymidylate synthetase Homo sapiens 0-20 16619549-2 2006 Thymidylate synthase (TS) and dihydropyrimidine dehydrogenase (DPD) are the major determinants of individual sensitivity to 5-FU, and the impact of TS and DPD expression on prognosis and 5-FU efficacy has been studied in gastrointestinal carcinomas. Fluorouracil 187-191 thymidylate synthetase Homo sapiens 22-24 16317430-11 2006 Testing for TS and GSTP1 polymorphisms may allow identification of gastric cancer patients who will benefit from 5-FU/cisplatin chemotherapy, sparing others the side effects of this chemotherapy. Fluorouracil 113-117 thymidylate synthetase Homo sapiens 12-14 16317430-11 2006 Testing for TS and GSTP1 polymorphisms may allow identification of gastric cancer patients who will benefit from 5-FU/cisplatin chemotherapy, sparing others the side effects of this chemotherapy. Fluorouracil 113-117 glutathione S-transferase pi 1 Homo sapiens 19-24 16512989-0 2006 Polymorphisms in the thymidylate synthase gene predict response to 5-fluorouracil therapy in colorectal cancer. Fluorouracil 67-81 thymidylate synthetase Homo sapiens 21-41 21062732-1 2010 BACKGROUND: Dihydropyrimidine dehydrogenase (DPD), orotate phosphoribosyl transferase (OPRT), and thymidylate synthase (TS) levels correlate with sensitivity and resistance to 5-fluorouracil (5-FU). Fluorouracil 176-190 uridine monophosphate synthetase Homo sapiens 51-85 21062732-1 2010 BACKGROUND: Dihydropyrimidine dehydrogenase (DPD), orotate phosphoribosyl transferase (OPRT), and thymidylate synthase (TS) levels correlate with sensitivity and resistance to 5-fluorouracil (5-FU). Fluorouracil 176-190 uridine monophosphate synthetase Homo sapiens 87-91 21062732-1 2010 BACKGROUND: Dihydropyrimidine dehydrogenase (DPD), orotate phosphoribosyl transferase (OPRT), and thymidylate synthase (TS) levels correlate with sensitivity and resistance to 5-fluorouracil (5-FU). Fluorouracil 192-196 uridine monophosphate synthetase Homo sapiens 87-91 21084814-1 2010 We reported herein four resected cases with basaloid carcinoma of the esophagus and measured the activity of 5-FU related enzymes (TS, DPD, OPRT) in cancer tissue. Fluorouracil 109-113 thymidylate synthetase Homo sapiens 131-133 21224584-1 2010 PURPOSE: The aim of this study was to determine whether the expressions of excision repair cross-complementing-1 (ERCC1) and thymidylate synthase (TS) predict the clinical outcome of patients with esophageal squamous cell carcinoma treated with CDDP/5-FU chemoradiotherapy. Fluorouracil 250-254 ERCC excision repair 1, endonuclease non-catalytic subunit Homo sapiens 75-112 21224584-1 2010 PURPOSE: The aim of this study was to determine whether the expressions of excision repair cross-complementing-1 (ERCC1) and thymidylate synthase (TS) predict the clinical outcome of patients with esophageal squamous cell carcinoma treated with CDDP/5-FU chemoradiotherapy. Fluorouracil 250-254 ERCC excision repair 1, endonuclease non-catalytic subunit Homo sapiens 114-119 21224584-1 2010 PURPOSE: The aim of this study was to determine whether the expressions of excision repair cross-complementing-1 (ERCC1) and thymidylate synthase (TS) predict the clinical outcome of patients with esophageal squamous cell carcinoma treated with CDDP/5-FU chemoradiotherapy. Fluorouracil 250-254 thymidylate synthetase Homo sapiens 147-149 16424979-1 2006 To investigate the relationship between polymorphism in the 3"-untranslated region (3"-UTR) of the thymidylate synthase (TS) gene and sensitivity of gastric cancer to 5-fluorouracil (5-FU)-based chemotherapy, 106 cases of advanced gastric cancer were analyzed. Fluorouracil 167-181 thymidylate synthetase Homo sapiens 99-119 16424979-1 2006 To investigate the relationship between polymorphism in the 3"-untranslated region (3"-UTR) of the thymidylate synthase (TS) gene and sensitivity of gastric cancer to 5-fluorouracil (5-FU)-based chemotherapy, 106 cases of advanced gastric cancer were analyzed. Fluorouracil 167-181 thymidylate synthetase Homo sapiens 121-123 16424979-1 2006 To investigate the relationship between polymorphism in the 3"-untranslated region (3"-UTR) of the thymidylate synthase (TS) gene and sensitivity of gastric cancer to 5-fluorouracil (5-FU)-based chemotherapy, 106 cases of advanced gastric cancer were analyzed. Fluorouracil 183-187 thymidylate synthetase Homo sapiens 99-119 16424979-1 2006 To investigate the relationship between polymorphism in the 3"-untranslated region (3"-UTR) of the thymidylate synthase (TS) gene and sensitivity of gastric cancer to 5-fluorouracil (5-FU)-based chemotherapy, 106 cases of advanced gastric cancer were analyzed. Fluorouracil 183-187 thymidylate synthetase Homo sapiens 121-123 16424979-6 2006 These results show that the presence of the TS 3"-UTR 6 bp nucleotide fragment can be correlated with the sensitivity of gastric cancer to 5-FU-based chemotherapy, and that the TS 3"-UTR polymorphism profile can be used to guide the choice of 5-FU-based chemotherapy in advanced gastric cancer. Fluorouracil 139-143 thymidylate synthetase Homo sapiens 44-46 16424979-6 2006 These results show that the presence of the TS 3"-UTR 6 bp nucleotide fragment can be correlated with the sensitivity of gastric cancer to 5-FU-based chemotherapy, and that the TS 3"-UTR polymorphism profile can be used to guide the choice of 5-FU-based chemotherapy in advanced gastric cancer. Fluorouracil 243-247 thymidylate synthetase Homo sapiens 44-46 16424979-6 2006 These results show that the presence of the TS 3"-UTR 6 bp nucleotide fragment can be correlated with the sensitivity of gastric cancer to 5-FU-based chemotherapy, and that the TS 3"-UTR polymorphism profile can be used to guide the choice of 5-FU-based chemotherapy in advanced gastric cancer. Fluorouracil 243-247 thymidylate synthetase Homo sapiens 177-179 17162865-4 2005 Subconjunctiva injection of 5-Fu and Triamcinolone treat MAI in therapeutic group. Fluorouracil 28-32 glutathione S-transferase zeta 1 Homo sapiens 57-60 21224630-1 2010 Thymidylate synthase (TS) and excision repair complementing-1 (ERCC-1) were known to be important biomarkers to predict a tumor response to 5-fluorouracil (5-FU) and oxaliplatin, but the relationship between these expressions and tumor response were still unclear. Fluorouracil 140-154 thymidylate synthetase Homo sapiens 0-20 21224630-1 2010 Thymidylate synthase (TS) and excision repair complementing-1 (ERCC-1) were known to be important biomarkers to predict a tumor response to 5-fluorouracil (5-FU) and oxaliplatin, but the relationship between these expressions and tumor response were still unclear. Fluorouracil 140-154 thymidylate synthetase Homo sapiens 22-24 21224630-1 2010 Thymidylate synthase (TS) and excision repair complementing-1 (ERCC-1) were known to be important biomarkers to predict a tumor response to 5-fluorouracil (5-FU) and oxaliplatin, but the relationship between these expressions and tumor response were still unclear. Fluorouracil 140-154 ERCC excision repair 1, endonuclease non-catalytic subunit Homo sapiens 63-69 21224630-1 2010 Thymidylate synthase (TS) and excision repair complementing-1 (ERCC-1) were known to be important biomarkers to predict a tumor response to 5-fluorouracil (5-FU) and oxaliplatin, but the relationship between these expressions and tumor response were still unclear. Fluorouracil 156-160 thymidylate synthetase Homo sapiens 0-20 21224630-1 2010 Thymidylate synthase (TS) and excision repair complementing-1 (ERCC-1) were known to be important biomarkers to predict a tumor response to 5-fluorouracil (5-FU) and oxaliplatin, but the relationship between these expressions and tumor response were still unclear. Fluorouracil 156-160 thymidylate synthetase Homo sapiens 22-24 21224630-1 2010 Thymidylate synthase (TS) and excision repair complementing-1 (ERCC-1) were known to be important biomarkers to predict a tumor response to 5-fluorouracil (5-FU) and oxaliplatin, but the relationship between these expressions and tumor response were still unclear. Fluorouracil 156-160 ERCC excision repair 1, endonuclease non-catalytic subunit Homo sapiens 63-69 17162865-9 2005 CONCLUSION: The therapy of 5-Fu and Triamcinolone to treat the MAI after traumatic cataract surgery is safe and effective. Fluorouracil 27-31 glutathione S-transferase zeta 1 Homo sapiens 63-66 16282729-0 2005 [Expression of mRNA levels of thymidylate synthase, dihydropyrimidine dehydrogenase, and orotate phosphoribosyltransferase of colorectal cancer--relationships among mRNA levels in association with response to 5-FU based treatment]. Fluorouracil 209-213 thymidylate synthetase Homo sapiens 30-50 16282729-0 2005 [Expression of mRNA levels of thymidylate synthase, dihydropyrimidine dehydrogenase, and orotate phosphoribosyltransferase of colorectal cancer--relationships among mRNA levels in association with response to 5-FU based treatment]. Fluorouracil 209-213 uridine monophosphate synthetase Homo sapiens 89-122 16282061-8 2005 The level of serum alanine aminotransferase (ALT) was higher and the WBC and PLT counts in the peripheral blood were lower in 5-FU group than those in the control group (P<0.05). Fluorouracil 126-130 glutamic pyruvic transaminase, soluble Mus musculus 19-43 16282061-8 2005 The level of serum alanine aminotransferase (ALT) was higher and the WBC and PLT counts in the peripheral blood were lower in 5-FU group than those in the control group (P<0.05). Fluorouracil 126-130 glutamic pyruvic transaminase, soluble Mus musculus 45-48 16243820-4 2005 RNA expression levels of 5-FU metabolism-associated genes thymidylate synthase, thymidine phosphorylase, dihydropyrimidine dehydrogenase, methylenetetrahydrofolate reductase, MAP7, and ELF3, of platinum- and taxane-related genes caldesmon, ERCC1, ERCC4, HER-2/neu, and GADD45, and of multidrug resistance gene MRP1 were determined using real-time reverse transcriptase-PCR. Fluorouracil 25-29 E74 like ETS transcription factor 3 Homo sapiens 185-189 16243820-4 2005 RNA expression levels of 5-FU metabolism-associated genes thymidylate synthase, thymidine phosphorylase, dihydropyrimidine dehydrogenase, methylenetetrahydrofolate reductase, MAP7, and ELF3, of platinum- and taxane-related genes caldesmon, ERCC1, ERCC4, HER-2/neu, and GADD45, and of multidrug resistance gene MRP1 were determined using real-time reverse transcriptase-PCR. Fluorouracil 25-29 ERCC excision repair 1, endonuclease non-catalytic subunit Homo sapiens 240-245 16315867-6 2005 Radiation and 5-FU induce Th1-dominant state by inhibiting the OK-432-induced production of IL-10 and TGF-beta mediated by regulation of SOCS-1 and SOCS-3 expression, and are suggested to increase anti-cancer immunity. Fluorouracil 14-18 suppressor of cytokine signaling 1 Homo sapiens 137-143 16142362-1 2005 Orotate phosphoribosyl transferase (OPRT) is an essential nucleotide metabolic enzyme for cell proliferation and also a key enzyme for conversion of 5-FU to its active form in tumor tissue. Fluorouracil 149-153 uridine monophosphate synthetase Homo sapiens 0-34 16142362-1 2005 Orotate phosphoribosyl transferase (OPRT) is an essential nucleotide metabolic enzyme for cell proliferation and also a key enzyme for conversion of 5-FU to its active form in tumor tissue. Fluorouracil 149-153 uridine monophosphate synthetase Homo sapiens 36-40 16141798-1 2005 The present study aimed to prospectively investigate the influence of thymidylate synthase (TS) polymorphisms (5"-TSER, 3"-TSUTR) on the disease-free survival (DFS) and overall survival (OS) of patients with colorectal cancer (CRC) who were treated with adjuvant 5-fluorouracil (5-FU) therapy. Fluorouracil 263-277 thymidylate synthetase Homo sapiens 92-94 20165956-0 2010 Thymidylate synthase germline polymorphisms in rectal cancer patients treated with neoadjuvant chemoradiotherapy based on 5-fluorouracil. Fluorouracil 122-136 thymidylate synthetase Homo sapiens 0-20 20165956-10 2010 CONCLUSIONS: The thymidylate synthase genotype might help to identify patients with stage II/III rectal cancer who could benefit from pre- and postoperative fluorouracil-based chemotherapy. Fluorouracil 157-169 thymidylate synthetase Homo sapiens 17-37 22870098-7 2010 TS and OPRT expression were not related to various clinicopathological factors, but patients with a high TS mRNA expression showed a significantly poorer prognosis in cases where 5-FU was not administered. Fluorouracil 179-183 thymidylate synthetase Homo sapiens 105-107 22870098-8 2010 The efficacy of 5-FU was more significant when administered for more than 6 months in the group with a high TS mRNA expression. Fluorouracil 16-20 thymidylate synthetase Homo sapiens 108-110 22870098-9 2010 These data suggest that TS mRNA expression in breast cancer tissue is an ideal predictor of outcomes for patients with no administration of 5-FU, and of the efficacy of 5-FU. Fluorouracil 140-144 thymidylate synthetase Homo sapiens 24-26 22870098-9 2010 These data suggest that TS mRNA expression in breast cancer tissue is an ideal predictor of outcomes for patients with no administration of 5-FU, and of the efficacy of 5-FU. Fluorouracil 169-173 thymidylate synthetase Homo sapiens 24-26 21036767-2 2010 To explore the predictability of TYMS polymorphisms for the sensitivity and toxicity of 5-fluorouracil (5-FU) in breast cancer patients, this study investigated the association between TYMS polymorphisms and TYMS protein expression in normal and tumour tissue specimens from 49 lymph node-positive breast cancer patients. Fluorouracil 104-108 thymidylate synthetase Homo sapiens 33-37 21036767-5 2010 These findings suggest that breast cancer patients with the TYMS 3"-UTR +6 bp/+6 bp polymorphism whose tumours show a 6 bp deletion within TYMS 3"-UTR represent a group that may derive the most benefit from 5-FU chemotherapy. Fluorouracil 207-211 thymidylate synthetase Homo sapiens 60-64 21036767-5 2010 These findings suggest that breast cancer patients with the TYMS 3"-UTR +6 bp/+6 bp polymorphism whose tumours show a 6 bp deletion within TYMS 3"-UTR represent a group that may derive the most benefit from 5-FU chemotherapy. Fluorouracil 207-211 thymidylate synthetase Homo sapiens 139-143 21036698-0 2010 5-fluorouracil-induced death of Jurkat T-cells--a role for caspases and MCL-1. Fluorouracil 0-14 MCL1 apoptosis regulator, BCL2 family member Homo sapiens 72-77 21036698-7 2010 Furthermore, we observed 5-FU induced PARP cleavage and notably, reduced expression of antiapoptotic MCL-1L associated with the appearance of proapoptotic MCL-1S. Fluorouracil 25-29 MCL1 apoptosis regulator, BCL2 family member Homo sapiens 101-107 21036698-7 2010 Furthermore, we observed 5-FU induced PARP cleavage and notably, reduced expression of antiapoptotic MCL-1L associated with the appearance of proapoptotic MCL-1S. Fluorouracil 25-29 MCL1 apoptosis regulator, BCL2 family member Homo sapiens 155-161 20700687-9 2010 Enforced 14-3-3sigma expression can increase the sensitivity of MCF-7/5-FU cells to 5-FU and cDDP. Fluorouracil 70-74 stratifin Homo sapiens 9-20 20811661-0 2010 Irinotecan overcomes the resistance to 5-fluorouracil in human colon cancer xenografts by down-regulation of intratumoral thymidylate synthase. Fluorouracil 39-53 thymidylate synthetase Homo sapiens 122-142 16141798-1 2005 The present study aimed to prospectively investigate the influence of thymidylate synthase (TS) polymorphisms (5"-TSER, 3"-TSUTR) on the disease-free survival (DFS) and overall survival (OS) of patients with colorectal cancer (CRC) who were treated with adjuvant 5-fluorouracil (5-FU) therapy. Fluorouracil 279-283 thymidylate synthetase Homo sapiens 92-94 16207145-1 2005 Folate metabolism is the target of two major drug groups: folate antagonists (for example, methotrexate) and thymidylate synthase inhibitors (for example, 5-fluorouracil). Fluorouracil 155-169 thymidylate synthetase Homo sapiens 109-129 20920194-11 2010 The sensitivity of all the four cells to 5-FU also varied according to cell types, particularly with CL-6 cell (IC50=757 micromolar). Fluorouracil 41-45 insulin induced gene 1 Homo sapiens 101-105 20837458-1 2010 BACKGROUND: Thymidylate synthase (TS), thymidine phosphorylase (TP), and dihydropyrimidine dehydrogenase (DPD) are key enzymes in the 5-fluorouracil (5-FU) pathway. Fluorouracil 134-148 thymidylate synthetase Homo sapiens 12-32 20837458-1 2010 BACKGROUND: Thymidylate synthase (TS), thymidine phosphorylase (TP), and dihydropyrimidine dehydrogenase (DPD) are key enzymes in the 5-fluorouracil (5-FU) pathway. Fluorouracil 134-148 thymidylate synthetase Homo sapiens 34-36 20837458-1 2010 BACKGROUND: Thymidylate synthase (TS), thymidine phosphorylase (TP), and dihydropyrimidine dehydrogenase (DPD) are key enzymes in the 5-fluorouracil (5-FU) pathway. Fluorouracil 150-154 thymidylate synthetase Homo sapiens 12-32 20837458-1 2010 BACKGROUND: Thymidylate synthase (TS), thymidine phosphorylase (TP), and dihydropyrimidine dehydrogenase (DPD) are key enzymes in the 5-fluorouracil (5-FU) pathway. Fluorouracil 150-154 thymidylate synthetase Homo sapiens 34-36 21410037-8 2010 CONCLUSIONS: For the chemosensitivity of colorectal cancer to 5-Fluorouracil, the specimen should be excised from the invasive front of the tumor, and TS expression should be evaluated in it. Fluorouracil 62-76 thymidylate synthetase Homo sapiens 151-153 20697159-8 2010 In mouse xenograft models, combination of a CD13 inhibitor and the genotoxic chemotherapeutic fluorouracil (5-FU) drastically reduced tumor volume compared with either agent alone. Fluorouracil 108-112 alanyl (membrane) aminopeptidase Mus musculus 44-48 20697159-9 2010 5-FU inhibited CD90+ proliferating CSCs, some of which produce CD13+ semiquiescent CSCs, while CD13 inhibition suppressed the self-renewing and tumor-initiating ability of dormant CSCs. Fluorouracil 0-4 alanyl (membrane) aminopeptidase Mus musculus 63-67 16255377-2 2005 The fermented wheat germ extract (code name: MSC, trade name: Avemar) registered as a dietary food for special medical purposes for cancer patients to complement the active oncotherapy, exerted a growth inhibitory effect in HCR-25 human colon carcinoma xenograft, and had a synergistic effect with 5-FU in mouse C-38 colorectal carcinoma. Fluorouracil 298-302 coiled-coil alpha-helical rod protein 1 Homo sapiens 224-227 16182121-1 2005 Thymidylate synthase (TS) intratumoural expression may be a prognostic marker and predict outcome of 5-fluorouracil (5-FU)-based chemotherapy in colorectal cancer patients. Fluorouracil 101-115 thymidylate synthetase Homo sapiens 0-20 21098876-12 2010 Our results indicate that rHuEpo acts via EpoR to directly inhibit DLD-1 cell growth and indirectly modulate the cytostatics effects of 5-FU and SN-38. Fluorouracil 136-140 erythropoietin receptor Homo sapiens 42-46 20603394-0 2010 Obesity hormone leptin induces growth and interferes with the cytotoxic effects of 5-fluorouracil in colorectal tumor stem cells. Fluorouracil 83-97 leptin Homo sapiens 16-22 20603394-8 2010 Moreover, leptin counteracted cytotoxic effects of 5-fluorouracil, a common colon cancer therapeutic agent. Fluorouracil 51-65 leptin Homo sapiens 10-16 20628391-0 2010 UGT1A and TYMS genetic variants predict toxicity and response of colorectal cancer patients treated with first-line irinotecan and fluorouracil combination therapy. Fluorouracil 131-143 thymidylate synthetase Homo sapiens 10-14 20628391-9 2010 CONCLUSION: TYMS and UGT1A polymorphisms influence on tumour response and toxicities derived from irinotecan/5FU treatment in CRC patients. Fluorouracil 109-112 thymidylate synthetase Homo sapiens 12-16 16182121-1 2005 Thymidylate synthase (TS) intratumoural expression may be a prognostic marker and predict outcome of 5-fluorouracil (5-FU)-based chemotherapy in colorectal cancer patients. Fluorouracil 101-115 thymidylate synthetase Homo sapiens 22-24 16182121-1 2005 Thymidylate synthase (TS) intratumoural expression may be a prognostic marker and predict outcome of 5-fluorouracil (5-FU)-based chemotherapy in colorectal cancer patients. Fluorouracil 117-121 thymidylate synthetase Homo sapiens 0-20 16182121-1 2005 Thymidylate synthase (TS) intratumoural expression may be a prognostic marker and predict outcome of 5-fluorouracil (5-FU)-based chemotherapy in colorectal cancer patients. Fluorouracil 117-121 thymidylate synthetase Homo sapiens 22-24 16077970-6 2005 A significant association was found between tumour TS expression and response to treatment with 5-FU plus FA with irinotecan (p=0.05). Fluorouracil 96-100 thymidylate synthetase Homo sapiens 51-53 16077970-8 2005 Immunohistochemical TS expression levels might be used both as a prognostic marker and to help identify patients who would benefit from 5-FU based regime. Fluorouracil 136-140 thymidylate synthetase Homo sapiens 20-22 16009948-7 2005 In the subgroup of patients treated with surgery alone, the expression of TS in lymph node metastases also had a prognostic value for OS (P = .04) and DFS (P = .03), but this was not the case for the other subgroup who received adjuvant fluorouracil-based chemotherapy (OS, P = .5; DFS, P = .2). Fluorouracil 237-249 thymidylate synthetase Homo sapiens 74-76 19956517-0 2005 Thymidylate synthase, thymidine phosphorylase, VEGF and p53 protein expression in primary colorectal cancer for predicting response to 5-fluorouracil-based chemotherapy. Fluorouracil 135-149 thymidylate synthetase Homo sapiens 0-20 19956517-3 2005 The expression levels of thymidylate synthase (TS), thymidine phosphorylase (TP) and p53 have been known to be associated with the clinical response to 5-FU-based therapy as well as the prognosis, and that of vascular endothelial growth factor (VEGF) is associated with poor survival. Fluorouracil 152-156 thymidylate synthetase Homo sapiens 25-45 16010424-13 2005 The EGF labelling index was, however significantly lower in the tumours treated with triple therapy than those treated with 5-FU/LV. Fluorouracil 124-128 epidermal growth factor Homo sapiens 4-7 16026610-6 2005 RESULTS: In 8/16 paired esophageal biopsies, there was an increase in the expression of multi-drug resistance gene 1 (MDR1) following epirubicin + cisplatin + 5-fluorouracil (ECF) chemotherapy and this was accompanied by increased expression of the MDR-1 encoded protein, P-gp. Fluorouracil 159-173 phosphoglycolate phosphatase Homo sapiens 272-276 16081025-9 2005 Cutaneous LE lesions can also be induced in TCRalpha-/- mice treated with fluorouracil and ultraviolet B light irradiation. Fluorouracil 74-86 T cell receptor alpha chain Mus musculus 44-52 16030402-1 2005 BACKGROUND/AIMS: Thymidylate synthase (TS) is a target enzyme of 5-fluorouracil (5-FU) and has a polymorphic 28 bp tandem repeated sequence. Fluorouracil 65-79 thymidylate synthetase Homo sapiens 17-37 18931698-9 2009 Furthermore, reduced expression of CXXC4 by small interfering RNAs promoted cell proliferation and inhibited apoptosis after 5-FU and doxorubicin treatment in RCC cells. Fluorouracil 125-129 CXXC finger protein 4 Homo sapiens 35-40 19137262-6 2009 The present study demonstrates that galectin-3 stabilizes hnRNP Q via complex formation, and reduction in the hnRNP Q level leads to slow proliferation and less susceptibility to 5-FU. Fluorouracil 179-183 synaptotagmin binding cytoplasmic RNA interacting protein Homo sapiens 110-117 19023200-0 2009 Correlations between thymidylate synthase expression and chemosensitivity to 5-fluorouracil, cell proliferation and clinical outcome in head and neck squamous cell carcinoma. Fluorouracil 77-91 thymidylate synthetase Homo sapiens 21-41 19023200-3 2009 In this study, we examined whether TS expression is correlated with chemosensitivity to 5-FU, cell proliferation and clinical outcome in HNSCC. Fluorouracil 88-92 thymidylate synthetase Homo sapiens 35-37 19023200-9 2009 CONCLUSIONS: These results indicate that TS expression plays an important role in the sensitivity of HNSCC to 5-FU chemotherapy. Fluorouracil 110-114 thymidylate synthetase Homo sapiens 41-43 19082440-1 2009 Orotate phosphoribosyl transferase (OPRT) is the initial enzyme of 5-fluorouracil (5-FU) activation, in which 5-FU is converted to 5-fluorouridinemonophosphate. Fluorouracil 67-81 uridine monophosphate synthetase Homo sapiens 0-34 19082440-1 2009 Orotate phosphoribosyl transferase (OPRT) is the initial enzyme of 5-fluorouracil (5-FU) activation, in which 5-FU is converted to 5-fluorouridinemonophosphate. Fluorouracil 67-81 uridine monophosphate synthetase Homo sapiens 36-40 19082440-1 2009 Orotate phosphoribosyl transferase (OPRT) is the initial enzyme of 5-fluorouracil (5-FU) activation, in which 5-FU is converted to 5-fluorouridinemonophosphate. Fluorouracil 83-87 uridine monophosphate synthetase Homo sapiens 0-34 19082440-1 2009 Orotate phosphoribosyl transferase (OPRT) is the initial enzyme of 5-fluorouracil (5-FU) activation, in which 5-FU is converted to 5-fluorouridinemonophosphate. Fluorouracil 83-87 uridine monophosphate synthetase Homo sapiens 36-40 19082440-1 2009 Orotate phosphoribosyl transferase (OPRT) is the initial enzyme of 5-fluorouracil (5-FU) activation, in which 5-FU is converted to 5-fluorouridinemonophosphate. Fluorouracil 110-114 uridine monophosphate synthetase Homo sapiens 0-34 19082440-1 2009 Orotate phosphoribosyl transferase (OPRT) is the initial enzyme of 5-fluorouracil (5-FU) activation, in which 5-FU is converted to 5-fluorouridinemonophosphate. Fluorouracil 110-114 uridine monophosphate synthetase Homo sapiens 36-40 19307741-12 2009 CONCLUSION: High OPRT gene expression may be a predictive factor of CR to 5-fluorouracil/cisplatin-based CRT in esophageal cancer. Fluorouracil 74-88 uridine monophosphate synthetase Homo sapiens 17-21 16030402-1 2005 BACKGROUND/AIMS: Thymidylate synthase (TS) is a target enzyme of 5-fluorouracil (5-FU) and has a polymorphic 28 bp tandem repeated sequence. Fluorouracil 81-85 thymidylate synthetase Homo sapiens 17-37 15944796-7 2005 In addition, microsatellite instability did not correlate with the extent of chemotherapy benefit, although we observed a statistically non-significant favourable impact of 5-FU-based treatment in the MSI-H group compared to MSI-L/MSS patients. Fluorouracil 173-177 RB binding protein 4, chromatin remodeling factor Homo sapiens 201-204 15856030-10 2005 These data therefore demonstrate that Ras mutations increase sensitivity to 5-FU-induced apoptosis at least in part through the negative regulation of gelsolin expression. Fluorouracil 76-80 gelsolin Homo sapiens 151-159 15856030-11 2005 Our data indicate that Ras mutations promote apoptosis in response to 5-FU treatment and imply that tumors with Ras mutations and/or reduced expression of gelsolin may show enhanced apoptosis in response to 5-FU also in vivo. Fluorouracil 70-74 gelsolin Homo sapiens 155-163 15856030-11 2005 Our data indicate that Ras mutations promote apoptosis in response to 5-FU treatment and imply that tumors with Ras mutations and/or reduced expression of gelsolin may show enhanced apoptosis in response to 5-FU also in vivo. Fluorouracil 207-211 gelsolin Homo sapiens 155-163 15902309-3 2005 We were able to achieve restoration of their radiosensitivity and sensitivity to 5-fluorouracil and irinotecan by reexpression of SPARC in tumor xenografts. Fluorouracil 81-95 secreted protein acidic and cysteine rich Homo sapiens 130-135 15731169-4 2005 Furthermore, exposure of colorectal cancer cells to anti-periostin antibodies activates apoptosis and potentiates the effects of 5-fluorouracil chemotherapy. Fluorouracil 129-143 periostin Homo sapiens 57-66 15826316-0 2005 Phase III trial of postoperative cisplatin, interferon alpha-2b, and 5-FU combined with external radiation treatment versus 5-FU alone for patients with resected pancreatic adenocarcinoma -- CapRI: study protocol [ISRCTN62866759]. Fluorouracil 69-73 RAS p21 protein activator 4 Homo sapiens 191-196 19105824-1 2008 BACKGROUND: Over-expression of thymidylate synthase (TS) and dihydropyrimidine dehydrogenase (DPD) in tumor tissue is associated with insensitivity to 5-fluorouracil (5-FU). Fluorouracil 151-165 thymidylate synthetase Homo sapiens 53-55 19105824-1 2008 BACKGROUND: Over-expression of thymidylate synthase (TS) and dihydropyrimidine dehydrogenase (DPD) in tumor tissue is associated with insensitivity to 5-fluorouracil (5-FU). Fluorouracil 167-171 thymidylate synthetase Homo sapiens 31-51 19105824-1 2008 BACKGROUND: Over-expression of thymidylate synthase (TS) and dihydropyrimidine dehydrogenase (DPD) in tumor tissue is associated with insensitivity to 5-fluorouracil (5-FU). Fluorouracil 167-171 thymidylate synthetase Homo sapiens 53-55 15864374-1 2005 Response of colorectal cancers to 5-fluorouracil appears to be influenced by differences in thymidylate synthase (TS) expression. Fluorouracil 34-48 thymidylate synthetase Homo sapiens 92-112 15864374-1 2005 Response of colorectal cancers to 5-fluorouracil appears to be influenced by differences in thymidylate synthase (TS) expression. Fluorouracil 34-48 thymidylate synthetase Homo sapiens 114-116 15756440-4 2005 A significantly better outcome in the low-dose CDDP/5-FU group than in the surgery alone group was associated with pStage III disease (p<0.001), pN1 lymph node metastasis (p<0.001), and lymphatic invasion (p<0.01). Fluorouracil 52-56 serpin family E member 2 Homo sapiens 148-151 16833532-2 2005 Full geometry optimizations of the 5-fluorouracil-water complexes were carried out at the MP2/6-31+G(d,p) level of theory. Fluorouracil 35-49 tryptase pseudogene 1 Homo sapiens 90-98 16833532-9 2005 The minimum energy path (MP2/6-31+G(d,p)) for water-assisted proton transfer in trihydrated 5-fluorouracil was followed. Fluorouracil 92-106 tryptase pseudogene 1 Homo sapiens 25-28 15735113-0 2005 Thymidylate synthase and methylenetetrahydrofolate reductase gene polymorphism in normal tissue as predictors of fluorouracil sensitivity. Fluorouracil 113-125 thymidylate synthetase Homo sapiens 0-20 15735113-1 2005 PURPOSE: To analyze thymidylate synthase (TS) and methylenetetrahydrofolate reductase (MTHFR) gene polymorphism with respect to fluorouracil (FU) sensitivity. Fluorouracil 128-140 thymidylate synthetase Homo sapiens 20-40 15670580-0 2005 Modulation of 5-fluorouracil cytotoxicity through thymidylate synthase and NF-kappaB down-regulation and its application on the radiolabelled iododeoxyuridine therapy on human hepatoma cell. Fluorouracil 14-28 thymidylate synthetase Homo sapiens 50-70 15701575-0 2005 Pre-treatment with insulin-like growth factor-I partially ameliorates 5-fluorouracil-induced intestinal mucositis in rats. Fluorouracil 70-84 insulin-like growth factor 1 Rattus norvegicus 19-47 18722050-0 2008 Thymidylate synthase genotypes and tumour regression in stage II/III rectal cancer patients after neoadjuvant fluorouracil-based chemoradiation. Fluorouracil 110-122 thymidylate synthetase Homo sapiens 0-20 18851872-9 2008 In subgroup analysis with 39 patients who were treated with regimens containing 5-fluorouracil (5-FU), the genotypes of GGH-401Cytosine/Thymine were significantly associated with the response to NAC (P=0.039). Fluorouracil 80-94 gamma-glutamyl hydrolase Homo sapiens 120-123 18851872-9 2008 In subgroup analysis with 39 patients who were treated with regimens containing 5-fluorouracil (5-FU), the genotypes of GGH-401Cytosine/Thymine were significantly associated with the response to NAC (P=0.039). Fluorouracil 96-100 gamma-glutamyl hydrolase Homo sapiens 120-123 19020767-1 2008 It has been reported that the expression of thymidylate synthase (TS), dihydropyrimidine dehydrogenase (DPD) and orotate phosphoribosyltransferase (OPRT) may predict the clinical efficacy of 5-fluorouracil (5-FU)-based therapy in cancer patients. Fluorouracil 191-205 thymidylate synthetase Homo sapiens 66-68 19020767-1 2008 It has been reported that the expression of thymidylate synthase (TS), dihydropyrimidine dehydrogenase (DPD) and orotate phosphoribosyltransferase (OPRT) may predict the clinical efficacy of 5-fluorouracil (5-FU)-based therapy in cancer patients. Fluorouracil 191-205 uridine monophosphate synthetase Homo sapiens 113-146 19020767-1 2008 It has been reported that the expression of thymidylate synthase (TS), dihydropyrimidine dehydrogenase (DPD) and orotate phosphoribosyltransferase (OPRT) may predict the clinical efficacy of 5-fluorouracil (5-FU)-based therapy in cancer patients. Fluorouracil 191-205 uridine monophosphate synthetase Homo sapiens 148-152 19020767-1 2008 It has been reported that the expression of thymidylate synthase (TS), dihydropyrimidine dehydrogenase (DPD) and orotate phosphoribosyltransferase (OPRT) may predict the clinical efficacy of 5-fluorouracil (5-FU)-based therapy in cancer patients. Fluorouracil 207-211 thymidylate synthetase Homo sapiens 44-64 19020767-1 2008 It has been reported that the expression of thymidylate synthase (TS), dihydropyrimidine dehydrogenase (DPD) and orotate phosphoribosyltransferase (OPRT) may predict the clinical efficacy of 5-fluorouracil (5-FU)-based therapy in cancer patients. Fluorouracil 207-211 thymidylate synthetase Homo sapiens 66-68 19020767-1 2008 It has been reported that the expression of thymidylate synthase (TS), dihydropyrimidine dehydrogenase (DPD) and orotate phosphoribosyltransferase (OPRT) may predict the clinical efficacy of 5-fluorouracil (5-FU)-based therapy in cancer patients. Fluorouracil 207-211 uridine monophosphate synthetase Homo sapiens 113-146 19020767-1 2008 It has been reported that the expression of thymidylate synthase (TS), dihydropyrimidine dehydrogenase (DPD) and orotate phosphoribosyltransferase (OPRT) may predict the clinical efficacy of 5-fluorouracil (5-FU)-based therapy in cancer patients. Fluorouracil 207-211 uridine monophosphate synthetase Homo sapiens 148-152 15701575-9 2005 We conclude that IGF-I pre-treatment only partially attenuates features of intestinal mucositis when assessed 48 h after 5-FU chemotherapy. Fluorouracil 121-125 insulin-like growth factor 1 Rattus norvegicus 17-22 15608420-4 2005 Therefore we investigated whether the addition of monoclonal antibodies against the EGFR could enhance the response rate of cisplatin, 5-FU and docetaxel. Fluorouracil 135-139 epidermal growth factor receptor Mus musculus 84-88 16178783-4 2005 Thymidylate synthase (TS or ThyA) has long been considered as one of the best-known drug targets in the anti-cancer area, after which old and new drugs, such as 5-fluoro uracil and the anti-folate ZD1694, have been introduced into chemotherapy to treat solid tumours. Fluorouracil 161-176 thymidylate synthetase Homo sapiens 0-20 16254431-0 2005 Adjuvant 5-FU-based chemoradiotherapy for patients undergoing R-1/R-2 resections for pancreatic cancer. Fluorouracil 9-13 CD1b molecule Homo sapiens 62-65 15999119-1 2005 The enzymes thymidylate synthase (TS), dihydropyrimidine dehydrogenase (DPD), thymidine phosphorylase (TP), and orotate phosphoribosyl transferase (OPRT) are involved in the metabolism of the anticancer drug 5-fluorouracil. Fluorouracil 208-222 thymidylate synthetase Homo sapiens 12-32 15999119-1 2005 The enzymes thymidylate synthase (TS), dihydropyrimidine dehydrogenase (DPD), thymidine phosphorylase (TP), and orotate phosphoribosyl transferase (OPRT) are involved in the metabolism of the anticancer drug 5-fluorouracil. Fluorouracil 208-222 uridine monophosphate synthetase Homo sapiens 148-152 15534911-0 2004 The effect of adenovirus expressing wild-type p53 on 5-fluorouracil chemosensitivity is related to p53 status in pancreatic cancer cell lines. Fluorouracil 53-67 Wistar clone pR53P1 p53 pseudogene Rattus norvegicus 46-49 19093176-5 2008 Clinical and in vitro work has previously shown that high CH(2)FH(4) and low GGH expression levels correlate with good response to 5-FU. Fluorouracil 131-135 gamma-glutamyl hydrolase Homo sapiens 77-80 18594845-4 2008 Our study investigated the value of high degree of MSI (MSI-H) in patients treated with 5-FU/oxaliplatin-based chemotherapy which has been done by only one further study recently. Fluorouracil 88-92 RB binding protein 4, chromatin remodeling factor Homo sapiens 51-54 18612238-2 2008 The targeted pyrimidine biosynthesis pathway includes dihydropyrimidine dehydrogenase (DPD), which converts 5-FU to an inactive metabolite, and thymidylate synthase (TS), which is a major target of 5-FU. Fluorouracil 108-112 dihydropyrimidine dehydrogenase Mus musculus 87-90 18612238-2 2008 The targeted pyrimidine biosynthesis pathway includes dihydropyrimidine dehydrogenase (DPD), which converts 5-FU to an inactive metabolite, and thymidylate synthase (TS), which is a major target of 5-FU. Fluorouracil 198-202 dihydropyrimidine dehydrogenase Mus musculus 87-90 18612238-4 2008 Overexpression of the worm DPD and TS homologs (DPYD-1 and Y110A7A.4, respectively) suppressed germ cell death following 5-FU exposure. Fluorouracil 121-125 dihydropyrimidine dehydrogenase Mus musculus 27-30 18661526-1 2008 Thymidylate synthase (TS) is a potentially valuable marker for therapy response since it is the molecular target of 5-fluorouracil (5-FU). Fluorouracil 116-130 thymidylate synthetase Homo sapiens 0-20 18661526-1 2008 Thymidylate synthase (TS) is a potentially valuable marker for therapy response since it is the molecular target of 5-fluorouracil (5-FU). Fluorouracil 116-130 thymidylate synthetase Homo sapiens 22-24 18661526-1 2008 Thymidylate synthase (TS) is a potentially valuable marker for therapy response since it is the molecular target of 5-fluorouracil (5-FU). Fluorouracil 132-136 thymidylate synthetase Homo sapiens 0-20 18661526-1 2008 Thymidylate synthase (TS) is a potentially valuable marker for therapy response since it is the molecular target of 5-fluorouracil (5-FU). Fluorouracil 132-136 thymidylate synthetase Homo sapiens 22-24 15534911-0 2004 The effect of adenovirus expressing wild-type p53 on 5-fluorouracil chemosensitivity is related to p53 status in pancreatic cancer cell lines. Fluorouracil 53-67 Wistar clone pR53P1 p53 pseudogene Rattus norvegicus 99-102 15534911-1 2004 AIM: There are conflicting data about p53 function on cellular sensitivity to the cytotoxic action of 5-fluorouracil (5-FU). Fluorouracil 102-116 Wistar clone pR53P1 p53 pseudogene Rattus norvegicus 38-41 15534911-1 2004 AIM: There are conflicting data about p53 function on cellular sensitivity to the cytotoxic action of 5-fluorouracil (5-FU). Fluorouracil 118-122 Wistar clone pR53P1 p53 pseudogene Rattus norvegicus 38-41 15534911-9 2004 Both in vitro and in vivo analyses revealed that a sublethal dose of Ad-p53 augmented the apoptotic response induced by 5-FU. Fluorouracil 120-124 Wistar clone pR53P1 p53 pseudogene Rattus norvegicus 72-75 15534911-10 2004 CONCLUSION: Our results suggest that Ad-p53 may synergistically enhance 5-FU-chemosensitivity most strikingly in pancreatic cancer cells lacking p53 function. Fluorouracil 72-76 Wistar clone pR53P1 p53 pseudogene Rattus norvegicus 40-43 15386371-0 2004 Single nucleotide polymorphism in the 5" tandem repeat sequences of thymidylate synthase gene predicts for response to fluorouracil-based chemotherapy in advanced colorectal cancer patients. Fluorouracil 119-131 thymidylate synthetase Homo sapiens 68-88 15386371-1 2004 Thymidylate synthase (TS) is the primary target of 5-fluorouracil (5-FU). Fluorouracil 51-65 thymidylate synthetase Homo sapiens 0-20 15386371-1 2004 Thymidylate synthase (TS) is the primary target of 5-fluorouracil (5-FU). Fluorouracil 51-65 thymidylate synthetase Homo sapiens 22-24 15386371-1 2004 Thymidylate synthase (TS) is the primary target of 5-fluorouracil (5-FU). Fluorouracil 67-71 thymidylate synthetase Homo sapiens 0-20 15386371-1 2004 Thymidylate synthase (TS) is the primary target of 5-fluorouracil (5-FU). Fluorouracil 67-71 thymidylate synthetase Homo sapiens 22-24 15386371-2 2004 A VNTR polymorphism in the TS promoter region is associated with the efficacy of 5-FU-based chemotherapy in colorectal cancer. Fluorouracil 81-85 thymidylate synthetase Homo sapiens 27-29 15386371-14 2004 The selection of patients who are likely to respond to 5-FU therapy may be considerably improved if the TS genotype were to include both the VNTR and the SNP located within the promoter region of the gene. Fluorouracil 55-59 thymidylate synthetase Homo sapiens 104-106 15585071-5 2004 Similarly, in the multicenter prospective Chemo N0 trial, administration of cyclophosphamide/methotrexate/5-fluorouracil-based chemotherapy led to a substantial reduction in risk of disease recurrence in patients with high uPA/PAI-1. Fluorouracil 106-120 serpin family E member 1 Homo sapiens 227-232 15571969-1 2004 Thymidylate Synthase (TS) is the key enzyme for DNA synthesis pathways and is inhibited by 5-fluorouracil (5FU). Fluorouracil 91-105 thymidylate synthetase Homo sapiens 0-20 15571969-1 2004 Thymidylate Synthase (TS) is the key enzyme for DNA synthesis pathways and is inhibited by 5-fluorouracil (5FU). Fluorouracil 91-105 thymidylate synthetase Homo sapiens 22-24 15571969-1 2004 Thymidylate Synthase (TS) is the key enzyme for DNA synthesis pathways and is inhibited by 5-fluorouracil (5FU). Fluorouracil 107-110 thymidylate synthetase Homo sapiens 0-20 15571969-1 2004 Thymidylate Synthase (TS) is the key enzyme for DNA synthesis pathways and is inhibited by 5-fluorouracil (5FU). Fluorouracil 107-110 thymidylate synthetase Homo sapiens 22-24 15571969-7 2004 As TS is the key enzyme for DNA synthesis pathways and is inhibited by 5-fluorouracil (5FU), we can hypothesise that TS expression levels in the different histotypes of CRC could affect the potential responsiveness of these tumours to fluoropyrimidine chemotherapy, with a low efficacy being expected in signet ring cell areas. Fluorouracil 71-85 thymidylate synthetase Homo sapiens 3-5 15571969-7 2004 As TS is the key enzyme for DNA synthesis pathways and is inhibited by 5-fluorouracil (5FU), we can hypothesise that TS expression levels in the different histotypes of CRC could affect the potential responsiveness of these tumours to fluoropyrimidine chemotherapy, with a low efficacy being expected in signet ring cell areas. Fluorouracil 71-85 thymidylate synthetase Homo sapiens 117-119 15571969-7 2004 As TS is the key enzyme for DNA synthesis pathways and is inhibited by 5-fluorouracil (5FU), we can hypothesise that TS expression levels in the different histotypes of CRC could affect the potential responsiveness of these tumours to fluoropyrimidine chemotherapy, with a low efficacy being expected in signet ring cell areas. Fluorouracil 87-90 thymidylate synthetase Homo sapiens 3-5 15571969-7 2004 As TS is the key enzyme for DNA synthesis pathways and is inhibited by 5-fluorouracil (5FU), we can hypothesise that TS expression levels in the different histotypes of CRC could affect the potential responsiveness of these tumours to fluoropyrimidine chemotherapy, with a low efficacy being expected in signet ring cell areas. Fluorouracil 87-90 thymidylate synthetase Homo sapiens 117-119 15542523-11 2004 Thus FPGS status may be an important predictor of chemosensitivity of colon cancer cells to 5-FU based chemotherapy, and FPGS gene transfer may increase the sensitivity of colon cancer cells to 5-FU-based chemotherapy. Fluorouracil 194-198 folylpolyglutamate synthase Homo sapiens 121-125 18691855-0 2008 Mitotic checkpoint genes, hsMAD2 and BubR1, in oesophageal squamous cancer cells and their association with 5-fluorouracil and cisplatin-based radiochemotherapy. Fluorouracil 108-122 mitotic arrest deficient 2 like 1 Homo sapiens 26-32 18691855-0 2008 Mitotic checkpoint genes, hsMAD2 and BubR1, in oesophageal squamous cancer cells and their association with 5-fluorouracil and cisplatin-based radiochemotherapy. Fluorouracil 108-122 BUB1 mitotic checkpoint serine/threonine kinase B Homo sapiens 37-42 15585135-7 2004 Our experiments showed that 5-FU engaged the mitochondrial apoptotic pathway involving cytosolic cytochrome c release and subsequent activation of caspase-9 and caspase-3 as well as the membrane death receptor (DR)-mediated apoptotic pathway involving activation of caspase-8 with an Apo-1/CD95 (Fas)-dependent fashion. Fluorouracil 28-32 caspase 9 Homo sapiens 147-156 15492820-9 2004 Vinorelbine suppressed the 5-FU-induced increase in TS protein in A549 cells. Fluorouracil 27-31 thymidylate synthetase Homo sapiens 52-54 17684476-0 2008 Transcription factor-binding sites in the thymidylate synthase gene: predictors of outcome in patients with metastatic colorectal cancer treated with 5-fluorouracil and oxaliplatin? Fluorouracil 150-164 thymidylate synthetase Homo sapiens 42-62 15688605-2 2004 An example of a drug for which clear predictive parameters have been identified is 5-fluorouracil (5FU): its antitumor activity is limited by either a high activity of the target enzyme thymidylate synthase (TS) and/or a high activity of its degrading enzyme, dihydropyrimidine dehydrogenase (DPD). Fluorouracil 83-97 thymidylate synthetase Homo sapiens 186-206 17684476-5 2008 Our results indicate that this new genetic parameter (the number of USF-binding sites) could be considered when evaluating the role of TS genotype in the efficacy of the 5-FU-based regimens. Fluorouracil 170-174 upstream transcription factor 1 Homo sapiens 68-71 17684476-5 2008 Our results indicate that this new genetic parameter (the number of USF-binding sites) could be considered when evaluating the role of TS genotype in the efficacy of the 5-FU-based regimens. Fluorouracil 170-174 thymidylate synthetase Homo sapiens 135-137 18728661-0 2008 Liver-only metastatic colorectal cancer patients and thymidylate synthase polymorphisms for predicting response to 5-fluorouracil-based chemotherapy. Fluorouracil 115-129 thymidylate synthetase Homo sapiens 53-73 18728661-1 2008 We investigated the association between thymidylate synthase (TS) germline polymorphisms and response to 5-fluorouracil-based chemotherapy in 80 patients with liver-only metastatic colorectal cancer (MCRC). Fluorouracil 105-119 thymidylate synthetase Homo sapiens 40-60 18776995-6 2008 The results indicated that the expression of SHh pathway target molecules at both messenger RNA and protein levels are evidently down-regulated in Hep3B cells treated with 5-FU. Fluorouracil 172-176 sonic hedgehog signaling molecule Homo sapiens 45-48 18776995-8 2008 Furthermore, 5-FU treatment affects the subcellular localization of PTC1 protein, a key member in SHh signaling pathway. Fluorouracil 13-17 sonic hedgehog signaling molecule Homo sapiens 98-101 18776995-9 2008 Our data showed that the down-regulation of SHh signaling pathway activity was involved in 5-FU-induced apoptosis and the inhibition of motility in hedgehog-activated HCC cell lines. Fluorouracil 91-95 sonic hedgehog signaling molecule Homo sapiens 44-47 18757417-4 2008 Promoter assays showed that the region with the Egr-1 binding site is critical for the induction of TSP-1 promoter activity by 5-FU. Fluorouracil 127-131 early growth response 1 Homo sapiens 48-53 18757417-5 2008 The binding of Egr-1 to the TSP-1 promoter was increased in KM12C cells treated with 5-FU. Fluorouracil 85-89 early growth response 1 Homo sapiens 15-20 18757417-6 2008 Immunofluorescence staining revealed that 5-FU significantly increased the level of Egr-1 in the nuclei of KM12C cells. Fluorouracil 42-46 early growth response 1 Homo sapiens 84-89 18757417-8 2008 Furthermore, 5-FU induced the phosphorylation of p38 mitogen-activated protein kinase (MAPK) and heat shock protein 27 (HSP27). Fluorouracil 13-17 heat shock protein family B (small) member 1 Homo sapiens 97-118 18757417-8 2008 Furthermore, 5-FU induced the phosphorylation of p38 mitogen-activated protein kinase (MAPK) and heat shock protein 27 (HSP27). Fluorouracil 13-17 heat shock protein family B (small) member 1 Homo sapiens 120-125 18695887-13 2008 In contrast, IAB-1 decreased the activity of thymidylate synthase (TS), which is a target enzyme of 5-FU. Fluorouracil 100-104 thymidylate synthetase Homo sapiens 45-65 18930000-2 2008 The commonly used anti-tumor drug, 5-fluorouracil (5-FU), blocks the cell cycle by inhibiting thymidylate synthase, and is also known to induce TXNIP gene expression. Fluorouracil 35-49 thymidylate synthetase Homo sapiens 94-114 18930000-2 2008 The commonly used anti-tumor drug, 5-fluorouracil (5-FU), blocks the cell cycle by inhibiting thymidylate synthase, and is also known to induce TXNIP gene expression. Fluorouracil 51-55 thymidylate synthetase Homo sapiens 94-114 18930000-6 2008 5-FU suppressed the expression of p27(kip1), p53, and cyclin E, whereas d-allose induced p53 and reduced cyclins D, A, and E. The expression of p27(kip1) remained unchanged by d-allose at transcriptional level, but increased at the protein level suggesting an increase in protein stability by TXNIP. Fluorouracil 0-4 interferon alpha inducible protein 27 Homo sapiens 34-37 18930000-6 2008 5-FU suppressed the expression of p27(kip1), p53, and cyclin E, whereas d-allose induced p53 and reduced cyclins D, A, and E. The expression of p27(kip1) remained unchanged by d-allose at transcriptional level, but increased at the protein level suggesting an increase in protein stability by TXNIP. Fluorouracil 0-4 cyclin dependent kinase inhibitor 1B Homo sapiens 38-42 18930000-6 2008 5-FU suppressed the expression of p27(kip1), p53, and cyclin E, whereas d-allose induced p53 and reduced cyclins D, A, and E. The expression of p27(kip1) remained unchanged by d-allose at transcriptional level, but increased at the protein level suggesting an increase in protein stability by TXNIP. Fluorouracil 0-4 interferon alpha inducible protein 27 Homo sapiens 144-147 18930000-6 2008 5-FU suppressed the expression of p27(kip1), p53, and cyclin E, whereas d-allose induced p53 and reduced cyclins D, A, and E. The expression of p27(kip1) remained unchanged by d-allose at transcriptional level, but increased at the protein level suggesting an increase in protein stability by TXNIP. Fluorouracil 0-4 cyclin dependent kinase inhibitor 1B Homo sapiens 148-152 18498133-10 2008 A SNP in codon 72 of TP53 was revealed to be a key regulator of 5-FU metabolizing genes such as DHFR and MTHFR, constituting 50% of all significant associations observed after FUMI therapy. Fluorouracil 64-68 dihydrofolate reductase Homo sapiens 96-100 18636193-5 2008 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium (MTT) assay indicated that overexpression of S100P sensitized OVCAR3 cells for chemotherapeutic drugs (paclitaxel, oxaliplatin, 5-fluorouracil, etoposide and epirubicin) induced cytotoxicity more than vector-only controls. Fluorouracil 181-195 S100 calcium binding protein P Homo sapiens 98-103 18652704-1 2008 BACKGROUND: Thymidylate synthase, dihydropyrimidine dehydrogenase, thymidine phosphorylase, and orotate phosphoribosyltransferase gene expressions are reported to be valid predictive markers for 5-fluorouracil sensitivity to gastrointestinal cancer. Fluorouracil 195-209 uridine monophosphate synthetase Homo sapiens 96-129 18751392-1 2008 BACKGROUND: 5-Fluorouracil (5-FU) is an antineoplastic drug that targets thymidylate synthase (TS). Fluorouracil 12-26 thymidylate synthetase Homo sapiens 73-93 18751392-1 2008 BACKGROUND: 5-Fluorouracil (5-FU) is an antineoplastic drug that targets thymidylate synthase (TS). Fluorouracil 12-26 thymidylate synthetase Homo sapiens 95-97 18751392-1 2008 BACKGROUND: 5-Fluorouracil (5-FU) is an antineoplastic drug that targets thymidylate synthase (TS). Fluorouracil 28-32 thymidylate synthetase Homo sapiens 73-93 18751392-1 2008 BACKGROUND: 5-Fluorouracil (5-FU) is an antineoplastic drug that targets thymidylate synthase (TS). Fluorouracil 28-32 thymidylate synthetase Homo sapiens 95-97 18633253-2 2008 Orotate phosphoribosyltransferase(OPRTEC 2.4.2.10)is a primary enzyme involved in the first-step phosphorylation process of 5-fluorouracil and is an important enzyme that possibly enables to predict sensitivity to S-1 irrespective of tissue DPD levels. Fluorouracil 124-138 uridine monophosphate synthetase Homo sapiens 0-33 18609706-11 2008 Furthermore, cells with reduced Bcl-x(L) or Mcl-1 expression was more sensitive towards oxaliplatin- and irinotecan-induced apoptosis, and in the case of Bcl-x(L) also towards 5-FU-induced apoptosis. Fluorouracil 176-180 MCL1 apoptosis regulator, BCL2 family member Homo sapiens 44-49 18575591-0 2008 Silencing of keratinocyte growth factor receptor restores 5-fluorouracil and tamoxifen efficacy on responsive cancer cells. Fluorouracil 58-72 fibroblast growth factor receptor 2 Homo sapiens 13-48 18575591-9 2008 The capacity of 5-FU to induce cell death is abrogated by co-treatment with KGF, whereas in KGFR silenced cells 5-FU efficiently induces cell death even combined to KGF, as determined by evaluating cell viability. Fluorouracil 112-116 fibroblast growth factor receptor 2 Homo sapiens 92-96 18360823-5 2008 The circulating levels of endostatin was analyzed in patients with pancreas cancer and compared to that of healthy controls, as well as after surgical treatment or in a group of nonoperable patients after intraperitoneal fluorouracil (5-FU) chemotherapy. Fluorouracil 221-233 collagen type XVIII alpha 1 chain Homo sapiens 26-36 18360823-5 2008 The circulating levels of endostatin was analyzed in patients with pancreas cancer and compared to that of healthy controls, as well as after surgical treatment or in a group of nonoperable patients after intraperitoneal fluorouracil (5-FU) chemotherapy. Fluorouracil 235-239 collagen type XVIII alpha 1 chain Homo sapiens 26-36 18074150-8 2008 Both paclitaxel and 5-FU are able to trigger apoptosis, and furthermore, to upregulate CD95, whereas only paclitaxel increases CD95 ligand expression. Fluorouracil 20-24 Fas cell surface death receptor Homo sapiens 87-91 18074150-11 2008 As evident from the differential response of our clonal ES subpopulations to paclitaxel and 5-FU, effective activation of the CD95 system depends on intrinsic properties of both the chemotherapeutic agent and target cell population. Fluorouracil 92-96 Fas cell surface death receptor Homo sapiens 126-130 18606591-4 2008 In the present work, we assessed the participation of Omi/Htra2 in the cell death induced by the chemotherapeutic drugs 5-fluorouracil (5-FU) and cisplatin (CDDP) in SW480 colon cancer cells. Fluorouracil 120-134 HtrA serine peptidase 2 Homo sapiens 58-63 18606591-4 2008 In the present work, we assessed the participation of Omi/Htra2 in the cell death induced by the chemotherapeutic drugs 5-fluorouracil (5-FU) and cisplatin (CDDP) in SW480 colon cancer cells. Fluorouracil 136-140 HtrA serine peptidase 2 Homo sapiens 58-63 18606591-7 2008 Exposure of cells to the Omi/Htra2 serine protease inhibitor UCF-101 prevented death p<0.0001 and partially suppressed reproductive cell death of cells exposed to cisplatin p<0.05, but not to 5-FU p=0.49. Fluorouracil 198-202 HtrA serine peptidase 2 Homo sapiens 29-34 18497967-0 2008 Expression of the hMLH1 gene is a possible predictor for the clinical response to 5-fluorouracil after a surgical resection in colorectal cancer. Fluorouracil 82-96 mutL homolog 1 Homo sapiens 18-23 18497967-3 2008 In the present study, we investigated whether the hMLH1 mRNA expression or promoter methylation is a prognostic factor in CRC patients treated with adjuvant 5-FU. Fluorouracil 157-161 mutL homolog 1 Homo sapiens 50-55 15688605-2 2004 An example of a drug for which clear predictive parameters have been identified is 5-fluorouracil (5FU): its antitumor activity is limited by either a high activity of the target enzyme thymidylate synthase (TS) and/or a high activity of its degrading enzyme, dihydropyrimidine dehydrogenase (DPD). Fluorouracil 83-97 thymidylate synthetase Homo sapiens 208-210 18497967-7 2008 Among the 35 patients receiving adjuvant 5-FU, the disease-free survival rate was significantly better in the patients demonstrating a low hMLH1 mRNA expression in the cancer cells in comparison to that of the patients with a high hMLH1 mRNA expression (p<0.01). Fluorouracil 41-45 mutL homolog 1 Homo sapiens 139-144 18497967-7 2008 Among the 35 patients receiving adjuvant 5-FU, the disease-free survival rate was significantly better in the patients demonstrating a low hMLH1 mRNA expression in the cancer cells in comparison to that of the patients with a high hMLH1 mRNA expression (p<0.01). Fluorouracil 41-45 mutL homolog 1 Homo sapiens 231-236 18497967-8 2008 Moreover, a multivariate analysis revealed that hMLH1 mRNA expression was a significant independent prognostic factor for tumor recurrence in CRC patients treated with adjuvant 5-FU. Fluorouracil 177-181 mutL homolog 1 Homo sapiens 48-53 15688605-2 2004 An example of a drug for which clear predictive parameters have been identified is 5-fluorouracil (5FU): its antitumor activity is limited by either a high activity of the target enzyme thymidylate synthase (TS) and/or a high activity of its degrading enzyme, dihydropyrimidine dehydrogenase (DPD). Fluorouracil 99-102 thymidylate synthetase Homo sapiens 186-206 18497967-10 2008 These data suggest that the hMLH1 mRNA quantitation in colorectal cancer cells may be helpful for evaluating the prognosis of CRC patients receiving 5-FU-based adjuvant chemotherapy after a surgical resection. Fluorouracil 149-153 mutL homolog 1 Homo sapiens 28-33 15688605-2 2004 An example of a drug for which clear predictive parameters have been identified is 5-fluorouracil (5FU): its antitumor activity is limited by either a high activity of the target enzyme thymidylate synthase (TS) and/or a high activity of its degrading enzyme, dihydropyrimidine dehydrogenase (DPD). Fluorouracil 99-102 thymidylate synthetase Homo sapiens 208-210 21136888-3 2008 Using proteome-fluorescence-based technology, we found that cetuximab is able to suppress the expression of thymidylate synthase (TS), which is involved in the mechanism of 5-FU action. Fluorouracil 173-177 thymidylate synthetase Homo sapiens 108-128 15375535-0 2004 Thymidylate synthase expression pattern is a prognostic factor in patients of colorectal cancer treated with 5-fluorouracil. Fluorouracil 109-123 thymidylate synthetase Homo sapiens 0-20 18630453-1 2008 BACKGROUND: In advanced colorectal cancer (CRC) a low expression of thymidylate synthase (TS) in metastases predicts a higher response to 5-fluorouracil (5-FU). Fluorouracil 138-152 thymidylate synthetase Homo sapiens 68-88 18630453-1 2008 BACKGROUND: In advanced colorectal cancer (CRC) a low expression of thymidylate synthase (TS) in metastases predicts a higher response to 5-fluorouracil (5-FU). Fluorouracil 138-152 thymidylate synthetase Homo sapiens 90-92 18630453-1 2008 BACKGROUND: In advanced colorectal cancer (CRC) a low expression of thymidylate synthase (TS) in metastases predicts a higher response to 5-fluorouracil (5-FU). Fluorouracil 154-158 thymidylate synthetase Homo sapiens 68-88 18630453-1 2008 BACKGROUND: In advanced colorectal cancer (CRC) a low expression of thymidylate synthase (TS) in metastases predicts a higher response to 5-fluorouracil (5-FU). Fluorouracil 154-158 thymidylate synthetase Homo sapiens 90-92 15355913-5 2004 RESULTS: We identified the following three genes coding for proliferation-related proteins: thymidylate synthase (TYMS), which is involved in chemoresistance (5-fluorouracil); 5"-aminoimidazole-4-carboxamide-1-beta-d-ribonucleotide transfolmylase/inosinicase (AICRT/I); and phosphoglycerate kinase 1 (PKG1), which was secreted by tumor cells and involved in the angiogenic process. Fluorouracil 161-173 thymidylate synthetase Homo sapiens 92-112 18425338-1 2008 Thymidylate synthase (TS) is a dNTP synthetic enzyme and is also a target enzyme of 5-fluorouracil (5-FU). Fluorouracil 84-98 thymidylate synthetase Homo sapiens 0-20 18425338-1 2008 Thymidylate synthase (TS) is a dNTP synthetic enzyme and is also a target enzyme of 5-fluorouracil (5-FU). Fluorouracil 84-98 thymidylate synthetase Homo sapiens 22-24 18425338-1 2008 Thymidylate synthase (TS) is a dNTP synthetic enzyme and is also a target enzyme of 5-fluorouracil (5-FU). Fluorouracil 100-104 thymidylate synthetase Homo sapiens 0-20 18425338-1 2008 Thymidylate synthase (TS) is a dNTP synthetic enzyme and is also a target enzyme of 5-fluorouracil (5-FU). Fluorouracil 100-104 thymidylate synthetase Homo sapiens 22-24 18425338-5 2008 The elevated expression of TS in cancer cells is a serious obstacle in the clinical use of 5-FU. Fluorouracil 91-95 thymidylate synthetase Homo sapiens 27-29 18425338-9 2008 Furthermore, the reduction of TS expression resulted in enhancement of the sensitivity to 5-FU in human colon cancer DLD-1 cells. Fluorouracil 90-94 thymidylate synthetase Homo sapiens 30-32 15355913-5 2004 RESULTS: We identified the following three genes coding for proliferation-related proteins: thymidylate synthase (TYMS), which is involved in chemoresistance (5-fluorouracil); 5"-aminoimidazole-4-carboxamide-1-beta-d-ribonucleotide transfolmylase/inosinicase (AICRT/I); and phosphoglycerate kinase 1 (PKG1), which was secreted by tumor cells and involved in the angiogenic process. Fluorouracil 161-173 thymidylate synthetase Homo sapiens 114-118 15355913-5 2004 RESULTS: We identified the following three genes coding for proliferation-related proteins: thymidylate synthase (TYMS), which is involved in chemoresistance (5-fluorouracil); 5"-aminoimidazole-4-carboxamide-1-beta-d-ribonucleotide transfolmylase/inosinicase (AICRT/I); and phosphoglycerate kinase 1 (PKG1), which was secreted by tumor cells and involved in the angiogenic process. Fluorouracil 161-173 phosphoglycerate kinase 1 Homo sapiens 260-299 15355913-9 2004 CONCLUSIONS: TYMS and PGK1, as well as their epitope peptides, might be appropriate target molecules for specific immunotherapy of HLA-A2(+) colon cancer patients because of the positive role of TYMS and PGK1 in chemoresistance (5-fluorouracil) and angiogenesis of tumor cells, respectively. Fluorouracil 229-243 thymidylate synthetase Homo sapiens 13-17 15355913-9 2004 CONCLUSIONS: TYMS and PGK1, as well as their epitope peptides, might be appropriate target molecules for specific immunotherapy of HLA-A2(+) colon cancer patients because of the positive role of TYMS and PGK1 in chemoresistance (5-fluorouracil) and angiogenesis of tumor cells, respectively. Fluorouracil 229-243 phosphoglycerate kinase 1 Homo sapiens 22-26 15355920-0 2004 Thymidylate synthase gene polymorphism predicts toxicity in colorectal cancer patients receiving 5-fluorouracil-based chemotherapy. Fluorouracil 97-111 thymidylate synthetase Homo sapiens 0-20 15355920-1 2004 PURPOSE: The target enzyme for 5-fluorouracil (5-FU) is thymidylate synthase (TS). Fluorouracil 31-45 thymidylate synthetase Homo sapiens 56-76 15355920-1 2004 PURPOSE: The target enzyme for 5-fluorouracil (5-FU) is thymidylate synthase (TS). Fluorouracil 31-45 thymidylate synthetase Homo sapiens 78-80 15355920-1 2004 PURPOSE: The target enzyme for 5-fluorouracil (5-FU) is thymidylate synthase (TS). Fluorouracil 47-51 thymidylate synthetase Homo sapiens 56-76 15355920-1 2004 PURPOSE: The target enzyme for 5-fluorouracil (5-FU) is thymidylate synthase (TS). Fluorouracil 47-51 thymidylate synthetase Homo sapiens 78-80 15355920-3 2004 TS expression predicts response to 5-FU-based chemotherapy, and the expression seems to be determined by the TYMS gene promoter. Fluorouracil 35-39 thymidylate synthetase Homo sapiens 0-2 15355920-4 2004 The aim of this study was to investigate the utility of determining these two TYMS gene polymorphisms to predict the toxicity and efficacy of 5-FU treatment in patients with colorectal cancer. Fluorouracil 142-146 thymidylate synthetase Homo sapiens 78-82 15355920-5 2004 EXPERIMENTAL DESIGN: The determination of TYMS genotypes was performed in tumor and normal tissues by PCR amplification from 90 patients with colorectal cancer who were treated with adjuvant or palliative 5-FU-based chemotherapy. Fluorouracil 205-209 thymidylate synthetase Homo sapiens 42-46 15355920-8 2004 RESULTS: Individuals who were homozygous for the double repeat in the TYMS promoter region had more severe side effects to 5-FU. Fluorouracil 123-127 thymidylate synthetase Homo sapiens 70-74 15355920-10 2004 The TYMS promoter and TYMS 3"-UTR polymorphisms were in linkage disequilibrium, and the haplotype 2R/ins 6-bp was significantly associated with a high risk of severe side effects to 5-FU. Fluorouracil 182-186 thymidylate synthetase Homo sapiens 4-8 15355920-10 2004 The TYMS promoter and TYMS 3"-UTR polymorphisms were in linkage disequilibrium, and the haplotype 2R/ins 6-bp was significantly associated with a high risk of severe side effects to 5-FU. Fluorouracil 182-186 thymidylate synthetase Homo sapiens 22-26 15355920-12 2004 CONCLUSIONS: This study demonstrated that TYMS genotyping could be of help in predicting toxicity to 5-FU-based chemotherapy. Fluorouracil 101-105 thymidylate synthetase Homo sapiens 42-46 15446572-11 2004 These results suggest that OPRT activity may be a good indicator of the malignant potential and sensitivity to 5-FU in bladder cancer. Fluorouracil 111-115 uridine monophosphate synthetase Homo sapiens 27-31 15301724-1 2004 BACKGROUND & OBJECTIVE: Methylenetrahydrofolate reductase (MTHFR) C677T polymorphism modifies enzyme activity and thus effects the level of 5, 10-methylenetetrahydrofolate (5,10-MTHR), which correlates with the tumor response to 5-fluorouracil (5-FU). Fluorouracil 233-247 DnaJ heat shock protein family (Hsp40) member C10 Homo sapiens 182-186 15301724-1 2004 BACKGROUND & OBJECTIVE: Methylenetrahydrofolate reductase (MTHFR) C677T polymorphism modifies enzyme activity and thus effects the level of 5, 10-methylenetetrahydrofolate (5,10-MTHR), which correlates with the tumor response to 5-fluorouracil (5-FU). Fluorouracil 249-253 DnaJ heat shock protein family (Hsp40) member C10 Homo sapiens 182-186 15330198-0 2004 Thymidylate synthetase (TS) genotype and TS/dihydropyrimidine dehydrogenase mRNA level as an indicator in determining chemosensitivity to 5-fluorouracil in advanced gastric carcinoma. Fluorouracil 138-152 thymidylate synthetase Homo sapiens 0-22 15330198-1 2004 BACKGROUND: One of the target enzymes of 5-fluorouracil (5-FU) is thymidylate synthetase (TS). Fluorouracil 41-55 thymidylate synthetase Homo sapiens 66-88 15330198-1 2004 BACKGROUND: One of the target enzymes of 5-fluorouracil (5-FU) is thymidylate synthetase (TS). Fluorouracil 57-61 thymidylate synthetase Homo sapiens 66-88 15235111-0 2004 c-myb Heterozygous mice are hypersensitive to 5-fluorouracil and ionizing radiation. Fluorouracil 46-60 myeloblastosis oncogene Mus musculus 0-5 22504509-1 2008 The objective of this study was to determine the effects of ionization, current density and penetration enhancers on the iontophoretic delivery of 5-fluorouracil (5-FU) through excised human stratum corneum (HSC). Fluorouracil 147-161 fucosyltransferase 1 (H blood group) Homo sapiens 208-211 22504509-1 2008 The objective of this study was to determine the effects of ionization, current density and penetration enhancers on the iontophoretic delivery of 5-fluorouracil (5-FU) through excised human stratum corneum (HSC). Fluorouracil 163-167 fucosyltransferase 1 (H blood group) Homo sapiens 208-211 15060742-1 2004 PURPOSE: Expression of thymidylate synthase (TS) and the 5-fluorouracil (5-FU) metabolic enzymes, including dihydropyrimidine dehydrogenase (DPD), orotate phosphoribosyl transferase (OPRT), thymidine phosphorylase (TP), and uridine phosphorylase (UP), has been reported to be associated with the sensitivity to 5-FU-based chemotherapy in colorectal cancer. Fluorouracil 73-77 uridine monophosphate synthetase Homo sapiens 147-181 15060742-1 2004 PURPOSE: Expression of thymidylate synthase (TS) and the 5-fluorouracil (5-FU) metabolic enzymes, including dihydropyrimidine dehydrogenase (DPD), orotate phosphoribosyl transferase (OPRT), thymidine phosphorylase (TP), and uridine phosphorylase (UP), has been reported to be associated with the sensitivity to 5-FU-based chemotherapy in colorectal cancer. Fluorouracil 73-77 uridine monophosphate synthetase Homo sapiens 183-187 15060742-1 2004 PURPOSE: Expression of thymidylate synthase (TS) and the 5-fluorouracil (5-FU) metabolic enzymes, including dihydropyrimidine dehydrogenase (DPD), orotate phosphoribosyl transferase (OPRT), thymidine phosphorylase (TP), and uridine phosphorylase (UP), has been reported to be associated with the sensitivity to 5-FU-based chemotherapy in colorectal cancer. Fluorouracil 311-315 thymidylate synthetase Homo sapiens 23-43 15060742-1 2004 PURPOSE: Expression of thymidylate synthase (TS) and the 5-fluorouracil (5-FU) metabolic enzymes, including dihydropyrimidine dehydrogenase (DPD), orotate phosphoribosyl transferase (OPRT), thymidine phosphorylase (TP), and uridine phosphorylase (UP), has been reported to be associated with the sensitivity to 5-FU-based chemotherapy in colorectal cancer. Fluorouracil 311-315 thymidylate synthetase Homo sapiens 45-47 15100168-5 2004 In addition to these substrates, we found that several organic compounds such as prostaglandin E(2), prostaglandin F(2alpha), allopurinol, 6-mercaptopurine (6-MP), 5-fluorouracil (5-FU), and l-carnitine are substrates of mOat3, compounds identified for the first time. Fluorouracil 164-178 solute carrier family 22 (organic anion transporter), member 8 Mus musculus 221-226 18059034-7 2008 In addition, hSRBC elevated apoptotic sensitivity of tumor cells to genotoxic agents, such as 5-FU, etoposide and ultraviolet. Fluorouracil 94-98 caveolae associated protein 3 Homo sapiens 13-18 18357371-1 2008 Expression of thymidylate synthase (TS) in tumor cells is frequently suggested as an important prognostic factor for patients scheduled for chemotherapy with 5-fluorouracil (5-FU). Fluorouracil 158-172 thymidylate synthetase Homo sapiens 14-34 18357371-1 2008 Expression of thymidylate synthase (TS) in tumor cells is frequently suggested as an important prognostic factor for patients scheduled for chemotherapy with 5-fluorouracil (5-FU). Fluorouracil 158-172 thymidylate synthetase Homo sapiens 36-38 18357371-1 2008 Expression of thymidylate synthase (TS) in tumor cells is frequently suggested as an important prognostic factor for patients scheduled for chemotherapy with 5-fluorouracil (5-FU). Fluorouracil 174-178 thymidylate synthetase Homo sapiens 14-34 18357371-1 2008 Expression of thymidylate synthase (TS) in tumor cells is frequently suggested as an important prognostic factor for patients scheduled for chemotherapy with 5-fluorouracil (5-FU). Fluorouracil 174-178 thymidylate synthetase Homo sapiens 36-38 21885003-5 2008 Several layers of evidence indicate that ERCC1 mRNA expression could be a predictive marker for cisplatin alone or in combination with certain drugs such as etoposide, gemcitabine, and 5-fluorouracil but not in combination with antimicrotubule drugs. Fluorouracil 185-199 ERCC excision repair 1, endonuclease non-catalytic subunit Homo sapiens 41-46 15100168-6 2004 The apparent K(m) values for the uptake of mOat3 that mediated the transport of 6-MP, 5-FU, and l-carnitine were 4.01 +/- 0.7 microM, 53.9 +/- 8.9 nM, and 61.9 +/- 1.1 nM, respectively. Fluorouracil 86-90 solute carrier family 22 (organic anion transporter), member 8 Mus musculus 43-48 15206578-3 2004 After repeated administration of 5-FU at 50 mg/kg/day for 1-5 days, a time-dependent decrease in cells expressing CD45Low, CD71 and CD90 was observed, whereas a decrease in the CD45High expressing cells was not observed. Fluorouracil 33-37 protein tyrosine phosphatase, receptor type, C Rattus norvegicus 114-118 15087029-12 2004 CONCLUSION: Combination of cryotherapy with 5-FU could enhance the apoptosis of G422 glioma cells presumably through modulating the HSP90alpha and p53 expression pattern. Fluorouracil 44-48 transformation related protein 53, pseudogene Mus musculus 147-150 15010882-2 2004 In this study we have investigated the association between the MSI status and the mRNA expression as well as the polymorphisms of the cellular target of 5-FU therapy, thymidylate synthase. Fluorouracil 153-157 thymidylate synthetase Homo sapiens 167-187 15014039-4 2004 Here, the newly discovered antiangiogenic drug rapamycin was combined with 5-FU to counteract the potential escape mechanism of dRib-induced angiogenesis. Fluorouracil 75-79 ribbon Drosophila melanogaster 128-132 15014039-14 2004 CONCLUSIONS: Inhibition of dRib-induced angiogenesis with rapamycin counteracts a potential TP-based escape mechanism for colorectal cancer under 5-FU therapy, introducing a novel, clinically feasible, combination treatment option for this common neoplasm. Fluorouracil 146-150 ribbon Drosophila melanogaster 27-31 14962716-2 2004 In vitro studies have shown that irinotecan downregulates thymidylate synthase (TS) expression in tumour cells, leading to synergy between irinotecan and 5-FU that is maximal when irinotecan is given 24 h prior to 5-FU. Fluorouracil 154-158 thymidylate synthetase Homo sapiens 58-78 17920123-6 2008 In the present studies, we examined the effects of chemopreventive agents, paclitaxel, etoposide and 5-fluorouracil, on the surface expression of programmed death-1-ligand 1 (PD-L1), a negative regulator of T cell anti-tumor immunity. Fluorouracil 101-115 CD274 molecule Homo sapiens 146-173 17920123-6 2008 In the present studies, we examined the effects of chemopreventive agents, paclitaxel, etoposide and 5-fluorouracil, on the surface expression of programmed death-1-ligand 1 (PD-L1), a negative regulator of T cell anti-tumor immunity. Fluorouracil 101-115 CD274 molecule Homo sapiens 175-180 18288408-2 2008 In this study, we aimed to clarify the prognostic value of the expression of the 5-FU metabolic enzyme genes, including orptate phosphoribosyl transferase (OPRT), dihydropyrimidine dehydrogenase (DPD), thymidylate synthetase (TS) and thymidylate phosphorylate (TP) genes in CRC patients treated with oral 5-FU-based adjuvant chemotherapy. Fluorouracil 81-85 uridine monophosphate synthetase Homo sapiens 120-154 18288408-2 2008 In this study, we aimed to clarify the prognostic value of the expression of the 5-FU metabolic enzyme genes, including orptate phosphoribosyl transferase (OPRT), dihydropyrimidine dehydrogenase (DPD), thymidylate synthetase (TS) and thymidylate phosphorylate (TP) genes in CRC patients treated with oral 5-FU-based adjuvant chemotherapy. Fluorouracil 81-85 uridine monophosphate synthetase Homo sapiens 156-160 18288408-2 2008 In this study, we aimed to clarify the prognostic value of the expression of the 5-FU metabolic enzyme genes, including orptate phosphoribosyl transferase (OPRT), dihydropyrimidine dehydrogenase (DPD), thymidylate synthetase (TS) and thymidylate phosphorylate (TP) genes in CRC patients treated with oral 5-FU-based adjuvant chemotherapy. Fluorouracil 81-85 thymidylate synthetase Homo sapiens 202-224 18288408-10 2008 These results suggest that the OPRT mRNA is a useful indicator in the prediction of disease-free and overall survival in Dukes" B and C stage CRC patients treated with oral 5-FU-based adjuvant chemotherapy. Fluorouracil 173-177 uridine monophosphate synthetase Homo sapiens 31-35 18082672-7 2008 Mechanistic studies demonstrated that the 5-FU plus scFv23/TNF combination specifically resulted in a down-regulation of HER-2/neu, p-Akt and Bcl-2 and up-regulation of TNF-R1. Fluorouracil 42-46 TNF receptor superfamily member 1A Homo sapiens 169-175 18047833-4 2008 Although LRCs expressed very low level of a well-known HSC marker, c-kit in normal circumstances, myeloablation by 5-FU treatment caused LRCs to abundantly express c-kit and proliferate actively. Fluorouracil 115-119 fucosyltransferase 1 (H blood group) Homo sapiens 55-58 18288923-2 2008 Methotrexate {MTX, (1)} and 5-fluorouracil (5-FU) were among the first clinically useful DHFR and TS inhibitors, respectively. Fluorouracil 28-42 dihydrofolate reductase Homo sapiens 89-93 18288923-2 2008 Methotrexate {MTX, (1)} and 5-fluorouracil (5-FU) were among the first clinically useful DHFR and TS inhibitors, respectively. Fluorouracil 28-42 thymidylate synthetase Homo sapiens 98-100 18288923-2 2008 Methotrexate {MTX, (1)} and 5-fluorouracil (5-FU) were among the first clinically useful DHFR and TS inhibitors, respectively. Fluorouracil 44-48 dihydrofolate reductase Homo sapiens 89-93 18288923-2 2008 Methotrexate {MTX, (1)} and 5-fluorouracil (5-FU) were among the first clinically useful DHFR and TS inhibitors, respectively. Fluorouracil 44-48 thymidylate synthetase Homo sapiens 98-100 18360075-1 2008 INTRODUCTION: Orotate phosphoribosyl transferase (OPRT), dihydropyrimidine dehydrogenase (DPD), and thymidylate synthase (TS) are initial key enzymes in the 5-fluorouracil (5-FU) metabolic pathway. Fluorouracil 157-171 uridine monophosphate synthetase Homo sapiens 14-48 18360075-1 2008 INTRODUCTION: Orotate phosphoribosyl transferase (OPRT), dihydropyrimidine dehydrogenase (DPD), and thymidylate synthase (TS) are initial key enzymes in the 5-fluorouracil (5-FU) metabolic pathway. Fluorouracil 157-171 uridine monophosphate synthetase Homo sapiens 50-54 18360075-1 2008 INTRODUCTION: Orotate phosphoribosyl transferase (OPRT), dihydropyrimidine dehydrogenase (DPD), and thymidylate synthase (TS) are initial key enzymes in the 5-fluorouracil (5-FU) metabolic pathway. Fluorouracil 157-171 thymidylate synthetase Homo sapiens 100-120 18360075-1 2008 INTRODUCTION: Orotate phosphoribosyl transferase (OPRT), dihydropyrimidine dehydrogenase (DPD), and thymidylate synthase (TS) are initial key enzymes in the 5-fluorouracil (5-FU) metabolic pathway. Fluorouracil 157-171 thymidylate synthetase Homo sapiens 122-124 18360075-1 2008 INTRODUCTION: Orotate phosphoribosyl transferase (OPRT), dihydropyrimidine dehydrogenase (DPD), and thymidylate synthase (TS) are initial key enzymes in the 5-fluorouracil (5-FU) metabolic pathway. Fluorouracil 173-177 uridine monophosphate synthetase Homo sapiens 14-48 18360075-1 2008 INTRODUCTION: Orotate phosphoribosyl transferase (OPRT), dihydropyrimidine dehydrogenase (DPD), and thymidylate synthase (TS) are initial key enzymes in the 5-fluorouracil (5-FU) metabolic pathway. Fluorouracil 173-177 uridine monophosphate synthetase Homo sapiens 50-54 18360075-1 2008 INTRODUCTION: Orotate phosphoribosyl transferase (OPRT), dihydropyrimidine dehydrogenase (DPD), and thymidylate synthase (TS) are initial key enzymes in the 5-fluorouracil (5-FU) metabolic pathway. Fluorouracil 173-177 thymidylate synthetase Homo sapiens 100-120 18360075-1 2008 INTRODUCTION: Orotate phosphoribosyl transferase (OPRT), dihydropyrimidine dehydrogenase (DPD), and thymidylate synthase (TS) are initial key enzymes in the 5-fluorouracil (5-FU) metabolic pathway. Fluorouracil 173-177 thymidylate synthetase Homo sapiens 122-124 18360075-10 2008 CONCLUSION: The response to 5-FU may be poor in patients with lymph-node metastasis, because of low OPRT activity, and in patients with poorly differentiated adenocarcinoma, because of high DPD activity. Fluorouracil 28-32 uridine monophosphate synthetase Homo sapiens 100-104 17943475-2 2008 Thymidylate synthase (TS) is inhibited by 5-FU, being another potential mediator of therapeutic resistance to 5-FU. Fluorouracil 42-46 thymidylate synthetase Homo sapiens 0-20 17943475-2 2008 Thymidylate synthase (TS) is inhibited by 5-FU, being another potential mediator of therapeutic resistance to 5-FU. Fluorouracil 42-46 thymidylate synthetase Homo sapiens 22-24 17943475-2 2008 Thymidylate synthase (TS) is inhibited by 5-FU, being another potential mediator of therapeutic resistance to 5-FU. Fluorouracil 110-114 thymidylate synthetase Homo sapiens 0-20 17943475-2 2008 Thymidylate synthase (TS) is inhibited by 5-FU, being another potential mediator of therapeutic resistance to 5-FU. Fluorouracil 110-114 thymidylate synthetase Homo sapiens 22-24 18607850-2 2008 This study aimed to assess the range of gene copies per nucleus of thymidylate synthase (TYMS), thymidine phosphorylase (TP) and dihydrofolate reductase (DHFR) in colorectal cancer, and to evaluate its prognostic significance following adjuvant chemotherapy, since these enzymes are closely related to efficacy of 5-fluorouracil (5FU). Fluorouracil 330-333 dihydrofolate reductase Homo sapiens 154-158 18607850-11 2008 CONCLUSION: Aberration of TYMS gene is of significance to expression of TYMS, which may influence the biology and 5-FU sensitivity of colorectal cancer. Fluorouracil 114-118 thymidylate synthetase Homo sapiens 26-30 18607850-11 2008 CONCLUSION: Aberration of TYMS gene is of significance to expression of TYMS, which may influence the biology and 5-FU sensitivity of colorectal cancer. Fluorouracil 114-118 thymidylate synthetase Homo sapiens 72-76 18661431-1 2008 INTRODUCTION: Increased expression of cytosine deaminase (CD) and uracil phosphoribosyltransferase (UPRT) may improve the antitumoral effect of 5-fluorouracil (5-FU) and 5-fluorocytosine (5-FC), and thereby enhance the potential of gene-directed enzyme prodrug therapy. Fluorouracil 144-158 uracil phosphoribosyltransferase Mus musculus 100-104 18661431-1 2008 INTRODUCTION: Increased expression of cytosine deaminase (CD) and uracil phosphoribosyltransferase (UPRT) may improve the antitumoral effect of 5-fluorouracil (5-FU) and 5-fluorocytosine (5-FC), and thereby enhance the potential of gene-directed enzyme prodrug therapy. Fluorouracil 160-164 uracil phosphoribosyltransferase Mus musculus 100-104 18661431-8 2008 RESULTS: Sensitivity to 5-FC and 5-FU was higher in cells stably expressing the CD/UPRT/mDsRed fusion gene than in cells stably expressing CD/mDsRed alone or wild-type cells. Fluorouracil 33-37 uracil phosphoribosyltransferase Mus musculus 83-87 18701820-1 2008 BACKGROUND: The combination of 5-fluorouracil (5-FU), cisplatin and interferon (IFN)-alpha was found to result in a high response rate in advanced esophageal squamous cell carcinoma (SCC). Fluorouracil 31-45 serpin family B member 3 Homo sapiens 183-186 18701820-1 2008 BACKGROUND: The combination of 5-fluorouracil (5-FU), cisplatin and interferon (IFN)-alpha was found to result in a high response rate in advanced esophageal squamous cell carcinoma (SCC). Fluorouracil 47-51 serpin family B member 3 Homo sapiens 183-186 17698398-8 2008 Furthermore, upon exposure to 5-Fluorouracil and UV irradiation, Cyr61 was rapidly induced in both p53(+/+) HepG2 and p53(-/-) Hep3B cells. Fluorouracil 30-44 cellular communication network factor 1 Homo sapiens 65-70 17640667-11 2008 The hydroxyproline levels were higher in the IGF-I and the IGF-I +5-FU groups as a result of the stimulating act of IGF-I. Fluorouracil 66-70 insulin-like growth factor 1 Rattus norvegicus 59-64 17640667-11 2008 The hydroxyproline levels were higher in the IGF-I and the IGF-I +5-FU groups as a result of the stimulating act of IGF-I. Fluorouracil 66-70 insulin-like growth factor 1 Rattus norvegicus 59-64 17640667-12 2008 CONCLUSION: IGF-I, when given intraperitoneally, seems to mediate some of the adverse effects of 5-FU on the colonic healing in rats. Fluorouracil 97-101 insulin-like growth factor 1 Rattus norvegicus 12-17 17951356-7 2008 We have demonstrated for the first time that Hmgb1 is an essential activator of cellular response to genotoxic stress caused by chemotherapeutic agents (thiopurines, cytarabine, and 5-fluorouracil), which acts at early steps of antimetabolite-induced stress by stimulating phosphorylation of two DNA damage markers, p53 and H2AX. Fluorouracil 182-196 transformation related protein 53, pseudogene Mus musculus 316-319 14962716-2 2004 In vitro studies have shown that irinotecan downregulates thymidylate synthase (TS) expression in tumour cells, leading to synergy between irinotecan and 5-FU that is maximal when irinotecan is given 24 h prior to 5-FU. Fluorouracil 214-218 thymidylate synthetase Homo sapiens 58-78 14735204-0 2004 Thymidylate synthase and methylenetetrahydrofolate reductase gene polymorphisms: relationships with 5-fluorouracil sensitivity. Fluorouracil 100-114 thymidylate synthetase Homo sapiens 0-20 17892912-0 2007 Quantitative double-fluorescence immunohistochemistry (qDFIHC), a novel technology to assess protein expression: a pilot study analyzing 5-FU sensitive markers thymidylate synthase, dihydropyrimidine dehydrogenase and orotate phosphoribosyl transferases in gastric cancer tissue specimens. Fluorouracil 137-141 thymidylate synthetase Homo sapiens 160-180 18031615-3 2007 The enhanced cytotoxicity of the combined treatment of ZD55-Smac with cisplatin or 5-fluorouracil (5-FU) was evaluated in several HCC cell lines. Fluorouracil 99-103 diablo IAP-binding mitochondrial protein Homo sapiens 60-64 17982676-7 2007 Alterations in gene expression in 5-FU-treated TP53-depleted HCT116 cultures confirmed previously-reported TP53 target genes and suggested potentially novel TP53 target genes (e.g. APOBEC3C, BIRC3, JMJD2B, LAMP3, MYO1E, PRRG1, SULF2, TACSTD2, TncRNA, ZFYVE20) that may play a role in mediating the 5-FU-induced DNA damage response in TP53-proficient cells. Fluorouracil 34-38 baculoviral IAP repeat containing 3 Homo sapiens 191-196 17982676-7 2007 Alterations in gene expression in 5-FU-treated TP53-depleted HCT116 cultures confirmed previously-reported TP53 target genes and suggested potentially novel TP53 target genes (e.g. APOBEC3C, BIRC3, JMJD2B, LAMP3, MYO1E, PRRG1, SULF2, TACSTD2, TncRNA, ZFYVE20) that may play a role in mediating the 5-FU-induced DNA damage response in TP53-proficient cells. Fluorouracil 34-38 proline rich and Gla domain 1 Homo sapiens 220-225 17982676-7 2007 Alterations in gene expression in 5-FU-treated TP53-depleted HCT116 cultures confirmed previously-reported TP53 target genes and suggested potentially novel TP53 target genes (e.g. APOBEC3C, BIRC3, JMJD2B, LAMP3, MYO1E, PRRG1, SULF2, TACSTD2, TncRNA, ZFYVE20) that may play a role in mediating the 5-FU-induced DNA damage response in TP53-proficient cells. Fluorouracil 34-38 sulfatase 2 Homo sapiens 227-232 14654948-0 2004 The role of p53 in the chemotherapeutic responses to cisplatin, doxorubicin and 5-fluorouracil treatment. Fluorouracil 80-94 transformation related protein 53, pseudogene Mus musculus 12-15 14654948-14 2004 However, a significant difference in specific growth delay was seen between the two groups when treated with doxorubicin or 5-fluorouracil (P=0.05), indicating a role for p53 protein in modulating the in vivo efficacy of these agents. Fluorouracil 124-138 transformation related protein 53, pseudogene Mus musculus 171-174 15043163-3 2004 The magnitude and duration of TS inhibition following exposure of HT29 cells to FdUMP[10] at 1 x 10(-8) M was greater than that which occurred following exposure of these cells to 5FU at 1 x 10(-6) M. FdUMP[10] exposure also resulted in much more extensive DNA damage to HT29 cells than occurred following exposure to 100-fold higher concentrations of 5FU. Fluorouracil 180-183 thymidylate synthetase Homo sapiens 30-32 17854773-0 2007 Orotate phosphoribosyltransferase expression level in tumors is a potential determinant of the efficacy of 5-fluorouracil. Fluorouracil 107-121 uridine monophosphate synthetase Homo sapiens 0-33 17854773-1 2007 Although the intratumoral expression levels of thymidylate synthase (TS) and dihydropyrimidine dehydrogenase (DPD) are known to affect the antitumor activity of 5-fluorouracil (5-FU), the importance of orotate phosphoribosyltransferase (OPRT) has remained unclear. Fluorouracil 161-175 thymidylate synthetase Homo sapiens 47-67 17854773-1 2007 Although the intratumoral expression levels of thymidylate synthase (TS) and dihydropyrimidine dehydrogenase (DPD) are known to affect the antitumor activity of 5-fluorouracil (5-FU), the importance of orotate phosphoribosyltransferase (OPRT) has remained unclear. Fluorouracil 177-181 thymidylate synthetase Homo sapiens 47-67 17854773-1 2007 Although the intratumoral expression levels of thymidylate synthase (TS) and dihydropyrimidine dehydrogenase (DPD) are known to affect the antitumor activity of 5-fluorouracil (5-FU), the importance of orotate phosphoribosyltransferase (OPRT) has remained unclear. Fluorouracil 177-181 uridine monophosphate synthetase Homo sapiens 202-235 17854773-1 2007 Although the intratumoral expression levels of thymidylate synthase (TS) and dihydropyrimidine dehydrogenase (DPD) are known to affect the antitumor activity of 5-fluorouracil (5-FU), the importance of orotate phosphoribosyltransferase (OPRT) has remained unclear. Fluorouracil 177-181 uridine monophosphate synthetase Homo sapiens 237-241 17854773-2 2007 This study investigated the relationship between intratumoral OPRT expression and the antitumor activity of 5-FU using human NCI60 cell lines with similar levels of TS and DPD messenger RNAs, as well as 31 tumor xenografts. Fluorouracil 108-112 uridine monophosphate synthetase Homo sapiens 62-66 17854773-3 2007 The OPRT mRNA level was positively correlated with the 5-FU efficacy in these cell lines. Fluorouracil 55-59 uridine monophosphate synthetase Homo sapiens 4-8 17854773-4 2007 In vitro, the 50% growth-inhibitory concentrations of 5-FU were closely correlated with the OPRT mRNA levels in cancer cell lines with similar levels of TS mRNAs when combined with a DPD inhibitor. Fluorouracil 54-58 uridine monophosphate synthetase Homo sapiens 92-96 17854773-5 2007 Moreover, downregulation of OPRT with small-interfering RNA decreased the sensitivities of the cultured tumor cells to 5-FU. Fluorouracil 119-123 uridine monophosphate synthetase Homo sapiens 28-32 17854773-6 2007 These results suggest that the OPRT expression level in tumors is an additional determinant of the efficacy of 5-FU. Fluorouracil 111-115 uridine monophosphate synthetase Homo sapiens 31-35 18219847-4 2007 In this study, we confirmed that an expression of E-selectin in human umbilical vein endothelial cells (HUVEC) was stimulated by 5-FU, and that the expression of E-selectin was inhibited by cimetidine which was a H2 receptor antagonist. Fluorouracil 129-133 selectin E Homo sapiens 50-60 15539918-0 2004 Thymidylate synthase expression in normal colonic mucosa: a predictive marker of toxicity in colorectal cancer patients receiving 5-fluorouracil-based adjuvant chemotherapy. Fluorouracil 130-144 thymidylate synthetase Homo sapiens 0-20 15539918-1 2004 OBJECTIVES: We retrospectively evaluated the relevance of thymidylate synthase (TS) expression in normal colonic mucosa as a predictive factor of toxicity in colorectal cancer patients receiving adjuvant fluorouracil (5-FU)-based chemotherapy. Fluorouracil 204-216 thymidylate synthetase Homo sapiens 58-78 15539918-1 2004 OBJECTIVES: We retrospectively evaluated the relevance of thymidylate synthase (TS) expression in normal colonic mucosa as a predictive factor of toxicity in colorectal cancer patients receiving adjuvant fluorouracil (5-FU)-based chemotherapy. Fluorouracil 204-216 thymidylate synthetase Homo sapiens 80-82 15539918-2 2004 METHODS: TS expression was immunohistochemically assessed on normal colonic mucosa from 50 patients with colorectal cancer Dukes" stages B (15 patients) and C (35 patients) treated with 5-FU-based adjuvant chemotherapy. Fluorouracil 186-190 thymidylate synthetase Homo sapiens 9-11 15539918-6 2004 CONCLUSIONS: Immunohistochemical TS expression in normal colonic mucosa may represent an important predictive parameter for identifying a subset of patients with a high risk of developing severe 5-FU-related toxicities. Fluorouracil 195-199 thymidylate synthetase Homo sapiens 33-35 13680162-1 2003 BACKGROUND/PURPOSE: Dihydropyrimidine dehydrogenase (DPD) and thymidylate synthase (TS) are key enzymes for predicting the efficacy of 5-FU in the treatment of malignant tumors. Fluorouracil 135-139 thymidylate synthetase Homo sapiens 62-82 13680162-1 2003 BACKGROUND/PURPOSE: Dihydropyrimidine dehydrogenase (DPD) and thymidylate synthase (TS) are key enzymes for predicting the efficacy of 5-FU in the treatment of malignant tumors. Fluorouracil 135-139 thymidylate synthetase Homo sapiens 84-86 13680162-14 2003 Some HCC patients may be good candidates for 5-FU-based chemotherapy based on measurements of tumor levels of DPD and TS. Fluorouracil 45-49 thymidylate synthetase Homo sapiens 118-120 14576935-2 2003 In the present study, the associations among phenotypic marker expression of gastric carcinomas, tumor thymidylate synthase (TS) expression, and the chemotherapeutic response to 5-fluorouracil (5-FU) were examined. Fluorouracil 178-192 thymidylate synthetase Homo sapiens 125-127 14576935-2 2003 In the present study, the associations among phenotypic marker expression of gastric carcinomas, tumor thymidylate synthase (TS) expression, and the chemotherapeutic response to 5-fluorouracil (5-FU) were examined. Fluorouracil 194-198 thymidylate synthetase Homo sapiens 103-123 14576935-2 2003 In the present study, the associations among phenotypic marker expression of gastric carcinomas, tumor thymidylate synthase (TS) expression, and the chemotherapeutic response to 5-fluorouracil (5-FU) were examined. Fluorouracil 194-198 thymidylate synthetase Homo sapiens 125-127 14576935-12 2003 CONCLUSIONS: These results indicate that postoperative chemotherapy with 5-FU could be effective for patients with the G-phenotype tumor, since the incidence of intratumoral expression of TS, the target enzyme of 5-FU, is significantly low in G-phenotype tumors. Fluorouracil 73-77 thymidylate synthetase Homo sapiens 188-190 14576935-12 2003 CONCLUSIONS: These results indicate that postoperative chemotherapy with 5-FU could be effective for patients with the G-phenotype tumor, since the incidence of intratumoral expression of TS, the target enzyme of 5-FU, is significantly low in G-phenotype tumors. Fluorouracil 213-217 thymidylate synthetase Homo sapiens 188-190 14981927-4 2003 Therefore we investigated whether the addition of monoclonal antibodies against the EGFR could enhance the response rate of cisplatin, 5-FU and docetaxel. Fluorouracil 135-139 epidermal growth factor receptor Mus musculus 84-88 12973835-0 2003 ErbB2 overexpression in human breast carcinoma is correlated with p21Cip1 up-regulation and tyrosine-15 hyperphosphorylation of p34Cdc2: poor responsiveness to chemotherapy with cyclophoshamide methotrexate, and 5-fluorouracil is associated with Erb2 overexpression and with p21Cip1 overexpression. Fluorouracil 212-226 cyclin dependent kinase 1 Homo sapiens 128-135 14614330-0 2003 Apoptotic response to 5-fluorouracil treatment is mediated by reduced polyamines, non-autocrine Fas ligand and induced tumor necrosis factor receptor 2. Fluorouracil 22-36 Fas ligand Homo sapiens 96-106 14614330-8 2003 Exposure to exogenous FasL increased 5-FU-induced apoptosis, and anti-TNFR2 antibody, but not anti-TNFR1, partially protected the sensitive cells. Fluorouracil 37-41 Fas ligand Homo sapiens 22-26 14614330-9 2003 Our combination of gene expression profiling and corroborative functional studies revealed that reduced polyamine levels, non-autocrine FasL originating exogenous to tumor cells, and induced TNFR2 are all functional mediators of apoptosis caused by 5-FU in colon carcinoma cells. Fluorouracil 249-253 Fas ligand Homo sapiens 136-140 12845668-0 2003 Overexpression of thymidylate synthase mediates desensitization for 5-fluorouracil of tumor cells. Fluorouracil 68-82 thymidylate synthetase Homo sapiens 18-38 12845668-2 2003 It has been suggested that the poor prognosis is partly due to a low sensitivity of TS-overexpressing tumors to TS-targeting 5-fluorouracil (5-FU). Fluorouracil 125-139 thymidylate synthetase Homo sapiens 84-86 12845668-2 2003 It has been suggested that the poor prognosis is partly due to a low sensitivity of TS-overexpressing tumors to TS-targeting 5-fluorouracil (5-FU). Fluorouracil 125-139 thymidylate synthetase Homo sapiens 112-114 12845668-2 2003 It has been suggested that the poor prognosis is partly due to a low sensitivity of TS-overexpressing tumors to TS-targeting 5-fluorouracil (5-FU). Fluorouracil 141-145 thymidylate synthetase Homo sapiens 84-86 18025275-3 2007 FPGS modulation affects the chemosensitivity of cancer cells to antifolates, such as methotrexate, and 5-fluorouracil (5FU) by altering polyglutamylation of antifolates and specific target intracellular folate cofactors. Fluorouracil 103-117 folylpolyglutamate synthase Homo sapiens 0-4 12845668-2 2003 It has been suggested that the poor prognosis is partly due to a low sensitivity of TS-overexpressing tumors to TS-targeting 5-fluorouracil (5-FU). Fluorouracil 141-145 thymidylate synthetase Homo sapiens 112-114 18025275-3 2007 FPGS modulation affects the chemosensitivity of cancer cells to antifolates, such as methotrexate, and 5-fluorouracil (5FU) by altering polyglutamylation of antifolates and specific target intracellular folate cofactors. Fluorouracil 119-122 folylpolyglutamate synthase Homo sapiens 0-4 12845668-3 2003 To investigate the relationship between TS expression and sensitivity to 5-FU, we used the TS-overexpressing cervical cancer cell line SKG-II/TS and SKG-I/TS that had been established by TS gene transfer. Fluorouracil 73-77 thymidylate synthetase Homo sapiens 40-42 18025275-5 2007 We generated an in vitro model of FPGS overexpression and inhibition in breast cancer cells by stably transfecting human MDA-MB-435 breast cancer cells with the sense FPGS cDNA or FPGS-targeted small interfering RNA, respectively, and investigated the effects of FPGS modulation on chemosensitivity to 5FU and methotrexate. Fluorouracil 302-305 folylpolyglutamate synthase Homo sapiens 34-38 12845668-4 2003 The 50% growth inhibitory concentration (IC(50)) of 5-FU for SKG-II/TS was 24 +/- 6.0 microM, which was 6 times as high as that for the control (4.0 +/- 1.1 microM), showing significantly decreased sensitivity to 5-FU (p < 0.01). Fluorouracil 52-56 thymidylate synthetase Homo sapiens 68-70 12845668-5 2003 The IC(50) of 5-FU for SKG-I/TS was 90 +/- 15 microM, which was over 2 times as high as that for the control (40 +/- 0.6 microM), showing significantly decreased sensitivity to 5-FU (p < 0.05). Fluorouracil 14-18 thymidylate synthetase Homo sapiens 29-31 12845668-5 2003 The IC(50) of 5-FU for SKG-I/TS was 90 +/- 15 microM, which was over 2 times as high as that for the control (40 +/- 0.6 microM), showing significantly decreased sensitivity to 5-FU (p < 0.05). Fluorouracil 177-181 thymidylate synthetase Homo sapiens 29-31 12845668-6 2003 Thus, TS-overexpressing tumors have decreased sensitivity to 5-FU, which may be one of the factors that determine the prognosis of these tumors. Fluorouracil 61-65 thymidylate synthetase Homo sapiens 6-8 12883718-2 2003 Thymidylate synthase (TS) is inhibited to form an inactive ternary complex by 5-fluoro-dUMP and is considered to be a target enzyme of 5-FU treatment. Fluorouracil 135-139 thymidylate synthetase Homo sapiens 0-20 17716984-0 2007 A dose escalation trial of adjuvant cyclophosphamide and epirubicin in combination with 5-fluorouracil using G-CSF support for premenopausal women with breast cancer involving four or more positive nodes. Fluorouracil 88-102 colony stimulating factor 3 Homo sapiens 109-114 17716984-8 2007 CONCLUSION: A dose-intense and dose-dense regimen of cyclophosphamide, epirubicin and 5-fluorouracil was delivered with G-CSF without apparent increase in acute toxicity. Fluorouracil 86-100 colony stimulating factor 3 Homo sapiens 120-125 12883718-2 2003 Thymidylate synthase (TS) is inhibited to form an inactive ternary complex by 5-fluoro-dUMP and is considered to be a target enzyme of 5-FU treatment. Fluorouracil 135-139 thymidylate synthetase Homo sapiens 22-24 17940834-11 2007 In NUGC-3/5FU/L, 5-FU-enhanced expression of TS mRNA was inhibited by the addition of CDHP. Fluorouracil 17-21 thymidylate synthetase Homo sapiens 45-47 12883718-3 2003 Two enzymes, DPD and TS, have been reported to be major determinants of individual sensitivity to 5-FU, and it has been reported that TS mRNA levels are modified by 5-FU treatment. Fluorouracil 98-102 thymidylate synthetase Homo sapiens 21-23 12883718-3 2003 Two enzymes, DPD and TS, have been reported to be major determinants of individual sensitivity to 5-FU, and it has been reported that TS mRNA levels are modified by 5-FU treatment. Fluorouracil 165-169 thymidylate synthetase Homo sapiens 134-136 17628013-2 2007 We found that specific c-Myc inhibition depleted cells of GSH by directly reducing the gene expression of both heavy and light subunits of the gamma-GCS enzyme and increased their susceptibility to antineoplastic drugs with different mechanisms of action, such as cisplatin (CDDP), staurosporine (STR), and 5-fluorouracil (5-FU). Fluorouracil 307-321 MYC proto-oncogene, bHLH transcription factor Homo sapiens 23-28 17628013-2 2007 We found that specific c-Myc inhibition depleted cells of GSH by directly reducing the gene expression of both heavy and light subunits of the gamma-GCS enzyme and increased their susceptibility to antineoplastic drugs with different mechanisms of action, such as cisplatin (CDDP), staurosporine (STR), and 5-fluorouracil (5-FU). Fluorouracil 323-327 MYC proto-oncogene, bHLH transcription factor Homo sapiens 23-28 12883718-6 2003 Furthermore inter-individual variations of TS mRNA levels after 5-FU treatment were found, and the individual TS induction varied between patients (0.2-2.4). Fluorouracil 64-68 thymidylate synthetase Homo sapiens 43-45 12883718-12 2003 These findings suggest that TS mRNA was induced by 5-FU treatment, and the overall induction level varied between individuals. Fluorouracil 51-55 thymidylate synthetase Homo sapiens 28-30 17896913-1 2007 Methotrexate {MTX, (1)} and 5-fluorouracil (5-FU) were among the first clinically useful DHFR and TS inhibitors, respectively. Fluorouracil 28-42 dihydrofolate reductase Homo sapiens 89-93 12883718-13 2003 Therefore, the estimation of TS mRNA induction may be useful to predict the efficacy of 5-FU treatment. Fluorouracil 88-92 thymidylate synthetase Homo sapiens 29-31 17896913-1 2007 Methotrexate {MTX, (1)} and 5-fluorouracil (5-FU) were among the first clinically useful DHFR and TS inhibitors, respectively. Fluorouracil 28-42 thymidylate synthetase Homo sapiens 98-100 15001837-5 2003 In the present study, we have investigated whether the inhibition of a growth-promoting gene, namely c-myb, affects the sensitivity of human colorectal cancer cells, in vitro, to conventional chemotherapeutic drugs: taxol, 5-fluorouracil, vinblastine and doxorubicin. Fluorouracil 223-237 MYB proto-oncogene, transcription factor Homo sapiens 101-106 17896913-1 2007 Methotrexate {MTX, (1)} and 5-fluorouracil (5-FU) were among the first clinically useful DHFR and TS inhibitors, respectively. Fluorouracil 44-48 dihydrofolate reductase Homo sapiens 89-93 17896913-1 2007 Methotrexate {MTX, (1)} and 5-fluorouracil (5-FU) were among the first clinically useful DHFR and TS inhibitors, respectively. Fluorouracil 44-48 thymidylate synthetase Homo sapiens 98-100 18019677-1 2007 BACKGROUND/AIMS: 5-fluorouracil (5-FU)-related metabolic enzymes, including dihydropyrimidine dehydrogenase (DPD), thymidylate synthase (TS), thymidylate phosphorylase (TP), and orotate phosphoribosyl transferase (OPRT) are initial, rate-limiting enzymes in the metabolism of 5-FU. Fluorouracil 17-31 thymidylate synthetase Homo sapiens 137-139 18019677-1 2007 BACKGROUND/AIMS: 5-fluorouracil (5-FU)-related metabolic enzymes, including dihydropyrimidine dehydrogenase (DPD), thymidylate synthase (TS), thymidylate phosphorylase (TP), and orotate phosphoribosyl transferase (OPRT) are initial, rate-limiting enzymes in the metabolism of 5-FU. Fluorouracil 17-31 uridine monophosphate synthetase Homo sapiens 178-212 18019677-1 2007 BACKGROUND/AIMS: 5-fluorouracil (5-FU)-related metabolic enzymes, including dihydropyrimidine dehydrogenase (DPD), thymidylate synthase (TS), thymidylate phosphorylase (TP), and orotate phosphoribosyl transferase (OPRT) are initial, rate-limiting enzymes in the metabolism of 5-FU. Fluorouracil 17-31 uridine monophosphate synthetase Homo sapiens 214-218 18019677-1 2007 BACKGROUND/AIMS: 5-fluorouracil (5-FU)-related metabolic enzymes, including dihydropyrimidine dehydrogenase (DPD), thymidylate synthase (TS), thymidylate phosphorylase (TP), and orotate phosphoribosyl transferase (OPRT) are initial, rate-limiting enzymes in the metabolism of 5-FU. Fluorouracil 33-37 thymidylate synthetase Homo sapiens 137-139 18019677-1 2007 BACKGROUND/AIMS: 5-fluorouracil (5-FU)-related metabolic enzymes, including dihydropyrimidine dehydrogenase (DPD), thymidylate synthase (TS), thymidylate phosphorylase (TP), and orotate phosphoribosyl transferase (OPRT) are initial, rate-limiting enzymes in the metabolism of 5-FU. Fluorouracil 33-37 uridine monophosphate synthetase Homo sapiens 178-212 18019677-1 2007 BACKGROUND/AIMS: 5-fluorouracil (5-FU)-related metabolic enzymes, including dihydropyrimidine dehydrogenase (DPD), thymidylate synthase (TS), thymidylate phosphorylase (TP), and orotate phosphoribosyl transferase (OPRT) are initial, rate-limiting enzymes in the metabolism of 5-FU. Fluorouracil 33-37 uridine monophosphate synthetase Homo sapiens 214-218 17702597-6 2007 In some instances, 5-FU up-regulates miR genes that are already over-expressed in neoplastic tissues, including, for example, miR-21 that is associated with anti-apoptotic functions characterizing malignant cells. Fluorouracil 19-23 microRNA 21 Homo sapiens 126-132 14680559-10 2003 When 5-FU or carboplatin was added, there was a significant difference in growth suppression rate between FasL positive and control cancer cells (t = 9.02, t = 11.93, P < 0.01). Fluorouracil 5-9 Fas ligand Homo sapiens 106-110 12819937-3 2003 5-Fluorouracil (5-FU) was synthesized in 1957 and represents the first class of antineoplastic agents to be developed as inhibitors of TS. Fluorouracil 0-14 thymidylate synthetase Homo sapiens 135-137 17609664-3 2007 Interestingly, S3 cells were fourfold more susceptible to 5-fluorouracil-induced cytotoxicity due to downregulation of thymidylate synthase. Fluorouracil 58-72 thymidylate synthetase Homo sapiens 119-139 17609664-11 2007 Downregulation of thymidylate synthase in S3 cells renders them more susceptible to 5-fluorouracil-induced cytotoxicity. Fluorouracil 84-98 thymidylate synthetase Homo sapiens 18-38 12819937-3 2003 5-Fluorouracil (5-FU) was synthesized in 1957 and represents the first class of antineoplastic agents to be developed as inhibitors of TS. Fluorouracil 16-20 thymidylate synthetase Homo sapiens 135-137 12929570-1 2003 BACKGROUND: Dihydropyrimidine dehydrogenase (DPD) is a rate-limiting enzyme in the catabolism of 5-fluorouracil (5-FU). Fluorouracil 97-111 dihydropyrimidine dehydrogenase Rattus norvegicus 12-43 17377791-1 2007 PURPOSE: It has been suggested that the gene expression levels of thymidylate synthase (TS) and dihydropyrimidine dehydrogenase (DPD) help in the prediction of the response to 5-fluorouracil (5-FU) in vivo and in vitro in gastric cancers. Fluorouracil 176-190 thymidylate synthetase Homo sapiens 66-86 17377791-1 2007 PURPOSE: It has been suggested that the gene expression levels of thymidylate synthase (TS) and dihydropyrimidine dehydrogenase (DPD) help in the prediction of the response to 5-fluorouracil (5-FU) in vivo and in vitro in gastric cancers. Fluorouracil 176-190 thymidylate synthetase Homo sapiens 88-90 17377791-1 2007 PURPOSE: It has been suggested that the gene expression levels of thymidylate synthase (TS) and dihydropyrimidine dehydrogenase (DPD) help in the prediction of the response to 5-fluorouracil (5-FU) in vivo and in vitro in gastric cancers. Fluorouracil 192-196 thymidylate synthetase Homo sapiens 66-86 17377791-1 2007 PURPOSE: It has been suggested that the gene expression levels of thymidylate synthase (TS) and dihydropyrimidine dehydrogenase (DPD) help in the prediction of the response to 5-fluorouracil (5-FU) in vivo and in vitro in gastric cancers. Fluorouracil 192-196 thymidylate synthetase Homo sapiens 88-90 17377791-5 2007 In differentiated tumors, TS gene expression levels were higher in the tumors with relative resistance to 5-FU, while in undifferentiated cases, DPD mRNA levels were higher in tumors that showed resistance to 5-FU in vitro (P = 0.043 and 0.007, respectively). Fluorouracil 106-110 thymidylate synthetase Homo sapiens 26-28 12929570-1 2003 BACKGROUND: Dihydropyrimidine dehydrogenase (DPD) is a rate-limiting enzyme in the catabolism of 5-fluorouracil (5-FU). Fluorouracil 97-111 dihydropyrimidine dehydrogenase Rattus norvegicus 45-48 12929570-1 2003 BACKGROUND: Dihydropyrimidine dehydrogenase (DPD) is a rate-limiting enzyme in the catabolism of 5-fluorouracil (5-FU). Fluorouracil 113-117 dihydropyrimidine dehydrogenase Rattus norvegicus 12-43 12929570-1 2003 BACKGROUND: Dihydropyrimidine dehydrogenase (DPD) is a rate-limiting enzyme in the catabolism of 5-fluorouracil (5-FU). Fluorouracil 113-117 dihydropyrimidine dehydrogenase Rattus norvegicus 45-48 12576456-8 2003 However, in the subgroup of patients treated with anthracycline-based chemotherapy (5-fluorouracil, Adriamycin/epirubicin, and cyclophosphamide), a correlation between response and the expression of BCRP and MRP1 (only PFS) was found, whereas such an association was not present in the cyclophosphamide, methotrexate, and 5-fluorouracil-treated group of patients. Fluorouracil 84-98 BCR pseudogene 1 Homo sapiens 199-203 12576456-8 2003 However, in the subgroup of patients treated with anthracycline-based chemotherapy (5-fluorouracil, Adriamycin/epirubicin, and cyclophosphamide), a correlation between response and the expression of BCRP and MRP1 (only PFS) was found, whereas such an association was not present in the cyclophosphamide, methotrexate, and 5-fluorouracil-treated group of patients. Fluorouracil 322-336 BCR pseudogene 1 Homo sapiens 199-203 12529547-2 2003 In mice, quiescent HSCs have been shown to be mostly CD34(-), but as a consequence of 5-fluorouracil treatment or cytokine stimulation, differentiate into CD34(+) cells. Fluorouracil 86-100 CD34 antigen Mus musculus 155-159 17347903-3 2007 We investigated whether the activation state of beta-catenin in the primary tumor is associated with differences in survival rates of patients with colon cancer undergoing immunochemotherapy with 5-fluorouracil plus polysaccharide K vs. chemotherapy with 5-fluorouracil alone. Fluorouracil 196-210 catenin beta 1 Homo sapiens 48-60 17347903-3 2007 We investigated whether the activation state of beta-catenin in the primary tumor is associated with differences in survival rates of patients with colon cancer undergoing immunochemotherapy with 5-fluorouracil plus polysaccharide K vs. chemotherapy with 5-fluorouracil alone. Fluorouracil 255-269 catenin beta 1 Homo sapiens 48-60 17237819-0 2007 Reg IV is a serum biomarker for gastric cancer patients and predicts response to 5-fluorouracil-based chemotherapy. Fluorouracil 81-95 regenerating family member 4 Homo sapiens 0-6 12616366-3 2003 METHODS: To predict tumor sensitivity to 5-fluorouracil (5-FU) in thymoma, we investigated the mRNA levels of thymidylate synthase (TS), the key enzyme that catalyzes the methylation of deoxyuridine monophosphate, and correlates with the resistance of 5-FU and dihydropyrimidine dehydrogenase (DPD), which degrades 5-FU in thymoma. Fluorouracil 41-55 thymidylate synthetase Homo sapiens 110-130 12616366-3 2003 METHODS: To predict tumor sensitivity to 5-fluorouracil (5-FU) in thymoma, we investigated the mRNA levels of thymidylate synthase (TS), the key enzyme that catalyzes the methylation of deoxyuridine monophosphate, and correlates with the resistance of 5-FU and dihydropyrimidine dehydrogenase (DPD), which degrades 5-FU in thymoma. Fluorouracil 41-55 thymidylate synthetase Homo sapiens 132-134 12616366-3 2003 METHODS: To predict tumor sensitivity to 5-fluorouracil (5-FU) in thymoma, we investigated the mRNA levels of thymidylate synthase (TS), the key enzyme that catalyzes the methylation of deoxyuridine monophosphate, and correlates with the resistance of 5-FU and dihydropyrimidine dehydrogenase (DPD), which degrades 5-FU in thymoma. Fluorouracil 57-61 thymidylate synthetase Homo sapiens 110-130 12616366-3 2003 METHODS: To predict tumor sensitivity to 5-fluorouracil (5-FU) in thymoma, we investigated the mRNA levels of thymidylate synthase (TS), the key enzyme that catalyzes the methylation of deoxyuridine monophosphate, and correlates with the resistance of 5-FU and dihydropyrimidine dehydrogenase (DPD), which degrades 5-FU in thymoma. Fluorouracil 57-61 thymidylate synthetase Homo sapiens 132-134 12616366-3 2003 METHODS: To predict tumor sensitivity to 5-fluorouracil (5-FU) in thymoma, we investigated the mRNA levels of thymidylate synthase (TS), the key enzyme that catalyzes the methylation of deoxyuridine monophosphate, and correlates with the resistance of 5-FU and dihydropyrimidine dehydrogenase (DPD), which degrades 5-FU in thymoma. Fluorouracil 252-256 thymidylate synthetase Homo sapiens 110-130 12616366-3 2003 METHODS: To predict tumor sensitivity to 5-fluorouracil (5-FU) in thymoma, we investigated the mRNA levels of thymidylate synthase (TS), the key enzyme that catalyzes the methylation of deoxyuridine monophosphate, and correlates with the resistance of 5-FU and dihydropyrimidine dehydrogenase (DPD), which degrades 5-FU in thymoma. Fluorouracil 252-256 thymidylate synthetase Homo sapiens 132-134 12616366-3 2003 METHODS: To predict tumor sensitivity to 5-fluorouracil (5-FU) in thymoma, we investigated the mRNA levels of thymidylate synthase (TS), the key enzyme that catalyzes the methylation of deoxyuridine monophosphate, and correlates with the resistance of 5-FU and dihydropyrimidine dehydrogenase (DPD), which degrades 5-FU in thymoma. Fluorouracil 252-256 thymidylate synthetase Homo sapiens 110-130 12616366-3 2003 METHODS: To predict tumor sensitivity to 5-fluorouracil (5-FU) in thymoma, we investigated the mRNA levels of thymidylate synthase (TS), the key enzyme that catalyzes the methylation of deoxyuridine monophosphate, and correlates with the resistance of 5-FU and dihydropyrimidine dehydrogenase (DPD), which degrades 5-FU in thymoma. Fluorouracil 252-256 thymidylate synthetase Homo sapiens 132-134 12616366-8 2003 CONCLUSIONS: The combined use of measurements of TS and DPD mRNA levels using real-time RT-PCR analyses may provide an indication of the selective cytoxicity of 5-FU on thymoma. Fluorouracil 161-165 thymidylate synthetase Homo sapiens 49-51 12453856-0 2002 Thymidylate synthase protein expression in colorectal cancer metastases predicts for clinical outcome to leucovorin-modulated bolus or infusional 5-fluorouracil but not methotrexate-modulated bolus 5-fluorouracil. Fluorouracil 146-160 thymidylate synthetase Homo sapiens 0-20 17551301-7 2007 For stage II/III patients, to have 2 or 3 polymorphisms of 3R/3R of 5"-TSER, a 6 bp of 3"-TSUTR, and GSTP1-Ile105Val resulted in an extensively longer survival (P = 0.020), although no difference was found between 2 groups, with respect to the plasma concentrations of 5-FU and clinicopathologic characteristics. Fluorouracil 269-273 glutathione S-transferase pi 1 Homo sapiens 101-106 12453856-1 2002 BACKGROUND: Different 5-fluorouracil (5-FU) schedules and/or biochemical modulators may result in different mechanisms of cytotoxicity, potentially affecting the correlation between thymidylate synthase (TS) expression and the clinical response to the fluoropyrimidine. Fluorouracil 22-36 thymidylate synthetase Homo sapiens 182-202 12453856-1 2002 BACKGROUND: Different 5-fluorouracil (5-FU) schedules and/or biochemical modulators may result in different mechanisms of cytotoxicity, potentially affecting the correlation between thymidylate synthase (TS) expression and the clinical response to the fluoropyrimidine. Fluorouracil 22-36 thymidylate synthetase Homo sapiens 204-206 12453856-1 2002 BACKGROUND: Different 5-fluorouracil (5-FU) schedules and/or biochemical modulators may result in different mechanisms of cytotoxicity, potentially affecting the correlation between thymidylate synthase (TS) expression and the clinical response to the fluoropyrimidine. Fluorouracil 38-42 thymidylate synthetase Homo sapiens 182-202 12453856-1 2002 BACKGROUND: Different 5-fluorouracil (5-FU) schedules and/or biochemical modulators may result in different mechanisms of cytotoxicity, potentially affecting the correlation between thymidylate synthase (TS) expression and the clinical response to the fluoropyrimidine. Fluorouracil 38-42 thymidylate synthetase Homo sapiens 204-206 12453856-6 2002 CONCLUSIONS: The correlation between intratumoral TS levels and the clinical response to 5-FU depends strongly on the schedule of administration/biochemical modulators that are used in different 5-FU regimens. Fluorouracil 89-93 thymidylate synthetase Homo sapiens 50-52 12453856-6 2002 CONCLUSIONS: The correlation between intratumoral TS levels and the clinical response to 5-FU depends strongly on the schedule of administration/biochemical modulators that are used in different 5-FU regimens. Fluorouracil 195-199 thymidylate synthetase Homo sapiens 50-52 12506474-1 2002 BACKGROUND: Orotate phosphoribosyl transferase (OPRT) is the initial key enzyme in the 5-FU metabolic pathway. Fluorouracil 87-91 uridine monophosphate synthetase Homo sapiens 12-46 12506474-1 2002 BACKGROUND: Orotate phosphoribosyl transferase (OPRT) is the initial key enzyme in the 5-FU metabolic pathway. Fluorouracil 87-91 uridine monophosphate synthetase Homo sapiens 48-52 12506474-3 2002 We have previously shown that there is a strong positive correlation between OPRT activity and the antitumor effects of 5-FU. Fluorouracil 120-124 uridine monophosphate synthetase Homo sapiens 77-81 12506474-10 2002 CONCLUSIONS: Further studies are necessary to develop techniques to measure OPRT activity in biopsies, in order to establish tailor-made therapies based on estimating the antitumor effect of 5-FU from OPRT, an enzyme related to 5-FU metabolism. Fluorouracil 228-232 uridine monophosphate synthetase Homo sapiens 201-205 12494248-1 2002 BACKGROUND: In tumor cells, the enzyme orotate phosphoribosyl transferase (OPRT) contributes to 5-fluorouracil (5-FU) phosphorylation and another enzyme, dihydropyrimidine dehydrogenase (DPD), is associated with 5-FU catabolic action. Fluorouracil 96-110 uridine monophosphate synthetase Homo sapiens 75-79 17545523-6 2007 CK18 levels were determined in serum from 61 breast cancer patients during docetaxel or cyclophosphamide/epirubicin/5-fluorouracil (CEF) therapy. Fluorouracil 116-130 keratin 18 Homo sapiens 0-4 12494248-1 2002 BACKGROUND: In tumor cells, the enzyme orotate phosphoribosyl transferase (OPRT) contributes to 5-fluorouracil (5-FU) phosphorylation and another enzyme, dihydropyrimidine dehydrogenase (DPD), is associated with 5-FU catabolic action. Fluorouracil 112-116 uridine monophosphate synthetase Homo sapiens 75-79 12494248-1 2002 BACKGROUND: In tumor cells, the enzyme orotate phosphoribosyl transferase (OPRT) contributes to 5-fluorouracil (5-FU) phosphorylation and another enzyme, dihydropyrimidine dehydrogenase (DPD), is associated with 5-FU catabolic action. Fluorouracil 212-216 uridine monophosphate synthetase Homo sapiens 75-79 12494248-12 2002 CONCLUSION: DPD and OPRT activities within cancer cells may predict positive sensitivity to 5-FU. Fluorouracil 92-96 uridine monophosphate synthetase Homo sapiens 20-24 12464897-1 2002 OBJECTIVE: Thymidylate synthase (TS) is the target enzyme for 5-fluorouracil (5-FU), and dihydropyrimidine dehydrogenase (DPD) is the first enzyme that metabolizes 5-fluorouracil. Fluorouracil 62-76 thymidylate synthetase Homo sapiens 11-31 12464897-1 2002 OBJECTIVE: Thymidylate synthase (TS) is the target enzyme for 5-fluorouracil (5-FU), and dihydropyrimidine dehydrogenase (DPD) is the first enzyme that metabolizes 5-fluorouracil. Fluorouracil 62-76 thymidylate synthetase Homo sapiens 33-35 12464897-1 2002 OBJECTIVE: Thymidylate synthase (TS) is the target enzyme for 5-fluorouracil (5-FU), and dihydropyrimidine dehydrogenase (DPD) is the first enzyme that metabolizes 5-fluorouracil. Fluorouracil 78-82 thymidylate synthetase Homo sapiens 11-31 12464897-1 2002 OBJECTIVE: Thymidylate synthase (TS) is the target enzyme for 5-fluorouracil (5-FU), and dihydropyrimidine dehydrogenase (DPD) is the first enzyme that metabolizes 5-fluorouracil. Fluorouracil 78-82 thymidylate synthetase Homo sapiens 33-35 12464897-1 2002 OBJECTIVE: Thymidylate synthase (TS) is the target enzyme for 5-fluorouracil (5-FU), and dihydropyrimidine dehydrogenase (DPD) is the first enzyme that metabolizes 5-fluorouracil. Fluorouracil 164-178 thymidylate synthetase Homo sapiens 11-31 12464897-1 2002 OBJECTIVE: Thymidylate synthase (TS) is the target enzyme for 5-fluorouracil (5-FU), and dihydropyrimidine dehydrogenase (DPD) is the first enzyme that metabolizes 5-fluorouracil. Fluorouracil 164-178 thymidylate synthetase Homo sapiens 33-35 12419434-6 2002 Seventeen patients who presented with pT4 or pN1 and/or pM1 received 5-fluorouracil-based chemotherapy postoperatively. Fluorouracil 69-83 serpin family E member 2 Homo sapiens 45-48 17463168-6 2007 Hematopoiesis was impaired in the absence of Cx32, and it was delayed during regeneration after chemical abrasion with 5-fluorouracil at 150 mg/kg body wt in Cx32-KO mice. Fluorouracil 119-133 gap junction protein, beta 1 Mus musculus 158-162 17278107-6 2007 This would severely decrease TS expression and may have implications for predicting efficacy and toxicity of therapy with commonly used fluorouracil-based therapy regimes. Fluorouracil 136-148 thymidylate synthetase Homo sapiens 29-31 17461503-7 2007 MK-AS significantly increased the inhibition rate of DDP, 5-FU and ADM. Additionally, synergism (Q 1.15) occurred at a lower concentration of ADM, 5-FU and DDP with combined MK-AS. Fluorouracil 147-151 translocase of inner mitochondrial membrane 8A Homo sapiens 53-56 17443278-1 2007 BACKGROUND: Thymidine phosphorylase (TP), orotate phosphoribosyltransferase (OPRT), and dihydropyrimidine dehydrogenase (DPD) are important enzymes related to the metabolism of 5-fluorouracil and its derivatives. Fluorouracil 177-191 uridine monophosphate synthetase Homo sapiens 42-75 17443278-1 2007 BACKGROUND: Thymidine phosphorylase (TP), orotate phosphoribosyltransferase (OPRT), and dihydropyrimidine dehydrogenase (DPD) are important enzymes related to the metabolism of 5-fluorouracil and its derivatives. Fluorouracil 177-191 uridine monophosphate synthetase Homo sapiens 77-81 17417073-11 2007 These findings suggest that there may be an important relationship between the TYMS haplotypes examined and 5-FU toxicity. Fluorouracil 108-112 thymidylate synthetase Homo sapiens 79-83 17364369-3 2007 BACKGROUND: Expression levels of the thymidylate synthase (TS) and 5-FU metabolic enzymes including dihydropyrimidine dehydrogenase (DPD), TP, and orotate phosphoribosyl transferase (OPRT), are reported to be associated with sensitivity to 5-FU-based chemotherapy in several cancers. Fluorouracil 67-71 uridine monophosphate synthetase Homo sapiens 183-187 17322540-0 2007 Prognostic value of expression of ERCC1, thymidylate synthase, and glutathione S-transferase P1 for 5-fluorouracil/oxaliplatin chemotherapy in advanced gastric cancer. Fluorouracil 100-114 ERCC excision repair 1, endonuclease non-catalytic subunit Homo sapiens 34-39 17322540-0 2007 Prognostic value of expression of ERCC1, thymidylate synthase, and glutathione S-transferase P1 for 5-fluorouracil/oxaliplatin chemotherapy in advanced gastric cancer. Fluorouracil 100-114 glutathione S-transferase pi 1 Homo sapiens 67-95 17322540-1 2007 BACKGROUND: The aim of this study was to determine whether expressions of the excision repair cross-complementing (ERCC1), thymidylate synthase (TS), and glutathione S-transferase P1 (GSTP1) predict clinical outcome in patients with advanced gastric cancer treated with fluorouracil (5-fluorouracil)/oxaliplatin chemotherapy. Fluorouracil 270-282 glutathione S-transferase pi 1 Homo sapiens 184-189 12482336-0 2002 Combination of 5-fluorouracil and irinotecan on modulation of thymidylate synthase and topoisomerase I expression and cell cycle regulation in human colon cancer LoVo cells: clinical relevance. Fluorouracil 15-29 thymidylate synthetase Homo sapiens 62-82 12482336-7 2002 The TS expression was decreased following 24 hours of 5-FU and it remained at reduced levels for > 24 hours after removal of 5-FU. Fluorouracil 54-58 thymidylate synthetase Homo sapiens 4-6 12482336-7 2002 The TS expression was decreased following 24 hours of 5-FU and it remained at reduced levels for > 24 hours after removal of 5-FU. Fluorouracil 128-132 thymidylate synthetase Homo sapiens 4-6 12402042-6 2002 In addition, BID-null mouse embryonic fibroblasts are more resistant than are wild-type fibroblasts to the DNA damaging agent adriamycin and the nucleotide analogue 5-fluorouracil, both of which stabilize endogenous p53. Fluorouracil 165-179 transformation related protein 53 Mus musculus 216-219 12677090-10 2002 Etoposide, cisplatin (CIS), and 5-fluorouracil (5-FU) showed the least cooperation (<or=11.5% over the additive single therapy values) with E2F-1. Fluorouracil 32-46 E2F transcription factor 1 Homo sapiens 143-148 12677090-10 2002 Etoposide, cisplatin (CIS), and 5-fluorouracil (5-FU) showed the least cooperation (<or=11.5% over the additive single therapy values) with E2F-1. Fluorouracil 48-52 E2F transcription factor 1 Homo sapiens 143-148 12677090-11 2002 Ad-E2F-1 treatment alone results in 3.4-fold increase of cyclin A kinase activity compared to Ad-LacZ control (p < 0.05); when combined with chemotherapeutic agents, cyclin A kinase activity was inhibited significantly by VIN, actinomycin D, and etoposide (p < 0.005), but not with CPT, CIS, and 5-FU (p > 0.1) compared to Ad-E2F-1 treatment alone. Fluorouracil 302-306 E2F transcription factor 1 Homo sapiens 3-8 12147691-1 2002 Thymidylate synthase (TS) catalyzes methylation of dUMP to dTMP and is the target of cancer chemotherapeutic agents (e.g. 5-fluorouracil). Fluorouracil 122-136 thymidylate synthetase Homo sapiens 0-20 12147691-1 2002 Thymidylate synthase (TS) catalyzes methylation of dUMP to dTMP and is the target of cancer chemotherapeutic agents (e.g. 5-fluorouracil). Fluorouracil 122-136 thymidylate synthetase Homo sapiens 22-24 12118326-0 2002 Role of retinoblastoma protein and E2F-1 transcription factor in the acquisition of 5-fluorouracil resistance by colon cancer cells. Fluorouracil 84-98 E2F transcription factor 1 Homo sapiens 35-40 12118326-3 2002 In vitro studies have demonstrated that the resistance to 5-FU is correlated with increased activity of thymidylate synthase (TS), whose gene has a E2F binding site in its promoter region. Fluorouracil 58-62 thymidylate synthetase Homo sapiens 104-124 12118326-8 2002 These results suggested that pRb and E2F-1 play important roles in the acquisition of 5-FU resistance by cancer cells and that cancer therapy targeting transcription factor E2F might be effective. Fluorouracil 86-90 E2F transcription factor 1 Homo sapiens 37-42 12067974-1 2002 Thymidylate synthase (TS) is a key enzyme in folate metabolism and the primary target of 5-fluorouracil. Fluorouracil 89-103 thymidylate synthetase Homo sapiens 0-20 12067974-1 2002 Thymidylate synthase (TS) is a key enzyme in folate metabolism and the primary target of 5-fluorouracil. Fluorouracil 89-103 thymidylate synthetase Homo sapiens 22-24 12085207-0 2002 Expression of multidrug resistance-associated protein1,P-glycoprotein, and thymidylate synthase in gastric cancer patients treated with 5-fluorouracil and doxorubicin-based adjuvant chemotherapy after curative resection. Fluorouracil 136-150 thymidylate synthetase Homo sapiens 75-95 12085207-2 2002 In a variety of malignancies, high expression of multidrug resistance-associated protein1 and P-glycoprotein has been associated with resistance to doxorubicin, whereas 5-fluorouracil resistance has correlated with the level of thymidylate synthase expression. Fluorouracil 169-183 thymidylate synthetase Homo sapiens 228-248 12116375-2 2002 Thymidylate synthase expression was tested in vitro, in vivo, and clinically as a prognostic factor for 5-fluorouracil (5FU) sensitivity. Fluorouracil 104-118 thymidylate synthetase Homo sapiens 0-20 12116375-2 2002 Thymidylate synthase expression was tested in vitro, in vivo, and clinically as a prognostic factor for 5-fluorouracil (5FU) sensitivity. Fluorouracil 120-123 thymidylate synthetase Homo sapiens 0-20 12052139-1 2002 Folate metabolism is the target of two major drug groups: folate antagonists (e.g., methotrexate) and thymidylate synthase inhibitors (for example, 5-fluorouracil). Fluorouracil 148-162 thymidylate synthetase Homo sapiens 102-122 12014648-0 2002 Roles of thymidylate synthase and dihydropyrimidine dehydrogenase in tumor progression and sensitivity to 5-fluorouracil in human gastric cancer. Fluorouracil 106-120 thymidylate synthetase Homo sapiens 9-29 12014648-1 2002 BACKGROUND: The role of thymidylate synthase (TS) and dihydropyrimidine dehydrogenase (DPD) enzyme activities in tumor progression and sensitivity to 5-fluorouracil (5-FU) were evaluated. Fluorouracil 150-164 thymidylate synthetase Homo sapiens 46-48 12014648-1 2002 BACKGROUND: The role of thymidylate synthase (TS) and dihydropyrimidine dehydrogenase (DPD) enzyme activities in tumor progression and sensitivity to 5-fluorouracil (5-FU) were evaluated. Fluorouracil 166-170 thymidylate synthetase Homo sapiens 24-44 12014648-1 2002 BACKGROUND: The role of thymidylate synthase (TS) and dihydropyrimidine dehydrogenase (DPD) enzyme activities in tumor progression and sensitivity to 5-fluorouracil (5-FU) were evaluated. Fluorouracil 166-170 thymidylate synthetase Homo sapiens 46-48 11872345-13 2002 These results suggest that high TS levels in resected metastases of colorectal cancer are associated with a poor outcome after surgery and 5-FU adjuvant therapy; therefore, a prospective assessment of TS levels in resected colorectal metastases could be useful to define which patients will most likely benefit from 5-FU adjuvant therapy after metastasectomy. Fluorouracil 139-143 thymidylate synthetase Homo sapiens 32-34 11915729-2 2002 The transfection of the gene for UPRT, a 5-FU-converting enzyme, resulted in a significant change in the sensitivity of pancreatic cancer cells against 5-FU, resulting in the decrease of the tumor volume disseminated in the abdominal cavity of mice. Fluorouracil 41-45 uracil phosphoribosyltransferase Mus musculus 33-37 11915729-2 2002 The transfection of the gene for UPRT, a 5-FU-converting enzyme, resulted in a significant change in the sensitivity of pancreatic cancer cells against 5-FU, resulting in the decrease of the tumor volume disseminated in the abdominal cavity of mice. Fluorouracil 152-156 uracil phosphoribosyltransferase Mus musculus 33-37 11836594-5 2002 The levels of TS and DPD activities in non-fixed fresh frozen bladder cancer specimens were determined biochemically by the 5-fluoro-2"-deoxyuridine 5"-monophosphate binding assay and the 5-fluorouracil degradation assay, respectively. Fluorouracil 188-202 thymidylate synthetase Homo sapiens 14-16 11816485-3 2002 Measurement of the expression of enzymes involved in 5-FU metabolism showed significantly higher activity of dihydropyrimidine dehydrogenase (DPD) and lower activity of thymidylate synthase (TS) in the MDA metastases than in the orthotopically implanted tumors. Fluorouracil 53-57 dihydropyrimidine dehydrogenase Mus musculus 109-140 17317154-1 2007 A significant association has been established, in clinical studies, between the expression or activity of thymidylate synthase (TYMS) and the efficiency of fluorouracil. Fluorouracil 157-169 thymidylate synthetase Homo sapiens 107-127 17317154-1 2007 A significant association has been established, in clinical studies, between the expression or activity of thymidylate synthase (TYMS) and the efficiency of fluorouracil. Fluorouracil 157-169 thymidylate synthetase Homo sapiens 129-133 17349846-1 2007 BACKGROUND: Orotate phosphoribosyl transferase (OPRT) is an essential enzyme for activation of 5-fluorouracil (5-FU) and its derivatives. Fluorouracil 95-109 uridine monophosphate synthetase Homo sapiens 12-46 17349846-1 2007 BACKGROUND: Orotate phosphoribosyl transferase (OPRT) is an essential enzyme for activation of 5-fluorouracil (5-FU) and its derivatives. Fluorouracil 95-109 uridine monophosphate synthetase Homo sapiens 48-52 17349846-1 2007 BACKGROUND: Orotate phosphoribosyl transferase (OPRT) is an essential enzyme for activation of 5-fluorouracil (5-FU) and its derivatives. Fluorouracil 111-115 uridine monophosphate synthetase Homo sapiens 12-46 17349846-1 2007 BACKGROUND: Orotate phosphoribosyl transferase (OPRT) is an essential enzyme for activation of 5-fluorouracil (5-FU) and its derivatives. Fluorouracil 111-115 uridine monophosphate synthetase Homo sapiens 48-52 17354198-0 2007 Leptin promotes the growth of Colon 38 cancer cells and interferes with the cytotoxic effect of fluorouracil in vitro. Fluorouracil 96-108 leptin Mus musculus 0-6 17354198-5 2007 The aim of our study was to examine the direct effect of leptin at various concentrations (from 10(-5) to 10(-12) M) when applied alone or jointly with fluorouracil (the classical cytotoxic drug for colon cancer) at two concentrations (0.25 mg/ml and 2.5 mg/ml) on the growth of murine Colon 38 cancer cells in vitro. Fluorouracil 152-164 leptin Mus musculus 57-63 17354198-12 2007 CONCLUSIONS: These data indicate that leptin is involved in the regulation of colon cancer growth and it may even heighten the cytotoxic effect of fluorouracil. Fluorouracil 147-159 leptin Mus musculus 38-44 17045692-11 2007 CONCLUSIONS: Our results indicated that IFNalpha/5-FU combination treatment enhances the induction of apoptosis and the cytotoxic effect of PBMCs via the Fas/FasL pathway. Fluorouracil 49-53 Fas ligand Homo sapiens 158-162 17045692-12 2007 The Fas/FasL pathway seems, at least in part, to contribute to the anti-tumor effects of IFNalpha/5-FU against HCCs. Fluorouracil 98-102 Fas ligand Homo sapiens 8-12 17607914-7 2007 Analysis of the expression of 5-fluorouracil (5-FU) (TS, DPD, TP)- and cisplatin (ERCC1, ERCC4, GADD45A, KU80)-related genes demonstrated an association of DPD expression with response and survival. Fluorouracil 30-44 ERCC excision repair 1, endonuclease non-catalytic subunit Homo sapiens 82-87 11816485-3 2002 Measurement of the expression of enzymes involved in 5-FU metabolism showed significantly higher activity of dihydropyrimidine dehydrogenase (DPD) and lower activity of thymidylate synthase (TS) in the MDA metastases than in the orthotopically implanted tumors. Fluorouracil 53-57 dihydropyrimidine dehydrogenase Mus musculus 142-145 12381902-3 2002 Thymidylate synthase is the target enzyme of both raltitrexed and 5-FU; however, the two drugs have distinct sites of action on the enzyme and the combination of the two agents may be synergistic. Fluorouracil 66-70 thymidylate synthetase Homo sapiens 0-20 11747337-1 2001 Thymidylate synthase (TS) is a key enzyme in DNA synthesis and is inhibited by metabolites of the chemotherapeutic agent 5-fluorouracil (5FU). Fluorouracil 121-135 thymidylate synthetase Homo sapiens 0-20 11747337-1 2001 Thymidylate synthase (TS) is a key enzyme in DNA synthesis and is inhibited by metabolites of the chemotherapeutic agent 5-fluorouracil (5FU). Fluorouracil 121-135 thymidylate synthetase Homo sapiens 22-24 11747337-1 2001 Thymidylate synthase (TS) is a key enzyme in DNA synthesis and is inhibited by metabolites of the chemotherapeutic agent 5-fluorouracil (5FU). Fluorouracil 137-140 thymidylate synthetase Homo sapiens 0-20 11747337-1 2001 Thymidylate synthase (TS) is a key enzyme in DNA synthesis and is inhibited by metabolites of the chemotherapeutic agent 5-fluorouracil (5FU). Fluorouracil 137-140 thymidylate synthetase Homo sapiens 22-24 11604993-1 2001 The measurement of the intra-tumoral level of thymidylate synthetase (TS), and dihydropyrimidine dehydrogenase (DPD), may be useful in predicting tumor sensitivity to 5-fluorouracil (5-FU). Fluorouracil 167-181 thymidylate synthetase Homo sapiens 46-68 17110929-5 2006 Furthermore, MDMX expression promotes resistance to the chemotherapeutic agent 5-fluorouracil (5-FU), which at low concentrations activates p53 by inducing ribosomal stress without significant DNA damage signaling. Fluorouracil 79-93 transformation related protein 53, pseudogene Mus musculus 140-143 17110929-5 2006 Furthermore, MDMX expression promotes resistance to the chemotherapeutic agent 5-fluorouracil (5-FU), which at low concentrations activates p53 by inducing ribosomal stress without significant DNA damage signaling. Fluorouracil 95-99 transformation related protein 53, pseudogene Mus musculus 140-143 17108726-4 2006 PURPOSE: This study was designed to investigate the effect of OPRT, DPD and TS in sensitivity to 5-FU. Fluorouracil 97-101 uridine monophosphate synthetase Homo sapiens 62-66 17108726-4 2006 PURPOSE: This study was designed to investigate the effect of OPRT, DPD and TS in sensitivity to 5-FU. Fluorouracil 97-101 thymidylate synthetase Homo sapiens 76-78 17016597-10 2006 RT-PCR showed that 5-FU post-treatment graduallly inhibited mRNA expression of ERCC1, which may affect recombination repair efficiency, accounting for the higher tumor sensitivity. Fluorouracil 19-23 ERCC excision repair 1, endonuclease non-catalytic subunit Homo sapiens 79-84 11604993-1 2001 The measurement of the intra-tumoral level of thymidylate synthetase (TS), and dihydropyrimidine dehydrogenase (DPD), may be useful in predicting tumor sensitivity to 5-fluorouracil (5-FU). Fluorouracil 183-187 thymidylate synthetase Homo sapiens 46-68 11604993-3 2001 Then we examined the correlation of the responsiveness of the patients with oral SCC to 5-FU with the intra-tumoral levels of DPD and TS mRNA. Fluorouracil 88-92 thymidylate synthetase Homo sapiens 134-136 11704815-3 2001 UPRT enhances the conversion of 5-FU into its active metabolites, which inhibit DNA and RNA synthesis. Fluorouracil 32-36 uracil phosphoribosyltransferase Mus musculus 0-4 17047489-8 2006 In-vitro results showed a higher sensitivity to 5-FU of cell lines with the lowest TS expression. Fluorouracil 48-52 thymidylate synthetase Homo sapiens 83-85 16949053-6 2006 In addition, Nutlin-3 increased expression of the p53 target genes Bax and PERP to a greater extent than doxorubicin or 5-FU, and triggered a G2/M phase arrest in these cells, compared to a G1 arrest triggered by doxorubicin and 5-FU. Fluorouracil 229-233 transformation related protein 53, pseudogene Mus musculus 50-53 16757204-0 2006 Orotate phosphoribosyl transferase mRNA expression in oral squamous cell carcinoma and its relationship with the dihydropyrimidine dehydrogenase expression and the clinical effect of 5-fluorouracil. Fluorouracil 183-197 uridine monophosphate synthetase Homo sapiens 0-34 16909101-6 2006 XAF1 expression enhanced the apoptotic response of tumor cells to chemotherapeutic agents, such as etoposide or 5-FU. Fluorouracil 112-116 XIAP associated factor 1 Homo sapiens 0-4 16951200-1 2006 The thymidylate synthase inhibitor 5-fluorouracil (5-FU) continues to play a pivotal role in the treatment of cancer. Fluorouracil 35-49 thymidylate synthetase Homo sapiens 4-24 11676864-0 2001 High expression of thymidylate synthase leads to resistance to 5-fluorouracil in biliary tract carcinoma in vitro. Fluorouracil 63-77 thymidylate synthetase Homo sapiens 19-39 16951200-1 2006 The thymidylate synthase inhibitor 5-fluorouracil (5-FU) continues to play a pivotal role in the treatment of cancer. Fluorouracil 51-55 thymidylate synthetase Homo sapiens 4-24 11556832-5 2001 These results demonstrate that a polymorphism within the TS gene, probably through its effect on TS expression levels, can influence the survival benefit obtained by CRC patients from 5-FU-based chemotherapy. Fluorouracil 184-188 thymidylate synthetase Homo sapiens 97-99 16912530-1 2006 Although orotate phosphoribosyltransferase (OPRT EC 2.4.2.10) is a key enzyme related to the first-step activation process of 5-fluorouracil, and therefore it has been shown to be an important enzyme that enables to predict sensitivity to 5-fluorouracil, the clinical and prognostic significance of protein and/or gene expression of OPRT has not been well established in gastric carcinoma. Fluorouracil 126-140 uridine monophosphate synthetase Homo sapiens 9-42 16912530-1 2006 Although orotate phosphoribosyltransferase (OPRT EC 2.4.2.10) is a key enzyme related to the first-step activation process of 5-fluorouracil, and therefore it has been shown to be an important enzyme that enables to predict sensitivity to 5-fluorouracil, the clinical and prognostic significance of protein and/or gene expression of OPRT has not been well established in gastric carcinoma. Fluorouracil 126-140 uridine monophosphate synthetase Homo sapiens 44-48 16912530-1 2006 Although orotate phosphoribosyltransferase (OPRT EC 2.4.2.10) is a key enzyme related to the first-step activation process of 5-fluorouracil, and therefore it has been shown to be an important enzyme that enables to predict sensitivity to 5-fluorouracil, the clinical and prognostic significance of protein and/or gene expression of OPRT has not been well established in gastric carcinoma. Fluorouracil 126-140 uridine monophosphate synthetase Homo sapiens 333-337 16912530-1 2006 Although orotate phosphoribosyltransferase (OPRT EC 2.4.2.10) is a key enzyme related to the first-step activation process of 5-fluorouracil, and therefore it has been shown to be an important enzyme that enables to predict sensitivity to 5-fluorouracil, the clinical and prognostic significance of protein and/or gene expression of OPRT has not been well established in gastric carcinoma. Fluorouracil 239-253 uridine monophosphate synthetase Homo sapiens 9-42 16912530-1 2006 Although orotate phosphoribosyltransferase (OPRT EC 2.4.2.10) is a key enzyme related to the first-step activation process of 5-fluorouracil, and therefore it has been shown to be an important enzyme that enables to predict sensitivity to 5-fluorouracil, the clinical and prognostic significance of protein and/or gene expression of OPRT has not been well established in gastric carcinoma. Fluorouracil 239-253 uridine monophosphate synthetase Homo sapiens 44-48 16912530-1 2006 Although orotate phosphoribosyltransferase (OPRT EC 2.4.2.10) is a key enzyme related to the first-step activation process of 5-fluorouracil, and therefore it has been shown to be an important enzyme that enables to predict sensitivity to 5-fluorouracil, the clinical and prognostic significance of protein and/or gene expression of OPRT has not been well established in gastric carcinoma. Fluorouracil 239-253 uridine monophosphate synthetase Homo sapiens 333-337 16804527-10 2006 Regional availability of p53-dependent and -independent apoptotic pathways in small and large intestine together with separate modulation of these pathways by antioxidants explains the different regional enterotoxicity following 5-FU therapy. Fluorouracil 229-233 transformation related protein 53, pseudogene Mus musculus 25-28 16886117-9 2006 Compared with 5-Fu alone, the growth suppression rate of FasL-positive colorectal carcinoma HR-8348 cells was significantly raised by sFas-Calphostin C combined with 5-Fu. Fluorouracil 14-18 Fas ligand Homo sapiens 57-61 16886117-9 2006 Compared with 5-Fu alone, the growth suppression rate of FasL-positive colorectal carcinoma HR-8348 cells was significantly raised by sFas-Calphostin C combined with 5-Fu. Fluorouracil 166-170 Fas ligand Homo sapiens 57-61 11493447-0 2001 Thrombocytopenic c-mpl(-/-) mice can produce a normal level of platelets after administration of 5-fluorouracil: the effect of age on the response. Fluorouracil 97-111 myeloproliferative leukemia virus oncogene Mus musculus 17-22 11493447-4 2001 A 5- to 6-fold increase in platelet levels in c-mpl(-/-) mice (to approximately 1000 x 10(9)/L) was observed on days 20 and 25 after 5-FU injection. Fluorouracil 133-137 myeloproliferative leukemia virus oncogene Mus musculus 46-51 11493447-6 2001 Administration of 5-FU also produced thrombocytosis in previously splenectomized c-mpl(-/-) mice. Fluorouracil 18-22 myeloproliferative leukemia virus oncogene Mus musculus 81-86 11493447-7 2001 Comparison of the platelet response to 5-FU in young (6-12 weeks) and old (33-46 weeks) c-mpl(-/-) mice found that older mice produced a much more marked response than younger mice, with a mean maximum platelet level of approximately 1700 x 10(9)/L. Fluorouracil 39-43 myeloproliferative leukemia virus oncogene Mus musculus 88-93 11493447-10 2001 These results indicate that c-mpl(-/-) mice can achieve a normal level of platelets after 5-FU injection, by means of a TPO-independent mechanism, and that they respond to 5-FU myelosuppression by producing large numbers of megakaryocytic, myeloid, and erythroid progenitors. Fluorouracil 90-94 myeloproliferative leukemia virus oncogene Mus musculus 28-33 12445371-2 2001 Treatment with 5-fluorouracil and leucovorin resulting in inhibition of DNA synthesis after inhibition of thymidylate synthase is the most common strategy for adjuvant and systemic chemotherapy in this disease. Fluorouracil 15-29 thymidylate synthetase Homo sapiens 106-126 11445849-1 2001 Thymidylate synthase (TS) is the target enzyme of 5-fluorouracil (5-FU), and dihydropyrimidine dehydrogenase (DPD) is the key enzyme in the 5-FU catabolic pathway. Fluorouracil 50-64 thymidylate synthetase Homo sapiens 0-20 11445849-1 2001 Thymidylate synthase (TS) is the target enzyme of 5-fluorouracil (5-FU), and dihydropyrimidine dehydrogenase (DPD) is the key enzyme in the 5-FU catabolic pathway. Fluorouracil 50-64 thymidylate synthetase Homo sapiens 22-24 11445849-1 2001 Thymidylate synthase (TS) is the target enzyme of 5-fluorouracil (5-FU), and dihydropyrimidine dehydrogenase (DPD) is the key enzyme in the 5-FU catabolic pathway. Fluorouracil 66-70 thymidylate synthetase Homo sapiens 0-20 11445849-1 2001 Thymidylate synthase (TS) is the target enzyme of 5-fluorouracil (5-FU), and dihydropyrimidine dehydrogenase (DPD) is the key enzyme in the 5-FU catabolic pathway. Fluorouracil 66-70 thymidylate synthetase Homo sapiens 22-24 11445849-1 2001 Thymidylate synthase (TS) is the target enzyme of 5-fluorouracil (5-FU), and dihydropyrimidine dehydrogenase (DPD) is the key enzyme in the 5-FU catabolic pathway. Fluorouracil 140-144 thymidylate synthetase Homo sapiens 0-20 16425285-0 2006 Prognostic impact of orotate phosphoribosyl transferase among 5-fluorouracil metabolic enzymes in resectable colorectal cancers treated by oral 5-fluorouracil-based adjuvant chemotherapy. Fluorouracil 62-76 uridine monophosphate synthetase Homo sapiens 21-55 11445849-1 2001 Thymidylate synthase (TS) is the target enzyme of 5-fluorouracil (5-FU), and dihydropyrimidine dehydrogenase (DPD) is the key enzyme in the 5-FU catabolic pathway. Fluorouracil 140-144 thymidylate synthetase Homo sapiens 22-24 16425285-0 2006 Prognostic impact of orotate phosphoribosyl transferase among 5-fluorouracil metabolic enzymes in resectable colorectal cancers treated by oral 5-fluorouracil-based adjuvant chemotherapy. Fluorouracil 144-158 uridine monophosphate synthetase Homo sapiens 21-55 11445854-0 2001 Apoptosis and thymidylate synthase inductions by 5-fluorouracil in gastric cancer cells with or without p53 mutation. Fluorouracil 49-63 thymidylate synthetase Homo sapiens 14-34 16425285-1 2006 Orotate phosphoribosyl transferase (OPRT) is the main enzyme that involves in phosphoribosylation of 5-fluorouracil (5-FU), an essential step that leads to tumor growth inhibition. Fluorouracil 101-115 uridine monophosphate synthetase Homo sapiens 0-34 11445854-1 2001 We studied apoptosis and thymidylate synthase (TS) inductions by 5-fluorouracil (5-FU) in gastric cancer cells with wild-type p53 (MKN-45 and MKN-74) and with mutated p53 (MKN-28 and KATO-III). Fluorouracil 65-79 thymidylate synthetase Homo sapiens 25-45 16425285-1 2006 Orotate phosphoribosyl transferase (OPRT) is the main enzyme that involves in phosphoribosylation of 5-fluorouracil (5-FU), an essential step that leads to tumor growth inhibition. Fluorouracil 101-115 uridine monophosphate synthetase Homo sapiens 36-40 16425285-1 2006 Orotate phosphoribosyl transferase (OPRT) is the main enzyme that involves in phosphoribosylation of 5-fluorouracil (5-FU), an essential step that leads to tumor growth inhibition. Fluorouracil 117-121 uridine monophosphate synthetase Homo sapiens 0-34 16425285-1 2006 Orotate phosphoribosyl transferase (OPRT) is the main enzyme that involves in phosphoribosylation of 5-fluorouracil (5-FU), an essential step that leads to tumor growth inhibition. Fluorouracil 117-121 uridine monophosphate synthetase Homo sapiens 36-40 16425285-8 2006 OPRT activity in tumor tissue was a predictor of prognosis in resectable CRC patients treated by oral 5-FU-based adjuvant chemotherapy, and was useful to pick-up high risk patients independent from known prognosis factors. Fluorouracil 102-106 uridine monophosphate synthetase Homo sapiens 0-4 11445854-1 2001 We studied apoptosis and thymidylate synthase (TS) inductions by 5-fluorouracil (5-FU) in gastric cancer cells with wild-type p53 (MKN-45 and MKN-74) and with mutated p53 (MKN-28 and KATO-III). Fluorouracil 81-85 thymidylate synthetase Homo sapiens 25-45 11445856-1 2001 Thymidylate synthase (TS) is an important target for chemotherapy drugs such as 5-fluorouracil and raltitrexed. Fluorouracil 80-94 thymidylate synthetase Homo sapiens 0-20 11445856-1 2001 Thymidylate synthase (TS) is an important target for chemotherapy drugs such as 5-fluorouracil and raltitrexed. Fluorouracil 80-94 thymidylate synthetase Homo sapiens 22-24 11389880-7 2001 The results clearly showed that normal rat tissues activated 5-FU mainly via the Rib1-P pathway, and to a lesser extent via the PRPP pathway. Fluorouracil 61-65 ribonuclease A family member 1, pancreatic Rattus norvegicus 81-85 16467204-3 2006 In this study, stress induced by 5-fluorouracil or phenylhydrazine revealed a delay in the recovery of erythroid progenitors, early precursors, and normal hematocrits in Cul4A(+/-) mice. Fluorouracil 33-47 cullin 4A Mus musculus 170-175 11431359-4 2001 Human MLH1(-) and MMR-deficient HCT116 colon cancer cells were 18-fold more resistant to 7.5 microM 5-fluorouracil (continuous treatment) and 17-fold more resistant to 7.5 microM FdUrd in clonogenic survival assays compared with genetically matched, MLH1(+) and MMR-proficient HCT116 3-6 cells. Fluorouracil 100-114 mutL homolog 1 Homo sapiens 6-13 11404490-1 2001 The purpose of this phase II trial was to evaluate the toxicity of a sequential chemoradiotherapy approach using docetaxel, cisplatin, and 5-fluorouracil (5-FU) (DCF) with granulocyte colony-stimulating factor support in previously untreated patients with locally advanced head and neck cancer (HNC). Fluorouracil 139-153 colony stimulating factor 3 Homo sapiens 172-209 11404490-1 2001 The purpose of this phase II trial was to evaluate the toxicity of a sequential chemoradiotherapy approach using docetaxel, cisplatin, and 5-fluorouracil (5-FU) (DCF) with granulocyte colony-stimulating factor support in previously untreated patients with locally advanced head and neck cancer (HNC). Fluorouracil 155-159 colony stimulating factor 3 Homo sapiens 172-209 11484952-10 2001 The anti-apoptotic protein mcl-1 was the only factor, which correlated with response to 5-FU treatment. Fluorouracil 88-92 MCL1 apoptosis regulator, BCL2 family member Homo sapiens 27-32 11376565-2 2001 The circadian-dependent efficacy and toxicity of 5-FU are related to the circadian variation in the activity of dihydropyrimidine dehydrogenase (DPD), which is a rate-limiting enzyme in the pyrimidine catabolic pathway. Fluorouracil 49-53 dihydropyrimidine dehydrogenase Mus musculus 112-143 11376565-2 2001 The circadian-dependent efficacy and toxicity of 5-FU are related to the circadian variation in the activity of dihydropyrimidine dehydrogenase (DPD), which is a rate-limiting enzyme in the pyrimidine catabolic pathway. Fluorouracil 49-53 dihydropyrimidine dehydrogenase Mus musculus 145-148 11376565-9 2001 Modulation of the circadian rhythm of DPD by CPT-11 may be a factor in optimizing the combination of 5-FU and CPT-11. Fluorouracil 101-105 dihydropyrimidine dehydrogenase Mus musculus 38-41 11400231-1 2001 BACKGROUND: We have shown that rIL-2 administration in recurrent head and neck cancers induces a tumor-specific T-lymphocyte reactivity and tumor regression; in a pilot study we have shown a safe and effective administration of rIL2 after cisplatin + 5-fluorouracil. Fluorouracil 251-265 interleukin 2 Rattus norvegicus 31-36 16918130-7 2006 The cell lines without synergism between 5-FU +TDDP/CDDP had lower thymidylate synthase (TS) activities than those with synergism, suggesting TS might be attributable to the synergistic mechanism. Fluorouracil 41-45 thymidylate synthetase Homo sapiens 67-87 16818496-8 2006 Recent pharmacogenetic studies focused on genes encoding proteins directly involved in drug activity, showing the role of thymidylate synthase and human equilibrative nucleoside transporter-1 as prognostic factor in 5-fluorouracil- and gemcitabine-treated patients, respectively. Fluorouracil 216-230 thymidylate synthetase Homo sapiens 122-142 16827120-3 2006 Previous studies from this laboratory have shown that raloxifene (RAL) attenuation of 5-fluorouracil/methotrexate (5-FU/MTX) cytotoxicity to breast cancer cells was sequence-dependent. Fluorouracil 86-100 metaxin 1 Homo sapiens 120-123 16827120-5 2006 MATERIALS AND METHODS: The sequence-dependent interaction among MTX, 5-FU and RAL on the proliferation and viability of human bone marrow HS-5 cells was determined by the MTT assay and the Trypan blue dye exclusion assay by exposing the cells to MTX, 5-FU and RAL alone, RAL 24 h prior to 5-FU followed 2 h later by MTX, and 5-FU 2 h prior to MTX followed 24 h later by RAL. Fluorouracil 251-255 metaxin 1 Homo sapiens 64-67 16827120-5 2006 MATERIALS AND METHODS: The sequence-dependent interaction among MTX, 5-FU and RAL on the proliferation and viability of human bone marrow HS-5 cells was determined by the MTT assay and the Trypan blue dye exclusion assay by exposing the cells to MTX, 5-FU and RAL alone, RAL 24 h prior to 5-FU followed 2 h later by MTX, and 5-FU 2 h prior to MTX followed 24 h later by RAL. Fluorouracil 251-255 metaxin 1 Homo sapiens 64-67 16677934-8 2006 Furthermore, we show that treatment with 5-FU and ultrasound increased the levels of the Bax and p27kip1 proteins, but the addition of Optison appears to suppress apoptotic protein expression. Fluorouracil 41-45 cyclin dependent kinase inhibitor 1B Homo sapiens 97-104 16809149-1 2006 UNLABELLED: Thymidylate synthase (TS), dihydropyrimidine dehydrogenase (DPD), and vascular endothelial growth factor (VEGF) are associated with the effect of 5-fluorouracil (5-FU) based adjuvant chemotherapy. Fluorouracil 174-178 thymidylate synthetase Homo sapiens 34-36 16809149-11 2006 CONCLUSION: Neoadjuvant chemotherapy for primary gastric cancer with one cycle of 5-FU and cisplatin was associated with histological findings in patients with low baseline TS and DPD. Fluorouracil 82-86 thymidylate synthetase Homo sapiens 173-175 16563096-3 2006 For example: 5-fluorouracil-derived agents would be used for tumors with a low expression of thymidylate synthase; gefitinib and erlotinib for tumors with epidermal growth factor receptor (EGFR) mutations or increased EGFR gene copy numbers; cisplatin and carboplatin for tumors with a low expression of excision repair cross complementing-1; and gemcitabine for tumors with a low expression of ribonucleotide reductase. Fluorouracil 13-27 thymidylate synthetase Homo sapiens 93-113 16280240-7 2006 Maintenance adjuvant chemotherapy by oral 5-fluorouracil (5-FU) significantly improved DFS and OS in patients with a TS 1+/2+ tumour (DFS: P = 0.0027, OS: P = 0.0398). Fluorouracil 42-56 thymidylate synthetase Homo sapiens 117-119 16280240-7 2006 Maintenance adjuvant chemotherapy by oral 5-fluorouracil (5-FU) significantly improved DFS and OS in patients with a TS 1+/2+ tumour (DFS: P = 0.0027, OS: P = 0.0398). Fluorouracil 58-62 thymidylate synthetase Homo sapiens 117-119 16280240-8 2006 These data suggest that the level of immunohistochemical TS expression is an independent prognosticator in patients with tongue SCC, and may be useful in the selection of patients who would benefit from oral 5-FU adjuvant chemotherapy. Fluorouracil 208-212 thymidylate synthetase Homo sapiens 57-59 16391809-1 2006 Thymidylate synthase (TS), dihydropyrimidine dehydrogenase (DPD) and thymidine phosphorylase (TP) are predictive markers for tumor response to 5-fluorouracil-based therapies. Fluorouracil 143-157 thymidylate synthetase Homo sapiens 0-20 16391809-1 2006 Thymidylate synthase (TS), dihydropyrimidine dehydrogenase (DPD) and thymidine phosphorylase (TP) are predictive markers for tumor response to 5-fluorouracil-based therapies. Fluorouracil 143-157 thymidylate synthetase Homo sapiens 22-24 16251201-1 2006 BACKGROUND: Thymidylate synthase (TS) and dihydropyrimidine dehydrogenase (DPD) are essential enzymes for 5-fluorouracil (5-FU) metabolism. Fluorouracil 106-120 thymidylate synthetase Homo sapiens 12-32 16251201-1 2006 BACKGROUND: Thymidylate synthase (TS) and dihydropyrimidine dehydrogenase (DPD) are essential enzymes for 5-fluorouracil (5-FU) metabolism. Fluorouracil 106-120 thymidylate synthetase Homo sapiens 34-36 16251201-1 2006 BACKGROUND: Thymidylate synthase (TS) and dihydropyrimidine dehydrogenase (DPD) are essential enzymes for 5-fluorouracil (5-FU) metabolism. Fluorouracil 122-126 thymidylate synthetase Homo sapiens 12-32 16251201-1 2006 BACKGROUND: Thymidylate synthase (TS) and dihydropyrimidine dehydrogenase (DPD) are essential enzymes for 5-fluorouracil (5-FU) metabolism. Fluorouracil 122-126 thymidylate synthetase Homo sapiens 34-36 16251201-2 2006 In patients with advanced colorectal cancer (ACRC), retrospective studies have shown that low expression levels of TS and DPD correlated with response to 5-FU. Fluorouracil 154-158 thymidylate synthetase Homo sapiens 115-117 16251201-12 2006 CONCLUSIONS: Prospective selection of 5-FU/LV chemotherapy based on low TS and DPD expression in patients with ACRC did not confirm the high response rates reported in retrospective studies. Fluorouracil 38-42 thymidylate synthetase Homo sapiens 72-74 16617381-1 2006 AIM: Thymidylate synthase (TS) is a rate-limiting enzyme in the DNA synthetic pathway, and represents a cellular target of antimetabolite drug 5-fluorouracil. Fluorouracil 143-157 thymidylate synthetase Homo sapiens 5-25 16617381-1 2006 AIM: Thymidylate synthase (TS) is a rate-limiting enzyme in the DNA synthetic pathway, and represents a cellular target of antimetabolite drug 5-fluorouracil. Fluorouracil 143-157 thymidylate synthetase Homo sapiens 27-29 16617381-5 2006 Developing resistance against 5-fluorouracil (FURA) based drugs might be due to the failure of inhibition of thymidylate synthase enzyme function. Fluorouracil 30-44 thymidylate synthetase Homo sapiens 109-129 16617381-5 2006 Developing resistance against 5-fluorouracil (FURA) based drugs might be due to the failure of inhibition of thymidylate synthase enzyme function. Fluorouracil 46-50 thymidylate synthetase Homo sapiens 109-129 16617381-13 2006 This facts indicate that the analysis of promoter polymorphism of thymidylate synthase gene might be a useful target to examine before FURA-based chemotherapy, and might allow to go into the direction of individualized treatment of head and neck cancer. Fluorouracil 135-139 thymidylate synthetase Homo sapiens 66-86 17065089-4 2006 TS is the main target of 5-fluorouracil (5-FU) activity, and its overexpression is one of the mechanisms of 5-FU drug resistance; however, in some studies its absence is responsible for a worse response to 5-FU. Fluorouracil 25-39 thymidylate synthetase Homo sapiens 0-2 17237621-0 2006 Overexpression of the orotate phosphoribosyl-transferase gene enhances the effect of 5-fluorouracil on gastric cancer cell lines. Fluorouracil 85-99 uridine monophosphate synthetase Homo sapiens 22-56 17237621-1 2006 OBJECTIVE: Orotate phosphoribosyl-transferase (OPRT) is the initial enzyme of the 5-fluorouracil (5-FU) metabolic pathway, converting 5-FU into 5-fluorouridinemonophosphate, which is the most important mechanism of 5-FU activation. Fluorouracil 82-96 uridine monophosphate synthetase Homo sapiens 11-45 17237621-1 2006 OBJECTIVE: Orotate phosphoribosyl-transferase (OPRT) is the initial enzyme of the 5-fluorouracil (5-FU) metabolic pathway, converting 5-FU into 5-fluorouridinemonophosphate, which is the most important mechanism of 5-FU activation. Fluorouracil 82-96 uridine monophosphate synthetase Homo sapiens 47-51 17237621-1 2006 OBJECTIVE: Orotate phosphoribosyl-transferase (OPRT) is the initial enzyme of the 5-fluorouracil (5-FU) metabolic pathway, converting 5-FU into 5-fluorouridinemonophosphate, which is the most important mechanism of 5-FU activation. Fluorouracil 98-102 uridine monophosphate synthetase Homo sapiens 11-45 17237621-1 2006 OBJECTIVE: Orotate phosphoribosyl-transferase (OPRT) is the initial enzyme of the 5-fluorouracil (5-FU) metabolic pathway, converting 5-FU into 5-fluorouridinemonophosphate, which is the most important mechanism of 5-FU activation. Fluorouracil 98-102 uridine monophosphate synthetase Homo sapiens 47-51 17237621-1 2006 OBJECTIVE: Orotate phosphoribosyl-transferase (OPRT) is the initial enzyme of the 5-fluorouracil (5-FU) metabolic pathway, converting 5-FU into 5-fluorouridinemonophosphate, which is the most important mechanism of 5-FU activation. Fluorouracil 134-138 uridine monophosphate synthetase Homo sapiens 11-45 17237621-1 2006 OBJECTIVE: Orotate phosphoribosyl-transferase (OPRT) is the initial enzyme of the 5-fluorouracil (5-FU) metabolic pathway, converting 5-FU into 5-fluorouridinemonophosphate, which is the most important mechanism of 5-FU activation. Fluorouracil 134-138 uridine monophosphate synthetase Homo sapiens 47-51 17237621-1 2006 OBJECTIVE: Orotate phosphoribosyl-transferase (OPRT) is the initial enzyme of the 5-fluorouracil (5-FU) metabolic pathway, converting 5-FU into 5-fluorouridinemonophosphate, which is the most important mechanism of 5-FU activation. Fluorouracil 134-138 uridine monophosphate synthetase Homo sapiens 11-45 17237621-1 2006 OBJECTIVE: Orotate phosphoribosyl-transferase (OPRT) is the initial enzyme of the 5-fluorouracil (5-FU) metabolic pathway, converting 5-FU into 5-fluorouridinemonophosphate, which is the most important mechanism of 5-FU activation. Fluorouracil 134-138 uridine monophosphate synthetase Homo sapiens 47-51 17237621-2 2006 We therefore investigated whether overexpression of the OPRT gene enhances sensitivity to 5-FU. Fluorouracil 90-94 uridine monophosphate synthetase Homo sapiens 56-60 11400231-1 2001 BACKGROUND: We have shown that rIL-2 administration in recurrent head and neck cancers induces a tumor-specific T-lymphocyte reactivity and tumor regression; in a pilot study we have shown a safe and effective administration of rIL2 after cisplatin + 5-fluorouracil. Fluorouracil 251-265 interleukin 2 Rattus norvegicus 228-232 11265402-1 2001 Orotate phosphoribosyl transferase (OPRT) is an enzyme that converts the pyrimidine fluoride-class anticancer drug 5-fluorouracil (5-FU) into the active nucleotide form. Fluorouracil 115-129 uridine monophosphate synthetase Homo sapiens 0-34 17237621-9 2006 CONCLUSION: The results indicate that overexpression of the OPRT gene plays an important role in the antiproliferative effect of 5-FU and might therefore be a predictive factor of response to 5-FU in gastric cancer patients. Fluorouracil 129-133 uridine monophosphate synthetase Homo sapiens 60-64 17237621-9 2006 CONCLUSION: The results indicate that overexpression of the OPRT gene plays an important role in the antiproliferative effect of 5-FU and might therefore be a predictive factor of response to 5-FU in gastric cancer patients. Fluorouracil 192-196 uridine monophosphate synthetase Homo sapiens 60-64 16739880-4 2006 The main target of 5-fluorouracil (5-FU) treatment is thymidylate synthase (TS). Fluorouracil 19-33 thymidylate synthetase Homo sapiens 54-74 16739880-4 2006 The main target of 5-fluorouracil (5-FU) treatment is thymidylate synthase (TS). Fluorouracil 35-39 thymidylate synthetase Homo sapiens 54-74 11265402-1 2001 Orotate phosphoribosyl transferase (OPRT) is an enzyme that converts the pyrimidine fluoride-class anticancer drug 5-fluorouracil (5-FU) into the active nucleotide form. Fluorouracil 115-129 uridine monophosphate synthetase Homo sapiens 36-40 11265402-1 2001 Orotate phosphoribosyl transferase (OPRT) is an enzyme that converts the pyrimidine fluoride-class anticancer drug 5-fluorouracil (5-FU) into the active nucleotide form. Fluorouracil 131-135 uridine monophosphate synthetase Homo sapiens 0-34 11265402-1 2001 Orotate phosphoribosyl transferase (OPRT) is an enzyme that converts the pyrimidine fluoride-class anticancer drug 5-fluorouracil (5-FU) into the active nucleotide form. Fluorouracil 131-135 uridine monophosphate synthetase Homo sapiens 36-40 11265402-8 2001 A decrease of OPRT activity in tumor tissue is a possible reason for the equivocal results of 5-FU-based chemotherapy in advanced gastric carcinoma. Fluorouracil 94-98 uridine monophosphate synthetase Homo sapiens 14-18 11300326-1 2001 BACKGROUND: In vitro, thymidylate synthase (TS) inhibition by 5-fluorouracil (5-FU) induces thymineless apoptosis possibly via Fas receptor Fas ligand interactions and cell-cycle arrest. Fluorouracil 62-76 thymidylate synthetase Homo sapiens 22-42 11300326-1 2001 BACKGROUND: In vitro, thymidylate synthase (TS) inhibition by 5-fluorouracil (5-FU) induces thymineless apoptosis possibly via Fas receptor Fas ligand interactions and cell-cycle arrest. Fluorouracil 62-76 Fas ligand Homo sapiens 140-150 11300326-1 2001 BACKGROUND: In vitro, thymidylate synthase (TS) inhibition by 5-fluorouracil (5-FU) induces thymineless apoptosis possibly via Fas receptor Fas ligand interactions and cell-cycle arrest. Fluorouracil 78-82 thymidylate synthetase Homo sapiens 22-42 11300326-1 2001 BACKGROUND: In vitro, thymidylate synthase (TS) inhibition by 5-fluorouracil (5-FU) induces thymineless apoptosis possibly via Fas receptor Fas ligand interactions and cell-cycle arrest. Fluorouracil 78-82 Fas ligand Homo sapiens 140-150 11163332-5 2001 NB1011 was synthesized and found to be at least 10-fold more cytotoxic to 5-FU-resistant, TS-overexpressing colorectal tumor cells than to normal cells. Fluorouracil 74-78 thymidylate synthetase Homo sapiens 90-92 11299739-6 2001 We therefore concluded that immunohistochemical studies for p53 and p21 were useful for predicting the chemosensitivities of colon and gastric cancer to MMC and 5-FU. Fluorouracil 161-165 H3 histone pseudogene 16 Homo sapiens 68-71 11201382-7 2001 In such situations, sufficient TS inhibition cannot be obtained if 5-FU is administered without supplementation of reduced folate. Fluorouracil 67-71 thymidylate synthetase Homo sapiens 31-33 11501504-0 2001 Dihydropyrimidine dehydrogenase activity and thymidylate synthase level are associated with response to 5-fluorouracil in human colorectal cancer. Fluorouracil 104-118 thymidylate synthetase Homo sapiens 45-65 11501504-1 2001 In the recent studies associated with the modulation of 5-fluorouracil (5-FU) and the development of new antifolates, attentions have been focused on the expression of the target enzymes, thymidylate synthase (TS) and dihydropyrimidine dehydrogenase (DPD), that affect tumor sensitivity and resistance to drugs. Fluorouracil 56-70 thymidylate synthetase Homo sapiens 188-208 20020992-0 2006 Changes of serum erythropoietin during Cisplatin- or 5-Fluorouracil-induced anemia in rats. Fluorouracil 53-67 erythropoietin Rattus norvegicus 17-31 20020992-1 2006 The aim of the present work was to investigate changes of serum erythropoietin (Epo) during cisplatin (DDP)-or 5-Fluorouracil (5-Fu)-induced anemia in rats. Fluorouracil 111-125 erythropoietin Rattus norvegicus 64-78 20020992-1 2006 The aim of the present work was to investigate changes of serum erythropoietin (Epo) during cisplatin (DDP)-or 5-Fluorouracil (5-Fu)-induced anemia in rats. Fluorouracil 111-125 erythropoietin Rattus norvegicus 80-83 20020992-1 2006 The aim of the present work was to investigate changes of serum erythropoietin (Epo) during cisplatin (DDP)-or 5-Fluorouracil (5-Fu)-induced anemia in rats. Fluorouracil 127-131 erythropoietin Rattus norvegicus 64-78 20020992-1 2006 The aim of the present work was to investigate changes of serum erythropoietin (Epo) during cisplatin (DDP)-or 5-Fluorouracil (5-Fu)-induced anemia in rats. Fluorouracil 127-131 erythropoietin Rattus norvegicus 80-83 20020992-5 2006 A single injection of 5-Fu decreased Ret counts and Hb concentration and increased serum Epo levels. Fluorouracil 22-26 erythropoietin Rattus norvegicus 89-92 20020992-10 2006 These results suggest that in 5-Fu-induced anemia, the elevated serum Epo level was due to the feedback response to anemia. Fluorouracil 30-34 erythropoietin Rattus norvegicus 70-73 16273130-8 2005 The results reveal that yCDglyTK is expressed in CNE-2 cells, the CEyCDglyTK/5-FC system has a potent anti-tumor action in NPC, and the radio-sensitization of Egr-1 promoter plays a key role in the killing of CNE-2 cells and in the conversion of 5-FC to 5-FU. Fluorouracil 254-258 early growth response 1 Homo sapiens 159-164 15918040-5 2005 In this study, correlation between the polymorphic tandem repeat sequences of the TYMS gene and the antitumor activities of 5-fluorouracil (5-FU) and 5-fluoro-2"-deoxyuridine (FUdR) were investigated with 30 established human cell lines derived from solid tumors. Fluorouracil 124-138 thymidylate synthetase Homo sapiens 82-86 15918040-5 2005 In this study, correlation between the polymorphic tandem repeat sequences of the TYMS gene and the antitumor activities of 5-fluorouracil (5-FU) and 5-fluoro-2"-deoxyuridine (FUdR) were investigated with 30 established human cell lines derived from solid tumors. Fluorouracil 140-144 thymidylate synthetase Homo sapiens 82-86 16282729-1 2005 We semiquantificated the mRNA levels of thymidylate synthase (TS), dihydropyrimidine dehydrogenase (DPD), and orotate phosphoribosyltransferase(OPRT) from the frozen tissue of colorectal cancer, in order to examine the relationships among these enzymes and the efficacy for 5-fluorouracil (FU)-based treatment in terms of the combinations of the expression levels of these enzymes. Fluorouracil 274-288 uridine monophosphate synthetase Homo sapiens 144-148 16282729-3 2005 In 39 patients who received 5-FU-based chemotherapy with evaluable lesions, patients with low TS expression (n = 23) showed a higher response rate (52%) as compared to those with high TS expression (13%, p = 0.02). Fluorouracil 28-32 thymidylate synthetase Homo sapiens 94-96 16282729-3 2005 In 39 patients who received 5-FU-based chemotherapy with evaluable lesions, patients with low TS expression (n = 23) showed a higher response rate (52%) as compared to those with high TS expression (13%, p = 0.02). Fluorouracil 28-32 thymidylate synthetase Homo sapiens 184-186 16282729-6 2005 In conclusion, low TS expression followed by low DPD expression is important to predict the efficacy of 5-FU-based treatment for colorectal cancer. Fluorouracil 104-108 thymidylate synthetase Homo sapiens 19-21 16249645-9 2005 Both patients were positive for genotypes of thymidylate synthase -- the target enzyme of 5-FU -- that are associated with improved drug response. Fluorouracil 90-94 thymidylate synthetase Homo sapiens 45-65 16012177-1 2005 BACKGROUND: The predictive value of thymidylate synthase (TS) and dihydropyrimidine dehydrogenase (DPD) expression on long-term survival by influencing 5-fluorouracil (5-FU) effect were determined in primary tumours and node metastases of stage III colon cancer patients treated adjuvantly with 5-FU regimens (n=391). Fluorouracil 152-166 thymidylate synthetase Homo sapiens 36-56 16012177-1 2005 BACKGROUND: The predictive value of thymidylate synthase (TS) and dihydropyrimidine dehydrogenase (DPD) expression on long-term survival by influencing 5-fluorouracil (5-FU) effect were determined in primary tumours and node metastases of stage III colon cancer patients treated adjuvantly with 5-FU regimens (n=391). Fluorouracil 152-166 thymidylate synthetase Homo sapiens 58-60 16012177-1 2005 BACKGROUND: The predictive value of thymidylate synthase (TS) and dihydropyrimidine dehydrogenase (DPD) expression on long-term survival by influencing 5-fluorouracil (5-FU) effect were determined in primary tumours and node metastases of stage III colon cancer patients treated adjuvantly with 5-FU regimens (n=391). Fluorouracil 168-172 thymidylate synthetase Homo sapiens 36-56 16227744-8 2005 The antitumor effect in the MTD-administered group was the strongest of all of the tested anticancer drug groups (cyclophosphamide, mitomycin C, fluorouracil, cisplatin, doxorubicin). Fluorouracil 145-157 metallothionein 1E Homo sapiens 28-31 11913730-0 2001 Thymidylate synthase gene polymorphism determines response and toxicity of 5-FU chemotherapy. Fluorouracil 75-79 thymidylate synthetase Homo sapiens 0-20 11913730-9 2001 The data suggest that genotyping for the TS polymorphism may have the potential to identify patients more likely to respond to 5-FU based chemotherapy. Fluorouracil 127-131 thymidylate synthetase Homo sapiens 41-43 11291709-1 2001 We report herein the case of a 40-year-old man with grade II invasive ductal carcinoma of the breast (pT1, pN0, M0: stage I) in whom a recurrence developed shortly after completion of a 2-year course of tamoxifen and 5-fluorouracil therapy following a mastectomy. Fluorouracil 217-231 zinc finger protein 77 Homo sapiens 102-105 16144923-0 2005 ERCC1 codon 118 polymorphism is a predictive factor for the tumor response to oxaliplatin/5-fluorouracil combination chemotherapy in patients with advanced colorectal cancer. Fluorouracil 90-104 ERCC excision repair 1, endonuclease non-catalytic subunit Homo sapiens 0-5 16012756-1 2005 Orotate phosphoribosyltransferase (OPRT) is a key enzyme in the anabolism of 5-fluorouracil (5-FU), and its expression in tumors is thought to increase the efficacy of 5-FU against the tumor. Fluorouracil 77-91 uridine monophosphate synthetase Homo sapiens 0-33 16012756-1 2005 Orotate phosphoribosyltransferase (OPRT) is a key enzyme in the anabolism of 5-fluorouracil (5-FU), and its expression in tumors is thought to increase the efficacy of 5-FU against the tumor. Fluorouracil 77-91 uridine monophosphate synthetase Homo sapiens 35-39 16012756-1 2005 Orotate phosphoribosyltransferase (OPRT) is a key enzyme in the anabolism of 5-fluorouracil (5-FU), and its expression in tumors is thought to increase the efficacy of 5-FU against the tumor. Fluorouracil 93-97 uridine monophosphate synthetase Homo sapiens 0-33 16012756-1 2005 Orotate phosphoribosyltransferase (OPRT) is a key enzyme in the anabolism of 5-fluorouracil (5-FU), and its expression in tumors is thought to increase the efficacy of 5-FU against the tumor. Fluorouracil 93-97 uridine monophosphate synthetase Homo sapiens 35-39 16012756-1 2005 Orotate phosphoribosyltransferase (OPRT) is a key enzyme in the anabolism of 5-fluorouracil (5-FU), and its expression in tumors is thought to increase the efficacy of 5-FU against the tumor. Fluorouracil 168-172 uridine monophosphate synthetase Homo sapiens 0-33 16012756-1 2005 Orotate phosphoribosyltransferase (OPRT) is a key enzyme in the anabolism of 5-fluorouracil (5-FU), and its expression in tumors is thought to increase the efficacy of 5-FU against the tumor. Fluorouracil 168-172 uridine monophosphate synthetase Homo sapiens 35-39 16012756-4 2005 These results suggest that immunohistochemical detection of tumoral OPRT protein expression with our anti-OPRT antibodies may provide a useful method for predicting the clinical response to 5-FU-based chemotherapy. Fluorouracil 190-194 uridine monophosphate synthetase Homo sapiens 68-72 16012756-4 2005 These results suggest that immunohistochemical detection of tumoral OPRT protein expression with our anti-OPRT antibodies may provide a useful method for predicting the clinical response to 5-FU-based chemotherapy. Fluorouracil 190-194 uridine monophosphate synthetase Homo sapiens 106-110 16044965-2 2005 Among them, orotate phosphoribosyltransferase (OPRT EC 2.4.2.10) is a key enzyme related to the first-step activation process of 5-fluorouracil and therefore it has been shown to be an important enzyme for the prediction of sensitivity to 5-fluorouracil and its related derivatives. Fluorouracil 129-143 uridine monophosphate synthetase Homo sapiens 12-45 16044965-2 2005 Among them, orotate phosphoribosyltransferase (OPRT EC 2.4.2.10) is a key enzyme related to the first-step activation process of 5-fluorouracil and therefore it has been shown to be an important enzyme for the prediction of sensitivity to 5-fluorouracil and its related derivatives. Fluorouracil 129-143 uridine monophosphate synthetase Homo sapiens 47-51 16044965-2 2005 Among them, orotate phosphoribosyltransferase (OPRT EC 2.4.2.10) is a key enzyme related to the first-step activation process of 5-fluorouracil and therefore it has been shown to be an important enzyme for the prediction of sensitivity to 5-fluorouracil and its related derivatives. Fluorouracil 239-253 uridine monophosphate synthetase Homo sapiens 12-45 16044965-2 2005 Among them, orotate phosphoribosyltransferase (OPRT EC 2.4.2.10) is a key enzyme related to the first-step activation process of 5-fluorouracil and therefore it has been shown to be an important enzyme for the prediction of sensitivity to 5-fluorouracil and its related derivatives. Fluorouracil 239-253 uridine monophosphate synthetase Homo sapiens 47-51 16044965-5 2005 OPRT levels were measured in 8 human cancer xenografts transplanted in nude mice and 58 gastric cancer tissues using both a newly established ELISA and a conventional enzyme assay using radiolabeled 5-fluorouracil as a substrate. Fluorouracil 199-213 uridine monophosphate synthetase Homo sapiens 0-4 16044965-8 2005 The ELISA system developed for the measurement of OPRT required a minimal amount of carcinoma tissue samples, which could be an easy-of-use assay system to predict sensitivity to 5-fluorouracil in gastric carcinoma. Fluorouracil 179-193 uridine monophosphate synthetase Homo sapiens 50-54 15897576-1 2005 PURPOSE: To investigate the prognostic role of thymidylate synthase (TS) polymorphisms in gastric cancer patients treated with radical surgery and fluorouracil-based adjuvant chemotherapy. Fluorouracil 147-159 thymidylate synthetase Homo sapiens 47-67 15897576-1 2005 PURPOSE: To investigate the prognostic role of thymidylate synthase (TS) polymorphisms in gastric cancer patients treated with radical surgery and fluorouracil-based adjuvant chemotherapy. Fluorouracil 147-159 thymidylate synthetase Homo sapiens 69-71 11321346-7 2001 Immunohistochemically, the thymidylate synthase expression level was very low in the tumor tissues, which might account for the good response to the combination chemotherapy with 5-FU and CDDP observed in the present case. Fluorouracil 179-183 thymidylate synthetase Homo sapiens 27-47 15918566-1 2005 Orotate phosphoribosyl transferase (OPRT, EC 2.4.2.10) is a key enzyme in the anabolism of 5-fluorouracil (5 FU), and its expression in tumor is thought to increase the efficacy of 5-FU against the tumor. Fluorouracil 91-105 uridine monophosphate synthetase Homo sapiens 0-34 15918566-1 2005 Orotate phosphoribosyl transferase (OPRT, EC 2.4.2.10) is a key enzyme in the anabolism of 5-fluorouracil (5 FU), and its expression in tumor is thought to increase the efficacy of 5-FU against the tumor. Fluorouracil 91-105 uridine monophosphate synthetase Homo sapiens 36-40 15918566-1 2005 Orotate phosphoribosyl transferase (OPRT, EC 2.4.2.10) is a key enzyme in the anabolism of 5-fluorouracil (5 FU), and its expression in tumor is thought to increase the efficacy of 5-FU against the tumor. Fluorouracil 181-185 uridine monophosphate synthetase Homo sapiens 0-34 15918566-1 2005 Orotate phosphoribosyl transferase (OPRT, EC 2.4.2.10) is a key enzyme in the anabolism of 5-fluorouracil (5 FU), and its expression in tumor is thought to increase the efficacy of 5-FU against the tumor. Fluorouracil 181-185 uridine monophosphate synthetase Homo sapiens 36-40 15918566-5 2005 These results suggest that immunohistochemical detection of tumoral OPRT protein expression using our anti-OPRT antibody may provide useful methods to predict the clinical response to 5-FU-based chemotherapy. Fluorouracil 184-188 uridine monophosphate synthetase Homo sapiens 68-72 15918566-5 2005 These results suggest that immunohistochemical detection of tumoral OPRT protein expression using our anti-OPRT antibody may provide useful methods to predict the clinical response to 5-FU-based chemotherapy. Fluorouracil 184-188 uridine monophosphate synthetase Homo sapiens 107-111 15952572-10 2005 CONCLUSION: The NPC patients with LRP and TS expression may be less sensitive to chemotherapy with DDP + 5-FU. Fluorouracil 105-109 thymidylate synthetase Homo sapiens 42-44 11156237-0 2000 Thymidylate synthase protein expression in primary colorectal cancer compared with the corresponding distant metastases and relationship with the clinical response to 5-fluorouracil. Fluorouracil 167-181 thymidylate synthetase Homo sapiens 0-20 15608686-5 2005 Similarly, constitutive hTERT expression inhibited wild-type p53-dependent apoptosis in response to mitomycin C or 5-fluorouracil in HCT116 colon carcinoma cells carrying endogenous p53. Fluorouracil 115-129 telomerase reverse transcriptase Homo sapiens 24-29 15670580-1 2005 The inhibition of thymidylate synthase (TS) by 5-fluorouracil (5-FU) was known to increase the incorporation of radiolabelled iododeoxyuridine (IdUrd) into DNA. Fluorouracil 47-61 thymidylate synthetase Homo sapiens 18-38 15670580-1 2005 The inhibition of thymidylate synthase (TS) by 5-fluorouracil (5-FU) was known to increase the incorporation of radiolabelled iododeoxyuridine (IdUrd) into DNA. Fluorouracil 47-61 thymidylate synthetase Homo sapiens 40-42 15670580-1 2005 The inhibition of thymidylate synthase (TS) by 5-fluorouracil (5-FU) was known to increase the incorporation of radiolabelled iododeoxyuridine (IdUrd) into DNA. Fluorouracil 63-67 thymidylate synthetase Homo sapiens 18-38 15670580-1 2005 The inhibition of thymidylate synthase (TS) by 5-fluorouracil (5-FU) was known to increase the incorporation of radiolabelled iododeoxyuridine (IdUrd) into DNA. Fluorouracil 63-67 thymidylate synthetase Homo sapiens 40-42 11156237-1 2000 Thymidylate synthase (TS) expression in colorectal cancer metastases has been shown to predict for the clinical response to 5-fluorouracil. Fluorouracil 124-138 thymidylate synthetase Homo sapiens 0-20 15546879-1 2005 The thymidylate synthase inhibitor 5-fluorouracil (5-FU) is used widely for chemotherapy of colorectal carcinoma. Fluorouracil 35-49 thymidylate synthetase Homo sapiens 4-24 15546879-1 2005 The thymidylate synthase inhibitor 5-fluorouracil (5-FU) is used widely for chemotherapy of colorectal carcinoma. Fluorouracil 51-55 thymidylate synthetase Homo sapiens 4-24 11156237-1 2000 Thymidylate synthase (TS) expression in colorectal cancer metastases has been shown to predict for the clinical response to 5-fluorouracil. Fluorouracil 124-138 thymidylate synthetase Homo sapiens 22-24 15546879-7 2005 Protein and transcriptome expression analysis showed that combined 5-FU and DENSPM treatment activated caspase 9, but not caspase 3, and significantly suppressed NADH dehydrogenases and cytochrome c oxidases, consistent with the observed increase in hydrogen peroxide, loss of mitochondrial membrane potential, and release of cytochrome c. Fluorouracil 67-71 caspase 9 Homo sapiens 103-112 11095583-3 2000 In fourteen cDNA-expressed human P450 enzymes having measurable activities, CYP1A2, CYP2A6, CYP2E1, and CYP3A5 were highly active in catalyzing 5-FU formation at a tegafur concentration of 100 microM. Fluorouracil 144-148 cytochrome P450 family 1 subfamily A member 2 Homo sapiens 76-82 11095583-4 2000 Kinetic analysis revealed that CYP1A2 had the highest V(max)/K(m) value and that the V(max) value of CYP2A6 was high in 5-FU formation. Fluorouracil 120-124 cytochrome P450 family 1 subfamily A member 2 Homo sapiens 31-37 11095583-9 2000 Polyclonal anti-CYP1A2 antibody, monoclonal anti-CYP2A6, and anti-CYP2C8 antibodies inhibited 5-FU formation activities to different extents in those two microsomal samples. Fluorouracil 94-98 cytochrome P450 family 1 subfamily A member 2 Homo sapiens 16-22 15846068-5 2005 Upregulation of RPL6 was associated with enhanced resistance to multiple anticancer drugs (adriamycin, vincristine, etoposide, 5-fluorouracil and cisplatin) and to adriamycin-induced apoptosis. Fluorouracil 127-141 ribosomal protein L6 Homo sapiens 16-20 11095583-10 2000 These results suggest that CYP1A2, CYP2A6, and CYP2C8 have important roles in human liver microsomal 5-FU formation and that the involvement of these three P450 forms differs among individual humans. Fluorouracil 101-105 cytochrome P450 family 1 subfamily A member 2 Homo sapiens 27-33 10975677-0 2000 Antitumoral effect of a nonviral interleukin-2 gene therapy is enhanced by combination with 5-fluorouracil. Fluorouracil 92-106 interleukin 2 Mus musculus 33-46 15770397-0 2005 Expression level of thymidylate synthase is a good predictor of chemosensitivity to 5-fluorouracil in colorectal cancer. Fluorouracil 84-98 thymidylate synthetase Homo sapiens 20-40 15770397-5 2005 RESULTS: A significant increase in the TS expression score was observed in 5-FU-sensitive colorectal cancers (0.57 +/- 0.19) compared to 5-FU-resistant ones (1.16 +/- 0.98; P = 0.029), whereas no significant differences in DPD expression scores were observed in 5-FU-sensitive colorectal cancers (0.86 +/- 1.19) compared to 5-FU-resistant ones (0.56 +/- 1.05; P = 0.603). Fluorouracil 75-79 thymidylate synthetase Homo sapiens 5-7 15655543-6 2005 Quantitative expression levels of drug pathway genes were determined using TaqMan RT-PCR (5-fluorouracil (5-FU): TYMS, DPYD, ECGF1; oxaliplatin: GSTP1 (glutathione S-transferase pi), ERCC1 and 2; irinotecan: ABCB1, ABCG2, CYP3A4, UGT1A1, CES2, TOP1). Fluorouracil 90-104 thymidylate synthetase Homo sapiens 113-117 15655543-6 2005 Quantitative expression levels of drug pathway genes were determined using TaqMan RT-PCR (5-fluorouracil (5-FU): TYMS, DPYD, ECGF1; oxaliplatin: GSTP1 (glutathione S-transferase pi), ERCC1 and 2; irinotecan: ABCB1, ABCG2, CYP3A4, UGT1A1, CES2, TOP1). Fluorouracil 106-110 thymidylate synthetase Homo sapiens 113-117 15695398-9 2005 The present study shows that the CRAd expressing UPRT was a more potent sensitizer of biliary cancer to 5-FU, than was a nonreplicative UPRT-encoding vector or a CRAd without UPRT gene, even at a lower dose of the vector, and that timing of 5-FU administration was a key factor to maximize the efficacy. Fluorouracil 104-108 uracil phosphoribosyltransferase Mus musculus 49-53 15695398-9 2005 The present study shows that the CRAd expressing UPRT was a more potent sensitizer of biliary cancer to 5-FU, than was a nonreplicative UPRT-encoding vector or a CRAd without UPRT gene, even at a lower dose of the vector, and that timing of 5-FU administration was a key factor to maximize the efficacy. Fluorouracil 241-245 uracil phosphoribosyltransferase Mus musculus 49-53 10853017-0 2000 Intratumoral expression of thymidylate synthase and dihydropyrimidine dehydrogenase in non-small cell lung cancer patients treated with 5-FU-based chemotherapy. Fluorouracil 136-140 thymidylate synthetase Homo sapiens 27-47 15638735-2 2005 TS was established as the principal target of the widely used anticancer drug 5-fluorouracil (5FU). Fluorouracil 78-92 thymidylate synthetase Homo sapiens 0-2 15638735-2 2005 TS was established as the principal target of the widely used anticancer drug 5-fluorouracil (5FU). Fluorouracil 94-97 thymidylate synthetase Homo sapiens 0-2 15638735-5 2005 5FU is non-ideal as a TS-inhibitory drug because it is only inefficiently converted to FdUMP, while the remainder of the administered dose is converted to toxic metabolites. Fluorouracil 0-3 thymidylate synthetase Homo sapiens 22-24 15534929-7 2004 PTEN transfection is associated with 5-Fu treatment effect and has a cooperatively cytotoxic effect. Fluorouracil 37-41 phosphatase and tensin homolog Homo sapiens 0-4 15585621-7 2004 5-FU had synergistic effect on TRAIL in HLF and additive effect in four other HCC cell lines. Fluorouracil 0-4 HLF transcription factor, PAR bZIP family member Homo sapiens 40-43 15585621-9 2004 Treatment of effector cells by IFNalpha and target HCC cells by 5-FU enhanced the cytotoxicity of CD14(+) monocytes and CD56(+) NK cells against HCC cells via a TRAIL-mediated pathway. Fluorouracil 64-68 neural cell adhesion molecule 1 Homo sapiens 120-124 15538739-3 2004 Thymidylate synthase (TS), thymidine phosphorylase (TP), and dihydropyrimidine dehydrogenase (DPD) are thought to be important predictors for the efficiency of 5-FU-based treatment. Fluorouracil 160-164 thymidylate synthetase Homo sapiens 0-20 15538739-3 2004 Thymidylate synthase (TS), thymidine phosphorylase (TP), and dihydropyrimidine dehydrogenase (DPD) are thought to be important predictors for the efficiency of 5-FU-based treatment. Fluorouracil 160-164 thymidylate synthetase Homo sapiens 22-24 15538739-4 2004 The aim of this study was to determine the correlation between TS-, TP-, and DPD-gene expression and the response to 5-FU-based long-term pre-operative chemoradiotherapy assessed by histopathological tumour regression. Fluorouracil 117-121 thymidylate synthetase Homo sapiens 63-65 15538739-12 2004 In conclusion, this study shows that TS gene expression in a pretreatment biopsy predicts the response of local rectal cancer to neo-adjuvant 5-FU-based chemoradiotherapy in a high percentage. Fluorouracil 142-146 thymidylate synthetase Homo sapiens 37-39 15585135-7 2004 Our experiments showed that 5-FU engaged the mitochondrial apoptotic pathway involving cytosolic cytochrome c release and subsequent activation of caspase-9 and caspase-3 as well as the membrane death receptor (DR)-mediated apoptotic pathway involving activation of caspase-8 with an Apo-1/CD95 (Fas)-dependent fashion. Fluorouracil 28-32 Fas cell surface death receptor Homo sapiens 284-289 15585135-7 2004 Our experiments showed that 5-FU engaged the mitochondrial apoptotic pathway involving cytosolic cytochrome c release and subsequent activation of caspase-9 and caspase-3 as well as the membrane death receptor (DR)-mediated apoptotic pathway involving activation of caspase-8 with an Apo-1/CD95 (Fas)-dependent fashion. Fluorouracil 28-32 Fas cell surface death receptor Homo sapiens 290-294 15492780-10 2004 High concentrations of CDHP may prevent 5-FU degradation in peritoneal dissemination and its surrounding fibrous tissue. Fluorouracil 40-44 cadherin 3 Mus musculus 23-27 15591457-0 2004 Immunohistochemical evaluation of thymidylate synthase (TS) and p16INK4a in advanced colorectal cancer: implication of TS expression in 5-FU-based adjuvant chemotherapy. Fluorouracil 136-140 thymidylate synthetase Homo sapiens 119-121 15591457-1 2004 BACKGROUND: Our previous analyses on the expression of thymidylate synthase (TS) and p16(INK4a) in colorectal cancer patients administered 5-fluorouracil (5-FU) pre-operatively demonstrated that a high level of TS expression was a predictor of 5-FU resistance, and that the combination of a low level of TS expression and induction of p16(INK4a) after chemotherapy implicated chemosensitivity. Fluorouracil 139-153 thymidylate synthetase Homo sapiens 55-75 15591457-1 2004 BACKGROUND: Our previous analyses on the expression of thymidylate synthase (TS) and p16(INK4a) in colorectal cancer patients administered 5-fluorouracil (5-FU) pre-operatively demonstrated that a high level of TS expression was a predictor of 5-FU resistance, and that the combination of a low level of TS expression and induction of p16(INK4a) after chemotherapy implicated chemosensitivity. Fluorouracil 139-153 thymidylate synthetase Homo sapiens 77-79 15591457-1 2004 BACKGROUND: Our previous analyses on the expression of thymidylate synthase (TS) and p16(INK4a) in colorectal cancer patients administered 5-fluorouracil (5-FU) pre-operatively demonstrated that a high level of TS expression was a predictor of 5-FU resistance, and that the combination of a low level of TS expression and induction of p16(INK4a) after chemotherapy implicated chemosensitivity. Fluorouracil 139-153 thymidylate synthetase Homo sapiens 211-213 15591457-1 2004 BACKGROUND: Our previous analyses on the expression of thymidylate synthase (TS) and p16(INK4a) in colorectal cancer patients administered 5-fluorouracil (5-FU) pre-operatively demonstrated that a high level of TS expression was a predictor of 5-FU resistance, and that the combination of a low level of TS expression and induction of p16(INK4a) after chemotherapy implicated chemosensitivity. Fluorouracil 139-153 thymidylate synthetase Homo sapiens 211-213 15591457-1 2004 BACKGROUND: Our previous analyses on the expression of thymidylate synthase (TS) and p16(INK4a) in colorectal cancer patients administered 5-fluorouracil (5-FU) pre-operatively demonstrated that a high level of TS expression was a predictor of 5-FU resistance, and that the combination of a low level of TS expression and induction of p16(INK4a) after chemotherapy implicated chemosensitivity. Fluorouracil 155-159 thymidylate synthetase Homo sapiens 55-75 15591457-1 2004 BACKGROUND: Our previous analyses on the expression of thymidylate synthase (TS) and p16(INK4a) in colorectal cancer patients administered 5-fluorouracil (5-FU) pre-operatively demonstrated that a high level of TS expression was a predictor of 5-FU resistance, and that the combination of a low level of TS expression and induction of p16(INK4a) after chemotherapy implicated chemosensitivity. Fluorouracil 155-159 thymidylate synthetase Homo sapiens 77-79 15591457-1 2004 BACKGROUND: Our previous analyses on the expression of thymidylate synthase (TS) and p16(INK4a) in colorectal cancer patients administered 5-fluorouracil (5-FU) pre-operatively demonstrated that a high level of TS expression was a predictor of 5-FU resistance, and that the combination of a low level of TS expression and induction of p16(INK4a) after chemotherapy implicated chemosensitivity. Fluorouracil 155-159 thymidylate synthetase Homo sapiens 211-213 15591457-1 2004 BACKGROUND: Our previous analyses on the expression of thymidylate synthase (TS) and p16(INK4a) in colorectal cancer patients administered 5-fluorouracil (5-FU) pre-operatively demonstrated that a high level of TS expression was a predictor of 5-FU resistance, and that the combination of a low level of TS expression and induction of p16(INK4a) after chemotherapy implicated chemosensitivity. Fluorouracil 155-159 thymidylate synthetase Homo sapiens 211-213 15591457-1 2004 BACKGROUND: Our previous analyses on the expression of thymidylate synthase (TS) and p16(INK4a) in colorectal cancer patients administered 5-fluorouracil (5-FU) pre-operatively demonstrated that a high level of TS expression was a predictor of 5-FU resistance, and that the combination of a low level of TS expression and induction of p16(INK4a) after chemotherapy implicated chemosensitivity. Fluorouracil 244-248 thymidylate synthetase Homo sapiens 55-75 15591457-1 2004 BACKGROUND: Our previous analyses on the expression of thymidylate synthase (TS) and p16(INK4a) in colorectal cancer patients administered 5-fluorouracil (5-FU) pre-operatively demonstrated that a high level of TS expression was a predictor of 5-FU resistance, and that the combination of a low level of TS expression and induction of p16(INK4a) after chemotherapy implicated chemosensitivity. Fluorouracil 244-248 thymidylate synthetase Homo sapiens 77-79 15591457-2 2004 The present study aimed to assess the relationship between the biological behavior of advanced colorectal cancer treated post-operatively by 5-FU-based chemotherapy and the expression of TS and p16(INK4a) in primary tumors. Fluorouracil 141-145 thymidylate synthetase Homo sapiens 187-189 15591457-10 2004 We suggest that, in the Dukes" C group, a 5-FU-based regimen can be chosen as a first-line chemotherapy for low TS expressors. Fluorouracil 42-46 thymidylate synthetase Homo sapiens 112-114 15571286-1 2004 The action of 5-Fluorouracil (5-FU) is mediated by inhibition of thymidylate synthase (TS), which is regulated by cell cycle proteins controlled by protein phosphorylation. Fluorouracil 14-28 thymidylate synthetase Homo sapiens 65-85 15571286-1 2004 The action of 5-Fluorouracil (5-FU) is mediated by inhibition of thymidylate synthase (TS), which is regulated by cell cycle proteins controlled by protein phosphorylation. Fluorouracil 30-34 thymidylate synthetase Homo sapiens 65-85 15571286-2 2004 We studied the effects of staurosporine and its analogue UCN-01, inhibitors of protein kinase C (PKC) on 5-FU cytotoxicity in Lovo colon cancer cells. Fluorouracil 105-109 urocortin Homo sapiens 57-60 15262975-0 2004 Antiapoptotic protein partners fortilin and MCL1 independently protect cells from 5-fluorouracil-induced cytotoxicity. Fluorouracil 82-96 tumor protein, translationally-controlled 1 Homo sapiens 31-39 15262975-0 2004 Antiapoptotic protein partners fortilin and MCL1 independently protect cells from 5-fluorouracil-induced cytotoxicity. Fluorouracil 82-96 MCL1 apoptosis regulator, BCL2 family member Homo sapiens 44-48 15262975-10 2004 When MCL1 was silenced by MCL1-targeted siRNA, fortilin was still able to protect cells from 5-FU-induced cytotoxicity in a dose-dependent manner. Fluorouracil 93-97 MCL1 apoptosis regulator, BCL2 family member Homo sapiens 5-9 15262975-10 2004 When MCL1 was silenced by MCL1-targeted siRNA, fortilin was still able to protect cells from 5-FU-induced cytotoxicity in a dose-dependent manner. Fluorouracil 93-97 MCL1 apoptosis regulator, BCL2 family member Homo sapiens 26-30 15262975-10 2004 When MCL1 was silenced by MCL1-targeted siRNA, fortilin was still able to protect cells from 5-FU-induced cytotoxicity in a dose-dependent manner. Fluorouracil 93-97 tumor protein, translationally-controlled 1 Homo sapiens 47-55 15262975-11 2004 Conversely, when fortilin was silenced by fortilin-targeted siRNA, MCL1 was also able to protect cells from 5-FU-induced cytotoxicity in a dose-dependent manner. Fluorouracil 108-112 tumor protein, translationally-controlled 1 Homo sapiens 17-25 15262975-11 2004 Conversely, when fortilin was silenced by fortilin-targeted siRNA, MCL1 was also able to protect cells from 5-FU-induced cytotoxicity in a dose-dependent manner. Fluorouracil 108-112 MCL1 apoptosis regulator, BCL2 family member Homo sapiens 67-71 15374982-0 2004 Inducible silencing of KILLER/DR5 in vivo promotes bioluminescent colon tumor xenograft growth and confers resistance to chemotherapeutic agent 5-fluorouracil. Fluorouracil 144-158 TNF receptor superfamily member 10b Homo sapiens 23-33 15342418-7 2004 P21Cip1, cdk1, cdk2, and cyclin E mRNA expression increased coincident with S-phase accumulation in HT29 cells treated with ZD9331 or 5fluorouracil/leucovorin, as demonstrated by cDNA microarray analyses. Fluorouracil 134-147 cyclin dependent kinase 1 Homo sapiens 9-13 15353301-1 2004 Cancer drugs such as 5-fluorouracil (5-FU) that target the enzyme thymidylate synthase (TS) have been and are still being widely used in cancer treatment, but as with other anti-cancer drugs, the majority of tumors do not respond to the treatment, whereas the patients still suffer drug-related toxicity. Fluorouracil 21-35 thymidylate synthetase Homo sapiens 66-86 15353301-1 2004 Cancer drugs such as 5-fluorouracil (5-FU) that target the enzyme thymidylate synthase (TS) have been and are still being widely used in cancer treatment, but as with other anti-cancer drugs, the majority of tumors do not respond to the treatment, whereas the patients still suffer drug-related toxicity. Fluorouracil 21-35 thymidylate synthetase Homo sapiens 88-90 15353301-1 2004 Cancer drugs such as 5-fluorouracil (5-FU) that target the enzyme thymidylate synthase (TS) have been and are still being widely used in cancer treatment, but as with other anti-cancer drugs, the majority of tumors do not respond to the treatment, whereas the patients still suffer drug-related toxicity. Fluorouracil 37-41 thymidylate synthetase Homo sapiens 66-86 15353301-1 2004 Cancer drugs such as 5-fluorouracil (5-FU) that target the enzyme thymidylate synthase (TS) have been and are still being widely used in cancer treatment, but as with other anti-cancer drugs, the majority of tumors do not respond to the treatment, whereas the patients still suffer drug-related toxicity. Fluorouracil 37-41 thymidylate synthetase Homo sapiens 88-90 15353301-5 2004 Thus, considerable interest was generated by data suggesting that the variable number of a 28 base-pair (bp) segment in the promoter region of the TS gene was associated with TS gene expression and/or protein expression, as well as with tumor response to 5-FU therapy, toxicity and patient survival. Fluorouracil 255-259 thymidylate synthetase Homo sapiens 147-149 10785598-1 2000 Inhibition of the key enzyme in DNA synthesis, thymidylate synthase (TS), by 5-fluorouracil (5-FU) and the novel antifolate raltitrexed (Tomudex; ZD1694), induces dTTP depletion, resulting in DNA strand breaks, which can initiate pathways leading to an apoptotic mode of cell death. Fluorouracil 77-91 thymidylate synthetase Homo sapiens 47-67 10785598-1 2000 Inhibition of the key enzyme in DNA synthesis, thymidylate synthase (TS), by 5-fluorouracil (5-FU) and the novel antifolate raltitrexed (Tomudex; ZD1694), induces dTTP depletion, resulting in DNA strand breaks, which can initiate pathways leading to an apoptotic mode of cell death. Fluorouracil 77-91 thymidylate synthetase Homo sapiens 69-71 10785598-1 2000 Inhibition of the key enzyme in DNA synthesis, thymidylate synthase (TS), by 5-fluorouracil (5-FU) and the novel antifolate raltitrexed (Tomudex; ZD1694), induces dTTP depletion, resulting in DNA strand breaks, which can initiate pathways leading to an apoptotic mode of cell death. Fluorouracil 93-97 thymidylate synthetase Homo sapiens 47-67 10785598-1 2000 Inhibition of the key enzyme in DNA synthesis, thymidylate synthase (TS), by 5-fluorouracil (5-FU) and the novel antifolate raltitrexed (Tomudex; ZD1694), induces dTTP depletion, resulting in DNA strand breaks, which can initiate pathways leading to an apoptotic mode of cell death. Fluorouracil 93-97 thymidylate synthetase Homo sapiens 69-71 10785598-2 2000 We studied 5-FU- and ZD1694-induced TS inhibition in relation to the expression of p53, p21, Bcl-2 and Bax in six colon carcinoma cell lines, two with a wild-type (wt) p53 (Lovo, LS174T) and four with a mutant (mt) p53 (WiDr, WiDr/F, HT29 and SW948) phenotype. Fluorouracil 11-15 thymidylate synthetase Homo sapiens 36-38 10785598-4 2000 Exposure to 5-FU (50 and 100 microM) and ZD1694 (50 and 100 nM) for 24 and 48 h induced p53 and p21 expression in wt p53 cells, but not in mt p53 cells. Fluorouracil 12-16 H3 histone pseudogene 16 Homo sapiens 96-99 10785598-7 2000 After 5-FU treatment, TS was present both as the free enzyme and in the ternary complex; however, predominantly as the ternary complex between TS, FdUMP and 5,10-methylenetetrahydrofolate. Fluorouracil 6-10 thymidylate synthetase Homo sapiens 22-24 10777249-2 2000 Treatment with 5-FU lowered the activities of cardiac superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) accompanied by higher catalase (CAT) activity. Fluorouracil 15-19 catalase Cavia porcellus 139-147 10777249-2 2000 Treatment with 5-FU lowered the activities of cardiac superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) accompanied by higher catalase (CAT) activity. Fluorouracil 15-19 catalase Cavia porcellus 149-152 10791849-1 2000 BACKGROUND: Thymidylate synthase (TS) is regarded as a parameter of 5-fluorouracil (5-FU) chemosensitivity for colorectal carcinoma. Fluorouracil 68-82 thymidylate synthetase Homo sapiens 12-32 10791849-1 2000 BACKGROUND: Thymidylate synthase (TS) is regarded as a parameter of 5-fluorouracil (5-FU) chemosensitivity for colorectal carcinoma. Fluorouracil 68-82 thymidylate synthetase Homo sapiens 34-36 10791849-1 2000 BACKGROUND: Thymidylate synthase (TS) is regarded as a parameter of 5-fluorouracil (5-FU) chemosensitivity for colorectal carcinoma. Fluorouracil 84-88 thymidylate synthetase Homo sapiens 12-32 10791849-1 2000 BACKGROUND: Thymidylate synthase (TS) is regarded as a parameter of 5-fluorouracil (5-FU) chemosensitivity for colorectal carcinoma. Fluorouracil 84-88 thymidylate synthetase Homo sapiens 34-36 10791849-2 2000 Recent researchers indicate that the chemosensitivity of 5-FU for colorectal carcinoma with low expression of TS is better than tumors with high expression of TS. Fluorouracil 57-61 thymidylate synthetase Homo sapiens 110-112 10791849-11 2000 CONCLUSIONS: TS, itself, may be a prognostic factor for colon carcinoma; and 5-FU adjuvant chemotherapy may be appropriate for colon carcinoma with high expression of TS. Fluorouracil 77-81 thymidylate synthetase Homo sapiens 167-169 10725316-7 2000 In rats, DPD was predicted to be completely inactivated by administration of BVU and the area under the curve of 5-FU was predicted to increase 11-fold, which agreed well with the reported data. Fluorouracil 113-117 dihydropyrimidine dehydrogenase Rattus norvegicus 9-12 15197779-0 2004 Topoisomerase-I, thymidylate synthase primary tumour expression and clinical efficacy of 5-FU/CPT-11 chemotherapy in advanced colorectal cancer patients. Fluorouracil 89-93 thymidylate synthetase Homo sapiens 17-37 15197779-1 2004 While several studies have reported that thymidylate synthase (TS) tumour expression can be a reliable predictive marker of clinical response to 5-Fluorouracil (5-FU) for advanced colorectal cancer patients, only a few studies that searched for predictive factors of irinotecan (CPT-11) clinical response are available. Fluorouracil 145-159 thymidylate synthetase Homo sapiens 41-61 15197779-1 2004 While several studies have reported that thymidylate synthase (TS) tumour expression can be a reliable predictive marker of clinical response to 5-Fluorouracil (5-FU) for advanced colorectal cancer patients, only a few studies that searched for predictive factors of irinotecan (CPT-11) clinical response are available. Fluorouracil 161-165 thymidylate synthetase Homo sapiens 41-61 10789559-12 2000 CONCLUSION: In our experience single agent, weekly, high dose 5-FU is well tolerated, but is ineffective as second-line treatment for metastatic colorectal cancer, and has only a marginal effect on CEA level. Fluorouracil 62-66 CEA cell adhesion molecule 5 Homo sapiens 198-201 15205195-0 2004 5-Fluorouracil incorporation into RNA and DNA in relation to thymidylate synthase inhibition of human colorectal cancers. Fluorouracil 0-14 thymidylate synthetase Homo sapiens 61-81 15205195-1 2004 BACKGROUND: The mechanism of action of 5-fluorouracil (5-FU) has been associated with inhibition of thymidylate synthase (TS) and incorporation of 5-FU into RNA and DNA, but limited data are available in human tumor tissue for the latter. Fluorouracil 39-53 thymidylate synthetase Homo sapiens 100-120 15205195-1 2004 BACKGROUND: The mechanism of action of 5-fluorouracil (5-FU) has been associated with inhibition of thymidylate synthase (TS) and incorporation of 5-FU into RNA and DNA, but limited data are available in human tumor tissue for the latter. Fluorouracil 39-53 thymidylate synthetase Homo sapiens 122-124 15205195-1 2004 BACKGROUND: The mechanism of action of 5-fluorouracil (5-FU) has been associated with inhibition of thymidylate synthase (TS) and incorporation of 5-FU into RNA and DNA, but limited data are available in human tumor tissue for the latter. Fluorouracil 55-59 thymidylate synthetase Homo sapiens 100-120 15205195-1 2004 BACKGROUND: The mechanism of action of 5-fluorouracil (5-FU) has been associated with inhibition of thymidylate synthase (TS) and incorporation of 5-FU into RNA and DNA, but limited data are available in human tumor tissue for the latter. Fluorouracil 55-59 thymidylate synthetase Homo sapiens 122-124 10639590-1 2000 The expression of thymidylate synthase (TS) in human cancer tissues has been suggested to be a prognostic factor for patients receiving 5-fluorouracil-based chemotherapy. Fluorouracil 136-150 thymidylate synthetase Homo sapiens 18-38 10639590-1 2000 The expression of thymidylate synthase (TS) in human cancer tissues has been suggested to be a prognostic factor for patients receiving 5-fluorouracil-based chemotherapy. Fluorouracil 136-150 thymidylate synthetase Homo sapiens 40-42 10752654-0 2000 Changes in thymidylate synthase mRNA in blood leukocytes from patients with colorectal cancer after bolus administration of 5-fluorouracil. Fluorouracil 124-138 thymidylate synthetase Homo sapiens 11-31 10752654-4 2000 bolus 5-FU 500-600 mg/m2 on the 5-FU target enzyme, thymidylate synthase (TS) mRNA, in blood leukocytes before and after courses 1 and 3 in 21 patients with colorectal cancer. Fluorouracil 6-10 thymidylate synthetase Homo sapiens 52-72 10752654-4 2000 bolus 5-FU 500-600 mg/m2 on the 5-FU target enzyme, thymidylate synthase (TS) mRNA, in blood leukocytes before and after courses 1 and 3 in 21 patients with colorectal cancer. Fluorouracil 6-10 thymidylate synthetase Homo sapiens 74-76 11129987-3 2000 When the MTX and 5-FU concentrations are 10 microM, antiproliferative effects of MTX 2 hr before 5-FU (MTX/5-FU) and 5-FU 2 h before MTX (5-FU/MTX) are 25.17+/-1.23% and 25.60+/-1.28% of the control rate, respectively. Fluorouracil 17-21 metaxin 1 Homo sapiens 81-84 11129987-3 2000 When the MTX and 5-FU concentrations are 10 microM, antiproliferative effects of MTX 2 hr before 5-FU (MTX/5-FU) and 5-FU 2 h before MTX (5-FU/MTX) are 25.17+/-1.23% and 25.60+/-1.28% of the control rate, respectively. Fluorouracil 17-21 metaxin 1 Homo sapiens 81-84 11129987-5 2000 The growth rates of MDA-MB-436 cells in 100 microM MTX and 10 microM 5-FU are 15.19+/-0.62% (MTX/5-FU) and 16.53+/-0.85% (5-FU/MTX) of the control rate. Fluorouracil 69-73 metaxin 1 Homo sapiens 93-96 11129987-5 2000 The growth rates of MDA-MB-436 cells in 100 microM MTX and 10 microM 5-FU are 15.19+/-0.62% (MTX/5-FU) and 16.53+/-0.85% (5-FU/MTX) of the control rate. Fluorouracil 69-73 metaxin 1 Homo sapiens 93-96 11129987-5 2000 The growth rates of MDA-MB-436 cells in 100 microM MTX and 10 microM 5-FU are 15.19+/-0.62% (MTX/5-FU) and 16.53+/-0.85% (5-FU/MTX) of the control rate. Fluorouracil 97-101 metaxin 1 Homo sapiens 51-54 11129987-5 2000 The growth rates of MDA-MB-436 cells in 100 microM MTX and 10 microM 5-FU are 15.19+/-0.62% (MTX/5-FU) and 16.53+/-0.85% (5-FU/MTX) of the control rate. Fluorouracil 97-101 metaxin 1 Homo sapiens 51-54 11417748-1 2000 Thymidylate synthase (TS) is an important target for chemotherapy and can be inhibited by 5-fluorouracil (5-FU) and the antifolates, AG337 (Nolatrexed) and multitargeted antifolate (MTA or Pemetrexed). Fluorouracil 90-104 thymidylate synthetase Homo sapiens 0-20 11417748-1 2000 Thymidylate synthase (TS) is an important target for chemotherapy and can be inhibited by 5-fluorouracil (5-FU) and the antifolates, AG337 (Nolatrexed) and multitargeted antifolate (MTA or Pemetrexed). Fluorouracil 90-104 thymidylate synthetase Homo sapiens 22-24 11417748-1 2000 Thymidylate synthase (TS) is an important target for chemotherapy and can be inhibited by 5-fluorouracil (5-FU) and the antifolates, AG337 (Nolatrexed) and multitargeted antifolate (MTA or Pemetrexed). Fluorouracil 106-110 thymidylate synthetase Homo sapiens 0-20 11417748-1 2000 Thymidylate synthase (TS) is an important target for chemotherapy and can be inhibited by 5-fluorouracil (5-FU) and the antifolates, AG337 (Nolatrexed) and multitargeted antifolate (MTA or Pemetrexed). Fluorouracil 106-110 thymidylate synthetase Homo sapiens 22-24 10643981-4 2000 p53 function was determined to be defective in each cell line as indicated by the lack of induction of p53-responsive genes, p21 and mdm2, following treatment with 5-fluorouracil. Fluorouracil 164-178 transformation related protein 53, pseudogene Mus musculus 0-3 15272584-6 2004 The DPD activity of mucinous adenocarcinoma is related to catabolism of 5-FU is equal to that of adenocarcinoma, however, the OPRT activity is related to a main pathway of 5-FU phosphorylation is significantly lower. Fluorouracil 172-176 uridine monophosphate synthetase Homo sapiens 126-130 15114696-2 2004 Dihydropyrimidine dehydrogenase (DPD) which catalyzes 5-fluorouracil (5-FU), thymidine phosphorylase (TP), responsible for catalyzing doxifluridine to 5-FU, and thymidylate synthase (TS) were estimated for breast cancer. Fluorouracil 54-68 thymidylate synthetase Homo sapiens 161-181 15114696-2 2004 Dihydropyrimidine dehydrogenase (DPD) which catalyzes 5-fluorouracil (5-FU), thymidine phosphorylase (TP), responsible for catalyzing doxifluridine to 5-FU, and thymidylate synthase (TS) were estimated for breast cancer. Fluorouracil 54-68 thymidylate synthetase Homo sapiens 183-185 15114696-2 2004 Dihydropyrimidine dehydrogenase (DPD) which catalyzes 5-fluorouracil (5-FU), thymidine phosphorylase (TP), responsible for catalyzing doxifluridine to 5-FU, and thymidylate synthase (TS) were estimated for breast cancer. Fluorouracil 70-74 thymidylate synthetase Homo sapiens 161-181 15114696-2 2004 Dihydropyrimidine dehydrogenase (DPD) which catalyzes 5-fluorouracil (5-FU), thymidine phosphorylase (TP), responsible for catalyzing doxifluridine to 5-FU, and thymidylate synthase (TS) were estimated for breast cancer. Fluorouracil 70-74 thymidylate synthetase Homo sapiens 183-185 15114696-2 2004 Dihydropyrimidine dehydrogenase (DPD) which catalyzes 5-fluorouracil (5-FU), thymidine phosphorylase (TP), responsible for catalyzing doxifluridine to 5-FU, and thymidylate synthase (TS) were estimated for breast cancer. Fluorouracil 151-155 thymidylate synthetase Homo sapiens 161-181 15114696-2 2004 Dihydropyrimidine dehydrogenase (DPD) which catalyzes 5-fluorouracil (5-FU), thymidine phosphorylase (TP), responsible for catalyzing doxifluridine to 5-FU, and thymidylate synthase (TS) were estimated for breast cancer. Fluorouracil 151-155 thymidylate synthetase Homo sapiens 183-185 14770427-2 2004 5-FU is a prodrug, and orotate phosphoribosyltransferase (OPRT) is the principal enzyme that converts 5-FU directly into an active antitumor metabolite, 5-fluoro-2"-deoxyuridine 5"-monophosphate. Fluorouracil 0-4 uridine monophosphate synthetase Homo sapiens 58-62 14770427-2 2004 5-FU is a prodrug, and orotate phosphoribosyltransferase (OPRT) is the principal enzyme that converts 5-FU directly into an active antitumor metabolite, 5-fluoro-2"-deoxyuridine 5"-monophosphate. Fluorouracil 102-106 uridine monophosphate synthetase Homo sapiens 23-56 14770427-2 2004 5-FU is a prodrug, and orotate phosphoribosyltransferase (OPRT) is the principal enzyme that converts 5-FU directly into an active antitumor metabolite, 5-fluoro-2"-deoxyuridine 5"-monophosphate. Fluorouracil 102-106 uridine monophosphate synthetase Homo sapiens 58-62 14770427-7 2004 METHODS: OPRT activity levels in nonfixed, fresh-frozen specimens of bladder carcinoma and normal bladder were determined enzymatically using a 5-FU phosphorylation assay. Fluorouracil 144-148 uridine monophosphate synthetase Homo sapiens 9-13 14770427-15 2004 OPRT activity in bladder carcinoma cells was correlated positively with their sensitivity to 5-FU. Fluorouracil 93-97 uridine monophosphate synthetase Homo sapiens 0-4 14770427-17 2004 In addition, high OPRT activity levels in patients with superficial bladder carcinoma predicted early recurrence and high sensitivity to 5-FU. Fluorouracil 137-141 uridine monophosphate synthetase Homo sapiens 18-22 10643981-4 2000 p53 function was determined to be defective in each cell line as indicated by the lack of induction of p53-responsive genes, p21 and mdm2, following treatment with 5-fluorouracil. Fluorouracil 164-178 transformed mouse 3T3 cell double minute 2 Mus musculus 133-137 10592098-5 1999 Apoptosis within primary tumors and lung metastatic foci, as detected by the terminal-deoxynucleotidyltransferase-mediated dUTP nick-end labeling method, was found to be significantly enhanced by HCFU as well as 5-FU administration at doses of more than 100 mg kg(-1) day(-1) and 50 mg kg(-1) day(-1) respectively. Fluorouracil 212-216 deoxynucleotidyltransferase, terminal Mus musculus 77-113 10515856-5 1999 We then observed that, after the injection of 150 mg/kg 5-fluorouracil (5-FU), stem cells may be found in both CD34(-) and CD34(+) cell populations. Fluorouracil 56-70 CD34 antigen Mus musculus 111-115 14770427-18 2004 These results suggest that the level of OPRT activity may be used both as a prognostic parameter and as a predictive indicator for 5-FU efficacy in patients with bladder carcinoma and that OPRT may be a molecular therapeutic target in bladder carcinoma. Fluorouracil 131-135 uridine monophosphate synthetase Homo sapiens 40-44 14713770-2 2004 It is a prodrug and orotate phosphoribosyltransferase (OPRT) is the principal enzyme that directly converts 5-FU to the active anticancer metabolite 5-fluoro-2"-deoxyuridine 5"-monophosphate. Fluorouracil 108-112 uridine monophosphate synthetase Homo sapiens 20-53 14713770-2 2004 It is a prodrug and orotate phosphoribosyltransferase (OPRT) is the principal enzyme that directly converts 5-FU to the active anticancer metabolite 5-fluoro-2"-deoxyuridine 5"-monophosphate. Fluorouracil 108-112 uridine monophosphate synthetase Homo sapiens 55-59 14713770-6 2004 The relationship between OPRT activity in RCC cells and their sensitivity to 5-FU was also examined. Fluorouracil 77-81 uridine monophosphate synthetase Homo sapiens 25-29 14713770-7 2004 MATERIALS AND METHODS: OPRT activity in nonfixed, fresh frozen RCC and normal kidney was determined enzymatically by the 5-FU phosphorylation assay. Fluorouracil 121-125 uridine monophosphate synthetase Homo sapiens 23-27 14713770-13 2004 OPRT activity in RCC cells positively correlated with their sensitivity to 5-FU. Fluorouracil 75-79 uridine monophosphate synthetase Homo sapiens 0-4 14713770-15 2004 In addition, higher OPRT activity in RCC predicted worse prognosis and higher sensitivity to 5-FU. Fluorouracil 93-97 uridine monophosphate synthetase Homo sapiens 20-24 14713770-16 2004 These results suggest that the level of OPRT activity may be used as a prognostic parameter and predictive indicator for 5-FU efficacy in RCC and OPRT may be a molecular therapeutic target in RCC. Fluorouracil 121-125 uridine monophosphate synthetase Homo sapiens 40-44 14716816-0 2004 Correlation of thymidylate synthase, thymidine phosphorylase and dihydropyrimidine dehydrogenase with sensitivity of gastrointestinal cancer cells to 5-fluorouracil and 5-fluoro-2"-deoxyuridine. Fluorouracil 150-164 thymidylate synthetase Homo sapiens 15-35 14716816-1 2004 AIM: To determine the expression levels of three metabolic enzymes of fluoropyrimidines: thymidylate synthase (TS), thymidine phosphorylase (TP) and dihydropyrimidine dehydrogenase (DPD) in seven human gastrointestinal cancer cell lines, and to compare the enzyme levels with the sensitivity to 5-fluorouracil (5-FU) and 5-fluoro-2"-deoxyuridine (FdUrd). Fluorouracil 295-309 thymidylate synthetase Homo sapiens 89-109 14716816-1 2004 AIM: To determine the expression levels of three metabolic enzymes of fluoropyrimidines: thymidylate synthase (TS), thymidine phosphorylase (TP) and dihydropyrimidine dehydrogenase (DPD) in seven human gastrointestinal cancer cell lines, and to compare the enzyme levels with the sensitivity to 5-fluorouracil (5-FU) and 5-fluoro-2"-deoxyuridine (FdUrd). Fluorouracil 311-315 thymidylate synthetase Homo sapiens 89-109 14679120-1 2004 BACKGROUND: The level of the enzyme thymidylate synthase (TS) is known to inversely correlate with the clinical activity of 5-fluorouracil (FU) in advanced colorectal cancer patients. Fluorouracil 124-138 thymidylate synthetase Homo sapiens 36-56 15001844-6 2004 However, Neu5Ac-Gal-IL-1alpha exhibited comparable activity to IL-1alpha in improvement of the recovery of peripheral white blood cells from myelosuppression in 5-fluorouracil-treated mice. Fluorouracil 161-175 interleukin 1 alpha Homo sapiens 20-29 15001844-6 2004 However, Neu5Ac-Gal-IL-1alpha exhibited comparable activity to IL-1alpha in improvement of the recovery of peripheral white blood cells from myelosuppression in 5-fluorouracil-treated mice. Fluorouracil 161-175 interleukin 1 alpha Mus musculus 63-72 14654960-0 2004 The transfection of thymidylate synthase antisense suppresses oncogenic properties of a human colon cancer cell line and augments the antitumor effect of fluorouracil. Fluorouracil 154-166 thymidylate synthetase Homo sapiens 20-40 14654960-3 2004 The aim of this study was to determine if antisense TS technology could augment the chemosensitivity of human cancer cells to 5-FU. Fluorouracil 126-130 thymidylate synthetase Homo sapiens 52-54 14654960-8 2004 The 50% inhibition values of 5-FU on DLD-1/anti-TS were approximately one forth that on parental cells. Fluorouracil 29-33 thymidylate synthetase Homo sapiens 48-50 14654960-10 2004 The tumor growth of DLD-1/anti-TS cells was suppressed significantly more than that of DLD-1 cells by the 5-FU. Fluorouracil 106-110 thymidylate synthetase Homo sapiens 31-33 14654960-11 2004 The expression and activity of TS in human colon cancer cells were effectively inhibited by TS antisense treatment and the effect of 5-FU to cancer cells can be augmented. Fluorouracil 133-137 thymidylate synthetase Homo sapiens 31-33 14703431-1 2003 OBJECTIVE: To investigate the relationship between apoptosis induced by CD3epsilon and 5-fluorouracil (5-FU), and study the P53 expression in the apoptosis process provide a novel insight and useful information of the apoptosis signaling pathway induced by CD3epsilon and/or 5-FU, and an important implication for the treatment of T-lymphocyte leukemia. Fluorouracil 87-101 CD3 epsilon subunit of T-cell receptor complex Homo sapiens 72-82 14703431-1 2003 OBJECTIVE: To investigate the relationship between apoptosis induced by CD3epsilon and 5-fluorouracil (5-FU), and study the P53 expression in the apoptosis process provide a novel insight and useful information of the apoptosis signaling pathway induced by CD3epsilon and/or 5-FU, and an important implication for the treatment of T-lymphocyte leukemia. Fluorouracil 103-107 CD3 epsilon subunit of T-cell receptor complex Homo sapiens 72-82 14703431-1 2003 OBJECTIVE: To investigate the relationship between apoptosis induced by CD3epsilon and 5-fluorouracil (5-FU), and study the P53 expression in the apoptosis process provide a novel insight and useful information of the apoptosis signaling pathway induced by CD3epsilon and/or 5-FU, and an important implication for the treatment of T-lymphocyte leukemia. Fluorouracil 103-107 CD3 epsilon subunit of T-cell receptor complex Homo sapiens 257-267 14703431-1 2003 OBJECTIVE: To investigate the relationship between apoptosis induced by CD3epsilon and 5-fluorouracil (5-FU), and study the P53 expression in the apoptosis process provide a novel insight and useful information of the apoptosis signaling pathway induced by CD3epsilon and/or 5-FU, and an important implication for the treatment of T-lymphocyte leukemia. Fluorouracil 275-279 CD3 epsilon subunit of T-cell receptor complex Homo sapiens 72-82 14703431-8 2003 CONCLUSION: Co-treatment of CD3epsilon and 5-FU increases the apoptosis and p53 expression, suggesting that there is a synergetic role of CD3epsilon and 5-FU on T lymphocytes. Fluorouracil 153-157 CD3 epsilon subunit of T-cell receptor complex Homo sapiens 28-38 14570375-1 2003 Although the expression of thymidylate synthase (TS) in metastatic colorectal cancer (CRC) may be a better predictor of response to 5-fluorouracil chemotherapy than TS expression in primary CRC, this enzyme has not been well studied in tumor-draining regional lymph nodes. Fluorouracil 132-146 thymidylate synthetase Homo sapiens 27-47 14570375-1 2003 Although the expression of thymidylate synthase (TS) in metastatic colorectal cancer (CRC) may be a better predictor of response to 5-fluorouracil chemotherapy than TS expression in primary CRC, this enzyme has not been well studied in tumor-draining regional lymph nodes. Fluorouracil 132-146 thymidylate synthetase Homo sapiens 49-51 14570375-9 2003 Nodal expression of TS may be important in predicting response to 5-fluorouracil when a primary CRC is TS-negative. Fluorouracil 66-80 thymidylate synthetase Homo sapiens 20-22 14570375-9 2003 Nodal expression of TS may be important in predicting response to 5-fluorouracil when a primary CRC is TS-negative. Fluorouracil 66-80 thymidylate synthetase Homo sapiens 103-105 14519634-0 2003 Thymidylate synthase and dihydropyrimidine dehydrogenase mRNA expression levels: predictors for survival in colorectal cancer patients receiving adjuvant 5-fluorouracil. Fluorouracil 154-168 thymidylate synthetase Homo sapiens 0-20 14519634-2 2003 In this study, we determined the prognostic value of thymidylate synthase (TS) and dihydropyrimidine dehydrogenase (DPD) expression in colorectal cancer patients treated with adjuvant 5-FU. Fluorouracil 184-188 thymidylate synthetase Homo sapiens 53-73 14519634-2 2003 In this study, we determined the prognostic value of thymidylate synthase (TS) and dihydropyrimidine dehydrogenase (DPD) expression in colorectal cancer patients treated with adjuvant 5-FU. Fluorouracil 184-188 thymidylate synthetase Homo sapiens 75-77 14519634-7 2003 Among the patients receiving adjuvant 5-FU therapy, those with high TS survived longer than those with low TS, and in each TS subgroup, the ones with low DPD survived longer than the ones with high DPD levels. Fluorouracil 38-42 thymidylate synthetase Homo sapiens 68-70 14519634-7 2003 Among the patients receiving adjuvant 5-FU therapy, those with high TS survived longer than those with low TS, and in each TS subgroup, the ones with low DPD survived longer than the ones with high DPD levels. Fluorouracil 38-42 thymidylate synthetase Homo sapiens 107-109 14519634-7 2003 Among the patients receiving adjuvant 5-FU therapy, those with high TS survived longer than those with low TS, and in each TS subgroup, the ones with low DPD survived longer than the ones with high DPD levels. Fluorouracil 38-42 thymidylate synthetase Homo sapiens 107-109 10515856-5 1999 We then observed that, after the injection of 150 mg/kg 5-fluorouracil (5-FU), stem cells may be found in both CD34(-) and CD34(+) cell populations. Fluorouracil 56-70 CD34 antigen Mus musculus 123-127 14519634-9 2003 CONCLUSIONS: This suggests that TS and DPD quantitation may be helpful to evaluate prognosis of patients receiving adjuvant 5-FU and that patients with high TS and low DPD may benefit from adjuvant 5-FU chemotherapy. Fluorouracil 198-202 thymidylate synthetase Homo sapiens 157-159 14519641-0 2003 Thymidylate synthase expression predicts the response to 5-fluorouracil-based adjuvant therapy in pancreatic cancer. Fluorouracil 57-71 thymidylate synthetase Homo sapiens 0-20 14519641-1 2003 PURPOSE: Thymidylate synthase (TS) is the target enzyme for 5-fluorouracil (5-FU), and TS expression may determine clinical response and survival after therapy with 5-FU in colorectal cancer. Fluorouracil 60-74 thymidylate synthetase Homo sapiens 9-29 10515856-5 1999 We then observed that, after the injection of 150 mg/kg 5-fluorouracil (5-FU), stem cells may be found in both CD34(-) and CD34(+) cell populations. Fluorouracil 72-76 CD34 antigen Mus musculus 111-115 14519641-1 2003 PURPOSE: Thymidylate synthase (TS) is the target enzyme for 5-fluorouracil (5-FU), and TS expression may determine clinical response and survival after therapy with 5-FU in colorectal cancer. Fluorouracil 60-74 thymidylate synthetase Homo sapiens 31-33 14519641-1 2003 PURPOSE: Thymidylate synthase (TS) is the target enzyme for 5-fluorouracil (5-FU), and TS expression may determine clinical response and survival after therapy with 5-FU in colorectal cancer. Fluorouracil 76-80 thymidylate synthetase Homo sapiens 9-29 14519641-1 2003 PURPOSE: Thymidylate synthase (TS) is the target enzyme for 5-fluorouracil (5-FU), and TS expression may determine clinical response and survival after therapy with 5-FU in colorectal cancer. Fluorouracil 76-80 thymidylate synthetase Homo sapiens 31-33 14519641-1 2003 PURPOSE: Thymidylate synthase (TS) is the target enzyme for 5-fluorouracil (5-FU), and TS expression may determine clinical response and survival after therapy with 5-FU in colorectal cancer. Fluorouracil 165-169 thymidylate synthetase Homo sapiens 9-29 14519641-1 2003 PURPOSE: Thymidylate synthase (TS) is the target enzyme for 5-fluorouracil (5-FU), and TS expression may determine clinical response and survival after therapy with 5-FU in colorectal cancer. Fluorouracil 165-169 thymidylate synthetase Homo sapiens 31-33 14519641-1 2003 PURPOSE: Thymidylate synthase (TS) is the target enzyme for 5-fluorouracil (5-FU), and TS expression may determine clinical response and survival after therapy with 5-FU in colorectal cancer. Fluorouracil 165-169 thymidylate synthetase Homo sapiens 87-89 10515856-5 1999 We then observed that, after the injection of 150 mg/kg 5-fluorouracil (5-FU), stem cells may be found in both CD34(-) and CD34(+) cell populations. Fluorouracil 72-76 CD34 antigen Mus musculus 123-127 10555156-1 1999 Interaction between 5-fluorouracil (5-FU) and FdUMP[10], a novel pro-drug formulation of the thymidylate synthase (TS) inhibitory nucleotide 5-fluoro-2"-deoxyuridine-5"-O-monophosphate (FdUMP), was investigated to evaluate the feasibility of using these two forms of fluorinated pyrimidine in combination chemotherapy regimens. Fluorouracil 36-40 thymidylate synthetase Homo sapiens 93-113 12948860-4 2003 5-Fluorouracil is known to inhibit thymidylate synthase (TS), a key enzyme that transfers a methyl group from 5,10-methylene-tetrahydrofolate to dUMP during nucleotide biosynthesis. Fluorouracil 0-14 thymidylate synthetase Homo sapiens 35-55 12948860-4 2003 5-Fluorouracil is known to inhibit thymidylate synthase (TS), a key enzyme that transfers a methyl group from 5,10-methylene-tetrahydrofolate to dUMP during nucleotide biosynthesis. Fluorouracil 0-14 thymidylate synthetase Homo sapiens 57-59 10499610-0 1999 A pilot study of interferon alpha-2a, fluorouracil, and leucovorin given with granulocyte-macrophage colony stimulating factor in advanced gastrointestinal adenocarcinoma. Fluorouracil 38-50 colony stimulating factor 2 Homo sapiens 78-126 12948860-7 2003 In contrast, 5-fluorouracil inhibited TS activity by >90% but increased TS protein levels. Fluorouracil 13-27 thymidylate synthetase Homo sapiens 38-40 12948860-7 2003 In contrast, 5-fluorouracil inhibited TS activity by >90% but increased TS protein levels. Fluorouracil 13-27 thymidylate synthetase Homo sapiens 75-77 12948860-11 2003 These results suggest that synergy between methionine restriction and 5-fluorouracil is attributable to multiple factors, including depletion of reduced folates, selective inhibition of TS, and creation of an imbalanced nucleotide pool. Fluorouracil 70-84 thymidylate synthetase Homo sapiens 186-188 10499610-1 1999 We reported previously that the addition of recombinant Escherichia coli human granulocyte-macrophage colony stimulating factor (GM-CSF) to a 5-fluorouracil (5-FU) and leucovorin (LV) regimen seemed to ameliorate diarrhea and permit increased 5-FU dose intensity (J. L. Grem et al., J. Clin. Fluorouracil 142-156 colony stimulating factor 2 Homo sapiens 79-127 12967482-1 2003 We previously demonstrated that epidermal growth factor (EGF) induces a decrease in dihydropyrimidine dehydrogenase (DPD), which is the first and rate-limiting enzyme in the catabolism of 5-fluorouracil (5-FU), in EGF receptor (EGFR)-positive human SKG-IIIb uterine cervical carcinoma cells, and thereby increased the sensitivity of the cells to 5-FU. Fluorouracil 188-202 epidermal growth factor Homo sapiens 32-55 10499610-1 1999 We reported previously that the addition of recombinant Escherichia coli human granulocyte-macrophage colony stimulating factor (GM-CSF) to a 5-fluorouracil (5-FU) and leucovorin (LV) regimen seemed to ameliorate diarrhea and permit increased 5-FU dose intensity (J. L. Grem et al., J. Clin. Fluorouracil 142-156 colony stimulating factor 2 Homo sapiens 129-135 12967482-1 2003 We previously demonstrated that epidermal growth factor (EGF) induces a decrease in dihydropyrimidine dehydrogenase (DPD), which is the first and rate-limiting enzyme in the catabolism of 5-fluorouracil (5-FU), in EGF receptor (EGFR)-positive human SKG-IIIb uterine cervical carcinoma cells, and thereby increased the sensitivity of the cells to 5-FU. Fluorouracil 204-208 epidermal growth factor Homo sapiens 32-55 12967482-1 2003 We previously demonstrated that epidermal growth factor (EGF) induces a decrease in dihydropyrimidine dehydrogenase (DPD), which is the first and rate-limiting enzyme in the catabolism of 5-fluorouracil (5-FU), in EGF receptor (EGFR)-positive human SKG-IIIb uterine cervical carcinoma cells, and thereby increased the sensitivity of the cells to 5-FU. Fluorouracil 346-350 epidermal growth factor Homo sapiens 32-55 10499610-1 1999 We reported previously that the addition of recombinant Escherichia coli human granulocyte-macrophage colony stimulating factor (GM-CSF) to a 5-fluorouracil (5-FU) and leucovorin (LV) regimen seemed to ameliorate diarrhea and permit increased 5-FU dose intensity (J. L. Grem et al., J. Clin. Fluorouracil 158-162 colony stimulating factor 2 Homo sapiens 79-127 12904931-4 2003 METHODS: The inhibitory effect of 5-FU on CYP1A2, CYP2C9, CYP2C19, CYP2C8, CYP2E1, CYP2D6, and CYP3A4 activities was examined with specific probe drugs in human liver microsomes. Fluorouracil 34-38 cytochrome P450 family 1 subfamily A member 2 Homo sapiens 42-48 10499610-1 1999 We reported previously that the addition of recombinant Escherichia coli human granulocyte-macrophage colony stimulating factor (GM-CSF) to a 5-fluorouracil (5-FU) and leucovorin (LV) regimen seemed to ameliorate diarrhea and permit increased 5-FU dose intensity (J. L. Grem et al., J. Clin. Fluorouracil 243-247 colony stimulating factor 2 Homo sapiens 79-127 12904931-4 2003 METHODS: The inhibitory effect of 5-FU on CYP1A2, CYP2C9, CYP2C19, CYP2C8, CYP2E1, CYP2D6, and CYP3A4 activities was examined with specific probe drugs in human liver microsomes. Fluorouracil 34-38 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 50-56 10499610-1 1999 We reported previously that the addition of recombinant Escherichia coli human granulocyte-macrophage colony stimulating factor (GM-CSF) to a 5-fluorouracil (5-FU) and leucovorin (LV) regimen seemed to ameliorate diarrhea and permit increased 5-FU dose intensity (J. L. Grem et al., J. Clin. Fluorouracil 243-247 colony stimulating factor 2 Homo sapiens 129-135 10473077-0 1999 Thymidylate synthase protein expression in advanced colon cancer: correlation with the site of metastasis and the clinical response to leucovorin-modulated bolus 5-fluorouracil. Fluorouracil 162-176 thymidylate synthetase Homo sapiens 0-20 10473077-1 1999 Recently, we have demonstrated that thymidylate synthase (TS) protein expression predicts for the clinical response to a regimen of infusional 5-fluorouracil (5FU) in advanced colorectal cancer patients. Fluorouracil 143-157 thymidylate synthetase Homo sapiens 36-56 10473077-1 1999 Recently, we have demonstrated that thymidylate synthase (TS) protein expression predicts for the clinical response to a regimen of infusional 5-fluorouracil (5FU) in advanced colorectal cancer patients. Fluorouracil 143-157 thymidylate synthetase Homo sapiens 58-60 12794758-0 2003 Role of hMLH1 promoter hypermethylation in drug resistance to 5-fluorouracil in colorectal cancer cell lines. Fluorouracil 62-76 mutL homolog 1 Homo sapiens 8-13 12794758-2 2003 We tested the hypothesis that demethylation of the hMLH1 promoter in hypermethylated colorectal cancer cells would restore MMR proficiency and drug sensitivity to 5-FU. Fluorouracil 163-167 mutL homolog 1 Homo sapiens 51-56 12794758-12 2003 We demonstrate that in vitro resistance to 5-FU can be overcome by reexpression of hMLH1 protein through 5 aza-dC-induced demethylation in hypermethylated cell lines. Fluorouracil 43-47 mutL homolog 1 Homo sapiens 83-88 10473077-4 1999 A secondary aim was to compare TS levels between liver metastases and abdominal recurrences from colon cancer, because these sites have a distinctly different responsiveness to 5FU chemotherapy. Fluorouracil 177-180 thymidylate synthetase Homo sapiens 31-33 10473077-10 1999 The higher TS levels observed in abdominal compared with liver metastases may account for their different responsiveness to 5FU chemotherapy. Fluorouracil 124-127 thymidylate synthetase Homo sapiens 11-13 12707718-11 2003 Thymidylate synthase ternary complex formation was demonstrated in bone marrow mononuclear cells isolated 24 h after the first oral 5-FU dose; the average was 66.5% bound. Fluorouracil 132-136 thymidylate synthetase Homo sapiens 0-20 10348793-3 1999 In the present study, the influence of liver damage induced by bile duct ligation on dihydropyrimidine dehydrogenase (DPD), a rate-limiting enzyme in 5-FU catabolism, CYP2B, and 5-FU pharmacokinetics were compared in male Sprague-Dawley rats. Fluorouracil 150-154 dihydropyrimidine dehydrogenase Rattus norvegicus 85-116 10348793-3 1999 In the present study, the influence of liver damage induced by bile duct ligation on dihydropyrimidine dehydrogenase (DPD), a rate-limiting enzyme in 5-FU catabolism, CYP2B, and 5-FU pharmacokinetics were compared in male Sprague-Dawley rats. Fluorouracil 150-154 dihydropyrimidine dehydrogenase Rattus norvegicus 118-121 19761066-0 2003 Recommendation preoperative 5-FU/RT fir T1-3, N0 disease. Fluorouracil 28-32 ankyrin repeat domain containing 11 Homo sapiens 40-44 10348793-3 1999 In the present study, the influence of liver damage induced by bile duct ligation on dihydropyrimidine dehydrogenase (DPD), a rate-limiting enzyme in 5-FU catabolism, CYP2B, and 5-FU pharmacokinetics were compared in male Sprague-Dawley rats. Fluorouracil 178-182 dihydropyrimidine dehydrogenase Rattus norvegicus 85-116 12829029-9 2003 Moderate reductions in L-selectin and CD11a expression were observed on stem cells of 5-FU-treated mice. Fluorouracil 86-90 integrin alpha L Mus musculus 38-43 10348793-3 1999 In the present study, the influence of liver damage induced by bile duct ligation on dihydropyrimidine dehydrogenase (DPD), a rate-limiting enzyme in 5-FU catabolism, CYP2B, and 5-FU pharmacokinetics were compared in male Sprague-Dawley rats. Fluorouracil 178-182 dihydropyrimidine dehydrogenase Rattus norvegicus 118-121 10561213-0 1999 Immunohistochemical quantitation of thymidylate synthase expression in colorectal cancer metastases predicts for clinical outcome to fluorouracil-based chemotherapy. Fluorouracil 133-145 thymidylate synthetase Homo sapiens 36-56 12824904-11 2003 For 5-FU resistance, dihydropyrimidine dehydrogenase and HB-EGF-like growth factor genes were also suggested to be resistance-related genes. Fluorouracil 4-8 heparin binding EGF like growth factor Homo sapiens 57-63 10561213-1 1999 PURPOSE: To determine whether immunohistochemical thymidylate synthase (TS) quantitation predicts for clinical outcome in patients with advanced colorectal cancer treated by fluorouracil (FUra)-based chemotherapy. Fluorouracil 188-192 thymidylate synthetase Homo sapiens 72-74 10645207-3 1999 Raltitrexed and 5-fluorouracil (5-FU) are specific and non-specific inhibitors, respectively, of thymidylate synthase, a critical enzyme in the de novo synthesis of DNA. Fluorouracil 16-30 thymidylate synthetase Homo sapiens 97-117 12651209-1 2003 Dihydropyrimidine dehydrogenase (DPD) is the rate-limiting enzyme of 5-fluorouracil (FU) catabolism. Fluorouracil 69-83 dihydropyrimidine dehydrogenase Mus musculus 0-31 12651209-1 2003 Dihydropyrimidine dehydrogenase (DPD) is the rate-limiting enzyme of 5-fluorouracil (FU) catabolism. Fluorouracil 69-83 dihydropyrimidine dehydrogenase Mus musculus 33-36 10645207-3 1999 Raltitrexed and 5-fluorouracil (5-FU) are specific and non-specific inhibitors, respectively, of thymidylate synthase, a critical enzyme in the de novo synthesis of DNA. Fluorouracil 32-36 thymidylate synthetase Homo sapiens 97-117 10370652-1 1999 BACKGROUND/AIMS: Thymidylate synthase (TS) is a target enzyme for 5-fluorouracil (5-FU). Fluorouracil 66-80 thymidylate synthetase Homo sapiens 17-37 12536082-3 2003 Both dThdPase and TS levels seemed to be related to response to 5-fluorouracil (5-FU) therapy in different types of human solid tumors. Fluorouracil 64-78 thymidylate synthetase Homo sapiens 18-20 12536082-3 2003 Both dThdPase and TS levels seemed to be related to response to 5-fluorouracil (5-FU) therapy in different types of human solid tumors. Fluorouracil 80-84 thymidylate synthetase Homo sapiens 18-20 10370652-1 1999 BACKGROUND/AIMS: Thymidylate synthase (TS) is a target enzyme for 5-fluorouracil (5-FU). Fluorouracil 66-80 thymidylate synthetase Homo sapiens 39-41 12536082-7 2003 These imply that immunohistochemical analysis of dThdPase and TS is available for selection of patients who will be received 5-FU based chemotherapy. Fluorouracil 125-129 thymidylate synthetase Homo sapiens 62-64 10370652-1 1999 BACKGROUND/AIMS: Thymidylate synthase (TS) is a target enzyme for 5-fluorouracil (5-FU). Fluorouracil 82-86 thymidylate synthetase Homo sapiens 17-37 10370652-1 1999 BACKGROUND/AIMS: Thymidylate synthase (TS) is a target enzyme for 5-fluorouracil (5-FU). Fluorouracil 82-86 thymidylate synthetase Homo sapiens 39-41 9748254-1 1998 Thymidylate synthase (TS) catalyzes the methylation of dUMP to dTMP and is the target for the widely used chemotherapeutic agent 5-fluorouracil. Fluorouracil 129-143 thymidylate synthetase Homo sapiens 0-20 9796967-5 1998 We had shown previously that high expression of thymidylate synthase (TS), the target enzyme of 5-FUra, was also a predictor of nonresponse to 5-FUra (L. Leichman et al, J. Clin. Fluorouracil 96-102 thymidylate synthetase Homo sapiens 48-68 9796967-5 1998 We had shown previously that high expression of thymidylate synthase (TS), the target enzyme of 5-FUra, was also a predictor of nonresponse to 5-FUra (L. Leichman et al, J. Clin. Fluorouracil 96-102 thymidylate synthetase Homo sapiens 70-72 9796967-5 1998 We had shown previously that high expression of thymidylate synthase (TS), the target enzyme of 5-FUra, was also a predictor of nonresponse to 5-FUra (L. Leichman et al, J. Clin. Fluorouracil 143-149 thymidylate synthetase Homo sapiens 48-68 9796967-5 1998 We had shown previously that high expression of thymidylate synthase (TS), the target enzyme of 5-FUra, was also a predictor of nonresponse to 5-FUra (L. Leichman et al, J. Clin. Fluorouracil 143-149 thymidylate synthetase Homo sapiens 70-72 9796967-7 1998 TP and TS expressions were found to be independent variables in these tumors, so that low expression levels of both TS and TP in tumors predicted a very high response rate (11 of 14) to 5-FUra/LV as well as a significantly longer survival, whereas none (0 of 24) of the patients with high expression of either TP or TS were responders. Fluorouracil 186-192 thymidylate synthetase Homo sapiens 116-118 9796967-7 1998 TP and TS expressions were found to be independent variables in these tumors, so that low expression levels of both TS and TP in tumors predicted a very high response rate (11 of 14) to 5-FUra/LV as well as a significantly longer survival, whereas none (0 of 24) of the patients with high expression of either TP or TS were responders. Fluorouracil 186-192 thymidylate synthetase Homo sapiens 116-118 10200532-10 1998 Furthermore, as observed with DXR and VP-16, both the CD95L-sensitive and the CD95L-resistant cell lines resulted equally sensitive to the cytotoxic effects of a number of different cytotoxic drugs (vincristine, camptothecin, 5-fluorouracil and methotrexate). Fluorouracil 226-240 Fas ligand Homo sapiens 78-83 9893640-2 1998 This study determined the influence of 5-FU on dihydropyrimidine dehydrogenase (DPD) activity, the enzyme responsible for its in vivo degradation. Fluorouracil 39-43 dihydropyrimidine dehydrogenase Rattus norvegicus 47-78 9893640-2 1998 This study determined the influence of 5-FU on dihydropyrimidine dehydrogenase (DPD) activity, the enzyme responsible for its in vivo degradation. Fluorouracil 39-43 dihydropyrimidine dehydrogenase Rattus norvegicus 80-83 9698077-0 1998 5-fluorouracil-mediated thymidylate synthase induction in malignant and nonmalignant human cells. Fluorouracil 0-14 thymidylate synthetase Homo sapiens 24-44 9596684-1 1998 Thymidylate synthase (TS) inhibition causes cell death, and this enzyme is the target for the important chemotherapy regime 5-fluorouracil/leucovorin. Fluorouracil 124-138 thymidylate synthetase Homo sapiens 0-20 9596684-1 1998 Thymidylate synthase (TS) inhibition causes cell death, and this enzyme is the target for the important chemotherapy regime 5-fluorouracil/leucovorin. Fluorouracil 124-138 thymidylate synthetase Homo sapiens 22-24 9673363-1 1998 Inhibition of Thymidylate Synthase (TS) by the 5-Fluorouracil (5Fu) active metabolite Fluoro-deoxy-uridine-monophosphate (FdUMP) is considered to be the main mechanism of action of 5Fu. Fluorouracil 63-66 thymidylate synthetase Homo sapiens 14-34 9673363-1 1998 Inhibition of Thymidylate Synthase (TS) by the 5-Fluorouracil (5Fu) active metabolite Fluoro-deoxy-uridine-monophosphate (FdUMP) is considered to be the main mechanism of action of 5Fu. Fluorouracil 63-66 thymidylate synthetase Homo sapiens 36-38 9673363-1 1998 Inhibition of Thymidylate Synthase (TS) by the 5-Fluorouracil (5Fu) active metabolite Fluoro-deoxy-uridine-monophosphate (FdUMP) is considered to be the main mechanism of action of 5Fu. Fluorouracil 181-184 thymidylate synthetase Homo sapiens 14-34 9673363-1 1998 Inhibition of Thymidylate Synthase (TS) by the 5-Fluorouracil (5Fu) active metabolite Fluoro-deoxy-uridine-monophosphate (FdUMP) is considered to be the main mechanism of action of 5Fu. Fluorouracil 181-184 thymidylate synthetase Homo sapiens 36-38 9607583-2 1998 Therefore, we determined p53 status in 36 patients with disseminated colorectal cancer by cDNA sequencing and immunohistochemical staining, as well as by the gene expression level of thymidylate synthase (TS), the target enzyme of 5-fluorouracil (5-FU), by reverse transcription-PCR. Fluorouracil 231-245 thymidylate synthetase Homo sapiens 183-203 9607583-2 1998 Therefore, we determined p53 status in 36 patients with disseminated colorectal cancer by cDNA sequencing and immunohistochemical staining, as well as by the gene expression level of thymidylate synthase (TS), the target enzyme of 5-fluorouracil (5-FU), by reverse transcription-PCR. Fluorouracil 231-245 thymidylate synthetase Homo sapiens 205-207 9607583-2 1998 Therefore, we determined p53 status in 36 patients with disseminated colorectal cancer by cDNA sequencing and immunohistochemical staining, as well as by the gene expression level of thymidylate synthase (TS), the target enzyme of 5-fluorouracil (5-FU), by reverse transcription-PCR. Fluorouracil 247-251 thymidylate synthetase Homo sapiens 205-207 9563485-6 1998 In contrast, IL-2 (400 microg/kg) significantly potentiated the toxicity of FUra administered as a single i.v. Fluorouracil 76-80 interleukin 2 Rattus norvegicus 13-17 9528843-1 1998 Two patients with proven 5-fluorouracil (5-FU)-associated cardiotoxicity were treated with the specific thymidylate synthase inhibitor raltitrexed safely, without evidence of cardiotoxicity. Fluorouracil 25-39 thymidylate synthetase Homo sapiens 104-124 9528843-1 1998 Two patients with proven 5-fluorouracil (5-FU)-associated cardiotoxicity were treated with the specific thymidylate synthase inhibitor raltitrexed safely, without evidence of cardiotoxicity. Fluorouracil 41-45 thymidylate synthetase Homo sapiens 104-124 9463483-8 1998 FUra-mediated thymidylate synthase inhibition was accompanied by a 124-fold increase in total deoxyuridylate immunoreactivity and a 31-fold increase in dUTP pools, but the addition of IFN-alpha + gamma attenuated the accumulation. Fluorouracil 0-4 thymidylate synthetase Homo sapiens 14-34 12625878-1 2003 It has been found in clinical practice that the serum level of phenytoin, of which metabolism is mediated by hepatic CYP2C enzymes, was markedly elevated by co-administration of 5-fluorouracil (5-FU) and doxifluridine (5"-deoxy-5-fluorouridine; 5"-DFUR), a prodrug of 5-FU, but the detailed mechanisms are unclear. Fluorouracil 178-192 cytochrome P450, subfamily 2, polypeptide 11 Rattus norvegicus 117-122 9743457-0 1998 Cisplatin-induced inhibition of p34cdc2 is abolished by 5-fluorouracil. Fluorouracil 56-70 cyclin dependent kinase 1 Homo sapiens 32-39 12625878-1 2003 It has been found in clinical practice that the serum level of phenytoin, of which metabolism is mediated by hepatic CYP2C enzymes, was markedly elevated by co-administration of 5-fluorouracil (5-FU) and doxifluridine (5"-deoxy-5-fluorouridine; 5"-DFUR), a prodrug of 5-FU, but the detailed mechanisms are unclear. Fluorouracil 194-198 cytochrome P450, subfamily 2, polypeptide 11 Rattus norvegicus 117-122 12625878-1 2003 It has been found in clinical practice that the serum level of phenytoin, of which metabolism is mediated by hepatic CYP2C enzymes, was markedly elevated by co-administration of 5-fluorouracil (5-FU) and doxifluridine (5"-deoxy-5-fluorouridine; 5"-DFUR), a prodrug of 5-FU, but the detailed mechanisms are unclear. Fluorouracil 268-272 cytochrome P450, subfamily 2, polypeptide 11 Rattus norvegicus 117-122 12625878-12 2003 The present study suggested that the down-regulation of hepatic CYP2C enzymes occurs by 5-FU exposure even at a low level, and provided a fundamental explanation for the drug interaction encountered in clinical practice. Fluorouracil 88-92 cytochrome P450, subfamily 2, polypeptide 11 Rattus norvegicus 64-69 9598142-0 1998 Dihydropyrimidine dehydrogenase in livers from mouse and rat, and in human liver, colon tumors, and mucosa in relation to anabolism of 5-fluorouracil. Fluorouracil 135-149 dihydropyrimidine dehydrogenase Mus musculus 0-31 12488549-8 2003 Treatment of H630-C6 cells with 5-FU, FUrd, FUdR, TFT, AG331, AG337, ZD1694, and methotrexate up-regulated TS levels as determined by Western blot analysis, although TS mRNA levels remained unchanged as determined by reverse transcription-polymerase chain reaction. Fluorouracil 32-36 thymidylate synthetase Homo sapiens 107-109 12488549-8 2003 Treatment of H630-C6 cells with 5-FU, FUrd, FUdR, TFT, AG331, AG337, ZD1694, and methotrexate up-regulated TS levels as determined by Western blot analysis, although TS mRNA levels remained unchanged as determined by reverse transcription-polymerase chain reaction. Fluorouracil 32-36 thymidylate synthetase Homo sapiens 166-168 12469154-2 2003 On the other hand, variability of 5-FU sensitivity of the tumors is also presumed to depend on the enzymes of 5-FU metabolism (e.g. dihydropyrimidine dehydrogenase; DPD, rate limiting enzyme of catabolism) and action target (e.g. thymidylate synthase; TS). Fluorouracil 34-38 thymidylate synthetase Homo sapiens 230-250 12469154-2 2003 On the other hand, variability of 5-FU sensitivity of the tumors is also presumed to depend on the enzymes of 5-FU metabolism (e.g. dihydropyrimidine dehydrogenase; DPD, rate limiting enzyme of catabolism) and action target (e.g. thymidylate synthase; TS). Fluorouracil 110-114 thymidylate synthetase Homo sapiens 230-250 9624255-1 1998 The main clinically relevant cellular target of 5-fluorouracil (5-FU) is the enzyme thymidylate synthase (TS). Fluorouracil 48-62 thymidylate synthetase Homo sapiens 84-104 12759532-0 2003 Subcutaneous granulocyte-macrophage colony-stimulating factor in mucositis induced by an adjuvant 5-fluorouracil plus leucovorin regimen. Fluorouracil 98-112 colony stimulating factor 2 Homo sapiens 13-61 12759532-2 2003 OBJECTIVE: To test the activity of subcutaneous granulocyte-macrophage colony-stimulating factor (GM-CSF) administration in patients with colorectal cancer treated with adjuvant 5-fluorouracil (5-FU) plus leucovorin (LV) and suffering from mucositis. Fluorouracil 178-192 colony stimulating factor 2 Homo sapiens 48-96 12759532-2 2003 OBJECTIVE: To test the activity of subcutaneous granulocyte-macrophage colony-stimulating factor (GM-CSF) administration in patients with colorectal cancer treated with adjuvant 5-fluorouracil (5-FU) plus leucovorin (LV) and suffering from mucositis. Fluorouracil 178-192 colony stimulating factor 2 Homo sapiens 98-104 12759532-2 2003 OBJECTIVE: To test the activity of subcutaneous granulocyte-macrophage colony-stimulating factor (GM-CSF) administration in patients with colorectal cancer treated with adjuvant 5-fluorouracil (5-FU) plus leucovorin (LV) and suffering from mucositis. Fluorouracil 194-198 colony stimulating factor 2 Homo sapiens 48-96 12759532-2 2003 OBJECTIVE: To test the activity of subcutaneous granulocyte-macrophage colony-stimulating factor (GM-CSF) administration in patients with colorectal cancer treated with adjuvant 5-fluorouracil (5-FU) plus leucovorin (LV) and suffering from mucositis. Fluorouracil 194-198 colony stimulating factor 2 Homo sapiens 98-104 12759532-13 2003 CONCLUSIONS: The subcutaneous administration of GM-CSF relieved patients from symptoms of 5-FU/LV-induced mucositis with acceptable side effects permitting the maintenance of full-dose chemotherapy. Fluorouracil 90-94 colony stimulating factor 2 Homo sapiens 48-54 9624255-1 1998 The main clinically relevant cellular target of 5-fluorouracil (5-FU) is the enzyme thymidylate synthase (TS). Fluorouracil 48-62 thymidylate synthetase Homo sapiens 106-108 9624255-1 1998 The main clinically relevant cellular target of 5-fluorouracil (5-FU) is the enzyme thymidylate synthase (TS). Fluorouracil 64-68 thymidylate synthetase Homo sapiens 84-104 9624255-1 1998 The main clinically relevant cellular target of 5-fluorouracil (5-FU) is the enzyme thymidylate synthase (TS). Fluorouracil 64-68 thymidylate synthetase Homo sapiens 106-108 12457437-13 2002 Future advances in the effective use of TS inhibitors may be forthcoming in the form of improved dosing, fewer untoward effects and increased tumour selectivity with novel fluorouracil prodrug formulations. Fluorouracil 172-184 thymidylate synthetase Homo sapiens 40-42 9624255-2 1998 Both preclinical data and clinical data in digestive tract cancer indicate that an increased amount of TS in tumours can predict for 5-FU resistance. Fluorouracil 133-137 thymidylate synthetase Homo sapiens 103-105 12439919-15 2002 CONCLUSION: The continuous exposure of Bel(7402) cells to 5-FU led to overexpression of TS and MRP, as well as increased intracellular GSH content and total GST activity. Fluorouracil 58-62 thymidylate synthetase Homo sapiens 88-90 9440758-0 1998 ERCC1 mRNA levels complement thymidylate synthase mRNA levels in predicting response and survival for gastric cancer patients receiving combination cisplatin and fluorouracil chemotherapy. Fluorouracil 162-174 ERCC excision repair 1, endonuclease non-catalytic subunit Homo sapiens 0-5 12484012-8 2002 Arterial infusion was performed 16 times, with the total amount of 5-FU administered being 20 g. A lowering of CEA levels and reduction of tumor size were achieved, and hepatic resection was performed. Fluorouracil 67-71 pregnancy specific beta-1-glycoprotein 2 Homo sapiens 111-114 9440758-1 1998 PURPOSE: We have previously shown that relative thymidylate synthase (TS) mRNA levels in primary gastric adenocarcinomas treated with fluorouracil (5-FU) and cisplatin are inversely associated with response and survival. Fluorouracil 134-146 thymidylate synthetase Homo sapiens 48-68 12353234-4 2002 The antitumor effect of 5FU is enhanced by augmenting 5-fluorodeoxyuridine monophosphate (FdUMP) converted from FUMP, which inhibits thymidylate synthetase (TS). Fluorouracil 24-27 thymidylate synthetase Homo sapiens 133-155 9440758-1 1998 PURPOSE: We have previously shown that relative thymidylate synthase (TS) mRNA levels in primary gastric adenocarcinomas treated with fluorouracil (5-FU) and cisplatin are inversely associated with response and survival. Fluorouracil 134-146 thymidylate synthetase Homo sapiens 70-72 9440758-1 1998 PURPOSE: We have previously shown that relative thymidylate synthase (TS) mRNA levels in primary gastric adenocarcinomas treated with fluorouracil (5-FU) and cisplatin are inversely associated with response and survival. Fluorouracil 148-152 thymidylate synthetase Homo sapiens 48-68 9440758-1 1998 PURPOSE: We have previously shown that relative thymidylate synthase (TS) mRNA levels in primary gastric adenocarcinomas treated with fluorouracil (5-FU) and cisplatin are inversely associated with response and survival. Fluorouracil 148-152 thymidylate synthetase Homo sapiens 70-72 9440758-2 1998 This is a presumed function of TS as a target for 5-FU activity. Fluorouracil 50-54 thymidylate synthetase Homo sapiens 31-33 12355219-9 2002 In addition, administration of 5-fluorouracil, which decreased anastomotic MPO levels, increased anastomotic leakage. Fluorouracil 31-45 myeloperoxidase Rattus norvegicus 75-78 9345027-8 1997 When lineage (Lin)-Sca-1(+) cells sorted from BMC of 5-FU-treated mice were incubated in serum-free culture, leptin synergized with SCF in the formation of blast cell colonies, which efficiently produced secondary colonies including a large proportion of multilineage colonies in the replating experiment. Fluorouracil 53-57 leptin Mus musculus 109-115 12460463-2 2002 The repeat length is associated with TS protein expression, which suggests that we may be able to predict the efficacy of 5-fluorouracil (5-FU)-based chemotherapy from a patient"s TS genotype determined through analysis of normal tissue obtained non-invasively. Fluorouracil 122-136 thymidylate synthetase Homo sapiens 37-39 12460463-2 2002 The repeat length is associated with TS protein expression, which suggests that we may be able to predict the efficacy of 5-fluorouracil (5-FU)-based chemotherapy from a patient"s TS genotype determined through analysis of normal tissue obtained non-invasively. Fluorouracil 122-136 thymidylate synthetase Homo sapiens 180-182 12460463-2 2002 The repeat length is associated with TS protein expression, which suggests that we may be able to predict the efficacy of 5-fluorouracil (5-FU)-based chemotherapy from a patient"s TS genotype determined through analysis of normal tissue obtained non-invasively. Fluorouracil 138-142 thymidylate synthetase Homo sapiens 37-39 12460463-2 2002 The repeat length is associated with TS protein expression, which suggests that we may be able to predict the efficacy of 5-fluorouracil (5-FU)-based chemotherapy from a patient"s TS genotype determined through analysis of normal tissue obtained non-invasively. Fluorouracil 138-142 thymidylate synthetase Homo sapiens 180-182 12422306-1 2002 In the last 50 years, 5-fluorouracil-based therapy has been the mainstay of adjuvant and palliative treatment for colorectal cancer but response rates and median survival have been dismal despite the introduction of thymidylate synthase modulators such as leucovorin. Fluorouracil 22-36 thymidylate synthetase Homo sapiens 216-236 9345027-8 1997 When lineage (Lin)-Sca-1(+) cells sorted from BMC of 5-FU-treated mice were incubated in serum-free culture, leptin synergized with SCF in the formation of blast cell colonies, which efficiently produced secondary colonies including a large proportion of multilineage colonies in the replating experiment. Fluorouracil 53-57 kit ligand Mus musculus 132-135 9223329-8 1997 FasL expression also correlated with acute apoptosis induced in parental GC3/cl cells, commencing at 48 hr, following thymidylate synthase inhibition by 5-fluorouracil/leucovorin exposure. Fluorouracil 153-167 Fas ligand Homo sapiens 0-4 12530000-1 2002 Thymidylate synthase (TS) is a target enzyme of 5-fluorouracil (5-FU). Fluorouracil 48-62 thymidylate synthetase Homo sapiens 0-20 9223329-8 1997 FasL expression also correlated with acute apoptosis induced in parental GC3/cl cells, commencing at 48 hr, following thymidylate synthase inhibition by 5-fluorouracil/leucovorin exposure. Fluorouracil 153-167 thymidylate synthetase Homo sapiens 118-138 9217040-0 1997 Hyperfractionated radiation therapy and 5-fluorouracil, cisplatin, and mitomycin-C (+/- granulocyte-colony stimulating factor) in the treatment of patients with locally advanced head and neck carcinoma. Fluorouracil 40-54 colony stimulating factor 3 Homo sapiens 88-125 12183426-10 2002 We hypothesize that potentiation of FUra cytotoxicity by rMETase may result from increased inhibition of thymidylate synthase, together with DNA hypomethylation and enhanced DNA repair that could be involved in cell responses to drug-induced damage. Fluorouracil 36-40 thymidylate synthetase Homo sapiens 105-125 21590122-0 1997 Preparation of the antibodies against recombinant human thymidylate synthase for the detection of its intratumoral levels and the application to sensitivity-study of 5-fluorouracil. Fluorouracil 166-180 thymidylate synthetase Homo sapiens 56-76 9262988-5 1997 Incubation with IL1+IL3+SCF caused an increase (fold expansion) in committed (28.6 +/- 8.1), immature (5.8 +/- 1.8), and primitive progenitors (4.1 +/- 0.8) among control CB MNC compared to a decrease in committed progenitors (0 +/- 0) but an increase in both immature (8.4 +/- 4.8) and primitive progenitors (7 +/- 2.9) among 5-FU resistant CB MNC. Fluorouracil 327-331 interleukin 1 alpha Homo sapiens 16-19 12478888-2 2002 This study was designed to investigate if antitumor activation of 5-FU could be enhanced by transfection of uracil phosphoribosyltransferase(UPRT) gene. Fluorouracil 66-70 uracil phosphoribosyltransferase Mus musculus 141-145 12478888-4 2002 The sensitivity of MFC transfected with UPRT gene to 5-FU was determined by MTT method. Fluorouracil 53-57 uracil phosphoribosyltransferase Mus musculus 40-44 12478888-6 2002 RESULTS: The 5-FU sensitivity in MFC transfected with the UPRT gene increased 17.26-fold compared to the control cells. Fluorouracil 13-17 uracil phosphoribosyltransferase Mus musculus 58-62 12478888-7 2002 In situ transfection of the UPRT gene mediated by retrovirus vector followed by the administration of 5-FU (10 mg/kg) significantly inhibited the tumor growth (P < 0.005) with an inhibition rate of 87.18% and prolonged the survival. Fluorouracil 102-106 uracil phosphoribosyltransferase Mus musculus 28-32 12478888-8 2002 CONCLUSION: Transfection of UPRT gene can render the murine gastric cancer cell line MFC be more sensitive to low concentration of 5-FU and significantly improve the antitumor effect of 5-FU both in vitro and in vivo. Fluorouracil 131-135 uracil phosphoribosyltransferase Mus musculus 28-32 12478888-8 2002 CONCLUSION: Transfection of UPRT gene can render the murine gastric cancer cell line MFC be more sensitive to low concentration of 5-FU and significantly improve the antitumor effect of 5-FU both in vitro and in vivo. Fluorouracil 186-190 uracil phosphoribosyltransferase Mus musculus 28-32 9262988-5 1997 Incubation with IL1+IL3+SCF caused an increase (fold expansion) in committed (28.6 +/- 8.1), immature (5.8 +/- 1.8), and primitive progenitors (4.1 +/- 0.8) among control CB MNC compared to a decrease in committed progenitors (0 +/- 0) but an increase in both immature (8.4 +/- 4.8) and primitive progenitors (7 +/- 2.9) among 5-FU resistant CB MNC. Fluorouracil 327-331 interleukin 3 Homo sapiens 20-23 12084458-7 2002 Studies thus far involving colorectal tumors obtained from patients have focused predominantly on the predictive value of levels of TS expression and p53 mutations in determining response to 5-FU. Fluorouracil 191-195 thymidylate synthetase Homo sapiens 132-134 9116281-1 1997 Administration of kit-ligand (KL) before and after doses of 5-fluorouracil (5-FU) results in marrow failure in mice, presumably because of enhanced KL-induced cycling of stem cells, which makes them more susceptible to the effects of 5-FU. Fluorouracil 76-80 kit ligand Mus musculus 18-28 12090040-1 2002 Dihydropyrimidine dehydrogenase (DPD) and thymidylate synthase (TS) in cancer are considered to play key roles in the sensitivity to 5-FU-based chemotherapy. Fluorouracil 133-137 thymidylate synthetase Homo sapiens 42-62 11978162-8 2002 The interaction of fluorouracil and phenytoin is known in clinical practice, and it is reported that the expression of hepatic CYP2C enzymes is depressed by exposure of rats to fluorouracil. Fluorouracil 19-31 cytochrome P450, subfamily 2, polypeptide 11 Rattus norvegicus 127-132 11978162-8 2002 The interaction of fluorouracil and phenytoin is known in clinical practice, and it is reported that the expression of hepatic CYP2C enzymes is depressed by exposure of rats to fluorouracil. Fluorouracil 177-189 cytochrome P450, subfamily 2, polypeptide 11 Rattus norvegicus 127-132 11980662-0 2002 The role of thymidylate synthase induction in modulating p53-regulated gene expression in response to 5-fluorouracil and antifolates. Fluorouracil 102-116 thymidylate synthetase Homo sapiens 12-32 11980662-1 2002 Thymidylate synthase (TS) is a critical target for chemotherapeutic agents such as 5-fluorouracil (5-FU) and antifolates such as tomudex (TDX),multitargeted antifolate, and ZD9331. Fluorouracil 83-97 thymidylate synthetase Homo sapiens 0-20 11980662-1 2002 Thymidylate synthase (TS) is a critical target for chemotherapeutic agents such as 5-fluorouracil (5-FU) and antifolates such as tomudex (TDX),multitargeted antifolate, and ZD9331. Fluorouracil 83-97 thymidylate synthetase Homo sapiens 22-24 11980662-1 2002 Thymidylate synthase (TS) is a critical target for chemotherapeutic agents such as 5-fluorouracil (5-FU) and antifolates such as tomudex (TDX),multitargeted antifolate, and ZD9331. Fluorouracil 99-103 thymidylate synthetase Homo sapiens 0-20 11980662-1 2002 Thymidylate synthase (TS) is a critical target for chemotherapeutic agents such as 5-fluorouracil (5-FU) and antifolates such as tomudex (TDX),multitargeted antifolate, and ZD9331. Fluorouracil 99-103 thymidylate synthetase Homo sapiens 22-24 12031098-5 2002 Addition of cytokines that augment these functions, mainly granulocyte macrophage-cerebrospinal fluid (GM-CSF), seemed to improve the clinical efficacy as well as chemotherapeutic agents (5-Fu). Fluorouracil 188-192 colony stimulating factor 2 Homo sapiens 103-109 11919227-0 2002 Thymidylate synthase expression in colorectal cancer: a prognostic and predictive marker of benefit from adjuvant fluorouracil-based chemotherapy. Fluorouracil 114-126 thymidylate synthetase Homo sapiens 0-20 11919227-8 2002 The study indicates that patients with high TS levels may benefit from adjuvant 5-FU-based chemotherapy. Fluorouracil 80-84 thymidylate synthetase Homo sapiens 44-46 12023789-6 2002 5-FU is equally interesting because it permits investigation of thymidylate synthase (TS) levels as a genetic target for predicting response and survival. Fluorouracil 0-4 thymidylate synthetase Homo sapiens 64-84 12023789-6 2002 5-FU is equally interesting because it permits investigation of thymidylate synthase (TS) levels as a genetic target for predicting response and survival. Fluorouracil 0-4 thymidylate synthetase Homo sapiens 86-88 11862424-9 2002 The cytotoxicity of FUra alone or in combination with MCLR, but not that of PPIs alone, was abrogated almost completely by exogenous thymidine (dThd), suggesting that inhibition of thymidylate synthetase (TS) is the growth-limiting event in the cytotoxic action of FUra even in combination with MCLR. Fluorouracil 20-24 thymidylate synthetase Homo sapiens 181-203 12027413-1 2002 Thymidylate Synthase (TS) is a rate-limiting enzyme in the DNA synthetic pathway and represents the cellular target of the antimetabolite drug 5-fluorouracil (FUra). Fluorouracil 143-157 thymidylate synthetase Homo sapiens 0-20 12027413-1 2002 Thymidylate Synthase (TS) is a rate-limiting enzyme in the DNA synthetic pathway and represents the cellular target of the antimetabolite drug 5-fluorouracil (FUra). Fluorouracil 143-157 thymidylate synthetase Homo sapiens 22-24 12027413-1 2002 Thymidylate Synthase (TS) is a rate-limiting enzyme in the DNA synthetic pathway and represents the cellular target of the antimetabolite drug 5-fluorouracil (FUra). Fluorouracil 159-163 thymidylate synthetase Homo sapiens 0-20 12027413-1 2002 Thymidylate Synthase (TS) is a rate-limiting enzyme in the DNA synthetic pathway and represents the cellular target of the antimetabolite drug 5-fluorouracil (FUra). Fluorouracil 159-163 thymidylate synthetase Homo sapiens 22-24 12027413-3 2002 In particular, five recent studies have consistently demonstrated an inverse correlation between the level of TS gene or protein expression measured in colorectal cancer metastases and the clinical response to either FUra or 5-fluorodeoxyuridine (FUdR). Fluorouracil 217-221 thymidylate synthetase Homo sapiens 110-112 12027413-7 2002 In this review preclinical and clinical data supporting the use of TS quantitation to predict for the clinical response to FUra will be described and unresolved problems including assays standardization, response prediction based on TS levels measured in primary tumors, intrapatient variations in TS levels and biological/biochemical limitations of this strategy will be discussed. Fluorouracil 123-127 thymidylate synthetase Homo sapiens 67-69 12450420-3 2002 As the first TS inhibitor in clinical use, 5-fluorouracil (5-FU) remains widely used for the treatment of colorectal, pancreatic, breast, head and neck, gastric, and ovarian cancers. Fluorouracil 43-57 thymidylate synthetase Homo sapiens 13-15 12450420-3 2002 As the first TS inhibitor in clinical use, 5-fluorouracil (5-FU) remains widely used for the treatment of colorectal, pancreatic, breast, head and neck, gastric, and ovarian cancers. Fluorouracil 59-63 thymidylate synthetase Homo sapiens 13-15 11841784-7 2002 A two-reaction pathway, composed of ribokinase and phosphopentomutase, appears to be responsible of the Rib1-P formation, needed to salvage uracil to uracil-nucleotides and to activate 5-FU to cytotoxic 5-FU-ribonucleotides. Fluorouracil 185-189 ribonuclease A family member 1, pancreatic Rattus norvegicus 104-108 11914638-8 2002 Dipyridamole and p-nitrobenzylthioinosine (NBMPR), potent inhibitors of equilibrative nucleoside transport, synergized with NB1011 selectively against 5-fluorouracil (5-FU)-resistant H630R10 colon carcinoma cells [combination index (CI)=0.75 and 0.35] and Tomudex-resistant MCF7TDX breast carcinoma cells (CI=0.51 and 0.57), both TS overexpressing cell lines. Fluorouracil 151-165 thymidylate synthetase Homo sapiens 330-332 11801545-1 2002 5-Fluorouracil (5-FU) exerts cytotoxic effects through inhibition of thymidylate synthase (TS) and incorporation of metabolites into RNA. Fluorouracil 0-14 thymidylate synthetase Homo sapiens 69-89 11801545-1 2002 5-Fluorouracil (5-FU) exerts cytotoxic effects through inhibition of thymidylate synthase (TS) and incorporation of metabolites into RNA. Fluorouracil 0-14 thymidylate synthetase Homo sapiens 91-93 11801545-1 2002 5-Fluorouracil (5-FU) exerts cytotoxic effects through inhibition of thymidylate synthase (TS) and incorporation of metabolites into RNA. Fluorouracil 16-20 thymidylate synthetase Homo sapiens 69-89 11801545-1 2002 5-Fluorouracil (5-FU) exerts cytotoxic effects through inhibition of thymidylate synthase (TS) and incorporation of metabolites into RNA. Fluorouracil 16-20 thymidylate synthetase Homo sapiens 91-93 11801545-2 2002 TS inhibition may be greater for infusional 5-FU, with bolus regimens more likely to cause RNA effects. Fluorouracil 44-48 thymidylate synthetase Homo sapiens 0-2 11801545-11 2002 Thus, both 5-FU regimens inhibit TS, and prolonged TS inhibition is achieved by CI 5-FU without significant toxicity. Fluorouracil 83-87 thymidylate synthetase Homo sapiens 51-53 11918083-8 2002 Collagen 1, fibronectin and fibroblast-derived ECM rendered LiM6 cells, but not LS174T, more sensitive to the harmful effect of 5-FU. Fluorouracil 128-132 multimerin 1 Homo sapiens 47-50 11748451-0 2002 5-FU improves p27-related poor prognosis in patients with Astler-Coller B2-C colorectal carcinoma. Fluorouracil 0-4 interferon alpha inducible protein 27 Homo sapiens 14-17 11748451-4 2002 UFT, 5-FU masked compound may improve the p27-related poor prognosis in colorectal cancer patients. Fluorouracil 5-9 interferon alpha inducible protein 27 Homo sapiens 42-45 9116281-1 1997 Administration of kit-ligand (KL) before and after doses of 5-fluorouracil (5-FU) results in marrow failure in mice, presumably because of enhanced KL-induced cycling of stem cells, which makes them more susceptible to the effects of 5-FU. Fluorouracil 234-238 kit ligand Mus musculus 18-28 9815719-1 1997 Thymidylate synthase (TS) is the main target for fluorouracil (FU). Fluorouracil 49-61 thymidylate synthetase Homo sapiens 0-20 11731512-0 2001 ERCC1 and thymidylate synthase mRNA levels predict survival for colorectal cancer patients receiving combination oxaliplatin and fluorouracil chemotherapy. Fluorouracil 129-141 ERCC excision repair 1, endonuclease non-catalytic subunit Homo sapiens 0-5 11731512-0 2001 ERCC1 and thymidylate synthase mRNA levels predict survival for colorectal cancer patients receiving combination oxaliplatin and fluorouracil chemotherapy. Fluorouracil 129-141 thymidylate synthetase Homo sapiens 10-30 11731512-1 2001 PURPOSE: To test the hypotheses of whether the relative mRNA expression of the thymidylate synthase (TS) gene and the excision cross-complementing (ERCC1) gene are associated with response to and survival of fluorouracil (5-FU)/oxaliplatin chemotherapy in metastatic colorectal cancer. Fluorouracil 208-220 thymidylate synthetase Homo sapiens 79-99 11731512-1 2001 PURPOSE: To test the hypotheses of whether the relative mRNA expression of the thymidylate synthase (TS) gene and the excision cross-complementing (ERCC1) gene are associated with response to and survival of fluorouracil (5-FU)/oxaliplatin chemotherapy in metastatic colorectal cancer. Fluorouracil 208-220 thymidylate synthetase Homo sapiens 101-103 11731512-10 2001 CONCLUSION: These data suggest that intratumoral ERCC1 mRNA and TS mRNA expression levels are independent predictive markers of survival for 5-FU and oxaliplatin combination chemotherapy in 5-FU-resistant metastatic colorectal cancer. Fluorouracil 141-145 ERCC excision repair 1, endonuclease non-catalytic subunit Homo sapiens 49-54 11731512-10 2001 CONCLUSION: These data suggest that intratumoral ERCC1 mRNA and TS mRNA expression levels are independent predictive markers of survival for 5-FU and oxaliplatin combination chemotherapy in 5-FU-resistant metastatic colorectal cancer. Fluorouracil 190-194 ERCC excision repair 1, endonuclease non-catalytic subunit Homo sapiens 49-54 9126308-5 1997 These results suggest that our anti-TS polyclonal antibody (IgG) is suitable for clinical prospective and retrospective studies on TS expression in various cancers as a prognostic factor and 5-FU response-predicting parameter. Fluorouracil 191-195 thymidylate synthetase Homo sapiens 36-38 9113088-5 1997 However, LV significantly (P < 0.01) potentiated the inhibition of TS activity in situ in HCT-8 cells at 24 hr after a 2-hr treatment with either 5-FU or 5-FdUrd, but had no such activity in the FL2h and FL72h sublines (P > 0.1). Fluorouracil 149-153 thymidylate synthetase Homo sapiens 70-72 9050858-2 1997 Administration of 40 mg/kg 5-fluorouracil (5-FU) to BDF-1 p53+/+ mice resulted in an increase in p53 protein at cell positions in the crypts that were also those subjected to an apoptotic cell death. Fluorouracil 27-41 transformation related protein 53, pseudogene Mus musculus 58-61 9050858-2 1997 Administration of 40 mg/kg 5-fluorouracil (5-FU) to BDF-1 p53+/+ mice resulted in an increase in p53 protein at cell positions in the crypts that were also those subjected to an apoptotic cell death. Fluorouracil 27-41 transformation related protein 53, pseudogene Mus musculus 97-100 9050858-2 1997 Administration of 40 mg/kg 5-fluorouracil (5-FU) to BDF-1 p53+/+ mice resulted in an increase in p53 protein at cell positions in the crypts that were also those subjected to an apoptotic cell death. Fluorouracil 43-47 transformation related protein 53, pseudogene Mus musculus 58-61 9050858-2 1997 Administration of 40 mg/kg 5-fluorouracil (5-FU) to BDF-1 p53+/+ mice resulted in an increase in p53 protein at cell positions in the crypts that were also those subjected to an apoptotic cell death. Fluorouracil 43-47 transformation related protein 53, pseudogene Mus musculus 97-100 9050858-7 1997 p53-Dependent cell death induced by 5-FU was only inhibited by administration of uridine. Fluorouracil 36-40 transformation related protein 53, pseudogene Mus musculus 0-3 9050858-10 1997 The data show that 5-FU-induced cell death of intestinal epithelial cells is p53-dependent and suggests that changes in RNA metabolism initiate events culminating in the expression of p53. Fluorouracil 19-23 transformation related protein 53, pseudogene Mus musculus 77-80 9050858-10 1997 The data show that 5-FU-induced cell death of intestinal epithelial cells is p53-dependent and suggests that changes in RNA metabolism initiate events culminating in the expression of p53. Fluorouracil 19-23 transformation related protein 53, pseudogene Mus musculus 184-187 9137428-2 1997 We found that the production of interleukin (IL)-1 alpha and prostaglandin E2(PGE2) in whole spleen cell cultures from mice given a sublethal dose of 5-Fu was induced in the week after treatment, and subsequently the production of IL-4 and IL-IO was induced. Fluorouracil 150-154 interleukin 1 alpha Mus musculus 32-56 9137428-2 1997 We found that the production of interleukin (IL)-1 alpha and prostaglandin E2(PGE2) in whole spleen cell cultures from mice given a sublethal dose of 5-Fu was induced in the week after treatment, and subsequently the production of IL-4 and IL-IO was induced. Fluorouracil 150-154 interleukin 4 Mus musculus 231-235 9137428-3 1997 The administration of 5-Fu and CNG suppressed the production of IL-1 alpha and PGE2, and induced the production of IL-4 and IL-10 earlier than 5-Fu alone did. Fluorouracil 22-26 interleukin 1 alpha Mus musculus 64-74 9137428-3 1997 The administration of 5-Fu and CNG suppressed the production of IL-1 alpha and PGE2, and induced the production of IL-4 and IL-10 earlier than 5-Fu alone did. Fluorouracil 22-26 interleukin 4 Mus musculus 115-119 9048835-2 1997 PURPOSE: We evaluated relationships between the level and/or pattern of tumor TS expression and response to fluorouracil (5-FU)-based neoadjuvant chemotherapy in patients with advanced head and neck cancer. Fluorouracil 108-120 thymidylate synthetase Homo sapiens 78-80 11714538-0 2001 Thymidylate synthase and dihydropyrimidine dehydrogenase activities in non-small cell lung cancer tissues: relationship with in vitro sensitivity to 5-fluorouracil. Fluorouracil 149-163 thymidylate synthetase Homo sapiens 0-20 11714538-1 2001 We examined enzymatic activities of thymidylate synthase (TS) and dihydropyrimidine dehydrogenase (DPD) in non-small cell lung cancer (NSCLC) tissues to determine the relationship to tumor sensitivity to 5-fluorouracil (5-FU). Fluorouracil 204-218 thymidylate synthetase Homo sapiens 36-56 11714538-1 2001 We examined enzymatic activities of thymidylate synthase (TS) and dihydropyrimidine dehydrogenase (DPD) in non-small cell lung cancer (NSCLC) tissues to determine the relationship to tumor sensitivity to 5-fluorouracil (5-FU). Fluorouracil 220-224 thymidylate synthetase Homo sapiens 36-56 12467230-8 2001 This potentiation of tumor response was accompanied by a total change in the FUra anabolic pathway with a 5000% increase of cytosolic fluorodeoxyuridine monophosphate, a stronger and longer inhibition of thymidylate synthase, and 300% augmentation of DNA damage. Fluorouracil 77-81 thymidylate synthetase Homo sapiens 204-224 11705873-3 2001 We have demonstrated that inducible expression of TS increased the IC(50) dose of the TS-targeted therapeutic agents 5-FU, TDX, and ZD9331 by 2-, 9- and 24-fold respectively. Fluorouracil 117-121 thymidylate synthetase Homo sapiens 50-52 11705873-3 2001 We have demonstrated that inducible expression of TS increased the IC(50) dose of the TS-targeted therapeutic agents 5-FU, TDX, and ZD9331 by 2-, 9- and 24-fold respectively. Fluorouracil 117-121 thymidylate synthetase Homo sapiens 86-88 11705873-6 2001 Cell cycle analyses revealed that IC(50) doses of 5-FU, TDX and MTA caused an S-phase arrest in cells that did not overexpress TS, and this arrest was overcome when TS was up-regulated. Fluorouracil 50-54 thymidylate synthetase Homo sapiens 127-129 11705873-6 2001 Cell cycle analyses revealed that IC(50) doses of 5-FU, TDX and MTA caused an S-phase arrest in cells that did not overexpress TS, and this arrest was overcome when TS was up-regulated. Fluorouracil 50-54 thymidylate synthetase Homo sapiens 165-167 9048835-2 1997 PURPOSE: We evaluated relationships between the level and/or pattern of tumor TS expression and response to fluorouracil (5-FU)-based neoadjuvant chemotherapy in patients with advanced head and neck cancer. Fluorouracil 122-126 thymidylate synthetase Homo sapiens 78-80 1591724-9 1992 Resistance to 5-fluorouracil was associated with significantly increased thymidylate synthase activity (P less than 0.01), but this was not reflected in altered gene expression, while increased sensitivity to methotrexate was accompanied by increased drug uptake but by unaltered activity and expression of dihydrofolate reductase. Fluorouracil 14-28 dihydrofolate reductase Homo sapiens 307-330 12450430-1 2001 Thymidylate synthase (TS) expression has been identified as an important predictor of response to 5-fluorouracil (5-FU). Fluorouracil 98-112 thymidylate synthetase Homo sapiens 0-20 12450430-1 2001 Thymidylate synthase (TS) expression has been identified as an important predictor of response to 5-fluorouracil (5-FU). Fluorouracil 98-112 thymidylate synthetase Homo sapiens 22-24 12450430-1 2001 Thymidylate synthase (TS) expression has been identified as an important predictor of response to 5-fluorouracil (5-FU). Fluorouracil 114-118 thymidylate synthetase Homo sapiens 0-20 12450430-1 2001 Thymidylate synthase (TS) expression has been identified as an important predictor of response to 5-fluorouracil (5-FU). Fluorouracil 114-118 thymidylate synthetase Homo sapiens 22-24 12450430-9 2001 The discordant TS expression between primary and metastatic tumors is a critical factor that must be taken into account when TS is being used as a predictive biomarker for the antitumor effect of 5-FU-based chemotherapy. Fluorouracil 196-200 thymidylate synthetase Homo sapiens 15-17 12450430-9 2001 The discordant TS expression between primary and metastatic tumors is a critical factor that must be taken into account when TS is being used as a predictive biomarker for the antitumor effect of 5-FU-based chemotherapy. Fluorouracil 196-200 thymidylate synthetase Homo sapiens 125-127 1587305-1 1992 The ability of highly purified, recombinant human macrophage colony-stimulating factor (M-CSF) and recombinant human interleukin 1 alpha (IL-1) to rescue hematopoietic activity from the myelosuppressive effects of 5-fluorouracil (5-FU) was investigated in the C57Bl/6 mouse. Fluorouracil 214-228 interleukin 1 alpha Homo sapiens 138-142 1587305-1 1992 The ability of highly purified, recombinant human macrophage colony-stimulating factor (M-CSF) and recombinant human interleukin 1 alpha (IL-1) to rescue hematopoietic activity from the myelosuppressive effects of 5-fluorouracil (5-FU) was investigated in the C57Bl/6 mouse. Fluorouracil 230-234 interleukin 1 alpha Homo sapiens 138-142 1587305-2 1992 IL-1 (q24 h x 4) stimulated granulopoietic recovery in the 5-FU-treated animals and reduced the period of severe neutropenia associated with this drug by 7 days. Fluorouracil 59-63 interleukin 1 alpha Homo sapiens 0-4 1587305-5 1992 Unexpectedly, the combination of IL-1 plus M-CSF (q24 h, days 1-4) followed by M-CSF (q24 h, days 5-14) resulted in a more than additive stimulation of progenitor recovery in both the marrow and the spleen that was observed as early as day 3 following 5-FU treatment. Fluorouracil 252-256 interleukin 1 alpha Homo sapiens 33-37 1587305-5 1992 Unexpectedly, the combination of IL-1 plus M-CSF (q24 h, days 1-4) followed by M-CSF (q24 h, days 5-14) resulted in a more than additive stimulation of progenitor recovery in both the marrow and the spleen that was observed as early as day 3 following 5-FU treatment. Fluorouracil 252-256 colony stimulating factor 1 Homo sapiens 43-48 1587305-5 1992 Unexpectedly, the combination of IL-1 plus M-CSF (q24 h, days 1-4) followed by M-CSF (q24 h, days 5-14) resulted in a more than additive stimulation of progenitor recovery in both the marrow and the spleen that was observed as early as day 3 following 5-FU treatment. Fluorouracil 252-256 colony stimulating factor 1 Homo sapiens 79-84 1587305-6 1992 Furthermore, in the absence of protracted M-CSF administration on days 5-14, the 4-day rescue with a combination of IL-1 plus M-CSF also resulted in a more than additive effect on the recovery from 5-FU-induced neutropenia. Fluorouracil 198-202 interleukin 1 alpha Homo sapiens 116-120 1587305-6 1992 Furthermore, in the absence of protracted M-CSF administration on days 5-14, the 4-day rescue with a combination of IL-1 plus M-CSF also resulted in a more than additive effect on the recovery from 5-FU-induced neutropenia. Fluorouracil 198-202 colony stimulating factor 1 Homo sapiens 126-131 1587305-7 1992 Collectively, these observations demonstrated that IL-1 and M-CSF can interact synergistically to stimulate granulopoietic recovery in the 5-FU-treated animal. Fluorouracil 139-143 interleukin 1 alpha Homo sapiens 51-55 1587305-7 1992 Collectively, these observations demonstrated that IL-1 and M-CSF can interact synergistically to stimulate granulopoietic recovery in the 5-FU-treated animal. Fluorouracil 139-143 colony stimulating factor 1 Homo sapiens 60-65 1641659-8 1992 High levels of deoxyuridine monophosphate that have been associated with resistance to 5-fluorouracil can be suppressed by hydroxyurea, leading to greater inhibition of thymidylate synthase. Fluorouracil 87-101 thymidylate synthetase Homo sapiens 169-189 1533568-1 1992 We have previously shown that interleukin-2 (IL-2) is able to induce the generation of natural killer (NK) activity in bone marrow (BM) cell cultures from mice pretreated with 5-fluorouracil (5-FU). Fluorouracil 176-190 interleukin 2 Mus musculus 30-43 1533568-1 1992 We have previously shown that interleukin-2 (IL-2) is able to induce the generation of natural killer (NK) activity in bone marrow (BM) cell cultures from mice pretreated with 5-fluorouracil (5-FU). Fluorouracil 176-190 interleukin 2 Mus musculus 45-49 1533568-1 1992 We have previously shown that interleukin-2 (IL-2) is able to induce the generation of natural killer (NK) activity in bone marrow (BM) cell cultures from mice pretreated with 5-fluorouracil (5-FU). Fluorouracil 192-196 interleukin 2 Mus musculus 30-43 1533568-1 1992 We have previously shown that interleukin-2 (IL-2) is able to induce the generation of natural killer (NK) activity in bone marrow (BM) cell cultures from mice pretreated with 5-fluorouracil (5-FU). Fluorouracil 192-196 interleukin 2 Mus musculus 45-49 1532671-3 1992 Sufficient levels of CH2-THF enhance the inhibition of the enzyme thymidylate synthase by the 5-FU metabolite FdUMP. Fluorouracil 94-98 thin fur Mus musculus 25-28 12450432-1 2001 Thymidylate synthase (TS) is an important target for chemotherapy drugs, such as 5-fluorouracil (5-FU), 5-fluorodeoxyuridine (FUDR), oral 5-FU prodrugs (e.g., uracil/tegafur [UFT], S-1, and capecitabine), and other novel folate-based drugs (e.g., raltitrexed, pemetrexed, and nolatrexed). Fluorouracil 81-95 thymidylate synthetase Homo sapiens 0-20 12450432-1 2001 Thymidylate synthase (TS) is an important target for chemotherapy drugs, such as 5-fluorouracil (5-FU), 5-fluorodeoxyuridine (FUDR), oral 5-FU prodrugs (e.g., uracil/tegafur [UFT], S-1, and capecitabine), and other novel folate-based drugs (e.g., raltitrexed, pemetrexed, and nolatrexed). Fluorouracil 81-95 thymidylate synthetase Homo sapiens 22-24 1557655-0 1992 Time course of inhibition of thymidylate synthase in patients treated with fluorouracil and leucovorin. Fluorouracil 75-87 thymidylate synthetase Homo sapiens 29-49 12450432-1 2001 Thymidylate synthase (TS) is an important target for chemotherapy drugs, such as 5-fluorouracil (5-FU), 5-fluorodeoxyuridine (FUDR), oral 5-FU prodrugs (e.g., uracil/tegafur [UFT], S-1, and capecitabine), and other novel folate-based drugs (e.g., raltitrexed, pemetrexed, and nolatrexed). Fluorouracil 97-101 thymidylate synthetase Homo sapiens 0-20 12450432-1 2001 Thymidylate synthase (TS) is an important target for chemotherapy drugs, such as 5-fluorouracil (5-FU), 5-fluorodeoxyuridine (FUDR), oral 5-FU prodrugs (e.g., uracil/tegafur [UFT], S-1, and capecitabine), and other novel folate-based drugs (e.g., raltitrexed, pemetrexed, and nolatrexed). Fluorouracil 97-101 thymidylate synthetase Homo sapiens 22-24 12450432-1 2001 Thymidylate synthase (TS) is an important target for chemotherapy drugs, such as 5-fluorouracil (5-FU), 5-fluorodeoxyuridine (FUDR), oral 5-FU prodrugs (e.g., uracil/tegafur [UFT], S-1, and capecitabine), and other novel folate-based drugs (e.g., raltitrexed, pemetrexed, and nolatrexed). Fluorouracil 138-142 thymidylate synthetase Homo sapiens 0-20 1557655-1 1992 The inhibition of thymidylate synthase (TS) by the fluorouracil (5-FU) metabolite 5-fluoro-2"-deoxyuridine-5"-monophosphate (FdUMP) is considered to be one of the main mechanisms of action of 5-FU. Fluorouracil 51-63 thymidylate synthetase Homo sapiens 18-38 12450432-1 2001 Thymidylate synthase (TS) is an important target for chemotherapy drugs, such as 5-fluorouracil (5-FU), 5-fluorodeoxyuridine (FUDR), oral 5-FU prodrugs (e.g., uracil/tegafur [UFT], S-1, and capecitabine), and other novel folate-based drugs (e.g., raltitrexed, pemetrexed, and nolatrexed). Fluorouracil 138-142 thymidylate synthetase Homo sapiens 22-24 1557655-1 1992 The inhibition of thymidylate synthase (TS) by the fluorouracil (5-FU) metabolite 5-fluoro-2"-deoxyuridine-5"-monophosphate (FdUMP) is considered to be one of the main mechanisms of action of 5-FU. Fluorouracil 51-63 thymidylate synthetase Homo sapiens 40-42 11676864-7 2001 TS content in the cell lines significantly correlated with 5-FU sensitivity, but DPD activity did not. Fluorouracil 59-63 thymidylate synthetase Homo sapiens 0-2 1557655-1 1992 The inhibition of thymidylate synthase (TS) by the fluorouracil (5-FU) metabolite 5-fluoro-2"-deoxyuridine-5"-monophosphate (FdUMP) is considered to be one of the main mechanisms of action of 5-FU. Fluorouracil 65-69 thymidylate synthetase Homo sapiens 18-38 11676864-8 2001 Therefore, in the present study, TS expression was concluded to influence the high resistance to 5-FU of biliary tract carcinoma in comparison with the carcinomas of the other digestive organs. Fluorouracil 97-101 thymidylate synthetase Homo sapiens 33-35 1557655-1 1992 The inhibition of thymidylate synthase (TS) by the fluorouracil (5-FU) metabolite 5-fluoro-2"-deoxyuridine-5"-monophosphate (FdUMP) is considered to be one of the main mechanisms of action of 5-FU. Fluorouracil 65-69 thymidylate synthetase Homo sapiens 40-42 1557655-1 1992 The inhibition of thymidylate synthase (TS) by the fluorouracil (5-FU) metabolite 5-fluoro-2"-deoxyuridine-5"-monophosphate (FdUMP) is considered to be one of the main mechanisms of action of 5-FU. Fluorouracil 192-196 thymidylate synthetase Homo sapiens 18-38 11556832-0 2001 A polymorphism in the enhancer region of the thymidylate synthase promoter influences the survival of colorectal cancer patients treated with 5-fluorouracil. Fluorouracil 142-156 thymidylate synthetase Homo sapiens 45-65 11556832-1 2001 High levels of thymidylate synthase (TS) expression have been associated with poor survival of colorectal cancer (CRC) patients to 5-fluorouracil (5-FU)-based chemotherapy. Fluorouracil 131-145 thymidylate synthetase Homo sapiens 15-35 11556832-1 2001 High levels of thymidylate synthase (TS) expression have been associated with poor survival of colorectal cancer (CRC) patients to 5-fluorouracil (5-FU)-based chemotherapy. Fluorouracil 131-145 thymidylate synthetase Homo sapiens 37-39 11556832-1 2001 High levels of thymidylate synthase (TS) expression have been associated with poor survival of colorectal cancer (CRC) patients to 5-fluorouracil (5-FU)-based chemotherapy. Fluorouracil 147-151 thymidylate synthetase Homo sapiens 15-35 1557655-1 1992 The inhibition of thymidylate synthase (TS) by the fluorouracil (5-FU) metabolite 5-fluoro-2"-deoxyuridine-5"-monophosphate (FdUMP) is considered to be one of the main mechanisms of action of 5-FU. Fluorouracil 192-196 thymidylate synthetase Homo sapiens 40-42 11556832-1 2001 High levels of thymidylate synthase (TS) expression have been associated with poor survival of colorectal cancer (CRC) patients to 5-fluorouracil (5-FU)-based chemotherapy. Fluorouracil 147-151 thymidylate synthetase Homo sapiens 37-39 11556832-5 2001 These results demonstrate that a polymorphism within the TS gene, probably through its effect on TS expression levels, can influence the survival benefit obtained by CRC patients from 5-FU-based chemotherapy. Fluorouracil 184-188 thymidylate synthetase Homo sapiens 57-59 1557655-13 1992 At least eight patients with an undetectable TS-free showed response to subsequent intraarterial treatment with 5-FU. Fluorouracil 112-116 thymidylate synthetase Homo sapiens 45-47 1557655-17 1992 The large variation in TS may be related to the observed variation in clinical response to 5-FU treatment. Fluorouracil 91-95 thymidylate synthetase Homo sapiens 23-25 1557656-7 1992 Interferon gamma interacts with 5-FU in H630 colon cancer cells at the level of thymidylate synthase and enhances cytotoxicity of 5-FU by eliminating the 5-FU-induced acute overexpression of the target enzyme. Fluorouracil 32-36 thymidylate synthetase Homo sapiens 80-100 1372030-1 1992 In agar culture of post 5-fluorouracil mouse bone marrow cells (FUBM), recombinant rat stem cell factor (rrSCF) synergizes with granulocyte colony-stimulating factor (G-CSF), interleukin-3 (IL-3) or interleukin-6 (IL-6) to stimulate primitive progenitor cells (HPP-CFCs). Fluorouracil 24-38 KIT ligand Rattus norvegicus 87-103 11545425-6 2001 RESULTS: Exposure to 5-FU for 1 and 5 min resulted in a similar and significant inhibition of the culture-induced increase in stromal cell density (P < 0.01), a significant reduction in the percentage of viable cells (P < 0.02), and reduced PCNA indices, compared with controls. Fluorouracil 21-25 proliferating cell nuclear antigen Homo sapiens 247-251 11406570-0 2001 c-myc/p53 interaction determines sensitivity of human colon carcinoma cells to 5-fluorouracil in vitro and in vivo. Fluorouracil 79-93 MYC proto-oncogene, bHLH transcription factor Homo sapiens 0-5 11406570-1 2001 Colon carcinoma cells overexpress c-myc due to defective Wnt signaling, but only patients whose tumors have an amplified c-myc gene show improved disease-free and overall survival in response to 5-fluoruracil (5FU). Fluorouracil 195-208 MYC proto-oncogene, bHLH transcription factor Homo sapiens 121-126 11406570-6 2001 Finally, the in vitro data predicted that only patients with both amplified c-myc and wild-type p53 in their primary tumors would be responsive to 5FU-based therapy, which was borne out by analysis of tumors from 135 patients entered into a Phase III clinical trial of 5FU-based adjuvant therapy. Fluorouracil 147-150 MYC proto-oncogene, bHLH transcription factor Homo sapiens 76-81 11510034-8 2001 Gemcitabine/CTX/5-fluorouracil/folinic acid is well tolerated by metastatic breast cancer patients pretreated with anthracyclines/taxanes, up to a CTX dose of 800 mg/m(2). Fluorouracil 16-30 cytochrome P450 family 27 subfamily A member 1 Homo sapiens 147-150 1564955-2 1992 Multilineage colony formation from mice that had been treated with 150 mg/kg 5-fluorouracil was assayed in cultures containing interleukin-3, interleukin-6, and erythropoietin. Fluorouracil 77-91 erythropoietin Mus musculus 161-175 1371964-3 1992 The daily administration of IL-1 alpha (100 ng/mouse/day) after 5-FU treatment markedly accelerated the recovery of bone marrow CFU-C. Fluorouracil 64-68 interleukin 1 alpha Mus musculus 28-38 1727369-10 1992 Those tumors with the lowest thymidylate synthase expression had the best response to both the 5-fluorouracil-leucovorin and 5-fluorouracil-cisplatin combinations. Fluorouracil 95-109 thymidylate synthetase Homo sapiens 29-49 1425012-5 1992 Injections of LIF also marginally accelerated platelet regeneration in mice pre-injected with 5-fluorouracil or subjected to whole-body irradiation and transplantation of marrow cells. Fluorouracil 94-108 leukemia inhibitory factor Mus musculus 14-17 1727111-6 1992 The MTD for combined-RT/chemotherapy was 250 mg/m2; therefore, the recommended dose of 5-FU is 200 mg/m2. Fluorouracil 87-91 metallothionein 1E Homo sapiens 4-7 1727111-7 1992 The MTD for post-RT chemotherapy was 375 mg/m2; therefore, the recommended dose of 5-FU is 325 mg/m2. Fluorouracil 83-87 metallothionein 1E Homo sapiens 4-7 1596583-6 1992 In patients treated with a combination of 5-fluorouracil and leucovorin, mRNA levels for TS increased approximately an order of magnitude in tumor samples 4 and 24 hr after drug treatment, whereas TS levels decreased. Fluorouracil 42-56 thymidylate synthetase Homo sapiens 89-91 11383214-6 2001 In vitro chemosensitivity to 5-FU in the lung and lymph node metastases was tested using CD-DST, and the enzymatic activities of thymidine synthetase (TS) and dihydropyrimidine dehydrogenase (DPD) in the lung and lymph node metastases were measured. Fluorouracil 29-33 dihydropyrimidine dehydrogenase Rattus norvegicus 192-195 11383215-0 2001 [Correlation between 5-fluorouracil (5-FU) sensitivity as measured by collagen gel droplet embedded culture drug sensitivity test (CD-DST) and expression of orotate phosphoribosyl transferase (OPRT), thymidylate synthase (TS), and dihydropyrimidine dehydrogenase (DPD) in colorectal cancer]. Fluorouracil 37-41 uridine monophosphate synthetase Homo sapiens 193-197 11383215-0 2001 [Correlation between 5-fluorouracil (5-FU) sensitivity as measured by collagen gel droplet embedded culture drug sensitivity test (CD-DST) and expression of orotate phosphoribosyl transferase (OPRT), thymidylate synthase (TS), and dihydropyrimidine dehydrogenase (DPD) in colorectal cancer]. Fluorouracil 37-41 thymidylate synthetase Homo sapiens 200-220 1596583-6 1992 In patients treated with a combination of 5-fluorouracil and leucovorin, mRNA levels for TS increased approximately an order of magnitude in tumor samples 4 and 24 hr after drug treatment, whereas TS levels decreased. Fluorouracil 42-56 thymidylate synthetase Homo sapiens 197-199 1421872-3 1992 Although IFN, given as 600,000 units/mouse daily sc x 14, and 5-FU, given as 60 mg/kg q4d x 3 ip, showed additive antitumor activity against Co-4, the thymidylate synthetase (TS) inhibition rate was unchanged in the tumors treated with the IFN/5-FU combination in comparison with those treated with 5-FU alone. Fluorouracil 62-66 complement C4A (Rodgers blood group) Homo sapiens 141-145 11274973-1 2001 Potentiation of the cytotoxic activity of 5-fluorouracil (FUra) by folinic acid (5-HCO-H4folate) is due to elevation of the methylene tetrahydrofolate (CH2-H4folate) level, which increases the stability of the ternary complex of thymidylate synthase (TS), fluorodeoxyuridine monophosphate, and CH2-H4folate that inactivates the TS. Fluorouracil 42-56 thymidylate synthetase Homo sapiens 229-249 11274973-1 2001 Potentiation of the cytotoxic activity of 5-fluorouracil (FUra) by folinic acid (5-HCO-H4folate) is due to elevation of the methylene tetrahydrofolate (CH2-H4folate) level, which increases the stability of the ternary complex of thymidylate synthase (TS), fluorodeoxyuridine monophosphate, and CH2-H4folate that inactivates the TS. Fluorouracil 58-62 thymidylate synthetase Homo sapiens 229-249 11706756-2 2001 The aim of this study was to determine the predictive value of p53 mutation or the expression of GML, a target of p53, for sensitivity to 5-FU and MMC. Fluorouracil 138-142 glycosylphosphatidylinositol anchored molecule like Homo sapiens 97-100 11706756-8 2001 However, when RPMI4788-GML were exposed to 5-FU for 24 h, the sensitivity of RPMI4788-GML was slightly increased compared with that of the parental cells, but was slightly lower than that of HCT116. Fluorouracil 43-47 glycosylphosphatidylinositol anchored molecule like Homo sapiens 23-26 11706756-8 2001 However, when RPMI4788-GML were exposed to 5-FU for 24 h, the sensitivity of RPMI4788-GML was slightly increased compared with that of the parental cells, but was slightly lower than that of HCT116. Fluorouracil 43-47 glycosylphosphatidylinositol anchored molecule like Homo sapiens 86-89 11706756-9 2001 CONCLUSION: GML expression and p53 mutation in colorectal cancer may be useful predictive genetic markers for sensitivity to MMC and 5-FU, respectively. Fluorouracil 133-137 glycosylphosphatidylinositol anchored molecule like Homo sapiens 12-15 1720706-10 1991 Quantitation of TS by Western blot analysis and biochemical FdUMP binding assay in 5-fluorouracil-resistant colon carcinoma cell lines (NCI H630R10, NCI H630R1) and a sensitive colon carcinoma cell line (NCI H630) revealed a 36- and 6-fold increase in TS in the resistant cell line as measured by the biochemical assay compared to a 39- and 10.6-fold increase as measured by densitometric analysis of the Western blot. Fluorouracil 83-97 thymidylate synthetase Homo sapiens 16-18 11245445-1 2001 Thymidylate synthase (TS) is a crucial target for 5-fluorouracil (5-FU) in the de novo pathway of pyrimidine synthesis, which is necessary for DNA synthesis. Fluorouracil 50-64 thymidylate synthetase Homo sapiens 0-20 11245445-1 2001 Thymidylate synthase (TS) is a crucial target for 5-fluorouracil (5-FU) in the de novo pathway of pyrimidine synthesis, which is necessary for DNA synthesis. Fluorouracil 66-70 thymidylate synthetase Homo sapiens 0-20 11180520-1 2001 The aim of the study was to evaluate the efficacy, tolerability and quality of life in 5-fluorouracil (5-FU) pretreated colorectal cancer patients after combined 5-FU and Ginkgo biloba extract GBE 761 ONC (i.e. the Ginkgo biloba special extract EGb 761(R)) therapy. Fluorouracil 87-101 1,4-alpha-glucan branching enzyme 1 Homo sapiens 193-196 11180520-1 2001 The aim of the study was to evaluate the efficacy, tolerability and quality of life in 5-fluorouracil (5-FU) pretreated colorectal cancer patients after combined 5-FU and Ginkgo biloba extract GBE 761 ONC (i.e. the Ginkgo biloba special extract EGb 761(R)) therapy. Fluorouracil 103-107 1,4-alpha-glucan branching enzyme 1 Homo sapiens 193-196 11212266-3 2001 In the cell, 5-FU is metabolized to 5-fluoro-2"-deoxyuridine 5"-monophosphate, a tight binding covalent inhibitor of thymidylate synthase. Fluorouracil 13-17 thymidylate synthetase Homo sapiens 117-137 11115547-1 2001 We examined whether a suicide gene/prodrug system using the uracil phosphoribosyltransferase (UPRT) of E. coli origin and 5-fluorouracil (5-FU) could achieve a bystander effect in two rodent tumor cell lines, murine colon carcinoma (Colon 26) and rat gliosarcoma (9L) cells. Fluorouracil 138-142 uracil phosphoribosyltransferase Mus musculus 94-98 1937958-7 1991 Resistance to FUra is acquired through gene amplification as substantiated by a 4- to 6-fold increase of thymidylate synthase gene copies in cells stably adapted to the drug. Fluorouracil 14-18 thymidylate synthetase Homo sapiens 105-125 1913647-6 1991 However, the clone which expressed the highest level of HSP27 was as sensitive as control cells to the cytotoxic action of bis-chloronitrosourea and 5-fluorouracil. Fluorouracil 149-163 heat shock protein family B (small) member 1 Homo sapiens 56-61 11142426-4 2000 TS is also a major target for cancer chemotherapeutic drugs, especially the widely used 5-fluorouracil. Fluorouracil 88-102 thymidylate synthetase Homo sapiens 0-2 11106258-3 2000 We have investigated whether this strain difference in response to raltitrexed is related to differential susceptibilities of intestinal mucosae to undergo apoptosis and also whether p53 expression, a critical factor in 5-fluorouracil-induced intestinal apoptosis and toxicity, modulates this response. Fluorouracil 220-234 transformation related protein 53, pseudogene Mus musculus 183-186 10914738-0 2000 Augmentation of antitumor activity of 5-fluorouracil by interferon alpha is associated with up-regulation of p27Kip1 in human hepatocellular carcinoma cells. Fluorouracil 38-52 cyclin dependent kinase inhibitor 1B Homo sapiens 109-116 1832057-3 1991 We have now examined the synergistic interactions between IL-11 and IL-4 in support of colony formation from marrow cells of mice treated 2 days before with 150 mg/kg 5-fluorouracil. Fluorouracil 167-181 interleukin 4 Mus musculus 68-72 1925442-4 1991 Leucovorin (LV) prolongs the inhibition of the key enzyme, thymidylate synthetase, by stabilizing the ternary complex with activated 5-FU, thus leading to "thymidine-less" death. Fluorouracil 133-137 thymidylate synthetase Homo sapiens 59-81 10854535-5 2000 Furthermore, intraperitoneal injection of 5-fluorouracil (5-FU) markedly inhibited the growth of the TSC-22-expressing TYS tumors, but did not affect the growth of control tumors. Fluorouracil 42-56 TSC22 domain family member 1 Homo sapiens 101-107 10854535-5 2000 Furthermore, intraperitoneal injection of 5-fluorouracil (5-FU) markedly inhibited the growth of the TSC-22-expressing TYS tumors, but did not affect the growth of control tumors. Fluorouracil 58-62 TSC22 domain family member 1 Homo sapiens 101-107 10854535-6 2000 It was found by TUNEL assay that TSC-22-expressing TYS tumors were induced to undergo apoptosis by 5-FU treatment. Fluorouracil 99-103 TSC22 domain family member 1 Homo sapiens 33-39 10854535-7 2000 These findings suggest that overexpression of TSC-22 protein in TYS cells enhances the in vivo chemosensitivity of the cells to 5-FU via induction of apoptosis. Fluorouracil 128-132 TSC22 domain family member 1 Homo sapiens 46-52 2060020-1 1991 We have previously shown that interleukin-2 (IL-2) is able to induce the generation of natural killer (NK) activity in bone marrow (BM) cells from mice pretreated with 5-fluorouracil. Fluorouracil 168-182 interleukin 2 Mus musculus 30-43 10820149-13 2000 A study on a larger scale is ongoing to determine the role of TS as a predictive parameter in patients with colorectal cancer treated either with postoperative adjuvant 5FU/levamisole or with surgery only. Fluorouracil 169-172 thymidylate synthetase Homo sapiens 62-64 10779637-3 2000 In this report, we demonstrate that 5-fluorouracil (5-FU)-induced early apoptotic cells are characterized by (i) ultracondensed mitochondria, (ii) no change in the microvilli or nucleus, (iii) a high mitochondrial transmembrane potential (Deltapsi(m)), and (iv) being annexin V(negative). Fluorouracil 36-50 annexin A5 Homo sapiens 268-277 10779637-3 2000 In this report, we demonstrate that 5-fluorouracil (5-FU)-induced early apoptotic cells are characterized by (i) ultracondensed mitochondria, (ii) no change in the microvilli or nucleus, (iii) a high mitochondrial transmembrane potential (Deltapsi(m)), and (iv) being annexin V(negative). Fluorouracil 52-56 annexin A5 Homo sapiens 268-277 10832438-0 2000 [Thymidylate synthase activity after preoperative administration of 5-FU in patients with gastric or colorectal cancer]. Fluorouracil 68-72 thymidylate synthetase Homo sapiens 1-21 2060020-1 1991 We have previously shown that interleukin-2 (IL-2) is able to induce the generation of natural killer (NK) activity in bone marrow (BM) cells from mice pretreated with 5-fluorouracil. Fluorouracil 168-182 interleukin 2 Mus musculus 45-49 2060021-0 1991 Accelerated recovery of antigen-presenting cell activity by the administration of interleukin 1 alpha in 5-fluorouracil-treated mice. Fluorouracil 105-119 interleukin 1 alpha Mus musculus 82-101 2060021-1 1991 In this study, we investigated the effect of human recombinant interleukin-1 alpha (IL-1 alpha) on antigen-presenting cell (APC) activity of spleen cells in mice treated with 5-fluorouracil (5-FU). Fluorouracil 175-189 interleukin 1 alpha Homo sapiens 84-94 2060021-1 1991 In this study, we investigated the effect of human recombinant interleukin-1 alpha (IL-1 alpha) on antigen-presenting cell (APC) activity of spleen cells in mice treated with 5-fluorouracil (5-FU). Fluorouracil 191-195 interleukin 1 alpha Homo sapiens 63-82 2060021-5 1991 The most accelerated recovery was observed when these mice were administered with IL-1 alpha both before and after the 5-FU treatment. Fluorouracil 119-123 interleukin 1 alpha Mus musculus 82-92 2060021-6 1991 The recovery was also accelerated when the mice were injected with IL-1 alpha after the 5-FU treatment, but not when injected before the 5-FU treatment. Fluorouracil 88-92 interleukin 1 alpha Mus musculus 67-77 2064349-8 1991 When administered as single agents, 5-FU and 2.0 Gy resulted in only a modest response by the LLca tumor (TGDs = 1.0 day), while LV had no effect on tumor growth. Fluorouracil 36-40 TDP-glucose 4,6-dehydratase Mus musculus 106-110 1789191-0 1991 Effect of leucovorin on 5-fluorouracil induced inhibition of thymidylate synthase in patients with colon cancer. Fluorouracil 24-38 thymidylate synthetase Homo sapiens 61-81 10857990-5 2000 Certain cell lines demonstrated synergistic interactions with combinations of UCN-01 (20-150 nM) and thiotepa, mitomycin C, cisplatin, melphalan, topotecan, gemcitabine, fludarabine or 5-fluorouracil. Fluorouracil 185-199 urocortin Homo sapiens 78-81 10778986-5 2000 Anti-Fas and anti-FasL antibodies both partly reversed this increase of cell sensitivity, thus confirming the role Fas plays in the modulation of FUra toxicity by d-Ino. Fluorouracil 146-150 Fas ligand Homo sapiens 18-22 1899039-4 1991 Inhibition rates of the antitumor drugs (mitomycin C, doxorubicin, cisplatin, cyclophosphamide, and 5-fluorouracil) for both the murine tumors were more or less raised by coadministration of rHu IL-1 alpha irrespective of medication schedules and combination timings. Fluorouracil 100-114 interleukin 1 alpha Mus musculus 195-205 10739875-10 2000 GH is being evaluated as an intracellular target for inhibition in order to enhance the therapeutic activity of antifolates and fluorouracil. Fluorouracil 128-140 gamma-glutamyl hydrolase Homo sapiens 0-2 11129987-11 2000 (Significant protection occurred in bone marrow cells exposed to 5-FU/TMQ and 5-FU/MTX.) Fluorouracil 65-69 metaxin 1 Homo sapiens 83-86 11129987-11 2000 (Significant protection occurred in bone marrow cells exposed to 5-FU/TMQ and 5-FU/MTX.) Fluorouracil 78-82 metaxin 1 Homo sapiens 83-86 11129987-14 2000 Hence, these studies suggest that a priming and nontoxic dose of 5-FU before high-dose MTX sustains MTX cytotoxicity in breast cancer and protects against MTX toxicity to bone marrow progenitor cells. Fluorouracil 65-69 metaxin 1 Homo sapiens 100-103 11129987-14 2000 Hence, these studies suggest that a priming and nontoxic dose of 5-FU before high-dose MTX sustains MTX cytotoxicity in breast cancer and protects against MTX toxicity to bone marrow progenitor cells. Fluorouracil 65-69 metaxin 1 Homo sapiens 100-103 10635300-1 1999 The relationship of 5-FU-sensitivity to thymidylate synthase (TS) was investigated in a total of 82 gastric cancers of stage III or IV. Fluorouracil 20-24 thymidylate synthetase Homo sapiens 40-60 10635300-1 1999 The relationship of 5-FU-sensitivity to thymidylate synthase (TS) was investigated in a total of 82 gastric cancers of stage III or IV. Fluorouracil 20-24 thymidylate synthetase Homo sapiens 62-64 10635300-7 1999 In the present study, the ratio of patients negative for TS among the high 5-FU-sensitivity group both was 65.2%, both of which have been reported as producing high survival rates. Fluorouracil 75-79 thymidylate synthetase Homo sapiens 57-59 10635300-8 1999 In contrast, the ratio of patients positive for TS in the low 5-FU-sensitivity group was 22.0%. Fluorouracil 62-66 thymidylate synthetase Homo sapiens 48-50 10635300-9 1999 From these results, TS is considered to be responsible for approximately 40-50% of either high or low 5-FU-sensitivity, respectively, when the lower TS expression in the present study was taken into consideration and corrected. Fluorouracil 102-106 thymidylate synthetase Homo sapiens 20-22 10697629-2 1999 5-FU is metabolically converted to 5-fluorouracil-2"-deoxyuridine-5"-monophosphate-(FdUMP) which is believed to inhibit DNA synthesis in neoplastic cells by forming a tightly bound ternary complex with thymidylate synthase (TS). Fluorouracil 0-4 thymidylate synthetase Homo sapiens 202-222 10697629-2 1999 5-FU is metabolically converted to 5-fluorouracil-2"-deoxyuridine-5"-monophosphate-(FdUMP) which is believed to inhibit DNA synthesis in neoplastic cells by forming a tightly bound ternary complex with thymidylate synthase (TS). Fluorouracil 0-4 thymidylate synthetase Homo sapiens 224-226 10697629-8 1999 The effectiveness of adjuvant 5-FU derivatives chemotherapy was reflected in a higher disease-free survival rate in node (+) cases showing TS levels between 5 and 10 pmol/g (p < 0.1), but not in node (-) cases. Fluorouracil 30-34 thymidylate synthetase Homo sapiens 139-141 10697629-10 1999 Breast cancers with extremely high TS levels were accompanied by an unfavorable prognosis; however, those with moderately high TS levels tended to respond to adjuvant chemotherapy with 5-FU derivatives. Fluorouracil 185-189 thymidylate synthetase Homo sapiens 127-129 2116122-4 1990 Investigation of the relationship between the tumor growth inhibition rate determined by subrenal capsule assay and the above parameters (TS inhibition, serum and tissue 5-Fu levels) showed that TS inhibition and tumor growth inhibition were well correlated (r = 0.73). Fluorouracil 170-174 thymidylate synthetase Homo sapiens 195-197 10526171-3 1999 The elevated expression of calpastatin resulted in decreased survival in the presence of okadaic acid (OA) but in no apparent alteration in the sensitivity toward other drugs such as 5-fluorouracil, mitomycin C and methotrexate. Fluorouracil 183-197 calpastatin Homo sapiens 27-38 10545786-3 1999 TS has been used as a target for cancer chemotherapy in the development of fluoropyrimidines such as 5-fluorouracil (5FU) and 5-fluorodeoxyuridine and novel folate-based TS inhibitors such as ZD1694 (Tomudex, Raltitrexed), LY231514, AG337 (Thymitaq) and GW1843U89. Fluorouracil 101-115 thymidylate synthetase Homo sapiens 0-2 10545786-3 1999 TS has been used as a target for cancer chemotherapy in the development of fluoropyrimidines such as 5-fluorouracil (5FU) and 5-fluorodeoxyuridine and novel folate-based TS inhibitors such as ZD1694 (Tomudex, Raltitrexed), LY231514, AG337 (Thymitaq) and GW1843U89. Fluorouracil 117-120 thymidylate synthetase Homo sapiens 0-2 1697091-3 1990 In serum-free cultures, IL-4 inhibited CFU-GM colony formation stimulated by G-CSF, GM-CSF or IL-3 from whole bone marrow cells (whole BM cells), nonadherent, nonphagocytic and T cell-depleted BM cells (fractionated BM cells) or whole BM cells of 5-Fluorouracil (5-FU) treated mice. Fluorouracil 247-261 interleukin 4 Mus musculus 24-28 10471740-2 1999 In the cell, 5-FU is metabolized to 5-fluorodeoxyuridylate (5-FdUMP), a tight binding covalent inhibitor of thymidylate synthase (TS). Fluorouracil 13-17 thymidylate synthetase Homo sapiens 108-128 10471740-2 1999 In the cell, 5-FU is metabolized to 5-fluorodeoxyuridylate (5-FdUMP), a tight binding covalent inhibitor of thymidylate synthase (TS). Fluorouracil 13-17 thymidylate synthetase Homo sapiens 130-132 1697091-3 1990 In serum-free cultures, IL-4 inhibited CFU-GM colony formation stimulated by G-CSF, GM-CSF or IL-3 from whole bone marrow cells (whole BM cells), nonadherent, nonphagocytic and T cell-depleted BM cells (fractionated BM cells) or whole BM cells of 5-Fluorouracil (5-FU) treated mice. Fluorouracil 263-267 interleukin 4 Mus musculus 24-28 2396254-11 1990 The increase of methylene THF, together with the increase of TS, might result in the resistance of the cells to 5-FU. Fluorouracil 112-116 thin fur Mus musculus 26-29 10628354-5 1999 RESULTS: The sequential administration of 5-FU prior to NDP or CDDP (FN or FC therapy) resulted in enhanced inhibition of tumor growth in comparison with NDP, CDDP or 5-FU monotherapy against KB3-1, OCC-1-JCK and LJC-1-JCK squamous carcinomas. Fluorouracil 42-46 chromosome 12 open reading frame 75 Homo sapiens 199-204 10628354-5 1999 RESULTS: The sequential administration of 5-FU prior to NDP or CDDP (FN or FC therapy) resulted in enhanced inhibition of tumor growth in comparison with NDP, CDDP or 5-FU monotherapy against KB3-1, OCC-1-JCK and LJC-1-JCK squamous carcinomas. Fluorouracil 42-46 NIMA related kinase 8 Homo sapiens 205-208 10628354-5 1999 RESULTS: The sequential administration of 5-FU prior to NDP or CDDP (FN or FC therapy) resulted in enhanced inhibition of tumor growth in comparison with NDP, CDDP or 5-FU monotherapy against KB3-1, OCC-1-JCK and LJC-1-JCK squamous carcinomas. Fluorouracil 42-46 NIMA related kinase 8 Homo sapiens 213-222 2117064-1 1990 We previously demonstrated that the antitumor efficacy of various antitumor agents such as 5-fluorouracil and cisplatin against experimental solid tumors was enhanced by pre- or simultaneous administration of human epidermal growth factor (hEGF). Fluorouracil 91-105 epidermal growth factor Homo sapiens 215-238 10499641-5 1999 Additionally, 5-FU revealed a drastically increased thymidylate synthase (TS) gene expression in 5-FU-resistant cells. Fluorouracil 14-18 thymidylate synthetase Homo sapiens 52-72 10499641-5 1999 Additionally, 5-FU revealed a drastically increased thymidylate synthase (TS) gene expression in 5-FU-resistant cells. Fluorouracil 14-18 thymidylate synthetase Homo sapiens 74-76 10499641-5 1999 Additionally, 5-FU revealed a drastically increased thymidylate synthase (TS) gene expression in 5-FU-resistant cells. Fluorouracil 97-101 thymidylate synthetase Homo sapiens 52-72 10499641-5 1999 Additionally, 5-FU revealed a drastically increased thymidylate synthase (TS) gene expression in 5-FU-resistant cells. Fluorouracil 97-101 thymidylate synthetase Homo sapiens 74-76 10499641-6 1999 However, the increasing actions of CDDP and 5-FU on GSTpi, DPD, MRP, and TS expression varied according to the exposure time, concentration, and schedule. Fluorouracil 44-48 thymidylate synthetase Homo sapiens 73-75 10499641-7 1999 A low concentration of CDDP (1 microg/ml, 30 min) followed by 5-FU (0.5 microg/ml, 72 h) was found to cause a less increased expression of DPD, MRP, GSTpi, and TS than either drug alone, thus resulting in synergistic cytotoxicity in 5-FU-resistant COLO201 and CDDP-resistant HCC-48 cells. Fluorouracil 62-66 thymidylate synthetase Homo sapiens 160-162 10424768-6 1999 FUra exposure resulted in transient induction of p53 and p21, which returned to basal levels 24 hr after drug removal. Fluorouracil 0-4 H3 histone pseudogene 16 Homo sapiens 57-60 2117064-1 1990 We previously demonstrated that the antitumor efficacy of various antitumor agents such as 5-fluorouracil and cisplatin against experimental solid tumors was enhanced by pre- or simultaneous administration of human epidermal growth factor (hEGF). Fluorouracil 91-105 epidermal growth factor Homo sapiens 240-244 33766090-9 2021 RESULTS: IRF8 expression can precisely predict the complete pathological response to monoclonal antibody therapy or to select combinations of chemotherapy such as FAC (fluorouracil, adriamycin, and cytoxan) in ER-negative BC subtypes. Fluorouracil 168-180 interferon regulatory factor 8 Homo sapiens 9-13 33810186-4 2021 The oncomiR microRNA-19b (miR-19b) has been reported to functionally play oncogenic roles in colorectal cancer (CRC) cells as well as regulate 5-FU sensitivity and determine outcome in CRC patients. Fluorouracil 143-147 microRNA 19b-1 Homo sapiens 12-24 33810186-4 2021 The oncomiR microRNA-19b (miR-19b) has been reported to functionally play oncogenic roles in colorectal cancer (CRC) cells as well as regulate 5-FU sensitivity and determine outcome in CRC patients. Fluorouracil 143-147 microRNA 19b-1 Homo sapiens 26-33 33793771-9 2021 Furthermore, the miR-424-5p mimic downregulated vimentin and upregulated E-cadherin in 5-fluorouracil-resistant HT-29 cells, whereas the miR-424-5p inhibitor exhibited opposite effects. Fluorouracil 87-101 vimentin Homo sapiens 48-56 33030957-8 2021 Knockout of PD-L1 was shown to attenuate the induction of DNA double-strand breaks (pH2AX) and caspase-3 cleavage by 5-fluorouracil (5-FU) and paclitaxel compared to parental CRC cells. Fluorouracil 117-131 CD274 molecule Homo sapiens 12-17 33030957-8 2021 Knockout of PD-L1 was shown to attenuate the induction of DNA double-strand breaks (pH2AX) and caspase-3 cleavage by 5-fluorouracil (5-FU) and paclitaxel compared to parental CRC cells. Fluorouracil 133-137 CD274 molecule Homo sapiens 12-17 22233820-2 2011 5-FU blocks thymidylate synthase (TS) which cross-links p53 mRNA, inhibiting its synthesis. Fluorouracil 0-4 thymidylate synthetase Homo sapiens 12-32 22233820-2 2011 5-FU blocks thymidylate synthase (TS) which cross-links p53 mRNA, inhibiting its synthesis. Fluorouracil 0-4 thymidylate synthetase Homo sapiens 34-36 34883427-2 2022 Manuka honey, alone and more in combination with 5-Fu, reduced the weight, the diameter and mass density of the spheroids and induced apoptosis through the downregulation of many apoptosis inhibitors, including IAPs (Livin, Survivin, XIAP), IGFs (IGF-I, IGF-II and IGF-IR) and HSPs (HSP-27, HSP-60 and HSP-70). Fluorouracil 49-53 insulin like growth factor 2 Homo sapiens 254-260 34883427-2 2022 Manuka honey, alone and more in combination with 5-Fu, reduced the weight, the diameter and mass density of the spheroids and induced apoptosis through the downregulation of many apoptosis inhibitors, including IAPs (Livin, Survivin, XIAP), IGFs (IGF-I, IGF-II and IGF-IR) and HSPs (HSP-27, HSP-60 and HSP-70). Fluorouracil 49-53 heat shock protein family B (small) member 1 Homo sapiens 283-289 34749259-0 2022 Molecular insights into the interaction of 5-fluorouracil and Fe3O4 nanoparticles with beta-casein: An experimental and theoretical study. Fluorouracil 43-57 casein beta Homo sapiens 87-98 34749259-1 2022 We investigated the potential carrier of milk beta-casein (beta-CN) and its interactions with 5-fluorouracil (5-FU) and iron oxide nanoparticles (Fe3O4 NPs). Fluorouracil 94-108 casein beta Homo sapiens 46-57 34749259-1 2022 We investigated the potential carrier of milk beta-casein (beta-CN) and its interactions with 5-fluorouracil (5-FU) and iron oxide nanoparticles (Fe3O4 NPs). Fluorouracil 94-108 apoptotic chromatin condensation inducer 1 Homo sapiens 59-66 34749259-1 2022 We investigated the potential carrier of milk beta-casein (beta-CN) and its interactions with 5-fluorouracil (5-FU) and iron oxide nanoparticles (Fe3O4 NPs). Fluorouracil 110-114 casein beta Homo sapiens 46-57 34370147-3 2022 The purpose of the study was to investigate the combined treatment of gastric tumorigenesis using Rapamycin and Fluorouracil (5-Fu) through interfering with the Akt/mTOR pathway in a mouse model with PTEN conditional deletion. Fluorouracil 112-124 mechanistic target of rapamycin kinase Mus musculus 165-169 34370147-3 2022 The purpose of the study was to investigate the combined treatment of gastric tumorigenesis using Rapamycin and Fluorouracil (5-Fu) through interfering with the Akt/mTOR pathway in a mouse model with PTEN conditional deletion. Fluorouracil 126-130 mechanistic target of rapamycin kinase Mus musculus 165-169 34370147-7 2022 The combined Rapamycin administration with 5-Fu resulted in better outcomes than their separate administration for the treatment of gastric cancer by inhibiting the mTOR signal pathway. Fluorouracil 43-47 mechanistic target of rapamycin kinase Mus musculus 165-169 34370147-8 2022 Our study indicates that Rapamycin has a synergistic interaction with chemotherapeutic 5-Fu, and demonstrates a potential therapeutic combination treatment on glandular stomach tumor with PTEN functional absence or aberrantly activated Akt/mTOR pathway. Fluorouracil 87-91 mechanistic target of rapamycin kinase Mus musculus 240-244 34785778-7 2022 Specifically, NAA40 stimulates transcription of the one-carbon metabolic gene thymidylate synthase (TYMS), whose product is targeted by 5-fluorouracil (5-FU) and accordingly in primary CRC tumours NAA40 expression associates with TYMS levels and poorer 5-FU response. Fluorouracil 136-150 N-alpha-acetyltransferase 40, NatD catalytic subunit Homo sapiens 14-19 34785778-7 2022 Specifically, NAA40 stimulates transcription of the one-carbon metabolic gene thymidylate synthase (TYMS), whose product is targeted by 5-fluorouracil (5-FU) and accordingly in primary CRC tumours NAA40 expression associates with TYMS levels and poorer 5-FU response. Fluorouracil 136-150 thymidylate synthetase Homo sapiens 78-98 34785778-7 2022 Specifically, NAA40 stimulates transcription of the one-carbon metabolic gene thymidylate synthase (TYMS), whose product is targeted by 5-fluorouracil (5-FU) and accordingly in primary CRC tumours NAA40 expression associates with TYMS levels and poorer 5-FU response. Fluorouracil 136-150 thymidylate synthetase Homo sapiens 100-104 34785778-7 2022 Specifically, NAA40 stimulates transcription of the one-carbon metabolic gene thymidylate synthase (TYMS), whose product is targeted by 5-fluorouracil (5-FU) and accordingly in primary CRC tumours NAA40 expression associates with TYMS levels and poorer 5-FU response. Fluorouracil 152-156 N-alpha-acetyltransferase 40, NatD catalytic subunit Homo sapiens 14-19 34785778-7 2022 Specifically, NAA40 stimulates transcription of the one-carbon metabolic gene thymidylate synthase (TYMS), whose product is targeted by 5-fluorouracil (5-FU) and accordingly in primary CRC tumours NAA40 expression associates with TYMS levels and poorer 5-FU response. Fluorouracil 152-156 thymidylate synthetase Homo sapiens 78-98 34785778-7 2022 Specifically, NAA40 stimulates transcription of the one-carbon metabolic gene thymidylate synthase (TYMS), whose product is targeted by 5-fluorouracil (5-FU) and accordingly in primary CRC tumours NAA40 expression associates with TYMS levels and poorer 5-FU response. Fluorouracil 152-156 thymidylate synthetase Homo sapiens 100-104 34785778-7 2022 Specifically, NAA40 stimulates transcription of the one-carbon metabolic gene thymidylate synthase (TYMS), whose product is targeted by 5-fluorouracil (5-FU) and accordingly in primary CRC tumours NAA40 expression associates with TYMS levels and poorer 5-FU response. Fluorouracil 253-257 N-alpha-acetyltransferase 40, NatD catalytic subunit Homo sapiens 14-19 34821902-6 2021 Moreover, GA could up-regulate the expression of neuronal survival and growth-related proteins, such as BDNF, p-ERK, p-CREB, p-Akt, p-GSK3beta, Nrf2, p-mTOR, and p-S6, in the hippocampi of 5-FU-treated mice. Fluorouracil 189-193 brain derived neurotrophic factor Mus musculus 104-108 34821902-6 2021 Moreover, GA could up-regulate the expression of neuronal survival and growth-related proteins, such as BDNF, p-ERK, p-CREB, p-Akt, p-GSK3beta, Nrf2, p-mTOR, and p-S6, in the hippocampi of 5-FU-treated mice. Fluorouracil 189-193 mechanistic target of rapamycin kinase Mus musculus 152-156 34034636-8 2021 Results showed that insulin combined with 5-FU suppressed cell viability by 30% in JEG-3 and 43% in JAR compared with 5-FU alone in 72 h. What"s more, insulin combined with 5-FU promoted cell apoptosis, inhibited cell proliferation, migration, and phosphorylation of survivin at residue threonine 34 (Thr34) and drug resistance-related proteins, P-GP and MRP1 levels (p < 0.05). Fluorouracil 42-46 phosphoglycolate phosphatase Homo sapiens 346-350 34034636-8 2021 Results showed that insulin combined with 5-FU suppressed cell viability by 30% in JEG-3 and 43% in JAR compared with 5-FU alone in 72 h. What"s more, insulin combined with 5-FU promoted cell apoptosis, inhibited cell proliferation, migration, and phosphorylation of survivin at residue threonine 34 (Thr34) and drug resistance-related proteins, P-GP and MRP1 levels (p < 0.05). Fluorouracil 118-122 phosphoglycolate phosphatase Homo sapiens 346-350 10482907-0 1999 Antisense down-regulation of thymidylate synthase to suppress growth and enhance cytotoxicity of 5-FUdR, 5-FU and Tomudex in HeLa cells. Fluorouracil 97-101 thymidylate synthetase Homo sapiens 29-49 34034636-8 2021 Results showed that insulin combined with 5-FU suppressed cell viability by 30% in JEG-3 and 43% in JAR compared with 5-FU alone in 72 h. What"s more, insulin combined with 5-FU promoted cell apoptosis, inhibited cell proliferation, migration, and phosphorylation of survivin at residue threonine 34 (Thr34) and drug resistance-related proteins, P-GP and MRP1 levels (p < 0.05). Fluorouracil 173-177 phosphoglycolate phosphatase Homo sapiens 346-350 34167427-0 2021 Novel mutual prodrug of 5-fluorouracil and heme oxygenase-1 inhibitor (5-FU/HO-1 hybrid): design and preliminary in vitro evaluation. Fluorouracil 24-38 heme oxygenase 1 Homo sapiens 43-59 10885904-3 1999 Several other enzymes of pyrimidine metabolism, i.e. thymidylate synthase (TS), thymidine kinase (TK) and pyrimidine nucleoside phosphorylase (PNP), which might be involved in the 5-FU action were also studied to elucidate their potential role in the modulation of 5-FU cytotoxicity. Fluorouracil 180-184 thymidylate synthetase Homo sapiens 53-73 10885904-3 1999 Several other enzymes of pyrimidine metabolism, i.e. thymidylate synthase (TS), thymidine kinase (TK) and pyrimidine nucleoside phosphorylase (PNP), which might be involved in the 5-FU action were also studied to elucidate their potential role in the modulation of 5-FU cytotoxicity. Fluorouracil 265-269 thymidylate synthetase Homo sapiens 53-73 10427537-1 1999 Colchicine, corticosteroids, daunomycin, fluorouracil, heparin and retinoids have been used in man and show an effect in different stages of the development of PVR. Fluorouracil 41-53 PVR cell adhesion molecule Homo sapiens 160-163 34167427-0 2021 Novel mutual prodrug of 5-fluorouracil and heme oxygenase-1 inhibitor (5-FU/HO-1 hybrid): design and preliminary in vitro evaluation. Fluorouracil 24-38 heme oxygenase 1 Homo sapiens 76-80 34167427-0 2021 Novel mutual prodrug of 5-fluorouracil and heme oxygenase-1 inhibitor (5-FU/HO-1 hybrid): design and preliminary in vitro evaluation. Fluorouracil 71-75 heme oxygenase 1 Homo sapiens 43-59 34167427-0 2021 Novel mutual prodrug of 5-fluorouracil and heme oxygenase-1 inhibitor (5-FU/HO-1 hybrid): design and preliminary in vitro evaluation. Fluorouracil 71-75 heme oxygenase 1 Homo sapiens 76-80 10200349-0 1999 Proliferating cell nuclear antigen as a predictor of therapeutic effect of continuous 5-fluorouracil administration in gastric cancer. Fluorouracil 86-100 proliferating cell nuclear antigen Homo sapiens 0-34 34167427-1 2021 In this work, the first mutual prodrug of 5-fluorouracil and heme oxygenase1 inhibitor (5-FU/HO-1 hybrid) has been designed, synthesised, and evaluated for its in vitro chemical and enzymatic hydrolysis stability. Fluorouracil 42-56 heme oxygenase 1 Homo sapiens 61-76 10200349-1 1999 The change of proliferating cell nuclear antigen (PCNA) expression was examined in three gastric cancer cell lines, MKN28, MKN45 and MKN74, during continuous or bolus exposure to 5-fluorouracil (5-FU). Fluorouracil 179-193 proliferating cell nuclear antigen Homo sapiens 14-48 10200349-1 1999 The change of proliferating cell nuclear antigen (PCNA) expression was examined in three gastric cancer cell lines, MKN28, MKN45 and MKN74, during continuous or bolus exposure to 5-fluorouracil (5-FU). Fluorouracil 179-193 proliferating cell nuclear antigen Homo sapiens 50-54 10200349-3 1999 PCNA expression was higher at 24 and 72 h after continuous 5-FU treatment than before treatment. Fluorouracil 59-63 proliferating cell nuclear antigen Homo sapiens 0-4 10200349-4 1999 Continuous 5-FU treatment of cells revealed higher expression of PCNA protein and mRNA than did bolus treatment. Fluorouracil 11-15 proliferating cell nuclear antigen Homo sapiens 65-69 10200349-8 1999 Thus PCNA values just after chemotherapy of gastric cancer may be useful in predicting the therapeutic effects of continuous 5-FU administration. Fluorouracil 125-129 proliferating cell nuclear antigen Homo sapiens 5-9 34167427-1 2021 In this work, the first mutual prodrug of 5-fluorouracil and heme oxygenase1 inhibitor (5-FU/HO-1 hybrid) has been designed, synthesised, and evaluated for its in vitro chemical and enzymatic hydrolysis stability. Fluorouracil 42-56 heme oxygenase 1 Homo sapiens 93-97 34167427-1 2021 In this work, the first mutual prodrug of 5-fluorouracil and heme oxygenase1 inhibitor (5-FU/HO-1 hybrid) has been designed, synthesised, and evaluated for its in vitro chemical and enzymatic hydrolysis stability. Fluorouracil 88-92 heme oxygenase 1 Homo sapiens 61-76 10212232-4 1999 The fluoropyrimidines 5-fluorouracil and 5-fluoro-2"-deoxyuridine are cytotoxic as a consequence of inhibition of TS by the metabolite 5-fluoro-2"-deoxyuridine 5"-monophosphate (FdUMP). Fluorouracil 22-36 thymidylate synthetase Homo sapiens 114-116 34167427-1 2021 In this work, the first mutual prodrug of 5-fluorouracil and heme oxygenase1 inhibitor (5-FU/HO-1 hybrid) has been designed, synthesised, and evaluated for its in vitro chemical and enzymatic hydrolysis stability. Fluorouracil 88-92 heme oxygenase 1 Homo sapiens 93-97 10206306-0 1999 A multifactorial approach including tumoural epidermal growth factor receptor, p53, thymidylate synthase and dihydropyrimidine dehydrogenase to predict treatment outcome in head and neck cancer patients receiving 5-fluorouracil. Fluorouracil 213-227 thymidylate synthetase Homo sapiens 84-104 34167427-6 2021 Altogether our results served as an initial proof-of-concept to develop 5-FU/HO-1 mutual prodrugs as potential novel anticancer agents. Fluorouracil 72-76 heme oxygenase 1 Homo sapiens 77-81 34901834-9 2021 Factors other than DPYD polymorphisms (e.g., miR-27a, TYMS, ENOSF1, p53) also affect 5-FU toxicity. Fluorouracil 85-89 thymidylate synthetase Homo sapiens 54-58 34844630-16 2021 CONCLUSIONS: CRART16 confers 5-FU resistance in CRC cells through the CRART16/miR-193b-5p/HMGA2/MAPK pathway. Fluorouracil 29-33 high mobility group AT-hook 2 Homo sapiens 90-95 34826159-2 2022 The results indicated that OSCC cells overexpressing GDF15 were sensitive to docetaxel, cisplatin, and 5-fluorouracil through a caspase-9-dependent pathway both in vitro and in vivo. Fluorouracil 103-117 caspase 9 Homo sapiens 128-137 10213225-12 1999 DPD levels were significantly correlated with 5-FU sensitivity, with high DPD activity and high DPD mRNA level resulting in low sensitivity to 5-FU. Fluorouracil 46-50 dihydropyrimidine dehydrogenase Mus musculus 0-3 10213225-12 1999 DPD levels were significantly correlated with 5-FU sensitivity, with high DPD activity and high DPD mRNA level resulting in low sensitivity to 5-FU. Fluorouracil 143-147 dihydropyrimidine dehydrogenase Mus musculus 0-3 10213225-14 1999 Tumoral DPD activity and DPD mRNA level may be useful indicators in predicting the antitumor activity of 5-FU. Fluorouracil 105-109 dihydropyrimidine dehydrogenase Mus musculus 8-11 10213225-14 1999 Tumoral DPD activity and DPD mRNA level may be useful indicators in predicting the antitumor activity of 5-FU. Fluorouracil 105-109 dihydropyrimidine dehydrogenase Mus musculus 25-28 34830244-9 2021 p130Cas was inducible by 5-fluorouracil (5-FU) and FOLFIRI (folinic acid, 5-FU, irinotecan), and p130Cas and EREG were upregulated in distant metastases (GSE121418). Fluorouracil 74-78 BCAR1 scaffold protein, Cas family member Homo sapiens 0-7 34775646-0 2021 EGF-functionalized lipid-polymer hybrid nanoparticles of 5-Fluorouracil and Sulphoraphane with enhanced bioavailability and anticancer activity against colon carcinoma. Fluorouracil 57-71 epidermal growth factor Homo sapiens 0-3 34775646-2 2021 The epidermal growth factor (EGF)-functionalized LPHNPs co-loaded with 5-fluorouracil (FU) and Sulforaphane (SFN) were prepared by one-step nanoprecipitation method. Fluorouracil 71-85 epidermal growth factor Homo sapiens 4-27 34775646-2 2021 The epidermal growth factor (EGF)-functionalized LPHNPs co-loaded with 5-fluorouracil (FU) and Sulforaphane (SFN) were prepared by one-step nanoprecipitation method. Fluorouracil 71-85 epidermal growth factor Homo sapiens 29-32 34605226-7 2021 Moreover, NK-1R antagonists enhance the efficacy of chemotherapy by increasing the sensitivity and overcoming resistance to 5-fluorouracil in CRC cells through the induction of sustained ER stress and the consequent suppression of ERK-c-Myc signaling both in vitro and in vivo. Fluorouracil 124-138 tachykinin receptor 1 Homo sapiens 10-15 34605226-7 2021 Moreover, NK-1R antagonists enhance the efficacy of chemotherapy by increasing the sensitivity and overcoming resistance to 5-fluorouracil in CRC cells through the induction of sustained ER stress and the consequent suppression of ERK-c-Myc signaling both in vitro and in vivo. Fluorouracil 124-138 MYC proto-oncogene, bHLH transcription factor Homo sapiens 235-240 34594423-0 2021 NDRG4 sensitizes CRC cells to 5-FU by upregulating DDIT3 expression. Fluorouracil 30-34 NDRG family member 4 Homo sapiens 0-5 34594423-2 2021 Our previous study reported that N-myc downstream-regulated gene 4 (NDRG4) plays a tumor-suppressive role in CRC, but the mechanisms associated with NDRG4 and 5-FU chemosensitivity remain unclear. Fluorouracil 159-163 NDRG family member 4 Homo sapiens 33-66 34594423-2 2021 Our previous study reported that N-myc downstream-regulated gene 4 (NDRG4) plays a tumor-suppressive role in CRC, but the mechanisms associated with NDRG4 and 5-FU chemosensitivity remain unclear. Fluorouracil 159-163 NDRG family member 4 Homo sapiens 68-73 34594423-3 2021 The results of the present study demonstrate that NDRG4 sensitized CRC cells to 5-FU by upregulating DNA damage inducible transcript 3 (DDIT3). Fluorouracil 80-84 NDRG family member 4 Homo sapiens 50-55 34594423-5 2021 Furthermore, NDRG4 promoted CRC cell apoptosis induced by 5-FU. Fluorouracil 58-62 NDRG family member 4 Homo sapiens 13-18 34594423-6 2021 Mechanistic analyses revealed that NDRG4 upregulated DDIT3 expression, and that the proapoptotic effect of NDRG4 under 5-FU treatment conditions was dependent on DDIT3. Fluorouracil 119-123 NDRG family member 4 Homo sapiens 107-112 34594423-7 2021 These findings support the biological value of the association between NDRG4, DDIT3 and 5-FU chemosensitivity in CRC, and may advance the clinical treatment of CRC in the future. Fluorouracil 88-92 NDRG family member 4 Homo sapiens 71-76 34718327-9 2021 Referring to the data from GEO dataset we verified GPER activation restored ERK1/2 activity in CIM and 5-fluorouracil-treated IEC-6 cells. Fluorouracil 103-117 G protein-coupled estrogen receptor 1 Rattus norvegicus 51-55 34082069-0 2021 Mice with Dysfunctional TGF-beta Signaling Develop Altered Intestinal Microbiome and Colorectal Cancer Resistant to 5FU. Fluorouracil 116-119 transforming growth factor alpha Mus musculus 24-32 34082069-5 2021 Using these mice, we evaluated the intestinal microbiome and determined the effect of dysfunctional TGF-beta signaling on the response to the chemotherapeutic agent 5-Fluoro-uracil (5FU) after induction of CRC. Fluorouracil 165-180 transforming growth factor alpha Mus musculus 100-108 34082069-5 2021 Using these mice, we evaluated the intestinal microbiome and determined the effect of dysfunctional TGF-beta signaling on the response to the chemotherapeutic agent 5-Fluoro-uracil (5FU) after induction of CRC. Fluorouracil 182-185 transforming growth factor alpha Mus musculus 100-108 34082069-9 2021 were significantly reduced in mice with CRC, these species only recovered to basal amounts after 5FU treatment in WT mice, suggesting that the alterations in the intestinal microbiome resulting from compromised TGF-beta signaling impaired the response to 5FU. Fluorouracil 97-100 transforming growth factor alpha Mus musculus 211-219 34082069-9 2021 were significantly reduced in mice with CRC, these species only recovered to basal amounts after 5FU treatment in WT mice, suggesting that the alterations in the intestinal microbiome resulting from compromised TGF-beta signaling impaired the response to 5FU. Fluorouracil 255-258 transforming growth factor alpha Mus musculus 211-219 34720803-3 2021 Methods: IGKC expression was immunohistochemically analyzed in 193 breast cancer patients who were treated with adjuvant chemotherapy, either with cyclophosphamide, methotrexate, and 5-fluorouracil (CMF) or 5-fluorouracil, epirubicin, and cyclophosphamide (FEC) between 1993 and 2001 with a median follow-up of 11 years. Fluorouracil 183-197 immunoglobulin kappa constant Homo sapiens 9-13 34720803-3 2021 Methods: IGKC expression was immunohistochemically analyzed in 193 breast cancer patients who were treated with adjuvant chemotherapy, either with cyclophosphamide, methotrexate, and 5-fluorouracil (CMF) or 5-fluorouracil, epirubicin, and cyclophosphamide (FEC) between 1993 and 2001 with a median follow-up of 11 years. Fluorouracil 207-221 immunoglobulin kappa constant Homo sapiens 9-13 34621107-12 2021 The present results demonstrated that p53-mediated apoptosis was induced in all phases of the cell cycle of the NPCs in the early stage after 5-FU treatment. Fluorouracil 142-146 Wistar clone pR53P1 p53 pseudogene Rattus norvegicus 38-41 34396431-10 2021 Overall, isolates of the CSC population CD44+ resistant to 5FU and oxaliplatin demonstrated different expression profiles; however, the present study was able to identify overexpression of the KRT-18 gene, in most of the isolates. Fluorouracil 59-62 keratin 18 Homo sapiens 193-199 34396431-11 2021 In conclusion, the results of the present study showed overexpression of KRT-18 in CD44+ cells is associated with chemoresistance to 5FU and oxaliplatin in CRAC. Fluorouracil 133-136 keratin 18 Homo sapiens 73-79 34391754-6 2021 Finally, we verified that 5-FU significantly activated the NLR Family Pyrin Domain Containing 3 (NLRP3) inflammasome in myeloid-derived suppressor cells (MDSCs) and that andrographolide sulfonate reversed this process to sensitize cells to 5-FU. Fluorouracil 26-30 NLR family, pyrin domain containing 3 Mus musculus 59-95 10096558-3 1999 OGT 719 has been designed to reduce the systemic toxicity normally associated with 5-FU while retaining activity against disease localized in the liver, in which it may be preferentially localized through the asialoglycoprotein receptor (ASGP-R). Fluorouracil 83-87 O-linked N-acetylglucosamine (GlcNAc) transferase Homo sapiens 0-3 34391754-6 2021 Finally, we verified that 5-FU significantly activated the NLR Family Pyrin Domain Containing 3 (NLRP3) inflammasome in myeloid-derived suppressor cells (MDSCs) and that andrographolide sulfonate reversed this process to sensitize cells to 5-FU. Fluorouracil 26-30 NLR family, pyrin domain containing 3 Mus musculus 97-102 10089915-0 1999 Marrow sensitization to 5-fluorouracil using the ligands for Flt-3 and c-Kit. Fluorouracil 24-38 KIT proto-oncogene receptor tyrosine kinase Mus musculus 71-76 34391754-7 2021 In summary, andrographolide sulfonate synergistically enhanced antitumor effects and improved antitumor immunity by inhibiting 5-FU-induced NLRP3 activation in MDSCs. Fluorouracil 127-131 NLR family, pyrin domain containing 3 Mus musculus 140-145 10089915-1 1999 In vivo administration of c-kit ligand (KL) expands early hemopoietic progenitors and stem cells and sensitizes clonogenic progenitors to 5-FU-mediated cell death. Fluorouracil 138-142 kit ligand Mus musculus 26-38 34728031-1 2021 Objective To establish a human colon cancer cell line HCT-116/5-FU resistant to 5-fluorouracil(5-FU)and explore the relationship between runt-related transcription factor 3(RUNX3)and drug resistance of colorectal cancer.Methods The human colon cancer cell line HCT-116/5-FU with resistance to 5-FU was established by low concentration gradient increment combined with high-dose intermittent shock.CCK-8 method was used to determine the half maximal inhibitory concentration(IC50)of 5-FU on the parent line HCT-116 and drug-resistant line HCT-116/5-FU.The cell growth curve was established for the calculation of population doubling time(TD).The mRNA levels and protein levels of RUNX3,P-glycoprotein(P-gp),multidrug resistance-associated protein 1(MRP1),and lung resistance-related protein(LRP)in HCT-116 and HCT-116/5-FU cells were determined by qRT-PCR and Western blotting,respectively.The RUNX3 expression in HCT-116 cells was knocked down by siRNA technique,and the cells were divided into RUNX3 knockdown groups(si-RUNX3-1 group and si-RUNX3-2 group)and negative control group(si-NC group).The knockdown efficiency was verified by qRT-PCR at the mRNA level and Western blotting at the protein level.The IC50 in si-RUNX3 groups and si-NC group was determined with CCK-8 method,and the expression of P-gp,MRP1,and LRP in the two groups was detected by Western blotting.Results A stable human colon cancer drug-resistant cell line HCT-116/5-FU was successfully constructed.HCT-116/5-FU showed the TD 1.38 times as long as that of HCT-116(P=0.002)and changed morphology.The mRNA level of RUNX3 in HCT-116/5-FU cells was significantly lower than that in HCT-116 cells(P=0.048),and those of P-gp(P=0.008),MRP1(P=0.001),and LRP(P=0.001)showed the opposite trend.The protein level of RUNX3 in HCT-116/5-FU cells was significantly lower than that in HCT-116(P<0.001),and those of P-gp,MRP1,and LRP presented the opposite trend(all P<0.001).The HCT-116 cell model with low expression of RUNX3 was successfully established.The mRNA level of RUNX3 had no significant difference between si-RUNX3-1 group and si-NC group(P=0.064),while the level in si-RUNX3-2 group was significantly lower than that in si-NC group(P=0.034).The protein levels of RUNX3 in si-RUNX3-1 group and si-RUNX3-2 group were lower than that in si-NC group(both P<0.001).The results demonstrated higher knocking efficiency in si-RUNX3-2 group,which was thus selected to complete the follow-up test.The IC50 of si-RUNX3 group was significantly higher than that of si-NC group(P<0.001),which indicated that the down-regulated expression of RUNX3 could reduce the sensitivity of HCT-116 cells to 5-FU.The relative protein levels of P-gp,MRP1,and LRP in si-RUNX3 group were significantly higher than those in si-NC group(all P<0.001).Conclusion The down-regulation of RUNX3 expression can reduce the sensitivity of HCT-116 cells to 5-FU,which is considered to be related to the up-regulated expression of P-gp,MRP1,and LRP. Fluorouracil 293-297 RUNX family transcription factor 3 Homo sapiens 137-172 10089915-1 1999 In vivo administration of c-kit ligand (KL) expands early hemopoietic progenitors and stem cells and sensitizes clonogenic progenitors to 5-FU-mediated cell death. Fluorouracil 138-142 kit ligand Mus musculus 40-42 10089915-8 1999 In the femur, 5-FU-mediated reductions in CFU-C were enhanced 3- to 30-fold in the presence of concomitant KL, FL or KL + FL administration. Fluorouracil 14-18 kit ligand Mus musculus 107-109 10089915-8 1999 In the femur, 5-FU-mediated reductions in CFU-C were enhanced 3- to 30-fold in the presence of concomitant KL, FL or KL + FL administration. Fluorouracil 14-18 kit ligand Mus musculus 117-119 10024690-0 1999 Dihydropyrimidine dehydrogenase, multidrug resistance-associated protein, and thymidylate synthase gene expression levels can predict 5-fluorouracil resistance in human gastrointestinal cancer cells. Fluorouracil 134-148 thymidylate synthetase Homo sapiens 78-98 10024690-2 1999 Although mRNA and protein levels of thymidylate synthase (TS) did not relate to the resistance, 5-FU treatment revealed a remarkable increase of TS expression. Fluorouracil 96-100 thymidylate synthetase Homo sapiens 145-147 10024690-3 1999 Such enhanced TS expression was more significant than DPD and MRP, and observed less in 5-FU sensitive cells. Fluorouracil 88-92 thymidylate synthetase Homo sapiens 14-16 10024690-4 1999 DPD and MRP expression levels can predict primary 5-FU resistance, and TS may be a potent predictor of cellular 5-FU resistance after 5-FU treatment. Fluorouracil 112-116 thymidylate synthetase Homo sapiens 71-73 10024690-4 1999 DPD and MRP expression levels can predict primary 5-FU resistance, and TS may be a potent predictor of cellular 5-FU resistance after 5-FU treatment. Fluorouracil 112-116 thymidylate synthetase Homo sapiens 71-73 34728031-1 2021 Objective To establish a human colon cancer cell line HCT-116/5-FU resistant to 5-fluorouracil(5-FU)and explore the relationship between runt-related transcription factor 3(RUNX3)and drug resistance of colorectal cancer.Methods The human colon cancer cell line HCT-116/5-FU with resistance to 5-FU was established by low concentration gradient increment combined with high-dose intermittent shock.CCK-8 method was used to determine the half maximal inhibitory concentration(IC50)of 5-FU on the parent line HCT-116 and drug-resistant line HCT-116/5-FU.The cell growth curve was established for the calculation of population doubling time(TD).The mRNA levels and protein levels of RUNX3,P-glycoprotein(P-gp),multidrug resistance-associated protein 1(MRP1),and lung resistance-related protein(LRP)in HCT-116 and HCT-116/5-FU cells were determined by qRT-PCR and Western blotting,respectively.The RUNX3 expression in HCT-116 cells was knocked down by siRNA technique,and the cells were divided into RUNX3 knockdown groups(si-RUNX3-1 group and si-RUNX3-2 group)and negative control group(si-NC group).The knockdown efficiency was verified by qRT-PCR at the mRNA level and Western blotting at the protein level.The IC50 in si-RUNX3 groups and si-NC group was determined with CCK-8 method,and the expression of P-gp,MRP1,and LRP in the two groups was detected by Western blotting.Results A stable human colon cancer drug-resistant cell line HCT-116/5-FU was successfully constructed.HCT-116/5-FU showed the TD 1.38 times as long as that of HCT-116(P=0.002)and changed morphology.The mRNA level of RUNX3 in HCT-116/5-FU cells was significantly lower than that in HCT-116 cells(P=0.048),and those of P-gp(P=0.008),MRP1(P=0.001),and LRP(P=0.001)showed the opposite trend.The protein level of RUNX3 in HCT-116/5-FU cells was significantly lower than that in HCT-116(P<0.001),and those of P-gp,MRP1,and LRP presented the opposite trend(all P<0.001).The HCT-116 cell model with low expression of RUNX3 was successfully established.The mRNA level of RUNX3 had no significant difference between si-RUNX3-1 group and si-NC group(P=0.064),while the level in si-RUNX3-2 group was significantly lower than that in si-NC group(P=0.034).The protein levels of RUNX3 in si-RUNX3-1 group and si-RUNX3-2 group were lower than that in si-NC group(both P<0.001).The results demonstrated higher knocking efficiency in si-RUNX3-2 group,which was thus selected to complete the follow-up test.The IC50 of si-RUNX3 group was significantly higher than that of si-NC group(P<0.001),which indicated that the down-regulated expression of RUNX3 could reduce the sensitivity of HCT-116 cells to 5-FU.The relative protein levels of P-gp,MRP1,and LRP in si-RUNX3 group were significantly higher than those in si-NC group(all P<0.001).Conclusion The down-regulation of RUNX3 expression can reduce the sensitivity of HCT-116 cells to 5-FU,which is considered to be related to the up-regulated expression of P-gp,MRP1,and LRP. Fluorouracil 293-297 RUNX family transcription factor 3 Homo sapiens 173-178 9890899-2 1999 This stem-loop structure is thought to be important in the regulation of TS translation, which is itself an important target for anticancer drugs, such as 5-fluorouracil. Fluorouracil 155-169 thymidylate synthetase Homo sapiens 73-75 34659884-5 2021 Therefore, the aim of this study was to clarify the role of leptin and the underlying mechanisms in mediating 5-fluorouracil (5-FU) resistance in CRC. Fluorouracil 110-124 leptin Homo sapiens 60-66 34659884-5 2021 Therefore, the aim of this study was to clarify the role of leptin and the underlying mechanisms in mediating 5-fluorouracil (5-FU) resistance in CRC. Fluorouracil 126-130 leptin Homo sapiens 60-66 10216492-2 1999 In a pilot phase II study, in order to improve the immune function during chemotherapy, we combined to cisplatin (CDDP) and 5-fluorouracil (5-FU) two biological response modifiers, retinyl palmitate (R) and Thymopentin (TP-5) for the treatment of SCC. Fluorouracil 124-138 serpin family B member 3 Homo sapiens 247-250 34659884-9 2021 Notably, this increase in resistance to 5-FU was through the elevated production and secretion of leptin. Fluorouracil 40-44 leptin Homo sapiens 98-104 34659884-13 2021 Furthermore, leptin neutralization rescued the sensitivity of CRC tumors to 5-FU in mice fed on a high-fat diet (HFD). Fluorouracil 76-80 leptin Mus musculus 13-19 10226579-3 1999 MCF-7 human breast and H630 human colon carcinoma cells selected for resistance to tomudex and 5-fluorouracil, respectively via thymidylate synthase (TS) amplification demonstrated only modest resistance to LY231514 compared to tomudex. Fluorouracil 95-109 thymidylate synthetase Homo sapiens 128-148 34659884-14 2021 These results indicated that leptin mediated 5-FU resistance through YAP-dependent AXL overexpression in CRC. Fluorouracil 45-49 leptin Mus musculus 29-35 34659884-14 2021 These results indicated that leptin mediated 5-FU resistance through YAP-dependent AXL overexpression in CRC. Fluorouracil 45-49 AXL receptor tyrosine kinase Homo sapiens 83-86 2685478-0 1989 In vivo effects of interleukin-1 alpha on regenerating mouse bone marrow myeloid colony-forming cells after treatment with 5-fluorouracil. Fluorouracil 123-137 interleukin 1 alpha Mus musculus 19-38 10999043-0 1999 Phase I and pharmacokinetic study of weekly 5-fluorouracil administered with granulocyte-macrophage colony-stimulating factor and high-dose leucovorin: a potential role for growth factor as mucosal protectant. Fluorouracil 44-58 colony stimulating factor 2 Homo sapiens 77-125 10999043-11 1999 In a weekly schedule with high-dose LV and GM-CSF, the MTD of 5-FU and 5-FU delivered dose intensity were higher than previously reported with 5-FU and LV administered without GM-CSF. Fluorouracil 62-66 colony stimulating factor 2 Homo sapiens 43-49 10999043-11 1999 In a weekly schedule with high-dose LV and GM-CSF, the MTD of 5-FU and 5-FU delivered dose intensity were higher than previously reported with 5-FU and LV administered without GM-CSF. Fluorouracil 71-75 colony stimulating factor 2 Homo sapiens 43-49 10999043-11 1999 In a weekly schedule with high-dose LV and GM-CSF, the MTD of 5-FU and 5-FU delivered dose intensity were higher than previously reported with 5-FU and LV administered without GM-CSF. Fluorouracil 71-75 colony stimulating factor 2 Homo sapiens 43-49 2685478-1 1989 Injection of a single dose of recombinant human interleukin-1 alpha (r-hu-IL-1 alpha) into mice 24 hr after 5-fluorouracil (FU) treatment resulted in an increased rate of recovery of three types of colony-forming cells (CFCs) in the bone marrow. Fluorouracil 108-122 interleukin 1 alpha Homo sapiens 48-67 9923446-2 1999 Thy-1.2lo Sca-1+ H-2Khi stem cells enriched from the bone marrow of 5-fluorouracil-treated (Ly5-2) mice were infected with the bcl-2 retrovirus and injected into (Ly5-1) irradiated recipients. Fluorouracil 68-82 CD24a antigen Mus musculus 92-97 2813219-5 1989 The addition of leucovorin increases fluorouracil"s ability to inhibit thymidylate synthase and thus colon cancer cell replication. Fluorouracil 37-49 thymidylate synthetase Homo sapiens 71-91 2783128-1 1989 In order to better understand the synergistic antiproliferative effects of interferon in combination with fluorouracil (FUra), we studied effects of alpha 2-interferon upon FUra induced inhibition of thymidylate synthase of HL-60 cells. Fluorouracil 173-177 thymidylate synthetase Homo sapiens 200-220 2783128-5 1989 These results suggest that interferon can sensitize cells to FUra inhibition of thymidylate synthase by enhancing accumulation of FdUMP. Fluorouracil 61-65 thymidylate synthetase Homo sapiens 80-100 2786878-3 1989 IL-4 supported the formation of blast cell colonies and small granulocyte/macrophage (GM) colonies in cultures of marrow and spleen cells of normal mice as well as spleen cells of mice treated with 150 mg/kg 5-fluorouracil (5-FU) 4 days earlier. Fluorouracil 208-222 interleukin 4 Mus musculus 0-4 2786878-3 1989 IL-4 supported the formation of blast cell colonies and small granulocyte/macrophage (GM) colonies in cultures of marrow and spleen cells of normal mice as well as spleen cells of mice treated with 150 mg/kg 5-fluorouracil (5-FU) 4 days earlier. Fluorouracil 224-228 interleukin 4 Mus musculus 0-4 2543331-0 1989 [Effect of human epidermal factor (hEGF) on antitumor activity of 5-fluorouracil (5-FU) in human gastric cancer cell lines]. Fluorouracil 66-80 epidermal growth factor Homo sapiens 35-39 2543331-0 1989 [Effect of human epidermal factor (hEGF) on antitumor activity of 5-fluorouracil (5-FU) in human gastric cancer cell lines]. Fluorouracil 82-86 epidermal growth factor Homo sapiens 35-39 2500406-1 1989 Thymidylate synthase (TS) is the enzyme target of 5-fluorouracil (FUra) that recent laboratory and clinical studies with folinic acid (calcium leucovorin) suggest may mediate important antitumor cytotoxicity. Fluorouracil 50-64 thymidylate synthetase Homo sapiens 0-20 2500406-1 1989 Thymidylate synthase (TS) is the enzyme target of 5-fluorouracil (FUra) that recent laboratory and clinical studies with folinic acid (calcium leucovorin) suggest may mediate important antitumor cytotoxicity. Fluorouracil 66-70 thymidylate synthetase Homo sapiens 0-20 3264195-1 1988 Serial observations of blast cell colony development from spleen cells of mice treated with 5-fluorouracil (5-FU) four days earlier revealed that either form of human interleukin-1 (IL-1 alpha or IL-1 beta) hastens the emergence of interleukin-3 (IL-3)-dependent blast cell colonies. Fluorouracil 92-106 interleukin 1 alpha Homo sapiens 167-180 3264195-1 1988 Serial observations of blast cell colony development from spleen cells of mice treated with 5-fluorouracil (5-FU) four days earlier revealed that either form of human interleukin-1 (IL-1 alpha or IL-1 beta) hastens the emergence of interleukin-3 (IL-3)-dependent blast cell colonies. Fluorouracil 92-106 interleukin 1 alpha Homo sapiens 182-192 3264195-1 1988 Serial observations of blast cell colony development from spleen cells of mice treated with 5-fluorouracil (5-FU) four days earlier revealed that either form of human interleukin-1 (IL-1 alpha or IL-1 beta) hastens the emergence of interleukin-3 (IL-3)-dependent blast cell colonies. Fluorouracil 92-106 interleukin 3 Homo sapiens 232-245 3264195-1 1988 Serial observations of blast cell colony development from spleen cells of mice treated with 5-fluorouracil (5-FU) four days earlier revealed that either form of human interleukin-1 (IL-1 alpha or IL-1 beta) hastens the emergence of interleukin-3 (IL-3)-dependent blast cell colonies. Fluorouracil 92-106 interleukin 3 Homo sapiens 247-251 3264195-1 1988 Serial observations of blast cell colony development from spleen cells of mice treated with 5-fluorouracil (5-FU) four days earlier revealed that either form of human interleukin-1 (IL-1 alpha or IL-1 beta) hastens the emergence of interleukin-3 (IL-3)-dependent blast cell colonies. Fluorouracil 108-112 interleukin 1 alpha Homo sapiens 167-180 3167844-0 1988 Mechanisms of innate resistance to thymidylate synthase inhibition after 5-fluorouracil. Fluorouracil 73-87 thymidylate synthetase Homo sapiens 35-55 11938799-2 1999 The cell or colony counting and transgene RT-PCR analysis showed that the proliferation, colony formation and transgene expression of the bone marrow cells were advanced in the combinative culture of mSCF with mIL-3, but they were significantly inhibited in the culture without any growth factors, or with mSCF, mIL-3 and Hu or 5-Fu. Fluorouracil 328-332 kit ligand Mus musculus 200-204 11817332-4 1999 5-FU also caused significant redistribution of cathepsin B activity from the lysosomal fraction to the zymogen fraction in pancreatic subcellular fractionation study. Fluorouracil 0-4 cathepsin B Rattus norvegicus 47-58 11817332-6 1999 These results suggest that the exocrine pancreas might be injured by 5-FU, and that lysosomal enzymes seem to play an important role in the pathogenesis of the pancreatic injuries induced by 5-FU, since cathepsin B can activate trypsinogen. Fluorouracil 191-195 cathepsin B Rattus norvegicus 203-214 3263940-5 1988 The biochemical properties of peak 1 were similar to those of murine IL-3 and stimulated multi-potential stem cell development in soft agar cultures of BM cells from rats treated with 5-fluorouracil (which enriches for haemopoietic stem cells). Fluorouracil 184-198 pseudopodium-enriched atypical kinase 1 Mus musculus 30-36 2837988-0 1988 [The role of thymidylate synthetase in sequential dose of MTX and 5-FU in the advanced scirrhous type gastric cancer]. Fluorouracil 66-70 thymidylate synthetase Homo sapiens 13-35 10555123-3 1999 Gemcitabine may potentiate fluorouracil"s inhibition of thymidylate synthase. Fluorouracil 27-39 thymidylate synthetase Homo sapiens 56-76 21374032-5 1999 However, the majority of an administered 5-FU dose undergoes metabolism to inactive species through a three-enzyme process, which is initiated and rate-limited by dihydropyrimidine dehydrogenase (DPD; EC 1.3.1.2). Fluorouracil 41-45 dihydropyrimidine dehydrogenase Mus musculus 163-194 21374032-5 1999 However, the majority of an administered 5-FU dose undergoes metabolism to inactive species through a three-enzyme process, which is initiated and rate-limited by dihydropyrimidine dehydrogenase (DPD; EC 1.3.1.2). Fluorouracil 41-45 dihydropyrimidine dehydrogenase Mus musculus 196-199 21374032-6 1999 Following a bolus injection of 5-FU, 80% is degraded via DPD after 24 h after administration (2). Fluorouracil 31-35 dihydropyrimidine dehydrogenase Mus musculus 57-60 2837988-1 1988 The biochemical rationale for the potentiation of the effects of 5-FU by MTX is based on an increased PRPP level or MTX polyglutamate produced by MTX. Fluorouracil 65-69 metaxin 1 Homo sapiens 73-76 2837988-1 1988 The biochemical rationale for the potentiation of the effects of 5-FU by MTX is based on an increased PRPP level or MTX polyglutamate produced by MTX. Fluorouracil 65-69 metaxin 1 Homo sapiens 116-119 2837988-1 1988 The biochemical rationale for the potentiation of the effects of 5-FU by MTX is based on an increased PRPP level or MTX polyglutamate produced by MTX. Fluorouracil 65-69 metaxin 1 Homo sapiens 116-119 3389839-5 1988 Increase in PRPP level by inhibition of the de novo purine synthetic pathway, and greater production of cytotoxic 5-FU-containing nucleotides (MTX, MMPR) 3. Fluorouracil 114-118 metaxin 1 Homo sapiens 143-146 10741375-5 1999 The MPO activity and FD-4 permeation were significantly increased by the administration of 5-FU to rats for 4 days, while on the coadministration of 5-FU and OP-1206, they were similar to those of control rats treated with saline solution alone, respectively. Fluorouracil 91-95 myeloperoxidase Rattus norvegicus 4-7 10030740-6 1999 The changes in free thymidylate synthetase (TS) concentration indicated TS synthesis after the administration of 5-FU to be more greatly suppressed in the combination group than in the 5-FU group. Fluorouracil 113-117 thymidylate synthetase Homo sapiens 20-42 3263749-3 1988 On the other hand in the presence of IL-2, NK cells are generated in cultures of BM from mice pretreated with 5-fluorouracil (5-FU, 150 mg/kg iv 4 days before harvesting), a treatment which has been shown to eliminate more differentiated but spare less differentiated BM precursors. Fluorouracil 110-124 interleukin 2 Mus musculus 37-41 10022227-2 1998 The enterotoxic antimetabolite 5-fluorouracil (5-FU) induced acute p53-dependent apoptosis in the crypts of both small intestine and midcolon. Fluorouracil 31-45 transformation related protein 53, pseudogene Mus musculus 67-70 10022227-2 1998 The enterotoxic antimetabolite 5-fluorouracil (5-FU) induced acute p53-dependent apoptosis in the crypts of both small intestine and midcolon. Fluorouracil 47-51 transformation related protein 53, pseudogene Mus musculus 67-70 10022227-6 1998 In p53 null (-/-) mice significant reductions in 5-FU-induced apoptosis and relief from the inhibition of cell cycle progression permitted retention of crypt integrity after 5-FU. Fluorouracil 49-53 transformation related protein 53, pseudogene Mus musculus 3-6 10022227-9 1998 Importantly, the tissue toxicity of 5-fluorouracil was genetically determined at a locus (p53) separate from that directly associated with toxin action. Fluorouracil 36-50 transformation related protein 53, pseudogene Mus musculus 90-93 2969304-1 1988 Uridine (UR) inhibits the metabolic activation of 5"-deoxy-5-fluorouridine (dFUR) to 5-fluorouracil (FU) by the intestinal pyrimidine nucleoside phosphorylases and could potentially reduce its intestinal toxicity. Fluorouracil 85-99 fur Drosophila melanogaster 76-80 9845529-5 1998 hG-CSF also had stimulatory effects on the formation of blast cell colonies in cultures using 5-fluorouracil-resistant hematopoietic progenitors and clone-sorted Lin-c-Kit+Sca-1(+) primitive hematopoietic cells. Fluorouracil 94-108 colony stimulating factor 3 Homo sapiens 0-6 9833767-0 1998 Interleukin-2/sodium butyrate treatment cures rats bearing liver tumors after acquired 5-fluorouracil resistance. Fluorouracil 87-101 interleukin 2 Rattus norvegicus 0-13 9833767-1 1998 We studied the effect of immunotherapy using recombinant interleukin-2 (rIL-2) in combination with a differentiating agent, sodium butyrate (NaBut), on experimental 5-fluorouracil (5-FU)-resistant liver metastasis from colorectal cancer in rats. Fluorouracil 165-179 interleukin 2 Rattus norvegicus 57-70 3499607-1 1987 The human bladder carcinoma cell line 5637 produces hematopoietic growth factors [granulocyte and granulocyte/macrophage colony-stimulating factors (G-CSF and GM-CSF)] and hemopoietin 1, which synergizes with CSFs to stimulate colony formation by primitive hematopoietic stem cells in 5-fluorouracil-treated mouse bone marrow. Fluorouracil 285-299 colony stimulating factor 2 Homo sapiens 159-185 9850079-0 1998 The relationships between p53-dependent apoptosis, inhibition of proliferation, and 5-fluorouracil-induced histopathology in murine intestinal epithelia. Fluorouracil 84-98 transformation related protein 53, pseudogene Mus musculus 26-29 9850079-2 1998 Administration of the enterotoxin 5-fluorouracil (5-FU) at either 40 or 400 mg/kg to BDF1 mice induced an acute p53-dependent apoptosis in the crypts of both small intestine and midcolon. Fluorouracil 34-48 transformation related protein 53, pseudogene Mus musculus 112-115 9850079-2 1998 Administration of the enterotoxin 5-fluorouracil (5-FU) at either 40 or 400 mg/kg to BDF1 mice induced an acute p53-dependent apoptosis in the crypts of both small intestine and midcolon. Fluorouracil 50-54 transformation related protein 53, pseudogene Mus musculus 112-115 9850079-4 1998 Only after the administration of 400 mg/kg 5-FU were mitotic index and DNA synthesis significantly suppressed in both small intestinal and midcolonic crypts at 24 h. This correlated with a prolonged, p53-dependent expression of p21waf-1/cip1. Fluorouracil 43-47 transformation related protein 53, pseudogene Mus musculus 200-203 3499607-3 1987 When bone marrow cells from 5-fluorouracil-treated mice were cultured in suspension for 7 days with recombinant human IL-1 alpha and/or G-CSF, it was found that the two factors synergized to enhance recovery of myelopoietic cells and colony-forming cells of both high and low proliferative potential. Fluorouracil 28-42 interleukin 1 alpha Homo sapiens 118-128 9850079-5 1998 In p53 null (-/-) mice, significant reductions in both 5-FU-induced apoptosis and inhibition of cell cycle progression allowed retention of crypt integrity 96 h after 5-FU. Fluorouracil 55-59 transformation related protein 53, pseudogene Mus musculus 3-6 9850079-5 1998 In p53 null (-/-) mice, significant reductions in both 5-FU-induced apoptosis and inhibition of cell cycle progression allowed retention of crypt integrity 96 h after 5-FU. Fluorouracil 167-171 transformation related protein 53, pseudogene Mus musculus 3-6 9850079-8 1998 Importantly, the tissue toxicity of 5-FU was genetically determined at a locus (p53) separate from that directly associated with drug action. Fluorouracil 36-40 transformation related protein 53, pseudogene Mus musculus 80-83 3499607-3 1987 When bone marrow cells from 5-fluorouracil-treated mice were cultured in suspension for 7 days with recombinant human IL-1 alpha and/or G-CSF, it was found that the two factors synergized to enhance recovery of myelopoietic cells and colony-forming cells of both high and low proliferative potential. Fluorouracil 28-42 colony stimulating factor 3 Homo sapiens 136-141 10081495-5 1998 EGF and TGF-alpha up-regulated thymidine phosphorylase (dThdPase) expression of tumor cells and consequently enhanced the antiproliferative action of 5"-dFUrd, which is converted to 5-fluorouracil by dThdPase. Fluorouracil 182-196 epidermal growth factor Homo sapiens 0-3 3499607-6 1987 Daily administration of recombinant human G-CSF or recombinant human IL-1 alpha accelerated recovery of stem cells, progenitor cells, and blood neutrophils by up to 4 days in 5-fluorouracil-treated C3H/HeJ and B6D2F1 mice. Fluorouracil 175-189 colony stimulating factor 3 Homo sapiens 42-47 3499607-6 1987 Daily administration of recombinant human G-CSF or recombinant human IL-1 alpha accelerated recovery of stem cells, progenitor cells, and blood neutrophils by up to 4 days in 5-fluorouracil-treated C3H/HeJ and B6D2F1 mice. Fluorouracil 175-189 interleukin 1 alpha Homo sapiens 69-79 3585449-1 1987 Seventeen patients with advanced or recurrent salivary gland cancer were treated with cisplatin, doxorubicin, and 5-fluorouracil combination chemotherapy (PAF). Fluorouracil 114-128 PCNA clamp associated factor Homo sapiens 155-158 9809460-6 1998 To date, the prediction of primary resistance to 5-FU in the clinic is limited to few studies focusing mainly on the key enzyme thymidylate synthase. Fluorouracil 49-53 thymidylate synthetase Homo sapiens 128-148 3032931-0 1987 5-Fluorouracil augmentation of dihydrofolate reductase RNA containing contiguous exon and intron sequences in KB7B cells. Fluorouracil 0-14 dihydrofolate reductase Homo sapiens 31-54 9951876-2 1998 Thymidylate synthase (TS) and dihydropyrimidine dehydrogenase (DPD) are key enzymes involved in the biochemical functions of the antimetabolite 5-fluorouracil (5-FU). Fluorouracil 144-158 thymidylate synthetase Homo sapiens 0-20 9951876-2 1998 Thymidylate synthase (TS) and dihydropyrimidine dehydrogenase (DPD) are key enzymes involved in the biochemical functions of the antimetabolite 5-fluorouracil (5-FU). Fluorouracil 160-164 thymidylate synthetase Homo sapiens 0-20 3032931-2 1987 Dihydrofolate reductase RNA containing both exon 1 and intron I, or exon 5 and a portion of intron V, increased up to 5-fold in cells grown in the presence of 2.0 to 3.0 microM 5-fluorouracil. Fluorouracil 177-191 dihydrofolate reductase Homo sapiens 0-23 3032931-3 1987 Dihydrofolate reductase RNA containing exon 1 or exon 5, but lacking intron I or intron V, respectively, increased 2-fold in cells grown in the presence of 0.65 to 3.0 microM 5-fluorouracil. Fluorouracil 175-189 dihydrofolate reductase Homo sapiens 0-23 3032931-5 1987 The results of these studies demonstrate that 5-fluorouracil alters the metabolism of dihydrofolate reductase precursor mRNA and/or processing intermediates. Fluorouracil 46-60 dihydrofolate reductase Homo sapiens 86-109 3502358-2 1987 Results indicate that both IL-1 alpha and IL-1 beta (1-10 U/ml) are able to stimulate the generation of NK cells from 5-fluorouracil (5-FU) resistant BM progenitors. Fluorouracil 118-132 interleukin 1 alpha Mus musculus 27-37 3502358-2 1987 Results indicate that both IL-1 alpha and IL-1 beta (1-10 U/ml) are able to stimulate the generation of NK cells from 5-fluorouracil (5-FU) resistant BM progenitors. Fluorouracil 134-138 interleukin 1 alpha Mus musculus 27-37 3756862-2 1986 In a study using fewer cell lines, Mer- cells were also sensitive to methotrexate but not to seven other agents including the antimetabolites 1-beta-D-arabinofuranosylcytosine and 5-fluorouracil. Fluorouracil 180-194 MER proto-oncogene, tyrosine kinase Homo sapiens 35-38 9808711-6 1998 The extreme enhancement of the tissue 5-FU levels was attributable to the facile inactivation by (E)-5-(2-bromovinyl)uracil (BVU) of hepatic dihydropyrimidine dehydrogenase (DPD), a key enzyme regulating the systemic 5-FU level in the rat and human. Fluorouracil 38-42 dihydropyrimidine dehydrogenase Rattus norvegicus 174-177 9930367-0 1998 p53- and p21-independent apoptosis of squamous cell carcinoma cells induced by 5-fluorouracil and radiation. Fluorouracil 79-93 H3 histone pseudogene 16 Homo sapiens 9-12 9930367-12 1998 These findings indicate that 5-FU and gamma-rays induce apoptosis of squamous cell carcinoma cells in p53- and p21-independent manners, in the S and G2/M phases, respectively. Fluorouracil 29-33 H3 histone pseudogene 16 Homo sapiens 111-114 9766655-4 1998 Associated with an up-regulation of TS, E2F-1-transfected cells were more resistant to 5-fluorouracil than were untransfected cells. Fluorouracil 87-101 E2F transcription factor 1 Homo sapiens 40-45 9793000-5 1998 RESULTS: The 5-FU treatment dramatically decreased the BM concentrations of AcSDKP by 73% and increased the ACE activity in plasma by 50% during the period of active BM regeneration. Fluorouracil 13-17 angiotensin I converting enzyme (peptidyl-dipeptidase A) 1 Mus musculus 108-111 2423519-4 1986 Under conditions to examine only RNA synthesized during the drug exposure, FUra was found to markedly enhance the level of newly synthesized nuclear DHFR-mRNA in a dose-dependent manner, while also producing an apparent dose-dependent reduction in the cytoplasmic DHFR-mRNA. Fluorouracil 75-79 dihydrofolate reductase Homo sapiens 149-153 2423519-4 1986 Under conditions to examine only RNA synthesized during the drug exposure, FUra was found to markedly enhance the level of newly synthesized nuclear DHFR-mRNA in a dose-dependent manner, while also producing an apparent dose-dependent reduction in the cytoplasmic DHFR-mRNA. Fluorouracil 75-79 dihydrofolate reductase Homo sapiens 264-268 2423519-6 1986 Following a 24-h FUra exposure, a dose-dependent loss of the 0.8-kilobase DHFR-mRNA was observed. Fluorouracil 17-21 dihydrofolate reductase Homo sapiens 74-78 2423519-7 1986 The combined results of these experiments indicate that FUra treatment reduces the ability of nascent DHFR-mRNA to relocate to the cytoplasm, suggesting either an inhibition of mRNA processing or nuclear-cytoplasmic transport. Fluorouracil 56-60 dihydrofolate reductase Homo sapiens 102-106 3713705-0 1986 5-Fluorouracil augmentation of dihydrofolate reductase gene transcripts containing intervening sequences in methotrexate-resistant KB cells. Fluorouracil 0-14 dihydrofolate reductase Homo sapiens 31-54 9688315-8 1998 Non-confluent HT29 cells over-expressing p27Kip1 are also more resistant to doxorubicin, etoposide and 5-fluorouracil. Fluorouracil 103-117 cyclin dependent kinase inhibitor 1B Homo sapiens 41-48 3713705-6 1986 Subsequent solution hybridization studies revealed a disproportionate 5-fluorouracil-induced increase in dihydrofolate reductase intron-containing RNA over dihydrofolate reductase mRNA. Fluorouracil 70-84 dihydrofolate reductase Homo sapiens 105-128 9773807-6 1998 Furthermore, elevations of thymidylate synthase were seen in all cell lines with resistance to 24 h of 5-FU but also in one cell line with resistance to a bolus schedule. Fluorouracil 103-107 thymidylate synthetase Homo sapiens 27-47 3713705-6 1986 Subsequent solution hybridization studies revealed a disproportionate 5-fluorouracil-induced increase in dihydrofolate reductase intron-containing RNA over dihydrofolate reductase mRNA. Fluorouracil 70-84 dihydrofolate reductase Homo sapiens 156-179 3943086-0 1986 Effect of (E)-5-(2-bromovinyl)uracil on the catabolism and antitumor activity of 5-fluorouracil in rats and leukemic mice. Fluorouracil 81-95 Rho guanine nucleotide exchange factor 15 Rattus norvegicus 10-15 9662252-0 1998 Thymidylate synthase expression and activity: relation to S-phase parameters and 5-fluorouracil sensitivity. Fluorouracil 81-95 thymidylate synthetase Homo sapiens 0-20 3958510-12 1986 These data suggest that multi-CSA and SA may be expressed by different factors and that 5-FU pre-treated marrow contains: a population of primitive multipotential progenitors which form large, mixed colonies in the presence of SCM + Epo, and a larger Epo-sensitive population which also requires HPCM + PMUE to form mixed colonies. Fluorouracil 88-92 erythropoietin Mus musculus 233-236 3958510-12 1986 These data suggest that multi-CSA and SA may be expressed by different factors and that 5-FU pre-treated marrow contains: a population of primitive multipotential progenitors which form large, mixed colonies in the presence of SCM + Epo, and a larger Epo-sensitive population which also requires HPCM + PMUE to form mixed colonies. Fluorouracil 88-92 erythropoietin Mus musculus 251-254 3940219-6 1986 Cytochrome P-450-independent metabolism of [14C]5-fluorouracil, measured by means of [14C]CO2 in the breath over 3 h, was decreased to 21% of the dose administered by 8 days after tumor cell administration, compared with 31% of the dose in control mice. Fluorouracil 48-62 cytochrome P450, family 21, subfamily a, polypeptide 1 Mus musculus 0-16 6426401-1 1984 The relationship between the antitumor activity and the inhibition of thymidylate synthase after oral administration of 5-FU, FT-207 or UFT was examined. Fluorouracil 120-124 thymidylate synthetase Homo sapiens 70-90 6426401-3 1984 It was found that the inhibition of thymidylate synthase in sarcoma-180 tumor tissue after single oral administration of 5-FU (20 mg/kg), FT-207 (30 or 120 mg/kg) or UFT (30 mg/kg) were about 45%, 20%, 50% or 65%, respectively, but the activities of other enzymes involved in DNA synthesis were not almost inhibited. Fluorouracil 121-125 thymidylate synthetase Homo sapiens 36-56 6426401-7 1984 These results suggest that the inhibition of thymidylate synthase by FdUMP converted from 5-FU, FT-207 or UFT plays a major role in their antitumor actions. Fluorouracil 90-94 thymidylate synthetase Homo sapiens 45-65 6409396-1 1983 There are two major R,S-1-(tetrahydro-2-furanyl)-5-fluorouracil (ftorafur) activation pathways to 5-fluorouracil, one that is mediated by microsomal cytochrome P-450 oxidation at C-5" of the tetrahydrofuran moiety and one that is mediated by soluble enzymes. Fluorouracil 49-63 complement C5 Homo sapiens 179-182 6409396-2 1983 This report demonstrates that the soluble enzyme pathway proceeds via enzymatic cleavage (possibly hydrolytic) of the N-1--C-2" bond to yield 5-fluorouracil and 4-hydroxybutanal, which is immediately further metabolized to gamma-butyrolactone or gamma-hydroxybutyric acid. Fluorouracil 142-156 complement C2 Homo sapiens 123-126 9657039-3 1998 When exposed to 5-FU, DLD-1/5-FU cells exhibited marked resistance to in situ thymidylate synthase (TS) inhibition by 5-FU as compared to DLD-1 cells, and incorporation of 5-FU into cellular RNA in DLD-1/5-FU cells decreased to 25% of that in DLD-1 cells. Fluorouracil 16-20 thymidylate synthetase Homo sapiens 78-98 9657039-3 1998 When exposed to 5-FU, DLD-1/5-FU cells exhibited marked resistance to in situ thymidylate synthase (TS) inhibition by 5-FU as compared to DLD-1 cells, and incorporation of 5-FU into cellular RNA in DLD-1/5-FU cells decreased to 25% of that in DLD-1 cells. Fluorouracil 28-32 thymidylate synthetase Homo sapiens 78-98 9657039-3 1998 When exposed to 5-FU, DLD-1/5-FU cells exhibited marked resistance to in situ thymidylate synthase (TS) inhibition by 5-FU as compared to DLD-1 cells, and incorporation of 5-FU into cellular RNA in DLD-1/5-FU cells decreased to 25% of that in DLD-1 cells. Fluorouracil 28-32 thymidylate synthetase Homo sapiens 78-98 9657039-3 1998 When exposed to 5-FU, DLD-1/5-FU cells exhibited marked resistance to in situ thymidylate synthase (TS) inhibition by 5-FU as compared to DLD-1 cells, and incorporation of 5-FU into cellular RNA in DLD-1/5-FU cells decreased to 25% of that in DLD-1 cells. Fluorouracil 28-32 thymidylate synthetase Homo sapiens 78-98 9657039-3 1998 When exposed to 5-FU, DLD-1/5-FU cells exhibited marked resistance to in situ thymidylate synthase (TS) inhibition by 5-FU as compared to DLD-1 cells, and incorporation of 5-FU into cellular RNA in DLD-1/5-FU cells decreased to 25% of that in DLD-1 cells. Fluorouracil 28-32 thymidylate synthetase Homo sapiens 78-98 6191988-1 1983 Hypoxanthine (Hx) and allopurinol (HPP) have been shown experimentally to reduce the conversion of 5-fluorouracil (FUra) to FUMP by orotate phosphoribosyltransferase (OPRTase). Fluorouracil 99-113 uridine monophosphate synthetase Homo sapiens 132-165 6191988-1 1983 Hypoxanthine (Hx) and allopurinol (HPP) have been shown experimentally to reduce the conversion of 5-fluorouracil (FUra) to FUMP by orotate phosphoribosyltransferase (OPRTase). Fluorouracil 99-113 uridine monophosphate synthetase Homo sapiens 167-174 6191988-1 1983 Hypoxanthine (Hx) and allopurinol (HPP) have been shown experimentally to reduce the conversion of 5-fluorouracil (FUra) to FUMP by orotate phosphoribosyltransferase (OPRTase). Fluorouracil 115-119 uridine monophosphate synthetase Homo sapiens 132-165 6191988-1 1983 Hypoxanthine (Hx) and allopurinol (HPP) have been shown experimentally to reduce the conversion of 5-fluorouracil (FUra) to FUMP by orotate phosphoribosyltransferase (OPRTase). Fluorouracil 115-119 uridine monophosphate synthetase Homo sapiens 167-174 98910-4 1978 Acceleration of tumour cell proliferation following 5-fluorouracil treatment was inhibited by treating animals either with the antiseritoninergic drug BW501 or with the histamine H2-receptor blocking drug Cimetidine. Fluorouracil 52-66 histamine receptor H 2 Rattus norvegicus 169-190 9741839-7 1998 EPO, pEPO, marrow responsiveness, or red cell volume were altered by either injections of rh-EPO, 5-fluorouracil, or phenylhydrazine, or by bleeding, or red cell transfusion. Fluorouracil 98-112 erythropoietin Mus musculus 0-3 5668151-0 1968 Effect of erythropoietin on early recovery of erythropoiesis in mice after sublethal dose of 5-fluorouracil. Fluorouracil 93-107 erythropoietin Mus musculus 10-24 9644315-1 1998 We analyzed the relationship between clinical response to neo-adjuvant chemotherapy including 5-fluorouracil (5-FU) in patients with hypopharyngeal carcinoma (HPC) and thymidylate synthase (TS) expression in their tumors. Fluorouracil 110-114 thymidylate synthetase Homo sapiens 168-188 9673356-0 1998 Detection and quantitation of thymidylate synthase mRNA in human colon adenocarcinoma cell line resistant to 5-fluorouracil by competitive PCR. Fluorouracil 109-123 thymidylate synthetase Homo sapiens 30-50 9673363-1 1998 Inhibition of Thymidylate Synthase (TS) by the 5-Fluorouracil (5Fu) active metabolite Fluoro-deoxy-uridine-monophosphate (FdUMP) is considered to be the main mechanism of action of 5Fu. Fluorouracil 47-61 thymidylate synthetase Homo sapiens 14-34 9673363-1 1998 Inhibition of Thymidylate Synthase (TS) by the 5-Fluorouracil (5Fu) active metabolite Fluoro-deoxy-uridine-monophosphate (FdUMP) is considered to be the main mechanism of action of 5Fu. Fluorouracil 47-61 thymidylate synthetase Homo sapiens 36-38 9673408-8 1998 As a result, cytokine intervention in animals treated with AdR, DDP or CTx resulted in only a modest, transient increase in the HPP-CFC and total granulocyte subpopulations when compared with their effect on 5FU--treated animals. Fluorouracil 208-211 V-set and immunoglobulin domain containing 2 Mus musculus 71-74 9576280-0 1998 High expression of thymidylate synthase is associated with the drug resistance of gastric carcinoma to high dose 5-fluorouracil-based systemic chemotherapy. Fluorouracil 113-127 thymidylate synthetase Homo sapiens 19-39 9576280-2 1998 This has enabled them to explore the possibility that the level of expression of thymidylate synthase (TS), the target enzyme of 5-FU, is related to the drug sensitivity of gastric carcinoma to 5-FU-based chemotherapy. Fluorouracil 129-133 thymidylate synthetase Homo sapiens 81-101 9576280-2 1998 This has enabled them to explore the possibility that the level of expression of thymidylate synthase (TS), the target enzyme of 5-FU, is related to the drug sensitivity of gastric carcinoma to 5-FU-based chemotherapy. Fluorouracil 129-133 thymidylate synthetase Homo sapiens 103-105 9576280-2 1998 This has enabled them to explore the possibility that the level of expression of thymidylate synthase (TS), the target enzyme of 5-FU, is related to the drug sensitivity of gastric carcinoma to 5-FU-based chemotherapy. Fluorouracil 194-198 thymidylate synthetase Homo sapiens 81-101 9576280-2 1998 This has enabled them to explore the possibility that the level of expression of thymidylate synthase (TS), the target enzyme of 5-FU, is related to the drug sensitivity of gastric carcinoma to 5-FU-based chemotherapy. Fluorouracil 194-198 thymidylate synthetase Homo sapiens 103-105 9576280-10 1998 CONCLUSIONS: The data from this study suggest that the expression of TS, as determined by immunohistochemistry, is a relatively reliable indicator of whether 5-FU should be used in the treatment of patients with gastric carcinoma. Fluorouracil 158-162 thymidylate synthetase Homo sapiens 69-71 9516392-0 1998 Regulation of the PepT1 peptide transporter in the rat small intestine in response to 5-fluorouracil-induced injury. Fluorouracil 86-100 solute carrier family 15 member 1 Rattus norvegicus 18-23 9516392-2 1998 The mechanism of this resistance was investigated by examining the activity level and expression of the peptide transporter PepT1 in the intestine of rats treated with 5-fluorouracil. Fluorouracil 168-182 solute carrier family 15 member 1 Rattus norvegicus 124-129 9516392-6 1998 Immunohistochemical analysis also showed that the PepT1 immunoreactivity level was preserved in the brush border membrane of the remaining villi of 5-fluorouracil-treated rats. Fluorouracil 148-162 solute carrier family 15 member 1 Rattus norvegicus 50-55 9589051-0 1998 [Effect of low-dose CDDP/5-FU therapy on thymidylate synthase content]. Fluorouracil 25-29 thymidylate synthetase Homo sapiens 41-61 9600127-6 1998 In contrast, the HT-29/5-FU/S cells were more sensitive to the inhibition of in situ thymidylate synthase (TS) by 5-FU than were the parent cells. Fluorouracil 23-27 thymidylate synthetase Homo sapiens 85-105 9472799-2 1998 Analysis of cultures established with BM cells collected 2 and 4 days after 5-FU treatment (2d and 4d 5-FU BM, respectively) and stimulated with IL-3 + IL-6 and IL-3 + SCF resulted in the generation of samples highly enriched for colony-forming units granulocyte/macrophage (CFU-GMs). Fluorouracil 76-80 kit ligand Mus musculus 168-171 9472799-2 1998 Analysis of cultures established with BM cells collected 2 and 4 days after 5-FU treatment (2d and 4d 5-FU BM, respectively) and stimulated with IL-3 + IL-6 and IL-3 + SCF resulted in the generation of samples highly enriched for colony-forming units granulocyte/macrophage (CFU-GMs). Fluorouracil 102-106 kit ligand Mus musculus 168-171 33907844-3 2021 It has been reported that NNMT inhibits apoptosis and enhances resistance to 5-fluorouracil (5-Fu) via inhibition of the apoptosis signal regulating kinase 1 (ASK1)-p38 MAPK pathway in CRC cells. Fluorouracil 93-97 mitogen-activated protein kinase kinase kinase 5 Homo sapiens 121-157 33907844-3 2021 It has been reported that NNMT inhibits apoptosis and enhances resistance to 5-fluorouracil (5-Fu) via inhibition of the apoptosis signal regulating kinase 1 (ASK1)-p38 MAPK pathway in CRC cells. Fluorouracil 93-97 mitogen-activated protein kinase kinase kinase 5 Homo sapiens 159-163 34035223-0 2021 Retraction Note to: FOXM1 modulates 5-fluorouracil sensitivity in cholangiocarcinoma through thymidylate synthase (TYMS): implications of FOXM1-TYMS axis uncoupling in 5-FU resistance. Fluorouracil 36-50 thymidylate synthetase Homo sapiens 93-113 34035223-0 2021 Retraction Note to: FOXM1 modulates 5-fluorouracil sensitivity in cholangiocarcinoma through thymidylate synthase (TYMS): implications of FOXM1-TYMS axis uncoupling in 5-FU resistance. Fluorouracil 36-50 thymidylate synthetase Homo sapiens 115-119 33983544-6 2021 The 5-FU-Tau-GO was more stable in neutral environment than in acidic environment, and with a certain PH response and sustained release effect. Fluorouracil 4-8 microtubule associated protein tau Homo sapiens 9-12 9416974-7 1997 In 5-FU naive cells, a stimulating effect of 5-FU on thymidylate synthase mRNA and ribonucleotide reductase mRNA expression was observed. Fluorouracil 3-7 thymidylate synthetase Homo sapiens 53-73 9416974-7 1997 In 5-FU naive cells, a stimulating effect of 5-FU on thymidylate synthase mRNA and ribonucleotide reductase mRNA expression was observed. Fluorouracil 45-49 thymidylate synthetase Homo sapiens 53-73 33983544-7 2021 In vivo, we compared oral and intravenous administrations of 5-FU and 5-FU-Tau-GO, respectively, using pharmacokinetic tests and related parameters and showed that 5-FU-Tau-GO oral or intravenous administration prolongs the action time of 5-FU in the body and improves its bioavailability. Fluorouracil 61-65 microtubule associated protein tau Homo sapiens 169-172 33983544-7 2021 In vivo, we compared oral and intravenous administrations of 5-FU and 5-FU-Tau-GO, respectively, using pharmacokinetic tests and related parameters and showed that 5-FU-Tau-GO oral or intravenous administration prolongs the action time of 5-FU in the body and improves its bioavailability. Fluorouracil 70-74 microtubule associated protein tau Homo sapiens 75-78 33983544-7 2021 In vivo, we compared oral and intravenous administrations of 5-FU and 5-FU-Tau-GO, respectively, using pharmacokinetic tests and related parameters and showed that 5-FU-Tau-GO oral or intravenous administration prolongs the action time of 5-FU in the body and improves its bioavailability. Fluorouracil 70-74 microtubule associated protein tau Homo sapiens 169-172 33983544-7 2021 In vivo, we compared oral and intravenous administrations of 5-FU and 5-FU-Tau-GO, respectively, using pharmacokinetic tests and related parameters and showed that 5-FU-Tau-GO oral or intravenous administration prolongs the action time of 5-FU in the body and improves its bioavailability. Fluorouracil 70-74 microtubule associated protein tau Homo sapiens 75-78 33983544-7 2021 In vivo, we compared oral and intravenous administrations of 5-FU and 5-FU-Tau-GO, respectively, using pharmacokinetic tests and related parameters and showed that 5-FU-Tau-GO oral or intravenous administration prolongs the action time of 5-FU in the body and improves its bioavailability. Fluorouracil 70-74 microtubule associated protein tau Homo sapiens 169-172 33983544-8 2021 In addition, the inhibition of HepG2 cells that was measured by the MTT assay, showed that the IC50 value of 5-FU was 196 +- 8.73 mug/mL, and the IC50 value of 5-FU-Tau-GO was 65.2 +- 0.7 mug/mL, indicating that 5- FU-Tau-GO is more potent against HepG2 cells and has a stronger inhibitory effect on cancer cells. Fluorouracil 109-113 microtubule associated protein tau Homo sapiens 165-168 33983544-8 2021 In addition, the inhibition of HepG2 cells that was measured by the MTT assay, showed that the IC50 value of 5-FU was 196 +- 8.73 mug/mL, and the IC50 value of 5-FU-Tau-GO was 65.2 +- 0.7 mug/mL, indicating that 5- FU-Tau-GO is more potent against HepG2 cells and has a stronger inhibitory effect on cancer cells. Fluorouracil 109-113 microtubule associated protein tau Homo sapiens 218-221 33983544-8 2021 In addition, the inhibition of HepG2 cells that was measured by the MTT assay, showed that the IC50 value of 5-FU was 196 +- 8.73 mug/mL, and the IC50 value of 5-FU-Tau-GO was 65.2 +- 0.7 mug/mL, indicating that 5- FU-Tau-GO is more potent against HepG2 cells and has a stronger inhibitory effect on cancer cells. Fluorouracil 160-164 microtubule associated protein tau Homo sapiens 165-168 33983544-8 2021 In addition, the inhibition of HepG2 cells that was measured by the MTT assay, showed that the IC50 value of 5-FU was 196 +- 8.73 mug/mL, and the IC50 value of 5-FU-Tau-GO was 65.2 +- 0.7 mug/mL, indicating that 5- FU-Tau-GO is more potent against HepG2 cells and has a stronger inhibitory effect on cancer cells. Fluorouracil 160-164 microtubule associated protein tau Homo sapiens 218-221 33983544-8 2021 In addition, the inhibition of HepG2 cells that was measured by the MTT assay, showed that the IC50 value of 5-FU was 196 +- 8.73 mug/mL, and the IC50 value of 5-FU-Tau-GO was 65.2 +- 0.7 mug/mL, indicating that 5- FU-Tau-GO is more potent against HepG2 cells and has a stronger inhibitory effect on cancer cells. Fluorouracil 212-217 microtubule associated protein tau Homo sapiens 165-168 33983544-9 2021 The effect on cell morphology that was measured using the AO/EB staining also showed that 5-FU-Tau-GO not only disrupted cells, but also significantly induced apoptosis compared to 5-FU. Fluorouracil 90-94 microtubule associated protein tau Homo sapiens 95-98 33983544-10 2021 We also verified by computer aided design that Tau-GO can bind better to 5-FU than to the unmodified GO, and that the formed 5-FU-Tau-GO system is more stable, and conducive to the transfer and release of 5-FU in vivo. Fluorouracil 73-77 microtubule associated protein tau Homo sapiens 47-50 33983544-10 2021 We also verified by computer aided design that Tau-GO can bind better to 5-FU than to the unmodified GO, and that the formed 5-FU-Tau-GO system is more stable, and conducive to the transfer and release of 5-FU in vivo. Fluorouracil 73-77 microtubule associated protein tau Homo sapiens 130-133 33983544-10 2021 We also verified by computer aided design that Tau-GO can bind better to 5-FU than to the unmodified GO, and that the formed 5-FU-Tau-GO system is more stable, and conducive to the transfer and release of 5-FU in vivo. Fluorouracil 125-129 microtubule associated protein tau Homo sapiens 47-50 33983544-10 2021 We also verified by computer aided design that Tau-GO can bind better to 5-FU than to the unmodified GO, and that the formed 5-FU-Tau-GO system is more stable, and conducive to the transfer and release of 5-FU in vivo. Fluorouracil 125-129 microtubule associated protein tau Homo sapiens 130-133 33983544-10 2021 We also verified by computer aided design that Tau-GO can bind better to 5-FU than to the unmodified GO, and that the formed 5-FU-Tau-GO system is more stable, and conducive to the transfer and release of 5-FU in vivo. Fluorouracil 125-129 microtubule associated protein tau Homo sapiens 47-50 9467870-0 1997 Uteroferrin and recombinant bovine GM-CSF modulate the myelosuppressive effects of 5-fluorouracil in young female pigs (Sus scrofa). Fluorouracil 83-97 acid phosphatase 5, tartrate resistant Bos taurus 0-11 9467870-0 1997 Uteroferrin and recombinant bovine GM-CSF modulate the myelosuppressive effects of 5-fluorouracil in young female pigs (Sus scrofa). Fluorouracil 83-97 colony stimulating factor 2 Bos taurus 35-41 9467870-1 1997 The present study investigated the ability of uteroferrin and recombinant bovine granulocyte monocyte/macrophage-colony stimulating factor (rbGM-CSF) to modulate the myelosuppressive effects of 5-fluorouracil (5-FU) in young female pigs (Sus scrofa). Fluorouracil 194-208 acid phosphatase 5, tartrate resistant Bos taurus 46-57 33983544-10 2021 We also verified by computer aided design that Tau-GO can bind better to 5-FU than to the unmodified GO, and that the formed 5-FU-Tau-GO system is more stable, and conducive to the transfer and release of 5-FU in vivo. Fluorouracil 125-129 microtubule associated protein tau Homo sapiens 130-133 33199829-0 2021 Silencing of long non-coding RNA LINC01270 inhibits esophageal cancer progression and enhances chemosensitivity to 5-fluorouracil by mediating GSTP1methylation. Fluorouracil 115-129 glutathione S-transferase, pi 1 Mus musculus 143-148 9336359-0 1997 Quantitation of intratumoral thymidylate synthase expression predicts for disseminated colorectal cancer response and resistance to protracted-infusion fluorouracil and weekly leucovorin. Fluorouracil 152-164 thymidylate synthetase Homo sapiens 29-49 9336359-3 1997 Intratumoral thymidylate synthase (TS) quantitation may be among the most important determinants of sensitivity or resistance to 5-FU. Fluorouracil 129-133 thymidylate synthetase Homo sapiens 13-33 9336359-3 1997 Intratumoral thymidylate synthase (TS) quantitation may be among the most important determinants of sensitivity or resistance to 5-FU. Fluorouracil 129-133 thymidylate synthetase Homo sapiens 35-37 33199829-10 2021 Moreover, GSTP1 overexpression was observed to reverse the effects of LINC01270 overexpression on EC cells and their response to 5-FU. Fluorouracil 129-133 glutathione S-transferase, pi 1 Mus musculus 10-15 33996571-0 2021 NGFR Increases the Chemosensitivity of Colorectal Cancer Cells by Enhancing the Apoptotic and Autophagic Effects of 5-fluorouracil via the Activation of S100A9. Fluorouracil 116-130 nerve growth factor receptor Homo sapiens 0-4 9446257-5 1997 In a randomized study by Ardizzoni et al., the administration of GM-CSF at the dose of 10 micrograms/kg following CEF program (cyclophosphamide, epirubicin and fluorouracil) was effective in reducing from 20 to 16 days the time interval among cycles. Fluorouracil 160-172 colony stimulating factor 2 Homo sapiens 65-71 9446257-8 1997 have observed that 3 micrograms/kg GM-CSF may allow the administration of 425 mg/m2 fluorouracil for five days; Reed et al. Fluorouracil 84-96 colony stimulating factor 2 Homo sapiens 35-41 33996571-4 2021 Our previous study indicated that NGFR acts as a tumor suppressor, and high expression is associated with better outcomes in patients receiving 5-FU-based adjuvant chemotherapy after surgery. Fluorouracil 144-148 nerve growth factor receptor Homo sapiens 34-38 33996571-12 2021 The results showed that the half maximal inhibitory concentration of NGFR-transfected cells was lower than that of controls in DLD1 and HCT8 cells after 5-FU treatment, and cell viability was lower than in empty-vector cells. Fluorouracil 153-157 nerve growth factor receptor Homo sapiens 69-73 9276707-9 1997 More potent inhibitors of thymidylate synthase (TS) such as tomudex and trimetrexate have been developed and are currently being evaluated in the clinic either alone or in combination with 5-FU. Fluorouracil 189-193 thymidylate synthetase Homo sapiens 26-46 33996571-15 2021 NGFR elevated the expression of S100A9 after 5-FU treatment. Fluorouracil 45-49 nerve growth factor receptor Homo sapiens 0-4 9276707-9 1997 More potent inhibitors of thymidylate synthase (TS) such as tomudex and trimetrexate have been developed and are currently being evaluated in the clinic either alone or in combination with 5-FU. Fluorouracil 189-193 thymidylate synthetase Homo sapiens 48-50 33954114-4 2021 Modulation of expression levels of microRNAs or long non-coding RNAs may be a suitable approach to sensitize tumor cells to 5-FU treatment via modulating multiple biological signaling pathways such as Hippo/YAP, Wnt/beta-catenin, Hedgehog, NF-kB, and Notch cascades. Fluorouracil 124-128 catenin beta 1 Homo sapiens 216-228 33948374-0 2021 Elevated LOXL2 expression by LINC01347/miR-328-5p axis contributes to 5-FU chemotherapy resistance of colorectal cancer. Fluorouracil 70-74 long intergenic non-protein coding RNA 1347 Homo sapiens 29-38 33948374-7 2021 Exogenous LINC01347 expression promoted cell proliferation and 5-FU resistance of CRC cells, while LINC01347 knockdown attenuated cell growth and 5-FU resistance in vitro and in vivo. Fluorouracil 63-67 long intergenic non-protein coding RNA 1347 Homo sapiens 10-19 9245489-0 1997 Mitigating effects of interleukin 11 on consecutive courses of 5-fluorouracil-induced ulcerative mucositis in hamsters. Fluorouracil 63-77 interleukin 11 Homo sapiens 22-36 33948374-7 2021 Exogenous LINC01347 expression promoted cell proliferation and 5-FU resistance of CRC cells, while LINC01347 knockdown attenuated cell growth and 5-FU resistance in vitro and in vivo. Fluorouracil 146-150 long intergenic non-protein coding RNA 1347 Homo sapiens 99-108 9245489-3 1997 Recently, we reported that recombinant human(rh) interleukin 11 (IL-11) favourably modified the course of mucositis following a single stomatotoxic regimen of 5-fluorouracil in hamsters. Fluorouracil 159-173 interleukin 11 Homo sapiens 49-63 9245489-3 1997 Recently, we reported that recombinant human(rh) interleukin 11 (IL-11) favourably modified the course of mucositis following a single stomatotoxic regimen of 5-fluorouracil in hamsters. Fluorouracil 159-173 interleukin 11 Homo sapiens 65-70 33948374-9 2021 LOXL2 knockdown impaired the LINC01347 overexpression induced 5-FU resistance in CRC cells. Fluorouracil 62-66 long intergenic non-protein coding RNA 1347 Homo sapiens 29-38 33948374-11 2021 Our study provided a molecular basis for the development of 5-FU based chemotherapy resistance in CRC by LINC01347/miR-328/LOXL2 axis. Fluorouracil 60-64 long intergenic non-protein coding RNA 1347 Homo sapiens 105-114 21590122-1 1997 Thymidylate synthase (TS) is a rate-limiting enzyme in de novo DNA biosynthesis and also a primary target for 5-fluorouracil (5-FU)-based chemotherapy. Fluorouracil 110-124 thymidylate synthetase Homo sapiens 0-20 33948374-12 2021 We identified LINC01347 as a prognostic biomarker and potential therapeutic target against 5-FU based chemotherapy resistance of CRC. Fluorouracil 91-95 long intergenic non-protein coding RNA 1347 Homo sapiens 14-23 21590122-1 1997 Thymidylate synthase (TS) is a rate-limiting enzyme in de novo DNA biosynthesis and also a primary target for 5-fluorouracil (5-FU)-based chemotherapy. Fluorouracil 110-124 thymidylate synthetase Homo sapiens 22-24 21590122-1 1997 Thymidylate synthase (TS) is a rate-limiting enzyme in de novo DNA biosynthesis and also a primary target for 5-fluorouracil (5-FU)-based chemotherapy. Fluorouracil 126-130 thymidylate synthetase Homo sapiens 0-20 32189577-2 2021 Among these compounds A2, A4, A11 and A14 possessed high inhibition activity against A-549 cell lines with IC50 values at 4.91, 3.22, 27.43 and 18.14 muM, respectively, better than that of 5-fluorouracil (IC50=59.27 muM). Fluorouracil 189-203 DXS435E Homo sapiens 30-33 21590122-1 1997 Thymidylate synthase (TS) is a rate-limiting enzyme in de novo DNA biosynthesis and also a primary target for 5-fluorouracil (5-FU)-based chemotherapy. Fluorouracil 126-130 thymidylate synthetase Homo sapiens 22-24 21590122-3 1997 Using this anti-TS antibody, it was revealed that the content of TS protein, as determined by Western blot analysis, correlated with the enzyme activity (gamma=0.973) and cytotoxicity of 5-FU, expressed as IC50 value (gamma=0.954) against human colon tumor cells, sensitive to and with acquired-resistance to 5-fluoropyrimidines and other cancer cells. Fluorouracil 187-191 thymidylate synthetase Homo sapiens 16-18 21590122-3 1997 Using this anti-TS antibody, it was revealed that the content of TS protein, as determined by Western blot analysis, correlated with the enzyme activity (gamma=0.973) and cytotoxicity of 5-FU, expressed as IC50 value (gamma=0.954) against human colon tumor cells, sensitive to and with acquired-resistance to 5-fluoropyrimidines and other cancer cells. Fluorouracil 187-191 thymidylate synthetase Homo sapiens 65-67 21590122-5 1997 These results indicate that this purified polyclonal antibody to rhTS is applicable to prospective and retrospective clinical studies on immunochemical TS expression in various tumors as a prognostic factor and 5-FU response-predicting parameter. Fluorouracil 211-215 thymidylate synthetase Homo sapiens 67-69 9238541-0 1997 Effect of 5-fluorouracil on interleukin-1 and interleukin-2 receptor expression. Fluorouracil 10-24 interleukin 1 alpha Homo sapiens 28-41 9238541-1 1997 We have studied the effect of anticancer drug 5-fluorouracil on the expression of human Interleukin-1 and Interleukin-2 receptor. Fluorouracil 46-60 interleukin 1 alpha Homo sapiens 88-101 9238541-2 1997 In this report, we show that 5-Fluorouracil increases the Interleukin-1 expression upto 2.66 folds without significantly affecting the levels of surface expression of p55 IL-2 receptor on human Peripheral blood mononuclear cells, CD4 and CD8 T cells. Fluorouracil 29-43 interleukin 1 alpha Homo sapiens 58-71 33841630-1 2021 First-generation immunological checkpoint inhibitors, such as CTLA-4, PD-L1 and PD-1 exhibit significant advantages over conventional cytotoxic drugs, such as oxaliplatin and 5-FU, for the treatment of colorectal cancer. Fluorouracil 175-179 cytotoxic T-lymphocyte associated protein 4 Homo sapiens 62-68 9238541-5 1997 Taken together, 5-fluorouracil differentially affects the expression of Interleukin-1, Interferon-gamma and Interleukin-2 receptor. Fluorouracil 16-30 interleukin 1 alpha Homo sapiens 72-85 9178824-7 1997 Flow cytometric analysis showed that Fas antigen expression of the cells increased upon incubation with 10 microg/ml of 5-FU. Fluorouracil 120-124 Fas cell surface death receptor Homo sapiens 37-48 33667525-4 2021 In contrast, 5-fluorouracil (5-FU) interferes with DNA biosynthesis by inhibiting thymidylate synthase(TS), which partly explains the absence of cross-resistance between TAS-102 and 5-FU. Fluorouracil 13-27 thymidylate synthetase Homo sapiens 82-102 9178824-10 1997 However, the relationship between 5-FU-mediated apoptosis and the Fas ligand/Fas system remains to be explored. Fluorouracil 34-38 Fas ligand Homo sapiens 66-76 33667525-4 2021 In contrast, 5-fluorouracil (5-FU) interferes with DNA biosynthesis by inhibiting thymidylate synthase(TS), which partly explains the absence of cross-resistance between TAS-102 and 5-FU. Fluorouracil 29-33 thymidylate synthetase Homo sapiens 82-102 32647340-9 2021 Overall, this study reveals a previously unrecognized mechanism of 5-FU resistance resulted from S1PR2 internalization-upregulated uracil generation in colorectal cancer, and provides the novel insight into the significance of S1PR2 localization in predicting the benefit of CRC patients from 5-FU-based chemotherapy. Fluorouracil 67-71 sphingosine-1-phosphate receptor 2 Homo sapiens 97-102 32647340-9 2021 Overall, this study reveals a previously unrecognized mechanism of 5-FU resistance resulted from S1PR2 internalization-upregulated uracil generation in colorectal cancer, and provides the novel insight into the significance of S1PR2 localization in predicting the benefit of CRC patients from 5-FU-based chemotherapy. Fluorouracil 67-71 sphingosine-1-phosphate receptor 2 Homo sapiens 227-232 32647340-9 2021 Overall, this study reveals a previously unrecognized mechanism of 5-FU resistance resulted from S1PR2 internalization-upregulated uracil generation in colorectal cancer, and provides the novel insight into the significance of S1PR2 localization in predicting the benefit of CRC patients from 5-FU-based chemotherapy. Fluorouracil 293-297 sphingosine-1-phosphate receptor 2 Homo sapiens 97-102 33788719-1 2021 BACKGROUND/AIM: In previous work we showed that expression of heat-shock protein 27 (HSP27; encoded by HSPB1) was associated with inherent resistance to 5-fluorouracil (5-FU). Fluorouracil 153-167 heat shock protein family B (small) member 1 Homo sapiens 85-90 33788719-1 2021 BACKGROUND/AIM: In previous work we showed that expression of heat-shock protein 27 (HSP27; encoded by HSPB1) was associated with inherent resistance to 5-fluorouracil (5-FU). Fluorouracil 153-167 heat shock protein family B (small) member 1 Homo sapiens 103-108 33788719-1 2021 BACKGROUND/AIM: In previous work we showed that expression of heat-shock protein 27 (HSP27; encoded by HSPB1) was associated with inherent resistance to 5-fluorouracil (5-FU). Fluorouracil 169-173 heat shock protein family B (small) member 1 Homo sapiens 62-83 33788719-1 2021 BACKGROUND/AIM: In previous work we showed that expression of heat-shock protein 27 (HSP27; encoded by HSPB1) was associated with inherent resistance to 5-fluorouracil (5-FU). Fluorouracil 169-173 heat shock protein family B (small) member 1 Homo sapiens 85-90 33788719-1 2021 BACKGROUND/AIM: In previous work we showed that expression of heat-shock protein 27 (HSP27; encoded by HSPB1) was associated with inherent resistance to 5-fluorouracil (5-FU). Fluorouracil 169-173 heat shock protein family B (small) member 1 Homo sapiens 103-108 33788719-6 2021 RESULTS: 5-FU-acquired resistance induced overexpression of HSP27 mRNA and protein levels in WiDr-R cells. Fluorouracil 9-13 heat shock protein family B (small) member 1 Homo sapiens 60-65 33788719-7 2021 Furthermore, siRNA knockdown of HSP27 in WiDr-R cells reduced 5-FU-acquired resistance. Fluorouracil 62-66 heat shock protein family B (small) member 1 Homo sapiens 32-37 33788719-8 2021 CONCLUSION: These findings demonstrate that HSP27 is associated with 5-FU resistance in human colon cancer cell cells and suggest that HSP27 regulation represents a novel approach to overcoming chemoresistance in colorectal cancer. Fluorouracil 69-73 heat shock protein family B (small) member 1 Homo sapiens 44-49 33788719-8 2021 CONCLUSION: These findings demonstrate that HSP27 is associated with 5-FU resistance in human colon cancer cell cells and suggest that HSP27 regulation represents a novel approach to overcoming chemoresistance in colorectal cancer. Fluorouracil 69-73 heat shock protein family B (small) member 1 Homo sapiens 135-140 33338532-0 2021 Voltage-gated sodium channel Nav1.5 promotes tumor progression and enhances chemosensitivity to 5-fluorouracil in colorectal cancer. Fluorouracil 96-110 sodium voltage-gated channel alpha subunit 5 Homo sapiens 29-35 33338532-4 2021 Elevated Nav1.5 expression was associated with poor prognosis in CRCs, whereas stage II/III patients with upregulated SCN5A expression could have better survival after receiving 5-FU-based adjuvant chemotherapy. Fluorouracil 178-182 sodium voltage-gated channel alpha subunit 5 Homo sapiens 118-123 33338532-8 2021 Meanwhile, SCN5A knockdown increased the 50% inhibitory concentration to 5-FU by upregulating 5-FU-stimulated apoptosis in CRCs. Fluorouracil 73-77 sodium voltage-gated channel alpha subunit 5 Homo sapiens 11-16 33338532-8 2021 Meanwhile, SCN5A knockdown increased the 50% inhibitory concentration to 5-FU by upregulating 5-FU-stimulated apoptosis in CRCs. Fluorouracil 94-98 sodium voltage-gated channel alpha subunit 5 Homo sapiens 11-16 33338532-9 2021 In conclusion, Nav1.5 could progress to proliferation and metastasis through Ca2+/calmodulin-dependent Ras signaling in CRC, and it could also enhance 5-FU-stimulated apoptosis. Fluorouracil 151-155 sodium voltage-gated channel alpha subunit 5 Homo sapiens 15-21 33574948-7 2021 AKT1/CTNNB1 mutations were also associated with oxaliplatin, irinotecan, SN-38 and 5-fluorouracil resistance. Fluorouracil 83-97 catenin beta 1 Homo sapiens 5-11 33613724-0 2021 MicroRNA-9-5p increases the sensitivity of colorectal cancer cells to 5-fluorouracil by downregulating high mobility group A2 expression. Fluorouracil 70-84 high mobility group AT-hook 2 Homo sapiens 103-125 33613724-10 2021 The present study indicated that miR-9-5p enhanced the sensitivity of CRC cells to 5-FU via downregulating HMGA2 expression. Fluorouracil 83-87 high mobility group AT-hook 2 Homo sapiens 107-112 33599179-0 2021 JAK2/STAT3 inhibitor reduced 5-FU resistance and autophagy through ATF6-mediated ER stress. Fluorouracil 29-33 activating transcription factor 6 Homo sapiens 67-71 33599179-11 2021 These findings indicated that the involvement of JAK2/STAT3 pathway in regulating ER stress affected the 5-FU resistance of AGS cells and autophagy, which was mediated by ATF6. Fluorouracil 105-109 activating transcription factor 6 Homo sapiens 171-175 33672989-2 2021 Fcy-hEGF fusion protein, composed of yeast cytosine deaminase (Fcy) and human EGF (hEGF), is capable of binding to EGFR and enzymatically convert 5-fluorocytosine (5-FC) to 1000-fold toxic 5-fluorocuracil (5-FU), thereby inhibiting the growth of EGFR-expressing tumor cells. Fluorouracil 206-210 epidermal growth factor Homo sapiens 4-8 33672989-2 2021 Fcy-hEGF fusion protein, composed of yeast cytosine deaminase (Fcy) and human EGF (hEGF), is capable of binding to EGFR and enzymatically convert 5-fluorocytosine (5-FC) to 1000-fold toxic 5-fluorocuracil (5-FU), thereby inhibiting the growth of EGFR-expressing tumor cells. Fluorouracil 206-210 epidermal growth factor Homo sapiens 5-8 33672989-2 2021 Fcy-hEGF fusion protein, composed of yeast cytosine deaminase (Fcy) and human EGF (hEGF), is capable of binding to EGFR and enzymatically convert 5-fluorocytosine (5-FC) to 1000-fold toxic 5-fluorocuracil (5-FU), thereby inhibiting the growth of EGFR-expressing tumor cells. Fluorouracil 206-210 epidermal growth factor Homo sapiens 83-87 32672083-5 2021 In the presence of LPA, the cell survival rate to 5-FU was significantly elevated by LPA5 knockdown. Fluorouracil 50-54 lysophosphatidic acid receptor 5 Homo sapiens 85-89 32672083-10 2021 The cell survival rate to 5-FU of DLD-5FU cells were significantly elevated by LPA5 knockdown. Fluorouracil 26-30 lysophosphatidic acid receptor 5 Homo sapiens 79-83 32672083-10 2021 The cell survival rate to 5-FU of DLD-5FU cells were significantly elevated by LPA5 knockdown. Fluorouracil 38-41 lysophosphatidic acid receptor 5 Homo sapiens 79-83 33645034-0 2021 [Curcumin mediates IL-6/STAT3 signaling pathway to repair intestinal mucosal injury induced by 5-FU chemotherapy for colon cancer]. Fluorouracil 95-99 signal transducer and activator of transcription 3 Rattus norvegicus 24-29 33645034-1 2021 This study aims to investigate the potential mechanism of curcumin in mediating interleukin-6(IL-6)/signal transducer and activator of transcription 3(STAT3) signaling pathway to repair intestinal mucosal injury induced by 5-fluorouracil(5-FU) chemotherapy for colon cancer. Fluorouracil 223-237 signal transducer and activator of transcription 3 Rattus norvegicus 100-150 33645034-1 2021 This study aims to investigate the potential mechanism of curcumin in mediating interleukin-6(IL-6)/signal transducer and activator of transcription 3(STAT3) signaling pathway to repair intestinal mucosal injury induced by 5-fluorouracil(5-FU) chemotherapy for colon cancer. Fluorouracil 223-237 signal transducer and activator of transcription 3 Rattus norvegicus 151-156 33645034-1 2021 This study aims to investigate the potential mechanism of curcumin in mediating interleukin-6(IL-6)/signal transducer and activator of transcription 3(STAT3) signaling pathway to repair intestinal mucosal injury induced by 5-fluorouracil(5-FU) chemotherapy for colon cancer. Fluorouracil 238-242 signal transducer and activator of transcription 3 Rattus norvegicus 100-150 33645034-1 2021 This study aims to investigate the potential mechanism of curcumin in mediating interleukin-6(IL-6)/signal transducer and activator of transcription 3(STAT3) signaling pathway to repair intestinal mucosal injury induced by 5-fluorouracil(5-FU) chemotherapy for colon cancer. Fluorouracil 238-242 signal transducer and activator of transcription 3 Rattus norvegicus 151-156 33039561-0 2021 Angiogenesis is promoted by exosomal DPP4 derived from 5-fluorouracil-resistant colon cancer cells. Fluorouracil 55-69 dipeptidyl peptidase 4 Homo sapiens 37-41 9135021-7 1997 c-myc status was not related to time to recurrence or death, but low levels of c-myc amplification identified a subset of patients who showed a statistically significant increase in disease-free survival, and a corresponding trend to longer overall survival, in response to adjuvant therapy with 5-fluorouracil plus levamisole. Fluorouracil 296-310 MYC proto-oncogene, bHLH transcription factor Homo sapiens 79-84 33039561-4 2021 Here, our study showed that the conditioned medium and exosomes from 5-FU-resistant colon cancer cells promoted angiogenesis, and we observed that exosomal dipeptidyl peptidase IV (DPP4) was a potent inducer of this angiogenesis. Fluorouracil 69-73 dipeptidyl peptidase 4 Homo sapiens 156-179 33039561-4 2021 Here, our study showed that the conditioned medium and exosomes from 5-FU-resistant colon cancer cells promoted angiogenesis, and we observed that exosomal dipeptidyl peptidase IV (DPP4) was a potent inducer of this angiogenesis. Fluorouracil 69-73 dipeptidyl peptidase 4 Homo sapiens 181-185 33039561-7 2021 These findings indicate that DPP4 may be a target for inhibiting angiogenesis in 5-FU-resistant colon cancer. Fluorouracil 81-85 dipeptidyl peptidase 4 Homo sapiens 29-33 33500399-2 2021 In this study, we observed that epithelial colorectal cancer (CRC) cells transiently exposed to 5-fluorouracil (5-FU) (a chemotherapeutic drug for CRC) as well as 5-FU-resistant cells (5-FU-R) develop EMT characters as evidenced by activation of Vimentin and augmented invasive properties. Fluorouracil 112-116 vimentin Homo sapiens 246-254 9620216-1 1997 We evaluated the effects of 5-fluorouracil (5FU) and leucovorin (LV) on thymidylate synthase (TS) in normal rapidly dividing tissues, which may contribute to toxic side-effects of treatment with 5FU and LV. Fluorouracil 28-42 thymidylate synthetase Homo sapiens 72-92 33500399-2 2021 In this study, we observed that epithelial colorectal cancer (CRC) cells transiently exposed to 5-fluorouracil (5-FU) (a chemotherapeutic drug for CRC) as well as 5-FU-resistant cells (5-FU-R) develop EMT characters as evidenced by activation of Vimentin and augmented invasive properties. Fluorouracil 163-167 vimentin Homo sapiens 246-254 9620216-1 1997 We evaluated the effects of 5-fluorouracil (5FU) and leucovorin (LV) on thymidylate synthase (TS) in normal rapidly dividing tissues, which may contribute to toxic side-effects of treatment with 5FU and LV. Fluorouracil 44-47 thymidylate synthetase Homo sapiens 72-92 33500399-2 2021 In this study, we observed that epithelial colorectal cancer (CRC) cells transiently exposed to 5-fluorouracil (5-FU) (a chemotherapeutic drug for CRC) as well as 5-FU-resistant cells (5-FU-R) develop EMT characters as evidenced by activation of Vimentin and augmented invasive properties. Fluorouracil 163-167 vimentin Homo sapiens 246-254 33500399-4 2021 Treatment with 4DPG restrains Vimentin phosphorylation (Ser38) in 5-FU-R cells, along with downregulation of mesenchymal markers Twist1 and MMP-2 while augmenting the expression of epithelial markers E-cadherin and TIMP-1. Fluorouracil 66-70 vimentin Homo sapiens 30-38 33500399-7 2021 Furthermore, immunoprecipitation analysis unveiled that 4DPG prevents complex formation between Vimentin and p53 resulting in the rescue of p53 and its nuclear localization in aggressive 5-FU-R cells. Fluorouracil 187-191 vimentin Homo sapiens 96-104 9045902-4 1997 The thymidylate synthase (TS) inhibition rate, an index of inhibition of the de novo pathway, was significantly higher in the 5-FU and 5-FU plus AZT groups than in the control group (P<0.01), but it did not differ from the control in the AZT group. Fluorouracil 126-130 thymidylate synthetase Homo sapiens 4-24 9045902-4 1997 The thymidylate synthase (TS) inhibition rate, an index of inhibition of the de novo pathway, was significantly higher in the 5-FU and 5-FU plus AZT groups than in the control group (P<0.01), but it did not differ from the control in the AZT group. Fluorouracil 135-139 thymidylate synthetase Homo sapiens 4-24 9268987-0 1997 Inhibition by 5-fluorouracil of ERCC1 and gamma-glutamylcysteine synthetase messenger RNA expression in a cisplatin-resistant HST-1 human squamous carcinoma cell line. Fluorouracil 14-28 ERCC excision repair 1, endonuclease non-catalytic subunit Homo sapiens 32-37 33131720-7 2021 In CD117 positive cells from wild type (WT) mouse bone marrow, 5-FU also enhanced the H2O2-induced [Ca2+]i increases, but not in cells from Trpm2 knockout (KO) mice. Fluorouracil 63-67 KIT proto-oncogene receptor tyrosine kinase Mus musculus 3-8 9253112-4 1997 A strong correlation between the number of CFU-Mk and HPP-CFC formation from 5-fluorouracil bone marrow cells was observed when these cells were stimulated with EPO in the presence of SCF and IL-3. Fluorouracil 77-91 erythropoietin Mus musculus 161-164 9253112-4 1997 A strong correlation between the number of CFU-Mk and HPP-CFC formation from 5-fluorouracil bone marrow cells was observed when these cells were stimulated with EPO in the presence of SCF and IL-3. Fluorouracil 77-91 kit ligand Mus musculus 184-187 8980242-4 1996 The probability of clinical response to biochemically modulated 5-FU was independent of p53 and PCNA expression. Fluorouracil 64-68 proliferating cell nuclear antigen Homo sapiens 96-100 8950202-1 1996 We estimate the influence of five 5-hydroxytryptamine receptor (5-HT3) antagonists on the activity of dihydropyrimidine dehydrogenase (DPDase), the rate-limiting enzyme in 5-fluorouracil (5FU) metabolism. Fluorouracil 172-186 dihydropyrimidine dehydrogenase Rattus norvegicus 102-133 8950202-1 1996 We estimate the influence of five 5-hydroxytryptamine receptor (5-HT3) antagonists on the activity of dihydropyrimidine dehydrogenase (DPDase), the rate-limiting enzyme in 5-fluorouracil (5FU) metabolism. Fluorouracil 172-186 dihydropyrimidine dehydrogenase Rattus norvegicus 135-141 8950202-1 1996 We estimate the influence of five 5-hydroxytryptamine receptor (5-HT3) antagonists on the activity of dihydropyrimidine dehydrogenase (DPDase), the rate-limiting enzyme in 5-fluorouracil (5FU) metabolism. Fluorouracil 188-191 dihydropyrimidine dehydrogenase Rattus norvegicus 102-133 8950202-1 1996 We estimate the influence of five 5-hydroxytryptamine receptor (5-HT3) antagonists on the activity of dihydropyrimidine dehydrogenase (DPDase), the rate-limiting enzyme in 5-fluorouracil (5FU) metabolism. Fluorouracil 188-191 dihydropyrimidine dehydrogenase Rattus norvegicus 135-141 8934221-6 1996 Preceding administration of pegylated stem cell factor (SCF), 100 micrograms/kg per day, increased CFU-C killing by a single dose of 5-fluorouracil (5-FU) 15- to 65-fold in the femur, and 5- to 15-fold in the spleen, consistent with previous reports. Fluorouracil 133-147 kit ligand Mus musculus 38-54 8934221-6 1996 Preceding administration of pegylated stem cell factor (SCF), 100 micrograms/kg per day, increased CFU-C killing by a single dose of 5-fluorouracil (5-FU) 15- to 65-fold in the femur, and 5- to 15-fold in the spleen, consistent with previous reports. Fluorouracil 133-147 kit ligand Mus musculus 56-59 8934221-6 1996 Preceding administration of pegylated stem cell factor (SCF), 100 micrograms/kg per day, increased CFU-C killing by a single dose of 5-fluorouracil (5-FU) 15- to 65-fold in the femur, and 5- to 15-fold in the spleen, consistent with previous reports. Fluorouracil 149-153 kit ligand Mus musculus 38-54 8934221-6 1996 Preceding administration of pegylated stem cell factor (SCF), 100 micrograms/kg per day, increased CFU-C killing by a single dose of 5-fluorouracil (5-FU) 15- to 65-fold in the femur, and 5- to 15-fold in the spleen, consistent with previous reports. Fluorouracil 149-153 kit ligand Mus musculus 56-59 8969073-12 1996 In conclusion, the BCM effect of LV on the antitumor effect of 5-FU was revealed in MC-1 and MPC-2 strains. Fluorouracil 63-67 mitochondrial pyruvate carrier 2 Homo sapiens 93-98 9275551-4 1996 RESULTS: COC1/DDP cells were of 6.5-fold resistance to DDP and displayed significant cross-resistant with carplatin and mitomycin C, but still remained sensitive to 5-fluorouracil and adriamycin. Fluorouracil 165-179 translocase of inner mitochondrial membrane 8A Homo sapiens 14-17 8759028-7 1996 The dose dependence of the EH of FUra and the effects of uracil and IL-2 on the EH of FUra corresponded with clinical findings. Fluorouracil 86-90 interleukin 2 Rattus norvegicus 68-72 8759880-5 1996 TPO in combination with the ligand for c-kit (SF) or interleukin-3 (IL-3) supported colony formation by marrow cells of 5-fluorouracil (5-FU)-treated mice whereas TPO alone yielded no colony. Fluorouracil 120-134 KIT proto-oncogene receptor tyrosine kinase Mus musculus 39-44 8759880-5 1996 TPO in combination with the ligand for c-kit (SF) or interleukin-3 (IL-3) supported colony formation by marrow cells of 5-fluorouracil (5-FU)-treated mice whereas TPO alone yielded no colony. Fluorouracil 136-140 KIT proto-oncogene receptor tyrosine kinase Mus musculus 39-44 33469286-12 2021 In addition, rapamycin liposomes and 5-FU can synergistically improve the efficacy of colorectal cancer via the Akt/mTOR and P53 pathways. Fluorouracil 37-41 mechanistic target of rapamycin kinase Mus musculus 116-120 33469286-12 2021 In addition, rapamycin liposomes and 5-FU can synergistically improve the efficacy of colorectal cancer via the Akt/mTOR and P53 pathways. Fluorouracil 37-41 transformation related protein 53, pseudogene Mus musculus 125-128 33489872-3 2020 Moreover, REG4-positive cancer cells show more frequent resistance to chemoradiotherapy, especially 5-FU-based chemotherapy. Fluorouracil 100-104 regenerating family member 4 Homo sapiens 10-14 32838723-13 2021 Moreover, western blotting and molecular docking revealed that compounds 3 or 5 might promote 5-FU-induced apoptosis by regulating the expression of Caspase 9 and PARP. Fluorouracil 94-98 caspase 9 Homo sapiens 149-158 33386794-7 2021 Besides, silencing of XIST not only diminished proliferative, migratory and invasive power of CRC cells (P< 0.05), but also enhanced sensitivity of CRC cells responding to 5-FU/cisplatin (P< 0.05). Fluorouracil 172-176 X inactive specific transcript Homo sapiens 22-26 32987433-11 2021 The combination of metformin with 5-FU or docetaxel significantly reduced the number of cells expressing the Shh protein compared to the 5-FU alone or docetaxel alone. Fluorouracil 34-38 sonic hedgehog signaling molecule Homo sapiens 109-112 32987433-11 2021 The combination of metformin with 5-FU or docetaxel significantly reduced the number of cells expressing the Shh protein compared to the 5-FU alone or docetaxel alone. Fluorouracil 137-141 sonic hedgehog signaling molecule Homo sapiens 109-112 33468749-4 2021 NAC with FOLFOXIRI(5-fluorouracil/oxaliplatin/leucovorin/irinotecan)plus bevacizumab(BEV)was inisiated as NAC. Fluorouracil 19-33 synuclein alpha Homo sapiens 0-3 33240430-9 2021 5-FU induced apoptosis through p53-p21 activity, while chrysin arrested the cell cycle in the G2/M phase. Fluorouracil 0-4 H3 histone pseudogene 16 Homo sapiens 35-38 33364975-13 2020 Interestingly, 5FU reduced bone marrow CD45+ immune cells and CD45+CD11b+ monocytes. Fluorouracil 15-18 protein tyrosine phosphatase, receptor type, C Mus musculus 39-43 33364975-13 2020 Interestingly, 5FU reduced bone marrow CD45+ immune cells and CD45+CD11b+ monocytes. Fluorouracil 15-18 protein tyrosine phosphatase, receptor type, C Mus musculus 62-66 33364975-14 2020 Our results demonstrate that 5FU induced body weight loss and decreased skeletal muscle CD45+ immune cells in association with a reduction in infiltrating Ly6cHigh monocytes. Fluorouracil 29-32 protein tyrosine phosphatase, receptor type, C Mus musculus 88-92 32814111-20 2020 Knockout of SLC25A22 in CRC cells that express mutant KRAS increased their sensitivity to 5-fluorouacil. Fluorouracil 90-103 solute carrier family 25 member 22 Homo sapiens 12-20 8765498-3 1996 When lymphohematopoietic progenitors isolated from 5-fluorouracil (5-FU)-treated mice were cultured in the presence of Steel factor (SF), IL-11, IL-7, and erythropoietin (Epo), B lymphopoiesis appeared to proceed through three stages: lymphohematopoietic proliferation, commitment, and early B lymphoid proliferation. Fluorouracil 67-71 kit ligand Mus musculus 119-131 32814111-22 2020 CONCLUSIONS: In CRC cells that express activated KRAS, SLC25A22 promotes accumulation of succinate, resulting in increased DNA methylation, activation of WNT signaling to beta-catenin, increased expression of LGR5, proliferation, stem cell features, and resistance to 5-fluorouacil. Fluorouracil 268-281 solute carrier family 25 member 22 Homo sapiens 55-63 8609072-4 1996 On the other hand, NUGC-3/5/5FU/L also showed resistance to in situ thymidylate synthase (TS) inhibition by 5-FU. Fluorouracil 108-112 thymidylate synthetase Homo sapiens 90-92 8609072-9 1996 2"-Deoxyinosine effectively enhanced TS inhibition by 5-FU in the resistant cells, thus markedly sensitizing them to 5-FU. Fluorouracil 54-58 thymidylate synthetase Homo sapiens 37-39 32835374-4 2020 We observed that combined treatment with andrographis was synergistic and resulted in a significant and dose-dependent increase in the efficacy of 5FU in HCT116 and SW480 5FUR cells (p&0.05), reduced clonogenic formation (p&0.01) and increased rates of caspase-9 mediated apoptosis (p&0.05). Fluorouracil 147-150 caspase 9 Homo sapiens 253-262 8823494-1 1996 Interferon (IFN) augments the anabolism of 5-fluorouracil (5FU) to its active metabolite, fluorodeoxyuridylate (FdUMP), which inhibits thymidylate synthase (TS). Fluorouracil 43-57 thymidylate synthetase Homo sapiens 135-155 8823494-1 1996 Interferon (IFN) augments the anabolism of 5-fluorouracil (5FU) to its active metabolite, fluorodeoxyuridylate (FdUMP), which inhibits thymidylate synthase (TS). Fluorouracil 59-62 thymidylate synthetase Homo sapiens 135-155 33046724-11 2020 HER2 receptors expression were markedly reduced in 5-FU-SLN4 treated mice compared with 5FU and liver and kidney tissues showed no toxicity at dose of 20 mg/kg. Fluorouracil 51-55 erb-b2 receptor tyrosine kinase 2 Mus musculus 0-4 8558194-1 1996 PURPOSE: We tested the hypothesis that polymerase chain reaction (PCR) quantitation of the enzyme thymidylate synthase (TS) within a primary adenocarcinoma of the stomach, has an inverse relationship to response and survival for patients who receive fluorouracil (5FU)-based chemotherapy. Fluorouracil 250-262 thymidylate synthetase Homo sapiens 98-118 8558194-1 1996 PURPOSE: We tested the hypothesis that polymerase chain reaction (PCR) quantitation of the enzyme thymidylate synthase (TS) within a primary adenocarcinoma of the stomach, has an inverse relationship to response and survival for patients who receive fluorouracil (5FU)-based chemotherapy. Fluorouracil 264-267 thymidylate synthetase Homo sapiens 98-118 10387999-5 1996 One of the critical mechanisms of resistance to 5-FU appears to be the acute induction in thymidylate synthase (TS) levels following therapy with inhibitors of this enzyme. Fluorouracil 48-52 thymidylate synthetase Homo sapiens 90-110 10387999-5 1996 One of the critical mechanisms of resistance to 5-FU appears to be the acute induction in thymidylate synthase (TS) levels following therapy with inhibitors of this enzyme. Fluorouracil 48-52 thymidylate synthetase Homo sapiens 112-114 31983282-7 2020 Taken together, our data suggest that PRKDC-mediated phosphorylation of PRKAG1 primes AMPK complex to the lysosomal activation by STK11 in cancer cells thereby linking DNA damage response to autophagy and cellular metabolism.Abbreviations: AXIN1: axin 1; 3-MA: 3-methyladenine; 5-FU: 5-fluorouracil; AA mutant: double alanine mutant (S192A, T284A) of PRKAG1; ACACA: acetyl-CoA carboxylase alpha; AICAR: 5-Aminoimidazole-4-carboxamide ribonucleotide; AMPK: AMP-activated protein kinase; ATG: autophagy-related; ATM: ataxia telangiectasia mutated; ATR: ATM serine/threonine kinase; AV: autophagic vacuole; AVd: degradative autophagic vacuole; AVi: initial autophagic vacuole; BECN1: beclin 1; BSA: bovine serum albumin; CBS: cystathionine beta-synthase; CDK7: cyclin dependent kinase 7; CDKN1A: cyclin dependent kinase inhibitor 1A; EGFP: enhanced green fluorescent protein; GAPDH: glyceraldehyde-3-phosphate dehydrogenase; GST: glutathione S transferase; H2AX/H2AFX: H2A.X variant histone; HBSS: Hanks balanced salt solution; IP: immunopurification; IR: ionizing radiation; MAP1LC3/LC3: microtubule associated protein 1 light chain 3; MAP3K9: mitogen-activated protein kinase kinase kinase 9; mRFP: monomeric red fluorescent protein; mCh: mCherry; MCM7: minichromosome maintenance complex component 7; MTORC1: mechanistic target of rapamycin kinase complex 1; NHEJ: non-homologous end joining; NRBP2: nuclear receptor binding protein 2; NTC: non-targeting control; NUAK1: NUAK family kinase 1; PBS: phosphate-buffered saline; PIK3AP1: phosphoinositide-3-kinase adaptor protein 1; PIK3CA: phosphatidylinositol-4,5-biphosphate 3-kinase catalytic subunit alpha; PIKK: phosphatidylinositol 3-kinase-related kinase; PRKAA: protein kinase AMP-activated catalytic subunit alpha; PRKAB: protein kinase AMP-activated non-catalytic subunit beta; PRKAG: protein kinase AMP-activated non-catalytic subunit gamma; PRKDC: protein kinase, DNA-activated, catalytic subunit; RLuc: Renilla luciferase; RPS6KB1: ribosomal protein S6 kinase B1; SQSTM1: sequestosome 1; STK11/LKB1: serine/threonine kinase 11; TP53: tumor protein p53; TSKS: testis specific serine kinase substrate; ULK1: unc-51 like autophagy activating kinase 1; WIPI2: WD repeat domain, phosphoinositide interacting 2; WT: wild type. Fluorouracil 278-282 serine/threonine kinase 11 Homo sapiens 130-135 8840428-8 1996 In the patients with 5-fluorouracil and cisplatin, PCNA-S was the most effective indicator of the histopathological response to PDC, as shown by a stepwise regression analysis. Fluorouracil 21-35 proliferating cell nuclear antigen Homo sapiens 51-55 8855506-4 1996 The HER of 5-FU was significantly increased (P < 0.01) in combination with IL-2 in a dose-dependent fashion while that of MMC also showed a tendency to increase. Fluorouracil 11-15 interleukin 2 Rattus norvegicus 78-82 31983282-7 2020 Taken together, our data suggest that PRKDC-mediated phosphorylation of PRKAG1 primes AMPK complex to the lysosomal activation by STK11 in cancer cells thereby linking DNA damage response to autophagy and cellular metabolism.Abbreviations: AXIN1: axin 1; 3-MA: 3-methyladenine; 5-FU: 5-fluorouracil; AA mutant: double alanine mutant (S192A, T284A) of PRKAG1; ACACA: acetyl-CoA carboxylase alpha; AICAR: 5-Aminoimidazole-4-carboxamide ribonucleotide; AMPK: AMP-activated protein kinase; ATG: autophagy-related; ATM: ataxia telangiectasia mutated; ATR: ATM serine/threonine kinase; AV: autophagic vacuole; AVd: degradative autophagic vacuole; AVi: initial autophagic vacuole; BECN1: beclin 1; BSA: bovine serum albumin; CBS: cystathionine beta-synthase; CDK7: cyclin dependent kinase 7; CDKN1A: cyclin dependent kinase inhibitor 1A; EGFP: enhanced green fluorescent protein; GAPDH: glyceraldehyde-3-phosphate dehydrogenase; GST: glutathione S transferase; H2AX/H2AFX: H2A.X variant histone; HBSS: Hanks balanced salt solution; IP: immunopurification; IR: ionizing radiation; MAP1LC3/LC3: microtubule associated protein 1 light chain 3; MAP3K9: mitogen-activated protein kinase kinase kinase 9; mRFP: monomeric red fluorescent protein; mCh: mCherry; MCM7: minichromosome maintenance complex component 7; MTORC1: mechanistic target of rapamycin kinase complex 1; NHEJ: non-homologous end joining; NRBP2: nuclear receptor binding protein 2; NTC: non-targeting control; NUAK1: NUAK family kinase 1; PBS: phosphate-buffered saline; PIK3AP1: phosphoinositide-3-kinase adaptor protein 1; PIK3CA: phosphatidylinositol-4,5-biphosphate 3-kinase catalytic subunit alpha; PIKK: phosphatidylinositol 3-kinase-related kinase; PRKAA: protein kinase AMP-activated catalytic subunit alpha; PRKAB: protein kinase AMP-activated non-catalytic subunit beta; PRKAG: protein kinase AMP-activated non-catalytic subunit gamma; PRKDC: protein kinase, DNA-activated, catalytic subunit; RLuc: Renilla luciferase; RPS6KB1: ribosomal protein S6 kinase B1; SQSTM1: sequestosome 1; STK11/LKB1: serine/threonine kinase 11; TP53: tumor protein p53; TSKS: testis specific serine kinase substrate; ULK1: unc-51 like autophagy activating kinase 1; WIPI2: WD repeat domain, phosphoinositide interacting 2; WT: wild type. Fluorouracil 284-298 protein kinase AMP-activated non-catalytic subunit gamma 1 Homo sapiens 72-78 8566832-6 1995 In the presence of 5-FU, a high degree of polymegathism and delay in actin and vinculin redistribution to the cell borders after wound closure was observed. Fluorouracil 19-23 vinculin Bos taurus 79-87 31983282-7 2020 Taken together, our data suggest that PRKDC-mediated phosphorylation of PRKAG1 primes AMPK complex to the lysosomal activation by STK11 in cancer cells thereby linking DNA damage response to autophagy and cellular metabolism.Abbreviations: AXIN1: axin 1; 3-MA: 3-methyladenine; 5-FU: 5-fluorouracil; AA mutant: double alanine mutant (S192A, T284A) of PRKAG1; ACACA: acetyl-CoA carboxylase alpha; AICAR: 5-Aminoimidazole-4-carboxamide ribonucleotide; AMPK: AMP-activated protein kinase; ATG: autophagy-related; ATM: ataxia telangiectasia mutated; ATR: ATM serine/threonine kinase; AV: autophagic vacuole; AVd: degradative autophagic vacuole; AVi: initial autophagic vacuole; BECN1: beclin 1; BSA: bovine serum albumin; CBS: cystathionine beta-synthase; CDK7: cyclin dependent kinase 7; CDKN1A: cyclin dependent kinase inhibitor 1A; EGFP: enhanced green fluorescent protein; GAPDH: glyceraldehyde-3-phosphate dehydrogenase; GST: glutathione S transferase; H2AX/H2AFX: H2A.X variant histone; HBSS: Hanks balanced salt solution; IP: immunopurification; IR: ionizing radiation; MAP1LC3/LC3: microtubule associated protein 1 light chain 3; MAP3K9: mitogen-activated protein kinase kinase kinase 9; mRFP: monomeric red fluorescent protein; mCh: mCherry; MCM7: minichromosome maintenance complex component 7; MTORC1: mechanistic target of rapamycin kinase complex 1; NHEJ: non-homologous end joining; NRBP2: nuclear receptor binding protein 2; NTC: non-targeting control; NUAK1: NUAK family kinase 1; PBS: phosphate-buffered saline; PIK3AP1: phosphoinositide-3-kinase adaptor protein 1; PIK3CA: phosphatidylinositol-4,5-biphosphate 3-kinase catalytic subunit alpha; PIKK: phosphatidylinositol 3-kinase-related kinase; PRKAA: protein kinase AMP-activated catalytic subunit alpha; PRKAB: protein kinase AMP-activated non-catalytic subunit beta; PRKAG: protein kinase AMP-activated non-catalytic subunit gamma; PRKDC: protein kinase, DNA-activated, catalytic subunit; RLuc: Renilla luciferase; RPS6KB1: ribosomal protein S6 kinase B1; SQSTM1: sequestosome 1; STK11/LKB1: serine/threonine kinase 11; TP53: tumor protein p53; TSKS: testis specific serine kinase substrate; ULK1: unc-51 like autophagy activating kinase 1; WIPI2: WD repeat domain, phosphoinositide interacting 2; WT: wild type. Fluorouracil 284-298 serine/threonine kinase 11 Homo sapiens 130-135 7579383-6 1995 Sequential IL-3 and GM-CSF (schedule B) was associated with higher platelet nadirs, shorter durations of platelet counts less than 50,000/microL, and the need for fewer platelet transfusions over five cycles of FLAC chemotherapy compared with concurrent cytokines, sequential IL-3 and GM-CSF schedule A, and GM-CSF alone. Fluorouracil 211-215 interleukin 3 Homo sapiens 11-15 7579383-6 1995 Sequential IL-3 and GM-CSF (schedule B) was associated with higher platelet nadirs, shorter durations of platelet counts less than 50,000/microL, and the need for fewer platelet transfusions over five cycles of FLAC chemotherapy compared with concurrent cytokines, sequential IL-3 and GM-CSF schedule A, and GM-CSF alone. Fluorouracil 211-215 colony stimulating factor 2 Homo sapiens 20-26 7579383-10 1995 The data from this phase I study suggest that sequential IL-3 and GM-CSF with IL-3 administered for 9 days before beginning GM-CSF may be superior to shorter durations of IL-3 administered sequentially with GM-CSF, to concurrent IL-3 and GM-CSF, and to either colony-stimulating factor alone in ameliorating the cumulative hematologic toxicity associated with multiple cycles of FLAC chemotherapy. Fluorouracil 379-383 colony stimulating factor 2 Homo sapiens 66-72 32683166-3 2020 In this study, we utilized the core structure 5-fluorouracil (5-FU) or tegafur, a 5-FU prodrug combined through different linkers with resorcinol to generate a series of fluoropyrimidin-2,4-dihydroxy-5-isopropylbenzamides which inhibit potent Heat Shock Protein 90 (HSP90). Fluorouracil 46-60 heat shock protein 90 alpha family class A member 1 Homo sapiens 243-264 7579383-10 1995 The data from this phase I study suggest that sequential IL-3 and GM-CSF with IL-3 administered for 9 days before beginning GM-CSF may be superior to shorter durations of IL-3 administered sequentially with GM-CSF, to concurrent IL-3 and GM-CSF, and to either colony-stimulating factor alone in ameliorating the cumulative hematologic toxicity associated with multiple cycles of FLAC chemotherapy. Fluorouracil 379-383 interleukin 3 Homo sapiens 78-82 7579383-10 1995 The data from this phase I study suggest that sequential IL-3 and GM-CSF with IL-3 administered for 9 days before beginning GM-CSF may be superior to shorter durations of IL-3 administered sequentially with GM-CSF, to concurrent IL-3 and GM-CSF, and to either colony-stimulating factor alone in ameliorating the cumulative hematologic toxicity associated with multiple cycles of FLAC chemotherapy. Fluorouracil 379-383 interleukin 3 Homo sapiens 78-82 7579383-10 1995 The data from this phase I study suggest that sequential IL-3 and GM-CSF with IL-3 administered for 9 days before beginning GM-CSF may be superior to shorter durations of IL-3 administered sequentially with GM-CSF, to concurrent IL-3 and GM-CSF, and to either colony-stimulating factor alone in ameliorating the cumulative hematologic toxicity associated with multiple cycles of FLAC chemotherapy. Fluorouracil 379-383 interleukin 3 Homo sapiens 78-82 32683166-3 2020 In this study, we utilized the core structure 5-fluorouracil (5-FU) or tegafur, a 5-FU prodrug combined through different linkers with resorcinol to generate a series of fluoropyrimidin-2,4-dihydroxy-5-isopropylbenzamides which inhibit potent Heat Shock Protein 90 (HSP90). Fluorouracil 46-60 heat shock protein 90 alpha family class A member 1 Homo sapiens 266-271 8528101-4 1995 Moreover, the number of BM MNC expressing c-kit on their surface from 5-FU-treated mice was markedly decreased relative to those from untreated controls. Fluorouracil 70-74 KIT proto-oncogene receptor tyrosine kinase Mus musculus 42-47 32683166-3 2020 In this study, we utilized the core structure 5-fluorouracil (5-FU) or tegafur, a 5-FU prodrug combined through different linkers with resorcinol to generate a series of fluoropyrimidin-2,4-dihydroxy-5-isopropylbenzamides which inhibit potent Heat Shock Protein 90 (HSP90). Fluorouracil 62-66 heat shock protein 90 alpha family class A member 1 Homo sapiens 243-264 8528101-6 1995 BM MNC of mice treated with 5-FU were separated on the basis of expression of the lineage-specific antigens (Lin), c-kit, and Ly6A/E. Fluorouracil 28-32 KIT proto-oncogene receptor tyrosine kinase Mus musculus 115-120 7634247-4 1995 Moreover, to investigate the usefulness of 5-fluorouracil (5FU) for combination with IFN-alpha therapy, we examined the effect of preincubation with 5FU on the susceptibility of ACHN. Fluorouracil 149-152 La ribonucleoprotein 6, translational regulator Homo sapiens 178-182 7634247-5 1995 IFN-alpha-induced protection of ACHN from lysis by IFN-alpha-activated NK cells weakened in the presence of 5FU at 0.2 microgram/ml. Fluorouracil 108-111 La ribonucleoprotein 6, translational regulator Homo sapiens 32-36 32683166-3 2020 In this study, we utilized the core structure 5-fluorouracil (5-FU) or tegafur, a 5-FU prodrug combined through different linkers with resorcinol to generate a series of fluoropyrimidin-2,4-dihydroxy-5-isopropylbenzamides which inhibit potent Heat Shock Protein 90 (HSP90). Fluorouracil 62-66 heat shock protein 90 alpha family class A member 1 Homo sapiens 266-271 7601257-4 1995 Similarly, murine post-5 fluorouracil (5-FU) bone marrow cells or fetal liver cells, induced to express EpoR and stimulated by Epo, displayed a significant enhancement of megakaryocyte colony formation, particularly of the BFU-megakaryocyte (BFU-Mk) colony type. Fluorouracil 25-37 erythropoietin receptor Mus musculus 104-108 7601257-4 1995 Similarly, murine post-5 fluorouracil (5-FU) bone marrow cells or fetal liver cells, induced to express EpoR and stimulated by Epo, displayed a significant enhancement of megakaryocyte colony formation, particularly of the BFU-megakaryocyte (BFU-Mk) colony type. Fluorouracil 25-37 erythropoietin Mus musculus 104-107 32945504-7 2020 We also found that combined treatment of Rg3 and 5-FU significantly enhanced the apoptosis of colon cancer cells by activating the Apaf1/caspase 9/caspase 3 pathway and arrested the cell cycle of the colon cancer cells in G0/G1 by promoting the expression of Cyclin D1, CDK2 and CDK4. Fluorouracil 49-53 caspase 9 Homo sapiens 137-146 7601257-4 1995 Similarly, murine post-5 fluorouracil (5-FU) bone marrow cells or fetal liver cells, induced to express EpoR and stimulated by Epo, displayed a significant enhancement of megakaryocyte colony formation, particularly of the BFU-megakaryocyte (BFU-Mk) colony type. Fluorouracil 39-43 erythropoietin receptor Mus musculus 104-108 7601257-4 1995 Similarly, murine post-5 fluorouracil (5-FU) bone marrow cells or fetal liver cells, induced to express EpoR and stimulated by Epo, displayed a significant enhancement of megakaryocyte colony formation, particularly of the BFU-megakaryocyte (BFU-Mk) colony type. Fluorouracil 39-43 erythropoietin Mus musculus 104-107 33533417-6 2020 In addition, the anodic peaks of 6-TG and fluorouracil (5-FU) in their mixture can be well separated using CuO/1E3MIBF4/CPE and simultaneous determination of them was studied. Fluorouracil 42-54 carboxypeptidase E Homo sapiens 120-123 33533417-6 2020 In addition, the anodic peaks of 6-TG and fluorouracil (5-FU) in their mixture can be well separated using CuO/1E3MIBF4/CPE and simultaneous determination of them was studied. Fluorouracil 56-60 carboxypeptidase E Homo sapiens 120-123 32887024-0 2020 Curcumin may reverse 5-fluorouracil resistance on colonic cancer cells by regulating TET1-NKD-Wnt signal pathway to inhibit the EMT progress. Fluorouracil 21-35 tet methylcytosine dioxygenase 1 Homo sapiens 85-89 32887024-13 2020 CONCLUSION: Curcumin might exert anti-resistant effect of 5-FU on HCT-116 cells by regulating the TET1-NKD2-WNT signal pathway to inhibit the EMT progress. Fluorouracil 58-62 tet methylcytosine dioxygenase 1 Homo sapiens 98-102 32887024-13 2020 CONCLUSION: Curcumin might exert anti-resistant effect of 5-FU on HCT-116 cells by regulating the TET1-NKD2-WNT signal pathway to inhibit the EMT progress. Fluorouracil 58-62 NKD inhibitor of WNT signaling pathway 2 Homo sapiens 103-107 32588739-8 2020 Further experiments were performed to explore the function of miR-185-3p in 5-FU-resistant cells through regulating aquaporin-5 (AQP5). Fluorouracil 76-80 aquaporin 5 Homo sapiens 116-127 21552807-1 1995 5-methyltetrahydrofolate (MTHF) is a main serum metabolite of 5-formyltetrahydrofolate (folinic acid, FA), a standard agent for potentiation of the cytotoxic activity of 5-fluorouracil (5-FU). Fluorouracil 170-184 thin fur Mus musculus 26-30 21552807-1 1995 5-methyltetrahydrofolate (MTHF) is a main serum metabolite of 5-formyltetrahydrofolate (folinic acid, FA), a standard agent for potentiation of the cytotoxic activity of 5-fluorouracil (5-FU). Fluorouracil 186-190 thin fur Mus musculus 26-30 7602356-1 1995 PURPOSE: The aim of the present study was to analyze the role of thymidylate synthase (TS; main cellular target of fluorouracil [FU]) and dihydropyrimidine dehydrogenase (DPD; rate-limiting enzyme of FU catabolism) in tumoral biopsies with respect to FU responsiveness. Fluorouracil 115-127 thymidylate synthetase Homo sapiens 65-85 7779703-8 1995 In these human carcinoma cell lines, the LCV dose and interval between 5-FU and LCV play a role in increased TS total protein and TS ternary complex; however, the amount of free TS is independent of the interval between 5-FU and LCV. Fluorouracil 71-75 thymidylate synthetase Homo sapiens 130-132 7779703-8 1995 In these human carcinoma cell lines, the LCV dose and interval between 5-FU and LCV play a role in increased TS total protein and TS ternary complex; however, the amount of free TS is independent of the interval between 5-FU and LCV. Fluorouracil 71-75 thymidylate synthetase Homo sapiens 130-132 7763285-0 1995 Thymidylate synthase gene amplification in human colon cancer cell lines resistant to 5-fluorouracil. Fluorouracil 86-100 thymidylate synthetase Homo sapiens 0-20 7763285-7 1995 Although no major rearrangements of the TS gene were noted by Southern analysis, there was significant amplification of the TS gene in 5-FU-resistant cells, which was confirmed by DNA slot blot analysis. Fluorouracil 135-139 thymidylate synthetase Homo sapiens 124-126 7759157-1 1995 5"-deoxy-5-fluorouridine (5"-FUdR) is a cytostatic that is biotransformed to 5-fluorouracil (5-FUra) by pyrimidine nucleoside phosphorylase (PyNPase), the expression of which is up-regulated by tumor necrosis factor alpha (TNF alpha), interleukin-1 alpha (IL-1 alpha) and interferon gamma (IFN gamma). Fluorouracil 77-91 interleukin 1 alpha Mus musculus 235-254 7759157-1 1995 5"-deoxy-5-fluorouridine (5"-FUdR) is a cytostatic that is biotransformed to 5-fluorouracil (5-FUra) by pyrimidine nucleoside phosphorylase (PyNPase), the expression of which is up-regulated by tumor necrosis factor alpha (TNF alpha), interleukin-1 alpha (IL-1 alpha) and interferon gamma (IFN gamma). Fluorouracil 77-91 interleukin 1 alpha Mus musculus 256-266 7759157-1 1995 5"-deoxy-5-fluorouridine (5"-FUdR) is a cytostatic that is biotransformed to 5-fluorouracil (5-FUra) by pyrimidine nucleoside phosphorylase (PyNPase), the expression of which is up-regulated by tumor necrosis factor alpha (TNF alpha), interleukin-1 alpha (IL-1 alpha) and interferon gamma (IFN gamma). Fluorouracil 93-99 interleukin 1 alpha Mus musculus 235-254 7759157-1 1995 5"-deoxy-5-fluorouridine (5"-FUdR) is a cytostatic that is biotransformed to 5-fluorouracil (5-FUra) by pyrimidine nucleoside phosphorylase (PyNPase), the expression of which is up-regulated by tumor necrosis factor alpha (TNF alpha), interleukin-1 alpha (IL-1 alpha) and interferon gamma (IFN gamma). Fluorouracil 93-99 interleukin 1 alpha Mus musculus 256-266 32588739-8 2020 Further experiments were performed to explore the function of miR-185-3p in 5-FU-resistant cells through regulating aquaporin-5 (AQP5). Fluorouracil 76-80 aquaporin 5 Homo sapiens 129-133 32588739-11 2020 MiR-185-3p was low-expressed in CRC tissues and 5-FU-resistance cells, and it targeted and regulated the expression of AQP5, which was found up-regulated in CRC and 5-FU-resistance CRC cells (r = -0.29, P < .05). Fluorouracil 165-169 aquaporin 5 Homo sapiens 119-123 32473828-0 2020 Corrigendum to "S1PR2 inhibitors potently reverse 5-FU resistance by downregulating DPD expression in colorectal cancer" [Pharmacol Res. Fluorouracil 50-54 sphingosine-1-phosphate receptor 2 Homo sapiens 16-21 32727780-3 2020 MATERIALS AND METHODS: Changes in the expression levels of CRH-related peptides and their receptors in HCT116, DLD-1, and SW480 cell lines after fluorouracil (5-FU) loading were evaluated. Fluorouracil 145-157 corticotropin releasing hormone Homo sapiens 59-62 7645979-1 1995 5-Fluorouracil is the drug chosen for the treatment of patients with advanced colorectal carcinoma; its major site of action is thymidylate synthase (TS), resulting in pronounced and prolonged inhibition of DNA synthesis. Fluorouracil 0-14 thymidylate synthetase Homo sapiens 128-148 7645979-1 1995 5-Fluorouracil is the drug chosen for the treatment of patients with advanced colorectal carcinoma; its major site of action is thymidylate synthase (TS), resulting in pronounced and prolonged inhibition of DNA synthesis. Fluorouracil 0-14 thymidylate synthetase Homo sapiens 150-152 9166454-8 1995 After exposure to fluorouracil, levels of free thymidylate synthase were significantly lower and the percent bound thymidylate synthase was higher in responders than in nonresponders. Fluorouracil 18-30 thymidylate synthetase Homo sapiens 47-67 9166454-8 1995 After exposure to fluorouracil, levels of free thymidylate synthase were significantly lower and the percent bound thymidylate synthase was higher in responders than in nonresponders. Fluorouracil 18-30 thymidylate synthetase Homo sapiens 115-135 9166454-10 1995 CONCLUSIONS: These preliminary results indicate that a response to neoadjuvant fluorouracil-based therapy may be associated with decreased levels of total thymidylate synthase before therapy and free thymidylate synthase after exposure to fluorouracil in patients with locally advanced gastric cancer. Fluorouracil 79-91 thymidylate synthetase Homo sapiens 155-175 9166454-10 1995 CONCLUSIONS: These preliminary results indicate that a response to neoadjuvant fluorouracil-based therapy may be associated with decreased levels of total thymidylate synthase before therapy and free thymidylate synthase after exposure to fluorouracil in patients with locally advanced gastric cancer. Fluorouracil 79-91 thymidylate synthetase Homo sapiens 200-220 9166454-10 1995 CONCLUSIONS: These preliminary results indicate that a response to neoadjuvant fluorouracil-based therapy may be associated with decreased levels of total thymidylate synthase before therapy and free thymidylate synthase after exposure to fluorouracil in patients with locally advanced gastric cancer. Fluorouracil 239-251 thymidylate synthetase Homo sapiens 155-175 9166454-10 1995 CONCLUSIONS: These preliminary results indicate that a response to neoadjuvant fluorouracil-based therapy may be associated with decreased levels of total thymidylate synthase before therapy and free thymidylate synthase after exposure to fluorouracil in patients with locally advanced gastric cancer. Fluorouracil 239-251 thymidylate synthetase Homo sapiens 200-220 9166454-11 1995 Quantification of thymidylate synthase protein expression before and after exposure to fluorouracil may provide a method to select patients for fluorouracil therapy in the neoadjuvant, adjuvant, or advanced-disease setting based upon the fundamental sensitivity of the tumor. Fluorouracil 87-99 thymidylate synthetase Homo sapiens 18-38 9166454-11 1995 Quantification of thymidylate synthase protein expression before and after exposure to fluorouracil may provide a method to select patients for fluorouracil therapy in the neoadjuvant, adjuvant, or advanced-disease setting based upon the fundamental sensitivity of the tumor. Fluorouracil 144-156 thymidylate synthetase Homo sapiens 18-38 7790321-2 1995 In this study, the effect of Met-depleting TPN with 5-FU upon thymidylate synthase (TS) activity was examined, and the histological effect of this treatment on human gastric cancer was evaluated. Fluorouracil 52-56 thymidylate synthetase Homo sapiens 62-82 7882343-0 1995 Thymidylate synthase gene and protein expression correlate and are associated with response to 5-fluorouracil in human colorectal and gastric tumors. Fluorouracil 95-109 thymidylate synthetase Homo sapiens 0-20 7882343-1 1995 Thymidylate synthase (TS) is the target enzyme for 5-fluorouracil (5-FU). Fluorouracil 51-65 thymidylate synthetase Homo sapiens 0-20 7882343-1 1995 Thymidylate synthase (TS) is the target enzyme for 5-fluorouracil (5-FU). Fluorouracil 51-65 thymidylate synthetase Homo sapiens 22-24 7882343-1 1995 Thymidylate synthase (TS) is the target enzyme for 5-fluorouracil (5-FU). Fluorouracil 67-71 thymidylate synthetase Homo sapiens 0-20 7882343-1 1995 Thymidylate synthase (TS) is the target enzyme for 5-fluorouracil (5-FU). Fluorouracil 67-71 thymidylate synthetase Homo sapiens 22-24 7882343-2 1995 We have correlated TS protein and gene expression with the response in patients with colorectal (n = 9) and gastric cancer (n = 12) treated with infusional 5-FU plus leucovorin (LV) or infusional 5-FU/LV and cisplatin, respectively. Fluorouracil 156-160 thymidylate synthetase Homo sapiens 19-21 7882343-2 1995 We have correlated TS protein and gene expression with the response in patients with colorectal (n = 9) and gastric cancer (n = 12) treated with infusional 5-FU plus leucovorin (LV) or infusional 5-FU/LV and cisplatin, respectively. Fluorouracil 196-200 thymidylate synthetase Homo sapiens 19-21 7882343-8 1995 Both the TS protein level and TS gene expression were significantly associated with response to 5-FU-based therapy. Fluorouracil 96-100 thymidylate synthetase Homo sapiens 9-11 7882343-8 1995 Both the TS protein level and TS gene expression were significantly associated with response to 5-FU-based therapy. Fluorouracil 96-100 thymidylate synthetase Homo sapiens 30-32 32727780-3 2020 MATERIALS AND METHODS: Changes in the expression levels of CRH-related peptides and their receptors in HCT116, DLD-1, and SW480 cell lines after fluorouracil (5-FU) loading were evaluated. Fluorouracil 159-163 corticotropin releasing hormone Homo sapiens 59-62 32096264-10 2020 Moreover, in vivo experiment verified that the silence of TRIM14 reduced the tumor size and weight, and inhibited the migration and proliferation of GC cells in 5-FU-resistant GC mice. Fluorouracil 161-165 tripartite motif-containing 14 Mus musculus 58-64 32751071-6 2020 Beyond the well-established role for inhibiting thymidylate synthase (TS) by the 5-FU metabolite 5-fluoro-2"-deoxyuridine-5"-O-monophosphate (FdUMP), recent studies have implicated new roles for RNA modifying enzymes that are inhibited by 5-FU substitution including tRNA methyltransferase 2 homolog A (TRMT2A) and pseudouridylate synthase in 5-FU cytotoxicity. Fluorouracil 81-85 thymidylate synthetase Homo sapiens 48-68 32751071-6 2020 Beyond the well-established role for inhibiting thymidylate synthase (TS) by the 5-FU metabolite 5-fluoro-2"-deoxyuridine-5"-O-monophosphate (FdUMP), recent studies have implicated new roles for RNA modifying enzymes that are inhibited by 5-FU substitution including tRNA methyltransferase 2 homolog A (TRMT2A) and pseudouridylate synthase in 5-FU cytotoxicity. Fluorouracil 81-85 thymidylate synthetase Homo sapiens 70-72 32546724-0 2020 SphK2 confers 5-fluorouracil resistance to colorectal cancer via upregulating H3K56ac-mediated DPD expression. Fluorouracil 14-28 dihydropyrimidine dehydrogenase Mus musculus 95-98 32546724-5 2020 Assays of ChIP-Seq and luciferase reporter gene demonstrated that high SphK2 upregulated DPD through promoting the HDAC1-mediated H3K56ac, leading to the degradation of intracellular 5-FU into inactive alpha-fluoro-beta-alanine (FBAL). Fluorouracil 183-187 dihydropyrimidine dehydrogenase Mus musculus 89-92 32546724-5 2020 Assays of ChIP-Seq and luciferase reporter gene demonstrated that high SphK2 upregulated DPD through promoting the HDAC1-mediated H3K56ac, leading to the degradation of intracellular 5-FU into inactive alpha-fluoro-beta-alanine (FBAL). Fluorouracil 183-187 histone deacetylase 1 Mus musculus 115-120 32601379-9 2020 Immunofluorescence and cellular ultrastructure experiments using antibodies against TGN38 protein, a trans-Golgi network marker, showed that 5-FU and doxorubicin treatments result in an apoptosis-independent stacks dispersal of the Golgi ribbon structure in both HCT-15 and SW-480 cells. Fluorouracil 141-145 trans-golgi network protein 2 Homo sapiens 84-89 32601379-12 2020 Moreover, we found that after treatment with 5-FU, TGN38 factor coimmunolocalizes with beclin-1 autophagic protein in discrete structures associated with the fragmented Golgi, suggesting that the activation of pro-survival autophagy is linked to loss of Golgi integrity. Fluorouracil 45-49 trans-golgi network protein 2 Homo sapiens 51-56 32586310-4 2020 By comparing gene and protein expression and identifying cell survival rates after knockdown or high expression of FEN1, the correlation between FEN1 high expression and 5-Fluorouracil (5-Fu) drug resistance was revealed. Fluorouracil 170-184 flap structure-specific endonuclease 1 Homo sapiens 115-119 32586310-4 2020 By comparing gene and protein expression and identifying cell survival rates after knockdown or high expression of FEN1, the correlation between FEN1 high expression and 5-Fluorouracil (5-Fu) drug resistance was revealed. Fluorouracil 170-184 flap structure-specific endonuclease 1 Homo sapiens 145-149 32586310-4 2020 By comparing gene and protein expression and identifying cell survival rates after knockdown or high expression of FEN1, the correlation between FEN1 high expression and 5-Fluorouracil (5-Fu) drug resistance was revealed. Fluorouracil 186-190 flap structure-specific endonuclease 1 Homo sapiens 115-119 32586310-4 2020 By comparing gene and protein expression and identifying cell survival rates after knockdown or high expression of FEN1, the correlation between FEN1 high expression and 5-Fluorouracil (5-Fu) drug resistance was revealed. Fluorouracil 186-190 flap structure-specific endonuclease 1 Homo sapiens 145-149 32586310-7 2020 FEN1 was highly expressed in BGC823/5-Fu regardless of gene level(P < 0.001) or protein level. Fluorouracil 36-40 flap structure-specific endonuclease 1 Homo sapiens 0-4 7869049-5 1995 IL-5 also supported formation of both multi-lineage and blast cell colonies from dormant progenitors of the 5-fluorouracil-treated transgenic mice. Fluorouracil 108-122 interleukin 5 Mus musculus 0-4 7733626-0 1995 Recombinant human interferon alpha-2a increases the antitumor activity of 5-fluorouracil on human colon carcinoma xenograft Co-4 without any change in 5-FU pharmacokinetics. Fluorouracil 74-88 complement C4A (Rodgers blood group) Homo sapiens 124-128 7733626-1 1995 We investigated the modulating effect of recombinant human interferon alpha-2a (IFN-alpha) on the antitumor activity of 5-fluorouracil (5-FU) against a human colon carcinoma xenograft (Co-4) in nude mice with reference to changes in the pharmacokinetic pattern of 5-FU. Fluorouracil 120-134 complement C4A (Rodgers blood group) Homo sapiens 185-189 7733626-2 1995 Mice bearing Co-4 received 5-FU ip at a dose of 90 mg/kg once with or without IFN-alpha, which was administered sc at a dose of 60.000 IU/mouse daily for 7 days before 5-FU treatment. Fluorouracil 27-31 complement C4A (Rodgers blood group) Homo sapiens 13-17 7805178-3 1995 Exogenous leucovorin, on the other hand, which enhances thymidylate synthase inhibition, appears to increase the clinical toxicity of 5-FU in a dose-dependent manner. Fluorouracil 134-138 thymidylate synthetase Homo sapiens 56-76 32586310-8 2020 Furthermore, manipulating FEN1 altered the sensitivity of cancer cells to chemotherapeutic drug 5-Fu. Fluorouracil 96-100 flap structure-specific endonuclease 1 Homo sapiens 26-30 32586310-11 2020 The decrease of FEN1 expression in BGC823/5-Fu had a concentration dependent relationship with JYPW. Fluorouracil 42-46 flap structure-specific endonuclease 1 Homo sapiens 16-20 32586310-13 2020 CONCLUSION: FEN1 was highly expressed in drug-resistance gastric cancer cells BGC823/5-Fu, which leading to BGC823 resistant to (5-Fu) by acting on DNA damage repair. Fluorouracil 85-89 flap structure-specific endonuclease 1 Homo sapiens 12-16 32586310-13 2020 CONCLUSION: FEN1 was highly expressed in drug-resistance gastric cancer cells BGC823/5-Fu, which leading to BGC823 resistant to (5-Fu) by acting on DNA damage repair. Fluorouracil 129-133 flap structure-specific endonuclease 1 Homo sapiens 12-16 32580513-3 2020 The tumor suppressor microRNA (miR)-199b directly targets the PP2A inhibitor SET, which has been involved in 5-FU resistance, and its downregulation has been found to correlate with poor outcome in metastatic colorectal cancer. Fluorouracil 109-113 protein phosphatase 2 phosphatase activator Homo sapiens 62-66 32464550-0 2020 lncRNA HOTAIR Contributes to 5FU Resistance through Suppressing miR-218 and Activating NF-kappaB/TS Signaling in Colorectal Cancer. Fluorouracil 29-32 HOX transcript antisense RNA Homo sapiens 7-13 32382150-0 2020 LncRNA SNORD3A specifically sensitizes breast cancer cells to 5-FU by sponging miR-185-5p to enhance UMPS expression. Fluorouracil 62-66 uridine monophosphate synthetase Homo sapiens 101-105 32382150-12 2020 Our findings indicate that Meis1-regulated SNORD3A specifically sensitizes breast cancer cells to 5-FU via enhancing UMPS expression. Fluorouracil 98-102 uridine monophosphate synthetase Homo sapiens 117-121 32382150-13 2020 The SNORD3A-UMPS axis may serve as a potential biomarker and therapeutic target to improve the efficacy of 5-FU-based chemotherapy for breast cancer patients. Fluorouracil 107-111 uridine monophosphate synthetase Homo sapiens 12-16 32088343-0 2020 S1PR2 inhibitors potently reverse 5-FU resistance by downregulating DPD expression in colorectal cancer. Fluorouracil 34-38 sphingosine-1-phosphate receptor 2 Homo sapiens 0-5 32088343-1 2020 In this study, S1PR2 was reckoned as a brand-new GPCR target for designing inhibitors to reverse 5-FU resistance. Fluorouracil 97-101 sphingosine-1-phosphate receptor 2 Homo sapiens 15-20 32088343-4 2020 The underlying mechanism was uncovered that JTE-013 demonstrated an anti-FU-resistance activity by blocking S1PR2 internalization to the endoplasmic reticulum (ER), which inhibited the degradation of 5-FU into alpha-fluoro-beta-alanine (FBAL) by downregulating tumoral DPD expression. Fluorouracil 200-204 sphingosine-1-phosphate receptor 2 Homo sapiens 108-113 32088343-6 2020 SIGNIFICANCE: This study provides novel insights that S1PR2 inhibitors could sensitize 5-FU therapy in colorectal cancer. Fluorouracil 87-91 sphingosine-1-phosphate receptor 2 Homo sapiens 54-59 32345258-0 2020 Enhanced antitumor efficacy in colon cancer using EGF functionalized PLGA nanoparticles loaded with 5-Fluorouracil and perfluorocarbon. Fluorouracil 100-114 epidermal growth factor Homo sapiens 50-53 32345258-5 2020 METHODS: We developed epidermal growth factor (EGF) functionalized PLGA nanoparticles (NPs) co-loaded with 5-fluorouracil (5Fu) and perfluorocarbon (PFC) (EGF-PLGA@5Fu/PFC) for targeted treatment of colon cancer. Fluorouracil 107-121 epidermal growth factor Homo sapiens 22-45 32345258-5 2020 METHODS: We developed epidermal growth factor (EGF) functionalized PLGA nanoparticles (NPs) co-loaded with 5-fluorouracil (5Fu) and perfluorocarbon (PFC) (EGF-PLGA@5Fu/PFC) for targeted treatment of colon cancer. Fluorouracil 107-121 epidermal growth factor Homo sapiens 47-50 32345258-5 2020 METHODS: We developed epidermal growth factor (EGF) functionalized PLGA nanoparticles (NPs) co-loaded with 5-fluorouracil (5Fu) and perfluorocarbon (PFC) (EGF-PLGA@5Fu/PFC) for targeted treatment of colon cancer. Fluorouracil 123-126 epidermal growth factor Homo sapiens 22-45 32345258-5 2020 METHODS: We developed epidermal growth factor (EGF) functionalized PLGA nanoparticles (NPs) co-loaded with 5-fluorouracil (5Fu) and perfluorocarbon (PFC) (EGF-PLGA@5Fu/PFC) for targeted treatment of colon cancer. Fluorouracil 123-126 epidermal growth factor Homo sapiens 47-50 32345258-8 2020 RESULTS: The findings showed that EGF-PLGA@5Fu /PFC NPs had an average size 200 nm and a 5Fu-loading efficiency of 7.29%. Fluorouracil 43-46 epidermal growth factor Homo sapiens 34-37 32345258-12 2020 In tumor xenografted mice, EGF-PLGA@5Fu/PFC NPs suppressed tumor growth more effectively than 5Fu, PLGA@5Fu or PLGA@5Fu/PFC NPs. Fluorouracil 36-39 epidermal growth factor Mus musculus 27-30 32004938-0 2020 Patchouli alcohol attenuates 5-fluorouracil-induced intestinal mucositis via TLR2/MyD88/NF-kB pathway and regulation of microbiota. Fluorouracil 29-43 MYD88, innate immune signal transduction adaptor Rattus norvegicus 82-87 32004938-0 2020 Patchouli alcohol attenuates 5-fluorouracil-induced intestinal mucositis via TLR2/MyD88/NF-kB pathway and regulation of microbiota. Fluorouracil 29-43 nuclear factor kappa B subunit 1 Rattus norvegicus 88-93 7483142-3 1995 The antimetabolite 5-fluorouracil (5-FU) has been shown to be active in prostate cancer, acting via inhibition of thymidylate synthase, an essential enzyme in DNA de novo synthesis. Fluorouracil 19-33 thymidylate synthetase Homo sapiens 114-134 7483142-3 1995 The antimetabolite 5-fluorouracil (5-FU) has been shown to be active in prostate cancer, acting via inhibition of thymidylate synthase, an essential enzyme in DNA de novo synthesis. Fluorouracil 35-39 thymidylate synthetase Homo sapiens 114-134 31587155-0 2020 Ubiquitin-Specific Protease 22/Silent Information Regulator 1 Axis Plays a Pivotal Role in the Prognosis and 5-Fluorouracil Resistance in Hepatocellular Carcinoma. Fluorouracil 109-123 ubiquitin specific peptidase 22 Homo sapiens 0-30 31587155-3 2020 However, it is still unknown whether USP22 and SIRT1 co-expression is associated with disease progression and 5-Fluorouracil (5-FU) resistance in HCC. Fluorouracil 110-124 ubiquitin specific peptidase 22 Homo sapiens 37-42 31587155-11 2020 The SIRT1 inhibitor EX-527 dramatically inhibited the expression of Cyclin B1 and resistance-associated protein 3 (MRP3) to reduce 5-FU drug resistance in vivo. Fluorouracil 131-135 cyclin B1 Homo sapiens 68-113 7538704-0 1995 Intensive weekly chemotherapy for elderly gastric cancer patients, using 5-fluorouracil, cisplatin, epi-doxorubicin, 6S-leucovorin and glutathione with the support of G-CSF. Fluorouracil 73-87 colony stimulating factor 3 Homo sapiens 167-172 30693808-5 2020 Moreover, cepharanthine could prevent 5-fluorouracil-induced BCRP and MRP1 expression. Fluorouracil 38-52 BCR pseudogene 1 Homo sapiens 61-65 30693808-5 2020 Moreover, cepharanthine could prevent 5-fluorouracil-induced BCRP and MRP1 expression. Fluorouracil 38-52 MDM4 regulator of p53 Homo sapiens 70-74 32256983-9 2020 Therefore, FPGS and GGH affect chemosensitivity to antifolates and 5-fluorouracil by altering intracellular retention status of antifolates and folate cofactors such as 5,10-methylenetetrahydrofolate, subsequently influencing the cytotoxic effects of 5-fluorouracil, respectively. Fluorouracil 251-265 gamma-glutamyl hydrolase Homo sapiens 20-23 7977167-10 1994 CONCLUSIONS: Adding GM-CSF to the combination of cisplatin and 5-fluorouracil allowed to increase 5-fluorouracil dose up to 50% over the conventional dosage. Fluorouracil 63-77 colony stimulating factor 2 Homo sapiens 20-26 7977167-10 1994 CONCLUSIONS: Adding GM-CSF to the combination of cisplatin and 5-fluorouracil allowed to increase 5-fluorouracil dose up to 50% over the conventional dosage. Fluorouracil 98-112 colony stimulating factor 2 Homo sapiens 20-26 32256983-10 2020 Generally, high FPGS and/or low GGH activity is associated with increased chemosensitivity of cancer cells to methotrexate and 5-fluorouracil, while low FPGS and/or high GGH activity seems to correspond to resistance to these drugs. Fluorouracil 127-141 folylpolyglutamate synthase Homo sapiens 16-20 32256983-10 2020 Generally, high FPGS and/or low GGH activity is associated with increased chemosensitivity of cancer cells to methotrexate and 5-fluorouracil, while low FPGS and/or high GGH activity seems to correspond to resistance to these drugs. Fluorouracil 127-141 gamma-glutamyl hydrolase Homo sapiens 32-35 7923012-9 1994 Treatment of T24 cells with the c-myc antisense oligonucleotide in combination with mitomycin C, Adriamycin, or 5-fluorouracil (5-FU) did not overcome their resistance to these anticancer chemotherapeutic agents. Fluorouracil 112-126 MYC proto-oncogene, bHLH transcription factor Homo sapiens 32-37 32216815-14 2020 We further found that down-regulation of LTBP1 enhanced ESCC cells" sensitivity to 5-FU treatment. Fluorouracil 83-87 latent transforming growth factor beta binding protein 1 Homo sapiens 41-46 7923012-9 1994 Treatment of T24 cells with the c-myc antisense oligonucleotide in combination with mitomycin C, Adriamycin, or 5-fluorouracil (5-FU) did not overcome their resistance to these anticancer chemotherapeutic agents. Fluorouracil 128-132 MYC proto-oncogene, bHLH transcription factor Homo sapiens 32-37 7923012-14 1994 Incubation of T24 or T24/CDDP cells with the c-myc antisense oligonucleotide increased the intracellular accumulation of CDDP, but not the accumulation of 5-FU. Fluorouracil 155-159 MYC proto-oncogene, bHLH transcription factor Homo sapiens 45-50 7525886-17 1994 CONCLUSION: The addition of cisplatin to 5-FU, HU, and concomitant radiotherapy is feasible using G-CSF. Fluorouracil 41-45 colony stimulating factor 3 Homo sapiens 98-103 7858238-3 1994 We have investigated CD43 expression by hemopoietic progenitors of normal and 5-fluorouracil(5-FU)-treated mice. Fluorouracil 78-92 sialophorin Mus musculus 21-25 7858238-3 1994 We have investigated CD43 expression by hemopoietic progenitors of normal and 5-fluorouracil(5-FU)-treated mice. Fluorouracil 93-97 sialophorin Mus musculus 21-25 7847809-6 1994 Moreover, treatment with IFN-alpha, 5-FU or IFN-alpha + 5-FU resulted in a marked increase in the number of HT-29 cells positive for the CEA surface antigen. Fluorouracil 36-40 CEA cell adhesion molecule 5 Homo sapiens 137-140 7847809-6 1994 Moreover, treatment with IFN-alpha, 5-FU or IFN-alpha + 5-FU resulted in a marked increase in the number of HT-29 cells positive for the CEA surface antigen. Fluorouracil 56-60 CEA cell adhesion molecule 5 Homo sapiens 137-140 8053919-1 1994 5-Ethynyluracil (776C85) is a potent mechanism-based inactivator of dihydropyrimidine dehydrogenase (DPD), the enzyme that catalyzes the rapid catabolism of 5-fluorouracil (5-FU). Fluorouracil 157-171 dihydropyrimidine dehydrogenase Canis lupus familiaris 68-99 8053919-1 1994 5-Ethynyluracil (776C85) is a potent mechanism-based inactivator of dihydropyrimidine dehydrogenase (DPD), the enzyme that catalyzes the rapid catabolism of 5-fluorouracil (5-FU). Fluorouracil 157-171 dihydropyrimidine dehydrogenase Canis lupus familiaris 101-104 8053919-1 1994 5-Ethynyluracil (776C85) is a potent mechanism-based inactivator of dihydropyrimidine dehydrogenase (DPD), the enzyme that catalyzes the rapid catabolism of 5-fluorouracil (5-FU). Fluorouracil 173-177 dihydropyrimidine dehydrogenase Canis lupus familiaris 68-99 8053919-1 1994 5-Ethynyluracil (776C85) is a potent mechanism-based inactivator of dihydropyrimidine dehydrogenase (DPD), the enzyme that catalyzes the rapid catabolism of 5-fluorouracil (5-FU). Fluorouracil 173-177 dihydropyrimidine dehydrogenase Canis lupus familiaris 101-104 8005809-7 1994 CONCLUSION: These findings support the concept that the manipulation of FUra"s DNA-dependent actions, for example, through modulators of thymidylate synthase (TS) activity, may increase radiosensitization in clinical trials in the treatment of gastrointestinal cancers. Fluorouracil 72-76 thymidylate synthetase Homo sapiens 137-157 8005809-7 1994 CONCLUSION: These findings support the concept that the manipulation of FUra"s DNA-dependent actions, for example, through modulators of thymidylate synthase (TS) activity, may increase radiosensitization in clinical trials in the treatment of gastrointestinal cancers. Fluorouracil 72-76 thymidylate synthetase Homo sapiens 159-161 8206932-1 1994 The synthesis of thymidylate synthase (TS) from 5-fluorouracil (FUra)- and 5-bromouracil (BrUra)-substituted mRNAs was examined to investigate the effect of incorporation of uracil (Ura) analogs on translation. Fluorouracil 48-62 thymidylate synthetase Homo sapiens 17-37 8206932-1 1994 The synthesis of thymidylate synthase (TS) from 5-fluorouracil (FUra)- and 5-bromouracil (BrUra)-substituted mRNAs was examined to investigate the effect of incorporation of uracil (Ura) analogs on translation. Fluorouracil 48-62 thymidylate synthetase Homo sapiens 39-41 8206932-1 1994 The synthesis of thymidylate synthase (TS) from 5-fluorouracil (FUra)- and 5-bromouracil (BrUra)-substituted mRNAs was examined to investigate the effect of incorporation of uracil (Ura) analogs on translation. Fluorouracil 64-68 thymidylate synthetase Homo sapiens 17-37 8206932-1 1994 The synthesis of thymidylate synthase (TS) from 5-fluorouracil (FUra)- and 5-bromouracil (BrUra)-substituted mRNAs was examined to investigate the effect of incorporation of uracil (Ura) analogs on translation. Fluorouracil 64-68 thymidylate synthetase Homo sapiens 39-41 8141112-1 1994 The use of leucovorin to modulate 5-fluorouracil (FUra)-mediated inhibition of thymidylate synthase has been shown both in vitro and in vivo to improve the antitumor activity of FUra. Fluorouracil 34-48 thymidylate synthetase Homo sapiens 79-99 8141112-1 1994 The use of leucovorin to modulate 5-fluorouracil (FUra)-mediated inhibition of thymidylate synthase has been shown both in vitro and in vivo to improve the antitumor activity of FUra. Fluorouracil 50-54 thymidylate synthetase Homo sapiens 79-99 8141112-1 1994 The use of leucovorin to modulate 5-fluorouracil (FUra)-mediated inhibition of thymidylate synthase has been shown both in vitro and in vivo to improve the antitumor activity of FUra. Fluorouracil 178-182 thymidylate synthetase Homo sapiens 79-99 8168119-6 1994 In euthymic mice injected with IL-2 (5 x 10(4) Cetus units twice daily for 4-5 days), 5-FU augmented (up to 37-fold, days 1-9) and CY reduced (up to day 6) LAK activity, as compared with that in the IL-2 control. Fluorouracil 86-90 interleukin 2 Mus musculus 31-35 32244885-0 2020 Use of STAT6 Phosphorylation Inhibitor and Trimethylglycine as New Adjuvant Therapies for 5-Fluorouracil in Colitis-Associated Tumorigenesis. Fluorouracil 90-104 signal transducer and activator of transcription 6 Homo sapiens 7-12 32244885-5 2020 We found that these adjuvant therapies induced a remarkable reduction of tumor growth when administrated together with 5-FU, correlating with a reduction in STAT6-phosphorylation. Fluorouracil 119-123 signal transducer and activator of transcription 6 Homo sapiens 157-162 32244885-6 2020 This reduction upgraded the effect of 5-FU by increasing both levels of apoptosis and markers of cell adhesion such as E-cadherin, whereas decreased epithelial-mesenchymal transition markers were associated with aggressive phenotypes and drug resistance, such as beta-catenin nuclear translocation and Zinc finger protein SNAI1 (SNAI1). Fluorouracil 38-42 catenin beta 1 Homo sapiens 263-275 31917964-8 2020 Our data showed that 5FU treatment significantly decreased numbers of Olfm4+ ISCs and goblet cells in intestine, which could be ameliorated by dmPGE2 treatment. Fluorouracil 21-24 olfactomedin 4 Mus musculus 70-75 32269848-7 2020 AGS and NCI-N87 cells transfected with si-RNA-Bcl-3 (si-Bcl-3) showed significantly reduced migratory ability and increased chemosensitivity to oxaliplatin, 5-fluorouracil, and irinotecan. Fluorouracil 157-171 BCL3 transcription coactivator Homo sapiens 46-51 32005975-5 2020 Silencing or loss of C1GALT1 inhibited cell viability, migration, invasion, tumor growth and metastasis, as well as increased apoptosis and cytotoxicity of 5-fluorouracil in AGS and MKN45 cells. Fluorouracil 156-170 core 1 synthase, glycoprotein-N-acetylgalactosamine 3-beta-galactosyltransferase 1 Homo sapiens 21-28 32076068-4 2020 Compared to nal-IRI/5-FU/LV treatment, combining nal-IRI/5-FU/LV with vactosertib, a TGF-beta signalling inhibitor, significantly improved long-term survival rates and effectively suppressed invasion to surrounding tissues. Fluorouracil 57-61 transforming growth factor alpha Mus musculus 85-93 32076068-6 2020 Particularly, the expression of tumour-suppressing gene Ccdc80 was induced by vactosertib and further induced by vactosertib in combination with nal-IRI/5-FU/LV. Fluorouracil 153-157 coiled-coil domain containing 80 Mus musculus 56-62 31313286-11 2020 Taken together, our data indicated that modification of ERRFI1 by KHSRP occurs through miR-501-5p, an essential mechanism driving CRC proliferation and 5-FU resistance. Fluorouracil 152-156 microRNA 501 Homo sapiens 87-94 31966052-6 2020 A total of 26 patients exhibited highly methylated PD-L1; in this group, the median progression-free survival time of patients receiving platinum/fluorouracil chemotherapy was 4.2 months longer than those receiving paclitaxel/fluorouracil chemotherapy, and the risk of disease progression in patients receiving paclitaxel/fluorouracil chemotherapy was 5.009 times higher compared with patients who received platinum/fluorouracil chemotherapy. Fluorouracil 146-158 CD274 molecule Homo sapiens 51-56 31966052-6 2020 A total of 26 patients exhibited highly methylated PD-L1; in this group, the median progression-free survival time of patients receiving platinum/fluorouracil chemotherapy was 4.2 months longer than those receiving paclitaxel/fluorouracil chemotherapy, and the risk of disease progression in patients receiving paclitaxel/fluorouracil chemotherapy was 5.009 times higher compared with patients who received platinum/fluorouracil chemotherapy. Fluorouracil 226-238 CD274 molecule Homo sapiens 51-56 31966052-6 2020 A total of 26 patients exhibited highly methylated PD-L1; in this group, the median progression-free survival time of patients receiving platinum/fluorouracil chemotherapy was 4.2 months longer than those receiving paclitaxel/fluorouracil chemotherapy, and the risk of disease progression in patients receiving paclitaxel/fluorouracil chemotherapy was 5.009 times higher compared with patients who received platinum/fluorouracil chemotherapy. Fluorouracil 226-238 CD274 molecule Homo sapiens 51-56 31966052-6 2020 A total of 26 patients exhibited highly methylated PD-L1; in this group, the median progression-free survival time of patients receiving platinum/fluorouracil chemotherapy was 4.2 months longer than those receiving paclitaxel/fluorouracil chemotherapy, and the risk of disease progression in patients receiving paclitaxel/fluorouracil chemotherapy was 5.009 times higher compared with patients who received platinum/fluorouracil chemotherapy. Fluorouracil 226-238 CD274 molecule Homo sapiens 51-56 31563901-13 2020 Moreover, these transfectants showed a significantly lower apoptosis rate in response to 5-fluorouracil and gemcitabine with a decrease of BOK expression, suggesting a role of miR-296-5p in drug resistance. Fluorouracil 89-103 microRNA 296 Homo sapiens 176-183 8123839-6 1994 The physiologic relevance of NGF in early hematopoiesis was confirmed by showing that 12% to 15% of progenitor blood cells from mice treated with 5-fluorouracil expressed TrkA and that these cells could be induced to proliferate and differentiate in response to NGF in association with macrophage colony-stimulating factor. Fluorouracil 146-160 neurotrophic tyrosine kinase, receptor, type 1 Mus musculus 171-175 8021136-2 1994 Because the glutathione (GSH) system and thymidylate synthase (TS) are involved in the resistance to the main drugs used in HNSCC (cisplatin and 5-FU), we studied these systems in tumors and normal mucosae. Fluorouracil 145-149 thymidylate synthetase Homo sapiens 63-65 7833111-0 1994 A role for dihydropyrimidine dehydrogenase and thymidylate synthase in tumour sensitivity to fluorouracil. Fluorouracil 93-105 thymidylate synthetase Homo sapiens 47-67 8246030-0 1993 Phase I trial of recombinant human granulocyte-macrophage colony-stimulating factor derived from yeast in patients with breast cancer receiving cyclophosphamide, doxorubicin, and fluorouracil. Fluorouracil 179-191 colony stimulating factor 2 Homo sapiens 35-83 7691257-1 1993 We have analyzed c-kit expression by hematopoietic progenitors from normal and 5-fluorouracil (5-FU)-treated mice by staining with monoclonal anti-c-kit antibody ACK-4. Fluorouracil 79-93 KIT proto-oncogene receptor tyrosine kinase Mus musculus 17-22 7691257-1 1993 We have analyzed c-kit expression by hematopoietic progenitors from normal and 5-fluorouracil (5-FU)-treated mice by staining with monoclonal anti-c-kit antibody ACK-4. Fluorouracil 79-93 KIT proto-oncogene receptor tyrosine kinase Mus musculus 147-152 7691257-1 1993 We have analyzed c-kit expression by hematopoietic progenitors from normal and 5-fluorouracil (5-FU)-treated mice by staining with monoclonal anti-c-kit antibody ACK-4. Fluorouracil 95-99 KIT proto-oncogene receptor tyrosine kinase Mus musculus 17-22 7691257-1 1993 We have analyzed c-kit expression by hematopoietic progenitors from normal and 5-fluorouracil (5-FU)-treated mice by staining with monoclonal anti-c-kit antibody ACK-4. Fluorouracil 95-99 KIT proto-oncogene receptor tyrosine kinase Mus musculus 147-152 7691257-3 1993 The majority of colony-forming cells from normal mice were in c-kit(high) population, whereas most of the progenitors from 5-FU-treated mice were in the c-kit(low) population. Fluorouracil 123-127 KIT proto-oncogene receptor tyrosine kinase Mus musculus 153-158 7691257-4 1993 Optimal colony formation from c-kit(low) cells from 5-FU-treated mice required the interactions of at least two factors among interleukin-3 (IL-3), IL-11 and steel factor (SF) whereas colony formation from c-kit(high) cells of normal mice was supported well by IL-3 alone. Fluorouracil 52-56 KIT proto-oncogene receptor tyrosine kinase Mus musculus 30-35 7691257-4 1993 Optimal colony formation from c-kit(low) cells from 5-FU-treated mice required the interactions of at least two factors among interleukin-3 (IL-3), IL-11 and steel factor (SF) whereas colony formation from c-kit(high) cells of normal mice was supported well by IL-3 alone. Fluorouracil 52-56 kit ligand Mus musculus 158-170 7691257-4 1993 Optimal colony formation from c-kit(low) cells from 5-FU-treated mice required the interactions of at least two factors among interleukin-3 (IL-3), IL-11 and steel factor (SF) whereas colony formation from c-kit(high) cells of normal mice was supported well by IL-3 alone. Fluorouracil 52-56 kit ligand Mus musculus 172-174 8104229-1 1993 Post 5-fluorouracil-treated murine bone marrow cells infected with a recombinant retrovirus (murine stem cell virus-interleukin 11 [MSCV-IL-11]) bearing a human IL-11 gene were transplanted into lethally irradiated syngeneic mice. Fluorouracil 5-19 interleukin 11 Homo sapiens 137-142 8104229-1 1993 Post 5-fluorouracil-treated murine bone marrow cells infected with a recombinant retrovirus (murine stem cell virus-interleukin 11 [MSCV-IL-11]) bearing a human IL-11 gene were transplanted into lethally irradiated syngeneic mice. Fluorouracil 5-19 interleukin 11 Homo sapiens 161-166 8242472-1 1993 1,25-Dihydroxyvitamin D3 (1,25(OH)2D3) was recently shown to promote maturation of 5-fluorouracil (5FU)-treated bone marrow cells by up-regulating macrophage-colony stimulating factor (M-CSF) receptors in the presence of interleukin 1 alpha (IL-1 alpha). Fluorouracil 99-102 interleukin 1 alpha Mus musculus 221-240 8242472-1 1993 1,25-Dihydroxyvitamin D3 (1,25(OH)2D3) was recently shown to promote maturation of 5-fluorouracil (5FU)-treated bone marrow cells by up-regulating macrophage-colony stimulating factor (M-CSF) receptors in the presence of interleukin 1 alpha (IL-1 alpha). Fluorouracil 99-102 interleukin 1 alpha Mus musculus 242-252 8339275-6 1993 These findings indicate that low-dose continuous exposure schedules to FUra are cytotoxic primarily due to inhibition of thymidylate synthase and underscores the role of 5,10-methylenetetrahydrofolate polyglutamates in this inhibition. Fluorouracil 71-75 thymidylate synthetase Homo sapiens 121-141 8400344-2 1993 One of the principal mechanisms of action of 5-fluorouracil (5-FU) is the inhibition of TS by formation of a ternary covalent complex consisting of TS-5-fluorodeoxyuridylate-5,10-methylenetetrahydrofolate. Fluorouracil 45-59 thymidylate synthetase Homo sapiens 88-90 8400344-2 1993 One of the principal mechanisms of action of 5-fluorouracil (5-FU) is the inhibition of TS by formation of a ternary covalent complex consisting of TS-5-fluorodeoxyuridylate-5,10-methylenetetrahydrofolate. Fluorouracil 45-59 thymidylate synthetase Homo sapiens 148-150 8400344-2 1993 One of the principal mechanisms of action of 5-fluorouracil (5-FU) is the inhibition of TS by formation of a ternary covalent complex consisting of TS-5-fluorodeoxyuridylate-5,10-methylenetetrahydrofolate. Fluorouracil 61-65 thymidylate synthetase Homo sapiens 88-90 8400344-2 1993 One of the principal mechanisms of action of 5-fluorouracil (5-FU) is the inhibition of TS by formation of a ternary covalent complex consisting of TS-5-fluorodeoxyuridylate-5,10-methylenetetrahydrofolate. Fluorouracil 61-65 thymidylate synthetase Homo sapiens 148-150 8400344-8 1993 The ratio of complex to free TS was up to 2-fold greater in 5-FU/leucovorin-treated cells compared to those treated with 5-FU alone. Fluorouracil 60-64 thymidylate synthetase Homo sapiens 29-31 8400344-8 1993 The ratio of complex to free TS was up to 2-fold greater in 5-FU/leucovorin-treated cells compared to those treated with 5-FU alone. Fluorouracil 121-125 thymidylate synthetase Homo sapiens 29-31 8355668-1 1993 A major mechanism underlying the cytotoxicity of fluoropyrimidine analogs such as 5-fluorouracil and 5-fluoro-2"-deoxyuridine (FdUrd) occurs via the formation of 5-fluoro-2"-deoxyuridylate (FdUMP), a tight-binding inhibitor of thymidylate synthase (TS). Fluorouracil 82-96 thymidylate synthetase Homo sapiens 227-247 7686504-1 1993 The monoclonal rat anti-c-kit antibody (ACK2), which abrogates colony growth supported by stem cell factor (SCF), significantly inhibited the interleukin-6 (IL-6)-dependent growth of hematopoietic progenitors derived from spleen cells of normal and 5-fluorouracil (5-FU)-treated mice and from bone marrow cells of normal mice in serum-containing culture. Fluorouracil 249-263 KIT proto-oncogene receptor tyrosine kinase Mus musculus 24-29 7686504-1 1993 The monoclonal rat anti-c-kit antibody (ACK2), which abrogates colony growth supported by stem cell factor (SCF), significantly inhibited the interleukin-6 (IL-6)-dependent growth of hematopoietic progenitors derived from spleen cells of normal and 5-fluorouracil (5-FU)-treated mice and from bone marrow cells of normal mice in serum-containing culture. Fluorouracil 265-269 KIT proto-oncogene receptor tyrosine kinase Mus musculus 24-29 31736281-5 2020 Of these genes, ABCG2, AHNAK2, BCL2, FZD1, and TP73 are associated with published evidence for resistance to 5-fluorouracil and cisplatin. Fluorouracil 109-123 AHNAK nucleoprotein 2 Homo sapiens 23-29 31856090-4 2020 We present the case of a 44-year-old woman with ATM-mutated PC who achieved stable disease as the best response to first-line fluorouracil, leucovorin, irinotecan, and oxaliplatin, followed by progression on a PARP inhibitor. Fluorouracil 126-138 ATM serine/threonine kinase Homo sapiens 48-51 7689417-0 1993 Incorporation of 5-fluorouracil into RNA by Mycobacterium avium complex strain LM1. Fluorouracil 17-31 lymphomyeloid antigen 1 Mus musculus 79-82 7689417-1 1993 The incorporation of 5-fluorouracil (FUra) into RNA of Mycobacterium avium complex strain LM1 was evaluated. Fluorouracil 21-35 lymphomyeloid antigen 1 Mus musculus 90-93 7689417-1 1993 The incorporation of 5-fluorouracil (FUra) into RNA of Mycobacterium avium complex strain LM1 was evaluated. Fluorouracil 37-41 lymphomyeloid antigen 1 Mus musculus 90-93 31858276-7 2019 Combination of 5-FU+ss-lap resulted in lower cell viability; most notably, 5-FU/ss-lap-loaded mesoporous silica nanoparticles (FNQ-MSN) exhibited significantly lower cell viability compared with that of any of the individual drug or physical combinations. Fluorouracil 15-19 LAP Homo sapiens 83-86 31858276-7 2019 Combination of 5-FU+ss-lap resulted in lower cell viability; most notably, 5-FU/ss-lap-loaded mesoporous silica nanoparticles (FNQ-MSN) exhibited significantly lower cell viability compared with that of any of the individual drug or physical combinations. Fluorouracil 75-79 LAP Homo sapiens 23-26 31858276-7 2019 Combination of 5-FU+ss-lap resulted in lower cell viability; most notably, 5-FU/ss-lap-loaded mesoporous silica nanoparticles (FNQ-MSN) exhibited significantly lower cell viability compared with that of any of the individual drug or physical combinations. Fluorouracil 75-79 LAP Homo sapiens 83-86 31858276-10 2019 Notable decrease in tumor volume was observed with the physical mixture of 5-FU+ss-lap; however, combined treatment of carrier-based 5-FU and ss-lap (FNQ-MSN) significantly delayed the tumor growth and prolonged the survival of tumor-bearing xenograft mice. Fluorouracil 133-137 moesin Mus musculus 154-157 31018249-5 2019 Treatment of PIK3CA-mutant cells with fisetin and 5-FU reduced the expression of PI3K, phosphorylation of AKT, mTOR, its target proteins, constituents of mTOR signaling complex and this treatment increased the phosphorylation of AMPKalpha. Fluorouracil 50-54 mechanistic target of rapamycin kinase Mus musculus 111-115 31018249-5 2019 Treatment of PIK3CA-mutant cells with fisetin and 5-FU reduced the expression of PI3K, phosphorylation of AKT, mTOR, its target proteins, constituents of mTOR signaling complex and this treatment increased the phosphorylation of AMPKalpha. Fluorouracil 50-54 mechanistic target of rapamycin kinase Mus musculus 154-158 31767795-8 2019 Patients with tumor PD-L1 >= 1% had a significantly longer DFS in sequential chemotherapy than in than 5-FU/LV arm (interaction p = .04) and a trend for OS (interaction p = .12). Fluorouracil 103-107 CD274 molecule Homo sapiens 20-25 31767795-12 2019 Moreover, tumor PD-L1 expression >=1% was associated with greater benefit from intensive sequential chemotherapy compared with 5-fluorouracil plus leucovorin (5-FU/LV), whereas PD-L1 expression <1% was not, conditioning a statistically significant interaction between such biomarker and treatment arms. Fluorouracil 127-141 CD274 molecule Homo sapiens 16-21 31767795-12 2019 Moreover, tumor PD-L1 expression >=1% was associated with greater benefit from intensive sequential chemotherapy compared with 5-fluorouracil plus leucovorin (5-FU/LV), whereas PD-L1 expression <1% was not, conditioning a statistically significant interaction between such biomarker and treatment arms. Fluorouracil 159-163 CD274 molecule Homo sapiens 16-21 31521892-10 2019 Furthermore, according to the accumulation and efflux of rhodamine 123 in Bel7402/5-FU resistant cells and Bel7402 sensitive cells, CP-25 could reverse the resistance of MTX in Bel7402/5-FU cells compared with Bel7402 cells, which was reflected by the reduced IC50 values of MTX. Fluorouracil 82-86 homeobox C6 Homo sapiens 132-137 31521892-10 2019 Furthermore, according to the accumulation and efflux of rhodamine 123 in Bel7402/5-FU resistant cells and Bel7402 sensitive cells, CP-25 could reverse the resistance of MTX in Bel7402/5-FU cells compared with Bel7402 cells, which was reflected by the reduced IC50 values of MTX. Fluorouracil 185-189 homeobox C6 Homo sapiens 132-137 31521892-11 2019 Further study indicated that CP-25 could decrease P-gp expression and inhibit P-gp function in Bel7402/5-FU cells. Fluorouracil 103-107 homeobox C6 Homo sapiens 29-34 31799650-0 2019 MiR-335 promotes cell proliferation by inhibiting MEF2D and sensitizes cells to 5-Fu treatment in gallbladder carcinoma. Fluorouracil 80-84 microRNA 335 Mus musculus 0-7 31664952-7 2019 DPP-4 inhibitor (50 mg/kg) was administered orally for four days starting the day before 5-FU administration. Fluorouracil 89-93 dipeptidylpeptidase 4 Mus musculus 0-5 31664952-17 2019 CONCLUSION: DPP-4 inhibitor can improve 5-FU induced AM and, therefore, has potential as an alternative treatment for chemotherapy-induced AM. Fluorouracil 40-44 dipeptidylpeptidase 4 Mus musculus 12-17 31695423-0 2019 Nitrogen Permease Regulator-Like-2 Exhibited Anti-Tumor Effects And Enhanced The Sensitivity Of Colorectal Cancer Cells To Oxaliplatin And 5-Fluorouracil. Fluorouracil 139-153 NPR2 like, GATOR1 complex subunit Homo sapiens 0-34 7683729-0 1993 Granulocyte colony-stimulating factor: effective in ameliorating fluorouracil-based myelosuppression? Fluorouracil 65-77 colony stimulating factor 3 Homo sapiens 0-37 31695423-7 2019 To further explore whether NPRL2 could reduce drug resistance of CRC cells against oxaliplatin (L-OHP) and 5-fluorouracil (5-FU), we constructed a tumor model using HT29 cells. Fluorouracil 107-121 NPR2 like, GATOR1 complex subunit Homo sapiens 27-32 31695423-11 2019 Our results also confirmed that NPRL2 enhanced the sensitivity of CRC cells to L-OHP and 5-FU. Fluorouracil 89-93 NPR2 like, GATOR1 complex subunit Homo sapiens 32-37 31695423-13 2019 Conclusion: Our present work demonstrated that NPRL2 exhibited anti-tumor effects and enhanced the sensitivities of CRC cells to L-OHP and 5-FU through the P-gp and MRP1 pathways. Fluorouracil 139-143 NPR2 like, GATOR1 complex subunit Homo sapiens 47-52 31302419-0 2019 Matrix metalloproteinase 1 promotes tumorigenesis and inhibits the sensitivity to 5-fluorouracil of nasopharyngeal carcinoma. Fluorouracil 82-96 matrix metallopeptidase 1 Homo sapiens 0-26 8517641-2 1993 In this study, effects of immunochemotherapy using OK-432, 5-fluorouracil (5-FU) and mitomycin C (MMC) on Col-2-JCK, a human colon cancer xenograft, were evaluated using this model. Fluorouracil 75-79 NIMA related kinase 8 Homo sapiens 112-115 8422641-1 1993 BACKGROUND AND METHODS: Various factors, including thymidylate synthase, thymidine kinase, 5-fluorouracil phosphorylation and degradation pathways, folate concentrations, and the stability of ternary complex, which influence thymidylate synthase inhibition rate of fluoropyrimidines, were studied in 87 human adenocarcinoma tissues. Fluorouracil 91-105 thymidylate synthetase Homo sapiens 225-245 31302419-3 2019 This research was aimed to study the effects of matrix metalloproteinase 1 (MMP1) gene on nasopharyngeal carcinoma (NPC) cell proliferation, viability, invasiveness, apoptosis, and sensitivity to 5-FU. Fluorouracil 196-200 matrix metallopeptidase 1 Homo sapiens 48-74 8369613-1 1993 We investigated the modulating effect of L-leucovorin (LV) on the antitumor effect of 5-fluorouracil (5-FU) against human colon carcinoma cells (C-1) in vitro and human colon carcinoma xenografts (Co-4) in nude mice. Fluorouracil 86-100 heterogeneous nuclear ribonucleoprotein C Homo sapiens 145-148 1281687-11 1992 The population ratio of c-kit+Sca-1+ to c-kit+Sca-1- increased 2 and 4 days after exposure to 5-fluorouracil (5-FU). Fluorouracil 94-108 KIT proto-oncogene receptor tyrosine kinase Mus musculus 24-29 1281687-11 1992 The population ratio of c-kit+Sca-1+ to c-kit+Sca-1- increased 2 and 4 days after exposure to 5-fluorouracil (5-FU). Fluorouracil 94-108 KIT proto-oncogene receptor tyrosine kinase Mus musculus 40-45 1281687-11 1992 The population ratio of c-kit+Sca-1+ to c-kit+Sca-1- increased 2 and 4 days after exposure to 5-fluorouracil (5-FU). Fluorouracil 110-114 KIT proto-oncogene receptor tyrosine kinase Mus musculus 24-29 1281687-11 1992 The population ratio of c-kit+Sca-1+ to c-kit+Sca-1- increased 2 and 4 days after exposure to 5-fluorouracil (5-FU). Fluorouracil 110-114 KIT proto-oncogene receptor tyrosine kinase Mus musculus 40-45 1451052-0 1992 Schedule-dependent inhibition of thymidylate synthase by 5-fluorouracil in gastric cancer. Fluorouracil 57-71 thymidylate synthetase Homo sapiens 33-53 1451052-2 1992 METHODS: A randomized study was conducted to investigate schedule-dependent thymidylate synthase (TS) inhibition by 5-FU in 16 patients with gastric cancer who underwent surgical resection. Fluorouracil 116-120 thymidylate synthetase Homo sapiens 76-96 1451052-2 1992 METHODS: A randomized study was conducted to investigate schedule-dependent thymidylate synthase (TS) inhibition by 5-FU in 16 patients with gastric cancer who underwent surgical resection. Fluorouracil 116-120 thymidylate synthetase Homo sapiens 98-100 31302419-3 2019 This research was aimed to study the effects of matrix metalloproteinase 1 (MMP1) gene on nasopharyngeal carcinoma (NPC) cell proliferation, viability, invasiveness, apoptosis, and sensitivity to 5-FU. Fluorouracil 196-200 matrix metallopeptidase 1 Homo sapiens 76-80 31302419-11 2019 When 5-FU was not a player, the forced overexpression of MMP1 gene led to enhanced growth and invasion of CNE1 and HNE1 cell lines, whereas MMP1 gene knockdown resulted in the opposite outcome. Fluorouracil 5-9 matrix metallopeptidase 1 Homo sapiens 57-61 31302419-12 2019 When 5-FU was added, MMP1 gene knockdown led to significantly suppressed cell proliferation and enhanced cell apoptosis. Fluorouracil 5-9 matrix metallopeptidase 1 Homo sapiens 21-25 31302419-14 2019 CONCLUSION: Not only the knockdown of MMP1 gene led to suppressed proliferation and invasion but also increased the sensitivity to 5-FU of CNE1 and HNE1 cells. Fluorouracil 131-135 matrix metallopeptidase 1 Homo sapiens 38-42 31302419-15 2019 Our results provided convincing evidence that MMP1 gene knockdown could offer a favorable sensitivity approach for NPC with 5-FU treatment. Fluorouracil 124-128 matrix metallopeptidase 1 Homo sapiens 46-50 31662984-0 2019 Spica Prunellae Extract Enhances Fluorouracil Sensitivity of 5-Fluorouracil-Resistant Human Colon Carcinoma HCT-8/5-FU Cells via TOP2alpha and miR-494. Fluorouracil 33-45 microRNA 494 Homo sapiens 143-150 1457523-3 1992 Advances in analytical methodology should facilitate quantitation of thymidylate synthase content in tumor tissue prior to and following fluorouracil-based therapy. Fluorouracil 137-149 thymidylate synthetase Homo sapiens 69-89 1280628-1 1992 A comparison with recombinant human granulocyte colony-stimulating factor in 5-fluorouracil-treated mice. Fluorouracil 77-91 colony stimulating factor 3 Homo sapiens 36-73 31662984-0 2019 Spica Prunellae Extract Enhances Fluorouracil Sensitivity of 5-Fluorouracil-Resistant Human Colon Carcinoma HCT-8/5-FU Cells via TOP2alpha and miR-494. Fluorouracil 61-75 DNA topoisomerase II alpha Homo sapiens 129-138 1638519-2 1992 The results presented herein demonstrate that the pretreatment of mice with recombinant human interleukin 1 alpha (rhIL-1 alpha) protects mice from the lethal effects of several myelotoxic chemotherapeutic drugs, including 5-fluorouracil (5FUra), cyclophosphamide, cis-diammine(1,1-cyclobutanedicarboxylato)platinum(II), and 1,3-bis-(2-chloroethyl)-1-nitrosourea. Fluorouracil 239-244 interleukin 1 alpha Homo sapiens 94-113 31662984-0 2019 Spica Prunellae Extract Enhances Fluorouracil Sensitivity of 5-Fluorouracil-Resistant Human Colon Carcinoma HCT-8/5-FU Cells via TOP2alpha and miR-494. Fluorouracil 61-75 microRNA 494 Homo sapiens 143-150 31662984-0 2019 Spica Prunellae Extract Enhances Fluorouracil Sensitivity of 5-Fluorouracil-Resistant Human Colon Carcinoma HCT-8/5-FU Cells via TOP2alpha and miR-494. Fluorouracil 114-118 DNA topoisomerase II alpha Homo sapiens 129-138 31662984-4 2019 Modules of the hub genes in protein-protein interaction networks gathered to TOP2alpha showed a decrease in HCT-8 cells but an increase in 5-FU-resistant HCT-8/5-FU cells with 5-FU exposure. Fluorouracil 139-143 DNA topoisomerase II alpha Homo sapiens 77-86 31662984-4 2019 Modules of the hub genes in protein-protein interaction networks gathered to TOP2alpha showed a decrease in HCT-8 cells but an increase in 5-FU-resistant HCT-8/5-FU cells with 5-FU exposure. Fluorouracil 160-164 DNA topoisomerase II alpha Homo sapiens 77-86 31662984-4 2019 Modules of the hub genes in protein-protein interaction networks gathered to TOP2alpha showed a decrease in HCT-8 cells but an increase in 5-FU-resistant HCT-8/5-FU cells with 5-FU exposure. Fluorouracil 160-164 DNA topoisomerase II alpha Homo sapiens 77-86 1828154-4 1991 5-Benzyloxybenzyluracil (BBU) is a potent inhibitor of dihydropyrimidine dehydrogenase (DPD), the initial enzyme in FUra catabolism (Naguib FMN, el Kouni MH and Cha S, Biochem Pharmacol 38: 1471-1480, 1989). Fluorouracil 116-120 dihydropyrimidine dehydrogenase Rattus norvegicus 88-91 31662984-5 2019 Downregulation of TOP2alpha with siRNA or miR-494 transfection resulted in an increase of cytotoxicity and decrease of cell colonies to 5-FU for HCT-8/5-FU cells. Fluorouracil 136-140 DNA topoisomerase II alpha Homo sapiens 18-27 1828154-9 1991 Further studies utilizing short-term (20 min) infusion of BBU prior to administration of FUra suggested that the inhibition of DPD was reversible. Fluorouracil 89-93 dihydropyrimidine dehydrogenase Rattus norvegicus 127-130 31662984-5 2019 Downregulation of TOP2alpha with siRNA or miR-494 transfection resulted in an increase of cytotoxicity and decrease of cell colonies to 5-FU for HCT-8/5-FU cells. Fluorouracil 136-140 microRNA 494 Homo sapiens 42-49 31662984-5 2019 Downregulation of TOP2alpha with siRNA or miR-494 transfection resulted in an increase of cytotoxicity and decrease of cell colonies to 5-FU for HCT-8/5-FU cells. Fluorouracil 151-155 DNA topoisomerase II alpha Homo sapiens 18-27 31662984-5 2019 Downregulation of TOP2alpha with siRNA or miR-494 transfection resulted in an increase of cytotoxicity and decrease of cell colonies to 5-FU for HCT-8/5-FU cells. Fluorouracil 151-155 microRNA 494 Homo sapiens 42-49 31662984-7 2019 It significantly helped suppress cell growth and induced cell apoptosis in HCT-8/5-FU cells with the expression of TOP2alpha being significantly suppressed, which increased by 5-FU. Fluorouracil 81-85 DNA topoisomerase II alpha Homo sapiens 115-124 1992915-2 1991 FdUMP, a metabolite of 5-fluorouracil(5-FU), is known to have an inhibitory activity of thymidylate synthase (TS). Fluorouracil 23-37 thymidylate synthetase Homo sapiens 88-108 31662984-7 2019 It significantly helped suppress cell growth and induced cell apoptosis in HCT-8/5-FU cells with the expression of TOP2alpha being significantly suppressed, which increased by 5-FU. Fluorouracil 176-180 DNA topoisomerase II alpha Homo sapiens 115-124 1992915-2 1991 FdUMP, a metabolite of 5-fluorouracil(5-FU), is known to have an inhibitory activity of thymidylate synthase (TS). Fluorouracil 23-37 thymidylate synthetase Homo sapiens 110-112 31662984-8 2019 Consistently, miR-494, which reportedly regulates TOP2alpha, exhibited reverse trends in EESP/5-FU combination treatment. Fluorouracil 94-98 microRNA 494 Homo sapiens 14-21 1992915-2 1991 FdUMP, a metabolite of 5-fluorouracil(5-FU), is known to have an inhibitory activity of thymidylate synthase (TS). Fluorouracil 38-42 thymidylate synthetase Homo sapiens 88-108 1992915-2 1991 FdUMP, a metabolite of 5-fluorouracil(5-FU), is known to have an inhibitory activity of thymidylate synthase (TS). Fluorouracil 38-42 thymidylate synthetase Homo sapiens 110-112 31662984-8 2019 Consistently, miR-494, which reportedly regulates TOP2alpha, exhibited reverse trends in EESP/5-FU combination treatment. Fluorouracil 94-98 DNA topoisomerase II alpha Homo sapiens 50-59 31536574-1 2019 Metronomic chemotherapy using the 5-FU prodrug uracil-tegafur (UFT) and cyclophosphamide (CTX) was previously shown to only modestly delay primary tumor growth, but nevertheless markedly suppressed the development of micro-metastasis in an orthotopic breast cancer xenograft model, using the metastatic variant of the MDA-MB-231 cell line, 231/LM2-4. Fluorouracil 34-38 cytochrome P450 family 27 subfamily A member 1 Homo sapiens 90-93 1674889-6 1991 CMT, but not RNT, inhibited cytosolic dihydropyrimidine dehydrogenase (DPD), the enzyme responsible for 5-FUra catabolism. Fluorouracil 104-110 dihydropyrimidine dehydrogenase Rattus norvegicus 38-69 1674889-6 1991 CMT, but not RNT, inhibited cytosolic dihydropyrimidine dehydrogenase (DPD), the enzyme responsible for 5-FUra catabolism. Fluorouracil 104-110 dihydropyrimidine dehydrogenase Rattus norvegicus 71-74 1674889-7 1991 It is proposed that the observed effects of CMT on 5-FUra kinetics are the result of inhibition of DPD. Fluorouracil 51-57 dihydropyrimidine dehydrogenase Rattus norvegicus 99-102 1827310-1 1991 Inhibition of thymidylate synthase (TS) by the 5-fluorouracil (5-FU) metabolite FdUMP is considered to be the main mechanism of action of 5-FU. Fluorouracil 47-61 thymidylate synthetase Homo sapiens 14-34 31288002-7 2019 RESULTS: combined administration of luteolin and 5-FU in SEC model increased levels of p53, p21, caspase 3, DRAM and survivability while, tumor volume, weight, thioredoxin reductase one (TR1) activity and cyclin D1 expression showed the reverse with restoration of oxidant/antioxidant indices. Fluorouracil 49-53 transformation related protein 53, pseudogene Mus musculus 87-90 1827310-1 1991 Inhibition of thymidylate synthase (TS) by the 5-fluorouracil (5-FU) metabolite FdUMP is considered to be the main mechanism of action of 5-FU. Fluorouracil 63-67 thymidylate synthetase Homo sapiens 14-34 1827310-1 1991 Inhibition of thymidylate synthase (TS) by the 5-fluorouracil (5-FU) metabolite FdUMP is considered to be the main mechanism of action of 5-FU. Fluorouracil 138-142 thymidylate synthetase Homo sapiens 14-34 31020694-8 2019 JEG-3 cells were treated with MTX or 5-FU for and quantitative real-time polymerase chain reaction assay revealed that H19 messenger RNA expression increased. Fluorouracil 37-41 H19 imprinted maternally expressed transcript Homo sapiens 119-122 1832538-4 1991 Following 5-fluorouracil activation to 5-fluorodeoxyuridine monophosphates, its binding to thymidylate synthase is stabilized by the active cofactor, 5,10 methylene tetrahydrofolate and its polyglutamate forms. Fluorouracil 10-24 thymidylate synthetase Homo sapiens 91-111 31463333-11 2019 An additional 2.1 +- 0.8 cycles for 5-FU and 1.2 +- 0.4 months for IFN were needed to achieve HR-OCT resolution of OSSN. Fluorouracil 36-40 plexin A2 Homo sapiens 97-100 2258610-2 1990 In this study, recombinant human IL-1 alpha (rhIL-1 alpha) was used to protect normal and tumor-bearing BALB/c mice from the acute toxicity caused by lethal doses of cyclophosphamide (Cy) and 5-fluorouracil. Fluorouracil 192-206 interleukin 1 alpha Homo sapiens 33-43 2128782-6 1990 After treatment, the estrogen receptor (ER) and progesterone receptor (PgR) levels decreased significantly in the groups treated with TAM alone and the combination of 5-FU and TAM but remained unchanged in the group treated with 5-FU alone. Fluorouracil 167-171 estrogen receptor 1 Rattus norvegicus 21-38 31162779-0 2019 Induced miR-31 by 5-fluorouracil exposure contributes to the resistance in colorectal tumors. Fluorouracil 18-32 microRNA 31 Homo sapiens 8-14 2128782-6 1990 After treatment, the estrogen receptor (ER) and progesterone receptor (PgR) levels decreased significantly in the groups treated with TAM alone and the combination of 5-FU and TAM but remained unchanged in the group treated with 5-FU alone. Fluorouracil 167-171 estrogen receptor 1 Rattus norvegicus 40-42 2128782-6 1990 After treatment, the estrogen receptor (ER) and progesterone receptor (PgR) levels decreased significantly in the groups treated with TAM alone and the combination of 5-FU and TAM but remained unchanged in the group treated with 5-FU alone. Fluorouracil 167-171 progesterone receptor Rattus norvegicus 48-69 2128782-6 1990 After treatment, the estrogen receptor (ER) and progesterone receptor (PgR) levels decreased significantly in the groups treated with TAM alone and the combination of 5-FU and TAM but remained unchanged in the group treated with 5-FU alone. Fluorouracil 167-171 progesterone receptor Rattus norvegicus 71-74 2128782-7 1990 The decreases in the ER and PgR levels in responsive tumors after treatment were considerably greater in the groups greated with TAM alone and the combination of 5-FU and TAM than in the group treated with 5-FU alone. Fluorouracil 162-166 estrogen receptor 1 Rattus norvegicus 21-23 31162779-8 2019 The ectopic expression of mimic miR-31 showed significant 5-FU resistance in the parental DLD-1 cells, while anti-miR-31 caused significant growth inhibition in DLD/F cells; that is, 5-FU-resistant colon cancer cell line DLD-1 under exposure to 5-FU. Fluorouracil 58-62 microRNA 31 Homo sapiens 32-38 2208278-1 1990 We have identified a novel growth factor, stem cell factor (SCF), for primitive hematopoietic progenitors based on its activity on bone marrow cells derived from mice treated with 5-fluorouracil. Fluorouracil 180-194 kit ligand Mus musculus 42-58 31162779-8 2019 The ectopic expression of mimic miR-31 showed significant 5-FU resistance in the parental DLD-1 cells, while anti-miR-31 caused significant growth inhibition in DLD/F cells; that is, 5-FU-resistant colon cancer cell line DLD-1 under exposure to 5-FU. Fluorouracil 183-187 microRNA 31 Homo sapiens 32-38 2208278-1 1990 We have identified a novel growth factor, stem cell factor (SCF), for primitive hematopoietic progenitors based on its activity on bone marrow cells derived from mice treated with 5-fluorouracil. Fluorouracil 180-194 kit ligand Mus musculus 60-63 31162779-8 2019 The ectopic expression of mimic miR-31 showed significant 5-FU resistance in the parental DLD-1 cells, while anti-miR-31 caused significant growth inhibition in DLD/F cells; that is, 5-FU-resistant colon cancer cell line DLD-1 under exposure to 5-FU. Fluorouracil 183-187 microRNA 31 Homo sapiens 114-120 2354443-0 1990 Influence of dose of [6RS]leucovorin on reduced folate pools and 5-fluorouracil-mediated thymidylate synthase inhibition in human colon adenocarcinoma xenografts. Fluorouracil 65-79 thymidylate synthetase Homo sapiens 89-109 31162779-8 2019 The ectopic expression of mimic miR-31 showed significant 5-FU resistance in the parental DLD-1 cells, while anti-miR-31 caused significant growth inhibition in DLD/F cells; that is, 5-FU-resistant colon cancer cell line DLD-1 under exposure to 5-FU. Fluorouracil 183-187 microRNA 31 Homo sapiens 32-38 31162779-8 2019 The ectopic expression of mimic miR-31 showed significant 5-FU resistance in the parental DLD-1 cells, while anti-miR-31 caused significant growth inhibition in DLD/F cells; that is, 5-FU-resistant colon cancer cell line DLD-1 under exposure to 5-FU. Fluorouracil 183-187 microRNA 31 Homo sapiens 114-120 31162779-9 2019 When we exposed high doses of 5-FU to parent or 5-FU-resistant cells, the expression levels of miR-31 were raised higher than those of controls. Fluorouracil 30-34 microRNA 31 Homo sapiens 95-101 31162779-9 2019 When we exposed high doses of 5-FU to parent or 5-FU-resistant cells, the expression levels of miR-31 were raised higher than those of controls. Fluorouracil 48-52 microRNA 31 Homo sapiens 95-101 31162779-12 2019 This study provides evidence supporting the association of miR-31 with 5-FU drug resistance and clinical stages of colorectal tumors. Fluorouracil 71-75 microRNA 31 Homo sapiens 59-65 33814416-7 2021 We investigated whether the ETS transcription factor ETV2 (aka ER71), critical for vascular development and regeneration, can promote angiogenesis and hair regrowth in a 5-FU-induced alopecia mouse model. Fluorouracil 170-174 ets variant 2 Mus musculus 53-57 33814416-9 2021 Following 5-FU treatment, Tie2-Cre; Etv2 CKO mice revealed a significant reduction in capillary density, anagen induction, and hair restoration when compared with controls. Fluorouracil 10-14 ets variant 2 Mus musculus 36-40 31285549-10 2019 5"-fluorouracil was found to be very effective in reducing the expression of KIAA1429 and CDK1 in breast cancer. Fluorouracil 0-15 vir like m6A methyltransferase associated Homo sapiens 77-85 33814416-10 2021 Mice receiving lentiviral Etv2 injection after 5-FU treatment showed significantly improved anagen induction and hair regrowth. Fluorouracil 47-51 ets variant 2 Mus musculus 26-30 33814416-11 2021 Two-photon laser scanning microscopy revealed that enforced Etv2 expression restored normal vessel morphology after 5-FU mediated vessel injury. Fluorouracil 116-120 ets variant 2 Mus musculus 60-64 33808326-7 2021 Substitution of either of these two residues to alanine or inhibition of ATR/ATM kinase activity abolished nuclear localization of SRPK1 and conferred tolerance to 5-FU treatment. Fluorouracil 164-168 ATM serine/threonine kinase Homo sapiens 77-80 31285549-10 2019 5"-fluorouracil was found to be very effective in reducing the expression of KIAA1429 and CDK1 in breast cancer. Fluorouracil 0-15 cyclin dependent kinase 1 Homo sapiens 90-94 31357665-7 2019 Moreover, HCC cells with silenced SHIP2 had increased expression of mesenchymal markers, which promotes cell migration, enhances glucose uptake, and leads to resistance to the chemotherapy drug (5-Fluorouracil, 5-FU). Fluorouracil 195-209 inositol polyphosphate phosphatase like 1 Homo sapiens 34-39 31357665-7 2019 Moreover, HCC cells with silenced SHIP2 had increased expression of mesenchymal markers, which promotes cell migration, enhances glucose uptake, and leads to resistance to the chemotherapy drug (5-Fluorouracil, 5-FU). Fluorouracil 211-215 inositol polyphosphate phosphatase like 1 Homo sapiens 34-39 31317696-8 2019 Finally, interference of FOXA1 or KRT7 increased the chemosensitivity of AGS and SGC-7901 cells to 5-fluorouracil (5-Fu) treatment by suppressing cell proliferation. Fluorouracil 99-113 forkhead box A1 Homo sapiens 25-30 31317696-8 2019 Finally, interference of FOXA1 or KRT7 increased the chemosensitivity of AGS and SGC-7901 cells to 5-fluorouracil (5-Fu) treatment by suppressing cell proliferation. Fluorouracil 99-113 jagged canonical Notch ligand 1 Homo sapiens 73-76 31317696-8 2019 Finally, interference of FOXA1 or KRT7 increased the chemosensitivity of AGS and SGC-7901 cells to 5-fluorouracil (5-Fu) treatment by suppressing cell proliferation. Fluorouracil 115-119 forkhead box A1 Homo sapiens 25-30 31317696-8 2019 Finally, interference of FOXA1 or KRT7 increased the chemosensitivity of AGS and SGC-7901 cells to 5-fluorouracil (5-Fu) treatment by suppressing cell proliferation. Fluorouracil 115-119 jagged canonical Notch ligand 1 Homo sapiens 73-76 31317696-9 2019 In conclusion, these data indicate that FOXA1 promoted proliferation, migration, invasion, and decreased chemosensitivity of GC cells to 5-Fu treatment through transcriptional activator KRT7. Fluorouracil 137-141 forkhead box A1 Homo sapiens 40-45 31115533-0 2019 TFAP2E methylation promotes 5-fluorouracil resistance via exosomal miR-106a-5p and miR-421 in gastric cancer MGC-803 cells. Fluorouracil 28-42 microRNA 421 Homo sapiens 83-90 31217433-0 2019 Docosahexaenoic acid inhibits both NLRP3 inflammasome assembly and JNK-mediated mature IL-1beta secretion in 5-fluorouracil-treated MDSC: implication in cancer treatment. Fluorouracil 109-123 interleukin 1 alpha Mus musculus 87-95 31217433-1 2019 Limitation of 5-fluorouracil (5-FU) anticancer efficacy is due to IL-1beta secretion by myeloid-derived suppressor cells (MDSC), according to a previous pre-clinical report. Fluorouracil 14-28 interleukin 1 alpha Mus musculus 66-74 31217433-1 2019 Limitation of 5-fluorouracil (5-FU) anticancer efficacy is due to IL-1beta secretion by myeloid-derived suppressor cells (MDSC), according to a previous pre-clinical report. Fluorouracil 30-34 interleukin 1 alpha Mus musculus 66-74 31217433-2 2019 Release of mature IL-1beta is a consequence of 5-FU-mediated NLRP3 activation and subsequent caspase-1 activity in MDSC. Fluorouracil 47-51 interleukin 1 alpha Mus musculus 18-26 31217433-2 2019 Release of mature IL-1beta is a consequence of 5-FU-mediated NLRP3 activation and subsequent caspase-1 activity in MDSC. Fluorouracil 47-51 NLR family, pyrin domain containing 3 Mus musculus 61-66 31217433-3 2019 IL-1beta sustains tumor growth recovery in 5-FU-treated mice. Fluorouracil 43-47 interleukin 1 alpha Mus musculus 0-8 31217433-5 2019 Here, we demonstrate that DHA inhibits 5-FU-induced IL-1beta secretion and caspase-1 activity in a MDSC cell line (MSC-2). Fluorouracil 39-43 interleukin 1 alpha Mus musculus 52-60 31217433-6 2019 Accordingly, we showed that DHA-enriched diet reduces circulating IL-1beta concentration and tumor recurrence in 5-FU-treated tumor-bearing mice. Fluorouracil 113-117 interleukin 1 alpha Mus musculus 66-74 30478896-9 2019 When treated with 5-fluorouracil, the expressions of stem cell markers, including Oct4, Sox2, and CD49F, were maximally maintained in the recellularized scaffold with decreased apoptosis rates compared with monolayer cells. Fluorouracil 18-32 POU class 5 homeobox 1 Homo sapiens 82-86 33806077-0 2021 Coptidis Rhizoma Extract Reverses 5-Fluorouracil Resistance in HCT116 Human Colorectal Cancer Cells via Modulation of Thymidylate Synthase. Fluorouracil 34-48 thymidylate synthetase Homo sapiens 118-138 33806077-4 2021 A well-known thymidylate synthase (TS) inhibitor, 5-fluorouracil (5-FU), is frequently prescribed to CRC patients; however, drug resistance is a critical limitation of its clinical application. Fluorouracil 50-64 thymidylate synthetase Homo sapiens 13-33 33806077-4 2021 A well-known thymidylate synthase (TS) inhibitor, 5-fluorouracil (5-FU), is frequently prescribed to CRC patients; however, drug resistance is a critical limitation of its clinical application. Fluorouracil 50-64 thymidylate synthetase Homo sapiens 35-37 33806077-4 2021 A well-known thymidylate synthase (TS) inhibitor, 5-fluorouracil (5-FU), is frequently prescribed to CRC patients; however, drug resistance is a critical limitation of its clinical application. Fluorouracil 66-70 thymidylate synthetase Homo sapiens 13-33 33806077-4 2021 A well-known thymidylate synthase (TS) inhibitor, 5-fluorouracil (5-FU), is frequently prescribed to CRC patients; however, drug resistance is a critical limitation of its clinical application. Fluorouracil 66-70 thymidylate synthetase Homo sapiens 35-37 33806077-8 2021 In addition, the combination of CRE and 5-FU notably suppressed the activity of TS, which was overexpressed in HCT116/R cells, as compared to HCT116/WT cells. Fluorouracil 40-44 thymidylate synthetase Homo sapiens 80-82 33802784-6 2021 Special attention was paid to the determination of the influence of pH and ionic strength as well as presence of co-contaminants (cadmium (Cd2+) and another pharmaceutical-metoprolol (MET)) on the sorption of 5-FU and MTX onto soil. Fluorouracil 209-213 SAFB like transcription modulator Homo sapiens 184-187 33802784-11 2021 The investigated co-contaminant (MET) caused around 25-fold increased sorption of 5-FU, whereas diminished sorption of MTX. Fluorouracil 82-86 SAFB like transcription modulator Homo sapiens 33-36 33033767-2 2020 Our study aims to design a number of analogues of 5-FU and evaluate their effectiveness against thymidylate synthase (TS) in silico compared to parent 5-FU with an effort to obtain better hit(s). Fluorouracil 50-54 thymidylate synthetase Homo sapiens 96-116 25721610-0 2015 Thymidylate synthase expression in circulating tumor cells: a new tool to predict 5-fluorouracil resistance in metastatic colorectal cancer patients. Fluorouracil 82-96 thymidylate synthetase Homo sapiens 0-20 25721610-1 2015 Thymidylate synthase (TYMS) is an important enzyme for 5-fluorouracil (5-FU) metabolism in metastatic colorectal cancer (mCRC) patients. Fluorouracil 55-69 thymidylate synthetase Homo sapiens 0-20 25721610-1 2015 Thymidylate synthase (TYMS) is an important enzyme for 5-fluorouracil (5-FU) metabolism in metastatic colorectal cancer (mCRC) patients. Fluorouracil 55-69 thymidylate synthetase Homo sapiens 22-26 25721610-1 2015 Thymidylate synthase (TYMS) is an important enzyme for 5-fluorouracil (5-FU) metabolism in metastatic colorectal cancer (mCRC) patients. Fluorouracil 71-75 thymidylate synthetase Homo sapiens 0-20 25721610-1 2015 Thymidylate synthase (TYMS) is an important enzyme for 5-fluorouracil (5-FU) metabolism in metastatic colorectal cancer (mCRC) patients. Fluorouracil 71-75 thymidylate synthetase Homo sapiens 22-26 25721610-14 2015 Our results searching for TYMS staining in CTCs, primary tumors and metastases suggest that the analysis of TYMS can be useful tool as a 5-FU resistance predictor biomarker if analyzed in CTCs from mCRC patients. Fluorouracil 137-141 thymidylate synthetase Homo sapiens 26-30 25721610-14 2015 Our results searching for TYMS staining in CTCs, primary tumors and metastases suggest that the analysis of TYMS can be useful tool as a 5-FU resistance predictor biomarker if analyzed in CTCs from mCRC patients. Fluorouracil 137-141 thymidylate synthetase Homo sapiens 108-112 30760080-5 2019 RNA profiling of synchronized 5-FU treated yeast cells and protein assays reveal that the drug specifically inhibits a set of cell cycle regulated genes involved in mitotic division, by decreasing levels of the paralogous Swi5 and Ace2 transcriptional activators. Fluorouracil 30-34 DNA-binding transcription factor ACE2 Saccharomyces cerevisiae S288C 231-235 26516361-0 2015 High Expression of Pyruvate Kinase M2 is Associated with Chemosensitivity to Epirubicin and 5-Fluorouracil in Breast Cancer. Fluorouracil 92-106 pyruvate kinase M1/2 Homo sapiens 19-37 26516361-5 2015 RESULTS: We found high PKM2 expression was significantly associated with in vitro chemosensitivity to epirubicin (EPI) (P=0.019) and 5-fluorouracil (5-Fu) (P=0.009) in breast cancer patients. Fluorouracil 133-147 pyruvate kinase M1/2 Homo sapiens 23-27 26516361-5 2015 RESULTS: We found high PKM2 expression was significantly associated with in vitro chemosensitivity to epirubicin (EPI) (P=0.019) and 5-fluorouracil (5-Fu) (P=0.009) in breast cancer patients. Fluorouracil 149-153 pyruvate kinase M1/2 Homo sapiens 23-27 26516361-7 2015 Although univariate and multivariate analysis indicated that high PKM2 was a poor independent predictor of progression free survival (PFS) and overall survival (OS) in breast cancer, patients with PKM2 high expression who received EPI-based or EPI plus 5-Fu chemotherapy were found to have a longer PFS (P=0.003, P=0.013) and OS (P=0.003, P=0.004) than patients treated with non-EPI/5-Fu-based regimens, respectively. Fluorouracil 253-257 pyruvate kinase M1/2 Homo sapiens 66-70 26516361-7 2015 Although univariate and multivariate analysis indicated that high PKM2 was a poor independent predictor of progression free survival (PFS) and overall survival (OS) in breast cancer, patients with PKM2 high expression who received EPI-based or EPI plus 5-Fu chemotherapy were found to have a longer PFS (P=0.003, P=0.013) and OS (P=0.003, P=0.004) than patients treated with non-EPI/5-Fu-based regimens, respectively. Fluorouracil 383-387 pyruvate kinase M1/2 Homo sapiens 66-70 26516361-8 2015 CONCLUSIONS: Our findings confirmed the poor prognosis of high PKM2 expression in breast cancer patients and revealed the predictive value of high PKM2 in the therapeutic response to EPI and 5-Fu. Fluorouracil 191-195 pyruvate kinase M1/2 Homo sapiens 147-151 34633539-9 2022 Groups with EP and treated with 5-FU or CIS showed high immunolabelling pattern of RANKL, TNF-alpha, and IL-1beta, moderate of BAX, and low of HIF-1alpha. Fluorouracil 32-36 BCL2 associated X, apoptosis regulator Rattus norvegicus 127-130 34592338-15 2022 AFE also efficiently regressed CT26-derived solid tumor in Balb/c mice acting alone or in synergy with 5FU through inducing autophagy as a major mechanism of action as indicated by upregulation of Beclin 1 and phospho-AMPK, and inhibition of phosphor-S6K1 levels in the tumor tissue lysates. Fluorouracil 103-106 beclin 1, autophagy related Mus musculus 197-205 34800596-7 2022 Our data revealed that 5-FU could induce cardiotoxicity which was detected as significant increases of troponin I, lactate dehydrogenase (LDH), creatine kinase- MB (CK-MB), endothelin receptors, malondialdehyde (MDA), toll like receptor4 (TLR4), myeloid differentiation primary response 88 (MyD88), nuclear factor kappa B (NFkappaB), and caspase 3 levels. Fluorouracil 23-27 MYD88, innate immune signal transduction adaptor Rattus norvegicus 246-289 34800596-7 2022 Our data revealed that 5-FU could induce cardiotoxicity which was detected as significant increases of troponin I, lactate dehydrogenase (LDH), creatine kinase- MB (CK-MB), endothelin receptors, malondialdehyde (MDA), toll like receptor4 (TLR4), myeloid differentiation primary response 88 (MyD88), nuclear factor kappa B (NFkappaB), and caspase 3 levels. Fluorouracil 23-27 MYD88, innate immune signal transduction adaptor Rattus norvegicus 291-296 30716387-8 2019 Based on these observations, we infer that inhibition of MALAT1 suppressed CRC progression and metastasis and improved the sensitivity of cancer cells to 5-FU. Fluorouracil 154-158 metastasis associated lung adenocarcinoma transcript 1 Homo sapiens 57-63 31115003-0 2019 MiR-195 reverses 5-FU resistance through targeting HMGA1 in gastric cancer cells. Fluorouracil 17-21 high mobility group AT-hook 1 Homo sapiens 51-56 31115003-10 2019 CONCLUSIONS: The down-regulation of miR-195 induces the resistance to 5-FU in gastric cancer through promoting the expression of HMGA1. Fluorouracil 70-74 high mobility group AT-hook 1 Homo sapiens 129-134 30944635-3 2019 Tegafur-uracil is an oral form of 5-fluorouracil whose efficacy is influenced by the activities of enzymes associated with its metabolism, such as dihydropyrimidine dehydrogenase (DPD), orotatephosphoribosyltransferase (OPRT) and thymidylate synthase (TS). Fluorouracil 34-48 thymidylate synthetase Homo sapiens 230-250 30944635-3 2019 Tegafur-uracil is an oral form of 5-fluorouracil whose efficacy is influenced by the activities of enzymes associated with its metabolism, such as dihydropyrimidine dehydrogenase (DPD), orotatephosphoribosyltransferase (OPRT) and thymidylate synthase (TS). Fluorouracil 34-48 thymidylate synthetase Homo sapiens 252-254 31022917-7 2019 Inhibition of P-gp and MRP1 increased the 5-FU drug sensitivity in HCV infected Huh7.5.1 cells. Fluorouracil 42-46 phosphoglycolate phosphatase Homo sapiens 14-18 31039730-0 2019 Downregulation of lncRNA CCAT1 enhances 5-fluorouracil sensitivity in human colon cancer cells. Fluorouracil 40-54 colon cancer associated transcript 1 Homo sapiens 25-30 31039730-1 2019 BACKGROUND: The purpose of this study was to determine the aberrant expression of the long noncoding RNA (lncRNA) colon cancer-associated transcript 1 (CCAT1) in 5-fluorouracil-resistant colonic neoplasm cells and to elucidate its effects on the 5-fluorouracil sensitivity of human colonic neoplasm cells. Fluorouracil 162-176 colon cancer associated transcript 1 Homo sapiens 152-157 31039730-1 2019 BACKGROUND: The purpose of this study was to determine the aberrant expression of the long noncoding RNA (lncRNA) colon cancer-associated transcript 1 (CCAT1) in 5-fluorouracil-resistant colonic neoplasm cells and to elucidate its effects on the 5-fluorouracil sensitivity of human colonic neoplasm cells. Fluorouracil 246-260 colon cancer associated transcript 1 Homo sapiens 152-157 31039730-8 2019 Moreover, the expression levels of CCAT1 were high in HCT 116/5-FU and HT-29/5-FU cell lines, whose apoptosis rates induced by 5-FU were lower than those in corresponding parental cells. Fluorouracil 62-66 colon cancer associated transcript 1 Homo sapiens 35-40 31039730-8 2019 Moreover, the expression levels of CCAT1 were high in HCT 116/5-FU and HT-29/5-FU cell lines, whose apoptosis rates induced by 5-FU were lower than those in corresponding parental cells. Fluorouracil 77-81 colon cancer associated transcript 1 Homo sapiens 35-40 31039730-8 2019 Moreover, the expression levels of CCAT1 were high in HCT 116/5-FU and HT-29/5-FU cell lines, whose apoptosis rates induced by 5-FU were lower than those in corresponding parental cells. Fluorouracil 77-81 colon cancer associated transcript 1 Homo sapiens 35-40 31039730-9 2019 The results of qRT-PCR and CCK-8 assay showed that enhancement of lncRNA CCAT1 expression levels in HCT 116 and HT-29 cell lines increased their IC50 of 5-FU and decreased their apoptosis rates. Fluorouracil 153-157 colon cancer associated transcript 1 Homo sapiens 73-78 31039730-10 2019 Meanwhile, siRNA-CCAT1 effectively inhibited the expression of CCAT1 and enhanced the 5-FU-sensitivity of HCT 116/5-FU and HT-29/5-FU, in which apoptosis rates were increased at the same time. Fluorouracil 86-90 colon cancer associated transcript 1 Homo sapiens 17-22 31039730-10 2019 Meanwhile, siRNA-CCAT1 effectively inhibited the expression of CCAT1 and enhanced the 5-FU-sensitivity of HCT 116/5-FU and HT-29/5-FU, in which apoptosis rates were increased at the same time. Fluorouracil 114-118 colon cancer associated transcript 1 Homo sapiens 17-22 31039730-10 2019 Meanwhile, siRNA-CCAT1 effectively inhibited the expression of CCAT1 and enhanced the 5-FU-sensitivity of HCT 116/5-FU and HT-29/5-FU, in which apoptosis rates were increased at the same time. Fluorouracil 114-118 colon cancer associated transcript 1 Homo sapiens 17-22 31039730-11 2019 CONCLUSIONS: Downregulation of CCAT1 effectively reversed the resistance of HCT 116/5-FU and HT-29/5-FU cells to 5-FU chemotherapeutic, opening a new avenue in colon cancer therapy. Fluorouracil 84-88 colon cancer associated transcript 1 Homo sapiens 31-36 31039730-11 2019 CONCLUSIONS: Downregulation of CCAT1 effectively reversed the resistance of HCT 116/5-FU and HT-29/5-FU cells to 5-FU chemotherapeutic, opening a new avenue in colon cancer therapy. Fluorouracil 99-103 colon cancer associated transcript 1 Homo sapiens 31-36 31039730-11 2019 CONCLUSIONS: Downregulation of CCAT1 effectively reversed the resistance of HCT 116/5-FU and HT-29/5-FU cells to 5-FU chemotherapeutic, opening a new avenue in colon cancer therapy. Fluorouracil 99-103 colon cancer associated transcript 1 Homo sapiens 31-36 31019568-0 2019 Overexpression of long noncoding RNA LINC01419 in esophageal squamous cell carcinoma and its relation to the sensitivity to 5-fluorouracil by mediating GSTP1 methylation. Fluorouracil 124-138 glutathione S-transferase pi 1 Homo sapiens 152-157 31019568-2 2019 Herein, this study elucidates the role and mechanism by which LINC01419 regulates the DNA methylation of glutathione S-transferase pi 1 (GSTP1) in relation to ESCC progression and the sensitivity of ESCC cells to 5-fluorouracil (5-FU). Fluorouracil 213-227 glutathione S-transferase pi 1 Homo sapiens 105-135 31019568-2 2019 Herein, this study elucidates the role and mechanism by which LINC01419 regulates the DNA methylation of glutathione S-transferase pi 1 (GSTP1) in relation to ESCC progression and the sensitivity of ESCC cells to 5-fluorouracil (5-FU). Fluorouracil 213-227 glutathione S-transferase pi 1 Homo sapiens 137-142 31019568-2 2019 Herein, this study elucidates the role and mechanism by which LINC01419 regulates the DNA methylation of glutathione S-transferase pi 1 (GSTP1) in relation to ESCC progression and the sensitivity of ESCC cells to 5-fluorouracil (5-FU). Fluorouracil 229-233 glutathione S-transferase pi 1 Homo sapiens 105-135 31019568-2 2019 Herein, this study elucidates the role and mechanism by which LINC01419 regulates the DNA methylation of glutathione S-transferase pi 1 (GSTP1) in relation to ESCC progression and the sensitivity of ESCC cells to 5-fluorouracil (5-FU). Fluorouracil 229-233 glutathione S-transferase pi 1 Homo sapiens 137-142 31019568-7 2019 Notably, LINC01419 could bind to the promoter region of the GSTP1 gene, resulting in elevated GSTP1 methylation and reduced GSTP1 levels via the recruitment of DNA methyltransferase among ESCC cells, whereby ESCC progression was stimulated accompanied by reduced ESCC cell sensitivity to 5-FU. Fluorouracil 288-292 glutathione S-transferase pi 1 Homo sapiens 60-65 31019568-8 2019 GSTP1 demethylation by 5-Aza-CdR was observed to reverse the effects of LINC01419 overexpression in ESCC cells and the response to 5-FU. Fluorouracil 131-135 glutathione S-transferase pi 1 Homo sapiens 0-5 31019568-9 2019 Conclusion: Highly expressed LINC01419 in ESCC promotes GSTP1 methylation, which ultimately acts to promote the event of ESCC and diminish the sensitivity of ESCC cells to 5-FU, highlighting a novel potential strategy to improve 5-FU-based chemotherapy in ESCC. Fluorouracil 172-176 glutathione S-transferase pi 1 Homo sapiens 56-61 31019568-9 2019 Conclusion: Highly expressed LINC01419 in ESCC promotes GSTP1 methylation, which ultimately acts to promote the event of ESCC and diminish the sensitivity of ESCC cells to 5-FU, highlighting a novel potential strategy to improve 5-FU-based chemotherapy in ESCC. Fluorouracil 229-233 glutathione S-transferase pi 1 Homo sapiens 56-61 30895944-1 2019 BACKGROUND: Topical calcipotriol plus 5-fluorouracil (5-FU) combination is an effective immunotherapy against actinic keratosis (AK), which is a precursor to squamous cell carcinoma (SCC). Fluorouracil 38-52 serpin family B member 3 Homo sapiens 183-186 30895944-1 2019 BACKGROUND: Topical calcipotriol plus 5-fluorouracil (5-FU) combination is an effective immunotherapy against actinic keratosis (AK), which is a precursor to squamous cell carcinoma (SCC). Fluorouracil 54-58 serpin family B member 3 Homo sapiens 183-186 30895944-10 2019 CONCLUSION: A short course of calcipotriol plus 5-FU treatment on the face and scalp is associated with induction of robust T cell immunity and Trm formation against AKs and significantly lowers the risk of SCC development within 3 years of treatment. Fluorouracil 48-52 serpin family B member 3 Homo sapiens 207-210 30936724-0 2019 Nonhomologous end joining key factor XLF enhances both 5-florouracil and oxaliplatin resistance in colorectal cancer. Fluorouracil 55-68 non-homologous end joining factor 1 Homo sapiens 37-40 34688013-1 2022 Sphingosine-1-phosphate receptor 2 (S1PR2) has been identified as a brand-new GPCR target for designing antagonists to reverse 5-FU resistance. Fluorouracil 127-131 sphingosine-1-phosphate receptor 2 Homo sapiens 0-34 34688013-1 2022 Sphingosine-1-phosphate receptor 2 (S1PR2) has been identified as a brand-new GPCR target for designing antagonists to reverse 5-FU resistance. Fluorouracil 127-131 sphingosine-1-phosphate receptor 2 Homo sapiens 36-41 34970530-8 2021 Mechanistically, 2b induced apoptosis-dependent anticancer effect (43%) higher than that of 5-fluorouracil (34.95%) in three studied cancer cell lines, activated p53 (47%), downregulated the Bcl2 gene (1.25-fold), and upregulated p21 (2-fold) in the treated cancer cells. Fluorouracil 92-106 H3 histone pseudogene 16 Homo sapiens 230-233 34411894-0 2021 Design, synthesis and biological evaluation of sphingosine-1-phosphate receptor 2 antagonists as potent 5-FU-resistance reversal agents for the treatment of colorectal cancer. Fluorouracil 104-108 sphingosine-1-phosphate receptor 2 Homo sapiens 47-81 34411894-4 2021 Sphingosine-1-phosphate receptor 2 (S1PR2) was proved to be a potential target for reversing 5-FU resistance, but the activity of known S1PR2 antagonists JTE-013 were weak in 5-FU-resistant cell lines. Fluorouracil 93-97 sphingosine-1-phosphate receptor 2 Homo sapiens 0-34 34411894-4 2021 Sphingosine-1-phosphate receptor 2 (S1PR2) was proved to be a potential target for reversing 5-FU resistance, but the activity of known S1PR2 antagonists JTE-013 were weak in 5-FU-resistant cell lines. Fluorouracil 93-97 sphingosine-1-phosphate receptor 2 Homo sapiens 36-41 34411894-4 2021 Sphingosine-1-phosphate receptor 2 (S1PR2) was proved to be a potential target for reversing 5-FU resistance, but the activity of known S1PR2 antagonists JTE-013 were weak in 5-FU-resistant cell lines. Fluorouracil 175-179 sphingosine-1-phosphate receptor 2 Homo sapiens 0-34 34411894-5 2021 To develop more potent S1PR2 antagonists to treat 5-FU-resistant cancer, a series of JTE-013 derivatives were designed and synthesized. Fluorouracil 50-54 sphingosine-1-phosphate receptor 2 Homo sapiens 23-28 34546854-0 2021 Exosomal-mediated transfer of APCDD1L-AS1 induces 5-fluorouracil resistance in oral squamous cell carcinoma via miR-1224-5p/nuclear receptor binding SET domain protein 2 (NSD2) axis. Fluorouracil 50-64 APC down-regulated 1 like Homo sapiens 30-37 34546854-3 2021 However, the role of APCDD1L-AS1 in 5-fluorouracil (5-FU) resistance regulation within OSCC is still obscure. Fluorouracil 52-56 APC down-regulated 1 like Homo sapiens 21-28 34546854-9 2021 APCDD1L-AS1 knockdown impaired 5-FU resistance in 5-FU-resistant OSCC cells by reducing IC50 value, suppressing cell viability, and accelerating cell apoptosis. Fluorouracil 31-35 APC down-regulated 1 like Homo sapiens 0-7 34546854-9 2021 APCDD1L-AS1 knockdown impaired 5-FU resistance in 5-FU-resistant OSCC cells by reducing IC50 value, suppressing cell viability, and accelerating cell apoptosis. Fluorouracil 50-54 APC down-regulated 1 like Homo sapiens 0-7 34546854-11 2021 Besides, miR-1224-5p was a molecular target of APCDD1L-AS1 and directly targeted NSD2 in 5-FU-resistant cells. Fluorouracil 89-93 microRNA 1224 Homo sapiens 9-17 34546854-12 2021 MiR-1224-5p exhibited a much lower level in 5-FU-resistant tissues and increased 5-FU sensitivity in 5-FU-resistant OSCC cells. Fluorouracil 44-48 microRNA 1224 Homo sapiens 0-8 34546854-12 2021 MiR-1224-5p exhibited a much lower level in 5-FU-resistant tissues and increased 5-FU sensitivity in 5-FU-resistant OSCC cells. Fluorouracil 81-85 microRNA 1224 Homo sapiens 0-8 34546854-12 2021 MiR-1224-5p exhibited a much lower level in 5-FU-resistant tissues and increased 5-FU sensitivity in 5-FU-resistant OSCC cells. Fluorouracil 101-105 microRNA 1224 Homo sapiens 0-8 34688691-0 2021 FOXM1 inhibitor, Siomycin A, synergizes and restores 5-FU cytotoxicity in human cholangiocarcinoma cell lines via targeting thymidylate synthase. Fluorouracil 53-57 thymidylate synthetase Homo sapiens 124-144 34688691-1 2021 AIMS: 5-Fluorouracil (5-FU), a thymidylate synthase (TS) inhibitor, has been used as the first-line chemotherapeutic drug for cholangiocarcinoma (CCA). Fluorouracil 6-20 thymidylate synthetase Homo sapiens 31-51 34688691-1 2021 AIMS: 5-Fluorouracil (5-FU), a thymidylate synthase (TS) inhibitor, has been used as the first-line chemotherapeutic drug for cholangiocarcinoma (CCA). Fluorouracil 6-20 thymidylate synthetase Homo sapiens 53-55 34688691-1 2021 AIMS: 5-Fluorouracil (5-FU), a thymidylate synthase (TS) inhibitor, has been used as the first-line chemotherapeutic drug for cholangiocarcinoma (CCA). Fluorouracil 22-26 thymidylate synthetase Homo sapiens 31-51 34688691-1 2021 AIMS: 5-Fluorouracil (5-FU), a thymidylate synthase (TS) inhibitor, has been used as the first-line chemotherapeutic drug for cholangiocarcinoma (CCA). Fluorouracil 22-26 thymidylate synthetase Homo sapiens 53-55 34688691-3 2021 Upregulation of Forkhead box M1 (FOXM1) and TS were shown to play a significant role in 5-FU resistance. Fluorouracil 88-92 thymidylate synthetase Homo sapiens 44-46 34688691-12 2021 FOXM1 and TS expression were increased in the 5-FU treated cells but were suppressed in the SioA treated cells. Fluorouracil 46-50 thymidylate synthetase Homo sapiens 10-12 34637097-7 2021 The combination of 5-FU and Quer compared to 5-FU alone improved apoptosis by increasing the gene expression of Bax and p53 and caspase-9 activity and decreasing the Bcl2 gene expression. Fluorouracil 19-23 caspase 9 Homo sapiens 128-137 34637097-7 2021 The combination of 5-FU and Quer compared to 5-FU alone improved apoptosis by increasing the gene expression of Bax and p53 and caspase-9 activity and decreasing the Bcl2 gene expression. Fluorouracil 45-49 caspase 9 Homo sapiens 128-137 34888232-7 2021 Results: 5-FU-treated SPAK-KO mice exhibited milder intestinal mucositis, reduced pro-inflammatory cytokine expression, increased villus length, good maintenance of proliferative indices of villus cells, decreased apoptotic index of enterocytes, reduced gut permeability, and restoration of tight junction protein expression (vs. 5-FU-treated wild-type mice). Fluorouracil 9-13 serine/threonine kinase 39 Mus musculus 22-26 34830244-9 2021 p130Cas was inducible by 5-fluorouracil (5-FU) and FOLFIRI (folinic acid, 5-FU, irinotecan), and p130Cas and EREG were upregulated in distant metastases (GSE121418). Fluorouracil 25-39 BCAR1 scaffold protein, Cas family member Homo sapiens 0-7 34830244-9 2021 p130Cas was inducible by 5-fluorouracil (5-FU) and FOLFIRI (folinic acid, 5-FU, irinotecan), and p130Cas and EREG were upregulated in distant metastases (GSE121418). Fluorouracil 41-45 BCAR1 scaffold protein, Cas family member Homo sapiens 0-7 34773342-5 2022 We investigated the influence of chemotherapeutic drugs (cisplatin and fluorouracil) on PD-L1/L2 expression and PD-L1/L2-related pathways in vitro. Fluorouracil 71-83 CD274 molecule Homo sapiens 112-117 34773342-11 2022 Fluorouracil increased PD-L1 and PD-L2 expression. Fluorouracil 0-12 CD274 molecule Homo sapiens 23-28 34528330-3 2021 A significant positive correlation was observed between AEG-1, TS, ERCC1, EGFR, and VEGF gene expression levels in CRC cell lines, and low AEG-1 and TS expression were highly sensitive to 5-fluorouracil treatment. Fluorouracil 188-202 thymidylate synthetase Homo sapiens 63-65 34528330-3 2021 A significant positive correlation was observed between AEG-1, TS, ERCC1, EGFR, and VEGF gene expression levels in CRC cell lines, and low AEG-1 and TS expression were highly sensitive to 5-fluorouracil treatment. Fluorouracil 188-202 thymidylate synthetase Homo sapiens 149-151 30842415-0 2019 ABHD5 blunts the sensitivity of colorectal cancer to fluorouracil via promoting autophagic uracil yield. Fluorouracil 53-65 abhydrolase domain containing 5, lysophosphatidic acid acyltransferase Homo sapiens 0-5 28942723-3 2019 Dihydropyrimidine dehydrogenase and thymidylate synthase play a major role in fluorouracil and capecitabine activity and toxicity. Fluorouracil 78-90 thymidylate synthetase Homo sapiens 36-56 34694685-2 2022 Deoxythymidine monophosphate (dTMP) is synthesized by the combined action of three enzymes: serine hydroxymethyltransferase (SHMT), dihydrofolate reductase (DHFR) and thymidylate synthase (TYMS), with the latter two being targets of widely used chemotherapeutics such as antifolates and 5-fluorouracil. Fluorouracil 287-301 serine hydroxymethyltransferase 1 Homo sapiens 92-123 34694685-2 2022 Deoxythymidine monophosphate (dTMP) is synthesized by the combined action of three enzymes: serine hydroxymethyltransferase (SHMT), dihydrofolate reductase (DHFR) and thymidylate synthase (TYMS), with the latter two being targets of widely used chemotherapeutics such as antifolates and 5-fluorouracil. Fluorouracil 287-301 serine hydroxymethyltransferase 1 Homo sapiens 125-129 34694685-2 2022 Deoxythymidine monophosphate (dTMP) is synthesized by the combined action of three enzymes: serine hydroxymethyltransferase (SHMT), dihydrofolate reductase (DHFR) and thymidylate synthase (TYMS), with the latter two being targets of widely used chemotherapeutics such as antifolates and 5-fluorouracil. Fluorouracil 287-301 dihydrofolate reductase Homo sapiens 132-155 34694685-2 2022 Deoxythymidine monophosphate (dTMP) is synthesized by the combined action of three enzymes: serine hydroxymethyltransferase (SHMT), dihydrofolate reductase (DHFR) and thymidylate synthase (TYMS), with the latter two being targets of widely used chemotherapeutics such as antifolates and 5-fluorouracil. Fluorouracil 287-301 dihydrofolate reductase Homo sapiens 157-161 34694685-2 2022 Deoxythymidine monophosphate (dTMP) is synthesized by the combined action of three enzymes: serine hydroxymethyltransferase (SHMT), dihydrofolate reductase (DHFR) and thymidylate synthase (TYMS), with the latter two being targets of widely used chemotherapeutics such as antifolates and 5-fluorouracil. Fluorouracil 287-301 thymidylate synthetase Homo sapiens 167-187 34694685-2 2022 Deoxythymidine monophosphate (dTMP) is synthesized by the combined action of three enzymes: serine hydroxymethyltransferase (SHMT), dihydrofolate reductase (DHFR) and thymidylate synthase (TYMS), with the latter two being targets of widely used chemotherapeutics such as antifolates and 5-fluorouracil. Fluorouracil 287-301 thymidylate synthetase Homo sapiens 189-193 34685438-0 2021 6-Shogaol Antagonizes the Adipocyte-Conditioned Medium-Initiated 5-Fluorouracil Resistance in Human Colorectal Cancer Cells through Controlling the SREBP-1 Level. Fluorouracil 65-79 sterol regulatory element binding transcription factor 1 Homo sapiens 148-155 34685438-5 2021 It was shown that the level of sterol-regulatory element-binding protein-1 (SREBP-1), a critical transcription factor involved in lipid synthesis and metabolism, would be upregulated through Akt and p70S6K signaling pathways while CRC cells are cultured in ACM, which subsequently decreases the cell sensitivity to 5-FU cytotoxicity. Fluorouracil 315-319 sterol regulatory element binding transcription factor 1 Homo sapiens 31-74 34685438-5 2021 It was shown that the level of sterol-regulatory element-binding protein-1 (SREBP-1), a critical transcription factor involved in lipid synthesis and metabolism, would be upregulated through Akt and p70S6K signaling pathways while CRC cells are cultured in ACM, which subsequently decreases the cell sensitivity to 5-FU cytotoxicity. Fluorouracil 315-319 sterol regulatory element binding transcription factor 1 Homo sapiens 76-83 34685438-5 2021 It was shown that the level of sterol-regulatory element-binding protein-1 (SREBP-1), a critical transcription factor involved in lipid synthesis and metabolism, would be upregulated through Akt and p70S6K signaling pathways while CRC cells are cultured in ACM, which subsequently decreases the cell sensitivity to 5-FU cytotoxicity. Fluorouracil 315-319 ribosomal protein S6 kinase B1 Homo sapiens 199-205 34685438-7 2021 Overall, the present study elucidated the role of adipocyte-containing microenvironment in 5-FU resistance development of CRC through controlling the SREBP-1 level and further enhanced the concept of clinical application of 6-shogaol and AMPK signaling in CRC therapy. Fluorouracil 91-95 sterol regulatory element binding transcription factor 1 Homo sapiens 150-157 34728031-0 2021 (Expression of Runt-related Transcription Factor 3 in Human Colon Cancer Cell Line HCT-116 Resistant to 5-Fluorouracil and the Mechanism of Drug Resistance). Fluorouracil 104-118 RUNX family transcription factor 3 Homo sapiens 15-50 34728031-1 2021 Objective To establish a human colon cancer cell line HCT-116/5-FU resistant to 5-fluorouracil(5-FU)and explore the relationship between runt-related transcription factor 3(RUNX3)and drug resistance of colorectal cancer.Methods The human colon cancer cell line HCT-116/5-FU with resistance to 5-FU was established by low concentration gradient increment combined with high-dose intermittent shock.CCK-8 method was used to determine the half maximal inhibitory concentration(IC50)of 5-FU on the parent line HCT-116 and drug-resistant line HCT-116/5-FU.The cell growth curve was established for the calculation of population doubling time(TD).The mRNA levels and protein levels of RUNX3,P-glycoprotein(P-gp),multidrug resistance-associated protein 1(MRP1),and lung resistance-related protein(LRP)in HCT-116 and HCT-116/5-FU cells were determined by qRT-PCR and Western blotting,respectively.The RUNX3 expression in HCT-116 cells was knocked down by siRNA technique,and the cells were divided into RUNX3 knockdown groups(si-RUNX3-1 group and si-RUNX3-2 group)and negative control group(si-NC group).The knockdown efficiency was verified by qRT-PCR at the mRNA level and Western blotting at the protein level.The IC50 in si-RUNX3 groups and si-NC group was determined with CCK-8 method,and the expression of P-gp,MRP1,and LRP in the two groups was detected by Western blotting.Results A stable human colon cancer drug-resistant cell line HCT-116/5-FU was successfully constructed.HCT-116/5-FU showed the TD 1.38 times as long as that of HCT-116(P=0.002)and changed morphology.The mRNA level of RUNX3 in HCT-116/5-FU cells was significantly lower than that in HCT-116 cells(P=0.048),and those of P-gp(P=0.008),MRP1(P=0.001),and LRP(P=0.001)showed the opposite trend.The protein level of RUNX3 in HCT-116/5-FU cells was significantly lower than that in HCT-116(P<0.001),and those of P-gp,MRP1,and LRP presented the opposite trend(all P<0.001).The HCT-116 cell model with low expression of RUNX3 was successfully established.The mRNA level of RUNX3 had no significant difference between si-RUNX3-1 group and si-NC group(P=0.064),while the level in si-RUNX3-2 group was significantly lower than that in si-NC group(P=0.034).The protein levels of RUNX3 in si-RUNX3-1 group and si-RUNX3-2 group were lower than that in si-NC group(both P<0.001).The results demonstrated higher knocking efficiency in si-RUNX3-2 group,which was thus selected to complete the follow-up test.The IC50 of si-RUNX3 group was significantly higher than that of si-NC group(P<0.001),which indicated that the down-regulated expression of RUNX3 could reduce the sensitivity of HCT-116 cells to 5-FU.The relative protein levels of P-gp,MRP1,and LRP in si-RUNX3 group were significantly higher than those in si-NC group(all P<0.001).Conclusion The down-regulation of RUNX3 expression can reduce the sensitivity of HCT-116 cells to 5-FU,which is considered to be related to the up-regulated expression of P-gp,MRP1,and LRP. Fluorouracil 269-273 RUNX family transcription factor 3 Homo sapiens 137-172 34091433-0 2021 Corrigendum to "Voltage-gated sodium channel Nav1.5 promotes tumor progression and enhances chemosensitivity to 5-fluorouracil in colorectal cancer" (Canc. Fluorouracil 112-126 sodium voltage-gated channel alpha subunit 5 Homo sapiens 45-51 30803213-0 2019 Study of Thymidylate Synthase (TS) and Dihydropyrimidine Dehydrogenase (DPD) Expressions on 5-Fluorouracil in Oral Squamous Cell Carcinoma Background: The study aims to analyze Thymidylate Synthase (TS) and Dihydropyrimidine Dehydrogenase(DPD) Expressions on 5-Fluorouracil in Oral Squamous Cell Carcinoma (OSCC). Fluorouracil 92-106 thymidylate synthetase Homo sapiens 9-29 34611476-8 2021 TRAILR2 was down-regulated by oxaliplatin and 5-FU, was not affected by CPT-11, and was increased by cisplatin. Fluorouracil 46-50 TNF receptor superfamily member 10b Homo sapiens 0-7 30803213-0 2019 Study of Thymidylate Synthase (TS) and Dihydropyrimidine Dehydrogenase (DPD) Expressions on 5-Fluorouracil in Oral Squamous Cell Carcinoma Background: The study aims to analyze Thymidylate Synthase (TS) and Dihydropyrimidine Dehydrogenase(DPD) Expressions on 5-Fluorouracil in Oral Squamous Cell Carcinoma (OSCC). Fluorouracil 92-106 thymidylate synthetase Homo sapiens 31-33 30803213-0 2019 Study of Thymidylate Synthase (TS) and Dihydropyrimidine Dehydrogenase (DPD) Expressions on 5-Fluorouracil in Oral Squamous Cell Carcinoma Background: The study aims to analyze Thymidylate Synthase (TS) and Dihydropyrimidine Dehydrogenase(DPD) Expressions on 5-Fluorouracil in Oral Squamous Cell Carcinoma (OSCC). Fluorouracil 92-106 thymidylate synthetase Homo sapiens 177-197 30803213-7 2019 TS levels are not only predictiveof 5-FU response, but also prognostic in clinical value of non-treated cancer patients. Fluorouracil 36-40 thymidylate synthetase Homo sapiens 0-2 30915355-7 2019 In addition, Ubenimex downregulates expression of membrane transport proteins, such as P-gp and MRP1, by inhibiting phosphorylation in the PI3K/AKT/mTOR pathway to increase intracellular accumulations of 5-fluorouracil and oxaliplatin, a process for which downregulation of CD13 expression is essential. Fluorouracil 204-218 phosphoglycolate phosphatase Homo sapiens 87-91 34640443-3 2021 5-fluorouracil and its prodrugs affect neoplastic cells in multiple ways by impairing their proliferation, principally through the inhibition of thymidylate synthase. Fluorouracil 0-14 thymidylate synthetase Homo sapiens 145-165 30488540-0 2019 Augmented antitumor activity of 5-fluorouracil by double knockdown of MDM4 and MDM2 in colon and gastric cancer cells. Fluorouracil 32-46 MDM4 regulator of p53 Homo sapiens 70-74 30488540-5 2019 In the present study, MDM4/MDM2 double knockdown with the siRNAs enhanced 5-fluorouracil (5-FU)-induced p53 activation, arrested the cell cycle at G1 phase, and potentiated the antitumor effect of 5-FU in wtTP53/highMDM4 human colon (HCT116 and LoVo) and gastric (SNU-1 and NUGC-4) cancer cells. Fluorouracil 74-88 MDM4 regulator of p53 Homo sapiens 22-26 30488540-5 2019 In the present study, MDM4/MDM2 double knockdown with the siRNAs enhanced 5-fluorouracil (5-FU)-induced p53 activation, arrested the cell cycle at G1 phase, and potentiated the antitumor effect of 5-FU in wtTP53/highMDM4 human colon (HCT116 and LoVo) and gastric (SNU-1 and NUGC-4) cancer cells. Fluorouracil 90-94 MDM4 regulator of p53 Homo sapiens 22-26 30488540-5 2019 In the present study, MDM4/MDM2 double knockdown with the siRNAs enhanced 5-fluorouracil (5-FU)-induced p53 activation, arrested the cell cycle at G1 phase, and potentiated the antitumor effect of 5-FU in wtTP53/highMDM4 human colon (HCT116 and LoVo) and gastric (SNU-1 and NUGC-4) cancer cells. Fluorouracil 197-201 MDM4 regulator of p53 Homo sapiens 22-26 30488540-7 2019 As p53-MDM2 forms a negative feedback loop, enhancement of the antitumor effect of 5-FU by MDM4/MDM2 double knockdown could be attributed to blocking of the feedback mechanism in addition to direct suppression of these p53 antagonists. Fluorouracil 83-87 MDM4 regulator of p53 Homo sapiens 91-95 30488540-8 2019 Intratumor injection of the MDM4/MDM2 siRNAs suppressed in vivo tumor growth and boosted the antitumor effect of 5-FU in an athymic mouse xenograft model using HCT116 cells. Fluorouracil 113-117 transformed mouse 3T3 cell double minute 2 Mus musculus 33-37 30583087-4 2019 In this study we have shown that the increase in exogenous IL-1alpha signaling increases chemosensitivity of both chemosensitive and chemoresistant colorectal cancer cell lines, treated with a widely used cytotoxic antimetabolite 5-fluorouracil (5-FU). Fluorouracil 230-244 interleukin 1 alpha Homo sapiens 59-68 30583087-4 2019 In this study we have shown that the increase in exogenous IL-1alpha signaling increases chemosensitivity of both chemosensitive and chemoresistant colorectal cancer cell lines, treated with a widely used cytotoxic antimetabolite 5-fluorouracil (5-FU). Fluorouracil 246-250 interleukin 1 alpha Homo sapiens 59-68 30226808-6 2019 The levels of LINC00261 were reduced among the cancerous tissues obtained from patients exhibiting resistance to 5-FU. Fluorouracil 113-117 long intergenic non-protein coding RNA 261 Homo sapiens 14-23 34552494-7 2021 In this study, murine CRC cells (CT26) and a murine model of CRC were used to examine the anti-tumor properties of ABP and explore the mechanism underlying the synergistic interactions between ABP and 5-FU. Fluorouracil 201-205 amine oxidase, copper-containing 1 Mus musculus 193-196 34552494-12 2021 Together, these data suggest that ABP exhibits anti-neoplastic activity and can effectively enhance the efficacy of 5-FU in CRC treatment. Fluorouracil 116-120 amine oxidase, copper-containing 1 Mus musculus 34-37 30226808-7 2019 Overexpression of LINC00261 was determined to dramatically inhibit proliferation and resistance to apoptosis among 5-FU-resistant TE-1 and -5 cells, whereas silencing of LINC00261 was determined to enhance proliferation and resistance to apoptosis among the TE-1 and -5 cells. Fluorouracil 115-119 long intergenic non-protein coding RNA 261 Homo sapiens 18-27 34659526-9 2021 RUNX1 enhanced CRC cell resistance to 5-fluorouracil (5-FU), promoted proliferation, and inhibited 5-FU-induced apoptosis. Fluorouracil 38-52 RUNX family transcription factor 1 Homo sapiens 0-5 30226808-8 2019 DPYD, a confirmed target of LINC00261, displayed a greater incidence of DNA methylation among patient"s sensitive to 5-FU. Fluorouracil 117-121 long intergenic non-protein coding RNA 261 Homo sapiens 28-37 34659526-9 2021 RUNX1 enhanced CRC cell resistance to 5-fluorouracil (5-FU), promoted proliferation, and inhibited 5-FU-induced apoptosis. Fluorouracil 54-58 RUNX family transcription factor 1 Homo sapiens 0-5 30226808-9 2019 A key finding revealed that overexpressed LINC00261 could increase the methylation of the DPYD promoter through the recruitment of DNA methyltransferase (DNMT), which, in turn, acts to decrease DPYD activity in 5-FU-resistant TE-1 cells, whereas a reversible change was recorded once the demethylation reagent 5-aza-2"-deoxyctidine was employed to treat the 5-FU-resistant TE-1 cells. Fluorouracil 211-215 long intergenic non-protein coding RNA 261 Homo sapiens 42-51 34659526-9 2021 RUNX1 enhanced CRC cell resistance to 5-fluorouracil (5-FU), promoted proliferation, and inhibited 5-FU-induced apoptosis. Fluorouracil 99-103 RUNX family transcription factor 1 Homo sapiens 0-5 30226808-9 2019 A key finding revealed that overexpressed LINC00261 could increase the methylation of the DPYD promoter through the recruitment of DNA methyltransferase (DNMT), which, in turn, acts to decrease DPYD activity in 5-FU-resistant TE-1 cells, whereas a reversible change was recorded once the demethylation reagent 5-aza-2"-deoxyctidine was employed to treat the 5-FU-resistant TE-1 cells. Fluorouracil 358-362 long intergenic non-protein coding RNA 261 Homo sapiens 42-51 34097885-5 2021 RESULTS: 5FU-EGFR-aptamers reduced proliferation in a concentration-dependent manner in mouse and human pancreatic cancer cell lines. Fluorouracil 9-12 epidermal growth factor receptor Mus musculus 13-17 30226808-10 2019 Taken together, the results of the study provided evidence emphasizing the distinct antitumor ability of LINC00261 in cases of esophageal cancer, which was manifested by overexpression of LINC00261 detected to increase the sensitivity of human esophageal cancer cells to 5-FU by mediating methylation-dependent repression of DPYD. Fluorouracil 271-275 long intergenic non-protein coding RNA 261 Homo sapiens 105-114 34097885-10 2021 CONCLUSION: Tumor-specific targeted delivery of 5FU using EGFR-aptamers as carrier achieved high target specificity, overcame 5FU resistance, proved to be effective in a syngeneic orthotopic transplantation model, in KPC mice, in a CDX model as well as PDOs and therefore represents a promising backbone for pancreatic cancer chemotherapy in patients. Fluorouracil 48-51 epidermal growth factor receptor Mus musculus 58-62 30226808-10 2019 Taken together, the results of the study provided evidence emphasizing the distinct antitumor ability of LINC00261 in cases of esophageal cancer, which was manifested by overexpression of LINC00261 detected to increase the sensitivity of human esophageal cancer cells to 5-FU by mediating methylation-dependent repression of DPYD. Fluorouracil 271-275 long intergenic non-protein coding RNA 261 Homo sapiens 188-197 34389694-3 2021 We found that elevated expression of cIAP1 and cIAP2 (but not XIAP) significantly correlated with poor prognosis in patients with microsatellite stable (MSS) stage III colorectal cancer treated with 5-fluorouracil (5FU)-based adjuvant chemotherapy, suggesting their involvement in promoting chemoresistance. Fluorouracil 199-213 baculoviral IAP repeat containing 3 Homo sapiens 47-52 30531622-8 2019 Through this analysis, the authors found a set of genes, including YAP1 and CCL-2, whose expression changes predict 5-fluorouracil therapy status and include genes that have not previously been associated with keloid biology and are of unknown function. Fluorouracil 116-130 C-C motif chemokine ligand 2 Homo sapiens 76-81 34389694-3 2021 We found that elevated expression of cIAP1 and cIAP2 (but not XIAP) significantly correlated with poor prognosis in patients with microsatellite stable (MSS) stage III colorectal cancer treated with 5-fluorouracil (5FU)-based adjuvant chemotherapy, suggesting their involvement in promoting chemoresistance. Fluorouracil 215-218 baculoviral IAP repeat containing 3 Homo sapiens 47-52 30465515-0 2019 Single-chain Antibody Against Reg4 Suppresses Gastric Cancer Cell Growth and Enhances 5-FU-induced Cell Death in vitro. Fluorouracil 86-90 regenerating family member 4 Homo sapiens 30-34 30465515-2 2019 Pathological hyper-expression or artificial over-expression of Reg4 causes acceleration of tumor growth, migration, and resistance to chemotherapeutic 5-Fluorouracil (5-FU). Fluorouracil 151-165 regenerating family member 4 Homo sapiens 63-67 30465515-2 2019 Pathological hyper-expression or artificial over-expression of Reg4 causes acceleration of tumor growth, migration, and resistance to chemotherapeutic 5-Fluorouracil (5-FU). Fluorouracil 167-171 regenerating family member 4 Homo sapiens 63-67 30465515-12 2019 CONCLUSION: The single-chain antibody (scFv-Reg4) significantly inhibited gastric cancer cell proliferation and synergistically enhanced the lethal effect of 5-FU. Fluorouracil 158-162 regenerating family member 4 Homo sapiens 44-48 30342137-4 2019 Additionally, a strength effect was also observed in regulating immune function of GP11 and 5-Fu simultaneous administration, such as enhancing serum interleukin-2 (IL-2) and tumor necrosis factor-alpha (TNF-alpha) secretion, and increasing immune organs weights. Fluorouracil 92-96 interleukin 2 Mus musculus 150-163 30342137-4 2019 Additionally, a strength effect was also observed in regulating immune function of GP11 and 5-Fu simultaneous administration, such as enhancing serum interleukin-2 (IL-2) and tumor necrosis factor-alpha (TNF-alpha) secretion, and increasing immune organs weights. Fluorouracil 92-96 interleukin 2 Mus musculus 165-169 30806287-2 2019 MSI is a good predictor for efficacy of 5-fluorouracil (FU)-based chemotherapy in the treatment of colorectal cancer. Fluorouracil 40-54 RB binding protein 4, chromatin remodeling factor Homo sapiens 0-3 30806287-4 2019 However, other studies suggest that high-frequency MSI (MSI-H) status reduced survival in patients receiving 5-FU-based adjuvant chemotherapy. Fluorouracil 109-113 RB binding protein 4, chromatin remodeling factor Homo sapiens 51-54 30806287-5 2019 Thus, the correlation between MSI status and efficacy of 5-FU-based adjuvant chemotherapy for gastric cancer remains controversial. Fluorouracil 57-61 RB binding protein 4, chromatin remodeling factor Homo sapiens 30-33 30806287-6 2019 We performed a PubMed, Embase, and Cochrane search to retrieve studies that explore the correlation between MSI status and 5-FU-based adjuvant chemotherapy efficacy in gastric cancer. Fluorouracil 123-127 RB binding protein 4, chromatin remodeling factor Homo sapiens 108-111 30806287-14 2019 Although MSI can effectively predict efficacy of 5-FU-based chemotherapy in patients with colorectal cancer, the correlation between MSI status and efficacy of 5-FU-based adjuvant chemotherapy for gastric cancer remains controversial. Fluorouracil 160-164 RB binding protein 4, chromatin remodeling factor Homo sapiens 133-136 30207288-0 2018 Early disease relapse in a patient with colorectal cancer who harbors genetic variants of DPYD, TYMS, MTHFR and DHFR after treatment with 5-fluorouracil-based chemotherapy. Fluorouracil 138-152 thymidylate synthetase Homo sapiens 96-100 30207288-0 2018 Early disease relapse in a patient with colorectal cancer who harbors genetic variants of DPYD, TYMS, MTHFR and DHFR after treatment with 5-fluorouracil-based chemotherapy. Fluorouracil 138-152 dihydrofolate reductase Homo sapiens 112-116 30538221-2 2018 Development of 5-FU resistance is associated with elevated expression of its cellular target, thymidylate synthase (TYMS). Fluorouracil 15-19 thymidylate synthetase Homo sapiens 94-114 34603888-5 2021 We present a case of a 47-year-old Caucasian female with rectal SCC who is under remission for two years after being treated with upfront chemoradiation with mitomycin and 5-fluorouracil (5-FU). Fluorouracil 172-186 serpin family B member 3 Homo sapiens 64-67 34603888-5 2021 We present a case of a 47-year-old Caucasian female with rectal SCC who is under remission for two years after being treated with upfront chemoradiation with mitomycin and 5-fluorouracil (5-FU). Fluorouracil 188-192 serpin family B member 3 Homo sapiens 64-67 34422665-0 2021 ARTEMIN Promotes Oncogenicity and Resistance to 5-Fluorouracil in Colorectal Carcinoma by p44/42 MAPK Dependent Expression of CDH2. Fluorouracil 48-62 artemin Homo sapiens 0-7 34422665-5 2021 Forced expression of ARTN reduced the sensitivity of CRC cells to 5-FU treatment; and 5-FU resistant CRC cells harbored enhanced expression of ARTN. Fluorouracil 66-70 artemin Homo sapiens 21-25 34422665-5 2021 Forced expression of ARTN reduced the sensitivity of CRC cells to 5-FU treatment; and 5-FU resistant CRC cells harbored enhanced expression of ARTN. Fluorouracil 86-90 artemin Homo sapiens 143-147 34452150-3 2021 5-FU activity leads to caspase-1 activation, secretion and maturation of interleukins (IL)-1, IL-18 and reactive oxygen species (ROS) generation. Fluorouracil 0-4 interleukin 1 alpha Homo sapiens 73-92 34367280-11 2021 We also found that downregulation of ECT2 increased 5-FU sensitivity in GC cells by downregulating P-gp, MRP1, and Bcl-2. Fluorouracil 52-56 phosphoglycolate phosphatase Homo sapiens 99-103 34360807-7 2021 In Caco-2 cells, LMWF enhanced the suppressive effects of 5-FU on cell viability through both the c-mesenchymal-epithelial transition (MET)/Kirsten rat sarcoma virus (KRAS)/extracellular signal-regulated kinase (ERK) and the c-MET/phosphatidyl-inositol 3-kinases (PI3K)/protein kinase B (AKT) signaling pathways. Fluorouracil 58-62 SAFB like transcription modulator Homo sapiens 135-138 34309458-9 2022 The increase in p53, Bax, p38 MAPK, and PTEN gene expression levels compared to the control group was 1.71, 1.42, 3.26, and 3.29-fold with 5-FU + L treatment, respectively, while this increase was 8.43, 1.65, 3.55, and 3.54-fold with 5-FU + Q treatment, respectively. Fluorouracil 139-143 phosphatase and tensin homolog Homo sapiens 40-44 34309458-9 2022 The increase in p53, Bax, p38 MAPK, and PTEN gene expression levels compared to the control group was 1.71, 1.42, 3.26, and 3.29-fold with 5-FU + L treatment, respectively, while this increase was 8.43, 1.65, 3.55, and 3.54-fold with 5-FU + Q treatment, respectively. Fluorouracil 234-238 phosphatase and tensin homolog Homo sapiens 40-44 34281530-11 2021 In the terms of mechanism, miR-216b could be sponged by circFBXL5, and its inhibitor could also reverse the influence of circFBXL5 silencing on the 5-FU resistance of breast cancer cells. Fluorouracil 148-152 microRNA 216b Homo sapiens 27-35 34281530-12 2021 In addition, HMGA2 was a target of miR-216b, and its overexpression also reversed the regulation of miR-216b overexpression on the 5-FU resistance of breast cancer. Fluorouracil 131-135 high mobility group AT-hook 2 Homo sapiens 13-18 34281530-12 2021 In addition, HMGA2 was a target of miR-216b, and its overexpression also reversed the regulation of miR-216b overexpression on the 5-FU resistance of breast cancer. Fluorouracil 131-135 microRNA 216b Homo sapiens 35-43 34281530-12 2021 In addition, HMGA2 was a target of miR-216b, and its overexpression also reversed the regulation of miR-216b overexpression on the 5-FU resistance of breast cancer. Fluorouracil 131-135 microRNA 216b Homo sapiens 100-108 34281530-14 2021 CONCLUSION: Our data showed that circFBXL5 could promote the 5-FU resistance of breast cancer by regulating miR-216b/HMGA2 axis. Fluorouracil 61-65 microRNA 216b Homo sapiens 108-116 34359989-8 2021 The potential effects of OPN isoforms on cisplatin and 5-Fu were evaluated by detecting cellular reactive oxygen species (ROS) levels in the HGC-27-derived cell lines. Fluorouracil 55-59 secreted phosphoprotein 1 Homo sapiens 25-28 34589581-0 2021 Targeting EGFR sensitizes 5-Fu-resistant colon cancer cells through modification of the lncRNA-FGD5-AS1-miR-330-3p-Hexokinase 2 axis. Fluorouracil 26-30 microRNA 330 Homo sapiens 104-111 34589581-9 2021 Rescue experiments demonstrated that FGD5-AS1 promotes glycolysis through modulating the miR-330-3p-HK2 axis, leading to 5-Fu resistance of CRC cancer cells. Fluorouracil 121-125 microRNA 330 Homo sapiens 89-96 34276810-2 2021 Genetic mutations in two major metabolizing enzymes for 5-FU; dihydropyrimidine dehydrogenase (DPYD and thymidylate synthetase (TYMS), have been associated with clinical response and toxicity. Fluorouracil 56-60 thymidylate synthetase Homo sapiens 104-126 34276810-2 2021 Genetic mutations in two major metabolizing enzymes for 5-FU; dihydropyrimidine dehydrogenase (DPYD and thymidylate synthetase (TYMS), have been associated with clinical response and toxicity. Fluorouracil 56-60 thymidylate synthetase Homo sapiens 128-132 34276810-14 2021 Conclusions: Molecular testing for DPYD and TYMS genes can allow us to identify patients who are most likely to respond or face severe toxicity to 5-FU in a potentially curable cancer. Fluorouracil 147-151 thymidylate synthetase Homo sapiens 44-48 30538221-2 2018 Development of 5-FU resistance is associated with elevated expression of its cellular target, thymidylate synthase (TYMS). Fluorouracil 15-19 thymidylate synthetase Homo sapiens 116-120 30538221-5 2018 In agreement, RT-qPCR and western blot analyses of four human CCA cell lines at the baseline level and in response to high doses of 5-FU revealed good correlations between FOXM1 and TYMS expression in the CCA cell lines tested, except for the highly 5-FU-resistant HuCCA cells. Fluorouracil 132-136 thymidylate synthetase Homo sapiens 182-186 30538221-7 2018 Interestingly, silencing of TYMS sensitized both KKU-D131 and HuCCA to 5-FU treatment, suggesting that resistance to very high levels of 5-FU is due to the inability of the genotoxic sensor FOXM1 to modulate TYMS expression. Fluorouracil 71-75 thymidylate synthetase Homo sapiens 28-32 30538221-7 2018 Interestingly, silencing of TYMS sensitized both KKU-D131 and HuCCA to 5-FU treatment, suggesting that resistance to very high levels of 5-FU is due to the inability of the genotoxic sensor FOXM1 to modulate TYMS expression. Fluorouracil 137-141 thymidylate synthetase Homo sapiens 28-32 30155759-0 2018 Enhancing 5-fluorouracil efficacy through suppression of PKM2 in colorectal cancer cells. Fluorouracil 10-24 pyruvate kinase M1/2 Homo sapiens 57-61 30155759-4 2018 Here, the role of PKM2 in the anticancer efficacy of 5-fluorouracil (5-FU) was evaluated in colorectal cancer (CRC). Fluorouracil 53-67 pyruvate kinase M1/2 Homo sapiens 18-22 34128315-6 2021 However, when treated with 5-FU, CHOP deficiency resulted in higher survival rates, associated with an increased number of HSCs and reduced level of apoptosis. Fluorouracil 27-31 DNA-damage inducible transcript 3 Mus musculus 33-37 34564977-0 2021 RNF38 enhances 5-Fluorouracil resistance in colorectal cancer by activating the Wnt pathway. Fluorouracil 15-29 ring finger protein 38 Homo sapiens 0-5 34564977-6 2021 The roles of RNF38 and Wnt signaling in 5-FU-resistant CRC were further illustrated. Fluorouracil 40-44 ring finger protein 38 Homo sapiens 13-18 34564977-9 2021 Next, the regulatory effect of RNF38 on 5-FU resistance in CRC was mainly explored. Fluorouracil 40-44 ring finger protein 38 Homo sapiens 31-36 34564977-15 2021 CONCLUSIONS: Overexpression of RNF38 enhanced 5-FU resistance in CRC. Fluorouracil 46-50 ring finger protein 38 Homo sapiens 31-36 34564977-16 2021 Furthermore, Wnt signaling was activated by RNF38 and involved in 5-FU resistance in CRC. Fluorouracil 66-70 ring finger protein 38 Homo sapiens 44-49 34279763-4 2021 METHODS AND RESULTS: According to our MTT assay results, Resveratrol (RSV), Nutlin3a and Suramin was found to be more effective in HCT-116 p53+/+ cells and these differences were evaluated together with the effect of 5-FU on the SIRT5, FOXO3a and Bim protein expressions in HCT-116 p53 +/+ and HCT-116 p53 -/- cells. Fluorouracil 217-221 BCL2 like 11 Homo sapiens 247-250 34893156-7 2021 The polymorphism rs1695 of the GSTP1 gene has been associated with the effectiveness and toxicity of fluorouracil, cyclophosphamide and epirubicin therapy. Fluorouracil 101-113 glutathione S-transferase pi 1 Homo sapiens 31-36 34100299-0 2021 Gender-dependent association of TYMS-TSER polymorphism with 5-fluorouracil or capecitabine based chemotherapy toxicity. Fluorouracil 60-74 thymidylate synthetase Homo sapiens 32-36 34100299-1 2021 Aim: TYMS gene encodes for TS enzyme involved in 5-fluorouracil (5-FU) and capecitabine (CAP) metabolism. Fluorouracil 49-63 thymidylate synthetase Homo sapiens 5-9 34100299-1 2021 Aim: TYMS gene encodes for TS enzyme involved in 5-fluorouracil (5-FU) and capecitabine (CAP) metabolism. Fluorouracil 65-69 thymidylate synthetase Homo sapiens 5-9 34100299-2 2021 This study assessed the association of TYMS-TSER and 3RG>C polymorphisms with 5-FU/CAP adverse event (AE) incidence. Fluorouracil 78-82 thymidylate synthetase Homo sapiens 39-43 34100299-3 2021 Materials & methods: TYMS-TSER and 3RG>C polymorphisms were analyzed by use of PCR/PCR-RFLP in 313 5-FU/CAP-treated cancer patients. Fluorouracil 99-103 thymidylate synthetase Homo sapiens 21-25 34100299-4 2021 Results: Female TYMS-TSER 2R carriers were at increased risk for 5-FU/CAP AEs (odds ratio: 2.195; p = 0.032). Fluorouracil 65-69 thymidylate synthetase Homo sapiens 16-20 34170813-7 2022 TQ was found to be more effective in increasing and BAX/BCL-2 ratio), while 5-FU was more effective in inhibiting thymidylate synthase. Fluorouracil 76-80 thymidylate synthetase Homo sapiens 114-134 34257696-0 2021 Erteng-Sanjie Capsule Enhances Chemosensitivity of 5-Fluorouracil in Tumor-Bearing Nude Mice with Gastric Cancer by Inhibiting Notch1/Hes1 Signaling Pathway. Fluorouracil 51-65 notch 1 Mus musculus 127-133 34257696-14 2021 In conclusion, the findings of the study showed that ETSJC improved the chemosensitivity of 5-FU by blocking Notch1/Hes1 signaling pathway in gastric cancer-bearing mice. Fluorouracil 92-96 notch 1 Mus musculus 109-115 34168463-7 2021 Results: Both 5-Fu and CDDP result in the apoptosis of A549 and NCI-H226 cells and improve the expressions of has-miR-134 and has-miR-296. Fluorouracil 14-18 microRNA 296 Homo sapiens 130-137 34168463-8 2021 However, 5-Fu enhances the expression of OCT3/4 in A549 cells, and the change of methyltransferase genes and BSP results suggested some genetic differences between CDDP and 5-Fu treatment in A549 cells. Fluorouracil 9-13 POU class 5 homeobox 1 Homo sapiens 41-47 34168463-8 2021 However, 5-Fu enhances the expression of OCT3/4 in A549 cells, and the change of methyltransferase genes and BSP results suggested some genetic differences between CDDP and 5-Fu treatment in A549 cells. Fluorouracil 173-177 POU class 5 homeobox 1 Homo sapiens 41-47 34168463-11 2021 The enrichment of A549 lung cancer stem cells with 5-Fu might be related to the methylation of OCT3/4 promoter and the expression of H3K9Me3 and H3K9Ace. Fluorouracil 51-55 POU class 5 homeobox 1 Homo sapiens 95-101 30155759-4 2018 Here, the role of PKM2 in the anticancer efficacy of 5-fluorouracil (5-FU) was evaluated in colorectal cancer (CRC). Fluorouracil 69-73 pyruvate kinase M1/2 Homo sapiens 18-22 30155759-7 2018 A CRC subcutaneous tumor model was performed to investigate the effect of PKM2 inhibition on 5-FU efficacy in vivo. Fluorouracil 93-97 pyruvate kinase M1/2 Homo sapiens 74-78 29948238-1 2018 BACKGROUND: The efficacy of primary prophylactic granulocyte colony-stimulating factor (G-CSF) in preventing febrile neutropenia (FN) in patients treated with docetaxel, cisplatin, and 5-fluorouracil (TPF) chemotherapy remains controversial. Fluorouracil 185-199 colony stimulating factor 3 Homo sapiens 49-86 34199777-3 2021 Using an in vitro model, we demonstrated that HO-1 overexpression regulates stemness and resistance to 5-FU treatment, regardless of p53. Fluorouracil 103-107 heme oxygenase 1 Homo sapiens 46-50 29948238-1 2018 BACKGROUND: The efficacy of primary prophylactic granulocyte colony-stimulating factor (G-CSF) in preventing febrile neutropenia (FN) in patients treated with docetaxel, cisplatin, and 5-fluorouracil (TPF) chemotherapy remains controversial. Fluorouracil 185-199 colony stimulating factor 3 Homo sapiens 88-93 31949649-13 2018 Additionally, cell invasion was promoted by miR-106a-5p overexpression in the HT-29 cells and was inhibited by miR-106a-5p knockdown in the 5-FU resistant HT-29 cells; miR-106a-5p overexpression contributed to migration by increasing vimentin expression and by decreasing E-cadherin expression in the HT-29 cells; miR-106a-5p functioned by directly binding to TGFbetaR2. Fluorouracil 140-144 microRNA 106a Homo sapiens 111-119 31949649-16 2018 CONCLUSION: The up-regulation of miR-106a-5p contributes to the pathomechanism of colorectal cancer by promoting 5-FU resistance and metastasis via inhibiting target TGFbetaR2. Fluorouracil 113-117 microRNA 106a Homo sapiens 33-41 31949649-17 2018 Our findings provide new promising ways for the clinical application of the TGFbetaR2-miR-106a axis in clinical chemotherapy for 5-FU resistant colorectal cancer. Fluorouracil 129-133 microRNA 106a Homo sapiens 86-94 30010221-0 2018 Targeting glypican-4 overcomes 5-FU resistance and attenuates stem cell-like properties via suppression of Wnt/beta-catenin pathway in pancreatic cancer cells. Fluorouracil 31-35 glypican 4 Homo sapiens 10-20 30010221-4 2018 In this study, we are the first to demonstrate that GPC4 was involved in 5-fluorouracil (5-FU) resistance and pancreatic cancer stemness through comprehensive bioinformatical analysis. Fluorouracil 73-87 glypican 4 Homo sapiens 52-56 30010221-4 2018 In this study, we are the first to demonstrate that GPC4 was involved in 5-fluorouracil (5-FU) resistance and pancreatic cancer stemness through comprehensive bioinformatical analysis. Fluorouracil 89-93 glypican 4 Homo sapiens 52-56 30010221-5 2018 Functional experiments showed that knockdown of GPC4 sensitized pancreatic cancer cells to 5-FU and attenuated stem cell-like properties. Fluorouracil 91-95 glypican 4 Homo sapiens 48-52 30011079-0 2018 Effect of 5-fluorouracil on excision repair cross-complementing 1 expression and consequent cytotoxicity regulation in human gastric cancer cells. Fluorouracil 10-24 ERCC excision repair 1, endonuclease non-catalytic subunit Homo sapiens 28-65 30011079-5 2018 Thus, this study was aimed to investigate whether ERCC1 expression could be regulated, and its role in gastric cancer cells treated with 5-FU and the underlying mechanism. Fluorouracil 137-141 ERCC excision repair 1, endonuclease non-catalytic subunit Homo sapiens 50-55 30011079-7 2018 It was shown that ERCC1 expression could be upregulated in AGS cells treated with 5-FU and this upregulation could subsequently attenuate the cytotoxicity of 5-FU in AGS cells. Fluorouracil 82-86 ERCC excision repair 1, endonuclease non-catalytic subunit Homo sapiens 18-23 30011079-7 2018 It was shown that ERCC1 expression could be upregulated in AGS cells treated with 5-FU and this upregulation could subsequently attenuate the cytotoxicity of 5-FU in AGS cells. Fluorouracil 158-162 ERCC excision repair 1, endonuclease non-catalytic subunit Homo sapiens 18-23 30011079-8 2018 Moreover, 5-FU-upregulated ERCC1 expression was regulated by extracellular signal-regulated kinase (ERK) 1/2 and p38 signaling through activating the transcription factor c-jun/activator protein (AP)-1. Fluorouracil 10-14 ERCC excision repair 1, endonuclease non-catalytic subunit Homo sapiens 27-32 30011079-9 2018 These results indicated the role of ERCC1 in the development of drug resistance to 5-FU in AGS cells. Fluorouracil 83-87 ERCC excision repair 1, endonuclease non-catalytic subunit Homo sapiens 36-41 30305667-4 2018 In previous work, we demonstrated that either Lactococcus lactis NZ9000 or a recombinant strain expressing an antimicrobial peptide involved in human gut homeostasis, the Pancreatitis-associated Protein (PAP), could ameliorate 5-FU-induced mucositis in mice. Fluorouracil 227-231 regenerating family member 3 alpha Homo sapiens 171-202 34205990-3 2021 However, the efficacy of 5-FU is limited by drug resistance, and bone marrow toxicity through high-level expression of thymidylate synthase, justifying the need for improvement of the therapeutic index. Fluorouracil 25-29 thymidylate synthetase Homo sapiens 119-139 30305667-4 2018 In previous work, we demonstrated that either Lactococcus lactis NZ9000 or a recombinant strain expressing an antimicrobial peptide involved in human gut homeostasis, the Pancreatitis-associated Protein (PAP), could ameliorate 5-FU-induced mucositis in mice. Fluorouracil 227-231 regenerating family member 3 alpha Homo sapiens 204-207 30305667-9 2018 We conclude the strain secreting antimicrobial PAP was more effective in the control of 5-FU-dysbiosis. Fluorouracil 88-92 regenerating family member 3 alpha Homo sapiens 47-50 29390193-0 2018 Knockdown of aquaporin-5 sensitizes colorectal cancer cells to 5-fluorouracil via inhibition of the Wnt-beta-catenin signaling pathway. Fluorouracil 63-77 aquaporin 5 Homo sapiens 13-24 29390193-3 2018 Hence, this study investigated the effect of AQP5 silencing in CRC cells on 5-fluorouracil (5-FU) sensitivity and attempted to elucidate the underlying mechanisms. Fluorouracil 76-90 aquaporin 5 Homo sapiens 45-49 29390193-3 2018 Hence, this study investigated the effect of AQP5 silencing in CRC cells on 5-fluorouracil (5-FU) sensitivity and attempted to elucidate the underlying mechanisms. Fluorouracil 92-96 aquaporin 5 Homo sapiens 45-49 29390193-7 2018 The results showed that silencing of AQP5 increased the chemosensitivity of CRC cells to 5-FU, facilitated 5-FU-mediated apoptosis, suppressed tumor growth, and reduced 5-FU chemoresistance in vivo. Fluorouracil 89-93 aquaporin 5 Homo sapiens 37-41 29390193-7 2018 The results showed that silencing of AQP5 increased the chemosensitivity of CRC cells to 5-FU, facilitated 5-FU-mediated apoptosis, suppressed tumor growth, and reduced 5-FU chemoresistance in vivo. Fluorouracil 107-111 aquaporin 5 Homo sapiens 37-41 29390193-7 2018 The results showed that silencing of AQP5 increased the chemosensitivity of CRC cells to 5-FU, facilitated 5-FU-mediated apoptosis, suppressed tumor growth, and reduced 5-FU chemoresistance in vivo. Fluorouracil 107-111 aquaporin 5 Homo sapiens 37-41 29390193-10 2018 Taken together, these results suggest that AQP5 silencing enhances the sensitivity of CRC cells to 5-FU, and the underlying mechanism is related to inhibition of the Wnt-beta-catenin pathway. Fluorouracil 99-103 aquaporin 5 Homo sapiens 43-47 30510364-2 2018 5-FU acts by inhibiting thymidylate synthase (TS), and high levels of TS correlate with resistance to treatment with fluoropyrimidines. Fluorouracil 0-4 thymidylate synthetase Homo sapiens 24-44 30510364-2 2018 5-FU acts by inhibiting thymidylate synthase (TS), and high levels of TS correlate with resistance to treatment with fluoropyrimidines. Fluorouracil 0-4 thymidylate synthetase Homo sapiens 46-48 30510364-3 2018 The aim of this study was to evaluate the expression of TS in GC patients, and its relation with clinicopathological characteristics and prognosis in adjuvant chemotherapy with 5-FU. Fluorouracil 177-181 thymidylate synthetase Homo sapiens 56-58 30510364-12 2018 In survival analysis, TS-high was associated with worse disease-free survival (DFS) in stage III GC patients who received 5-FU-based chemotherapy (P=0.007). Fluorouracil 122-126 thymidylate synthetase Homo sapiens 22-24 30250581-4 2018 The present study aimed to investigate the effect of miR-1260b inhibitor on CRC cells, and their chemosensitivity to 5-FU, by treating them with the miR-1260b inhibitor. Fluorouracil 117-121 microRNA 1260b Homo sapiens 149-158 30250581-9 2018 Notably, miR-1260b inhibitor could significantly enhanced the chemoresponse of HCT116 cells to 5-FU via reduced proliferation, increased apoptosis, and downregulation of PDCD4, p-Akt and p-ERK protein expression. Fluorouracil 95-99 microRNA 1260b Homo sapiens 9-18 30250581-9 2018 Notably, miR-1260b inhibitor could significantly enhanced the chemoresponse of HCT116 cells to 5-FU via reduced proliferation, increased apoptosis, and downregulation of PDCD4, p-Akt and p-ERK protein expression. Fluorouracil 95-99 eukaryotic translation initiation factor 2 alpha kinase 3 Homo sapiens 187-192 34094932-0 2021 HOXA13, Negatively Regulated by miR-139-5p, Decreases the Sensitivity of Gastric Cancer to 5-Fluorouracil Possibly by Targeting ABCC4. Fluorouracil 91-105 homeobox A13 Homo sapiens 0-6 30250224-5 2018 Additionally, in vivo and in vitro studies showed that depleting PGAM5 expression inhibited tumor growth and increased the 5-fluorouracil sensitivity of HCC cells. Fluorouracil 123-137 PGAM family member 5, mitochondrial serine/threonine protein phosphatase Homo sapiens 65-70 34094932-5 2021 The Kaplan-Meier plotter database was mined for prognosis analysis of GC patients with different HOXA13 expression receiving 5-Fluorouracil (5-FU) therapy. Fluorouracil 125-139 homeobox A13 Homo sapiens 97-103 34094932-5 2021 The Kaplan-Meier plotter database was mined for prognosis analysis of GC patients with different HOXA13 expression receiving 5-Fluorouracil (5-FU) therapy. Fluorouracil 141-145 homeobox A13 Homo sapiens 97-103 30250224-6 2018 Conversely, restoring PGAM5 expression in PGAM5-knockdown cells dramatically enhanced HCC cell resistance to 5-fluorouracil. Fluorouracil 109-123 PGAM family member 5, mitochondrial serine/threonine protein phosphatase Homo sapiens 22-27 34094932-6 2021 The effects of HOXA13 on sensitivity of GC cells to 5-FU were investigated by Cell Counting Kit-8 (CCK-8), 5-Ethynyl-2"-deoxyuridine (EdU) incorporation, flow cytometry and experiment in vivo. Fluorouracil 52-56 homeobox A13 Homo sapiens 15-21 34094932-7 2021 RNA-Sequencing analysis was performed to explore the underlying mechanism of HOXA13-mediated 5-FU resistance in GC. Fluorouracil 93-97 homeobox A13 Homo sapiens 77-83 30250224-6 2018 Conversely, restoring PGAM5 expression in PGAM5-knockdown cells dramatically enhanced HCC cell resistance to 5-fluorouracil. Fluorouracil 109-123 PGAM family member 5, mitochondrial serine/threonine protein phosphatase Homo sapiens 42-47 34094932-10 2021 Results: HOXA13 was upregulated in GC and its high expression was associated with poor prognosis of GC patients with 5-FU treatment. Fluorouracil 117-121 homeobox A13 Homo sapiens 9-15 30250224-7 2018 Importantly, we demonstrated that the mechanism of 5-fluorouracil resistance conferred to HCC cells by PGAM5 was via inhibiting BAX- and cytochrome C-mediated apoptotic signaling by interacting and stabilizing Bcl-xL. Fluorouracil 51-65 PGAM family member 5, mitochondrial serine/threonine protein phosphatase Homo sapiens 103-108 34094932-11 2021 Overexpression of HOXA13 impaired the inhibitory effects of 5-FU on GC cells proliferation in vitro and vivo, and knockdown of HOXA13 exacerbated 5-FU-induced GC cells apoptosis. Fluorouracil 60-64 homeobox A13 Homo sapiens 18-24 30345013-3 2018 In patients with pN1 and pT1-pT3 tumors, 3 months of treatment with 5-fluorouracil and oxaliplatin is comparable with respect to 3-year survival rate to 6 months of treatment. Fluorouracil 68-82 zinc finger protein 77 Homo sapiens 25-28 34094932-11 2021 Overexpression of HOXA13 impaired the inhibitory effects of 5-FU on GC cells proliferation in vitro and vivo, and knockdown of HOXA13 exacerbated 5-FU-induced GC cells apoptosis. Fluorouracil 146-150 homeobox A13 Homo sapiens 127-133 34094932-12 2021 Mechanistically, HOXA13, directly targeted by miR-139-5p in GC, might upregulate ABCC4 expression, thereby accentuating 5-FU resistance of GC cells. Fluorouracil 120-124 homeobox A13 Homo sapiens 17-23 34094932-13 2021 Conclusion: Our study suggests that HOXA13 attenuates 5-FU sensitivity of GC possibly by upregulating ABCC4. Fluorouracil 54-58 homeobox A13 Homo sapiens 36-42 30250641-12 2018 Resveratrol and 5-FU treatments inhibited STAT3 phosphorylation and its binding to the promoter region of human telomerase reverse transcriptase (hTERT). Fluorouracil 16-20 telomerase reverse transcriptase Homo sapiens 112-144 34067869-8 2021 5FU reduced the expression of the key cytoskeletal proteins, desmin and dystrophin, which was not prevented by BGP-15. Fluorouracil 0-3 desmin Mus musculus 61-67 30250641-12 2018 Resveratrol and 5-FU treatments inhibited STAT3 phosphorylation and its binding to the promoter region of human telomerase reverse transcriptase (hTERT). Fluorouracil 16-20 telomerase reverse transcriptase Homo sapiens 146-151 30068336-10 2018 Further studies where colorectal cancer (CRC) cells were subjected to 5-fluorouracil (5FU) treatment revealed a sharp increase in MASTL expression upon chemotherapy, along with increases in Bcl-xL and Survivin expression. Fluorouracil 70-84 microtubule associated serine/threonine kinase like Homo sapiens 130-135 34981469-9 2021 The expression levels of all tested genes were altered in all treatment groups compared to the control, with that of WNT1, CTNNB1, TCF, MTOR, AKT1, BIRC5, and CCND1 showing the most robust changes in the combined curcumin/berberine/5-FU treatment. Fluorouracil 232-236 catenin beta 1 Homo sapiens 123-129 30068336-10 2018 Further studies where colorectal cancer (CRC) cells were subjected to 5-fluorouracil (5FU) treatment revealed a sharp increase in MASTL expression upon chemotherapy, along with increases in Bcl-xL and Survivin expression. Fluorouracil 86-89 microtubule associated serine/threonine kinase like Homo sapiens 130-135 28950928-0 2018 Downregulation of MicroRNA-147 Inhibits Cell Proliferation and Increases the Chemosensitivity of Gastric Cancer Cells to 5-Fluorouracil by Directly Targeting PTEN. Fluorouracil 121-135 microRNA 147a Homo sapiens 18-30 35276696-12 2022 Mechanistically, circSAMD4A knockdown-induced 5-Fu sensitivity was mediated by miR-545-3p/PFKFB3 axis. Fluorouracil 46-50 6-phosphofructo-2-kinase/fructose-2,6-biphosphatase 3 Homo sapiens 90-96 35276696-14 2022 CircSAMD4A contributed to 5-Fu resistance of CRC cells partly through upregulating PFKFB3 expression by sponging miR-545-3p, providing a possible circRNA-targeted therapy for CRC. Fluorouracil 26-30 6-phosphofructo-2-kinase/fructose-2,6-biphosphatase 3 Homo sapiens 83-89 28950928-0 2018 Downregulation of MicroRNA-147 Inhibits Cell Proliferation and Increases the Chemosensitivity of Gastric Cancer Cells to 5-Fluorouracil by Directly Targeting PTEN. Fluorouracil 121-135 phosphatase and tensin homolog Homo sapiens 158-162 28950928-4 2018 Downregulation of miR-147 decreased cell proliferation and enhanced the chemosensitivity of gastric cancer cells to 5-fluorouracil (5-FU) through the cell apoptosis pathway. Fluorouracil 116-130 microRNA 147a Homo sapiens 18-25 28950928-4 2018 Downregulation of miR-147 decreased cell proliferation and enhanced the chemosensitivity of gastric cancer cells to 5-fluorouracil (5-FU) through the cell apoptosis pathway. Fluorouracil 132-136 microRNA 147a Homo sapiens 18-25 35609368-8 2022 In addition, C3G alone or combined with 5-FU affected the expression of the tumor microenvironment-related factors Ki67, CD45, PDL1, and CD73. Fluorouracil 40-44 protein tyrosine phosphatase, receptor type, C Mus musculus 121-125 35609368-8 2022 In addition, C3G alone or combined with 5-FU affected the expression of the tumor microenvironment-related factors Ki67, CD45, PDL1, and CD73. Fluorouracil 40-44 5' nucleotidase, ecto Mus musculus 137-141 28950928-6 2018 PTEN knockdown reversed the effects of miR-147 downregulation on the proliferation, chemosensitivity, and 5-FU-induced apoptosis of gastric cancer cells. Fluorouracil 106-110 phosphatase and tensin homolog Homo sapiens 0-4 35609368-9 2022 Compared with the mice treated with 5-FU or C3G alone, those treated with both C3G and 5-FU exhibited significantly impaired tumor growth, decreased tumor sizes, and increased tumor inhibition. Fluorouracil 36-40 Rap guanine nucleotide exchange factor (GEF) 1 Mus musculus 79-82 35609368-9 2022 Compared with the mice treated with 5-FU or C3G alone, those treated with both C3G and 5-FU exhibited significantly impaired tumor growth, decreased tumor sizes, and increased tumor inhibition. Fluorouracil 87-91 Rap guanine nucleotide exchange factor (GEF) 1 Mus musculus 44-47 28950928-6 2018 PTEN knockdown reversed the effects of miR-147 downregulation on the proliferation, chemosensitivity, and 5-FU-induced apoptosis of gastric cancer cells. Fluorouracil 106-110 microRNA 147a Homo sapiens 39-46 28950928-8 2018 In conclusion, miR-147 suppressed the proliferation and enhanced the chemosensitivity of gastric cancer cells to 5-FU by promoting cell apoptosis through directly targeting PTEN and regulating the PI3K/AKT signaling pathway. Fluorouracil 113-117 microRNA 147a Homo sapiens 15-22 28950928-8 2018 In conclusion, miR-147 suppressed the proliferation and enhanced the chemosensitivity of gastric cancer cells to 5-FU by promoting cell apoptosis through directly targeting PTEN and regulating the PI3K/AKT signaling pathway. Fluorouracil 113-117 phosphatase and tensin homolog Homo sapiens 173-177 30013790-0 2018 Uridine triacetate for severe 5-fluorouracil toxicity in a patient with thymidylate synthase gene variation: Potential pharmacogenomic implications. Fluorouracil 30-44 thymidylate synthetase Homo sapiens 72-92 35427566-5 2022 Thymidylate synthase (TYMS), the major target of chemotherapeutic drugs 5-FU or other fluoropyrimidines, which catalyzes the conversion of dUMP to dTMP and provides the sole de novo source of thymidylate for DNA synthesis. Fluorouracil 72-76 thymidylate synthetase Homo sapiens 0-20 35427566-5 2022 Thymidylate synthase (TYMS), the major target of chemotherapeutic drugs 5-FU or other fluoropyrimidines, which catalyzes the conversion of dUMP to dTMP and provides the sole de novo source of thymidylate for DNA synthesis. Fluorouracil 72-76 thymidylate synthetase Homo sapiens 22-26 30013790-3 2018 Genetic variations in the dihydropyrimidine dehydrogenase and thymidylate synthase genes have been shown to increase the risk of 5-fluorouracil toxicity. Fluorouracil 129-143 thymidylate synthetase Homo sapiens 62-82 35405270-4 2022 In addition, Met could inhibit 5-Fu-induced high expression of endoplasmic reticulum stress(ERS)-related proteins GRP78 and CHOP. Fluorouracil 31-35 DNA-damage inducible transcript 3 Mus musculus 124-128 31949703-8 2018 As atractyloside synergized with 5-Fluoruracil (5-FU) to suppress colorectal cancer cell proliferation, we concluded that the inhibition of BORIS downstream by atractyloside amplifies the effect of 5-FU by promoting DNA damage. Fluorouracil 33-46 CCCTC-binding factor like Homo sapiens 140-145 35483272-4 2022 FNR associated genes (GPX4, SLC7A11, and FTH1) and STAT3 are upregulated in 5-FU resistant cells and xenografts. Fluorouracil 76-80 glutathione peroxidase 4 Homo sapiens 22-26 35483272-4 2022 FNR associated genes (GPX4, SLC7A11, and FTH1) and STAT3 are upregulated in 5-FU resistant cells and xenografts. Fluorouracil 76-80 solute carrier family 7 member 11 Homo sapiens 28-35 35483272-4 2022 FNR associated genes (GPX4, SLC7A11, and FTH1) and STAT3 are upregulated in 5-FU resistant cells and xenografts. Fluorouracil 76-80 ferritin heavy chain 1 Homo sapiens 41-45 35608750-0 2022 The epigenetic modifier HDAC2 and the checkpoint kinase ATM determine the responses of microsatellite instable colorectal cancer cells to 5-fluorouracil. Fluorouracil 138-152 ATM serine/threonine kinase Homo sapiens 56-59 35608750-11 2022 Pharmacological inhibition of ATM sensitizes RKO cells to cytotoxic effects of 5-fluorouracil. Fluorouracil 79-93 ATM serine/threonine kinase Homo sapiens 30-33 31949703-8 2018 As atractyloside synergized with 5-Fluoruracil (5-FU) to suppress colorectal cancer cell proliferation, we concluded that the inhibition of BORIS downstream by atractyloside amplifies the effect of 5-FU by promoting DNA damage. Fluorouracil 48-52 CCCTC-binding factor like Homo sapiens 140-145 35608750-12 2022 These findings demonstrate that HDAC2 and ATM modulate the responses of colorectal cancer cells towards 5-FU. Fluorouracil 104-108 ATM serine/threonine kinase Homo sapiens 42-45 31949703-8 2018 As atractyloside synergized with 5-Fluoruracil (5-FU) to suppress colorectal cancer cell proliferation, we concluded that the inhibition of BORIS downstream by atractyloside amplifies the effect of 5-FU by promoting DNA damage. Fluorouracil 198-202 CCCTC-binding factor like Homo sapiens 140-145 29702091-5 2018 Significantly, MALAT1 deletion sensitized HepG2 cells to 5-FU-induced cell cycle arrest in G1 phase, as evidenced by the significant reduction in Cyclin D1 and CDK4 and increase in p53, p21 and p27 protein levels. Fluorouracil 57-61 metastasis associated lung adenocarcinoma transcript 1 Homo sapiens 15-21 29702091-5 2018 Significantly, MALAT1 deletion sensitized HepG2 cells to 5-FU-induced cell cycle arrest in G1 phase, as evidenced by the significant reduction in Cyclin D1 and CDK4 and increase in p53, p21 and p27 protein levels. Fluorouracil 57-61 H3 histone pseudogene 16 Homo sapiens 186-189 29702091-5 2018 Significantly, MALAT1 deletion sensitized HepG2 cells to 5-FU-induced cell cycle arrest in G1 phase, as evidenced by the significant reduction in Cyclin D1 and CDK4 and increase in p53, p21 and p27 protein levels. Fluorouracil 57-61 interferon alpha inducible protein 27 Homo sapiens 194-197 35597840-2 2022 The current study aims to identify and validate reliable markers that can predict pathological complete response (pCR) in fluorouracil, epirubicin, and cyclophosphamide (FEC)-based neoadjuvant therapy with (NACT/RT) and without concurrent radiation (NACT). Fluorouracil 122-134 solute carrier family 13 member 5 Homo sapiens 207-211 35597840-2 2022 The current study aims to identify and validate reliable markers that can predict pathological complete response (pCR) in fluorouracil, epirubicin, and cyclophosphamide (FEC)-based neoadjuvant therapy with (NACT/RT) and without concurrent radiation (NACT). Fluorouracil 122-134 solute carrier family 13 member 5 Homo sapiens 250-254 29702091-6 2018 In addition, MALAT1 knockdown triggered 5-FU induced apoptosis in HepG2 cells by inducing intrinsic apoptosis-related signals, including Cyto-c, Apaf-1, cleaved Caspase-9/-7/-3 and poly (ADP-ribose) polymerase (PARP). Fluorouracil 40-44 metastasis associated lung adenocarcinoma transcript 1 Homo sapiens 13-19 29702091-10 2018 Therefore, our data supplied a potential mechanism by which knockdown of MALAT1 might play an important role in augmenting sensitivity of HepG2 cells to 5-FU in therapeutic approaches, demonstrating suppressing of MALAT1 may serve as a combination with chemotherapeutic agents in liver cancer treatment. Fluorouracil 153-157 metastasis associated lung adenocarcinoma transcript 1 Homo sapiens 73-79 29777330-0 2018 Down-regulating IL-6/GP130 targets improved the anti-tumor effects of 5-fluorouracil in colon cancer. Fluorouracil 70-84 interleukin 6 cytokine family signal transducer Homo sapiens 21-26 29777330-4 2018 Thus, we speculated that in colon cancer, the anti-tumor efficacy of 5-FU might be increased in combination with IL-6/GP130 inhibitors. Fluorouracil 69-73 interleukin 6 cytokine family signal transducer Homo sapiens 118-123 29777330-15 2018 Further mechanistic studies determined that BZA treatment enhanced 5-FU anti-tumor activation by inhibiting the IL-6/GP130 signaling pathway and the phosphorylation status of the downstream effectors AKT, ERK and STAT3. Fluorouracil 67-71 interleukin 6 cytokine family signal transducer Homo sapiens 117-122 29777330-16 2018 In contrast, IL-6 can attenuate 5-FU function via activating IL-6R/GP130 signaling and the P-AKT, P-ERK and P-STAT3 levels. Fluorouracil 32-36 interleukin 6 cytokine family signal transducer Homo sapiens 67-72 28899623-0 2018 TYMS Gene Polymorphisms in Breast Cancer Patients Receiving 5-Fluorouracil-Based Chemotherapy. Fluorouracil 60-74 thymidylate synthetase Homo sapiens 0-4 29436749-0 2018 HOXA13 contributes to gastric carcinogenesis through DHRS2 interacting with MDM2 and confers 5-FU resistance by a p53-dependent pathway. Fluorouracil 93-97 homeobox A13 Homo sapiens 0-6 29436749-6 2018 The patients with HOXA13 overexpression were closely related with poor prognosis and more prone to be resistant to 5-FU. Fluorouracil 115-119 homeobox A13 Homo sapiens 18-24 29436749-9 2018 Furthermore, HOXA13 conferred 5-FU resistance through MRP1 by a p53-dependent pathway. Fluorouracil 30-34 homeobox A13 Homo sapiens 13-19 29436749-9 2018 Furthermore, HOXA13 conferred 5-FU resistance through MRP1 by a p53-dependent pathway. Fluorouracil 30-34 MDM4 regulator of p53 Homo sapiens 54-58 29436749-10 2018 Therefore, HOXA13 might serve as a potential signature that recognized patients who were insensitive to 5-FU, and timely recommended them to other chemotherapy regimens. Fluorouracil 104-108 homeobox A13 Homo sapiens 11-17 29795190-3 2018 Our study showed that miR-181a expression was significantly increased after 5-fluorouracil (5-FU) treatment in renal mesangial cells and kidney tissue, which was associated with decreased baculoviral inhibition of apoptosis protein repeat-containing 6 (BIRC6) expression and increased apoptotic rate. Fluorouracil 76-90 baculoviral IAP repeat containing 6 Homo sapiens 253-258 29795190-3 2018 Our study showed that miR-181a expression was significantly increased after 5-fluorouracil (5-FU) treatment in renal mesangial cells and kidney tissue, which was associated with decreased baculoviral inhibition of apoptosis protein repeat-containing 6 (BIRC6) expression and increased apoptotic rate. Fluorouracil 92-96 baculoviral IAP repeat containing 6 Homo sapiens 253-258 29795190-4 2018 Enforced miR-181a expression enhanced 5-FU-induced p53-dependent mitochondrial apoptosis, including declined Bcl-2/Bax ratio, loss of mitochondrial membrane potential, cytochrome c release, and caspase-9 and caspase-3 activation. Fluorouracil 38-42 caspase 9 Homo sapiens 194-203 29483219-9 2018 In addition, we identified an FDA-approved bacteriostatic antibiotic, fusidic acid sodium salt (fusidic acid or FA) as an inhibitor of PRPK, and show that FA combined with 5-fluorouracil (5-FU) inhibited PRPK activity and colon cancer metastasis to the lung in mice. Fluorouracil 172-186 transformation related protein 53 regulating kinase B Mus musculus 204-208 35577773-7 2022 We found that SFMBT1 is up-regulated in CRC and its expression is further amplified in 5-FU resistance. Fluorouracil 87-91 Scm like with four mbt domains 1 Homo sapiens 14-20 35577773-8 2022 SFMBT1 drives 5-FU resistance and CRC proliferation, migration and invasion. Fluorouracil 14-18 Scm like with four mbt domains 1 Homo sapiens 0-6 35577773-13 2022 Our results indicate that the SFMBT1/HMG20A axis could be targeted to increase the resistance of CRC cells to 5-FU. Fluorouracil 110-114 Scm like with four mbt domains 1 Homo sapiens 30-36 35634282-9 2022 The combination of 5-FU with ICB augmented an inflammatory tumor microenvironment with markedly increased CD8+ T cell activation and upregulation of IFNgamma, TNFalpha and IL-1beta signaling. Fluorouracil 19-23 interleukin 1 alpha Homo sapiens 172-180 35634282-10 2022 The effective anti-tumor immune response of 5-FU chemo-immunotherapy was dependent on CD8+ T cells but was unaffected when TNFalpha or IL-1beta cytokine signaling pathways were blocked. Fluorouracil 44-48 interleukin 1 alpha Homo sapiens 135-143 29483219-9 2018 In addition, we identified an FDA-approved bacteriostatic antibiotic, fusidic acid sodium salt (fusidic acid or FA) as an inhibitor of PRPK, and show that FA combined with 5-fluorouracil (5-FU) inhibited PRPK activity and colon cancer metastasis to the lung in mice. Fluorouracil 188-192 transformation related protein 53 regulating kinase B Mus musculus 204-208 29497124-7 2018 Finally, we found that USP27 expression is inhibited by 5-fluorouracil (5-FU) treatment and USP27 depletion sensitizes Hep3B cells to 5-FU-induced apoptosis. Fluorouracil 56-70 ubiquitin specific peptidase 27 X-linked Homo sapiens 23-28 29497124-7 2018 Finally, we found that USP27 expression is inhibited by 5-fluorouracil (5-FU) treatment and USP27 depletion sensitizes Hep3B cells to 5-FU-induced apoptosis. Fluorouracil 72-76 ubiquitin specific peptidase 27 X-linked Homo sapiens 23-28 29497124-7 2018 Finally, we found that USP27 expression is inhibited by 5-fluorouracil (5-FU) treatment and USP27 depletion sensitizes Hep3B cells to 5-FU-induced apoptosis. Fluorouracil 134-138 ubiquitin specific peptidase 27 X-linked Homo sapiens 23-28 29497124-7 2018 Finally, we found that USP27 expression is inhibited by 5-fluorouracil (5-FU) treatment and USP27 depletion sensitizes Hep3B cells to 5-FU-induced apoptosis. Fluorouracil 134-138 ubiquitin specific peptidase 27 X-linked Homo sapiens 92-97 29849804-8 2018 Additionally, bufalin combined with 5-FU reduced the expression levels of anti-apoptotic proteins, such as Mcl-1, XIAP and Bcl-2 and upregulated the levels of the pro-apoptotic proteins, Bax and Bad. Fluorouracil 36-40 MCL1 apoptosis regulator, BCL2 family member Homo sapiens 107-112 29352327-11 2018 In addition, immunofluorescence analysis showed increased expression of active cofilin, LIMK1, LIMK2, and SSH1 in HT29 colon cancer cells resistant to 5-fluorouracil compared to parental HT29 cells. Fluorouracil 151-165 slingshot protein phosphatase 1 Homo sapiens 106-110 29719602-0 2018 Leptin-Notch axis impairs 5-fluorouracil effects on pancreatic cancer. Fluorouracil 26-40 leptin Homo sapiens 0-6 29719602-2 2018 Obesity is a risk factor for PC that could affect 5-FU effectiveness through the adipokine leptin, which is a known proliferation, survival factor and Notch inducer. Fluorouracil 50-54 leptin Homo sapiens 91-97 29719602-5 2018 Leptin treatment decreased 5-FU cytotoxicity, and increased cell proliferation, colony forming ability, stem cell, pluripotency, EMT markers, drug efflux proteins (ABCC5, ABCC11) and Notch. Fluorouracil 27-31 leptin Homo sapiens 0-6 29719602-6 2018 In addition, leptin reduced the 5-FU effects on apoptosis by decreasing pro-apoptotic (Bax, Caspase-3 activation and PARP degradation) and increasing anti-apoptotic factors (RIP and Bcl-XL). Fluorouracil 32-36 leptin Homo sapiens 13-19 29719602-7 2018 Leptin"s effects on PC tumorspheres treated with 5-FU were reduced by IONP-LPrA2 and were mainly Notch signaling- dependent and more evident in MiaPaCa-2-derived tumorspheres. Fluorouracil 49-53 leptin Homo sapiens 0-6 29719602-8 2018 Present results suggest that leptin could impair 5-FU cytotoxicity and promote chemoresistance. Fluorouracil 49-53 leptin Homo sapiens 29-35 29719602-9 2018 Therefore, targeting the leptin-Notch axis could be a novel way to improve 5-FU therapy for PC patients, especially in obesity context. Fluorouracil 75-79 leptin Homo sapiens 25-31 29331415-2 2018 Previously, we found that NgBR promotes the membrane translocation and activation of Ras in breast cancer cells and enhances the chemoresistance of hepatocellular carcinoma cells to 5-fluorouracil. Fluorouracil 182-196 NUS1 dehydrodolichyl diphosphate synthase subunit Homo sapiens 26-30 29432052-7 2018 Furthermore, the 5-FU-induced increase of proinflammatory cytokine interleukin (IL)-2 and the decrease of anti-inflammatory cytokine IL-10 level in the peripheral blood were significantly attenuated by OPNF administration. Fluorouracil 17-21 interleukin 10 Rattus norvegicus 133-138 35579160-2 2022 5-FU acts mainly by inhibiting thymidylate synthase, thereby interfering with deoxyribonucleic acid (DNA) replication or by 5-FU incorporating into DNA, causing damage to the sequence of nucleotides. Fluorouracil 0-4 thymidylate synthetase Homo sapiens 31-51 35505494-0 2022 Retraction notice to Downregulation of MicroRNA-147 Inhibits Cell Proliferation and Increases the Chemosensitivity of Gastric Cancer Cells to 5-Fluorouracil by Directly Targeting PTEN (Oncology Research 26(6) (2018) 901911). Fluorouracil 142-156 phosphatase and tensin homolog Homo sapiens 179-183 29605826-12 2018 The expression of SphK1 was positively correlated with poor overall survival (OS) and progression-free survival (PFS), as well as poor response to 5-FU and doxorubicin. Fluorouracil 147-151 sphingosine kinase 1 Homo sapiens 18-23 29605826-14 2018 Furthermore, silencing of SphK1 by Ad-SPHK1-siRNA or SphK1 inhibitor PF543 sensitized TNBCs to 5-FU and doxorubicin. Fluorouracil 95-99 sphingosine kinase 1 Homo sapiens 26-31 29605826-14 2018 Furthermore, silencing of SphK1 by Ad-SPHK1-siRNA or SphK1 inhibitor PF543 sensitized TNBCs to 5-FU and doxorubicin. Fluorouracil 95-99 sphingosine kinase 1 Homo sapiens 53-58 28026832-13 2018 Inhibition of SYT8 expression by GC cells correlated with decreased invasion, migration, and fluorouracil resistance. Fluorouracil 93-105 synaptotagmin 8 Homo sapiens 14-18 29491068-1 2018 BACKGROUND/AIM: Trifluridine/tipiracil (FTD/TPI) is used for metastatic colorectal cancer, that is refractory to 5-fluorouracil (5-FU)-based therapies. Fluorouracil 113-127 triosephosphate isomerase 1 Mus musculus 44-47 35218806-4 2022 Here, we introduced a pH-responsive micellar hydrogel system based on deoxycholic acid micelle (DCA Mic) and carboxymethyl chitosan hydrogel (CMC Hyd) to enhance 5-FU efficacy against skin cancer and reduce its systemic side effects by improving its delivery into the skin. Fluorouracil 162-166 ubiquitin protein ligase E3 component n-recognin 5 Homo sapiens 146-149 35218806-8 2022 The 5-FU@Mic-Hyd could be a promising delivery platform with enhanced efficacy in the management of skin cancer without systemic toxicity. Fluorouracil 4-8 ubiquitin protein ligase E3 component n-recognin 5 Homo sapiens 13-16 35449812-8 2022 The effect of 5-FU and ZER on the cell viability was investigated by MTT assay in a dose and time-dependent manner, after that, the expression of vimentin, beta-catenin, and survivin was quantified. Fluorouracil 14-18 vimentin Homo sapiens 146-154 35449812-8 2022 The effect of 5-FU and ZER on the cell viability was investigated by MTT assay in a dose and time-dependent manner, after that, the expression of vimentin, beta-catenin, and survivin was quantified. Fluorouracil 14-18 catenin beta 1 Homo sapiens 156-168 29491068-1 2018 BACKGROUND/AIM: Trifluridine/tipiracil (FTD/TPI) is used for metastatic colorectal cancer, that is refractory to 5-fluorouracil (5-FU)-based therapies. Fluorouracil 129-133 triosephosphate isomerase 1 Mus musculus 44-47 29259071-3 2018 Baseline prostate-specific antigen values declined from 1,890 ng/mL to <1 ng/mL after 5-FU therapy. Fluorouracil 89-93 kallikrein related peptidase 3 Homo sapiens 9-34 30359298-0 2018 The new 6q27 tumor suppressor DACT2, frequently silenced by CpG methylation, sensitizes nasopharyngeal cancer cells to paclitaxel and 5-FU toxicity via beta-catenin/Cdc25c signaling and G2/M arrest. Fluorouracil 134-138 catenin beta 1 Homo sapiens 152-164 30359298-0 2018 The new 6q27 tumor suppressor DACT2, frequently silenced by CpG methylation, sensitizes nasopharyngeal cancer cells to paclitaxel and 5-FU toxicity via beta-catenin/Cdc25c signaling and G2/M arrest. Fluorouracil 134-138 cell division cycle 25C Homo sapiens 165-171 29479997-1 2018 Thymidylate synthase (TS) is an enzyme involved in DNA synthesis and is associatedwith resistance of tumor cells to 5-fluorouracil. Fluorouracil 116-130 thymidylate synthetase Homo sapiens 0-20 35395805-7 2022 Additionally, the patients with TET1 mutations were found to be more sensitive to lapatinib and 5-fluorouracil. Fluorouracil 96-110 tet methylcytosine dioxygenase 1 Homo sapiens 32-36 29479997-1 2018 Thymidylate synthase (TS) is an enzyme involved in DNA synthesis and is associatedwith resistance of tumor cells to 5-fluorouracil. Fluorouracil 116-130 thymidylate synthetase Homo sapiens 22-24 29458395-0 2018 Herbal formula Huang Qin Ge Gen Tang enhances 5-fluorouracil antitumor activity through modulation of the E2F1/TS pathway. Fluorouracil 46-60 E2F transcription factor 1 Homo sapiens 106-110 29318904-0 2018 Thymidylate synthase: a predictive biomarker in resected colorectal liver metastases receiving 5-FU treatment. Fluorouracil 95-99 thymidylate synthetase Homo sapiens 0-20 29318904-8 2018 CONCLUSION: TS appears to be a clinically relevant predictive biomarker in patients with resected CRLM receiving systemic 5-FU. Fluorouracil 122-126 thymidylate synthetase Homo sapiens 12-14 29042284-5 2018 Furthermore, Se-GP11 could enhance the immune functions during the tumor inhibition process of 5-Fu for increasing the cytokines secretion (IL-2 and TNF-alpha) and immune organs weights. Fluorouracil 95-99 interleukin 2 Mus musculus 140-144 29399358-9 2018 The findings suggest that ERCC1 expression could be a predictive biomarker for chemotherapy response to 5-FU/cisplatin in HNSCC. Fluorouracil 104-108 ERCC excision repair 1, endonuclease non-catalytic subunit Homo sapiens 26-31 35415017-7 2022 We hypothesize that hsacirc_004413 makes gastric cancer cells resistant to 5-Fu mainly through adsorption of miR-145-5p. Fluorouracil 75-79 microRNA 145 Homo sapiens 109-116 35346989-7 2022 RESULTS: ANXA10 knockout GC cells showed significantly increased proliferation, invasion, and sensitivity to 5-FU. Fluorouracil 109-113 annexin A10 Homo sapiens 9-15 35346989-8 2022 The overall survival of ANXA10-positive cases was considerably lower than that of ANXA10-negative cases in GC patients who received 5-FU-based chemotherapy. Fluorouracil 132-136 annexin A10 Homo sapiens 82-88 35346989-10 2022 CONCLUSION: ANXA10 knockout increased the susceptibility of GC cell lines to 5-FU; ANXA10 may be a predictive indicator for response to 5-FU treatment in GC cases. Fluorouracil 77-81 annexin A10 Homo sapiens 12-18 35346989-10 2022 CONCLUSION: ANXA10 knockout increased the susceptibility of GC cell lines to 5-FU; ANXA10 may be a predictive indicator for response to 5-FU treatment in GC cases. Fluorouracil 77-81 annexin A10 Homo sapiens 83-89 35346989-10 2022 CONCLUSION: ANXA10 knockout increased the susceptibility of GC cell lines to 5-FU; ANXA10 may be a predictive indicator for response to 5-FU treatment in GC cases. Fluorouracil 136-140 annexin A10 Homo sapiens 12-18 35346989-10 2022 CONCLUSION: ANXA10 knockout increased the susceptibility of GC cell lines to 5-FU; ANXA10 may be a predictive indicator for response to 5-FU treatment in GC cases. Fluorouracil 136-140 annexin A10 Homo sapiens 83-89 29434918-5 2018 Furthermore, knockdown of Arf6 was associated with elevated chemosensitivity of SGC-7901 cells to 5-fluorouracil through inactivation of the ERK1/2 signaling pathway. Fluorouracil 98-112 ADP ribosylation factor 6 Homo sapiens 26-30 29362023-10 2018 Our in vivo xenograft results also suggested that transfection of TAp73 affects the tumor suppression effect of 5-FU. Fluorouracil 112-116 transformation related protein 73 Mus musculus 66-71 35133490-7 2022 Further study reveals 5-FU disrupts sNASP/TNF receptor-associated factor 6 (TRAF6) complex, potentiates cellular sensitivity to 5-FU via NK-kB. Fluorouracil 22-26 TNF receptor associated factor 6 Homo sapiens 36-74 35133490-7 2022 Further study reveals 5-FU disrupts sNASP/TNF receptor-associated factor 6 (TRAF6) complex, potentiates cellular sensitivity to 5-FU via NK-kB. Fluorouracil 22-26 TNF receptor associated factor 6 Homo sapiens 76-81 35133490-7 2022 Further study reveals 5-FU disrupts sNASP/TNF receptor-associated factor 6 (TRAF6) complex, potentiates cellular sensitivity to 5-FU via NK-kB. Fluorouracil 128-132 TNF receptor associated factor 6 Homo sapiens 36-74 29053388-7 2018 The cells treated with 5-FU or IRINO exhibited several hallmarks of SIPS: growth arrest, increased size and granularity, polyploidization, augmented activity of the SA-beta-galactosidase, accumulation of P21 and CYCLIN D1 proteins, and the senescence-associated secretory phenotype. Fluorouracil 23-27 H3 histone pseudogene 16 Homo sapiens 204-207 35133490-7 2022 Further study reveals 5-FU disrupts sNASP/TNF receptor-associated factor 6 (TRAF6) complex, potentiates cellular sensitivity to 5-FU via NK-kB. Fluorouracil 128-132 TNF receptor associated factor 6 Homo sapiens 76-81 35092904-0 2022 Long non-coding RNA HNF1A-AS1 induces 5-FU resistance of gastric cancer through miR-30b-5p/EIF5A2 pathway. Fluorouracil 38-42 microRNA 30b Mus musculus 80-87 29475390-8 2018 Knockdown of NME2 restored 5-FU sensitivity in 5-FU-resistant CRC cells, reduced cell survival and increased cell apoptosis; and overexpression of NME2 in HCT-8 cells results in the acquisition of resistance to 5-FU, this alteration enhanced HCT-8 cells growth abilities and reduced apoptosis. Fluorouracil 27-31 NME/NM23 nucleoside diphosphate kinase 2 Homo sapiens 13-17 35092904-3 2022 The current study sought to explore the mechanism of lncRNA HNF1A antisense RNA 1 (HNF1A-AS1) in mediating 5-fluorouracil (5-FU) resistance of GC. Fluorouracil 107-121 HNF1 homeobox A Mus musculus 60-92 35092904-3 2022 The current study sought to explore the mechanism of lncRNA HNF1A antisense RNA 1 (HNF1A-AS1) in mediating 5-fluorouracil (5-FU) resistance of GC. Fluorouracil 123-127 HNF1 homeobox A Mus musculus 60-92 35092904-13 2022 CONCLUSIONS: The findings from the current study showed HNF1A-AS1 promoted 5-FU resistance by acting as a ceRNA of miR-30b-5p and promoting EIF5A2-induced EMT process in GC. Fluorouracil 75-79 microRNA 30b Mus musculus 115-122 29475390-8 2018 Knockdown of NME2 restored 5-FU sensitivity in 5-FU-resistant CRC cells, reduced cell survival and increased cell apoptosis; and overexpression of NME2 in HCT-8 cells results in the acquisition of resistance to 5-FU, this alteration enhanced HCT-8 cells growth abilities and reduced apoptosis. Fluorouracil 47-51 NME/NM23 nucleoside diphosphate kinase 2 Homo sapiens 13-17 29475390-8 2018 Knockdown of NME2 restored 5-FU sensitivity in 5-FU-resistant CRC cells, reduced cell survival and increased cell apoptosis; and overexpression of NME2 in HCT-8 cells results in the acquisition of resistance to 5-FU, this alteration enhanced HCT-8 cells growth abilities and reduced apoptosis. Fluorouracil 47-51 NME/NM23 nucleoside diphosphate kinase 2 Homo sapiens 13-17 29475390-9 2018 These findings suggest that NME2 mediates chemoresistance to 5-FU in CRC and that specific NME2 inhibition could optimize 5-FU-based chemotherapy of CRC. Fluorouracil 61-65 NME/NM23 nucleoside diphosphate kinase 2 Homo sapiens 28-32 29475390-9 2018 These findings suggest that NME2 mediates chemoresistance to 5-FU in CRC and that specific NME2 inhibition could optimize 5-FU-based chemotherapy of CRC. Fluorouracil 122-126 NME/NM23 nucleoside diphosphate kinase 2 Homo sapiens 91-95 35354250-4 2022 Consistently, PFKFB3 overexpression triggered BM EPC damage after 5FU treatment and impaired hematopoiesis-supporting ability in vitro. Fluorouracil 66-69 6-phosphofructo-2-kinase/fructose-2,6-biphosphatase 3 Homo sapiens 14-20 28722177-4 2018 We show that this is due to global alterations in nucleotide metabolism, including elevated expression of thymidylate synthase and thymidine kinase 1 (established 5-FU resistance mechanisms), which likely result in an increase in intracellular dTTP pools and a "dilution" of 5-FU anabolites. Fluorouracil 163-167 thymidylate synthetase Homo sapiens 106-126 35354250-5 2022 Mechanismly, PFKFB3 facilitated pro-apoptotic transcription factor FOXO3A and its downstream gene expressions, including p21, p27, FAS after 5FU treatment in vitro. Fluorouracil 141-144 6-phosphofructo-2-kinase/fructose-2,6-biphosphatase 3 Homo sapiens 13-19 28722177-4 2018 We show that this is due to global alterations in nucleotide metabolism, including elevated expression of thymidylate synthase and thymidine kinase 1 (established 5-FU resistance mechanisms), which likely result in an increase in intracellular dTTP pools and a "dilution" of 5-FU anabolites. Fluorouracil 275-279 thymidylate synthetase Homo sapiens 106-126 35354250-5 2022 Mechanismly, PFKFB3 facilitated pro-apoptotic transcription factor FOXO3A and its downstream gene expressions, including p21, p27, FAS after 5FU treatment in vitro. Fluorouracil 141-144 H3 histone pseudogene 16 Homo sapiens 121-124 27871087-0 2018 The HDM2 (MDM2) Inhibitor NVP-CGM097 Inhibits Tumor Cell Proliferation and Shows Additive Effects with 5-Fluorouracil on the p53-p21-Rb-E2F1 Cascade in the p53wild type Neuroendocrine Tumor Cell Line GOT1. Fluorouracil 103-117 H3 histone pseudogene 16 Homo sapiens 129-132 27871087-0 2018 The HDM2 (MDM2) Inhibitor NVP-CGM097 Inhibits Tumor Cell Proliferation and Shows Additive Effects with 5-Fluorouracil on the p53-p21-Rb-E2F1 Cascade in the p53wild type Neuroendocrine Tumor Cell Line GOT1. Fluorouracil 103-117 E2F transcription factor 1 Homo sapiens 136-140 35408903-0 2022 Kaempferol Can Reverse the 5-Fu Resistance of Colorectal Cancer Cells by Inhibiting PKM2-Mediated Glycolysis. Fluorouracil 27-31 pyruvate kinase M1/2 Homo sapiens 84-88 27871087-0 2018 The HDM2 (MDM2) Inhibitor NVP-CGM097 Inhibits Tumor Cell Proliferation and Shows Additive Effects with 5-Fluorouracil on the p53-p21-Rb-E2F1 Cascade in the p53wild type Neuroendocrine Tumor Cell Line GOT1. Fluorouracil 103-117 glutamic-oxaloacetic transaminase 1 Homo sapiens 200-204 27871087-9 2018 Experiments of co-incubation of NVP-CGM097 with 5-fluorouracil, temozolomide, or everolimus each showed additive antiproliferative effects in GOT1 cells. Fluorouracil 48-62 glutamic-oxaloacetic transaminase 1 Homo sapiens 142-146 35408903-8 2022 In terms of mechanism, kaempferol promotes the expression of microRNA-326 (miR-326) in colon cancer cells, and miR-326 could inhibit the process of glycolysis by directly targeting pyruvate kinase M2 isoform (PKM2) 3"-UTR (untranslated region) to inhibit the expression of PKM2 or indirectly block the alternative splicing factors of PKM mRNA, and then reverse the resistance of colorectal cancer cells to 5-Fu. Fluorouracil 406-410 pyruvate kinase M1/2 Homo sapiens 181-207 27871087-10 2018 NVP-CGM097 and 5-fluorouracil increased p53 and p21 expression in an additive manner. Fluorouracil 15-29 H3 histone pseudogene 16 Homo sapiens 48-51 35408903-9 2022 Taken together, our data suggest that kaempferol may play an important role in overcoming resistance to 5-Fu therapy by regulating the miR-326-hnRNPA1/A2/PTBP1-PKM2 axis. Fluorouracil 104-108 pyruvate kinase M1/2 Homo sapiens 160-164 29115526-7 2018 Notably, miR-31 was upregulated in 5-FU-resistant CRC cells, and knockdown of miR-31 increased the chemosensitivity of 5-FU-resistant CRC cells. Fluorouracil 35-39 microRNA 31 Homo sapiens 9-15 35151644-6 2022 In the clinic, 5-FU could increase cell apoptosis and cause oral mucosa damage while increasing the expression of the ERS marker genes GRP78 and C/EBP-homologous protein (CHOP). Fluorouracil 15-19 DNA-damage inducible transcript 3 Mus musculus 145-169 35151644-6 2022 In the clinic, 5-FU could increase cell apoptosis and cause oral mucosa damage while increasing the expression of the ERS marker genes GRP78 and C/EBP-homologous protein (CHOP). Fluorouracil 15-19 DNA-damage inducible transcript 3 Mus musculus 171-175 35151644-7 2022 Our study found that 5-FU could induce severe ERS, upregulate the expression of GRP78 and CHOP, raise oxidative stress and increase the expression of inflammatory factors by activating the NF-kappaB pathway, thus causing cell apoptosis and finally leading to oral mucosal injury. Fluorouracil 21-25 DNA-damage inducible transcript 3 Mus musculus 90-94 35170195-0 2022 Long noncoding RNA CCAT2 reduces chemosensitivity to 5-fluorouracil in breast cancer cells by activating the mTOR axis. Fluorouracil 53-67 colon cancer associated transcript 2 Homo sapiens 19-24 35170195-4 2022 This study explored whether BC cell drug sensitivity to 5-Fu was related to lncRNA CCAT2-regulated mTOR pathway. Fluorouracil 56-60 colon cancer associated transcript 2 Homo sapiens 83-88 29115526-7 2018 Notably, miR-31 was upregulated in 5-FU-resistant CRC cells, and knockdown of miR-31 increased the chemosensitivity of 5-FU-resistant CRC cells. Fluorouracil 119-123 microRNA 31 Homo sapiens 9-15 29115526-7 2018 Notably, miR-31 was upregulated in 5-FU-resistant CRC cells, and knockdown of miR-31 increased the chemosensitivity of 5-FU-resistant CRC cells. Fluorouracil 119-123 microRNA 31 Homo sapiens 78-84 29115526-8 2018 Furthermore, we demonstrated that ENST00000547547 reduced the chemoresistance of 5-FU via competitive binding to miR-31 in 5-FU-resistant CRC cell lines. Fluorouracil 81-85 microRNA 31 Homo sapiens 113-119 29115526-8 2018 Furthermore, we demonstrated that ENST00000547547 reduced the chemoresistance of 5-FU via competitive binding to miR-31 in 5-FU-resistant CRC cell lines. Fluorouracil 123-127 microRNA 31 Homo sapiens 113-119 29115526-9 2018 Collectively, our findings revealed that ENST00000547547 reduced chemoresistance in 5-FU of 5-FU-resistant CRC cells through competitive binding to miR-31 and has the potential to serve as a therapeutic target in CRC patients. Fluorouracil 84-88 microRNA 31 Homo sapiens 148-154 29115526-9 2018 Collectively, our findings revealed that ENST00000547547 reduced chemoresistance in 5-FU of 5-FU-resistant CRC cells through competitive binding to miR-31 and has the potential to serve as a therapeutic target in CRC patients. Fluorouracil 92-96 microRNA 31 Homo sapiens 148-154 29484125-8 2018 The in vitro study showed that the knockdown of YTHDF1 resulted in the suppression of cancer proliferation and sensitization to the exposure of anticancer drugs such as fluorouracil and oxaliplatin. Fluorouracil 169-181 YTH N6-methyladenosine RNA binding protein 1 Homo sapiens 48-54 28713155-6 2017 In 5-FU-treated HCC cells, hypoxia reduced the levels of basal thymidylate synthase (TS) and functional TS, leading to decreased dTMP synthesis and DNA replication. Fluorouracil 3-7 thymidylate synthetase Homo sapiens 63-83 29373881-0 2017 The Impact of Thymidylate Synthase and Methylenetetrahydrofolate Reductase Genotypes on Sensitivity to 5-Fluorouracil Treatment in Colorectal Cancer Cells. Fluorouracil 103-117 thymidylate synthetase Homo sapiens 14-34 35191417-12 2022 Re-expression of PAX5 sensitized ESCC cell lines KYSE150 and KYSE30 to fluorouracil and docetaxel. Fluorouracil 71-83 paired box 5 Mus musculus 17-21 35180871-0 2022 MeCP2 confers 5-fluorouracil resistance in gastric cancer via upregulating the NOX4/PKM2 pathway. Fluorouracil 14-28 pyruvate kinase M1/2 Homo sapiens 84-88 29373881-2 2017 Given the known relationship between thymidylate synthase (TS) and methylenetetrahydrofolate reductase (MTHFR) activity and 5-FU metabolism, this study investigated the impact of selected functional polymorphisms of the TS and MTHFR genes on chemotherapy resistance in 5 human CRC cell lines. Fluorouracil 124-128 thymidylate synthetase Homo sapiens 59-61 35180871-9 2022 Silencing NOX4 rescued the inductive effect of MeCP2 overexpression on 5-FU sensitivity of GC cells and reduced the expression of NOX4 and PKM2 in MeCP2 overexpressed 5-FU-resistant GC cells. Fluorouracil 167-171 pyruvate kinase M1/2 Homo sapiens 139-143 29098552-12 2017 Moreover, sensitivity of HCC cell line SP cells to 5-fluorouracil was substantially increased by overexpression of BTG2. Fluorouracil 51-65 BTG anti-proliferation factor 2 Homo sapiens 115-119 28836853-5 2017 Induction of miR-31 in MKN-45 followed by suppression of RhoA expression resulted in increased sensitivity to 5-fluorouracil, inhibition of cell proliferation, and invasion compared to the control groups. Fluorouracil 110-124 microRNA 31 Homo sapiens 13-19 28836853-13 2017 In addition, induction of miR-31 increased sensitivity to 5-FU; thus, increasing its tissue concentrations could be a potential target for treatment of gastric cancer in the future. Fluorouracil 58-62 microRNA 31 Homo sapiens 26-32 29206996-6 2017 Results: With a median follow-up of 50 months, the addition of oxaliplatin to fluorouracil-based CRT led to statistically significantly improved three-year DFS (75.9%, 95% CI = 72.3 to 79.5, vs 71.3%, 95% CI = 67.6 to 74.9, P = .04, PC 1) and a shift toward more advanced TRG groups ( P < .001, PC 2) compared with CRT with fluorouracil alone. Fluorouracil 78-90 proprotein convertase subtilisin/kexin type 1 Homo sapiens 233-237 29206996-6 2017 Results: With a median follow-up of 50 months, the addition of oxaliplatin to fluorouracil-based CRT led to statistically significantly improved three-year DFS (75.9%, 95% CI = 72.3 to 79.5, vs 71.3%, 95% CI = 67.6 to 74.9, P = .04, PC 1) and a shift toward more advanced TRG groups ( P < .001, PC 2) compared with CRT with fluorouracil alone. Fluorouracil 78-90 chromobox 4 Homo sapiens 298-302 29545913-5 2018 And we established 5-fluorouracil-refractory hMLH1-deficient cells and analyzed trifluridine cytotoxicity. Fluorouracil 19-33 mutL homolog 1 Homo sapiens 45-50 29545913-7 2018 5-Fluorouracil-refractory hMLH1-deficient cells treated with trifluridine showed an equal or greater sensitivity than non-5-fluorouracil-refractory cells. Fluorouracil 0-14 mutL homolog 1 Homo sapiens 26-31 29545913-7 2018 5-Fluorouracil-refractory hMLH1-deficient cells treated with trifluridine showed an equal or greater sensitivity than non-5-fluorouracil-refractory cells. Fluorouracil 122-136 mutL homolog 1 Homo sapiens 26-31 28886238-7 2017 This results in the accumulation or activation of CRL4 substrates including LATS1 and p73, which contribute to cell apoptosis induced by actinomycin D and 5-fluorouracil. Fluorouracil 155-169 interleukin 17 receptor B Homo sapiens 50-54 28886238-7 2017 This results in the accumulation or activation of CRL4 substrates including LATS1 and p73, which contribute to cell apoptosis induced by actinomycin D and 5-fluorouracil. Fluorouracil 155-169 large tumor suppressor kinase 1 Homo sapiens 76-81 29138379-2 2017 She received 3 courses of neoadjuvant chemotherapy(NAC)with docetaxel, cisplatin, and 5- fluorouracil(the DCF regimen)and achieved an excellent response. Fluorouracil 86-101 synuclein alpha Homo sapiens 51-54 35215344-12 2022 In conclusion, FEB pre-treatment reduced 5-FU-induced parotid salivary gland damage not only through its powerful anti-inflammatory and antioxidant effects, but also through its effect on the TRPC1/CHOP signalling pathway. Fluorouracil 41-45 DNA-damage inducible transcript 3 Rattus norvegicus 198-202 35198633-10 2022 5-FU treatment also decreased body weight, TAC (total antioxidant capacity) values, VEGF (vascular endothelial growth factor) expression, blood cells, and hemoglobin (Hb) levels. Fluorouracil 0-4 vascular endothelial growth factor A Rattus norvegicus 84-88 35198633-10 2022 5-FU treatment also decreased body weight, TAC (total antioxidant capacity) values, VEGF (vascular endothelial growth factor) expression, blood cells, and hemoglobin (Hb) levels. Fluorouracil 0-4 vascular endothelial growth factor A Rattus norvegicus 90-124 29124041-6 2017 While tight junction protein occludin was reduced, however, zonula occludens-1 (ZO-1) and junctional adhesion molecule-A (JAM-A) were increased in colonic tissues of 5-Fu treated mice. Fluorouracil 166-170 F11 receptor Mus musculus 90-120 29124041-6 2017 While tight junction protein occludin was reduced, however, zonula occludens-1 (ZO-1) and junctional adhesion molecule-A (JAM-A) were increased in colonic tissues of 5-Fu treated mice. Fluorouracil 166-170 F11 receptor Mus musculus 122-127 29340219-3 2017 In the in vitro enzyme-prodrug cancer gene therapy scheme, ARE-hTERT promoter-driven expression of CD : UPRT (yeast cytosine deaminase : uracil phosphoribosyltransferase) chimeric protein induced a more pronounced death of cancer cells either upon treatment with 5-fluorouracil (5FC) alone or when 5FC was combined with chemotherapeutic drugs as compared to the hTERT promoter. Fluorouracil 263-277 telomerase reverse transcriptase Homo sapiens 63-68 29340219-3 2017 In the in vitro enzyme-prodrug cancer gene therapy scheme, ARE-hTERT promoter-driven expression of CD : UPRT (yeast cytosine deaminase : uracil phosphoribosyltransferase) chimeric protein induced a more pronounced death of cancer cells either upon treatment with 5-fluorouracil (5FC) alone or when 5FC was combined with chemotherapeutic drugs as compared to the hTERT promoter. Fluorouracil 263-277 telomerase reverse transcriptase Homo sapiens 362-367 28979703-13 2017 In conclusion, inhibition of miR-205-5p may reverse chemotherapeutic resistance to 5-Fu, and this may occur via the PTEN/JNK/ANXA3 pathway. Fluorouracil 83-87 phosphatase and tensin homolog Homo sapiens 116-120 28883649-5 2017 We found that high CEACAM6 expression was associated with a better OS in early-stage or well-differentiated GC, or who were treated without 5-fluorouracil (5-FU). Fluorouracil 140-154 CEA cell adhesion molecule 6 Homo sapiens 19-26 35196761-1 2022 Objective: To evaluate the roles of G Protein-Coupled Receptor 68 (GPR68) and tumor infiltrating lymphocytes (TIL) in TPF-(paclitaxel, cisplatin and 5-fluorouracil) induced chemotherapy for middle-advanced hypopharyngeal squamous cell carcinomas. Fluorouracil 149-163 G protein-coupled receptor 68 Homo sapiens 67-72 35039826-0 2022 Correction: Down-regulation of miR-543 expression increases the sensitivity of colorectal cancer cells to 5-Fluorouracil through the PTEN/PI3K/AKT pathway. Fluorouracil 106-120 microRNA 543 Homo sapiens 31-38 35039826-0 2022 Correction: Down-regulation of miR-543 expression increases the sensitivity of colorectal cancer cells to 5-Fluorouracil through the PTEN/PI3K/AKT pathway. Fluorouracil 106-120 phosphatase and tensin homolog Homo sapiens 133-137 35083139-8 2021 Silence of CCDC144NL-AS1 and LINC01614 both significantly suppressed the cell proliferation and migration of gastric cancer cells, and also promoted the chemosensitivity of gastric cancer cells to 5-fluorouracil. Fluorouracil 197-211 long intergenic non-protein coding RNA 1614 Homo sapiens 29-38 35035999-0 2022 Evaluating serum level of thymidylate synthase in post burn keloid patients before and after intralesional injection of 5-fluorouracil. Fluorouracil 120-134 thymidylate synthetase Homo sapiens 26-46 35035999-3 2022 5-fluorouracil (5-FU) is a fluorinated pyrimidine analogue acting as an anti-metabolic agent that inhibits thymidylate synthase and interferes with ribo-nucleic acid (RNA) synthesis. Fluorouracil 0-14 thymidylate synthetase Homo sapiens 107-127 35035999-3 2022 5-fluorouracil (5-FU) is a fluorinated pyrimidine analogue acting as an anti-metabolic agent that inhibits thymidylate synthase and interferes with ribo-nucleic acid (RNA) synthesis. Fluorouracil 16-20 thymidylate synthetase Homo sapiens 107-127 35035999-4 2022 Objectives: we aimed to evaluate the level of thymidylate synthase in post burn keloid patients before and after intralesional injection of 5-fluorouracil. Fluorouracil 140-154 thymidylate synthetase Homo sapiens 46-66 35035999-6 2022 Serum TS was estimated using commercially available enzyme-linked immunosorbent assay (ELISA) kits before and after treatment with 5-fluorouracil. Fluorouracil 131-145 thymidylate synthetase Homo sapiens 6-8 35035999-7 2022 Results: There was a statistically significant difference in TS levels before and after 5-FU treatment (p < 0.05). Fluorouracil 88-92 thymidylate synthetase Homo sapiens 61-63 34998404-0 2022 ROS/PI3K/Akt and Wnt/beta-catenin signalings activate HIF-1alpha-induced metabolic reprogramming to impart 5-fluorouracil resistance in colorectal cancer. Fluorouracil 107-121 catenin beta 1 Homo sapiens 21-33 34998404-12 2022 Upregulation of HIF-1alpha in 5-FU-resistant CRC occurred through non-oxygen-dependent mechanisms of reactive oxygen species-mediated activation of PI3K/Akt signaling and aberrant activation of beta-catenin in the nucleus. Fluorouracil 30-34 catenin beta 1 Homo sapiens 194-206 28883649-5 2017 We found that high CEACAM6 expression was associated with a better OS in early-stage or well-differentiated GC, or who were treated without 5-fluorouracil (5-FU). Fluorouracil 156-160 CEA cell adhesion molecule 6 Homo sapiens 19-26 28883649-6 2017 Conversely, high CEACAM6 expression was associated with a poor OS in advanced-stage GC, poorly differentiated tumors, or who were treated with 5-FU. Fluorouracil 143-147 CEA cell adhesion molecule 6 Homo sapiens 17-24 28883649-8 2017 In addition, CEACAM6 overexpression in GC cells increased apoptotic resistance to 5-FU. Fluorouracil 82-86 CEA cell adhesion molecule 6 Homo sapiens 13-20 29088858-9 2017 In addition, we demonstrated that metformin treatment also impaired the cross-resistance of A549/R and PC9/R to cisplatin, etoposide and 5-fluorouracil. Fluorouracil 137-151 proprotein convertase subtilisin/kexin type 9 Homo sapiens 103-106 29137307-0 2017 Reversal of 5-fluorouracil resistance by EGCG is mediate by inactivation of TFAP2A/VEGF signaling pathway and down-regulation of MDR-1 and P-gp expression in gastric cancer. Fluorouracil 12-26 phosphoglycolate phosphatase Homo sapiens 139-143 28816773-5 2017 In our study, combined 3-BP and 5-FU treatment upregulated p53 and p21, whereas cyclin-dependent kinase CDK4 and CDK2 were downregulated, which led to G0/G1 phase arrest. Fluorouracil 32-36 H3 histone pseudogene 16 Homo sapiens 67-70 27325420-10 2017 Patients with basal-like GATA6low tumours have a shorter survival and have a distinctly poor response to adjuvant 5-fluorouracil (5-FU)/leucovorin. Fluorouracil 114-128 GATA binding protein 6 Homo sapiens 25-30 35195263-1 2022 BACKGROUND: Perioperative FLOT (fluorouracil plus leucovorin, oxaliplatin, and docetaxel) chemotherapy is a recent regimen used to treat resectable oesophagogastric (OG) adenocarcinoma, associated with improved overall survival versus earlier chemotherapy strategies. Fluorouracil 32-44 flotillin 1 Homo sapiens 26-30 35103981-11 2022 5-FU suppressed the stemness maintenance of CSCs in PANC-1 cells, as demonstrated by the inhibition of tumorsphere formation, the decrease in CD44+CD133+ cells" fraction, and downregulation of OCT4, Nanog, and SOX2 expression. Fluorouracil 0-4 POU class 5 homeobox 1 Homo sapiens 193-197 27325420-10 2017 Patients with basal-like GATA6low tumours have a shorter survival and have a distinctly poor response to adjuvant 5-fluorouracil (5-FU)/leucovorin. Fluorouracil 130-134 GATA binding protein 6 Homo sapiens 25-30 28927061-1 2017 The mechanism of 5-fluorouracil (5FU) resistance was investigated, focusing on the level of thymidylate synthase (TS) ternary complex formed with fluoro-deoxyuridine monophosphate (FdUMP). Fluorouracil 17-31 thymidylate synthetase Homo sapiens 92-112 28927061-1 2017 The mechanism of 5-fluorouracil (5FU) resistance was investigated, focusing on the level of thymidylate synthase (TS) ternary complex formed with fluoro-deoxyuridine monophosphate (FdUMP). Fluorouracil 17-31 thymidylate synthetase Homo sapiens 114-116 28977993-4 2017 Here we show that tumoroid cultures from a CRC patient are highly sensitive to the thymidylate synthase inhibitor 5-fluorouracil (adrucil) but less sensitive to the combination of nucleoside analog trifluridine and thymidine phosphorylase inhibitor tipiracil (Lonsurf). Fluorouracil 114-128 thymidylate synthetase Homo sapiens 83-103 28977993-4 2017 Here we show that tumoroid cultures from a CRC patient are highly sensitive to the thymidylate synthase inhibitor 5-fluorouracil (adrucil) but less sensitive to the combination of nucleoside analog trifluridine and thymidine phosphorylase inhibitor tipiracil (Lonsurf). Fluorouracil 130-137 thymidylate synthetase Homo sapiens 83-103 28739692-0 2017 WNT/beta-Catenin Signaling Inhibitor IC-2 Suppresses Sphere Formation and Sensitizes Colorectal Cancer Cells to 5-Fluorouracil. Fluorouracil 112-126 catenin beta 1 Homo sapiens 4-16 28304151-8 2017 Furthermore, we showed that CITED4, a key regulator for cardiomyocyte proliferation, was blocked by 5-FU. Fluorouracil 100-104 Cbp/p300-interacting transactivator, with Glu/Asp-rich carboxy-terminal domain, 4 Mus musculus 28-34 2480245-1 1989 Cis-platinum, 5-fluorouracil and bleomycin are active agents in head and neck SCC. Fluorouracil 14-28 serpin family B member 3 Homo sapiens 78-81 2473792-3 1989 Cultures of unseparated bone marrow, harvested from patients four to six days after administration of 5-fluorouracil (5-FU), resulted in additive GM colony formation with GM-CSF plus G-CSF, GM-CSF plus IL-3, and G-CSF plus IL-3. Fluorouracil 118-122 colony stimulating factor 2 Homo sapiens 171-177 2473792-3 1989 Cultures of unseparated bone marrow, harvested from patients four to six days after administration of 5-fluorouracil (5-FU), resulted in additive GM colony formation with GM-CSF plus G-CSF, GM-CSF plus IL-3, and G-CSF plus IL-3. Fluorouracil 118-122 colony stimulating factor 2 Homo sapiens 190-196 2473792-3 1989 Cultures of unseparated bone marrow, harvested from patients four to six days after administration of 5-fluorouracil (5-FU), resulted in additive GM colony formation with GM-CSF plus G-CSF, GM-CSF plus IL-3, and G-CSF plus IL-3. Fluorouracil 118-122 interleukin 3 Homo sapiens 202-206 2473792-3 1989 Cultures of unseparated bone marrow, harvested from patients four to six days after administration of 5-fluorouracil (5-FU), resulted in additive GM colony formation with GM-CSF plus G-CSF, GM-CSF plus IL-3, and G-CSF plus IL-3. Fluorouracil 118-122 colony stimulating factor 3 Homo sapiens 212-217 2473792-3 1989 Cultures of unseparated bone marrow, harvested from patients four to six days after administration of 5-fluorouracil (5-FU), resulted in additive GM colony formation with GM-CSF plus G-CSF, GM-CSF plus IL-3, and G-CSF plus IL-3. Fluorouracil 118-122 interleukin 3 Homo sapiens 223-227 2507490-2 1989 Recently we observed that the antitumor efficacy of various antitumor agents (5-fluorouracil, tegafur, adriamycin, mitomycin C, cyclophosphamide, and cisplatin) against experimental solid tumors was enhanced by prior or simultaneous administration of human epidermal growth factor (EGF). Fluorouracil 78-92 epidermal growth factor Homo sapiens 257-280 2507490-2 1989 Recently we observed that the antitumor efficacy of various antitumor agents (5-fluorouracil, tegafur, adriamycin, mitomycin C, cyclophosphamide, and cisplatin) against experimental solid tumors was enhanced by prior or simultaneous administration of human epidermal growth factor (EGF). Fluorouracil 78-92 epidermal growth factor Homo sapiens 282-285 2507490-5 1989 In a dose-dependent manner, human EGF enhanced the efficacy of an antitumor agent (5-FU) treatment against human epidermoid carcinoma A431 transplanted sc in athymic nude mice [ED50 = 2.9 (0.2-49.7, 95% confidence interval) microgram/kg, sc]. Fluorouracil 83-87 epidermal growth factor Homo sapiens 34-37 2507490-7 1989 The degrees of enhancement were directly proportional to the numbers of human EGF binding sites present on tumor cell plasma membrane (threshold of binding site density = 1.5 X 10(3) sites/cell) using 5-FU or cisplatin as an antitumor agent, thus suggesting that the binding of EGF to the receptors on tumor cells is an essential process in enhancing the susceptibility of tumor cells to antitumor agents. Fluorouracil 201-205 epidermal growth factor Homo sapiens 78-81 2495166-0 1989 5-Fluorouracil and UFT-sensitive gastric carcinoma has a high level of thymidylate synthase. Fluorouracil 0-14 thymidylate synthetase Homo sapiens 71-91 2495166-1 1989 The authors examined the relationship between the level of thymidylate synthase (TS) and the sensitivity to 5-fluorouracil (5-FU) and UFT, a combined oral preparation of 1-(2-tetrahydrofuryl)-5-fluorouracil (tegafur) and uracil in a molar ratio of 1:4. Fluorouracil 108-122 thymidylate synthetase Homo sapiens 59-79 2495166-1 1989 The authors examined the relationship between the level of thymidylate synthase (TS) and the sensitivity to 5-fluorouracil (5-FU) and UFT, a combined oral preparation of 1-(2-tetrahydrofuryl)-5-fluorouracil (tegafur) and uracil in a molar ratio of 1:4. Fluorouracil 108-122 thymidylate synthetase Homo sapiens 81-83 2495166-1 1989 The authors examined the relationship between the level of thymidylate synthase (TS) and the sensitivity to 5-fluorouracil (5-FU) and UFT, a combined oral preparation of 1-(2-tetrahydrofuryl)-5-fluorouracil (tegafur) and uracil in a molar ratio of 1:4. Fluorouracil 124-128 thymidylate synthetase Homo sapiens 59-79 2495166-1 1989 The authors examined the relationship between the level of thymidylate synthase (TS) and the sensitivity to 5-fluorouracil (5-FU) and UFT, a combined oral preparation of 1-(2-tetrahydrofuryl)-5-fluorouracil (tegafur) and uracil in a molar ratio of 1:4. Fluorouracil 124-128 thymidylate synthetase Homo sapiens 81-83 2495166-8 1989 A correlation was noted between the TS level and decrease in size of the tumor exposed to 5-FU (r = -0.671) or UFT (r = -0.758): gastric cancer tissue with higher level of TS is more sensitive to 5-FU and UFT than is that with a lower TS level. Fluorouracil 90-94 thymidylate synthetase Homo sapiens 36-38 2495166-8 1989 A correlation was noted between the TS level and decrease in size of the tumor exposed to 5-FU (r = -0.671) or UFT (r = -0.758): gastric cancer tissue with higher level of TS is more sensitive to 5-FU and UFT than is that with a lower TS level. Fluorouracil 90-94 thymidylate synthetase Homo sapiens 172-174 2495166-8 1989 A correlation was noted between the TS level and decrease in size of the tumor exposed to 5-FU (r = -0.671) or UFT (r = -0.758): gastric cancer tissue with higher level of TS is more sensitive to 5-FU and UFT than is that with a lower TS level. Fluorouracil 90-94 thymidylate synthetase Homo sapiens 172-174 2495166-8 1989 A correlation was noted between the TS level and decrease in size of the tumor exposed to 5-FU (r = -0.671) or UFT (r = -0.758): gastric cancer tissue with higher level of TS is more sensitive to 5-FU and UFT than is that with a lower TS level. Fluorouracil 196-200 thymidylate synthetase Homo sapiens 36-38 2495166-8 1989 A correlation was noted between the TS level and decrease in size of the tumor exposed to 5-FU (r = -0.671) or UFT (r = -0.758): gastric cancer tissue with higher level of TS is more sensitive to 5-FU and UFT than is that with a lower TS level. Fluorouracil 196-200 thymidylate synthetase Homo sapiens 172-174 2495166-8 1989 A correlation was noted between the TS level and decrease in size of the tumor exposed to 5-FU (r = -0.671) or UFT (r = -0.758): gastric cancer tissue with higher level of TS is more sensitive to 5-FU and UFT than is that with a lower TS level. Fluorouracil 196-200 thymidylate synthetase Homo sapiens 172-174 2495166-9 1989 These findings show that the sensitivity to 5-FU and UFT of gastric cancer tissue is related to the TS level and that UFT shows promise for the treatment of patients with gastric cancer. Fluorouracil 44-48 thymidylate synthetase Homo sapiens 100-102 2731961-3 1989 Following administration of a cytotoxic dose of 5-fluorouracil, or lethal irradiation and transplantation of normal donor marrow, the levels of Thy-1 and Qa-m7 antigen expression rapidly increase, reaching a peak at the onset of regeneration: the nadir of marrow cellularity. Fluorouracil 48-62 Thy-1 cell surface antigen Homo sapiens 144-149 2624224-0 1989 In vitro and in vivo inhibition of thymidylate synthase of human colon cancer by 5-fluorouracil. Fluorouracil 81-95 thymidylate synthetase Homo sapiens 35-55 2846313-2 1988 Succinate dehydrogenase activity in the PHC was significantly decreased by adriamycin (ADM), mitomycin C (MMC), aclacinomycin A (ACR) (P less than 0.01), and 5-fluorouracil (5-FU), cisplatin (DDP) and carboquone (CQ) (P less than 0.05), as compared to findings in tissues from the metastatic liver tumors. Fluorouracil 174-178 acrosin Homo sapiens 129-132 3281726-1 1988 Marrow cells from 5-fluorouracil (5-FU)-treated mice formed few or no mixed erythroid colonies when plated in semisolid medium with interleukin 3 (IL 3) and erythropoietin (Ep) alone. Fluorouracil 18-32 erythropoietin Mus musculus 157-171 3281726-1 1988 Marrow cells from 5-fluorouracil (5-FU)-treated mice formed few or no mixed erythroid colonies when plated in semisolid medium with interleukin 3 (IL 3) and erythropoietin (Ep) alone. Fluorouracil 34-38 erythropoietin Mus musculus 157-171 3263749-3 1988 On the other hand in the presence of IL-2, NK cells are generated in cultures of BM from mice pretreated with 5-fluorouracil (5-FU, 150 mg/kg iv 4 days before harvesting), a treatment which has been shown to eliminate more differentiated but spare less differentiated BM precursors. Fluorouracil 126-130 interleukin 2 Mus musculus 37-41 28714970-5 2017 Scf deletion using Adipoq-Cre/ER inhibited haematopoietic regeneration after irradiation or 5-fluorouracil treatment, depleting HSCs and reducing mouse survival. Fluorouracil 92-106 kit ligand Mus musculus 0-3 3257232-6 1988 Bone marrow from mice pre-treated with 5-fluorouracil is greatly depleted of progenitor cells directly responsive to IL-3 or IL-5. Fluorouracil 39-53 interleukin 5 Mus musculus 125-129 3284210-4 1988 Recent laboratory studies have indicated that leucovorin can enhance the cytotoxicity of fluorouracil in vitro, evidently by enhancing inhibition of the key enzyme, thymidylate synthetase, by the fluorouracil metabolite, FdUMP (fluorodeoxyuridine monophosphate; a stable inactive FdUMP-reduced folate-thymidylate synthetase complex is formed). Fluorouracil 89-101 thymidylate synthetase Homo sapiens 165-187 3284210-4 1988 Recent laboratory studies have indicated that leucovorin can enhance the cytotoxicity of fluorouracil in vitro, evidently by enhancing inhibition of the key enzyme, thymidylate synthetase, by the fluorouracil metabolite, FdUMP (fluorodeoxyuridine monophosphate; a stable inactive FdUMP-reduced folate-thymidylate synthetase complex is formed). Fluorouracil 89-101 thymidylate synthetase Homo sapiens 301-323 3284210-4 1988 Recent laboratory studies have indicated that leucovorin can enhance the cytotoxicity of fluorouracil in vitro, evidently by enhancing inhibition of the key enzyme, thymidylate synthetase, by the fluorouracil metabolite, FdUMP (fluorodeoxyuridine monophosphate; a stable inactive FdUMP-reduced folate-thymidylate synthetase complex is formed). Fluorouracil 196-208 thymidylate synthetase Homo sapiens 165-187 28714373-7 2017 Finally, we assessed the role of miR-21 in mediating renal cell carcinoma chemoresistance and further showed that miR-21 silencing significantly (1) increased chemosensitivity of paclitaxel, 5-fluorouracil, oxaliplatin, and dovitinib; (2) decreased expression of multi-drug resistance genes; and (4) increased SLC22A1/OCT1, SLC22A2/OCT2, and SLC31A1/CTR1 platinum influx transporter expression. Fluorouracil 191-205 microRNA 21 Homo sapiens 114-120 28336806-0 2017 Fluorouracil Enhances Photodynamic Therapy of Squamous Cell Carcinoma via a p53-Independent Mechanism that Increases Protoporphyrin IX levels and Tumor Cell Death. Fluorouracil 0-12 transformation related protein 53, pseudogene Mus musculus 76-79 2977647-1 1987 The activity of 5"-deoxy-5-fluorouridine (dFUR) depends on its activation to 5-fluorouracil (FU) by pyrimidine nucleoside phosphorylases. Fluorouracil 77-91 fur Drosophila melanogaster 42-46 3815393-1 1987 We have identified amplification of the thymidylate synthase gene in a colonic tumor that had developed resistance to 5-fluorouracil/leucovorin combination chemotherapy. Fluorouracil 118-132 thymidylate synthetase Homo sapiens 40-60 3815393-3 1987 Since thymidylate synthase is a target enzyme for 5-fluorouracil, it is likely that the observed gene amplification is responsible for the resistance. Fluorouracil 50-64 thymidylate synthetase Homo sapiens 6-26 28336806-7 2017 Second, a 3- to 6-fold induction of p53 in 5-FU-pretreated tumors was noted. Fluorouracil 43-47 transformation related protein 53, pseudogene Mus musculus 36-39 28336806-9 2017 Furthermore, 5-FU pretreatment of 4T1 tumors (cells that completely lack p53), still led to significant beneficial inductions, that is, 2.5-fold for both PpIX and PDT-induced cell death. Fluorouracil 13-17 transformation related protein 53, pseudogene Mus musculus 73-76 28336806-10 2017 Thus, neoadjuvantal 5-FU combined with PDT represents a new therapeutic approach that appears useful even for p53-mutant and p53-null tumors. Fluorouracil 20-24 transformation related protein 53, pseudogene Mus musculus 110-113 28336806-10 2017 Thus, neoadjuvantal 5-FU combined with PDT represents a new therapeutic approach that appears useful even for p53-mutant and p53-null tumors. Fluorouracil 20-24 transformation related protein 53, pseudogene Mus musculus 125-128 28596680-12 2017 AXL silencing showed a subtle trend to restore colon cancer cell sensitivity to 5FU or irinotecan. Fluorouracil 80-83 AXL receptor tyrosine kinase Homo sapiens 0-3 28881661-8 2017 Through inducing ROS-mediated degradation of Mcl-1 ubiquitination, the triple combination of 5-FU, DTN and DHA resulted in the elevated apoptosis in CRC cells, thus to reduce the tumor size and weight. Fluorouracil 93-97 MCL1 apoptosis regulator, BCL2 family member Homo sapiens 45-50 28881661-9 2017 Taken together, this study suggests the triple combination of 5-FU+DTN+DHA exhibits an effective anticancer activity of overcoming drug resistance in colorectal cancer, mechanism as the elevated apoptosis mediated by an increase of ROS and Mcl-1 ubiquitination, may be a novel strategy for clinical colon cancer treatment. Fluorouracil 62-66 MCL1 apoptosis regulator, BCL2 family member Homo sapiens 240-245 27853901-1 2017 BACKGROUND: The impact of microsatellite instability (MSI) on survival in stage III colon cancer treated with adjuvant 5-fluorouracil-oxaliplatin combination (FOLFOX) chemotherapy is not clear. Fluorouracil 119-133 RB binding protein 4, chromatin remodeling factor Homo sapiens 54-57 3489636-1 1986 Bone marrow cells taken from mice treated eight days previously with 5-fluorouracil, formed colonies consisting of 10-100 cells after four days of incubation in methylcellulose cultures containing only 500 cells/dish, in the presence of partially purified synergistic factor from human placental-conditioned medium (SFHPlac) and macrophage colony-stimulating factor (CSF-1). Fluorouracil 69-83 colony stimulating factor 1 Homo sapiens 367-372 2947416-0 1986 Passage of 5"-dFUrd and its metabolites 5-FU and 5-FUH2 to CSF in a clinical phase 1 study. Fluorouracil 40-44 colony stimulating factor 2 Homo sapiens 59-62 2947416-2 1986 5"-dFUrd, 5"FU, and 5-FUH2 were shown to cross the blood-brain barrier to CSF. Fluorouracil 10-14 colony stimulating factor 2 Homo sapiens 74-77 3008760-6 1986 Subsequent to administration of FUra, thymidylate synthase activity was reduced greater than 75% in all tumors, but it recovered rapidly in tumors resistant to FUra. Fluorouracil 32-36 thymidylate synthetase Homo sapiens 38-58 27187663-4 2017 However, 5-FU, but not MTX, lowered the presence of DHFR-TS complex in the nucleus by 2.5-fold. Fluorouracil 9-13 dihydrofolate reductase Homo sapiens 52-56 2415245-9 1986 In several cell lines activities of nucleotide-degrading enzymes were rather high and interfered with the measurement of orotate phosphoribosyl transferase (OPRT) with FUra as substrate. Fluorouracil 168-172 uridine monophosphate synthetase Homo sapiens 121-155 2415245-9 1986 In several cell lines activities of nucleotide-degrading enzymes were rather high and interfered with the measurement of orotate phosphoribosyl transferase (OPRT) with FUra as substrate. Fluorouracil 168-172 uridine monophosphate synthetase Homo sapiens 157-161 27187663-4 2017 However, 5-FU, but not MTX, lowered the presence of DHFR-TS complex in the nucleus by 2.5-fold. Fluorouracil 9-13 thymidylate synthetase Homo sapiens 57-59 2415245-11 1986 The WiDr cell line had a relatively high OPRT activity which could explain its sensitivity to FUra. Fluorouracil 94-98 uridine monophosphate synthetase Homo sapiens 41-45 28521444-0 2017 MicroRNA-330 inhibited cell proliferation and enhanced chemosensitivity to 5-fluorouracil in colorectal cancer by directly targeting thymidylate synthase. Fluorouracil 75-89 thymidylate synthetase Homo sapiens 133-153 28521444-6 2017 Ectopic miR-330 expression decreased cell proliferation and enhanced cell chemosensitivity to 5-FU via the cell apoptosis pathway in CRC. Fluorouracil 94-98 microRNA 330 Homo sapiens 8-15 28521444-8 2017 Knockdown of TYMS inhibited CRC cell proliferation, and enhanced cell chemosensitivity to 5-FU by promoting cell apoptosis. Fluorouracil 90-94 thymidylate synthetase Homo sapiens 13-17 28521444-9 2017 In conclusion, the results of the present study indicated that miR-330 targeted TYMS to inhibit the proliferation and enhance the chemosensitivity of CRC cells to 5-FU by promoting cell apoptosis. Fluorouracil 163-167 microRNA 330 Homo sapiens 63-70 28521444-9 2017 In conclusion, the results of the present study indicated that miR-330 targeted TYMS to inhibit the proliferation and enhance the chemosensitivity of CRC cells to 5-FU by promoting cell apoptosis. Fluorouracil 163-167 thymidylate synthetase Homo sapiens 80-84 28207045-6 2017 Treatment with miR-21 and miR-30d antagonists sensitized hypoxic CRC cells to 5-FU. Fluorouracil 78-82 microRNA 21 Homo sapiens 15-21 28445968-0 2017 USP22 knockdown enhanced chemosensitivity of hepatocellular carcinoma cells to 5-Fu by up-regulation of Smad4 and suppression of Akt. Fluorouracil 79-83 ubiquitin specific peptidase 22 Homo sapiens 0-5 28388410-5 2017 We find that uric acid directly inhibits uridine monophosphate synthase (UMPS) and consequently reduces the sensitivity of cancer cells to the chemotherapeutic agent 5-fluorouracil. Fluorouracil 166-180 uridine monophosphate synthetase Homo sapiens 41-71 28388410-5 2017 We find that uric acid directly inhibits uridine monophosphate synthase (UMPS) and consequently reduces the sensitivity of cancer cells to the chemotherapeutic agent 5-fluorouracil. Fluorouracil 166-180 uridine monophosphate synthetase Homo sapiens 73-77 28069878-10 2017 Finally, the interaction between lncRNA MALAT1 and miR-218 was observed, which further indicated its prognostic value in patients who received standard FOLFOX (oxaliplatin combine with 5-fluorouracil and leucovorin) treatment. Fluorouracil 185-199 metastasis associated lung adenocarcinoma transcript 1 Homo sapiens 40-46 4053028-0 1985 Effects of uridine and thymidine on the degradation of 5-fluorouracil, uracil, and thymine by rat liver dihydropyrimidine dehydrogenase. Fluorouracil 55-69 dihydropyrimidine dehydrogenase Rattus norvegicus 104-135 4053028-1 1985 The kinetic properties and control mechanisms of 5-fluorouracil (5-FU), uracil, and thymine degradation by rat liver dihydropyrimidine dehydrogenase were studied in vitro. Fluorouracil 49-63 dihydropyrimidine dehydrogenase Rattus norvegicus 117-148 4053028-1 1985 The kinetic properties and control mechanisms of 5-fluorouracil (5-FU), uracil, and thymine degradation by rat liver dihydropyrimidine dehydrogenase were studied in vitro. Fluorouracil 65-69 dihydropyrimidine dehydrogenase Rattus norvegicus 117-148 4053028-4 1985 The specific activities of dihydropyrimidine dehydrogenase (nmol/min/mg of protein) for 5-FU, uracil, and thymine were 0.82, 0.68, and 0.56, respectively. Fluorouracil 88-92 dihydropyrimidine dehydrogenase Rattus norvegicus 27-58 28222070-11 2017 This was mediated by reduced expression of histone deacetylase 6 (HDAC6), which further inhibited the phosphorylation of Akt and the expression of thymidylate synthase (TYMS), the critical determinant of 5-FU cytotoxicity. Fluorouracil 204-208 thymidylate synthetase Homo sapiens 147-167 28222070-11 2017 This was mediated by reduced expression of histone deacetylase 6 (HDAC6), which further inhibited the phosphorylation of Akt and the expression of thymidylate synthase (TYMS), the critical determinant of 5-FU cytotoxicity. Fluorouracil 204-208 thymidylate synthetase Homo sapiens 169-173 27878398-0 2017 HSP90 is a promising target in gemcitabine and 5-fluorouracil resistant pancreatic cancer. Fluorouracil 47-61 heat shock protein 90 alpha family class A member 1 Homo sapiens 0-5 6744325-0 1984 Thymidylate synthetase inhibition in malignant tumors and normal liver of patients given intravenous 5-fluorouracil. Fluorouracil 101-115 thymidylate synthetase Homo sapiens 0-22 27878398-4 2017 The aim of this study was to evaluate the efficacy of different HSP90 inhibitors in gemcitabine and 5-FU resistant PC. Fluorouracil 100-104 heat shock protein 90 alpha family class A member 1 Homo sapiens 64-69 27878398-16 2017 HSP90 inhibition disrupts multiple signaling cascades in gemcitabine and 5-FU resistant PC simultaneously and promotes cancer cell apoptosis. Fluorouracil 73-77 heat shock protein 90 alpha family class A member 1 Homo sapiens 0-5 28000054-4 2017 We demonstrate that 5-FU, but not topotecan, increases NPC permeability, and disrupts Ran-mediated nuclear transport before the disruption of the NPC. Fluorouracil 20-24 RAN, member RAS oncogene family Homo sapiens 86-89 28000054-12 2017 Our results reveal a new mechanism of action for these therapeutics during apoptosis, opening the door to other potential combination chemotherapies that employ 5-FU as a calcium mediated inhibitor of Crm1-induced nuclear export of tumor suppressors. Fluorouracil 161-165 exportin 1 Homo sapiens 201-205 28382142-7 2017 Results: Ectopic expression of PRC1 significantly increased the chemoresistance, promoted the tumor growth and abrogated 5-FU-induced G2/M phase arrest via p21/p27-pRBs pathway. Fluorouracil 121-125 H3 histone pseudogene 16 Homo sapiens 156-159 28382142-7 2017 Results: Ectopic expression of PRC1 significantly increased the chemoresistance, promoted the tumor growth and abrogated 5-FU-induced G2/M phase arrest via p21/p27-pRBs pathway. Fluorouracil 121-125 interferon alpha inducible protein 27 Homo sapiens 160-163 27912078-8 2017 Although cancer therapeutic agents 5-fluorouracil and doxorubicin could not induce a robust p53 activation in the wild-type oocytes, they induced p53 nuclear accumulation in the Mdm2 and Mdm4 double heterozygous oocytes. Fluorouracil 35-49 transformation related protein 53, pseudogene Mus musculus 146-149 28352348-10 2017 5-FU+GA further decreased P53, survivin and TS mRNA and protein levels in the two CRC cell lines compared with single drugs, whereas increased P53 protein levels were observed in HCT116 cells. Fluorouracil 0-4 thymidylate synthetase Homo sapiens 44-46 28356933-5 2017 Analysis of cell viability in the control and DKK4 over-expressing cell lines, following treatment with 5-fluorouracil (5-Fu), YN968D1 or both, indicated that DKK4 over-expressing cells exhibit increased drug resistance. Fluorouracil 104-118 dickkopf WNT signaling pathway inhibitor 4 Homo sapiens 159-163 28356933-5 2017 Analysis of cell viability in the control and DKK4 over-expressing cell lines, following treatment with 5-fluorouracil (5-Fu), YN968D1 or both, indicated that DKK4 over-expressing cells exhibit increased drug resistance. Fluorouracil 120-124 dickkopf WNT signaling pathway inhibitor 4 Homo sapiens 159-163 28356933-8 2017 The present data suggested that DKK4 may enhance the resistance of colorectal cancer cells to 5-Fu and YN968D1 treatment, when used alone or in combination. Fluorouracil 94-98 dickkopf WNT signaling pathway inhibitor 4 Homo sapiens 32-36 28025107-7 2017 RESULTS: 5-FU and/or apigenin caused significant increase in tissue levels of Beclin-1, caspases 3, 9 and JNK activities, MDA with significant decrease in tumor volume, Mcl-1expression, tissue glutathione peroxidase and total antioxidant capacity and alleviated the histopathological changes with significant decrease of Ki-67 proliferation index compared to vehicle treated SEC control group. Fluorouracil 9-13 beclin 1, autophagy related Mus musculus 78-109 28051999-0 2017 FOXM1 evokes 5-fluorouracil resistance in colorectal cancer depending on ABCC10. Fluorouracil 13-27 ATP binding cassette subfamily C member 10 Homo sapiens 73-79 12865-1 1976 The influence of intracellular pH (pHi) upon 5-fluorouracil (5-FU) uptake has been studied in slices of Walker 256 carcinosarcoma and rat liver. Fluorouracil 45-59 glucose-6-phosphate isomerase Rattus norvegicus 35-38 12865-1 1976 The influence of intracellular pH (pHi) upon 5-fluorouracil (5-FU) uptake has been studied in slices of Walker 256 carcinosarcoma and rat liver. Fluorouracil 61-65 glucose-6-phosphate isomerase Rattus norvegicus 35-38 12865-4 1976 Uptake of 5-FU by liver slices appeared to follow a pattern predictable from the pHi and the pK of the drug. Fluorouracil 10-14 glucose-6-phosphate isomerase Rattus norvegicus 81-84 28051999-8 2017 Notably, treatment with ABCC10 inhibitor reversed FOXM1-induced resistance to 5-FU in vivo. Fluorouracil 78-82 ATP binding cassette subfamily C member 10 Homo sapiens 24-30 28051999-10 2017 Therefore, FOXM1 promotes 5-FU resistance by upregulating ABCC10, suggesting that FOXM1/ABCC10 axis may serve as a potential therapeutic target for 5-FU resistance in CRC patients. Fluorouracil 26-30 ATP binding cassette subfamily C member 10 Homo sapiens 58-64 28051999-10 2017 Therefore, FOXM1 promotes 5-FU resistance by upregulating ABCC10, suggesting that FOXM1/ABCC10 axis may serve as a potential therapeutic target for 5-FU resistance in CRC patients. Fluorouracil 26-30 ATP binding cassette subfamily C member 10 Homo sapiens 88-94 28051999-10 2017 Therefore, FOXM1 promotes 5-FU resistance by upregulating ABCC10, suggesting that FOXM1/ABCC10 axis may serve as a potential therapeutic target for 5-FU resistance in CRC patients. Fluorouracil 148-152 ATP binding cassette subfamily C member 10 Homo sapiens 58-64 28051999-10 2017 Therefore, FOXM1 promotes 5-FU resistance by upregulating ABCC10, suggesting that FOXM1/ABCC10 axis may serve as a potential therapeutic target for 5-FU resistance in CRC patients. Fluorouracil 148-152 ATP binding cassette subfamily C member 10 Homo sapiens 88-94 28098226-9 2017 Sensitivity of colorectal cancer cells to 5-fluorouracil (5-FU) was inversely correlated with BORIS expression. Fluorouracil 42-56 CCCTC-binding factor like Homo sapiens 94-99 6051753-0 1967 Coliphage MS2 containing 5-fluorouracil. Fluorouracil 25-39 MS2 Homo sapiens 10-13 28098226-9 2017 Sensitivity of colorectal cancer cells to 5-fluorouracil (5-FU) was inversely correlated with BORIS expression. Fluorouracil 58-62 CCCTC-binding factor like Homo sapiens 94-99 28098226-11 2017 BORIS silencing induced reactive oxygen species (ROS) production and apoptosis, whereas BORIS supplementation inhibited apoptosis induced by BORIS short interfering RNA (siRNA), hydrogen peroxide (H2O2) or 5-FU. Fluorouracil 206-210 CCCTC-binding factor like Homo sapiens 88-93 28098226-11 2017 BORIS silencing induced reactive oxygen species (ROS) production and apoptosis, whereas BORIS supplementation inhibited apoptosis induced by BORIS short interfering RNA (siRNA), hydrogen peroxide (H2O2) or 5-FU. Fluorouracil 206-210 CCCTC-binding factor like Homo sapiens 88-93 27924828-0 2016 rpL3 promotes the apoptosis of p53 mutated lung cancer cells by down-regulating CBS and NFkappaB upon 5-FU treatment. Fluorouracil 102-106 ribosomal protein L3 Homo sapiens 0-4 14343285-0 1965 COLIPHAGE MS2 CONTAINING 5-FLUOROURACIL. Fluorouracil 25-39 MS2 Homo sapiens 10-13 27924828-2 2016 In the present study, we reporte that rpL3 induced by 5-FU treatment in Calu-6 cells represses CBS transcription and reduces CBS protein stability leading to a decrease of CBS protein levels. Fluorouracil 54-58 ribosomal protein L3 Homo sapiens 38-42 27924828-4 2016 Furthermore, we demonstrate that rpL3 significantly enhances the apoptosis of 5-FU treated Calu-6 cells promoting the overexpression of the pro-apoptotic proteins Bax and the inhibition of the anti-apoptotic protein Bcl-2. Fluorouracil 78-82 ribosomal protein L3 Homo sapiens 33-37 27924828-5 2016 We finally demonstrate that rpL3 potentiates 5-FU efficacy inhibiting cell migration and invasion. Fluorouracil 45-49 ribosomal protein L3 Homo sapiens 28-32 27924828-6 2016 Our results suggest that combination of rpL3 and 5-FU is a promising strategy for chemotherapy of lung cancers lacking functional p53 that are resistant to 5-FU. Fluorouracil 156-160 ribosomal protein L3 Homo sapiens 40-44 27917904-6 2016 Furthermore, among TNM II and III gp130-high patients, those who were treated with 5-fluorouracil (5-FU) based adjuvant chemotherapy had better OS (P < 0.001). Fluorouracil 83-97 interleukin 6 cytokine family signal transducer Homo sapiens 34-39 27917904-6 2016 Furthermore, among TNM II and III gp130-high patients, those who were treated with 5-fluorouracil (5-FU) based adjuvant chemotherapy had better OS (P < 0.001). Fluorouracil 99-103 interleukin 6 cytokine family signal transducer Homo sapiens 34-39 28042500-6 2016 We found overexpressing miR-147 significantly inhibited HCC in vitro proliferation and migration, increased 5-FU chemosensitivity, and reduced in vivo tumorigenicity. Fluorouracil 108-112 microRNA 147a Homo sapiens 24-31 33910127-0 2021 SPARC enhances 5-FU chemosensitivity in gastric cancer by modulating epithelial-mesenchymal transition and apoptosis. Fluorouracil 15-19 secreted protein acidic and cysteine rich Homo sapiens 0-5 33910127-2 2021 In fact, SPARC proteins may have an effect on the chemoresistance of gastric cancer cells to 5-Fluorouracil (5-FU), which needs further research in the future. Fluorouracil 93-107 secreted protein acidic and cysteine rich Homo sapiens 9-14 27501171-12 2016 CONCLUSION: MiR-221 controls 5-FU resistance of EC partly via modulation of Wnt/beta-catenin-EMT pathways by direct targeting of DKK2 expression. Fluorouracil 29-33 microRNA 221 Homo sapiens 12-19 33910127-2 2021 In fact, SPARC proteins may have an effect on the chemoresistance of gastric cancer cells to 5-Fluorouracil (5-FU), which needs further research in the future. Fluorouracil 109-113 secreted protein acidic and cysteine rich Homo sapiens 9-14 33910127-3 2021 Therefore, the purpose of this study was to explore the relationship between SPARC proteins and the chemosensitivity of gastric cancer cells to 5-FU. Fluorouracil 144-148 secreted protein acidic and cysteine rich Homo sapiens 77-82 27501171-12 2016 CONCLUSION: MiR-221 controls 5-FU resistance of EC partly via modulation of Wnt/beta-catenin-EMT pathways by direct targeting of DKK2 expression. Fluorouracil 29-33 catenin beta 1 Homo sapiens 80-92 27501171-13 2016 MiR-221 may serve as a prognostic marker and therapeutic target for patients with 5-FU resistant EAC. Fluorouracil 82-86 microRNA 221 Homo sapiens 0-7 27569869-5 2016 In addition, variants in genes of the 5-FU metabolic pathway, including TYMS, MTHFR and DPYD also influenced capecitabine efficacy and toxicity. Fluorouracil 38-42 thymidylate synthetase Homo sapiens 72-76 27895768-1 2016 The present study aimed to investigate the interaction between miR-196 and its target gene homeobox B8 (HoxB8) in colorectal cancer (CRC) cells, and the sensitivity of miR-196 and HoxB8 to fluorouracil, leucovorin and oxaliplatin (FOLFOX4) chemotherapy (1,200 mg/m2 fluorouracil, 200 mg/m2 leucovorin and 85 mg/m2 oxaliplatin). Fluorouracil 189-201 homeobox B8 Homo sapiens 180-185 27895768-1 2016 The present study aimed to investigate the interaction between miR-196 and its target gene homeobox B8 (HoxB8) in colorectal cancer (CRC) cells, and the sensitivity of miR-196 and HoxB8 to fluorouracil, leucovorin and oxaliplatin (FOLFOX4) chemotherapy (1,200 mg/m2 fluorouracil, 200 mg/m2 leucovorin and 85 mg/m2 oxaliplatin). Fluorouracil 266-278 homeobox B8 Homo sapiens 91-102 33910127-4 2021 In vitro, after SPARC protein levels were regulated by plasmid, siRNA and human recombinant SPARC protein transfection in MGC-803, SGC-7901 and BGC-823 cells, we detected epithelial-mesenchymal transition (EMT), apoptosis markers and cell viability after 5-FU treatment. Fluorouracil 255-259 secreted protein acidic and cysteine rich Homo sapiens 16-21 27895768-1 2016 The present study aimed to investigate the interaction between miR-196 and its target gene homeobox B8 (HoxB8) in colorectal cancer (CRC) cells, and the sensitivity of miR-196 and HoxB8 to fluorouracil, leucovorin and oxaliplatin (FOLFOX4) chemotherapy (1,200 mg/m2 fluorouracil, 200 mg/m2 leucovorin and 85 mg/m2 oxaliplatin). Fluorouracil 266-278 homeobox B8 Homo sapiens 104-109 33910127-11 2021 Our results show that the SPARC protein could enhance 5-FU chemosensitivity in gastric cancer cell lines by inhibiting EMT and promoting cell apoptosis. Fluorouracil 54-58 secreted protein acidic and cysteine rich Homo sapiens 26-31 27651161-12 2016 Additionally, functional studies indicated that over-expression of RAD51B promoted cell proliferation, aneuploidy, and drug resistance, while RAD51B knockdown led to G1 arrest and sensitized cells to 5-fluorouracil (5-FU). Fluorouracil 216-220 RAD51 paralog B Mus musculus 67-73 27651161-12 2016 Additionally, functional studies indicated that over-expression of RAD51B promoted cell proliferation, aneuploidy, and drug resistance, while RAD51B knockdown led to G1 arrest and sensitized cells to 5-fluorouracil (5-FU). Fluorouracil 216-220 RAD51 paralog B Mus musculus 142-148 33866038-10 2021 Moreover, PAI-1 inhibitor treatment significantly alleviated the impaired hematopoietic regeneration in obese mice both after 5-fluorouracil injection and HSCT. Fluorouracil 126-140 serine (or cysteine) peptidase inhibitor, clade E, member 1 Mus musculus 10-15 27777774-0 2016 5-Fluorouracil upregulates cell surface B7-H1 (PD-L1) expression in gastrointestinal cancers. Fluorouracil 0-14 CD274 molecule Homo sapiens 40-45 27777774-0 2016 5-Fluorouracil upregulates cell surface B7-H1 (PD-L1) expression in gastrointestinal cancers. Fluorouracil 0-14 CD274 molecule Homo sapiens 47-52 27777774-7 2016 RESULTS: B7-H1 expression in human HCT 116 p53+/+ and HCT 116 p53-/- CRC cells lines, while low at baseline, can be induced by treatment with 5-FU. Fluorouracil 142-146 CD274 molecule Homo sapiens 9-14 34035223-0 2021 Retraction Note to: FOXM1 modulates 5-fluorouracil sensitivity in cholangiocarcinoma through thymidylate synthase (TYMS): implications of FOXM1-TYMS axis uncoupling in 5-FU resistance. Fluorouracil 168-172 thymidylate synthetase Homo sapiens 115-119 27777774-8 2016 OE33 baseline B7-H1 expression exceeded CRC cell maximal expression and could be further increased in a dose dependent manner following 5-FU treatment in the absence of immune cells. Fluorouracil 136-140 CD274 molecule Homo sapiens 14-19 27777774-11 2016 CONCLUSIONS: B7-H1/PD-L1 expression can be increased following treatment with 5-FU in gastrointestinal cancer cell lines, suggesting alternative mechanisms to classic immune-mediated upregulation. Fluorouracil 78-82 CD274 molecule Homo sapiens 13-18 27777774-11 2016 CONCLUSIONS: B7-H1/PD-L1 expression can be increased following treatment with 5-FU in gastrointestinal cancer cell lines, suggesting alternative mechanisms to classic immune-mediated upregulation. Fluorouracil 78-82 CD274 molecule Homo sapiens 19-24 27733154-6 2016 Low RRM2 transcript level significantly associated with poor response to the first-line palliative 5-FU-based chemotherapy in the testing set and with poor disease-free interval of patients in the validation set irrespective of 5-FU treatment. Fluorouracil 99-103 ribonucleotide reductase regulatory subunit M2 Homo sapiens 4-8 27733154-6 2016 Low RRM2 transcript level significantly associated with poor response to the first-line palliative 5-FU-based chemotherapy in the testing set and with poor disease-free interval of patients in the validation set irrespective of 5-FU treatment. Fluorouracil 228-232 ribonucleotide reductase regulatory subunit M2 Homo sapiens 4-8 27798882-13 2016 CONCLUSION: The synergistic effect of vandetanib with 5-FU is related to vandetanib-induced reduction of TYMS via down-regulation of cyclin D1. Fluorouracil 54-58 thymidylate synthetase Homo sapiens 105-109 27138786-13 2016 TS mRNA expression showed potentially predictive value in 5-fluorouracil treatment, and personalized treatment based on pharmacokinetics and pharmacodynamics proved to be clinically beneficial and is worthy of further clinical studies. Fluorouracil 58-72 thymidylate synthetase Homo sapiens 0-2 34040446-10 2021 There was an inverse relationship between the frequency of G-CSF use and the RDI of continuous infusion 5FU, r=-0.26 (p<0.001). Fluorouracil 104-107 colony stimulating factor 3 Homo sapiens 59-64 33986804-5 2021 The effect of E2F1 on gastric cancer cell sensitivity of 5-Fu was evaluated using cell viability assay and TdT-mediated dUTP Nick-End Labeling staining. Fluorouracil 57-61 DNA nucleotidylexotransferase L homeolog Xenopus laevis 107-110 27637357-3 2016 In the treatment of cancer with 5-fluorouracil, the administration of folates mechanistically leads to the formation of [6R]-5,10-methylene-tetrahydrofolate, and the increased concentration of this molecule leads to stabilization of the ternary complex comprising thymidylate synthase, 2"-deoxy-uridine-5"-monophosphate, and [6R]-5,10-methylene-tetrahydrofolate. Fluorouracil 32-46 thymidylate synthetase Homo sapiens 264-284 33986804-11 2021 E2F1 enhanced 5-Fu resistance in gastric cancer cells, and the E2F1 expression level was correlated with the prognosis of gastric cancer patients receiving 5-Fu therapy. Fluorouracil 14-18 E2F transcription factor 1 Homo sapiens 0-4 33986804-11 2021 E2F1 enhanced 5-Fu resistance in gastric cancer cells, and the E2F1 expression level was correlated with the prognosis of gastric cancer patients receiving 5-Fu therapy. Fluorouracil 156-160 E2F transcription factor 1 Homo sapiens 0-4 33986804-11 2021 E2F1 enhanced 5-Fu resistance in gastric cancer cells, and the E2F1 expression level was correlated with the prognosis of gastric cancer patients receiving 5-Fu therapy. Fluorouracil 156-160 E2F transcription factor 1 Homo sapiens 63-67 33753854-11 2021 C1TC and SAHH have been shown to be useful biomarkers for predicting 5-FU sensitivity as a substitute for the CD-DST in adjuvant chemotherapy for PDAC. Fluorouracil 69-73 adenosylhomocysteinase Homo sapiens 9-13 33731881-7 2021 The median expression of 5-FU-related genes TYMS, TYMP, and DYPD was significantly higher in mucinous CRC compared to non-mucinous CRC (p < 0.001, p = 0.003, p < 0.001, respectively). Fluorouracil 25-29 thymidylate synthetase Homo sapiens 44-48 27618153-6 2016 Myeloperoxidase activity was significantly increased in the jejunum and ileum following 5-FU, compared to saline controls. Fluorouracil 88-92 myeloperoxidase Rattus norvegicus 0-15 32647340-0 2021 Increased S1P induces S1PR2 internalization to blunt the sensitivity of colorectal cancer to 5-fluorouracil via promoting intracellular uracil generation. Fluorouracil 93-107 sphingosine-1-phosphate receptor 2 Homo sapiens 22-27 32647340-2 2021 In this study we investigated the role of S1PR2 internalization in 5-fluorouracil (5-FU) resistance in human colorectal cancer (CRC). Fluorouracil 67-81 sphingosine-1-phosphate receptor 2 Homo sapiens 42-47 32647340-2 2021 In this study we investigated the role of S1PR2 internalization in 5-fluorouracil (5-FU) resistance in human colorectal cancer (CRC). Fluorouracil 83-87 sphingosine-1-phosphate receptor 2 Homo sapiens 42-47 32647340-6 2021 In HCT116 and HT-29 cells, application of S1P (10 muM) empowered S1PR2 to internalize from PM to ER, thus inducing 5-FU resistance, whereas the specific S1PR2 inhibitor JTE-013 (10 muM) effectively inhibited S1P-induced S1PR2 internalization. Fluorouracil 115-119 sphingosine-1-phosphate receptor 2 Homo sapiens 65-70 33788740-7 2021 MDM4-transduced NUGC4 cells formed twice as many colonies and had a higher 50% inhibitory concentration for 5-fluorouracil and oxaliplatin than did the control cells. Fluorouracil 108-122 MDM4 regulator of p53 Homo sapiens 0-4 30990333-3 2021 The combination of PGG and 5-FU had synergistic effects on reversal the aggressive phenotypes of HepG2 cells, increasing the proportion of Bax/Bcl-2, promoting the activation of caspase-9 and caspase-3, and inducing apoptosis. Fluorouracil 27-31 caspase 9 Homo sapiens 178-187 27671231-5 2016 Co-treatment of DY and 5-FU significantly elevated ROS levels, up-regulated Bax/Bcl-2 ratio and triggered mitochondrial dysfunction, followed by a release of cytochrome c and up-regulation of proteins such as cleaved-caspase-9/3 and cleaved-PARP. Fluorouracil 23-27 caspase 9 Homo sapiens 217-226 27524242-9 2016 Flow cytometric analysis showed that 3-MA treatment, MALAT1 siRNA and miR-216b mimics all promoted 5-FU induced apoptosis in BEL-7402/5-FU cells. Fluorouracil 99-103 metastasis associated lung adenocarcinoma transcript 1 Homo sapiens 53-59 27524242-9 2016 Flow cytometric analysis showed that 3-MA treatment, MALAT1 siRNA and miR-216b mimics all promoted 5-FU induced apoptosis in BEL-7402/5-FU cells. Fluorouracil 99-103 microRNA 216b Homo sapiens 70-78 27517750-1 2016 5-fluorodeoxyuridine (5-FdU, floxuridine) is active against multiple cancers through the inhibition of thymidylate synthase, which consequently introduces uracil and 5-FU incorporation into the genome. Fluorouracil 166-170 thymidylate synthetase Homo sapiens 103-123 27404124-9 2016 These results suggest that the induction of GATA-6 dysfunction may be more effective for chemotherapy for colorectal cancer, although the mechanism underlying the synergistic effect of 5-FU and anisomycin remains unknown. Fluorouracil 185-189 GATA binding protein 6 Homo sapiens 44-50 33658938-0 2020 Higher ETV5 Expression Associates With Poor 5-Florouracil-Based Adjuvant Therapy Response in Colon Cancer. Fluorouracil 44-57 ETS variant transcription factor 5 Homo sapiens 7-11 33658938-6 2020 The present study suggests ETV5 expression as a strong predictive biomarker for 5-FU-based adjCTX response in stage II/III CC patients. Fluorouracil 80-84 ETS variant transcription factor 5 Homo sapiens 27-31 33147611-0 2021 A management of neutropenia using granulocyte colony stimulating factor support for chemotherapy consisted of docetaxel, cisplatin and 5-fluorouracil in patients with oesophageal squamous cell carcinoma. Fluorouracil 135-149 colony stimulating factor 3 Homo sapiens 34-71 33147611-1 2021 BACKGROUND: An exploratory study was designed to evaluate the efficacy of granulocyte colony stimulating factor support for chemotherapy consisting of docetaxel, cisplatin and 5-fluorouracil chemotherapy in patients with oesophageal cancer. Fluorouracil 176-190 colony stimulating factor 3 Homo sapiens 74-111 33147611-12 2021 CONCLUSIONS: Granulocyte colony stimulating factor support including secondary prophylactic usage may be feasible for maintaining the intensity of docetaxel, cisplatin and 5-fluorouracil chemotherapy in patients with oesophageal cancer. Fluorouracil 172-186 colony stimulating factor 3 Homo sapiens 13-50 33373916-0 2021 Neutrophil elastase inhibitor (MPH-966) improves intestinal mucosal damage and gut microbiota in a mouse model of 5-fluorouracil-induced intestinal mucositis. Fluorouracil 114-128 elastase, neutrophil expressed Mus musculus 0-19 33641785-8 2021 JSD caused down-regulated HIF-1alpha, PI3K, AKT/p-AKT, HKII and Glut1, as well as up-regulated Caspase3 and Caspase9 in HCT-8/5-FU cells and tumor tissues. Fluorouracil 126-130 caspase 9 Homo sapiens 108-116 33634982-8 2021 Synergistic inhibition of the LIF/JAK1/STAT3 and NF-kB signaling pathways by ATO and 5-FU/cisplatin is a potential molecular mechanism underlying the differentiation effect. Fluorouracil 85-89 LIF interleukin 6 family cytokine Homo sapiens 30-33 33634982-9 2021 CONCLUSIONS: ATO induced the differentiation of HCC CSCs and potentiated the cytotoxic effects of 5-FU/cisplatin through synergistic inhibition of the LIF/JAK1/STAT3 and NF-kB signaling pathways. Fluorouracil 98-102 LIF interleukin 6 family cytokine Homo sapiens 151-154 33552264-7 2021 The silencing of P4HA1 resulted in decreased cell proliferation, cell cycle arrest in the G1 phase, decreased tumorsphere formation, decreased tumorsphere volume, increased susceptibility to 5-fluorouracil and increased caspase-3 activity. Fluorouracil 191-205 prolyl 4-hydroxylase subunit alpha 1 Homo sapiens 17-22 33569416-16 2021 Conclusions: Our results demonstrated that 5-FU treatment upregulated miR-21, which directly repressed PDCD4, and subsequently activated the JNK pathway, leading to the upregulation of ABCG2 in CRC cells. Fluorouracil 43-47 microRNA 21 Homo sapiens 70-76 27220321-4 2016 Cell Counting Kit-8 (CCK-8) assay showed that transfection of pCDNA3.1(+)-SH3GL1 increased while transfection of SH3GL1 siRNA decreased cell viability in response to 5-fluorouracil (5-FU) treatment (P < 0.05). Fluorouracil 166-180 SH3-domain GRB2-like 1 Mus musculus 113-119 33140501-2 2021 5-Fluorouracil (5-FU) is an anticancer nucleoside analog that both inhibits thymidylate synthase (TS) and causes DNA damage via the misincorporation of FdUTP and dUTP into DNA under the conditions of dTTP depletion. Fluorouracil 0-14 thymidylate synthetase Homo sapiens 76-96 31846964-3 2021 The objective of this study was to determine the role of the NLRP3 inflammasome in 5-FU-induced small intestinal mucositis. Fluorouracil 83-87 NLR family, pyrin domain containing 3 Mus musculus 61-66 31846964-4 2021 METHODS: Small intestinal mucositis was induced in wild-type, NLRP3-/-, and caspase-1-/- mice by intraperitoneal injection of 5-FU. Fluorouracil 126-130 NLR family, pyrin domain containing 3 Mus musculus 62-67 31846964-9 2021 NLRP3-/- mice exhibited less severe 5-FU-induced mucositis, and this phenotype was mimicked by genetic depletion or pharmacological inhibition of caspase-1. Fluorouracil 36-40 NLR family, pyrin domain containing 3 Mus musculus 0-5 27220321-4 2016 Cell Counting Kit-8 (CCK-8) assay showed that transfection of pCDNA3.1(+)-SH3GL1 increased while transfection of SH3GL1 siRNA decreased cell viability in response to 5-fluorouracil (5-FU) treatment (P < 0.05). Fluorouracil 182-186 SH3-domain GRB2-like 1 Mus musculus 113-119 27486820-6 2016 Upon chemotherapy macrophages increase Gas6 synthesis, which significantly attenuates the cytotoxic effect of 5-FU chemotherapy on tumor cells. Fluorouracil 110-114 growth arrest specific 6 Homo sapiens 39-43 31846964-13 2021 CONCLUSIONS: NLRP3 inflammasome activation may exacerbate 5-FU-induced small intestinal mucositis via IL-1beta maturation. Fluorouracil 58-62 NLR family, pyrin domain containing 3 Mus musculus 13-18 27648358-3 2016 In the present study, we show that miR-122 confers resistance to 5-fluorouracil induced hepatocellular carcinoma cell apoptosis in vitro and reduces the potency of 5-fluorouracil in the inhibition of tumor growth in a mouse xenograft model in vivo. Fluorouracil 65-79 microRNA 122 Mus musculus 35-42 33285053-2 2021 As the target enzyme for capecitabine, thymidylate synthase (TYMS) plays a key role for 5-fluorouracil metabolism and has been associated with some side effects caused by capecitabine. Fluorouracil 88-102 thymidylate synthetase Homo sapiens 39-59 27648358-3 2016 In the present study, we show that miR-122 confers resistance to 5-fluorouracil induced hepatocellular carcinoma cell apoptosis in vitro and reduces the potency of 5-fluorouracil in the inhibition of tumor growth in a mouse xenograft model in vivo. Fluorouracil 164-178 microRNA 122 Mus musculus 35-42 33285053-2 2021 As the target enzyme for capecitabine, thymidylate synthase (TYMS) plays a key role for 5-fluorouracil metabolism and has been associated with some side effects caused by capecitabine. Fluorouracil 88-102 thymidylate synthetase Homo sapiens 61-65 27385266-9 2016 Methylation of IGFBP3, mir148a and PTEN are found to be predictive markers for 5-FU and EGFR therapy respectively. Fluorouracil 79-83 insulin like growth factor binding protein 3 Homo sapiens 15-21 33051247-3 2020 Interestingly, we found that let-7c exhibited a strong synergism with 5-fluorouracil (5-FU) in the inhibition of HCC cell viability, as manifested by average combination indices of 0.3 and 0.5 in Hep3B and Huh7 cells, respectively. Fluorouracil 86-90 microRNA let-7c Homo sapiens 29-35 33051247-5 2020 Further studies showed that protein levels of multidrug resistance-associated protein 5 (MRP5/ABCC5), a 5-FU efflux transporter, were reduced around 50% by let-7c in HCC cells. Fluorouracil 104-108 microRNA let-7c Homo sapiens 156-162 33051247-7 2020 Since 5-FU is an irreversible inhibitor of thymidylate synthetase (TS), we investigated the interactions of let-7c with 5-FU at pharmacodynamic level. Fluorouracil 120-124 microRNA let-7c Homo sapiens 108-114 33051247-9 2020 Collectively, these results indicate that let-7c interacts with 5-FU at both pharmacokinetic and pharmacodynamic levels, and these findings shall offer insight into molecular mechanisms of synergistic drug combinations. Fluorouracil 64-68 microRNA let-7c Homo sapiens 42-48 33051247-12 2020 In particular, let-7c enhances 5-FU exposure (via suppressing ABCC5/MRP5 expression) and co-targets thymidylate synthase with 5-FU (let-7c reduces protein expression while 5-FU irreversibly inactivates enzyme). Fluorouracil 31-35 microRNA let-7c Homo sapiens 15-21 33051247-12 2020 In particular, let-7c enhances 5-FU exposure (via suppressing ABCC5/MRP5 expression) and co-targets thymidylate synthase with 5-FU (let-7c reduces protein expression while 5-FU irreversibly inactivates enzyme). Fluorouracil 126-130 microRNA let-7c Homo sapiens 15-21 33051247-12 2020 In particular, let-7c enhances 5-FU exposure (via suppressing ABCC5/MRP5 expression) and co-targets thymidylate synthase with 5-FU (let-7c reduces protein expression while 5-FU irreversibly inactivates enzyme). Fluorouracil 126-130 thymidylate synthetase Homo sapiens 100-120 27385266-9 2016 Methylation of IGFBP3, mir148a and PTEN are found to be predictive markers for 5-FU and EGFR therapy respectively. Fluorouracil 79-83 microRNA 148a Homo sapiens 23-30 33051247-12 2020 In particular, let-7c enhances 5-FU exposure (via suppressing ABCC5/MRP5 expression) and co-targets thymidylate synthase with 5-FU (let-7c reduces protein expression while 5-FU irreversibly inactivates enzyme). Fluorouracil 126-130 microRNA let-7c Homo sapiens 132-138 27385266-9 2016 Methylation of IGFBP3, mir148a and PTEN are found to be predictive markers for 5-FU and EGFR therapy respectively. Fluorouracil 79-83 phosphatase and tensin homolog Homo sapiens 35-39 33051247-12 2020 In particular, let-7c enhances 5-FU exposure (via suppressing ABCC5/MRP5 expression) and co-targets thymidylate synthase with 5-FU (let-7c reduces protein expression while 5-FU irreversibly inactivates enzyme). Fluorouracil 126-130 microRNA let-7c Homo sapiens 15-21 26392091-4 2016 The analysis of the changes in the expression of genes involved in the response to DNA damage (CDKN1A, GADD45A, MDM2), apoptosis (BAX, BCL2) and oncogenesis (MYC, JUN) showed that 5-FU, CDDP and ET upregulated the genes involved in DNA damage response, while the anti-apoptotic gene BCL2 and oncogene MYC were downregulated. Fluorouracil 180-184 MYC proto-oncogene, bHLH transcription factor Homo sapiens 158-161 32377978-3 2020 DFP-11207 is a novel oral cytotoxic agent that combines a 5-FU pro-drug with a reversible DPD inhibitor and a potent inhibitor of OPRT, resulting in enhanced pharmacological activity of 5-FU with decreased gastrointestinal and myelosuppressive toxicities. Fluorouracil 186-190 uridine monophosphate synthetase Homo sapiens 130-134 26392091-4 2016 The analysis of the changes in the expression of genes involved in the response to DNA damage (CDKN1A, GADD45A, MDM2), apoptosis (BAX, BCL2) and oncogenesis (MYC, JUN) showed that 5-FU, CDDP and ET upregulated the genes involved in DNA damage response, while the anti-apoptotic gene BCL2 and oncogene MYC were downregulated. Fluorouracil 180-184 MYC proto-oncogene, bHLH transcription factor Homo sapiens 301-304 27446402-3 2016 In a previous study, it was demonstrated that STK17A, a proapoptotic gene, was significantly downregulated in acquired resistance phenotypes of colon cancer cells that are resistant to oxaliplatin and 5-fluorouracil. Fluorouracil 201-215 serine/threonine kinase 17a Homo sapiens 46-52 26883251-7 2016 Under different concentrations of 5-FU and paclitaxel in MDA-MB231 cell, E-cadherin mRNA and protein expressions increased gradually with the increase of concentrations, and Vimentin and N-cadherin mRNA and protein expressions decreased gradually with the decrease of concentrations (all P < 0.05). Fluorouracil 34-38 vimentin Homo sapiens 174-182 33098378-0 2020 Loganetin and 5-fluorouracil synergistically inhibit the carcinogenesis of gastric cancer cells via down-regulation of the Wnt/beta-catenin pathway. Fluorouracil 14-28 catenin beta 1 Homo sapiens 127-139 26886287-1 2016 This work aims to evaluate the impact of 2-morpholino-8-phenyl-4H-chromen-4-one (LY294002) combined 5-fluorouracil (5-FU) for the activity of CD90+ liver cancer cells derived from the human liver cancer cell line MHCC97H. Fluorouracil 100-114 Thy-1 cell surface antigen Homo sapiens 142-146 26886287-1 2016 This work aims to evaluate the impact of 2-morpholino-8-phenyl-4H-chromen-4-one (LY294002) combined 5-fluorouracil (5-FU) for the activity of CD90+ liver cancer cells derived from the human liver cancer cell line MHCC97H. Fluorouracil 116-120 Thy-1 cell surface antigen Homo sapiens 142-146 27323852-0 2016 Nicotinamide N-methyltransferase enhances resistance to 5-fluorouracil in colorectal cancer cells through inhibition of the ASK1-p38 MAPK pathway. Fluorouracil 56-70 mitogen-activated protein kinase kinase kinase 5 Homo sapiens 124-128 33261601-5 2020 CSN8 overexpression arrested cell proliferation, upregulated key dormancy marker (NR2F1, DEC2, p27) and hypoxia response genes (HIF-1alpha, GLUT1), and dramatically enhanced survival under hypoxia, serum deprivation, or chemo-drug 5-fluorouracil treatment conditions. Fluorouracil 231-245 COP9 signalosome subunit 8 Homo sapiens 0-4 27400751-4 2016 RESULTS: We found from Cox hazard models, logrank test and Wilcoxon test that osteopontin exon 4 was associated with a favorable response to tamoxifen, but a poor response to chemotherapy with CMF (cyclophosphamide, methotrexate, fluorouracil). Fluorouracil 230-242 secreted phosphoprotein 1 Homo sapiens 78-89 33312758-5 2020 We manifested that intratumoral CD103+CD4+ T cells in gastric cancer predicted poor overall survival and inferior responsiveness to fluorouracil-based ACT. Fluorouracil 132-144 integrin subunit alpha E Homo sapiens 32-37 33312758-8 2020 Overall, this study revealed that intratumoral CD103+CD4+T cell infiltration defined immunoevasive contexture and predicted poor prognosis and inferior responsiveness to fluorouracil-based ACT. Fluorouracil 170-182 integrin subunit alpha E Homo sapiens 47-52 33312377-9 2020 Gemcitabine and 5-FU and doxorubicin reacted favourably with most concentrations of bromelain and NAC investigated. Fluorouracil 16-20 synuclein alpha Homo sapiens 98-101 27085973-13 2016 This will help in selecting the best therapeutic option, 5-fluorouracil in combination with XK469, for patients overexpressing GAS2 in CRC cells. Fluorouracil 57-71 growth arrest specific 2 Homo sapiens 127-131 32977944-7 2020 Generally speaking, our results indicated that miR-149 contributes to resistance of 5-FU in gastric cancer via targeting TREM2 and regulating beta-catenin pathway. Fluorouracil 84-88 microRNA 149 Homo sapiens 47-54 32977944-7 2020 Generally speaking, our results indicated that miR-149 contributes to resistance of 5-FU in gastric cancer via targeting TREM2 and regulating beta-catenin pathway. Fluorouracil 84-88 catenin beta 1 Homo sapiens 142-154 33177877-0 2020 Inhibition of CDK1 Reverses the Resistance of 5-Fu in Colorectal Cancer. Fluorouracil 46-50 cyclin dependent kinase 1 Homo sapiens 14-18 33177877-4 2020 This study aimed to clarify the correlation between cyclin-dependent kinase 1 (CDK1) and 5-Fu-induced tumor resistance. Fluorouracil 89-93 cyclin dependent kinase 1 Homo sapiens 52-77 33177877-4 2020 This study aimed to clarify the correlation between cyclin-dependent kinase 1 (CDK1) and 5-Fu-induced tumor resistance. Fluorouracil 89-93 cyclin dependent kinase 1 Homo sapiens 79-83 33177877-5 2020 Materials and Methods: Cell proliferation and invasion experiments showed that down-regulation of CDK1 inhibited fluorouracil-resistant CRC cell proliferation. Fluorouracil 113-125 cyclin dependent kinase 1 Homo sapiens 98-102 33177877-6 2020 The expression level of CDK1 was detected in 5-Fu-resistant CRC cells in vitro. Fluorouracil 45-49 cyclin dependent kinase 1 Homo sapiens 24-28 32118594-2 2020 In addition, we aim to assess the correlation between TS and ERCC-1 expression and the response of these cases to oxaliplatin and 5-fluorouracil chemotherapy (FOLFOX). Fluorouracil 130-144 thymidylate synthetase Homo sapiens 54-56 32118594-2 2020 In addition, we aim to assess the correlation between TS and ERCC-1 expression and the response of these cases to oxaliplatin and 5-fluorouracil chemotherapy (FOLFOX). Fluorouracil 130-144 ERCC excision repair 1, endonuclease non-catalytic subunit Homo sapiens 61-67 33000179-0 2020 Role of ARID1A in epithelial-mesenchymal transition in breast cancer and its effect on cell sensitivity to 5-FU. Fluorouracil 107-111 AT-rich interaction domain 1A Homo sapiens 8-14 33000179-6 2020 Proliferation assay revealed that ARID1A silencing increased cell viability and partially reversed the inhibitory effects of 5-fluorouracil (5-FU) on the MCF7 cells, while ARID1A overexpression exerted an opposite effect on the MDA-MB-231 cells. Fluorouracil 125-139 AT-rich interaction domain 1A Homo sapiens 34-40 33000179-6 2020 Proliferation assay revealed that ARID1A silencing increased cell viability and partially reversed the inhibitory effects of 5-fluorouracil (5-FU) on the MCF7 cells, while ARID1A overexpression exerted an opposite effect on the MDA-MB-231 cells. Fluorouracil 141-145 AT-rich interaction domain 1A Homo sapiens 34-40 33000179-7 2020 ARID1A silencing promoted proliferation, migration, invasion and angiogenesis, and partly reversed the inhibitory effects of 5-FU on cell biological behaviors, while the overexpression of ARID1A further enhanced the inhibitory effect of 5-FU on the cells. Fluorouracil 125-129 AT-rich interaction domain 1A Homo sapiens 0-6 33000179-7 2020 ARID1A silencing promoted proliferation, migration, invasion and angiogenesis, and partly reversed the inhibitory effects of 5-FU on cell biological behaviors, while the overexpression of ARID1A further enhanced the inhibitory effect of 5-FU on the cells. Fluorouracil 237-241 AT-rich interaction domain 1A Homo sapiens 0-6 33000179-7 2020 ARID1A silencing promoted proliferation, migration, invasion and angiogenesis, and partly reversed the inhibitory effects of 5-FU on cell biological behaviors, while the overexpression of ARID1A further enhanced the inhibitory effect of 5-FU on the cells. Fluorouracil 237-241 AT-rich interaction domain 1A Homo sapiens 188-194 33000179-9 2020 On the whole, the findings of the present study demonstrate that ARID1A exerts an antitumor effect on breast cancer, and its overexpression can enhance the sensitivity of breast cancer cells to 5-FU. Fluorouracil 194-198 AT-rich interaction domain 1A Homo sapiens 65-71 33087710-0 2020 5-FU promotes stemness of colorectal cancer via p53-mediated WNT/beta-catenin pathway activation. Fluorouracil 0-4 catenin beta 1 Homo sapiens 65-77 33087710-6 2020 These findings indicate p53 as a critical mediator of 5-FU-induced CSC activation via the WNT/beta-catenin signaling pathway and highlight the significance of combinatorial treatment of WNT inhibitor and 5-FU as a compelling therapeutic strategy to improve the poor outcomes of current 5-FU-based therapies for CRC patients. Fluorouracil 54-58 catenin beta 1 Homo sapiens 94-106 33086767-1 2020 Inhibition of thymidylate synthase (TS) is the primary mode of action for 5-fluorouracil (5FU) chemotherapy. Fluorouracil 74-88 thymidylate synthetase Homo sapiens 14-34 33086767-1 2020 Inhibition of thymidylate synthase (TS) is the primary mode of action for 5-fluorouracil (5FU) chemotherapy. Fluorouracil 74-88 thymidylate synthetase Homo sapiens 36-38 33086767-1 2020 Inhibition of thymidylate synthase (TS) is the primary mode of action for 5-fluorouracil (5FU) chemotherapy. Fluorouracil 90-93 thymidylate synthetase Homo sapiens 14-34 33086767-1 2020 Inhibition of thymidylate synthase (TS) is the primary mode of action for 5-fluorouracil (5FU) chemotherapy. Fluorouracil 90-93 thymidylate synthetase Homo sapiens 36-38 33086767-8 2020 After applying this comprehensive naming system to our data, we demonstrated that the number of upstream stimulatory factor (USF1-)binding sites in the TSER was significantly associated with gastrointestinal toxicity in 5FU treatment. Fluorouracil 220-223 upstream transcription factor 1 Homo sapiens 125-129 33193874-14 2020 Conclusions: Our study reveals the molecular regulation of angiogenesis in 5-FU-resistant colon cancer and suggests that the GDF15-POSTN axis may be a novel target for anti-angiogenic therapies in colon cancer. Fluorouracil 75-79 periostin Homo sapiens 131-136 31983282-7 2020 Taken together, our data suggest that PRKDC-mediated phosphorylation of PRKAG1 primes AMPK complex to the lysosomal activation by STK11 in cancer cells thereby linking DNA damage response to autophagy and cellular metabolism.Abbreviations: AXIN1: axin 1; 3-MA: 3-methyladenine; 5-FU: 5-fluorouracil; AA mutant: double alanine mutant (S192A, T284A) of PRKAG1; ACACA: acetyl-CoA carboxylase alpha; AICAR: 5-Aminoimidazole-4-carboxamide ribonucleotide; AMPK: AMP-activated protein kinase; ATG: autophagy-related; ATM: ataxia telangiectasia mutated; ATR: ATM serine/threonine kinase; AV: autophagic vacuole; AVd: degradative autophagic vacuole; AVi: initial autophagic vacuole; BECN1: beclin 1; BSA: bovine serum albumin; CBS: cystathionine beta-synthase; CDK7: cyclin dependent kinase 7; CDKN1A: cyclin dependent kinase inhibitor 1A; EGFP: enhanced green fluorescent protein; GAPDH: glyceraldehyde-3-phosphate dehydrogenase; GST: glutathione S transferase; H2AX/H2AFX: H2A.X variant histone; HBSS: Hanks balanced salt solution; IP: immunopurification; IR: ionizing radiation; MAP1LC3/LC3: microtubule associated protein 1 light chain 3; MAP3K9: mitogen-activated protein kinase kinase kinase 9; mRFP: monomeric red fluorescent protein; mCh: mCherry; MCM7: minichromosome maintenance complex component 7; MTORC1: mechanistic target of rapamycin kinase complex 1; NHEJ: non-homologous end joining; NRBP2: nuclear receptor binding protein 2; NTC: non-targeting control; NUAK1: NUAK family kinase 1; PBS: phosphate-buffered saline; PIK3AP1: phosphoinositide-3-kinase adaptor protein 1; PIK3CA: phosphatidylinositol-4,5-biphosphate 3-kinase catalytic subunit alpha; PIKK: phosphatidylinositol 3-kinase-related kinase; PRKAA: protein kinase AMP-activated catalytic subunit alpha; PRKAB: protein kinase AMP-activated non-catalytic subunit beta; PRKAG: protein kinase AMP-activated non-catalytic subunit gamma; PRKDC: protein kinase, DNA-activated, catalytic subunit; RLuc: Renilla luciferase; RPS6KB1: ribosomal protein S6 kinase B1; SQSTM1: sequestosome 1; STK11/LKB1: serine/threonine kinase 11; TP53: tumor protein p53; TSKS: testis specific serine kinase substrate; ULK1: unc-51 like autophagy activating kinase 1; WIPI2: WD repeat domain, phosphoinositide interacting 2; WT: wild type. Fluorouracil 278-282 protein kinase AMP-activated non-catalytic subunit gamma 1 Homo sapiens 72-78 27101738-9 2016 D5D knockdown along with DGLA treatment also enhanced the cytotoxicities of various chemotherapeutic drugs, including 5-fluorouracil, regorafenib, and irinotecan, potentially through the activation of pro-apoptotic proteins, e.g. p53 and caspase 9. Fluorouracil 118-132 fatty acid desaturase 1 Homo sapiens 0-3 32944000-0 2020 Epigenetic regulation of osteopontin splicing isoform c defines its role as a microenvironmental factor to promote the survival of colon cancer cells from 5-FU treatment. Fluorouracil 155-159 secreted phosphoprotein 1 Homo sapiens 25-36 32944000-5 2020 Methods: We assayed precisely the abundance of major OPN splicing isoforms under 5-FU treatments in colon cancer cell lines with different sensitivities to 5-FU, and also evaluated the effects of the condition medium from OPN splicing isoforms overexpressed cells on cell functions. Fluorouracil 81-85 secreted phosphoprotein 1 Homo sapiens 53-56 32944000-8 2020 OPNc as a secretory protein in the conditioned medium exerted a more potent effect to promote cell survival in 5-FU than other OPN isoforms. Fluorouracil 111-115 secreted phosphoprotein 1 Homo sapiens 0-3 32675286-2 2020 5-FU is thought to inhibit the enzyme thymidylate synthase, which plays a role in nucleotide synthesis and has been found to induce single- and double-strand DNA breaks. Fluorouracil 0-4 thymidylate synthetase Homo sapiens 38-58 32838518-6 2020 Western blot analysis reveals the formation of ternary complex of thymidylate synthase, which shows the intracellular conversion of tegafur into 5-FU after its release from PFL. Fluorouracil 145-149 thymidylate synthetase Homo sapiens 66-86 32270916-11 2020 Based on these findings, we may suggest that 5-FU combined with casticin treatment increased apoptotic cell death in WEHI-3 mouse leukemia cells that may undergo mitochondria and caspases signaling pathways in vitro. Fluorouracil 45-49 caspase 8 Mus musculus 179-187 32753651-8 2020 In vitro and in vivo functional studies performed by silencing or overexpressing TET1 suggested that TET1 is able to suppress epithelial-mesenchymal transition (EMT) and sensitize PDAC cells to 5FU and gemcitabine. Fluorouracil 194-197 tet methylcytosine dioxygenase 1 Homo sapiens 101-105 33463109-6 2020 The effects of LPS and 5-FU on cytotoxicity, apoptosis, and gene expression in NF-kappaB, ERK, and AKT signaling pathways were evaluated by MTT assay, Annexin V/propidium iodide (PI) apoptosis assay, and qRT-PCR, respectively. Fluorouracil 23-27 EPH receptor B2 Homo sapiens 90-93 33463109-6 2020 The effects of LPS and 5-FU on cytotoxicity, apoptosis, and gene expression in NF-kappaB, ERK, and AKT signaling pathways were evaluated by MTT assay, Annexin V/propidium iodide (PI) apoptosis assay, and qRT-PCR, respectively. Fluorouracil 23-27 annexin A5 Homo sapiens 151-160 32879665-3 2020 AIM: To detect whether interleukin (IL)-1 receptor antagonist (IL-1RA) could increase the chemosensitivity to 5-FU by decreasing the activation of the NF-kappaB pathway and reducing the proliferation of colon cancer cells. Fluorouracil 110-114 interleukin 1 receptor antagonist Homo sapiens 23-61 32879665-3 2020 AIM: To detect whether interleukin (IL)-1 receptor antagonist (IL-1RA) could increase the chemosensitivity to 5-FU by decreasing the activation of the NF-kappaB pathway and reducing the proliferation of colon cancer cells. Fluorouracil 110-114 interleukin 1 receptor antagonist Homo sapiens 63-69 32879665-8 2020 Treatment with 5-FU combined with IL-1RA could increase the chemosensitivity of the SW620 cell line, and decreased expression of the TAK1/NF-kappaB and MEK pathways resulted in limited proliferation in the SW620 cell line. Fluorouracil 15-19 mitogen-activated protein kinase kinase kinase 7 Homo sapiens 133-137 32922964-10 2020 Polymorphisms of the glucocorticoid receptor and variants of CCL2, YAP1, miR-21-5p and NF-kappabeta might be responsible for different responses to treatments used in keloid scars such as 5-fluorouracil. Fluorouracil 188-202 C-C motif chemokine ligand 2 Homo sapiens 61-65 27685916-0 2016 Thymidylate synthase polymorphism in Mexican patients with colon cancer treated with 5-fluorouracil. Fluorouracil 85-99 thymidylate synthetase Homo sapiens 0-20 33117504-0 2020 Correlation between polymorphism of TYMS gene and toxicity response to treatment with 5-fluoruracil and capecitabine. Fluorouracil 86-99 thymidylate synthetase Homo sapiens 36-40 32096264-2 2020 METHODS: The expression of TRIM14 in 5-fluorouracil (5-FU)- and oxaliplation (L-OHP)-resistant GC tissues and cells were determined by qRT-PCR and western blotting. Fluorouracil 37-51 tripartite motif containing 14 Homo sapiens 27-33 32096264-2 2020 METHODS: The expression of TRIM14 in 5-fluorouracil (5-FU)- and oxaliplation (L-OHP)-resistant GC tissues and cells were determined by qRT-PCR and western blotting. Fluorouracil 53-57 tripartite motif containing 14 Homo sapiens 27-33 32096264-8 2020 RESULTS: TRIM14 was significantly upregulated in 5-FU- and L-OHP-resistant GC tissues and cells. Fluorouracil 49-53 tripartite motif containing 14 Homo sapiens 9-15 32751071-6 2020 Beyond the well-established role for inhibiting thymidylate synthase (TS) by the 5-FU metabolite 5-fluoro-2"-deoxyuridine-5"-O-monophosphate (FdUMP), recent studies have implicated new roles for RNA modifying enzymes that are inhibited by 5-FU substitution including tRNA methyltransferase 2 homolog A (TRMT2A) and pseudouridylate synthase in 5-FU cytotoxicity. Fluorouracil 239-243 thymidylate synthetase Homo sapiens 48-68 32751071-6 2020 Beyond the well-established role for inhibiting thymidylate synthase (TS) by the 5-FU metabolite 5-fluoro-2"-deoxyuridine-5"-O-monophosphate (FdUMP), recent studies have implicated new roles for RNA modifying enzymes that are inhibited by 5-FU substitution including tRNA methyltransferase 2 homolog A (TRMT2A) and pseudouridylate synthase in 5-FU cytotoxicity. Fluorouracil 239-243 thymidylate synthetase Homo sapiens 70-72 32751071-6 2020 Beyond the well-established role for inhibiting thymidylate synthase (TS) by the 5-FU metabolite 5-fluoro-2"-deoxyuridine-5"-O-monophosphate (FdUMP), recent studies have implicated new roles for RNA modifying enzymes that are inhibited by 5-FU substitution including tRNA methyltransferase 2 homolog A (TRMT2A) and pseudouridylate synthase in 5-FU cytotoxicity. Fluorouracil 239-243 thymidylate synthetase Homo sapiens 48-68 32751071-6 2020 Beyond the well-established role for inhibiting thymidylate synthase (TS) by the 5-FU metabolite 5-fluoro-2"-deoxyuridine-5"-O-monophosphate (FdUMP), recent studies have implicated new roles for RNA modifying enzymes that are inhibited by 5-FU substitution including tRNA methyltransferase 2 homolog A (TRMT2A) and pseudouridylate synthase in 5-FU cytotoxicity. Fluorouracil 239-243 thymidylate synthetase Homo sapiens 70-72 32708710-2 2020 TYMS inhibitors (e.g., 5-Fluorouracil) can lead to drug resistance through an autoregulatory mechanism of TYMS that causes its overexpression. Fluorouracil 23-37 thymidylate synthetase Homo sapiens 0-4 32708710-2 2020 TYMS inhibitors (e.g., 5-Fluorouracil) can lead to drug resistance through an autoregulatory mechanism of TYMS that causes its overexpression. Fluorouracil 23-37 thymidylate synthetase Homo sapiens 106-110 32653028-0 2020 LncRNA HOTAIR-mediated MTHFR methylation inhibits 5-fluorouracil sensitivity in esophageal cancer cells. Fluorouracil 50-64 HOX transcript antisense RNA Homo sapiens 7-13 32653028-3 2020 In the present study, we focus on exploring the role of long non-coding RNA (lncRNA) HOTAIR in EC progression and sensitivity of EC cells to 5-FU. Fluorouracil 141-145 HOX transcript antisense RNA Homo sapiens 85-91 32653028-10 2020 Interference with lncRNA HOTAIR enhanced 5-FU-induced apoptosis, exhibited anti-proliferative activity, and reduced promoter methylation of the MTHFR in EC cells. Fluorouracil 41-45 HOX transcript antisense RNA Homo sapiens 25-31 32664186-0 2020 Effectiveness of a Controlled 5-FU Delivery Based on FZD10 Antibody-Conjugated Liposomes in Colorectal Cancer In vitro Models. Fluorouracil 30-34 frizzled class receptor 10 Homo sapiens 53-58 32664186-3 2020 Here, the anticancer effect of novel immuno-liposomes loaded with 5-Fluorouracil (5-FU), decorated with an antibody against FZD10 (anti-FZD10/5-FU/LPs), was evaluated in vitro on two different CRC cell lines, namely metastatic CoLo-205 and nonmetastatic CaCo-2 cells, that were found to overexpress FZD10. Fluorouracil 66-80 frizzled class receptor 10 Homo sapiens 124-129 32664186-3 2020 Here, the anticancer effect of novel immuno-liposomes loaded with 5-Fluorouracil (5-FU), decorated with an antibody against FZD10 (anti-FZD10/5-FU/LPs), was evaluated in vitro on two different CRC cell lines, namely metastatic CoLo-205 and nonmetastatic CaCo-2 cells, that were found to overexpress FZD10. Fluorouracil 66-80 frizzled class receptor 10 Homo sapiens 136-141 32664186-3 2020 Here, the anticancer effect of novel immuno-liposomes loaded with 5-Fluorouracil (5-FU), decorated with an antibody against FZD10 (anti-FZD10/5-FU/LPs), was evaluated in vitro on two different CRC cell lines, namely metastatic CoLo-205 and nonmetastatic CaCo-2 cells, that were found to overexpress FZD10. Fluorouracil 66-80 frizzled class receptor 10 Homo sapiens 136-141 32664186-3 2020 Here, the anticancer effect of novel immuno-liposomes loaded with 5-Fluorouracil (5-FU), decorated with an antibody against FZD10 (anti-FZD10/5-FU/LPs), was evaluated in vitro on two different CRC cell lines, namely metastatic CoLo-205 and nonmetastatic CaCo-2 cells, that were found to overexpress FZD10. Fluorouracil 82-86 frizzled class receptor 10 Homo sapiens 136-141 32664186-3 2020 Here, the anticancer effect of novel immuno-liposomes loaded with 5-Fluorouracil (5-FU), decorated with an antibody against FZD10 (anti-FZD10/5-FU/LPs), was evaluated in vitro on two different CRC cell lines, namely metastatic CoLo-205 and nonmetastatic CaCo-2 cells, that were found to overexpress FZD10. Fluorouracil 82-86 frizzled class receptor 10 Homo sapiens 136-141 32664186-5 2020 The results highlighted that the cytotoxic activity of 5-FU was enhanced when encapsulated in the anti-FZD10 /5-FU/LPs at the lowest tested concentrations, as compared to the free 5-FU counterparts. Fluorouracil 55-59 frizzled class receptor 10 Homo sapiens 103-108 32664186-5 2020 The results highlighted that the cytotoxic activity of 5-FU was enhanced when encapsulated in the anti-FZD10 /5-FU/LPs at the lowest tested concentrations, as compared to the free 5-FU counterparts. Fluorouracil 110-114 frizzled class receptor 10 Homo sapiens 103-108 32664186-5 2020 The results highlighted that the cytotoxic activity of 5-FU was enhanced when encapsulated in the anti-FZD10 /5-FU/LPs at the lowest tested concentrations, as compared to the free 5-FU counterparts. Fluorouracil 110-114 frizzled class receptor 10 Homo sapiens 103-108 26831819-0 2016 E2F1/TS Immunophenotype and Survival of Patients with Colorectal Cancer Treated with 5FU-Based Adjuvant Therapy. Fluorouracil 85-88 E2F transcription factor 1 Homo sapiens 0-4 33024525-0 2020 Relationship between the Expression of the Thymidylate Synthase and the Prognosis of Gastric Cancer Patients Treated with Combinational Chemotherapy Regimen Including Fluorouracil, Docetaxel and Cisplatin. Fluorouracil 167-179 thymidylate synthetase Homo sapiens 43-63 33024525-1 2020 Background: Thymidylate synthase is one of the target enzymes of 5-fluorouracil. Fluorouracil 65-79 thymidylate synthetase Homo sapiens 12-32 32377720-11 2020 Furthermore, the overexpression of XPD significantly increased the chemosensitivity of EC9706 and EC109 cells to cisplatin or fluorouracil. Fluorouracil 126-138 ERCC excision repair 2, TFIIH core complex helicase subunit Homo sapiens 35-38 32377720-13 2020 On the whole, the findings of the present study demonstrate that XPD inhibits the growth and invasion of EC9706 and EC109 cells, whilst also enhancing the chemosensitivity of EC9706 and EC109 cells to cisplatin or fluorouracil by regulating the PI3K/AKT signaling pathway. Fluorouracil 214-226 ERCC excision repair 2, TFIIH core complex helicase subunit Homo sapiens 65-68 32319648-10 2020 Notably, the CRC cells with low MUC1 expression levels and high expression levels of the other MUCs (MUC2, MU4 and MUC5AC) were shown to benefit from 5-FU treatment. Fluorouracil 150-154 adaptor related protein complex 4 subunit mu 1 Homo sapiens 107-110 32319648-10 2020 Notably, the CRC cells with low MUC1 expression levels and high expression levels of the other MUCs (MUC2, MU4 and MUC5AC) were shown to benefit from 5-FU treatment. Fluorouracil 150-154 mucin 5AC, oligomeric mucus/gel-forming Homo sapiens 115-121 26831819-0 2016 E2F1/TS Immunophenotype and Survival of Patients with Colorectal Cancer Treated with 5FU-Based Adjuvant Therapy. Fluorouracil 85-88 thymidylate synthetase Homo sapiens 5-7 26831819-3 2016 The purpose of this study is to assess the correlation between expression of both E2F1 and TS in CRCs and survival of patients administered adjuvant 5FU-based chemotherapy, in order to find a better predictor of treatment outcome than expression of TS or E2F1 alone. Fluorouracil 149-152 E2F transcription factor 1 Homo sapiens 82-86 26831819-3 2016 The purpose of this study is to assess the correlation between expression of both E2F1 and TS in CRCs and survival of patients administered adjuvant 5FU-based chemotherapy, in order to find a better predictor of treatment outcome than expression of TS or E2F1 alone. Fluorouracil 149-152 thymidylate synthetase Homo sapiens 91-93 26831819-8 2016 The E2F1+TS+ immunophenotype may be a marker of poor prognosis (the worst DFS and OS) of patients with colon cancer treated with 5FU-based adjuvant therapy. Fluorouracil 129-132 E2F transcription factor 1 Homo sapiens 4-8 26831819-8 2016 The E2F1+TS+ immunophenotype may be a marker of poor prognosis (the worst DFS and OS) of patients with colon cancer treated with 5FU-based adjuvant therapy. Fluorouracil 129-132 thymidylate synthetase Homo sapiens 9-11 26810069-4 2016 Knockdown of TXNDC5 by siRNAs inhibits the cell growth, migration, and invasion of ccRCC cells as well as sensitizes ccRCC cells to chemotherapeutic drugs, such as Camptothecin and 5-Fluorouracil. Fluorouracil 181-195 thioredoxin domain containing 5 Homo sapiens 13-19 27493479-0 2016 Wnt/Beta-Catenin Signal Inhibitor HC-1 Sensitizes Oral Squamous Cell Carcinoma Cells to 5-Fluorouracil through Reduction of CD44-Positive Population. Fluorouracil 88-102 catenin beta 1 Homo sapiens 4-16 27144434-0 2016 MEK5/ERK5 signaling inhibition increases colon cancer cell sensitivity to 5-fluorouracil through a p53-dependent mechanism. Fluorouracil 74-88 mitogen-activated protein kinase 7 Homo sapiens 5-9 27144434-2 2016 Here, we evaluated the impact of the MEK5/ERK5 cascade in colon cancer cell sensitivity to 5-fluorouracil (5-FU). Fluorouracil 91-105 mitogen-activated protein kinase 7 Homo sapiens 42-46 26261061-0 2016 AGXT and ERCC2 polymorphisms are associated with clinical outcome in metastatic colorectal cancer patients treated with 5-FU/oxaliplatin. Fluorouracil 120-124 alanine--glyoxylate and serine--pyruvate aminotransferase Homo sapiens 0-4 32067389-0 2020 Proteomic Analysis Reveals That EPHX1 Contributes to 5-Fluorouracil Resistance in a Human Hepatocellular Carcinoma Cell Line. Fluorouracil 53-67 epoxide hydrolase 1 Homo sapiens 32-37 32647090-8 2020 A 5-FU group revealed marked ileal mucosal damage associated with a significant decrease in the mean body weight, AQP-4 level and area percent of PAS and AQP-4 positive reaction. Fluorouracil 2-6 aquaporin 4 Rattus norvegicus 114-119 32647090-8 2020 A 5-FU group revealed marked ileal mucosal damage associated with a significant decrease in the mean body weight, AQP-4 level and area percent of PAS and AQP-4 positive reaction. Fluorouracil 2-6 aquaporin 4 Rattus norvegicus 154-159 32647090-11 2020 A 5-FU resulted in severe ileal mucositis through TNF-alpha, NF-kappaB, MMP-9, and AQP-4 disturbances. Fluorouracil 2-6 aquaporin 4 Rattus norvegicus 83-88 32665777-10 2020 Moreover, qPCR analyses showed that CASP3 and CASP9 mRNA levels significantly increased after pre-treatment with Pxd followed by 5-Fu and 1-OHP treatments, compared to 5-Fu with 1-OHP alone. Fluorouracil 129-133 caspase 9 Homo sapiens 46-51 32629871-6 2020 NRF2 knockdown reversed 5-FU resistance of PDAC cells via suppression of ABCG2 and HO-1. Fluorouracil 24-28 heme oxygenase 1 Homo sapiens 83-87 32511132-7 2022 RESULTS: High LAP expression predicted poor overall survival (P < 0.001, P < 0.001, and P = 0.022) and inferior therapeutic responsiveness to fluorouracil-based adjuvant chemotherapy (P = 0.008 for interaction) in gastric cancer. Fluorouracil 142-154 LAP Homo sapiens 14-17 26261061-0 2016 AGXT and ERCC2 polymorphisms are associated with clinical outcome in metastatic colorectal cancer patients treated with 5-FU/oxaliplatin. Fluorouracil 120-124 ERCC excision repair 2, TFIIH core complex helicase subunit Homo sapiens 9-14 27178693-8 2016 Treatments of SCC include electrodesiccation and curettage, surgical resection, cryosurgery, radiation, and systemic chemotherapy such as 5-fluorouracil and cetuximab. Fluorouracil 138-152 serpin family B member 3 Homo sapiens 14-17 32142918-11 2020 Drosha wild type GCSCs with SHMT2 are sensitive to 5-fluorouracil; however, Drosha low-expressing GCSCs with SHMT1 are 5-FU-resistant. Fluorouracil 119-123 serine hydroxymethyltransferase 1 Homo sapiens 109-114 32142918-12 2020 The loss of miR-6778-5p or SHMT1 notably mitigates GCSC sphere formation and increases sensitivity to 5-fluorouracil in Drosha-knockdown gastric cancer cells. Fluorouracil 102-116 microRNA 6778 Homo sapiens 12-20 32142918-12 2020 The loss of miR-6778-5p or SHMT1 notably mitigates GCSC sphere formation and increases sensitivity to 5-fluorouracil in Drosha-knockdown gastric cancer cells. Fluorouracil 102-116 serine hydroxymethyltransferase 1 Homo sapiens 27-32 26687645-5 2016 Co-treatment with OMT and 5-Fu caused G0/G1 phase arrest by upregulating P21 and P27 and downregulating cyclin D, and induced apoptosis through increasing the production of reactive oxygen species (ROS) and decreasing the levels of p-ERK. Fluorouracil 26-30 H3 histone pseudogene 16 Homo sapiens 73-76 26687645-5 2016 Co-treatment with OMT and 5-Fu caused G0/G1 phase arrest by upregulating P21 and P27 and downregulating cyclin D, and induced apoptosis through increasing the production of reactive oxygen species (ROS) and decreasing the levels of p-ERK. Fluorouracil 26-30 interferon alpha inducible protein 27 Homo sapiens 81-84 26687645-5 2016 Co-treatment with OMT and 5-Fu caused G0/G1 phase arrest by upregulating P21 and P27 and downregulating cyclin D, and induced apoptosis through increasing the production of reactive oxygen species (ROS) and decreasing the levels of p-ERK. Fluorouracil 26-30 eukaryotic translation initiation factor 2 alpha kinase 3 Homo sapiens 232-237 27183638-6 2016 In addition, Dok1/Dok2 deficiency induces resistance to 5-FU-induced hematopoietic stem cell exhaustion. Fluorouracil 56-60 docking protein 2 Mus musculus 18-22 26387536-8 2016 Importantly, pharmacological inhibition of HuR by MS-444 inhibits HuR homodimerization and its cytoplasmic translocation, abrogates hypoxia-induced PIM1 overexpression and markedly enhances PDA cell sensitivity to oxaliplatin and 5-fluorouracil under physiologic low oxygen conditions. Fluorouracil 230-244 ELAV like RNA binding protein 1 Homo sapiens 43-46 32382808-2 2020 The biological activity of the 5-FU degrading enzyme, dihydropyrimidine dehydrogenase (DPD), and the target enzyme thymidylate synthase (TS), are subject to circadian rhythmicity in healthy volunteers. Fluorouracil 31-35 thymidylate synthetase Homo sapiens 115-135 26985715-0 2016 Loss of Runt-related transcription factor 3 induces resistance to 5-fluorouracil and cisplatin in hepatocellular carcinoma. Fluorouracil 66-80 RUNX family transcription factor 3 Homo sapiens 8-43 32382808-2 2020 The biological activity of the 5-FU degrading enzyme, dihydropyrimidine dehydrogenase (DPD), and the target enzyme thymidylate synthase (TS), are subject to circadian rhythmicity in healthy volunteers. Fluorouracil 31-35 thymidylate synthetase Homo sapiens 137-139 26985715-6 2016 MTT assays were used to determine the effects of RUNX3 expression on 5-fluorouracil (5-FU) and cisplatin (CDDP) sensitivity. Fluorouracil 69-83 RUNX family transcription factor 3 Homo sapiens 49-54 26985715-6 2016 MTT assays were used to determine the effects of RUNX3 expression on 5-fluorouracil (5-FU) and cisplatin (CDDP) sensitivity. Fluorouracil 85-89 RUNX family transcription factor 3 Homo sapiens 49-54 26985715-10 2016 Importantly, loss of RUNX3 expression contributed to 5-FU and CDDP resistance by inducing MRP expression. Fluorouracil 53-57 RUNX family transcription factor 3 Homo sapiens 21-26 26662569-8 2016 The expression of PCNA and Bcl-XL is remarkably decreased, and the expression of Caspase-3 and cleaved Caspase-3 is obviously increased in GC cells treated with the single and combination of 5-Fu and PD. Fluorouracil 191-195 proliferating cell nuclear antigen Homo sapiens 18-22 26864640-0 2016 MicroRNA-21 induces 5-fluorouracil resistance in human pancreatic cancer cells by regulating PTEN and PDCD4. Fluorouracil 20-34 phosphatase and tensin homolog Homo sapiens 93-97 26864640-2 2016 The objective of this study was to delineate the mechanism by which miR-21 induces drug resistance to 5-fluorouracil (5-FU) in human pancreatic cancer cells (PATU8988 and PANC-1). Fluorouracil 102-116 microRNA 21 Homo sapiens 68-74 26864640-2 2016 The objective of this study was to delineate the mechanism by which miR-21 induces drug resistance to 5-fluorouracil (5-FU) in human pancreatic cancer cells (PATU8988 and PANC-1). Fluorouracil 118-122 microRNA 21 Homo sapiens 68-74 26864640-3 2016 We report that PATU8988 cells resistant to 5-FU express high levels of miR-21 in comparison to sensitive primary PATU8988 cells. Fluorouracil 43-47 microRNA 21 Homo sapiens 71-77 26864640-4 2016 Suppression of miR-21 expression in 5-Fu-resistant PATU8988 cells can alleviate its 5-FU resistance. Fluorouracil 36-40 microRNA 21 Homo sapiens 15-21 26864640-4 2016 Suppression of miR-21 expression in 5-Fu-resistant PATU8988 cells can alleviate its 5-FU resistance. Fluorouracil 84-88 microRNA 21 Homo sapiens 15-21 26864640-5 2016 Meanwhile, lentiviral vector-mediated overexpression of miR-21 not only conferred resistance to 5-FU but also promoted proliferation, migration, and invasion of PATU8988 and PANC-1 cells. Fluorouracil 96-100 microRNA 21 Homo sapiens 56-62 26864640-7 2016 Overexpression of PTEN and PDCD4 antagonized miR-21-induced resistance to 5-FU and migration activity. Fluorouracil 74-78 phosphatase and tensin homolog Homo sapiens 18-22 26864640-7 2016 Overexpression of PTEN and PDCD4 antagonized miR-21-induced resistance to 5-FU and migration activity. Fluorouracil 74-78 microRNA 21 Homo sapiens 45-51 26864640-8 2016 Our work demonstrates that miR-21 can confer drug resistance to 5-FU in pancreatic cancer cells by regulating the expression of tumor suppressor genes, as the target genes of miR-21, PTEN and PDCD4 can rescue 5-FU sensitivity and the phenotypic characteristics disrupted by miR-21. Fluorouracil 64-68 microRNA 21 Homo sapiens 27-33 26864640-8 2016 Our work demonstrates that miR-21 can confer drug resistance to 5-FU in pancreatic cancer cells by regulating the expression of tumor suppressor genes, as the target genes of miR-21, PTEN and PDCD4 can rescue 5-FU sensitivity and the phenotypic characteristics disrupted by miR-21. Fluorouracil 64-68 microRNA 21 Homo sapiens 175-181 26864640-8 2016 Our work demonstrates that miR-21 can confer drug resistance to 5-FU in pancreatic cancer cells by regulating the expression of tumor suppressor genes, as the target genes of miR-21, PTEN and PDCD4 can rescue 5-FU sensitivity and the phenotypic characteristics disrupted by miR-21. Fluorouracil 64-68 phosphatase and tensin homolog Homo sapiens 183-187 26864640-8 2016 Our work demonstrates that miR-21 can confer drug resistance to 5-FU in pancreatic cancer cells by regulating the expression of tumor suppressor genes, as the target genes of miR-21, PTEN and PDCD4 can rescue 5-FU sensitivity and the phenotypic characteristics disrupted by miR-21. Fluorouracil 64-68 microRNA 21 Homo sapiens 175-181 26864640-8 2016 Our work demonstrates that miR-21 can confer drug resistance to 5-FU in pancreatic cancer cells by regulating the expression of tumor suppressor genes, as the target genes of miR-21, PTEN and PDCD4 can rescue 5-FU sensitivity and the phenotypic characteristics disrupted by miR-21. Fluorouracil 209-213 microRNA 21 Homo sapiens 27-33 26864640-8 2016 Our work demonstrates that miR-21 can confer drug resistance to 5-FU in pancreatic cancer cells by regulating the expression of tumor suppressor genes, as the target genes of miR-21, PTEN and PDCD4 can rescue 5-FU sensitivity and the phenotypic characteristics disrupted by miR-21. Fluorouracil 209-213 microRNA 21 Homo sapiens 175-181 26864640-8 2016 Our work demonstrates that miR-21 can confer drug resistance to 5-FU in pancreatic cancer cells by regulating the expression of tumor suppressor genes, as the target genes of miR-21, PTEN and PDCD4 can rescue 5-FU sensitivity and the phenotypic characteristics disrupted by miR-21. Fluorouracil 209-213 phosphatase and tensin homolog Homo sapiens 183-187 26864640-8 2016 Our work demonstrates that miR-21 can confer drug resistance to 5-FU in pancreatic cancer cells by regulating the expression of tumor suppressor genes, as the target genes of miR-21, PTEN and PDCD4 can rescue 5-FU sensitivity and the phenotypic characteristics disrupted by miR-21. Fluorouracil 209-213 microRNA 21 Homo sapiens 175-181 26785286-7 2016 Pretreatment with a general caspase inhibitor (Z-VAD-FMK), a caspase-8 inhibitor (Z-IETD-FMK), and a caspase-9 inhibitor (Z-LEHD-FMK) reversed 5-FU-induced cellular damage. Fluorouracil 143-147 caspase 9 Homo sapiens 101-110 26785286-10 2016 CONCLUSION: These data reveal that 5-FU-induced cellular apoptosis in corneal epithelial cells may be mediated through caspase-8, caspase-9, and mitochondria-regulated pathways, as well as by upregulation of p21 and downregulation of Bcl-2-dependent signal transduction pathways. Fluorouracil 35-39 caspase 9 Homo sapiens 130-139 26785286-10 2016 CONCLUSION: These data reveal that 5-FU-induced cellular apoptosis in corneal epithelial cells may be mediated through caspase-8, caspase-9, and mitochondria-regulated pathways, as well as by upregulation of p21 and downregulation of Bcl-2-dependent signal transduction pathways. Fluorouracil 35-39 H3 histone pseudogene 16 Homo sapiens 208-211 26908448-0 2016 ANXA11 regulates the tumorigenesis, lymph node metastasis and 5-fluorouracil sensitivity of murine hepatocarcinoma Hca-P cells by targeting c-Jun. Fluorouracil 62-76 annexin A11 Mus musculus 0-6 26908448-3 2016 Here, ANXA11 acted as a suppressor for the tumorigenicity, LNM and 5-FU resistance of Hca-P via c-Jun. Fluorouracil 67-71 annexin A11 Mus musculus 6-12 26908448-9 2016 ANXA11 knockdown enhanced the chemoresistance of Hca-P cells specifically toward 5-FU instead of cisplatin. Fluorouracil 81-85 annexin A11 Mus musculus 0-6 26908448-11 2016 Interestingly, compared with scramble-Hca-P cells, the levels of c-Jun and c-Jun (pSer73) in shRNA-Anxa11-Hca-P cells were upregulated in the presences of 0.1 and 1.0 mg/L 5-FU. Fluorouracil 172-176 annexin A11 Mus musculus 99-105 26475334-2 2016 We found that fluorouracil (5-FU)-resistant esophageal squamous cell carcinoma cell lines, established through exposure to increasing concentrations of 5-FU, showed upregulation of Id1, IGF2, and E2F1. Fluorouracil 14-26 insulin like growth factor 2 Homo sapiens 186-190 26475334-2 2016 We found that fluorouracil (5-FU)-resistant esophageal squamous cell carcinoma cell lines, established through exposure to increasing concentrations of 5-FU, showed upregulation of Id1, IGF2, and E2F1. Fluorouracil 14-26 E2F transcription factor 1 Homo sapiens 196-200 26475334-2 2016 We found that fluorouracil (5-FU)-resistant esophageal squamous cell carcinoma cell lines, established through exposure to increasing concentrations of 5-FU, showed upregulation of Id1, IGF2, and E2F1. Fluorouracil 28-32 insulin like growth factor 2 Homo sapiens 186-190 26475334-2 2016 We found that fluorouracil (5-FU)-resistant esophageal squamous cell carcinoma cell lines, established through exposure to increasing concentrations of 5-FU, showed upregulation of Id1, IGF2, and E2F1. Fluorouracil 28-32 E2F transcription factor 1 Homo sapiens 196-200 26475334-2 2016 We found that fluorouracil (5-FU)-resistant esophageal squamous cell carcinoma cell lines, established through exposure to increasing concentrations of 5-FU, showed upregulation of Id1, IGF2, and E2F1. Fluorouracil 152-156 insulin like growth factor 2 Homo sapiens 186-190 26475334-2 2016 We found that fluorouracil (5-FU)-resistant esophageal squamous cell carcinoma cell lines, established through exposure to increasing concentrations of 5-FU, showed upregulation of Id1, IGF2, and E2F1. Fluorouracil 152-156 E2F transcription factor 1 Homo sapiens 196-200 26725729-10 2016 CONCLUSIONS: Results of this study suggest that the RECQ1 A159C genotype may be a prognostic or predictive factor for resectable pancreatic cancer patients who are treated with adjuvant 5-FU before and after 5-FU-based chemoradiation. Fluorouracil 186-190 RecQ like helicase Homo sapiens 52-57 26725729-10 2016 CONCLUSIONS: Results of this study suggest that the RECQ1 A159C genotype may be a prognostic or predictive factor for resectable pancreatic cancer patients who are treated with adjuvant 5-FU before and after 5-FU-based chemoradiation. Fluorouracil 208-212 RecQ like helicase Homo sapiens 52-57 26691173-2 2016 BACKGROUND: Combined chemoradiation with infusional 5-FU and mitomycin is the standard treatment for localized squamous cell carcinoma (SCC) of the anal canal. Fluorouracil 52-56 serpin family B member 3 Homo sapiens 136-139 26691173-4 2016 However, the efficacy of the substitution of 5-FU for capecitabine in anal SCC needs confirmation. Fluorouracil 45-49 serpin family B member 3 Homo sapiens 75-78 26895662-8 2016 In both the FPGS-overexpressed HCT116 and MDA-MB-435 cell lines, we identified several differentially expressed genes involved in folate biosynthesis and one-carbon metabolism, which might in part have contributed to the observed increased efficacy of 5-fluorouracil in response to FPGS overexpression. Fluorouracil 252-266 folylpolyglutamate synthase Homo sapiens 12-16 26895662-8 2016 In both the FPGS-overexpressed HCT116 and MDA-MB-435 cell lines, we identified several differentially expressed genes involved in folate biosynthesis and one-carbon metabolism, which might in part have contributed to the observed increased efficacy of 5-fluorouracil in response to FPGS overexpression. Fluorouracil 252-266 folylpolyglutamate synthase Homo sapiens 282-286 26647806-0 2016 Smad4 sensitizes colorectal cancer to 5-fluorouracil through cell cycle arrest by inhibiting the PI3K/Akt/CDC2/survivin cascade. Fluorouracil 38-52 SMAD family member 4 Mus musculus 0-5 26647806-9 2016 Smad4 deficiency in CT26 and SW620 cells induced chemoresistance to 5-FU both in vitro and in vivo. Fluorouracil 68-72 SMAD family member 4 Mus musculus 0-5 32028241-7 2020 In conclusion, FAM83H-AS1 is related with the CDDP and 5-FU insensitivity of GC patients, silence of FAM83H-AS1 promotes chemosensitivity of GC through Wnt/beta-catenin signaling pathway. Fluorouracil 55-59 catenin beta 1 Homo sapiens 156-168 26432329-8 2016 The single and combination of 5-Fu and BGJ398 decreased the expressions of PCNA, Bcl-xl, and FLIP while increased the expression of caspase-3 in GC cells, especially in shRNA groups. Fluorouracil 30-34 proliferating cell nuclear antigen Homo sapiens 75-79 26840457-3 2016 Here, we show that both in vitro and in vivo increased expression of NgBR contributes to the increased chemoresistance of Bel7402/5FU cells, a stable 5-FU (5-Fluorouracil) resistant cell line related Bel7402 cells. Fluorouracil 150-154 NUS1 dehydrodolichyl diphosphate synthase subunit Homo sapiens 69-73 26840457-3 2016 Here, we show that both in vitro and in vivo increased expression of NgBR contributes to the increased chemoresistance of Bel7402/5FU cells, a stable 5-FU (5-Fluorouracil) resistant cell line related Bel7402 cells. Fluorouracil 156-170 NUS1 dehydrodolichyl diphosphate synthase subunit Homo sapiens 69-73 26840457-5 2016 In addition, NgBR suppresses p53 protein levels through activation of the PI3K/Akt/MDM2 pathway, which promotes p53 degradation via the ubiquitin proteasome pathway and thus increases the resistance of human hepatocellular cancer cells to 5-FU. Fluorouracil 239-243 NUS1 dehydrodolichyl diphosphate synthase subunit Homo sapiens 13-17 26840457-7 2016 These results suggest that targeting NgBR in combination with chemotherapeutic drugs, such as 5-FU, could improve the efficacy of current anticancer treatments. Fluorouracil 94-98 NUS1 dehydrodolichyl diphosphate synthase subunit Homo sapiens 37-41 26844701-10 2016 Exposure of explant cultures to 5FU-based CT increased the percentage of cells positive for active Caspase-3 and Terminal Deoxynucleotidyl Transferase dUTP Nick end Labelling (TUNEL), but also the expression of regeneration and proliferation markers beta-Catenin and Ki-67, as well as cyclooxygenase-2 (COX-2). Fluorouracil 32-35 catenin beta 1 Homo sapiens 250-262 26714930-1 2016 As a critical endonuclease in DNA repair, Mus81 is traditionally regarded as a tumor suppressor, but recently correlated with the sensitivity of mitomycin C and 5-fluorouracil in colon cancer and breast cancer cells. Fluorouracil 161-175 MUS81 structure-specific endonuclease subunit Homo sapiens 42-47 26691280-12 2016 Results indicated that 5-FU decreased H-ras, Rho-A, p53, Stat1 and increased Bax gene expression in Tumor2 and decreased Rac1, Rho-A, NF-kappaB and increased Bax and caspase-3 protein expression in Tumor2. Fluorouracil 23-27 HRas proto-oncogene, GTPase Homo sapiens 38-43 26691280-13 2016 5-FU decreased H-ras, Bcl-xL and NF-kappaB and increased Bax gene expression. Fluorouracil 0-4 HRas proto-oncogene, GTPase Homo sapiens 15-20 26538346-2 2016 OBJECTIVE: To non-invasively assess the pharmacodynamic changes induced by treatment with low dose 5-fluorouracil and 10% salicylic acid by means of RCM and high-definition OCT in field cancerization and actinic keratosis. Fluorouracil 99-113 plexin A2 Homo sapiens 173-176 26538346-7 2016 CONCLUSIONS: Evaluation of AK and subclinical AK by RCM and HD-OCT showed objective improvement after treatment with 5-fluorouracil and 10% salicylic acid. Fluorouracil 117-131 plexin A2 Homo sapiens 63-66 26893778-0 2016 Downregulation of Foxc2 enhances apoptosis induced by 5-fluorouracil through activation of MAPK and AKT pathways in colorectal cancer. Fluorouracil 54-68 forkhead box C2 Homo sapiens 18-23 26893778-4 2016 The Foxc2-shRNA cells were treated with 5-FU and the cell viability was determined by an MTT assay. Fluorouracil 40-44 forkhead box C2 Homo sapiens 4-9 26893778-6 2016 The present study identified that 5-FU increased the percentage of apoptotic CRC cells among the Foxc2/RNA interference-transfected cells compared with cells transfected with an empty vector. Fluorouracil 34-38 forkhead box C2 Homo sapiens 97-102 26893778-7 2016 Therefore, the downregulation of Foxc2, induced by 5-FU, may enhance apoptosis by the downregulation of apoptotic factors, including B cell lymphoma-2 and pro-caspase-3, in Foxc2-shRNA CRC cells. Fluorouracil 51-55 forkhead box C2 Homo sapiens 33-38 26893778-7 2016 Therefore, the downregulation of Foxc2, induced by 5-FU, may enhance apoptosis by the downregulation of apoptotic factors, including B cell lymphoma-2 and pro-caspase-3, in Foxc2-shRNA CRC cells. Fluorouracil 51-55 forkhead box C2 Homo sapiens 173-178 26893778-8 2016 Furthermore, the mitogen-activated protein kinase (MAPK) and phosphatidylinositide 3-kinases/protein kinase B (PI3K/AKT) pathways were essential for the sensitization effect of Foxc2 to 5-FU treatment. Fluorouracil 186-190 forkhead box C2 Homo sapiens 177-182 26893778-9 2016 Overall, these findings reveal the mechanisms behind Foxc2 depletion and 5-FU treatment of CRC and suggest that Foxc2 enhances resistance to apoptosis, induced by 5-FU, through the activation of MAPK and P13K/AKT pathways, and may serve as a valuable clinical prognostic marker for CRC. Fluorouracil 163-167 forkhead box C2 Homo sapiens 112-117 25867072-4 2016 We now show that apoptosis plays a key role in their anti-tumor activities in colon cancer cells and xenografts through the DR5, FADD and caspase-8 axis, and is strongly enhanced by tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) and 5-fluorouracil. Fluorouracil 250-264 Fas associated via death domain Homo sapiens 129-133 26751376-5 2016 Cytotoxicity assays with inhibitors of de novo adenine synthesis (5-FU, AZA and MTX) after MTAP gene knockdown showed an increased sensitivity, mainly to 5-FU. Fluorouracil 154-158 metaxin 1 Homo sapiens 80-83 32073706-0 2020 MicroRNA-375-3p Enhances Chemosensitivity to 5-Fluorouracil by Targeting Thymidylate Synthase in Colorectal Cancer. Fluorouracil 45-59 thymidylate synthetase Homo sapiens 73-93 32073706-5 2020 Thymidylate synthase (TYMS) was demonstrated to be a direct target of miR-375-3p, and TYMS knockdown exerted similar effects as miR-375-3p overexpression on the CRC cellular response to 5-FU. Fluorouracil 186-190 thymidylate synthetase Homo sapiens 0-20 32073706-5 2020 Thymidylate synthase (TYMS) was demonstrated to be a direct target of miR-375-3p, and TYMS knockdown exerted similar effects as miR-375-3p overexpression on the CRC cellular response to 5-FU. Fluorouracil 186-190 thymidylate synthetase Homo sapiens 22-26 32385145-1 2020 BACKGROUND: We have previously shown that 5-fluorouracil (5-FU) selectively kills myeloid-derived suppressor cells (MDSCs) and activates NLRP3 (NOD-leucine rich repeat and pyrin containing protein 3) inflammasome. Fluorouracil 42-56 NLR family, pyrin domain containing 3 Mus musculus 137-142 32385145-1 2020 BACKGROUND: We have previously shown that 5-fluorouracil (5-FU) selectively kills myeloid-derived suppressor cells (MDSCs) and activates NLRP3 (NOD-leucine rich repeat and pyrin containing protein 3) inflammasome. Fluorouracil 58-62 NLR family, pyrin domain containing 3 Mus musculus 137-142 32385145-10 2020 IL-1beta injection is able to bypass HS+5-FU antitumor effects. Fluorouracil 40-44 interleukin 1 alpha Mus musculus 0-8 32385145-13 2020 Finally, the effects of 5-FU on tumor growth can be restored by inhibiting IL-1beta, using anakinra. Fluorouracil 24-28 interleukin 1 alpha Mus musculus 75-83 32348733-1 2020 The major molecular mode of action of the cytotoxic drug 5-fluorouracil (5-FU) is generally considered to result from thymidylate synthase inhibition. Fluorouracil 57-71 thymidylate synthetase Homo sapiens 118-138 32348733-1 2020 The major molecular mode of action of the cytotoxic drug 5-fluorouracil (5-FU) is generally considered to result from thymidylate synthase inhibition. Fluorouracil 73-77 thymidylate synthetase Homo sapiens 118-138 32061752-6 2020 We found that the anticancer drugs such as 5-fluorouracil (5-FU) activated the IRE1alpha-XBP1 pathway to induce the expression of ABCB1, ABCC1 and ABCG2 in colon cancer cells. Fluorouracil 43-57 X-box binding protein 1 Homo sapiens 89-93 32061752-6 2020 We found that the anticancer drugs such as 5-fluorouracil (5-FU) activated the IRE1alpha-XBP1 pathway to induce the expression of ABCB1, ABCC1 and ABCG2 in colon cancer cells. Fluorouracil 59-63 X-box binding protein 1 Homo sapiens 89-93 32061753-6 2020 Moreover, F5446 increased 5-FU-resistant human CRC sensitivity to both 5-FU- and FasL-induced apoptosis and inhibited tumor cell growth in vitro. Fluorouracil 26-30 Fas ligand Homo sapiens 81-85 26588055-8 2016 Moreover, miR-671-5p sensitized breast cancer cells to cisplatin, 5-fluorouracil (5-FU) and epirubicin exposure. Fluorouracil 66-80 microRNA 671 Homo sapiens 10-17 26588055-8 2016 Moreover, miR-671-5p sensitized breast cancer cells to cisplatin, 5-fluorouracil (5-FU) and epirubicin exposure. Fluorouracil 82-86 microRNA 671 Homo sapiens 10-17 25724421-8 2016 We observed marked elevation in the myeloperoxidase (MPO) activity after 5-FU administration, which was reversed by Tau pretreatment. Fluorouracil 73-77 myeloperoxidase Rattus norvegicus 36-51 32391259-0 2020 5-FU-Induced Upregulation of Exosomal PD-L1 Causes Immunosuppression in Advanced Gastric Cancer Patients. Fluorouracil 0-4 CD274 molecule Homo sapiens 38-43 32391259-1 2020 Although the cytotoxic chemotherapeutic agent 5-fluorouracil (5-FU) is generally considered to directly kill cancer cells and exert immunostimulatory effects in advanced gastric cancer, accumulating evidence indicates that it upregulates the expression of PD-L1, a representative immune checkpoint blockade molecule involved in negative regulation of the immune response. Fluorouracil 46-60 CD274 molecule Homo sapiens 256-261 32391259-1 2020 Although the cytotoxic chemotherapeutic agent 5-fluorouracil (5-FU) is generally considered to directly kill cancer cells and exert immunostimulatory effects in advanced gastric cancer, accumulating evidence indicates that it upregulates the expression of PD-L1, a representative immune checkpoint blockade molecule involved in negative regulation of the immune response. Fluorouracil 62-66 CD274 molecule Homo sapiens 256-261 32391259-3 2020 However, whether 5-FU alters the expression of exosomal PD-L1 and induces immunosuppression in gastric cancer remains unclear. Fluorouracil 17-21 CD274 molecule Homo sapiens 56-61 32391259-4 2020 Herein, we found that 5-FU increased gastric cancer-derived exosomal PD-L1. Fluorouracil 22-26 CD274 molecule Homo sapiens 69-74 32391259-8 2020 These results suggested that 5-FU-induced upregulation of exosomal PD-L1 causes systemic immunosuppression in advanced gastric cancer following multiple cycles of chemotherapy, especially after two cycles. Fluorouracil 29-33 CD274 molecule Homo sapiens 67-72 32218415-1 2020 BACKGROUND This study was performed to estimate the genetic effects of HtrA1 polymorphisms rs1049331 and rs11200638 on treatment response in stage III colon cancer patients receiving 5-FU-based chemotherapy. Fluorouracil 183-187 HtrA serine peptidase 1 Homo sapiens 71-76 32218415-9 2020 CONCLUSIONS HtrA1 rs1049331 polymorphism, but not rs11200638 polymorphism, can influence individual sensitivity to 5-FU-based treatment in stage III colon cancer patients. Fluorouracil 115-119 HtrA serine peptidase 1 Homo sapiens 12-17 32266092-7 2020 Additionally, the combined treatment of WA and 5-FU mediated ER stress induces autophagy and apoptosis, which were confirmed by immunoblotting, acridine orange (AO) staining and annexin-V FITC by flow cytometry. Fluorouracil 47-51 annexin A5 Homo sapiens 178-187 32266092-11 2020 In summary, the combination of WA and 5-FU decreases cell viability by inducing ER stress-mediated induction of autophagy and apoptosis, inhibiting the beta-catenin pathway and arresting the cell cycle at a G2M phase in CRC cells. Fluorouracil 38-42 catenin beta 1 Homo sapiens 152-164 25724421-8 2016 We observed marked elevation in the myeloperoxidase (MPO) activity after 5-FU administration, which was reversed by Tau pretreatment. Fluorouracil 73-77 myeloperoxidase Rattus norvegicus 53-56 32266094-0 2020 Endoplasmic reticulum stress confers 5-fluorouracil resistance in breast cancer cell via the GRP78/OCT4/lncRNA MIAT/AKT pathway. Fluorouracil 37-51 POU class 5 homeobox 1 Homo sapiens 99-103 27061538-4 2016 Apoptosis induced by bornyl acetate and 5-FU was evaluated by Annexin V binding assay using flow cytometer. Fluorouracil 40-44 annexin A5 Homo sapiens 62-71 31911552-7 2020 In contrast, MDSC depletion by either gemcitabine or 5-fluorouracil treatment in OB-Runx2-/- mice prevented these effects and inhibited MM tumor growth in BM. Fluorouracil 53-67 runt related transcription factor 2 Mus musculus 84-89 26774139-8 2016 In addition, chidamide alone or in combination with 5-Fu increased the p53, phosphorylated-p53 (p-p53), p21 and gammaH2AX levels, but suppressed cyclin dependent kinase 4 (CDK4) expression in tumor cells. Fluorouracil 52-56 H3 histone pseudogene 16 Homo sapiens 104-107 26692822-13 2015 In addition, As2O3 in combination with 5-FU treatment caused up-regulation of DR5, caspase 3, caspase 8, and caspase 9, and down-regulation of BCL-2, but had no effect of DR4. Fluorouracil 39-43 TNF receptor superfamily member 10b Homo sapiens 78-81 31788833-5 2020 This study aimed to investigate the key role of TMEM45A in CRC by knockdown of its expression in 5-FU-resistant CRC cells (HCT-8/5-FU and SW480/5-FU) and their parental cells (HCT-8 and SW480). Fluorouracil 97-101 transmembrane protein 45A Homo sapiens 48-55 31788833-5 2020 This study aimed to investigate the key role of TMEM45A in CRC by knockdown of its expression in 5-FU-resistant CRC cells (HCT-8/5-FU and SW480/5-FU) and their parental cells (HCT-8 and SW480). Fluorouracil 129-133 transmembrane protein 45A Homo sapiens 48-55 26692822-13 2015 In addition, As2O3 in combination with 5-FU treatment caused up-regulation of DR5, caspase 3, caspase 8, and caspase 9, and down-regulation of BCL-2, but had no effect of DR4. Fluorouracil 39-43 caspase 9 Homo sapiens 109-118 31788833-5 2020 This study aimed to investigate the key role of TMEM45A in CRC by knockdown of its expression in 5-FU-resistant CRC cells (HCT-8/5-FU and SW480/5-FU) and their parental cells (HCT-8 and SW480). Fluorouracil 129-133 transmembrane protein 45A Homo sapiens 48-55 26527315-4 2015 5-FU treatment-resistant cells show a de novo expression of pyruvate kinase M1 (PKM1) and repression of PKM2, correlating with repression of the pentose phosphate pathway, decrease in NADPH level and in antioxidant defenses, promoting PKM2 oxidation and acquisition of stem-like phenotype. Fluorouracil 0-4 pyruvate kinase M1/2 Homo sapiens 104-108 31788833-6 2020 Data showed that TMEM45A was significantly up-regulated in HCT-8/5-FU and SW480/5-FU cells in comparison with their parental HCT-8 and SW480 cells. Fluorouracil 65-69 transmembrane protein 45A Homo sapiens 17-24 31788833-6 2020 Data showed that TMEM45A was significantly up-regulated in HCT-8/5-FU and SW480/5-FU cells in comparison with their parental HCT-8 and SW480 cells. Fluorouracil 80-84 transmembrane protein 45A Homo sapiens 17-24 31788833-7 2020 Knockdown of TMEM45A enhanced 5-FU sensitivity and 5-FU-induced apoptosis in HCT-8/5-FU and SW480/5-FU cells. Fluorouracil 30-34 transmembrane protein 45A Homo sapiens 13-20 31788833-7 2020 Knockdown of TMEM45A enhanced 5-FU sensitivity and 5-FU-induced apoptosis in HCT-8/5-FU and SW480/5-FU cells. Fluorouracil 51-55 transmembrane protein 45A Homo sapiens 13-20 31788833-7 2020 Knockdown of TMEM45A enhanced 5-FU sensitivity and 5-FU-induced apoptosis in HCT-8/5-FU and SW480/5-FU cells. Fluorouracil 51-55 transmembrane protein 45A Homo sapiens 13-20 31788833-7 2020 Knockdown of TMEM45A enhanced 5-FU sensitivity and 5-FU-induced apoptosis in HCT-8/5-FU and SW480/5-FU cells. Fluorouracil 51-55 transmembrane protein 45A Homo sapiens 13-20 31788833-8 2020 It was also found that inhibition of TMEM45A increased the intracellular accumulation of Rhodamine-123 and down-regulated the expression of MDR1 in HCT-8/5-FU and SW480/5-FU cells. Fluorouracil 154-158 transmembrane protein 45A Homo sapiens 37-44 31788833-8 2020 It was also found that inhibition of TMEM45A increased the intracellular accumulation of Rhodamine-123 and down-regulated the expression of MDR1 in HCT-8/5-FU and SW480/5-FU cells. Fluorouracil 169-173 transmembrane protein 45A Homo sapiens 37-44 31788833-9 2020 In addition, knockdown of TMEM45A suppressed migration and invasion of HCT-8/5-FU and SW480/5-FU cells. Fluorouracil 77-81 transmembrane protein 45A Homo sapiens 26-33 31788833-9 2020 In addition, knockdown of TMEM45A suppressed migration and invasion of HCT-8/5-FU and SW480/5-FU cells. Fluorouracil 92-96 transmembrane protein 45A Homo sapiens 26-33 31788833-10 2020 Furthermore, knockdown of TMEM45A not only attenuated MDR-enhanced epithelial-mesenchymal transition (EMT), but also suppressed MDR-enhanced activation of TGF-beta signaling pathway in HCT-8/5-FU and SW480/5-FU cells. Fluorouracil 191-195 transmembrane protein 45A Homo sapiens 26-33 31788833-10 2020 Furthermore, knockdown of TMEM45A not only attenuated MDR-enhanced epithelial-mesenchymal transition (EMT), but also suppressed MDR-enhanced activation of TGF-beta signaling pathway in HCT-8/5-FU and SW480/5-FU cells. Fluorouracil 206-210 transmembrane protein 45A Homo sapiens 26-33 32152581-5 2020 In mice treated with topical 5-fluorouracil, use of STAR particles increased the efficacy of the drug in suppressing the growth of subcutaneous melanoma tumors and prolonging survival. Fluorouracil 29-43 steroidogenic acute regulatory protein Mus musculus 52-56 32162808-8 2020 Patients with tumor PD-L1 >= 1% had a significantly longer DFS in sequential chemotherapy than in than 5-FU/LV arm (interaction p = .04) and a trend for OS (interaction p = .12). Fluorouracil 103-107 CD274 molecule Homo sapiens 20-25 32162808-12 2020 Moreover, tumor PD-L1 expression >=1% was associated with greater benefit from intensive sequential chemotherapy compared with 5-fluorouracil plus leucovorin (5-FU/LV), whereas PD-L1 expression <1% was not, conditioning a statistically significant interaction between such biomarker and treatment arms. Fluorouracil 127-141 CD274 molecule Homo sapiens 16-21 32162808-12 2020 Moreover, tumor PD-L1 expression >=1% was associated with greater benefit from intensive sequential chemotherapy compared with 5-fluorouracil plus leucovorin (5-FU/LV), whereas PD-L1 expression <1% was not, conditioning a statistically significant interaction between such biomarker and treatment arms. Fluorouracil 159-163 CD274 molecule Homo sapiens 16-21 32194698-7 2020 The results revealed that suppression of HSP27 expression significantly increased cell apoptosis, inhibited tumor growth and enhanced sensitivity to the anti-cancer agents 5-fluorouracil (5-FU) and vincristine (VCR). Fluorouracil 172-186 heat shock protein family B (small) member 1 Homo sapiens 41-46 32194698-7 2020 The results revealed that suppression of HSP27 expression significantly increased cell apoptosis, inhibited tumor growth and enhanced sensitivity to the anti-cancer agents 5-fluorouracil (5-FU) and vincristine (VCR). Fluorouracil 188-192 heat shock protein family B (small) member 1 Homo sapiens 41-46 32005407-8 2020 High expression of COL4A1, COL4A2, COL6A1, COL6A2, and COL6A3 was correlated with poorer prognosis of GC patients treated by surgery only, while higher expression of COL4A1 and COL11A1 correlated with poorer survival of patients treated by 5-fluorouracil-based adjuvant therapy. Fluorouracil 240-254 collagen type IV alpha 1 chain Homo sapiens 19-25 32185127-2 2020 Herein, we provide mechanistic rationale for acquired or inherent chemotherapeutic resistance to the anti-tumor effects of 5-fluorouracil (5-FU) that is linked to oncogenic GLI1 transcription activity and NBS1 overexpression. Fluorouracil 123-137 nibrin Homo sapiens 205-209 32185127-2 2020 Herein, we provide mechanistic rationale for acquired or inherent chemotherapeutic resistance to the anti-tumor effects of 5-fluorouracil (5-FU) that is linked to oncogenic GLI1 transcription activity and NBS1 overexpression. Fluorouracil 139-143 nibrin Homo sapiens 205-209 26527315-4 2015 5-FU treatment-resistant cells show a de novo expression of pyruvate kinase M1 (PKM1) and repression of PKM2, correlating with repression of the pentose phosphate pathway, decrease in NADPH level and in antioxidant defenses, promoting PKM2 oxidation and acquisition of stem-like phenotype. Fluorouracil 0-4 pyruvate kinase M1/2 Homo sapiens 235-239 26453961-3 2015 Here, we describe that DNA methylation levels at CpG loci of hyaluronoglucosaminidase 2 (HYLA2) could be used to identify stage II and III colon cancer patients who are most likely to benefit from 5-flourouracil (5-FU) chemotherapy with respect to overall survival and progression-free survival. Fluorouracil 213-217 hyaluronidase 2 Homo sapiens 61-87 26453961-3 2015 Here, we describe that DNA methylation levels at CpG loci of hyaluronoglucosaminidase 2 (HYLA2) could be used to identify stage II and III colon cancer patients who are most likely to benefit from 5-flourouracil (5-FU) chemotherapy with respect to overall survival and progression-free survival. Fluorouracil 213-217 hyaluronidase 2 Homo sapiens 89-94 26788191-0 2015 Functional mechanism of the enhancement of 5-fluorouracil sensitivity by TUSC4 in colon cancer cells. Fluorouracil 43-57 NPR2 like, GATOR1 complex subunit Homo sapiens 73-78 26788191-3 2015 The aim of the present study was to investigate the functional mechanism by which TUSC4 affects sensitivity to 5-FU and to determine its clinical significance in CRC. Fluorouracil 111-115 NPR2 like, GATOR1 complex subunit Homo sapiens 82-87 26788191-4 2015 The results of the present study demonstrated that TUSC4 overexpression increases the sensitivity of HCT116 cells to 5-FU. Fluorouracil 117-121 NPR2 like, GATOR1 complex subunit Homo sapiens 51-56 26788191-5 2015 The IC50 of 5-FU was reduced in cells transduced with TUSC4 compared with negative control (NC) cells, and the effect of TUSC4 on 5-FU sensitivity was time dependent. Fluorouracil 12-16 NPR2 like, GATOR1 complex subunit Homo sapiens 54-59 26788191-5 2015 The IC50 of 5-FU was reduced in cells transduced with TUSC4 compared with negative control (NC) cells, and the effect of TUSC4 on 5-FU sensitivity was time dependent. Fluorouracil 130-134 NPR2 like, GATOR1 complex subunit Homo sapiens 54-59 26788191-5 2015 The IC50 of 5-FU was reduced in cells transduced with TUSC4 compared with negative control (NC) cells, and the effect of TUSC4 on 5-FU sensitivity was time dependent. Fluorouracil 130-134 NPR2 like, GATOR1 complex subunit Homo sapiens 121-126 26788191-8 2015 The mechanism through which TUSC4 overexpression enhances 5-FU sensitivity involves the downregulation of the function of the PI3K/Akt/mTOR network. Fluorouracil 58-62 NPR2 like, GATOR1 complex subunit Homo sapiens 28-33 26788191-9 2015 Furthermore, 5-FU upregulated caspase-3 and caspase-9, promoting apoptosis in TUSC4-overexpressing cells compared with cells that were transduced with TUSC4 or treated with 5-FU and NC cells. Fluorouracil 13-17 caspase 9 Homo sapiens 44-53 26788191-9 2015 Furthermore, 5-FU upregulated caspase-3 and caspase-9, promoting apoptosis in TUSC4-overexpressing cells compared with cells that were transduced with TUSC4 or treated with 5-FU and NC cells. Fluorouracil 13-17 NPR2 like, GATOR1 complex subunit Homo sapiens 78-83 26788191-10 2015 The findings of the present study indicate that TUSC4 has potential as a biomarker for the prediction of the response to 5-FU and prognosis in patients with colorectal cancer and other types of human cancer. Fluorouracil 121-125 NPR2 like, GATOR1 complex subunit Homo sapiens 48-53 26788191-11 2015 TUSC4 may also act as a molecular therapeutic agent for enhancing the patient"s response to 5-FU treatment. Fluorouracil 92-96 NPR2 like, GATOR1 complex subunit Homo sapiens 0-5 26108995-0 2015 Suberoylanilide hydroxamic acid enhances chemosensitivity to 5-fluorouracil in hepatocellular carcinoma via inhibition of thymidylate synthase. Fluorouracil 61-75 thymidylate synthetase Homo sapiens 122-142 26108995-7 2015 Our results indicate that SAHA and 5-FU act synergistically to inhibit cell growth and tumorigenicity in HCC via the induction of cell-cycle arrest and apoptosis through a mechanism involving the inhibition of thymidylate synthase, suggesting that combination treatment with 5-FU and SAHA may be beneficial for the treatment of inoperable HCC. Fluorouracil 35-39 thymidylate synthetase Homo sapiens 210-230 26136123-11 2015 Survival and antiapoptosis signaling (pAkt, Akt, Mcl-1 and Bcl-2) was downregulated, and the proapoptotic proteins (Bad and Bax) were upregulated in 5-FU-treated control cells but expression levels of Bcl-2, Bad, and Bad were not altered in 5-FU-treated A7-nAChR-KD cells. Fluorouracil 149-153 MCL1 apoptosis regulator, BCL2 family member Homo sapiens 49-54 26142736-3 2015 As a target of 5-FU, thymidylate synthase (TS) expression level might be influenced by irinotecan. Fluorouracil 15-19 thymidylate synthetase Homo sapiens 21-41 26142736-3 2015 As a target of 5-FU, thymidylate synthase (TS) expression level might be influenced by irinotecan. Fluorouracil 15-19 thymidylate synthetase Homo sapiens 43-45 26807186-8 2015 After inhibiting Mcl-1, the cell migration and invasion decreased (P<0.05), the resistance to VCR, DDP and 5-Fu was reversed to different extents (P<0.05), TS mRNA expression increased significantly (P<0.05), MDR1 remained unchanged (P>0.05), but DPD and TOP2A decreased significantly (P<0.05). Fluorouracil 110-114 MCL1 apoptosis regulator, BCL2 family member Homo sapiens 17-22 26807186-8 2015 After inhibiting Mcl-1, the cell migration and invasion decreased (P<0.05), the resistance to VCR, DDP and 5-Fu was reversed to different extents (P<0.05), TS mRNA expression increased significantly (P<0.05), MDR1 remained unchanged (P>0.05), but DPD and TOP2A decreased significantly (P<0.05). Fluorouracil 110-114 DNA topoisomerase II alpha Homo sapiens 267-272 26428513-5 2015 While both FTD and 5-FU inhibit thymidylate synthase (TS), a central enzyme in DNA synthesis, sufficient TS inhibition by FTD requires continuous infusion; therefore, it is not considered a clinically relevant mechanism with oral dosing. Fluorouracil 19-23 thymidylate synthetase Homo sapiens 32-52 26428513-5 2015 While both FTD and 5-FU inhibit thymidylate synthase (TS), a central enzyme in DNA synthesis, sufficient TS inhibition by FTD requires continuous infusion; therefore, it is not considered a clinically relevant mechanism with oral dosing. Fluorouracil 19-23 thymidylate synthetase Homo sapiens 54-56 26293216-9 2015 SPAG9 overxpression also increased chemoresistance to 5--fluorouracil (5-FU) in SGC-7901 cells. Fluorouracil 54-69 sperm associated antigen 9 Homo sapiens 0-5 31188741-7 2020 Additionally, TMEM100 expression restored the sensitivity of GC cells to chemotherapeutic drugs such as 5-fluouracil (5-FU) and cisplatin. Fluorouracil 118-122 transmembrane protein 100 Mus musculus 14-21 32098629-12 2020 Finally, we observed that up-regulation of MUC5AC conferred resistance to 5-FU through down-regulation of p53 and its target gene p21 and up-regulation of beta-catenin and its target genes CD44 and Lgr5. Fluorouracil 74-78 transformation related protein 53, pseudogene Mus musculus 106-109 32076068-8 2020 Collectively, these results indicate that combination treatment of vactosertib with nal-IRI/5-FU/LV improves overall survival rates in a mouse model of pancreatic cancer by suppressing invasion through CCDC80. Fluorouracil 92-96 coiled-coil domain containing 80 Mus musculus 202-208 31605153-11 2020 CONCLUSIONS: Reduction of the total liver DPD following major hepatectomy caused increased plasma 5-FU levels and 5-FU-associated toxicity. Fluorouracil 98-102 dihydropyrimidine dehydrogenase Rattus norvegicus 42-45 31605153-11 2020 CONCLUSIONS: Reduction of the total liver DPD following major hepatectomy caused increased plasma 5-FU levels and 5-FU-associated toxicity. Fluorouracil 114-118 dihydropyrimidine dehydrogenase Rattus norvegicus 42-45 31313286-0 2020 Inhibition of KHSRP sensitizes colorectal cancer to 5-fluoruracil through miR-501-5p-mediated ERRFI1 mRNA degradation. Fluorouracil 52-65 microRNA 501 Homo sapiens 74-81 31872284-7 2020 Collectively, these data indicated that NOD1 suppressed proliferation and enhanced response to sorafenib or 5-FU treatment through inhibiting SRC-MAPK axis in hepatocellular carcinoma. Fluorouracil 108-112 nucleotide binding oligomerization domain containing 1 Homo sapiens 40-44 31746054-5 2020 Exposure to specific TLR2/6 or TLR5 ligands enhanced the expression of mesenchymal markers as well as the migratory activity of oxaliplatin- or 5-fluorouracil-resistant colon cancer cells. Fluorouracil 144-158 toll like receptor 5 Homo sapiens 31-35 31918721-7 2020 The results showed that the engineered exosome-based 5-FU and miR-21i co-delivery system could efficiently facilitate cellular uptake and significantly down-regulate miR-21 expression in 5-FU resistant HCT-1165FR cell lines. Fluorouracil 187-191 microRNA 21 Homo sapiens 62-68 31896739-0 2020 Over-expression of EGFR regulated by RARA contributes to 5-FU resistance in colon cancer. Fluorouracil 57-61 retinoic acid receptor alpha Homo sapiens 37-41 31896739-9 2020 EGFR contributed to 5-FU resistance in colon cancer cells through autophagy induction, and EGFR overexpression in 5-FU resistant colon cancer was regulated by RARA. Fluorouracil 114-118 retinoic acid receptor alpha Homo sapiens 159-163 26293216-9 2015 SPAG9 overxpression also increased chemoresistance to 5--fluorouracil (5-FU) in SGC-7901 cells. Fluorouracil 71-75 sperm associated antigen 9 Homo sapiens 0-5 26457704-0 2015 MicroRNA-302b Enhances the Sensitivity of Hepatocellular Carcinoma Cell Lines to 5-FU via Targeting Mcl-1 and DPYD. Fluorouracil 81-85 MCL1 apoptosis regulator, BCL2 family member Homo sapiens 100-105 26457704-3 2015 However, the role that miR-302b plays in the 5-Fluorouracil (5-FU) sensitivity of HCC has not been known. Fluorouracil 45-59 microRNA 302b Homo sapiens 23-31 26457704-3 2015 However, the role that miR-302b plays in the 5-Fluorouracil (5-FU) sensitivity of HCC has not been known. Fluorouracil 61-65 microRNA 302b Homo sapiens 23-31 26457704-4 2015 This study showed that miR-302b could enhance the sensitivity to 5-FU in HCC cell lines and verified its two putative targeted genes responsible for its 5-FU sensitivity. Fluorouracil 65-69 microRNA 302b Homo sapiens 23-31 26457704-4 2015 This study showed that miR-302b could enhance the sensitivity to 5-FU in HCC cell lines and verified its two putative targeted genes responsible for its 5-FU sensitivity. Fluorouracil 153-157 microRNA 302b Homo sapiens 23-31 26617970-2 2015 C-5-Furan-2-yl uracil derivative 6 was shown to be more potent against MCF-7 than the reference drug 5-fluorouracil (5-FU), while C-5-alkynyl uracil derivatives 9c and 9e exhibited antibreast cancer activities comparable to 5-FU. Fluorouracil 101-115 complement C5 Homo sapiens 0-3 32964213-12 2020 Conclusion: This is the first case series that reports the safety and feasibility of s-MOX in patients with mCRC who developed cardiac toxicity to 5-FU or capecitabine. Fluorouracil 147-151 monooxygenase DBH like 1 Homo sapiens 87-90 26617970-2 2015 C-5-Furan-2-yl uracil derivative 6 was shown to be more potent against MCF-7 than the reference drug 5-fluorouracil (5-FU), while C-5-alkynyl uracil derivatives 9c and 9e exhibited antibreast cancer activities comparable to 5-FU. Fluorouracil 117-121 complement C5 Homo sapiens 0-3 26617970-2 2015 C-5-Furan-2-yl uracil derivative 6 was shown to be more potent against MCF-7 than the reference drug 5-fluorouracil (5-FU), while C-5-alkynyl uracil derivatives 9c and 9e exhibited antibreast cancer activities comparable to 5-FU. Fluorouracil 224-228 complement C5 Homo sapiens 0-3 26316041-8 2015 Knockdown of beta-catenin significantly increased chemosensitivity to 5-fluorouracil and irinotecan in HCT116 3D cultures and LoVo 3D cultures. Fluorouracil 70-84 catenin beta 1 Homo sapiens 13-25 26418978-0 2015 [Drug resistance of colon cancer cells to 5-fluorouracil mediated by microRNA-21]. Fluorouracil 42-56 microRNA 21 Homo sapiens 69-80 26418978-1 2015 OBJECTIVE To explore downstream regulatory pathway of microRNA-21 (miR-21) in colon cancer cells (RKO) through detecting miR-21 and its target PDCD4, and the influence of miR-21 regulation on the sensitivity of RKO cells to 5-fluorouracil (5-FU). Fluorouracil 224-238 microRNA 21 Homo sapiens 54-65 26418978-1 2015 OBJECTIVE To explore downstream regulatory pathway of microRNA-21 (miR-21) in colon cancer cells (RKO) through detecting miR-21 and its target PDCD4, and the influence of miR-21 regulation on the sensitivity of RKO cells to 5-fluorouracil (5-FU). Fluorouracil 224-238 microRNA 21 Homo sapiens 67-73 26418978-1 2015 OBJECTIVE To explore downstream regulatory pathway of microRNA-21 (miR-21) in colon cancer cells (RKO) through detecting miR-21 and its target PDCD4, and the influence of miR-21 regulation on the sensitivity of RKO cells to 5-fluorouracil (5-FU). Fluorouracil 240-244 microRNA 21 Homo sapiens 54-65 26418978-1 2015 OBJECTIVE To explore downstream regulatory pathway of microRNA-21 (miR-21) in colon cancer cells (RKO) through detecting miR-21 and its target PDCD4, and the influence of miR-21 regulation on the sensitivity of RKO cells to 5-fluorouracil (5-FU). Fluorouracil 240-244 microRNA 21 Homo sapiens 67-73 26418978-4 2015 RESULTS MTT assay reveals that the IC50 of 5-FU in RKO-WT cells (52.82 +- 0.06 umol/L) was about 67% higher than in miR-21 knockout cells (32.23 +- 0.05 umol/L) (P < 0.05), and the apoptosis ratio elevated after knockout of miR-21. Fluorouracil 43-47 microRNA 21 Homo sapiens 227-233 26418978-6 2015 CONCLUSION MiR-21 can mediate the drug resistance to 5-FU by inhibiting its target PDCD4, which can regulate the expression of ABCC5 and CD44 genes. Fluorouracil 53-57 microRNA 21 Homo sapiens 11-17 26291056-4 2015 The BIRC3 mRNA expression was measured by qRT-PCR in 65 pretreatment frozen biopsies from patients receiving preoperatively docetaxel, cisplatin, 5-fluorouracil, and concurrent radiotherapy. Fluorouracil 146-160 baculoviral IAP repeat containing 3 Homo sapiens 4-9 25956534-4 2015 In this study, in vitro 5-FU not only directly blocked both stromal cell- and RANKL-induced osteoclastogenesis through NF-kappaB pathway, but also indirectly inhibited osteoclast formation and angiogenesis by suppressing the expression of osteoclast-activating factors including IL-1beta, MCP-1 and tumor angiogenesis factor VEGF in stromal cells. Fluorouracil 24-28 tumor necrosis factor superfamily member 11 Gallus gallus 78-83 25956534-4 2015 In this study, in vitro 5-FU not only directly blocked both stromal cell- and RANKL-induced osteoclastogenesis through NF-kappaB pathway, but also indirectly inhibited osteoclast formation and angiogenesis by suppressing the expression of osteoclast-activating factors including IL-1beta, MCP-1 and tumor angiogenesis factor VEGF in stromal cells. Fluorouracil 24-28 interleukin 1, beta Gallus gallus 279-287 26208739-0 2015 Gossypol sensitizes the antitumor activity of 5-FU through down-regulation of thymidylate synthase in human colon carcinoma cells. Fluorouracil 46-50 thymidylate synthetase Homo sapiens 78-98 26210704-0 2015 Long Survival and Severe Toxicity Under 5-Fluorouracil-Based Therapy in a Patient With Colorectal Cancer Who Harbors a Germline Codon-Stop Mutation in TYMS. Fluorouracil 40-54 thymidylate synthetase Homo sapiens 151-155 26622665-10 2015 In conclusion, the results indicated that 5-FU-induced ROS production resulted in the upregulation of TET1 expression and function. Fluorouracil 42-46 tet methylcytosine dioxygenase 1 Homo sapiens 102-106 25861021-7 2015 We found that silencing the expression of beta-catenin with lentiviruses could delay cell proliferation, promote apoptosis, weaken the invasive power of GC cells, and increase the sensitivity of GC cells to 5-fluorouracil in vitro. Fluorouracil 207-221 catenin beta 1 Homo sapiens 42-54 26247730-5 2015 Knockdown of PPP2R1B expression increases AKT phosphorylation, which leads to elevated XIAP expression and enhanced 5-FU resistance; whereas rescue of PPP2R1B expression in miR-587-expressing cells decreases AKT phosphorylation/XIAP expression, re-sensitizing colon cancer cells to 5-FU-induced apoptosis. Fluorouracil 116-120 microRNA 587 Homo sapiens 173-180 26247730-5 2015 Knockdown of PPP2R1B expression increases AKT phosphorylation, which leads to elevated XIAP expression and enhanced 5-FU resistance; whereas rescue of PPP2R1B expression in miR-587-expressing cells decreases AKT phosphorylation/XIAP expression, re-sensitizing colon cancer cells to 5-FU-induced apoptosis. Fluorouracil 282-286 microRNA 587 Homo sapiens 173-180 26247730-6 2015 Moreover, a specific and potent AKT inhibitor, MK2206, reverses miR-587-conferred 5-FU resistance. Fluorouracil 82-86 microRNA 587 Homo sapiens 64-71 26247730-9 2015 A major implication of our study is that inhibition of miR-587 or restoration of PPP2R1B expression may have significant therapeutic potential to overcome drug resistance in colorectal cancer patients and that the combined use of an AKT inhibitor with 5-FU may increase efficacy in colorectal cancer treatment. Fluorouracil 252-256 microRNA 587 Homo sapiens 55-62 32262584-8 2015 This drastically facilitated unhindered vertical diffusion with selective binding of uracil and 5-fluorouracil and their sensitive analysis using differential pulse anodic stripping voltammetry, with detection limits as low as 0.50 and 0.33 ng mL-1 (S/N = 3), respectively. Fluorouracil 96-110 L1 cell adhesion molecule Mus musculus 244-248 31911300-3 2020 Compounds A2, A9, A10 exhibited significant cytotoxic activities compared to their parent compounds and standard drug 5-fluorouracil. Fluorouracil 118-132 immunoglobulin kappa variable 6D-21 (non-functional) Homo sapiens 18-21 31542354-0 2019 Inhibition of hydrogen sulfide synthesis reverses acquired resistance to 5-FU through miR-215-5p-EREG/TYMS axis in colon cancer cells. Fluorouracil 73-77 thymidylate synthetase Homo sapiens 102-106 32156869-1 2019 BACKGROUND: In Japan, pre-operative 5-FU and cisplatin(CDDP)(FP)combination therapy has been the standard neoadjuvant chemotherapy(NAC)for advanced resectable esophageal cancer(EC); furthermore, the efficacy of the docetaxel (DTX)-containing triplet regimen, FP plus DTX, has been reported. Fluorouracil 36-40 synuclein alpha Homo sapiens 131-134 26205949-11 2015 Mechanistically, vitamin D3/5-FU co-therapy significantly decreased the expression of Wnt, beta-catenin, iNOS, COX-2 and HSP-90 and significantly increased the expression of DKK-1, TGF-beta1, TGF-betaR2, smad4 (P < 0.05), in comparison with their corresponding monotherapy groups. Fluorouracil 28-32 catenin beta 1 Rattus norvegicus 91-103 26276288-1 2015 OBJECTIVE: To study the effect of lipoteichoic acid (LTA) and 5-FU on the expression of caspase-3, EGFR, TGF-alpha proteins of tumor tissue of H22 cancer bearing mice and its anti-tumor mechanism. Fluorouracil 62-66 epidermal growth factor receptor Mus musculus 99-103 26276288-1 2015 OBJECTIVE: To study the effect of lipoteichoic acid (LTA) and 5-FU on the expression of caspase-3, EGFR, TGF-alpha proteins of tumor tissue of H22 cancer bearing mice and its anti-tumor mechanism. Fluorouracil 62-66 transforming growth factor alpha Mus musculus 105-114 26276288-9 2015 CONCLUSIONS: LTA combined with 5-FU can effectively inhibit the tumorigenesis of H22 tumor bearing mice, increase the caspase-3 protein expression, inhibit TGF-alpha and EGFR protein expression, further promote tumor cell apoptosis and play a synergistic antitumor effect. Fluorouracil 31-35 transforming growth factor alpha Mus musculus 156-165 26276288-9 2015 CONCLUSIONS: LTA combined with 5-FU can effectively inhibit the tumorigenesis of H22 tumor bearing mice, increase the caspase-3 protein expression, inhibit TGF-alpha and EGFR protein expression, further promote tumor cell apoptosis and play a synergistic antitumor effect. Fluorouracil 31-35 epidermal growth factor receptor Mus musculus 170-174 25112781-1 2015 BACKGROUND: The efficacy of 5-fluorouracil (5FU)-based therapy, which remains the cornerstone of gastrointestinal cancer treatment, depends upon the expression of enzymes involved in pyrimidine metabolism, including thymidylate synthase (TS), dihydropyrimidine dehydrogenase (DPD), thymidine phosphorylase (TP), and orotate phosphoribosyltransferase (OPRT). Fluorouracil 44-47 uridine monophosphate synthetase Homo sapiens 316-349 25112781-1 2015 BACKGROUND: The efficacy of 5-fluorouracil (5FU)-based therapy, which remains the cornerstone of gastrointestinal cancer treatment, depends upon the expression of enzymes involved in pyrimidine metabolism, including thymidylate synthase (TS), dihydropyrimidine dehydrogenase (DPD), thymidine phosphorylase (TP), and orotate phosphoribosyltransferase (OPRT). Fluorouracil 44-47 uridine monophosphate synthetase Homo sapiens 351-355 25953218-3 2015 MicroRNA-21 has been related to acquisition of 5-fluorouracil resistance; however, its potential predictive value of response to preoperative chemoradiotherapy in locally advanced rectal cancer remains unknown. Fluorouracil 47-61 microRNA 21 Homo sapiens 0-11 25689483-0 2015 The c-MYC-ABCB5 axis plays a pivotal role in 5-fluorouracil resistance in human colon cancer cells. Fluorouracil 45-59 MYC proto-oncogene, bHLH transcription factor Homo sapiens 4-9 25689483-3 2015 In this study, we found that the c-MYC expression level in primary colorectal cancer tissues correlated with the recurrence rate following 5-fluorouracil (5-FU)-based adjuvant chemotherapy. Fluorouracil 139-153 MYC proto-oncogene, bHLH transcription factor Homo sapiens 33-38 25689483-3 2015 In this study, we found that the c-MYC expression level in primary colorectal cancer tissues correlated with the recurrence rate following 5-fluorouracil (5-FU)-based adjuvant chemotherapy. Fluorouracil 155-159 MYC proto-oncogene, bHLH transcription factor Homo sapiens 33-38 25689483-4 2015 Supporting this finding, overexpression of exogenous c-MYC increased the survival rate following 5-FU treatment in human colon cancer cells, and knockdown of endogenous c-MYC decreased it. Fluorouracil 97-101 MYC proto-oncogene, bHLH transcription factor Homo sapiens 53-58 25689483-5 2015 Furthermore, c-MYC knockdown decreased the expression level of ABCB5, which is involved in 5-FU resistance. Fluorouracil 91-95 MYC proto-oncogene, bHLH transcription factor Homo sapiens 13-18 25689483-12 2015 Taken together, these results suggest that c-MYC confers resistance to 5-FU through regulating ABCB5 expression in human colon cancer cells. Fluorouracil 71-75 MYC proto-oncogene, bHLH transcription factor Homo sapiens 43-48 26166093-2 2015 These polymorphisms have been related to the risk of suffering different cancers, for example leukemia, breast or gastric cancer, and response to different drugs, among which are methotrexate glutamates, stavudine, and specifically 5-fluorouracil (5-FU), as TYMS is its direct target. Fluorouracil 232-246 thymidylate synthetase Homo sapiens 258-262 26166093-2 2015 These polymorphisms have been related to the risk of suffering different cancers, for example leukemia, breast or gastric cancer, and response to different drugs, among which are methotrexate glutamates, stavudine, and specifically 5-fluorouracil (5-FU), as TYMS is its direct target. Fluorouracil 248-252 thymidylate synthetase Homo sapiens 258-262 26166093-4 2015 Estimates of the extent to which these polymorphisms influence in TYMS expression have in the past been based on functional analysis by luciferase assays and quantification of TYMS mRNA, but both these studies, as the association studies with cancer risk or with toxicity or response to 5-FU, are very contradictory. Fluorouracil 287-291 thymidylate synthetase Homo sapiens 66-70 31612261-4 2019 RESULTS: The Keynote-048 study showed an improvement in overall survival with pembrolizumab monotherapy for patients with measurable programmed cell death ligand 1 (PD-L1) expression according to the combined positive score (CPS), and for the whole cohort with the combination of pembrolizumab and platin/5-fluorouracil (FU). Fluorouracil 305-319 CD274 molecule Homo sapiens 165-170 25940810-6 2015 We report the case of a 15-year-old immunocompromised girl with severe recalcitrant condyloma that resolved after a course of systemic 5-fluorouracil, mitomycin C, and radiation therapy for SCC. Fluorouracil 135-149 serpin family B member 3 Homo sapiens 190-193 31638183-0 2019 In vitro and in vivo studies on the association of long non-coding RNAs H19 and urothelial cancer associated 1 with the susceptibility to 5-fluorouracil in rectal cancer. Fluorouracil 138-152 H19 imprinted maternally expressed transcript Homo sapiens 72-75 31638183-4 2019 Bioinformatic analysis identified H19 and urothelial cancer associated 1 (UCA1) as candidate biomarkers for 5FU susceptibility. Fluorouracil 108-111 H19 imprinted maternally expressed transcript Homo sapiens 34-37 31638183-6 2019 The ratios of changes of H19 and UCA1 expression in response to 5FU were low in cells resistant to 5FU, whereas ratios were high in cells susceptible to 5FU. Fluorouracil 64-67 H19 imprinted maternally expressed transcript Homo sapiens 25-28 31638183-6 2019 The ratios of changes of H19 and UCA1 expression in response to 5FU were low in cells resistant to 5FU, whereas ratios were high in cells susceptible to 5FU. Fluorouracil 99-102 H19 imprinted maternally expressed transcript Homo sapiens 25-28 31638183-6 2019 The ratios of changes of H19 and UCA1 expression in response to 5FU were low in cells resistant to 5FU, whereas ratios were high in cells susceptible to 5FU. Fluorouracil 99-102 H19 imprinted maternally expressed transcript Homo sapiens 25-28 25753067-7 2015 On increased demand of platelet production after 5-FU treatment, a part of CD41(+) LSK population expressed CD42b on the surface, and 90% of them showed unipotent megakaryopoietic capacity in single cell culture and predominantly produced platelets in vivo at the early phase after transplantation. Fluorouracil 49-53 integrin alpha 2b Mus musculus 75-79 31638183-11 2019 The increase in H19 and UCA1 expression may represent the response to impaired cell cycle in cells susceptible to 5FU. Fluorouracil 114-117 H19 imprinted maternally expressed transcript Homo sapiens 16-19 31638183-12 2019 Our results indicate that changes in H19 and UCA1 expression may be considered for predicting the susceptibility to 5FU-based NAC in rectal cancer. Fluorouracil 116-119 H19 imprinted maternally expressed transcript Homo sapiens 37-40 31581233-7 2019 This link between RPL22L1 induction and 5-Fluorouracil resistance appears to be causal, because ectopic expression or knockdown of RPL22L1 in cell lines increases and decreases 5-Fluorouracil resistance, respectively, and this is associated with changes in expression of the DNA-repair genes, MGMT and MLH1. Fluorouracil 40-54 mutL homolog 1 Homo sapiens 302-306 25913620-9 2015 Also of interest, suppression of RAD18 by miR-145 enhanced DNA damage in CRC cells after 5-FU treatment. Fluorouracil 89-93 microRNA 145 Homo sapiens 42-49 31173642-11 2019 Consistent with these results, iPTH treatment inhibited 5-fluorouracil- or ovariectomy (OVX)-induced LepR+ MSPC-derived adipogenesis in BM and increased LepR+ MSPC-derived osteoblasts, even under the adipocyte-induced conditions. Fluorouracil 56-70 leptin receptor Mus musculus 101-105 31261026-0 2019 The long non-coding RNA HOTAIRM1 suppresses cell progression via sponging endogenous miR-17-5p/ B-cell translocation gene 3 (BTG3) axis in 5-fluorouracil resistant colorectal cancer cells. Fluorouracil 139-153 BTG anti-proliferation factor 3 Homo sapiens 96-123 31261026-0 2019 The long non-coding RNA HOTAIRM1 suppresses cell progression via sponging endogenous miR-17-5p/ B-cell translocation gene 3 (BTG3) axis in 5-fluorouracil resistant colorectal cancer cells. Fluorouracil 139-153 BTG anti-proliferation factor 3 Homo sapiens 125-129 25913620-10 2015 Finally, the 5-FU-resistant cancer cells could be selectively ablated by treatment with miR-145. Fluorouracil 13-17 microRNA 145 Homo sapiens 88-95 25270617-1 2015 PURPOSE: To describe the use of a pulse-dose topical 5-fluorouracil (5-FU) treatment regimen in a Pug dog with corneal squamous cell carcinoma (SCC). Fluorouracil 53-67 serpin family B member 3 Homo sapiens 144-147 25270617-1 2015 PURPOSE: To describe the use of a pulse-dose topical 5-fluorouracil (5-FU) treatment regimen in a Pug dog with corneal squamous cell carcinoma (SCC). Fluorouracil 69-73 serpin family B member 3 Homo sapiens 144-147 25423960-5 2015 The expression of thymidylate synthase (TYMS) involved in 5-FU metabolism was also examined in protein and mRNA levels. Fluorouracil 58-62 thymidylate synthetase Homo sapiens 18-38 25423960-5 2015 The expression of thymidylate synthase (TYMS) involved in 5-FU metabolism was also examined in protein and mRNA levels. Fluorouracil 58-62 thymidylate synthetase Homo sapiens 40-44 25323586-0 2015 Bcl-2 stabilization by paxillin confers 5-fluorouracil resistance in colorectal cancer. Fluorouracil 40-54 paxillin Homo sapiens 23-31 25323586-4 2015 We thus hypothesized that pPXN-Y31/Y118 may be required for Bcl-2 protein stability via PXN interacting with Bcl-2 to confer 5-FU resistance in colorectal cancer. Fluorouracil 125-129 paxillin Homo sapiens 27-30 25323586-7 2015 An increase in Bcl-2 expression by PXN is responsible for resistance to 5-FU. Fluorouracil 72-76 paxillin Homo sapiens 35-38 25323586-10 2015 Patients with high PXN/high Bcl-2 or high pPXN-S272/high Bcl-2 tumors are commonly to have an unfavorable response to 5-FU-based chemotherapy, compared with patients who have high PXN, high pPXN-S272 or high Bcl-2 tumors alone. Fluorouracil 118-122 paxillin Homo sapiens 19-22 25323586-10 2015 Patients with high PXN/high Bcl-2 or high pPXN-S272/high Bcl-2 tumors are commonly to have an unfavorable response to 5-FU-based chemotherapy, compared with patients who have high PXN, high pPXN-S272 or high Bcl-2 tumors alone. Fluorouracil 118-122 paxillin Homo sapiens 43-46 25323586-11 2015 Therefore, we suggest that Src, PAK1 or Bcl-2 inhibitor may potentially overcome the resistance of 5-FU-based chemotherapy and consequently to improve outcomes in patients with PXN/Bcl-2 and pPXN-S272/Bcl-2-positive tumors. Fluorouracil 99-103 paxillin Homo sapiens 177-180 25433307-9 2015 Furthermore, belinostat attenuated the 5-fluorouracil mediated induction of thymidylate synthase via HSP90 hyperacetylation. Fluorouracil 39-53 thymidylate synthetase Homo sapiens 76-96 25433307-9 2015 Furthermore, belinostat attenuated the 5-fluorouracil mediated induction of thymidylate synthase via HSP90 hyperacetylation. Fluorouracil 39-53 heat shock protein 90 alpha family class A member 1 Homo sapiens 101-106 25433307-11 2015 CONCLUSIONS: In combination with 5-fluorouracil the targeted inhibitor of histone deacetylase synergistically inhibited renal cancer cell growth by the blockade of thymidylate synthase induction and the induction of reactive oxygen species mediated DNA damage in vitro and in vivo. Fluorouracil 33-47 thymidylate synthetase Homo sapiens 164-184 25919696-6 2015 5-FU chemosensitivity was significantly increased in miR-224 knockdown cells, and in NIH3T3 cells expressing KRAS and BRAF mutant proteins. Fluorouracil 0-4 Kirsten rat sarcoma viral oncogene homolog Mus musculus 109-113 25919696-6 2015 5-FU chemosensitivity was significantly increased in miR-224 knockdown cells, and in NIH3T3 cells expressing KRAS and BRAF mutant proteins. Fluorouracil 0-4 Braf transforming gene Mus musculus 118-122 25826088-1 2015 Stabilization of Bcl-2 protein by paxillin (PXN)-mediated ERK activation was recently reported to cause an unfavorable response to 5-Fluorouracil-based chemotherapy. Fluorouracil 131-145 paxillin Homo sapiens 34-42 31602272-4 2019 Moreover, the clonogenic survival fraction and cell apoptosis experiments showed that knockdown of AIB1 substantially increased cervical cancer cells sensitivity to ionizing radiation (IR) or cisplatin/5-fluorouracil. Fluorouracil 202-216 HEAT repeat containing 6 Homo sapiens 99-103 25826088-1 2015 Stabilization of Bcl-2 protein by paxillin (PXN)-mediated ERK activation was recently reported to cause an unfavorable response to 5-Fluorouracil-based chemotherapy. Fluorouracil 131-145 paxillin Homo sapiens 44-47 25881233-4 2015 Thymidylate synthase (TS) expression is a long-standing candidate as a biomarker for 5-fluorouracil (5-FU) treatment of cancer patients. Fluorouracil 85-99 thymidylate synthetase Homo sapiens 0-20 31366557-1 2019 BACKGROUND/AIM: The aim of this study was to investigate PD-L1 expression and its association with prognosis in esophageal squamous cell carcinoma (ESCC) before and after neoadjuvant chemotherapy (5-fluorouracil and cisplatin, NAC-FP). Fluorouracil 197-211 CD274 molecule Homo sapiens 57-62 31028570-9 2019 Combinatorial treatment of 5-FU and CEA aptamer augmented caspase-8 activity in the 5-FU-resistant colon cancer cell line via aptamer-mediated disruption of CEA interaction with death receptor 5 and in mouse xenograft tumors. Fluorouracil 27-31 caspase 8 Mus musculus 58-67 31028570-9 2019 Combinatorial treatment of 5-FU and CEA aptamer augmented caspase-8 activity in the 5-FU-resistant colon cancer cell line via aptamer-mediated disruption of CEA interaction with death receptor 5 and in mouse xenograft tumors. Fluorouracil 84-88 caspase 8 Mus musculus 58-67 31366086-10 2019 Intriguingly, the combination of LA and anticancer drugs (doxorubicin, 5-fluorouracil) attenuated p53-mediated stabilization of p21 and resulted in synergistic killing in CRC cells in a p53-dependant manner. Fluorouracil 71-85 H3 histone pseudogene 16 Homo sapiens 128-131 25881233-4 2015 Thymidylate synthase (TS) expression is a long-standing candidate as a biomarker for 5-fluorouracil (5-FU) treatment of cancer patients. Fluorouracil 85-99 thymidylate synthetase Homo sapiens 22-24 25881233-4 2015 Thymidylate synthase (TS) expression is a long-standing candidate as a biomarker for 5-fluorouracil (5-FU) treatment of cancer patients. Fluorouracil 101-105 thymidylate synthetase Homo sapiens 0-20 25881233-4 2015 Thymidylate synthase (TS) expression is a long-standing candidate as a biomarker for 5-fluorouracil (5-FU) treatment of cancer patients. Fluorouracil 101-105 thymidylate synthetase Homo sapiens 22-24 25881233-7 2015 5-FU sensitivity of the transformant cells significantly increased in response to downregulated TS expression, although being not examined in the full dynamic range because of the doxycycline toxicity. Fluorouracil 0-4 thymidylate synthetase Homo sapiens 96-98 25881233-8 2015 Intriguingly, our in vitro data suggest that there is a linear relationship between TS expression and the 5-FU sensitivity in cells. Fluorouracil 106-110 thymidylate synthetase Homo sapiens 84-86 25881233-10 2015 Thus, our in vitro and in vivo observations suggest that TS expression is a determinant of 5-FU sensitivity in cells, at least in this specific genetic background, and, therefore, support the possibility of TS expression as a biomarker for 5-FU-based cancer chemotherapy. Fluorouracil 91-95 thymidylate synthetase Homo sapiens 57-59 25762627-1 2015 Thymidylate synthase (TYMS) plays a role in DNA synthesis and is a target for 5-fluorouracil. Fluorouracil 78-92 thymidylate synthetase Homo sapiens 0-20 25762627-1 2015 Thymidylate synthase (TYMS) plays a role in DNA synthesis and is a target for 5-fluorouracil. Fluorouracil 78-92 thymidylate synthetase Homo sapiens 22-26 25227897-0 2015 Nuclear maspin expression as a predictive marker for fluorouracil treatment response in colon cancer. Fluorouracil 53-65 serpin family B member 5 Homo sapiens 8-14 31384313-6 2019 The effects of BAY1143572 and 5-FU on MCL-1 in vitro were analyzed by Western blotting, quantitative real-time polymerase chain reaction, and chromatin immunoprecipitation assay. Fluorouracil 30-34 MCL1 apoptosis regulator, BCL2 family member Homo sapiens 38-43 31384313-11 2019 5-FU enhanced BAY1143572-induced MCL-1 downregulation and stable MCL-1 overexpression reduced the apoptosis induced by BAY1143572 and 5-FU in vitro. Fluorouracil 0-4 MCL1 apoptosis regulator, BCL2 family member Homo sapiens 33-38 31384313-11 2019 5-FU enhanced BAY1143572-induced MCL-1 downregulation and stable MCL-1 overexpression reduced the apoptosis induced by BAY1143572 and 5-FU in vitro. Fluorouracil 134-138 MCL1 apoptosis regulator, BCL2 family member Homo sapiens 65-70 30841957-0 2019 PAR2 Inhibition Enhanced the Sensitivity of Colorectal Cancer Cells to 5-FU and Reduced EMT Signaling. Fluorouracil 71-75 coagulation factor II (thrombin) receptor-like 1 Mus musculus 0-4 30841957-1 2019 The aim of this study was to investigate the underlying mechanisms that transforming growth factor-beta (TGF-beta)-mediated epithelial-to-mesenchymal transition (EMT) in tumor cells contributes to 5-FU resistance. Fluorouracil 197-201 transforming growth factor alpha Mus musculus 105-113 30841957-4 2019 In this study, we found that protease-activated receptor 2 (PAR2) induction in 5-FU therapy is correlated with TGF-beta-mediated EMT and apoptosis resistance. Fluorouracil 79-83 coagulation factor II (thrombin) receptor-like 1 Mus musculus 29-58 30841957-4 2019 In this study, we found that protease-activated receptor 2 (PAR2) induction in 5-FU therapy is correlated with TGF-beta-mediated EMT and apoptosis resistance. Fluorouracil 79-83 coagulation factor II (thrombin) receptor-like 1 Mus musculus 60-64 30841957-4 2019 In this study, we found that protease-activated receptor 2 (PAR2) induction in 5-FU therapy is correlated with TGF-beta-mediated EMT and apoptosis resistance. Fluorouracil 79-83 transforming growth factor alpha Mus musculus 111-119 30841957-5 2019 PAR2 and TGF-beta were both activated in response to 5-FU treatment in vivo and in vitro, and whereas TGF-beta inhibition sensitized CRC cells to 5-FU and suppressed cell migration, PAR2 activation eliminated the effect of TGF-beta inhibition. Fluorouracil 53-57 coagulation factor II (thrombin) receptor-like 1 Mus musculus 0-4 30841957-5 2019 PAR2 and TGF-beta were both activated in response to 5-FU treatment in vivo and in vitro, and whereas TGF-beta inhibition sensitized CRC cells to 5-FU and suppressed cell migration, PAR2 activation eliminated the effect of TGF-beta inhibition. Fluorouracil 53-57 transforming growth factor alpha Mus musculus 9-17 30841957-6 2019 Conversely, siRNA-mediated PAR2 depletion or PAR2 inhibition with a specific inhibitor produced a similar phenotype as TGF-beta signal inhibition: 5-FU sensitization and cell migration suppression. Fluorouracil 147-151 coagulation factor II (thrombin) receptor-like 1 Mus musculus 27-31 30841957-6 2019 Conversely, siRNA-mediated PAR2 depletion or PAR2 inhibition with a specific inhibitor produced a similar phenotype as TGF-beta signal inhibition: 5-FU sensitization and cell migration suppression. Fluorouracil 147-151 coagulation factor II (thrombin) receptor-like 1 Mus musculus 45-49 30841957-6 2019 Conversely, siRNA-mediated PAR2 depletion or PAR2 inhibition with a specific inhibitor produced a similar phenotype as TGF-beta signal inhibition: 5-FU sensitization and cell migration suppression. Fluorouracil 147-151 transforming growth factor alpha Mus musculus 119-127 30841957-7 2019 Moreover, the results of xenograft experiments indicated that the PAR2 inhibitor can enhance cell killing by 5-FU in vivo and suppress EMT signaling. Fluorouracil 109-113 coagulation factor II (thrombin) receptor-like 1 Mus musculus 66-70 30841957-8 2019 Our results reveal that the TGF-beta effects require the coordinating action of PAR2, suggesting that PAR2 inhibition could be a new therapeutic strategy to combat 5-FU resistance in CRC. Fluorouracil 164-168 transforming growth factor alpha Mus musculus 28-36 30841957-8 2019 Our results reveal that the TGF-beta effects require the coordinating action of PAR2, suggesting that PAR2 inhibition could be a new therapeutic strategy to combat 5-FU resistance in CRC. Fluorouracil 164-168 coagulation factor II (thrombin) receptor-like 1 Mus musculus 80-84 30841957-8 2019 Our results reveal that the TGF-beta effects require the coordinating action of PAR2, suggesting that PAR2 inhibition could be a new therapeutic strategy to combat 5-FU resistance in CRC. Fluorouracil 164-168 coagulation factor II (thrombin) receptor-like 1 Mus musculus 102-106 30920880-3 2019 The patients in the paclitaxel plus fluorouracil group were treated with paclitaxel and fluorouracil one cycle per week in dCRT for five cycles followed by paclitaxel and fluorouracil one cycle per month in consolidation chemotherapy for two cycles. Fluorouracil 36-48 crt Drosophila melanogaster 123-127 30920880-4 2019 The patients in the cisplatin/5-fluorouracil group were treated with cisplatin and fluorouracil one cycle per month in dCRT for two cycles followed by two cycles in consolidation chemotherapy. Fluorouracil 30-44 crt Drosophila melanogaster 119-123 30920880-4 2019 The patients in the cisplatin/5-fluorouracil group were treated with cisplatin and fluorouracil one cycle per month in dCRT for two cycles followed by two cycles in consolidation chemotherapy. Fluorouracil 32-44 crt Drosophila melanogaster 119-123 31262877-1 2019 BACKGROUND/AIM: Recently, we demonstrated the ability of inhibitors of protein kinase 2 (casein kinase II; CK2) to enhance the efficacy of 5-fluorouracil, a thymidylate synthase (TYMS)-directed drug for anticancer treatment. Fluorouracil 139-153 thymidylate synthetase Homo sapiens 157-177 31262877-1 2019 BACKGROUND/AIM: Recently, we demonstrated the ability of inhibitors of protein kinase 2 (casein kinase II; CK2) to enhance the efficacy of 5-fluorouracil, a thymidylate synthase (TYMS)-directed drug for anticancer treatment. Fluorouracil 139-153 thymidylate synthetase Homo sapiens 179-183 31180555-11 2019 The present study demonstrated that kaempferol has a synergistic effect with 5-FU by inhibiting cell proliferation and inducing apoptosis in colorectal cancer cells via suppression of TS or attenuation of p-Akt activation. Fluorouracil 77-81 thymidylate synthetase Homo sapiens 184-186 31072625-0 2019 miR-145 Regulates the sensitivity of esophageal squamous cell carcinoma cells to 5-FU via targeting REV3L. Fluorouracil 81-85 microRNA 145 Homo sapiens 0-7 31072625-2 2019 However, the underlying role and molecular mechanism of miR-145 in the sensitivity of esophageal squamous cell carcinoma (ESCC) to 5-FU remained largely unknown. Fluorouracil 131-135 microRNA 145 Homo sapiens 56-63 31072625-11 2019 Overexpressed miR-145 significantly inhibited cell viability and elevated cell apoptosis rate upon 5-FU treatment. Fluorouracil 99-103 microRNA 145 Homo sapiens 14-21 31072625-12 2019 Additionally, transfection of miR-145 mimic further altered expression of key genes involved in cell apoptosis (Bcl-2, Bax, Caspase3) in ESCC cells treated with 5-FU. Fluorouracil 161-165 microRNA 145 Homo sapiens 30-37 31243264-6 2019 We found that the interaction between GRP78 and SPARC increased during exposure to 5-FU, CPT-11, and tunicamycin, resulting in an attenuation of GRP78"s inhibition of apoptosis. Fluorouracil 83-87 secreted protein acidic and cysteine rich Homo sapiens 48-53 25611552-3 2015 In this study, we investigated BAF57 expression in ovarian cancer cell lines and their sensitivities to cisplatin, doxorubicin, paclitaxel, and 5-fluorouracil. Fluorouracil 144-158 SWI/SNF related, matrix associated, actin dependent regulator of chromatin, subfamily e, member 1 Homo sapiens 31-36 31243264-8 2019 In line with these findings, a lower expression of GRP78 relative to SPARC in CRC is associated with a lower IC50 for 5-FU in either sensitive or therapy-refractory CRC cells. Fluorouracil 118-122 secreted protein acidic and cysteine rich Homo sapiens 69-74 31000196-0 2019 Ribavirin sensitizes nasopharyngeal carcinoma to 5-fluorouracil through suppressing 5-fluorouracil-induced ERK-dependent-eIF4E activation. Fluorouracil 49-63 eukaryotic translation initiation factor 4E Mus musculus 121-126 31000196-0 2019 Ribavirin sensitizes nasopharyngeal carcinoma to 5-fluorouracil through suppressing 5-fluorouracil-induced ERK-dependent-eIF4E activation. Fluorouracil 84-98 eukaryotic translation initiation factor 4E Mus musculus 121-126 31000196-2 2019 In this work, we demonstrate that eIF4E inhibition using both ribavirin and siRNA targets NPC cells and enhances the efficacy of 5-fluorouracil (5-FU). Fluorouracil 129-143 eukaryotic translation initiation factor 4E Mus musculus 34-39 31000196-2 2019 In this work, we demonstrate that eIF4E inhibition using both ribavirin and siRNA targets NPC cells and enhances the efficacy of 5-fluorouracil (5-FU). Fluorouracil 145-149 eukaryotic translation initiation factor 4E Mus musculus 34-39 31000196-3 2019 Mechanism studies indicate that 5-FU treatment increases phosphorylation of eIF4E in NPC cells, and this is dependent on ERK activation. Fluorouracil 32-36 eukaryotic translation initiation factor 4E Mus musculus 76-81 25611552-4 2015 BAF57 expression was strongly correlated with sensitivities to cisplatin, doxorubicin, and 5-fluorouracil in 10 ovarian cancer cell lines. Fluorouracil 91-105 SWI/SNF related, matrix associated, actin dependent regulator of chromatin, subfamily e, member 1 Homo sapiens 0-5 25683168-8 2015 LoVo and SW480 cells with upregulated PTEN were sensitive to apoptosis induced by 5-FU. Fluorouracil 82-86 phosphatase and tensin homolog Homo sapiens 38-42 25836926-3 2015 MSI-H is highly correlated with loss of MMR protein expression, is commonly diploid, is often located in the right side of the colon, prognosticates good patient outcome, and predicts poor efficacy with 5-fluorouracil treatment. Fluorouracil 203-217 RB binding protein 4, chromatin remodeling factor Homo sapiens 0-3 31360112-0 2019 TLX3 repressed SNAI1-induced epithelial-mesenchymal transition by directly constraining STAT3 phosphorylation and functionally sensitized 5-FU chemotherapy in hepatocellular carcinoma. Fluorouracil 138-142 T cell leukemia, homeobox 3 Mus musculus 0-4 31360112-6 2019 TLX3 over-expression inhibited HCC cell viability, proliferation, migration, invasion and enhanced 5-FU treatment, whereas silencing TLX3 produced the opposite results. Fluorouracil 99-103 T cell leukemia, homeobox 3 Mus musculus 0-4 31360112-8 2019 In vivo experiments showed that knockdown of TLX3 promoted the growth of HCC xenografts and attenuated the anti-tumor effects of 5-FU treatment. Fluorouracil 129-133 T cell leukemia, homeobox 3 Mus musculus 45-49 31360112-11 2019 Taken together, loss of expression of TLX3 induces EMT by enhancing IL-6/STAT3/SNAI1 signaling, and accelerates HCC progression while also attenuated the effect of 5-FU on HCCs. Fluorouracil 164-168 T cell leukemia, homeobox 3 Mus musculus 38-42 30823845-0 2019 Thymidylate synthase gene polymorphism predicts disease free survival in stage II-III rectal adenocarcinoma patients receiving adjuvant 5-FU-based chemotherapy. Fluorouracil 136-140 thymidylate synthetase Homo sapiens 0-20 30823845-1 2019 BACKGROUND: The objective is to investigate whether thymidylate synthase gene TS 5"-UTR polymorphism of peripheral blood mononuclear cells are associated with clinical outcomes of patients with stage II-III rectal adenocarcinoma treated with adjuvant 5-fluorouracil (5-FU) chemotherapy in Chinese population. Fluorouracil 251-265 thymidylate synthetase Homo sapiens 52-72 30823845-1 2019 BACKGROUND: The objective is to investigate whether thymidylate synthase gene TS 5"-UTR polymorphism of peripheral blood mononuclear cells are associated with clinical outcomes of patients with stage II-III rectal adenocarcinoma treated with adjuvant 5-fluorouracil (5-FU) chemotherapy in Chinese population. Fluorouracil 267-271 thymidylate synthetase Homo sapiens 52-72 25747889-17 2015 Compared to NS group, mRNA and proteins expression of Foxp3 and TIM-3 down regulated in BLTA and 5-FU group (P<0.01). Fluorouracil 97-101 forkhead box P3 Mus musculus 54-59 25385370-0 2015 Annexin A2 knockdown inhibits hepatoma cell growth and sensitizes hepatoma cells to 5-fluorouracil by regulating beta-catenin and cyclin D1 expression. Fluorouracil 84-98 annexin A2 Homo sapiens 0-10 31151160-10 2019 Finally, using a specific HIF-2alpha inhibitor alone or in combination with drugs in patient-derived primary colon cancer cells, overcame their resistance to 5-FU or CCI-779, thus emphasizing the crucial role played by HIF-2alpha in promoting resistance and cell survival. Fluorouracil 158-162 endothelial PAS domain protein 1 Homo sapiens 26-36 25385370-5 2015 We also investigated the role of ANXA2 in chemotherapeutic treatment with 5-FU. Fluorouracil 74-78 annexin A2 Homo sapiens 33-38 31139014-0 2019 Low expression of SPARC in gastric cancer-associated fibroblasts leads to stemness transformation and 5-fluorouracil resistance in gastric cancer. Fluorouracil 102-116 secreted protein acidic and cysteine rich Homo sapiens 18-23 25385370-6 2015 5-FU inhibited hepatoma cell growth, while ANXA2 overexpression reduced, and knockdown enhanced, the effects of 5-FU on hepatoma cell growth. Fluorouracil 112-116 annexin A2 Homo sapiens 43-48 31139014-1 2019 Background: The aim of the present study was to clarify the correlations between SPARC expression in gastric cancer-associated fibroblasts (GCAFs) and the prognosis of patients with gastric cancer and to elucidate the role of GCAF-derived SPARC in stemness transformation and 5-fluorouracil resistance in gastric cancer. Fluorouracil 276-290 secreted protein acidic and cysteine rich Homo sapiens 81-86 31139014-13 2019 Low expression of GCAF-derived SPARC can lead to CSC transformation and 5-FU resistance. Fluorouracil 72-76 secreted protein acidic and cysteine rich Homo sapiens 31-36 25385370-8 2015 Taken together, our data suggest that the ANXA2 protein is a critical factor in HCC and that its downregulation can enhance chemotherapeutic treatment with 5-FU. Fluorouracil 156-160 annexin A2 Homo sapiens 42-47 25767396-2 2015 In this study, known antimetabolite drugs such as gemcitabine (ribonucleotide reductase inhibitor) and 5-fluorouracil (thymidylate synthase inhibitor) were compared with novel members of these two drug families in the treatment of a chemoresistant pancreatic cancer cell line PANC-1. Fluorouracil 103-117 thymidylate synthetase Homo sapiens 119-139 30590435-0 2019 Melatonin-mediated downregulation of thymidylate synthase as a novel mechanism for overcoming 5-fluorouracil associated chemoresistance in colorectal cancer cells. Fluorouracil 94-108 thymidylate synthetase Homo sapiens 37-57 30590435-12 2019 CONCLUSIONS: Melatonin facilitates overcoming 5-FU resistance through downregulation of TYMS. Fluorouracil 46-50 thymidylate synthetase Homo sapiens 88-92 30590435-13 2019 Melatonin may serve as a potential therapeutic option on its own, or in conjunction with 5-FU, in the treatment of patients with advanced or chemoresistant CRC.Melatonin inhibits the growth of 5-FU resistant colorectal cancer (CRC) cells through upregulation of miR-215-5p and a concomitant downregulation of TYMS. Fluorouracil 193-197 thymidylate synthetase Homo sapiens 309-313 30938104-0 2019 Long non-coding RNA PCAT6 targets miR-204 to modulate the chemoresistance of colorectal cancer cells to 5-fluorouracil-based treatment through HMGA2 signaling. Fluorouracil 104-118 microRNA 204 Homo sapiens 34-41 30938104-0 2019 Long non-coding RNA PCAT6 targets miR-204 to modulate the chemoresistance of colorectal cancer cells to 5-fluorouracil-based treatment through HMGA2 signaling. Fluorouracil 104-118 high mobility group AT-hook 2 Homo sapiens 143-148 30938104-2 2019 In our previous study, we revealed that miR-204 overexpression could sensitize CRC cell to 5-FU treatment through targeting HMGA2/PI3K signaling pathway; however, miR-204 expression in CRC tissues is abnormally downregulated. Fluorouracil 91-95 microRNA 204 Homo sapiens 40-47 30938104-2 2019 In our previous study, we revealed that miR-204 overexpression could sensitize CRC cell to 5-FU treatment through targeting HMGA2/PI3K signaling pathway; however, miR-204 expression in CRC tissues is abnormally downregulated. Fluorouracil 91-95 high mobility group AT-hook 2 Homo sapiens 124-129 30938104-2 2019 In our previous study, we revealed that miR-204 overexpression could sensitize CRC cell to 5-FU treatment through targeting HMGA2/PI3K signaling pathway; however, miR-204 expression in CRC tissues is abnormally downregulated. Fluorouracil 91-95 microRNA 204 Homo sapiens 163-170 30938104-7 2019 Furthermore, we revealed that PCAT6 knockdown attenuated CRC chemoresistance to 5-FU through miR-204/HMGA2/PI3K; miR-204 inhibition could partially reverse the effect of PCAT6 knockdown. Fluorouracil 80-84 microRNA 204 Homo sapiens 93-100 30938104-7 2019 Furthermore, we revealed that PCAT6 knockdown attenuated CRC chemoresistance to 5-FU through miR-204/HMGA2/PI3K; miR-204 inhibition could partially reverse the effect of PCAT6 knockdown. Fluorouracil 80-84 high mobility group AT-hook 2 Homo sapiens 101-106 30938104-7 2019 Furthermore, we revealed that PCAT6 knockdown attenuated CRC chemoresistance to 5-FU through miR-204/HMGA2/PI3K; miR-204 inhibition could partially reverse the effect of PCAT6 knockdown. Fluorouracil 80-84 microRNA 204 Homo sapiens 113-120 31007741-2 2019 The present study aimed to assess the association between pituitary homeobox paired homeodomain transcription 1 (PITX1) expression and the sensitivity of GC cells to the chemotherapeutic drugs 5-fluorouracil (5-FU) and cisplatin (CDDP). Fluorouracil 193-207 paired like homeodomain 1 Homo sapiens 113-118 31007741-2 2019 The present study aimed to assess the association between pituitary homeobox paired homeodomain transcription 1 (PITX1) expression and the sensitivity of GC cells to the chemotherapeutic drugs 5-fluorouracil (5-FU) and cisplatin (CDDP). Fluorouracil 209-213 paired like homeodomain 1 Homo sapiens 113-118 31007741-7 2019 A Cell Counting kit-8 assay was performed to determine the impact of PITX1 expression on the sensitivity of GC cells to 5-FU and CDDP. Fluorouracil 120-124 paired like homeodomain 1 Homo sapiens 69-74 31007741-8 2019 The Cancer Genome Atlas database was used to analyze the expression of PITX1 with GC prognosis in the Asian population and to assess the potential mechanism of PITX1 in 5-FU and CDDP resistance. Fluorouracil 169-173 paired like homeodomain 1 Homo sapiens 160-165 31007741-14 2019 The expression of PITX1 affected the sensitivity of GC cells to 5-FU/CDDP, indicating that PITX1 may increase the efficacy of treatment in GC patients. Fluorouracil 64-68 paired like homeodomain 1 Homo sapiens 18-23 31007741-14 2019 The expression of PITX1 affected the sensitivity of GC cells to 5-FU/CDDP, indicating that PITX1 may increase the efficacy of treatment in GC patients. Fluorouracil 64-68 paired like homeodomain 1 Homo sapiens 91-96 30276573-1 2019 BACKGROUND: 5FU can be converted to its active metabolite fluoro-deoxyuridine monophosphate (FdUMP) through two pathways: the orotate phosphoribosyl transferase-ribonucleotide reductase (OPRT-RR) pathway and the thymidine phosphorylase-thymidine kinase (TP-TK) pathway. Fluorouracil 12-15 uridine monophosphate synthetase Homo sapiens 187-191 31023384-7 2019 The cytotoxicity of T cells induced by CD3-HAC towards PD-L1-positive cells was detected in vitro and in vivo in combination with 5-FU. Fluorouracil 130-134 CD274 molecule Homo sapiens 55-60 31097925-0 2019 Coelomic Fluid of Lumbricus rubellus Synergistically Enhances Cytotoxic Effect of 5-Fluorouracil through Modulation of Focal Adhesion Kinase and p21 in HT-29 Cancer Cell Line. Fluorouracil 82-96 H3 histone pseudogene 16 Homo sapiens 145-148 31097925-3 2019 This study aims to investigate whether the combination of CFL and 5-fluorouracil could reduce FAK protein level and iCa2+ and enhance p21 level. Fluorouracil 66-80 H3 histone pseudogene 16 Homo sapiens 134-137 31097925-9 2019 Combination of CFL and 5-fluorouracil significantly decreased FAK expression (p<0.05), iCa2+ (p<0.05), and increased p21 expression (p<0.05) in HT-29 cells. Fluorouracil 23-37 H3 histone pseudogene 16 Homo sapiens 123-126 31353575-6 2019 Furthermore, we demonstrated that MIX enhances antiproliferative effect of common cytostatics: 5-fluorouracil and cisplatin. Fluorouracil 95-109 Mix paired-like homeobox Homo sapiens 34-37 31353575-12 2019 Furthermore, activity of the substances combined as MIX to influence antiproliferative potential of commonly used in colon cancer treatment cytostatics, 5-fluorouracil, and cisplatin was verified. Fluorouracil 153-167 Mix paired-like homeobox Homo sapiens 52-55 25581782-5 2015 Not surprisingly, several human cancers overexpress TSase, which makes it a common target for chemotherapy (e.g., 5-fluorouracil). Fluorouracil 114-128 thymidylate synthetase Homo sapiens 52-57 25802497-3 2015 Gastrointestinal toxicity has been previously reported in the setting of 5-fluorouracil (5-FU)-based chemotherapy with abnormal thymidylate synthase or dihydropyrimidine dehydrogenase activities. Fluorouracil 73-87 thymidylate synthetase Homo sapiens 128-148 30971955-0 2019 Gliclazide Prevents 5-FU-Induced Oral Mucositis by Reducing Oxidative Stress, Inflammation, and P-Selectin Adhesion Molecules. Fluorouracil 20-24 selectin P Homo sapiens 96-106 30915129-6 2019 Hsp27 also sensitized HT-29 and LoVo to 5-FU by enhancing cell apoptosis. Fluorouracil 40-44 heat shock protein family B (small) member 1 Homo sapiens 0-5 30915129-7 2019 Overexpression of Hsp27 could block miR-214 with an effect on the sensitivity of colon cancer cells to 5-FU. Fluorouracil 103-107 heat shock protein family B (small) member 1 Homo sapiens 18-23 30915129-8 2019 In conclusion, miR-214 sensitizes colon cancer cells to 5-FU by targeting Hsp27, indicating a significant role for this miRNA in colon cancer chemotherapy. Fluorouracil 56-60 heat shock protein family B (small) member 1 Homo sapiens 74-79 30783438-13 2019 These results indicate that downregulation of miR-183 can inhibit the growth of PC cells in vitro and in vivo, and increase cell sensitivity to 5-fluorouracil and gemcitabine through regulating the PTEN/PI3K/Akt signaling pathway. Fluorouracil 144-158 phosphatase and tensin homolog Homo sapiens 198-202 25802497-3 2015 Gastrointestinal toxicity has been previously reported in the setting of 5-fluorouracil (5-FU)-based chemotherapy with abnormal thymidylate synthase or dihydropyrimidine dehydrogenase activities. Fluorouracil 89-93 thymidylate synthetase Homo sapiens 128-148 25432336-4 2015 Interestingly, cell viability studies showed pronounced sensitivity of GMCSF overexpressing MCF-7 cells towards anticancer drugs, such as, doxorubicin, 5FU and cisplatin. Fluorouracil 152-155 colony stimulating factor 2 Homo sapiens 71-76 30873379-4 2019 Furthermore, knockout of uPAR decreases resistance to 5-FU, cisplatin, docetaxel, and doxorubicin in these cells. Fluorouracil 54-58 plasminogen activator, urokinase receptor Homo sapiens 25-29 30728402-0 2019 FOXM1 modulates 5-FU resistance in colorectal cancer through regulating TYMS expression. Fluorouracil 16-20 thymidylate synthetase Homo sapiens 72-76 30728402-1 2019 Resistance to 5-Fluoruracil (5-FU) has been linked to elevated expression of the main target, thymidylate synthase (TYMS), which catalyses the de novo pathway for production of deoxythymidine monophosphate. Fluorouracil 14-27 thymidylate synthetase Homo sapiens 94-114 30728402-1 2019 Resistance to 5-Fluoruracil (5-FU) has been linked to elevated expression of the main target, thymidylate synthase (TYMS), which catalyses the de novo pathway for production of deoxythymidine monophosphate. Fluorouracil 14-27 thymidylate synthetase Homo sapiens 116-120 30728402-1 2019 Resistance to 5-Fluoruracil (5-FU) has been linked to elevated expression of the main target, thymidylate synthase (TYMS), which catalyses the de novo pathway for production of deoxythymidine monophosphate. Fluorouracil 29-33 thymidylate synthetase Homo sapiens 94-114 30728402-1 2019 Resistance to 5-Fluoruracil (5-FU) has been linked to elevated expression of the main target, thymidylate synthase (TYMS), which catalyses the de novo pathway for production of deoxythymidine monophosphate. Fluorouracil 29-33 thymidylate synthetase Homo sapiens 116-120 30728402-5 2019 ChIP and global ChIP-seq data also confirms that FOXM1 can also potentially regulate other 5-FU targets, such as TYMS, thymidine kinase 1 (TK-1) and thymidine phosphorylase (TYMP). Fluorouracil 91-95 thymidylate synthetase Homo sapiens 113-117 30728402-10 2019 In summary, this research demonstrated that FOXM1 plays a pivotal role in 5-FU resistance at least partially through the regulation of TYMS. Fluorouracil 74-78 thymidylate synthetase Homo sapiens 135-139 30607648-7 2019 Altogether, these results indicated that DLEC1 protects cells against cell death induced by 5-FU through the attenuation of active proteins in caspase cascade and the up-regulation of BCL-XL. Fluorouracil 92-96 caspase 9 Homo sapiens 143-150 30538221-8 2018 Consistently, ChIP analysis revealed that FOXM1 binds efficiently to the TYMS promoter and modulates TYMS expression at the promoter level upon 5-FU treatment in KKU-D131 but not in HuCCA cells. Fluorouracil 144-148 thymidylate synthetase Homo sapiens 101-105 30538221-10 2018 In conclusion, our data show that FOXM1 regulates TYMS expression to modulate 5-FU resistance in CCA and that severe 5-FU resistance can be caused by the uncoupling of the regulation of TYMS by FOXM1. Fluorouracil 78-82 thymidylate synthetase Homo sapiens 50-54 30538221-10 2018 In conclusion, our data show that FOXM1 regulates TYMS expression to modulate 5-FU resistance in CCA and that severe 5-FU resistance can be caused by the uncoupling of the regulation of TYMS by FOXM1. Fluorouracil 117-121 thymidylate synthetase Homo sapiens 186-190 25444895-6 2015 Furthermore, OVA12 inhibited 5-FU-induced apoptosis through specific upregulation of Mcl-1 and survivin. Fluorouracil 29-33 MCL1 apoptosis regulator, BCL2 family member Homo sapiens 85-90 30155836-5 2018 Functionally, RARalpha knockdown suppressed the proliferation and metastasis of EC cells through downregulating the expression of PCNA, Ki67, MMP7, and MMP9, as well as enhanced drug susceptibility of EC cells to 5-fluorouracil and cisplatin. Fluorouracil 213-227 retinoic acid receptor alpha Homo sapiens 14-22 25788051-6 2015 Moreover, 41.58% of ES-2 and 20.86% of PLC/PRF/5 cell apoptosis was caused by the combination of the two, while 5-FU caused apoptosis of 20.86% of ES-2 cells and 8.85% of PLC/PRF/5 cells. Fluorouracil 112-116 heparan sulfate proteoglycan 2 Homo sapiens 171-174 30255549-0 2018 Increase of PRPP enhances chemosensitivity of PRPS1 mutant acute lymphoblastic leukemia cells to 5-Fluorouracil. Fluorouracil 97-111 phosphoribosyl pyrophosphate synthetase 1 Homo sapiens 46-51 30255549-3 2018 In this study, we found that PRPS1 mutant ALL cells specifically showed more chemosensitivity to 5-Fluorouracil (5-FU) than control cells, attributed to increased apoptosis of PRPS1 mutant cells by 5-FU. Fluorouracil 97-111 phosphoribosyl pyrophosphate synthetase 1 Homo sapiens 29-34 30255549-3 2018 In this study, we found that PRPS1 mutant ALL cells specifically showed more chemosensitivity to 5-Fluorouracil (5-FU) than control cells, attributed to increased apoptosis of PRPS1 mutant cells by 5-FU. Fluorouracil 97-111 phosphoribosyl pyrophosphate synthetase 1 Homo sapiens 176-181 30255549-3 2018 In this study, we found that PRPS1 mutant ALL cells specifically showed more chemosensitivity to 5-Fluorouracil (5-FU) than control cells, attributed to increased apoptosis of PRPS1 mutant cells by 5-FU. Fluorouracil 113-117 phosphoribosyl pyrophosphate synthetase 1 Homo sapiens 29-34 25482885-0 2015 miR-203 enhances chemosensitivity to 5-fluorouracil by targeting thymidylate synthase in colorectal cancer. Fluorouracil 37-51 thymidylate synthetase Homo sapiens 65-85 30255549-3 2018 In this study, we found that PRPS1 mutant ALL cells specifically showed more chemosensitivity to 5-Fluorouracil (5-FU) than control cells, attributed to increased apoptosis of PRPS1 mutant cells by 5-FU. Fluorouracil 113-117 phosphoribosyl pyrophosphate synthetase 1 Homo sapiens 176-181 30255549-3 2018 In this study, we found that PRPS1 mutant ALL cells specifically showed more chemosensitivity to 5-Fluorouracil (5-FU) than control cells, attributed to increased apoptosis of PRPS1 mutant cells by 5-FU. Fluorouracil 198-202 phosphoribosyl pyrophosphate synthetase 1 Homo sapiens 29-34 30255549-3 2018 In this study, we found that PRPS1 mutant ALL cells specifically showed more chemosensitivity to 5-Fluorouracil (5-FU) than control cells, attributed to increased apoptosis of PRPS1 mutant cells by 5-FU. Fluorouracil 198-202 phosphoribosyl pyrophosphate synthetase 1 Homo sapiens 176-181 25482885-6 2015 Silencing of TYMS enhanced 5-FU chemosensitivity, similar to the roles of miR-203. Fluorouracil 27-31 thymidylate synthetase Homo sapiens 13-17 30255549-4 2018 Mechanistically, PRPS1 mutants increase the level of intracellular phosphoribosyl pyrophosphate (PRPP), which causes the apt conversion of 5-FU to FUMP and FUTP in Reh cells, to promote 5-FU-induced DNA damage and apoptosis. Fluorouracil 139-143 phosphoribosyl pyrophosphate synthetase 1 Homo sapiens 17-22 25482885-8 2015 Overall, our data indicate that miR-203 enhances 5-FU chemosensitivity via the downregulation of TYMS in colorectal cancer and provide important insight into the mechanism of 5-FU resistance in colorectal cancer patients. Fluorouracil 49-53 thymidylate synthetase Homo sapiens 97-101 30255549-4 2018 Mechanistically, PRPS1 mutants increase the level of intracellular phosphoribosyl pyrophosphate (PRPP), which causes the apt conversion of 5-FU to FUMP and FUTP in Reh cells, to promote 5-FU-induced DNA damage and apoptosis. Fluorouracil 186-190 phosphoribosyl pyrophosphate synthetase 1 Homo sapiens 17-22 30255549-5 2018 Our study not only provides mechanistic rationale for re-targeting drug resistant cells in ALL, but also implicates that ALL patients who harbor relapse-specific mutations of PRPS1 might benefit from 5-FU-based chemotherapy in clinical settings. Fluorouracil 200-204 phosphoribosyl pyrophosphate synthetase 1 Homo sapiens 175-180 25482885-8 2015 Overall, our data indicate that miR-203 enhances 5-FU chemosensitivity via the downregulation of TYMS in colorectal cancer and provide important insight into the mechanism of 5-FU resistance in colorectal cancer patients. Fluorouracil 175-179 thymidylate synthetase Homo sapiens 97-101 25329760-7 2015 Hematopoietic stress, induced by 5-fluorouracil ablation, revealed that in this circumstance c-Myb-expressing cells become critical for multilineage repopulation. Fluorouracil 33-47 myeloblastosis oncogene Mus musculus 93-98 30538567-13 2018 In addition, we found that a KIF20A inhibitor, genistein, could enhance the antitumor activity of cisplatin and fluorouracil, which might be considered as a chemosensitive agent in GC. Fluorouracil 112-124 kinesin family member 20A Homo sapiens 29-35 30451890-7 2018 Further, corresponding to CD44v6 knockdown cells, 5FU+ Silibinin treatment significantly decreased CD44v6, Nanog, CTNNB1 and CDKN2A expression whereas increased E-cadherin expression in HCT116 derived CD44+ cells. Fluorouracil 50-53 catenin beta 1 Homo sapiens 114-120 24999837-0 2015 Exogenous IL-1Ra attenuates intestinal mucositis induced by oxaliplatin and 5-fluorouracil through suppression of p53-dependent apoptosis. Fluorouracil 76-90 transformation related protein 53, pseudogene Mus musculus 114-117 30396933-0 2018 Inhibiting xCT Improves 5-Fluorouracil Resistance of Gastric Cancer Induced by CD44 Variant 9 Expression. Fluorouracil 24-38 solute carrier family 7 member 11 Homo sapiens 11-14 24999837-4 2015 Our previous studies showed the protective effect of recombinant human interleukin-1 receptor antagonist (rhIL-1Ra) on the intestine in mice after 5-fluorouracil chemotherapy. Fluorouracil 147-161 interleukin 1 receptor antagonist Homo sapiens 71-104 26700594-0 2015 Orotate phosphoribosyltransferase localizes to the Golgi complex and its expression levels affect the sensitivity to anti-cancer drug 5-fluorouracil. Fluorouracil 134-148 uridine monophosphate synthetase Homo sapiens 0-33 30344717-9 2018 Furthermore, it was revealed that PARP-3 overexpression was associated with shorter survival time in patients with cyclophosphamide/doxorubicin or epirubicin/5-fluorouracil (CAF/CEF) chemotherapy compared with low PARP-3 expression, but not in patients with CAF/CEF + docetaxel chemotherapy. Fluorouracil 158-172 poly(ADP-ribose) polymerase family member 3 Homo sapiens 34-40 30340556-10 2018 Increased expression of osteopontin (p = 0.019) and low density of CD8-positive T-cells (p = 0.043) were significantly associated with unfavourable response to 5-FU. Fluorouracil 160-164 secreted phosphoprotein 1 Homo sapiens 24-35 30258365-6 2018 Meanwhile, CD13-targeting siRNA and neutralizing antibody can enhance the cytotoxic effect of 5-fluorouracil (5FU). Fluorouracil 94-108 alanyl (membrane) aminopeptidase Mus musculus 11-15 30258365-6 2018 Meanwhile, CD13-targeting siRNA and neutralizing antibody can enhance the cytotoxic effect of 5-fluorouracil (5FU). Fluorouracil 110-113 alanyl (membrane) aminopeptidase Mus musculus 11-15 26700594-4 2015 Furthermore, chemotherapeutic drug 5-fluorouracil (5-FU) is taken up into cancer cells and is converted to 5-fluoro-UMP (FUMP) by OPRT or to 5-fluoro-dUMP (FdUMP) through intermediary molecules by thymidine phosphorylase. Fluorouracil 35-49 uridine monophosphate synthetase Homo sapiens 130-134 30042169-9 2018 Notably, overexpression of miR-629-5p also conferred 5-fluorouracil sensitivity, which was partly abrogated by coexpression of CXXC4. Fluorouracil 53-67 CXXC finger protein 4 Homo sapiens 127-132 30042169-10 2018 Overall, the results presented here suggest that miR-629-5p functions as a tumor promoter by improving proliferation and migration and repressing apoptosis and 5-FU sensitivity in colorectal cancer progression by directly down-regulating CXXC4. Fluorouracil 160-164 CXXC finger protein 4 Homo sapiens 238-243 26700594-4 2015 Furthermore, chemotherapeutic drug 5-fluorouracil (5-FU) is taken up into cancer cells and is converted to 5-fluoro-UMP (FUMP) by OPRT or to 5-fluoro-dUMP (FdUMP) through intermediary molecules by thymidine phosphorylase. Fluorouracil 51-55 uridine monophosphate synthetase Homo sapiens 130-134 30096914-11 2018 Administration with both AA and 5-FU in prevention and throughout was able to prevent decreases in Notch1 SOX2, nestin, DCX, and Nrf2 caused by 5-FU. Fluorouracil 144-148 notch receptor 1 Rattus norvegicus 99-105 26700594-6 2015 However, it remains unclear how the subcellular localization of OPRT and how its variable expression levels affect the response to 5-FU at the cellular level. Fluorouracil 131-135 uridine monophosphate synthetase Homo sapiens 64-68 30096914-11 2018 Administration with both AA and 5-FU in prevention and throughout was able to prevent decreases in Notch1 SOX2, nestin, DCX, and Nrf2 caused by 5-FU. Fluorouracil 144-148 SRY-box transcription factor 2 Rattus norvegicus 106-110 26700594-8 2015 Results also show that not only overexpression but also downregulation of OPRT render cells susceptible to 5-FU exposure, but it has no effect on DNA damaging agent doxorubicin. Fluorouracil 107-111 uridine monophosphate synthetase Homo sapiens 74-78 26700594-9 2015 This study provides clues to elucidate the cellular response to 5-FU chemotherapy in relation to the OPRT expression level. Fluorouracil 64-68 uridine monophosphate synthetase Homo sapiens 101-105 25524944-9 2015 Based on TS-targeted drug use status, TS expression was significantly associated with OS in pemetrexed (HR=0.42) and 5-Fluorouracil subgroups (HR=0.34), but not in no TS-targeted drug subgroup. Fluorouracil 117-131 thymidylate synthetase Homo sapiens 38-40 30014319-0 2018 Evaluation of Antiproliferative Activity, Safety and Biodistribution of Oxaliplatin and 5-Fluorouracil Loaded Lactoferrin Nanoparticles for the Management of Colon Adenocarcinoma: an In Vitro and an In Vivo Study. Fluorouracil 88-102 lactotransferrin Rattus norvegicus 110-121 30014319-3 2018 The present study is based on evaluation of anti-proliferative potential, pharmacokinetics parameters, safety profile, biodistribution and efficacy of 5-FU/oxaliplatin loaded lactoferrin nanoparticles in cell lines and wistar rats in order to overcome the above limitation. Fluorouracil 151-155 lactotransferrin Rattus norvegicus 175-186 30014319-8 2018 Lactoferrin nanoparticles also improve the pharmacokinetics profile, safety parameters and efficacy of 5-FU and Oxaliplatin. Fluorouracil 103-107 lactotransferrin Rattus norvegicus 0-11 30014319-9 2018 CONCLUSION: Lactoferrin nanoparticles demonstrated an attractive drug delivery module to manage the colon adenocarcinoma as it has improved the antiproliferative activity of 5-FU and Oxaliplatin against colon adenocarcinoma cells. Fluorouracil 174-178 lactotransferrin Rattus norvegicus 12-23 25348515-9 2015 CBL knockdown increased PDAC resistance to gemcitabine and 5-fluorouracil (5-FU) by upregulating pEGFR (Y1068), pERK, and pAKT. Fluorouracil 59-73 Cbl proto-oncogene Homo sapiens 0-3 25348515-9 2015 CBL knockdown increased PDAC resistance to gemcitabine and 5-fluorouracil (5-FU) by upregulating pEGFR (Y1068), pERK, and pAKT. Fluorouracil 75-79 Cbl proto-oncogene Homo sapiens 0-3 25348515-9 2015 CBL knockdown increased PDAC resistance to gemcitabine and 5-fluorouracil (5-FU) by upregulating pEGFR (Y1068), pERK, and pAKT. Fluorouracil 75-79 eukaryotic translation initiation factor 2 alpha kinase 3 Homo sapiens 112-116 26557771-4 2015 Reg IV treatment inhibits 5-fluorouracil induced apoptosis, at least two mechanisms are involved in inhibition of apoptosis by Reg IV, including Bcl-2 and dihydropyrimidine dehydrogenase (DPD). Fluorouracil 26-40 regenerating family member 4 Homo sapiens 0-6 25755712-8 2015 Treatment of BA-responsive RMS-13 cells with 5-FU and BA combination resulted in inhibition of GLI1, GLI2, PTCH1, and IGF2 genes. Fluorouracil 45-49 insulin like growth factor 2 Homo sapiens 118-122 25310623-5 2015 5-FU treatment induced DNA damage and activation of ataxia telangiectasia mutated (ATM) and Chk1, leading to S-phase arrest, and Chk1 inhibition using SB218078 reduced S-phase arrest and increased apoptosis in the presence of 5-FU. Fluorouracil 226-230 ATM serine/threonine kinase Homo sapiens 52-81 25310623-5 2015 5-FU treatment induced DNA damage and activation of ataxia telangiectasia mutated (ATM) and Chk1, leading to S-phase arrest, and Chk1 inhibition using SB218078 reduced S-phase arrest and increased apoptosis in the presence of 5-FU. Fluorouracil 226-230 ATM serine/threonine kinase Homo sapiens 83-86 25333998-9 2015 Moreover, 5-FU partly recovered Hsp90 client proteins, including Akt, p-Akt, inhibitor of kappaB kinase (IKK)alpha, extracellular signal-regulated kinase (ERK)1/2, and glycogen synthase kinase (GSK)-3beta, which SNX-2112 had downregulated. Fluorouracil 10-14 heat shock protein 90 alpha family class A member 1 Homo sapiens 32-37 25317679-4 2015 Compartments of the bone marrow progenitor cells for granulocytes/macrophages and erythrocytes were enhanced in the control, as well as in the 5-FU-administered A(3)AR KO mice. Fluorouracil 143-147 cytochrome P450, family 19, subfamily a, polypeptide 1 Mus musculus 165-170 25317679-5 2015 5-FU-induced hematopoietic suppression, evaluated on day 2 after the administration of the cytotoxic drug, was found to be significantly deeper in the A(3)AR KO mice compared with their WT counterparts, as measured at the level of the bone marrow progenitor cells. Fluorouracil 0-4 cytochrome P450, family 19, subfamily a, polypeptide 1 Mus musculus 155-160 25317679-7 2015 The increased depth of 5-FU-induced suppression in the compartments of the hematopoietic progenitor cells in the A(3)AR KO mice represents probably a hitherto undescribed further consequence of the lack of adenosine A(3) receptors and indicates its synergism with the pharmacologically induced cytotoxic action of 5-FU. Fluorouracil 23-27 cytochrome P450, family 19, subfamily a, polypeptide 1 Mus musculus 117-122 25460919-6 2014 5-FU increased the expression of APC and decreased the expression of FEN1 in HCT-116 and HT-29 cells, which were sensitized to 5-FU when compared to LOVO cells. Fluorouracil 0-4 flap structure-specific endonuclease 1 Homo sapiens 69-73 29582366-5 2018 Ginsenoside Rh2 could enhance the cytotoxicity of 5-FU in drug-resistant CRC cells (LoVo/5-FU and HCT-8/5-FU). Fluorouracil 50-54 Rh associated glycoprotein Homo sapiens 12-15 29902974-10 2018 Subsequently the molecular inhibition of specific isoforms of ALDH by ALDH1A1 or ALDH1A3 siRNA led to sensitizing of cell lines HT-29/eGFP, HCT-116/eGFP to capecitabine and 5-FU. Fluorouracil 173-177 aldehyde dehydrogenase 1 family member A1 Homo sapiens 62-66 29859044-8 2018 Moreover, Slit3-repression induced chemoresistance to sorafenib, oxaliplatin and 5-FU through impairment of beta-catenin degradation and induction of cyclin D3 and survivin levels. Fluorouracil 81-85 catenin beta 1 Homo sapiens 108-120 29463559-8 2018 Prior treatment of a responder PDX with 5-FU increased expression of thymidylate synthase and decreased efficacy of capecitabine. Fluorouracil 40-44 thymidylate synthetase Homo sapiens 69-89 29693171-4 2018 To determine the association between PVT1 expression and 5-fluorouracil (5-FU) resistance in CRC, the expression levels of PVT1 mRNA in 5-FU-resistant CRC tissues and cell lines (HCT-8/5-FU and HCT-116/5-FU) were assessed by a reverse transcription-quantitative polymerase chain reaction (RT-qPCR). Fluorouracil 136-140 Pvt1 oncogene Homo sapiens 123-127 29693171-6 2018 In the present study, PVT1 mRNA was highly expressed in 5-FU-resistant CRC tissues and cell lines. Fluorouracil 56-60 Pvt1 oncogene Homo sapiens 22-26 29693171-7 2018 HCT-8/5-FU and HCT-116/5-FU cells transfected with small interfering RNA PVT1 and treated with 5-FU exhibited higher apoptotic rates and lower survival rates. Fluorouracil 23-27 Pvt1 oncogene Homo sapiens 73-77 29693171-8 2018 By contrast, overexpression of PVT1 in HCT-8 and HCT-116 cells transfected with lentiviral vector-PVT1-green fluorescent protein and treated with 5-FU exhibited lower apoptosis rates and higher survival rates. Fluorouracil 146-150 Pvt1 oncogene Homo sapiens 31-35 29693171-8 2018 By contrast, overexpression of PVT1 in HCT-8 and HCT-116 cells transfected with lentiviral vector-PVT1-green fluorescent protein and treated with 5-FU exhibited lower apoptosis rates and higher survival rates. Fluorouracil 146-150 Pvt1 oncogene Homo sapiens 98-102 29844931-0 2018 Dasatinib reduces 5-Fu-triggered apoptosis in colon carcinoma by directly modulating Src-dependent caspase-9 phosphorylation. Fluorouracil 18-22 caspase 9 Homo sapiens 99-108 31938347-7 2018 Furthermore, 5-FU-induced apoptosis of CD44high/ESAhigh cells was significantly increased in the presence of an inhibitor of the PGE2 receptors (EP1/EP2) when CD44high/ESAhigh cells were co-cultured with CD44high/ESAlow cells. Fluorouracil 13-17 prostaglandin E receptor 1 Homo sapiens 145-152 29512753-11 2018 Additionally, a Cell Counting Kit-8 assay demonstrated that specific inhibitors of NOS3 and BDNF/neurotrophic receptor tyrosine kinase, type 2 signaling reduced the IC50 of MCF-7/MDR cells in response to various anticancer drugs, including adriamycin, cisplatin and 5-fluorouracil. Fluorouracil 266-280 ret proto-oncogene Homo sapiens 110-134 29414586-3 2018 However, it also plays an active role in cancer treatment, through its contribution in the conversion of the anti-cancer drug 5-fluorouracil (5-FU) to an irreversible inhibitor of thymidylate synthase (TS), responsible of the inhibition of the DNA synthesis. Fluorouracil 126-140 thymidylate synthetase Homo sapiens 180-200 29414586-3 2018 However, it also plays an active role in cancer treatment, through its contribution in the conversion of the anti-cancer drug 5-fluorouracil (5-FU) to an irreversible inhibitor of thymidylate synthase (TS), responsible of the inhibition of the DNA synthesis. Fluorouracil 142-146 thymidylate synthetase Homo sapiens 180-200 25460919-6 2014 5-FU increased the expression of APC and decreased the expression of FEN1 in HCT-116 and HT-29 cells, which were sensitized to 5-FU when compared to LOVO cells. Fluorouracil 127-131 flap structure-specific endonuclease 1 Homo sapiens 69-73 29893327-12 2018 Conclusion: We determined that uPAR and CAIX levels were higher in the fluorouracil, epirubicin, and cyclophosphamide (FEC) chemotherapy group than in the control group, but there was no difference between the FEC and epirubicin/adriamycin chemotherapy groups in terms of basal and postchemotherapy uPAR, CAIX levels. Fluorouracil 71-83 plasminogen activator, urokinase receptor Homo sapiens 31-35 25132574-6 2014 CONCLUSIONS: MiR-21 expression in CAFs was associated with decreased OS in PDAC patients who received 5-FU, but not gemcitabine. Fluorouracil 102-106 microRNA 21 Homo sapiens 13-19 29155481-7 2018 The RGZ reduced leukocyte infiltration, preserved tissue structure, and dampened the 5-FU-induced expression of p53 and matrix metalloproteinase (Mmp)-2 after 5 days, and of Mmp-2 and interleukin (Il-1beta after 15 days. Fluorouracil 85-89 transformation related protein 53, pseudogene Mus musculus 112-115 25132574-0 2014 Stromal microRNA-21 levels predict response to 5-fluorouracil in patients with pancreatic cancer. Fluorouracil 47-61 microRNA 21 Homo sapiens 8-19 29330293-7 2018 The LIN28B-long isoform-expressing cells demonstrated increased drug resistance to 5-fluorouracil and cisplatin through the upregulation of ERCC1, a DNA repair gene, in a LET-7-dependent manner. Fluorouracil 83-97 ERCC excision repair 1, endonuclease non-catalytic subunit Homo sapiens 140-145 25132574-2 2014 We studied the predictive value of miR-21 levels for gemcitabine or 5-fluorouracil (5-FU) response in tumor cells (TCs) or cancer associated fibroblasts (CAFs) in a cohort of PDAC patients from the RTOG 9704 trial. Fluorouracil 68-82 microRNA 21 Homo sapiens 35-41 25132574-2 2014 We studied the predictive value of miR-21 levels for gemcitabine or 5-fluorouracil (5-FU) response in tumor cells (TCs) or cancer associated fibroblasts (CAFs) in a cohort of PDAC patients from the RTOG 9704 trial. Fluorouracil 84-88 microRNA 21 Homo sapiens 35-41 25453619-2 2014 Meanwhile, leucovorin enhances the efficacy of 5-fluorouracil by inhibiting thymidylate synthase. Fluorouracil 47-61 thymidylate synthetase Homo sapiens 76-96 25063586-0 2014 Unbiased proteomic and transcript analyses reveal that stathmin-1 silencing inhibits colorectal cancer metastasis and sensitizes to 5-fluorouracil treatment. Fluorouracil 132-146 stathmin 1 Homo sapiens 55-65 25230779-13 2014 Therefore, CD133 may inhibit 5-FU-induced apoptosis by regulating the expression of P-gp and Bcl-2 family mediated by phosphoinositide 3-kinase/Akt/p70S6K pathway in GC cells. Fluorouracil 29-33 ribosomal protein S6 kinase B1 Homo sapiens 148-154 25425972-6 2014 Low ATM protein level was significantly associated with poor survival including in patients with ER-negative tumors who received adjuvant anthracycline or cyclophosphamide, methotrexate, and 5-fluorouracil-based adjuvant chemotherapy (Ps < .05). Fluorouracil 191-205 ATM serine/threonine kinase Homo sapiens 4-7 29515783-0 2018 HMGA2 enhances 5-fluorouracil chemoresistance in colorectal cancer via the Dvl2/Wnt pathway. Fluorouracil 15-29 high mobility group AT-hook 2 Homo sapiens 0-5 29515783-3 2018 Here, we demonstrate a strong correlation between HMGA2 expression and chemosensitivity to 5-fluorouracil (5-FU), a widely used first-line systemic chemotherapy regimen for colorectal cancer (CRC) patients. Fluorouracil 91-105 high mobility group AT-hook 2 Homo sapiens 50-55 29515783-3 2018 Here, we demonstrate a strong correlation between HMGA2 expression and chemosensitivity to 5-fluorouracil (5-FU), a widely used first-line systemic chemotherapy regimen for colorectal cancer (CRC) patients. Fluorouracil 107-111 high mobility group AT-hook 2 Homo sapiens 50-55 29515783-6 2018 Taken together, our data suggest that HMGA2 enhances the chemoresistance to 5-FU in CRC via activating the Dvl2/Wnt pathway. Fluorouracil 76-80 high mobility group AT-hook 2 Homo sapiens 38-43 25520880-1 2014 We have previous found a positive correlation between post-therapy TCR repertoire normalization and remission of colorectal cancer (CRC) patients following fluorouracil, leucovorin, and irinotecan (FOLFIRI) plus bevacizumab or Rh-endostatin therapy. Fluorouracil 156-168 T cell receptor beta variable 20/OR9-2 (non-functional) Homo sapiens 67-70 30261494-11 2018 Compared to SIRT2- cells, SIRT2+ cells formed more tumor spheres, appeared to be more resistant towards fluorouracil-induced apoptosis, and generated bigger tumors with higher frequency after serial adoptive transplantation. Fluorouracil 104-116 sirtuin 2 Homo sapiens 26-31 25178657-0 2014 5-Fluorouracil causes severe CNS demyelination by disruption of TCF7L2/HDAC1/HDAC2 complex in adolescent mice. Fluorouracil 0-14 histone deacetylase 1 Mus musculus 71-76 25178657-5 2014 5-FU-decreased TCF7L2 results in disruption of the interaction between TCF7L2 and HDAC1/2. Fluorouracil 0-4 histone deacetylase 1 Mus musculus 82-89 25178657-6 2014 Inhibition of crucial myelination-promoting factors by 5-FU is more significantly antagonized by co-transfection of TCF7L2, HDAC1 and HDAC2 than TCF7L2 alone. Fluorouracil 55-59 histone deacetylase 1 Mus musculus 124-129 25178657-7 2014 Our findings reveal that 5-FU could acutely induce the severe myelin degeneration in adolescence and disruption of TCF7L2/HDAC1/HDAC2 complex is at least partially involved in 5-FU-induced demyelination. Fluorouracil 176-180 histone deacetylase 1 Mus musculus 122-127 25366763-7 2014 In conclusion, this study reports that the ERCC1 rs11615 TT polymorphism can be used as a prognostic marker to determine the clinical outcome of gastric cancer patients treated with 5-fluorouracil-based chemotherapy. Fluorouracil 182-196 ERCC excision repair 1, endonuclease non-catalytic subunit Homo sapiens 43-48 29843139-11 2018 Blocking extracellular HOP with neutralizing antibody reduced proliferation and enhanced fluorouracil-induced apoptosis of GC cells. Fluorouracil 89-101 stress induced phosphoprotein 1 Homo sapiens 23-26 30121640-0 2018 Role of Urotensin-2 in 5-Fluorouracil-Related Arterial Vasoconstriction in Cancer Patients. Fluorouracil 23-37 urotensin 2 Homo sapiens 8-19 30121640-1 2018 BACKGROUND: The aim of this study was to identify the possible relationship of 5-fluorouracil (5-FU)-related arterial vasoconstriction with urotensin-2 (UT-2), which has a high potential as an endogenic vasoconstrictor. Fluorouracil 79-93 urotensin 2 Homo sapiens 140-151 30121640-1 2018 BACKGROUND: The aim of this study was to identify the possible relationship of 5-fluorouracil (5-FU)-related arterial vasoconstriction with urotensin-2 (UT-2), which has a high potential as an endogenic vasoconstrictor. Fluorouracil 79-93 urotensin 2 Homo sapiens 153-157 30121640-1 2018 BACKGROUND: The aim of this study was to identify the possible relationship of 5-fluorouracil (5-FU)-related arterial vasoconstriction with urotensin-2 (UT-2), which has a high potential as an endogenic vasoconstrictor. Fluorouracil 95-99 urotensin 2 Homo sapiens 140-151 30121640-1 2018 BACKGROUND: The aim of this study was to identify the possible relationship of 5-fluorouracil (5-FU)-related arterial vasoconstriction with urotensin-2 (UT-2), which has a high potential as an endogenic vasoconstrictor. Fluorouracil 95-99 urotensin 2 Homo sapiens 153-157 30121640-9 2018 Increased UT-2 levels are likely to play a role in 5-FU-related cardiac toxicity pathogenesis. Fluorouracil 51-55 urotensin 2 Homo sapiens 10-14 29371950-0 2017 Overexpression of miR-489 enhances efficacy of 5-fluorouracil-based treatment in breast cancer stem cells by targeting XIAP. Fluorouracil 47-61 microRNA 489 Homo sapiens 18-25 29371950-7 2017 Furthermore, overexpression of miR-489 was found to increase the cytotoxicity of 5-fluorouracil to BCSCs. Fluorouracil 81-95 microRNA 489 Homo sapiens 31-38 29371950-9 2017 We found that enforced expression of XIAP through its recombinant expression vector abolished the effect of miR-489 on reversing the 5-fluorouracil resistance. Fluorouracil 133-147 microRNA 489 Homo sapiens 108-115 29371950-11 2017 In summary, our data demonstrate that introduction with miR-489 represents a novel strategy to enhance efficacy of 5-fluorouracil-based treatment in BCSCs. Fluorouracil 115-129 microRNA 489 Homo sapiens 56-63 25364260-0 2014 Inhibition of Mus81 by siRNA enhances sensitivity to 5-FU in breast carcinoma cell lines. Fluorouracil 53-57 MUS81 structure-specific endonuclease subunit Homo sapiens 14-19 28990068-5 2017 According to the results of the present study, MACC1 was depleted in two colon cancer cell lines resistant to 5-FU; subsequently, CSC-like properties and 5-FU sensitivity were investigated. Fluorouracil 110-114 MET transcriptional regulator MACC1 Homo sapiens 47-52 28990068-6 2017 Within 5-FU-resistant cells, cell death was facilitated by MACC1 knockdown. Fluorouracil 7-11 MET transcriptional regulator MACC1 Homo sapiens 59-64 28990068-8 2017 Additionally, it was indicated that the phosphoinositide 3-kinase/protein kinase B signaling pathway may be associated with 5-FU resistance and CSC-like properties via MACC1. Fluorouracil 124-128 protein tyrosine kinase 2 beta Homo sapiens 66-82 28990068-8 2017 Additionally, it was indicated that the phosphoinositide 3-kinase/protein kinase B signaling pathway may be associated with 5-FU resistance and CSC-like properties via MACC1. Fluorouracil 124-128 MET transcriptional regulator MACC1 Homo sapiens 168-173 30512606-7 2017 There are forms of SCC in situ or Bowen disease, cutaneous or mucosal, accessible to cryotherapy, 5-FU, imiquimod or dynamic phototherapy as an alternative to surgery. Fluorouracil 98-102 serpin family B member 3 Homo sapiens 19-22 29113258-0 2017 Combination of calcineurin B subunit (CnB) and 5-fluorouracil reverses 5-fluorouracil-induced immunosuppressive effect and enhances the antitumor activity in hepatocellular carcinoma. Fluorouracil 71-85 protein phosphatase 3 regulatory subunit B, alpha Homo sapiens 15-36 29113258-0 2017 Combination of calcineurin B subunit (CnB) and 5-fluorouracil reverses 5-fluorouracil-induced immunosuppressive effect and enhances the antitumor activity in hepatocellular carcinoma. Fluorouracil 71-85 protein phosphatase 3 regulatory subunit B, alpha Homo sapiens 38-41 29113258-5 2017 It was demonstrated that combined treatment of 5-FU and CnB led to increased tumor-suppressive effects, as indicated by reduced tumor volume and weight when compared with 5-FU or CnB treatment alone in a hepatoma xenograph model. Fluorouracil 171-175 protein phosphatase 3 regulatory subunit B, alpha Homo sapiens 56-59 29113258-7 2017 Notably, the addition of CnB to 5-FU-based therapy completely reversed the immunosuppressive effect of 5-FU. Fluorouracil 32-36 protein phosphatase 3 regulatory subunit B, alpha Homo sapiens 25-28 29113258-7 2017 Notably, the addition of CnB to 5-FU-based therapy completely reversed the immunosuppressive effect of 5-FU. Fluorouracil 103-107 protein phosphatase 3 regulatory subunit B, alpha Homo sapiens 25-28 29113258-9 2017 Furthermore, pathological examinations indicated that CnB attenuated 5-FU-induced organ damage. Fluorouracil 69-73 protein phosphatase 3 regulatory subunit B, alpha Homo sapiens 54-57 29113258-10 2017 Based on these findings, it is proposed that CnB may serve as a novel and promising drug candidate for the improvement of 5-FU-based chemotherapy. Fluorouracil 122-126 protein phosphatase 3 regulatory subunit B, alpha Homo sapiens 45-48 30082548-2 2017 Earlier studies have demonstrated that arsenic trioxide (ATO) can significantly resensitize resistant colon cancer to 5-fluorouracil (5-FU) by downregulating thymidylate synthase (TS). Fluorouracil 134-138 thymidylate synthetase Homo sapiens 158-178 28860825-5 2017 ARID1A-knockdown cells were treated with AKT inhibitor (GSK690693), 5-fluorouracil, or cisplatin, alone or in combination. Fluorouracil 68-82 AT-rich interaction domain 1A Homo sapiens 0-6 28109077-6 2017 In contrast, the sequential combination of both folinate salts and 5-FU was antagonistic at 24 and 72 h. The simultaneous combination of 5-FU and NaLV or CaLV inhibited TYMS gene expression at 24 h, whereas the sequential combination reduced SLC19A1 gene expression. Fluorouracil 67-71 thymidylate synthetase Homo sapiens 169-173 28109077-6 2017 In contrast, the sequential combination of both folinate salts and 5-FU was antagonistic at 24 and 72 h. The simultaneous combination of 5-FU and NaLV or CaLV inhibited TYMS gene expression at 24 h, whereas the sequential combination reduced SLC19A1 gene expression. Fluorouracil 137-141 thymidylate synthetase Homo sapiens 169-173 25364260-5 2014 The present study aimed to investigate the role of Mus81 on the chemosensitivity of breast carcinoma cells in response to 5-fluorouracil (5-FU), a chemotherapeutic drug that is widely used for treatment of breast malignancies. Fluorouracil 122-136 MUS81 structure-specific endonuclease subunit Homo sapiens 51-56 25364260-5 2014 The present study aimed to investigate the role of Mus81 on the chemosensitivity of breast carcinoma cells in response to 5-fluorouracil (5-FU), a chemotherapeutic drug that is widely used for treatment of breast malignancies. Fluorouracil 138-142 MUS81 structure-specific endonuclease subunit Homo sapiens 51-56 25364260-11 2014 We found that the Mus81-silenced MCF-7 and T47D cells exhibited decreased cell viability and clonogenic survival, but increased G2 accumulation, in response to 5-FU. Fluorouracil 160-164 MUS81 structure-specific endonuclease subunit Homo sapiens 18-23 25364260-14 2014 CONCLUSION: Taken together, our data suggest that Mus81 inhibition significantly increased the chemosensitivity of MCF-7 and T47D cells in response to 5-FU. Fluorouracil 151-155 MUS81 structure-specific endonuclease subunit Homo sapiens 50-55 25232828-1 2014 BACKGROUND: Retrospective studies indicate associations between TSER (thymidylate synthase enhancer region) genotypes and clinical outcomes in patients receiving 5-FU based chemotherapy, but well-controlled prospective validation has been lacking. Fluorouracil 162-166 thymidylate synthetase Homo sapiens 70-90 28435028-14 2017 Increased expression of PPP1R11 in p53-deficient CRC cells was required for hypoxia-induced EMT, invasion, migration, and resistance to 5-fluorouracil, as well as metastasis of xenograft tumors to lungs of mice. Fluorouracil 136-150 protein phosphatase 1, regulatory inhibitor subunit 11 Mus musculus 24-31 28435028-14 2017 Increased expression of PPP1R11 in p53-deficient CRC cells was required for hypoxia-induced EMT, invasion, migration, and resistance to 5-fluorouracil, as well as metastasis of xenograft tumors to lungs of mice. Fluorouracil 136-150 transformation related protein 53, pseudogene Mus musculus 35-38 25223338-0 2014 Joint detection of ERCC1, TUBB3, and TYMS guidance selection of docetaxel, 5-fluorouracil and cisplatin (DDP) individual chemotherapy in advanced gastric cancer patients. Fluorouracil 75-89 thymidylate synthetase Homo sapiens 37-41 28652707-2 2017 In vitro studies of DFP-11207 indicated that it strongly inhibited the degradation of 5-FU by dihydropyrimidine dehydrogenase (DPD) in homogenates of the rat liver, and also inhibited the phosphorylation of 5-FU by orotate phosphoribosyltransferase (OPRT) in tumor tissues in a similar magnitude of potency by CDHP and CTA, respectively. Fluorouracil 86-90 dihydropyrimidine dehydrogenase Rattus norvegicus 127-130 28389232-10 2017 The mechanisms of AOG on enhancing the growth inhibitory effect of 5-FU may be through the influence of TLR-4/NF-kappaB pathway. Fluorouracil 67-71 toll like receptor 4 Homo sapiens 104-109 28150434-4 2017 5-Fluorouracil (5-FU)-resistant SW480 cells (SW480/5-FU) were found to have elevated levels of miR-577. Fluorouracil 0-14 microRNA 577 Homo sapiens 95-102 28150434-4 2017 5-Fluorouracil (5-FU)-resistant SW480 cells (SW480/5-FU) were found to have elevated levels of miR-577. Fluorouracil 16-20 microRNA 577 Homo sapiens 95-102 28150434-4 2017 5-Fluorouracil (5-FU)-resistant SW480 cells (SW480/5-FU) were found to have elevated levels of miR-577. Fluorouracil 51-55 microRNA 577 Homo sapiens 95-102 28150434-5 2017 Ectopic expression of miR-577 enhanced 5-FU sensitivity in SW480/5-FU cells. Fluorouracil 39-43 microRNA 577 Homo sapiens 22-29 28150434-5 2017 Ectopic expression of miR-577 enhanced 5-FU sensitivity in SW480/5-FU cells. Fluorouracil 65-69 microRNA 577 Homo sapiens 22-29 28150434-7 2017 Enforced expression of HSP27 reversed the effects of miR-577 on CRC cell growth and 5-FU sensitivity. Fluorouracil 84-88 heat shock protein family B (small) member 1 Homo sapiens 23-28 28067150-0 2017 Low-dose 5-fluorouracil sensitizes HepG2 cells to TRAIL through TRAIL receptor DR5 and survivin-dependent mechanisms. Fluorouracil 9-23 TNF receptor superfamily member 10b Homo sapiens 79-82 28067150-5 2017 The enhanced induction of cell death by the 5-FU/TRAIL combination was mediated by DR5 up-regulation and survivin down-regulation. Fluorouracil 44-48 TNF receptor superfamily member 10b Homo sapiens 83-86 28378512-4 2017 5-FU induced significant weight loss, shortened villi height, and increased histological severity, IL-1beta expression, and MPO activity compared to the normal control group. Fluorouracil 0-4 myeloperoxidase Rattus norvegicus 124-127 28588704-7 2017 Furthermore, the expression levels of survivin, which is a direct transcriptional target of Wnt/beta-catenin and an inhibitor of apoptosis, were markedly elevated when Ell3 OE cells were treated with 5-FU, as detected by western blot analysis. Fluorouracil 200-204 elongation factor for RNA polymerase II 3 Homo sapiens 168-172 28542590-0 2017 The MTH1 inhibitor TH588 demonstrates anti-tumoral effects alone and in combination with everolimus, 5-FU and gamma-irradiation in neuroendocrine tumor cells. Fluorouracil 101-105 nudix hydrolase 1 Homo sapiens 4-8 27983919-5 2017 Overexpression of PER3 could strengthen 5-FU-induced inhibitory effects on colorectal CSCs, but knockdown of PER3 decreased its inhibition of colorectal CSCs. Fluorouracil 40-44 period circadian regulator 3 Homo sapiens 18-22 25232494-2 2014 Organic anion transporter 2 (OAT2) and organic cation transporter 2 (OCT2) are critical determinants in uptake of 5-FU and oxaliplatin, respectively. Fluorouracil 114-118 solute carrier family 22 member 2 Homo sapiens 39-67 27911869-1 2017 AIMS AND BACKGROUND: This study was designed to compare the efficacy and safety of paclitaxel/oxaliplatin/fluorouracil (TOF) regimen and S-1/oxaliplatin (SOX) regimen for metastatic gastric cancer (GC) patients. Fluorouracil 106-118 FEZ family zinc finger 2 Homo sapiens 120-123 28393242-10 2017 Moreover, Srcin1 suppression sensitized cancer cells to 5-fluorouracil (5-FU)-induced apoptosis in vitro and in vivo. Fluorouracil 56-70 SRC kinase signaling inhibitor 1 Homo sapiens 10-16 28393242-10 2017 Moreover, Srcin1 suppression sensitized cancer cells to 5-fluorouracil (5-FU)-induced apoptosis in vitro and in vivo. Fluorouracil 72-76 SRC kinase signaling inhibitor 1 Homo sapiens 10-16 28515926-1 2017 Treatment with 5-fluorouracil (5-FU) and cisplatin (PF regimen) remains the most frequently used chemotherapy for esophageal squamous cell carcinoma (SCC). Fluorouracil 15-29 serpin family B member 3 Homo sapiens 150-153 28515926-1 2017 Treatment with 5-fluorouracil (5-FU) and cisplatin (PF regimen) remains the most frequently used chemotherapy for esophageal squamous cell carcinoma (SCC). Fluorouracil 31-35 serpin family B member 3 Homo sapiens 150-153 28428709-10 2017 The severity of 5-FU-induced diarrhea was lower in IL-13Ralpha1 KO mice, indicating major role for IL-13 signaling via IL-13Ralpha1 in pathogenesis. Fluorouracil 16-20 interleukin 13 receptor, alpha 1 Mus musculus 51-63 28428709-10 2017 The severity of 5-FU-induced diarrhea was lower in IL-13Ralpha1 KO mice, indicating major role for IL-13 signaling via IL-13Ralpha1 in pathogenesis. Fluorouracil 16-20 interleukin 13 receptor, alpha 1 Mus musculus 119-131 28428709-12 2017 IL-13Ralpha2 was upregulated in the ileum of 5-FU-treated Fn14 KO mice. Fluorouracil 45-49 interleukin 13 receptor, alpha 2 Mus musculus 0-12 28428709-14 2017 CONCLUSION: Disruption of the TWEAK/Fn14 pathway affects several interconnected pathways, including those associated with IL-13, IL-33, and IL-13Ralpha2, to attenuate 5-FU-induced intestinal side effects. Fluorouracil 167-171 interleukin 13 receptor, alpha 2 Mus musculus 140-152 28381166-8 2017 Lentivirus-induced miR-181d downregulation decreased pancreatic cancer proliferation, migration, and fluorouracil resistance in vitro and inhibited the growth of cancer explant in vivo. Fluorouracil 101-113 microRNA 181d Homo sapiens 19-27 28325302-3 2017 To this end, P19 was incorporated with gemcitabine and 5-fluorouracil (5-FU), or conjugated to monomethyl auristatin E (MMAE) and derivative of maytansine 1 (DM1). Fluorouracil 55-69 interleukin 23 subunit alpha Homo sapiens 13-16 28325302-3 2017 To this end, P19 was incorporated with gemcitabine and 5-fluorouracil (5-FU), or conjugated to monomethyl auristatin E (MMAE) and derivative of maytansine 1 (DM1). Fluorouracil 71-75 interleukin 23 subunit alpha Homo sapiens 13-16 28255900-9 2017 The differences between HSPC1 inhibitors were also reflected in combination treatment-17-DMAG was more effective compared with NVP-AUY922 in potentiating the cytotoxic effects of 5-fluorouracil, oxaliplatin and irinotecan. Fluorouracil 179-193 heat shock protein 90 alpha family class A member 1 Homo sapiens 24-29 28112370-3 2017 In the present study, we evaluated the influence of anticancer agents 5-fluorouracil, gemcitabine and paclitaxel on PD-L1 expression in human pancreatic cancer cell lines MIA PaCa-2 and AsPC-1 and in murine pancreatic cancer cell line Pan02. Fluorouracil 70-84 CD274 molecule Homo sapiens 116-121 28112370-5 2017 We observed that when AsPC-1, MIA PaCa-2 and Pan02 cells were stimulated by 5-fluorouracil, gemcitabine or paclitaxel, PD-L1 surface protein expression was enhanced. Fluorouracil 76-90 CD274 molecule Homo sapiens 119-124 28848656-1 2016 BACKGROUND: In the cetuximab after progression in KRAS wild-type colorectal cancer patients (CAPRI) trial patients with metastatic colorectal cancer (mCRC) received 5-fluorouracil, folinic acid and irinotecan (FOLFIRI) and cetuximab in first line followed by 5-Fluorouracil, folinic acid, oxaliplatin (FOLFOX) with or without cetuximab until progression. Fluorouracil 165-179 RAS p21 protein activator 4 Homo sapiens 93-98 28193209-6 2017 Hence, in this study we sought to evaluate the protective effects of LL-PAP on 5-FU-induced experimental mucositis in BALB/c mice as a novel approach to treat the disease. Fluorouracil 79-83 regenerating family member 3 alpha Homo sapiens 69-75 28193209-9 2017 Recombinant lactococci carrying antimicrobial PAP did not improve those markers of inflammation, although its expression was associated with villous architecture preservation and increased secretory granules density inside Paneth cells in response to 5-FU inflammation. Fluorouracil 251-255 regenerating family member 3 alpha Homo sapiens 46-49 27009482-1 2017 BACKGROUND: Thymidylate synthase (TS) is the major target for fluoropyrimidine drugs like 5-Fluorouracil (5-FU). Fluorouracil 90-104 thymidylate synthetase Homo sapiens 12-32 27009482-1 2017 BACKGROUND: Thymidylate synthase (TS) is the major target for fluoropyrimidine drugs like 5-Fluorouracil (5-FU). Fluorouracil 106-110 thymidylate synthetase Homo sapiens 12-32 27864056-0 2017 Lactoferrin nanoparticle mediated targeted delivery of 5-fluorouracil for enhanced therapeutic efficacy. Fluorouracil 55-69 lactotransferrin Mus musculus 0-11 27864056-5 2017 The study aimed to efficiently entrap 5-FU in lactoferrin nanoparticles (LfNPs) in an attempt to enhance its therapeutic efficacy. Fluorouracil 38-42 lactotransferrin Mus musculus 46-57 27935870-7 2017 Our data indicate that Oct3/4, Sox2, and Nanog are transiently expressed in response to 5-FU-induced injury, and then they are gradually silenced as the cells differentiate. Fluorouracil 88-92 solute carrier family 22 member 8 Rattus norvegicus 23-29 27935870-7 2017 Our data indicate that Oct3/4, Sox2, and Nanog are transiently expressed in response to 5-FU-induced injury, and then they are gradually silenced as the cells differentiate. Fluorouracil 88-92 SRY-box transcription factor 2 Rattus norvegicus 31-35 27935870-9 2017 Treatment with 5-FU reversed the methylation of the Oct3/4, Nanog, and Sox2 promoters, which corresponded to increases in Oct3/4, Nanog, and Sox2 mRNA and protein. Fluorouracil 15-19 solute carrier family 22 member 8 Rattus norvegicus 52-58 27935870-9 2017 Treatment with 5-FU reversed the methylation of the Oct3/4, Nanog, and Sox2 promoters, which corresponded to increases in Oct3/4, Nanog, and Sox2 mRNA and protein. Fluorouracil 15-19 SRY-box transcription factor 2 Rattus norvegicus 71-75 27935870-9 2017 Treatment with 5-FU reversed the methylation of the Oct3/4, Nanog, and Sox2 promoters, which corresponded to increases in Oct3/4, Nanog, and Sox2 mRNA and protein. Fluorouracil 15-19 solute carrier family 22 member 8 Rattus norvegicus 122-128 27935870-9 2017 Treatment with 5-FU reversed the methylation of the Oct3/4, Nanog, and Sox2 promoters, which corresponded to increases in Oct3/4, Nanog, and Sox2 mRNA and protein. Fluorouracil 15-19 SRY-box transcription factor 2 Rattus norvegicus 141-145 27869649-11 2017 Importantly, calcipotriol plus 5-FU treatment induced TSLP, HLA class II, and natural killer cell group 2D (NKG2D) ligand expression in the lesional keratinocytes associated with a marked CD4+ T cell infiltration, which peaked on days 10-11 after treatment, without pain, crusting, or ulceration. Fluorouracil 31-35 thymic stromal lymphopoietin Homo sapiens 54-58 28011480-6 2017 In contrast, treatment with CaLa (2.5 mM), alone and in combination with 5-FU, exerted antitumor activity against both anchored and unanchored CRC cells via calcium-mediated FAK proteolysis and inhibition of EMT markers, such as vimentin and SNAIL. Fluorouracil 73-77 vimentin Homo sapiens 229-237 25232494-2 2014 Organic anion transporter 2 (OAT2) and organic cation transporter 2 (OCT2) are critical determinants in uptake of 5-FU and oxaliplatin, respectively. Fluorouracil 114-118 solute carrier family 22 member 2 Homo sapiens 69-73 27840990-5 2017 In this study, we used two human colon cancer cell lines, HCT116 and HT29, and evaluated the influence of miR-302a on 5-fluorouracil (5-FU)-induced cell death and viability inhibition. Fluorouracil 118-132 microRNA 302a Homo sapiens 106-114 27840990-5 2017 In this study, we used two human colon cancer cell lines, HCT116 and HT29, and evaluated the influence of miR-302a on 5-fluorouracil (5-FU)-induced cell death and viability inhibition. Fluorouracil 134-138 microRNA 302a Homo sapiens 106-114 24970398-11 2014 Finally, knockdown of GSTP-1 promoted the sensitivity of SNU-407 cells to the anticancer agent 5-fluorouracil. Fluorouracil 95-109 glutathione S-transferase pi 1 Homo sapiens 22-28 27840990-7 2017 Then, we designed siRNA against IGF-1R and found that si-IGF-1R resembled the effect of miR-302a on 5-FU treatment. Fluorouracil 100-104 microRNA 302a Homo sapiens 88-96 27840990-9 2017 In conclusion, miR-302a targeted IGF-1R and enhanced 5-FU-induced cell death and viability inhibition in human colon cancer cells. Fluorouracil 53-57 microRNA 302a Homo sapiens 15-23 27936107-2 2016 KSHV encodes functional thymidylate synthase, which is a target for anticancer drugs such as raltitrexed or 5-fluorouracil. Fluorouracil 108-122 ORF70 Human gammaherpesvirus 8 24-44 27906628-0 2016 Role of genomic factors beyond thymidylate synthase in the prediction of response to 5-fluorouracil. Fluorouracil 85-99 thymidylate synthetase Homo sapiens 31-51 24800927-11 2014 Taken together, activation of CXCL4 expression by 5-FU in mice participates in 5-FU-induced intestinal mucositis through upregulation of p53 via activation of p38-MAPK, and CXCL4mab is potentially beneficial in preventing CIM in the intestinal tract. Fluorouracil 79-83 transformation related protein 53, pseudogene Mus musculus 137-140 24919507-9 2014 In in vitro studies, we observed increased expression of p21 and p-ERK1/2 diminution via use of both analogs as compared to use of 5-FU alone. Fluorouracil 131-135 H3 histone pseudogene 16 Homo sapiens 57-60 24919507-12 2014 Our results suggest that the mechanism of potentiation of 5-FU antitumor action by both analogs is realized via increased p21 expression and decreased p-ERK1/2 level which may lead to diminution of thymidylate synthase expression. Fluorouracil 58-62 H3 histone pseudogene 16 Homo sapiens 122-125 24595405-2 2014 PURPOSE: Primary prophylaxis with granulocyte colony-stimulating factor (G-CSF) is used in many institutions across the UK due to unacceptable febrile neutropenia (FN) rates with FEC-D (fluorouracil, epirubicin, cyclophosphamide-docetaxel). Fluorouracil 186-198 colony stimulating factor 3 Homo sapiens 34-71 24595405-2 2014 PURPOSE: Primary prophylaxis with granulocyte colony-stimulating factor (G-CSF) is used in many institutions across the UK due to unacceptable febrile neutropenia (FN) rates with FEC-D (fluorouracil, epirubicin, cyclophosphamide-docetaxel). Fluorouracil 186-198 colony stimulating factor 3 Homo sapiens 73-78 24595405-2 2014 PURPOSE: Primary prophylaxis with granulocyte colony-stimulating factor (G-CSF) is used in many institutions across the UK due to unacceptable febrile neutropenia (FN) rates with FEC-D (fluorouracil, epirubicin, cyclophosphamide-docetaxel). Fluorouracil 186-198 collagen type VIII alpha 2 chain Homo sapiens 179-184 24833095-0 2014 Decreased ARID1A expression facilitates cell proliferation and inhibits 5-fluorouracil-induced apoptosis in colorectal carcinoma. Fluorouracil 72-86 AT-rich interaction domain 1A Homo sapiens 10-16 24833095-6 2014 ARID1A overexpression by plasmid transfection in SW620 cell line inhibited proliferation and facilitated 5-fluorouracil-induced apoptosis. Fluorouracil 105-119 AT-rich interaction domain 1A Homo sapiens 0-6 24833095-7 2014 ARID1A depletion by siRNA in SW480 cell line promoted proliferation ability and inhibited 5-fluorouracil-induced apoptosis. Fluorouracil 90-104 AT-rich interaction domain 1A Homo sapiens 0-6 24982337-4 2014 RESULTS: Rapamycin combined with 5-fluorouracil significantly reduced tumor size, suppressed expression of B-cell lymphoma 2, increased tumor apoptosis, and inhibited mTOR signaling activity by de-phosphorylation of S6K. Fluorouracil 33-47 mechanistic target of rapamycin kinase Mus musculus 167-171 23376192-10 2014 Overall, we present examples of how Pharmaco-miR provides possible explanations for previously published observations, including how the cisplatin and 5-fluorouracil resistance induced by miR-148a may be caused by miR-148a targeting of the gene KIT. Fluorouracil 151-165 microRNA 148a Homo sapiens 188-196 27882131-10 2016 PADI4 siRNA coupled with 5-Fu significantly enhanced its inhibitory effect on the proliferation of gastric cancer cells. Fluorouracil 25-29 peptidyl arginine deiminase 4 Homo sapiens 0-5 27726102-0 2016 MiRNA-221-3p desensitizes pancreatic cancer cells to 5-fluorouracil by targeting RB1. Fluorouracil 53-67 microRNA 221 Homo sapiens 0-9 27726102-4 2016 But the detailed molecular mechanism about miR-221-3p regulating 5-fluorouracil (5-FU) resistance in human pancreatic cancer remains to be clarified. Fluorouracil 65-79 microRNA 221 Homo sapiens 43-50 27726102-4 2016 But the detailed molecular mechanism about miR-221-3p regulating 5-fluorouracil (5-FU) resistance in human pancreatic cancer remains to be clarified. Fluorouracil 81-85 microRNA 221 Homo sapiens 43-50 27726102-5 2016 In this study, we investigated the association between miR-221-3p expression and 5-FU sensitivity. Fluorouracil 81-85 microRNA 221 Homo sapiens 55-62 27427897-8 2016 Mice receiving 5-FU +- SCF showed intact ovarian function and fertility. Fluorouracil 15-19 kit ligand Mus musculus 23-26 27760966-1 2016 The loss of mismatch repair(MMR)function as a result of MLH1 promoter methylation is closely correlated with high frequency microsatellite instability, and tumors with such characteristics are resistant to anticancer drugs such as 5-FU. Fluorouracil 231-235 mutL homolog 1 Homo sapiens 56-60 27698820-6 2016 These findings indicate that low-dose 5-Fu treatment may efficiently enrich the CSC-like cell population in PLC/RAF/5 cells. Fluorouracil 38-42 heparan sulfate proteoglycan 2 Homo sapiens 108-111 27752409-0 2016 The First Case of Severe Takotsubo Cardiomyopathy Associated with 5-Fluorouracil in a Patient with Abnormalities of Both Dihydropyrimidine Dehydrogenase (DPYD) and Thymidylate Synthase (TYMS) Genes. Fluorouracil 66-80 thymidylate synthetase Homo sapiens 164-184 27752409-0 2016 The First Case of Severe Takotsubo Cardiomyopathy Associated with 5-Fluorouracil in a Patient with Abnormalities of Both Dihydropyrimidine Dehydrogenase (DPYD) and Thymidylate Synthase (TYMS) Genes. Fluorouracil 66-80 thymidylate synthetase Homo sapiens 186-190 27752409-12 2016 In this paper, we describe the first case of cardiomyopathy related to DPD deficiency and homozygous polymorphism of TYMS in a patient with colon cancer following 5-FU containing regimen. Fluorouracil 163-167 thymidylate synthetase Homo sapiens 117-121 23376192-10 2014 Overall, we present examples of how Pharmaco-miR provides possible explanations for previously published observations, including how the cisplatin and 5-fluorouracil resistance induced by miR-148a may be caused by miR-148a targeting of the gene KIT. Fluorouracil 151-165 microRNA 148a Homo sapiens 214-222 24752576-5 2014 Conversely, knockdown of AQP5 in HT-29 human colon cancer cells increased inhibition rates of cancer chemotherapeutic drugs such as 5-FU and DDP. Fluorouracil 132-136 aquaporin 5 Homo sapiens 25-29 24515389-5 2014 It"s found the inhibition rate of 5-FU, L-OHP to well-differentiated GC tissues and cell line was lower than that in the poorly differentiated tissues and cell line; expressions of ZNF139 and MDR1/P-gp, MRP1 and Bcl-2 in well-differentiated GC tissues and cell line MKN28 were higher, while Bax expression was lower. Fluorouracil 34-38 phosphoglycolate phosphatase Homo sapiens 197-201 24634414-2 2014 In this article, we show that overexpression of the MT1G isoform sensitizes colorectal cell lines to the chemotherapeutic agents oxaliplatin (OXA) and 5-fluorouracil (5-FU), in part through enhancing p53 and repressing NF-kappaB activity. Fluorouracil 151-165 metallothionein 1G Homo sapiens 52-56 24634414-2 2014 In this article, we show that overexpression of the MT1G isoform sensitizes colorectal cell lines to the chemotherapeutic agents oxaliplatin (OXA) and 5-fluorouracil (5-FU), in part through enhancing p53 and repressing NF-kappaB activity. Fluorouracil 167-171 metallothionein 1G Homo sapiens 52-56 24486618-9 2014 The possible mechanism of 5-FU induced renal toxicity is the induction of oxidative stress; activation of apoptotic pathway by upregulation of p53, bax, caspase-3 and down regulating Bcl-2. Fluorouracil 26-30 Wistar clone pR53P1 p53 pseudogene Rattus norvegicus 143-146 24486618-9 2014 The possible mechanism of 5-FU induced renal toxicity is the induction of oxidative stress; activation of apoptotic pathway by upregulation of p53, bax, caspase-3 and down regulating Bcl-2. Fluorouracil 26-30 BCL2 associated X, apoptosis regulator Rattus norvegicus 148-151 24381058-0 2014 Overexpression of S100P promotes colorectal cancer metastasis and decreases chemosensitivity to 5-FU in vitro. Fluorouracil 96-100 S100 calcium binding protein P Homo sapiens 18-23 24381058-7 2014 Ectopic expression of S100P promotes SW480 cancer cells migration and invasion, decreases chemosensitivity to 5-FU in vitro. Fluorouracil 110-114 S100 calcium binding protein P Homo sapiens 22-27 24357118-8 2014 In vivo, megakaryocyte expression of fibronectin and basement membrane components was upregulated during bone marrow reconstitution upon 5-fluorouracil induced myelosuppression, while only type IV collagen resulted upregulated upon induced thrombocytopenia. Fluorouracil 137-151 fibronectin 1 Mus musculus 37-48 27417318-0 2016 Effects of a bolus injection of 5-fluorouracil on dihydropyrimidine dehydrogenase activity in rats receiving continuous infusion of 5-fluorouracil. Fluorouracil 32-46 dihydropyrimidine dehydrogenase Rattus norvegicus 50-81 27417318-2 2016 We examined the effects of a 5-FU bolus injection on the activity of dihydropyrimidine dehydrogenase (DPD), which is the first and rate-limiting enzyme of 5-FU catabolism, in rats. Fluorouracil 29-33 dihydropyrimidine dehydrogenase Rattus norvegicus 69-100 27417318-2 2016 We examined the effects of a 5-FU bolus injection on the activity of dihydropyrimidine dehydrogenase (DPD), which is the first and rate-limiting enzyme of 5-FU catabolism, in rats. Fluorouracil 29-33 dihydropyrimidine dehydrogenase Rattus norvegicus 102-105 27417318-2 2016 We examined the effects of a 5-FU bolus injection on the activity of dihydropyrimidine dehydrogenase (DPD), which is the first and rate-limiting enzyme of 5-FU catabolism, in rats. Fluorouracil 155-159 dihydropyrimidine dehydrogenase Rattus norvegicus 69-100 27417318-2 2016 We examined the effects of a 5-FU bolus injection on the activity of dihydropyrimidine dehydrogenase (DPD), which is the first and rate-limiting enzyme of 5-FU catabolism, in rats. Fluorouracil 155-159 dihydropyrimidine dehydrogenase Rattus norvegicus 102-105 27417318-6 2016 The plasma UH2/Ura ratio, an indirect biomarker of hepatic DPD activity, tended to be lower in the rats that had received a 5-FU bolus injection than in those that had not, and it remained low after infusion ended. Fluorouracil 124-128 dihydropyrimidine dehydrogenase Rattus norvegicus 59-62 27417318-9 2016 CONCLUSIONS: A bolus injection suppresses hepatic DPD activity and its effects are dependent on dosage, resulting in slower elimination of 5-FU from the blood and contributing to long-term systemic exposure to 5-FU. Fluorouracil 139-143 dihydropyrimidine dehydrogenase Rattus norvegicus 50-53 27417318-9 2016 CONCLUSIONS: A bolus injection suppresses hepatic DPD activity and its effects are dependent on dosage, resulting in slower elimination of 5-FU from the blood and contributing to long-term systemic exposure to 5-FU. Fluorouracil 210-214 dihydropyrimidine dehydrogenase Rattus norvegicus 50-53 24548858-9 2014 Colorectal cancer cells with RAD21 knockdown exhibited enhanced sensitivity to 5-fluorouracil, either alone or in combination with oxaliplatin. Fluorouracil 79-93 RAD21 cohesin complex component Homo sapiens 29-34 27390048-4 2016 METHODS: We developed the phenytoin-capecitabine interaction model on the assumption that fluorouracil (5-FU) inhibits cytochrome P450 (CYP) 2C9 synthesis in a concentration- dependent manner. Fluorouracil 90-102 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 119-144 27390048-4 2016 METHODS: We developed the phenytoin-capecitabine interaction model on the assumption that fluorouracil (5-FU) inhibits cytochrome P450 (CYP) 2C9 synthesis in a concentration- dependent manner. Fluorouracil 104-108 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 119-144 27390048-9 2016 The 50% inhibitory 5-FU concentration for CYP2C9 synthesis and the degradation rate constant of CYP2C9 were estimated to be 0.00310 ng/mL and 0.0768 day-1, respectively. Fluorouracil 19-23 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 42-48 27390048-9 2016 The 50% inhibitory 5-FU concentration for CYP2C9 synthesis and the degradation rate constant of CYP2C9 were estimated to be 0.00310 ng/mL and 0.0768 day-1, respectively. Fluorouracil 19-23 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 96-102 27338638-4 2016 By testing the synergistic effects of conventional therapeutics, BPTES combined with 5-fluorouracil (5-FU), an irreversible inhibitor of thymidylate synthase, significant effects were observed on cell growth arrest in NSCLC. Fluorouracil 85-99 thymidylate synthetase Homo sapiens 137-157 27338638-4 2016 By testing the synergistic effects of conventional therapeutics, BPTES combined with 5-fluorouracil (5-FU), an irreversible inhibitor of thymidylate synthase, significant effects were observed on cell growth arrest in NSCLC. Fluorouracil 101-105 thymidylate synthetase Homo sapiens 137-157 27280393-7 2016 Kmt2d depletion in KC/KPC cell lines also led to an increased response to the nucleoside analogue 5-fluorouracil, suggesting that lower levels of this methyltransferase may mediate the sensitivity of PDAC to particular treatments. Fluorouracil 98-112 lysine methyltransferase 2D Homo sapiens 0-5 24357147-6 2014 5-FU up-regulated the expression of Fas and immunogenic cell death markers in MB49 cells and cytotoxic T lymphocytes from mice receiving RAd-CD40L immunotherapy efficiently lysed 5-FU treated MB49 cells in a Fas ligand-dependent manner. Fluorouracil 0-4 CD40 ligand Mus musculus 141-146 24357147-6 2014 5-FU up-regulated the expression of Fas and immunogenic cell death markers in MB49 cells and cytotoxic T lymphocytes from mice receiving RAd-CD40L immunotherapy efficiently lysed 5-FU treated MB49 cells in a Fas ligand-dependent manner. Fluorouracil 179-183 CD40 ligand Mus musculus 141-146 27119506-4 2016 Lentiviral-mediated re-expression of miR-320c (representative member of the miR-320 family) inhibited HCT116 CRC growth and migration in vitro, sensitized CRC cells to 5-Fluorouracil (5-FU), and inhibited tumor formation in SCID mice. Fluorouracil 168-182 microRNA 320 Mus musculus 37-44 27119506-4 2016 Lentiviral-mediated re-expression of miR-320c (representative member of the miR-320 family) inhibited HCT116 CRC growth and migration in vitro, sensitized CRC cells to 5-Fluorouracil (5-FU), and inhibited tumor formation in SCID mice. Fluorouracil 184-188 microRNA 320 Mus musculus 37-44 24357147-8 2014 Collectively, these data suggest that RAd-CD40L gene therapy is a promising adjuvant treatment to 5-FU for the management of bladder cancer. Fluorouracil 98-102 CD40 ligand Mus musculus 42-47 24572701-10 2014 Inhibition of SphK1 also enhanced the sensitivity of colon cancer cells to 5-FU. Fluorouracil 75-79 sphingosine kinase 1 Homo sapiens 14-19 27144434-2 2016 Here, we evaluated the impact of the MEK5/ERK5 cascade in colon cancer cell sensitivity to 5-fluorouracil (5-FU). Fluorouracil 107-111 mitogen-activated protein kinase 7 Homo sapiens 42-46 27144434-4 2016 In colon cancer cells, 5-FU exposure impaired endogenous KRAS/MEK5/ERK5 expression and/or activation. Fluorouracil 23-27 mitogen-activated protein kinase 7 Homo sapiens 67-71 27144434-6 2016 Using genetic and pharmacological approaches, we showed that ERK5 inhibition increased caspase-3/7 activity and apoptosis following 5-FU exposure. Fluorouracil 132-136 mitogen-activated protein kinase 7 Homo sapiens 61-65 27144434-8 2016 In addition, ERK5 inhibition increased the response of HCT116 p53+/+ cells to 5-FU, but failed to sensitize HCT116 p53-/- cells to the cytotoxic effects of this chemotherapeutic agent, suggesting a p53-dependent axis mediating 5-FU sensitization. Fluorouracil 78-82 mitogen-activated protein kinase 7 Homo sapiens 13-17 24450514-1 2014 Thymidylate synthase (TS) is a target for pemetrexed and the prodrug 5-fluorouracil (5-FU) that inhibit the protein by binding at its active site. Fluorouracil 69-83 thymidylate synthetase Homo sapiens 0-20 27144434-10 2016 Collectively, our results suggest that ERK5-targeted inhibition provides a promising therapeutic approach to overcome resistance to 5-FU-based chemotherapy and improve colon cancer treatment. Fluorouracil 132-136 mitogen-activated protein kinase 7 Homo sapiens 39-43 27020656-9 2016 Mechanistically, paricalcitol and 5-FU had cooperated together to repress the expression of procancerous Wnt, beta-catenin, NF-kappaB, COX-2, iNOS, VEGF, and HSP-90 more, and to upregulate the expression of antitumorigenesis DKK-1 and CDNK-1A, compared with their monotherapies. Fluorouracil 34-38 catenin beta 1 Rattus norvegicus 110-122 27020656-9 2016 Mechanistically, paricalcitol and 5-FU had cooperated together to repress the expression of procancerous Wnt, beta-catenin, NF-kappaB, COX-2, iNOS, VEGF, and HSP-90 more, and to upregulate the expression of antitumorigenesis DKK-1 and CDNK-1A, compared with their monotherapies. Fluorouracil 34-38 vascular endothelial growth factor A Rattus norvegicus 148-152 26799587-8 2016 In addition, BDH2 or lncRNA TP73-AS1 knockdown enhanced the chemosensitivity of esophageal cancer cells to 5-FU and cisplatin. Fluorouracil 107-111 3-hydroxybutyrate dehydrogenase 2 Homo sapiens 13-17 24450514-1 2014 Thymidylate synthase (TS) is a target for pemetrexed and the prodrug 5-fluorouracil (5-FU) that inhibit the protein by binding at its active site. Fluorouracil 85-89 thymidylate synthetase Homo sapiens 0-20 24583651-0 2014 Toll-like receptor-5 agonist Entolimod broadens the therapeutic window of 5-fluorouracil by reducing its toxicity to normal tissues in mice. Fluorouracil 74-88 toll-like receptor 5 Mus musculus 0-20 27274438-5 2016 Orotate phosphoribosyltransferase (OPRT) is a key enzyme related to the first step activation of 5-fluorouracil (5-FU) for inhibiting RNA synthesis. Fluorouracil 97-111 uridine monophosphate synthetase Homo sapiens 0-33 27274438-5 2016 Orotate phosphoribosyltransferase (OPRT) is a key enzyme related to the first step activation of 5-fluorouracil (5-FU) for inhibiting RNA synthesis. Fluorouracil 97-111 uridine monophosphate synthetase Homo sapiens 35-39 27274438-5 2016 Orotate phosphoribosyltransferase (OPRT) is a key enzyme related to the first step activation of 5-fluorouracil (5-FU) for inhibiting RNA synthesis. Fluorouracil 113-117 uridine monophosphate synthetase Homo sapiens 0-33 27274438-5 2016 Orotate phosphoribosyltransferase (OPRT) is a key enzyme related to the first step activation of 5-fluorouracil (5-FU) for inhibiting RNA synthesis. Fluorouracil 113-117 uridine monophosphate synthetase Homo sapiens 35-39 27274438-7 2016 We examined the protein levels of 5-FU metabolism-related enzymes (TS, DPD, OPRT, and thymidine phosphorylase [TP]) in 14 cases RESULTS: High TS, DPD, OPRT, and TP expressions were seen in 28.6%, 71.4%, 85.7%, and 35.7% of patients, respectively. Fluorouracil 34-38 thymidylate synthetase Homo sapiens 67-69 27274438-7 2016 We examined the protein levels of 5-FU metabolism-related enzymes (TS, DPD, OPRT, and thymidine phosphorylase [TP]) in 14 cases RESULTS: High TS, DPD, OPRT, and TP expressions were seen in 28.6%, 71.4%, 85.7%, and 35.7% of patients, respectively. Fluorouracil 34-38 thymidylate synthetase Homo sapiens 133-135 27274438-7 2016 We examined the protein levels of 5-FU metabolism-related enzymes (TS, DPD, OPRT, and thymidine phosphorylase [TP]) in 14 cases RESULTS: High TS, DPD, OPRT, and TP expressions were seen in 28.6%, 71.4%, 85.7%, and 35.7% of patients, respectively. Fluorouracil 34-38 uridine monophosphate synthetase Homo sapiens 151-155 26908448-13 2016 ANXA11 level regulates LNM and 5-FU resistance of Hca-P via c-Jun pathway. Fluorouracil 31-35 annexin A11 Mus musculus 0-6 26998056-10 2016 miRNA levels increased with cancer progression, and lapatinib and 5-fluorouracil (5-FU; the active form of capecitabine) treatment increased the miRNA levels (specifically miR-210 and miR-221) in the treatment-resistant pancreatic cancer PANC-1 and MIA PaCa-2 cell lines. Fluorouracil 66-80 microRNA 221 Homo sapiens 184-191 26998056-10 2016 miRNA levels increased with cancer progression, and lapatinib and 5-fluorouracil (5-FU; the active form of capecitabine) treatment increased the miRNA levels (specifically miR-210 and miR-221) in the treatment-resistant pancreatic cancer PANC-1 and MIA PaCa-2 cell lines. Fluorouracil 82-86 microRNA 221 Homo sapiens 184-191 26453116-6 2016 HNRNPC expression was negatively correlated with OS of GC patients treated with 5FU-based drugs and with time to progression (TTP) of GC patients treated with CF regimen. Fluorouracil 80-83 heterogeneous nuclear ribonucleoprotein C Homo sapiens 0-6 26716512-6 2016 Treatment of breast cancer cells with 5-fluorouracil (5-FU) increased the expression of pro-apoptotic and anti-proliferative factor, BAX and p21 protein through phosphorylation of p53 and p38. Fluorouracil 38-52 transformation related protein 53, pseudogene Mus musculus 180-183 26716512-6 2016 Treatment of breast cancer cells with 5-fluorouracil (5-FU) increased the expression of pro-apoptotic and anti-proliferative factor, BAX and p21 protein through phosphorylation of p53 and p38. Fluorouracil 54-58 transformation related protein 53, pseudogene Mus musculus 180-183 24277474-0 2014 Thymidylate synthase expression and p21(WAF1)/p53 phenotype of colon cancers identify patients who may benefit from 5-fluorouracil based therapy. Fluorouracil 116-130 thymidylate synthetase Homo sapiens 0-20 24277474-2 2014 Here, we assessed the prognostic significance of TS expression in Astler-Coller stage B2 and C CRCs defined by a p21(WAF1)/p53 immunophenotype in patients subjected to 5-fluorouracil (5FU)-based adjuvant therapy. Fluorouracil 168-182 thymidylate synthetase Homo sapiens 49-51 24277474-2 2014 Here, we assessed the prognostic significance of TS expression in Astler-Coller stage B2 and C CRCs defined by a p21(WAF1)/p53 immunophenotype in patients subjected to 5-fluorouracil (5FU)-based adjuvant therapy. Fluorouracil 184-187 thymidylate synthetase Homo sapiens 49-51 24281197-1 2014 PURPOSE: The purpose of the study is to analyze the relationship between tumor thymidylate synthase (TS) mRNA expression levels and raltitrexed/pemetrexed/5-FU sensitivity. Fluorouracil 155-159 thymidylate synthetase Homo sapiens 79-99 24415354-0 2014 Thymidylate synthase polymorphism in sporadic colorectal and gastric cancer in Tunisian population: a predictive role in 5-fluorouracil based chemotherapy treatment. Fluorouracil 121-135 thymidylate synthetase Homo sapiens 0-20 26893678-5 2016 The inhibitory effect of DDP and 5-FU alone or combined with h-R3 on EC1 or EC9706 cell proliferation was detected using an MTT assay. Fluorouracil 33-37 Susceptibility to lysis by alloreactive natural killer cells Homo sapiens 69-72 24415354-2 2014 Because thymidylate synthase provides an effective prediction of chemotherapy treatment based on 5-fluorouracil, our interest in this study was focused on finding an eventual interaction between thymidylate synthase polymorphism and treatment of sporadic colorectal and gastric cancer. Fluorouracil 97-111 thymidylate synthetase Homo sapiens 8-28 24415354-2 2014 Because thymidylate synthase provides an effective prediction of chemotherapy treatment based on 5-fluorouracil, our interest in this study was focused on finding an eventual interaction between thymidylate synthase polymorphism and treatment of sporadic colorectal and gastric cancer. Fluorouracil 97-111 thymidylate synthetase Homo sapiens 195-215 24415354-7 2014 Furthermore, we found a correlation of thymidylate synthase polymorphism with the fluorouracil-based therapy regimes and also with preoperatory radiation in patients with colorectal cancer. Fluorouracil 82-94 thymidylate synthetase Homo sapiens 39-59 24447928-7 2014 The exposure of both cell lines to 5-FU significantly increased the intracellular levels of miR-145 and miR-34a in the 5-FU-sensitive DLD-1 cells, whereas the level of neither miR was elevated in the DLD-1/5FU cells. Fluorouracil 35-39 microRNA 145 Homo sapiens 92-99 24447928-7 2014 The exposure of both cell lines to 5-FU significantly increased the intracellular levels of miR-145 and miR-34a in the 5-FU-sensitive DLD-1 cells, whereas the level of neither miR was elevated in the DLD-1/5FU cells. Fluorouracil 35-39 myosin regulatory light chain interacting protein Homo sapiens 92-95 24447928-7 2014 The exposure of both cell lines to 5-FU significantly increased the intracellular levels of miR-145 and miR-34a in the 5-FU-sensitive DLD-1 cells, whereas the level of neither miR was elevated in the DLD-1/5FU cells. Fluorouracil 119-123 microRNA 145 Homo sapiens 92-99 24447928-7 2014 The exposure of both cell lines to 5-FU significantly increased the intracellular levels of miR-145 and miR-34a in the 5-FU-sensitive DLD-1 cells, whereas the level of neither miR was elevated in the DLD-1/5FU cells. Fluorouracil 119-123 myosin regulatory light chain interacting protein Homo sapiens 92-95 24447928-8 2014 Interestingly, the amount of miR-145 detected in the small MVs shed into the medium of the parental cells was reduced after the treatment with 5-FU. Fluorouracil 143-147 microRNA 145 Homo sapiens 29-36 24447928-11 2014 Thus, the intra- and extracellular miR-145 and -34a were closely associated with 5-FU resistance, and the resistance was in part due to the enhanced secretion of miR-145 and -34a via MVs, resulting in low intracellular levels of both miRNAs. Fluorouracil 81-85 microRNA 145 Homo sapiens 35-42 24447928-11 2014 Thus, the intra- and extracellular miR-145 and -34a were closely associated with 5-FU resistance, and the resistance was in part due to the enhanced secretion of miR-145 and -34a via MVs, resulting in low intracellular levels of both miRNAs. Fluorouracil 81-85 microRNA 145 Homo sapiens 162-169 24275137-5 2014 We showed that forced expression of miR-21 significantly inhibited apoptosis, enhanced cell proliferation, invasion, and colony formation ability, promoted G1/S cell cycle transition and increased the resistance of tumor cells to 5-FU and X radiation in HT-29 colon cancer cells. Fluorouracil 230-234 microRNA 21 Homo sapiens 36-42 26768731-10 2016 Moreover, they showed reduced apoptosis, increased proliferation and different response to 5-fluorouracil and oxaliplatin upon CRY1 and CRY2 ectopic expression. Fluorouracil 91-105 cryptochrome circadian regulator 1 Homo sapiens 127-131 24275137-6 2014 Furthermore, knockdown of miR-21 reversed these effects on HT-29 cells and increased the sensitivity of HT-29/5-FU to 5-FU chemotherapy. Fluorouracil 110-114 microRNA 21 Homo sapiens 26-32 24275137-6 2014 Furthermore, knockdown of miR-21 reversed these effects on HT-29 cells and increased the sensitivity of HT-29/5-FU to 5-FU chemotherapy. Fluorouracil 118-122 microRNA 21 Homo sapiens 26-32 24275137-8 2014 These results demonstrate that miR-21 may play an important role in the 5-FU resistance of colon cancer cells. Fluorouracil 72-76 microRNA 21 Homo sapiens 31-37 24100087-1 2014 BACKGROUND: 5-Fluorouracil (5-FU) is a cornerstone of chemotherapy for colorectal cancer (CRC), and the major targets of 5-FU are thymidylate synthase (TS), methylenetetrahydrofolate reductase (MTHFR), and reduced folate carrier 1 (RFC1). Fluorouracil 12-26 thymidylate synthetase Homo sapiens 152-154 27415661-3 2016 The aim of this study is to investigate whether miR-149 targets FOXM1 to regulate the 5-FU resistance of CRC. Fluorouracil 86-90 microRNA 149 Homo sapiens 48-55 27415661-5 2016 Also, the effects of miR-149 expression on the sensitivity of CRC cells to 5-FU were determined by gain- and loss-of-function assays. Fluorouracil 75-79 microRNA 149 Homo sapiens 21-28 27415661-8 2016 Re-expression of miR-149 could enhance the 5-FU sensitivity of 5-FU-resistant CRC cells by increasing 5-FU-inducing apoptosis, while downregulation of miR-149 could decrease the 5-FU sensitivity of parental CRC cells by decreasing 5-FU-inducing apoptosis. Fluorouracil 43-47 microRNA 149 Homo sapiens 17-24 27415661-8 2016 Re-expression of miR-149 could enhance the 5-FU sensitivity of 5-FU-resistant CRC cells by increasing 5-FU-inducing apoptosis, while downregulation of miR-149 could decrease the 5-FU sensitivity of parental CRC cells by decreasing 5-FU-inducing apoptosis. Fluorouracil 63-67 microRNA 149 Homo sapiens 17-24 27415661-8 2016 Re-expression of miR-149 could enhance the 5-FU sensitivity of 5-FU-resistant CRC cells by increasing 5-FU-inducing apoptosis, while downregulation of miR-149 could decrease the 5-FU sensitivity of parental CRC cells by decreasing 5-FU-inducing apoptosis. Fluorouracil 63-67 microRNA 149 Homo sapiens 17-24 27415661-8 2016 Re-expression of miR-149 could enhance the 5-FU sensitivity of 5-FU-resistant CRC cells by increasing 5-FU-inducing apoptosis, while downregulation of miR-149 could decrease the 5-FU sensitivity of parental CRC cells by decreasing 5-FU-inducing apoptosis. Fluorouracil 63-67 microRNA 149 Homo sapiens 17-24 24100087-1 2014 BACKGROUND: 5-Fluorouracil (5-FU) is a cornerstone of chemotherapy for colorectal cancer (CRC), and the major targets of 5-FU are thymidylate synthase (TS), methylenetetrahydrofolate reductase (MTHFR), and reduced folate carrier 1 (RFC1). Fluorouracil 28-32 thymidylate synthetase Homo sapiens 152-154 27415661-8 2016 Re-expression of miR-149 could enhance the 5-FU sensitivity of 5-FU-resistant CRC cells by increasing 5-FU-inducing apoptosis, while downregulation of miR-149 could decrease the 5-FU sensitivity of parental CRC cells by decreasing 5-FU-inducing apoptosis. Fluorouracil 63-67 microRNA 149 Homo sapiens 17-24 27415661-10 2016 The silencing of FOXM1 could mimic the effect of miR-149 upregulation on the 5-FU resistance of 5-FU-resistant CRC cells. Fluorouracil 77-81 microRNA 149 Homo sapiens 49-56 24100087-1 2014 BACKGROUND: 5-Fluorouracil (5-FU) is a cornerstone of chemotherapy for colorectal cancer (CRC), and the major targets of 5-FU are thymidylate synthase (TS), methylenetetrahydrofolate reductase (MTHFR), and reduced folate carrier 1 (RFC1). Fluorouracil 121-125 thymidylate synthetase Homo sapiens 130-150 27415661-10 2016 The silencing of FOXM1 could mimic the effect of miR-149 upregulation on the 5-FU resistance of 5-FU-resistant CRC cells. Fluorouracil 96-100 microRNA 149 Homo sapiens 49-56 24100087-1 2014 BACKGROUND: 5-Fluorouracil (5-FU) is a cornerstone of chemotherapy for colorectal cancer (CRC), and the major targets of 5-FU are thymidylate synthase (TS), methylenetetrahydrofolate reductase (MTHFR), and reduced folate carrier 1 (RFC1). Fluorouracil 121-125 thymidylate synthetase Homo sapiens 152-154 27415661-11 2016 Furthermore, the expression of miR-149 in the 5-FU-responding CRC tissues was significantly higher than that in the non-responding tissues and inversely correlated with FOXM1 mRNA level. Fluorouracil 46-50 microRNA 149 Homo sapiens 31-38 24052409-0 2014 Mahanine synergistically enhances cytotoxicity of 5-fluorouracil through ROS-mediated activation of PTEN and p53/p73 in colon carcinoma. Fluorouracil 50-64 phosphatase and tensin homolog Homo sapiens 100-104 27415661-12 2016 CONCLUSIONS: MiR-149 reverses the resistance of CRC cells to 5-FU by directly targeting FOXM1. Fluorouracil 61-65 microRNA 149 Homo sapiens 13-20 27415661-13 2016 Thus, targeting miR-149/FOXM1 signaling will be a potential strategy in the treatment of 5-FU-chemoresistant CRC. Fluorouracil 89-93 microRNA 149 Homo sapiens 16-23 24403450-2 2014 In the present study, we evaluated ERCC1 expression levels in uterine cervical adenocarcinoma cell lines to assess whether they are affected by treatment with cisplatin with and without 5-fluorouracil (5-FU). Fluorouracil 186-200 ERCC excision repair 1, endonuclease non-catalytic subunit Homo sapiens 35-40 24403450-2 2014 In the present study, we evaluated ERCC1 expression levels in uterine cervical adenocarcinoma cell lines to assess whether they are affected by treatment with cisplatin with and without 5-fluorouracil (5-FU). Fluorouracil 202-206 ERCC excision repair 1, endonuclease non-catalytic subunit Homo sapiens 35-40 24403450-6 2014 ERCC1 mRNA expression levels were investigated using quantitative RT-PCR following treatment with cisplatin with and without 5-FU. Fluorouracil 125-129 ERCC excision repair 1, endonuclease non-catalytic subunit Homo sapiens 0-5 24403450-9 2014 ERCC1 expression was significantly elevated by cisplatin treatment, which was reduced by co-administration of 5-FU in HCA-1, TCO-2 and HCA-1R cells. Fluorouracil 110-114 ERCC excision repair 1, endonuclease non-catalytic subunit Homo sapiens 0-5 24403450-11 2014 Co-administration of cisplatin and 5-FU revealed synergistic or additive effects through inhibition of ERCC1 expression in cervical adenocarcinoma cells. Fluorouracil 35-39 ERCC excision repair 1, endonuclease non-catalytic subunit Homo sapiens 103-108 24403450-12 2014 Therefore, it is possible that a combination therapy of cisplatin and 5-FU or 5-FU derivatives constitutes an ideal treatment regimen, from the ERCC1 inhibition point of view in cervical adenocarcinoma. Fluorouracil 70-74 ERCC excision repair 1, endonuclease non-catalytic subunit Homo sapiens 144-149 24403450-12 2014 Therefore, it is possible that a combination therapy of cisplatin and 5-FU or 5-FU derivatives constitutes an ideal treatment regimen, from the ERCC1 inhibition point of view in cervical adenocarcinoma. Fluorouracil 78-82 ERCC excision repair 1, endonuclease non-catalytic subunit Homo sapiens 144-149 24434574-10 2014 These data collectively suggest that Ad-mda-7 induced apoptosis despite Akt activation and that the combinatory antitumor effects with 5-FU were produced partly by downregulating the Ad-mda-7-induced Akt activation. Fluorouracil 135-139 interleukin 24 Homo sapiens 40-45 24434574-10 2014 These data collectively suggest that Ad-mda-7 induced apoptosis despite Akt activation and that the combinatory antitumor effects with 5-FU were produced partly by downregulating the Ad-mda-7-induced Akt activation. Fluorouracil 135-139 interleukin 24 Homo sapiens 186-191 24520224-0 2014 Combination of TRAP1 and ERCC1 Expression Predicts Clinical Outcomes in Metastatic Colorectal Cancer Treated with Oxaliplatin/5-Fluorouracil. Fluorouracil 126-140 ERCC excision repair 1, endonuclease non-catalytic subunit Homo sapiens 25-30 24520224-2 2014 Excision repair cross-complementation group 1 (ERCC1) expression levels in tumor tissues also predict clinical outcomes in metastatic CRC patients receiving combination oxaliplatin and 5-fluorouracil treatment. Fluorouracil 185-199 ERCC excision repair 1, endonuclease non-catalytic subunit Homo sapiens 0-45 24520224-2 2014 Excision repair cross-complementation group 1 (ERCC1) expression levels in tumor tissues also predict clinical outcomes in metastatic CRC patients receiving combination oxaliplatin and 5-fluorouracil treatment. Fluorouracil 185-199 ERCC excision repair 1, endonuclease non-catalytic subunit Homo sapiens 47-52 24520224-12 2014 CONCLUSION: The present study demonstrates that the combination of TRAP1 and ERCC1 expression predicts the survival of metastatic CRC patients who were treated with oxaliplatin/5-fluorouracil. Fluorouracil 177-191 ERCC excision repair 1, endonuclease non-catalytic subunit Homo sapiens 77-82 24170546-10 2014 Importantly, 5-FU treatment resulted in significantly increased migration and invasion, and targeting AXL using pharmacologic inhibition or RNA interference (RNAi) approaches suppressed basal and 5-FU-induced migration and invasion. Fluorouracil 196-200 AXL receptor tyrosine kinase Homo sapiens 102-105 23530500-6 2014 Furthermore, down-regulation of PRDX6 and PSMB7 enhanced SMMC-7721/5-FU cells to 5-FU sensitivity. Fluorouracil 67-71 proteasome 20S subunit beta 7 Homo sapiens 42-47 23530500-7 2014 CONCLUSIONS: Our study suggests that targeting drug resistant genes such as PRDX6 and PSMB7 could be a novel approach to overcome 5-FU resistance in HCC cells. Fluorouracil 130-134 proteasome 20S subunit beta 7 Homo sapiens 86-91 24190362-0 2014 Overexpression of human telomerase reverse transcriptase C-terminal polypeptide sensitizes HeLa cells to 5-fluorouracil-induced growth inhibition and apoptosis. Fluorouracil 105-119 telomerase reverse transcriptase Homo sapiens 24-56 26629940-4 2014 It suggested that, compared to the control, body weight gain, the ratio of ovarian wet weight to body weight, primary follicle numbers, and the levels of AMH were significantly decreased, while the concentration of E2 and FSH was heavily increased following 5-FU administration. Fluorouracil 258-262 anti-Mullerian hormone Rattus norvegicus 154-157 26629940-5 2014 In contrast, after coadministration of triptorelin with 5-FU, the ratio of ovarian wet weight to body weight and the levels of AMH were significantly increased, whereas the level of E2 and FSH was decreased significantly when compared with the 5-FU group. Fluorouracil 56-60 anti-Mullerian hormone Rattus norvegicus 127-130 26629940-6 2014 Furthermore, at indicated times, 5-FU led to the reduced Bcl-2 and NF-kappaB expression and increased Bax expression while triptorelin plus 5-FU increased Bcl-2 and NF-kappaB expression and decreased Bax expression. Fluorouracil 33-37 BCL2 associated X, apoptosis regulator Rattus norvegicus 102-105 24239965-0 2014 A complex interplay between PGC-1 co-activators and mTORC1 regulates hematopoietic recovery following 5-fluorouracil treatment. Fluorouracil 102-116 PPARG coactivator 1 alpha Sus scrofa 28-33 24239965-4 2014 Moreover, expression of PGC-1 family members, proteins that regulate mitochondrial biogenesis, in HSPCs following 5-fluorouracil treatment changes; also, these proteins play a stage specific role in hematopoietic recovery. Fluorouracil 114-128 PPARG coactivator 1 alpha Sus scrofa 24-29 24033642-7 2013 Comparable increases in RAD51 foci formation were observed after each combined treatment with cisplatin and either 3-aminobenzamide (3-AB) or 5-FU in three human esophageal cancer cell lines, TE11, TE14, and TE15. Fluorouracil 142-146 RAD51 recombinase Homo sapiens 24-29 26695693-7 2016 Overexpression of miR-1914* and -1915 in chemoresistant CRC cells reduced resistance to 5-FU and Oxaliplatin in vitro. Fluorouracil 88-92 microRNA 1914 Homo sapiens 18-26 27200415-1 2016 The objective of the study was to investigate the pharmacokinetics and efficacy of 5-FU entrapped pH-sensitive liposomal nanoparticles with surface-modified anti-epidermal growth factor receptor (EGFR) antibody (pHLNps-5-FU) delivery system. Fluorouracil 83-87 epidermal growth factor receptor Mus musculus 157-194 27200415-1 2016 The objective of the study was to investigate the pharmacokinetics and efficacy of 5-FU entrapped pH-sensitive liposomal nanoparticles with surface-modified anti-epidermal growth factor receptor (EGFR) antibody (pHLNps-5-FU) delivery system. Fluorouracil 83-87 epidermal growth factor receptor Mus musculus 196-200 27141384-1 2016 Thymidylate synthase (TS) is a tumor-associated enzyme critical for DNA replication and main 5"-fluorouracil (5"-FU) target. Fluorouracil 93-108 thymidylate synthetase Homo sapiens 0-20 27141384-1 2016 Thymidylate synthase (TS) is a tumor-associated enzyme critical for DNA replication and main 5"-fluorouracil (5"-FU) target. Fluorouracil 110-115 thymidylate synthetase Homo sapiens 0-20 30263026-2 2015 5-Fluorouracil, an anticancer agent clinically used against various cancers, including prostate cancer, inhibits DNA synthesis by binding TS. Fluorouracil 0-14 thymidylate synthetase Homo sapiens 138-140 26788158-7 2015 On the basis of the combination of interfering plasmid and 5-FU, the additional GH did not increase the incidence of liver metastases (P>0.05), but improved the weight loss of the mice (P<0.05) induced by the inhibition of GHR and toxicity of 5-FU. Fluorouracil 249-253 growth hormone Mus musculus 80-82 26572487-2 2015 Recently, murine Retn was found to be a possibly potential regulator of hematopoiesis in mice shown in the screening results of a set of gene chips which mapped the expression level of murine genes during regeneration of impaired bone marrow (BM) by 5-fluorouracil. Fluorouracil 250-264 resistin Mus musculus 17-21 26552750-4 2015 RESULTS: 5-Fluorouracil, oxaliplatin and SN-38 (the active metabolite of irinotecan), as well as cisplatin, methotrexate and vinblastine, each caused decreases in cell-surface CXCR4 and concomitant increases in CD26 on HT-29, T84, HRT-18, SW480 and SW620 CRC cell lines. Fluorouracil 9-23 dipeptidyl peptidase 4 Homo sapiens 211-215 26552750-7 2015 Orthotopic HT-29 xenografts treated with standard CRC chemotherapeutics 5-fluorouracil, irinotecan, or oxaliplatin showed dramatic increases in CD26 compared to untreated tumors. Fluorouracil 72-86 dipeptidyl peptidase 4 Homo sapiens 144-148 26552750-9 2015 Analysis of cancer-initiating cell CD44 and CD133 subsets revealed drug-dependent responses of CD26/CD44/CD133 populations, suggesting that the benefits of combining standard chemotherapies 5-fluoruracil and oxaliplatin may be derived from their complementary elimination of cell populations. Fluorouracil 190-203 dipeptidyl peptidase 4 Homo sapiens 95-99 26055341-0 2015 MicroRNA-197 influences 5-fluorouracil resistance via thymidylate synthase in colorectal cancer. Fluorouracil 24-38 thymidylate synthetase Homo sapiens 54-74 26416450-0 2015 Acquired resistance to 5-fluorouracil via HSP90/Src-mediated increase in thymidylate synthase expression in colon cancer. Fluorouracil 23-37 heat shock protein 90 alpha family class A member 1 Homo sapiens 42-47 26416450-0 2015 Acquired resistance to 5-fluorouracil via HSP90/Src-mediated increase in thymidylate synthase expression in colon cancer. Fluorouracil 23-37 thymidylate synthetase Homo sapiens 73-93 26416450-2 2015 The expression of thymidylate synthase (TYMS) has been reported to be associated with the resistance to 5-FU. Fluorouracil 104-108 thymidylate synthetase Homo sapiens 18-38 26416450-2 2015 The expression of thymidylate synthase (TYMS) has been reported to be associated with the resistance to 5-FU. Fluorouracil 104-108 thymidylate synthetase Homo sapiens 40-44 26416450-3 2015 Here, we demonstrate that the enhanced HSP90 function and subsequent activation of Src induce expression of TYMS and acquired resistance to 5-FU in colon cancer. Fluorouracil 140-144 heat shock protein 90 alpha family class A member 1 Homo sapiens 39-44 26416450-5 2015 HCT116/R, a HCT116 colon cancer cell subline carrying acquired resistance to 5-FU, showed increased expression and activation of HSP90"s client proteins and transcriptional up-regulation of TYMS. Fluorouracil 77-81 heat shock protein 90 alpha family class A member 1 Homo sapiens 129-134 26416450-5 2015 HCT116/R, a HCT116 colon cancer cell subline carrying acquired resistance to 5-FU, showed increased expression and activation of HSP90"s client proteins and transcriptional up-regulation of TYMS. Fluorouracil 77-81 thymidylate synthetase Homo sapiens 190-194 26416450-7 2015 Conversely, pharmacological blockade of HSP90 or Src in HCT116/R cells effectively suppressed the changes involved in 5-FU resistance in vitro and xenograft tumor growth, hematogenous spread, and metastatic tumor development in vivo. Fluorouracil 118-122 heat shock protein 90 alpha family class A member 1 Homo sapiens 40-45 26416450-8 2015 This study suggests a novel function of HSP90-Src pathway in regulation of TYMS expression and acquisition of 5-FU resistance. Fluorouracil 110-114 heat shock protein 90 alpha family class A member 1 Homo sapiens 40-45 25873048-1 2015 BACKGROUND: Thymidylate synthase (TS) is an enzyme involved in DNA synthesis, and it is a target for 5-fluorouracil. Fluorouracil 101-115 thymidylate synthetase Homo sapiens 12-32 25873048-1 2015 BACKGROUND: Thymidylate synthase (TS) is an enzyme involved in DNA synthesis, and it is a target for 5-fluorouracil. Fluorouracil 101-115 thymidylate synthetase Homo sapiens 34-36 26722420-0 2015 Correlations between expression levels of thymidylate synthase, thymidine phosphorylase and dihydropyrimidine dehydrogenase, and efficacy of 5-fluorouracil-based chemotherapy for advanced colorectal cancer. Fluorouracil 141-155 thymidylate synthetase Homo sapiens 42-62 26722420-6 2015 Therefore, TS, TP, and DPD mRNA levels appear to be suitable indicators of the efficacy of 5-FU-based chemotherapy and prognosis of CRC. Fluorouracil 91-95 thymidylate synthetase Homo sapiens 11-13 26368019-8 2015 Annexin V-PE/7-AAD staining indicates 5-Fu + Gyp could induce SW-480 cell apoptosis. Fluorouracil 38-42 annexin A5 Homo sapiens 0-9 26025778-4 2015 We have previously reported that use of low-dose arsenic (LDA) temporarily and reversibly suppresses p53 activation, thereby ameliorating normal tissue toxicity from exposure to 5-fluorouracil and X rays. Fluorouracil 178-192 transformation related protein 53, pseudogene Mus musculus 101-104 26205949-11 2015 Mechanistically, vitamin D3/5-FU co-therapy significantly decreased the expression of Wnt, beta-catenin, iNOS, COX-2 and HSP-90 and significantly increased the expression of DKK-1, TGF-beta1, TGF-betaR2, smad4 (P < 0.05), in comparison with their corresponding monotherapy groups. Fluorouracil 28-32 SMAD family member 4 Rattus norvegicus 204-209 26205949-12 2015 CONCLUSIONS: Vitamin D3 and 5-FU synergise together and exhibit better anticancer effects by modulating Wnt/beta-catenin pathway, TGF-beta1 signals, iNOS, COX-2 and HSP-90. Fluorouracil 28-32 catenin beta 1 Rattus norvegicus 108-120 26193446-8 2015 We conclude that SLC46A1/PCFT and SLC19A1/RFC-1 are associated with DFS of patients with colorectal cancer and hypothesize that poor response to 5-fluorouracil plus leucovorin therapy in some patients may be linked to low expression of these genes. Fluorouracil 145-159 solute carrier family 46 member 1 Homo sapiens 17-24 26193446-8 2015 We conclude that SLC46A1/PCFT and SLC19A1/RFC-1 are associated with DFS of patients with colorectal cancer and hypothesize that poor response to 5-fluorouracil plus leucovorin therapy in some patients may be linked to low expression of these genes. Fluorouracil 145-159 solute carrier family 46 member 1 Homo sapiens 25-29 26328013-0 2015 HOTAIR is a predictive and prognostic biomarker for patients with advanced gastric adenocarcinoma receiving fluorouracil and platinum combination chemotherapy. Fluorouracil 108-120 HOX transcript antisense RNA Homo sapiens 0-6 26328013-4 2015 This study aimed to evaluate the association of HOTAIR expression with the prognosis of patients with advanced gastric adenocarcinoma (GA) receiving fluorouracil and platinum based chemotherapy. Fluorouracil 149-161 HOX transcript antisense RNA Homo sapiens 48-54 26328013-5 2015 We examined the levels of HOTAIR in 168 GA samples using quantitative real-time PCR and analyzed its relationship with clinical features and prognosis of patients with advanced GA treated with fluorouracil and platinum based chemotherapy. Fluorouracil 193-205 HOX transcript antisense RNA Homo sapiens 26-32 26328013-8 2015 In conclusion, our results provide first evidence that HOTAIR may be served as a biomarker that predicts which patient with advanced GA will benefit from fluorouracil and platinum combination chemotherapy. Fluorouracil 154-166 HOX transcript antisense RNA Homo sapiens 55-61 25112781-1 2015 BACKGROUND: The efficacy of 5-fluorouracil (5FU)-based therapy, which remains the cornerstone of gastrointestinal cancer treatment, depends upon the expression of enzymes involved in pyrimidine metabolism, including thymidylate synthase (TS), dihydropyrimidine dehydrogenase (DPD), thymidine phosphorylase (TP), and orotate phosphoribosyltransferase (OPRT). Fluorouracil 28-42 thymidylate synthetase Homo sapiens 216-236 25112781-1 2015 BACKGROUND: The efficacy of 5-fluorouracil (5FU)-based therapy, which remains the cornerstone of gastrointestinal cancer treatment, depends upon the expression of enzymes involved in pyrimidine metabolism, including thymidylate synthase (TS), dihydropyrimidine dehydrogenase (DPD), thymidine phosphorylase (TP), and orotate phosphoribosyltransferase (OPRT). Fluorouracil 28-42 thymidylate synthetase Homo sapiens 238-240 25112781-1 2015 BACKGROUND: The efficacy of 5-fluorouracil (5FU)-based therapy, which remains the cornerstone of gastrointestinal cancer treatment, depends upon the expression of enzymes involved in pyrimidine metabolism, including thymidylate synthase (TS), dihydropyrimidine dehydrogenase (DPD), thymidine phosphorylase (TP), and orotate phosphoribosyltransferase (OPRT). Fluorouracil 28-42 uridine monophosphate synthetase Homo sapiens 316-349 25112781-1 2015 BACKGROUND: The efficacy of 5-fluorouracil (5FU)-based therapy, which remains the cornerstone of gastrointestinal cancer treatment, depends upon the expression of enzymes involved in pyrimidine metabolism, including thymidylate synthase (TS), dihydropyrimidine dehydrogenase (DPD), thymidine phosphorylase (TP), and orotate phosphoribosyltransferase (OPRT). Fluorouracil 28-42 uridine monophosphate synthetase Homo sapiens 351-355 25112781-1 2015 BACKGROUND: The efficacy of 5-fluorouracil (5FU)-based therapy, which remains the cornerstone of gastrointestinal cancer treatment, depends upon the expression of enzymes involved in pyrimidine metabolism, including thymidylate synthase (TS), dihydropyrimidine dehydrogenase (DPD), thymidine phosphorylase (TP), and orotate phosphoribosyltransferase (OPRT). Fluorouracil 44-47 thymidylate synthetase Homo sapiens 216-236 25112781-1 2015 BACKGROUND: The efficacy of 5-fluorouracil (5FU)-based therapy, which remains the cornerstone of gastrointestinal cancer treatment, depends upon the expression of enzymes involved in pyrimidine metabolism, including thymidylate synthase (TS), dihydropyrimidine dehydrogenase (DPD), thymidine phosphorylase (TP), and orotate phosphoribosyltransferase (OPRT). Fluorouracil 44-47 thymidylate synthetase Homo sapiens 238-240 25519757-7 2015 RESULTS: In the 5-FU/EP and 5-FU/EP/SRP groups, there was less PBF, greater breakdown of periodontal tissues and increased immunostaining for RANKL compared with the EP and EP/SRP groups. Fluorouracil 16-20 PTTG1 interacting protein Rattus norvegicus 63-66 25519757-7 2015 RESULTS: In the 5-FU/EP and 5-FU/EP/SRP groups, there was less PBF, greater breakdown of periodontal tissues and increased immunostaining for RANKL compared with the EP and EP/SRP groups. Fluorouracil 28-32 PTTG1 interacting protein Rattus norvegicus 63-66 25677905-1 2015 The most important cytotoxic drug namely, cyclophosphamide used in breast cancer along with epirubicin and 5-fluorouracil, is transported by ABCC transporters and detoxified by glutathione S-transferases (GSTs). Fluorouracil 107-121 glutathione S-transferase pi 1 Homo sapiens 205-209 25889180-8 2015 Whole genome transcriptomic analysis of liver samples of F1 generation zebrafish exposed to 0.01 mug/L and 1 mug/L 5-FU revealed dose-dependent increases in the number of differentially expressed genes, including up-regulation of several DNA-damage-responsive genes and oncogenes (i.e., jun, myca). Fluorouracil 115-119 MYC proto-oncogene, bHLH transcription factor a Danio rerio 292-296 25909168-0 2015 Epigenetic silencing of BCL6B inactivates p53 signaling and causes human hepatocellular carcinoma cell resist to 5-FU. Fluorouracil 113-117 BCL6B transcription repressor Homo sapiens 24-29 25909168-11 2015 Re-expression of BCL6B activated p53 signaling and sensitized HCC cells to 5-fluorouracil. Fluorouracil 75-89 BCL6B transcription repressor Homo sapiens 17-22 25951903-10 2015 Transfection of let-7b or let-7c combined with 5-FU inhibited proliferation and potentiated the antitumor efficacies of 5-FU at tolerated concentration. Fluorouracil 120-124 microRNA let-7c Homo sapiens 26-32 25951903-12 2015 Overexpression of let-7b and let-7c reduced Akt2 expression, and Akt2 inhibition enhanced the sensitivity to 5-FU by affecting apoptotic pathway. Fluorouracil 109-113 AKT serine/threonine kinase 2 Homo sapiens 65-69 25951903-14 2015 The dysregulation of let-7b and let-7c may be involved in chemoresistance of RCC cells to 5-FU by down-regulating Akt2. Fluorouracil 90-94 microRNA let-7c Homo sapiens 32-38 25951903-14 2015 The dysregulation of let-7b and let-7c may be involved in chemoresistance of RCC cells to 5-FU by down-regulating Akt2. Fluorouracil 90-94 AKT serine/threonine kinase 2 Homo sapiens 114-118 24033642-9 2013 Our findings suggested that the homologous recombinational repair pathway may be involved in the synergism between cisplatin and either 3-AB or 5-FU, and that 3-AB and 5-FU may similarly modify the cisplatin-induced DNA damage to types requiring the recruitment of RAD51 proteins for their repair. Fluorouracil 144-148 RAD51 recombinase Homo sapiens 265-270 24293316-3 2013 We show here that Doxorubicin, 5-Fluorouracil, Paclitaxel and Cisplatin treatments trigger, in various human cancer cell lines, an increase of netrin-1 expression which is accompanied by netrin-1 receptors increase. Fluorouracil 31-45 netrin 1 Homo sapiens 143-151 24293316-5 2013 We show that candidate drugs interfering with netrin-1/netrin-1 receptors interactions potentiate Doxorubicin, Cisplatin or 5-Fluorouracil-induced cancer cell death in vitro. Fluorouracil 124-138 netrin 1 Homo sapiens 46-54 24293316-5 2013 We show that candidate drugs interfering with netrin-1/netrin-1 receptors interactions potentiate Doxorubicin, Cisplatin or 5-Fluorouracil-induced cancer cell death in vitro. Fluorouracil 124-138 netrin 1 Homo sapiens 55-63 25337561-11 2013 The expressions of occludin and claudin-1, not ZO-1 protein expressions in 200 mg/kg 5-FU treated animals were significantly reduced compared to those of the control group or 100 mg/kg 5-FU group. Fluorouracil 85-89 claudin 1 Mus musculus 32-41 24100378-6 2013 In the presence of PBMCs, PSK augmented the inhibitory effects of 5-FU and 5"-DFUR on HCT116 cell proliferation. Fluorouracil 66-70 TAO kinase 2 Homo sapiens 26-29 24100378-11 2013 The present results propose the possibility that PSK induces PBMCs to express IFN-alpha which inhibits DPD expression, and consequently augments the antitumor effect of 5-FU or 5"-DFUR. Fluorouracil 169-173 TAO kinase 2 Homo sapiens 49-52 24211581-10 2013 Moreover, we found that 5-aza-2"-deoxycytidine-mediated or enforced up-regulation of BNIP3 in DLD-1 cells results in KRas-dependent resistance to 5-Fluorouracil. Fluorouracil 146-160 KRAS proto-oncogene, GTPase Homo sapiens 117-121 24372557-2 2015 Reverse-transcription polymerase chain reaction and Western blot analyses were employed to detect periostin expression in SW480 and HT-29 colon cancer cells treated with oxaliplatin or fluorouracil (5-FU). Fluorouracil 185-197 periostin Homo sapiens 98-107 23982118-8 2013 The exploratory pharmacokinetic/pharmacogenetic study showed that CYP2A6 variants (*4, *7, *9) are associated with a lower metabolic ratio of S-1 (exposure ratio of 5-fluorouracil to tegafur). Fluorouracil 165-179 cytochrome P450 family 2 subfamily A member 6 Homo sapiens 66-72 24372557-2 2015 Reverse-transcription polymerase chain reaction and Western blot analyses were employed to detect periostin expression in SW480 and HT-29 colon cancer cells treated with oxaliplatin or fluorouracil (5-FU). Fluorouracil 199-203 periostin Homo sapiens 98-107 24372557-5 2015 The results showed that treatment with oxaliplatin or 5-FU elevated both the mRNA and protein levels of periostin in SW480 and HT-29 cells. Fluorouracil 54-58 periostin Homo sapiens 104-113 23809767-3 2013 METHODS: NR4A2 was transfected into CRC cells to investigate its effects on chemo-resistance to 5-fluorouracil and oxaliplatin and chemotherapeutics-induced apoptosis. Fluorouracil 96-110 nuclear receptor subfamily 4, group A, member 2 Mus musculus 9-14 24200057-8 2013 RESULTS: The killing rates of docetaxel, epirubicin and fluorouracil on CD55(high) subgroup MCF-7 cells were much lower than on total MCF-7 cells. Fluorouracil 56-68 CD55 molecule (Cromer blood group) Homo sapiens 72-76 26137071-5 2015 Furthermore, exposure to 5-fluorouracil significantly increased the proportion of CD26+ cells in vitro. Fluorouracil 25-39 dipeptidyl peptidase 4 Homo sapiens 82-86 25933112-8 2015 Moreover, the decrease in AKT and S6 phosphorylation induced by 5-FU was effectively reversed by capsaicin, indicating that capsaicin inhibits 5-FU-induced autophagy by activating the phosphoinositide 3-kinase (PI3K)/protein kinase B (AKT)/mammalian target of rapamycin (mTOR) pathway in CCA cells. Fluorouracil 64-68 phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit delta Homo sapiens 184-209 25933112-8 2015 Moreover, the decrease in AKT and S6 phosphorylation induced by 5-FU was effectively reversed by capsaicin, indicating that capsaicin inhibits 5-FU-induced autophagy by activating the phosphoinositide 3-kinase (PI3K)/protein kinase B (AKT)/mammalian target of rapamycin (mTOR) pathway in CCA cells. Fluorouracil 64-68 protein tyrosine kinase 2 beta Homo sapiens 217-233 25933112-8 2015 Moreover, the decrease in AKT and S6 phosphorylation induced by 5-FU was effectively reversed by capsaicin, indicating that capsaicin inhibits 5-FU-induced autophagy by activating the phosphoinositide 3-kinase (PI3K)/protein kinase B (AKT)/mammalian target of rapamycin (mTOR) pathway in CCA cells. Fluorouracil 143-147 phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit delta Homo sapiens 184-209 25933112-8 2015 Moreover, the decrease in AKT and S6 phosphorylation induced by 5-FU was effectively reversed by capsaicin, indicating that capsaicin inhibits 5-FU-induced autophagy by activating the phosphoinositide 3-kinase (PI3K)/protein kinase B (AKT)/mammalian target of rapamycin (mTOR) pathway in CCA cells. Fluorouracil 143-147 protein tyrosine kinase 2 beta Homo sapiens 217-233 25995742-6 2015 RESULTS: It was noted that combined treatment of 5-FU + PUFAs on gastric carcinoma (MGC and SGC) cells produced a significant growth inhibitory action compared with either agent alone by inhibiting the production of TNF-alpha and VEGF and a simultaneous increase in the expression of LPL, PPAR-gamma, and C/EBP. Fluorouracil 49-53 lipoprotein lipase Homo sapiens 284-287 25906152-6 2015 5-FU treatment led to the formation of a z-VAD-resistant pro-caspase-8/RIP1/FADD complex, which was strongly stabilized by caspase-3 KO. Fluorouracil 0-4 receptor interacting serine/threonine kinase 1 Homo sapiens 71-75 25906152-6 2015 5-FU treatment led to the formation of a z-VAD-resistant pro-caspase-8/RIP1/FADD complex, which was strongly stabilized by caspase-3 KO. Fluorouracil 0-4 Fas associated via death domain Homo sapiens 76-80 23975242-1 2013 PURPOSE: Capecitabine (CAP), a prodrug, needs to be converted to 5-fluorouracil by several key enzymes, including thymidine phosphorylase (TP). Fluorouracil 65-79 thymidine phosphorylase Mus musculus 114-137 25886460-9 2015 In contrast, 5-FU enhanced formation of PGE2, LTB4 and mPGES expression, but suppressed LXA4 synthesis and COX-2 expression. Fluorouracil 13-17 prostaglandin E synthase Mus musculus 55-60 25227897-3 2015 MATERIAL AND METHODS: Maspin expression was assessed using immunohistochemistry on tissue microarrays obtained from 380 patients with stage II and III colorectal cancer randomized to adjuvant chemotherapy with fluorouracil and levamisole (5-FU/Lev) or to surgery only (control), with scores (0-300) based on presence (0-100) and intensity (0-3) of maspin expression. Fluorouracil 239-243 serpin family B member 5 Homo sapiens 22-28 25227897-10 2015 CONCLUSIONS: In patients with colon cancer a low nuclear maspin expression was an independent predictor of benefit from adjuvant chemotherapy with 5-FU/Lev. Fluorouracil 147-151 serpin family B member 5 Homo sapiens 57-63 23975242-1 2013 PURPOSE: Capecitabine (CAP), a prodrug, needs to be converted to 5-fluorouracil by several key enzymes, including thymidine phosphorylase (TP). Fluorouracil 65-79 thymidine phosphorylase Mus musculus 139-141 25861418-11 2015 Radioimmunoassay showed that mice treated with AHCC plus 5-FU had the highest serum levels of IL-2 and TNFalpha compared with the vehicle group and 5-FU group. Fluorouracil 57-61 interleukin 2 Mus musculus 94-98 23822592-9 2013 EGFR mAbs combined with oxaliplatin and an infusional 5-FU regimen was associated with significantly improved RR, PFS and OS as first-line treatment in KRAS wild-type mCRC. Fluorouracil 54-58 KRAS proto-oncogene, GTPase Homo sapiens 152-156 25888862-0 2015 Retraction note: Joint detection of ERCC1, TUBB3, and TYMS guidance selection of docetaxel, 5-fluorouracil and cisplatin (DDP) individual chemotherapy in advanced gastric cancer patients. Fluorouracil 92-106 thymidylate synthetase Homo sapiens 54-58 23355500-6 2013 Especially, Second generated dendrimer (G-2)/5-FU conjugates showed excellent in vivo antitumor as well as antiangiogenic activities evaluated by the embryo chorioallantoic membrane assay due to slow hydrolysis rate and the amount of 5-FU released. Fluorouracil 45-49 proline-rich coiled-coil 2A Mus musculus 40-43 24434920-1 2015 5-Fluorouracil (5-FU), the mainstay of solid tumor chemotherapy over the past 40 years, induces grade III-IV toxicities in up to 15% of patients with polymorphisms in the dihydropyrimidine dehydrogenase (DPYD), thymidylate synthase (TYMS), and methylenetetrahydrofolate reductase (MTHFR) genes. Fluorouracil 0-14 thymidylate synthetase Homo sapiens 211-231 24434920-1 2015 5-Fluorouracil (5-FU), the mainstay of solid tumor chemotherapy over the past 40 years, induces grade III-IV toxicities in up to 15% of patients with polymorphisms in the dihydropyrimidine dehydrogenase (DPYD), thymidylate synthase (TYMS), and methylenetetrahydrofolate reductase (MTHFR) genes. Fluorouracil 0-14 thymidylate synthetase Homo sapiens 233-237 24434920-1 2015 5-Fluorouracil (5-FU), the mainstay of solid tumor chemotherapy over the past 40 years, induces grade III-IV toxicities in up to 15% of patients with polymorphisms in the dihydropyrimidine dehydrogenase (DPYD), thymidylate synthase (TYMS), and methylenetetrahydrofolate reductase (MTHFR) genes. Fluorouracil 16-20 thymidylate synthetase Homo sapiens 211-231 23355500-6 2013 Especially, Second generated dendrimer (G-2)/5-FU conjugates showed excellent in vivo antitumor as well as antiangiogenic activities evaluated by the embryo chorioallantoic membrane assay due to slow hydrolysis rate and the amount of 5-FU released. Fluorouracil 234-238 proline-rich coiled-coil 2A Mus musculus 40-43 24434920-1 2015 5-Fluorouracil (5-FU), the mainstay of solid tumor chemotherapy over the past 40 years, induces grade III-IV toxicities in up to 15% of patients with polymorphisms in the dihydropyrimidine dehydrogenase (DPYD), thymidylate synthase (TYMS), and methylenetetrahydrofolate reductase (MTHFR) genes. Fluorouracil 16-20 thymidylate synthetase Homo sapiens 233-237 23960437-1 2013 Dihydropyrimidine dehydrogenase (DPYD) is an enzyme that regulates the rate-limiting step in pyrimidine metabolism, especially catabolism of fluorouracil, a chemotherapeutic agent for cancer. Fluorouracil 141-153 dihydropyrimidine dehydrogenase Homo sapiens 0-31 23960437-1 2013 Dihydropyrimidine dehydrogenase (DPYD) is an enzyme that regulates the rate-limiting step in pyrimidine metabolism, especially catabolism of fluorouracil, a chemotherapeutic agent for cancer. Fluorouracil 141-153 dihydropyrimidine dehydrogenase Homo sapiens 33-37 23894404-8 2013 CONCLUSION: The XPD and XRCC1 allelic variants may be prognostic markers for CRC patients receiving 5-FU based chemotherapy. Fluorouracil 100-104 X-ray repair cross complementing 1 Homo sapiens 24-29 23864778-4 2013 The influence of downregulation of CDX2 on MDR was assessed by measuring IC50 of SGC7901/DDP cells to cisplatin, doxorubicin, and 5-fluorouracil, rate of doxorubicin efflux, apoptosis, and cell cycle progression detected by flow cytometry. Fluorouracil 130-144 caudal type homeobox 2 Homo sapiens 35-39 25380796-7 2015 The results showed that the 5-FU + B. infantis group demonstrated a higher body weight and villus height, increased expression of PCNA, reduced expression of NF-kappaB and pro-inflammatory factors, and lower MPO concentration compared to the 5-FU group. Fluorouracil 28-32 myeloperoxidase Rattus norvegicus 208-211 23861589-1 2013 PURPOSE: To determine whether 5-fluorouracil (5-FU) sensitivity is associated with the mRNA expressions of thymidylate synthase (TS), dihydropyrimidine dehydrogenase (DPD), and thymidine phosphorylase (TP) in patients with hepatocellular carcinoma (HCC) treated with 5-FU-based transarterial chemoembolization (TACE). Fluorouracil 46-50 dihydropyrimidine dehydrogenase Homo sapiens 134-165 23861589-1 2013 PURPOSE: To determine whether 5-fluorouracil (5-FU) sensitivity is associated with the mRNA expressions of thymidylate synthase (TS), dihydropyrimidine dehydrogenase (DPD), and thymidine phosphorylase (TP) in patients with hepatocellular carcinoma (HCC) treated with 5-FU-based transarterial chemoembolization (TACE). Fluorouracil 46-50 dihydropyrimidine dehydrogenase Homo sapiens 167-170 23861589-1 2013 PURPOSE: To determine whether 5-fluorouracil (5-FU) sensitivity is associated with the mRNA expressions of thymidylate synthase (TS), dihydropyrimidine dehydrogenase (DPD), and thymidine phosphorylase (TP) in patients with hepatocellular carcinoma (HCC) treated with 5-FU-based transarterial chemoembolization (TACE). Fluorouracil 267-271 dihydropyrimidine dehydrogenase Homo sapiens 167-170 23861589-7 2013 CONCLUSION: DPD mRNA expression level was negatively correlated with the clinical outcomes of HCC patients treated with 5-FU-based TACE. Fluorouracil 120-124 dihydropyrimidine dehydrogenase Homo sapiens 12-15 23861589-8 2013 These results provide indirect evidence that high DPD mRNA expression is a predictive marker of treatment resistance for 5-FU. Fluorouracil 121-125 dihydropyrimidine dehydrogenase Homo sapiens 50-53 23575907-10 2013 Also, 2 dose-limiting toxicities occurred at DL2 at 300 mg/m(2), resulting in expansion of DL1 at 200 mg/m(2) 5-FU, the eventual MTD. Fluorouracil 110-114 delta like canonical Notch ligand 1 Homo sapiens 91-94 23588312-2 2013 The responses to 5-FU, with respect to both toxicity and efficacy, vary among racial groups, potentially because of variability in the activity levels of the enzyme dihydropyrimidine dehydrogenase (DPD, encoded by the DPYD gene). Fluorouracil 17-21 dihydropyrimidine dehydrogenase Homo sapiens 198-201 23588312-2 2013 The responses to 5-FU, with respect to both toxicity and efficacy, vary among racial groups, potentially because of variability in the activity levels of the enzyme dihydropyrimidine dehydrogenase (DPD, encoded by the DPYD gene). Fluorouracil 17-21 dihydropyrimidine dehydrogenase Homo sapiens 218-222 23588312-4 2013 The DPYD-Y186C variant was unique to individuals of African ancestry, and DPD activity was 46% lower in carriers as compared with noncarriers (279 +- 35 vs. 514 +- 168 pmol 5-FU min(-1) mg(-1); P = 0.00029). Fluorouracil 173-177 dihydropyrimidine dehydrogenase Homo sapiens 4-8 23588312-4 2013 The DPYD-Y186C variant was unique to individuals of African ancestry, and DPD activity was 46% lower in carriers as compared with noncarriers (279 +- 35 vs. 514 +- 168 pmol 5-FU min(-1) mg(-1); P = 0.00029). Fluorouracil 173-177 dihydropyrimidine dehydrogenase Homo sapiens 74-77 23852891-0 2013 Knockdown of PLA2G2A sensitizes gastric cancer cells to 5-FU in vitro. Fluorouracil 56-60 phospholipase A2 group IIA Homo sapiens 13-20 23852891-10 2013 The effects of 5-FU on PLA2G2A expression were determined in vitro. Fluorouracil 15-19 phospholipase A2 group IIA Homo sapiens 23-30 23852891-12 2013 PLA2G2A was overexpressed by transfection of full-long PLA2G2A cDNA in vitro, and the effects were evaluated on 5-FU sensitivity. Fluorouracil 112-116 phospholipase A2 group IIA Homo sapiens 0-7 23852891-15 2013 Silencing of PLA2G2A increased 5-FU killing in 5-FU-treated cells, and overexpression of PLA2G2A decreased 5-FU killing in 5-FU-treated cells. Fluorouracil 31-35 phospholipase A2 group IIA Homo sapiens 13-20 23852891-15 2013 Silencing of PLA2G2A increased 5-FU killing in 5-FU-treated cells, and overexpression of PLA2G2A decreased 5-FU killing in 5-FU-treated cells. Fluorouracil 47-51 phospholipase A2 group IIA Homo sapiens 13-20 23852891-15 2013 Silencing of PLA2G2A increased 5-FU killing in 5-FU-treated cells, and overexpression of PLA2G2A decreased 5-FU killing in 5-FU-treated cells. Fluorouracil 47-51 phospholipase A2 group IIA Homo sapiens 13-20 23852891-15 2013 Silencing of PLA2G2A increased 5-FU killing in 5-FU-treated cells, and overexpression of PLA2G2A decreased 5-FU killing in 5-FU-treated cells. Fluorouracil 47-51 phospholipase A2 group IIA Homo sapiens 13-20 23852891-16 2013 CONCLUSIONS: PLA2G2A was correlated with sensitivity to 5-FU. Fluorouracil 56-60 phospholipase A2 group IIA Homo sapiens 13-20 23852891-17 2013 Silencing of PLA2G2A was sensitive to 5-FU treatment. Fluorouracil 38-42 phospholipase A2 group IIA Homo sapiens 13-20 23730514-9 2013 For two patients, KRAS mutation status changed after application of neoadjuvant 5-FU radiochemotherapy. Fluorouracil 80-84 KRAS proto-oncogene, GTPase Homo sapiens 18-22 23730514-12 2013 CONCLUSIONS: So one can conclude that (I) KRAS mutations status may change after neoadjuvant 5-FU radiochemotherapy relevant for further therapeutic decisions; (II) MSI-H patients do not respond to neoadjuvant 5-FU radiochemotherapy. Fluorouracil 93-97 KRAS proto-oncogene, GTPase Homo sapiens 42-46 23661467-9 2013 Deficiencies in Nhp10 and CR combined with deficiencies in HR or PRR increased 5-FU sensitivity; however, combined deficiencies of HAT, HR, and PRR did not. Fluorouracil 79-83 Nhp10p Saccharomyces cerevisiae S288C 16-21 23315170-10 2013 The administration of PGE(2) or an EP4 agonist facilitated the recovery of HSPCs from 5-fluorouracil (5-FU)-induced myelosuppression, indicating a role for PGE(2)/EP4 signaling in this process. Fluorouracil 86-100 prostaglandin E receptor 4 (subtype EP4) Mus musculus 35-38 25873402-3 2015 Here we constructed a fluorouracil (5-Fu) resistant SW480 cell line (SW480/5-Fu) and discovered that miRNA miR-494 was down-regulated in the drug resistant cells compared with the parental cells. Fluorouracil 22-34 microRNA 494 Homo sapiens 107-114 25873402-3 2015 Here we constructed a fluorouracil (5-Fu) resistant SW480 cell line (SW480/5-Fu) and discovered that miRNA miR-494 was down-regulated in the drug resistant cells compared with the parental cells. Fluorouracil 36-40 microRNA 494 Homo sapiens 107-114 25873402-4 2015 miR-494 level was found to be correlated with 5-Fu sensitivity in colon cancer cells, and artificial alteration of miR-494 affects the sensitivity of colon cancer cell lines to 5-Fu. Fluorouracil 46-50 microRNA 494 Homo sapiens 0-7 25873402-4 2015 miR-494 level was found to be correlated with 5-Fu sensitivity in colon cancer cells, and artificial alteration of miR-494 affects the sensitivity of colon cancer cell lines to 5-Fu. Fluorouracil 177-181 microRNA 494 Homo sapiens 115-122 25873402-5 2015 miR-494 also promoted apoptosis of colon cancer cells at present of 5-Fu. Fluorouracil 68-72 microRNA 494 Homo sapiens 0-7 25873402-8 2015 Overexpression or knockdown of DPYD could attenuate miR-494 mediated 5-Fu sensitivity regulation, suggesting the dependence of DPYD regulation in miR-494 activity. Fluorouracil 69-73 microRNA 494 Homo sapiens 52-59 25873402-8 2015 Overexpression or knockdown of DPYD could attenuate miR-494 mediated 5-Fu sensitivity regulation, suggesting the dependence of DPYD regulation in miR-494 activity. Fluorouracil 69-73 microRNA 494 Homo sapiens 146-153 25873402-9 2015 miR-494 inhibited SW480/5-Fu derived xenograft tumors growth in vivo at present of 5-Fu. Fluorouracil 24-28 microRNA 494 Homo sapiens 0-7 25873402-9 2015 miR-494 inhibited SW480/5-Fu derived xenograft tumors growth in vivo at present of 5-Fu. Fluorouracil 83-87 microRNA 494 Homo sapiens 0-7 25873402-10 2015 Thus, we concluded that in colon cancer cells, tumor suppressor miR-494 enhanced 5-Fu sensitivity via regulation of DPYD expression. Fluorouracil 81-85 microRNA 494 Homo sapiens 64-71 25169655-6 2015 METHODS: CD44(high) /ESA(low), CD44(high) /ESA(high) and CD44(low) cells were FACS sorted from the HNSCC cell line LUC4, and 5-FU-induced apoptosis was analysed by Annexin V staining followed by flow cytometry analysis. Fluorouracil 125-129 annexin A5 Homo sapiens 164-173 25744837-9 2015 Compared with HT-29 cells, HT-29/5-FU cells showed remarkable reduction of cell proliferation and colony formation, higher expressions of TS and DPD, higher percentage of cells in the S phase, and stronger ability of resistance to apoptosis induced by 5-FU. Fluorouracil 33-37 thymidylate synthetase Homo sapiens 138-140 25544773-0 2015 Targeting the microRNA-21/AP1 axis by 5-fluorouracil and pirarubicin in human hepatocellular carcinoma. Fluorouracil 38-52 microRNA 21 Homo sapiens 14-25 25544773-3 2015 Here, we investigated the correlation between microRNA-21 expression and hepatic arterial infusion chemotherapy with 5-fluorouracil and pirarubicin (HAIC) for hepatocellular carcinoma (HCC). Fluorouracil 117-131 microRNA 21 Homo sapiens 46-57 25502560-5 2015 When the level of miR-96 increased, the expression of the anti-apoptotic regulator XIAP and p53 stability regulator UBE2N decreased, resulting in increased apoptosis and growth inhibition following 5-FU exposure. Fluorouracil 198-202 ubiquitin conjugating enzyme E2 N Homo sapiens 116-121 25351347-8 2015 mRNA and protein expression levels of HIF-2alpha, ABCG2 and Oct-4 were significantly lower in the celecoxib and 5-FU/celecoxib combination groups (P<0.01) compared with those of the hypoxia control and 5-FU groups. Fluorouracil 112-116 endothelial PAS domain protein 1 Homo sapiens 38-48 25351347-8 2015 mRNA and protein expression levels of HIF-2alpha, ABCG2 and Oct-4 were significantly lower in the celecoxib and 5-FU/celecoxib combination groups (P<0.01) compared with those of the hypoxia control and 5-FU groups. Fluorouracil 112-116 POU class 5 homeobox 1 Homo sapiens 60-65 25351347-8 2015 mRNA and protein expression levels of HIF-2alpha, ABCG2 and Oct-4 were significantly lower in the celecoxib and 5-FU/celecoxib combination groups (P<0.01) compared with those of the hypoxia control and 5-FU groups. Fluorouracil 205-209 endothelial PAS domain protein 1 Homo sapiens 38-48 23315170-10 2013 The administration of PGE(2) or an EP4 agonist facilitated the recovery of HSPCs from 5-fluorouracil (5-FU)-induced myelosuppression, indicating a role for PGE(2)/EP4 signaling in this process. Fluorouracil 86-100 prostaglandin E receptor 4 (subtype EP4) Mus musculus 163-166 23315170-10 2013 The administration of PGE(2) or an EP4 agonist facilitated the recovery of HSPCs from 5-fluorouracil (5-FU)-induced myelosuppression, indicating a role for PGE(2)/EP4 signaling in this process. Fluorouracil 102-106 prostaglandin E receptor 4 (subtype EP4) Mus musculus 35-38 23433850-3 2013 Our previous studies showed the protective effect of recombinant murine IL-1Ra on hematopoiesis in mice after treatment with chemotherapeutic agent 5-fluorouracil. Fluorouracil 148-162 interleukin 1 receptor antagonist Mus musculus 72-78 25550184-4 2015 Here we assumed that DCN silencing cells increase chemosusceptibility to S-1, consisted of tegafur, prodrug of 5-fluorouracil. Fluorouracil 111-125 decorin Homo sapiens 21-24 23519428-9 2013 HBV replication or 5-fluorouracil-induced cell death was suppressed by treatment of IFN-lambda or IL-22 in an IL-10RB K47E-independent manner. Fluorouracil 19-33 interleukin 22 Homo sapiens 98-103 24133626-2 2013 shRNA-mediated PDE3B depletion in CDDP-resistant cells derived from SCC cells and Hela cells and induced CDDP sensitivity and inhibited tumor growth with elevated cyclic GMP induction resulting in upregulation of the multidrug-resistant molecule, but this did not occur in the 5-fluorouracil-resistant hepatocellular carcinoma cell lines. Fluorouracil 277-291 phosphodiesterase 3B Homo sapiens 15-20 25973304-11 2015 BCL6B activated P53 signaling and induced apoptosis, Re-expression of BCL6B sensitized RKO and HT29 cells to 5-fluorouracil. Fluorouracil 109-123 BCL6B transcription repressor Homo sapiens 0-5 25973304-11 2015 BCL6B activated P53 signaling and induced apoptosis, Re-expression of BCL6B sensitized RKO and HT29 cells to 5-fluorouracil. Fluorouracil 109-123 BCL6B transcription repressor Homo sapiens 70-75 25524944-9 2015 Based on TS-targeted drug use status, TS expression was significantly associated with OS in pemetrexed (HR=0.42) and 5-Fluorouracil subgroups (HR=0.34), but not in no TS-targeted drug subgroup. Fluorouracil 117-131 thymidylate synthetase Homo sapiens 38-40 23420099-5 2013 mRNA levels of four transporters, SLC22A2, SLC23A2, ABCB1 and ABCC2, two DNA repair-related enzymes, Rad51 and MSH2, and one metabolic enzyme, dihydropyrimidine dehydrogenase (DPYD), showed a strong correlation ( r >0.7) with IC(50) values for 5-FU. Fluorouracil 247-251 dihydropyrimidine dehydrogenase Homo sapiens 143-174 26237679-2 2015 Here we show that Cdk5-depleted (Cdk5-shRNA) HeLa cells show higher sensitivity to S-phase irradiation, chronic hydroxyurea exposure, and 5-fluorouracil and 6-thioguanine treatment, with hydroxyurea and IR sensitivity also seen in Cdk5-depleted U2OS cells. Fluorouracil 138-152 cyclin dependent kinase 5 Homo sapiens 18-22 23420099-7 2013 Gimeracil, a DPYD inhibitor, enhanced the sensitivity of some cells to 5-FU but decreased the sensitivity of all the cells to CDDP. Fluorouracil 71-75 dihydropyrimidine dehydrogenase Homo sapiens 13-17 26237679-2 2015 Here we show that Cdk5-depleted (Cdk5-shRNA) HeLa cells show higher sensitivity to S-phase irradiation, chronic hydroxyurea exposure, and 5-fluorouracil and 6-thioguanine treatment, with hydroxyurea and IR sensitivity also seen in Cdk5-depleted U2OS cells. Fluorouracil 138-152 cyclin dependent kinase 5 Homo sapiens 33-37 26237679-2 2015 Here we show that Cdk5-depleted (Cdk5-shRNA) HeLa cells show higher sensitivity to S-phase irradiation, chronic hydroxyurea exposure, and 5-fluorouracil and 6-thioguanine treatment, with hydroxyurea and IR sensitivity also seen in Cdk5-depleted U2OS cells. Fluorouracil 138-152 cyclin dependent kinase 5 Homo sapiens 33-37 23420099-9 2013 In conclusion, mRNA levels of SLC22A2, SLC23A2, ABCB1, ABCC2, Rad51, MSH2 and DPYD were confirmed to be strongly correlated with IC50 values for 5-FU, and mRNA levels of ABCC2, MSH2 and DPYD were confirmed to be strongly correlated with IC(50) values for CDDP. Fluorouracil 145-149 ATP binding cassette subfamily C member 2 Homo sapiens 55-60 25643258-6 2015 Our study suggests that PHA- 767491 could enhance the efficacy of 5-FU by inhibiting Chk1 phosphorylation and down-regulating Mcl1 expression through inhibition of Cdc7 and Cdk9, thus combinational administration of PHA-767491 with 5-FU could be potentially beneficial to patients with advanced and resistant HCC. Fluorouracil 66-70 MCL1 apoptosis regulator, BCL2 family member Homo sapiens 126-130 23420099-9 2013 In conclusion, mRNA levels of SLC22A2, SLC23A2, ABCB1, ABCC2, Rad51, MSH2 and DPYD were confirmed to be strongly correlated with IC50 values for 5-FU, and mRNA levels of ABCC2, MSH2 and DPYD were confirmed to be strongly correlated with IC(50) values for CDDP. Fluorouracil 145-149 RAD51 recombinase Homo sapiens 62-67 23420099-9 2013 In conclusion, mRNA levels of SLC22A2, SLC23A2, ABCB1, ABCC2, Rad51, MSH2 and DPYD were confirmed to be strongly correlated with IC50 values for 5-FU, and mRNA levels of ABCC2, MSH2 and DPYD were confirmed to be strongly correlated with IC(50) values for CDDP. Fluorouracil 145-149 dihydropyrimidine dehydrogenase Homo sapiens 78-82 23420099-9 2013 In conclusion, mRNA levels of SLC22A2, SLC23A2, ABCB1, ABCC2, Rad51, MSH2 and DPYD were confirmed to be strongly correlated with IC50 values for 5-FU, and mRNA levels of ABCC2, MSH2 and DPYD were confirmed to be strongly correlated with IC(50) values for CDDP. Fluorouracil 145-149 ATP binding cassette subfamily C member 2 Homo sapiens 170-175 23420099-9 2013 In conclusion, mRNA levels of SLC22A2, SLC23A2, ABCB1, ABCC2, Rad51, MSH2 and DPYD were confirmed to be strongly correlated with IC50 values for 5-FU, and mRNA levels of ABCC2, MSH2 and DPYD were confirmed to be strongly correlated with IC(50) values for CDDP. Fluorouracil 145-149 dihydropyrimidine dehydrogenase Homo sapiens 186-190 23335937-6 2012 This is the first report in Spain of a case of 5-FU-induced lethal toxicity associated with a genetic defect that results in the complete loss of the DPD enzyme. Fluorouracil 47-51 dihydropyrimidine dehydrogenase Homo sapiens 150-153 25633488-4 2015 He had been previously treated by topical 5-fluorouracil for an adjacent microinvasive squamous cell carcinoma (SCC), with complete clinical response. Fluorouracil 42-56 serpin family B member 3 Homo sapiens 112-115 25466507-8 2015 Three chemotherapeutic agents with different mechanism of action (5-fluorouracil, bortezomib and paclitaxel) significantly induced GCNT3 expression in several cancer cells, being observed the correlation between antitumour action and GCNT3 modulation, whereas this gene was not modulated in cells that do not respond to treatment. Fluorouracil 66-80 glucosaminyl (N-acetyl) transferase 3, mucin type Homo sapiens 131-136 25466507-8 2015 Three chemotherapeutic agents with different mechanism of action (5-fluorouracil, bortezomib and paclitaxel) significantly induced GCNT3 expression in several cancer cells, being observed the correlation between antitumour action and GCNT3 modulation, whereas this gene was not modulated in cells that do not respond to treatment. Fluorouracil 66-80 glucosaminyl (N-acetyl) transferase 3, mucin type Homo sapiens 234-239 22454320-2 2013 Response to 5-FU treatment is variable with 10-30% of patients experiencing serious toxicity partly explained by reduced activity of dihydropyrimidine dehydrogenase (DPD). Fluorouracil 12-16 dihydropyrimidine dehydrogenase Homo sapiens 133-164 22454320-2 2013 Response to 5-FU treatment is variable with 10-30% of patients experiencing serious toxicity partly explained by reduced activity of dihydropyrimidine dehydrogenase (DPD). Fluorouracil 12-16 dihydropyrimidine dehydrogenase Homo sapiens 166-169 22454320-12 2013 The present method merges the analysis of 5-FU pharmacokinetics and DPD activity into a single assay representing a valuable tool to improve the efficacy and safety of 5-FU-based chemotherapy. Fluorouracil 168-172 dihydropyrimidine dehydrogenase Homo sapiens 68-71 23202296-6 2013 Accordingly, Gem and 5FU exerted higher antitumor effects when tumors were established in Nlrp3(-/-) or Casp1(-/-) mice or wild-type mice treated with interleukin-1 receptor antagonist (IL-1Ra). Fluorouracil 21-24 interleukin 1 receptor antagonist Mus musculus 151-184 23202296-6 2013 Accordingly, Gem and 5FU exerted higher antitumor effects when tumors were established in Nlrp3(-/-) or Casp1(-/-) mice or wild-type mice treated with interleukin-1 receptor antagonist (IL-1Ra). Fluorouracil 21-24 interleukin 1 receptor antagonist Mus musculus 186-192 23555026-9 2013 These results suggest that combining ISC-4 and cetuximab should be explored in patients with 5-FU-resistant colon cancer harboring wild-type KRAS. Fluorouracil 93-97 KRAS proto-oncogene, GTPase Homo sapiens 141-145 23441212-5 2013 5-FU treatment could lead to the conversion of LC3 I/II, the up-regulation of Beclin-1, the down-regulation of p62 and the formation of acidic vesicular organelles (AVOs) in A549 cells. Fluorouracil 0-4 beclin 1 Homo sapiens 78-86 23441212-5 2013 5-FU treatment could lead to the conversion of LC3 I/II, the up-regulation of Beclin-1, the down-regulation of p62 and the formation of acidic vesicular organelles (AVOs) in A549 cells. Fluorouracil 0-4 nucleoporin 62 Homo sapiens 111-114 23441212-7 2013 Furthermore, the inhibition of autophagy also stimulated ROS formation and scavenging of ROS by antioxidant NAC inhibited caspase-3 activity, prevented the release of cyt-c from mitochondria and eventually rescued cancer cells from 5-FU-mediated apoptosis. Fluorouracil 232-236 X-linked Kx blood group Homo sapiens 108-111 22322955-2 2012 We investigated the clinical significance of miR-10b and its involvement in chemotherapeutic resistance to 5-fluorouracil (5-FU), which is a key component of common chemotherapy regimens in colorectal cancer. Fluorouracil 123-127 microRNA 10b Homo sapiens 45-52 22322955-4 2012 We also investigated the chemotherapeutic sensitivity to 5-FU in miR-10b-overexpressing colorectal cancer cells. Fluorouracil 57-61 microRNA 10b Homo sapiens 65-72 22322955-10 2012 Moreover, the expression of miR-10b is a potential indicator of chemosensitivity to the common 5-FU-based chemotherapy regimen. Fluorouracil 95-99 microRNA 10b Homo sapiens 28-35 22993328-7 2012 RESULTS: The frequency of cells that were capable of initiating spheres was higher in 5-FU-pre treated cells, which also overexpressed stem cell marker genes, OCT4 and NANOG. Fluorouracil 86-90 Nanog homeobox Homo sapiens 168-173 22480411-1 2012 OBJECTIVE: Levels of 5-FU metabolic or related enzymes, particularly thymidine phosphorylase (TP) and dihydropyrimidine dehydrogenase (DPD), have been investigated in various cancer types, including uterine cervical cancer. Fluorouracil 21-25 dihydropyrimidine dehydrogenase Homo sapiens 135-138 24647007-3 2015 The few proven genetic biomarkers of 5-FU toxicity are rare variants and polymorphisms, respectively, at candidate loci dihydropyrimidine dehydrogenase (DPYD) and thymidylate synthase (TYMS). Fluorouracil 37-41 thymidylate synthetase Homo sapiens 163-183 24647007-3 2015 The few proven genetic biomarkers of 5-FU toxicity are rare variants and polymorphisms, respectively, at candidate loci dihydropyrimidine dehydrogenase (DPYD) and thymidylate synthase (TYMS). Fluorouracil 37-41 thymidylate synthetase Homo sapiens 185-189 25310623-5 2015 5-FU treatment induced DNA damage and activation of ataxia telangiectasia mutated (ATM) and Chk1, leading to S-phase arrest, and Chk1 inhibition using SB218078 reduced S-phase arrest and increased apoptosis in the presence of 5-FU. Fluorouracil 0-4 ATM serine/threonine kinase Homo sapiens 52-81 25310623-5 2015 5-FU treatment induced DNA damage and activation of ataxia telangiectasia mutated (ATM) and Chk1, leading to S-phase arrest, and Chk1 inhibition using SB218078 reduced S-phase arrest and increased apoptosis in the presence of 5-FU. Fluorouracil 0-4 ATM serine/threonine kinase Homo sapiens 83-86 25333998-10 2015 Taken together, this is the first report that the combination of SNX-2112 with 5-FU exhibited antagonistic effect in esophageal cancer cells by affecting growth inhibition, cell cycle, apoptosis, and Hsp90 client proteins, suggesting that care is required in the clinical application of combined SNX-2112 and 5-FU. Fluorouracil 79-83 heat shock protein 90 alpha family class A member 1 Homo sapiens 200-205 22641663-1 2012 AIM: The activity of the widely used anticancer drug 5-fluorouracil (5-FU) is determined by the presence of several enzymes, including dihydropyrimidine dehydrogenase (DPD), orotate phosphoribosyl transferase (OPRT), and thymidylate synthase (TS). Fluorouracil 53-67 dihydropyrimidine dehydrogenase Homo sapiens 135-166 22641663-1 2012 AIM: The activity of the widely used anticancer drug 5-fluorouracil (5-FU) is determined by the presence of several enzymes, including dihydropyrimidine dehydrogenase (DPD), orotate phosphoribosyl transferase (OPRT), and thymidylate synthase (TS). Fluorouracil 53-67 dihydropyrimidine dehydrogenase Homo sapiens 168-171 22641663-1 2012 AIM: The activity of the widely used anticancer drug 5-fluorouracil (5-FU) is determined by the presence of several enzymes, including dihydropyrimidine dehydrogenase (DPD), orotate phosphoribosyl transferase (OPRT), and thymidylate synthase (TS). Fluorouracil 69-73 dihydropyrimidine dehydrogenase Homo sapiens 135-166 22641663-1 2012 AIM: The activity of the widely used anticancer drug 5-fluorouracil (5-FU) is determined by the presence of several enzymes, including dihydropyrimidine dehydrogenase (DPD), orotate phosphoribosyl transferase (OPRT), and thymidylate synthase (TS). Fluorouracil 69-73 dihydropyrimidine dehydrogenase Homo sapiens 168-171 22020693-2 2012 5-FU competes with the natural occurring pyrimidine uracil (Ura) as a substrate for dihydropyrimidine dehydrogenase (DPD; enzyme commission number 1.3.1.2). Fluorouracil 0-4 dihydropyrimidine dehydrogenase Homo sapiens 84-115 22020693-2 2012 5-FU competes with the natural occurring pyrimidine uracil (Ura) as a substrate for dihydropyrimidine dehydrogenase (DPD; enzyme commission number 1.3.1.2). Fluorouracil 0-4 dihydropyrimidine dehydrogenase Homo sapiens 117-120 22580644-8 2012 CONCLUSIONS: This study is first to report that the XRCC1 and XRCC3 gene polymorphisms are useful as a surrogate marker of clinical outcome in colorectal cancer with 5-FU/oxaliplatin combination chemotherapy in the Chinese population. Fluorouracil 166-170 X-ray repair cross complementing 1 Homo sapiens 52-57 22580644-8 2012 CONCLUSIONS: This study is first to report that the XRCC1 and XRCC3 gene polymorphisms are useful as a surrogate marker of clinical outcome in colorectal cancer with 5-FU/oxaliplatin combination chemotherapy in the Chinese population. Fluorouracil 166-170 X-ray repair cross complementing 3 Homo sapiens 62-67 22736131-13 2012 CONCLUSIONS: Triplets regimens (epirubicin, platins and fluorouracil) show benefit on disease-free survival for the stage III( gastric cancer patients staged by TNM staging 2010 edition. Fluorouracil 56-68 teneurin transmembrane protein 1 Homo sapiens 161-164 22522606-12 2012 But CD4(+) T cells also decreased in spleen cells of tumor-bearing mice by alone 5-FU treated, splenic NK cell and CTL activity also degraded, while CD4(+) T cells and splenic NK cell and CTL activity significantly increased by BLTA treated. Fluorouracil 81-85 CD4 antigen Mus musculus 4-7 25468199-4 2015 RESULTS AND CONCLUSION: Among 5-FU target enzymes, TS was the only one that showed a significant difference in the level of gene expression between the high and low gene expression groups, for both disease-free survival (DFS) and overall survival (OS), when patients were divided according to median values; 5-year DFS rates in high/low TS gene expression were 60.4% and 72.6%, respectively (p=0.050), 5-year OS rates were 78.1% and 88.6%, respectively (p=0.011). Fluorouracil 30-34 thymidylate synthetase Homo sapiens 51-53 25352209-0 2015 Knockdown of Merm1/Wbscr22 attenuates sensitivity of H460 non-small cell lung cancer cells to SN-38 and 5-FU without alteration to p53 expression levels. Fluorouracil 104-108 BUD23 rRNA methyltransferase and ribosome maturation factor Homo sapiens 13-18 25352209-0 2015 Knockdown of Merm1/Wbscr22 attenuates sensitivity of H460 non-small cell lung cancer cells to SN-38 and 5-FU without alteration to p53 expression levels. Fluorouracil 104-108 BUD23 rRNA methyltransferase and ribosome maturation factor Homo sapiens 19-26 25352209-7 2015 Downregulation of Merm1/Wbscr22 did not affect H1299 sensitivity to any of the six antitumor agents, whereas attenuated H460 sensitivity to SN-38 and 5-FU, without significant alteration in p53 at both mRNA and protein levels, was identified. Fluorouracil 150-154 BUD23 rRNA methyltransferase and ribosome maturation factor Homo sapiens 18-23 25352209-11 2015 In conclusion, shRNA-mediated knockdown of Merm1/Wbscr22 attenuates H460 sensitivity to SN-38 and 5-FU, suggesting Merm1/Wbscr22 is involved in chemosensitivity to SN-38 and 5-FU in H460 cells. Fluorouracil 98-102 BUD23 rRNA methyltransferase and ribosome maturation factor Homo sapiens 43-48 25352209-11 2015 In conclusion, shRNA-mediated knockdown of Merm1/Wbscr22 attenuates H460 sensitivity to SN-38 and 5-FU, suggesting Merm1/Wbscr22 is involved in chemosensitivity to SN-38 and 5-FU in H460 cells. Fluorouracil 98-102 BUD23 rRNA methyltransferase and ribosome maturation factor Homo sapiens 49-56 25352209-11 2015 In conclusion, shRNA-mediated knockdown of Merm1/Wbscr22 attenuates H460 sensitivity to SN-38 and 5-FU, suggesting Merm1/Wbscr22 is involved in chemosensitivity to SN-38 and 5-FU in H460 cells. Fluorouracil 98-102 BUD23 rRNA methyltransferase and ribosome maturation factor Homo sapiens 115-120 25352209-11 2015 In conclusion, shRNA-mediated knockdown of Merm1/Wbscr22 attenuates H460 sensitivity to SN-38 and 5-FU, suggesting Merm1/Wbscr22 is involved in chemosensitivity to SN-38 and 5-FU in H460 cells. Fluorouracil 98-102 BUD23 rRNA methyltransferase and ribosome maturation factor Homo sapiens 121-128 25352209-11 2015 In conclusion, shRNA-mediated knockdown of Merm1/Wbscr22 attenuates H460 sensitivity to SN-38 and 5-FU, suggesting Merm1/Wbscr22 is involved in chemosensitivity to SN-38 and 5-FU in H460 cells. Fluorouracil 174-178 BUD23 rRNA methyltransferase and ribosome maturation factor Homo sapiens 43-48 25352209-11 2015 In conclusion, shRNA-mediated knockdown of Merm1/Wbscr22 attenuates H460 sensitivity to SN-38 and 5-FU, suggesting Merm1/Wbscr22 is involved in chemosensitivity to SN-38 and 5-FU in H460 cells. Fluorouracil 174-178 BUD23 rRNA methyltransferase and ribosome maturation factor Homo sapiens 49-56 25352209-11 2015 In conclusion, shRNA-mediated knockdown of Merm1/Wbscr22 attenuates H460 sensitivity to SN-38 and 5-FU, suggesting Merm1/Wbscr22 is involved in chemosensitivity to SN-38 and 5-FU in H460 cells. Fluorouracil 174-178 BUD23 rRNA methyltransferase and ribosome maturation factor Homo sapiens 115-120 25352209-11 2015 In conclusion, shRNA-mediated knockdown of Merm1/Wbscr22 attenuates H460 sensitivity to SN-38 and 5-FU, suggesting Merm1/Wbscr22 is involved in chemosensitivity to SN-38 and 5-FU in H460 cells. Fluorouracil 174-178 BUD23 rRNA methyltransferase and ribosome maturation factor Homo sapiens 121-128 22522606-13 2012 BLTA in combination with 5-FU could also enhance the ratio of CD4(+) T cells and splenic NK cell and CTL activity. Fluorouracil 25-29 CD4 antigen Mus musculus 62-65 21782419-9 2012 In the mice receiving with or without 5-FU, the serum levels of monocyte chemoattractant protein-1 (MCP-1) increased by all means but otherwise decreased when the herbal combination was administrated. Fluorouracil 38-42 chemokine (C-C motif) ligand 2 Mus musculus 64-98 25252848-0 2015 Re-sensitization of 5-FU resistance by SPARC through negative regulation of glucose metabolism in hepatocellular carcinoma. Fluorouracil 20-24 secreted protein acidic and cysteine rich Homo sapiens 39-44 25252848-7 2015 Interestingly, the 5-fluorouracil (5-FU)-resistant HepG2 cells showed increased glucose metabolism and downregulated SPARC levels. Fluorouracil 19-33 secreted protein acidic and cysteine rich Homo sapiens 117-122 25252848-7 2015 Interestingly, the 5-fluorouracil (5-FU)-resistant HepG2 cells showed increased glucose metabolism and downregulated SPARC levels. Fluorouracil 35-39 secreted protein acidic and cysteine rich Homo sapiens 117-122 25252848-8 2015 Finally, we reported the overexpression of SPARC re-sensitize 5-FU-resistant cells to 5-FU through inhibition of glycolysis both in vitro and in vivo. Fluorouracil 62-66 secreted protein acidic and cysteine rich Homo sapiens 43-48 25252848-8 2015 Finally, we reported the overexpression of SPARC re-sensitize 5-FU-resistant cells to 5-FU through inhibition of glycolysis both in vitro and in vivo. Fluorouracil 86-90 secreted protein acidic and cysteine rich Homo sapiens 43-48 25294903-0 2014 DNA methylation status of key cell-cycle regulators such as CDKNA2/p16 and CCNA1 correlates with treatment response to doxorubicin and 5-fluorouracil in locally advanced breast tumors. Fluorouracil 135-149 cyclin A1 Homo sapiens 75-80 21782419-9 2012 In the mice receiving with or without 5-FU, the serum levels of monocyte chemoattractant protein-1 (MCP-1) increased by all means but otherwise decreased when the herbal combination was administrated. Fluorouracil 38-42 chemokine (C-C motif) ligand 2 Mus musculus 100-105 22328001-10 2012 Knockdown of CIP2A decreased the resistance of the cells to 5-fluorouracil, oxaliplatin, and SN38 (an active metabolite of irinotecan). Fluorouracil 60-74 cellular inhibitor of PP2A Homo sapiens 13-18 22328001-11 2012 Treatment with 5-fluorouracil, oxaliplatin, and SN38 decreased CIP2A expression. Fluorouracil 15-29 cellular inhibitor of PP2A Homo sapiens 63-68 22328001-13 2012 The knockdown of CIP2A reduced proliferation and anchorage-independent colony formation and increased 5-fluorouracil, oxaliplatin, and SN38 efficacy in colon cancer cell lines. Fluorouracil 102-116 cellular inhibitor of PP2A Homo sapiens 17-22 22339362-1 2012 Inhibition of human deoxyuridine triphosphatase (dUTPase) has been identified as a promising approach to enhance the efficacy of 5-fluorouracil (5-FU)-based chemotherapy. Fluorouracil 129-143 deoxyuridine triphosphatase Homo sapiens 20-47 22339362-1 2012 Inhibition of human deoxyuridine triphosphatase (dUTPase) has been identified as a promising approach to enhance the efficacy of 5-fluorouracil (5-FU)-based chemotherapy. Fluorouracil 129-143 Deoxyuridine triphosphatase Drosophila melanogaster 49-56 22339362-1 2012 Inhibition of human deoxyuridine triphosphatase (dUTPase) has been identified as a promising approach to enhance the efficacy of 5-fluorouracil (5-FU)-based chemotherapy. Fluorouracil 145-149 deoxyuridine triphosphatase Homo sapiens 20-47 22339362-1 2012 Inhibition of human deoxyuridine triphosphatase (dUTPase) has been identified as a promising approach to enhance the efficacy of 5-fluorouracil (5-FU)-based chemotherapy. Fluorouracil 145-149 Deoxyuridine triphosphatase Drosophila melanogaster 49-56 22404301-1 2012 Recently, deoxyuridine triphosphatase (dUTPase) has emerged as a potential target for drug development as part of a new strategy of 5-fluorouracil-based combination chemotherapy. Fluorouracil 132-146 deoxyuridine triphosphatase Homo sapiens 10-37 22404301-1 2012 Recently, deoxyuridine triphosphatase (dUTPase) has emerged as a potential target for drug development as part of a new strategy of 5-fluorouracil-based combination chemotherapy. Fluorouracil 132-146 Deoxyuridine triphosphatase Drosophila melanogaster 39-46 22291191-11 2012 Together, our findings suggested that immunosuppression by 5-FU-MSC is mediated by a combination of elevated IL-1ra, IL-10, and PGE(2), anti-inflammatory Th2 cytokines, and decreased IL-17. Fluorouracil 59-63 interleukin 1 receptor antagonist Mus musculus 109-115 22291191-11 2012 Together, our findings suggested that immunosuppression by 5-FU-MSC is mediated by a combination of elevated IL-1ra, IL-10, and PGE(2), anti-inflammatory Th2 cytokines, and decreased IL-17. Fluorouracil 59-63 interleukin 17A Mus musculus 183-188 22309939-15 2012 Finally, whereas paclitaxel, doxorubicin, and 5-fluorouracil enriched the CD44high/CD24-/low population compared with control in SUM149, subsequent treatment with BI 2536 killed the emergent population, suggesting that it could potentially be used to prevent relapse. Fluorouracil 46-60 CD44 molecule (Indian blood group) Homo sapiens 74-78 25466554-9 2014 The influence of overexpression of E2F1 on anticancer drug resistance was assessed by measuring IC50 of SGC7901/DDP cells to cisplatin, doxorubicin, and 5-fluorouracil, as well as the rate of doxorubicin efflux, apoptosis, and cell cycle progression detected by flow cytometry. Fluorouracil 153-167 E2F transcription factor 1 Homo sapiens 35-39 25466554-11 2014 RESULTS: The SGC7901/DDP gastric cancer cell line stably overexpressing E2F1 exhibited significantly inhibited sensitivity to cisplatin, doxorubicin, and 5-fluorouracil. Fluorouracil 154-168 E2F transcription factor 1 Homo sapiens 72-76 23317245-1 2012 We conducted this study to detect associations between XRCC1 Arg399Gln and XPD Lys751Gln genotypes and survival of colorectal cancer patients treated with 5-FU/oxalipatin chemotherapy. Fluorouracil 155-159 X-ray repair cross complementing 1 Homo sapiens 55-60 25364415-1 2014 The aim of the present study was to investigate whether the inhibition of HSP27 phosphorylation, which affects certain cellular functions, modulates sensitivity to 5-fluorouracil (5-FU) in colorectal cancer cells. Fluorouracil 164-178 heat shock protein family B (small) member 1 Homo sapiens 74-79 25364415-1 2014 The aim of the present study was to investigate whether the inhibition of HSP27 phosphorylation, which affects certain cellular functions, modulates sensitivity to 5-fluorouracil (5-FU) in colorectal cancer cells. Fluorouracil 180-184 heat shock protein family B (small) member 1 Homo sapiens 74-79 23317245-8 2012 In conclusion, it is suggested that the XRCC1 Arg399Gln and XPD Lys751Gln polymorphisms should be routinely assessed to determine colorectal patients who are more likely to benefit from 5-FU/oxalipatin chemotherapy. Fluorouracil 186-190 X-ray repair cross complementing 1 Homo sapiens 40-45 25364415-2 2014 Exposure to 5-FU in HCT116 and HCT15 cells expressing high levels of HSP27 with a low 5-FU sensitivity caused a minimal change in HSP27 expression, but induced the upregulation of HSP27 phosphorylation, particularly at Ser78. Fluorouracil 12-16 heat shock protein family B (small) member 1 Homo sapiens 69-74 23238479-1 2012 BACKGROUND: An impairment of the 5-fluorouracil (5-FU) catabolic pathway, represented by alterations in the dihydropyrimidine dehydrogenase (DPYD) gene, is considered a crucial factor contributing to the development of 5-FU-related toxicity. Fluorouracil 33-47 dihydropyrimidine dehydrogenase Homo sapiens 108-139 25364415-2 2014 Exposure to 5-FU in HCT116 and HCT15 cells expressing high levels of HSP27 with a low 5-FU sensitivity caused a minimal change in HSP27 expression, but induced the upregulation of HSP27 phosphorylation, particularly at Ser78. Fluorouracil 12-16 heat shock protein family B (small) member 1 Homo sapiens 130-135 25364415-2 2014 Exposure to 5-FU in HCT116 and HCT15 cells expressing high levels of HSP27 with a low 5-FU sensitivity caused a minimal change in HSP27 expression, but induced the upregulation of HSP27 phosphorylation, particularly at Ser78. Fluorouracil 12-16 heat shock protein family B (small) member 1 Homo sapiens 130-135 25364415-2 2014 Exposure to 5-FU in HCT116 and HCT15 cells expressing high levels of HSP27 with a low 5-FU sensitivity caused a minimal change in HSP27 expression, but induced the upregulation of HSP27 phosphorylation, particularly at Ser78. Fluorouracil 86-90 heat shock protein family B (small) member 1 Homo sapiens 69-74 25364415-3 2014 By contrast, exposure to 5-FU in HT29 cells expressing a low level of HSP27 with a high 5-FU sensitivity marginally increased HSP27 expression, with minimal phosphorylation. Fluorouracil 25-29 heat shock protein family B (small) member 1 Homo sapiens 70-75 23238479-1 2012 BACKGROUND: An impairment of the 5-fluorouracil (5-FU) catabolic pathway, represented by alterations in the dihydropyrimidine dehydrogenase (DPYD) gene, is considered a crucial factor contributing to the development of 5-FU-related toxicity. Fluorouracil 33-47 dihydropyrimidine dehydrogenase Homo sapiens 141-145 25364415-3 2014 By contrast, exposure to 5-FU in HT29 cells expressing a low level of HSP27 with a high 5-FU sensitivity marginally increased HSP27 expression, with minimal phosphorylation. Fluorouracil 25-29 heat shock protein family B (small) member 1 Homo sapiens 126-131 23284920-6 2012 We observed that survival of Atrx-null cells were similar to wild type cells in response to serum withdrawal, anti-Fas antibody, C2 ceramide or dexamethasone treatment but were more sensitive to 5-fluorouracil (5-FU). Fluorouracil 195-209 ATRX, chromatin remodeler Mus musculus 29-33 25364415-3 2014 By contrast, exposure to 5-FU in HT29 cells expressing a low level of HSP27 with a high 5-FU sensitivity marginally increased HSP27 expression, with minimal phosphorylation. Fluorouracil 88-92 heat shock protein family B (small) member 1 Homo sapiens 70-75 25364415-4 2014 Treatment with a selective inhibitor, p38 mitogen-activated protein kinase (MAPK; SB203580), caused the dose-dependent suppression of HSP27 phosphorylation, which was upregulated by 5-FU, reducing the half maximal inhibitory concentration values of 5-FU in the HCT116 and HCT15 cells. Fluorouracil 182-186 heat shock protein family B (small) member 1 Homo sapiens 134-139 25364415-4 2014 Treatment with a selective inhibitor, p38 mitogen-activated protein kinase (MAPK; SB203580), caused the dose-dependent suppression of HSP27 phosphorylation, which was upregulated by 5-FU, reducing the half maximal inhibitory concentration values of 5-FU in the HCT116 and HCT15 cells. Fluorouracil 249-253 heat shock protein family B (small) member 1 Homo sapiens 134-139 25364415-6 2014 In conclusion, this study indicated that the inhibition of HSP27 phosphorylation by a selective inhibitor of p38 MAPK promotes 5-FU sensitivity without causing cytotoxicity in colorectal cancer cells. Fluorouracil 127-131 heat shock protein family B (small) member 1 Homo sapiens 59-64 23284920-6 2012 We observed that survival of Atrx-null cells were similar to wild type cells in response to serum withdrawal, anti-Fas antibody, C2 ceramide or dexamethasone treatment but were more sensitive to 5-fluorouracil (5-FU). Fluorouracil 211-215 ATRX, chromatin remodeler Mus musculus 29-33 21550686-11 2011 A positive expression of TS, DPD and OPRT might be an important factor in predicting the effectiveness of 5-FU based chemotherapy in this disease. Fluorouracil 106-110 dihydropyrimidine dehydrogenase Homo sapiens 29-32 22011696-6 2011 However, individual differences in the metabolic production of 5-FU from FT because of genetic polymorphisms in CYP2A6 and individual variation in the levels of renal function may lead to complications when 5-FU is coadministered with warfarin as compared to when 5-FU is administered alone. Fluorouracil 63-67 cytochrome P450 family 2 subfamily A member 6 Homo sapiens 112-118 21807902-8 2011 Interestingly, treatment of cells with the ribosomal stress-inducing agent actinomycin D or 5-fluorouracil significantly decreased the c-myc mRNA levels in an L11- and Ago2-dependent manner. Fluorouracil 92-106 ribosomal protein L11 Homo sapiens 159-162 21868518-7 2011 CONCLUSION: Expression level of TS, OPRT, ERCC1, BRCA1 and MVD in resected colorectal lung metastases may play an important role for predicting outcome after 5-fluorouracil-based adjuvant therapy. Fluorouracil 158-172 BRCA1 DNA repair associated Homo sapiens 49-54 21855038-1 2011 BACKGROUND: This prospective analysis evaluated the effect of tumor KRAS status on efficacy of second-line panitumumab plus folinic acid/5-fluorouracil/irinotecan (FOLFIRI). Fluorouracil 137-151 KRAS proto-oncogene, GTPase Homo sapiens 68-72 25473889-0 2014 Human rpL3 plays a crucial role in cell response to nucleolar stress induced by 5-FU and L-OHP. Fluorouracil 80-84 ribosomal protein L3 Homo sapiens 6-10 25473889-2 2014 Here, we demonstrate that in lung and colon cancer cell lines devoid of p53, the efficacy of 5-FU and L-OHP chemotherapy depends on rpL3 status. Fluorouracil 93-97 ribosomal protein L3 Homo sapiens 132-136 25473889-3 2014 Specifically, we demonstrate that ribosomal stress induced by 5-FU and L-OHP is associated to up-regulation of rpL3 and its accumulation as ribosome-free form. Fluorouracil 62-66 ribosomal protein L3 Homo sapiens 111-115 25473889-6 2014 It is noteworthy that silencing of rpL3 abolishes the cytotoxic effects of 5-FU and L-OH indicating that the loss of rpL3 makes chemotherapy drugs ineffective. Fluorouracil 75-79 ribosomal protein L3 Homo sapiens 35-39 21710497-5 2011 Ad-FZ33 expressing uracil phosphoribosyl transferase (UPRT), an enzyme which greatly enhances the toxicity of 5-fluorouracil (FU), combined with antibodies against EpCAM or EGFR, remarkably enhanced the sensitivity of biliary cancer cells to 5-FU. Fluorouracil 110-124 uracil phosphoribosyltransferase homolog Homo sapiens 19-52 21710497-5 2011 Ad-FZ33 expressing uracil phosphoribosyl transferase (UPRT), an enzyme which greatly enhances the toxicity of 5-fluorouracil (FU), combined with antibodies against EpCAM or EGFR, remarkably enhanced the sensitivity of biliary cancer cells to 5-FU. Fluorouracil 110-124 uracil phosphoribosyltransferase homolog Homo sapiens 54-58 21710497-5 2011 Ad-FZ33 expressing uracil phosphoribosyl transferase (UPRT), an enzyme which greatly enhances the toxicity of 5-fluorouracil (FU), combined with antibodies against EpCAM or EGFR, remarkably enhanced the sensitivity of biliary cancer cells to 5-FU. Fluorouracil 242-246 uracil phosphoribosyltransferase homolog Homo sapiens 19-52 21710497-5 2011 Ad-FZ33 expressing uracil phosphoribosyl transferase (UPRT), an enzyme which greatly enhances the toxicity of 5-fluorouracil (FU), combined with antibodies against EpCAM or EGFR, remarkably enhanced the sensitivity of biliary cancer cells to 5-FU. Fluorouracil 242-246 uracil phosphoribosyltransferase homolog Homo sapiens 54-58 21570764-0 2011 PGE2 targets squamous cell carcinoma cell with the activated epidermal growth factor receptor family for survival against 5-fluorouracil through NR4A2 induction. Fluorouracil 122-136 nuclear receptor subfamily 4, group A, member 2 Mus musculus 145-150 21723691-0 2011 Interleukin 1 receptor antagonist reduces lethality and intestinal toxicity of 5-Fluorouracil in a mouse mucositis model. Fluorouracil 79-93 interleukin 1 receptor antagonist Mus musculus 0-33 21723691-6 2011 Administration of recombinant IL-1Ra to the mouse model of intestinal mucositis induced by 5-Fu demonstrated its therapeutic effects to the symptoms and pathology of the disease. Fluorouracil 91-95 interleukin 1 receptor antagonist Mus musculus 30-36 20972872-3 2011 The aim of this study was to evaluate the association between k-ras status and addition of oxaliplatin to fluorouracil plus leucovorin (FOLFOX) chemotherapy in CRC patients with curative surgical resection. Fluorouracil 106-118 KRAS proto-oncogene, GTPase Homo sapiens 62-67 25367337-12 2014 The AGR2 knockdown also increased the sensitivity of the cells to chemotherapeutic drugs, including gemcitabine, 5-fluorouracil and cisplatin. Fluorouracil 113-127 anterior gradient 2, protein disulphide isomerase family member Homo sapiens 4-8 21228335-1 2011 BACKGROUND: The randomized phase II OPUS (Oxaliplatin and Cetuximab in First-Line Treatment of Metastatic Colorectal Cancer) study showed that tumor KRAS mutation status was predictive for outcome in patients receiving cetuximab plus FOLFOX-4 (oxaliplatin/5-fluorouracil/folinic acid) as first-line therapy for metastatic colorectal cancer (mCRC). Fluorouracil 256-270 KRAS proto-oncogene, GTPase Homo sapiens 149-153 20844880-0 2011 Interleukin-1 receptor antagonist reduced apoptosis and attenuated intestinal mucositis in a 5-fluorouracil chemotherapy model in mice. Fluorouracil 93-107 interleukin 1 receptor antagonist Mus musculus 0-33 20844880-2 2011 And we further determine whether interleukin-1 receptor antagonist (IL-1Ra) reduces apoptosis in vivo after 5-fluorouracil (5-FU) chemotherapy in the small intestine. Fluorouracil 108-122 interleukin 1 receptor antagonist Mus musculus 33-66 20844880-2 2011 And we further determine whether interleukin-1 receptor antagonist (IL-1Ra) reduces apoptosis in vivo after 5-fluorouracil (5-FU) chemotherapy in the small intestine. Fluorouracil 108-122 interleukin 1 receptor antagonist Mus musculus 68-74 20844880-2 2011 And we further determine whether interleukin-1 receptor antagonist (IL-1Ra) reduces apoptosis in vivo after 5-fluorouracil (5-FU) chemotherapy in the small intestine. Fluorouracil 124-128 interleukin 1 receptor antagonist Mus musculus 33-66 20844880-2 2011 And we further determine whether interleukin-1 receptor antagonist (IL-1Ra) reduces apoptosis in vivo after 5-fluorouracil (5-FU) chemotherapy in the small intestine. Fluorouracil 124-128 interleukin 1 receptor antagonist Mus musculus 68-74 20844880-15 2011 Moreover, IL-1Ra attenuated the severity of intestinal mucositis induced by 5-FU and enhanced intestinal crypt proliferation. Fluorouracil 76-80 interleukin 1 receptor antagonist Mus musculus 10-16 20844880-16 2011 In vitro experiments showed that IL-1Ra suppressed apoptosis and increased cell viability in enterocyte IEC-6 cells treated with 5-FU. Fluorouracil 129-133 interleukin 1 receptor antagonist Rattus norvegicus 33-39 20844880-19 2011 Administered with IL-1Ra protects mice against intestinal apoptosis induced by 5-FU, relieves mucosal impairment of the small intestine, and facilitates the recovery of the intestinal mucosa. Fluorouracil 79-83 interleukin 1 receptor antagonist Mus musculus 18-24 21635146-0 2011 GALNT14 SNP as a potential predictor of response to combination chemotherapy using 5-FU, mitoxantrone and cisplatin in advanced HCC. Fluorouracil 83-87 polypeptide N-acetylgalactosaminyltransferase 14 Homo sapiens 0-7 21471424-9 2011 CONCLUSIONS: Our results indicate that MTHFR activity and a specific combination of the MTHFR 1298A>C and TYMS 3"-UTR ins/del polymorphisms are possible predictors of 5-FU treatment-related toxicity. Fluorouracil 170-174 methylenetetrahydrofolate reductase Homo sapiens 39-44 21471424-9 2011 CONCLUSIONS: Our results indicate that MTHFR activity and a specific combination of the MTHFR 1298A>C and TYMS 3"-UTR ins/del polymorphisms are possible predictors of 5-FU treatment-related toxicity. Fluorouracil 170-174 methylenetetrahydrofolate reductase Homo sapiens 88-93 21780905-3 2011 Repression of dUTPase induced specific expression level increments for thymidylate kinase and thymidine kinase, and also an increased sensitization to 5-fluoro-2"-deoxyuridine and 5-fluoro-uracil. Fluorouracil 180-195 Deoxyuridine triphosphatase Drosophila melanogaster 14-21 24367220-1 2011 BACKGROUND: Type 1 interferon alpha receptor 2 (IFNAR2) in the liver has been reported to be a predictive factor for the response to intra-arterial 5-fluorouracil (5-FU) + systemic interferon (IFN)-alpha combination therapy in patients with advanced hepatocellular carcinoma. Fluorouracil 148-162 interferon alpha and beta receptor subunit 2 Homo sapiens 48-54 24367220-1 2011 BACKGROUND: Type 1 interferon alpha receptor 2 (IFNAR2) in the liver has been reported to be a predictive factor for the response to intra-arterial 5-fluorouracil (5-FU) + systemic interferon (IFN)-alpha combination therapy in patients with advanced hepatocellular carcinoma. Fluorouracil 164-168 interferon alpha and beta receptor subunit 2 Homo sapiens 48-54 24367220-2 2011 We tested whether IFNAR2 expression in peripheral blood mononuclear cells could predict the response to 5-FU + IFN. Fluorouracil 104-108 interferon alpha and beta receptor subunit 2 Homo sapiens 18-24 24367220-10 2011 CONCLUSION: IFNAR2 expression in peripheral blood mononuclear cells may predict the response to 5-FU + IFN therapy in patients with advanced hepatocellular carcinoma, although these data are preliminary. Fluorouracil 96-100 interferon alpha and beta receptor subunit 2 Homo sapiens 12-18 21291546-2 2011 METHODS: TNM staged anal squamous-cell cancer patients were treated with pelvic radiotherapy concomitant to continuous infusion fluorouracil plus cisplatin for at least 2 cycles. Fluorouracil 128-140 teneurin transmembrane protein 1 Homo sapiens 9-12 25279168-0 2014 beta-catenin knockdown enhances the effects of fluorouracil in the breast cancer cell line MDA-MB-468. Fluorouracil 47-59 catenin beta 1 Homo sapiens 0-12 25279168-5 2014 Knockdown of beta-catenin enhanced the effects of fluorouracil (5-FU) chemotherapy on the proliferation of MDA-MB-468 cells. Fluorouracil 50-62 catenin beta 1 Homo sapiens 13-25 25279168-5 2014 Knockdown of beta-catenin enhanced the effects of fluorouracil (5-FU) chemotherapy on the proliferation of MDA-MB-468 cells. Fluorouracil 64-68 catenin beta 1 Homo sapiens 13-25 25279168-6 2014 Thus, these preliminary results indicate that beta-catenin knockdown enhanced 5-FU-induced proliferation inhibition in the breast cancer cell line MDA-MB-468, and indicate that combining 5-FU with gene silencing could be an advantageous option for enhancing the curative effect of chemotherapy in breast cancer and other malignancies. Fluorouracil 78-82 catenin beta 1 Homo sapiens 46-58 25279168-6 2014 Thus, these preliminary results indicate that beta-catenin knockdown enhanced 5-FU-induced proliferation inhibition in the breast cancer cell line MDA-MB-468, and indicate that combining 5-FU with gene silencing could be an advantageous option for enhancing the curative effect of chemotherapy in breast cancer and other malignancies. Fluorouracil 187-191 catenin beta 1 Homo sapiens 46-58 24898807-0 2014 Overexpression of microRNA-122 re-sensitizes 5-FU-resistant colon cancer cells to 5-FU through the inhibition of PKM2 in vitro and in vivo. Fluorouracil 45-49 pyruvate kinase M1/2 Homo sapiens 113-117 24898807-0 2014 Overexpression of microRNA-122 re-sensitizes 5-FU-resistant colon cancer cells to 5-FU through the inhibition of PKM2 in vitro and in vivo. Fluorouracil 82-86 pyruvate kinase M1/2 Homo sapiens 113-117 24898807-8 2014 Importantly, overexpression of miR-122 in 5-FU-resistant cells resensitizes 5-FU resistance through the inhibition of PKM2 both in vitro and in vivo. Fluorouracil 42-46 pyruvate kinase M1/2 Homo sapiens 118-122 24898807-8 2014 Importantly, overexpression of miR-122 in 5-FU-resistant cells resensitizes 5-FU resistance through the inhibition of PKM2 both in vitro and in vivo. Fluorouracil 76-80 pyruvate kinase M1/2 Homo sapiens 118-122 25249558-2 2014 Therefore, we hypothesized that SNAI2 (Slug) may mediate 5-fluorouracil (5FU) chemotherapy resistance through inhibition of miR145 in colorectal cancer and thus represents a novel therapeutic target to enhance current colorectal cancer treatment strategies. Fluorouracil 57-71 microRNA 145 Homo sapiens 124-130 25249558-2 2014 Therefore, we hypothesized that SNAI2 (Slug) may mediate 5-fluorouracil (5FU) chemotherapy resistance through inhibition of miR145 in colorectal cancer and thus represents a novel therapeutic target to enhance current colorectal cancer treatment strategies. Fluorouracil 73-76 microRNA 145 Homo sapiens 124-130 25249558-8 2014 In pretreatment rectal cancer patient biopsy samples, low miR145 expression levels correlated with poor response to neoadjuvant 5FU-based chemoradiation. Fluorouracil 128-131 microRNA 145 Homo sapiens 58-64 20811948-0 2011 Tyrosine kinase inhibitor PTK/ZK enhances the antitumor effects of interferon-alpha/5-fluorouracil therapy for hepatocellular carcinoma cells. Fluorouracil 84-98 TXK tyrosine kinase Homo sapiens 0-15 21044746-0 2010 Methylenetetrahydrofolate reductase polymorphism (677 C>T) predicts long time to progression in metastatic colon cancer treated with 5-fluorouracil and folinic acid. Fluorouracil 136-150 methylenetetrahydrofolate reductase Homo sapiens 0-35 25296971-0 2014 HSP90 inhibition downregulates thymidylate synthase and sensitizes colorectal cancer cell lines to the effect of 5FU-based chemotherapy. Fluorouracil 113-116 heat shock protein 90 alpha family class A member 1 Homo sapiens 0-5 25296971-3 2014 We tested the hypothesis that HSP90 transcriptional and functional inhibition can inhibit cell cycle progression, downregulate TS levels and sensitize colorectal cancer (CRC) cell lines to the effects of 5FU. Fluorouracil 204-207 heat shock protein 90 alpha family class A member 1 Homo sapiens 30-35 25550778-6 2014 CD147 overexpression increased the 5-Fluorouracil (5-FU) resistance, enhanced the invasion and EMT of CRC cells by regulating EMT markers and MMPs. Fluorouracil 35-49 basigin (Ok blood group) Homo sapiens 0-5 25550778-6 2014 CD147 overexpression increased the 5-Fluorouracil (5-FU) resistance, enhanced the invasion and EMT of CRC cells by regulating EMT markers and MMPs. Fluorouracil 51-55 basigin (Ok blood group) Homo sapiens 0-5 25550778-9 2014 Taken together, our study indicates that CD147 promotes the 5-FU resistance, and MAPK/ERK signaling pathway is involved in CD147-promoted invasion and EMT of CRC cells. Fluorouracil 60-64 basigin (Ok blood group) Homo sapiens 41-46 24821366-0 2014 Efficacy and safety of early G-CSF administration in patients with head and neck cancer treated by docetaxel-cisplatin and 5-fluorouracil (DCF protocol): a retrospective study. Fluorouracil 123-137 colony stimulating factor 3 Homo sapiens 29-34 25202077-11 2014 CONCLUSION: These findings indicate a possible prognostic role of TYMS mRNA expression and highlight a cluster of genes associated with nodal metastases that warrant further investigation in a larger cohort of patients with colorectal cancer treated with 5-FU-based adjuvant chemotherapy. Fluorouracil 255-259 thymidylate synthetase Homo sapiens 66-70 21044746-4 2010 The polymorphism 677C>T of the methylenetetrahydrofolate reductase (MTHFR) gene seems to influence the effectiveness of treatment with 5-FU. Fluorouracil 138-142 methylenetetrahydrofolate reductase Homo sapiens 34-69 21044746-4 2010 The polymorphism 677C>T of the methylenetetrahydrofolate reductase (MTHFR) gene seems to influence the effectiveness of treatment with 5-FU. Fluorouracil 138-142 methylenetetrahydrofolate reductase Homo sapiens 71-76 21044746-5 2010 We undertook this study to evaluate the frequency of MTHFR 677C>T polymorphism and its relationship to the time to progression (TTP) and overall survival (OS) in m-CRC treated with 5-FU/FA. Fluorouracil 184-188 methylenetetrahydrofolate reductase Homo sapiens 53-58 21044746-12 2010 The results of this study appear to show that the presence of the MTHFR 677C>T polymorphism is associated with longer TTP and OS in m-CRC treated with 5-FU/FA. Fluorouracil 154-158 methylenetetrahydrofolate reductase Homo sapiens 66-71 20500514-7 2010 COLM-5 cells showed expression pattern of 5-FU metabolizing enzymes such as high dihydropyrimidine dehydrogenase (DPD) and low thymidylate synthase (TS)/orotate phosphoribosyltransferase (OPRT) both in vitro and in vivo. Fluorouracil 42-46 dihydropyrimidine dehydrogenase Homo sapiens 81-112 20500514-7 2010 COLM-5 cells showed expression pattern of 5-FU metabolizing enzymes such as high dihydropyrimidine dehydrogenase (DPD) and low thymidylate synthase (TS)/orotate phosphoribosyltransferase (OPRT) both in vitro and in vivo. Fluorouracil 42-46 dihydropyrimidine dehydrogenase Homo sapiens 114-117 20463005-9 2010 Furthermore, the amount of 5-FU and GBL/GHB formed in the hepatic S9 was markedly decreased in the presence of a CYP2A6 inhibitor, suggesting that GBL/GHB may be mainly generated through the CYP2A6-mediated formation of SA. Fluorouracil 27-31 cytochrome P450 family 2 subfamily A member 6 Homo sapiens 113-119 20463005-9 2010 Furthermore, the amount of 5-FU and GBL/GHB formed in the hepatic S9 was markedly decreased in the presence of a CYP2A6 inhibitor, suggesting that GBL/GHB may be mainly generated through the CYP2A6-mediated formation of SA. Fluorouracil 27-31 cytochrome P450 family 2 subfamily A member 6 Homo sapiens 191-197 20646319-0 2010 TNFRSF1B A1466G genotype is predictive of clinical efficacy after treatment with a definitive 5-fluorouracil/cisplatin-based chemoradiotherapy in Japanese patients with esophageal squamous cell carcinoma. Fluorouracil 94-108 TNF receptor superfamily member 1B Homo sapiens 0-8 25148895-6 2014 Moreover, knockdown of CRM1 disturbed the expression of tumor suppressor proteins and inhibited NF-kappaB activity in ESCC cell lines, especially if the cell line was treated with 5-fluorouracil. Fluorouracil 180-194 exportin 1 Homo sapiens 23-27 24994673-2 2014 Since 5-FU is converted into active or inactive forms by orotate phosphoribosyltransferase (OPRT) or dihydropyrimidine dehydrogenase (DPD), a correlation between these enzymes and response to 5-FU has been suggested. Fluorouracil 6-10 uridine monophosphate synthetase Homo sapiens 57-90 24994673-2 2014 Since 5-FU is converted into active or inactive forms by orotate phosphoribosyltransferase (OPRT) or dihydropyrimidine dehydrogenase (DPD), a correlation between these enzymes and response to 5-FU has been suggested. Fluorouracil 6-10 uridine monophosphate synthetase Homo sapiens 92-96 24994673-2 2014 Since 5-FU is converted into active or inactive forms by orotate phosphoribosyltransferase (OPRT) or dihydropyrimidine dehydrogenase (DPD), a correlation between these enzymes and response to 5-FU has been suggested. Fluorouracil 192-196 uridine monophosphate synthetase Homo sapiens 57-90 24994673-2 2014 Since 5-FU is converted into active or inactive forms by orotate phosphoribosyltransferase (OPRT) or dihydropyrimidine dehydrogenase (DPD), a correlation between these enzymes and response to 5-FU has been suggested. Fluorouracil 192-196 uridine monophosphate synthetase Homo sapiens 92-96 24994673-4 2014 Therefore, in the present study, we aimed to prospectively evaluate whether OPRT and DPD were predictive factors of the response to 5-FU treatment in patients with resectable CRC. Fluorouracil 132-136 uridine monophosphate synthetase Homo sapiens 76-80 24994673-15 2014 In conclusion, our results suggest that the OPRT/DPD ratio could be a predictive factor for response to 5-FU/LV adjuvant chemotherapy. Fluorouracil 104-108 uridine monophosphate synthetase Homo sapiens 44-48 24972040-13 2014 These findings provide evidence that neutrophil recruitment and neutrophil elastase may decrease the levels of AQP 4 and 8 in the colon of mice treated with 5-FU and contribute to the pathophysiology of 5-FU-induced body weight loss and diarrhea. Fluorouracil 157-161 elastase, neutrophil expressed Mus musculus 64-83 24972040-13 2014 These findings provide evidence that neutrophil recruitment and neutrophil elastase may decrease the levels of AQP 4 and 8 in the colon of mice treated with 5-FU and contribute to the pathophysiology of 5-FU-induced body weight loss and diarrhea. Fluorouracil 203-207 elastase, neutrophil expressed Mus musculus 64-83 25175730-0 2014 Association between ERCC1 and TS mRNA levels and disease free survival in colorectal cancer patients receiving oxaliplatin and fluorouracil (5-FU) adjuvant chemotherapy. Fluorouracil 127-139 ERCC excision repair 1, endonuclease non-catalytic subunit Homo sapiens 20-25 25175730-0 2014 Association between ERCC1 and TS mRNA levels and disease free survival in colorectal cancer patients receiving oxaliplatin and fluorouracil (5-FU) adjuvant chemotherapy. Fluorouracil 141-145 ERCC excision repair 1, endonuclease non-catalytic subunit Homo sapiens 20-25 25175730-1 2014 BACKGROUND: Aim was to explore the association of ERCC1 and TS mRNA levels with the disease free survival (DFS) in Chinese colorectal cancer (CRC) patients receiving oxaliplatin and 5-FU based adjuvant chemotherapy. Fluorouracil 182-186 ERCC excision repair 1, endonuclease non-catalytic subunit Homo sapiens 50-55 24962565-8 2014 Compared with forced expression of wild type TDG, CRL4(Cdt2)- resistant TDG (DeltaPIP) slows cell proliferation and slightly increases the toxicity of 5-FU. Fluorouracil 151-155 interleukin 17 receptor B Homo sapiens 50-54 24800927-0 2014 Activation of p38-MAPK by CXCL4/CXCR3 axis contributes to p53-dependent intestinal apoptosis initiated by 5-fluorouracil. Fluorouracil 106-120 chemokine (C-X-C motif) receptor 3 Mus musculus 32-37 24800927-0 2014 Activation of p38-MAPK by CXCL4/CXCR3 axis contributes to p53-dependent intestinal apoptosis initiated by 5-fluorouracil. Fluorouracil 106-120 transformation related protein 53, pseudogene Mus musculus 58-61 24800927-6 2014 CXCL4 and its receptor CXCR3 were confirmed at both the gene and protein levels to be homeostatically regulated during 5-FU-induced mucositis. Fluorouracil 119-123 chemokine (C-X-C motif) receptor 3 Mus musculus 23-28 24800927-8 2014 Mechanistically, CXCL4mab reduced the apoptosis of the crypt epithelia by suppression of the 5-FU-induced expression of p53 and Bax through its receptor CXCR3. Fluorouracil 93-97 transformation related protein 53, pseudogene Mus musculus 120-123 24800927-8 2014 Mechanistically, CXCL4mab reduced the apoptosis of the crypt epithelia by suppression of the 5-FU-induced expression of p53 and Bax through its receptor CXCR3. Fluorouracil 93-97 chemokine (C-X-C motif) receptor 3 Mus musculus 153-158 24800927-11 2014 Taken together, activation of CXCL4 expression by 5-FU in mice participates in 5-FU-induced intestinal mucositis through upregulation of p53 via activation of p38-MAPK, and CXCL4mab is potentially beneficial in preventing CIM in the intestinal tract. Fluorouracil 50-54 transformation related protein 53, pseudogene Mus musculus 137-140 20646319-4 2010 In this study, genetic polymorphisms of TNFRSF1B gene were evaluated Japanese esophageal squamous cell carcinoma (ESCC) patients treated with the definitive 5-FU/CDDP-based chemoradiotherapy and their predictive values of prognosis or severe acute toxicities were assessed. Fluorouracil 157-161 TNF receptor superfamily member 1B Homo sapiens 40-48 20646319-9 2010 CONCLUSIONS: Genetic polymorphism of TNFRSF1B A1466G was found to be predictive response in Japanese ESCC patients with a definitive 5-FU/CDDP-based chemoradiotherapy. Fluorouracil 133-137 TNF receptor superfamily member 1B Homo sapiens 37-45 20637356-4 2010 The phenotyping of DPD and UGT1A1 activities, and to a lesser extent, its genotyping, appears as the most useful tool in terms of prediction of toxicities induced by two major drugs: 5-FU and irinotecan. Fluorouracil 183-187 dihydropyrimidine dehydrogenase Homo sapiens 19-22 20637356-4 2010 The phenotyping of DPD and UGT1A1 activities, and to a lesser extent, its genotyping, appears as the most useful tool in terms of prediction of toxicities induced by two major drugs: 5-FU and irinotecan. Fluorouracil 183-187 UDP glucuronosyltransferase family 1 member A1 Homo sapiens 27-33 19830428-0 2010 Enhanced 5-fluorouracil cytotoxicity in high cyclooxygenase-2 expressing colorectal cancer cells and xenografts induced by non-steroidal anti-inflammatory drugs via downregulation of dihydropyrimidine dehydrogenase. Fluorouracil 9-23 dihydropyrimidine dehydrogenase Homo sapiens 183-214 19830428-1 2010 PURPOSE: To prove that 5-FU cytotoxicity could be increased by combination with low-dose non-steroidal anti-inflammatory drugs (NSAIDs) (indomethacin or NS-398) in high cyclooxygenase-2- (COX-2) expressing cells and xenografts through the modulation of dihydropyrimidine dehydrogenase (DPD) mRNA expression and/or enzyme activity. Fluorouracil 23-27 dihydropyrimidine dehydrogenase Homo sapiens 253-284 19830428-1 2010 PURPOSE: To prove that 5-FU cytotoxicity could be increased by combination with low-dose non-steroidal anti-inflammatory drugs (NSAIDs) (indomethacin or NS-398) in high cyclooxygenase-2- (COX-2) expressing cells and xenografts through the modulation of dihydropyrimidine dehydrogenase (DPD) mRNA expression and/or enzyme activity. Fluorouracil 23-27 dihydropyrimidine dehydrogenase Homo sapiens 286-289 19830428-10 2010 Downregulation of DPD was observed after 5-FU monotherapy, but the combined effect of NSAIDs and 5-FU on DPD mRNA expression, and enzyme activity was superior to the effect of 5-FU alone. Fluorouracil 41-45 dihydropyrimidine dehydrogenase Homo sapiens 18-21 19830428-10 2010 Downregulation of DPD was observed after 5-FU monotherapy, but the combined effect of NSAIDs and 5-FU on DPD mRNA expression, and enzyme activity was superior to the effect of 5-FU alone. Fluorouracil 97-101 dihydropyrimidine dehydrogenase Homo sapiens 105-108 20231086-5 2010 The autophagy activation induced by 5-FU treatment was revealed by microtubule-associated protein 1 light chain 3 (LC3) immunofluorescence and immunoblotting and p62 immunoblotting. Fluorouracil 36-40 microtubule associated protein 1 light chain 3 alpha Homo sapiens 115-118 20231086-5 2010 The autophagy activation induced by 5-FU treatment was revealed by microtubule-associated protein 1 light chain 3 (LC3) immunofluorescence and immunoblotting and p62 immunoblotting. Fluorouracil 36-40 nucleoporin 62 Homo sapiens 162-165 25083297-21 2014 It should include markers such as ERCC1 predicting response to 5-fluorouracil and platinum based chemotherapy, to enable individualizing therapy for this cancer. Fluorouracil 63-77 ERCC excision repair 1, endonuclease non-catalytic subunit Homo sapiens 34-39 20647713-7 2010 Hence, DPD inhibitory fluorouracil, such as S-1, may have potent therapeutic efficacy for poorly-differentiated adenocarcinoma of the colorectum. Fluorouracil 22-34 dihydropyrimidine dehydrogenase Homo sapiens 7-10 25013487-0 2014 5-Fluorouracil-induced apoptosis in colorectal cancer cells is caspase-9-dependent and mediated by activation of protein kinase C-delta Elucidation of the molecular mechanisms by which 5-fluorouracil (5-FU) induces apoptosis is required in order to understand the resistance of colorectal cancer (CRC) cells to 5-FU. Fluorouracil 0-14 caspase 9 Homo sapiens 63-72 25013487-0 2014 5-Fluorouracil-induced apoptosis in colorectal cancer cells is caspase-9-dependent and mediated by activation of protein kinase C-delta Elucidation of the molecular mechanisms by which 5-fluorouracil (5-FU) induces apoptosis is required in order to understand the resistance of colorectal cancer (CRC) cells to 5-FU. Fluorouracil 185-199 caspase 9 Homo sapiens 63-72 25013487-0 2014 5-Fluorouracil-induced apoptosis in colorectal cancer cells is caspase-9-dependent and mediated by activation of protein kinase C-delta Elucidation of the molecular mechanisms by which 5-fluorouracil (5-FU) induces apoptosis is required in order to understand the resistance of colorectal cancer (CRC) cells to 5-FU. Fluorouracil 201-205 caspase 9 Homo sapiens 63-72 25013487-4 2014 In addition, 5-FU-induced apoptosis was caspase-dependent as it appeared to be initiated by caspase-9. Fluorouracil 13-17 caspase 9 Homo sapiens 92-101 21029695-10 2010 CONCLUSION: Genetic polymorphisms of ERCC1-118, XRCC1-399 and GSTP1-105 are associated with TTP and OS of advanced gastric cancer patients treated with oxaliplatin/5-Fu-based combination chemotherapy as the first-line chemotherapy. Fluorouracil 164-168 X-ray repair cross complementing 1 Homo sapiens 48-53 25013487-8 2014 These results indicated that 5-FU induces apoptosis in CRC by the activation of PKCdelta and caspase-9. Fluorouracil 29-33 caspase 9 Homo sapiens 93-102 20384633-6 2010 Both the mRNA and protein expression levels of thymidylate synthase (TS), dihydropyrimidine dehydrogenase (DPD), and orotate phosphoribosyltransferase (OPRT), which are associated with 5-FU sensitivity/response, were analyzed in the cells undergoing treatment. Fluorouracil 185-189 dihydropyrimidine dehydrogenase Homo sapiens 74-105 20384633-10 2010 We conclude that combination therapy with SAHA and S-1 in lung cancer may be promising due to its potential to overcome S-1 resistance via modulation of 5-FU/S-1 sensitivity-associated biomarker (TS) by HDAC inhibitor. Fluorouracil 153-157 histone deacetylase 9 Homo sapiens 203-207 25199288-10 2014 CONCLUSION: SJAMP and 5-FU can via decrease the expressions of PCNA protein, P53, Cyclin D1 and CDK4 proteins and mRNAs, increase the expressions of P21 proteins and mRNAs, to inhibit the growth of H22 tumor in mice. Fluorouracil 22-26 transformation related protein 53, pseudogene Mus musculus 77-80 20567103-1 2010 Thymidylate synthase(TS), dihydropyrimidine dehydrogenase(DPD), and orotate phosphoribosyl transferase(OPRT)are initial key enzymes in the 5-fluorouracil(5-FU)metabolic pathway. Fluorouracil 139-153 dihydropyrimidine dehydrogenase Homo sapiens 58-61 20567103-1 2010 Thymidylate synthase(TS), dihydropyrimidine dehydrogenase(DPD), and orotate phosphoribosyl transferase(OPRT)are initial key enzymes in the 5-fluorouracil(5-FU)metabolic pathway. Fluorouracil 154-158 dihydropyrimidine dehydrogenase Homo sapiens 58-61 20458768-6 2010 RESULTS: The SK-Hep-1/CDDP cells (IC(50) = 70.61 +/- 1.06 microg/mL) was 13.76 times more resistant to CDDP than the SK-Hep-1 cells (IC(50) = 5.13 +/- 0.09 microg/mL), and CDDP-resistant cells also demonstrated cross-resistance to many anti-tumor agents such as doxorubicin, 5-fluorouracil and vincristine. Fluorouracil 275-289 DNL-type zinc finger Homo sapiens 16-21 24922653-0 2014 Cell-cycle distribution and Thymidilate Synthatase (TS) expression correlate with 5-FU resistance in head and neck carcinoma cells. Fluorouracil 82-86 thymidylate synthetase Homo sapiens 52-54 24922653-2 2014 The main action of 5-FU is the suppression of DNA replication by inhibiting Thymidylate Synthase (TS). Fluorouracil 19-23 thymidylate synthetase Homo sapiens 76-96 24922653-2 2014 The main action of 5-FU is the suppression of DNA replication by inhibiting Thymidylate Synthase (TS). Fluorouracil 19-23 thymidylate synthetase Homo sapiens 98-100 24922653-7 2014 RESULTS: There was a remarkable increase in TS protein expression levels in UM-SCC-23/WR following 5-FU treatment. Fluorouracil 99-103 thymidylate synthetase Homo sapiens 5-7 24922653-9 2014 CONCLUSION: The cell-cycle perturbation or elevation of TS protein expression may be involved in acquired 5-FU resistance and identifies 5-FU resistance mechanisms in the two different 5-FU treatment regimens. Fluorouracil 106-110 thymidylate synthetase Homo sapiens 56-58 24922653-9 2014 CONCLUSION: The cell-cycle perturbation or elevation of TS protein expression may be involved in acquired 5-FU resistance and identifies 5-FU resistance mechanisms in the two different 5-FU treatment regimens. Fluorouracil 137-141 thymidylate synthetase Homo sapiens 56-58 24922653-9 2014 CONCLUSION: The cell-cycle perturbation or elevation of TS protein expression may be involved in acquired 5-FU resistance and identifies 5-FU resistance mechanisms in the two different 5-FU treatment regimens. Fluorouracil 137-141 thymidylate synthetase Homo sapiens 56-58 24751000-3 2014 METHODS: To elucidate the mechanisms of variations to 5-FU outcome, the authors investigated MTHFR, DHFR, TYMS and SLC19A1 folate genes expression for 5-FU response in laryngeal cancer cell line (Hep-2). Fluorouracil 151-155 dihydrofolate reductase Homo sapiens 100-104 24751000-3 2014 METHODS: To elucidate the mechanisms of variations to 5-FU outcome, the authors investigated MTHFR, DHFR, TYMS and SLC19A1 folate genes expression for 5-FU response in laryngeal cancer cell line (Hep-2). Fluorouracil 151-155 thymidylate synthetase Homo sapiens 106-110 24751000-8 2014 Statistical analysis showed significant association between control group and increased expression for TYMS gene in cells treated with 100 ng/mL/5-FU chemotherapy (P<0.05). Fluorouracil 145-149 thymidylate synthetase Homo sapiens 103-107 24751000-9 2014 CONCLUSIONS: The authors found association between the highest 5-FU dose chemotherapy and increased expression levels for TYMS folate gene in laryngeal cancer cell line. Fluorouracil 63-67 thymidylate synthetase Homo sapiens 122-126 20485548-2 2010 In this report, the effects of 5-fluorouracil (5-FU) and ZD1694 on the regulation of TS gene expression were evaluated in zebrafish embryos. Fluorouracil 31-45 thymidylate synthetase Danio rerio 85-87 24618665-2 2014 The present study investigates the prognostic and predictive value of dCK and HuR expression levels for sensitivity to gemcitabine and 5-fluorouracil (5-FU) in a large phase III adjuvant trial with chemoradiation backbone in pancreatic ductal adenocarcinoma (PDA). Fluorouracil 135-149 ELAV like RNA binding protein 1 Homo sapiens 78-81 24618665-2 2014 The present study investigates the prognostic and predictive value of dCK and HuR expression levels for sensitivity to gemcitabine and 5-fluorouracil (5-FU) in a large phase III adjuvant trial with chemoradiation backbone in pancreatic ductal adenocarcinoma (PDA). Fluorouracil 151-155 ELAV like RNA binding protein 1 Homo sapiens 78-81 20485548-2 2010 In this report, the effects of 5-fluorouracil (5-FU) and ZD1694 on the regulation of TS gene expression were evaluated in zebrafish embryos. Fluorouracil 47-51 thymidylate synthetase Danio rerio 85-87 24618665-11 2014 Finally, we demonstrate that 5-FU can increase HuR function by enhancing HuR translocation from the nucleus to the cytoplasm, similar to the effect of gemcitabine in PDA cells. Fluorouracil 29-33 ELAV like RNA binding protein 1 Homo sapiens 47-50 24618665-11 2014 Finally, we demonstrate that 5-FU can increase HuR function by enhancing HuR translocation from the nucleus to the cytoplasm, similar to the effect of gemcitabine in PDA cells. Fluorouracil 29-33 ELAV like RNA binding protein 1 Homo sapiens 73-76 20485548-3 2010 Our results revealed that the expression of TS was increased by about six-fold when embryos were treated with 1.0 microM 5-FU and there was a greater than 10-fold increase in the TS protein level after treatment with 0.4 microM ZD1694. Fluorouracil 121-125 thymidylate synthetase Danio rerio 44-46 24992758-8 2014 Serum levels of TNF-alpha, IL-2, and IFN-gamma, frequencies of CD4 + and CD8+ T cells in the spleen, and splenic NK and CTL activities were also significantly increased in mice treated with 5-FU+PL or 5-FU+PTM compared with mice treated with 5-FU alone (P < 0.05). Fluorouracil 190-194 interleukin 2 Mus musculus 27-31 20485548-10 2010 Additionally, a TS stability experiment confirmed that treatment of zebrafish embryos with 5-FU could increase the TS stability significantly, and the half life of TS protein was about 2.7 times longer than in untreated embryos. Fluorouracil 91-95 thymidylate synthetase Danio rerio 16-18 24816638-5 2014 Sal reversed the 5-FU-induced increase in CD133(+) EPCAM(+) cells, epithelial-mesenchymal transition and activation of the Wnt/beta-catenin signaling pathway. Fluorouracil 17-21 catenin beta 1 Homo sapiens 127-139 20485548-10 2010 Additionally, a TS stability experiment confirmed that treatment of zebrafish embryos with 5-FU could increase the TS stability significantly, and the half life of TS protein was about 2.7 times longer than in untreated embryos. Fluorouracil 91-95 thymidylate synthetase Danio rerio 115-117 20485548-10 2010 Additionally, a TS stability experiment confirmed that treatment of zebrafish embryos with 5-FU could increase the TS stability significantly, and the half life of TS protein was about 2.7 times longer than in untreated embryos. Fluorouracil 91-95 thymidylate synthetase Danio rerio 115-117 20485548-12 2010 These findings also demonstrated that the increase in TS protein induced by 5-FU occurs at the post-transcriptional level and that increased stability and translation efficiency both contributed to the increase in TS protein levels induced by TS inhibitors. Fluorouracil 76-80 thymidylate synthetase Danio rerio 54-56 20819423-0 2010 Variants in the dihydropyrimidine dehydrogenase, methylenetetrahydrofolate reductase and thymidylate synthase genes predict early toxicity of 5-fluorouracil in colorectal cancer patients. Fluorouracil 142-156 dihydropyrimidine dehydrogenase Homo sapiens 16-47 20819423-0 2010 Variants in the dihydropyrimidine dehydrogenase, methylenetetrahydrofolate reductase and thymidylate synthase genes predict early toxicity of 5-fluorouracil in colorectal cancer patients. Fluorouracil 142-156 methylenetetrahydrofolate reductase Homo sapiens 49-84 20819423-1 2010 Adverse drug reactions to 5-fluorouracil (5-FU)-based chemotherapy have been reported to be due, in part, to genetic variants of the genes for the drug-related enzymes thymidylate synthase (TS; TYMS gene), methylenetetrahydrofolate reductase (MTHFR gene) and dihydropyrimidine dehydrogenase (DPD; DPYD gene). Fluorouracil 26-40 methylenetetrahydrofolate reductase Homo sapiens 206-241 24851048-2 2014 Based on its function of binding specifically to ganglioside GM1 on the surface of cells, a novel nanoparticle (NP) composed of a mixture of bovine serum albumin (BSA) and LTB was designed for targeted delivery of 5-fluorouracil to tumor cells. Fluorouracil 214-228 lymphotoxin beta Homo sapiens 172-175 20819423-1 2010 Adverse drug reactions to 5-fluorouracil (5-FU)-based chemotherapy have been reported to be due, in part, to genetic variants of the genes for the drug-related enzymes thymidylate synthase (TS; TYMS gene), methylenetetrahydrofolate reductase (MTHFR gene) and dihydropyrimidine dehydrogenase (DPD; DPYD gene). Fluorouracil 26-40 methylenetetrahydrofolate reductase Homo sapiens 243-248 24851048-9 2014 Hence, the results indicate that BSA-LTB NPs could be a potential nanocarrier to improve targeted delivery of 5-fluorouracil to tumor cells via mediation of LTB. Fluorouracil 110-124 lymphotoxin beta Homo sapiens 37-40 24851048-9 2014 Hence, the results indicate that BSA-LTB NPs could be a potential nanocarrier to improve targeted delivery of 5-fluorouracil to tumor cells via mediation of LTB. Fluorouracil 110-124 lymphotoxin beta Homo sapiens 157-160 20819423-1 2010 Adverse drug reactions to 5-fluorouracil (5-FU)-based chemotherapy have been reported to be due, in part, to genetic variants of the genes for the drug-related enzymes thymidylate synthase (TS; TYMS gene), methylenetetrahydrofolate reductase (MTHFR gene) and dihydropyrimidine dehydrogenase (DPD; DPYD gene). Fluorouracil 26-40 dihydropyrimidine dehydrogenase Homo sapiens 259-290 24325353-0 2014 A low Dicer expression is associated with resistance to 5-FU-based chemoradiotherapy and a shorter overall survival in patients with oral squamous cell carcinoma. Fluorouracil 56-60 dicer 1, ribonuclease III Homo sapiens 6-11 24325353-11 2014 CONCLUSION: These results suggest that Dicer is a potential biomarker for predicting the clinical response to 5-FU-based chemoradiotherapy and the overall survival in patients with OSCC. Fluorouracil 110-114 dicer 1, ribonuclease III Homo sapiens 39-44 20819423-1 2010 Adverse drug reactions to 5-fluorouracil (5-FU)-based chemotherapy have been reported to be due, in part, to genetic variants of the genes for the drug-related enzymes thymidylate synthase (TS; TYMS gene), methylenetetrahydrofolate reductase (MTHFR gene) and dihydropyrimidine dehydrogenase (DPD; DPYD gene). Fluorouracil 26-40 dihydropyrimidine dehydrogenase Homo sapiens 292-295 20819423-1 2010 Adverse drug reactions to 5-fluorouracil (5-FU)-based chemotherapy have been reported to be due, in part, to genetic variants of the genes for the drug-related enzymes thymidylate synthase (TS; TYMS gene), methylenetetrahydrofolate reductase (MTHFR gene) and dihydropyrimidine dehydrogenase (DPD; DPYD gene). Fluorouracil 26-40 dihydropyrimidine dehydrogenase Homo sapiens 297-301 20819423-1 2010 Adverse drug reactions to 5-fluorouracil (5-FU)-based chemotherapy have been reported to be due, in part, to genetic variants of the genes for the drug-related enzymes thymidylate synthase (TS; TYMS gene), methylenetetrahydrofolate reductase (MTHFR gene) and dihydropyrimidine dehydrogenase (DPD; DPYD gene). Fluorouracil 42-46 methylenetetrahydrofolate reductase Homo sapiens 206-241 20819423-1 2010 Adverse drug reactions to 5-fluorouracil (5-FU)-based chemotherapy have been reported to be due, in part, to genetic variants of the genes for the drug-related enzymes thymidylate synthase (TS; TYMS gene), methylenetetrahydrofolate reductase (MTHFR gene) and dihydropyrimidine dehydrogenase (DPD; DPYD gene). Fluorouracil 42-46 methylenetetrahydrofolate reductase Homo sapiens 243-248 20819423-1 2010 Adverse drug reactions to 5-fluorouracil (5-FU)-based chemotherapy have been reported to be due, in part, to genetic variants of the genes for the drug-related enzymes thymidylate synthase (TS; TYMS gene), methylenetetrahydrofolate reductase (MTHFR gene) and dihydropyrimidine dehydrogenase (DPD; DPYD gene). Fluorouracil 42-46 dihydropyrimidine dehydrogenase Homo sapiens 259-290 20819423-1 2010 Adverse drug reactions to 5-fluorouracil (5-FU)-based chemotherapy have been reported to be due, in part, to genetic variants of the genes for the drug-related enzymes thymidylate synthase (TS; TYMS gene), methylenetetrahydrofolate reductase (MTHFR gene) and dihydropyrimidine dehydrogenase (DPD; DPYD gene). Fluorouracil 42-46 dihydropyrimidine dehydrogenase Homo sapiens 292-295 20819423-1 2010 Adverse drug reactions to 5-fluorouracil (5-FU)-based chemotherapy have been reported to be due, in part, to genetic variants of the genes for the drug-related enzymes thymidylate synthase (TS; TYMS gene), methylenetetrahydrofolate reductase (MTHFR gene) and dihydropyrimidine dehydrogenase (DPD; DPYD gene). Fluorouracil 42-46 dihydropyrimidine dehydrogenase Homo sapiens 297-301 20513938-3 2010 Patients with genetic variations in UGT1A1 and DPYD genes are hypersensitive to Irinotecan and 5-Fluorouracil (5FU) respectively. Fluorouracil 95-109 UDP glucuronosyltransferase family 1 member A1 Homo sapiens 36-42 20513938-3 2010 Patients with genetic variations in UGT1A1 and DPYD genes are hypersensitive to Irinotecan and 5-Fluorouracil (5FU) respectively. Fluorouracil 95-109 dihydropyrimidine dehydrogenase Homo sapiens 47-51 20513938-3 2010 Patients with genetic variations in UGT1A1 and DPYD genes are hypersensitive to Irinotecan and 5-Fluorouracil (5FU) respectively. Fluorouracil 111-114 UDP glucuronosyltransferase family 1 member A1 Homo sapiens 36-42 20513938-3 2010 Patients with genetic variations in UGT1A1 and DPYD genes are hypersensitive to Irinotecan and 5-Fluorouracil (5FU) respectively. Fluorouracil 111-114 dihydropyrimidine dehydrogenase Homo sapiens 47-51 20107315-0 2010 MK-1775, a small molecule Wee1 inhibitor, enhances anti-tumor efficacy of various DNA-damaging agents, including 5-fluorouracil. Fluorouracil 113-127 WEE1 G2 checkpoint kinase Homo sapiens 26-30 19711345-3 2010 In this study, immunohistochemical expression of MIB1 was studied in a well-characterised series of early (Stages I and II) node-negative breast carcinoma cases (n = 100) with long-term follow-up that have received adjuvant chemotherapy (cyclophosphamide/methotrexate/5-fluorouracil regimen). Fluorouracil 268-282 MIB E3 ubiquitin protein ligase 1 Homo sapiens 49-53 20056608-0 2010 Arabidopsis uracil DNA glycosylase (UNG) is required for base excision repair of uracil and increases plant sensitivity to 5-fluorouracil. Fluorouracil 123-137 uracil dna glycosylase Arabidopsis thaliana 36-39 20056608-7 2010 AtUNG-deficient plants do not display any apparent phenotype, but show increased resistance to 5-fluorouracil (5-FU), a cytostatic drug that favors dUMP misincorporation into DNA. Fluorouracil 95-109 uracil dna glycosylase Arabidopsis thaliana 0-5 20056608-7 2010 AtUNG-deficient plants do not display any apparent phenotype, but show increased resistance to 5-fluorouracil (5-FU), a cytostatic drug that favors dUMP misincorporation into DNA. Fluorouracil 111-115 uracil dna glycosylase Arabidopsis thaliana 0-5 20056608-8 2010 The resistance of atung(-/-) mutants to 5-FU is accompanied by the accumulation of uracil residues in DNA. Fluorouracil 40-44 uracil dna glycosylase Arabidopsis thaliana 18-23 20023572-0 2010 Differential effects of 5-fluorouracil on glucose transport and expressions of glucose transporter proteins in gastric cancer cells. Fluorouracil 24-38 solute carrier family 2 member 1 Homo sapiens 42-59 20023572-2 2010 We hypothesized that the sensitivity of gastric cancer to 5-FU treatment might be related to the rate of glucose transport (GLUT), and investigated the expressions of GLUT1, 2, 3, and 4 in two different gastric cancer cells (SNU-216, moderately differentiated gastric adenocarcinoma; and SNU-668, signet ring cell gastric carcinoma). Fluorouracil 58-62 solute carrier family 2 member 1 Homo sapiens 105-122 20023572-2 2010 We hypothesized that the sensitivity of gastric cancer to 5-FU treatment might be related to the rate of glucose transport (GLUT), and investigated the expressions of GLUT1, 2, 3, and 4 in two different gastric cancer cells (SNU-216, moderately differentiated gastric adenocarcinoma; and SNU-668, signet ring cell gastric carcinoma). Fluorouracil 58-62 solute carrier family 2 member 1 Homo sapiens 124-128 20023572-2 2010 We hypothesized that the sensitivity of gastric cancer to 5-FU treatment might be related to the rate of glucose transport (GLUT), and investigated the expressions of GLUT1, 2, 3, and 4 in two different gastric cancer cells (SNU-216, moderately differentiated gastric adenocarcinoma; and SNU-668, signet ring cell gastric carcinoma). Fluorouracil 58-62 solute carrier family 2 member 1 Homo sapiens 167-178 20023572-5 2010 We found that 5-FU suppressed glucose uptake in SNU-216, while it stimulated GLUT in SNU-668. Fluorouracil 14-18 solute carrier family 2 member 1 Homo sapiens 77-81 20023572-6 2010 Further analysis revealed that 5-FU decreased the expression levels of GLUT1, 2, and 4 in SNU-216 cells and increased the expression levels of GLUT1, 2, and 4 in SNU-668 cells. Fluorouracil 31-35 solute carrier family 2 member 1 Homo sapiens 71-76 20023572-6 2010 Further analysis revealed that 5-FU decreased the expression levels of GLUT1, 2, and 4 in SNU-216 cells and increased the expression levels of GLUT1, 2, and 4 in SNU-668 cells. Fluorouracil 31-35 solute carrier family 2 member 1 Homo sapiens 143-148 20023572-10 2010 Taken together, these results suggest that 5-FU exerts differential effects on GLUT depending on gastric cancer cell types, which may indicate a possible explanation, at least in part, for the differing responses to 5-FU chemotherapy in gastric cancer. Fluorouracil 43-47 solute carrier family 2 member 1 Homo sapiens 79-83 20023572-10 2010 Taken together, these results suggest that 5-FU exerts differential effects on GLUT depending on gastric cancer cell types, which may indicate a possible explanation, at least in part, for the differing responses to 5-FU chemotherapy in gastric cancer. Fluorouracil 216-220 solute carrier family 2 member 1 Homo sapiens 79-83 20179204-0 2010 Suppression of cyclin D1 by hypoxia-inducible factor-1 via direct mechanism inhibits the proliferation and 5-fluorouracil-induced apoptosis of A549 cells. Fluorouracil 107-121 cyclin D1 Mus musculus 15-24 24772313-2 2014 In order to reveal the effects of smoking and alcohol consumption on the 5-fluorouracil (5-FU)-related metabolic enzymes, namely thymidylate synthase, dihydropyrimidine dehydrogenase (DPD; a sole catabolic enzyme of 5-FU), orotate phosphoribosyl transferase (OPRT) and thymidine phosphorylase, in oral squamous cell carcinomas, the mRNA expression of these enzymes was investigated in 29 surgical specimens and compared by the Brinkman index and drinking years. Fluorouracil 89-93 thymidylate synthetase Homo sapiens 129-149 24772313-2 2014 In order to reveal the effects of smoking and alcohol consumption on the 5-fluorouracil (5-FU)-related metabolic enzymes, namely thymidylate synthase, dihydropyrimidine dehydrogenase (DPD; a sole catabolic enzyme of 5-FU), orotate phosphoribosyl transferase (OPRT) and thymidine phosphorylase, in oral squamous cell carcinomas, the mRNA expression of these enzymes was investigated in 29 surgical specimens and compared by the Brinkman index and drinking years. Fluorouracil 89-93 uridine monophosphate synthetase Homo sapiens 223-257 24772313-2 2014 In order to reveal the effects of smoking and alcohol consumption on the 5-fluorouracil (5-FU)-related metabolic enzymes, namely thymidylate synthase, dihydropyrimidine dehydrogenase (DPD; a sole catabolic enzyme of 5-FU), orotate phosphoribosyl transferase (OPRT) and thymidine phosphorylase, in oral squamous cell carcinomas, the mRNA expression of these enzymes was investigated in 29 surgical specimens and compared by the Brinkman index and drinking years. Fluorouracil 89-93 uridine monophosphate synthetase Homo sapiens 259-263 24743738-8 2014 The siRNA- or shRNA-mediated knockdown of Nrf2 or HO-1 significantly suppressed cancer cell viability and tumor growth in vitro and in vivo, resulting in enhanced 5-FU sensitivity. Fluorouracil 163-167 heme oxygenase 1 Homo sapiens 50-54 24743738-11 2014 ROS generated by 5-FU upregulated TET1 expression and function, whereas antioxidant had the opposite effect. Fluorouracil 17-21 tet methylcytosine dioxygenase 1 Homo sapiens 34-38 24743738-12 2014 These results suggested that the mechanism underlying the acquisition of 5-FU resistance in CRC involves the upregulation of Nrf2 and HO-1 expression via epigenetic modifications of DNA demethylation. Fluorouracil 73-77 heme oxygenase 1 Homo sapiens 134-138 24708484-0 2014 P21 and CD166 as predictive markers of poor response and outcome after fluorouracil-based chemoradiotherapy for the patients with rectal cancer. Fluorouracil 71-83 H3 histone pseudogene 16 Homo sapiens 0-3 24708484-9 2014 CONCLUSION: These show high p21 and CD166 expression at the pretreatment biopsy were associated with tumor regression and poor prognosis in patients treated with 5-FU based CRT. Fluorouracil 162-166 H3 histone pseudogene 16 Homo sapiens 28-31 24535229-10 2014 Following treatment with the COX-2 inhibitor and 5-FU, the OPRT expression was upregulated and the DPD expression was downregulated in the resistant cells. Fluorouracil 49-53 uridine monophosphate synthetase Homo sapiens 59-63 24249161-0 2014 MicroRNA-23a antisense enhances 5-fluorouracil chemosensitivity through APAF-1/caspase-9 apoptotic pathway in colorectal cancer cells. Fluorouracil 32-46 caspase 9 Homo sapiens 79-88 24249161-9 2014 The activation of the caspases-3 and 7 was increased in miR-23a antisense and 5-FU-treated colon cancer cells compared to negative control. Fluorouracil 78-82 caspase 9 Homo sapiens 22-30 20179204-9 2010 Moreover, we found that 5-fluorouracil-triggered apoptosis of DN-HIF-transfected A549 cells was reduced by sicyclin D1 (cyclin D1-specific interference RNA) introduction, suggesting that clinical observation of HIF-1 overexpression-associated chemoresistance might be, at least partially, due to the negative regulation of cyclin D1. Fluorouracil 24-38 cyclin D1 Mus musculus 109-118 24249161-13 2014 This study shows that miR-23a antisense enhanced 5-FU-induced apoptosis in colorectal cancer cells through the APAF-1/caspase-9 apoptotic pathway. Fluorouracil 49-53 caspase 9 Homo sapiens 118-127 20179204-9 2010 Moreover, we found that 5-fluorouracil-triggered apoptosis of DN-HIF-transfected A549 cells was reduced by sicyclin D1 (cyclin D1-specific interference RNA) introduction, suggesting that clinical observation of HIF-1 overexpression-associated chemoresistance might be, at least partially, due to the negative regulation of cyclin D1. Fluorouracil 24-38 cyclin D1 Mus musculus 120-129 20219304-5 2010 5-FU is metabolised by the dihydopyrimydine dehydrogenase (DPD). Fluorouracil 0-4 dihydropyrimidine dehydrogenase Homo sapiens 27-57 23817222-9 2014 This study shows that the WNT5B germline variant rs2010851 was significantly identified as a stage-dependent prognostic marker for CC patients after 5-fluorouracil-based adjuvant therapy. Fluorouracil 149-163 Wnt family member 5B Homo sapiens 26-31 24791593-0 2014 Let-7 g microRNA sensitizes fluorouracil-resistant human hepatoma cells. Fluorouracil 28-40 microRNA let-7g Homo sapiens 0-7 24791593-2 2014 This study investigated the inhibitory effect of the let-7g microRNA on the expression of the HMGA2 gene in the fluorouracil (5-Fu)-resistant human hepatoma cell line Bel-7402/5-Fu, and the effect of let-7 g microRNA on drug sensitization in Bel-7402/5-Fu cells. Fluorouracil 112-124 microRNA let-7g Homo sapiens 53-59 24791593-2 2014 This study investigated the inhibitory effect of the let-7g microRNA on the expression of the HMGA2 gene in the fluorouracil (5-Fu)-resistant human hepatoma cell line Bel-7402/5-Fu, and the effect of let-7 g microRNA on drug sensitization in Bel-7402/5-Fu cells. Fluorouracil 112-124 high mobility group AT-hook 2 Homo sapiens 94-99 24791593-2 2014 This study investigated the inhibitory effect of the let-7g microRNA on the expression of the HMGA2 gene in the fluorouracil (5-Fu)-resistant human hepatoma cell line Bel-7402/5-Fu, and the effect of let-7 g microRNA on drug sensitization in Bel-7402/5-Fu cells. Fluorouracil 126-130 high mobility group AT-hook 2 Homo sapiens 94-99 24791593-7 2014 In addition, cyclin A was down-regulated in the let-7 g transfectants cells.The results showed that let-7 g microRNA contributed to an increase of 5-Fu-induced cell cycle inhibit in human hepatoma cell and sensitized cells to 5-Fu, leading to increased the effectiveness of the drug in treating hepatoma cancer. Fluorouracil 147-151 microRNA let-7g Homo sapiens 48-55 24791593-7 2014 In addition, cyclin A was down-regulated in the let-7 g transfectants cells.The results showed that let-7 g microRNA contributed to an increase of 5-Fu-induced cell cycle inhibit in human hepatoma cell and sensitized cells to 5-Fu, leading to increased the effectiveness of the drug in treating hepatoma cancer. Fluorouracil 147-151 microRNA let-7g Homo sapiens 100-107 24791593-7 2014 In addition, cyclin A was down-regulated in the let-7 g transfectants cells.The results showed that let-7 g microRNA contributed to an increase of 5-Fu-induced cell cycle inhibit in human hepatoma cell and sensitized cells to 5-Fu, leading to increased the effectiveness of the drug in treating hepatoma cancer. Fluorouracil 226-230 microRNA let-7g Homo sapiens 48-55 24791593-7 2014 In addition, cyclin A was down-regulated in the let-7 g transfectants cells.The results showed that let-7 g microRNA contributed to an increase of 5-Fu-induced cell cycle inhibit in human hepatoma cell and sensitized cells to 5-Fu, leading to increased the effectiveness of the drug in treating hepatoma cancer. Fluorouracil 226-230 microRNA let-7g Homo sapiens 100-107 24318989-10 2014 This study reported a carriage of ERCC1 rs11615, and rs2298881 polymorphism can be used as a predictor of response to folinic acid/5-fluorouracil (5-FU)/oxaliplatin (FOLFOX)-based chemotherapy in gastric cancer patients. Fluorouracil 131-145 ERCC excision repair 1, endonuclease non-catalytic subunit Homo sapiens 34-39 24318989-10 2014 This study reported a carriage of ERCC1 rs11615, and rs2298881 polymorphism can be used as a predictor of response to folinic acid/5-fluorouracil (5-FU)/oxaliplatin (FOLFOX)-based chemotherapy in gastric cancer patients. Fluorouracil 147-151 ERCC excision repair 1, endonuclease non-catalytic subunit Homo sapiens 34-39 24469951-0 2014 Matrix metalloproteinase 7 is a useful marker for 5-fluorouracil-based adjuvant chemotherapy in stage II and stage III colorectal cancer patients. Fluorouracil 50-64 matrix metallopeptidase 7 Homo sapiens 0-26 24469951-2 2014 The mechanism of cell killing associated with 5-FU treatment in colon cancer was also closely related to Fas-induced apoptosis, which implied that the expression level of MMP7 in colorectal cancer may be associated with the sensitivity of 5-FU treatment. Fluorouracil 46-50 matrix metallopeptidase 7 Homo sapiens 171-175 24469951-2 2014 The mechanism of cell killing associated with 5-FU treatment in colon cancer was also closely related to Fas-induced apoptosis, which implied that the expression level of MMP7 in colorectal cancer may be associated with the sensitivity of 5-FU treatment. Fluorouracil 239-243 matrix metallopeptidase 7 Homo sapiens 171-175 24469951-3 2014 To prove the hypothesis, first we verified the negative relevance between the colorectal cancer cells apoptosis in response to 5-FU treatment and MMP7 level by MTT and flow cytometry assay in vitro. Fluorouracil 127-131 matrix metallopeptidase 7 Homo sapiens 146-150 24469951-5 2014 We found that increased level of MMP7 resulted in the enhanced drug resistance in SW620 colon cancer cells treated with 5-FU in vitro. Fluorouracil 120-124 matrix metallopeptidase 7 Homo sapiens 33-37 24469951-9 2014 These data suggested that MMP7 is a useful marker for 5-FU chemotherapy sensitivity in patients with stage II-III colorectal cancer. Fluorouracil 54-58 matrix metallopeptidase 7 Homo sapiens 26-30 24281197-1 2014 PURPOSE: The purpose of the study is to analyze the relationship between tumor thymidylate synthase (TS) mRNA expression levels and raltitrexed/pemetrexed/5-FU sensitivity. Fluorouracil 155-159 thymidylate synthetase Homo sapiens 101-103 23086188-0 2014 Knockdown of MMP-7 inhibits cell proliferation and enhances sensitivity to 5-Fluorouracil and X-ray irradiation in colon cancer cells. Fluorouracil 75-89 matrix metallopeptidase 7 Homo sapiens 13-18 23086188-7 2014 We showed that the down regulation of MMP-7 inhibits colon cancer cell proliferation and sensitizes tumour cells to 5-FU and IR (P < 0.05). Fluorouracil 116-120 matrix metallopeptidase 7 Homo sapiens 38-43 24189396-4 2014 Moreover, a increased effect was also observed in boosting immunity functions when the Heps-bearing mice receiving SCPP11 combination with 5-Fu administration, including increased in thymus indexes and enhancing serum IL-2 and TNF-alpha secretion. Fluorouracil 139-143 interleukin 2 Mus musculus 218-222 24396484-3 2014 The present study revealed that the expression levels of the three antitumor miRNAs, miR-122a, miR-145 and miR-205, were significantly elevated in MDA-MB-453 LAR-type TNBC tumor cells treated with 5-fluorouracil together with ixabepilone. Fluorouracil 197-211 microRNA 145 Homo sapiens 95-102 20219304-5 2010 5-FU is metabolised by the dihydopyrimydine dehydrogenase (DPD). Fluorouracil 0-4 dihydropyrimidine dehydrogenase Homo sapiens 59-62 19968781-7 2010 Suppression of dUTPase expression using short interfering RNAs inhibited cell proliferation and sensitized HuH7 cells to 5-fluorouracil treatment. Fluorouracil 121-135 Deoxyuridine triphosphatase Drosophila melanogaster 15-22 24497922-1 2014 OBJECTIVE: To explore genes of the killer-cell immunoglobulin-like receptor (KIR) and of the HLA ligand and their relationship with the outcome of metastatic colorectal cancer (mCRC) patients treated with first-line 5-fluorouracil, leucovorin, and irinotecan (FOLFIRI). Fluorouracil 216-230 killer cell immunoglobulin like receptor, two Ig domains and short cytoplasmic tail 4 Homo sapiens 35-75 24497922-1 2014 OBJECTIVE: To explore genes of the killer-cell immunoglobulin-like receptor (KIR) and of the HLA ligand and their relationship with the outcome of metastatic colorectal cancer (mCRC) patients treated with first-line 5-fluorouracil, leucovorin, and irinotecan (FOLFIRI). Fluorouracil 216-230 killer cell immunoglobulin like receptor, two Ig domains and short cytoplasmic tail 4 Homo sapiens 77-80 24407236-0 2014 Antioxidants decrease the apoptotic effect of 5-Fu in colon cancer by regulating Src-dependent caspase-7 phosphorylation. Fluorouracil 46-50 caspase 7 Homo sapiens 95-104 19585117-4 2010 The mRNA levels of thymidine synthetase (TS) and dihydropyrimidine dehydrogenase (DPD) in HepG2 cells after oroxylin A and 5-FU combination treatment were observed by quantitative real-time PCR. Fluorouracil 123-127 dihydropyrimidine dehydrogenase Homo sapiens 82-85 24407236-7 2014 Mouse embryonic fibroblasts that are deficient in Src showed a clear resistance to 5-Fu, and knocking down Src protein expression in colon cancer cells also decreased 5-Fu-induced apoptosis. Fluorouracil 83-87 Rous sarcoma oncogene Mus musculus 50-53 24407236-7 2014 Mouse embryonic fibroblasts that are deficient in Src showed a clear resistance to 5-Fu, and knocking down Src protein expression in colon cancer cells also decreased 5-Fu-induced apoptosis. Fluorouracil 167-171 Rous sarcoma oncogene Mus musculus 107-110 19669769-2 2010 We analyze the relationship of MTHFR C677T and A1298C polymorphisms with biological, clinicopathological, genetic and epigenetic features of tumors, and the patient outcome after treatment with 5-FU-based chemotherapy to determine the contribution of MTHFR genotypes in the risk of colorectal cancer (CRC) and in the response to therapy. Fluorouracil 194-198 methylenetetrahydrofolate reductase Homo sapiens 31-36 25081659-0 2014 Liposome-mediated induction of apoptosis of human hepatoma cells by c-myc antisense phosphorothioate oligodeoxynucleotide and 5-fluorouracil. Fluorouracil 126-140 MYC proto-oncogene, bHLH transcription factor Homo sapiens 68-73 25081659-1 2014 BACKGROUND: The aim of this study was to investigate the effect of a c-myc antisense oligodeoxynucleotide and 5-fluorouracil on the expression of c-myc, invasion and proliferation of HEPG-2 liver cancer cells. Fluorouracil 110-124 MYC proto-oncogene, bHLH transcription factor Homo sapiens 146-151 25081659-8 2014 The percentage of c-myc-protein- positive cells were significantly lower in antisense oligodeoxynucleotide, 5-fluorouracil and combination groups than that in the control group (P<0.01). Fluorouracil 108-122 MYC proto-oncogene, bHLH transcription factor Homo sapiens 18-23 19669769-7 2010 MTHFR 677T allele carriers responded better to 5-FU-based chemotherapy than patients with the wild CC genotype (log rank, p = 0.05). Fluorouracil 47-51 methylenetetrahydrofolate reductase Homo sapiens 0-5 25081659-9 2014 CONCLUSIONS: A liposome-mediated c-myc antisense oligodeoxynucleotide and 5-fluorouracil can inhibit the proliferation and invasion of liver cancer cells by reducing the expression of c-myc. Fluorouracil 74-88 MYC proto-oncogene, bHLH transcription factor Homo sapiens 33-38 25081659-9 2014 CONCLUSIONS: A liposome-mediated c-myc antisense oligodeoxynucleotide and 5-fluorouracil can inhibit the proliferation and invasion of liver cancer cells by reducing the expression of c-myc. Fluorouracil 74-88 MYC proto-oncogene, bHLH transcription factor Homo sapiens 184-189 25081659-10 2014 A c-myc antisense oligodeoxynucleotide can increase the sensitivity of liver cancer cells to 5-fluorouracil and decrease the dosage of the agent necessary for efficacy, providing an experimental basis for the clinical therapy of liver cancer. Fluorouracil 93-107 MYC proto-oncogene, bHLH transcription factor Homo sapiens 2-7 20146975-1 2010 Dihydropyrimidine dehydrogenase (DPD) is a key enzyme in the metabolic catabolism of fluoropyrimidines, such as 5-Fluorouracil and its oral prodrugs derivatives, including capecitabine and ftorafur (UFT, S1). Fluorouracil 112-126 dihydropyrimidine dehydrogenase Homo sapiens 0-31 25169518-8 2014 The results of annexin V-FITC /PI staining and Hoechst 33258 staining showed that the percentage of apoptotic cells induced by SIN and 5-FU combined or alone was significantly higher than the control group (p<0.05). Fluorouracil 135-139 annexin A5 Homo sapiens 15-24 25087947-8 2014 Furthermore, combination treatment of GNA and 5-FU showed up-regulated of caspase-3, caspase-9, bax, RIP1, apoptosis-inducing factor (AIF), voltage-dependent anion channel (VDAC), cytochrome c and cyclophilin D and down-regulated bcl-2. Fluorouracil 46-50 caspase 9 Homo sapiens 85-94 25087947-8 2014 Furthermore, combination treatment of GNA and 5-FU showed up-regulated of caspase-3, caspase-9, bax, RIP1, apoptosis-inducing factor (AIF), voltage-dependent anion channel (VDAC), cytochrome c and cyclophilin D and down-regulated bcl-2. Fluorouracil 46-50 receptor interacting serine/threonine kinase 1 Homo sapiens 101-105 24434574-4 2014 We thereby investigated a possible combination of Ad-mda-7 and anticancer agents and found that Ad-mda-7 with 5-fluorouracil (5-FU), cisplatin, mitomycin C or etoposide produced greater cytotoxic effects than those by Ad-mda-7 or the agent alone. Fluorouracil 110-124 interleukin 24 Homo sapiens 53-58 20146975-1 2010 Dihydropyrimidine dehydrogenase (DPD) is a key enzyme in the metabolic catabolism of fluoropyrimidines, such as 5-Fluorouracil and its oral prodrugs derivatives, including capecitabine and ftorafur (UFT, S1). Fluorouracil 112-126 dihydropyrimidine dehydrogenase Homo sapiens 33-36 24434574-4 2014 We thereby investigated a possible combination of Ad-mda-7 and anticancer agents and found that Ad-mda-7 with 5-fluorouracil (5-FU), cisplatin, mitomycin C or etoposide produced greater cytotoxic effects than those by Ad-mda-7 or the agent alone. Fluorouracil 110-124 interleukin 24 Homo sapiens 99-104 24434574-4 2014 We thereby investigated a possible combination of Ad-mda-7 and anticancer agents and found that Ad-mda-7 with 5-fluorouracil (5-FU), cisplatin, mitomycin C or etoposide produced greater cytotoxic effects than those by Ad-mda-7 or the agent alone. Fluorouracil 110-124 interleukin 24 Homo sapiens 99-104 20407238-1 2010 BACKGROUND: Expression levels of thymidylate synthase (TS), dihydropyrimidine dehydrogenase (DPD), and orotate phosphoribosyltransferase (OPRT) have been reported to be associated with tumor response to 5-fluorouracil (5-FU). Fluorouracil 203-217 dihydropyrimidine dehydrogenase Homo sapiens 60-91 24434574-4 2014 We thereby investigated a possible combination of Ad-mda-7 and anticancer agents and found that Ad-mda-7 with 5-fluorouracil (5-FU), cisplatin, mitomycin C or etoposide produced greater cytotoxic effects than those by Ad-mda-7 or the agent alone. Fluorouracil 126-130 interleukin 24 Homo sapiens 99-104 24434574-4 2014 We thereby investigated a possible combination of Ad-mda-7 and anticancer agents and found that Ad-mda-7 with 5-fluorouracil (5-FU), cisplatin, mitomycin C or etoposide produced greater cytotoxic effects than those by Ad-mda-7 or the agent alone. Fluorouracil 126-130 interleukin 24 Homo sapiens 99-104 20407238-1 2010 BACKGROUND: Expression levels of thymidylate synthase (TS), dihydropyrimidine dehydrogenase (DPD), and orotate phosphoribosyltransferase (OPRT) have been reported to be associated with tumor response to 5-fluorouracil (5-FU). Fluorouracil 219-223 dihydropyrimidine dehydrogenase Homo sapiens 60-91 20407238-8 2010 CONCLUSION: DPD and OPRT protein levels in CRC suggest that female gender and colonic tumors are positive prognostic factors in patients who receive chemotherapy with 5-FU. Fluorouracil 167-171 dihydropyrimidine dehydrogenase Homo sapiens 12-15 20058135-1 2010 UFT and S-1 are oral 5-fluorouracil (5-FU) derivative drugs containing an inhibitor of dihydropyrimidine dehydrogenase (DPD); they are defined as DPD-inhibitory fluoropyrimidine (DIF). Fluorouracil 37-41 dihydropyrimidine dehydrogenase Homo sapiens 146-149 24846461-9 2014 We here show that this temporal separation of pro- and anti-apoptotic signaling induced by inhibition of Dicer1 is synergistic and synthetic lethal to low-dose 5-FU chemotherapy in p53-mutated HACAT cells. Fluorouracil 160-164 dicer 1, ribonuclease III Homo sapiens 105-111 20058135-2 2010 Because DPD is the key enzyme of 5-FU degradation, 5-FU is not active in primary lung cancers with high DPD activity, which causes rapid degradation of 5-FU. Fluorouracil 33-37 dihydropyrimidine dehydrogenase Homo sapiens 8-11 20058135-3 2010 Thus, theoretically, a DIF can overcome a cancer"s resistance to 5-FU through inhibiting the enzyme activity of DPD, with the result that 5-FU may be active in primary lung cancer. Fluorouracil 65-69 dihydropyrimidine dehydrogenase Homo sapiens 112-115 20058135-3 2010 Thus, theoretically, a DIF can overcome a cancer"s resistance to 5-FU through inhibiting the enzyme activity of DPD, with the result that 5-FU may be active in primary lung cancer. Fluorouracil 138-142 dihydropyrimidine dehydrogenase Homo sapiens 112-115 20087047-8 2010 The expression level of DPD was significantly low, so we suggested that the severe bone marrow suppression might have been caused by the disordered metabolism of 5-FU. Fluorouracil 162-166 dihydropyrimidine dehydrogenase Homo sapiens 24-27 23834160-5 2014 Compared to the control, all used six doses (10, 50, 100, 150, 250 and 250 microM) of 5-FU, colchicine and licofelone, which were cytotoxic and reduced the number of H-Ras transformed 5RP7 cells by as much as 78, 72 and 92%, respectively. Fluorouracil 86-90 HRas proto-oncogene, GTPase Rattus norvegicus 166-171 19669768-8 2010 The effect of the 5-fluorouracil (5-FU)-induced cell death by knockdown of IGF-IR was also investigated by methyl thiazolyl tetrazolium assay. Fluorouracil 18-32 insulin like growth factor 1 receptor Homo sapiens 75-81 23494117-0 2014 Enhancement of 5-fluorouracil-induced cytotoxicity by leucovorin in 5-fluorouracil-resistant gastric cancer cells with upregulated expression of thymidylate synthase. Fluorouracil 15-29 thymidylate synthetase Homo sapiens 145-165 23494117-0 2014 Enhancement of 5-fluorouracil-induced cytotoxicity by leucovorin in 5-fluorouracil-resistant gastric cancer cells with upregulated expression of thymidylate synthase. Fluorouracil 68-82 thymidylate synthetase Homo sapiens 145-165 19669768-8 2010 The effect of the 5-fluorouracil (5-FU)-induced cell death by knockdown of IGF-IR was also investigated by methyl thiazolyl tetrazolium assay. Fluorouracil 34-38 insulin like growth factor 1 receptor Homo sapiens 75-81 19709902-7 2009 Our results show that IL-21 therapy can be successfully combined with agents from different chemotherapeutic drug classes, i.e. topoisomerase II inhibitors (PLD), anti-metabolites (5-FU) and platinum analogs (oxaliplatin) provided that IL-21 therapy is delayed relative to chemotherapy. Fluorouracil 181-185 interleukin 21 Mus musculus 22-27 25150310-11 2014 After knock-down ANXA2 expression using ANXA2 small interfering RNA, the drug sensitivity of SGC7901/DDP cells to doxorubicin, 5-FU and DDP increased. Fluorouracil 127-131 annexin A2 Homo sapiens 17-22 26629940-6 2014 Furthermore, at indicated times, 5-FU led to the reduced Bcl-2 and NF-kappaB expression and increased Bax expression while triptorelin plus 5-FU increased Bcl-2 and NF-kappaB expression and decreased Bax expression. Fluorouracil 140-144 BCL2 associated X, apoptosis regulator Rattus norvegicus 200-203 24391839-0 2013 Amelioration of cancer stem cells in macrophage colony stimulating factor-expressing U87MG-human glioblastoma upon 5-fluorouracil therapy. Fluorouracil 115-129 colony stimulating factor 1 Homo sapiens 37-73 24391839-4 2013 Cytotoxicity of anti-cancer drug 5-fluorouracil (5-FU) was evaluated on both U87MG and U87-MCSF cells. Fluorouracil 33-47 colony stimulating factor 1 Homo sapiens 91-95 24391839-4 2013 Cytotoxicity of anti-cancer drug 5-fluorouracil (5-FU) was evaluated on both U87MG and U87-MCSF cells. Fluorouracil 49-53 colony stimulating factor 1 Homo sapiens 91-95 24391839-5 2013 Interestingly, the proliferation of U87-MCSF cells was less (p<0.001) than that of U87MG cells alone, after treatment with 5-FU. Fluorouracil 126-130 colony stimulating factor 1 Homo sapiens 40-44 24391839-6 2013 Significant decrease in expression levels of cyclin E and A2 quantified by real time PCR analysis corroborated the reduced proliferation of 5-FU treated U87-MCSF cells. Fluorouracil 140-144 colony stimulating factor 1 Homo sapiens 157-161 24391839-8 2013 Notch-1 upregulation induced a possible epithelial-mesenchymal transition in U87-MCSF cells, which accounted for an increase in the proportion of CD24(high)/CD44(less) cancer stem cells in U87-MCSF cells after 5-FU treatment. Fluorouracil 210-214 colony stimulating factor 1 Homo sapiens 81-85 24391839-9 2013 The elevated resistance of U87-MCSF cells towards 5-FU was due to the increase in the expressions (10.2 and 6 fold) of ABCB1 and mdm2, respectively. Fluorouracil 50-54 colony stimulating factor 1 Homo sapiens 31-35 24391839-11 2013 Our studies provided mechanistic insights into drug resistance of U87MG cells and also described the pivotal role played by MCSF in augmenting the resistance of U87MG cells to 5-FU. Fluorouracil 176-180 colony stimulating factor 1 Homo sapiens 124-128 19949674-2 2009 Adenosine triphosphate-based chemotherapy response assay (ATP-CRA) was employed to retrieve chemoresponse to 5-fluorouracil (5-FU), doxetaxel, doxorubicin, epirubicin, and paclitaxel in 49 patients. Fluorouracil 109-123 myotubularin related protein 11 Homo sapiens 62-65 19949674-2 2009 Adenosine triphosphate-based chemotherapy response assay (ATP-CRA) was employed to retrieve chemoresponse to 5-fluorouracil (5-FU), doxetaxel, doxorubicin, epirubicin, and paclitaxel in 49 patients. Fluorouracil 125-129 myotubularin related protein 11 Homo sapiens 62-65 19839788-1 2009 In the present investigation, testosterone (T) was evaluated as a targeting ligand to direct the site-specific delivery of 5-Fluorouracil (5-FU) bearing liposomes to the androgen receptor (ARs) positive tumors and other organs like prostate, brain, and testis. Fluorouracil 123-137 androgen receptor Rattus norvegicus 170-187 19839788-1 2009 In the present investigation, testosterone (T) was evaluated as a targeting ligand to direct the site-specific delivery of 5-Fluorouracil (5-FU) bearing liposomes to the androgen receptor (ARs) positive tumors and other organs like prostate, brain, and testis. Fluorouracil 139-143 androgen receptor Rattus norvegicus 170-187 19465420-1 2009 BACKGROUND: Methylenetetrahydrofolate reductase is a pivotal enzyme in folate metabolism and 5-fluorouracil (5-FU) cytotoxicity. Fluorouracil 93-107 methylenetetrahydrofolate reductase Homo sapiens 12-47 19342154-1 2009 Among gene therapy strategies elaborated to kill cancer cells, one uses the CodA gene, coding for cytosine deaminase (CD) that converts 5-fluorocytosine (5-FC) into toxic 5-fluorouracil (5-FU). Fluorouracil 171-185 CODA Homo sapiens 76-80 19342154-1 2009 Among gene therapy strategies elaborated to kill cancer cells, one uses the CodA gene, coding for cytosine deaminase (CD) that converts 5-fluorocytosine (5-FC) into toxic 5-fluorouracil (5-FU). Fluorouracil 187-191 CODA Homo sapiens 76-80 19663627-1 2009 BACKGROUND: Dihydropyrimidine dehydrogenase (DPD) is the first rate limiting enzyme that catabolizes 5-fluorouracil. Fluorouracil 101-115 dihydropyrimidine dehydrogenase Homo sapiens 12-43 19663627-1 2009 BACKGROUND: Dihydropyrimidine dehydrogenase (DPD) is the first rate limiting enzyme that catabolizes 5-fluorouracil. Fluorouracil 101-115 dihydropyrimidine dehydrogenase Homo sapiens 45-48 19645718-10 2009 UPP-1 functions as a key regulator of the pyrimidine salvage pathway in C. elegans, as mutation of upp-1 results in strong 5-FU resistance. Fluorouracil 123-127 Uridine and thymidine phosphorylase Caenorhabditis elegans 0-5 19645718-10 2009 UPP-1 functions as a key regulator of the pyrimidine salvage pathway in C. elegans, as mutation of upp-1 results in strong 5-FU resistance. Fluorouracil 123-127 Uridine and thymidine phosphorylase Caenorhabditis elegans 99-104 19531543-4 2009 In vitro ATP-CRA was used to analyze chemosensitivity for 5-fluorouracil (5-FU), docetaxel, doxorubicin, epirubicin, vinorelbine, gemcitabine, methotrexate (MTX), oxaliplatin and paclitaxel. Fluorouracil 58-72 myotubularin related protein 11 Homo sapiens 13-16 19531543-4 2009 In vitro ATP-CRA was used to analyze chemosensitivity for 5-fluorouracil (5-FU), docetaxel, doxorubicin, epirubicin, vinorelbine, gemcitabine, methotrexate (MTX), oxaliplatin and paclitaxel. Fluorouracil 74-78 myotubularin related protein 11 Homo sapiens 13-16 19048402-7 2009 The HT-29 cell line was found to be homozygous for TS 2R and 1494ins6 and T homozygous for MTHFR 677 polymorphisms predicting high 5-FU sensitivity (IC(50): 10 microM). Fluorouracil 131-135 methylenetetrahydrofolate reductase Homo sapiens 91-96 19048402-8 2009 TS 3R homozygosity, TS 1496del6 and MTHFR 677CT heterozygosity may explain the modest 5-FU sensitivity (IC(50): 1.1 mM) of the HCA-7 cell line. Fluorouracil 86-90 methylenetetrahydrofolate reductase Homo sapiens 36-41 19714313-2 2009 However, the majority of administered 5-FU is known to be catabolized in vivo in the liver where Dihydropyrimidine dehydrogenase (DPD) is abundantly expressed to degrade 5-FU. Fluorouracil 38-42 dihydropyrimidine dehydrogenase Homo sapiens 97-128 19714313-2 2009 However, the majority of administered 5-FU is known to be catabolized in vivo in the liver where Dihydropyrimidine dehydrogenase (DPD) is abundantly expressed to degrade 5-FU. Fluorouracil 38-42 dihydropyrimidine dehydrogenase Homo sapiens 130-133 19714313-2 2009 However, the majority of administered 5-FU is known to be catabolized in vivo in the liver where Dihydropyrimidine dehydrogenase (DPD) is abundantly expressed to degrade 5-FU. Fluorouracil 170-174 dihydropyrimidine dehydrogenase Homo sapiens 97-128 19714313-2 2009 However, the majority of administered 5-FU is known to be catabolized in vivo in the liver where Dihydropyrimidine dehydrogenase (DPD) is abundantly expressed to degrade 5-FU. Fluorouracil 170-174 dihydropyrimidine dehydrogenase Homo sapiens 130-133 19622726-4 2009 In addition, AEG-1 enhances the expression of dihydropyrimidine dehydrogenase (DPYD) that catalyzes the initial and rate-limiting step in the catabolism of 5-FU. Fluorouracil 156-160 metadherin Mus musculus 13-18 19622726-5 2009 siRNA-mediated inhibition of AEG-1, LSF, or DPYD significantly increased the sensitivity of HCC cells to 5-FU in vitro and a lentivirus delivering AEG-1 siRNA in combination with 5-FU markedly inhibited growth of HCC cells xenotransplanted in athymic nude mice when compared to either agent alone. Fluorouracil 105-109 metadherin Mus musculus 29-34 19622726-5 2009 siRNA-mediated inhibition of AEG-1, LSF, or DPYD significantly increased the sensitivity of HCC cells to 5-FU in vitro and a lentivirus delivering AEG-1 siRNA in combination with 5-FU markedly inhibited growth of HCC cells xenotransplanted in athymic nude mice when compared to either agent alone. Fluorouracil 179-183 metadherin Mus musculus 29-34 18980827-4 2009 Here, we demonstrate that IL-1Ra expression in BM cells and in circulation was elevated temporarily during 5-Fu-induced myelosuppression. Fluorouracil 107-111 interleukin 1 receptor antagonist Mus musculus 26-32 18980827-6 2009 Due perhaps to its reversible suppression of the cell cycle progression of BM cells, pretreatment of normal mice with exogenous IL-1Ra reduced the acute lethal toxicity and BM suppression of 5-Fu, and accelerated the recoveries of BM cells and platelets following 5-Fu treatment. Fluorouracil 191-195 interleukin 1 receptor antagonist Mus musculus 128-134 18980827-6 2009 Due perhaps to its reversible suppression of the cell cycle progression of BM cells, pretreatment of normal mice with exogenous IL-1Ra reduced the acute lethal toxicity and BM suppression of 5-Fu, and accelerated the recoveries of BM cells and platelets following 5-Fu treatment. Fluorouracil 264-268 interleukin 1 receptor antagonist Mus musculus 128-134 19574900-7 2009 Clinical resolution of the neoplasm obtained using topical 5-FU was accompanied by a reduction in the expression of MMP-2, MMP-9, and TIMP-1 in tears and dysplastic conjunctival epithelium. Fluorouracil 59-63 matrix metallopeptidase 9 Homo sapiens 123-128 19584296-6 2009 Independent validation experiment using five new pancreatic cancer cell lines confirmed that an inverse correlation between E-cadherin and Zeb-1 correlated closely with resistance to gemcitabine, 5-FU, and cisplatin. Fluorouracil 196-200 zinc finger E-box binding homeobox 1 Homo sapiens 139-144 18830594-0 2009 Zebularine suppresses the apoptotic potential of 5-fluorouracil via cAMP/PKA/CREB pathway against human oral squamous cell carcinoma cells. Fluorouracil 49-63 cAMP responsive element binding protein 1 Homo sapiens 77-81 18830594-3 2009 METHOD: We investigated the effect of a DNA methyltransferase (DNMT) inhibitor, zebularine (Zeb), on the chemosensitivity of 5-FU and cisplatin (CDDP) by MTT and TUNEL methods, and compared the molecular mechanism of action with those of a GSK3beta inhibitor, LiCl, and an Hsp90 inhibitor, 17-AAG. Fluorouracil 125-129 DNA methyltransferase 1 Homo sapiens 40-61 18830594-3 2009 METHOD: We investigated the effect of a DNA methyltransferase (DNMT) inhibitor, zebularine (Zeb), on the chemosensitivity of 5-FU and cisplatin (CDDP) by MTT and TUNEL methods, and compared the molecular mechanism of action with those of a GSK3beta inhibitor, LiCl, and an Hsp90 inhibitor, 17-AAG. Fluorouracil 125-129 DNA methyltransferase 1 Homo sapiens 63-67 19217205-6 2009 Furthermore, 5-FU has significantly lower inhibition effect on Huh7-EGFRvIII cells then on both Huh-7 and Huh7-EGFR cells in vitro and in vivo. Fluorouracil 13-17 MIR7-3 host gene Homo sapiens 63-67 19217205-6 2009 Furthermore, 5-FU has significantly lower inhibition effect on Huh7-EGFRvIII cells then on both Huh-7 and Huh7-EGFR cells in vitro and in vivo. Fluorouracil 13-17 MIR7-3 host gene Homo sapiens 96-101 19217205-6 2009 Furthermore, 5-FU has significantly lower inhibition effect on Huh7-EGFRvIII cells then on both Huh-7 and Huh7-EGFR cells in vitro and in vivo. Fluorouracil 13-17 MIR7-3 host gene Homo sapiens 106-110 19217207-3 2009 Accordingly, TRAP1 levels were increased in HT-29 colorectal carcinoma cells resistant to 5-fluorouracil, oxaliplatin and irinotecan. Fluorouracil 90-104 TNF receptor associated protein 1 Homo sapiens 13-18 19217207-5 2009 Interestingly, TRAP1 overexpression leads to 5-fluorouracil-, oxaliplatin- and irinotecan-resistant phenotypes in different neoplastic cells. Fluorouracil 45-59 TNF receptor associated protein 1 Homo sapiens 15-20 19567146-7 2009 Re-expression of wild-type RASSF1A could enhance the inhibition of cell proliferation and the percentage of apoptotic cells following cell treatment with mitomycin, but had no significant effect when combined with adriamycin, etoposide, 5-fluorouracil and cisplatin treatment. Fluorouracil 237-251 Ras association domain family member 1 Homo sapiens 27-34 19219653-7 2009 Earlier studies revealed that the transcription of genes for key enzymes like thymidylate synthase, thymidine kinase, and dihydropyrimidine dehydrogenase are regulated by 5-FU. Fluorouracil 171-175 dihydropyrimidine dehydrogenase Homo sapiens 78-153 19509240-8 2009 IGF1R depletion induced apoptosis, blocked cell survival, and sensitized to 5-fluorouracil and etoposide. Fluorouracil 76-90 insulin like growth factor 1 receptor Homo sapiens 0-5 19530960-2 2009 This study aims to assess the predictive value of DPYD variation with respect to previously described DPYD variants for 5-FU toxicity. Fluorouracil 120-124 dihydropyrimidine dehydrogenase Homo sapiens 102-106 19530960-5 2009 DPYD haplotypes were inferred and their associations with severe 5-FU toxicity were assessed. Fluorouracil 65-69 dihydropyrimidine dehydrogenase Homo sapiens 0-4 19530960-9 2009 Furthermore, a comparison with other studies suggests that the relative importance of particular DPYD mutations (IVS14+1G>A and c.2846A>T) for predicting severe 5-FU toxicity differs geographically across Europe. Fluorouracil 167-171 dihydropyrimidine dehydrogenase Homo sapiens 97-101 19478948-12 2009 The combination of MTA with 5-FU or 6-TG, in the treatment of MTAP-negative tumors, may produce a significantly improved therapeutic index. Fluorouracil 28-32 methylthioadenosine phosphorylase Homo sapiens 62-66 19595187-0 2009 [Effect of Fluorouracil-inducible GM-CSF gene therapy regulated by Egr-1 promoter on chemotherapeutic hematopoietic damage of tumor-bearing mice]. Fluorouracil 11-23 colony stimulating factor 2 (granulocyte-macrophage) Mus musculus 34-40 19595187-8 2009 The effect of N-acetylcysteine (a free radical scavenger) on GM-CSF production post-exposure to 5-Fu was examined. Fluorouracil 96-100 colony stimulating factor 2 (granulocyte-macrophage) Mus musculus 61-67 19595187-14 2009 RESULTS: The results indicated that the activity of EGFP and the amounts of secreted GM-CSF in HFCL/EG cells exposed to 5-Fu increased as compared to non-5-Fu group with flow cytometry, RT-PCR and ELISA respectively. Fluorouracil 120-124 colony stimulating factor 2 (granulocyte-macrophage) Mus musculus 85-91 19595187-15 2009 N-acetylcysteine significantly decreased the concentration of GM-CSF in HFCL/EG cells treated with 5-FU. Fluorouracil 99-103 colony stimulating factor 2 (granulocyte-macrophage) Mus musculus 62-68 19450180-6 2009 In addition, a growing body of in vitro and clinical evidence suggests that the MTHFR SNPs may be an important pharmacogenetic determinant of response to and toxicity of 5-fluorouracil (5FU) and methotrexate (MTX)-based cancer and anti-inflammatory chemotherapy. Fluorouracil 170-184 methylenetetrahydrofolate reductase Homo sapiens 80-85 24324676-7 2013 In addition, in tumor-bearing mice, the relationship between the therapeutic effects of chemotherapy (5-FU) and the tumor accumulation of (99m)Tc-C3(BHam)2-annexin A5 just after the first treatment of 5-FU was evaluated. Fluorouracil 102-106 annexin A5 Mus musculus 156-166 24324676-13 2013 Accumulation of (99m)Tc-C3(BHam)2-annexin A5 in tumors significantly increased after 5-FU treatment. Fluorouracil 85-89 annexin A5 Mus musculus 34-44 19450180-6 2009 In addition, a growing body of in vitro and clinical evidence suggests that the MTHFR SNPs may be an important pharmacogenetic determinant of response to and toxicity of 5-fluorouracil (5FU) and methotrexate (MTX)-based cancer and anti-inflammatory chemotherapy. Fluorouracil 186-189 methylenetetrahydrofolate reductase Homo sapiens 80-85 24091730-5 2013 Ccne1(-/-) mice showed normal hematopoiesis in vivo under homeostatic conditions but a severe impairment following myeloablative stress induced by 5-fluorouracil (5-FU). Fluorouracil 147-161 cyclin E1 Mus musculus 0-5 19179360-6 2009 However, HPs, but not HSCs, can be induced to express VASH1 after BM suppression by 5-FU. Fluorouracil 84-88 vasohibin 1 Homo sapiens 54-59 24091730-5 2013 Ccne1(-/-) mice showed normal hematopoiesis in vivo under homeostatic conditions but a severe impairment following myeloablative stress induced by 5-fluorouracil (5-FU). Fluorouracil 163-167 cyclin E1 Mus musculus 0-5 24091730-6 2013 Under these conditions, Ccne1(-/-) HSCs were less efficient in entering the cell cycle, resulting in decreased hematopoiesis and reduced survival of mutant mice upon weekly 5-FU treatment. Fluorouracil 173-177 cyclin E1 Mus musculus 24-29 24132143-6 2013 Overexpression of exogenous ACLy by lentivirus transduction in chemo-naive colorectal cancer cells led to significant chemoresistance to SN38 but not to 5-fluorouracil or oxaliplatin. Fluorouracil 153-167 ATP citrate lyase Homo sapiens 28-32 24394000-0 2013 [A case of good response in a rectal cancer patient with decreased dihydropyrimidine dehydrogenase activity because of strict control of the 5-fluorouracil dose]. Fluorouracil 141-155 dihydropyrimidine dehydrogenase Homo sapiens 67-98 24161202-0 2013 CpG oligodeoxynucleotides enhance chemosensitivity of 5-fluorouracil in HepG2 human hepatoma cells via downregulation of the antiapoptotic factors survivin and livin. Fluorouracil 54-68 baculoviral IAP repeat containing 7 Homo sapiens 160-165 24161202-7 2013 The mRNA expression of Livin and Survivin decreased in cells treated with CpG-ODN alone but increased in cells treated with 5-FU alone. Fluorouracil 124-128 baculoviral IAP repeat containing 7 Homo sapiens 23-28 24161202-8 2013 However, CpG-ODN in combination with 5-FU could down-regulate the mRNA expression of Livin and Survivin within HepG2 cells. Fluorouracil 37-41 baculoviral IAP repeat containing 7 Homo sapiens 85-90 24161202-9 2013 CONCLUSIONS: Our finding demonstrated that CpG-ODN enhanced the chemosentivity of 5-FU in HepG2 human hepatoma cells at least in part by down-regulating the expression of Livin and Survivin, leading to apoptosis and further inducing cell cycle arrest at S phase. Fluorouracil 82-86 baculoviral IAP repeat containing 7 Homo sapiens 171-176 24124444-6 2013 Our results suggest that CPA1, CPA2, and HMS1 confer 5-FU resistance by stimulating pyrimidine biosynthesis. Fluorouracil 53-57 Hms1p Saccharomyces cerevisiae S288C 41-45 24124444-8 2013 In contrast, HAM1 and YJL055W confer 5-FU resistance in a ura2 mutant, and selectively inhibit incorporation into RNA of 5-FU but not uracil. Fluorouracil 37-41 bifunctional carbamoylphosphate synthetase/aspartate transcarbamylase Saccharomyces cerevisiae S288C 58-62 23821160-3 2013 METHODS: NR4A2 was transfected into GC cells to investigate its effects on chemoresistance to 5-fluorouracil and the tumorigenicity in nude mice. Fluorouracil 94-108 nuclear receptor subfamily 4, group A, member 2 Mus musculus 9-14 23821160-7 2013 RESULTS: Ectopic expression of NR4A2 significantly increased the chemoresistance and attenuated 5-fluorouracil-induced apoptosis. Fluorouracil 96-110 nuclear receptor subfamily 4 group A member 2 Homo sapiens 31-36 23821160-11 2013 High expression of NR4A2 (immunoreactive score >= 3) in cancer cells significantly predicted an unfavorable postoperative disease-specific survival of patients with stage I to III GC (P = .011), especially for those who received 5-fluorouracil-based chemotherapy (P = .016). Fluorouracil 232-246 nuclear receptor subfamily 4 group A member 2 Homo sapiens 19-24 23821160-14 2013 CONCLUSIONS: High NR4A2 expression in GC cells confers chemoresistance, attenuates 5-fluorouracil-induced apoptosis, and predicts an unfavorable survival, especially for those who received chemotherapy. Fluorouracil 83-97 nuclear receptor subfamily 4, group A, member 2 Mus musculus 18-23 23856855-1 2013 5-Fluorouracil (5-FU) is rapidly degraded by dihyropyrimidine dehydrogenase (DPD). Fluorouracil 0-14 dihydropyrimidine dehydrogenase Homo sapiens 45-75 23856855-1 2013 5-Fluorouracil (5-FU) is rapidly degraded by dihyropyrimidine dehydrogenase (DPD). Fluorouracil 0-14 dihydropyrimidine dehydrogenase Homo sapiens 77-80 23856855-1 2013 5-Fluorouracil (5-FU) is rapidly degraded by dihyropyrimidine dehydrogenase (DPD). Fluorouracil 16-20 dihydropyrimidine dehydrogenase Homo sapiens 45-75 23856855-1 2013 5-Fluorouracil (5-FU) is rapidly degraded by dihyropyrimidine dehydrogenase (DPD). Fluorouracil 16-20 dihydropyrimidine dehydrogenase Homo sapiens 77-80 24024896-0 2013 ABCC11/MRP8 polymorphisms affect 5-fluorouracil-induced severe toxicity and hepatic expression. Fluorouracil 33-47 ATP binding cassette subfamily C member 11 Homo sapiens 0-6 24024896-0 2013 ABCC11/MRP8 polymorphisms affect 5-fluorouracil-induced severe toxicity and hepatic expression. Fluorouracil 33-47 ATP binding cassette subfamily C member 11 Homo sapiens 7-11 24024896-1 2013 AIM: Because 5-fluorodeoxyuridine monophosphate (5-FdUMP), an anabolic active metabolite of 5-fluorouracil (5-FU), is a substrate of MRP8 (encoded by ABCC11), we investigated whether ABCC11 polymorphisms play a role in severe toxicity of 5-FU. Fluorouracil 92-106 ATP binding cassette subfamily C member 11 Homo sapiens 133-137 24024896-1 2013 AIM: Because 5-fluorodeoxyuridine monophosphate (5-FdUMP), an anabolic active metabolite of 5-fluorouracil (5-FU), is a substrate of MRP8 (encoded by ABCC11), we investigated whether ABCC11 polymorphisms play a role in severe toxicity of 5-FU. Fluorouracil 92-106 ATP binding cassette subfamily C member 11 Homo sapiens 150-156 24024896-1 2013 AIM: Because 5-fluorodeoxyuridine monophosphate (5-FdUMP), an anabolic active metabolite of 5-fluorouracil (5-FU), is a substrate of MRP8 (encoded by ABCC11), we investigated whether ABCC11 polymorphisms play a role in severe toxicity of 5-FU. Fluorouracil 92-106 ATP binding cassette subfamily C member 11 Homo sapiens 183-189 24024896-1 2013 AIM: Because 5-fluorodeoxyuridine monophosphate (5-FdUMP), an anabolic active metabolite of 5-fluorouracil (5-FU), is a substrate of MRP8 (encoded by ABCC11), we investigated whether ABCC11 polymorphisms play a role in severe toxicity of 5-FU. Fluorouracil 108-112 ATP binding cassette subfamily C member 11 Homo sapiens 133-137 24024896-1 2013 AIM: Because 5-fluorodeoxyuridine monophosphate (5-FdUMP), an anabolic active metabolite of 5-fluorouracil (5-FU), is a substrate of MRP8 (encoded by ABCC11), we investigated whether ABCC11 polymorphisms play a role in severe toxicity of 5-FU. Fluorouracil 108-112 ATP binding cassette subfamily C member 11 Homo sapiens 150-156 24024896-1 2013 AIM: Because 5-fluorodeoxyuridine monophosphate (5-FdUMP), an anabolic active metabolite of 5-fluorouracil (5-FU), is a substrate of MRP8 (encoded by ABCC11), we investigated whether ABCC11 polymorphisms play a role in severe toxicity of 5-FU. Fluorouracil 108-112 ATP binding cassette subfamily C member 11 Homo sapiens 183-189 24024896-1 2013 AIM: Because 5-fluorodeoxyuridine monophosphate (5-FdUMP), an anabolic active metabolite of 5-fluorouracil (5-FU), is a substrate of MRP8 (encoded by ABCC11), we investigated whether ABCC11 polymorphisms play a role in severe toxicity of 5-FU. Fluorouracil 238-242 ATP binding cassette subfamily C member 11 Homo sapiens 133-137 24024896-1 2013 AIM: Because 5-fluorodeoxyuridine monophosphate (5-FdUMP), an anabolic active metabolite of 5-fluorouracil (5-FU), is a substrate of MRP8 (encoded by ABCC11), we investigated whether ABCC11 polymorphisms play a role in severe toxicity of 5-FU. Fluorouracil 238-242 ATP binding cassette subfamily C member 11 Homo sapiens 150-156 24024896-1 2013 AIM: Because 5-fluorodeoxyuridine monophosphate (5-FdUMP), an anabolic active metabolite of 5-fluorouracil (5-FU), is a substrate of MRP8 (encoded by ABCC11), we investigated whether ABCC11 polymorphisms play a role in severe toxicity of 5-FU. Fluorouracil 238-242 ATP binding cassette subfamily C member 11 Homo sapiens 183-189 19383847-5 2009 Resistance to bolus 5-FU was associated with lower expression of UMP kinase (UMPK), an enzyme that plays an important role in the activation of 5-FU to 5-FUTP and its incorporation into RNA. Fluorouracil 20-24 cytidine/uridine monophosphate kinase 1 Homo sapiens 65-75 19383847-5 2009 Resistance to bolus 5-FU was associated with lower expression of UMP kinase (UMPK), an enzyme that plays an important role in the activation of 5-FU to 5-FUTP and its incorporation into RNA. Fluorouracil 20-24 cytidine/uridine monophosphate kinase 1 Homo sapiens 77-81 19383847-5 2009 Resistance to bolus 5-FU was associated with lower expression of UMP kinase (UMPK), an enzyme that plays an important role in the activation of 5-FU to 5-FUTP and its incorporation into RNA. Fluorouracil 144-148 cytidine/uridine monophosphate kinase 1 Homo sapiens 65-75 19383847-5 2009 Resistance to bolus 5-FU was associated with lower expression of UMP kinase (UMPK), an enzyme that plays an important role in the activation of 5-FU to 5-FUTP and its incorporation into RNA. Fluorouracil 144-148 cytidine/uridine monophosphate kinase 1 Homo sapiens 77-81 19383847-7 2009 Herein, we show that UMPK down-regulation in 5-FU-sensitive cells (HCT-8/P) induces resistance to bolus 5-FU treatment. Fluorouracil 45-49 cytidine/uridine monophosphate kinase 1 Homo sapiens 21-25 19383847-7 2009 Herein, we show that UMPK down-regulation in 5-FU-sensitive cells (HCT-8/P) induces resistance to bolus 5-FU treatment. Fluorouracil 104-108 cytidine/uridine monophosphate kinase 1 Homo sapiens 21-25 19383847-9 2009 Importantly, colorectal cancer hepatic metastases isolated from patients clinically resistant to weekly bolus 5-FU/leucovorin treatment exhibited decreased mRNA expression of UMPK but not thymidylate synthase or dihydropyrimidine dehydrogenase compared with tumor samples of patients not previously exposed to 5-FU. Fluorouracil 110-114 cytidine/uridine monophosphate kinase 1 Homo sapiens 175-179 19383847-9 2009 Importantly, colorectal cancer hepatic metastases isolated from patients clinically resistant to weekly bolus 5-FU/leucovorin treatment exhibited decreased mRNA expression of UMPK but not thymidylate synthase or dihydropyrimidine dehydrogenase compared with tumor samples of patients not previously exposed to 5-FU. Fluorouracil 310-314 cytidine/uridine monophosphate kinase 1 Homo sapiens 175-179 19383847-10 2009 Our findings provide new insights into the mechanisms of acquired resistance to 5-FU in colorectal cancer and implicate UMPK as an important mechanism of clinical resistance to pulse 5-FU treatment in some patients. Fluorouracil 183-187 cytidine/uridine monophosphate kinase 1 Homo sapiens 120-124 19435561-9 2009 The metastasis rates in Baihe Recipe group, 5-FU group and untreated group were 33.33%, 35.71% and 80.00% respectively, with significant difference (P<0.05), and the expressions of VEGF and p53 proteins in tumor tissues in the Baihe Recipe group were lower than those in the untreated group and the 5-FU group (P<0.01, P<0.05). Fluorouracil 302-306 vascular endothelial growth factor A Mus musculus 184-188 18704422-0 2009 The polymorphisms of TS and MTHFR predict survival of gastric cancer patients treated with fluorouracil-based adjuvant chemotherapy in Chinese population. Fluorouracil 91-103 methylenetetrahydrofolate reductase Homo sapiens 28-33 18704422-1 2009 PURPOSE: The aim of this study was to investigate the association of the thymidylate synthase (TS) and methylenetetrahydrofolate reductase (MTHFR) polymorphisms with the clinical outcomes of gastric cancer patients treated with 5-FU-based adjuvant chemotherapy. Fluorouracil 228-232 methylenetetrahydrofolate reductase Homo sapiens 140-145 18704422-8 2009 CONCLUSION: The polymorphisms of TS 3"-UTR ins6/del6 and MTHFR C677T appear to be potential prognostic factors in gastric cancer patients treated with 5-FU-based adjuvant chemotherapy, which may allow identification of gastric cancer patients who will benefit from 5-FU chemotherapy. Fluorouracil 151-155 methylenetetrahydrofolate reductase Homo sapiens 57-62 18704422-8 2009 CONCLUSION: The polymorphisms of TS 3"-UTR ins6/del6 and MTHFR C677T appear to be potential prognostic factors in gastric cancer patients treated with 5-FU-based adjuvant chemotherapy, which may allow identification of gastric cancer patients who will benefit from 5-FU chemotherapy. Fluorouracil 265-269 methylenetetrahydrofolate reductase Homo sapiens 57-62 19288006-1 2009 The enzymes thymidylate synthase (TS), dihydropyrimidine dehydrogenase (DPD) and orotate phosphoribosyl transferase (OPRT) are involved in the metabolism of the anticancer drug 5-fluorouracil (FU). Fluorouracil 177-191 dihydropyrimidine dehydrogenase Homo sapiens 39-70 19288006-1 2009 The enzymes thymidylate synthase (TS), dihydropyrimidine dehydrogenase (DPD) and orotate phosphoribosyl transferase (OPRT) are involved in the metabolism of the anticancer drug 5-fluorouracil (FU). Fluorouracil 177-191 dihydropyrimidine dehydrogenase Homo sapiens 72-75 19288006-2 2009 Expression of TS, DPD and OPRT in cancer tissue has been reported to be associated with sensitivity and/or resistance to 5-FU therapy. Fluorouracil 121-125 dihydropyrimidine dehydrogenase Homo sapiens 18-21 19287123-0 2009 Cardiotoxicity of 5-fluorouracil and capecitabine in a pancreatic cancer patient with a novel mutation in the dihydropyrimidine dehydrogenase gene. Fluorouracil 18-32 dihydropyrimidine dehydrogenase Homo sapiens 110-141 19287123-11 2009 Genetic variations such as polymorphic abnormality of DPYD are potential causative factors for a significant portion of serious adverse reactions to 5-fluorouracil-based therapy. Fluorouracil 149-163 dihydropyrimidine dehydrogenase Homo sapiens 54-58 19179402-6 2009 RSpo1 administration also substantially alleviated tongue mucositis in the oral cavity of mice receiving concomitant 5-fluorouracil and x-ray radiation. Fluorouracil 117-131 R-spondin 1 Mus musculus 0-5 23715169-7 2013 Thereafter, in the scaffold model, we found that the chemotherapeutic regimen of docetaxel, cisplatin and fluorouracil unleashed a stronger capability than the regimen comprising cisplatin and fluorouracil to deplete the CD44(+) subpopulation. Fluorouracil 106-118 CD44 molecule (Indian blood group) Homo sapiens 221-225 18818388-3 2009 Bone marrow cells from Mll5-deficient mice were defective in spleen colony-forming assays, and the mutant mice showed enhanced susceptibility to 5-fluorouracil-induced myelosuppression. Fluorouracil 145-159 lysine (K)-specific methyltransferase 2E Mus musculus 23-27 23760813-3 2013 Although several reports have shown the detrimental effect of some dihydropyrimidine dehydrogenase (DPYD) and thymidylate synthase (TYMS) gene polymorphisms in patients undergoing 5-FU-based treatment, they account for only a minority of toxicities. Fluorouracil 180-184 dihydropyrimidine dehydrogenase Homo sapiens 67-98 23760813-3 2013 Although several reports have shown the detrimental effect of some dihydropyrimidine dehydrogenase (DPYD) and thymidylate synthase (TYMS) gene polymorphisms in patients undergoing 5-FU-based treatment, they account for only a minority of toxicities. Fluorouracil 180-184 dihydropyrimidine dehydrogenase Homo sapiens 100-104 23760813-7 2013 However, other polymorphisms could account for 5-FU-induced toxicity, with the CHST1 rs9787901 and GSTM3 rs1799735 having the strongest association. Fluorouracil 47-51 glutathione S-transferase mu 3 Homo sapiens 99-104 23816136-0 2013 miR-381, a novel intrinsic WEE1 inhibitor, sensitizes renal cancer cells to 5-FU by up-regulation of Cdc2 activities in 786-O. Fluorouracil 76-80 WEE1 G2 checkpoint kinase Homo sapiens 27-31 23816136-7 2013 miR-381 combined with 5-FU led to Cdc2 activation, mitotic catastrophe, and cell apoptosis through inhibitory WEE1. Fluorouracil 22-26 WEE1 G2 checkpoint kinase Homo sapiens 110-114 23816136-10 2013 CONCLUSION: miR-381 increases sensitivity of 786-O cells to 5-FU by inhibitory WEE1 and increase of Cdc2 activity. Fluorouracil 60-64 WEE1 G2 checkpoint kinase Homo sapiens 79-83 23216104-10 2013 Cells treated with 5-FU also exhibited tumorigenic potential, based on tumor formation assays in nude mice, and Oct3/4-positive cell aggregates were identified in the resulting tumors. Fluorouracil 19-23 POU domain, class 5, transcription factor 1 Mus musculus 112-116 23216104-11 2013 In this study, we have shown that 5-FU treatment enriched the population of cells expressing the putative embryonic markers Oct3/4 and Sox2 and exhibiting nuclear accumulation of beta-catenin. Fluorouracil 34-38 SRY-box transcription factor 2 Homo sapiens 135-139 23689915-3 2013 METHODS: Newly diagnosed K-RAS wild-type colorectal cancer patients with unresectable liver-only metastases were treated with 5-fluorouracil, leucovorin, and oxaliplatin (FOLFOX6) plus cetuximab every 2 weeks for a maximum of 12 cycles. Fluorouracil 126-140 KRAS proto-oncogene, GTPase Homo sapiens 25-30 19143760-6 2009 RESULTS: Expression levels of Notch3, Jagged1, and Hey1 were increased in rat tracheal epithelial cells after treatment with 5-FU. Fluorouracil 125-129 jagged canonical Notch ligand 1 Rattus norvegicus 38-45 18620897-0 2009 The role of dihydropyrimidine dehydrogenase expression in resistance to 5-fluorouracil in head and neck squamous cell carcinoma cells. Fluorouracil 72-86 dihydropyrimidine dehydrogenase Homo sapiens 12-43 23507524-8 2013 Following an initial decrease in stem cell number, 5-FU treated mice had profound thrombopoietin (Tpo) dependent stem cell rebound above baseline levels. Fluorouracil 51-55 thrombopoietin Mus musculus 82-96 23507524-8 2013 Following an initial decrease in stem cell number, 5-FU treated mice had profound thrombopoietin (Tpo) dependent stem cell rebound above baseline levels. Fluorouracil 51-55 thrombopoietin Mus musculus 98-101 24649225-3 2013 Organic anion transporter 2 (OAT2) and reduced folate carrier 1 (RFC1) are the major uptake transporters of 5-fluorouracil (5-FU) and LV, respectively. Fluorouracil 108-122 solute carrier family 22 member 7 Homo sapiens 0-27 24649225-3 2013 Organic anion transporter 2 (OAT2) and reduced folate carrier 1 (RFC1) are the major uptake transporters of 5-fluorouracil (5-FU) and LV, respectively. Fluorouracil 108-122 solute carrier family 22 member 7 Homo sapiens 29-33 24649225-3 2013 Organic anion transporter 2 (OAT2) and reduced folate carrier 1 (RFC1) are the major uptake transporters of 5-fluorouracil (5-FU) and LV, respectively. Fluorouracil 124-128 solute carrier family 22 member 7 Homo sapiens 0-27 24649225-3 2013 Organic anion transporter 2 (OAT2) and reduced folate carrier 1 (RFC1) are the major uptake transporters of 5-fluorouracil (5-FU) and LV, respectively. Fluorouracil 124-128 solute carrier family 22 member 7 Homo sapiens 29-33 23814492-6 2013 OK-432-induced IL-10 and TGF-beta but not Th1 cytokines were significantly inhibited by 5-FU and/or X-ray. Fluorouracil 88-92 interleukin 10 Homo sapiens 15-20 18620897-3 2009 Dihydropyrimidine dehydrogenase (DPD) is the rate-limiting enzyme in the degradation of pyrimidine bases and is also responsible for the degradation of 5-FU. Fluorouracil 152-156 dihydropyrimidine dehydrogenase Homo sapiens 0-31 18620897-3 2009 Dihydropyrimidine dehydrogenase (DPD) is the rate-limiting enzyme in the degradation of pyrimidine bases and is also responsible for the degradation of 5-FU. Fluorouracil 152-156 dihydropyrimidine dehydrogenase Homo sapiens 33-36 18620897-4 2009 In this study, we examined whether DPD expression affects the cytotoxic activity of 5-FU against head and neck squamous cell carcinoma (HNSCC) and the role of DPD in the biological regulation of HNSCC. Fluorouracil 84-88 dihydropyrimidine dehydrogenase Homo sapiens 35-38 18620897-8 2009 DPD overexpression decreases the cytotoxicity of 5-FU. Fluorouracil 49-53 dihydropyrimidine dehydrogenase Homo sapiens 0-3 18620897-9 2009 CDHP, a strong DPD inhibitor, enhances the cytotoxic effect of 5-FU in HNSCC cells in vitro. Fluorouracil 63-67 cadherin 3 Homo sapiens 0-4 23478146-3 2013 In this study, we identified a subpopulation of CD44+ cells within the tumor of gastric cancer patients, which, upon treatment by chemotherapeutic agent 5-fluorouracil (5-FU), were markedly enriched. Fluorouracil 153-167 CD44 molecule (Indian blood group) Homo sapiens 48-52 18620897-9 2009 CDHP, a strong DPD inhibitor, enhances the cytotoxic effect of 5-FU in HNSCC cells in vitro. Fluorouracil 63-67 dihydropyrimidine dehydrogenase Homo sapiens 15-18 23478146-3 2013 In this study, we identified a subpopulation of CD44+ cells within the tumor of gastric cancer patients, which, upon treatment by chemotherapeutic agent 5-fluorouracil (5-FU), were markedly enriched. Fluorouracil 169-173 CD44 molecule (Indian blood group) Homo sapiens 48-52 23478146-9 2013 Upon enrichment by 5-FU, CD44+ cells harbored increased ALDH expression as compared with CD44- cells. Fluorouracil 19-23 CD44 molecule (Indian blood group) Homo sapiens 25-29 18620897-11 2009 The present results strongly indicate that DPD expression plays an important role in the sensitivity of HNSCC to 5-FU chemotherapy, suggesting the possibility of personalized chemotherapy including the prediction of response and adverse effects. Fluorouracil 113-117 dihydropyrimidine dehydrogenase Homo sapiens 43-46 23588527-6 2013 Moreover, the increased sensitivity and RAD51 focus formation induced by the combination treatment of 5-FU and CDDP were significantly repressed by RRM-1 depletion. Fluorouracil 102-106 RAD51 recombinase Homo sapiens 40-45 19309506-6 2009 RESULTS: TLE3 staining was associated with improved 5-year disease-free interval (DFI) in the overall cohort (n = 441, P < 0.004), in patients treated with cyclophosphamide (C), methotrexate, and 5-fluorouracil (n = 72, P < 0.02), and in those treated with regimens containing doxorubicin (A) and a T (n = 65, P < 0.04). Fluorouracil 199-213 TLE family member 3, transcriptional corepressor Homo sapiens 9-13 20037211-0 2009 TPMT and DPD polymorphisms: Efficient screening method for Indian patients considering taking Thiopurine and 5-FU drugs. Fluorouracil 109-113 dihydropyrimidine dehydrogenase Homo sapiens 9-12 23532818-7 2013 It seemed that patients with high expressions of miR-215 could benefit from 5-fluorouracil-containing adjuvant chemotherapy without significant difference, whereas this phenomenon was reverse in patients with low expressions of miR-215. Fluorouracil 76-90 microRNA 215 Homo sapiens 49-56 23718853-11 2013 The in vivo experiment also confirmed that the Huh7-HBx group was much more resistant to ADM or 5-FU than the control. Fluorouracil 96-100 MIR7-3 host gene Homo sapiens 47-51 19015148-2 2009 METHODS: We investigated the 5-FU-related gene expression levels of thymidylate synthase (TS), DPD, thymidine phosphorylase (TP) and orotate phosphoribosyl transferase (OPRT) in resected tumor specimens from 51 patients with adenocarcinomas and 47 with squamous cell carcinomas using quantitative reverse transcription-PCR, and compared those levels between the two histological types. Fluorouracil 29-33 dihydropyrimidine dehydrogenase Homo sapiens 95-98 19015155-3 2009 Importantly, uracil misincorporation is a mechanism of cytotoxicity induced by fluoropyrimidine chemotherapeutic agents including 5-fluorouracil (5-FU) and elevated expression of dUTPase is negatively correlated with clinical response to 5-FU-therapy. Fluorouracil 238-242 Deoxyuridine triphosphatase Drosophila melanogaster 179-186 23721525-10 2013 Moreover, the combination of HCPT and 5-fluorouracial (5-FU) synergistically induced apoptosis and downregulated the expression of survivin and XIAP. Fluorouracil 55-59 X-linked inhibitor of apoptosis Homo sapiens 144-148 19015155-9 2009 The novel observation that oxaliplatin downregulates dUTPase expression may provide a mechanistic basis contributing to the synergy observed between 5-FU and oxaliplatin in the clinic. Fluorouracil 149-153 Deoxyuridine triphosphatase Drosophila melanogaster 53-60 19082440-2 2009 Dihydropyrimidine dehydrogenase (DPD) is a degrading enzyme that catabolizes 5-FU. Fluorouracil 77-81 dihydropyrimidine dehydrogenase Homo sapiens 0-31 23626689-10 2013 Our results also suggest that the MTHFR Glu429Ala polymorphism may be an adverse prognostic marker in patients not treated with 5-FU. Fluorouracil 128-132 methylenetetrahydrofolate reductase Homo sapiens 34-39 19082440-2 2009 Dihydropyrimidine dehydrogenase (DPD) is a degrading enzyme that catabolizes 5-FU. Fluorouracil 77-81 dihydropyrimidine dehydrogenase Homo sapiens 33-36 19082440-10 2009 Furthermore, the OPRT/DPD expression ratio, a powerful predictive factor to evaluate 5-FU sensitivity, in the HRPC group was significantly higher than that in the low grade HSPC group. Fluorouracil 85-89 dihydropyrimidine dehydrogenase Homo sapiens 22-25 19077464-10 2009 Compared to parental Capan-1 cells, Capan-1 cells with acquired chemoresistance towards 5-fluorouracil showed an upregulated mRNA and protein expression of MRP3, MRP4, and MRP5. Fluorouracil 88-102 ATP binding cassette subfamily C member 4 Homo sapiens 162-166 19077464-12 2009 CONCLUSION: MRP3, MRP4, and MRP5 are upregulated in 5-fluorouracil-resistant cells, and MRP5 contributes to 5-FU resistance in pancreatic carcinoma cells. Fluorouracil 52-66 ATP binding cassette subfamily C member 4 Homo sapiens 18-22 18626508-3 2009 Taking advantage of this prostate cancer-specific property of PSMA(E/P), we successfully introduced bacterial UPRT into LNCaP cells where the tumoricidal effect of 5-fluorouracil (5-FU) was significantly increased when compared with the cells without the exogenous UPRT. Fluorouracil 164-178 uracil phosphoribosyltransferase homolog Homo sapiens 110-114 18626508-3 2009 Taking advantage of this prostate cancer-specific property of PSMA(E/P), we successfully introduced bacterial UPRT into LNCaP cells where the tumoricidal effect of 5-fluorouracil (5-FU) was significantly increased when compared with the cells without the exogenous UPRT. Fluorouracil 164-178 uracil phosphoribosyltransferase homolog Homo sapiens 265-269 18626508-3 2009 Taking advantage of this prostate cancer-specific property of PSMA(E/P), we successfully introduced bacterial UPRT into LNCaP cells where the tumoricidal effect of 5-fluorouracil (5-FU) was significantly increased when compared with the cells without the exogenous UPRT. Fluorouracil 180-184 uracil phosphoribosyltransferase homolog Homo sapiens 110-114 18626508-3 2009 Taking advantage of this prostate cancer-specific property of PSMA(E/P), we successfully introduced bacterial UPRT into LNCaP cells where the tumoricidal effect of 5-fluorouracil (5-FU) was significantly increased when compared with the cells without the exogenous UPRT. Fluorouracil 180-184 uracil phosphoribosyltransferase homolog Homo sapiens 265-269 18626508-4 2009 We conclude that the efficacy of 5-FU-based chemotherapy in prostate cancers can be significantly improved by targeted expression of the suicide gene UPRT under the control of PSMA(E/P). Fluorouracil 33-37 uracil phosphoribosyltransferase homolog Homo sapiens 150-154 19106633-7 2008 In vivo, TRAIL expression was induced in mouse natural killer cells at 24 hours after systemic treatment with 5-Fluorouracil. Fluorouracil 110-124 tumor necrosis factor (ligand) superfamily, member 10 Mus musculus 9-14 23407049-4 2013 Research on methylenetetrahydrofolate reductase (MTHFR) gene polymorphisms and fluoropyrimidine treatment outcome has focused on intravenous 5-fluorouracil and has yielded inconclusive results. Fluorouracil 141-155 methylenetetrahydrofolate reductase Homo sapiens 12-47 23407049-4 2013 Research on methylenetetrahydrofolate reductase (MTHFR) gene polymorphisms and fluoropyrimidine treatment outcome has focused on intravenous 5-fluorouracil and has yielded inconclusive results. Fluorouracil 141-155 methylenetetrahydrofolate reductase Homo sapiens 49-54 23328581-0 2013 Phenotypic profiling of DPYD variations relevant to 5-fluorouracil sensitivity using real-time cellular analysis and in vitro measurement of enzyme activity. Fluorouracil 52-66 dihydropyrimidine dehydrogenase Homo sapiens 24-28 23328581-3 2013 Dihydropyrimidine dehydrogenase (DPD, encoded by DPYD) rapidly degrades 85% of administered 5-FU, and as such, limits the amount of drug available for conversion into active metabolites. Fluorouracil 92-96 dihydropyrimidine dehydrogenase Homo sapiens 0-31 23328581-3 2013 Dihydropyrimidine dehydrogenase (DPD, encoded by DPYD) rapidly degrades 85% of administered 5-FU, and as such, limits the amount of drug available for conversion into active metabolites. Fluorouracil 92-96 dihydropyrimidine dehydrogenase Homo sapiens 33-36 23328581-3 2013 Dihydropyrimidine dehydrogenase (DPD, encoded by DPYD) rapidly degrades 85% of administered 5-FU, and as such, limits the amount of drug available for conversion into active metabolites. Fluorouracil 92-96 dihydropyrimidine dehydrogenase Homo sapiens 49-53 23328581-4 2013 Clinical studies have suggested that genetic variations in DPYD increase the risk for 5-FU toxicity, however, there is not a clear consensus about which variations are relevant predictors. Fluorouracil 86-90 dihydropyrimidine dehydrogenase Homo sapiens 59-63 23328581-6 2013 Relative sensitivity to 5-FU for cells expressing DPYD variations was also measured. Fluorouracil 24-28 dihydropyrimidine dehydrogenase Homo sapiens 50-54 23328581-10 2013 These findings support the hypothesis that selected DPYD alleles are protective against severe 5-FU toxicity, and, as a consequence, may decrease the effectiveness of 5-FU an antitumor drug in carriers. Fluorouracil 95-99 dihydropyrimidine dehydrogenase Homo sapiens 52-56 23328581-10 2013 These findings support the hypothesis that selected DPYD alleles are protective against severe 5-FU toxicity, and, as a consequence, may decrease the effectiveness of 5-FU an antitumor drug in carriers. Fluorouracil 167-171 dihydropyrimidine dehydrogenase Homo sapiens 52-56 19093184-8 2008 S-1 is a prodrug of 5-fluorouracil (5-FU), and contains 5-chloro-2-4-dihydroxypyridine (CDHP), an inhibitor of dihydropyrimidine dehydrogenase (DPD) that rapidly degrades 5-FU. Fluorouracil 171-175 dihydropyrimidine dehydrogenase Homo sapiens 111-142 19093184-12 2008 We suggest that the rapid degradation of 5-FU mediated by this high DPD in our patient was significantly blocked by the CDHP in S-1, and that the efficacy of 5-FU was consequently maintained at the maximum level. Fluorouracil 41-45 dihydropyrimidine dehydrogenase Homo sapiens 68-71 19093184-12 2008 We suggest that the rapid degradation of 5-FU mediated by this high DPD in our patient was significantly blocked by the CDHP in S-1, and that the efficacy of 5-FU was consequently maintained at the maximum level. Fluorouracil 158-162 dihydropyrimidine dehydrogenase Homo sapiens 68-71 19189665-5 2008 The effect of 5-FU correlated with an increase in the percentage of cells in the S-phase and caused an increased in CD4+ cells, a decrease in CD56+ cells and a shift of the cytokine secretion pattern from Th2 to Th1. Fluorouracil 14-18 negative elongation factor complex member C/D Homo sapiens 212-215 23181270-0 2013 Aberrant upregulation of ASCL2 by promoter demethylation promotes the growth and resistance to 5-fluorouracil of gastric cancer cells. Fluorouracil 95-109 achaete-scute family bHLH transcription factor 2 Homo sapiens 25-30 23181270-9 2013 Ectopic overexpression of ASCL2 showed that ASCL2 increased cell growth and promoted resistance to 5-fluorouracil in GC cells. Fluorouracil 99-113 achaete-scute family bHLH transcription factor 2 Homo sapiens 26-31 23181270-9 2013 Ectopic overexpression of ASCL2 showed that ASCL2 increased cell growth and promoted resistance to 5-fluorouracil in GC cells. Fluorouracil 99-113 achaete-scute family bHLH transcription factor 2 Homo sapiens 44-49 19031139-12 2008 The intestinal epithelial stem cells expressing msi-1 can regenerate the damage of intestinal mucosa induced by 5-FU. Fluorouracil 112-116 musashi RNA-binding protein 1 Mus musculus 48-53 23192274-8 2013 In a multivariable analysis adjusting for tumor grade, stage and patient age, Beclin 1 overexpression was independently associated with worse OS [hazard ratio (HR), 1.82; 95% confidence interval (CI), 1.0-3.3; p = 0.042] in patients who received 5-FU-based adjuvant therapy. Fluorouracil 246-250 beclin 1 Homo sapiens 78-86 23192274-10 2013 In conclusion, Beclin 1 overexpression was associated with reduced survival in colon cancer patients treated with adjuvant 5-FU. Fluorouracil 123-127 beclin 1 Homo sapiens 15-23 23229803-7 2013 The antitumor activity of capecitabine and 5"-DFUR correlated significantly with the mRNA levels of TP and with the TP/DPD ratio, whereas the activity of 5-FU correlated significantly with OPRT, TMPK, UMPK and CD. Fluorouracil 178-182 cytidine/uridine monophosphate kinase 1 Homo sapiens 225-229 23229803-8 2013 In a stepwise regression analysis, TP and DPD were found to be independent predictive factors of sensitivity to capecitabine and 5"-DFUR, and UMPK was predictive of sensitivity to 5-FU. Fluorouracil 216-220 cytidine/uridine monophosphate kinase 1 Homo sapiens 166-170 24324958-6 2013 Our results showed that there were significant synergistic effects of low dose 5-Fu and TRAIL on TRAIL-resistant AGS cells, and this effect was supposed to be mediated by decreasing DcR2 expression and increasing DR5 expression. Fluorouracil 79-83 TNF receptor superfamily member 10d Homo sapiens 182-186 23107827-9 2013 5-FU-induced epithelial damage increased the MPO activity (neutrophil number) and the level of pro-inflammatory cytokines (IL-4, TNF-alpha, IL-1beta and CXCL-8) in the duodenum. Fluorouracil 0-4 myeloperoxidase Mus musculus 45-48 23135628-5 2013 GLUT-1 and PDK-1 expression was significantly associated with tumor progression, although only PDK-1 expression was an independent prognostic factor for patients who received 5-FU adjuvant treatment. Fluorouracil 211-215 pyruvate dehydrogenase kinase 1 Homo sapiens 119-124 23135628-7 2013 However, DCA treatment reduced lactate production and increased responsiveness to 5-FU in MKN45 cells, which expressed high levels of PDK-1 in comparison to the other cell lines. Fluorouracil 94-98 pyruvate dehydrogenase kinase 1 Homo sapiens 158-163 22910294-5 2013 We demonstrated that MV-mediated delivery of CD-UPRT mRNA/protein by direct injection into schwannomas led to regression of these tumors upon systemic treatment with the prodrug (5-fluorocytosine (5-FC)), which is converted within tumor cells to 5-fluorouracil (5-FU)-an anticancer agent. Fluorouracil 246-260 uracil phosphoribosyltransferase homolog Homo sapiens 48-52 22910294-5 2013 We demonstrated that MV-mediated delivery of CD-UPRT mRNA/protein by direct injection into schwannomas led to regression of these tumors upon systemic treatment with the prodrug (5-fluorocytosine (5-FC)), which is converted within tumor cells to 5-fluorouracil (5-FU)-an anticancer agent. Fluorouracil 262-266 uracil phosphoribosyltransferase homolog Homo sapiens 48-52 24330851-8 2013 Simultaneous inhibition of XIAP and survivin expression in pancreatic cells significantly reduced cell proliferation, increased caspase-3/7 activity, and increased cell sensitization to 5-FU and gemcitabine treatments compared to inhibition of XIAP or survivin expression alone. Fluorouracil 186-190 X-linked inhibitor of apoptosis Homo sapiens 27-31 18813834-6 2008 LC-antisense molecules to EIF3EIP and AFP were simultaneously treated with 5-FU to Huh-7 cells. Fluorouracil 75-79 MIR7-3 host gene Homo sapiens 83-88 18546291-2 2008 The role of nonhomologous end joining (NHEJ) genes (Ku70, Ku80 and DNA-PKcs) in double-strand break (DSB) repair, genomic instability and apoptosis suggest a possible impact on tumor response to radiotherapy, 5-fluorouracil or cisplatin, as these agents are direct or indirect inductors of DSBs. Fluorouracil 209-223 X-ray repair cross complementing 6 Homo sapiens 52-56 18790783-7 2008 In this article, we present further evidence showing that elevated expression of dUTPase can protect breast cancer cells from the expansion of the intracellular uracil pool, translating to reduced growth inhibition following treatment with 5-FU. Fluorouracil 240-244 Deoxyuridine triphosphatase Drosophila melanogaster 81-88 18790783-9 2008 As 5-FU and the oral 5-FU prodrug capecitabine remain central agents in the treatment of a variety of malignancies, the clinical utility of a small-molecule inhibitor to dUTPase represents a viable strategy to improve the clinical efficacy of these mainstay chemotherapeutic agents. Fluorouracil 3-7 Deoxyuridine triphosphatase Drosophila melanogaster 170-177 18790783-9 2008 As 5-FU and the oral 5-FU prodrug capecitabine remain central agents in the treatment of a variety of malignancies, the clinical utility of a small-molecule inhibitor to dUTPase represents a viable strategy to improve the clinical efficacy of these mainstay chemotherapeutic agents. Fluorouracil 21-25 Deoxyuridine triphosphatase Drosophila melanogaster 170-177 18698031-0 2008 Checkpoint kinase 1 down-regulation by an inducible small interfering RNA expression system sensitized in vivo tumors to treatment with 5-fluorouracil. Fluorouracil 136-150 checkpoint kinase 1 Mus musculus 0-19 18698031-6 2008 Inhibition of Chk1 protein levels in inducible clones on induction with doxycycline correlated with an increased cisplatin and 5-FU activity. Fluorouracil 127-131 checkpoint kinase 1 Mus musculus 14-18 18698031-9 2008 More importantly, an increased 5-FU antitumor activity was found in tumors with the double Chk1 and p53 silencing. Fluorouracil 31-35 checkpoint kinase 1 Mus musculus 91-95 18702703-5 2008 We propose that systemically administered 5-Fu chemotherapy will cause deficits in hippocampal memory that are associated with altered BDNF levels and proliferating cells (particularly vascular-associated cells) in the dentate gyrus. Fluorouracil 42-46 brain-derived neurotrophic factor Rattus norvegicus 135-139 23236239-0 2012 UGT1A1 predicts outcome in colorectal cancer treated with irinotecan and fluorouracil. Fluorouracil 73-85 UDP glucuronosyltransferase family 1 member A1 Homo sapiens 0-6 18702703-8 2008 5-Fu-induced changes in hippocampal BDNF and doublecortin (DCX) protein levels were quantified using Western immunoblotting. Fluorouracil 0-4 brain-derived neurotrophic factor Rattus norvegicus 36-40 18702703-8 2008 5-Fu-induced changes in hippocampal BDNF and doublecortin (DCX) protein levels were quantified using Western immunoblotting. Fluorouracil 0-4 doublecortin Rattus norvegicus 45-57 18702703-8 2008 5-Fu-induced changes in hippocampal BDNF and doublecortin (DCX) protein levels were quantified using Western immunoblotting. Fluorouracil 0-4 doublecortin Rattus norvegicus 59-62 18702703-10 2008 In contrast, 5-Fu significantly reduced BDNF and DCX levels in the hippocampus, indicating alterations in neurotrophin levels and neurogenesis. Fluorouracil 13-17 brain-derived neurotrophic factor Rattus norvegicus 40-44 18702703-10 2008 In contrast, 5-Fu significantly reduced BDNF and DCX levels in the hippocampus, indicating alterations in neurotrophin levels and neurogenesis. Fluorouracil 13-17 doublecortin Rattus norvegicus 49-52 18575723-9 2008 Our results suggest that hsp27, Prx 6 and hsp70 are potential 5-FU response proteins and they may represent potential targets for further evaluation in other 5-FU-sensitive and -resistant CRC cell lines. Fluorouracil 62-66 heat shock protein family A (Hsp70) member 4 Homo sapiens 42-47 18575723-9 2008 Our results suggest that hsp27, Prx 6 and hsp70 are potential 5-FU response proteins and they may represent potential targets for further evaluation in other 5-FU-sensitive and -resistant CRC cell lines. Fluorouracil 158-162 heat shock protein family A (Hsp70) member 4 Homo sapiens 42-47 18553230-5 2008 The low level of dihydropyrimidine denhydrogenase (DPD), thymidylate synthase (TS) activities, and a high level of orotate phosphoribosyl-transferase (OPRT) activity enhance the antitumor effect of 5-FU and S-1. Fluorouracil 198-202 dihydropyrimidine dehydrogenase Homo sapiens 17-49 18452418-0 2008 Analysis of the DPYD gene implicated in 5-fluorouracil catabolism in Chinese cancer patients. Fluorouracil 40-54 dihydropyrimidine dehydrogenase Homo sapiens 16-20 18452418-2 2008 More than 85% of the 5-FU administered is catabolized by dihydropyrimidine dehydrogenase (DPD) in the liver. Fluorouracil 21-25 dihydropyrimidine dehydrogenase Homo sapiens 57-88 18452418-2 2008 More than 85% of the 5-FU administered is catabolized by dihydropyrimidine dehydrogenase (DPD) in the liver. Fluorouracil 21-25 dihydropyrimidine dehydrogenase Homo sapiens 90-93 18600532-0 2008 Altered dihydropyrimidine dehydrogenase activity associated with mild toxicity in patients treated with 5-fluorouracil containing chemotherapy. Fluorouracil 104-118 dihydropyrimidine dehydrogenase Homo sapiens 8-39 18600532-1 2008 Dihydropyrimidine dehydrogenase (DPD) plays a pivotal role in the metabolism of 5-fluorouracil (5FU). Fluorouracil 80-94 dihydropyrimidine dehydrogenase Homo sapiens 0-31 23236239-22 2012 CONCLUSION: A distinct distribution pattern of UGT1A1 genotypes in Chinese patients might contribute to relatively low toxicity associated with irinotecan and 5-fluorouracil in mCRC patients. Fluorouracil 159-173 UDP glucuronosyltransferase family 1 member A1 Homo sapiens 47-53 18600532-1 2008 Dihydropyrimidine dehydrogenase (DPD) plays a pivotal role in the metabolism of 5-fluorouracil (5FU). Fluorouracil 80-94 dihydropyrimidine dehydrogenase Homo sapiens 33-36 23169295-10 2012 In validation study, ERCC1 and DPD but not TOP1 expressions in cancer cells were significantly higher in FOLFOX (oxaliplatin, folinic acid, and 5-FU)-treated patients (N=24) than nontreated patients (N=21). Fluorouracil 144-148 dihydropyrimidine dehydrogenase Homo sapiens 31-34 18600532-1 2008 Dihydropyrimidine dehydrogenase (DPD) plays a pivotal role in the metabolism of 5-fluorouracil (5FU). Fluorouracil 96-99 dihydropyrimidine dehydrogenase Homo sapiens 0-31 18600532-1 2008 Dihydropyrimidine dehydrogenase (DPD) plays a pivotal role in the metabolism of 5-fluorouracil (5FU). Fluorouracil 96-99 dihydropyrimidine dehydrogenase Homo sapiens 33-36 18600532-2 2008 In patients treated with capecitabine or 5FU combined with other chemotherapeutic drugs, DPD activity in peripheral blood mononuclear cells was increased in patients experiencing grade I/II neutropenia. Fluorouracil 41-44 dihydropyrimidine dehydrogenase Homo sapiens 89-92 18600532-4 2008 Thus, patients with a low-normal or high-normal DPD activity proved to be at risk of developing mild toxicity upon treatment with 5FU-based chemotherapy, demonstrating the important role of DPD in the etiology of toxicity associated with 5FU and the catabolites of 5FU. Fluorouracil 130-133 dihydropyrimidine dehydrogenase Homo sapiens 48-51 18600532-4 2008 Thus, patients with a low-normal or high-normal DPD activity proved to be at risk of developing mild toxicity upon treatment with 5FU-based chemotherapy, demonstrating the important role of DPD in the etiology of toxicity associated with 5FU and the catabolites of 5FU. Fluorouracil 130-133 dihydropyrimidine dehydrogenase Homo sapiens 190-193 22770988-4 2012 Interestingly, when gef gene expression was combined with drugs of choice in the clinical treatment of colon cancer (5-fluorouracil, oxaliplatin and irinotecan), a strong synergistic effect was observed with approximately a 15-20% enhancement of the antiproliferative effect. Fluorouracil 117-131 Rho/Rac guanine nucleotide exchange factor 2 Homo sapiens 20-23 18600532-4 2008 Thus, patients with a low-normal or high-normal DPD activity proved to be at risk of developing mild toxicity upon treatment with 5FU-based chemotherapy, demonstrating the important role of DPD in the etiology of toxicity associated with 5FU and the catabolites of 5FU. Fluorouracil 238-241 dihydropyrimidine dehydrogenase Homo sapiens 48-51 18600532-4 2008 Thus, patients with a low-normal or high-normal DPD activity proved to be at risk of developing mild toxicity upon treatment with 5FU-based chemotherapy, demonstrating the important role of DPD in the etiology of toxicity associated with 5FU and the catabolites of 5FU. Fluorouracil 238-241 dihydropyrimidine dehydrogenase Homo sapiens 190-193 22842517-3 2012 The association between HSP27 protein expression levels and 5-FU sensitivity was evaluated in a mouse xenograft model. Fluorouracil 60-64 heat shock protein 1 Mus musculus 24-29 18600532-4 2008 Thus, patients with a low-normal or high-normal DPD activity proved to be at risk of developing mild toxicity upon treatment with 5FU-based chemotherapy, demonstrating the important role of DPD in the etiology of toxicity associated with 5FU and the catabolites of 5FU. Fluorouracil 238-241 dihydropyrimidine dehydrogenase Homo sapiens 48-51 18600532-4 2008 Thus, patients with a low-normal or high-normal DPD activity proved to be at risk of developing mild toxicity upon treatment with 5FU-based chemotherapy, demonstrating the important role of DPD in the etiology of toxicity associated with 5FU and the catabolites of 5FU. Fluorouracil 238-241 dihydropyrimidine dehydrogenase Homo sapiens 190-193 18245778-1 2008 BACKGROUND: Low tumour expression levels of thymidylate synthase (TS), dihydropyrimidine dehydrogenase (DPD) and thymidine phosphorylase (TP) have been linked with improved outcome for colorectal cancer (CRC) patients treated with 5-fluorouracil (5-FU). Fluorouracil 231-245 dihydropyrimidine dehydrogenase Homo sapiens 71-102 18245778-1 2008 BACKGROUND: Low tumour expression levels of thymidylate synthase (TS), dihydropyrimidine dehydrogenase (DPD) and thymidine phosphorylase (TP) have been linked with improved outcome for colorectal cancer (CRC) patients treated with 5-fluorouracil (5-FU). Fluorouracil 231-245 dihydropyrimidine dehydrogenase Homo sapiens 104-107 22512656-4 2012 In this study, a tripeptide NGR(NO2) was synthesized and conjugated with 5-fluorouracil. Fluorouracil 73-87 reticulon 4 receptor Homo sapiens 28-31 18245778-1 2008 BACKGROUND: Low tumour expression levels of thymidylate synthase (TS), dihydropyrimidine dehydrogenase (DPD) and thymidine phosphorylase (TP) have been linked with improved outcome for colorectal cancer (CRC) patients treated with 5-fluorouracil (5-FU). Fluorouracil 247-251 dihydropyrimidine dehydrogenase Homo sapiens 71-102 22998564-1 2012 BACKGROUND: Recently, S-1, a novel 5-fluorouracil (5-FU)-based agent containing the strong dihydropyrimidine dehydrogenase (DPD) inhibitor, 5-chloro-2,4-dihydropyrimidine (CDHP) has been clinically used to treat various non-urothelial carcinomas (UC). Fluorouracil 35-49 dihydropyrimidine dehydrogenase Homo sapiens 91-122 18245778-1 2008 BACKGROUND: Low tumour expression levels of thymidylate synthase (TS), dihydropyrimidine dehydrogenase (DPD) and thymidine phosphorylase (TP) have been linked with improved outcome for colorectal cancer (CRC) patients treated with 5-fluorouracil (5-FU). Fluorouracil 247-251 dihydropyrimidine dehydrogenase Homo sapiens 104-107 22998564-1 2012 BACKGROUND: Recently, S-1, a novel 5-fluorouracil (5-FU)-based agent containing the strong dihydropyrimidine dehydrogenase (DPD) inhibitor, 5-chloro-2,4-dihydropyrimidine (CDHP) has been clinically used to treat various non-urothelial carcinomas (UC). Fluorouracil 35-49 dihydropyrimidine dehydrogenase Homo sapiens 124-127 22998564-1 2012 BACKGROUND: Recently, S-1, a novel 5-fluorouracil (5-FU)-based agent containing the strong dihydropyrimidine dehydrogenase (DPD) inhibitor, 5-chloro-2,4-dihydropyrimidine (CDHP) has been clinically used to treat various non-urothelial carcinomas (UC). Fluorouracil 51-55 dihydropyrimidine dehydrogenase Homo sapiens 91-122 18245778-7 2008 These results provide indirect evidence that low TS, DPD and TP protein expression are predictive of good response to 5-FU chemotherapy. Fluorouracil 118-122 dihydropyrimidine dehydrogenase Homo sapiens 53-56 22998564-1 2012 BACKGROUND: Recently, S-1, a novel 5-fluorouracil (5-FU)-based agent containing the strong dihydropyrimidine dehydrogenase (DPD) inhibitor, 5-chloro-2,4-dihydropyrimidine (CDHP) has been clinically used to treat various non-urothelial carcinomas (UC). Fluorouracil 51-55 dihydropyrimidine dehydrogenase Homo sapiens 124-127 22322955-0 2012 MicroRNA-10b is a prognostic indicator in colorectal cancer and confers resistance to the chemotherapeutic agent 5-fluorouracil in colorectal cancer cells. Fluorouracil 113-127 microRNA 10b Homo sapiens 0-12 22322955-2 2012 We investigated the clinical significance of miR-10b and its involvement in chemotherapeutic resistance to 5-fluorouracil (5-FU), which is a key component of common chemotherapy regimens in colorectal cancer. Fluorouracil 107-121 microRNA 10b Homo sapiens 45-52 18473752-2 2008 The metabolism of 5FU requires the activity of thymidylate synthase (TS) and dihydropyrimidine dehydrogenase (DPD) among other enzymes. Fluorouracil 18-21 dihydropyrimidine dehydrogenase Homo sapiens 77-108 22684338-0 2012 Prospective impact of 5-FU in the induction of endoplasmic reticulum stress, modulation of GRP78 expression and autophagy in Sk-Hep1 cells. Fluorouracil 22-26 DNL-type zinc finger Homo sapiens 140-144 18473752-2 2008 The metabolism of 5FU requires the activity of thymidylate synthase (TS) and dihydropyrimidine dehydrogenase (DPD) among other enzymes. Fluorouracil 18-21 dihydropyrimidine dehydrogenase Homo sapiens 110-113 22684338-4 2012 In pursuit of a novel effective strategy, we have evaluated the potential of 5-FU to promote endoplasmic reticulum (ER) stress and autophagy in Sk-Hep1 HCC cells. Fluorouracil 89-93 DNL-type zinc finger Homo sapiens 171-175 18493057-0 2008 RNA-based 5-fluorouracil toxicity requires the pseudouridylation activity of Cbf5p. Fluorouracil 10-24 pseudouridine synthase CBF5 Saccharomyces cerevisiae S288C 77-82 22684338-5 2012 We found that 5-FU profoundly induces ER stress in Sk-Hep1 cells and upregulates p53 and activates CHOP/GADD153 and caspase-12. Fluorouracil 14-18 DNL-type zinc finger Homo sapiens 66-70 22684338-12 2012 Taken together, these results indicate that 5-FU-induced ER stress activates the mitochondrial apoptotic cell death pathway by downregulating GRP78 and protective autophagy proteins in Sk-Hep1 cells, raising the possibility of using 5-FU as a therapeutic agent to target human HCC. Fluorouracil 44-48 DNL-type zinc finger Homo sapiens 212-216 18452463-10 2008 The CD and UPRT gene system quickly and directly converted 5-FC into 5-FU, and then into toxic metabolites. Fluorouracil 69-73 uracil phosphoribosyltransferase homolog Homo sapiens 11-15 18575323-1 2008 OBJECTIVE: To study the bystander effect of Uracil Phosphoribosyltransferase (UPRT )/5-fluorouracil (5-FU) suicide gene system, which is regulated by PSMA enhancer/promoter, on prostate cancer cell. Fluorouracil 85-99 uracil phosphoribosyltransferase homolog Homo sapiens 78-82 18575323-1 2008 OBJECTIVE: To study the bystander effect of Uracil Phosphoribosyltransferase (UPRT )/5-fluorouracil (5-FU) suicide gene system, which is regulated by PSMA enhancer/promoter, on prostate cancer cell. Fluorouracil 101-105 uracil phosphoribosyltransferase homolog Homo sapiens 44-76 23070091-2 2012 Around 80% of administered dose of 5-FU is catabolized by dihydropirymidine dehydrogenase (DPD). Fluorouracil 35-39 dihydropyrimidine dehydrogenase Homo sapiens 58-89 18575323-1 2008 OBJECTIVE: To study the bystander effect of Uracil Phosphoribosyltransferase (UPRT )/5-fluorouracil (5-FU) suicide gene system, which is regulated by PSMA enhancer/promoter, on prostate cancer cell. Fluorouracil 101-105 uracil phosphoribosyltransferase homolog Homo sapiens 78-82 23070091-2 2012 Around 80% of administered dose of 5-FU is catabolized by dihydropirymidine dehydrogenase (DPD). Fluorouracil 35-39 dihydropyrimidine dehydrogenase Homo sapiens 91-94 18212800-7 2008 Furthermore, patients with the CYP2A6*4C allele had a significantly lower maximum plasma concentration (102.6 +/- 32.9 ng/ml) for 5-FU than patients without the CYP2A6*4C allele (157.0 +/- 65.5 ng/ml, P < 0.05). Fluorouracil 130-134 cytochrome P450 family 2 subfamily A member 6 Homo sapiens 31-37 22456329-4 2012 TACE was performed using Gemcitabine 1000mg/m2 (emulsified with lipiodol, 10-12mL), cisplatin 40 mg/m2 and 5-fluorouracil 500mg/m2 through the hepatic artery feeding the tumor. Fluorouracil 107-121 ADAM metallopeptidase domain 17 Homo sapiens 0-4 18202788-6 2008 In particular, cells with methylated TIMP3 had reduced mRNA levels and were significantly more sensitive to aphidicolin-glycinate, AraC and 5-FU than cells with unmethylated TIMP3. Fluorouracil 140-144 TIMP metallopeptidase inhibitor 3 Homo sapiens 37-42 22306127-1 2012 Dihydropyrimidine dehydrogenase (DPD) is important to the antitumor effect of 5-fluorouracil (5-FU). Fluorouracil 78-92 dihydropyrimidine dehydrogenase Homo sapiens 0-31 22306127-1 2012 Dihydropyrimidine dehydrogenase (DPD) is important to the antitumor effect of 5-fluorouracil (5-FU). Fluorouracil 78-92 dihydropyrimidine dehydrogenase Homo sapiens 33-36 22306127-1 2012 Dihydropyrimidine dehydrogenase (DPD) is important to the antitumor effect of 5-fluorouracil (5-FU). Fluorouracil 94-98 dihydropyrimidine dehydrogenase Homo sapiens 0-31 22306127-1 2012 Dihydropyrimidine dehydrogenase (DPD) is important to the antitumor effect of 5-fluorouracil (5-FU). Fluorouracil 94-98 dihydropyrimidine dehydrogenase Homo sapiens 33-36 22306127-2 2012 DPD gene (DPYD) expression in tumors is correlated with sensitivity to 5-FU. Fluorouracil 71-75 dihydropyrimidine dehydrogenase Homo sapiens 0-3 22306127-2 2012 DPD gene (DPYD) expression in tumors is correlated with sensitivity to 5-FU. Fluorouracil 71-75 dihydropyrimidine dehydrogenase Homo sapiens 10-14 22306127-3 2012 Because the 5-FU accumulated in cancer cells is also rapidly converted into inactivated metabolites through catabolic pathways mediated by DPD, high DPD activity in cancer cells is an important determinant of the response to 5-FU. Fluorouracil 12-16 dihydropyrimidine dehydrogenase Homo sapiens 139-142 22306127-3 2012 Because the 5-FU accumulated in cancer cells is also rapidly converted into inactivated metabolites through catabolic pathways mediated by DPD, high DPD activity in cancer cells is an important determinant of the response to 5-FU. Fluorouracil 12-16 dihydropyrimidine dehydrogenase Homo sapiens 149-152 22306127-3 2012 Because the 5-FU accumulated in cancer cells is also rapidly converted into inactivated metabolites through catabolic pathways mediated by DPD, high DPD activity in cancer cells is an important determinant of the response to 5-FU. Fluorouracil 225-229 dihydropyrimidine dehydrogenase Homo sapiens 139-142 22306127-3 2012 Because the 5-FU accumulated in cancer cells is also rapidly converted into inactivated metabolites through catabolic pathways mediated by DPD, high DPD activity in cancer cells is an important determinant of the response to 5-FU. Fluorouracil 225-229 dihydropyrimidine dehydrogenase Homo sapiens 149-152 22306127-4 2012 DPD activity is highly variable and reduced activity causes a high risk of 5-FU toxicity. Fluorouracil 75-79 dihydropyrimidine dehydrogenase Homo sapiens 0-3 22306127-14 2012 This study is the first to show that miRNAs regulate the DPD protein, and provides new insight into 5-FU-based chemotherapy. Fluorouracil 100-104 dihydropyrimidine dehydrogenase Homo sapiens 57-60 22522606-14 2012 CONCLUSION: The present study suggested that BLTA in combination with 5-FU could enhance antitumor effect, with inhibiting TIM-3/TIM-3L pathway, cutting down immunosuppressive activity of CD4(+)CD25(+) T(reg) and enhancing cell-mediated immunity. Fluorouracil 70-74 CD4 antigen Mus musculus 188-191 22388795-6 2012 A narrative summary is presented for 39 studies that describe three TYMS genotypes and two MTHFR genotypes associated with response to 5-FU-based chemotherapy. Fluorouracil 135-139 methylenetetrahydrofolate reductase Homo sapiens 91-96 17918158-0 2008 Curcumin enhances the effects of 5-fluorouracil and oxaliplatin in mediating growth inhibition of colon cancer cells by modulating EGFR and IGF-1R. Fluorouracil 33-47 insulin like growth factor 1 receptor Homo sapiens 140-146 18097780-1 2008 The aim of the study is to report the long-term outcome and secondary tumours of early breast cancer patients of adjuvant CNF (cyclophosphamide, mitoxantrone, and 5-fluorouracil) chemotherapy. Fluorouracil 163-177 NPHS1 adhesion molecule, nephrin Homo sapiens 122-125 18383853-1 2008 We established the optimal conditions for the induction of cell death by cisplatin (CDDP) and 5-fluorouracil (5-FU) in human oral squamous cell carcinoma (HSC-2, HSC-3, HSC-4) and human hepatocellular carcinoma (HepG2) cell lines. Fluorouracil 94-108 DnaJ heat shock protein family (Hsp40) member B7 Homo sapiens 162-167 21892263-7 2008 The main purpose of our study was to look for a correlation between the levels of expression of the genes for sensitivity to 5-FU (TS, TP, DPD) within the tumor and the clinical response observed after three courses of chemotherapy combining 5-FU/platinum salt in patients presenting with advanced cancer of the pharyngo-larynx. Fluorouracil 125-129 dihydropyrimidine dehydrogenase Homo sapiens 139-142 21892263-7 2008 The main purpose of our study was to look for a correlation between the levels of expression of the genes for sensitivity to 5-FU (TS, TP, DPD) within the tumor and the clinical response observed after three courses of chemotherapy combining 5-FU/platinum salt in patients presenting with advanced cancer of the pharyngo-larynx. Fluorouracil 242-246 dihydropyrimidine dehydrogenase Homo sapiens 139-142 18197934-2 2008 Gene expression of 5-FU metabolic enzymes such as thymidylate synthase (TS), thymidine phosphorylase (TP), dihydropyrimidine dehydrogenase (DPD) and orotate phosphoribosyl transferase (OPRT), has recently been investigated in order to predict the 5-FU sensitivity of several cancers. Fluorouracil 19-23 dihydropyrimidine dehydrogenase Homo sapiens 140-143 18197934-9 2008 TS and DPD mRNA expression levels may be useful indicators in predicting the anti-tumor activity of 5-FU in ESCC. Fluorouracil 100-104 dihydropyrimidine dehydrogenase Homo sapiens 7-10 18157009-6 2008 The addition of IFN-alpha to 5-FU-treatment decreased tumor volume, reduced serum level of VEGF, and down-regulated the expression of VEGF-receptor significantly. Fluorouracil 29-33 interferon alpha Mus musculus 16-25 22339448-0 2012 Evaluation of 5-fluorouracil pharmacokinetics in cancer patients with a c.1905+1G>A mutation in DPYD by means of a Bayesian limited sampling strategy. Fluorouracil 14-28 dihydropyrimidine dehydrogenase Homo sapiens 99-103 22339448-1 2012 BACKGROUND AND OBJECTIVE: Dihydropyrimidine dehydrogenase (DPD) is the initial enzyme in the catabolism of 5-fluorouracil (5FU) and DPD deficiency is an important pharmacogenetic syndrome. Fluorouracil 107-121 dihydropyrimidine dehydrogenase Homo sapiens 26-57 22339448-1 2012 BACKGROUND AND OBJECTIVE: Dihydropyrimidine dehydrogenase (DPD) is the initial enzyme in the catabolism of 5-fluorouracil (5FU) and DPD deficiency is an important pharmacogenetic syndrome. Fluorouracil 107-121 dihydropyrimidine dehydrogenase Homo sapiens 59-62 22339448-1 2012 BACKGROUND AND OBJECTIVE: Dihydropyrimidine dehydrogenase (DPD) is the initial enzyme in the catabolism of 5-fluorouracil (5FU) and DPD deficiency is an important pharmacogenetic syndrome. Fluorouracil 123-126 dihydropyrimidine dehydrogenase Homo sapiens 26-57 22339448-1 2012 BACKGROUND AND OBJECTIVE: Dihydropyrimidine dehydrogenase (DPD) is the initial enzyme in the catabolism of 5-fluorouracil (5FU) and DPD deficiency is an important pharmacogenetic syndrome. Fluorouracil 123-126 dihydropyrimidine dehydrogenase Homo sapiens 59-62 22339448-4 2012 METHODS: Thirty patients, heterozygous for the c.1905+1G>A mutation in DPYD, and 18 control patients received a dose of 5FU 300 mg/m2 and/or 5FU 450 mg/m2, followed by pharmacokinetic analysis of the 5FU plasma levels. Fluorouracil 123-126 dihydropyrimidine dehydrogenase Homo sapiens 74-78 22339448-4 2012 METHODS: Thirty patients, heterozygous for the c.1905+1G>A mutation in DPYD, and 18 control patients received a dose of 5FU 300 mg/m2 and/or 5FU 450 mg/m2, followed by pharmacokinetic analysis of the 5FU plasma levels. Fluorouracil 144-147 dihydropyrimidine dehydrogenase Homo sapiens 74-78 22188649-7 2012 5-FU-induced Chk1 phosphorylation was significantly impaired in Rad9- or Rad17-deficient cells, and severe gammaH2AX nuclear foci and DSBs were formed, which was followed by apoptosis. Fluorouracil 0-4 RAD17 checkpoint clamp loader component Gallus gallus 73-78 22188649-8 2012 Finally, inhibition of Chk1 kinase by UCN-01 increased 5-FU-induced gammaH2AX nuclear foci and enhanced 5-FU cytotoxicity in Rad9- or Rad17-deficient cells. Fluorouracil 55-59 RAD17 checkpoint clamp loader component Gallus gallus 134-139 22188649-9 2012 These results suggest that Rad9- and Rad17-independent activation of the ATR-Chk1 signaling pathway also significantly contributes to 5-FU tolerance. Fluorouracil 134-138 RAD17 checkpoint clamp loader component Gallus gallus 37-42 22101181-9 2012 Compared to 5-FU and P-FU, the HPMA copolymer containing the Hsp47/CBP2 binding peptide (P-FU-peptide) exhibited the highest cytotoxic efficacy to cell line of human head and neck squamous cell carcinoma (p<0.05) and was internalized much faster than P-FU, especially after being incubated for 30 min. Fluorouracil 12-16 serpin family H member 1 Homo sapiens 61-66 22978343-1 2012 PURPOSE: The anticancer drug 5-fluorouracile (5-FU) which is indicated for the treatment of a variety of solid malignancies such as colorectal, breast, head and neck neoplasms is extensively biotransformed to 5 fluoro-5,6- dihydrouracil (5-FDHU) by the dihydropyrimidine deshydrogenase enzyme (DPD). Fluorouracil 46-50 dihydropyrimidine dehydrogenase Homo sapiens 253-292 22978343-1 2012 PURPOSE: The anticancer drug 5-fluorouracile (5-FU) which is indicated for the treatment of a variety of solid malignancies such as colorectal, breast, head and neck neoplasms is extensively biotransformed to 5 fluoro-5,6- dihydrouracil (5-FDHU) by the dihydropyrimidine deshydrogenase enzyme (DPD). Fluorouracil 46-50 dihydropyrimidine dehydrogenase Homo sapiens 294-297 22978343-19 2012 This model has significant implications, to identify patients with potentially low DPD phenotype requiring earlier adjustment of the 5-FU dose. Fluorouracil 133-137 dihydropyrimidine dehydrogenase Homo sapiens 83-86 22205615-5 2012 Also, mock-knockdown and NANOG-knockdown cells were treated with 5-fluorouracil (5-FU) and survival rate was measured by MTT assay to evaluate drug sensitivity. Fluorouracil 65-79 Nanog homeobox Homo sapiens 25-30 22205615-5 2012 Also, mock-knockdown and NANOG-knockdown cells were treated with 5-fluorouracil (5-FU) and survival rate was measured by MTT assay to evaluate drug sensitivity. Fluorouracil 81-85 Nanog homeobox Homo sapiens 25-30 22205615-7 2012 NANOG knockdown suppressed proliferation, colony formation, and in vivo tumorigenicity but increased the sensitivity to 5-FU of SW620 cells. Fluorouracil 120-124 Nanog homeobox Homo sapiens 0-5 22205615-8 2012 5-FU treatment greatly inhibited the expression of the major stemness-associated genes NANOG, OCT4, and SOX2. Fluorouracil 0-4 Nanog homeobox Homo sapiens 87-92 22205615-8 2012 5-FU treatment greatly inhibited the expression of the major stemness-associated genes NANOG, OCT4, and SOX2. Fluorouracil 0-4 SRY-box transcription factor 2 Homo sapiens 104-108 23238479-1 2012 BACKGROUND: An impairment of the 5-fluorouracil (5-FU) catabolic pathway, represented by alterations in the dihydropyrimidine dehydrogenase (DPYD) gene, is considered a crucial factor contributing to the development of 5-FU-related toxicity. Fluorouracil 49-53 dihydropyrimidine dehydrogenase Homo sapiens 108-139 23238479-1 2012 BACKGROUND: An impairment of the 5-fluorouracil (5-FU) catabolic pathway, represented by alterations in the dihydropyrimidine dehydrogenase (DPYD) gene, is considered a crucial factor contributing to the development of 5-FU-related toxicity. Fluorouracil 49-53 dihydropyrimidine dehydrogenase Homo sapiens 141-145 23238479-1 2012 BACKGROUND: An impairment of the 5-fluorouracil (5-FU) catabolic pathway, represented by alterations in the dihydropyrimidine dehydrogenase (DPYD) gene, is considered a crucial factor contributing to the development of 5-FU-related toxicity. Fluorouracil 219-223 dihydropyrimidine dehydrogenase Homo sapiens 108-139 23238479-1 2012 BACKGROUND: An impairment of the 5-fluorouracil (5-FU) catabolic pathway, represented by alterations in the dihydropyrimidine dehydrogenase (DPYD) gene, is considered a crucial factor contributing to the development of 5-FU-related toxicity. Fluorouracil 219-223 dihydropyrimidine dehydrogenase Homo sapiens 141-145 23056627-1 2012 BACKGROUND: 5-fluorouracil, a commonly used chemotherapeutic agent, up-regulates expression of human thymidylate synthase (hTS). Fluorouracil 12-26 APC down-regulated 1 Homo sapiens 123-126 23056627-7 2012 Our data also suggest that the inhibition of the catalytic activity of hTS and the up-regulation of the hTS protein level are not causally linked, as the inactivated ternary complex, formed by hTS, deoxyuridine monophosphate and methylenetetrahydrofolate, was detected already 3 hours after 5-FU exposure, whereas substantial increase in global TS levels was detected only after 24 hours. Fluorouracil 291-295 APC down-regulated 1 Homo sapiens 71-74 23056627-7 2012 Our data also suggest that the inhibition of the catalytic activity of hTS and the up-regulation of the hTS protein level are not causally linked, as the inactivated ternary complex, formed by hTS, deoxyuridine monophosphate and methylenetetrahydrofolate, was detected already 3 hours after 5-FU exposure, whereas substantial increase in global TS levels was detected only after 24 hours. Fluorouracil 291-295 APC down-regulated 1 Homo sapiens 104-107 23056627-7 2012 Our data also suggest that the inhibition of the catalytic activity of hTS and the up-regulation of the hTS protein level are not causally linked, as the inactivated ternary complex, formed by hTS, deoxyuridine monophosphate and methylenetetrahydrofolate, was detected already 3 hours after 5-FU exposure, whereas substantial increase in global TS levels was detected only after 24 hours. Fluorouracil 291-295 APC down-regulated 1 Homo sapiens 104-107 23056627-7 2012 Our data also suggest that the inhibition of the catalytic activity of hTS and the up-regulation of the hTS protein level are not causally linked, as the inactivated ternary complex, formed by hTS, deoxyuridine monophosphate and methylenetetrahydrofolate, was detected already 3 hours after 5-FU exposure, whereas substantial increase in global TS levels was detected only after 24 hours. Fluorouracil 291-295 APC down-regulated 1 Homo sapiens 72-74 23056627-8 2012 CONCLUSIONS/SIGNIFICANCE: Altogether, our data indicate that constitutive TYMS mRNA transcription, cell cycle-induced hTS regulation and hTS enzyme stability are the three key mechanisms responsible for 5-fluorouracil induced up-regulation of human thymidylate synthase expression in the two ovarian cancer cell lines studied. Fluorouracil 203-217 APC down-regulated 1 Homo sapiens 118-121 23056627-8 2012 CONCLUSIONS/SIGNIFICANCE: Altogether, our data indicate that constitutive TYMS mRNA transcription, cell cycle-induced hTS regulation and hTS enzyme stability are the three key mechanisms responsible for 5-fluorouracil induced up-regulation of human thymidylate synthase expression in the two ovarian cancer cell lines studied. Fluorouracil 203-217 APC down-regulated 1 Homo sapiens 137-140 22199347-7 2011 CONCLUSION: Quantification of DPD mRNA levels is useful for determining the subgroup of lung AD patients who would benefit most from 5-FU after surgery. Fluorouracil 133-137 dihydropyrimidine dehydrogenase Homo sapiens 30-33 18157009-6 2008 The addition of IFN-alpha to 5-FU-treatment decreased tumor volume, reduced serum level of VEGF, and down-regulated the expression of VEGF-receptor significantly. Fluorouracil 29-33 vascular endothelial growth factor A Mus musculus 91-95 18157009-6 2008 The addition of IFN-alpha to 5-FU-treatment decreased tumor volume, reduced serum level of VEGF, and down-regulated the expression of VEGF-receptor significantly. Fluorouracil 29-33 vascular endothelial growth factor A Mus musculus 134-138 18157009-8 2008 IFN-alpha significantly improves the outcome of 5-FU-therapy in treating pancreatic carcinoma. Fluorouracil 48-52 interferon alpha Mus musculus 0-9 18157009-9 2008 This is at least partly mediated by IFN-alpha antiangiogenic properties, which acts along with 5-FU on the VEGF system, vessel density, and RGS-5 expression in pericytes. Fluorouracil 95-99 interferon alpha Mus musculus 36-45 18157009-9 2008 This is at least partly mediated by IFN-alpha antiangiogenic properties, which acts along with 5-FU on the VEGF system, vessel density, and RGS-5 expression in pericytes. Fluorouracil 95-99 vascular endothelial growth factor A Mus musculus 107-111 18216719-1 2008 OBJECTIVE: Approximately 30-40% of grade III-IV toxicity to 5-FU has been associated with partial or profound deficiency in dihydropyrimidine dehydrogenase (DPD), the first of three enzymes in the catabolic pathway of fluoropyrimidines. Fluorouracil 60-64 dihydropyrimidine dehydrogenase Homo sapiens 157-160 18415744-11 2008 Mucosal damage and reduced mucin content in stomach and small intestine were observed in rats receiving 5-FU alone. Fluorouracil 104-108 solute carrier family 13 member 2 Rattus norvegicus 27-32 21787270-5 2011 DPD represent the more studied 5-FU toxicity marker, followed by TS and OPRT. Fluorouracil 31-35 dihydropyrimidine dehydrogenase Homo sapiens 0-3 21954436-1 2011 Abrogation of uridine phosphorylase (UPase) leads to abnormalities in pyrimidine metabolism and host protection against 5-fluorouracil (5-FU) toxicity. Fluorouracil 120-134 uridine phosphorylase 1 Mus musculus 14-35 21954436-1 2011 Abrogation of uridine phosphorylase (UPase) leads to abnormalities in pyrimidine metabolism and host protection against 5-fluorouracil (5-FU) toxicity. Fluorouracil 120-134 uridine phosphorylase 1 Mus musculus 37-42 21954436-1 2011 Abrogation of uridine phosphorylase (UPase) leads to abnormalities in pyrimidine metabolism and host protection against 5-fluorouracil (5-FU) toxicity. Fluorouracil 136-140 uridine phosphorylase 1 Mus musculus 14-35 21954436-1 2011 Abrogation of uridine phosphorylase (UPase) leads to abnormalities in pyrimidine metabolism and host protection against 5-fluorouracil (5-FU) toxicity. Fluorouracil 136-140 uridine phosphorylase 1 Mus musculus 37-42 21954436-2 2011 We elucidated the effects on the metabolism and antitumor efficacy of 5-FU and capecitabine (N(4)-pentyloxycarbonyl-5"-deoxy-5-fluorocytidine) in our UPase knockout (UPase(-/-)) model. Fluorouracil 70-74 uridine phosphorylase 1 Mus musculus 150-176 21954436-5 2011 UPase expressing colon 38 tumors implanted in UPase(-/-) mice revealed an improved therapeutic efficacy when treated with 5-FU and capecitabine because of the higher maximum tolerated dose for fluoropyrimidines achievable in UPase(-/-) mice. Fluorouracil 122-126 uridine phosphorylase 1 Mus musculus 0-5 21954436-5 2011 UPase expressing colon 38 tumors implanted in UPase(-/-) mice revealed an improved therapeutic efficacy when treated with 5-FU and capecitabine because of the higher maximum tolerated dose for fluoropyrimidines achievable in UPase(-/-) mice. Fluorouracil 122-126 uridine phosphorylase 1 Mus musculus 46-56 21954436-5 2011 UPase expressing colon 38 tumors implanted in UPase(-/-) mice revealed an improved therapeutic efficacy when treated with 5-FU and capecitabine because of the higher maximum tolerated dose for fluoropyrimidines achievable in UPase(-/-) mice. Fluorouracil 122-126 uridine phosphorylase 1 Mus musculus 225-235 22312705-0 2011 MiR-122 increases sensitivity of drug-resistant BEL-7402/5-FU cells to 5-fluorouracil via down-regulation of bcl-2 family proteins. Fluorouracil 71-85 microRNA 122 Homo sapiens 0-7 22312705-7 2011 Accordingly, P53 protein expression showed a significant up-regulation; MTT results showed that after incubation with 5-FU, miR-122 transfectants had higher cell inhibitory rates than negative miRNA or untreated cells; flow cytometry results demonstrated that apoptosis rate increased in miR-122 transfected cells, compared with negative miRNA or untreated cells. Fluorouracil 118-122 microRNA 122 Homo sapiens 124-131 22312705-7 2011 Accordingly, P53 protein expression showed a significant up-regulation; MTT results showed that after incubation with 5-FU, miR-122 transfectants had higher cell inhibitory rates than negative miRNA or untreated cells; flow cytometry results demonstrated that apoptosis rate increased in miR-122 transfected cells, compared with negative miRNA or untreated cells. Fluorouracil 118-122 microRNA 122 Homo sapiens 288-295 22312705-8 2011 After addition of 5-FU (10 and 100 micromol/I), miR-122 transfected cells showed higher apoptosis rate than negative miRNA or untreated cells. Fluorouracil 18-22 microRNA 122 Homo sapiens 48-55 22312705-9 2011 MiR-122 can specifically down-regulate the expression of Bcl-2 and Bcl-XL, and increase P53 activity in BEL-7402/5-FU cells, which increased cells spontaneous apoptosis and sensitize cells to 5-FU. Fluorouracil 113-117 microRNA 122 Homo sapiens 0-7 18938749-2 2008 Although clinically this mucositis can be treated, data on the effect of CTon the mucosal defense mechanisms are scant, so the effects of 5-fluorouracil (5-FU) on mucin, one of the principal defense factors of the GI mucosa, were investigated. Fluorouracil 138-152 solute carrier family 13 member 2 Rattus norvegicus 163-168 22045187-0 2011 Methylenetetrahydrofolate reductase genetic polymorphisms and toxicity to 5-FU-based chemoradiation in rectal cancer. Fluorouracil 74-78 methylenetetrahydrofolate reductase Homo sapiens 0-35 22045187-6 2011 RESULTS: MTHFR 1298A>C and MTHFR diplotypes (for 677C>T and 1298A>C) were associated with chemoradiation-related toxicity when 5-FU was used alone. Fluorouracil 136-140 methylenetetrahydrofolate reductase Homo sapiens 9-14 22045187-6 2011 RESULTS: MTHFR 1298A>C and MTHFR diplotypes (for 677C>T and 1298A>C) were associated with chemoradiation-related toxicity when 5-FU was used alone. Fluorouracil 136-140 methylenetetrahydrofolate reductase Homo sapiens 30-35 22045187-9 2011 CONCLUSION: MTHFR polymorphisms can potentially predict toxicity in patients treated with 5-FU as a single chemotherapeutic drug. Fluorouracil 90-94 methylenetetrahydrofolate reductase Homo sapiens 12-17 21833589-3 2011 Since dihydropyrimidine dehydrogenase (DPD) is the main candidate for pharmacogenetic studies on 5-FU toxicity, the entire coding sequence and exon-flanking intronic regions of the DPYD gene were sequenced in the patient. Fluorouracil 97-101 dihydropyrimidine dehydrogenase Homo sapiens 6-37 21833589-3 2011 Since dihydropyrimidine dehydrogenase (DPD) is the main candidate for pharmacogenetic studies on 5-FU toxicity, the entire coding sequence and exon-flanking intronic regions of the DPYD gene were sequenced in the patient. Fluorouracil 97-101 dihydropyrimidine dehydrogenase Homo sapiens 39-42 21833589-3 2011 Since dihydropyrimidine dehydrogenase (DPD) is the main candidate for pharmacogenetic studies on 5-FU toxicity, the entire coding sequence and exon-flanking intronic regions of the DPYD gene were sequenced in the patient. Fluorouracil 97-101 dihydropyrimidine dehydrogenase Homo sapiens 181-185 21344302-1 2011 PURPOSE: Eniluracil (EU) is a potent dihydropyrimidine (DPD) inhibitor, which improves the oral bio-availability of 5-fluorouracil (5-FU) and may overcome fluoropyrimidine (FP) resistance in hepatocellular carcinoma (HCC). Fluorouracil 116-130 dihydropyrimidine dehydrogenase Homo sapiens 56-59 21344302-1 2011 PURPOSE: Eniluracil (EU) is a potent dihydropyrimidine (DPD) inhibitor, which improves the oral bio-availability of 5-fluorouracil (5-FU) and may overcome fluoropyrimidine (FP) resistance in hepatocellular carcinoma (HCC). Fluorouracil 132-136 dihydropyrimidine dehydrogenase Homo sapiens 56-59 18938749-2 2008 Although clinically this mucositis can be treated, data on the effect of CTon the mucosal defense mechanisms are scant, so the effects of 5-fluorouracil (5-FU) on mucin, one of the principal defense factors of the GI mucosa, were investigated. Fluorouracil 154-158 solute carrier family 13 member 2 Rattus norvegicus 163-168 18938749-7 2008 RESULTS: 5-FU caused significant alterations of the immunoreactivity and content of mucin in the rat GI mucosa, especially in the jejunum. Fluorouracil 9-13 solute carrier family 13 member 2 Rattus norvegicus 84-89 17971768-7 2007 The antitumour effects of combination treatment is due in part to the elevation by PEG-IFN of p53 protein and mRNA expression and in part to the DNA damage that is generated by 5-FU, which induces p53 serine46 phosphorylation, which in turn upregulates p53AIP1 expression. Fluorouracil 177-181 tumor protein p53 regulated apoptosis inducing protein 1 Homo sapiens 253-260 18056458-3 2007 Although RPS27L mRNA levels were consistently induced after diverse p53 activating signals, its change in protein level was stimuli-dependent: it was up-regulated when cells were arrested in response to DNA-damaging agents Adriamycin or VP16 but was down-regulated when cells underwent apoptosis in response to antimetabolite agent 5-fluorouracil. Fluorouracil 332-346 ribosomal protein S27 like Homo sapiens 9-15 17982671-4 2007 Treatment with CDDP or 5-FU either alone or in combination with Zeb or SAHA continued for 48 or 72 h. In HSC-3 cells, Zeb had chemosensitive efficacy with CDDP, but not 5-FU, whereas SAHA showed efficacy with both CDDP and 5-FU. Fluorouracil 23-27 DnaJ heat shock protein family (Hsp40) member B7 Homo sapiens 105-110 17982671-6 2007 Furthermore, DNA methylation could be a regulatory mechanism for dihydropyrimidine dehydrogenase (DPD), known to be a principal factor in 5-FU resistance. Fluorouracil 138-142 dihydropyrimidine dehydrogenase Homo sapiens 65-96 17982671-6 2007 Furthermore, DNA methylation could be a regulatory mechanism for dihydropyrimidine dehydrogenase (DPD), known to be a principal factor in 5-FU resistance. Fluorouracil 138-142 dihydropyrimidine dehydrogenase Homo sapiens 98-101 17982671-7 2007 CDHP (5-chloro-2,4-dihydroxypyridine), an inhibitor of DPD, had an enhancing effect on the apoptotic ability of 5-FU alone or 5-FU/Zeb combination. Fluorouracil 112-116 dihydropyrimidine dehydrogenase Homo sapiens 55-58 17982671-7 2007 CDHP (5-chloro-2,4-dihydroxypyridine), an inhibitor of DPD, had an enhancing effect on the apoptotic ability of 5-FU alone or 5-FU/Zeb combination. Fluorouracil 126-130 dihydropyrimidine dehydrogenase Homo sapiens 55-58 17982671-8 2007 In conclusion, the present study suggests that low-dose (IC20) Zeb may sensitize cancer cells to CDDP, which may be an important characteristic for solid cancer treatment, and that DPD and other agents activated by Zeb in cancer cells could be an inhibitory factor in the response to apoptosis induced by 5-FU. Fluorouracil 305-309 dihydropyrimidine dehydrogenase Homo sapiens 181-184 18159003-0 2007 [Expression of proliferating cell nuclear antigen in severely damaged small intestinal mucosa due to high-dose 5-FU exposure]. Fluorouracil 111-115 proliferating cell nuclear antigen Mus musculus 15-49 21931273-11 2011 Physiological and/or genetic differences underlying heterogeneity in 5-FU levels during dose optimization require further study of patient demographics, single nucleotide polymorphisms in Dihydropyrimidine Dehydrogenase (DPD), TS, or other genes that impact 5-FU metabolism and gene expression changes in liver after 5-FU therapy. Fluorouracil 258-262 dihydropyrimidine dehydrogenase Homo sapiens 221-224 21931273-11 2011 Physiological and/or genetic differences underlying heterogeneity in 5-FU levels during dose optimization require further study of patient demographics, single nucleotide polymorphisms in Dihydropyrimidine Dehydrogenase (DPD), TS, or other genes that impact 5-FU metabolism and gene expression changes in liver after 5-FU therapy. Fluorouracil 258-262 dihydropyrimidine dehydrogenase Homo sapiens 221-224 21153821-5 2011 METHODS: Wild-type mice or PAFR(-/-) mice were treated with 5-FU (450 mg/kg, i.p.). Fluorouracil 60-64 platelet-activating factor receptor Mus musculus 27-31 21153821-9 2011 RESULTS: 5-FU treatment decreased the duodenal villus height/crypt depth ratio, increased MPO activity, and increased the concentration of TNF-alpha, IL-1beta and KC in comparison with saline-treated animals. Fluorouracil 9-13 myeloperoxidase Mus musculus 90-93 21153821-10 2011 In PAFR(-/-) mice and PAFR antagonist-treated mice, 5-FU-dependent intestinal damage was reduced and a decrease in duodenal villus height/crypt depth ratio was attenuated. Fluorouracil 52-56 platelet-activating factor receptor Mus musculus 3-7 21153821-10 2011 In PAFR(-/-) mice and PAFR antagonist-treated mice, 5-FU-dependent intestinal damage was reduced and a decrease in duodenal villus height/crypt depth ratio was attenuated. Fluorouracil 52-56 platelet-activating factor receptor Mus musculus 22-26 21153821-11 2011 However, the 5-FU-dependent increase in duodenum MPO activity was not affected. Fluorouracil 13-17 myeloperoxidase Mus musculus 49-52 21153821-13 2011 CONCLUSIONS: In conclusion, our study establishes the role of PAFR activation in 5-FU-induced intestinal mucositis. Fluorouracil 81-85 platelet-activating factor receptor Mus musculus 62-66 18159003-1 2007 OBJECTIVE: To detect the expression of proliferating cell nuclear antigen (PCNA) in severely damaged intestinal mucosa due to high-dose 5-FU exposure. Fluorouracil 136-140 proliferating cell nuclear antigen Mus musculus 39-73 18159003-1 2007 OBJECTIVE: To detect the expression of proliferating cell nuclear antigen (PCNA) in severely damaged intestinal mucosa due to high-dose 5-FU exposure. Fluorouracil 136-140 proliferating cell nuclear antigen Mus musculus 75-79 18159003-4 2007 RESULTS: High-dose 5-FU exposure of the mice resulted in severe intestinal mucous damage, with complete destruction of the villi and crypts and significantly increased cells positive for PCNA expression (P<0.01). Fluorouracil 19-23 proliferating cell nuclear antigen Mus musculus 187-191 18159003-5 2007 CONCLUSION: High-dose 5-FU treatment can significantly increase the PCNA index, and the cells expressing PCNA can be closely associated with regeneration of the severely damaged mucosa due to the exposure. Fluorouracil 22-26 proliferating cell nuclear antigen Mus musculus 68-72 18225548-1 2007 BACKGROUND: Dihydropyrimidine dehydrogenase (DPD) is a critical enzyme in the catabolism of 5-fluorouracil (5-FU), a drug frequently used in cancer therapy. Fluorouracil 92-106 dihydropyrimidine dehydrogenase Homo sapiens 12-43 18225548-1 2007 BACKGROUND: Dihydropyrimidine dehydrogenase (DPD) is a critical enzyme in the catabolism of 5-fluorouracil (5-FU), a drug frequently used in cancer therapy. Fluorouracil 92-106 dihydropyrimidine dehydrogenase Homo sapiens 45-48 18225548-1 2007 BACKGROUND: Dihydropyrimidine dehydrogenase (DPD) is a critical enzyme in the catabolism of 5-fluorouracil (5-FU), a drug frequently used in cancer therapy. Fluorouracil 108-112 dihydropyrimidine dehydrogenase Homo sapiens 12-43 18225548-1 2007 BACKGROUND: Dihydropyrimidine dehydrogenase (DPD) is a critical enzyme in the catabolism of 5-fluorouracil (5-FU), a drug frequently used in cancer therapy. Fluorouracil 108-112 dihydropyrimidine dehydrogenase Homo sapiens 45-48 18225548-2 2007 One of the possible causes of severe 5-FU toxicity is genetic polymorphisms in the DPYD gene, such as IVS14+1G > A. Fluorouracil 37-41 dihydropyrimidine dehydrogenase Homo sapiens 83-87 17853063-2 2007 TRAP-1 mRNA expression is increased in DEM-adapted cells as well as in tumor cells resistant to 5-fluorouracil and to platin derivatives. Fluorouracil 96-110 TNF receptor associated protein 1 Homo sapiens 0-6 22040429-7 2011 The protein and mRNA levels of VEGF were down-regulated after being treated with ATRA and 5-FU compared to the control group (P < 0.05). Fluorouracil 90-94 vascular endothelial growth factor A Mus musculus 31-35 17988579-0 2007 [Study of the immunological mechanism of anti-tumor effects of 5-FU by establishing EL4 tumor-bearing mouse models]. Fluorouracil 63-67 epilepsy 4 Mus musculus 84-87 21791367-1 2011 INTRODUCTION/BACKGROUND: Pyrimidine antimetabolites" target molecules thymidylate synthase (TS) and flopropyrimidine-metabolising enzymes such as dihydropyrimidine dehydrogenase (DPD), thymidine phosphorylase (TP) and orotate phosphoribosyltransferase (OPRT) are known as biomarkers of 5-fluorouracil (5-FU) treatment. Fluorouracil 286-300 dihydropyrimidine dehydrogenase Homo sapiens 146-177 21791367-1 2011 INTRODUCTION/BACKGROUND: Pyrimidine antimetabolites" target molecules thymidylate synthase (TS) and flopropyrimidine-metabolising enzymes such as dihydropyrimidine dehydrogenase (DPD), thymidine phosphorylase (TP) and orotate phosphoribosyltransferase (OPRT) are known as biomarkers of 5-fluorouracil (5-FU) treatment. Fluorouracil 286-300 dihydropyrimidine dehydrogenase Homo sapiens 179-182 21791367-1 2011 INTRODUCTION/BACKGROUND: Pyrimidine antimetabolites" target molecules thymidylate synthase (TS) and flopropyrimidine-metabolising enzymes such as dihydropyrimidine dehydrogenase (DPD), thymidine phosphorylase (TP) and orotate phosphoribosyltransferase (OPRT) are known as biomarkers of 5-fluorouracil (5-FU) treatment. Fluorouracil 302-306 dihydropyrimidine dehydrogenase Homo sapiens 146-177 21791367-1 2011 INTRODUCTION/BACKGROUND: Pyrimidine antimetabolites" target molecules thymidylate synthase (TS) and flopropyrimidine-metabolising enzymes such as dihydropyrimidine dehydrogenase (DPD), thymidine phosphorylase (TP) and orotate phosphoribosyltransferase (OPRT) are known as biomarkers of 5-fluorouracil (5-FU) treatment. Fluorouracil 302-306 dihydropyrimidine dehydrogenase Homo sapiens 179-182 21919605-8 2011 Specific combinations of functional polymorphisms in DPYD and TYMS were demonstrated to be associated with DFS and overall survival in patients receiving adjuvant 5-FU-based treatment. Fluorouracil 163-167 dihydropyrimidine dehydrogenase Homo sapiens 53-57 21919607-0 2011 Dihydropyrimidine dehydrogenase gene as a major predictor of severe 5-fluorouracil toxicity. Fluorouracil 68-82 dihydropyrimidine dehydrogenase Homo sapiens 0-31 17988579-8 2007 RESULTS: A single dose of 5-FU (75 mg/kg) cured both the EL4 tumor-bearing wild type C57BL/6 mice and the EL4 tumor-bearing nude C57BL/6 mice in the first week. Fluorouracil 26-30 epilepsy 4 Mus musculus 57-60 21919607-1 2011 The importance of polymorphisms in the dihydropyrimidine dehydrogenase (DPD) gene (DPYD) for the prediction of severe toxicity in 5-fluorouracil (5-FU) based chemotherapy has been controversially debated. Fluorouracil 130-144 dihydropyrimidine dehydrogenase Homo sapiens 39-70 21919607-1 2011 The importance of polymorphisms in the dihydropyrimidine dehydrogenase (DPD) gene (DPYD) for the prediction of severe toxicity in 5-fluorouracil (5-FU) based chemotherapy has been controversially debated. Fluorouracil 130-144 dihydropyrimidine dehydrogenase Homo sapiens 72-75 17988579-8 2007 RESULTS: A single dose of 5-FU (75 mg/kg) cured both the EL4 tumor-bearing wild type C57BL/6 mice and the EL4 tumor-bearing nude C57BL/6 mice in the first week. Fluorouracil 26-30 epilepsy 4 Mus musculus 106-109 21919607-1 2011 The importance of polymorphisms in the dihydropyrimidine dehydrogenase (DPD) gene (DPYD) for the prediction of severe toxicity in 5-fluorouracil (5-FU) based chemotherapy has been controversially debated. Fluorouracil 130-144 dihydropyrimidine dehydrogenase Homo sapiens 83-87 17988579-10 2007 CONCLUSION: A single dose of 5-FU has marked anti-tumor effects on lymphoma EL4 tumor-bearing C57BL/6 mice with or without T lymphocytes. Fluorouracil 29-33 epilepsy 4 Mus musculus 76-79 21919607-1 2011 The importance of polymorphisms in the dihydropyrimidine dehydrogenase (DPD) gene (DPYD) for the prediction of severe toxicity in 5-fluorouracil (5-FU) based chemotherapy has been controversially debated. Fluorouracil 146-150 dihydropyrimidine dehydrogenase Homo sapiens 39-70 21919607-1 2011 The importance of polymorphisms in the dihydropyrimidine dehydrogenase (DPD) gene (DPYD) for the prediction of severe toxicity in 5-fluorouracil (5-FU) based chemotherapy has been controversially debated. Fluorouracil 146-150 dihydropyrimidine dehydrogenase Homo sapiens 72-75 21919607-1 2011 The importance of polymorphisms in the dihydropyrimidine dehydrogenase (DPD) gene (DPYD) for the prediction of severe toxicity in 5-fluorouracil (5-FU) based chemotherapy has been controversially debated. Fluorouracil 146-150 dihydropyrimidine dehydrogenase Homo sapiens 83-87 21919607-2 2011 As a key enzyme in the catabolism of 5-FU, DPD is the top candidate for pharmacogenetic studies on 5-FU toxicity, since a reduced DPD activity is thought to result in an increased half-life of the drug, and thus, an increased risk of toxicity. Fluorouracil 37-41 dihydropyrimidine dehydrogenase Homo sapiens 43-46 21919607-2 2011 As a key enzyme in the catabolism of 5-FU, DPD is the top candidate for pharmacogenetic studies on 5-FU toxicity, since a reduced DPD activity is thought to result in an increased half-life of the drug, and thus, an increased risk of toxicity. Fluorouracil 37-41 dihydropyrimidine dehydrogenase Homo sapiens 130-133 21919607-2 2011 As a key enzyme in the catabolism of 5-FU, DPD is the top candidate for pharmacogenetic studies on 5-FU toxicity, since a reduced DPD activity is thought to result in an increased half-life of the drug, and thus, an increased risk of toxicity. Fluorouracil 99-103 dihydropyrimidine dehydrogenase Homo sapiens 43-46 17390142-9 2007 In the HT-29 cell line, 5-FU treatment promoted an increase of 5.5 times in Hsp70 concentration after 12 h. Then, within 24 h, the increase in Hsp70 levels was still about two times. Fluorouracil 24-28 heat shock protein family A (Hsp70) member 4 Homo sapiens 143-148 21107571-0 2011 Determination of 5-fluorouracil and dihydrofluorouracil levels by using a liquid chromatography-tandem mass spectrometry method for evaluation of dihydropyrimidine dehydrogenase enzyme activity. Fluorouracil 17-31 dihydropyrimidine dehydrogenase Homo sapiens 146-177 21107571-2 2011 The key and rate-limiting enzyme in 5-FU catabolism is dihydropyrimidine dehydrogenase (DHPDH), whose partial or complete deficiency exposes to a severe 5-FU toxicity in patients. Fluorouracil 36-40 dihydropyrimidine dehydrogenase Homo sapiens 55-86 21107571-2 2011 The key and rate-limiting enzyme in 5-FU catabolism is dihydropyrimidine dehydrogenase (DHPDH), whose partial or complete deficiency exposes to a severe 5-FU toxicity in patients. Fluorouracil 36-40 dihydropyrimidine dehydrogenase Homo sapiens 88-93 21107571-2 2011 The key and rate-limiting enzyme in 5-FU catabolism is dihydropyrimidine dehydrogenase (DHPDH), whose partial or complete deficiency exposes to a severe 5-FU toxicity in patients. Fluorouracil 153-157 dihydropyrimidine dehydrogenase Homo sapiens 55-86 21107571-2 2011 The key and rate-limiting enzyme in 5-FU catabolism is dihydropyrimidine dehydrogenase (DHPDH), whose partial or complete deficiency exposes to a severe 5-FU toxicity in patients. Fluorouracil 153-157 dihydropyrimidine dehydrogenase Homo sapiens 88-93 21804305-1 2011 Capecitabine is an oral anticancer prodrug which is converted to 5-fluorouracil (5-FU) via 3 enzymatic steps, these being 5"-deoxy-5-fluorocytidine (5"-DFCR), 5"-deoxy-5-fluorouridine (5"-DFUR), and finally 5-FU by carboxylesterase (CES), cytidine deaminase (CDA), and thymidine phosphorylase (TP), respectively. Fluorouracil 65-79 thymidine phosphorylase Mus musculus 269-292 21804305-1 2011 Capecitabine is an oral anticancer prodrug which is converted to 5-fluorouracil (5-FU) via 3 enzymatic steps, these being 5"-deoxy-5-fluorocytidine (5"-DFCR), 5"-deoxy-5-fluorouridine (5"-DFUR), and finally 5-FU by carboxylesterase (CES), cytidine deaminase (CDA), and thymidine phosphorylase (TP), respectively. Fluorouracil 81-85 thymidine phosphorylase Mus musculus 269-292 21566437-0 2011 [Preventive effect of polaprezinc suspension dispersed in sodium alginate solution (P-AG) for stomatitis induced by Docetaxel/Cisplatin/Fluorouracil (DCF) chemotherapy in patients with head and neck cancer]. Fluorouracil 136-148 phosphoprotein membrane anchor with glycosphingolipid microdomains 1 Homo sapiens 84-88 17390142-10 2007 In contrast, in the SNU-C4 cell line, 5-FU induced an increase of about two times in the Hsp70 content after 12 h and, after 24 h, did not significantly affect Hsp70 content. Fluorouracil 38-42 heat shock protein family A (Hsp70) member 4 Homo sapiens 89-94 17390142-11 2007 CONCLUSIONS: These data suggest that 5-FU induced Hsp70 synthesis in the HT-29 resistant cell line and that this Hsp70 accumulation could protect against 5-FU-induced apoptosis. Fluorouracil 37-41 heat shock protein family A (Hsp70) member 4 Homo sapiens 50-55 21521021-0 2011 Association analysis of CYP2A6 genotypes and haplotypes with 5-fluorouracil formation from tegafur in human liver microsomes. Fluorouracil 61-75 cytochrome P450 family 2 subfamily A member 6 Homo sapiens 24-30 17390142-11 2007 CONCLUSIONS: These data suggest that 5-FU induced Hsp70 synthesis in the HT-29 resistant cell line and that this Hsp70 accumulation could protect against 5-FU-induced apoptosis. Fluorouracil 37-41 heat shock protein family A (Hsp70) member 4 Homo sapiens 113-118 21521021-1 2011 AIM: Tegafur is primarily converted to 5-fluorouracil (5-FU) by CYP2A6 in the human liver to exert its antitumor effect. Fluorouracil 39-53 cytochrome P450 family 2 subfamily A member 6 Homo sapiens 64-70 17390142-11 2007 CONCLUSIONS: These data suggest that 5-FU induced Hsp70 synthesis in the HT-29 resistant cell line and that this Hsp70 accumulation could protect against 5-FU-induced apoptosis. Fluorouracil 154-158 heat shock protein family A (Hsp70) member 4 Homo sapiens 113-118 21521021-1 2011 AIM: Tegafur is primarily converted to 5-fluorouracil (5-FU) by CYP2A6 in the human liver to exert its antitumor effect. Fluorouracil 55-59 cytochrome P450 family 2 subfamily A member 6 Homo sapiens 64-70 17390142-12 2007 Thus, Hsp70 protection against 5-FU-induced apoptosis might underlie colon cancer chemoresistance. Fluorouracil 31-35 heat shock protein family A (Hsp70) member 4 Homo sapiens 6-11 21521021-3 2011 MATERIALS & METHODS: Using a set of over 45 Chinese livers, the association between CYP2A6 genetic variations and 5-FU formation rates from tegafur, as well as CYP2A6 mRNA and protein levels, was determined. Fluorouracil 118-122 cytochrome P450 family 2 subfamily A member 6 Homo sapiens 88-94 18004243-0 2007 Dihydropyrimidine dehydrogenase activity correlates with fluorouracil sensitivity in breast cancer. Fluorouracil 57-69 dihydropyrimidine dehydrogenase Homo sapiens 0-31 21521021-5 2011 From genotype/haplotype-phenotype association tests, we demonstrated that CYP2A6*4 was the main allele responsible for the decreased 5-FU formation from tegafur and CYP2A6 expression in this population. Fluorouracil 133-137 cytochrome P450 family 2 subfamily A member 6 Homo sapiens 74-80 21521021-5 2011 From genotype/haplotype-phenotype association tests, we demonstrated that CYP2A6*4 was the main allele responsible for the decreased 5-FU formation from tegafur and CYP2A6 expression in this population. Fluorouracil 133-137 cytochrome P450 family 2 subfamily A member 6 Homo sapiens 165-171 21521021-6 2011 By contrast, haplotype 14 (a novel CYP2A6*1B allele) was associated with increased microsomal 5-FU formation activity and CYP2A6 expression, and this may be attributed to the combined effects of three single variants (g.22C>T, g.1620T>C and a gene conversion in the 3 -UTR) included in this haplotype. Fluorouracil 94-98 cytochrome P450 family 2 subfamily A member 6 Homo sapiens 35-41 21521021-7 2011 CONCLUSION: We concluded that CYP2A6*4 and the novel CYP2A6*1B variant were the major genetic determinants of interindividual variability in 5-FU formation from tegafur in Chinese livers. Fluorouracil 141-145 cytochrome P450 family 2 subfamily A member 6 Homo sapiens 30-36 21521021-7 2011 CONCLUSION: We concluded that CYP2A6*4 and the novel CYP2A6*1B variant were the major genetic determinants of interindividual variability in 5-FU formation from tegafur in Chinese livers. Fluorouracil 141-145 cytochrome P450 family 2 subfamily A member 6 Homo sapiens 53-59 21205074-11 2011 An in vivo antitumor effect of nutlin-3 alone and its additive augmentation by 5-fluorouracil were confirmed in an MDM2 overexpressed xenograft tumor model. Fluorouracil 79-93 MDM2 proto-oncogene Homo sapiens 115-119 21468552-7 2011 A similar reaction has also been observed in patients with the XRCC1 Arg399Gln polymorphism, while patients with the GSTP1 Ile105Val polymorphism have an improved response to oxaliplatin/5FU therapy. Fluorouracil 187-190 X-ray repair cross complementing 1 Homo sapiens 63-68 21222484-2 2011 In budding yeast, 5-FU promotes a large increase in the dUMP/dTMP ratio leading to massive polymerase-catalyzed incorporation of uracil (U) into genomic DNA, and to a lesser extent 5-FU, which are both excised by yeast uracil DNA glycosylase (UNG), leading to DNA fragmentation and cell death. Fluorouracil 18-22 uracil-DNA glycosylase Saccharomyces cerevisiae S288C 219-241 21378348-14 2011 Thus, the DPD inhibitory action of CDHP contributes to a decrease in 5-FU catabolism and to significantly higher blood levels of 5-FU compared to FT alone. Fluorouracil 69-73 dihydropyrimidine dehydrogenase Homo sapiens 10-13 21378348-14 2011 Thus, the DPD inhibitory action of CDHP contributes to a decrease in 5-FU catabolism and to significantly higher blood levels of 5-FU compared to FT alone. Fluorouracil 69-73 cadherin 3 Homo sapiens 35-39 21378348-14 2011 Thus, the DPD inhibitory action of CDHP contributes to a decrease in 5-FU catabolism and to significantly higher blood levels of 5-FU compared to FT alone. Fluorouracil 129-133 dihydropyrimidine dehydrogenase Homo sapiens 10-13 21378348-14 2011 Thus, the DPD inhibitory action of CDHP contributes to a decrease in 5-FU catabolism and to significantly higher blood levels of 5-FU compared to FT alone. Fluorouracil 129-133 cadherin 3 Homo sapiens 35-39 21143703-1 2011 S-1 is an oral fluoropyrimidine anti-neoplastic agent that is converted by CYP2A6 to 5-fluorouracil (5FU). Fluorouracil 85-99 cytochrome P450 family 2 subfamily A member 6 Homo sapiens 75-81 17335544-0 2007 Dihydropyrimidine dehydrogenase activity and the IVS14+1G>A mutation in patients developing 5FU-related toxicity. Fluorouracil 95-98 dihydropyrimidine dehydrogenase Homo sapiens 0-31 21043999-5 2011 SCDSF alone and in association with 5-Fu trigger both the extrinsic and the intrinsic apoptotic pathways, activating caspase-8, -3 and -7. Fluorouracil 36-40 caspase 8, apoptosis-related cysteine peptidase Danio rerio 117-137 21043999-6 2011 SCDSF and 5-Fu alone exerted opposite effects on Bax and Bcl-xL proteins, meanwhile SCDSF+5-Fu induced an almost complete suppression of Bcl-xL release and a dramatic increase in the Bax/Bcl-xL ratio. Fluorouracil 10-14 BCL2 like 1 Danio rerio 57-63 21043999-6 2011 SCDSF and 5-Fu alone exerted opposite effects on Bax and Bcl-xL proteins, meanwhile SCDSF+5-Fu induced an almost complete suppression of Bcl-xL release and a dramatic increase in the Bax/Bcl-xL ratio. Fluorouracil 90-94 BCL2 like 1 Danio rerio 137-143 21043999-6 2011 SCDSF and 5-Fu alone exerted opposite effects on Bax and Bcl-xL proteins, meanwhile SCDSF+5-Fu induced an almost complete suppression of Bcl-xL release and a dramatic increase in the Bax/Bcl-xL ratio. Fluorouracil 90-94 BCL2 like 1 Danio rerio 137-143 17335544-1 2007 AIMS: To examine retrospectively the relationship between DPD phenotype/genotype and the intensity of 5FU toxicity. Fluorouracil 102-105 dihydropyrimidine dehydrogenase Homo sapiens 58-61 20387074-2 2011 Several studies have evaluated in patients with colon cancer, either the role of genes involved in the 5-FU pathway, such as thymidylate synthase (TS), thymidine phosphorylase (TP) and dihydropyrimidine dehydrogenase (DPD) or the role of microsatellite instability (MSI) as prognostic or predictive markers for adjuvant chemotherapy efficacy, with discordant results. Fluorouracil 103-107 dihydropyrimidine dehydrogenase Homo sapiens 218-221 17699726-0 2007 Alteration of dihydropyrimidine dehydrogenase expression by IFN-alpha affects the antiproliferative effects of 5-fluorouracil in human hepatocellular carcinoma cells. Fluorouracil 111-125 dihydropyrimidine dehydrogenase Homo sapiens 14-45 17699726-1 2007 Dihydropyrimidine dehydrogenase (DPD) is the rate-limiting enzyme in the catabolism of 5-fluorouracil (5-FU) and its activity is closely associated with cellular sensitivity to 5-FU. Fluorouracil 87-101 dihydropyrimidine dehydrogenase Homo sapiens 0-31 17699726-1 2007 Dihydropyrimidine dehydrogenase (DPD) is the rate-limiting enzyme in the catabolism of 5-fluorouracil (5-FU) and its activity is closely associated with cellular sensitivity to 5-FU. Fluorouracil 87-101 dihydropyrimidine dehydrogenase Homo sapiens 33-36 17699726-1 2007 Dihydropyrimidine dehydrogenase (DPD) is the rate-limiting enzyme in the catabolism of 5-fluorouracil (5-FU) and its activity is closely associated with cellular sensitivity to 5-FU. Fluorouracil 103-107 dihydropyrimidine dehydrogenase Homo sapiens 0-31 17699726-1 2007 Dihydropyrimidine dehydrogenase (DPD) is the rate-limiting enzyme in the catabolism of 5-fluorouracil (5-FU) and its activity is closely associated with cellular sensitivity to 5-FU. Fluorouracil 103-107 dihydropyrimidine dehydrogenase Homo sapiens 33-36 17699726-1 2007 Dihydropyrimidine dehydrogenase (DPD) is the rate-limiting enzyme in the catabolism of 5-fluorouracil (5-FU) and its activity is closely associated with cellular sensitivity to 5-FU. Fluorouracil 177-181 dihydropyrimidine dehydrogenase Homo sapiens 0-31 17699726-1 2007 Dihydropyrimidine dehydrogenase (DPD) is the rate-limiting enzyme in the catabolism of 5-fluorouracil (5-FU) and its activity is closely associated with cellular sensitivity to 5-FU. Fluorouracil 177-181 dihydropyrimidine dehydrogenase Homo sapiens 33-36 17699726-2 2007 This study examines the role of DPD in the antiproliferative effects of 5-FU combined with IFN-alpha on hepatocellular carcinoma (HCC) cells in culture and asks whether IFN-alpha could affect DPD expression. Fluorouracil 72-76 dihydropyrimidine dehydrogenase Homo sapiens 32-35 17699726-7 2007 Coadministration of a selective DPD inhibitor, 5-chloro-2,4-dihydroxypyridine (CDHP), enhanced the antiproliferative effect of 5-FU and IFN-alpha on KYN-3 approximately 4-fold. Fluorouracil 127-131 dihydropyrimidine dehydrogenase Homo sapiens 32-35 17537404-5 2007 To elucidate the relationship between 5-FU-induced ROS production and Romo1 expression, Romo1 siRNA was used to inhibit 5-FU-triggered Romo1 induction. Fluorouracil 120-124 reactive oxygen species modulator 1 Homo sapiens 88-93 17537404-5 2007 To elucidate the relationship between 5-FU-induced ROS production and Romo1 expression, Romo1 siRNA was used to inhibit 5-FU-triggered Romo1 induction. Fluorouracil 120-124 reactive oxygen species modulator 1 Homo sapiens 88-93 17537404-6 2007 Romo1 siRNA treatment efficiently blocked 5-FU-induced ROS generation, demonstrating that 5-FU treatment stimulated ROS production through Romo1 induction. Fluorouracil 42-46 reactive oxygen species modulator 1 Homo sapiens 0-5 17537404-6 2007 Romo1 siRNA treatment efficiently blocked 5-FU-induced ROS generation, demonstrating that 5-FU treatment stimulated ROS production through Romo1 induction. Fluorouracil 42-46 reactive oxygen species modulator 1 Homo sapiens 139-144 17537404-6 2007 Romo1 siRNA treatment efficiently blocked 5-FU-induced ROS generation, demonstrating that 5-FU treatment stimulated ROS production through Romo1 induction. Fluorouracil 90-94 reactive oxygen species modulator 1 Homo sapiens 0-5 17537404-6 2007 Romo1 siRNA treatment efficiently blocked 5-FU-induced ROS generation, demonstrating that 5-FU treatment stimulated ROS production through Romo1 induction. Fluorouracil 90-94 reactive oxygen species modulator 1 Homo sapiens 139-144 17537404-7 2007 Based on these results we suggest that cellular adaptive response to Romo1-induced ROS is another mechanism of drug resistance to 5-FU and Romo1 expression may provide a new clinical implication in drug resistance of cancer chemotherapy. Fluorouracil 130-134 reactive oxygen species modulator 1 Homo sapiens 69-74 17725258-1 2007 A 68-year-old woman had had a TNM stage-III rectal carcinoma at the age of 54 for which she had undergone a low anterior resection followed by postoperative radiotherapy and adjuvant chemotherapy with fluorouracil and levamisol. Fluorouracil 201-213 teneurin transmembrane protein 1 Homo sapiens 30-33 17762391-6 2007 Moreover, the THC8307/L-OHP cells are also resistant to the other anticancer drug 5-fluorouracil, and the expression levels of the differentially regulated genes such as S100P, CAeta, STA15, TCF8 are constantly maintained. Fluorouracil 82-96 zinc finger E-box binding homeobox 1 Homo sapiens 191-195 17589894-0 2007 Effect of targeted magnetic nanoparticles containing 5-FU on expression of bcl-2, bax and caspase 3 in nude mice with transplanted human liver cancer. Fluorouracil 53-57 BCL2-associated X protein Mus musculus 82-85 17589894-0 2007 Effect of targeted magnetic nanoparticles containing 5-FU on expression of bcl-2, bax and caspase 3 in nude mice with transplanted human liver cancer. Fluorouracil 53-57 caspase 3 Mus musculus 90-99 17589894-9 2007 CONCLUSION: The targeted magnetic nanoparticles containing 5-FU can improve the chemotherapeutic effect of 5-FU against hepatocellular carcinoma by decreasing the expression of bcl-2 gene, and increasing the expression of bax and caspase 3 genes. Fluorouracil 59-63 BCL2-associated X protein Mus musculus 222-225 17589894-9 2007 CONCLUSION: The targeted magnetic nanoparticles containing 5-FU can improve the chemotherapeutic effect of 5-FU against hepatocellular carcinoma by decreasing the expression of bcl-2 gene, and increasing the expression of bax and caspase 3 genes. Fluorouracil 59-63 caspase 3 Mus musculus 230-239 17589894-9 2007 CONCLUSION: The targeted magnetic nanoparticles containing 5-FU can improve the chemotherapeutic effect of 5-FU against hepatocellular carcinoma by decreasing the expression of bcl-2 gene, and increasing the expression of bax and caspase 3 genes. Fluorouracil 107-111 BCL2-associated X protein Mus musculus 222-225 17589894-9 2007 CONCLUSION: The targeted magnetic nanoparticles containing 5-FU can improve the chemotherapeutic effect of 5-FU against hepatocellular carcinoma by decreasing the expression of bcl-2 gene, and increasing the expression of bax and caspase 3 genes. Fluorouracil 107-111 caspase 3 Mus musculus 230-239 17330233-1 2007 This study explores the effect of 5-fluorouracil (5FU) exposure on mRNA levels of its target enzyme thymidylate synthase (TS) and the rate-limiting catabolic enzyme dihydropyrimidine dehydrogenase (DPD) in tumors of colorectal cancer patients. Fluorouracil 34-48 dihydropyrimidine dehydrogenase Homo sapiens 198-201 17330233-1 2007 This study explores the effect of 5-fluorouracil (5FU) exposure on mRNA levels of its target enzyme thymidylate synthase (TS) and the rate-limiting catabolic enzyme dihydropyrimidine dehydrogenase (DPD) in tumors of colorectal cancer patients. Fluorouracil 50-53 dihydropyrimidine dehydrogenase Homo sapiens 198-201 17612628-1 2007 Dihydropyrimidine dehydrogenase (DPD) is one of the factors that determine the efficacy and toxicity of 5-fluorouracil. Fluorouracil 104-118 dihydropyrimidine dehydrogenase Homo sapiens 0-31 21456204-2 2011 5-FU administered in Plu-CLA hydrogel (P-FU) led to the significant enhancement of tumor growth suppression and cellular apoptosis. Fluorouracil 0-4 clasper Mus musculus 25-28 21456204-4 2011 Therefore, Plu-CLA could be a potential intraperitoneal carrier for hydrophilic 5-FU for the effective treatment of metastatic colon cancer. Fluorouracil 80-84 clasper Mus musculus 15-18 21067862-4 2011 Sirt1, which is one of the target genes for miR-34a and related to drug-resistance, was strikingly up-regulated in the 5-FU-resistant cells. Fluorouracil 119-123 sirtuin 1 Homo sapiens 0-5 21067862-5 2011 The ectopic expression of miR-34a in the 5-FU-resistant cells inhibited growth, as in the parental cells, and attenuated the resistance to 5-FU through the down-regulation of Sirt1 and E2F3. Fluorouracil 41-45 sirtuin 1 Homo sapiens 175-180 21067862-6 2011 Moreover, the silencing of Sirt1 significantly canceled the resistance to 5-FU in the 5-FU-resistant cells. Fluorouracil 74-78 sirtuin 1 Homo sapiens 27-32 21067862-6 2011 Moreover, the silencing of Sirt1 significantly canceled the resistance to 5-FU in the 5-FU-resistant cells. Fluorouracil 86-90 sirtuin 1 Homo sapiens 27-32 21067862-7 2011 These findings suggest that miR-34a targeting the Sirt1 and E2F3 genes could negatively regulate, at least in part, the resistance to 5-FU in human colorectal cancer DLD-1 cells. Fluorouracil 134-138 sirtuin 1 Homo sapiens 50-55 21881227-8 2011 5-FU treatment (400 mg/kg) also significantly downregurated expression levels of P-glycoprotein (P-gp) and breast cancer resistance protein (Bcrp) to 41.2 +- 14.7%, 15.7 +- 4.3% of control, respectively. Fluorouracil 0-4 ATP-binding cassette, subfamily B (MDR/TAP), member 1B Rattus norvegicus 81-95 21881227-8 2011 5-FU treatment (400 mg/kg) also significantly downregurated expression levels of P-glycoprotein (P-gp) and breast cancer resistance protein (Bcrp) to 41.2 +- 14.7%, 15.7 +- 4.3% of control, respectively. Fluorouracil 0-4 ATP-binding cassette, subfamily B (MDR/TAP), member 1B Rattus norvegicus 97-101 21881227-12 2011 5-FU treatment decreased expression levels of P-glycoprotein and Bcrp in intestine. Fluorouracil 0-4 ATP-binding cassette, subfamily B (MDR/TAP), member 1B Rattus norvegicus 46-60 17612628-1 2007 Dihydropyrimidine dehydrogenase (DPD) is one of the factors that determine the efficacy and toxicity of 5-fluorouracil. Fluorouracil 104-118 dihydropyrimidine dehydrogenase Homo sapiens 33-36 17612628-9 2007 The transcriptional suppression of DPYD by methylation may be responsible for the increased 5-fluorouracil sensitivity observed in some patients. Fluorouracil 92-106 dihydropyrimidine dehydrogenase Homo sapiens 35-39 17611394-5 2007 Treatment with XIAP siRNA in combination with Paclitaxel, Cisplatin, Fluorouracil and Etoposide enhanced chemosensitivity. Fluorouracil 69-81 X-linked inhibitor of apoptosis Homo sapiens 15-19 20204365-0 2011 DPD-based adaptive dosing of 5-FU in patients with head and neck cancer: impact on treatment efficacy and toxicity. Fluorouracil 29-33 dihydropyrimidine dehydrogenase Homo sapiens 0-3 20204365-3 2011 We have developed a simple, rapid, and inexpensive functional testing for DPD activity, as a means to identify deficient patients and to anticipate subsequent 5-FU-related toxicities. Fluorouracil 159-163 dihydropyrimidine dehydrogenase Homo sapiens 74-77 20204365-17 2011 CONCLUSIONS: Although non-randomized, this study strongly suggests that prospective determination of DPD status has an immediate clinical benefit by reducing the drug-induced toxicities incidence in patients treated with 5-FU, allowing an optimal administration of several courses in a row, while maintaining efficacy. Fluorouracil 221-225 dihydropyrimidine dehydrogenase Homo sapiens 101-104 20798686-6 2011 Furthermore, all patients who received cyclophosphamide (CP), epirubicin plus taxotere/CP, epirubicin plus 5-fluorouracil chemotherapy showed miR-448 suppression, an increased SATB1, Twist1 expression and acquisition of mesenchymal phenotypes. Fluorouracil 107-121 SATB homeobox 1 Homo sapiens 176-181 21634054-0 2011 Efficacy of irinotecan in combination with 5-fluorouracil (FOLFIRI) for metastatic gastric or gastroesophageal junction adenocarcinomas (MGA) treatment. Fluorouracil 44-58 MAX dimerization protein MGA Homo sapiens 139-142 21634054-1 2011 OBJECTIVES: The most commonly used schedules are 5-FU in combination with CDDP with or without epirubicin (ECF) or docetaxel (TCF) in treatment of MGA patients (pts), independently of HER status. Fluorouracil 49-53 MAX dimerization protein MGA Homo sapiens 147-150 20880064-1 2011 AIMS: Dihydropyrimidine dehydrogenase (DPD) and thymidylate synthase (TS) are key enzymes in the metabolism of 5-fluorouracil and have been implicated as possible prognostic markers for cancer patients. Fluorouracil 113-127 dihydropyrimidine dehydrogenase Homo sapiens 8-39 20880064-1 2011 AIMS: Dihydropyrimidine dehydrogenase (DPD) and thymidylate synthase (TS) are key enzymes in the metabolism of 5-fluorouracil and have been implicated as possible prognostic markers for cancer patients. Fluorouracil 113-127 dihydropyrimidine dehydrogenase Homo sapiens 41-44 21109933-6 2011 The specific down-regulation of CYLD resulted in increased resistance towards treatment with doxorubicin, 5-fluorouracil and cisplatin. Fluorouracil 106-120 CYLD lysine 63 deubiquitinase Homo sapiens 32-36 21761314-2 2011 Dihydropyrimidine dehydrogenase (DPD) is a degrading enzyme that catabolizes 5-FU. Fluorouracil 77-81 dihydropyrimidine dehydrogenase Homo sapiens 0-31 21761314-2 2011 Dihydropyrimidine dehydrogenase (DPD) is a degrading enzyme that catabolizes 5-FU. Fluorouracil 77-81 dihydropyrimidine dehydrogenase Homo sapiens 33-36 21761314-9 2011 Furthermore, the OPRT/ DPD expression ratio, a powerful predictive factor to evaluate 5-FU sensitivity, in the HRPC group was significantly higher than that in the low-grade HSPC group. Fluorouracil 86-90 dihydropyrimidine dehydrogenase Homo sapiens 23-26 22028766-8 2011 Furthermore, knockdown of NRP-2 sensitized CNDT 2.5 cells in vitro to 5FU toxicity. Fluorouracil 70-73 neuropilin 2 Homo sapiens 26-31 21887339-5 2011 PKR protein was activated by 5-FU treatment in a p53-independent manner, inducing phosphorylation of the protein synthesis translation initiation factor eIF-2alpha and cell death by apoptosis. Fluorouracil 29-33 eukaryotic translation initiation factor 2A Homo sapiens 153-163 21629657-9 2011 Gene expression of the autophagy-related LC3 gene as well as of Bad, Mdr-1, Atg12 and the vATPase was analysed after treatment of cells with 5-fluorouracil and omeprazole and confirmed the above mentioned results. Fluorouracil 141-155 microtubule associated protein 1 light chain 3 alpha Homo sapiens 41-44 20801641-2 2010 METHODS: Immunoreactivity of MMP-9 and TIMP-1 by carcinoma cells, lymphocytes and fibroblasts in archival specimens of paraffin-embedded primary tumours were retrospectively associated with outcome in 340 consecutive patients completely resected for CRC stages II-IV and subsequently treated with adjuvant 5-fluorouracil. Fluorouracil 306-320 matrix metallopeptidase 9 Homo sapiens 29-34 17611394-6 2007 These results suggest that XIAP might be helpful for diagnosis of ESCC and XIAP siRNA combined with Paclitaxel, Cisplatin, Fluorouracil and Etoposide may be a feasible strategy to enhance the effects of chemotherapy in patients with ESCC. Fluorouracil 123-135 X-linked inhibitor of apoptosis Homo sapiens 75-79 17565266-9 2007 Also, the combination of C-IFN +5-FU most downregulated DPD mRNA expression. Fluorouracil 32-36 dihydropyrimidine dehydrogenase Homo sapiens 56-59 17311258-7 2007 Using RNAi to downregulate these proteins we further confirmed that the levels of cIAP-2 and XIAP influence the response to the anti-cancer drugs, although only marginally for 5-FU. Fluorouracil 176-180 X-linked inhibitor of apoptosis Homo sapiens 93-97 17444856-4 2007 Wild-type RASSF1A cDNA was introduced into SMMC-7721; chemosensitivity to cisplatin, mitomycin and fluorouracil were analyzed using 3-[4, 5-dimethylthiazol-2-yl]-2, 5-diphenyltetrazolium bromide assay. Fluorouracil 99-111 Ras association domain family member 1 Homo sapiens 10-17 22811812-3 2010 In this study, we aimed to address the impact of KRAS on the pattern of metastatic disease at presentation and on RR and PFS with first-line 5-fluorouracil, leucovorin, and oxaliplatin (FOLFOX) chemotherapy. Fluorouracil 141-155 KRAS proto-oncogene, GTPase Homo sapiens 49-53 21163769-5 2010 The rate-limiting enzyme of 5-FU catabolism is dihydropyrimidine dehydrogenase (DPD) since more than 80% of the administered 5-FU is catabolized by DPD. Fluorouracil 28-32 dihydropyrimidine dehydrogenase Homo sapiens 80-83 21163769-5 2010 The rate-limiting enzyme of 5-FU catabolism is dihydropyrimidine dehydrogenase (DPD) since more than 80% of the administered 5-FU is catabolized by DPD. Fluorouracil 28-32 dihydropyrimidine dehydrogenase Homo sapiens 148-151 21163769-5 2010 The rate-limiting enzyme of 5-FU catabolism is dihydropyrimidine dehydrogenase (DPD) since more than 80% of the administered 5-FU is catabolized by DPD. Fluorouracil 125-129 dihydropyrimidine dehydrogenase Homo sapiens 80-83 21163769-5 2010 The rate-limiting enzyme of 5-FU catabolism is dihydropyrimidine dehydrogenase (DPD) since more than 80% of the administered 5-FU is catabolized by DPD. Fluorouracil 125-129 dihydropyrimidine dehydrogenase Homo sapiens 148-151 21163769-6 2010 Tumoral DPD has become of clinical interest because elevated intratumoral DPD can decrease the tumor response to 5-FU therapy. Fluorouracil 113-117 dihydropyrimidine dehydrogenase Homo sapiens 8-11 21163769-6 2010 Tumoral DPD has become of clinical interest because elevated intratumoral DPD can decrease the tumor response to 5-FU therapy. Fluorouracil 113-117 dihydropyrimidine dehydrogenase Homo sapiens 74-77 21163769-11 2010 Based on the fact that at the same time DPD activity was also increased it might be conceivable that a possible explanation for the decrease of 5-FU sensitivity is the co-existence of high COX-2 and DPD activity. Fluorouracil 144-148 dihydropyrimidine dehydrogenase Homo sapiens 40-43 21163769-11 2010 Based on the fact that at the same time DPD activity was also increased it might be conceivable that a possible explanation for the decrease of 5-FU sensitivity is the co-existence of high COX-2 and DPD activity. Fluorouracil 144-148 dihydropyrimidine dehydrogenase Homo sapiens 199-202 21163769-12 2010 Indomethacin or NS-398 enhanced in a simultaneous and significant manner the sensitivity and cytotoxic effect of 5-FU on high COX-2 expressing cells and xenografts through the modulation of DPD - decrease of its mRNA expression and/or enzyme activity. Fluorouracil 113-117 dihydropyrimidine dehydrogenase Homo sapiens 190-193 21163769-13 2010 Based on our results it could be presumable that 5-FU efficacy is limited by the COX-2 associated high DPD expression and activity in patients with colorectal cancer as well, therefore further clinical studies are warranted to decide if NSAIDs in the therapeutic protocol might improve the antitumor potency of 5-FU. Fluorouracil 49-53 dihydropyrimidine dehydrogenase Homo sapiens 103-106 17186550-2 2007 However, it is not fully understood to what extent NFkappaB contributes to induction of the metastasis-associated matrix metalloprotease-9 (MMP-9) gene and sensitivity to the commonly used chemotherapeutic 5-fluorouracil (5-Fu) in CRC. Fluorouracil 206-220 matrix metallopeptidase 9 Homo sapiens 114-138 17186550-2 2007 However, it is not fully understood to what extent NFkappaB contributes to induction of the metastasis-associated matrix metalloprotease-9 (MMP-9) gene and sensitivity to the commonly used chemotherapeutic 5-fluorouracil (5-Fu) in CRC. Fluorouracil 206-220 matrix metallopeptidase 9 Homo sapiens 140-145 17186550-2 2007 However, it is not fully understood to what extent NFkappaB contributes to induction of the metastasis-associated matrix metalloprotease-9 (MMP-9) gene and sensitivity to the commonly used chemotherapeutic 5-fluorouracil (5-Fu) in CRC. Fluorouracil 222-226 matrix metallopeptidase 9 Homo sapiens 114-138 17186550-2 2007 However, it is not fully understood to what extent NFkappaB contributes to induction of the metastasis-associated matrix metalloprotease-9 (MMP-9) gene and sensitivity to the commonly used chemotherapeutic 5-fluorouracil (5-Fu) in CRC. Fluorouracil 222-226 matrix metallopeptidase 9 Homo sapiens 140-145 17482957-4 2007 Its association with the expression of dihydropyrimidine dehydrogenase (DPD), a principal enzyme in the degradation of 5-FU and pyrimidine nucleotides, was also examined. Fluorouracil 119-123 dihydropyrimidine dehydrogenase Homo sapiens 39-70 17482957-4 2007 Its association with the expression of dihydropyrimidine dehydrogenase (DPD), a principal enzyme in the degradation of 5-FU and pyrimidine nucleotides, was also examined. Fluorouracil 119-123 dihydropyrimidine dehydrogenase Homo sapiens 72-75 17350823-1 2007 Dihydropyrimidine dehydrogenase (DPD) is a key enzyme in the metabolic catabolism of chemotherapeutic agent 5-fluorouracil (5FU) and its derivatives, including capecitabine. Fluorouracil 108-122 dihydropyrimidine dehydrogenase Homo sapiens 0-31 17350823-1 2007 Dihydropyrimidine dehydrogenase (DPD) is a key enzyme in the metabolic catabolism of chemotherapeutic agent 5-fluorouracil (5FU) and its derivatives, including capecitabine. Fluorouracil 108-122 dihydropyrimidine dehydrogenase Homo sapiens 33-36 17350823-1 2007 Dihydropyrimidine dehydrogenase (DPD) is a key enzyme in the metabolic catabolism of chemotherapeutic agent 5-fluorouracil (5FU) and its derivatives, including capecitabine. Fluorouracil 124-127 dihydropyrimidine dehydrogenase Homo sapiens 0-31 17417073-0 2007 Thymidylate synthase (TYMS) and dihydropyrimidine dehydrogenase (DPYD) polymorphisms in the Korean population for prediction of 5-fluorouracil-associated toxicity. Fluorouracil 128-142 dihydropyrimidine dehydrogenase Homo sapiens 32-63 17417073-0 2007 Thymidylate synthase (TYMS) and dihydropyrimidine dehydrogenase (DPYD) polymorphisms in the Korean population for prediction of 5-fluorouracil-associated toxicity. Fluorouracil 128-142 dihydropyrimidine dehydrogenase Homo sapiens 65-69 17417073-1 2007 The important cellular proteins for 5-fluorouracil (5-FU) metabolism are the major target enzymes, thymidylate synthase, and the rate-limiting enzyme in the degradation pathway, dihydropyrimidine dehydrogenase. Fluorouracil 36-50 dihydropyrimidine dehydrogenase Homo sapiens 178-209 17417073-1 2007 The important cellular proteins for 5-fluorouracil (5-FU) metabolism are the major target enzymes, thymidylate synthase, and the rate-limiting enzyme in the degradation pathway, dihydropyrimidine dehydrogenase. Fluorouracil 52-56 dihydropyrimidine dehydrogenase Homo sapiens 178-209 17417073-2 2007 Adverse drug reactions to 5-FU-based chemotherapy have been reported to be in part the result of polymorphisms in the thymidylate synthase (TYMS) and dihydropyrimidine dehydrogenase (DPYD) genes. Fluorouracil 26-30 dihydropyrimidine dehydrogenase Homo sapiens 150-181 17242401-0 2007 5-fluorouracil activation of p53 involves an MDM2-ribosomal protein interaction. Fluorouracil 0-14 MDM2 proto-oncogene Homo sapiens 45-49 17242401-4 2007 Here we report that 5-FU treatment leads to p53 stabilization and activation by blocking MDM2 feedback inhibition through ribosomal proteins. Fluorouracil 20-24 MDM2 proto-oncogene Homo sapiens 89-93 17242401-5 2007 5-FU treatment increased the fraction of ribosome-free L5, L11, and L23 ribosomal proteins and their interaction with MDM2, leading to p53 activation and G1/S arrest. Fluorouracil 0-4 ribosomal protein L11 Homo sapiens 59-62 17242401-5 2007 5-FU treatment increased the fraction of ribosome-free L5, L11, and L23 ribosomal proteins and their interaction with MDM2, leading to p53 activation and G1/S arrest. Fluorouracil 0-4 immunoglobulin kappa variable 1D-43 Homo sapiens 68-71 17242401-5 2007 5-FU treatment increased the fraction of ribosome-free L5, L11, and L23 ribosomal proteins and their interaction with MDM2, leading to p53 activation and G1/S arrest. Fluorouracil 0-4 MDM2 proto-oncogene Homo sapiens 118-122 17242401-7 2007 These results demonstrate that 5-FU treatment triggers a ribosomal stress response so that ribosomal proteins L5, L11, and L23 are released from ribosome to activate p53 by ablating the MDM2-p53 feedback circuit. Fluorouracil 31-35 ribosomal protein L11 Homo sapiens 114-117 17242401-7 2007 These results demonstrate that 5-FU treatment triggers a ribosomal stress response so that ribosomal proteins L5, L11, and L23 are released from ribosome to activate p53 by ablating the MDM2-p53 feedback circuit. Fluorouracil 31-35 immunoglobulin kappa variable 1D-43 Homo sapiens 123-126 17242401-7 2007 These results demonstrate that 5-FU treatment triggers a ribosomal stress response so that ribosomal proteins L5, L11, and L23 are released from ribosome to activate p53 by ablating the MDM2-p53 feedback circuit. Fluorouracil 31-35 MDM2 proto-oncogene Homo sapiens 186-190 17465211-9 2007 CONCLUSION: The DPD mRNA level and OPRT/DPD ratio evaluated from paraffin embedded specimens are candidates for further evaluation as predictors of response against 5-fluorouracil-based chemotherapy in colorectal cancer. Fluorouracil 165-179 dihydropyrimidine dehydrogenase Homo sapiens 16-19 17230597-2 2007 After intravenous administration of 5-fluorouracil at a dose of 30 mg/kg to NARs, the time-averaged nonrenal clearance (Clnr) of the drug was significantly faster than the controls (51.3 versus 28.8 ml/min/kg), possibly due to an increase in the expression and mRNA level of CYP1A2 in NARs. Fluorouracil 36-50 cytochrome P450, family 1, subfamily a, polypeptide 2 Rattus norvegicus 275-281 17230597-3 2007 In order to determine whether 5-fluorouracil is metabolized via CYP1A2 in male Sprague-Dawley rats, the rats were pretreated with 3-methylcholanthrene (a main inducer of CYP1A1/2 in rats). Fluorouracil 30-44 cytochrome P450, family 1, subfamily a, polypeptide 2 Rattus norvegicus 64-70 17092280-1 2007 OBJECTIVE: To measure dihydropyrimidine dehydrogenase (DPD), an enzyme involved in the metabolism of 5-fluorouracil (5-FU), expression in prostate cancer and determine whether 5-chloro-2,4-dihydroxypyridine (CDHP), a potent inhibitor of DPD, enhances the antitumoral activity of 5-FU against prostate cancer. Fluorouracil 101-115 dihydropyrimidine dehydrogenase Homo sapiens 22-53 17092280-1 2007 OBJECTIVE: To measure dihydropyrimidine dehydrogenase (DPD), an enzyme involved in the metabolism of 5-fluorouracil (5-FU), expression in prostate cancer and determine whether 5-chloro-2,4-dihydroxypyridine (CDHP), a potent inhibitor of DPD, enhances the antitumoral activity of 5-FU against prostate cancer. Fluorouracil 101-115 dihydropyrimidine dehydrogenase Homo sapiens 55-58 17092280-1 2007 OBJECTIVE: To measure dihydropyrimidine dehydrogenase (DPD), an enzyme involved in the metabolism of 5-fluorouracil (5-FU), expression in prostate cancer and determine whether 5-chloro-2,4-dihydroxypyridine (CDHP), a potent inhibitor of DPD, enhances the antitumoral activity of 5-FU against prostate cancer. Fluorouracil 117-121 dihydropyrimidine dehydrogenase Homo sapiens 22-53 17092280-1 2007 OBJECTIVE: To measure dihydropyrimidine dehydrogenase (DPD), an enzyme involved in the metabolism of 5-fluorouracil (5-FU), expression in prostate cancer and determine whether 5-chloro-2,4-dihydroxypyridine (CDHP), a potent inhibitor of DPD, enhances the antitumoral activity of 5-FU against prostate cancer. Fluorouracil 117-121 dihydropyrimidine dehydrogenase Homo sapiens 55-58 17092280-1 2007 OBJECTIVE: To measure dihydropyrimidine dehydrogenase (DPD), an enzyme involved in the metabolism of 5-fluorouracil (5-FU), expression in prostate cancer and determine whether 5-chloro-2,4-dihydroxypyridine (CDHP), a potent inhibitor of DPD, enhances the antitumoral activity of 5-FU against prostate cancer. Fluorouracil 117-121 dihydropyrimidine dehydrogenase Homo sapiens 237-240 17582310-3 2007 More than 80% of administered 5-FU is detoxified in 5-fluoro-5,6-dihydrouracil (5-FUH2) by an enzyme: dihydropyrimidine dehydrogenase (DPD). Fluorouracil 30-34 dihydropyrimidine dehydrogenase Homo sapiens 102-133 21223795-9 2010 The average gray value of caspase-3 protein expressed in the control group was 46.12 +- 0.33 and the relative expression of caspase-3 mRNA was 0.14 +- 0.03, both were significantly lower than that in the ATRA group, 5-Fu group and the two-drugs combination group (P < 0.05). Fluorouracil 216-220 caspase 3 Mus musculus 26-35 21223795-9 2010 The average gray value of caspase-3 protein expressed in the control group was 46.12 +- 0.33 and the relative expression of caspase-3 mRNA was 0.14 +- 0.03, both were significantly lower than that in the ATRA group, 5-Fu group and the two-drugs combination group (P < 0.05). Fluorouracil 216-220 caspase 3 Mus musculus 124-133 17582310-3 2007 More than 80% of administered 5-FU is detoxified in 5-fluoro-5,6-dihydrouracil (5-FUH2) by an enzyme: dihydropyrimidine dehydrogenase (DPD). Fluorouracil 30-34 dihydropyrimidine dehydrogenase Homo sapiens 135-138 17096352-1 2007 Cytotoxic effect of 5-fluorouracil 5-FU is mediated through inhibition of thymidylate synthase (TS), and 5-FU is catabolised by dihydropyrimidine dehydrogenase (DPD). Fluorouracil 20-34 dihydropyrimidine dehydrogenase Homo sapiens 128-159 17096352-1 2007 Cytotoxic effect of 5-fluorouracil 5-FU is mediated through inhibition of thymidylate synthase (TS), and 5-FU is catabolised by dihydropyrimidine dehydrogenase (DPD). Fluorouracil 20-34 dihydropyrimidine dehydrogenase Homo sapiens 161-164 17096352-1 2007 Cytotoxic effect of 5-fluorouracil 5-FU is mediated through inhibition of thymidylate synthase (TS), and 5-FU is catabolised by dihydropyrimidine dehydrogenase (DPD). Fluorouracil 35-39 dihydropyrimidine dehydrogenase Homo sapiens 161-164 17096352-1 2007 Cytotoxic effect of 5-fluorouracil 5-FU is mediated through inhibition of thymidylate synthase (TS), and 5-FU is catabolised by dihydropyrimidine dehydrogenase (DPD). Fluorouracil 105-109 dihydropyrimidine dehydrogenase Homo sapiens 128-159 17096352-1 2007 Cytotoxic effect of 5-fluorouracil 5-FU is mediated through inhibition of thymidylate synthase (TS), and 5-FU is catabolised by dihydropyrimidine dehydrogenase (DPD). Fluorouracil 105-109 dihydropyrimidine dehydrogenase Homo sapiens 161-164 17096352-2 2007 Efficacy of 5-FU may therefore depend on the TS and DPD activity of colorectal cancer. Fluorouracil 12-16 dihydropyrimidine dehydrogenase Homo sapiens 52-55 21152064-3 2010 In chemotherapeutic sensitivity screening assays, cells overexpressing pp32 were selectively resistant to the nucleoside analogs gemcitabine and cytarabine (ARA-C), but were sensitized to 5-fluorouracil; conversely, silencing pp32 in pancreatic cancer cells enhanced gemcitabine sensitivity. Fluorouracil 188-202 acidic nuclear phosphoprotein 32 family member A Homo sapiens 71-75 16868766-8 2007 Similar to the case for other MRPs that possess only two membrane spanning domains (MRP4 and MRP5), MRP8 is a cyclic nucleotide efflux pump that is able to confer resistance to nucleoside-based agents, such as PMEA and 5FU. Fluorouracil 219-222 ATP binding cassette subfamily C member 4 Homo sapiens 84-88 20723540-10 2010 In vivo dynamic [(18)F]FLT-PET and ex vivo analysis in HT29 tumor-bearing mice showed significantly increased [(18)F]FLT flux and TK1 activity of tumor tissue 24h after 5-FU administration (P<0.05). Fluorouracil 169-173 thymidine kinase 1 Mus musculus 130-133 16868766-8 2007 Similar to the case for other MRPs that possess only two membrane spanning domains (MRP4 and MRP5), MRP8 is a cyclic nucleotide efflux pump that is able to confer resistance to nucleoside-based agents, such as PMEA and 5FU. Fluorouracil 219-222 ATP binding cassette subfamily C member 11 Homo sapiens 100-104 17445431-0 2007 [The association between DPYD gene polymorphism and chemotherapeutic toxicity of 5-FU in gastric carcinoma and colonic carcinoma]. Fluorouracil 81-85 dihydropyrimidine dehydrogenase Homo sapiens 25-29 21062980-6 2010 This role is supported with the demonstration that HNF4alpha is functionally involved in the protection against spontaneous and 5-fluorouracil chemotherapy-induced production of ROS in colorectal cancer cell lines. Fluorouracil 128-142 hepatic nuclear factor 4, alpha Mus musculus 51-60 20888173-0 2010 Interleukin 1 receptor antagonist reduces lethality and intestinal toxicity of 5-fluorouracil in a mouse mucositis model. Fluorouracil 79-93 interleukin 1 receptor antagonist Mus musculus 0-33 20888173-6 2010 Administration of recombinant IL-1Ra to the mouse model of intestinal mucositis induced by 5-Fu demonstrated its therapeutic effects to the symptoms and pathology of the disease. Fluorouracil 91-95 interleukin 1 receptor antagonist Mus musculus 30-36 21062732-1 2010 BACKGROUND: Dihydropyrimidine dehydrogenase (DPD), orotate phosphoribosyl transferase (OPRT), and thymidylate synthase (TS) levels correlate with sensitivity and resistance to 5-fluorouracil (5-FU). Fluorouracil 176-190 dihydropyrimidine dehydrogenase Homo sapiens 12-43 21062732-1 2010 BACKGROUND: Dihydropyrimidine dehydrogenase (DPD), orotate phosphoribosyl transferase (OPRT), and thymidylate synthase (TS) levels correlate with sensitivity and resistance to 5-fluorouracil (5-FU). Fluorouracil 192-196 dihydropyrimidine dehydrogenase Homo sapiens 12-43 17445431-10 2007 CONCLUSION: DPYD*5 gene mutation contributes to reduced DPYD enzyme activity and 5-FU dyes metabolism, which is associated with accumulation of 5-FU and chemotherapeutic toxicity in patients with gastric and colonic carcinoma. Fluorouracil 81-85 dihydropyrimidine dehydrogenase Homo sapiens 12-16 17445431-10 2007 CONCLUSION: DPYD*5 gene mutation contributes to reduced DPYD enzyme activity and 5-FU dyes metabolism, which is associated with accumulation of 5-FU and chemotherapeutic toxicity in patients with gastric and colonic carcinoma. Fluorouracil 144-148 dihydropyrimidine dehydrogenase Homo sapiens 12-16 17445431-10 2007 CONCLUSION: DPYD*5 gene mutation contributes to reduced DPYD enzyme activity and 5-FU dyes metabolism, which is associated with accumulation of 5-FU and chemotherapeutic toxicity in patients with gastric and colonic carcinoma. Fluorouracil 144-148 dihydropyrimidine dehydrogenase Homo sapiens 56-60 17097873-6 2007 Patients with a high-normal DPD activity proved to be at risk of developing mild toxicity upon treatment with 5FU-leucovorin, suggesting an important role of DPD in the aetiology of toxicity associated with catabolites of 5FU. Fluorouracil 110-113 dihydropyrimidine dehydrogenase Homo sapiens 28-31 17097873-6 2007 Patients with a high-normal DPD activity proved to be at risk of developing mild toxicity upon treatment with 5FU-leucovorin, suggesting an important role of DPD in the aetiology of toxicity associated with catabolites of 5FU. Fluorouracil 110-113 dihydropyrimidine dehydrogenase Homo sapiens 158-161 17097873-6 2007 Patients with a high-normal DPD activity proved to be at risk of developing mild toxicity upon treatment with 5FU-leucovorin, suggesting an important role of DPD in the aetiology of toxicity associated with catabolites of 5FU. Fluorouracil 222-225 dihydropyrimidine dehydrogenase Homo sapiens 28-31 17097873-6 2007 Patients with a high-normal DPD activity proved to be at risk of developing mild toxicity upon treatment with 5FU-leucovorin, suggesting an important role of DPD in the aetiology of toxicity associated with catabolites of 5FU. Fluorouracil 222-225 dihydropyrimidine dehydrogenase Homo sapiens 158-161 17300701-2 2007 We reported that responders to IFN-alpha/5-fluorouracil combination therapy expressed higher IFN alpha receptor (IFNAR)2 in tumor. Fluorouracil 41-55 interferon alpha and beta receptor subunit 2 Homo sapiens 113-120 17660867-1 2007 The cytotoxic effect of 5-fluorouracil (5-FU) is mediated by the inhibition of thymidylate synthase (TS), however, at the same time 5-FU is catabolized by dihydropyrimidine dehydrogenase (DPD). Fluorouracil 24-38 dihydropyrimidine dehydrogenase Homo sapiens 155-186 17660867-1 2007 The cytotoxic effect of 5-fluorouracil (5-FU) is mediated by the inhibition of thymidylate synthase (TS), however, at the same time 5-FU is catabolized by dihydropyrimidine dehydrogenase (DPD). Fluorouracil 24-38 dihydropyrimidine dehydrogenase Homo sapiens 188-191 16929515-1 2006 We evaluated DNA polymorphisms in the thymidylate synthase (TS) and 5,10-methylene-tetrahydrofolate reductase (MTHFR) genes for an association with response and survival in locally advanced gastric cancer treated with 5-FU based preoperative chemotherapy (CTx). Fluorouracil 218-222 methylenetetrahydrofolate reductase Homo sapiens 68-109 16929515-1 2006 We evaluated DNA polymorphisms in the thymidylate synthase (TS) and 5,10-methylene-tetrahydrofolate reductase (MTHFR) genes for an association with response and survival in locally advanced gastric cancer treated with 5-FU based preoperative chemotherapy (CTx). Fluorouracil 218-222 methylenetetrahydrofolate reductase Homo sapiens 111-116 16969493-1 2006 Thymidine phosphorylase (TP) and dihydropyrimidine dehydrogenase (DPD) are the major catabolic enzymes of 5-FU. Fluorouracil 106-110 dihydropyrimidine dehydrogenase Homo sapiens 66-69 16969493-7 2006 In conclusion, chemotherapy with 5-FU may be more effective in squamous cell lung cancer patients than lung adenocarcinoma patients from the result of the ratio of TP to DPD. Fluorouracil 33-37 dihydropyrimidine dehydrogenase Homo sapiens 170-173 16880781-1 2006 The sensitivity to 5-fluorouracil (5-FU) has been reported to be associated with target molecule thymidylate synthase (TS), fluoropyrimidine-metabolising enzymes such as orotate phosphoribosyltransferase (OPRT), and dihydropyrimidine dehydrogenase (DPD). Fluorouracil 19-33 dihydropyrimidine dehydrogenase Homo sapiens 216-247 16880781-1 2006 The sensitivity to 5-fluorouracil (5-FU) has been reported to be associated with target molecule thymidylate synthase (TS), fluoropyrimidine-metabolising enzymes such as orotate phosphoribosyltransferase (OPRT), and dihydropyrimidine dehydrogenase (DPD). Fluorouracil 19-33 dihydropyrimidine dehydrogenase Homo sapiens 249-252 16880781-1 2006 The sensitivity to 5-fluorouracil (5-FU) has been reported to be associated with target molecule thymidylate synthase (TS), fluoropyrimidine-metabolising enzymes such as orotate phosphoribosyltransferase (OPRT), and dihydropyrimidine dehydrogenase (DPD). Fluorouracil 35-39 dihydropyrimidine dehydrogenase Homo sapiens 216-247 16880781-1 2006 The sensitivity to 5-fluorouracil (5-FU) has been reported to be associated with target molecule thymidylate synthase (TS), fluoropyrimidine-metabolising enzymes such as orotate phosphoribosyltransferase (OPRT), and dihydropyrimidine dehydrogenase (DPD). Fluorouracil 35-39 dihydropyrimidine dehydrogenase Homo sapiens 249-252 20803296-0 2010 Intragenic deletions and a deep intronic mutation affecting pre-mRNA splicing in the dihydropyrimidine dehydrogenase gene as novel mechanisms causing 5-fluorouracil toxicity. Fluorouracil 150-164 dihydropyrimidine dehydrogenase Homo sapiens 85-116 16557594-6 2006 High dose 5-FU also induced a higher regulation of the mitochondrial death genes APAF1, BAK1 and BCL2, and induction of genes of the ID family. Fluorouracil 10-14 BCL2 antagonist/killer 1 Homo sapiens 88-92 16785472-3 2006 RESULTS: In the Cox proportional hazards model, MTHFR Glu429Ala variant genotypes were associated with significantly improved survival (hazard ratio [HR] = 0.56; 95% CI, 0.35 to 0.89) in patients treated with fluorouracil (FU). Fluorouracil 209-221 methylenetetrahydrofolate reductase Homo sapiens 48-53 20803296-1 2010 Dihydropyrimidine dehydrogenase (DPD) is the initial enzyme acting in the catabolism of the widely used antineoplastic agent 5-fluorouracil (5FU). Fluorouracil 125-139 dihydropyrimidine dehydrogenase Homo sapiens 0-31 20803296-1 2010 Dihydropyrimidine dehydrogenase (DPD) is the initial enzyme acting in the catabolism of the widely used antineoplastic agent 5-fluorouracil (5FU). Fluorouracil 125-139 dihydropyrimidine dehydrogenase Homo sapiens 33-36 20803296-1 2010 Dihydropyrimidine dehydrogenase (DPD) is the initial enzyme acting in the catabolism of the widely used antineoplastic agent 5-fluorouracil (5FU). Fluorouracil 141-144 dihydropyrimidine dehydrogenase Homo sapiens 0-31 20803296-1 2010 Dihydropyrimidine dehydrogenase (DPD) is the initial enzyme acting in the catabolism of the widely used antineoplastic agent 5-fluorouracil (5FU). Fluorouracil 141-144 dihydropyrimidine dehydrogenase Homo sapiens 33-36 20920994-0 2010 Routine dihydropyrimidine dehydrogenase testing for anticipating 5-fluorouracil-related severe toxicities: hype or hope? Fluorouracil 65-79 dihydropyrimidine dehydrogenase Homo sapiens 8-39 20920994-3 2010 Several clinical reports have shown the deleterious effect of dihydropyrimidine dehydrogenase (DPD) genetic polymorphism, a condition that reduces the liver detoxification step of standard dosages of 5-FU, in patients undergoing fluoropyrimidine-based therapy. Fluorouracil 200-204 dihydropyrimidine dehydrogenase Homo sapiens 62-93 20920994-3 2010 Several clinical reports have shown the deleterious effect of dihydropyrimidine dehydrogenase (DPD) genetic polymorphism, a condition that reduces the liver detoxification step of standard dosages of 5-FU, in patients undergoing fluoropyrimidine-based therapy. Fluorouracil 200-204 dihydropyrimidine dehydrogenase Homo sapiens 95-98 16820886-0 2006 Deficient expression of the DPD gene is caused by epigenetic modification in biliary tract cancer cells, and induces high sensitivity to 5-FU treatment. Fluorouracil 137-141 dihydropyrimidine dehydrogenase Homo sapiens 28-31 20920994-6 2010 Consequently, no regulatory step has been undertaken yet to recommend DPD testing as part of routine clinical practice for securing the administration of 5-FU. Fluorouracil 154-158 dihydropyrimidine dehydrogenase Homo sapiens 70-73 20920994-7 2010 This review covers the limits and achievements of the various strategies proposed so far for determining DPD status in patients scheduled for 5-FU therapy. Fluorouracil 142-146 dihydropyrimidine dehydrogenase Homo sapiens 105-108 20811704-9 2010 The activity of Akt3/PKBgamma was inhibited with 5-FU alone and trastuzumab, indicating that trastuzumab may inhibit colon cancer growth through ErbB2-Akt3/PKBgamma signaling. Fluorouracil 49-53 AKT serine/threonine kinase 3 Homo sapiens 16-20 20811704-9 2010 The activity of Akt3/PKBgamma was inhibited with 5-FU alone and trastuzumab, indicating that trastuzumab may inhibit colon cancer growth through ErbB2-Akt3/PKBgamma signaling. Fluorouracil 49-53 AKT serine/threonine kinase 3 Homo sapiens 21-29 20811704-9 2010 The activity of Akt3/PKBgamma was inhibited with 5-FU alone and trastuzumab, indicating that trastuzumab may inhibit colon cancer growth through ErbB2-Akt3/PKBgamma signaling. Fluorouracil 49-53 AKT serine/threonine kinase 3 Homo sapiens 156-164 20809970-1 2010 BACKGROUND: Severe toxicity to 5-fluorouracil (5-FU) based chemotherapy in gastrointestinal cancer has been associated with constitutional genetic alterations of the dihydropyrimidine dehydrogenase gene (DPYD). Fluorouracil 31-45 dihydropyrimidine dehydrogenase Homo sapiens 166-197 20809970-1 2010 BACKGROUND: Severe toxicity to 5-fluorouracil (5-FU) based chemotherapy in gastrointestinal cancer has been associated with constitutional genetic alterations of the dihydropyrimidine dehydrogenase gene (DPYD). Fluorouracil 31-45 dihydropyrimidine dehydrogenase Homo sapiens 204-208 20809970-1 2010 BACKGROUND: Severe toxicity to 5-fluorouracil (5-FU) based chemotherapy in gastrointestinal cancer has been associated with constitutional genetic alterations of the dihydropyrimidine dehydrogenase gene (DPYD). Fluorouracil 47-51 dihydropyrimidine dehydrogenase Homo sapiens 166-197 20809970-1 2010 BACKGROUND: Severe toxicity to 5-fluorouracil (5-FU) based chemotherapy in gastrointestinal cancer has been associated with constitutional genetic alterations of the dihydropyrimidine dehydrogenase gene (DPYD). Fluorouracil 47-51 dihydropyrimidine dehydrogenase Homo sapiens 204-208 20837458-1 2010 BACKGROUND: Thymidylate synthase (TS), thymidine phosphorylase (TP), and dihydropyrimidine dehydrogenase (DPD) are key enzymes in the 5-fluorouracil (5-FU) pathway. Fluorouracil 134-148 dihydropyrimidine dehydrogenase Homo sapiens 73-104 20837458-1 2010 BACKGROUND: Thymidylate synthase (TS), thymidine phosphorylase (TP), and dihydropyrimidine dehydrogenase (DPD) are key enzymes in the 5-fluorouracil (5-FU) pathway. Fluorouracil 134-148 dihydropyrimidine dehydrogenase Homo sapiens 106-109 20837458-1 2010 BACKGROUND: Thymidylate synthase (TS), thymidine phosphorylase (TP), and dihydropyrimidine dehydrogenase (DPD) are key enzymes in the 5-fluorouracil (5-FU) pathway. Fluorouracil 150-154 dihydropyrimidine dehydrogenase Homo sapiens 73-104 20837458-1 2010 BACKGROUND: Thymidylate synthase (TS), thymidine phosphorylase (TP), and dihydropyrimidine dehydrogenase (DPD) are key enzymes in the 5-fluorouracil (5-FU) pathway. Fluorouracil 150-154 dihydropyrimidine dehydrogenase Homo sapiens 106-109 16820886-6 2006 DPD mRNA expression and DPD activity exhibited positive correlation with the IC50 for 5-FU (R=0.658, R=0.644, respectively), although these relationships were not statistically significant. Fluorouracil 86-90 dihydropyrimidine dehydrogenase Homo sapiens 0-3 16820886-6 2006 DPD mRNA expression and DPD activity exhibited positive correlation with the IC50 for 5-FU (R=0.658, R=0.644, respectively), although these relationships were not statistically significant. Fluorouracil 86-90 dihydropyrimidine dehydrogenase Homo sapiens 24-27 16820886-11 2006 In conclusion, these results may aid the selection of 5-FU chemotherapy following determination of DPD expression in biliary tract cancers. Fluorouracil 54-58 dihydropyrimidine dehydrogenase Homo sapiens 99-102 16584912-14 2006 5-FU is phosphorylated by OPRT and TP and detoxified by DPD. Fluorouracil 0-4 dihydropyrimidine dehydrogenase Homo sapiens 56-59 16897968-3 2006 As a single agent, S-1 showed higher antitumor activity with its low intestinal toxicity compared to continuous venous infusion 5-FU, the most effective dosing method of 5-FU, and/or to clinically available oral fluoropyrimidines such as UFT, doxyfluridine and capecitabine on various murine tumors and human tumor xenografts. Fluorouracil 170-174 proteasome (prosome, macropain) 26S subunit, non-ATPase, 1 Mus musculus 19-22 16709241-11 2006 Differential expression in response to 5-FU treatment was demonstrated for genes involved in regulation of nucleotide binding/metabolism (ATAD2, GNL2, GNL3, MATR3), amino acid metabolism (AHCY, GSS, IVD, OAT), cytoskeleton organization (KRT7, KRT8, KRT19, MAST1), transport (MTCH1, NCBP1, SNAPAP, VPS52), and oxygen metabolism (COX5A, COX7C). Fluorouracil 39-43 G protein nucleolar 2 Homo sapiens 145-149 16709241-11 2006 Differential expression in response to 5-FU treatment was demonstrated for genes involved in regulation of nucleotide binding/metabolism (ATAD2, GNL2, GNL3, MATR3), amino acid metabolism (AHCY, GSS, IVD, OAT), cytoskeleton organization (KRT7, KRT8, KRT19, MAST1), transport (MTCH1, NCBP1, SNAPAP, VPS52), and oxygen metabolism (COX5A, COX7C). Fluorouracil 39-43 matrin 3 Homo sapiens 157-162 16709241-11 2006 Differential expression in response to 5-FU treatment was demonstrated for genes involved in regulation of nucleotide binding/metabolism (ATAD2, GNL2, GNL3, MATR3), amino acid metabolism (AHCY, GSS, IVD, OAT), cytoskeleton organization (KRT7, KRT8, KRT19, MAST1), transport (MTCH1, NCBP1, SNAPAP, VPS52), and oxygen metabolism (COX5A, COX7C). Fluorouracil 39-43 keratin 8 Homo sapiens 243-247 16709241-11 2006 Differential expression in response to 5-FU treatment was demonstrated for genes involved in regulation of nucleotide binding/metabolism (ATAD2, GNL2, GNL3, MATR3), amino acid metabolism (AHCY, GSS, IVD, OAT), cytoskeleton organization (KRT7, KRT8, KRT19, MAST1), transport (MTCH1, NCBP1, SNAPAP, VPS52), and oxygen metabolism (COX5A, COX7C). Fluorouracil 39-43 cytochrome c oxidase subunit 7C Homo sapiens 335-340 16806531-1 2006 Dihydropyrimidine dehydrogenase (DPD), the initial and rate-limiting enzyme in the 5-fluorouracil (5-FU) catabolic pathway, has been implicated as one of the factors determining the efficacy and toxicity of the anticancer agent 5-FU. Fluorouracil 83-97 dihydropyrimidine dehydrogenase Homo sapiens 0-31 23199090-4 2010 The screening of genotypes, such as thymidylate synthase, dihydropyrimidine dehydrogenase, methylene tetrahydrofolate reductase, orotate phosphoribosyltransferase or glutathione S-transferase, could help identifying those patients with colorectal carcinoma who can actually benefit from a 5-FU-based therapy. Fluorouracil 289-293 methylenetetrahydrofolate reductase Homo sapiens 91-127 23199091-3 2010 5-FU undergoes complex metabolism, dihydropyrimidine dehydrogenase (DPD) being the rate-limiting enzyme of inactivation of 5-FU and its prodrugs. Fluorouracil 0-4 dihydropyrimidine dehydrogenase Homo sapiens 35-66 23199091-3 2010 5-FU undergoes complex metabolism, dihydropyrimidine dehydrogenase (DPD) being the rate-limiting enzyme of inactivation of 5-FU and its prodrugs. Fluorouracil 0-4 dihydropyrimidine dehydrogenase Homo sapiens 68-71 23199091-3 2010 5-FU undergoes complex metabolism, dihydropyrimidine dehydrogenase (DPD) being the rate-limiting enzyme of inactivation of 5-FU and its prodrugs. Fluorouracil 123-127 dihydropyrimidine dehydrogenase Homo sapiens 35-66 23199091-3 2010 5-FU undergoes complex metabolism, dihydropyrimidine dehydrogenase (DPD) being the rate-limiting enzyme of inactivation of 5-FU and its prodrugs. Fluorouracil 123-127 dihydropyrimidine dehydrogenase Homo sapiens 68-71 20570612-6 2010 Furthermore, WOG could decrease the mRNA levels of dihydropyrimidine dehydrogenase (DPD), the metabolic enzymes of 5-FU. Fluorouracil 115-119 dihydropyrimidine dehydrogenase Homo sapiens 51-82 20570612-6 2010 Furthermore, WOG could decrease the mRNA levels of dihydropyrimidine dehydrogenase (DPD), the metabolic enzymes of 5-FU. Fluorouracil 115-119 dihydropyrimidine dehydrogenase Homo sapiens 84-87 20635445-5 2010 RESULTS: While YD-9 cells showed high resistance to chemotherapeutic agents such as etoposide and 5-fluorouraci (5-FU), HSP70 antisense oligonucelotides sensitized chemoresistant YD-9 cells to etoposide and 5-FU. Fluorouracil 207-211 heat shock protein family A (Hsp70) member 4 Homo sapiens 120-125 16806531-1 2006 Dihydropyrimidine dehydrogenase (DPD), the initial and rate-limiting enzyme in the 5-fluorouracil (5-FU) catabolic pathway, has been implicated as one of the factors determining the efficacy and toxicity of the anticancer agent 5-FU. Fluorouracil 83-97 dihydropyrimidine dehydrogenase Homo sapiens 33-36 16806531-1 2006 Dihydropyrimidine dehydrogenase (DPD), the initial and rate-limiting enzyme in the 5-fluorouracil (5-FU) catabolic pathway, has been implicated as one of the factors determining the efficacy and toxicity of the anticancer agent 5-FU. Fluorouracil 99-103 dihydropyrimidine dehydrogenase Homo sapiens 0-31 16806531-1 2006 Dihydropyrimidine dehydrogenase (DPD), the initial and rate-limiting enzyme in the 5-fluorouracil (5-FU) catabolic pathway, has been implicated as one of the factors determining the efficacy and toxicity of the anticancer agent 5-FU. Fluorouracil 99-103 dihydropyrimidine dehydrogenase Homo sapiens 33-36 16806531-1 2006 Dihydropyrimidine dehydrogenase (DPD), the initial and rate-limiting enzyme in the 5-fluorouracil (5-FU) catabolic pathway, has been implicated as one of the factors determining the efficacy and toxicity of the anticancer agent 5-FU. Fluorouracil 228-232 dihydropyrimidine dehydrogenase Homo sapiens 0-31 20207475-3 2010 The MTT assay indicated that over-expression of Beclin1 sensitized CaSki cells to chemotherapeutic drugs (cisplatin, paclitaxel, 5-fluorouracil, and epirubicin) and induced greater degrees of cytotoxicity than vector-only controls. Fluorouracil 129-143 beclin 1 Homo sapiens 48-55 16806531-1 2006 Dihydropyrimidine dehydrogenase (DPD), the initial and rate-limiting enzyme in the 5-fluorouracil (5-FU) catabolic pathway, has been implicated as one of the factors determining the efficacy and toxicity of the anticancer agent 5-FU. Fluorouracil 228-232 dihydropyrimidine dehydrogenase Homo sapiens 33-36 16806531-9 2006 These studies provide further insight into the molecular mechanisms underlying the heterogeneity of DPD activity, and may facilitate the efficacy and safety of 5-FU-based chemotherapy. Fluorouracil 160-164 dihydropyrimidine dehydrogenase Homo sapiens 100-103 16596227-4 2006 In this study, RAD51 protein levels were quantified by immunohistochemistry in tumor samples from twelve head and neck cancer patients who received identical treatment with induction chemotherapy (paclitaxel and carboplatinum) followed by radiation therapy given concurrently with additional chemotherapy (paclitaxel, fluorouracil, hydroxyurea). Fluorouracil 318-330 RAD51 recombinase Homo sapiens 15-20 19208748-11 2009 Further, EFEMP1 expression decreased apoptosis and promoted cell cycle progression in response to serum starvation or exposure to gemcitabine, 5-fluorouracil, and irinotecan. Fluorouracil 143-157 EGF containing fibulin extracellular matrix protein 1 Homo sapiens 9-15 19105824-1 2008 BACKGROUND: Over-expression of thymidylate synthase (TS) and dihydropyrimidine dehydrogenase (DPD) in tumor tissue is associated with insensitivity to 5-fluorouracil (5-FU). Fluorouracil 167-171 dihydropyrimidine dehydrogenase Homo sapiens 61-92 19105824-1 2008 BACKGROUND: Over-expression of thymidylate synthase (TS) and dihydropyrimidine dehydrogenase (DPD) in tumor tissue is associated with insensitivity to 5-fluorouracil (5-FU). Fluorouracil 167-171 dihydropyrimidine dehydrogenase Homo sapiens 94-97 19020767-1 2008 It has been reported that the expression of thymidylate synthase (TS), dihydropyrimidine dehydrogenase (DPD) and orotate phosphoribosyltransferase (OPRT) may predict the clinical efficacy of 5-fluorouracil (5-FU)-based therapy in cancer patients. Fluorouracil 191-205 dihydropyrimidine dehydrogenase Homo sapiens 71-102 19020767-1 2008 It has been reported that the expression of thymidylate synthase (TS), dihydropyrimidine dehydrogenase (DPD) and orotate phosphoribosyltransferase (OPRT) may predict the clinical efficacy of 5-fluorouracil (5-FU)-based therapy in cancer patients. Fluorouracil 191-205 dihydropyrimidine dehydrogenase Homo sapiens 104-107 19020767-1 2008 It has been reported that the expression of thymidylate synthase (TS), dihydropyrimidine dehydrogenase (DPD) and orotate phosphoribosyltransferase (OPRT) may predict the clinical efficacy of 5-fluorouracil (5-FU)-based therapy in cancer patients. Fluorouracil 207-211 dihydropyrimidine dehydrogenase Homo sapiens 71-102 19020767-1 2008 It has been reported that the expression of thymidylate synthase (TS), dihydropyrimidine dehydrogenase (DPD) and orotate phosphoribosyltransferase (OPRT) may predict the clinical efficacy of 5-fluorouracil (5-FU)-based therapy in cancer patients. Fluorouracil 207-211 dihydropyrimidine dehydrogenase Homo sapiens 104-107 19106597-8 2008 But further cases would be needed to evaluate the effect of PSK with 5-FU-based adjuvant chemotherapy. Fluorouracil 69-73 TAO kinase 2 Homo sapiens 60-63 18937829-1 2008 BACKGROUND: The activity of dihydropyrimidine dehydrogenase (DPD), the key enzyme of pyrimidine catabolism, is thought to be an important determinant for the occurrence of severe toxic reactions to 5-fluorouracil (5-FU), which is one of the most commonly prescribed chemotherapeutic agents for the treatment of solid cancers. Fluorouracil 198-212 dihydropyrimidine dehydrogenase Homo sapiens 28-59 18937829-1 2008 BACKGROUND: The activity of dihydropyrimidine dehydrogenase (DPD), the key enzyme of pyrimidine catabolism, is thought to be an important determinant for the occurrence of severe toxic reactions to 5-fluorouracil (5-FU), which is one of the most commonly prescribed chemotherapeutic agents for the treatment of solid cancers. Fluorouracil 198-212 dihydropyrimidine dehydrogenase Homo sapiens 61-64 18937829-1 2008 BACKGROUND: The activity of dihydropyrimidine dehydrogenase (DPD), the key enzyme of pyrimidine catabolism, is thought to be an important determinant for the occurrence of severe toxic reactions to 5-fluorouracil (5-FU), which is one of the most commonly prescribed chemotherapeutic agents for the treatment of solid cancers. Fluorouracil 214-218 dihydropyrimidine dehydrogenase Homo sapiens 28-59 18937829-1 2008 BACKGROUND: The activity of dihydropyrimidine dehydrogenase (DPD), the key enzyme of pyrimidine catabolism, is thought to be an important determinant for the occurrence of severe toxic reactions to 5-fluorouracil (5-FU), which is one of the most commonly prescribed chemotherapeutic agents for the treatment of solid cancers. Fluorouracil 214-218 dihydropyrimidine dehydrogenase Homo sapiens 61-64 18937829-3 2008 However, only a small proportion of severe toxicities in 5-FU based chemotherapy can be explained with such rare deleterious DPYD mutations resulting in severe enzyme deficiencies. Fluorouracil 57-61 dihydropyrimidine dehydrogenase Homo sapiens 125-129 18937829-4 2008 Recently, hypermethylation of the DPYD promoter region has been proposed as an alternative mechanism for DPD deficiency and thus as a major cause of severe 5-FU toxicity. Fluorouracil 156-160 dihydropyrimidine dehydrogenase Homo sapiens 34-38 18266059-0 2008 In vivo 5-fluorouracil-[corrected]induced apoptosis on murine thymocytes: involvement of FAS, Bax and Caspase3. Fluorouracil 8-22 BCL2-associated X protein Mus musculus 94-97 18266059-0 2008 In vivo 5-fluorouracil-[corrected]induced apoptosis on murine thymocytes: involvement of FAS, Bax and Caspase3. Fluorouracil 8-22 caspase 3 Mus musculus 102-110 18266059-12 2008 This study revealed that in vivo apoptosis in normal thymus after 5-FU administration is related to FAS, Bax, and Caspase 3 co-expressions under the current experimental conditions, these findings, therefore, contribute to a new insight into the molecular mechanisms involved during 5-FU administration upon the thymus and the possible events committed in the lymphophenia associated with chemotherapy. Fluorouracil 66-70 BCL2-associated X protein Mus musculus 105-108 18266059-12 2008 This study revealed that in vivo apoptosis in normal thymus after 5-FU administration is related to FAS, Bax, and Caspase 3 co-expressions under the current experimental conditions, these findings, therefore, contribute to a new insight into the molecular mechanisms involved during 5-FU administration upon the thymus and the possible events committed in the lymphophenia associated with chemotherapy. Fluorouracil 66-70 caspase 3 Mus musculus 114-123 18776995-7 2008 The overexpression of Gli1 restores cell viability and, to some extent, the migration abilities inhibited by 5-FU. Fluorouracil 109-113 GLI family zinc finger 1 Homo sapiens 22-26 18270838-0 2008 The expression of Msi-1 and its significance in small intestinal mucosa severely damaged by high-dose 5-FU. Fluorouracil 102-106 musashi RNA-binding protein 1 Mus musculus 18-23 18270838-1 2008 OBJECTIVE: The purpose was to investigate the expression of musashi-1 (msi-1) and its significances in small intestinal mucosa that was severely damaged by high-dose 5-FU. Fluorouracil 166-170 musashi RNA-binding protein 1 Mus musculus 60-69 18270838-1 2008 OBJECTIVE: The purpose was to investigate the expression of musashi-1 (msi-1) and its significances in small intestinal mucosa that was severely damaged by high-dose 5-FU. Fluorouracil 166-170 musashi RNA-binding protein 1 Mus musculus 71-76 18270838-5 2008 RESULTS: After treatment with high-dose 5-FU, the intestinal mucosa suffered severe damage: the villi and crypts disappeared, the number of msi-1-positive cells increased greatly, the intestinal epithelial cells could be divided into two fractions by FACS, and the percentage of msi-1-positive cells was up to 67.75% in the fraction in which the value of FSC was higher. Fluorouracil 40-44 musashi RNA-binding protein 1 Mus musculus 140-145 18270838-5 2008 RESULTS: After treatment with high-dose 5-FU, the intestinal mucosa suffered severe damage: the villi and crypts disappeared, the number of msi-1-positive cells increased greatly, the intestinal epithelial cells could be divided into two fractions by FACS, and the percentage of msi-1-positive cells was up to 67.75% in the fraction in which the value of FSC was higher. Fluorouracil 40-44 musashi RNA-binding protein 1 Mus musculus 279-284 18930000-0 2008 Rare sugar D-allose enhances anti-tumor effect of 5-fluorouracil on the human hepatocellular carcinoma cell line HuH-7. Fluorouracil 50-64 MIR7-3 host gene Homo sapiens 113-118 18930000-4 2008 The treatment of HuH-7 cells with d-allose or 5-FU inhibited the cell growth in a dose-dependent manner (75.2+/-2.7% with 50 mM d-allose and 66.1+/-2.7% with 0.5 mug/ml 5-FU) and d-allose enhanced the anti-tumor effect of 5-FU (55.3+/-1.1 %). Fluorouracil 46-50 MIR7-3 host gene Homo sapiens 17-22 18930000-4 2008 The treatment of HuH-7 cells with d-allose or 5-FU inhibited the cell growth in a dose-dependent manner (75.2+/-2.7% with 50 mM d-allose and 66.1+/-2.7% with 0.5 mug/ml 5-FU) and d-allose enhanced the anti-tumor effect of 5-FU (55.3+/-1.1 %). Fluorouracil 169-173 MIR7-3 host gene Homo sapiens 17-22 18930000-4 2008 The treatment of HuH-7 cells with d-allose or 5-FU inhibited the cell growth in a dose-dependent manner (75.2+/-2.7% with 50 mM d-allose and 66.1+/-2.7% with 0.5 mug/ml 5-FU) and d-allose enhanced the anti-tumor effect of 5-FU (55.3+/-1.1 %). Fluorouracil 169-173 MIR7-3 host gene Homo sapiens 17-22 18690847-3 2008 The aim of the study was to investigate the induction by celecoxib of some multidrug resistance proteins, MRP1, MRP2, MRP4 and MRP5, involved in the transport of irinotecan and 5-FU. Fluorouracil 177-181 ATP binding cassette subfamily C member 2 Homo sapiens 112-116 18690847-3 2008 The aim of the study was to investigate the induction by celecoxib of some multidrug resistance proteins, MRP1, MRP2, MRP4 and MRP5, involved in the transport of irinotecan and 5-FU. Fluorouracil 177-181 ATP binding cassette subfamily C member 4 Homo sapiens 118-122 18498133-10 2008 A SNP in codon 72 of TP53 was revealed to be a key regulator of 5-FU metabolizing genes such as DHFR and MTHFR, constituting 50% of all significant associations observed after FUMI therapy. Fluorouracil 64-68 methylenetetrahydrofolate reductase Homo sapiens 105-110 18537153-1 2008 BACKGROUND AND OBJECTIVES: Single nucleotide polymorphisms of dihydropyrimidine dehydrogenases gene (DPYD) induces dihydropyrimidine dehydrogenase enzyme (DPD) deficiency resulting in increased activity of 5-fluorouracil derivatives. Fluorouracil 206-220 dihydropyrimidine dehydrogenase Homo sapiens 101-105 18537153-9 2008 CONCLUSIONS: Gene polymorphisms of DPYD and CDA predict survival of gastric cancer patients treated with 5-fluorouracil-based adjuvant chemotherapy. Fluorouracil 105-119 dihydropyrimidine dehydrogenase Homo sapiens 35-39 16809149-0 2006 Thymidylate synthase and dihydropyrimidine dehydrogenase are related to histological effects of 5-fluorouracil and cisplatin neoadjuvant chemotherapy for primary gastric cancer patients. Fluorouracil 96-110 dihydropyrimidine dehydrogenase Homo sapiens 25-56 16809149-1 2006 UNLABELLED: Thymidylate synthase (TS), dihydropyrimidine dehydrogenase (DPD), and vascular endothelial growth factor (VEGF) are associated with the effect of 5-fluorouracil (5-FU) based adjuvant chemotherapy. Fluorouracil 158-172 dihydropyrimidine dehydrogenase Homo sapiens 39-70 16809149-1 2006 UNLABELLED: Thymidylate synthase (TS), dihydropyrimidine dehydrogenase (DPD), and vascular endothelial growth factor (VEGF) are associated with the effect of 5-fluorouracil (5-FU) based adjuvant chemotherapy. Fluorouracil 158-172 dihydropyrimidine dehydrogenase Homo sapiens 72-75 16595493-3 2006 Glucose transporter-1 (Glut-1) and hexokinase II (HKII) proteins are highly expressed in many breast carcinomas, but their status while undergoing DOX or 5FU chemotherapy has not been systematically evaluated. Fluorouracil 154-157 solute carrier family 2 member 1 Homo sapiens 0-21 16595493-3 2006 Glucose transporter-1 (Glut-1) and hexokinase II (HKII) proteins are highly expressed in many breast carcinomas, but their status while undergoing DOX or 5FU chemotherapy has not been systematically evaluated. Fluorouracil 154-157 solute carrier family 2 member 1 Homo sapiens 23-29 16525674-6 2006 DPD and TP mRNA levels were significantly higher in metastatic liver tumors (DPD: 10.36+/-1.81 versus 3.95+/-0.99, p<0.01; and TP: 18.80+/-4.96 versus 7.28+/-1.23, p<0.05) and inversely correlated with 5-FU sensitivity (DPD: R=0.570, p<0.05; TP: R=0.600, p<0.05). Fluorouracil 208-212 dihydropyrimidine dehydrogenase Homo sapiens 0-3 18597209-3 2008 The systemic exposure to 5-FU is fundamentally determined by the genetically polymorphic enzyme dihydropyrimidine dehydrogenase (DPD). Fluorouracil 25-29 dihydropyrimidine dehydrogenase Homo sapiens 96-127 18597209-3 2008 The systemic exposure to 5-FU is fundamentally determined by the genetically polymorphic enzyme dihydropyrimidine dehydrogenase (DPD). Fluorouracil 25-29 dihydropyrimidine dehydrogenase Homo sapiens 129-132 18633250-8 2008 So far 39 mutations/ polymorphisms have been identified in dihydropyrimidine dehydrogenase(DPD)gene, a major catabolic enzyme of 5- FU. Fluorouracil 129-134 dihydropyrimidine dehydrogenase Homo sapiens 91-94 18633250-10 2008 A polymorphism that may influence the efficacy of 5-FU by influencing folate pools is that of the methylenetetrahydrofolate reductase(MTHFR)gene. Fluorouracil 50-54 methylenetetrahydrofolate reductase Homo sapiens 98-133 18633250-10 2008 A polymorphism that may influence the efficacy of 5-FU by influencing folate pools is that of the methylenetetrahydrofolate reductase(MTHFR)gene. Fluorouracil 50-54 methylenetetrahydrofolate reductase Homo sapiens 134-139 18633222-7 2008 We concluded from this study that the change in DPD activity due to an induction of DPD by 5-FU and metastasis of cancer caused the recurrence and lower a urinary value. Fluorouracil 91-95 dihydropyrimidine dehydrogenase Homo sapiens 48-51 18633222-7 2008 We concluded from this study that the change in DPD activity due to an induction of DPD by 5-FU and metastasis of cancer caused the recurrence and lower a urinary value. Fluorouracil 91-95 dihydropyrimidine dehydrogenase Homo sapiens 84-87 16525674-9 2006 DPD and TP may affect the acquisition of resistance to 5-FU during liver metastasis of colorectal cancer. Fluorouracil 55-59 dihydropyrimidine dehydrogenase Homo sapiens 0-3 16538173-2 2006 Common genetic polymorphisms in the human MTHFR gene are associated with individual variation in the efficacy and toxicity of chemotherapeutic agents, such as methotrexate and 5-fluorouracil. Fluorouracil 176-190 methylenetetrahydrofolate reductase Homo sapiens 42-47 18380793-0 2008 CYP2A6 and the plasma level of 5-chloro-2, 4-dihydroxypyridine are determinants of the pharmacokinetic variability of tegafur and 5-fluorouracil, respectively, in Japanese patients with cancer given S-1. Fluorouracil 130-144 cytochrome P450 family 2 subfamily A member 6 Homo sapiens 0-6 18380793-3 2008 CYP2A6 is involved in the biotransformation of FT to 5-FU. Fluorouracil 53-57 cytochrome P450 family 2 subfamily A member 6 Homo sapiens 0-6 18380793-13 2008 Although the CYP2A6 variants are the cause of the PK variability of FT, the AUC of CDHP affected by renal function is the key determinant of the variability in the PK of 5-FU. Fluorouracil 170-174 cytochrome P450 family 2 subfamily A member 6 Homo sapiens 13-19 18705276-1 2008 BACKGROUND/AIMS: Dihydropyrimidine dehydrogenase is the initial and rate-limiting enzyme in the catabolism of 5-fluorouracil. Fluorouracil 110-124 dihydropyrimidine dehydrogenase Homo sapiens 17-48 18575323-8 2008 CONCLUSION: pPSMA enhancer/promoter-UPRT/5-FU suicide gene system kills LNCaP cells in target, UPRT can transform 5-FU into toxic metabolites quickly and play the role of cytotoxicity. Fluorouracil 41-45 uracil phosphoribosyltransferase homolog Homo sapiens 95-99 18575323-8 2008 CONCLUSION: pPSMA enhancer/promoter-UPRT/5-FU suicide gene system kills LNCaP cells in target, UPRT can transform 5-FU into toxic metabolites quickly and play the role of cytotoxicity. Fluorouracil 114-118 uracil phosphoribosyltransferase homolog Homo sapiens 36-40 18575323-8 2008 CONCLUSION: pPSMA enhancer/promoter-UPRT/5-FU suicide gene system kills LNCaP cells in target, UPRT can transform 5-FU into toxic metabolites quickly and play the role of cytotoxicity. Fluorouracil 114-118 uracil phosphoribosyltransferase homolog Homo sapiens 95-99 18096571-3 2008 Employing the Mdm2 2A10 antibody and phosphatase treatment we found that Mdm2 accumulated in HepG2 cells when exposed to low concentrations of genotoxic compounds such as mitomycin C, etoposide, 5-fluorouracil, and benzo[a]pyrene (BP). Fluorouracil 195-209 MDM2 proto-oncogene Homo sapiens 73-77 16619549-2 2006 Thymidylate synthase (TS) and dihydropyrimidine dehydrogenase (DPD) are the major determinants of individual sensitivity to 5-FU, and the impact of TS and DPD expression on prognosis and 5-FU efficacy has been studied in gastrointestinal carcinomas. Fluorouracil 124-128 dihydropyrimidine dehydrogenase Homo sapiens 30-61 18326935-3 2008 While normal dihydropyrimidine dehydrogenase (DPD) enzyme activity is rate limiting in 5-fluorouracil (5-FU) catabolism, its deficiency could increase concentrations of bioavailable 5-FU anabolic products leading to 5-FU related toxicity syndrome. Fluorouracil 87-101 dihydropyrimidine dehydrogenase Homo sapiens 13-44 18326935-3 2008 While normal dihydropyrimidine dehydrogenase (DPD) enzyme activity is rate limiting in 5-fluorouracil (5-FU) catabolism, its deficiency could increase concentrations of bioavailable 5-FU anabolic products leading to 5-FU related toxicity syndrome. Fluorouracil 87-101 dihydropyrimidine dehydrogenase Homo sapiens 46-49 18326935-3 2008 While normal dihydropyrimidine dehydrogenase (DPD) enzyme activity is rate limiting in 5-fluorouracil (5-FU) catabolism, its deficiency could increase concentrations of bioavailable 5-FU anabolic products leading to 5-FU related toxicity syndrome. Fluorouracil 103-107 dihydropyrimidine dehydrogenase Homo sapiens 13-44 16619549-2 2006 Thymidylate synthase (TS) and dihydropyrimidine dehydrogenase (DPD) are the major determinants of individual sensitivity to 5-FU, and the impact of TS and DPD expression on prognosis and 5-FU efficacy has been studied in gastrointestinal carcinomas. Fluorouracil 124-128 dihydropyrimidine dehydrogenase Homo sapiens 63-66 18326935-3 2008 While normal dihydropyrimidine dehydrogenase (DPD) enzyme activity is rate limiting in 5-fluorouracil (5-FU) catabolism, its deficiency could increase concentrations of bioavailable 5-FU anabolic products leading to 5-FU related toxicity syndrome. Fluorouracil 103-107 dihydropyrimidine dehydrogenase Homo sapiens 46-49 16619549-2 2006 Thymidylate synthase (TS) and dihydropyrimidine dehydrogenase (DPD) are the major determinants of individual sensitivity to 5-FU, and the impact of TS and DPD expression on prognosis and 5-FU efficacy has been studied in gastrointestinal carcinomas. Fluorouracil 187-191 dihydropyrimidine dehydrogenase Homo sapiens 63-66 18326935-3 2008 While normal dihydropyrimidine dehydrogenase (DPD) enzyme activity is rate limiting in 5-fluorouracil (5-FU) catabolism, its deficiency could increase concentrations of bioavailable 5-FU anabolic products leading to 5-FU related toxicity syndrome. Fluorouracil 182-186 dihydropyrimidine dehydrogenase Homo sapiens 13-44 18326935-3 2008 While normal dihydropyrimidine dehydrogenase (DPD) enzyme activity is rate limiting in 5-fluorouracil (5-FU) catabolism, its deficiency could increase concentrations of bioavailable 5-FU anabolic products leading to 5-FU related toxicity syndrome. Fluorouracil 182-186 dihydropyrimidine dehydrogenase Homo sapiens 46-49 16537192-2 2006 Dihydropyrimidine dehydrogenase (DPD) plays a pivotal role in the metabolism of 5FU and as such, a deficiency of DPD has been recognized as an important risk factor, predisposing patients to the development of severe 5FU-associated toxicity. Fluorouracil 80-83 dihydropyrimidine dehydrogenase Homo sapiens 0-31 18326935-3 2008 While normal dihydropyrimidine dehydrogenase (DPD) enzyme activity is rate limiting in 5-fluorouracil (5-FU) catabolism, its deficiency could increase concentrations of bioavailable 5-FU anabolic products leading to 5-FU related toxicity syndrome. Fluorouracil 182-186 dihydropyrimidine dehydrogenase Homo sapiens 13-44 18326935-3 2008 While normal dihydropyrimidine dehydrogenase (DPD) enzyme activity is rate limiting in 5-fluorouracil (5-FU) catabolism, its deficiency could increase concentrations of bioavailable 5-FU anabolic products leading to 5-FU related toxicity syndrome. Fluorouracil 182-186 dihydropyrimidine dehydrogenase Homo sapiens 46-49 17637782-1 2008 Uracil-Ftorafur (UFT) combines the 5-fluorouracil (FU) prodrug tegafur with uracil (at a 1:4 molar ratio), which is a competitive inhibitor of dihydropyrimidine dehydrogenase (DPD), the limiting enzyme of FU catabolism. Fluorouracil 35-49 dihydropyrimidine dehydrogenase Homo sapiens 143-174 16537192-2 2006 Dihydropyrimidine dehydrogenase (DPD) plays a pivotal role in the metabolism of 5FU and as such, a deficiency of DPD has been recognized as an important risk factor, predisposing patients to the development of severe 5FU-associated toxicity. Fluorouracil 80-83 dihydropyrimidine dehydrogenase Homo sapiens 33-36 16537192-2 2006 Dihydropyrimidine dehydrogenase (DPD) plays a pivotal role in the metabolism of 5FU and as such, a deficiency of DPD has been recognized as an important risk factor, predisposing patients to the development of severe 5FU-associated toxicity. Fluorouracil 217-220 dihydropyrimidine dehydrogenase Homo sapiens 0-31 16537192-2 2006 Dihydropyrimidine dehydrogenase (DPD) plays a pivotal role in the metabolism of 5FU and as such, a deficiency of DPD has been recognized as an important risk factor, predisposing patients to the development of severe 5FU-associated toxicity. Fluorouracil 217-220 dihydropyrimidine dehydrogenase Homo sapiens 33-36 18310281-9 2008 Our findings support the notion that expression of ABCC11 in ER-alpha-positive breast cancers may contribute to decreased sensitivity to chemotherapy combinations that include 5-FU. Fluorouracil 176-180 ATP binding cassette subfamily C member 11 Homo sapiens 51-57 16646564-1 2006 Dihydropyrimidine dehydrogenase (DPD) is the initial and rate-limiting enzyme in the catabolism of 5-fluorouracil (5-FU). Fluorouracil 115-119 dihydropyrimidine dehydrogenase Homo sapiens 0-31 18288408-2 2008 In this study, we aimed to clarify the prognostic value of the expression of the 5-FU metabolic enzyme genes, including orptate phosphoribosyl transferase (OPRT), dihydropyrimidine dehydrogenase (DPD), thymidylate synthetase (TS) and thymidylate phosphorylate (TP) genes in CRC patients treated with oral 5-FU-based adjuvant chemotherapy. Fluorouracil 81-85 dihydropyrimidine dehydrogenase Homo sapiens 196-199 18443386-0 2008 5-Fluorouracil toxicity-attributable IVS14 + 1G > A mutation of the dihydropyrimidine dehydrogenase gene in Polish colorectal cancer patients. Fluorouracil 0-14 dihydropyrimidine dehydrogenase Homo sapiens 71-102 18443386-1 2008 DPYD gene encodes dihydropyrimidine dehydrogenase which is the initial and rate-limiting enzyme in the metabolism of 5-fluorouracil (5-FU). Fluorouracil 117-131 dihydropyrimidine dehydrogenase Homo sapiens 0-4 18443386-1 2008 DPYD gene encodes dihydropyrimidine dehydrogenase which is the initial and rate-limiting enzyme in the metabolism of 5-fluorouracil (5-FU). Fluorouracil 117-131 dihydropyrimidine dehydrogenase Homo sapiens 18-49 18443386-1 2008 DPYD gene encodes dihydropyrimidine dehydrogenase which is the initial and rate-limiting enzyme in the metabolism of 5-fluorouracil (5-FU). Fluorouracil 133-137 dihydropyrimidine dehydrogenase Homo sapiens 0-4 18443386-1 2008 DPYD gene encodes dihydropyrimidine dehydrogenase which is the initial and rate-limiting enzyme in the metabolism of 5-fluorouracil (5-FU). Fluorouracil 133-137 dihydropyrimidine dehydrogenase Homo sapiens 18-49 18443386-2 2008 The aim of our study was PCR-RFLP based-genetic testing for the most common 5-FU toxicity-attributable IVS14 + 1G > A DPYD mutation (DPYD(*)2A) in 252 Polish colorectal cancer (CRC) patients treated with this adjuvant chemotherapeutic regimen after surgery. Fluorouracil 76-80 dihydropyrimidine dehydrogenase Homo sapiens 121-125 18443386-2 2008 The aim of our study was PCR-RFLP based-genetic testing for the most common 5-FU toxicity-attributable IVS14 + 1G > A DPYD mutation (DPYD(*)2A) in 252 Polish colorectal cancer (CRC) patients treated with this adjuvant chemotherapeutic regimen after surgery. Fluorouracil 76-80 dihydropyrimidine dehydrogenase Homo sapiens 136-145 18443386-4 2008 We conclude that IVS14 + 1G > A DPYD (DPYD(*)2A) variant occurs in the Polish population and is responsible for a significant proportion of life-threatening toxicity of 5-FU. Fluorouracil 172-176 dihydropyrimidine dehydrogenase Homo sapiens 35-39 18443386-4 2008 We conclude that IVS14 + 1G > A DPYD (DPYD(*)2A) variant occurs in the Polish population and is responsible for a significant proportion of life-threatening toxicity of 5-FU. Fluorouracil 172-176 dihydropyrimidine dehydrogenase Homo sapiens 41-50 18360075-1 2008 INTRODUCTION: Orotate phosphoribosyl transferase (OPRT), dihydropyrimidine dehydrogenase (DPD), and thymidylate synthase (TS) are initial key enzymes in the 5-fluorouracil (5-FU) metabolic pathway. Fluorouracil 157-171 dihydropyrimidine dehydrogenase Homo sapiens 57-88 18360075-1 2008 INTRODUCTION: Orotate phosphoribosyl transferase (OPRT), dihydropyrimidine dehydrogenase (DPD), and thymidylate synthase (TS) are initial key enzymes in the 5-fluorouracil (5-FU) metabolic pathway. Fluorouracil 157-171 dihydropyrimidine dehydrogenase Homo sapiens 90-93 18360075-1 2008 INTRODUCTION: Orotate phosphoribosyl transferase (OPRT), dihydropyrimidine dehydrogenase (DPD), and thymidylate synthase (TS) are initial key enzymes in the 5-fluorouracil (5-FU) metabolic pathway. Fluorouracil 173-177 dihydropyrimidine dehydrogenase Homo sapiens 57-88 18360075-1 2008 INTRODUCTION: Orotate phosphoribosyl transferase (OPRT), dihydropyrimidine dehydrogenase (DPD), and thymidylate synthase (TS) are initial key enzymes in the 5-fluorouracil (5-FU) metabolic pathway. Fluorouracil 173-177 dihydropyrimidine dehydrogenase Homo sapiens 90-93 18360075-10 2008 CONCLUSION: The response to 5-FU may be poor in patients with lymph-node metastasis, because of low OPRT activity, and in patients with poorly differentiated adenocarcinoma, because of high DPD activity. Fluorouracil 28-32 dihydropyrimidine dehydrogenase Homo sapiens 190-193 18203291-11 2008 Furthermore, Gli-1 siRNA increased the cytotoxic effect of 5-Fu on Huh7 cell. Fluorouracil 59-63 GLI family zinc finger 1 Homo sapiens 13-18 18203291-11 2008 Furthermore, Gli-1 siRNA increased the cytotoxic effect of 5-Fu on Huh7 cell. Fluorouracil 59-63 MIR7-3 host gene Homo sapiens 67-71 18371424-4 2008 Overproliferating Lrg-47(-/-) HSCs are severely impaired in functional repopulation assays, and when challenged with hematopoietic ablation by 5-fluorouracil or infection with Mycobacterium avium, Lrg-47(-/-) mice fail to achieve the expected expansion response in stem and progenitor cell populations. Fluorouracil 143-157 immunity-related GTPase family M member 1 Mus musculus 18-24 17786445-7 2008 Patients who received regimens containing oxaliplatin and infusional 5-fluorouracil (5-FU) demonstrated mTTP up to 7 months and a mOS of 16 months. Fluorouracil 69-83 zinc finger protein 36 Mus musculus 104-108 17786445-7 2008 Patients who received regimens containing oxaliplatin and infusional 5-fluorouracil (5-FU) demonstrated mTTP up to 7 months and a mOS of 16 months. Fluorouracil 85-89 zinc finger protein 36 Mus musculus 104-108 16646564-1 2006 Dihydropyrimidine dehydrogenase (DPD) is the initial and rate-limiting enzyme in the catabolism of 5-fluorouracil (5-FU). Fluorouracil 115-119 dihydropyrimidine dehydrogenase Homo sapiens 33-36 16239320-12 2006 The HuH7 SP cells expressed a higher resistance to doxorubicin, 5-fluorouracil, and gemcitabine compared with non-SP cells. Fluorouracil 64-78 MIR7-3 host gene Homo sapiens 4-8 16555161-10 2006 Expression of VEGF in liver metastases was clearly inhibited by YH-16 in combination with 5-FU or 5-FU alone compared to the control group, and MVD in middle-dose and high-dose YH-16 group, 5-FU group and combination group was lower than that in control group (P< 0.05). Fluorouracil 98-102 vascular endothelial growth factor A Mus musculus 14-18 18172246-6 2008 DPD inhibitors were initially combined with fluoropyrimidines to increase the efficacy of the drugs by impairing the DPD-mediated catabolism of 5-FU. Fluorouracil 144-148 dihydropyrimidine dehydrogenase Homo sapiens 0-3 18172246-6 2008 DPD inhibitors were initially combined with fluoropyrimidines to increase the efficacy of the drugs by impairing the DPD-mediated catabolism of 5-FU. Fluorouracil 144-148 dihydropyrimidine dehydrogenase Homo sapiens 117-120 18077151-2 2008 5-FU is catabolised by DPD. Fluorouracil 0-4 dihydropyrimidine dehydrogenase Homo sapiens 23-26 18077151-8 2008 Tumour 5-FU concentration correlated with TP/DPD and with tumour response. Fluorouracil 7-11 dihydropyrimidine dehydrogenase Homo sapiens 45-48 19104657-1 2008 BACKGROUND: Cancer patients carrying mutations in the dihydropyrimidine dehydrogenase gene (DPYD) have a high risk to experience severe drug-adverse effects following chemotherapy with fluoropyrimidine drugs such as 5-fluorouracil (5-FU) or capecitabine. Fluorouracil 216-230 dihydropyrimidine dehydrogenase Homo sapiens 54-85 19104657-1 2008 BACKGROUND: Cancer patients carrying mutations in the dihydropyrimidine dehydrogenase gene (DPYD) have a high risk to experience severe drug-adverse effects following chemotherapy with fluoropyrimidine drugs such as 5-fluorouracil (5-FU) or capecitabine. Fluorouracil 216-230 dihydropyrimidine dehydrogenase Homo sapiens 92-96 19104657-1 2008 BACKGROUND: Cancer patients carrying mutations in the dihydropyrimidine dehydrogenase gene (DPYD) have a high risk to experience severe drug-adverse effects following chemotherapy with fluoropyrimidine drugs such as 5-fluorouracil (5-FU) or capecitabine. Fluorouracil 232-236 dihydropyrimidine dehydrogenase Homo sapiens 54-85 19104657-1 2008 BACKGROUND: Cancer patients carrying mutations in the dihydropyrimidine dehydrogenase gene (DPYD) have a high risk to experience severe drug-adverse effects following chemotherapy with fluoropyrimidine drugs such as 5-fluorouracil (5-FU) or capecitabine. Fluorouracil 232-236 dihydropyrimidine dehydrogenase Homo sapiens 92-96 17941012-10 2007 There was a significant difference in overall survival between patients with positive and negative IFNAR2 expression cases (P<.0025), and a significant correlation was observed between IFNAR2 expression and response to IFN/5-FU combination therapy (P=.0199). Fluorouracil 226-230 interferon alpha and beta receptor subunit 2 Homo sapiens 188-194 17982676-7 2007 Alterations in gene expression in 5-FU-treated TP53-depleted HCT116 cultures confirmed previously-reported TP53 target genes and suggested potentially novel TP53 target genes (e.g. APOBEC3C, BIRC3, JMJD2B, LAMP3, MYO1E, PRRG1, SULF2, TACSTD2, TncRNA, ZFYVE20) that may play a role in mediating the 5-FU-induced DNA damage response in TP53-proficient cells. Fluorouracil 34-38 apolipoprotein B mRNA editing enzyme catalytic subunit 3C Homo sapiens 181-189 17982676-7 2007 Alterations in gene expression in 5-FU-treated TP53-depleted HCT116 cultures confirmed previously-reported TP53 target genes and suggested potentially novel TP53 target genes (e.g. APOBEC3C, BIRC3, JMJD2B, LAMP3, MYO1E, PRRG1, SULF2, TACSTD2, TncRNA, ZFYVE20) that may play a role in mediating the 5-FU-induced DNA damage response in TP53-proficient cells. Fluorouracil 34-38 nuclear paraspeckle assembly transcript 1 Homo sapiens 243-249 17982676-7 2007 Alterations in gene expression in 5-FU-treated TP53-depleted HCT116 cultures confirmed previously-reported TP53 target genes and suggested potentially novel TP53 target genes (e.g. APOBEC3C, BIRC3, JMJD2B, LAMP3, MYO1E, PRRG1, SULF2, TACSTD2, TncRNA, ZFYVE20) that may play a role in mediating the 5-FU-induced DNA damage response in TP53-proficient cells. Fluorouracil 34-38 rabenosyn, RAB effector Homo sapiens 251-258 17854773-1 2007 Although the intratumoral expression levels of thymidylate synthase (TS) and dihydropyrimidine dehydrogenase (DPD) are known to affect the antitumor activity of 5-fluorouracil (5-FU), the importance of orotate phosphoribosyltransferase (OPRT) has remained unclear. Fluorouracil 161-175 dihydropyrimidine dehydrogenase Homo sapiens 77-108 17854773-1 2007 Although the intratumoral expression levels of thymidylate synthase (TS) and dihydropyrimidine dehydrogenase (DPD) are known to affect the antitumor activity of 5-fluorouracil (5-FU), the importance of orotate phosphoribosyltransferase (OPRT) has remained unclear. Fluorouracil 161-175 dihydropyrimidine dehydrogenase Homo sapiens 110-113 17854773-1 2007 Although the intratumoral expression levels of thymidylate synthase (TS) and dihydropyrimidine dehydrogenase (DPD) are known to affect the antitumor activity of 5-fluorouracil (5-FU), the importance of orotate phosphoribosyltransferase (OPRT) has remained unclear. Fluorouracil 177-181 dihydropyrimidine dehydrogenase Homo sapiens 77-108 17854773-1 2007 Although the intratumoral expression levels of thymidylate synthase (TS) and dihydropyrimidine dehydrogenase (DPD) are known to affect the antitumor activity of 5-fluorouracil (5-FU), the importance of orotate phosphoribosyltransferase (OPRT) has remained unclear. Fluorouracil 177-181 dihydropyrimidine dehydrogenase Homo sapiens 110-113 17854773-4 2007 In vitro, the 50% growth-inhibitory concentrations of 5-FU were closely correlated with the OPRT mRNA levels in cancer cell lines with similar levels of TS mRNAs when combined with a DPD inhibitor. Fluorouracil 54-58 dihydropyrimidine dehydrogenase Homo sapiens 183-186 17876700-3 2007 Mutation detection in the clinical setting depends on the development of automated technology, especially for large genes, such as the dihydropyrimidine dehydrogenase (DPYD) gene, which codes the initial, rate-limiting enzyme in the catabolism of 5-fluorouracil (5FU). Fluorouracil 247-261 dihydropyrimidine dehydrogenase Homo sapiens 135-166 17876700-3 2007 Mutation detection in the clinical setting depends on the development of automated technology, especially for large genes, such as the dihydropyrimidine dehydrogenase (DPYD) gene, which codes the initial, rate-limiting enzyme in the catabolism of 5-fluorouracil (5FU). Fluorouracil 247-261 dihydropyrimidine dehydrogenase Homo sapiens 168-172 17876700-3 2007 Mutation detection in the clinical setting depends on the development of automated technology, especially for large genes, such as the dihydropyrimidine dehydrogenase (DPYD) gene, which codes the initial, rate-limiting enzyme in the catabolism of 5-fluorouracil (5FU). Fluorouracil 263-266 dihydropyrimidine dehydrogenase Homo sapiens 135-166 17876700-3 2007 Mutation detection in the clinical setting depends on the development of automated technology, especially for large genes, such as the dihydropyrimidine dehydrogenase (DPYD) gene, which codes the initial, rate-limiting enzyme in the catabolism of 5-fluorouracil (5FU). Fluorouracil 263-266 dihydropyrimidine dehydrogenase Homo sapiens 168-172 17390142-0 2007 Hsp70 response to 5-fluorouracil treatment in human colon cancer cell lines. Fluorouracil 18-32 heat shock protein family A (Hsp70) member 4 Homo sapiens 0-5 17390142-5 2007 In the present study, we investigated whether the content of Hsp70 is associated to 5-FU resistance. Fluorouracil 84-88 heat shock protein family A (Hsp70) member 4 Homo sapiens 61-66 17390142-9 2007 In the HT-29 cell line, 5-FU treatment promoted an increase of 5.5 times in Hsp70 concentration after 12 h. Then, within 24 h, the increase in Hsp70 levels was still about two times. Fluorouracil 24-28 heat shock protein family A (Hsp70) member 4 Homo sapiens 76-81 17940834-0 2007 Synergistic antitumor effect of combined 5-fluorouracil (5-FU) with 5-chloro-2,4-dihydroxypyridine on 5-FU-resistant gastric cancer cells: possible role of a dihydropyrimidine dehydrogenase-independent mechanism. Fluorouracil 57-61 dihydropyrimidine dehydrogenase Homo sapiens 158-189 16568373-9 2006 Furthermore, although 5-FU itself increased DPD mRNA expression, a mechanism considered to be related to the acquisition of 5-FU resistance, the addition of cisplatin or camptothecin significantly inhibited the 5-FU-induced elevation of DPD. Fluorouracil 22-26 dihydropyrimidine dehydrogenase Homo sapiens 44-47 16568373-9 2006 Furthermore, although 5-FU itself increased DPD mRNA expression, a mechanism considered to be related to the acquisition of 5-FU resistance, the addition of cisplatin or camptothecin significantly inhibited the 5-FU-induced elevation of DPD. Fluorouracil 22-26 dihydropyrimidine dehydrogenase Homo sapiens 237-240 16568373-9 2006 Furthermore, although 5-FU itself increased DPD mRNA expression, a mechanism considered to be related to the acquisition of 5-FU resistance, the addition of cisplatin or camptothecin significantly inhibited the 5-FU-induced elevation of DPD. Fluorouracil 124-128 dihydropyrimidine dehydrogenase Homo sapiens 44-47 16568373-9 2006 Furthermore, although 5-FU itself increased DPD mRNA expression, a mechanism considered to be related to the acquisition of 5-FU resistance, the addition of cisplatin or camptothecin significantly inhibited the 5-FU-induced elevation of DPD. Fluorouracil 124-128 dihydropyrimidine dehydrogenase Homo sapiens 44-47 16568373-10 2006 CONCLUSIONS: 5-FU-associated enzymes in colon cancer cells were greatly influenced by various chemotherapeutic agents; in particular, DPD expression was depressed. Fluorouracil 13-17 dihydropyrimidine dehydrogenase Homo sapiens 134-137 17163168-9 2006 Tumors with high TS, TP, and DPD expression levels should be treated with such non-TS-directed anticancer drugs as irinotecan or oxaliplatin, or in combination with 5-FU. Fluorouracil 165-169 dihydropyrimidine dehydrogenase Homo sapiens 29-32 17786362-0 2007 Inhibition of Fatty Acid Synthase (FASN) synergistically enhances the efficacy of 5-fluorouracil in breast carcinoma cells. Fluorouracil 82-96 fatty acid synthase Homo sapiens 14-33 17786362-0 2007 Inhibition of Fatty Acid Synthase (FASN) synergistically enhances the efficacy of 5-fluorouracil in breast carcinoma cells. Fluorouracil 82-96 fatty acid synthase Homo sapiens 35-39 17786362-3 2007 Upon pharmacological inhibition of FASN activity using the natural antibiotic cerulenin [(2S,3R)-2,3-epoxy-4-oxo-7E,10E-dodecadienamide], we evaluated the role of FASN-catalyzed endogenous fatty acid biogenesis on the sensitivity of SK-Br3, MCF-7 and MDA-MB-231 breast cancer cell lines to the anti-metabolite 5-fluorouracil (5-FU). Fluorouracil 310-324 fatty acid synthase Homo sapiens 35-39 17786362-3 2007 Upon pharmacological inhibition of FASN activity using the natural antibiotic cerulenin [(2S,3R)-2,3-epoxy-4-oxo-7E,10E-dodecadienamide], we evaluated the role of FASN-catalyzed endogenous fatty acid biogenesis on the sensitivity of SK-Br3, MCF-7 and MDA-MB-231 breast cancer cell lines to the anti-metabolite 5-fluorouracil (5-FU). Fluorouracil 326-330 fatty acid synthase Homo sapiens 35-39 17786362-12 2007 Our current findings revealing a schedule-dependent synergistic interaction between 5-FU and cerulenin represents, to the best of our knowledge, the first evidence that FASN-catalyzed de novo FA biogenesis plays a key role in regulating breast cancer cell response to antimetabolite-based therapies. Fluorouracil 84-88 fatty acid synthase Homo sapiens 169-173 17165084-1 2007 BACKGROUND: Dihydropyrimidine dehydrogenase (DPD) enzyme is responsible for the elimination of approximately 80% of administered dose of 5-FU. Fluorouracil 137-141 dihydropyrimidine dehydrogenase Homo sapiens 12-43 17165084-1 2007 BACKGROUND: Dihydropyrimidine dehydrogenase (DPD) enzyme is responsible for the elimination of approximately 80% of administered dose of 5-FU. Fluorouracil 137-141 dihydropyrimidine dehydrogenase Homo sapiens 45-48 18019677-1 2007 BACKGROUND/AIMS: 5-fluorouracil (5-FU)-related metabolic enzymes, including dihydropyrimidine dehydrogenase (DPD), thymidylate synthase (TS), thymidylate phosphorylase (TP), and orotate phosphoribosyl transferase (OPRT) are initial, rate-limiting enzymes in the metabolism of 5-FU. Fluorouracil 17-31 dihydropyrimidine dehydrogenase Homo sapiens 76-107 18019677-1 2007 BACKGROUND/AIMS: 5-fluorouracil (5-FU)-related metabolic enzymes, including dihydropyrimidine dehydrogenase (DPD), thymidylate synthase (TS), thymidylate phosphorylase (TP), and orotate phosphoribosyl transferase (OPRT) are initial, rate-limiting enzymes in the metabolism of 5-FU. Fluorouracil 17-31 dihydropyrimidine dehydrogenase Homo sapiens 109-112 18019677-1 2007 BACKGROUND/AIMS: 5-fluorouracil (5-FU)-related metabolic enzymes, including dihydropyrimidine dehydrogenase (DPD), thymidylate synthase (TS), thymidylate phosphorylase (TP), and orotate phosphoribosyl transferase (OPRT) are initial, rate-limiting enzymes in the metabolism of 5-FU. Fluorouracil 33-37 dihydropyrimidine dehydrogenase Homo sapiens 109-112 17702597-0 2007 Modification of miR gene expression pattern in human colon cancer cells following exposure to 5-fluorouracil in vitro. Fluorouracil 94-108 membrane associated ring-CH-type finger 8 Homo sapiens 16-19 17702597-4 2007 Here we show that 5-fluorouracil (5-FU), a classical antimetabolite largely used in the clinic, is able to change significantly the expression of several miR genes. Fluorouracil 18-32 membrane associated ring-CH-type finger 8 Homo sapiens 154-157 17702597-4 2007 Here we show that 5-fluorouracil (5-FU), a classical antimetabolite largely used in the clinic, is able to change significantly the expression of several miR genes. Fluorouracil 34-38 membrane associated ring-CH-type finger 8 Homo sapiens 154-157 17702597-6 2007 In some instances, 5-FU up-regulates miR genes that are already over-expressed in neoplastic tissues, including, for example, miR-21 that is associated with anti-apoptotic functions characterizing malignant cells. Fluorouracil 19-23 membrane associated ring-CH-type finger 8 Homo sapiens 37-40 17450522-7 2007 Celecoxib, 5FU or 5FU/celecoxib significantly suppressed the VEGF content in tumor tissues. Fluorouracil 11-14 vascular endothelial growth factor A Mus musculus 61-65 17450522-7 2007 Celecoxib, 5FU or 5FU/celecoxib significantly suppressed the VEGF content in tumor tissues. Fluorouracil 18-21 vascular endothelial growth factor A Mus musculus 61-65 17697537-12 2007 The proportions of immune T cells were lower in 5-FU-pretreated PBMCs than in control PBMCs (0.7% vs. 2.1% for CD4+IFN-gamma+ T cells, 2.2% vs. 3.9% for CD8+IFN-gamma+ T cells, 0.7% vs. 2.5% for CD4+IL-2+ T cells, 0.2% vs. 0.4% for CD8+IL-2+ T cells). Fluorouracil 48-52 CD8a molecule Homo sapiens 153-166 17377791-1 2007 PURPOSE: It has been suggested that the gene expression levels of thymidylate synthase (TS) and dihydropyrimidine dehydrogenase (DPD) help in the prediction of the response to 5-fluorouracil (5-FU) in vivo and in vitro in gastric cancers. Fluorouracil 176-190 dihydropyrimidine dehydrogenase Homo sapiens 96-127 17377791-1 2007 PURPOSE: It has been suggested that the gene expression levels of thymidylate synthase (TS) and dihydropyrimidine dehydrogenase (DPD) help in the prediction of the response to 5-fluorouracil (5-FU) in vivo and in vitro in gastric cancers. Fluorouracil 176-190 dihydropyrimidine dehydrogenase Homo sapiens 129-132 17377791-1 2007 PURPOSE: It has been suggested that the gene expression levels of thymidylate synthase (TS) and dihydropyrimidine dehydrogenase (DPD) help in the prediction of the response to 5-fluorouracil (5-FU) in vivo and in vitro in gastric cancers. Fluorouracil 192-196 dihydropyrimidine dehydrogenase Homo sapiens 96-127 17377791-1 2007 PURPOSE: It has been suggested that the gene expression levels of thymidylate synthase (TS) and dihydropyrimidine dehydrogenase (DPD) help in the prediction of the response to 5-fluorouracil (5-FU) in vivo and in vitro in gastric cancers. Fluorouracil 192-196 dihydropyrimidine dehydrogenase Homo sapiens 129-132 17377791-2 2007 METHODS: In this study, intratumoral TS and DPD gene expressions were evaluated with real time reverse transcriptional polymerase chain reaction technique to determine the correlation between the expression of these two genes and in vitro sensitivity to 5-FU, assessed by the histoculture drug response assay on 87 patients with gastric adenocarcinoma. Fluorouracil 254-258 dihydropyrimidine dehydrogenase Homo sapiens 44-47 17377791-6 2007 DPD also had significant predictive value for 5-FU sensitivity in undifferentiated cases [R(S) = -0.401, P = 0.011]. Fluorouracil 46-50 dihydropyrimidine dehydrogenase Homo sapiens 0-3 17699726-9 2007 The antiproliferative effect of 5-FU could thus be modulated by IFN-alpha, possibly through DPD expression, in HCC cells. Fluorouracil 32-36 dihydropyrimidine dehydrogenase Homo sapiens 92-95 16397252-2 2006 To enhance the therapeutic efficacy of endostatin, we fused endostatin with cytosine deaminase, which converts a prodrug 5-flucytosine into a cytotoxic 5-fluorouracil. Fluorouracil 152-166 collagen, type XVIII, alpha 1 Mus musculus 39-49 16397252-2 2006 To enhance the therapeutic efficacy of endostatin, we fused endostatin with cytosine deaminase, which converts a prodrug 5-flucytosine into a cytotoxic 5-fluorouracil. Fluorouracil 152-166 collagen, type XVIII, alpha 1 Mus musculus 60-70 16509759-11 2006 Also, polymorphisms in the DPYD gene show a relation with fluorouracil-related toxicity; however, in most cases no clear association has been found for polymorphisms in drug-metabolising enzymes and drug transporters, and pharmacokinetics or pharmacodynamics of anti-cancer drugs. Fluorouracil 58-70 dihydropyrimidine dehydrogenase Homo sapiens 27-31 16554992-1 2006 PURPOSE: Thymidine phosphorylase (TP) and dihydropyrimidine dehydrogenase (DPD) are important enzymes related to the metabolism of 5-fluorouracil and its derivatives. Fluorouracil 131-145 dihydropyrimidine dehydrogenase Homo sapiens 75-78 16306860-6 2005 Because fluorouracil is minimally excreted by the renal route (about 10% of the dose) and is almost entirely metabolized by dihydropyrimidine dehydrogenase (DPD), it is suggested that plasma factors that accumulate during the interdialytic period and are removed by dialysis may inhibit DPD activity and, consequently, fluorouracil metabolic clearance. Fluorouracil 8-20 dihydropyrimidine dehydrogenase Homo sapiens 124-155 18210873-13 2007 IC50 of si-livin-treated SGC-7901 cells to 5-Fu and cisplatin was decreased (P < 0.05) and the cells were more susceptible to proapoptotic stimuli (5-Fu and cisplatin) than control groups (P < 0.05). Fluorouracil 43-47 baculoviral IAP repeat containing 7 Homo sapiens 11-16 18210873-13 2007 IC50 of si-livin-treated SGC-7901 cells to 5-Fu and cisplatin was decreased (P < 0.05) and the cells were more susceptible to proapoptotic stimuli (5-Fu and cisplatin) than control groups (P < 0.05). Fluorouracil 151-155 baculoviral IAP repeat containing 7 Homo sapiens 11-16 17537404-0 2007 Drug resistance to 5-FU linked to reactive oxygen species modulator 1. Fluorouracil 19-23 reactive oxygen species modulator 1 Homo sapiens 34-69 17537404-5 2007 To elucidate the relationship between 5-FU-induced ROS production and Romo1 expression, Romo1 siRNA was used to inhibit 5-FU-triggered Romo1 induction. Fluorouracil 38-42 reactive oxygen species modulator 1 Homo sapiens 70-75 17537404-5 2007 To elucidate the relationship between 5-FU-induced ROS production and Romo1 expression, Romo1 siRNA was used to inhibit 5-FU-triggered Romo1 induction. Fluorouracil 38-42 reactive oxygen species modulator 1 Homo sapiens 88-93 17537404-5 2007 To elucidate the relationship between 5-FU-induced ROS production and Romo1 expression, Romo1 siRNA was used to inhibit 5-FU-triggered Romo1 induction. Fluorouracil 38-42 reactive oxygen species modulator 1 Homo sapiens 88-93 17537404-5 2007 To elucidate the relationship between 5-FU-induced ROS production and Romo1 expression, Romo1 siRNA was used to inhibit 5-FU-triggered Romo1 induction. Fluorouracil 120-124 reactive oxygen species modulator 1 Homo sapiens 70-75 17549381-1 2007 FdUMP[10] is a multimer of FdUMP, a suicide inhibitor of thymidylate synthase (TS), and was designed to bypass resistance to 5-fluorouracil (5FU). Fluorouracil 141-144 thymidylate synthase Mus musculus 57-77 17558308-0 2007 Polymorphism of the DNA repair enzyme XRCC1 is associated with treatment prediction in anthracycline and cyclophosphamide/methotrexate/5-fluorouracil-based chemotherapy of patients with primary invasive breast cancer. Fluorouracil 135-149 X-ray repair cross complementing 1 Homo sapiens 38-43 17558308-14 2007 CONCLUSION: The DNA repair enzyme XRCC1 is a potential treatment predictor for the outcome and survival of anthracycline and cyclophosphamide/methotrexate/5-fluorouracil-based chemotherapy of invasive breast cancer. Fluorouracil 155-169 X-ray repair cross complementing 1 Homo sapiens 34-39 16306860-6 2005 Because fluorouracil is minimally excreted by the renal route (about 10% of the dose) and is almost entirely metabolized by dihydropyrimidine dehydrogenase (DPD), it is suggested that plasma factors that accumulate during the interdialytic period and are removed by dialysis may inhibit DPD activity and, consequently, fluorouracil metabolic clearance. Fluorouracil 8-20 dihydropyrimidine dehydrogenase Homo sapiens 157-160 16306860-6 2005 Because fluorouracil is minimally excreted by the renal route (about 10% of the dose) and is almost entirely metabolized by dihydropyrimidine dehydrogenase (DPD), it is suggested that plasma factors that accumulate during the interdialytic period and are removed by dialysis may inhibit DPD activity and, consequently, fluorouracil metabolic clearance. Fluorouracil 8-20 dihydropyrimidine dehydrogenase Homo sapiens 287-290 16306860-6 2005 Because fluorouracil is minimally excreted by the renal route (about 10% of the dose) and is almost entirely metabolized by dihydropyrimidine dehydrogenase (DPD), it is suggested that plasma factors that accumulate during the interdialytic period and are removed by dialysis may inhibit DPD activity and, consequently, fluorouracil metabolic clearance. Fluorouracil 319-331 dihydropyrimidine dehydrogenase Homo sapiens 157-160 16282729-0 2005 [Expression of mRNA levels of thymidylate synthase, dihydropyrimidine dehydrogenase, and orotate phosphoribosyltransferase of colorectal cancer--relationships among mRNA levels in association with response to 5-FU based treatment]. Fluorouracil 209-213 dihydropyrimidine dehydrogenase Homo sapiens 52-83 16334763-2 2005 Dihydropyrimidine dehydrogenase (DPD) is a rate-limiting enzyme for degradation of 5-FU. Fluorouracil 83-87 dihydropyrimidine dehydrogenase Homo sapiens 0-31 17464085-4 2007 In contrast, normal HSCs from 5-fluorouracil treated marrows cultured on the IL-10 secreting stroma displayed an enhanced repopulating activity compared with cells grown on control stroma, with ninefold higher numbers of donor-derived HSCs in the reconstituted recipient marrows. Fluorouracil 30-44 interleukin 10 Homo sapiens 77-82 16334763-2 2005 Dihydropyrimidine dehydrogenase (DPD) is a rate-limiting enzyme for degradation of 5-FU. Fluorouracil 83-87 dihydropyrimidine dehydrogenase Homo sapiens 33-36 16282061-7 2005 The levels of CD3, CD4, CD4/CD8, IgG, IgM in 5-FU group were lower (P<0.05), while those in the three Shengmai Injection combined with 5-FU groups were higher than those in the control group (P<0.05). Fluorouracil 45-49 CD4 antigen Mus musculus 19-22 16282061-7 2005 The levels of CD3, CD4, CD4/CD8, IgG, IgM in 5-FU group were lower (P<0.05), while those in the three Shengmai Injection combined with 5-FU groups were higher than those in the control group (P<0.05). Fluorouracil 45-49 CD4 antigen Mus musculus 24-27 16243820-4 2005 RNA expression levels of 5-FU metabolism-associated genes thymidylate synthase, thymidine phosphorylase, dihydropyrimidine dehydrogenase, methylenetetrahydrofolate reductase, MAP7, and ELF3, of platinum- and taxane-related genes caldesmon, ERCC1, ERCC4, HER-2/neu, and GADD45, and of multidrug resistance gene MRP1 were determined using real-time reverse transcriptase-PCR. Fluorouracil 25-29 dihydropyrimidine dehydrogenase Homo sapiens 58-136 16243820-4 2005 RNA expression levels of 5-FU metabolism-associated genes thymidylate synthase, thymidine phosphorylase, dihydropyrimidine dehydrogenase, methylenetetrahydrofolate reductase, MAP7, and ELF3, of platinum- and taxane-related genes caldesmon, ERCC1, ERCC4, HER-2/neu, and GADD45, and of multidrug resistance gene MRP1 were determined using real-time reverse transcriptase-PCR. Fluorouracil 25-29 methylenetetrahydrofolate reductase Homo sapiens 138-173 16243820-4 2005 RNA expression levels of 5-FU metabolism-associated genes thymidylate synthase, thymidine phosphorylase, dihydropyrimidine dehydrogenase, methylenetetrahydrofolate reductase, MAP7, and ELF3, of platinum- and taxane-related genes caldesmon, ERCC1, ERCC4, HER-2/neu, and GADD45, and of multidrug resistance gene MRP1 were determined using real-time reverse transcriptase-PCR. Fluorouracil 25-29 microtubule associated protein 7 Homo sapiens 175-179 16243820-4 2005 RNA expression levels of 5-FU metabolism-associated genes thymidylate synthase, thymidine phosphorylase, dihydropyrimidine dehydrogenase, methylenetetrahydrofolate reductase, MAP7, and ELF3, of platinum- and taxane-related genes caldesmon, ERCC1, ERCC4, HER-2/neu, and GADD45, and of multidrug resistance gene MRP1 were determined using real-time reverse transcriptase-PCR. Fluorouracil 25-29 ERCC excision repair 4, endonuclease catalytic subunit Homo sapiens 247-252 16012177-1 2005 BACKGROUND: The predictive value of thymidylate synthase (TS) and dihydropyrimidine dehydrogenase (DPD) expression on long-term survival by influencing 5-fluorouracil (5-FU) effect were determined in primary tumours and node metastases of stage III colon cancer patients treated adjuvantly with 5-FU regimens (n=391). Fluorouracil 168-172 dihydropyrimidine dehydrogenase Homo sapiens 66-97 16012177-1 2005 BACKGROUND: The predictive value of thymidylate synthase (TS) and dihydropyrimidine dehydrogenase (DPD) expression on long-term survival by influencing 5-fluorouracil (5-FU) effect were determined in primary tumours and node metastases of stage III colon cancer patients treated adjuvantly with 5-FU regimens (n=391). Fluorouracil 168-172 dihydropyrimidine dehydrogenase Homo sapiens 99-102 17603216-4 2007 METHODS: We developed a model incorporating the inhibition of DPD by gimeracil and uracil, and fitted the model to the observed kinetics of tegafur and 5-FU after the administration of TS-1 and UFT. Fluorouracil 152-156 dihydropyrimidine dehydrogenase Homo sapiens 62-65 16012177-1 2005 BACKGROUND: The predictive value of thymidylate synthase (TS) and dihydropyrimidine dehydrogenase (DPD) expression on long-term survival by influencing 5-fluorouracil (5-FU) effect were determined in primary tumours and node metastases of stage III colon cancer patients treated adjuvantly with 5-FU regimens (n=391). Fluorouracil 295-299 dihydropyrimidine dehydrogenase Homo sapiens 99-102 16315867-6 2005 Radiation and 5-FU induce Th1-dominant state by inhibiting the OK-432-induced production of IL-10 and TGF-beta mediated by regulation of SOCS-1 and SOCS-3 expression, and are suggested to increase anti-cancer immunity. Fluorouracil 14-18 negative elongation factor complex member C/D Homo sapiens 26-29 16315867-6 2005 Radiation and 5-FU induce Th1-dominant state by inhibiting the OK-432-induced production of IL-10 and TGF-beta mediated by regulation of SOCS-1 and SOCS-3 expression, and are suggested to increase anti-cancer immunity. Fluorouracil 14-18 interleukin 10 Homo sapiens 92-97 16315929-1 2005 TS-1 is an antitumor drug including 5-chloro-2,4 dihydroxypyridine (CDHP), which inhibits dihydriopyrimidine dehydrogenase (DPD) activity selectively in metabolism of 5-FU. Fluorouracil 167-171 dihydropyrimidine dehydrogenase Homo sapiens 90-122 16315929-1 2005 TS-1 is an antitumor drug including 5-chloro-2,4 dihydroxypyridine (CDHP), which inhibits dihydriopyrimidine dehydrogenase (DPD) activity selectively in metabolism of 5-FU. Fluorouracil 167-171 dihydropyrimidine dehydrogenase Homo sapiens 124-127 16106266-8 2005 There was a significant correlation between IFNAR2 expression and response to IFN-alpha/5-FU combination therapy in univariate analysis (P = 0.0070). Fluorouracil 88-92 interferon alpha and beta receptor subunit 2 Homo sapiens 44-50 16106266-9 2005 IFN-alpha/5-FU combination therapy is a promising modality for advanced HCC with tumour thrombi in the major portal branches and could significantly depend on IFNAR2 expression. Fluorouracil 10-14 interferon alpha and beta receptor subunit 2 Homo sapiens 159-165 16101138-5 2005 Among them, three IFN-related genes, an IFN receptor gene (IFNAR2) and two IFN-stimulated genes (ISG15K, ISG-54K), that were up-regulated following addition of 5-FU, were investigated. Fluorouracil 160-164 interferon alpha and beta receptor subunit 2 Homo sapiens 59-65 15975592-0 2005 The effect of granulocyte macrophage-colony stimulating factor on bacterial translocation after administration of 5-fluorouracil in rats. Fluorouracil 114-128 colony stimulating factor 2 Rattus norvegicus 14-62 15975592-10 2005 The plasma endotoxin, tumor necrosis factor-alpha and interleukin-6 levels in the 5-FU and GM-CSF groups were significantly increased at day 7 compared with the control groups (P < 0.01), but these levels were significantly lower in the GM-CSF group compared to the 5-FU group (P < 0.01). Fluorouracil 82-86 colony stimulating factor 2 Rattus norvegicus 240-246 15975592-10 2005 The plasma endotoxin, tumor necrosis factor-alpha and interleukin-6 levels in the 5-FU and GM-CSF groups were significantly increased at day 7 compared with the control groups (P < 0.01), but these levels were significantly lower in the GM-CSF group compared to the 5-FU group (P < 0.01). Fluorouracil 269-273 colony stimulating factor 2 Rattus norvegicus 91-97 15975592-12 2005 Compared with 5-FU group, GM-CSF decreased the bacterial translocation (P < 0.01). Fluorouracil 14-18 colony stimulating factor 2 Rattus norvegicus 26-32 16115930-1 2005 PURPOSE: Complete or partial loss of dihydropyrimidine dehydrogenase (DPD) function has been described in cancer patients with intolerance to fluoropyrimidine drugs like 5-fluorouracil (5-FU) or Xeloda. Fluorouracil 170-184 dihydropyrimidine dehydrogenase Homo sapiens 37-68 16115930-1 2005 PURPOSE: Complete or partial loss of dihydropyrimidine dehydrogenase (DPD) function has been described in cancer patients with intolerance to fluoropyrimidine drugs like 5-fluorouracil (5-FU) or Xeloda. Fluorouracil 170-184 dihydropyrimidine dehydrogenase Homo sapiens 70-73 16115930-1 2005 PURPOSE: Complete or partial loss of dihydropyrimidine dehydrogenase (DPD) function has been described in cancer patients with intolerance to fluoropyrimidine drugs like 5-fluorouracil (5-FU) or Xeloda. Fluorouracil 186-190 dihydropyrimidine dehydrogenase Homo sapiens 37-68 16115930-1 2005 PURPOSE: Complete or partial loss of dihydropyrimidine dehydrogenase (DPD) function has been described in cancer patients with intolerance to fluoropyrimidine drugs like 5-fluorouracil (5-FU) or Xeloda. Fluorouracil 186-190 dihydropyrimidine dehydrogenase Homo sapiens 70-73 16033824-1 2005 PURPOSE: Dihydropyrimidine dehydrogenase (DPD) is the initial and rate-limiting enzyme catalyzing the metabolic degradation of the anticancer drug 5-fluorouracil (5-FU). Fluorouracil 147-161 dihydropyrimidine dehydrogenase Homo sapiens 9-40 16033824-1 2005 PURPOSE: Dihydropyrimidine dehydrogenase (DPD) is the initial and rate-limiting enzyme catalyzing the metabolic degradation of the anticancer drug 5-fluorouracil (5-FU). Fluorouracil 147-161 dihydropyrimidine dehydrogenase Homo sapiens 42-45 16033824-1 2005 PURPOSE: Dihydropyrimidine dehydrogenase (DPD) is the initial and rate-limiting enzyme catalyzing the metabolic degradation of the anticancer drug 5-fluorouracil (5-FU). Fluorouracil 163-167 dihydropyrimidine dehydrogenase Homo sapiens 9-40 16033824-1 2005 PURPOSE: Dihydropyrimidine dehydrogenase (DPD) is the initial and rate-limiting enzyme catalyzing the metabolic degradation of the anticancer drug 5-fluorouracil (5-FU). Fluorouracil 163-167 dihydropyrimidine dehydrogenase Homo sapiens 42-45 16030402-11 2005 These results may suggest further large-scale study about TSER and MTHFR polymorphism for the prediction of efficacy of 5-FU-based chemotherapy in gastric cancer in Korea. Fluorouracil 120-124 methylenetetrahydrofolate reductase Homo sapiens 67-72 15944764-6 2005 There were inverse correlations between antitumor and DPD activities for 5"-DFUR (r=-0.79, P=0.034), capecitabine (r=-0.56, P=0.19) and 5-FU (r=-0.86, P=0.013). Fluorouracil 136-140 dihydropyrimidine dehydrogenase Homo sapiens 54-57 15930305-1 2005 FdUMP[10], a 10mer of 5-fluoro-2"-deoxyuridine 5"-monophosphate (FdUMP), the thymidylate synthase inhibitory metabolite of 5-fluorouracil (FU), is most closely correlated with the DNA topoisomerase I (Top1) inhibitor camptothecin in the National Cancer Institute COMPARE analysis, but not with FU. Fluorouracil 123-137 thymidylate synthase Mus musculus 77-97 15984520-2 2005 The biological anti-tumor effect of 5-FU depends on the activity of its metabolizing enzyme, dihydropyrimidine dehydrogenase (DPD). Fluorouracil 36-40 dihydropyrimidine dehydrogenase Homo sapiens 93-124 17629045-2 2007 While this reaction is taking place Dihydropyrimidine Dihydrogenase (DPD) catalyzes 5-FU to inactive molecules. Fluorouracil 84-88 dihydropyrimidine dehydrogenase Homo sapiens 36-67 17629045-2 2007 While this reaction is taking place Dihydropyrimidine Dihydrogenase (DPD) catalyzes 5-FU to inactive molecules. Fluorouracil 84-88 dihydropyrimidine dehydrogenase Homo sapiens 69-72 15984520-2 2005 The biological anti-tumor effect of 5-FU depends on the activity of its metabolizing enzyme, dihydropyrimidine dehydrogenase (DPD). Fluorouracil 36-40 dihydropyrimidine dehydrogenase Homo sapiens 126-129 15939134-1 2005 Dihydropyrimidine deshydrogenase (DPD) is the rate limiting enzyme of 5-fluorouracil (5-FU) catabolism and its activity is generally determined in peripheral blood mononuclear cells. Fluorouracil 70-84 dihydropyrimidine dehydrogenase Homo sapiens 0-32 17487405-0 2007 Depletion of O6-methylguanine-DNA methyltransferase by O6-benzylguanine enhances 5-FU cytotoxicity in colon and oral cancer cell lines. Fluorouracil 81-85 O-6-methylguanine-DNA methyltransferase Homo sapiens 13-51 17487405-3 2007 We have previously shown that the colorectal cancer patients treated with 5-fluorouracil (5-FU) as adjuvant chemotherapy had a better prognosis when the tumor revealed hypermethylation in its MGMT promoter. Fluorouracil 74-88 O-6-methylguanine-DNA methyltransferase Homo sapiens 192-196 17487405-3 2007 We have previously shown that the colorectal cancer patients treated with 5-fluorouracil (5-FU) as adjuvant chemotherapy had a better prognosis when the tumor revealed hypermethylation in its MGMT promoter. Fluorouracil 90-94 O-6-methylguanine-DNA methyltransferase Homo sapiens 192-196 17487405-4 2007 Therefore, we sought to investigate the relationship between the expression levels of MGMT and the anti-tumor effect of 5-FU in vitro by using two colon adenocarcinoma and four oral cancer cell lines with a variety of MGMT expression. Fluorouracil 120-124 O-6-methylguanine-DNA methyltransferase Homo sapiens 86-90 17487405-6 2007 The 5-FU treatment uniformly depleted protein and mRNA expression of MGMT in all cell lines examined. Fluorouracil 4-8 O-6-methylguanine-DNA methyltransferase Homo sapiens 69-73 17487405-7 2007 Cell lines expressing low levels of MGMT were sensitive to 5-FU. Fluorouracil 59-63 O-6-methylguanine-DNA methyltransferase Homo sapiens 36-40 17487405-8 2007 On the other hand, cells expressing high levels of MGMT were less sensitive to 5-FU. Fluorouracil 79-83 O-6-methylguanine-DNA methyltransferase Homo sapiens 51-55 17487405-9 2007 The 5-FU treatment exhibited a better antiproliferative effect on the cells expressing high levels of MGMT by the pretreatment of O6-BG. Fluorouracil 4-8 O-6-methylguanine-DNA methyltransferase Homo sapiens 102-106 17487405-10 2007 Depletion of MGMT by O6-BG enhanced the anti-tumor effect of 5-FU. Fluorouracil 61-65 O-6-methylguanine-DNA methyltransferase Homo sapiens 13-17 17487405-11 2007 Assessment of the levels of MGMT expression in cancer cells and the control of its expression could contribute to the effective chemotherapy by 5-FU especially in patients who previously were considered as low-responsive individuals whose tumors have high levels of MGMT. Fluorouracil 144-148 O-6-methylguanine-DNA methyltransferase Homo sapiens 28-32 17487405-11 2007 Assessment of the levels of MGMT expression in cancer cells and the control of its expression could contribute to the effective chemotherapy by 5-FU especially in patients who previously were considered as low-responsive individuals whose tumors have high levels of MGMT. Fluorouracil 144-148 O-6-methylguanine-DNA methyltransferase Homo sapiens 266-270 17443278-1 2007 BACKGROUND: Thymidine phosphorylase (TP), orotate phosphoribosyltransferase (OPRT), and dihydropyrimidine dehydrogenase (DPD) are important enzymes related to the metabolism of 5-fluorouracil and its derivatives. Fluorouracil 177-191 dihydropyrimidine dehydrogenase Homo sapiens 88-119 17417073-2 2007 Adverse drug reactions to 5-FU-based chemotherapy have been reported to be in part the result of polymorphisms in the thymidylate synthase (TYMS) and dihydropyrimidine dehydrogenase (DPYD) genes. Fluorouracil 26-30 dihydropyrimidine dehydrogenase Homo sapiens 183-187 15939134-1 2005 Dihydropyrimidine deshydrogenase (DPD) is the rate limiting enzyme of 5-fluorouracil (5-FU) catabolism and its activity is generally determined in peripheral blood mononuclear cells. Fluorouracil 86-90 dihydropyrimidine dehydrogenase Homo sapiens 0-32 17364369-3 2007 BACKGROUND: Expression levels of the thymidylate synthase (TS) and 5-FU metabolic enzymes including dihydropyrimidine dehydrogenase (DPD), TP, and orotate phosphoribosyl transferase (OPRT), are reported to be associated with sensitivity to 5-FU-based chemotherapy in several cancers. Fluorouracil 67-71 dihydropyrimidine dehydrogenase Homo sapiens 133-136 15901346-6 2005 Moreover, we observed that hOat2 mediates the transport of bumetanide, ES, glutarate, dehydroepiandrosterone sulfate, allopurinol, prostaglandin E2, 5-fluorouracil, paclitaxel and L-ascorbic acid. Fluorouracil 149-163 solute carrier family 22 member 7 Homo sapiens 27-32 17092280-1 2007 OBJECTIVE: To measure dihydropyrimidine dehydrogenase (DPD), an enzyme involved in the metabolism of 5-fluorouracil (5-FU), expression in prostate cancer and determine whether 5-chloro-2,4-dihydroxypyridine (CDHP), a potent inhibitor of DPD, enhances the antitumoral activity of 5-FU against prostate cancer. Fluorouracil 279-283 dihydropyrimidine dehydrogenase Homo sapiens 22-53 17092280-1 2007 OBJECTIVE: To measure dihydropyrimidine dehydrogenase (DPD), an enzyme involved in the metabolism of 5-fluorouracil (5-FU), expression in prostate cancer and determine whether 5-chloro-2,4-dihydroxypyridine (CDHP), a potent inhibitor of DPD, enhances the antitumoral activity of 5-FU against prostate cancer. Fluorouracil 279-283 dihydropyrimidine dehydrogenase Homo sapiens 55-58 17092280-11 2007 CONCLUSION: The present study showed that DPD expression is elevated in prostate cancer, and indicate that DPD inhibitors might enhance the antitumour activity of 5-FU against prostate cancer. Fluorouracil 163-167 dihydropyrimidine dehydrogenase Homo sapiens 42-45 17092280-11 2007 CONCLUSION: The present study showed that DPD expression is elevated in prostate cancer, and indicate that DPD inhibitors might enhance the antitumour activity of 5-FU against prostate cancer. Fluorouracil 163-167 dihydropyrimidine dehydrogenase Homo sapiens 107-110 15820075-2 2005 Serum level of dihydropyrimidine dehydrogenase (DPD) relates to efficacy and toxicities of chemotherapy containing 5-fluorouracil (5-FU). Fluorouracil 115-129 dihydropyrimidine dehydrogenase Homo sapiens 15-46 15820075-2 2005 Serum level of dihydropyrimidine dehydrogenase (DPD) relates to efficacy and toxicities of chemotherapy containing 5-fluorouracil (5-FU). Fluorouracil 115-129 dihydropyrimidine dehydrogenase Homo sapiens 48-51 15820075-2 2005 Serum level of dihydropyrimidine dehydrogenase (DPD) relates to efficacy and toxicities of chemotherapy containing 5-fluorouracil (5-FU). Fluorouracil 131-135 dihydropyrimidine dehydrogenase Homo sapiens 15-46 15820075-2 2005 Serum level of dihydropyrimidine dehydrogenase (DPD) relates to efficacy and toxicities of chemotherapy containing 5-fluorouracil (5-FU). Fluorouracil 131-135 dihydropyrimidine dehydrogenase Homo sapiens 48-51 15820075-3 2005 This study was to explore relationship of DPD to serum concentration of 5-FU in colorectal cancer patients treated with FOLFOX6 regimen, and their correlation to treatment response and adverse events. Fluorouracil 72-76 dihydropyrimidine dehydrogenase Homo sapiens 42-45 15820075-8 2005 Serum level of DPD was negatively correlated with serum concentration of 5-FU (r=-0.460, P < 0.01). Fluorouracil 73-77 dihydropyrimidine dehydrogenase Homo sapiens 15-18 15820075-14 2005 DPD level negatively correlates with serum 5-FU concentration. Fluorouracil 43-47 dihydropyrimidine dehydrogenase Homo sapiens 0-3 15899693-1 2005 Dihydropyrimidine dehydrogenase (DPD) is the initial and rate-limiting enzyme in the catabolism of the pyrimidine bases uracil and thymine, as well as of the widely used chemotherapeutic drug 5-fluorouracil (5FU). Fluorouracil 192-206 dihydropyrimidine dehydrogenase Homo sapiens 0-31 15899693-1 2005 Dihydropyrimidine dehydrogenase (DPD) is the initial and rate-limiting enzyme in the catabolism of the pyrimidine bases uracil and thymine, as well as of the widely used chemotherapeutic drug 5-fluorouracil (5FU). Fluorouracil 192-206 dihydropyrimidine dehydrogenase Homo sapiens 33-36 15899693-1 2005 Dihydropyrimidine dehydrogenase (DPD) is the initial and rate-limiting enzyme in the catabolism of the pyrimidine bases uracil and thymine, as well as of the widely used chemotherapeutic drug 5-fluorouracil (5FU). Fluorouracil 208-211 dihydropyrimidine dehydrogenase Homo sapiens 0-31 15899693-1 2005 Dihydropyrimidine dehydrogenase (DPD) is the initial and rate-limiting enzyme in the catabolism of the pyrimidine bases uracil and thymine, as well as of the widely used chemotherapeutic drug 5-fluorouracil (5FU). Fluorouracil 208-211 dihydropyrimidine dehydrogenase Homo sapiens 33-36 15899693-7 2005 The identification of these novel mutations in DPYD will allow the identification of patients with an increased risk of developing severe 5FU-associated toxicity. Fluorouracil 138-141 dihydropyrimidine dehydrogenase Homo sapiens 47-51 15949378-2 2005 METHODS: Spleen cells from C57 mice administrated with 5-fluorouracil were induced by IL-3, 6 and granulocyte-macrophage colony stimulating factor (GM-CSF), and 1alpha, 25-(OH)(2)D(3) to obtain massive OLCs. Fluorouracil 55-69 colony stimulating factor 2 (granulocyte-macrophage) Mus musculus 86-146 15949378-2 2005 METHODS: Spleen cells from C57 mice administrated with 5-fluorouracil were induced by IL-3, 6 and granulocyte-macrophage colony stimulating factor (GM-CSF), and 1alpha, 25-(OH)(2)D(3) to obtain massive OLCs. Fluorouracil 55-69 colony stimulating factor 2 (granulocyte-macrophage) Mus musculus 148-154 15868930-4 2005 RESULTS: CDDP and 5-FU were more potent drugs than MMC, ADR and VP-16. Fluorouracil 18-22 host cell factor C1 Homo sapiens 64-69 15735113-0 2005 Thymidylate synthase and methylenetetrahydrofolate reductase gene polymorphism in normal tissue as predictors of fluorouracil sensitivity. Fluorouracil 113-125 methylenetetrahydrofolate reductase Homo sapiens 25-60 15735113-1 2005 PURPOSE: To analyze thymidylate synthase (TS) and methylenetetrahydrofolate reductase (MTHFR) gene polymorphism with respect to fluorouracil (FU) sensitivity. Fluorouracil 128-140 methylenetetrahydrofolate reductase Homo sapiens 50-85 15735113-1 2005 PURPOSE: To analyze thymidylate synthase (TS) and methylenetetrahydrofolate reductase (MTHFR) gene polymorphism with respect to fluorouracil (FU) sensitivity. Fluorouracil 128-140 methylenetetrahydrofolate reductase Homo sapiens 87-92 15698412-0 2005 Consensus interferon enhances the anti-proliferative effect of 5-fluorouracil on human hepatoma cells via downregulation of dihydropyrimidine dehydrogenase expression. Fluorouracil 63-77 dihydropyrimidine dehydrogenase Homo sapiens 124-155 15698412-10 2005 CONCLUSIONS: C-IFN likely improves the anti-tumor effect of 5-FU via downregulation of DPD enzyme in hepatoma cells. Fluorouracil 60-64 dihydropyrimidine dehydrogenase Homo sapiens 87-90 15659287-7 2005 Because 5-fluorouracil is a cell cycle-specific drug damaging mainly cells in the S-phase, protective effects of CPA can be explained by its inhibitory action on the cell cycling. Fluorouracil 8-22 carboxypeptidase A1, pancreatic Mus musculus 113-116 15659287-8 2005 This interpretation was confirmed by experiments demonstrating that repeated administration of CPA in the hyperproliferation phase of the recovering haematopoiesis after 5-fluorouracil treatment inhibited transiently restoration of CFC-GM counts. Fluorouracil 170-184 carboxypeptidase A1, pancreatic Mus musculus 95-98 16254431-0 2005 Adjuvant 5-FU-based chemoradiotherapy for patients undergoing R-1/R-2 resections for pancreatic cancer. Fluorouracil 9-13 CD1e molecule Homo sapiens 66-69 16021908-1 2005 Dihydropyrimidine dehydrogenase (DPD), known as a rate-limiting metabolic enzyme in the catabolism of 5-fluorouracil (5-FU), degrades more than about 80% of the administered 5-FU in human liver. Fluorouracil 102-116 dihydropyrimidine dehydrogenase Homo sapiens 0-31 17324113-0 2007 Regulation of human dihydropyrimidine dehydrogenase: implications in the pharmacogenetics of 5-FU-based chemotherapy. Fluorouracil 93-97 dihydropyrimidine dehydrogenase Homo sapiens 20-51 17324113-1 2007 Dihydropyrimidine dehydrogenase is the enzyme that is critical for the efficacy and toxicity of the anticancer reagent 5-fluorouracil. Fluorouracil 119-133 dihydropyrimidine dehydrogenase Homo sapiens 0-31 17349846-2 2007 Dihydropyrimidine dehydrogenase (DPD) is a rate-limiting enzyme for degradation of 5-FU. Fluorouracil 83-87 dihydropyrimidine dehydrogenase Homo sapiens 0-31 17349846-2 2007 Dihydropyrimidine dehydrogenase (DPD) is a rate-limiting enzyme for degradation of 5-FU. Fluorouracil 83-87 dihydropyrimidine dehydrogenase Homo sapiens 33-36 16021908-1 2005 Dihydropyrimidine dehydrogenase (DPD), known as a rate-limiting metabolic enzyme in the catabolism of 5-fluorouracil (5-FU), degrades more than about 80% of the administered 5-FU in human liver. Fluorouracil 102-116 dihydropyrimidine dehydrogenase Homo sapiens 33-36 16021908-1 2005 Dihydropyrimidine dehydrogenase (DPD), known as a rate-limiting metabolic enzyme in the catabolism of 5-fluorouracil (5-FU), degrades more than about 80% of the administered 5-FU in human liver. Fluorouracil 118-122 dihydropyrimidine dehydrogenase Homo sapiens 0-31 16021908-1 2005 Dihydropyrimidine dehydrogenase (DPD), known as a rate-limiting metabolic enzyme in the catabolism of 5-fluorouracil (5-FU), degrades more than about 80% of the administered 5-FU in human liver. Fluorouracil 118-122 dihydropyrimidine dehydrogenase Homo sapiens 33-36 17046731-0 2007 Identification of a novel mutation in the dihydropyrimidine dehydrogenase gene in a patient with a lethal outcome following 5-fluorouracil administration and the determination of its frequency in a population of 500 patients with colorectal carcinoma. Fluorouracil 124-138 dihydropyrimidine dehydrogenase Homo sapiens 42-73 17046731-1 2007 OBJECTIVES: Life-threatening toxic side-effects following 5-FU exposure have been related to deficiency of dihydropyrimidine dehydrogenase (DPD), the rate-limiting enzyme in its catabolism. Fluorouracil 58-62 dihydropyrimidine dehydrogenase Homo sapiens 140-143 16021908-1 2005 Dihydropyrimidine dehydrogenase (DPD), known as a rate-limiting metabolic enzyme in the catabolism of 5-fluorouracil (5-FU), degrades more than about 80% of the administered 5-FU in human liver. Fluorouracil 174-178 dihydropyrimidine dehydrogenase Homo sapiens 0-31 17046731-2 2007 We presently report a new DPYD gene SNP in a Spanish woman who died from multivisceral 5-FU-induced toxicity. Fluorouracil 87-91 dihydropyrimidine dehydrogenase Homo sapiens 26-30 16021908-1 2005 Dihydropyrimidine dehydrogenase (DPD), known as a rate-limiting metabolic enzyme in the catabolism of 5-fluorouracil (5-FU), degrades more than about 80% of the administered 5-FU in human liver. Fluorouracil 174-178 dihydropyrimidine dehydrogenase Homo sapiens 33-36 16021908-2 2005 Since it was reported that the anticancer effects of 5-FU were observed in cancer patients with lower DPD activities, many attempts have been conducted to anticipate the expected anticancer effects of 5-FU based on expression of intracanceral DPD. Fluorouracil 53-57 dihydropyrimidine dehydrogenase Homo sapiens 102-105 16021908-2 2005 Since it was reported that the anticancer effects of 5-FU were observed in cancer patients with lower DPD activities, many attempts have been conducted to anticipate the expected anticancer effects of 5-FU based on expression of intracanceral DPD. Fluorouracil 201-205 dihydropyrimidine dehydrogenase Homo sapiens 243-246 16021908-10 2005 It is suggested that newly identified polymorphism of DPD gene might affect transcription of DPD, thereby providing influence on the clinical outcome of cancer patients treated with 5-FU. Fluorouracil 182-186 dihydropyrimidine dehydrogenase Homo sapiens 54-57 16021908-10 2005 It is suggested that newly identified polymorphism of DPD gene might affect transcription of DPD, thereby providing influence on the clinical outcome of cancer patients treated with 5-FU. Fluorouracil 182-186 dihydropyrimidine dehydrogenase Homo sapiens 93-96 15999119-1 2005 The enzymes thymidylate synthase (TS), dihydropyrimidine dehydrogenase (DPD), thymidine phosphorylase (TP), and orotate phosphoribosyl transferase (OPRT) are involved in the metabolism of the anticancer drug 5-fluorouracil. Fluorouracil 208-222 dihydropyrimidine dehydrogenase Homo sapiens 39-70 15628771-2 2004 In the meantime, TP and DPD are a converting enzyme of 5"-DFUR to 5-FU and the major catabolic enzyme of 5-FU, respectively. Fluorouracil 66-70 dihydropyrimidine dehydrogenase Homo sapiens 24-27 17308379-1 2007 BACKGROUND: This study was designed to measure the dihydrouracil (UH(2))/uracil (U) ratio in plasma as a surrogate marker for dihydropyrimidine dehydrogenase (DPD) activity and to investigate the relationships of the UH(2)/U ratios in plasma with the toxicities of 5-fluorouracil (5-FU)-based adjuvant chemotherapy and 5-FU plasma concentrations in colorectal cancer patients. Fluorouracil 265-279 dihydropyrimidine dehydrogenase Homo sapiens 159-162 17308379-1 2007 BACKGROUND: This study was designed to measure the dihydrouracil (UH(2))/uracil (U) ratio in plasma as a surrogate marker for dihydropyrimidine dehydrogenase (DPD) activity and to investigate the relationships of the UH(2)/U ratios in plasma with the toxicities of 5-fluorouracil (5-FU)-based adjuvant chemotherapy and 5-FU plasma concentrations in colorectal cancer patients. Fluorouracil 281-285 dihydropyrimidine dehydrogenase Homo sapiens 159-162 17308379-1 2007 BACKGROUND: This study was designed to measure the dihydrouracil (UH(2))/uracil (U) ratio in plasma as a surrogate marker for dihydropyrimidine dehydrogenase (DPD) activity and to investigate the relationships of the UH(2)/U ratios in plasma with the toxicities of 5-fluorouracil (5-FU)-based adjuvant chemotherapy and 5-FU plasma concentrations in colorectal cancer patients. Fluorouracil 319-323 dihydropyrimidine dehydrogenase Homo sapiens 159-162 17952005-1 2007 BACKGROUND: Dihydropyrimidine dehydrogenase (DPD) is a rate-limiting enzyme for the degradation of 5-fluorouracil. Fluorouracil 99-113 dihydropyrimidine dehydrogenase Homo sapiens 12-43 17952005-1 2007 BACKGROUND: Dihydropyrimidine dehydrogenase (DPD) is a rate-limiting enzyme for the degradation of 5-fluorouracil. Fluorouracil 99-113 dihydropyrimidine dehydrogenase Homo sapiens 45-48 17097873-0 2007 Increased dihydropyrimidine dehydrogenase activity associated with mild toxicity in patients treated with 5-fluorouracil and leucovorin. Fluorouracil 106-120 dihydropyrimidine dehydrogenase Homo sapiens 10-41 17097873-1 2007 Dihydropyrimidine dehydrogenase (DPD) plays a pivotal role in the metabolism of 5FU. Fluorouracil 80-83 dihydropyrimidine dehydrogenase Homo sapiens 0-31 17097873-1 2007 Dihydropyrimidine dehydrogenase (DPD) plays a pivotal role in the metabolism of 5FU. Fluorouracil 80-83 dihydropyrimidine dehydrogenase Homo sapiens 33-36 15628771-2 2004 In the meantime, TP and DPD are a converting enzyme of 5"-DFUR to 5-FU and the major catabolic enzyme of 5-FU, respectively. Fluorouracil 105-109 dihydropyrimidine dehydrogenase Homo sapiens 24-27 15628771-7 2004 The higher TP/DPD ratio, which appears to be a predictor of 5-fluorouracil sensitivity, was observed in ovarian cancers than in normal counterparts. Fluorouracil 60-74 dihydropyrimidine dehydrogenase Homo sapiens 11-17 15547687-2 2004 The activity of the 5-fluorouracil (5-FU)-degrading enzyme dihydropyrimidine dehydrogenase (DPD) was significantly higher in the metastatic tumors than in the primary tumors. Fluorouracil 20-34 dihydropyrimidine dehydrogenase Homo sapiens 92-95 17848752-2 2007 However, little is known of the relationship between DPYD gene polymorphism and metabolism and chemotherapeutic toxicity of 5-FU in gastric carcinoma and colon carcinoma. Fluorouracil 124-128 dihydropyrimidine dehydrogenase Homo sapiens 53-57 17848752-3 2007 The present genotyping study demonstrated the relationship between DPYD gene polymorphism among 75 gastric carcinoma and colon carcinoma patients and its impact on 5-FU pharmacokinetic and side effect. Fluorouracil 164-168 dihydropyrimidine dehydrogenase Homo sapiens 67-71 17848752-10 2007 CONCLUSIONS: DPYD*5 gene mutation contribute to reduced DPYD enzyme activity and 5-FU dysmetabolism, which is associated with the accumulation of 5-FU and the chemotherapeutic toxicity in gastric carcinoma and colon carcinoma. Fluorouracil 81-85 dihydropyrimidine dehydrogenase Homo sapiens 13-17 17848752-10 2007 CONCLUSIONS: DPYD*5 gene mutation contribute to reduced DPYD enzyme activity and 5-FU dysmetabolism, which is associated with the accumulation of 5-FU and the chemotherapeutic toxicity in gastric carcinoma and colon carcinoma. Fluorouracil 146-150 dihydropyrimidine dehydrogenase Homo sapiens 13-17 17848752-10 2007 CONCLUSIONS: DPYD*5 gene mutation contribute to reduced DPYD enzyme activity and 5-FU dysmetabolism, which is associated with the accumulation of 5-FU and the chemotherapeutic toxicity in gastric carcinoma and colon carcinoma. Fluorouracil 146-150 dihydropyrimidine dehydrogenase Homo sapiens 56-60 15547687-2 2004 The activity of the 5-fluorouracil (5-FU)-degrading enzyme dihydropyrimidine dehydrogenase (DPD) was significantly higher in the metastatic tumors than in the primary tumors. Fluorouracil 36-40 dihydropyrimidine dehydrogenase Homo sapiens 92-95 15591715-1 2004 BACKGROUND: Dihydropyrimidine dehydrogenase (DPD) is the initial and rate-limiting enzyme in the metabolism of the chemotherapeutic drug 5-fluorouracil (5-FU). Fluorouracil 137-151 dihydropyrimidine dehydrogenase Homo sapiens 12-43 18846242-2 2007 While normal DPD enzyme activity is rate limiting in 5-FU catabolism, its deficiency could increase concentrations of bioavailable 5-FU anabolic products leading to 5-FU related toxicity syndrome. Fluorouracil 53-57 dihydropyrimidine dehydrogenase Homo sapiens 13-16 18846242-2 2007 While normal DPD enzyme activity is rate limiting in 5-FU catabolism, its deficiency could increase concentrations of bioavailable 5-FU anabolic products leading to 5-FU related toxicity syndrome. Fluorouracil 131-135 dihydropyrimidine dehydrogenase Homo sapiens 13-16 18846242-2 2007 While normal DPD enzyme activity is rate limiting in 5-FU catabolism, its deficiency could increase concentrations of bioavailable 5-FU anabolic products leading to 5-FU related toxicity syndrome. Fluorouracil 131-135 dihydropyrimidine dehydrogenase Homo sapiens 13-16 18846242-5 2007 RESULTS: Of 23 patients with excessive toxicities from 5-FU and/or capecitabine, 7 (30%) were DPD deficient with a median age of 66 years, M:F ratio = 1.3:1 and ethnicities included Caucasian (71%), African-American (14%) and South-Asian (14%). Fluorouracil 55-59 dihydropyrimidine dehydrogenase Homo sapiens 94-97 18846242-14 2007 Screening patients for DPD deficiency prior to administration of 5-FU or capecitabine using UraBT could potentially lower risk of toxicity. Fluorouracil 65-69 dihydropyrimidine dehydrogenase Homo sapiens 23-26 17607914-7 2007 Analysis of the expression of 5-fluorouracil (5-FU) (TS, DPD, TP)- and cisplatin (ERCC1, ERCC4, GADD45A, KU80)-related genes demonstrated an association of DPD expression with response and survival. Fluorouracil 30-44 dihydropyrimidine dehydrogenase Homo sapiens 57-60 17607914-7 2007 Analysis of the expression of 5-fluorouracil (5-FU) (TS, DPD, TP)- and cisplatin (ERCC1, ERCC4, GADD45A, KU80)-related genes demonstrated an association of DPD expression with response and survival. Fluorouracil 30-44 ERCC excision repair 4, endonuclease catalytic subunit Homo sapiens 89-94 17607914-7 2007 Analysis of the expression of 5-fluorouracil (5-FU) (TS, DPD, TP)- and cisplatin (ERCC1, ERCC4, GADD45A, KU80)-related genes demonstrated an association of DPD expression with response and survival. Fluorouracil 30-44 dihydropyrimidine dehydrogenase Homo sapiens 156-159 17607914-7 2007 Analysis of the expression of 5-fluorouracil (5-FU) (TS, DPD, TP)- and cisplatin (ERCC1, ERCC4, GADD45A, KU80)-related genes demonstrated an association of DPD expression with response and survival. Fluorouracil 46-50 dihydropyrimidine dehydrogenase Homo sapiens 156-159 17110929-5 2006 Furthermore, MDMX expression promotes resistance to the chemotherapeutic agent 5-fluorouracil (5-FU), which at low concentrations activates p53 by inducing ribosomal stress without significant DNA damage signaling. Fluorouracil 79-93 transformed mouse 3T3 cell double minute 4 Mus musculus 13-17 17110929-5 2006 Furthermore, MDMX expression promotes resistance to the chemotherapeutic agent 5-fluorouracil (5-FU), which at low concentrations activates p53 by inducing ribosomal stress without significant DNA damage signaling. Fluorouracil 95-99 transformed mouse 3T3 cell double minute 4 Mus musculus 13-17 17110929-7 2006 MDMX overexpression does not accelerate tumor growth but increases resistance to 5-FU treatment in vivo. Fluorouracil 81-85 transformed mouse 3T3 cell double minute 4 Mus musculus 0-4 17009149-3 2006 The aim of the investigation reported here was to identify which gene polymorphism is a dominant factor in FOLFOX chemotherapy-the methylenetetrahydrofolate reductase (MTHFR) gene for 5-fluorouracil or the X-ray cross-complementing1 (XRCC1) gene for oxaliplatin. Fluorouracil 184-198 methylenetetrahydrofolate reductase Homo sapiens 131-166 15591715-1 2004 BACKGROUND: Dihydropyrimidine dehydrogenase (DPD) is the initial and rate-limiting enzyme in the metabolism of the chemotherapeutic drug 5-fluorouracil (5-FU). Fluorouracil 137-151 dihydropyrimidine dehydrogenase Homo sapiens 45-48 17009149-3 2006 The aim of the investigation reported here was to identify which gene polymorphism is a dominant factor in FOLFOX chemotherapy-the methylenetetrahydrofolate reductase (MTHFR) gene for 5-fluorouracil or the X-ray cross-complementing1 (XRCC1) gene for oxaliplatin. Fluorouracil 184-198 methylenetetrahydrofolate reductase Homo sapiens 168-173 15591715-1 2004 BACKGROUND: Dihydropyrimidine dehydrogenase (DPD) is the initial and rate-limiting enzyme in the metabolism of the chemotherapeutic drug 5-fluorouracil (5-FU). Fluorouracil 153-157 dihydropyrimidine dehydrogenase Homo sapiens 12-43 15591715-1 2004 BACKGROUND: Dihydropyrimidine dehydrogenase (DPD) is the initial and rate-limiting enzyme in the metabolism of the chemotherapeutic drug 5-fluorouracil (5-FU). Fluorouracil 153-157 dihydropyrimidine dehydrogenase Homo sapiens 45-48 15492566-1 2004 OBJECTIVE: To clarify the relationship between intratumoral dihydropyrimidine dehydrogenase (DPD) expression and response to 5-fluorouracil (5-FU) liver perfusion chemotherapy (LPC) in pancreatic cancer patients, we evaluated DPD expression immunohistochemically in resected pancreatic cancer tissues. Fluorouracil 125-139 dihydropyrimidine dehydrogenase Homo sapiens 93-96 15492566-1 2004 OBJECTIVE: To clarify the relationship between intratumoral dihydropyrimidine dehydrogenase (DPD) expression and response to 5-fluorouracil (5-FU) liver perfusion chemotherapy (LPC) in pancreatic cancer patients, we evaluated DPD expression immunohistochemically in resected pancreatic cancer tissues. Fluorouracil 141-145 dihydropyrimidine dehydrogenase Homo sapiens 93-96 15492566-12 2004 CONCLUSIONS: An immunohistochemical evaluation of intratumoral DPD expression might be useful in predicting responsiveness to 5-FU-based chemotherapy in pancreatic cancer patients. Fluorouracil 126-130 dihydropyrimidine dehydrogenase Homo sapiens 63-66 15492566-13 2004 In the DPD(-) group, liver perfusion chemotherapy using 5-FU via the portal vein is effective adjuvant therapy for pancreatic cancer once pancreatectomy has been performed. Fluorouracil 56-60 dihydropyrimidine dehydrogenase Homo sapiens 7-10 15688605-2 2004 An example of a drug for which clear predictive parameters have been identified is 5-fluorouracil (5FU): its antitumor activity is limited by either a high activity of the target enzyme thymidylate synthase (TS) and/or a high activity of its degrading enzyme, dihydropyrimidine dehydrogenase (DPD). Fluorouracil 83-97 dihydropyrimidine dehydrogenase Homo sapiens 260-291 15688605-2 2004 An example of a drug for which clear predictive parameters have been identified is 5-fluorouracil (5FU): its antitumor activity is limited by either a high activity of the target enzyme thymidylate synthase (TS) and/or a high activity of its degrading enzyme, dihydropyrimidine dehydrogenase (DPD). Fluorouracil 83-97 dihydropyrimidine dehydrogenase Homo sapiens 293-296 15688605-2 2004 An example of a drug for which clear predictive parameters have been identified is 5-fluorouracil (5FU): its antitumor activity is limited by either a high activity of the target enzyme thymidylate synthase (TS) and/or a high activity of its degrading enzyme, dihydropyrimidine dehydrogenase (DPD). Fluorouracil 99-102 dihydropyrimidine dehydrogenase Homo sapiens 260-291 15308648-0 2004 UPS1 and UPS2 from Arabidopsis mediate high affinity transport of uracil and 5-fluorouracil. Fluorouracil 77-91 ureide permease 2 Arabidopsis thaliana 9-13 15308648-7 2004 A detailed analysis of the substrate specificities of two members of the AtUPS family shows that AtUPS1 and AtUPS2 mediate high affinity uracil and 5-fluorouracil (a toxic uracil analogue) transport when expressed in yeast and Xenopus oocytes. Fluorouracil 148-162 ureide permease 2 Arabidopsis thaliana 108-114 15501990-0 2004 Aberrant methylation of DPYD promoter, DPYD expression, and cellular sensitivity to 5-fluorouracil in cancer cells. Fluorouracil 84-98 dihydropyrimidine dehydrogenase Homo sapiens 24-28 15501990-1 2004 PURPOSE: Dihydropyrimidine dehydrogenase (DPD), the initial rate-limiting enzyme in the degradation of 5-fluorouracil (5-FU), is known to be a principal factor in clinical responses to the anticancer agent 5-FU, and various reports have clearly demonstrated that DPD activity is closely correlated to mRNA levels. Fluorouracil 103-117 dihydropyrimidine dehydrogenase Homo sapiens 9-40 15501990-1 2004 PURPOSE: Dihydropyrimidine dehydrogenase (DPD), the initial rate-limiting enzyme in the degradation of 5-fluorouracil (5-FU), is known to be a principal factor in clinical responses to the anticancer agent 5-FU, and various reports have clearly demonstrated that DPD activity is closely correlated to mRNA levels. Fluorouracil 103-117 dihydropyrimidine dehydrogenase Homo sapiens 42-45 15501990-1 2004 PURPOSE: Dihydropyrimidine dehydrogenase (DPD), the initial rate-limiting enzyme in the degradation of 5-fluorouracil (5-FU), is known to be a principal factor in clinical responses to the anticancer agent 5-FU, and various reports have clearly demonstrated that DPD activity is closely correlated to mRNA levels. Fluorouracil 103-117 dihydropyrimidine dehydrogenase Homo sapiens 263-266 15501990-1 2004 PURPOSE: Dihydropyrimidine dehydrogenase (DPD), the initial rate-limiting enzyme in the degradation of 5-fluorouracil (5-FU), is known to be a principal factor in clinical responses to the anticancer agent 5-FU, and various reports have clearly demonstrated that DPD activity is closely correlated to mRNA levels. Fluorouracil 119-123 dihydropyrimidine dehydrogenase Homo sapiens 9-40 15501990-1 2004 PURPOSE: Dihydropyrimidine dehydrogenase (DPD), the initial rate-limiting enzyme in the degradation of 5-fluorouracil (5-FU), is known to be a principal factor in clinical responses to the anticancer agent 5-FU, and various reports have clearly demonstrated that DPD activity is closely correlated to mRNA levels. Fluorouracil 119-123 dihydropyrimidine dehydrogenase Homo sapiens 42-45 15501990-1 2004 PURPOSE: Dihydropyrimidine dehydrogenase (DPD), the initial rate-limiting enzyme in the degradation of 5-fluorouracil (5-FU), is known to be a principal factor in clinical responses to the anticancer agent 5-FU, and various reports have clearly demonstrated that DPD activity is closely correlated to mRNA levels. Fluorouracil 119-123 dihydropyrimidine dehydrogenase Homo sapiens 263-266 15501990-1 2004 PURPOSE: Dihydropyrimidine dehydrogenase (DPD), the initial rate-limiting enzyme in the degradation of 5-fluorouracil (5-FU), is known to be a principal factor in clinical responses to the anticancer agent 5-FU, and various reports have clearly demonstrated that DPD activity is closely correlated to mRNA levels. Fluorouracil 206-210 dihydropyrimidine dehydrogenase Homo sapiens 9-40 15501990-1 2004 PURPOSE: Dihydropyrimidine dehydrogenase (DPD), the initial rate-limiting enzyme in the degradation of 5-fluorouracil (5-FU), is known to be a principal factor in clinical responses to the anticancer agent 5-FU, and various reports have clearly demonstrated that DPD activity is closely correlated to mRNA levels. Fluorouracil 206-210 dihydropyrimidine dehydrogenase Homo sapiens 42-45 15501990-1 2004 PURPOSE: Dihydropyrimidine dehydrogenase (DPD), the initial rate-limiting enzyme in the degradation of 5-fluorouracil (5-FU), is known to be a principal factor in clinical responses to the anticancer agent 5-FU, and various reports have clearly demonstrated that DPD activity is closely correlated to mRNA levels. Fluorouracil 206-210 dihydropyrimidine dehydrogenase Homo sapiens 263-266 15501990-7 2004 In HepG2, in vitro methylation of the DPYD promoter directly decreased promoter activity, and 5-azacytidine treatment restored higher DPYD expression in a dose- and time-dependent manner, along with decreased sensitivity to 5-FU. Fluorouracil 224-228 dihydropyrimidine dehydrogenase Homo sapiens 38-42 15501990-8 2004 CONCLUSIONS: We found that DPD activity was controlled, at least in part, at the transcription level of DPYD and that aberrant methylation of the DPYD promoter region acted as one of the repressors of DPYD expression and affected sensitivity to 5-FU in cancer cells. Fluorouracil 245-249 dihydropyrimidine dehydrogenase Homo sapiens 27-30 15501990-8 2004 CONCLUSIONS: We found that DPD activity was controlled, at least in part, at the transcription level of DPYD and that aberrant methylation of the DPYD promoter region acted as one of the repressors of DPYD expression and affected sensitivity to 5-FU in cancer cells. Fluorouracil 245-249 dihydropyrimidine dehydrogenase Homo sapiens 146-150 15501990-8 2004 CONCLUSIONS: We found that DPD activity was controlled, at least in part, at the transcription level of DPYD and that aberrant methylation of the DPYD promoter region acted as one of the repressors of DPYD expression and affected sensitivity to 5-FU in cancer cells. Fluorouracil 245-249 dihydropyrimidine dehydrogenase Homo sapiens 146-150 15365072-1 2004 PURPOSE: To determine whether deleted in colon cancer (DCC) protein expression in colorectal cancer (CRC) metastases could predict outcome to palliative fluorouracil (FU)-based chemotherapy and to assess whether it is similar to that observed in the corresponding primary tumors. Fluorouracil 153-165 DCC netrin 1 receptor Homo sapiens 55-58 15142874-3 2004 Bone marrow (BM) from 5-fluorouracil (5FU)-treated BtkTec(-/-) mice was transduced with a retroviral vector expressing human Btk and transplanted into BtkTec(-/-) recipients. Fluorouracil 22-36 Bruton tyrosine kinase Homo sapiens 51-54 15142874-3 2004 Bone marrow (BM) from 5-fluorouracil (5FU)-treated BtkTec(-/-) mice was transduced with a retroviral vector expressing human Btk and transplanted into BtkTec(-/-) recipients. Fluorouracil 38-41 Bruton tyrosine kinase Homo sapiens 51-54 15301724-0 2004 [Relationship of methylenetetrahydrofolate reductase C677T polymorphism and chemosensitivity to 5-fluorouracil in gastric carcinoma]. Fluorouracil 96-110 methylenetetrahydrofolate reductase Homo sapiens 17-52 15301724-1 2004 BACKGROUND & OBJECTIVE: Methylenetrahydrofolate reductase (MTHFR) C677T polymorphism modifies enzyme activity and thus effects the level of 5, 10-methylenetetrahydrofolate (5,10-MTHR), which correlates with the tumor response to 5-fluorouracil (5-FU). Fluorouracil 233-247 methylenetetrahydrofolate reductase Homo sapiens 28-61 15301724-1 2004 BACKGROUND & OBJECTIVE: Methylenetrahydrofolate reductase (MTHFR) C677T polymorphism modifies enzyme activity and thus effects the level of 5, 10-methylenetetrahydrofolate (5,10-MTHR), which correlates with the tumor response to 5-fluorouracil (5-FU). Fluorouracil 233-247 methylenetetrahydrofolate reductase Homo sapiens 63-68 15301724-1 2004 BACKGROUND & OBJECTIVE: Methylenetrahydrofolate reductase (MTHFR) C677T polymorphism modifies enzyme activity and thus effects the level of 5, 10-methylenetetrahydrofolate (5,10-MTHR), which correlates with the tumor response to 5-fluorouracil (5-FU). Fluorouracil 249-253 methylenetetrahydrofolate reductase Homo sapiens 28-61 15301724-1 2004 BACKGROUND & OBJECTIVE: Methylenetrahydrofolate reductase (MTHFR) C677T polymorphism modifies enzyme activity and thus effects the level of 5, 10-methylenetetrahydrofolate (5,10-MTHR), which correlates with the tumor response to 5-fluorouracil (5-FU). Fluorouracil 249-253 methylenetetrahydrofolate reductase Homo sapiens 63-68 15301724-2 2004 This study was to evaluate the effect of MTHFR C677T polymorphism on chemosensitivity and toxicity to 5-FU in patients with gastric carcinoma. Fluorouracil 102-106 methylenetetrahydrofolate reductase Homo sapiens 41-46 15330198-11 2004 While no relationship between 5-FU chemosensitivity and TS genotype or mRNA expression was observed, cases with high DPD mRNA expression were resistant to 5-FU and exhibited poor survival outcomes. Fluorouracil 155-159 dihydropyrimidine dehydrogenase Homo sapiens 117-120 15330204-0 2004 Expression of dihydropyrimidine dehydrogenase in cancer cells but not in stromal cells predicts the efficacy of fluorouracil treatment in patients with gastric carcinoma. Fluorouracil 112-124 dihydropyrimidine dehydrogenase Homo sapiens 14-45 15493835-7 2004 SAA markedly potentiated the cytotoxicity of 5-FU and mitomycin C in KB cells as well as the cytotoxicity of MTX in human hepatoma BEL-7402 cells. Fluorouracil 45-49 serum amyloid A1 cluster Homo sapiens 0-3 17241513-5 2006 Dihydropyrimidine dehydrogenase is prone to marked circadian rhythms, drug-drug interactions, and genetic polymorphisms; influence of its erratic activity on 5-FU pharmacokinetics and toxicity profile has been extensively investigated, and it is now well known that DPD deficiency leads to severe toxicities with 5-FU or possibly capecitabine exposure. Fluorouracil 313-317 dihydropyrimidine dehydrogenase Homo sapiens 0-31 15217955-0 2004 Metabotropic glutamate receptor 4-mediated 5-Fluorouracil resistance in a human colon cancer cell line. Fluorouracil 43-57 glutamate metabotropic receptor 4 Homo sapiens 0-33 15217955-6 2004 RESULTS: 5-FU-resistant human colon cancer cells were found to overexpress metabotropic glutamate receptor 4 (mGluR4). Fluorouracil 9-13 glutamate metabotropic receptor 4 Homo sapiens 75-108 15217955-7 2004 Other experiments showed cellular resistance to 5-FU (i.e., cell survival) was altered by the mGluR4 agonist l-2-amino-4-phosphonobutyric acid (L-AP 4), and by the mGluR4 antagonist (S)-amino-2-methyl-4-phosphonobutanoic acid (MAP 4), in that L-AP 4 increased 5-FU resistance in SNU-769A cells, whereas MAP 4 ablated 5-FU resistance in 5-FU-resistant cells. Fluorouracil 48-52 microtubule associated protein 4 Homo sapiens 227-232 15217955-7 2004 Other experiments showed cellular resistance to 5-FU (i.e., cell survival) was altered by the mGluR4 agonist l-2-amino-4-phosphonobutyric acid (L-AP 4), and by the mGluR4 antagonist (S)-amino-2-methyl-4-phosphonobutanoic acid (MAP 4), in that L-AP 4 increased 5-FU resistance in SNU-769A cells, whereas MAP 4 ablated 5-FU resistance in 5-FU-resistant cells. Fluorouracil 48-52 microtubule associated protein 4 Homo sapiens 303-308 15162350-3 2004 METHODS: The expression of IL-18 was analyzed by reverse transcriptase-polymerase chain reaction, Western blot, and ELISA in untreated and 5-fluorouracil (5-FU)-treated HNSCC cell lines. Fluorouracil 139-153 interleukin 18 Homo sapiens 27-32 15162350-3 2004 METHODS: The expression of IL-18 was analyzed by reverse transcriptase-polymerase chain reaction, Western blot, and ELISA in untreated and 5-fluorouracil (5-FU)-treated HNSCC cell lines. Fluorouracil 155-159 interleukin 18 Homo sapiens 27-32 15162350-7 2004 After exposure to 5-FU, the processed form of IL-18 was detected in the supernatants of both HNSCC cell lines. Fluorouracil 18-22 interleukin 18 Homo sapiens 46-51 15274386-0 2004 5FU and oxaliplatin-containing chemotherapy in two dihydropyrimidine dehydrogenase-deficient patients. Fluorouracil 0-3 dihydropyrimidine dehydrogenase Homo sapiens 51-82 15274386-1 2004 Patients with a germline mutation leading to a deficiency of the dihydropyrimidine dehydrogenase (DPD) enzyme are at risk from developing severe toxicity on the administration of 5FU-containing chemotherapy. Fluorouracil 179-182 dihydropyrimidine dehydrogenase Homo sapiens 98-101 15060742-1 2004 PURPOSE: Expression of thymidylate synthase (TS) and the 5-fluorouracil (5-FU) metabolic enzymes, including dihydropyrimidine dehydrogenase (DPD), orotate phosphoribosyl transferase (OPRT), thymidine phosphorylase (TP), and uridine phosphorylase (UP), has been reported to be associated with the sensitivity to 5-FU-based chemotherapy in colorectal cancer. Fluorouracil 73-77 dihydropyrimidine dehydrogenase Homo sapiens 108-139 15132136-2 2004 Over 80% of the 5-FU administered is metabolized by dihydropyrimidine dehydrogenase (DPD) in the liver. Fluorouracil 16-20 dihydropyrimidine dehydrogenase Homo sapiens 85-88 14726695-6 2004 It was found that overexpression of ZNRD1 could sensitize SGC7901 cells to P-glycoprotein (P-gp)-related anticancer drugs (vincristine, adriamycin, etoposide) but not to P-gp-nonrelated drugs (5-fluorouracil and cisplatin), which was accompanied with significantly decreased adriamycin accumulation and retention and increased adriamycin releasing in SGC7901 cells. Fluorouracil 193-207 RNA polymerase I subunit H Homo sapiens 36-41 15084981-5 2004 It is reported that uracil phosphoribosyl transferase (UPRT) overcomes 5-FU resistance. Fluorouracil 71-75 uracil phosphoribosyltransferase homolog Homo sapiens 55-59 15017333-1 2004 PURPOSE: Dihydropyrimidine dehydrogenase is a critical enzyme in the catabolism of 5-Fluorouracil, a drug frequently used in cancer therapy. Fluorouracil 83-97 dihydropyrimidine dehydrogenase Homo sapiens 9-40 17212138-2 2006 TS-1 contains CDHP, which inhibits DPD activity and maintains a high blood concentration of 5-FU. Fluorouracil 92-96 cadherin 3 Homo sapiens 14-18 17108726-4 2006 PURPOSE: This study was designed to investigate the effect of OPRT, DPD and TS in sensitivity to 5-FU. Fluorouracil 97-101 dihydropyrimidine dehydrogenase Homo sapiens 68-71 17108726-9 2006 In contrast, there was a significant inverse correlation (r=-0.738) between DPD activity and 5-FU sensitivity. Fluorouracil 93-97 dihydropyrimidine dehydrogenase Homo sapiens 76-79 17108726-11 2006 CONCLUSION: Though measuring OPRT, DPD, TS activities is valuable for prediction of sensitivity to 5-FU, DPD is considered to be the most important predictive factor of 5-FU sensitivity. Fluorouracil 169-173 dihydropyrimidine dehydrogenase Homo sapiens 105-108 17121937-0 2006 Clinical relevance of different dihydropyrimidine dehydrogenase gene single nucleotide polymorphisms on 5-fluorouracil tolerance. Fluorouracil 104-118 dihydropyrimidine dehydrogenase Homo sapiens 32-63 17121937-1 2006 PURPOSE: Although single nucleotide polymorphisms (SNP) of the dihydropyrimidine dehydrogenase gene (DPYD) have been reported, which affect enzyme activity and the severity of 5-fluorouracil (5-FU) toxicity, no pretherapeutic detection has thus far been developed. Fluorouracil 176-190 dihydropyrimidine dehydrogenase Homo sapiens 63-94 17121937-1 2006 PURPOSE: Although single nucleotide polymorphisms (SNP) of the dihydropyrimidine dehydrogenase gene (DPYD) have been reported, which affect enzyme activity and the severity of 5-fluorouracil (5-FU) toxicity, no pretherapeutic detection has thus far been developed. Fluorouracil 176-190 dihydropyrimidine dehydrogenase Homo sapiens 101-105 17121937-1 2006 PURPOSE: Although single nucleotide polymorphisms (SNP) of the dihydropyrimidine dehydrogenase gene (DPYD) have been reported, which affect enzyme activity and the severity of 5-fluorouracil (5-FU) toxicity, no pretherapeutic detection has thus far been developed. Fluorouracil 192-196 dihydropyrimidine dehydrogenase Homo sapiens 63-94 17121937-1 2006 PURPOSE: Although single nucleotide polymorphisms (SNP) of the dihydropyrimidine dehydrogenase gene (DPYD) have been reported, which affect enzyme activity and the severity of 5-fluorouracil (5-FU) toxicity, no pretherapeutic detection has thus far been developed. Fluorouracil 192-196 dihydropyrimidine dehydrogenase Homo sapiens 101-105 15017333-2 2004 Patients with deficient dihydropyrimidine dehydrogenase activity are at risk of developing severe 5-Fluorouracil-associated toxicity. Fluorouracil 98-112 dihydropyrimidine dehydrogenase Homo sapiens 24-55 15017333-4 2004 METHODS: We evaluated the frequency of mutations in exon 14 of dihydropyrimidine dehydrogenase (DPYD) gene in 73 unselected colorectal cancer patients treated with 5-Fluorouracil after surgery at a Portuguese Cancer Institute. Fluorouracil 164-178 dihydropyrimidine dehydrogenase Homo sapiens 63-94 15017333-4 2004 METHODS: We evaluated the frequency of mutations in exon 14 of dihydropyrimidine dehydrogenase (DPYD) gene in 73 unselected colorectal cancer patients treated with 5-Fluorouracil after surgery at a Portuguese Cancer Institute. Fluorouracil 164-178 dihydropyrimidine dehydrogenase Homo sapiens 96-100 15017333-7 2004 CONCLUSION: We conclude that mutations in exon 14 of DPYD gene are responsible for a significant proportion of life-threatening toxicity to 5-Fluorouracil, and should therefore be excluded before its administration to cancer patients. Fluorouracil 140-154 dihydropyrimidine dehydrogenase Homo sapiens 53-57 14744539-8 2004 In conclusion, tumor DPD level is an efficacious marker in oral 5-FU based-adjuvant chemotherapy for colorectal cancer; however, low tumor DPD predicts reduced survival in patients treated with curative surgery alone. Fluorouracil 64-68 dihydropyrimidine dehydrogenase Homo sapiens 21-24 17016579-3 2006 We present a colon cancer patient with the UGT1A1 polymorphism (UGT1A1 *28) as a known high risk for irinotecan, who was treated with a combination of doxifluridine and irinotecan for peritoneal dissemination resulting in stable disease for 2 years without adverse reactions, although the patient initially developed severe adverse effects to the combination of the protracted venous infusion of 5-FU and irinotecan. Fluorouracil 396-400 UDP glucuronosyltransferase family 1 member A1 Homo sapiens 43-49 17016579-3 2006 We present a colon cancer patient with the UGT1A1 polymorphism (UGT1A1 *28) as a known high risk for irinotecan, who was treated with a combination of doxifluridine and irinotecan for peritoneal dissemination resulting in stable disease for 2 years without adverse reactions, although the patient initially developed severe adverse effects to the combination of the protracted venous infusion of 5-FU and irinotecan. Fluorouracil 396-400 UDP glucuronosyltransferase family 1 member A1 Homo sapiens 64-70 17015056-1 2006 BACKGROUND AND OBJECTIVES: Dihydropyrimidine dehydrogenase (DPD) plays a key role in the catabolism of 5-fluorouracil (5-FU) to 5-fluoro-5,6-dihydrouracil (5-FDHU), and as such, an impairment of DPD has been recognized as an important factor for altered 5-FU and 5-FDHU pharmacokinetics, predisposing patients to the development of severe 5-FU-associated toxicity. Fluorouracil 103-117 dihydropyrimidine dehydrogenase Homo sapiens 27-58 17015056-1 2006 BACKGROUND AND OBJECTIVES: Dihydropyrimidine dehydrogenase (DPD) plays a key role in the catabolism of 5-fluorouracil (5-FU) to 5-fluoro-5,6-dihydrouracil (5-FDHU), and as such, an impairment of DPD has been recognized as an important factor for altered 5-FU and 5-FDHU pharmacokinetics, predisposing patients to the development of severe 5-FU-associated toxicity. Fluorouracil 103-117 dihydropyrimidine dehydrogenase Homo sapiens 60-63 17015056-1 2006 BACKGROUND AND OBJECTIVES: Dihydropyrimidine dehydrogenase (DPD) plays a key role in the catabolism of 5-fluorouracil (5-FU) to 5-fluoro-5,6-dihydrouracil (5-FDHU), and as such, an impairment of DPD has been recognized as an important factor for altered 5-FU and 5-FDHU pharmacokinetics, predisposing patients to the development of severe 5-FU-associated toxicity. Fluorouracil 103-117 dihydropyrimidine dehydrogenase Homo sapiens 195-198 17015056-1 2006 BACKGROUND AND OBJECTIVES: Dihydropyrimidine dehydrogenase (DPD) plays a key role in the catabolism of 5-fluorouracil (5-FU) to 5-fluoro-5,6-dihydrouracil (5-FDHU), and as such, an impairment of DPD has been recognized as an important factor for altered 5-FU and 5-FDHU pharmacokinetics, predisposing patients to the development of severe 5-FU-associated toxicity. Fluorouracil 119-123 dihydropyrimidine dehydrogenase Homo sapiens 27-58 17015056-1 2006 BACKGROUND AND OBJECTIVES: Dihydropyrimidine dehydrogenase (DPD) plays a key role in the catabolism of 5-fluorouracil (5-FU) to 5-fluoro-5,6-dihydrouracil (5-FDHU), and as such, an impairment of DPD has been recognized as an important factor for altered 5-FU and 5-FDHU pharmacokinetics, predisposing patients to the development of severe 5-FU-associated toxicity. Fluorouracil 119-123 dihydropyrimidine dehydrogenase Homo sapiens 60-63 17015056-1 2006 BACKGROUND AND OBJECTIVES: Dihydropyrimidine dehydrogenase (DPD) plays a key role in the catabolism of 5-fluorouracil (5-FU) to 5-fluoro-5,6-dihydrouracil (5-FDHU), and as such, an impairment of DPD has been recognized as an important factor for altered 5-FU and 5-FDHU pharmacokinetics, predisposing patients to the development of severe 5-FU-associated toxicity. Fluorouracil 119-123 dihydropyrimidine dehydrogenase Homo sapiens 195-198 14614573-1 2004 PURPOSE: The aim of this study was to investigate the changes in two of the enzymes involved in fluorouracil metabolism, thymidine phosphorylase (TP) and dihydropyrimidine dehydrogenase (DPD), in uterine cervical squamous cell cancer tissue after radiotherapy. Fluorouracil 96-108 dihydropyrimidine dehydrogenase Homo sapiens 154-185 14614573-1 2004 PURPOSE: The aim of this study was to investigate the changes in two of the enzymes involved in fluorouracil metabolism, thymidine phosphorylase (TP) and dihydropyrimidine dehydrogenase (DPD), in uterine cervical squamous cell cancer tissue after radiotherapy. Fluorouracil 96-108 dihydropyrimidine dehydrogenase Homo sapiens 187-190 15025795-0 2004 Dihydropyrimidine dehydrogenase and thymidylate synthase polymorphisms and their association with 5-fluorouracil/leucovorin chemotherapy in colorectal cancer. Fluorouracil 98-112 dihydropyrimidine dehydrogenase Homo sapiens 0-31 14735204-0 2004 Thymidylate synthase and methylenetetrahydrofolate reductase gene polymorphisms: relationships with 5-fluorouracil sensitivity. Fluorouracil 100-114 methylenetetrahydrofolate reductase Homo sapiens 25-60 14735204-1 2004 The relationship of thymidylate synthase (TS) and methylenetetrahydrofolate reductase (MTHFR) gene polymorphisms on 5-fluorouracil (FU) sensitivity was tested on 19 human cancer cell lines (head and neck, breast, digestive tract) in the absence and presence of folinic acid (FA) supplementation. Fluorouracil 116-130 methylenetetrahydrofolate reductase Homo sapiens 87-92 15077928-0 2004 K562 cell sensitization to 5-fluorouracil- or interferon-alpha-induced apoptosis via cordycepin (3"-deoxyadenosine): fine control of cell apoptosis via poly(A) polymerase upregulation. Fluorouracil 27-41 poly(A) polymerase alpha Homo sapiens 152-170 17000684-3 2006 Dihydropyrimidine dehydrogenase (DPD), the initial and rate-limiting enzyme of 5-FU catabolism, has previously been shown to have significant interpatient variability in activity. Fluorouracil 79-83 dihydropyrimidine dehydrogenase Homo sapiens 0-31 17000684-3 2006 Dihydropyrimidine dehydrogenase (DPD), the initial and rate-limiting enzyme of 5-FU catabolism, has previously been shown to have significant interpatient variability in activity. Fluorouracil 79-83 dihydropyrimidine dehydrogenase Homo sapiens 33-36 17000684-4 2006 Several studies have linked reduced DPD activity to the development of 5-FU toxicity. Fluorouracil 71-75 dihydropyrimidine dehydrogenase Homo sapiens 36-39 17000684-10 2006 CONCLUSION: These results indicate that African-Americans, particularly African-American women, have significantly reduced DPD enzyme activity compared with Caucasians, which may predispose this population to more 5-FU toxicity. Fluorouracil 214-218 dihydropyrimidine dehydrogenase Homo sapiens 123-126 16951168-5 2006 dose of the thymidylate synthase inhibitor 5-fluorouracil (5-FU; 165 mg/kg) and imaged by [(18)F]FLT-PET at 1 to 2 hours after treatment. Fluorouracil 43-57 thymidylate synthase Mus musculus 12-32 16951168-12 2006 We conclude that [(18)F]FLT-PET can be used to measure thymidylate synthase inhibition as early as 1 to 2 hours after treatment with 5-FU by a mechanism involving redistribution of nucleoside transporters to the plasma membrane. Fluorouracil 133-137 thymidylate synthase Mus musculus 55-75 14654475-6 2003 As for IFN-alpha, synergistic effects were observed when combined with 5-FU and DOX on PLC/PRF/5 cells only, whereas IFN-beta showed synergistic effects with 5-FU and CDDP on HuH7 and PLC/PRF/5 cell lines. Fluorouracil 158-162 MIR7-3 host gene Homo sapiens 175-179 13680162-1 2003 BACKGROUND/PURPOSE: Dihydropyrimidine dehydrogenase (DPD) and thymidylate synthase (TS) are key enzymes for predicting the efficacy of 5-FU in the treatment of malignant tumors. Fluorouracil 135-139 dihydropyrimidine dehydrogenase Homo sapiens 20-51 13680162-1 2003 BACKGROUND/PURPOSE: Dihydropyrimidine dehydrogenase (DPD) and thymidylate synthase (TS) are key enzymes for predicting the efficacy of 5-FU in the treatment of malignant tumors. Fluorouracil 135-139 dihydropyrimidine dehydrogenase Homo sapiens 53-56 13680162-14 2003 Some HCC patients may be good candidates for 5-FU-based chemotherapy based on measurements of tumor levels of DPD and TS. Fluorouracil 45-49 dihydropyrimidine dehydrogenase Homo sapiens 110-113 14981911-0 2003 Up-regulation in dihydropyrimidine dehydrogenase activity by raltitrexed causes antagonism in combination with 5-fluorouracil. Fluorouracil 111-125 dihydropyrimidine dehydrogenase Homo sapiens 17-48 14981911-2 2003 Further, we investigated the combined effect of raltirexed and 5-fluorouracil (5-FU) on the in vitro anti-tumor effect and its correlation to the DPD activity and mRNA level. Fluorouracil 79-83 dihydropyrimidine dehydrogenase Homo sapiens 146-149 14981911-6 2003 CONCLUSION: Raltitrexed may up-regulate DPD activity in tumor cells, resulting in antagonism when combined with 5-FU. Fluorouracil 112-116 dihydropyrimidine dehydrogenase Homo sapiens 40-43 12904894-1 2003 PURPOSE: Catabolism of 5-fluorouracil (5-FU) is primarily regulated by DPD. Fluorouracil 23-37 dihydropyrimidine dehydrogenase Homo sapiens 71-74 16985049-14 2006 When NC65 cells were treated with TRAIL gene therapy in combination with 5-FU, stronger growth suppression was obtained. Fluorouracil 73-77 tumor necrosis factor (ligand) superfamily, member 10 Mus musculus 34-39 16912518-1 2006 Dihydropyrimidine dehydrogenase (DPD, EC 1.3.1.2) is the initial and rate-limiting enzyme in the catabolism of the pyrimidine bases, uracil and thymine, and is also known to be the key enzyme catalyzing the metabolic degradation of the anti-cancer drug 5-fluorouracil (5-FU). Fluorouracil 253-267 dihydropyrimidine dehydrogenase Homo sapiens 0-31 16912518-1 2006 Dihydropyrimidine dehydrogenase (DPD, EC 1.3.1.2) is the initial and rate-limiting enzyme in the catabolism of the pyrimidine bases, uracil and thymine, and is also known to be the key enzyme catalyzing the metabolic degradation of the anti-cancer drug 5-fluorouracil (5-FU). Fluorouracil 253-267 dihydropyrimidine dehydrogenase Homo sapiens 33-36 16912518-1 2006 Dihydropyrimidine dehydrogenase (DPD, EC 1.3.1.2) is the initial and rate-limiting enzyme in the catabolism of the pyrimidine bases, uracil and thymine, and is also known to be the key enzyme catalyzing the metabolic degradation of the anti-cancer drug 5-fluorouracil (5-FU). Fluorouracil 269-273 dihydropyrimidine dehydrogenase Homo sapiens 0-31 16912518-1 2006 Dihydropyrimidine dehydrogenase (DPD, EC 1.3.1.2) is the initial and rate-limiting enzyme in the catabolism of the pyrimidine bases, uracil and thymine, and is also known to be the key enzyme catalyzing the metabolic degradation of the anti-cancer drug 5-fluorouracil (5-FU). Fluorouracil 269-273 dihydropyrimidine dehydrogenase Homo sapiens 33-36 16912518-3 2006 More than 85% of the administered 5-FU is catabolized by DPD. Fluorouracil 34-38 dihydropyrimidine dehydrogenase Homo sapiens 57-60 16912518-4 2006 The clinical importance of DPD has been demonstrated with the identification of severe or lethal toxicity in patients administered 5-FU who are deficient in or have low levels of DPD activity in their peripheral blood mononuclear cells (PBMC). Fluorouracil 131-135 dihydropyrimidine dehydrogenase Homo sapiens 27-30 16912518-4 2006 The clinical importance of DPD has been demonstrated with the identification of severe or lethal toxicity in patients administered 5-FU who are deficient in or have low levels of DPD activity in their peripheral blood mononuclear cells (PBMC). Fluorouracil 131-135 dihydropyrimidine dehydrogenase Homo sapiens 179-182 16799960-0 2006 TIP30 inhibits growth of HCC cell lines and inhibits HCC xenografts in mice in combination with 5-FU. Fluorouracil 96-100 HIV-1 Tat interactive protein 2 Mus musculus 0-5 16897967-9 2006 S-1 is an oral anticancer agent in capsule, in which the following 2 modulators for 5-FU are combined to FT: one is CDHP(5-chloro-2,4-dihydroxypyridine) which increases blood concentrations and enhances pharmacological actions of 5-FU by potently inhibiting the degradation of 5-FU; and another is Oxo(potassium oxonate) which is localized in the mucosa of the gastrointestinal (GI) tract after oral administration and reduces GI toxicities provoked by 5-FU. Fluorouracil 84-88 cadherin 3 Homo sapiens 116-120 16897991-4 2006 The administration of the conventional dose of S-1 including dihydropyrimidine dehydrogenase (DPD), an metabolic inhibitor of 5-FU, results in exceeding the critical plasma concentration of 5-FU, and the long-term administration with high plasma concentration of 5-FU is considered to show clinical effectiveness in head and neck cancer. Fluorouracil 126-130 dihydropyrimidine dehydrogenase Homo sapiens 94-97 16897991-4 2006 The administration of the conventional dose of S-1 including dihydropyrimidine dehydrogenase (DPD), an metabolic inhibitor of 5-FU, results in exceeding the critical plasma concentration of 5-FU, and the long-term administration with high plasma concentration of 5-FU is considered to show clinical effectiveness in head and neck cancer. Fluorouracil 190-194 dihydropyrimidine dehydrogenase Homo sapiens 94-97 16897991-4 2006 The administration of the conventional dose of S-1 including dihydropyrimidine dehydrogenase (DPD), an metabolic inhibitor of 5-FU, results in exceeding the critical plasma concentration of 5-FU, and the long-term administration with high plasma concentration of 5-FU is considered to show clinical effectiveness in head and neck cancer. Fluorouracil 190-194 dihydropyrimidine dehydrogenase Homo sapiens 94-97 12904894-1 2003 PURPOSE: Catabolism of 5-fluorouracil (5-FU) is primarily regulated by DPD. Fluorouracil 39-43 dihydropyrimidine dehydrogenase Homo sapiens 71-74 12904894-2 2003 Inactivation of DPD using eniluracil is advantageous in that it renders 5-FU orally bioavailable with more predictable pharmacokinetics and blocks one of the major potential mechanisms of 5-FU chemoresistance. Fluorouracil 72-76 dihydropyrimidine dehydrogenase Homo sapiens 16-19 16641252-3 2006 Severe toxicity from 5-fluorouracil has been attributed to a deficiency in dihydropyrimidine dehydrogenase (DPD), but currently there is no widely used genetic test for DPD deficiency. Fluorouracil 21-35 dihydropyrimidine dehydrogenase Homo sapiens 75-106 14551502-2 2003 DPD-inhibiting oral fluoropyrimidines showing promise in early clinical studies included UFT (the 5-FU prodrug, tegafur, plus the DPD substrate, uracil), eniluracil (an irreversible DPD inhibitor that improves the oral bioavailability of 5-FU) and S-1 (tegafur plus a reversible DPD inhibitor, 5-chloro-2,4-dihydroxypyridine, and oxonic acid). Fluorouracil 238-242 dihydropyrimidine dehydrogenase Homo sapiens 0-3 16641252-3 2006 Severe toxicity from 5-fluorouracil has been attributed to a deficiency in dihydropyrimidine dehydrogenase (DPD), but currently there is no widely used genetic test for DPD deficiency. Fluorouracil 21-35 dihydropyrimidine dehydrogenase Homo sapiens 108-111 12967482-8 2003 Further, combination treatment inhibited DPD activity, as well as DPD protein and mRNA expression, more strongly than did treatment with 5-FU or EGF alone. Fluorouracil 137-141 dihydropyrimidine dehydrogenase Homo sapiens 66-69 12967482-10 2003 The above findings indicate that 5-FU and EGF act synergistically in suppressing DPD activity and that the use of 5-FU against tumors in which EGF plays an important role would maximize the potential of 5-FU as an anticancer drug. Fluorouracil 33-37 dihydropyrimidine dehydrogenase Homo sapiens 81-84 14614330-0 2003 Apoptotic response to 5-fluorouracil treatment is mediated by reduced polyamines, non-autocrine Fas ligand and induced tumor necrosis factor receptor 2. Fluorouracil 22-36 TNF receptor superfamily member 1B Homo sapiens 119-151 14614330-9 2003 Our combination of gene expression profiling and corroborative functional studies revealed that reduced polyamine levels, non-autocrine FasL originating exogenous to tumor cells, and induced TNFR2 are all functional mediators of apoptosis caused by 5-FU in colon carcinoma cells. Fluorouracil 249-253 TNF receptor superfamily member 1B Homo sapiens 191-196 12883718-1 2003 Dihydropyrimidine dehydrogenase (DPD) is the rate-limiting enzyme in 5-fluorouracil (5-FU) catabolism. Fluorouracil 69-83 dihydropyrimidine dehydrogenase Homo sapiens 0-31 12883718-1 2003 Dihydropyrimidine dehydrogenase (DPD) is the rate-limiting enzyme in 5-fluorouracil (5-FU) catabolism. Fluorouracil 69-83 dihydropyrimidine dehydrogenase Homo sapiens 33-36 12883718-1 2003 Dihydropyrimidine dehydrogenase (DPD) is the rate-limiting enzyme in 5-fluorouracil (5-FU) catabolism. Fluorouracil 85-89 dihydropyrimidine dehydrogenase Homo sapiens 0-31 12883718-1 2003 Dihydropyrimidine dehydrogenase (DPD) is the rate-limiting enzyme in 5-fluorouracil (5-FU) catabolism. Fluorouracil 85-89 dihydropyrimidine dehydrogenase Homo sapiens 33-36 12883718-3 2003 Two enzymes, DPD and TS, have been reported to be major determinants of individual sensitivity to 5-FU, and it has been reported that TS mRNA levels are modified by 5-FU treatment. Fluorouracil 98-102 dihydropyrimidine dehydrogenase Homo sapiens 13-16 12883718-3 2003 Two enzymes, DPD and TS, have been reported to be major determinants of individual sensitivity to 5-FU, and it has been reported that TS mRNA levels are modified by 5-FU treatment. Fluorouracil 165-169 dihydropyrimidine dehydrogenase Homo sapiens 13-16 12853891-1 2003 TS-1 contains tegaful (FT), 5-chloro-2,4-dihydroxypyridine (CDHP; an inhibitor of 5-fluorouracil (5-FU) degradation) and potassium oxonate (Oxo; an inhibitor of 5-FU assimilation mainly in the digestive tract) in a molar ratio of 1:0.4:1. Fluorouracil 161-165 Trichinella spiralis resistance 1 Mus musculus 0-4 12792736-1 2003 Dihydropyrimidine dehydrogenase (DPD) is the first and rate-limiting enzyme in the catabolism of 5-fluorouracil (5-FU). Fluorouracil 97-111 dihydropyrimidine dehydrogenase Homo sapiens 0-31 12792736-1 2003 Dihydropyrimidine dehydrogenase (DPD) is the first and rate-limiting enzyme in the catabolism of 5-fluorouracil (5-FU). Fluorouracil 97-111 dihydropyrimidine dehydrogenase Homo sapiens 33-36 12792736-1 2003 Dihydropyrimidine dehydrogenase (DPD) is the first and rate-limiting enzyme in the catabolism of 5-fluorouracil (5-FU). Fluorouracil 113-117 dihydropyrimidine dehydrogenase Homo sapiens 0-31 12792736-1 2003 Dihydropyrimidine dehydrogenase (DPD) is the first and rate-limiting enzyme in the catabolism of 5-fluorouracil (5-FU). Fluorouracil 113-117 dihydropyrimidine dehydrogenase Homo sapiens 33-36 12792736-2 2003 DPD activity in tumor tissue may consequently serve as a predictive factor for sensitivity to 5-FU. Fluorouracil 94-98 dihydropyrimidine dehydrogenase Homo sapiens 0-3 12852985-1 2003 UNLABELLED: Dihydropyrimidine dehydrogenase (DPD) is the rate limiting enzyme of 5-fluoro-uracil (5-FU) catabolism. Fluorouracil 81-96 dihydropyrimidine dehydrogenase Homo sapiens 12-43 12852985-1 2003 UNLABELLED: Dihydropyrimidine dehydrogenase (DPD) is the rate limiting enzyme of 5-fluoro-uracil (5-FU) catabolism. Fluorouracil 81-96 dihydropyrimidine dehydrogenase Homo sapiens 45-48 12852985-1 2003 UNLABELLED: Dihydropyrimidine dehydrogenase (DPD) is the rate limiting enzyme of 5-fluoro-uracil (5-FU) catabolism. Fluorouracil 98-102 dihydropyrimidine dehydrogenase Homo sapiens 12-43 12852985-1 2003 UNLABELLED: Dihydropyrimidine dehydrogenase (DPD) is the rate limiting enzyme of 5-fluoro-uracil (5-FU) catabolism. Fluorouracil 98-102 dihydropyrimidine dehydrogenase Homo sapiens 45-48 12852985-5 2003 PURPOSE: Titrate DPD activity in oral mucosa in healthy subjects, in oral mucosa which is the target of 5-FU, at 10:00 and midnight could help to understand toxicities in patients. Fluorouracil 104-108 dihydropyrimidine dehydrogenase Homo sapiens 17-20 12795105-4 2003 We thought that the continuous elevation of serum 5-FU concentration, due to the accumulation of DPD inhibitor from the renal dysfunction, led to the development of HFS, although the participation of 5-FU metabolites such as F-beta-alanine cannot be ruled out. Fluorouracil 50-54 dihydropyrimidine dehydrogenase Homo sapiens 97-100 12820392-2 2003 Previously, we reported that adenoviral transduction of the Escherichia coli (E. coli) uracil phosphoribosyltransferase (UPRT) gene induced marked sensitivity in human colon cancer cells to 5-FU. Fluorouracil 190-194 uracil phosphoribosyltransferase homolog Homo sapiens 121-125 12775023-1 2003 BACKGROUND: Dihydropyrimidine dehydrogenase (DPD) is an enzyme that catabolizes 5-fluorouracil (5-FU). Fluorouracil 80-94 dihydropyrimidine dehydrogenase Homo sapiens 12-43 12775023-1 2003 BACKGROUND: Dihydropyrimidine dehydrogenase (DPD) is an enzyme that catabolizes 5-fluorouracil (5-FU). Fluorouracil 80-94 dihydropyrimidine dehydrogenase Homo sapiens 45-48 12775023-1 2003 BACKGROUND: Dihydropyrimidine dehydrogenase (DPD) is an enzyme that catabolizes 5-fluorouracil (5-FU). Fluorouracil 96-100 dihydropyrimidine dehydrogenase Homo sapiens 12-43 12775023-1 2003 BACKGROUND: Dihydropyrimidine dehydrogenase (DPD) is an enzyme that catabolizes 5-fluorouracil (5-FU). Fluorouracil 96-100 dihydropyrimidine dehydrogenase Homo sapiens 45-48 12775024-8 2003 However, a weak inverse correlation was found between DPD activity and sensitivity to 5-FU. Fluorouracil 86-90 dihydropyrimidine dehydrogenase Homo sapiens 54-57 12775024-9 2003 High DPD activity in tumor resulted in poor prognosis, especially in patients who received 5-FU-based adjuvant chemotherapy. Fluorouracil 91-95 dihydropyrimidine dehydrogenase Homo sapiens 5-8 12775024-14 2003 CONCLUSION: DPD is considered to be a most important predictive factor of 5-FU sensitivity. Fluorouracil 74-78 dihydropyrimidine dehydrogenase Homo sapiens 12-15 16866026-1 2006 Methylenetetrahydrofolate reductase (MTHFR) C677T polymorphism may influence the chemosensitivity of colorectal cancers to fluorouracil (5-FU) by increasing intracellular 5,10-methylenetetrahydrofolate. Fluorouracil 123-135 methylenetetrahydrofolate reductase Homo sapiens 0-35 15361639-0 2003 Phase II clinical trial of 5-fluorouracil, trimetrexate, and leucovorin (NFL) in patients with advanced pancreatic cancer. Fluorouracil 27-41 neurofilament light chain Homo sapiens 73-76 16866026-1 2006 Methylenetetrahydrofolate reductase (MTHFR) C677T polymorphism may influence the chemosensitivity of colorectal cancers to fluorouracil (5-FU) by increasing intracellular 5,10-methylenetetrahydrofolate. Fluorouracil 123-135 methylenetetrahydrofolate reductase Homo sapiens 37-42 16866026-1 2006 Methylenetetrahydrofolate reductase (MTHFR) C677T polymorphism may influence the chemosensitivity of colorectal cancers to fluorouracil (5-FU) by increasing intracellular 5,10-methylenetetrahydrofolate. Fluorouracil 137-141 methylenetetrahydrofolate reductase Homo sapiens 0-35 16866026-1 2006 Methylenetetrahydrofolate reductase (MTHFR) C677T polymorphism may influence the chemosensitivity of colorectal cancers to fluorouracil (5-FU) by increasing intracellular 5,10-methylenetetrahydrofolate. Fluorouracil 137-141 methylenetetrahydrofolate reductase Homo sapiens 37-42 16809149-1 2006 UNLABELLED: Thymidylate synthase (TS), dihydropyrimidine dehydrogenase (DPD), and vascular endothelial growth factor (VEGF) are associated with the effect of 5-fluorouracil (5-FU) based adjuvant chemotherapy. Fluorouracil 174-178 dihydropyrimidine dehydrogenase Homo sapiens 39-70 16809149-1 2006 UNLABELLED: Thymidylate synthase (TS), dihydropyrimidine dehydrogenase (DPD), and vascular endothelial growth factor (VEGF) are associated with the effect of 5-fluorouracil (5-FU) based adjuvant chemotherapy. Fluorouracil 174-178 dihydropyrimidine dehydrogenase Homo sapiens 72-75 16809149-11 2006 CONCLUSION: Neoadjuvant chemotherapy for primary gastric cancer with one cycle of 5-FU and cisplatin was associated with histological findings in patients with low baseline TS and DPD. Fluorouracil 82-86 dihydropyrimidine dehydrogenase Homo sapiens 180-183 12516049-2 2003 E. coli uracil phosphoribosyltransferase (UPRT) is a pyrimidine salvage enzyme that directly converts 5-FU into 5-fluorouridine monophosphate and improves the antitumoral effect of 5-FU. Fluorouracil 102-106 uracil phosphoribosyltransferase homolog Homo sapiens 8-40 16628085-2 2006 METHODS: Pancreatic carcinoma cell line SW1990 was exposed to 5-fluorouracil (5-fu) with the concentrations of 1.0 and 10 mug/mL to increase the expression of XIAP. Fluorouracil 62-76 X-linked inhibitor of apoptosis Homo sapiens 159-163 16628085-2 2006 METHODS: Pancreatic carcinoma cell line SW1990 was exposed to 5-fluorouracil (5-fu) with the concentrations of 1.0 and 10 mug/mL to increase the expression of XIAP. Fluorouracil 78-82 X-linked inhibitor of apoptosis Homo sapiens 159-163 16628085-5 2006 RESULTS: XIAP of SW1990 can be up-regulated with the chemoresistance increasing 1.5- and 4-fold after 10 and 30 days induced by 5-fu. Fluorouracil 128-132 X-linked inhibitor of apoptosis Homo sapiens 9-13 16628085-7 2006 The cells apoptosis index induced by 5-fu and gemcitabine increased greatly after XIAP is inhibited by the RNAi plasmid vectors. Fluorouracil 37-41 X-linked inhibitor of apoptosis Homo sapiens 82-86 16761622-0 2006 Plasma level of a 5-fluorouracil metabolite, fluoro-beta-alanine correlates with dihydropyrimidine dehydrogenase activity of peripheral blood mononuclear cells in 5-fluorouracil treated patients. Fluorouracil 18-32 dihydropyrimidine dehydrogenase Homo sapiens 81-112 16761622-0 2006 Plasma level of a 5-fluorouracil metabolite, fluoro-beta-alanine correlates with dihydropyrimidine dehydrogenase activity of peripheral blood mononuclear cells in 5-fluorouracil treated patients. Fluorouracil 163-177 dihydropyrimidine dehydrogenase Homo sapiens 81-112 16761622-1 2006 5-fluorouracil (5-FU) is mostly metabolized after administration, and the metabolizing enzyme, dihydropyrimidine dehydrogenase (DPD), seems to be the rate-limiting factor. Fluorouracil 0-14 dihydropyrimidine dehydrogenase Homo sapiens 95-126 16761622-1 2006 5-fluorouracil (5-FU) is mostly metabolized after administration, and the metabolizing enzyme, dihydropyrimidine dehydrogenase (DPD), seems to be the rate-limiting factor. Fluorouracil 0-14 dihydropyrimidine dehydrogenase Homo sapiens 128-131 16761622-1 2006 5-fluorouracil (5-FU) is mostly metabolized after administration, and the metabolizing enzyme, dihydropyrimidine dehydrogenase (DPD), seems to be the rate-limiting factor. Fluorouracil 16-20 dihydropyrimidine dehydrogenase Homo sapiens 128-131 16646564-1 2006 Dihydropyrimidine dehydrogenase (DPD) is the initial and rate-limiting enzyme in the catabolism of 5-fluorouracil (5-FU). Fluorouracil 99-113 dihydropyrimidine dehydrogenase Homo sapiens 0-31 16646564-1 2006 Dihydropyrimidine dehydrogenase (DPD) is the initial and rate-limiting enzyme in the catabolism of 5-fluorouracil (5-FU). Fluorouracil 99-113 dihydropyrimidine dehydrogenase Homo sapiens 33-36 16391809-1 2006 Thymidylate synthase (TS), dihydropyrimidine dehydrogenase (DPD) and thymidine phosphorylase (TP) are predictive markers for tumor response to 5-fluorouracil-based therapies. Fluorouracil 143-157 dihydropyrimidine dehydrogenase Homo sapiens 27-58 16391809-1 2006 Thymidylate synthase (TS), dihydropyrimidine dehydrogenase (DPD) and thymidine phosphorylase (TP) are predictive markers for tumor response to 5-fluorouracil-based therapies. Fluorouracil 143-157 dihydropyrimidine dehydrogenase Homo sapiens 60-63 16251201-1 2006 BACKGROUND: Thymidylate synthase (TS) and dihydropyrimidine dehydrogenase (DPD) are essential enzymes for 5-fluorouracil (5-FU) metabolism. Fluorouracil 106-120 dihydropyrimidine dehydrogenase Homo sapiens 42-73 16251201-1 2006 BACKGROUND: Thymidylate synthase (TS) and dihydropyrimidine dehydrogenase (DPD) are essential enzymes for 5-fluorouracil (5-FU) metabolism. Fluorouracil 106-120 dihydropyrimidine dehydrogenase Homo sapiens 75-78 16251201-1 2006 BACKGROUND: Thymidylate synthase (TS) and dihydropyrimidine dehydrogenase (DPD) are essential enzymes for 5-fluorouracil (5-FU) metabolism. Fluorouracil 122-126 dihydropyrimidine dehydrogenase Homo sapiens 42-73 16251201-1 2006 BACKGROUND: Thymidylate synthase (TS) and dihydropyrimidine dehydrogenase (DPD) are essential enzymes for 5-fluorouracil (5-FU) metabolism. Fluorouracil 122-126 dihydropyrimidine dehydrogenase Homo sapiens 75-78 16251201-2 2006 In patients with advanced colorectal cancer (ACRC), retrospective studies have shown that low expression levels of TS and DPD correlated with response to 5-FU. Fluorouracil 154-158 dihydropyrimidine dehydrogenase Homo sapiens 122-125 16251201-12 2006 CONCLUSIONS: Prospective selection of 5-FU/LV chemotherapy based on low TS and DPD expression in patients with ACRC did not confirm the high response rates reported in retrospective studies. Fluorouracil 38-42 dihydropyrimidine dehydrogenase Homo sapiens 79-82 16719540-4 2006 To individualise fluorouracil administration before the first dose, assessment of the individual dihydropyrimidine dehydrogenase (DPD) activity may be useful, because this genetically highly polymorphic enzyme controls approximately 80% of fluorouracil elimination. Fluorouracil 17-29 dihydropyrimidine dehydrogenase Homo sapiens 97-128 16719540-4 2006 To individualise fluorouracil administration before the first dose, assessment of the individual dihydropyrimidine dehydrogenase (DPD) activity may be useful, because this genetically highly polymorphic enzyme controls approximately 80% of fluorouracil elimination. Fluorouracil 17-29 dihydropyrimidine dehydrogenase Homo sapiens 130-133 16719540-4 2006 To individualise fluorouracil administration before the first dose, assessment of the individual dihydropyrimidine dehydrogenase (DPD) activity may be useful, because this genetically highly polymorphic enzyme controls approximately 80% of fluorouracil elimination. Fluorouracil 240-252 dihydropyrimidine dehydrogenase Homo sapiens 97-128 16719540-4 2006 To individualise fluorouracil administration before the first dose, assessment of the individual dihydropyrimidine dehydrogenase (DPD) activity may be useful, because this genetically highly polymorphic enzyme controls approximately 80% of fluorouracil elimination. Fluorouracil 240-252 dihydropyrimidine dehydrogenase Homo sapiens 130-133 16719540-5 2006 A complete or partial loss of DPD activity in 0.1 and 3-5% of Caucasians, respectively, leads to increased fluorouracil exposure and toxicity. Fluorouracil 107-119 dihydropyrimidine dehydrogenase Homo sapiens 30-33 16719540-12 2006 Whether an adaptation of the fluorouracil starting dose to the results of two DPD activity tests before fluorouracil administration a priori, and the adaptation of doses to fluorouracil exposure a posteriori is a reasonable approach to better prevent toxicity and increase efficacy, remains to be evaluated in randomised clinical studies comparing these strategies to routine clinical safety monitoring. Fluorouracil 29-41 dihydropyrimidine dehydrogenase Homo sapiens 78-81 16361556-11 2005 DISCUSSION: Methylation of the DPYD promoter region is associated with down-regulation of DPD activity in clinical samples and should be considered as a potentially important regulatory mechanism of DPD activity and basis for 5-FU toxicity in cancer patients. Fluorouracil 226-230 dihydropyrimidine dehydrogenase Homo sapiens 31-35 16361556-11 2005 DISCUSSION: Methylation of the DPYD promoter region is associated with down-regulation of DPD activity in clinical samples and should be considered as a potentially important regulatory mechanism of DPD activity and basis for 5-FU toxicity in cancer patients. Fluorouracil 226-230 dihydropyrimidine dehydrogenase Homo sapiens 90-93 16361556-11 2005 DISCUSSION: Methylation of the DPYD promoter region is associated with down-regulation of DPD activity in clinical samples and should be considered as a potentially important regulatory mechanism of DPD activity and basis for 5-FU toxicity in cancer patients. Fluorouracil 226-230 dihydropyrimidine dehydrogenase Homo sapiens 199-202 16253763-4 2005 The transport activity and mRNA expression of the facilitative glucose transporter 1 (GLUT1) were significantly decreased by 5-fluorouracil treatment, but those of PEPT1 were slightly increased. Fluorouracil 125-139 solute carrier family 2 member 1 Homo sapiens 86-91 16305582-2 2005 The activity of the first enzyme in this scheme, dihydropyrimidine dehydrogenase (DPD), is reported to be the key determinant of the cytotoxicity and side-effects of 5-fluorouracil. Fluorouracil 166-180 dihydropyrimidine dehydrogenase Homo sapiens 49-80 16305582-2 2005 The activity of the first enzyme in this scheme, dihydropyrimidine dehydrogenase (DPD), is reported to be the key determinant of the cytotoxicity and side-effects of 5-fluorouracil. Fluorouracil 166-180 dihydropyrimidine dehydrogenase Homo sapiens 82-85 12516049-2 2003 E. coli uracil phosphoribosyltransferase (UPRT) is a pyrimidine salvage enzyme that directly converts 5-FU into 5-fluorouridine monophosphate and improves the antitumoral effect of 5-FU. Fluorouracil 102-106 uracil phosphoribosyltransferase homolog Homo sapiens 42-46 12516049-2 2003 E. coli uracil phosphoribosyltransferase (UPRT) is a pyrimidine salvage enzyme that directly converts 5-FU into 5-fluorouridine monophosphate and improves the antitumoral effect of 5-FU. Fluorouracil 181-185 uracil phosphoribosyltransferase homolog Homo sapiens 8-40 12516049-2 2003 E. coli uracil phosphoribosyltransferase (UPRT) is a pyrimidine salvage enzyme that directly converts 5-FU into 5-fluorouridine monophosphate and improves the antitumoral effect of 5-FU. Fluorouracil 181-185 uracil phosphoribosyltransferase homolog Homo sapiens 42-46 12516049-5 2003 RESULTS: Cells transfected with AdCA-UPRT showed approximately 57 times lower IC50 to 5-FU compared with those transfected with AdCA-LacZ. Fluorouracil 86-90 uracil phosphoribosyltransferase homolog Homo sapiens 37-41 12616366-8 2003 CONCLUSIONS: The combined use of measurements of TS and DPD mRNA levels using real-time RT-PCR analyses may provide an indication of the selective cytoxicity of 5-FU on thymoma. Fluorouracil 161-165 dihydropyrimidine dehydrogenase Homo sapiens 56-59 12494248-1 2002 BACKGROUND: In tumor cells, the enzyme orotate phosphoribosyl transferase (OPRT) contributes to 5-fluorouracil (5-FU) phosphorylation and another enzyme, dihydropyrimidine dehydrogenase (DPD), is associated with 5-FU catabolic action. Fluorouracil 96-110 dihydropyrimidine dehydrogenase Homo sapiens 187-190 12494248-1 2002 BACKGROUND: In tumor cells, the enzyme orotate phosphoribosyl transferase (OPRT) contributes to 5-fluorouracil (5-FU) phosphorylation and another enzyme, dihydropyrimidine dehydrogenase (DPD), is associated with 5-FU catabolic action. Fluorouracil 112-116 dihydropyrimidine dehydrogenase Homo sapiens 154-185 12494248-1 2002 BACKGROUND: In tumor cells, the enzyme orotate phosphoribosyl transferase (OPRT) contributes to 5-fluorouracil (5-FU) phosphorylation and another enzyme, dihydropyrimidine dehydrogenase (DPD), is associated with 5-FU catabolic action. Fluorouracil 112-116 dihydropyrimidine dehydrogenase Homo sapiens 187-190 12494248-1 2002 BACKGROUND: In tumor cells, the enzyme orotate phosphoribosyl transferase (OPRT) contributes to 5-fluorouracil (5-FU) phosphorylation and another enzyme, dihydropyrimidine dehydrogenase (DPD), is associated with 5-FU catabolic action. Fluorouracil 212-216 dihydropyrimidine dehydrogenase Homo sapiens 154-185 12494248-1 2002 BACKGROUND: In tumor cells, the enzyme orotate phosphoribosyl transferase (OPRT) contributes to 5-fluorouracil (5-FU) phosphorylation and another enzyme, dihydropyrimidine dehydrogenase (DPD), is associated with 5-FU catabolic action. Fluorouracil 212-216 dihydropyrimidine dehydrogenase Homo sapiens 187-190 12494248-11 2002 Of the patient specimens showing OPRT activity of 0.413 or above and DPD activity of 30 or below, 88.9% were positive for 5-FU sensitivity, suggesting the possibility that the combination of these two levels may be predictive of 5-FU positive sensitivity. Fluorouracil 122-126 dihydropyrimidine dehydrogenase Homo sapiens 69-72 12494248-12 2002 CONCLUSION: DPD and OPRT activities within cancer cells may predict positive sensitivity to 5-FU. Fluorouracil 92-96 dihydropyrimidine dehydrogenase Homo sapiens 12-15 12494252-1 2002 BACKGROUND: Dihydropyrimidine dehydrogenase (DPD) activity in tumor tissues is thought to play an important role in the antitumor effect of 5-fluorouracil (FU). Fluorouracil 140-154 dihydropyrimidine dehydrogenase Homo sapiens 12-43 12494252-1 2002 BACKGROUND: Dihydropyrimidine dehydrogenase (DPD) activity in tumor tissues is thought to play an important role in the antitumor effect of 5-fluorouracil (FU). Fluorouracil 140-154 dihydropyrimidine dehydrogenase Homo sapiens 45-48 12494252-2 2002 In order to define 5-FU-resistant nonsmall-cell lung cancer, we assessed the DPD level in tumor tissues with an enzyme immunoassay. Fluorouracil 19-23 dihydropyrimidine dehydrogenase Homo sapiens 77-80 12464897-1 2002 OBJECTIVE: Thymidylate synthase (TS) is the target enzyme for 5-fluorouracil (5-FU), and dihydropyrimidine dehydrogenase (DPD) is the first enzyme that metabolizes 5-fluorouracil. Fluorouracil 62-76 dihydropyrimidine dehydrogenase Homo sapiens 89-120 12464897-1 2002 OBJECTIVE: Thymidylate synthase (TS) is the target enzyme for 5-fluorouracil (5-FU), and dihydropyrimidine dehydrogenase (DPD) is the first enzyme that metabolizes 5-fluorouracil. Fluorouracil 62-76 dihydropyrimidine dehydrogenase Homo sapiens 122-125 12464897-1 2002 OBJECTIVE: Thymidylate synthase (TS) is the target enzyme for 5-fluorouracil (5-FU), and dihydropyrimidine dehydrogenase (DPD) is the first enzyme that metabolizes 5-fluorouracil. Fluorouracil 78-82 dihydropyrimidine dehydrogenase Homo sapiens 89-120 12464897-1 2002 OBJECTIVE: Thymidylate synthase (TS) is the target enzyme for 5-fluorouracil (5-FU), and dihydropyrimidine dehydrogenase (DPD) is the first enzyme that metabolizes 5-fluorouracil. Fluorouracil 164-178 dihydropyrimidine dehydrogenase Homo sapiens 89-120 12464897-1 2002 OBJECTIVE: Thymidylate synthase (TS) is the target enzyme for 5-fluorouracil (5-FU), and dihydropyrimidine dehydrogenase (DPD) is the first enzyme that metabolizes 5-fluorouracil. Fluorouracil 164-178 dihydropyrimidine dehydrogenase Homo sapiens 122-125 12822071-1 2002 Cancer patients developing severe side effects upon chemotherapy with 5-fluorouracil (5-FU) are assumed to display reduced activity of the enzyme dihydropyrimidine dehydrogenase (DPD). Fluorouracil 70-84 dihydropyrimidine dehydrogenase Homo sapiens 146-177 12822071-1 2002 Cancer patients developing severe side effects upon chemotherapy with 5-fluorouracil (5-FU) are assumed to display reduced activity of the enzyme dihydropyrimidine dehydrogenase (DPD). Fluorouracil 70-84 dihydropyrimidine dehydrogenase Homo sapiens 179-182 12822071-1 2002 Cancer patients developing severe side effects upon chemotherapy with 5-fluorouracil (5-FU) are assumed to display reduced activity of the enzyme dihydropyrimidine dehydrogenase (DPD). Fluorouracil 86-90 dihydropyrimidine dehydrogenase Homo sapiens 146-177 12822071-1 2002 Cancer patients developing severe side effects upon chemotherapy with 5-fluorouracil (5-FU) are assumed to display reduced activity of the enzyme dihydropyrimidine dehydrogenase (DPD). Fluorouracil 86-90 dihydropyrimidine dehydrogenase Homo sapiens 179-182 12822071-5 2002 Our aim is to develop a sensitive and efficient screening of tumor patients to identify patients with mutations in the DPYD gene which might be related to 5-FU-toxicity. Fluorouracil 155-159 dihydropyrimidine dehydrogenase Homo sapiens 119-123 12552994-1 2002 Dihydropyrimidine dehydrogenase (DPD) is the initial and rate-limiting enzyme involved in the degradation of 5-FU. Fluorouracil 109-113 dihydropyrimidine dehydrogenase Homo sapiens 0-31 12552994-1 2002 Dihydropyrimidine dehydrogenase (DPD) is the initial and rate-limiting enzyme involved in the degradation of 5-FU. Fluorouracil 109-113 dihydropyrimidine dehydrogenase Homo sapiens 33-36 12552994-2 2002 DPD activity in peripheral blood mononuclear cells of 30 esophageal cancer patients treated with 5-FU and low-dose CDDP with irradiation was determined at the beginning of each cytostatic cycle, the objective being to determine if DPD activity is related to the occurrence of side-effects and responses to therapy. Fluorouracil 97-101 dihydropyrimidine dehydrogenase Homo sapiens 0-3 12552994-4 2002 5-FU-related side-effects tended to be registered more frequently in patients with low DPD activity. Fluorouracil 0-4 dihydropyrimidine dehydrogenase Homo sapiens 87-90 12352929-1 2002 This study investigated the relationship among the pharmacokinetics of 5-fluorouracil (5-FU) and 5-fluoro-5,6-dihydrouracil (5-FDHU); the activity of dihydropyrimidine dehydrogenase (DPD) in peripheral blood mononuclear cells; and treatment-related toxicity in 26 patients with surgically resected colorectal cancer treated with short daily infusions of 5-FU adjuvant chemotherapy, each cycle consisting of 5 consecutive days every 4 weeks. Fluorouracil 71-85 dihydropyrimidine dehydrogenase Homo sapiens 150-181 16302736-2 2005 Dihydropyrimidine dehydrogenase (DPD) is the major catabolic enzyme of 5-fluorouracil (5-FU). Fluorouracil 71-85 dihydropyrimidine dehydrogenase Homo sapiens 0-31 16302736-2 2005 Dihydropyrimidine dehydrogenase (DPD) is the major catabolic enzyme of 5-fluorouracil (5-FU). Fluorouracil 71-85 dihydropyrimidine dehydrogenase Homo sapiens 33-36 16302736-2 2005 Dihydropyrimidine dehydrogenase (DPD) is the major catabolic enzyme of 5-fluorouracil (5-FU). Fluorouracil 87-91 dihydropyrimidine dehydrogenase Homo sapiens 0-31 16302736-2 2005 Dihydropyrimidine dehydrogenase (DPD) is the major catabolic enzyme of 5-fluorouracil (5-FU). Fluorouracil 87-91 dihydropyrimidine dehydrogenase Homo sapiens 33-36 16302736-12 2005 CONCLUSION: The difference in DPD expressions between gastric and colorectal cancer tissues may reflect the organ specificity of the carcinomas and a difference in chemotherapeutic sensitivity to 5-FU or its analogs. Fluorouracil 196-200 dihydropyrimidine dehydrogenase Homo sapiens 30-33 16282729-6 2005 In conclusion, low TS expression followed by low DPD expression is important to predict the efficacy of 5-FU-based treatment for colorectal cancer. Fluorouracil 104-108 dihydropyrimidine dehydrogenase Homo sapiens 49-52 12352929-1 2002 This study investigated the relationship among the pharmacokinetics of 5-fluorouracil (5-FU) and 5-fluoro-5,6-dihydrouracil (5-FDHU); the activity of dihydropyrimidine dehydrogenase (DPD) in peripheral blood mononuclear cells; and treatment-related toxicity in 26 patients with surgically resected colorectal cancer treated with short daily infusions of 5-FU adjuvant chemotherapy, each cycle consisting of 5 consecutive days every 4 weeks. Fluorouracil 71-85 dihydropyrimidine dehydrogenase Homo sapiens 183-186 12352929-1 2002 This study investigated the relationship among the pharmacokinetics of 5-fluorouracil (5-FU) and 5-fluoro-5,6-dihydrouracil (5-FDHU); the activity of dihydropyrimidine dehydrogenase (DPD) in peripheral blood mononuclear cells; and treatment-related toxicity in 26 patients with surgically resected colorectal cancer treated with short daily infusions of 5-FU adjuvant chemotherapy, each cycle consisting of 5 consecutive days every 4 weeks. Fluorouracil 87-91 dihydropyrimidine dehydrogenase Homo sapiens 150-181 12352929-1 2002 This study investigated the relationship among the pharmacokinetics of 5-fluorouracil (5-FU) and 5-fluoro-5,6-dihydrouracil (5-FDHU); the activity of dihydropyrimidine dehydrogenase (DPD) in peripheral blood mononuclear cells; and treatment-related toxicity in 26 patients with surgically resected colorectal cancer treated with short daily infusions of 5-FU adjuvant chemotherapy, each cycle consisting of 5 consecutive days every 4 weeks. Fluorouracil 87-91 dihydropyrimidine dehydrogenase Homo sapiens 183-186 12378627-1 2002 AIM: Our previous studies showed increased sensitivity to 5-FU in colon cancer cell lines with microsatellite instability, and considered that mutations of TGFbeta-R II, IGF IIR, RIZ gene might enhance the potentials of cell growth and proliferation, which increased the sensitivity to 5-FU. Fluorouracil 58-62 PR/SET domain 2 Homo sapiens 179-182 12378627-1 2002 AIM: Our previous studies showed increased sensitivity to 5-FU in colon cancer cell lines with microsatellite instability, and considered that mutations of TGFbeta-R II, IGF IIR, RIZ gene might enhance the potentials of cell growth and proliferation, which increased the sensitivity to 5-FU. Fluorouracil 286-290 PR/SET domain 2 Homo sapiens 179-182 12209976-1 2002 Dihydropyrimidine dehydrogenase (DPD) is the initial and rate-limiting enzyme in the catabolism of 5-fluorouracil (5-FU), and it is suggested that patients with a partial deficiency of this enzyme are at risk of developing severe 5-FU-associated toxicity. Fluorouracil 99-113 dihydropyrimidine dehydrogenase Homo sapiens 0-31 16204693-0 2005 5-fluorouracil-based chemotherapy enhances the antitumor activity of a thymidylate synthase-directed polyepitopic peptide vaccine. Fluorouracil 0-14 thymidylate synthase Mus musculus 71-91 16204693-2 2005 Some chemotherapeutic agents, such as 5-fluorouracil (5-FU), act by inhibiting TS expression. Fluorouracil 38-52 thymidylate synthase Mus musculus 79-81 16204693-2 2005 Some chemotherapeutic agents, such as 5-fluorouracil (5-FU), act by inhibiting TS expression. Fluorouracil 54-58 thymidylate synthase Mus musculus 79-81 12209976-1 2002 Dihydropyrimidine dehydrogenase (DPD) is the initial and rate-limiting enzyme in the catabolism of 5-fluorouracil (5-FU), and it is suggested that patients with a partial deficiency of this enzyme are at risk of developing severe 5-FU-associated toxicity. Fluorouracil 99-113 dihydropyrimidine dehydrogenase Homo sapiens 33-36 12209976-1 2002 Dihydropyrimidine dehydrogenase (DPD) is the initial and rate-limiting enzyme in the catabolism of 5-fluorouracil (5-FU), and it is suggested that patients with a partial deficiency of this enzyme are at risk of developing severe 5-FU-associated toxicity. Fluorouracil 115-119 dihydropyrimidine dehydrogenase Homo sapiens 0-31 12209976-1 2002 Dihydropyrimidine dehydrogenase (DPD) is the initial and rate-limiting enzyme in the catabolism of 5-fluorouracil (5-FU), and it is suggested that patients with a partial deficiency of this enzyme are at risk of developing severe 5-FU-associated toxicity. Fluorouracil 115-119 dihydropyrimidine dehydrogenase Homo sapiens 33-36 12209976-1 2002 Dihydropyrimidine dehydrogenase (DPD) is the initial and rate-limiting enzyme in the catabolism of 5-fluorouracil (5-FU), and it is suggested that patients with a partial deficiency of this enzyme are at risk of developing severe 5-FU-associated toxicity. Fluorouracil 230-234 dihydropyrimidine dehydrogenase Homo sapiens 0-31 12209976-1 2002 Dihydropyrimidine dehydrogenase (DPD) is the initial and rate-limiting enzyme in the catabolism of 5-fluorouracil (5-FU), and it is suggested that patients with a partial deficiency of this enzyme are at risk of developing severe 5-FU-associated toxicity. Fluorouracil 230-234 dihydropyrimidine dehydrogenase Homo sapiens 33-36 12209976-7 2002 Adopting a threshold level for DPD activity of 70% of that observed in the normal population, 14% of the population is prone to the development of severe 5-FU-associated toxicity. Fluorouracil 154-158 dihydropyrimidine dehydrogenase Homo sapiens 31-34 12104082-1 2002 BACKGROUND: Dihydropyrimidine dehydrogenase (DPD) is the initial and rate-limiting enzyme in catabolism of pyrimidines including 5-fluorouracil. Fluorouracil 129-143 dihydropyrimidine dehydrogenase Homo sapiens 12-43 12104082-1 2002 BACKGROUND: Dihydropyrimidine dehydrogenase (DPD) is the initial and rate-limiting enzyme in catabolism of pyrimidines including 5-fluorouracil. Fluorouracil 129-143 dihydropyrimidine dehydrogenase Homo sapiens 45-48 12187768-8 2002 Administration of a clinical dose of 5-FU or its prodrug to poor 5-FU metabolizers may cause death unless DPD activity is determined using their peripheral blood mononuclear cells prior to the administration of the anticancer drug. Fluorouracil 37-41 dihydropyrimidine dehydrogenase Homo sapiens 106-109 12076692-2 2002 Both 5-FU and uracil (U) are catabolised by dihydropyrimidine dehydrogenase (DPD) to form dihydrofluorouracil (FUH(2)) and dihydrouracil (UH(2)), respectively. Fluorouracil 5-9 dihydropyrimidine dehydrogenase Homo sapiens 44-75 16204693-10 2005 Furthermore, treatment of these mice with 5-FU delayed or prevented the occurrence of tumors formed by inoculation with autologous (TS+)EL-4/HHD lymphoma cells. Fluorouracil 42-46 thymidylate synthase Mus musculus 132-134 16204693-11 2005 CONCLUSIONS: The multiepitopic TS/PP vaccine induces a tumor-specific immune response in mice and is especially potent when used in combination with 5-FU-based chemotherapy. Fluorouracil 149-153 thymidylate synthase Mus musculus 31-33 16012177-1 2005 BACKGROUND: The predictive value of thymidylate synthase (TS) and dihydropyrimidine dehydrogenase (DPD) expression on long-term survival by influencing 5-fluorouracil (5-FU) effect were determined in primary tumours and node metastases of stage III colon cancer patients treated adjuvantly with 5-FU regimens (n=391). Fluorouracil 152-166 dihydropyrimidine dehydrogenase Homo sapiens 66-97 16012177-1 2005 BACKGROUND: The predictive value of thymidylate synthase (TS) and dihydropyrimidine dehydrogenase (DPD) expression on long-term survival by influencing 5-fluorouracil (5-FU) effect were determined in primary tumours and node metastases of stage III colon cancer patients treated adjuvantly with 5-FU regimens (n=391). Fluorouracil 152-166 dihydropyrimidine dehydrogenase Homo sapiens 99-102 12076692-2 2002 Both 5-FU and uracil (U) are catabolised by dihydropyrimidine dehydrogenase (DPD) to form dihydrofluorouracil (FUH(2)) and dihydrouracil (UH(2)), respectively. Fluorouracil 5-9 dihydropyrimidine dehydrogenase Homo sapiens 77-80 12042667-3 2002 Since cytochrome P450 2A6 (CYP2A6) has been reported to metabolize FT to yield 5-fluorouracil (5-FU), it was postulated that the poor metabolic phenotype of patient 1 was caused by mutations of the CYP2A6 gene. Fluorouracil 79-93 cytochrome P450 family 2 subfamily A member 6 Homo sapiens 6-25 17022150-10 2005 There were significant correlations between the IC50 of CDDP and Bcl-2, BCRP, GST-pi, and between that of 5-FU and MRP 2. Fluorouracil 106-110 ATP binding cassette subfamily C member 2 Homo sapiens 115-120 15993511-7 2005 Our results indicate that degradation of 5-FU due to DPD is an important determinant in 5-FU sensitivity, while induction of TS contributes to acquired resistance against 5-FU in lung cancer. Fluorouracil 88-92 dihydropyrimidine dehydrogenase Homo sapiens 53-56 15993511-7 2005 Our results indicate that degradation of 5-FU due to DPD is an important determinant in 5-FU sensitivity, while induction of TS contributes to acquired resistance against 5-FU in lung cancer. Fluorouracil 88-92 dihydropyrimidine dehydrogenase Homo sapiens 53-56 16012767-1 2005 Thymidylate synthase (TS) and dihydropyrimidine dehydrogenase (DPD) are enzymes involved in the metabolism of 5-fluorouracil (FU). Fluorouracil 110-124 dihydropyrimidine dehydrogenase Homo sapiens 63-66 15986457-7 2005 Sodium (Na(+)) glucose co-transporter 1 (SGLT1) expressions were also moderately elevated in 5-FU-treated mice. Fluorouracil 93-97 solute carrier family 5 (sodium/glucose cotransporter), member 1 Mus musculus 8-39 15986457-7 2005 Sodium (Na(+)) glucose co-transporter 1 (SGLT1) expressions were also moderately elevated in 5-FU-treated mice. Fluorouracil 93-97 solute carrier family 5 (sodium/glucose cotransporter), member 1 Mus musculus 41-46 15986457-9 2005 These results indicate that repeated oral administration of 5-FU did not hamper, but unexpectedly induced, SGLT1 and GLUT2 expression to enhance glucose absorption. Fluorouracil 60-64 solute carrier family 5 (sodium/glucose cotransporter), member 1 Mus musculus 107-112 15817675-6 2005 However, after 5-fluorouracil (5-FU) treatment, there was a rapid increase in plasma vascular endothelial growth factor A (VEGF-A) levels and expansion of Tie2-positive neovessels. Fluorouracil 15-29 vascular endothelial growth factor A Mus musculus 85-121 15817675-6 2005 However, after 5-fluorouracil (5-FU) treatment, there was a rapid increase in plasma vascular endothelial growth factor A (VEGF-A) levels and expansion of Tie2-positive neovessels. Fluorouracil 15-29 vascular endothelial growth factor A Mus musculus 123-129 15817675-6 2005 However, after 5-fluorouracil (5-FU) treatment, there was a rapid increase in plasma vascular endothelial growth factor A (VEGF-A) levels and expansion of Tie2-positive neovessels. Fluorouracil 31-35 vascular endothelial growth factor A Mus musculus 85-121 15817675-6 2005 However, after 5-fluorouracil (5-FU) treatment, there was a rapid increase in plasma vascular endothelial growth factor A (VEGF-A) levels and expansion of Tie2-positive neovessels. Fluorouracil 31-35 vascular endothelial growth factor A Mus musculus 123-129 15994970-4 2005 At its IC50 concentration, 3-oxo-C12-(L)-HSL reduces the apparent IC50 of 5-fluorouracil (5-FU) from 1 micromol/L to 80 nmol/L (12-fold) in a colony formation assay. Fluorouracil 74-88 lipase E, hormone sensitive type Homo sapiens 41-44 15994970-4 2005 At its IC50 concentration, 3-oxo-C12-(L)-HSL reduces the apparent IC50 of 5-fluorouracil (5-FU) from 1 micromol/L to 80 nmol/L (12-fold) in a colony formation assay. Fluorouracil 90-94 lipase E, hormone sensitive type Homo sapiens 41-44 12042667-3 2002 Since cytochrome P450 2A6 (CYP2A6) has been reported to metabolize FT to yield 5-fluorouracil (5-FU), it was postulated that the poor metabolic phenotype of patient 1 was caused by mutations of the CYP2A6 gene. Fluorouracil 79-93 cytochrome P450 family 2 subfamily A member 6 Homo sapiens 27-33 12042667-3 2002 Since cytochrome P450 2A6 (CYP2A6) has been reported to metabolize FT to yield 5-fluorouracil (5-FU), it was postulated that the poor metabolic phenotype of patient 1 was caused by mutations of the CYP2A6 gene. Fluorouracil 95-99 cytochrome P450 family 2 subfamily A member 6 Homo sapiens 6-25 12042667-3 2002 Since cytochrome P450 2A6 (CYP2A6) has been reported to metabolize FT to yield 5-fluorouracil (5-FU), it was postulated that the poor metabolic phenotype of patient 1 was caused by mutations of the CYP2A6 gene. Fluorouracil 95-99 cytochrome P450 family 2 subfamily A member 6 Homo sapiens 27-33 12006517-0 2002 Impact of two weekly schedules of oral eniluracil given with fluorouracil and leucovorin on the duration of dihydropyrimidine dehydrogenase inhibition. Fluorouracil 61-73 dihydropyrimidine dehydrogenase Homo sapiens 108-139 12006555-0 2002 Correspondence re: Raida, M. et al., prevalence of a common point mutation in the dihydropyrimidine dehydrogenase (DPD) gene within the 5"-splice donor site of intron 14 in patients with severe 5-fluorouracil (5-FU)-related toxicity compared with controls. Fluorouracil 194-208 dihydropyrimidine dehydrogenase Homo sapiens 82-113 15858133-2 2005 Dihydropyrimidine dehydrogenase (DPD) is the principal enzyme involved in the catabolic detoxification of 5-fluorouracil (5FU). Fluorouracil 106-120 dihydropyrimidine dehydrogenase Homo sapiens 0-31 15858133-2 2005 Dihydropyrimidine dehydrogenase (DPD) is the principal enzyme involved in the catabolic detoxification of 5-fluorouracil (5FU). Fluorouracil 106-120 dihydropyrimidine dehydrogenase Homo sapiens 33-36 15858133-2 2005 Dihydropyrimidine dehydrogenase (DPD) is the principal enzyme involved in the catabolic detoxification of 5-fluorouracil (5FU). Fluorouracil 122-125 dihydropyrimidine dehydrogenase Homo sapiens 0-31 15858133-2 2005 Dihydropyrimidine dehydrogenase (DPD) is the principal enzyme involved in the catabolic detoxification of 5-fluorouracil (5FU). Fluorouracil 122-125 dihydropyrimidine dehydrogenase Homo sapiens 33-36 15858133-3 2005 A heterozygous G > A transition at the 5" splicing donor consensus sequence in intron 14 leading to exon 14 skipping (IVS14+1 G > A, DPYD*2A) with partial loss of enzyme activity may be partly responsible for 5FU induced toxicity, whereas irinotecan associated toxicity may in part be explained by an aberrant UGT1A1 promoter (TA)(n) genotype underlying Gilbert"s syndrome with reduced liver glucuronidation activity. Fluorouracil 215-218 UDP glucuronosyltransferase family 1 member A1 Homo sapiens 316-322 15837757-11 2005 The association of DPD expression with response and survival underlines a predominant role of DPD to predict 5-FU sensitivity. Fluorouracil 109-113 dihydropyrimidine dehydrogenase Homo sapiens 19-22 15837757-11 2005 The association of DPD expression with response and survival underlines a predominant role of DPD to predict 5-FU sensitivity. Fluorouracil 109-113 dihydropyrimidine dehydrogenase Homo sapiens 94-97 15729713-2 2005 The sensitivity of cancer cells to capecitabine, which is an oral, tumor-selective pre-prodrug of 5-fluorouracil may correlate better to the TP/DPD ratio than to levels of either enzyme alone. Fluorouracil 98-112 dihydropyrimidine dehydrogenase Homo sapiens 144-147 12006555-0 2002 Correspondence re: Raida, M. et al., prevalence of a common point mutation in the dihydropyrimidine dehydrogenase (DPD) gene within the 5"-splice donor site of intron 14 in patients with severe 5-fluorouracil (5-FU)-related toxicity compared with controls. Fluorouracil 194-208 dihydropyrimidine dehydrogenase Homo sapiens 115-118 12006555-0 2002 Correspondence re: Raida, M. et al., prevalence of a common point mutation in the dihydropyrimidine dehydrogenase (DPD) gene within the 5"-splice donor site of intron 14 in patients with severe 5-fluorouracil (5-FU)-related toxicity compared with controls. Fluorouracil 210-214 dihydropyrimidine dehydrogenase Homo sapiens 82-113 12006555-0 2002 Correspondence re: Raida, M. et al., prevalence of a common point mutation in the dihydropyrimidine dehydrogenase (DPD) gene within the 5"-splice donor site of intron 14 in patients with severe 5-fluorouracil (5-FU)-related toxicity compared with controls. Fluorouracil 210-214 dihydropyrimidine dehydrogenase Homo sapiens 115-118 15771958-7 2005 In addition, ZD55-sflt-1 showed a synergic effect with the chemotherapeutic agent 5-FU. Fluorouracil 82-86 FMS-like tyrosine kinase 1 Mus musculus 18-24 12149568-7 2002 In vivo antitumor activity of the oligonucleotide occurred in a dose-dependent manner in both models and synergistically or additive therapeutic effects of MDM2 inhibition and the cancer chemotherapeutic agents 10-hydroxycamptothecin and 5-fluorouracil were also observed. Fluorouracil 238-252 MDM2 proto-oncogene Homo sapiens 156-160 15684607-0 2005 Human pancreatic carcinoma cells secrete bioactive interleukin-18 after treatment with 5-fluorouracil: implications for anti-tumor immune response. Fluorouracil 87-101 interleukin 18 Homo sapiens 51-65 15770397-4 2005 We then evaluated the relationship between TS and DPD gene expression levels and the sensitivity of colorectal cancers to 5-FU, as determined by histoculture drug response assay (HDRA). Fluorouracil 122-126 dihydropyrimidine dehydrogenase Homo sapiens 50-53 15770397-5 2005 RESULTS: A significant increase in the TS expression score was observed in 5-FU-sensitive colorectal cancers (0.57 +/- 0.19) compared to 5-FU-resistant ones (1.16 +/- 0.98; P = 0.029), whereas no significant differences in DPD expression scores were observed in 5-FU-sensitive colorectal cancers (0.86 +/- 1.19) compared to 5-FU-resistant ones (0.56 +/- 1.05; P = 0.603). Fluorouracil 75-79 dihydropyrimidine dehydrogenase Homo sapiens 223-226 16147904-1 2005 Dihydropyrimidine dehydrogenase (DPD) is a rate-limiting enzyme of 5-fluorouracil (5-FU) catabolism. Fluorouracil 83-87 dihydropyrimidine dehydrogenase Homo sapiens 0-31 16147904-1 2005 Dihydropyrimidine dehydrogenase (DPD) is a rate-limiting enzyme of 5-fluorouracil (5-FU) catabolism. Fluorouracil 83-87 dihydropyrimidine dehydrogenase Homo sapiens 33-36 12014648-0 2002 Roles of thymidylate synthase and dihydropyrimidine dehydrogenase in tumor progression and sensitivity to 5-fluorouracil in human gastric cancer. Fluorouracil 106-120 dihydropyrimidine dehydrogenase Homo sapiens 34-65 12014648-1 2002 BACKGROUND: The role of thymidylate synthase (TS) and dihydropyrimidine dehydrogenase (DPD) enzyme activities in tumor progression and sensitivity to 5-fluorouracil (5-FU) were evaluated. Fluorouracil 150-164 dihydropyrimidine dehydrogenase Homo sapiens 87-90 12014648-1 2002 BACKGROUND: The role of thymidylate synthase (TS) and dihydropyrimidine dehydrogenase (DPD) enzyme activities in tumor progression and sensitivity to 5-fluorouracil (5-FU) were evaluated. Fluorouracil 166-170 dihydropyrimidine dehydrogenase Homo sapiens 87-90 12014648-6 2002 However, a weak correlation was found between DPD activity and sensitivity to 5-FU. Fluorouracil 78-82 dihydropyrimidine dehydrogenase Homo sapiens 46-49 12014648-8 2002 Conversely, in a subgroup of patients who received 5-FU-based adjuvant chemotherapy, overall survival was poorer in patients with high DPD activity (p=0.0465). Fluorouracil 51-55 dihydropyrimidine dehydrogenase Homo sapiens 135-138 12014648-9 2002 CONCLUSION: These results suggest that TS has an important role in tumor progression and DPD may be the dominant predictor of 5-FU sensitivity in gastric cancer. Fluorouracil 126-130 dihydropyrimidine dehydrogenase Homo sapiens 89-92 11870563-0 2002 [Detection of DPD-exon-14 skipping before 5-fluorouracil treatment? Fluorouracil 42-56 dihydropyrimidine dehydrogenase Homo sapiens 14-17 11916544-3 2002 Moreover, recent findings pointed out that the methylenetetrahydrofolate reductase (MTHFR) C677T mutation might change patient susceptibility to the toxic effects of the cyclophosphamide, methotrexate, 5-fluorouracil (CMF) regimen and raltitrexed. Fluorouracil 202-216 methylenetetrahydrofolate reductase Homo sapiens 47-82 15911984-3 2005 Previous results have shown that the catabolic rate-limiting enzymes DPD and NT, which are important membranous transporter of nucleosides, may regulate the sensitivity to 5-FU. Fluorouracil 172-176 dihydropyrimidine dehydrogenase Homo sapiens 69-72 15547701-8 2004 We identified two proto-oncogenes, nuclear receptor of T-cells (NOT) and c-fos, that were up-regulated in doxifluridine- and irinotecan-related regimens but unchanged in the 5-FU-related regimen. Fluorouracil 174-178 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 73-78 15538739-0 2004 Thymidylate synthase, thymidine phosphorylase, dihydropyrimidine dehydrogenase expression, and histological tumour regression after 5-FU-based neo-adjuvant chemoradiotherapy in rectal cancer. Fluorouracil 132-136 dihydropyrimidine dehydrogenase Homo sapiens 0-78 15538739-3 2004 Thymidylate synthase (TS), thymidine phosphorylase (TP), and dihydropyrimidine dehydrogenase (DPD) are thought to be important predictors for the efficiency of 5-FU-based treatment. Fluorouracil 160-164 dihydropyrimidine dehydrogenase Homo sapiens 61-92 15538739-3 2004 Thymidylate synthase (TS), thymidine phosphorylase (TP), and dihydropyrimidine dehydrogenase (DPD) are thought to be important predictors for the efficiency of 5-FU-based treatment. Fluorouracil 160-164 dihydropyrimidine dehydrogenase Homo sapiens 94-97 15538739-4 2004 The aim of this study was to determine the correlation between TS-, TP-, and DPD-gene expression and the response to 5-FU-based long-term pre-operative chemoradiotherapy assessed by histopathological tumour regression. Fluorouracil 117-121 dihydropyrimidine dehydrogenase Homo sapiens 77-80 11916544-3 2002 Moreover, recent findings pointed out that the methylenetetrahydrofolate reductase (MTHFR) C677T mutation might change patient susceptibility to the toxic effects of the cyclophosphamide, methotrexate, 5-fluorouracil (CMF) regimen and raltitrexed. Fluorouracil 202-216 methylenetetrahydrofolate reductase Homo sapiens 84-89 11915731-1 2002 We measured the activity of orotate phosphoribosyl transferase (OPRT), the amount of thymidylate synthase (TS) enzyme, and the activity of dihydropyrimidine dehydrogenase (DPD) for individual tissue types in order to study the contribution of these substances to the effects of the pyrimidine fluoride anticancer drug 5-fluorouracil (5-FU). Fluorouracil 318-332 dihydropyrimidine dehydrogenase Homo sapiens 172-175 11915731-1 2002 We measured the activity of orotate phosphoribosyl transferase (OPRT), the amount of thymidylate synthase (TS) enzyme, and the activity of dihydropyrimidine dehydrogenase (DPD) for individual tissue types in order to study the contribution of these substances to the effects of the pyrimidine fluoride anticancer drug 5-fluorouracil (5-FU). Fluorouracil 334-338 dihydropyrimidine dehydrogenase Homo sapiens 172-175 11865631-1 2002 The rate-limiting enzyme to catabolize 5-fluorouracil (5-FU) is dihydropyrimidine dehydrogenase (DPD), which expression in cancerous tissue is reported to have a relation with anti-tumor effect for 5-FU. Fluorouracil 39-53 dihydropyrimidine dehydrogenase Homo sapiens 64-95 15608557-0 2004 Methylenetetrahydrofolate reductase gene polymorphisms and response to fluorouracil-based treatment in advanced colorectal cancer patients. Fluorouracil 71-83 methylenetetrahydrofolate reductase Homo sapiens 0-35 15608557-3 2004 Thus, mutated MTHFR tumours should, in theory, be more sensitive to 5-fluorouracil (5FU) than wild-type tumours. Fluorouracil 68-82 methylenetetrahydrofolate reductase Homo sapiens 14-19 15608557-3 2004 Thus, mutated MTHFR tumours should, in theory, be more sensitive to 5-fluorouracil (5FU) than wild-type tumours. Fluorouracil 84-87 methylenetetrahydrofolate reductase Homo sapiens 14-19 11865631-1 2002 The rate-limiting enzyme to catabolize 5-fluorouracil (5-FU) is dihydropyrimidine dehydrogenase (DPD), which expression in cancerous tissue is reported to have a relation with anti-tumor effect for 5-FU. Fluorouracil 39-53 dihydropyrimidine dehydrogenase Homo sapiens 97-100 11865631-1 2002 The rate-limiting enzyme to catabolize 5-fluorouracil (5-FU) is dihydropyrimidine dehydrogenase (DPD), which expression in cancerous tissue is reported to have a relation with anti-tumor effect for 5-FU. Fluorouracil 55-59 dihydropyrimidine dehydrogenase Homo sapiens 64-95 11865631-1 2002 The rate-limiting enzyme to catabolize 5-fluorouracil (5-FU) is dihydropyrimidine dehydrogenase (DPD), which expression in cancerous tissue is reported to have a relation with anti-tumor effect for 5-FU. Fluorouracil 55-59 dihydropyrimidine dehydrogenase Homo sapiens 97-100 15769364-1 2004 OBJECTIVE: To investigate the relationship between polymorphisms of the methylenetetrahydrofolate reductase (MTHFR) C677T or A1298C and the response to fluoropyrimidine (5-FU)-based chemotherapy in advanced stomach cancer (SC). Fluorouracil 170-174 methylenetetrahydrofolate reductase Homo sapiens 72-107 15769364-1 2004 OBJECTIVE: To investigate the relationship between polymorphisms of the methylenetetrahydrofolate reductase (MTHFR) C677T or A1298C and the response to fluoropyrimidine (5-FU)-based chemotherapy in advanced stomach cancer (SC). Fluorouracil 170-174 methylenetetrahydrofolate reductase Homo sapiens 109-114 15769364-12 2004 CONCLUSION: These results in the present study suggested that the polymorphisms of MTHFR were associated with clinical response to 5-FU-based chemotherapy, suggesting that MTHFR genotypes could identify advanced SC patients that would be responsive to 5-FU-based chemotherapy. Fluorouracil 131-135 methylenetetrahydrofolate reductase Homo sapiens 83-88 15769364-12 2004 CONCLUSION: These results in the present study suggested that the polymorphisms of MTHFR were associated with clinical response to 5-FU-based chemotherapy, suggesting that MTHFR genotypes could identify advanced SC patients that would be responsive to 5-FU-based chemotherapy. Fluorouracil 131-135 methylenetetrahydrofolate reductase Homo sapiens 172-177 11865631-1 2002 The rate-limiting enzyme to catabolize 5-fluorouracil (5-FU) is dihydropyrimidine dehydrogenase (DPD), which expression in cancerous tissue is reported to have a relation with anti-tumor effect for 5-FU. Fluorouracil 198-202 dihydropyrimidine dehydrogenase Homo sapiens 64-95 15769364-12 2004 CONCLUSION: These results in the present study suggested that the polymorphisms of MTHFR were associated with clinical response to 5-FU-based chemotherapy, suggesting that MTHFR genotypes could identify advanced SC patients that would be responsive to 5-FU-based chemotherapy. Fluorouracil 252-256 methylenetetrahydrofolate reductase Homo sapiens 83-88 15769364-12 2004 CONCLUSION: These results in the present study suggested that the polymorphisms of MTHFR were associated with clinical response to 5-FU-based chemotherapy, suggesting that MTHFR genotypes could identify advanced SC patients that would be responsive to 5-FU-based chemotherapy. Fluorouracil 252-256 methylenetetrahydrofolate reductase Homo sapiens 172-177 11865631-1 2002 The rate-limiting enzyme to catabolize 5-fluorouracil (5-FU) is dihydropyrimidine dehydrogenase (DPD), which expression in cancerous tissue is reported to have a relation with anti-tumor effect for 5-FU. Fluorouracil 198-202 dihydropyrimidine dehydrogenase Homo sapiens 97-100 11862480-1 2002 PURPOSE: The activity of dihydropyrimidine dehydrogenase (DPD) - the rate-limiting enzyme in fluorouracil (5-FU) catabolism - has been reported to vary according to the time of day. Fluorouracil 93-105 dihydropyrimidine dehydrogenase Homo sapiens 25-56 15509204-0 2004 Biochemical modulation of 5-fluorouracil with interferon alpha/beta and gamma on murine renal cell carcinoma. Fluorouracil 26-40 interferon alpha Mus musculus 46-77 15509204-6 2004 Total thymidylate synthase was decreased by triple combination therapy (5-FU, IFN alpha/beta and IFN gamma, P = 0.0019) and combination therapy (5-FU and IFN gamma, P = 0.0018) compared to 5-FU alone. Fluorouracil 72-76 thymidylate synthase Mus musculus 6-26 15509204-6 2004 Total thymidylate synthase was decreased by triple combination therapy (5-FU, IFN alpha/beta and IFN gamma, P = 0.0019) and combination therapy (5-FU and IFN gamma, P = 0.0018) compared to 5-FU alone. Fluorouracil 145-149 thymidylate synthase Mus musculus 6-26 15509204-6 2004 Total thymidylate synthase was decreased by triple combination therapy (5-FU, IFN alpha/beta and IFN gamma, P = 0.0019) and combination therapy (5-FU and IFN gamma, P = 0.0018) compared to 5-FU alone. Fluorouracil 145-149 thymidylate synthase Mus musculus 6-26 15509204-8 2004 The concentration of 5-FU incorporated into RENCA tumors was increased by triple combination therapy (P = 0.0132) and combination therapy (5-FU and IFN alpha/beta, P = 0.0124) compared to 5-FU alone. Fluorouracil 21-25 interferon alpha Mus musculus 148-157 11862480-1 2002 PURPOSE: The activity of dihydropyrimidine dehydrogenase (DPD) - the rate-limiting enzyme in fluorouracil (5-FU) catabolism - has been reported to vary according to the time of day. Fluorouracil 93-105 dihydropyrimidine dehydrogenase Homo sapiens 58-61 11862480-1 2002 PURPOSE: The activity of dihydropyrimidine dehydrogenase (DPD) - the rate-limiting enzyme in fluorouracil (5-FU) catabolism - has been reported to vary according to the time of day. Fluorouracil 107-111 dihydropyrimidine dehydrogenase Homo sapiens 25-56 15688605-2 2004 An example of a drug for which clear predictive parameters have been identified is 5-fluorouracil (5FU): its antitumor activity is limited by either a high activity of the target enzyme thymidylate synthase (TS) and/or a high activity of its degrading enzyme, dihydropyrimidine dehydrogenase (DPD). Fluorouracil 99-102 dihydropyrimidine dehydrogenase Homo sapiens 293-296 15688606-5 2004 Methylenetetrahydrofolate reductase (MTHFR) is a key enzyme in the folate cycle, presenting two common polymorphisms (677C>T and 1298 A>C) which have impact on toxicity and efficacy of methotrexate and 5-fluorouracil. Fluorouracil 208-222 methylenetetrahydrofolate reductase Homo sapiens 0-35 11862480-1 2002 PURPOSE: The activity of dihydropyrimidine dehydrogenase (DPD) - the rate-limiting enzyme in fluorouracil (5-FU) catabolism - has been reported to vary according to the time of day. Fluorouracil 107-111 dihydropyrimidine dehydrogenase Homo sapiens 58-61 15688606-5 2004 Methylenetetrahydrofolate reductase (MTHFR) is a key enzyme in the folate cycle, presenting two common polymorphisms (677C>T and 1298 A>C) which have impact on toxicity and efficacy of methotrexate and 5-fluorouracil. Fluorouracil 208-222 methylenetetrahydrofolate reductase Homo sapiens 37-42 11816485-3 2002 Measurement of the expression of enzymes involved in 5-FU metabolism showed significantly higher activity of dihydropyrimidine dehydrogenase (DPD) and lower activity of thymidylate synthase (TS) in the MDA metastases than in the orthotopically implanted tumors. Fluorouracil 53-57 thymidylate synthase Mus musculus 169-189 15492780-6 2004 The mean values of 5-fluorouracil (5-FU) concentrations in ascites of the S-1 group at 1-4 h were 414-580 ng/ml (n=5), and those of FT group were 70-87 ng/ml (n=5), with significant differences between the two groups at each observation time. Fluorouracil 19-33 proteasome (prosome, macropain) 26S subunit, non-ATPase, 1 Mus musculus 74-77 15492780-6 2004 The mean values of 5-fluorouracil (5-FU) concentrations in ascites of the S-1 group at 1-4 h were 414-580 ng/ml (n=5), and those of FT group were 70-87 ng/ml (n=5), with significant differences between the two groups at each observation time. Fluorouracil 35-39 proteasome (prosome, macropain) 26S subunit, non-ATPase, 1 Mus musculus 74-77 11834904-5 2002 The present study also suggested that we might be able to exclude cases of bladder cancer in which 5-fluorouracil group medicines would be inappropriate candidates in treatment options by measuring both TP and DPD levels in the tumor. Fluorouracil 99-113 dihydropyrimidine dehydrogenase Homo sapiens 210-213 15492780-9 2004 The high concentrations and long duration of 5-FU in the peritoneal cavity after S-1 administration suggest that S-1 may be effective against peritoneal dissemination. Fluorouracil 45-49 proteasome (prosome, macropain) 26S subunit, non-ATPase, 1 Mus musculus 113-116 15467752-10 2004 Moreover, we show by the use of EGFP-tagged Bax and Bak that TRAIL and 5-FU synergistically trigger oligomerization and clustering of Bax but not Bak. Fluorouracil 71-75 BCL2 antagonist/killer 1 Homo sapiens 52-55 15308648-9 2004 Arabidopsis ups2 insertion mutants and ups1 lines, in which transcript levels were reduced by post-transcriptional gene silencing, are more tolerant to 5-fluorouracil as compared with wild type plants. Fluorouracil 152-166 ureide permease 2 Arabidopsis thaliana 12-16 15475457-1 2004 PURPOSE: In colorectal, breast, and head and neck cancers, response to 5-fluorouracil is associated with low expression of thymidylate synthase. Fluorouracil 71-85 thymidylate synthase Mus musculus 123-143 11761438-3 2001 Here, in a human colon carcinoma cell model in vitro, we examined whether the anti-neoplastic agents 5-fluorouracil (5-FU), CPT-11 or cisplatin (CDDP) could upregulate the expression of specific tumor cell surface markers, which may then enhance productive lytic interactions between CD8+ CTL and Ag-bearing tumor cells. Fluorouracil 101-115 CD8a molecule Homo sapiens 284-287 11761438-5 2001 Pretreatment of the SW480 primary colon carcinoma cell line with IFN-gamma, 5-FU, CPT-11 or CDDP enhanced ICAM-1 and Fas expression, resulting in Ag-specific CTL-mediated lysis involving Fas-dependent and -independent mechanisms. Fluorouracil 76-80 intercellular adhesion molecule 1 Homo sapiens 106-112 11604993-0 2001 Dihydropyrimidine dehydrogenase mRNA level correlates with the response to 5-fluorouracil-based chemo-immuno-radiation therapy in human oral squamous cell cancer. Fluorouracil 75-89 dihydropyrimidine dehydrogenase Homo sapiens 0-31 11604993-1 2001 The measurement of the intra-tumoral level of thymidylate synthetase (TS), and dihydropyrimidine dehydrogenase (DPD), may be useful in predicting tumor sensitivity to 5-fluorouracil (5-FU). Fluorouracil 167-181 dihydropyrimidine dehydrogenase Homo sapiens 79-110 11604993-1 2001 The measurement of the intra-tumoral level of thymidylate synthetase (TS), and dihydropyrimidine dehydrogenase (DPD), may be useful in predicting tumor sensitivity to 5-fluorouracil (5-FU). Fluorouracil 167-181 dihydropyrimidine dehydrogenase Homo sapiens 112-115 11604993-1 2001 The measurement of the intra-tumoral level of thymidylate synthetase (TS), and dihydropyrimidine dehydrogenase (DPD), may be useful in predicting tumor sensitivity to 5-fluorouracil (5-FU). Fluorouracil 183-187 dihydropyrimidine dehydrogenase Homo sapiens 79-110 11604993-1 2001 The measurement of the intra-tumoral level of thymidylate synthetase (TS), and dihydropyrimidine dehydrogenase (DPD), may be useful in predicting tumor sensitivity to 5-fluorouracil (5-FU). Fluorouracil 183-187 dihydropyrimidine dehydrogenase Homo sapiens 112-115 11604993-3 2001 Then we examined the correlation of the responsiveness of the patients with oral SCC to 5-FU with the intra-tumoral levels of DPD and TS mRNA. Fluorouracil 88-92 dihydropyrimidine dehydrogenase Homo sapiens 126-129 11604993-8 2001 These observations suggest that intra-tumoral levels of DPD mRNA may predict the tumor response to 5-FU-based chemo-immuno-radiation therapy in the patients with oral SCC. Fluorouracil 99-103 dihydropyrimidine dehydrogenase Homo sapiens 56-59 15362800-5 2004 In a pharmacokinetic study, TS-1 was administered on day 10 and the 5-fluorouracil levels were retained and maintained for a longer time, in the ascites and tumor than in plasma. Fluorouracil 68-82 Trichinella spiralis resistance 1 Mus musculus 28-32 15362800-7 2004 CONCLUSIONS: TS-1 could be effective in treating peritoneal dissemination of gastric cancer, due to the supply of 5-fluorouracil in the tumor by systemic and intraperitoneal circulation. Fluorouracil 114-128 Trichinella spiralis resistance 1 Mus musculus 13-17 11678380-1 2001 The anticancer drug 5-fluorouracil (5FU) undergoes extensive biotransformation to 5-dihydrofluorouracil (5FUH2) by the enzyme dihydropyrimidine deshydrogenase (DPD). Fluorouracil 20-34 dihydropyrimidine dehydrogenase Homo sapiens 126-158 11678380-1 2001 The anticancer drug 5-fluorouracil (5FU) undergoes extensive biotransformation to 5-dihydrofluorouracil (5FUH2) by the enzyme dihydropyrimidine deshydrogenase (DPD). Fluorouracil 20-34 dihydropyrimidine dehydrogenase Homo sapiens 160-163 11678380-1 2001 The anticancer drug 5-fluorouracil (5FU) undergoes extensive biotransformation to 5-dihydrofluorouracil (5FUH2) by the enzyme dihydropyrimidine deshydrogenase (DPD). Fluorouracil 36-39 dihydropyrimidine dehydrogenase Homo sapiens 126-158 11678380-1 2001 The anticancer drug 5-fluorouracil (5FU) undergoes extensive biotransformation to 5-dihydrofluorouracil (5FUH2) by the enzyme dihydropyrimidine deshydrogenase (DPD). Fluorouracil 36-39 dihydropyrimidine dehydrogenase Homo sapiens 160-163 11697844-0 2001 Relationship between 5-fluorouracil disposition, toxicity and dihydropyrimidine dehydrogenase activity in cancer patients. Fluorouracil 21-35 dihydropyrimidine dehydrogenase Homo sapiens 62-93 15269599-3 2004 Recently described in this context was the dUTPase, which may confer resistance to fluoropyrimidine drugs such as 5-fluorouracil (5-FU). Fluorouracil 114-128 Deoxyuridine triphosphatase Drosophila melanogaster 43-50 15269599-3 2004 Recently described in this context was the dUTPase, which may confer resistance to fluoropyrimidine drugs such as 5-fluorouracil (5-FU). Fluorouracil 130-134 Deoxyuridine triphosphatase Drosophila melanogaster 43-50 16163233-1 2004 Through the use of pharmacogenetic studies, interindividual variability in response (efficacy and toxicity) to 5-fluorouracil (5-FU) chemotherapy has been linked to the rate-limiting enzyme in the drug"s catabolic pathway, known as dihydropyrimidine dehydrogenase (DPD). Fluorouracil 111-125 dihydropyrimidine dehydrogenase Homo sapiens 232-263 16163233-1 2004 Through the use of pharmacogenetic studies, interindividual variability in response (efficacy and toxicity) to 5-fluorouracil (5-FU) chemotherapy has been linked to the rate-limiting enzyme in the drug"s catabolic pathway, known as dihydropyrimidine dehydrogenase (DPD). Fluorouracil 111-125 dihydropyrimidine dehydrogenase Homo sapiens 265-268 16163233-1 2004 Through the use of pharmacogenetic studies, interindividual variability in response (efficacy and toxicity) to 5-fluorouracil (5-FU) chemotherapy has been linked to the rate-limiting enzyme in the drug"s catabolic pathway, known as dihydropyrimidine dehydrogenase (DPD). Fluorouracil 127-131 dihydropyrimidine dehydrogenase Homo sapiens 232-263 16163233-1 2004 Through the use of pharmacogenetic studies, interindividual variability in response (efficacy and toxicity) to 5-fluorouracil (5-FU) chemotherapy has been linked to the rate-limiting enzyme in the drug"s catabolic pathway, known as dihydropyrimidine dehydrogenase (DPD). Fluorouracil 127-131 dihydropyrimidine dehydrogenase Homo sapiens 265-268 11697844-2 2001 In order to study the predictivity of pharmacokinetics with respect to the occurrence of 5-FU toxicity, this study investigates the relationship between the pharmacokinetics of 5-FU and its metabolite 5-fluoro-5,6-dihydrouracil (5-FDHU), dihydropyrimidine dehydrogenase (DPD) activity in peripheral blood mononuclear cells (PBMNC) and treatment tolerability. Fluorouracil 177-181 dihydropyrimidine dehydrogenase Homo sapiens 238-269 11697844-2 2001 In order to study the predictivity of pharmacokinetics with respect to the occurrence of 5-FU toxicity, this study investigates the relationship between the pharmacokinetics of 5-FU and its metabolite 5-fluoro-5,6-dihydrouracil (5-FDHU), dihydropyrimidine dehydrogenase (DPD) activity in peripheral blood mononuclear cells (PBMNC) and treatment tolerability. Fluorouracil 177-181 dihydropyrimidine dehydrogenase Homo sapiens 271-274 11555593-1 2001 Dihydropyrimidine dehydrogenase (DPD) is the initial key enzyme in 5-fluorouracil (5-FU) catabolism. Fluorouracil 67-81 dihydropyrimidine dehydrogenase Homo sapiens 0-31 11555593-1 2001 Dihydropyrimidine dehydrogenase (DPD) is the initial key enzyme in 5-fluorouracil (5-FU) catabolism. Fluorouracil 67-81 dihydropyrimidine dehydrogenase Homo sapiens 33-36 11555593-1 2001 Dihydropyrimidine dehydrogenase (DPD) is the initial key enzyme in 5-fluorouracil (5-FU) catabolism. Fluorouracil 83-87 dihydropyrimidine dehydrogenase Homo sapiens 0-31 11555593-1 2001 Dihydropyrimidine dehydrogenase (DPD) is the initial key enzyme in 5-fluorouracil (5-FU) catabolism. Fluorouracil 83-87 dihydropyrimidine dehydrogenase Homo sapiens 33-36 11555593-4 2001 5-FU concentrations in tumors were higher than those in normal tissues (P < 0.05) and were inversely associated with DPD protein levels (r = -0.463; P < 0.05). Fluorouracil 0-4 dihydropyrimidine dehydrogenase Homo sapiens 120-123 11555593-8 2001 These results suggest DPD activities in tumors to be predictive of 5-FU levels in colorectal cancer tissues and are reflected by DPD mRNA levels as measured by reverse transcription-PCR. Fluorouracil 67-71 dihydropyrimidine dehydrogenase Homo sapiens 22-25 11555601-0 2001 Prevalence of a common point mutation in the dihydropyrimidine dehydrogenase (DPD) gene within the 5"-splice donor site of intron 14 in patients with severe 5-fluorouracil (5-FU)- related toxicity compared with controls. Fluorouracil 157-171 dihydropyrimidine dehydrogenase Homo sapiens 45-76 11555601-0 2001 Prevalence of a common point mutation in the dihydropyrimidine dehydrogenase (DPD) gene within the 5"-splice donor site of intron 14 in patients with severe 5-fluorouracil (5-FU)- related toxicity compared with controls. Fluorouracil 157-171 dihydropyrimidine dehydrogenase Homo sapiens 78-81 11555601-0 2001 Prevalence of a common point mutation in the dihydropyrimidine dehydrogenase (DPD) gene within the 5"-splice donor site of intron 14 in patients with severe 5-fluorouracil (5-FU)- related toxicity compared with controls. Fluorouracil 173-177 dihydropyrimidine dehydrogenase Homo sapiens 45-76 15246190-3 2004 When dichotomized at the mean TS and DPD mRNA level, patients with low-DPD tumors who were administered 5-FU had a significantly better prognosis than those who did not receive adjuvant treatment (p = 0.041). Fluorouracil 104-108 dihydropyrimidine dehydrogenase Homo sapiens 37-40 11555601-0 2001 Prevalence of a common point mutation in the dihydropyrimidine dehydrogenase (DPD) gene within the 5"-splice donor site of intron 14 in patients with severe 5-fluorouracil (5-FU)- related toxicity compared with controls. Fluorouracil 173-177 dihydropyrimidine dehydrogenase Homo sapiens 78-81 11555601-1 2001 Deficiency of dihydropyrimidine dehydrogenase (DPD), the rate-limiting enzyme in 5-fluorouracil (5-FU) catabolism, has been linked to toxic side effects of 5-FU. Fluorouracil 81-95 dihydropyrimidine dehydrogenase Homo sapiens 47-50 15272584-6 2004 The DPD activity of mucinous adenocarcinoma is related to catabolism of 5-FU is equal to that of adenocarcinoma, however, the OPRT activity is related to a main pathway of 5-FU phosphorylation is significantly lower. Fluorouracil 72-76 dihydropyrimidine dehydrogenase Homo sapiens 4-7 15272584-6 2004 The DPD activity of mucinous adenocarcinoma is related to catabolism of 5-FU is equal to that of adenocarcinoma, however, the OPRT activity is related to a main pathway of 5-FU phosphorylation is significantly lower. Fluorouracil 172-176 dihydropyrimidine dehydrogenase Homo sapiens 4-7 11555601-1 2001 Deficiency of dihydropyrimidine dehydrogenase (DPD), the rate-limiting enzyme in 5-fluorouracil (5-FU) catabolism, has been linked to toxic side effects of 5-FU. Fluorouracil 97-101 dihydropyrimidine dehydrogenase Homo sapiens 47-50 11555601-1 2001 Deficiency of dihydropyrimidine dehydrogenase (DPD), the rate-limiting enzyme in 5-fluorouracil (5-FU) catabolism, has been linked to toxic side effects of 5-FU. Fluorouracil 156-160 dihydropyrimidine dehydrogenase Homo sapiens 47-50 11555601-9 2001 We conclude that carriers of the DPD exon 14-skipping mutation are at significantly increased risk to experience life-threatening myelosuppression upon 5-FU treatment, even when the allelic status is heterozygous. Fluorouracil 152-156 dihydropyrimidine dehydrogenase Homo sapiens 33-36 11445849-1 2001 Thymidylate synthase (TS) is the target enzyme of 5-fluorouracil (5-FU), and dihydropyrimidine dehydrogenase (DPD) is the key enzyme in the 5-FU catabolic pathway. Fluorouracil 50-64 dihydropyrimidine dehydrogenase Homo sapiens 110-113 11445849-1 2001 Thymidylate synthase (TS) is the target enzyme of 5-fluorouracil (5-FU), and dihydropyrimidine dehydrogenase (DPD) is the key enzyme in the 5-FU catabolic pathway. Fluorouracil 66-70 dihydropyrimidine dehydrogenase Homo sapiens 110-113 11445849-1 2001 Thymidylate synthase (TS) is the target enzyme of 5-fluorouracil (5-FU), and dihydropyrimidine dehydrogenase (DPD) is the key enzyme in the 5-FU catabolic pathway. Fluorouracil 140-144 dihydropyrimidine dehydrogenase Homo sapiens 77-108 11445849-1 2001 Thymidylate synthase (TS) is the target enzyme of 5-fluorouracil (5-FU), and dihydropyrimidine dehydrogenase (DPD) is the key enzyme in the 5-FU catabolic pathway. Fluorouracil 140-144 dihydropyrimidine dehydrogenase Homo sapiens 110-113 11459999-3 2001 Two patients treated in a phase I trial of oral 5-FU, leucovorin and eniluracil, an inhibitor of dihydropyrimidine dehydrogenase (DPD), developed delayed onset symptoms of unsteady gait and reduced sensation in the legs. Fluorouracil 48-52 dihydropyrimidine dehydrogenase Homo sapiens 97-128 15069534-1 2004 Thymidilate synthase (TS) is a major target of 5-fluorouracil (5-FU) and dihydropyrimidine dehydrogenase (DPD) is a rate-limiting enzyme in the degradation of 5-FU. Fluorouracil 47-61 dihydropyrimidine dehydrogenase Homo sapiens 106-109 15069534-1 2004 Thymidilate synthase (TS) is a major target of 5-fluorouracil (5-FU) and dihydropyrimidine dehydrogenase (DPD) is a rate-limiting enzyme in the degradation of 5-FU. Fluorouracil 63-67 dihydropyrimidine dehydrogenase Homo sapiens 106-109 15069534-1 2004 Thymidilate synthase (TS) is a major target of 5-fluorouracil (5-FU) and dihydropyrimidine dehydrogenase (DPD) is a rate-limiting enzyme in the degradation of 5-FU. Fluorouracil 159-163 dihydropyrimidine dehydrogenase Homo sapiens 73-104 15069534-1 2004 Thymidilate synthase (TS) is a major target of 5-fluorouracil (5-FU) and dihydropyrimidine dehydrogenase (DPD) is a rate-limiting enzyme in the degradation of 5-FU. Fluorouracil 159-163 dihydropyrimidine dehydrogenase Homo sapiens 106-109 15114696-2 2004 Dihydropyrimidine dehydrogenase (DPD) which catalyzes 5-fluorouracil (5-FU), thymidine phosphorylase (TP), responsible for catalyzing doxifluridine to 5-FU, and thymidylate synthase (TS) were estimated for breast cancer. Fluorouracil 54-68 dihydropyrimidine dehydrogenase Homo sapiens 0-31 15114696-2 2004 Dihydropyrimidine dehydrogenase (DPD) which catalyzes 5-fluorouracil (5-FU), thymidine phosphorylase (TP), responsible for catalyzing doxifluridine to 5-FU, and thymidylate synthase (TS) were estimated for breast cancer. Fluorouracil 54-68 dihydropyrimidine dehydrogenase Homo sapiens 33-36 15114696-2 2004 Dihydropyrimidine dehydrogenase (DPD) which catalyzes 5-fluorouracil (5-FU), thymidine phosphorylase (TP), responsible for catalyzing doxifluridine to 5-FU, and thymidylate synthase (TS) were estimated for breast cancer. Fluorouracil 70-74 dihydropyrimidine dehydrogenase Homo sapiens 0-31 15114696-2 2004 Dihydropyrimidine dehydrogenase (DPD) which catalyzes 5-fluorouracil (5-FU), thymidine phosphorylase (TP), responsible for catalyzing doxifluridine to 5-FU, and thymidylate synthase (TS) were estimated for breast cancer. Fluorouracil 70-74 dihydropyrimidine dehydrogenase Homo sapiens 33-36 15114696-2 2004 Dihydropyrimidine dehydrogenase (DPD) which catalyzes 5-fluorouracil (5-FU), thymidine phosphorylase (TP), responsible for catalyzing doxifluridine to 5-FU, and thymidylate synthase (TS) were estimated for breast cancer. Fluorouracil 151-155 dihydropyrimidine dehydrogenase Homo sapiens 0-31 15114696-2 2004 Dihydropyrimidine dehydrogenase (DPD) which catalyzes 5-fluorouracil (5-FU), thymidine phosphorylase (TP), responsible for catalyzing doxifluridine to 5-FU, and thymidylate synthase (TS) were estimated for breast cancer. Fluorouracil 151-155 dihydropyrimidine dehydrogenase Homo sapiens 33-36 15154628-4 2004 DPD is the enzyme that converts 5-FU to inactive metabolites and therefore dictates the amount of 5-FU that is available to be metabolised to cytotoxic nucleotides. Fluorouracil 32-36 dihydropyrimidine dehydrogenase Homo sapiens 0-3 11459999-3 2001 Two patients treated in a phase I trial of oral 5-FU, leucovorin and eniluracil, an inhibitor of dihydropyrimidine dehydrogenase (DPD), developed delayed onset symptoms of unsteady gait and reduced sensation in the legs. Fluorouracil 48-52 dihydropyrimidine dehydrogenase Homo sapiens 130-133 15154628-4 2004 DPD is the enzyme that converts 5-FU to inactive metabolites and therefore dictates the amount of 5-FU that is available to be metabolised to cytotoxic nucleotides. Fluorouracil 98-102 dihydropyrimidine dehydrogenase Homo sapiens 0-3 11459999-11 2001 Since DPD was profoundly inhibited during eniluracil therapy in these two patients, it is likely that 5-FU or its active metabolites were contributing factors to the peripheral neuropathy. Fluorouracil 102-106 dihydropyrimidine dehydrogenase Homo sapiens 6-9 15014039-0 2004 Blockage of 2-deoxy-D-ribose-induced angiogenesis with rapamycin counteracts a thymidine phosphorylase-based escape mechanism available for colon cancer under 5-fluorouracil therapy. Fluorouracil 159-173 thymidine phosphorylase Mus musculus 79-102 11431359-4 2001 Human MLH1(-) and MMR-deficient HCT116 colon cancer cells were 18-fold more resistant to 7.5 microM 5-fluorouracil (continuous treatment) and 17-fold more resistant to 7.5 microM FdUrd in clonogenic survival assays compared with genetically matched, MLH1(+) and MMR-proficient HCT116 3-6 cells. Fluorouracil 100-114 mutL homolog 1 Mus musculus 6-10 15014039-2 2004 A recognized weakness of conventional 5-fluorouracil (5-FU) therapy relates to expression of the intracellular enzyme, thymidine phosphorylase (TP). Fluorouracil 38-52 thymidine phosphorylase Mus musculus 119-142 15014039-2 2004 A recognized weakness of conventional 5-fluorouracil (5-FU) therapy relates to expression of the intracellular enzyme, thymidine phosphorylase (TP). Fluorouracil 54-58 thymidine phosphorylase Mus musculus 119-142 11267993-4 2001 MED1 acts as a mismatch-specific DNA N-glycosylase active on thymine, uracil, 5-fluorouracil and, weakly, 3,N(4)-ethenocytosine paired with guanine. Fluorouracil 78-92 mediator complex subunit 1 Homo sapiens 0-4 15045945-1 2004 In humans, 80-90% of the administered dose of 5-fluorouracil (5-FU) is degraded by dihydropyrimidine dehydrogenase (DPD), the initial rate-limiting enzyme in pyrimidine catabolism. Fluorouracil 46-60 dihydropyrimidine dehydrogenase Homo sapiens 83-114 11376561-2 2001 CYP2A6-expressing cells (DLD-1 / CYP2A6 cells) more efficiently catalyzed the conversion of FT to 5-fluorouracil (5-FU) (2.6-fold) and the 7-hydroxylation of coumarin (7.9-fold) than cells transfected with a null construct (DLD-1 / null cells). Fluorouracil 98-112 cytochrome P450 family 2 subfamily A member 6 Homo sapiens 0-6 15045945-1 2004 In humans, 80-90% of the administered dose of 5-fluorouracil (5-FU) is degraded by dihydropyrimidine dehydrogenase (DPD), the initial rate-limiting enzyme in pyrimidine catabolism. Fluorouracil 46-60 dihydropyrimidine dehydrogenase Homo sapiens 116-119 15045945-1 2004 In humans, 80-90% of the administered dose of 5-fluorouracil (5-FU) is degraded by dihydropyrimidine dehydrogenase (DPD), the initial rate-limiting enzyme in pyrimidine catabolism. Fluorouracil 62-66 dihydropyrimidine dehydrogenase Homo sapiens 83-114 15045945-1 2004 In humans, 80-90% of the administered dose of 5-fluorouracil (5-FU) is degraded by dihydropyrimidine dehydrogenase (DPD), the initial rate-limiting enzyme in pyrimidine catabolism. Fluorouracil 62-66 dihydropyrimidine dehydrogenase Homo sapiens 116-119 11376561-2 2001 CYP2A6-expressing cells (DLD-1 / CYP2A6 cells) more efficiently catalyzed the conversion of FT to 5-fluorouracil (5-FU) (2.6-fold) and the 7-hydroxylation of coumarin (7.9-fold) than cells transfected with a null construct (DLD-1 / null cells). Fluorouracil 98-112 cytochrome P450 family 2 subfamily A member 6 Homo sapiens 33-39 14742277-7 2004 RG1503 blunted or abolished the following 5-FU-induced effects: increases in matrix metalloproteinase (MMP)-2, MMP-9, and plasmin, and decreases in tissue inhibitor of metalloproteinase (TIMP)-1 and TIMP-2. Fluorouracil 42-46 matrix metallopeptidase 9 Homo sapiens 111-116 11376561-2 2001 CYP2A6-expressing cells (DLD-1 / CYP2A6 cells) more efficiently catalyzed the conversion of FT to 5-fluorouracil (5-FU) (2.6-fold) and the 7-hydroxylation of coumarin (7.9-fold) than cells transfected with a null construct (DLD-1 / null cells). Fluorouracil 114-118 cytochrome P450 family 2 subfamily A member 6 Homo sapiens 0-6 14742277-7 2004 RG1503 blunted or abolished the following 5-FU-induced effects: increases in matrix metalloproteinase (MMP)-2, MMP-9, and plasmin, and decreases in tissue inhibitor of metalloproteinase (TIMP)-1 and TIMP-2. Fluorouracil 42-46 TIMP metallopeptidase inhibitor 2 Homo sapiens 199-205 11376561-2 2001 CYP2A6-expressing cells (DLD-1 / CYP2A6 cells) more efficiently catalyzed the conversion of FT to 5-fluorouracil (5-FU) (2.6-fold) and the 7-hydroxylation of coumarin (7.9-fold) than cells transfected with a null construct (DLD-1 / null cells). Fluorouracil 114-118 cytochrome P450 family 2 subfamily A member 6 Homo sapiens 33-39 11329775-1 2001 Dihydropyrimidine dehydrogenase (DPD) is the initial and rate-limiting enzyme in the (fluoro) pyrimidine catabolic pathway, and has an important role in 5-fluorouracil (5-FU) pharmacology. Fluorouracil 153-167 dihydropyrimidine dehydrogenase Homo sapiens 0-31 14734703-0 2004 Effect of the methylenetetrahydrofolate reductase C677T polymorphism on chemosensitivity of colon and breast cancer cells to 5-fluorouracil and methotrexate. Fluorouracil 125-139 methylenetetrahydrofolate reductase Homo sapiens 14-49 14716816-1 2004 AIM: To determine the expression levels of three metabolic enzymes of fluoropyrimidines: thymidylate synthase (TS), thymidine phosphorylase (TP) and dihydropyrimidine dehydrogenase (DPD) in seven human gastrointestinal cancer cell lines, and to compare the enzyme levels with the sensitivity to 5-fluorouracil (5-FU) and 5-fluoro-2"-deoxyuridine (FdUrd). Fluorouracil 295-309 dihydropyrimidine dehydrogenase Homo sapiens 182-185 14716816-1 2004 AIM: To determine the expression levels of three metabolic enzymes of fluoropyrimidines: thymidylate synthase (TS), thymidine phosphorylase (TP) and dihydropyrimidine dehydrogenase (DPD) in seven human gastrointestinal cancer cell lines, and to compare the enzyme levels with the sensitivity to 5-fluorouracil (5-FU) and 5-fluoro-2"-deoxyuridine (FdUrd). Fluorouracil 311-315 dihydropyrimidine dehydrogenase Homo sapiens 182-185 14716816-5 2004 Cell lines with lower DPD mRNA and protein levels tended to be more sensitive to 5-FU (P<0.05), but neither TS nor TP correlated with 5-FU IC50 (P>0.05). Fluorouracil 81-85 dihydropyrimidine dehydrogenase Homo sapiens 22-25 11329775-1 2001 Dihydropyrimidine dehydrogenase (DPD) is the initial and rate-limiting enzyme in the (fluoro) pyrimidine catabolic pathway, and has an important role in 5-fluorouracil (5-FU) pharmacology. Fluorouracil 153-167 dihydropyrimidine dehydrogenase Homo sapiens 33-36 14716816-8 2004 CONCLUSION: DPD and TS enzyme levels may be useful indicators in predicting the antitumor activity of 5-FU or FdUrd, respectively. Fluorouracil 102-106 dihydropyrimidine dehydrogenase Homo sapiens 12-15 11329775-1 2001 Dihydropyrimidine dehydrogenase (DPD) is the initial and rate-limiting enzyme in the (fluoro) pyrimidine catabolic pathway, and has an important role in 5-fluorouracil (5-FU) pharmacology. Fluorouracil 169-173 dihydropyrimidine dehydrogenase Homo sapiens 0-31 11329775-1 2001 Dihydropyrimidine dehydrogenase (DPD) is the initial and rate-limiting enzyme in the (fluoro) pyrimidine catabolic pathway, and has an important role in 5-fluorouracil (5-FU) pharmacology. Fluorouracil 169-173 dihydropyrimidine dehydrogenase Homo sapiens 33-36 12827409-8 2004 CONCLUSION: Considering also our own findings, this review presents the latest developments in the scientific discussion of the tumor suppressor/oncogenes p53, k-ras, and DCC, biochemical determinants of the 5-fluorouracil metabolism, and defects of the DNA repair system. Fluorouracil 208-222 KRAS proto-oncogene, GTPase Homo sapiens 160-165 12827409-8 2004 CONCLUSION: Considering also our own findings, this review presents the latest developments in the scientific discussion of the tumor suppressor/oncogenes p53, k-ras, and DCC, biochemical determinants of the 5-fluorouracil metabolism, and defects of the DNA repair system. Fluorouracil 208-222 DCC netrin 1 receptor Homo sapiens 171-174 11264006-7 2001 Moreover, when cells were treated with various concentrations of 5-FU for 12 h, the concentration of 2 microgram/ml efficiently inhibited the IKK activity as compared to 1, 5, or 10 microgram/ml. Fluorouracil 65-69 component of inhibitor of nuclear factor kappa B kinase complex Homo sapiens 142-145 11264006-10 2001 Thus, these results suggest that 5-FU induction of apoptosis in cl-1 cells may be mediated by suppression of NF-kappaB via inhibition of IKK activity. Fluorouracil 33-37 component of inhibitor of nuclear factor kappa B kinase complex Homo sapiens 137-140 14712769-0 2003 [Support of TS-1, 5-FU preparation containing potent DPD inhibitor by determination of urinary uracil/serum 5-FU clearance]. Fluorouracil 18-22 dihydropyrimidine dehydrogenase Homo sapiens 53-56 14712769-0 2003 [Support of TS-1, 5-FU preparation containing potent DPD inhibitor by determination of urinary uracil/serum 5-FU clearance]. Fluorouracil 108-112 dihydropyrimidine dehydrogenase Homo sapiens 53-56 11267945-2 2001 Over 80% of administered 5FU is metabolically degraded by dihydropyrimidine dehydrogenase (DPD), a primary and rate-limiting enzyme in the 5FU metabolic pathway. Fluorouracil 25-28 dihydropyrimidine dehydrogenase Homo sapiens 58-89 14520468-8 2003 The binding of [(125)I]SIB-annexin V to RIF-1 tumours increased by 2.3-fold at 48 h after a single intraperitoneal injection of 5-fluorouracil (165 mg kg(-1) body weight), compared to a 4.4-fold increase in TUNEL-positive cells measured by immunostaining. Fluorouracil 128-142 annexin A5 Mus musculus 27-36 14519634-0 2003 Thymidylate synthase and dihydropyrimidine dehydrogenase mRNA expression levels: predictors for survival in colorectal cancer patients receiving adjuvant 5-fluorouracil. Fluorouracil 154-168 dihydropyrimidine dehydrogenase Homo sapiens 25-56 14519634-2 2003 In this study, we determined the prognostic value of thymidylate synthase (TS) and dihydropyrimidine dehydrogenase (DPD) expression in colorectal cancer patients treated with adjuvant 5-FU. Fluorouracil 184-188 dihydropyrimidine dehydrogenase Homo sapiens 83-114 14519634-2 2003 In this study, we determined the prognostic value of thymidylate synthase (TS) and dihydropyrimidine dehydrogenase (DPD) expression in colorectal cancer patients treated with adjuvant 5-FU. Fluorouracil 184-188 dihydropyrimidine dehydrogenase Homo sapiens 116-119 14519634-7 2003 Among the patients receiving adjuvant 5-FU therapy, those with high TS survived longer than those with low TS, and in each TS subgroup, the ones with low DPD survived longer than the ones with high DPD levels. Fluorouracil 38-42 dihydropyrimidine dehydrogenase Homo sapiens 154-157 14519634-7 2003 Among the patients receiving adjuvant 5-FU therapy, those with high TS survived longer than those with low TS, and in each TS subgroup, the ones with low DPD survived longer than the ones with high DPD levels. Fluorouracil 38-42 dihydropyrimidine dehydrogenase Homo sapiens 198-201 14519634-9 2003 CONCLUSIONS: This suggests that TS and DPD quantitation may be helpful to evaluate prognosis of patients receiving adjuvant 5-FU and that patients with high TS and low DPD may benefit from adjuvant 5-FU chemotherapy. Fluorouracil 124-128 dihydropyrimidine dehydrogenase Homo sapiens 39-42 14519634-9 2003 CONCLUSIONS: This suggests that TS and DPD quantitation may be helpful to evaluate prognosis of patients receiving adjuvant 5-FU and that patients with high TS and low DPD may benefit from adjuvant 5-FU chemotherapy. Fluorouracil 198-202 dihydropyrimidine dehydrogenase Homo sapiens 168-171 12967482-0 2003 Effect of 5-fluorouracil and epidermal growth factor on cell growth and dihydropyrimidine dehydrogenase regulation in human uterine cervical carcinoma SKG-IIIb cells. Fluorouracil 10-24 dihydropyrimidine dehydrogenase Homo sapiens 72-103 12967482-1 2003 We previously demonstrated that epidermal growth factor (EGF) induces a decrease in dihydropyrimidine dehydrogenase (DPD), which is the first and rate-limiting enzyme in the catabolism of 5-fluorouracil (5-FU), in EGF receptor (EGFR)-positive human SKG-IIIb uterine cervical carcinoma cells, and thereby increased the sensitivity of the cells to 5-FU. Fluorouracil 188-202 dihydropyrimidine dehydrogenase Homo sapiens 84-115 12967482-1 2003 We previously demonstrated that epidermal growth factor (EGF) induces a decrease in dihydropyrimidine dehydrogenase (DPD), which is the first and rate-limiting enzyme in the catabolism of 5-fluorouracil (5-FU), in EGF receptor (EGFR)-positive human SKG-IIIb uterine cervical carcinoma cells, and thereby increased the sensitivity of the cells to 5-FU. Fluorouracil 188-202 dihydropyrimidine dehydrogenase Homo sapiens 117-120 12967482-1 2003 We previously demonstrated that epidermal growth factor (EGF) induces a decrease in dihydropyrimidine dehydrogenase (DPD), which is the first and rate-limiting enzyme in the catabolism of 5-fluorouracil (5-FU), in EGF receptor (EGFR)-positive human SKG-IIIb uterine cervical carcinoma cells, and thereby increased the sensitivity of the cells to 5-FU. Fluorouracil 204-208 dihydropyrimidine dehydrogenase Homo sapiens 84-115 12967482-1 2003 We previously demonstrated that epidermal growth factor (EGF) induces a decrease in dihydropyrimidine dehydrogenase (DPD), which is the first and rate-limiting enzyme in the catabolism of 5-fluorouracil (5-FU), in EGF receptor (EGFR)-positive human SKG-IIIb uterine cervical carcinoma cells, and thereby increased the sensitivity of the cells to 5-FU. Fluorouracil 204-208 dihydropyrimidine dehydrogenase Homo sapiens 117-120 12967482-1 2003 We previously demonstrated that epidermal growth factor (EGF) induces a decrease in dihydropyrimidine dehydrogenase (DPD), which is the first and rate-limiting enzyme in the catabolism of 5-fluorouracil (5-FU), in EGF receptor (EGFR)-positive human SKG-IIIb uterine cervical carcinoma cells, and thereby increased the sensitivity of the cells to 5-FU. Fluorouracil 346-350 dihydropyrimidine dehydrogenase Homo sapiens 84-115 12967482-1 2003 We previously demonstrated that epidermal growth factor (EGF) induces a decrease in dihydropyrimidine dehydrogenase (DPD), which is the first and rate-limiting enzyme in the catabolism of 5-fluorouracil (5-FU), in EGF receptor (EGFR)-positive human SKG-IIIb uterine cervical carcinoma cells, and thereby increased the sensitivity of the cells to 5-FU. Fluorouracil 346-350 dihydropyrimidine dehydrogenase Homo sapiens 117-120 12967482-7 2003 Expression of DPD mRNA was concentration-dependently inhibited by treatment with 5-FU and by EGF at a concentration that strongly stimulated cell growth. Fluorouracil 81-85 dihydropyrimidine dehydrogenase Homo sapiens 14-17 12967482-8 2003 Further, combination treatment inhibited DPD activity, as well as DPD protein and mRNA expression, more strongly than did treatment with 5-FU or EGF alone. Fluorouracil 137-141 dihydropyrimidine dehydrogenase Homo sapiens 41-44 12904931-4 2003 METHODS: The inhibitory effect of 5-FU on CYP1A2, CYP2C9, CYP2C19, CYP2C8, CYP2E1, CYP2D6, and CYP3A4 activities was examined with specific probe drugs in human liver microsomes. Fluorouracil 34-38 cytochrome P450 family 2 subfamily C member 19 Homo sapiens 58-65 11267945-2 2001 Over 80% of administered 5FU is metabolically degraded by dihydropyrimidine dehydrogenase (DPD), a primary and rate-limiting enzyme in the 5FU metabolic pathway. Fluorouracil 25-28 dihydropyrimidine dehydrogenase Homo sapiens 91-94 11267945-8 2001 We also studied the association between toxic response to 5FU and heterozygous frame shift or missense mutation of the DPYD gene among eight cancer patients who had received 5FU-based chemotherapy. Fluorouracil 58-61 dihydropyrimidine dehydrogenase Homo sapiens 119-123 11267945-10 2001 Our results indicate that a very small percentage, about 0.2%, of the Japanese population seems to carry homozygous mutations in DPYD gene, mutations which possibly indicate genetically increased toxicity of 5FU-based chemotherapy. Fluorouracil 208-211 dihydropyrimidine dehydrogenase Homo sapiens 129-133 11241325-2 2001 The recent availability of oral formulations of 5-FU in conjunction with the ability to modulate the anabolic and catabolic metabolism of 5-FU with leucovorin and dihydropyrimidine dehydrogenase (DPD) inhibitors, respectively, may provide a substantial improvement in the ease of administration and the efficacy of fluoropyrimidine therapy. Fluorouracil 138-142 dihydropyrimidine dehydrogenase Homo sapiens 148-194 11241325-2 2001 The recent availability of oral formulations of 5-FU in conjunction with the ability to modulate the anabolic and catabolic metabolism of 5-FU with leucovorin and dihydropyrimidine dehydrogenase (DPD) inhibitors, respectively, may provide a substantial improvement in the ease of administration and the efficacy of fluoropyrimidine therapy. Fluorouracil 138-142 dihydropyrimidine dehydrogenase Homo sapiens 196-199 11166452-7 2001 Experiments were performed to address this paradox: administration of 5-fluorouracil with consequent "expansion" of early hematopoietic cells resulted in the appearance of IL-11-responsive cells in mpl(-/-) mice when assayed in in vitro cultures. Fluorouracil 70-84 interleukin 11 Mus musculus 172-177 12914384-5 2003 TS (thymidilate synthase) and DPD (dihydropyrimidine dehydrogenase) polymorphisms are implicated in the development of toxicity and in the efficacy of 5-fluorouracil (5FU). Fluorouracil 151-165 dihydropyrimidine dehydrogenase Homo sapiens 30-33 12914384-5 2003 TS (thymidilate synthase) and DPD (dihydropyrimidine dehydrogenase) polymorphisms are implicated in the development of toxicity and in the efficacy of 5-fluorouracil (5FU). Fluorouracil 151-165 dihydropyrimidine dehydrogenase Homo sapiens 35-66 12914384-5 2003 TS (thymidilate synthase) and DPD (dihydropyrimidine dehydrogenase) polymorphisms are implicated in the development of toxicity and in the efficacy of 5-fluorouracil (5FU). Fluorouracil 167-170 dihydropyrimidine dehydrogenase Homo sapiens 30-33 12914384-5 2003 TS (thymidilate synthase) and DPD (dihydropyrimidine dehydrogenase) polymorphisms are implicated in the development of toxicity and in the efficacy of 5-fluorouracil (5FU). Fluorouracil 167-170 dihydropyrimidine dehydrogenase Homo sapiens 35-66 12915131-0 2003 Ha-ras overexpression mediated cell apoptosis in the presence of 5-fluorouracil. Fluorouracil 65-79 Harvey rat sarcoma virus oncogene Mus musculus 0-6 12915131-1 2003 By using a mouse NIH3T3 derivate designed 7-4 harboring the inducible Ha-ras oncogene, we demonstrated the close relationship between Ha-ras expression level and sensitization of 5-flurouracil (5-FU)-treated cells. Fluorouracil 194-198 Harvey rat sarcoma virus oncogene Mus musculus 70-76 12915131-1 2003 By using a mouse NIH3T3 derivate designed 7-4 harboring the inducible Ha-ras oncogene, we demonstrated the close relationship between Ha-ras expression level and sensitization of 5-flurouracil (5-FU)-treated cells. Fluorouracil 194-198 Harvey rat sarcoma virus oncogene Mus musculus 134-140 12915131-5 2003 These results indicate that Ras, Bcl-2, as well as Raf-1 and PI3K pathways play pivotal roles in 5-FU-induced apoptosis under Ha-ras-overexpressed condition. Fluorouracil 97-101 Harvey rat sarcoma virus oncogene Mus musculus 126-132 12915131-7 2003 Sensitization of Ha-ras-related cells to 5-FU was also demonstrated in human bladder cancer cells. Fluorouracil 41-45 Harvey rat sarcoma virus oncogene Mus musculus 17-23 12915131-8 2003 Through understanding the mechanism of 5-FU induced apoptosis in tumor cells, a new direction toward the treatment of Ha-ras oncogene-related cancers with 5-FU at more optimal dosages is possible and combinational therapy with other drugs that suppress PI3K and Bcl-2 activities can also be considered. Fluorouracil 39-43 Harvey rat sarcoma virus oncogene Mus musculus 118-124 12915131-8 2003 Through understanding the mechanism of 5-FU induced apoptosis in tumor cells, a new direction toward the treatment of Ha-ras oncogene-related cancers with 5-FU at more optimal dosages is possible and combinational therapy with other drugs that suppress PI3K and Bcl-2 activities can also be considered. Fluorouracil 155-159 Harvey rat sarcoma virus oncogene Mus musculus 118-124 12960741-2 2003 Previous studies indicated that measurement of dihydropyrimidine dehydrogenase (DPD) gene expression before treatment was valuable in determining the potential benefit of and toxicity to 5-FU treatment. Fluorouracil 187-191 dihydropyrimidine dehydrogenase Homo sapiens 47-78 12960741-2 2003 Previous studies indicated that measurement of dihydropyrimidine dehydrogenase (DPD) gene expression before treatment was valuable in determining the potential benefit of and toxicity to 5-FU treatment. Fluorouracil 187-191 dihydropyrimidine dehydrogenase Homo sapiens 80-83 11172899-8 2001 The SRB assay revealed a 8-fold increased IC(50) for cisplatin and a 2.5-fold increase for 5-FU in DU 145 MN1 as compared to DU 145 cells. Fluorouracil 91-95 chaperonin containing TCP1 subunit 4 Homo sapiens 4-7 11501504-0 2001 Dihydropyrimidine dehydrogenase activity and thymidylate synthase level are associated with response to 5-fluorouracil in human colorectal cancer. Fluorouracil 104-118 dihydropyrimidine dehydrogenase Homo sapiens 0-31 11501504-1 2001 In the recent studies associated with the modulation of 5-fluorouracil (5-FU) and the development of new antifolates, attentions have been focused on the expression of the target enzymes, thymidylate synthase (TS) and dihydropyrimidine dehydrogenase (DPD), that affect tumor sensitivity and resistance to drugs. Fluorouracil 72-76 dihydropyrimidine dehydrogenase Homo sapiens 218-249 11501504-2 2001 In order to evaluate predictability of therapeutic efficacy by intratumoral enzyme activity, we investigated the role of TS content and DPD activity in tumor sensitivity of 5-FU. Fluorouracil 173-177 dihydropyrimidine dehydrogenase Homo sapiens 136-139 11501504-9 2001 Four out of 24 patients, highly responsive to 5-FU, showed low levels in both DPD and TS. Fluorouracil 46-50 dihydropyrimidine dehydrogenase Homo sapiens 78-81 11197871-2 2001 The transfection of UPRT, a 5-FU converting enzyme, gene resulted in the significant change in sensitivity of pancreatic cancer cells against 5-FU. Fluorouracil 28-32 uracil phosphoribosyltransferase homolog Homo sapiens 20-24 12912951-0 2003 Denaturing high performance liquid chromatography analysis of the DPYD gene in patients with lethal 5-fluorouracil toxicity. Fluorouracil 100-114 dihydropyrimidine dehydrogenase Homo sapiens 66-70 11219973-0 2001 Clinical implications of dihydropyrimidine dehydrogenase on 5-FU pharmacology. Fluorouracil 60-64 dihydropyrimidine dehydrogenase Homo sapiens 25-56 12912951-4 2003 In the present study, we used this denaturing high performance liquid chromatography approach to examine the DPYD genotype of three patients who experienced lethal toxicity after administration of 5-FU. Fluorouracil 197-201 dihydropyrimidine dehydrogenase Homo sapiens 109-113 12853891-1 2003 TS-1 contains tegaful (FT), 5-chloro-2,4-dihydroxypyridine (CDHP; an inhibitor of 5-fluorouracil (5-FU) degradation) and potassium oxonate (Oxo; an inhibitor of 5-FU assimilation mainly in the digestive tract) in a molar ratio of 1:0.4:1. Fluorouracil 82-96 Trichinella spiralis resistance 1 Mus musculus 0-4 12853891-1 2003 TS-1 contains tegaful (FT), 5-chloro-2,4-dihydroxypyridine (CDHP; an inhibitor of 5-fluorouracil (5-FU) degradation) and potassium oxonate (Oxo; an inhibitor of 5-FU assimilation mainly in the digestive tract) in a molar ratio of 1:0.4:1. Fluorouracil 98-102 Trichinella spiralis resistance 1 Mus musculus 0-4 11219973-1 2001 Dihydropyrimidine dehydrogenase (DPD) is the initial rate-limiting enzyme in the catabolism of 5-fluorouracil (5-FU), accounting for catabolism of over 85% of an administered dose of 5-FU. Fluorouracil 95-109 dihydropyrimidine dehydrogenase Homo sapiens 0-31 12841874-9 2003 ROC curves indicated that DPD and NT mRNAs were possible predictors of sensitivity to 5-FU, with cutoff values of 0.6 and 0.4, respectively. Fluorouracil 86-90 dihydropyrimidine dehydrogenase Homo sapiens 26-29 11219973-1 2001 Dihydropyrimidine dehydrogenase (DPD) is the initial rate-limiting enzyme in the catabolism of 5-fluorouracil (5-FU), accounting for catabolism of over 85% of an administered dose of 5-FU. Fluorouracil 95-109 dihydropyrimidine dehydrogenase Homo sapiens 33-36 12841874-10 2003 The sensitivity of colorectal cancer to 5-FU may be regulated by DPD, the rate-limiting enzyme of catabolism, and NT, an important transmembrane transporter of nucleosides. Fluorouracil 40-44 dihydropyrimidine dehydrogenase Homo sapiens 65-68 11219973-1 2001 Dihydropyrimidine dehydrogenase (DPD) is the initial rate-limiting enzyme in the catabolism of 5-fluorouracil (5-FU), accounting for catabolism of over 85% of an administered dose of 5-FU. Fluorouracil 111-115 dihydropyrimidine dehydrogenase Homo sapiens 0-31 11219973-1 2001 Dihydropyrimidine dehydrogenase (DPD) is the initial rate-limiting enzyme in the catabolism of 5-fluorouracil (5-FU), accounting for catabolism of over 85% of an administered dose of 5-FU. Fluorouracil 111-115 dihydropyrimidine dehydrogenase Homo sapiens 33-36 11219973-1 2001 Dihydropyrimidine dehydrogenase (DPD) is the initial rate-limiting enzyme in the catabolism of 5-fluorouracil (5-FU), accounting for catabolism of over 85% of an administered dose of 5-FU. Fluorouracil 183-187 dihydropyrimidine dehydrogenase Homo sapiens 0-31 11219973-1 2001 Dihydropyrimidine dehydrogenase (DPD) is the initial rate-limiting enzyme in the catabolism of 5-fluorouracil (5-FU), accounting for catabolism of over 85% of an administered dose of 5-FU. Fluorouracil 183-187 dihydropyrimidine dehydrogenase Homo sapiens 33-36 11219973-2 2001 DPD plays an important role in regulating the availability of 5-FU for anabolism. Fluorouracil 62-66 dihydropyrimidine dehydrogenase Homo sapiens 0-3 11219973-3 2001 DPD also accounts for much of the variability observed with the therapeutic use of 5-FU. Fluorouracil 83-87 dihydropyrimidine dehydrogenase Homo sapiens 0-3 11219973-5 2001 Knowledge of the DPD level, as well as the levels of other potentially important molecular markers (e.g., thymidylate synthase), may permit adjustments or modulation of the 5-FU dose that can result in an increase in the therapeutic efficacy of 5-FU. Fluorouracil 173-177 dihydropyrimidine dehydrogenase Homo sapiens 17-20 11219978-2 2001 Tegafur, a prodrug of 5-fluorouracil (5-FU), is converted to 5-FU by the hepatic cytochrome P450 pathway, whereas uracil enhances the half-life of converted 5-FU leading to prolonged exposure and higher intracellular concentration of 5-FU by inhibiting dihydropyrimidine dehydrogenase (DPD), a rate-limiting enzyme in 5-FU catabolism. Fluorouracil 22-36 dihydropyrimidine dehydrogenase Homo sapiens 253-284 11219978-2 2001 Tegafur, a prodrug of 5-fluorouracil (5-FU), is converted to 5-FU by the hepatic cytochrome P450 pathway, whereas uracil enhances the half-life of converted 5-FU leading to prolonged exposure and higher intracellular concentration of 5-FU by inhibiting dihydropyrimidine dehydrogenase (DPD), a rate-limiting enzyme in 5-FU catabolism. Fluorouracil 22-36 dihydropyrimidine dehydrogenase Homo sapiens 286-289 11219978-2 2001 Tegafur, a prodrug of 5-fluorouracil (5-FU), is converted to 5-FU by the hepatic cytochrome P450 pathway, whereas uracil enhances the half-life of converted 5-FU leading to prolonged exposure and higher intracellular concentration of 5-FU by inhibiting dihydropyrimidine dehydrogenase (DPD), a rate-limiting enzyme in 5-FU catabolism. Fluorouracil 38-42 dihydropyrimidine dehydrogenase Homo sapiens 253-284 11219978-2 2001 Tegafur, a prodrug of 5-fluorouracil (5-FU), is converted to 5-FU by the hepatic cytochrome P450 pathway, whereas uracil enhances the half-life of converted 5-FU leading to prolonged exposure and higher intracellular concentration of 5-FU by inhibiting dihydropyrimidine dehydrogenase (DPD), a rate-limiting enzyme in 5-FU catabolism. Fluorouracil 38-42 dihydropyrimidine dehydrogenase Homo sapiens 286-289 11219979-1 2001 5-fluorouracil (5-FU) is irreversibly catabolized to dihydrofluorouracil, an inactive metabolite, by the enzyme dihydropyrimidine dehydrogenase (DPD). Fluorouracil 0-14 dihydropyrimidine dehydrogenase Homo sapiens 112-143 11219979-1 2001 5-fluorouracil (5-FU) is irreversibly catabolized to dihydrofluorouracil, an inactive metabolite, by the enzyme dihydropyrimidine dehydrogenase (DPD). Fluorouracil 0-14 dihydropyrimidine dehydrogenase Homo sapiens 145-148 11219979-1 2001 5-fluorouracil (5-FU) is irreversibly catabolized to dihydrofluorouracil, an inactive metabolite, by the enzyme dihydropyrimidine dehydrogenase (DPD). Fluorouracil 16-20 dihydropyrimidine dehydrogenase Homo sapiens 112-143 11219979-1 2001 5-fluorouracil (5-FU) is irreversibly catabolized to dihydrofluorouracil, an inactive metabolite, by the enzyme dihydropyrimidine dehydrogenase (DPD). Fluorouracil 16-20 dihydropyrimidine dehydrogenase Homo sapiens 145-148 11219979-3 2001 Inactivation of DPD, therefore, is an approach to enhance the availability of 5-FU for potential improved therapeutic effect. Fluorouracil 78-82 dihydropyrimidine dehydrogenase Homo sapiens 16-19 11334264-3 2001 Interactions between bropirimine and 5-fluorouracil (5-FU) were investigated on dihydropyrimidine dehydrogenase (DPD) activity, the rate-limiting enzyme of 5-FU metabolism, in human liver cytosol. Fluorouracil 37-51 dihydropyrimidine dehydrogenase Homo sapiens 80-111 11334264-3 2001 Interactions between bropirimine and 5-fluorouracil (5-FU) were investigated on dihydropyrimidine dehydrogenase (DPD) activity, the rate-limiting enzyme of 5-FU metabolism, in human liver cytosol. Fluorouracil 37-51 dihydropyrimidine dehydrogenase Homo sapiens 113-116 11156223-0 2000 Clinical implications of dihydropyrimidine dehydrogenase (DPD) deficiency in patients with severe 5-fluorouracil-associated toxicity: identification of new mutations in the DPD gene. Fluorouracil 98-112 dihydropyrimidine dehydrogenase Homo sapiens 58-61 11156223-1 2000 Dihydropyrimidine dehydrogenase (DPD) is the initial and rate-limiting enzyme in the catabolism of 5-fluorouracil (5FU), and it is suggested that patients with a partial deficiency of this enzyme are at risk for developing a severe 5FU-associated toxicity. Fluorouracil 99-113 dihydropyrimidine dehydrogenase Homo sapiens 0-31 11156223-1 2000 Dihydropyrimidine dehydrogenase (DPD) is the initial and rate-limiting enzyme in the catabolism of 5-fluorouracil (5FU), and it is suggested that patients with a partial deficiency of this enzyme are at risk for developing a severe 5FU-associated toxicity. Fluorouracil 99-113 dihydropyrimidine dehydrogenase Homo sapiens 33-36 11156223-1 2000 Dihydropyrimidine dehydrogenase (DPD) is the initial and rate-limiting enzyme in the catabolism of 5-fluorouracil (5FU), and it is suggested that patients with a partial deficiency of this enzyme are at risk for developing a severe 5FU-associated toxicity. Fluorouracil 115-118 dihydropyrimidine dehydrogenase Homo sapiens 0-31 11156223-1 2000 Dihydropyrimidine dehydrogenase (DPD) is the initial and rate-limiting enzyme in the catabolism of 5-fluorouracil (5FU), and it is suggested that patients with a partial deficiency of this enzyme are at risk for developing a severe 5FU-associated toxicity. Fluorouracil 115-118 dihydropyrimidine dehydrogenase Homo sapiens 33-36 11156223-1 2000 Dihydropyrimidine dehydrogenase (DPD) is the initial and rate-limiting enzyme in the catabolism of 5-fluorouracil (5FU), and it is suggested that patients with a partial deficiency of this enzyme are at risk for developing a severe 5FU-associated toxicity. Fluorouracil 232-235 dihydropyrimidine dehydrogenase Homo sapiens 0-31 11156223-1 2000 Dihydropyrimidine dehydrogenase (DPD) is the initial and rate-limiting enzyme in the catabolism of 5-fluorouracil (5FU), and it is suggested that patients with a partial deficiency of this enzyme are at risk for developing a severe 5FU-associated toxicity. Fluorouracil 232-235 dihydropyrimidine dehydrogenase Homo sapiens 33-36 11195061-5 2000 In the case of 5-FU, the quantitative expression levels of thymidylate synthase, thymidine phosphorylase, and dihydropyrimidine dehydrogenase were found to be associated with tumor response. Fluorouracil 15-19 dihydropyrimidine dehydrogenase Homo sapiens 59-141 11095583-3 2000 In fourteen cDNA-expressed human P450 enzymes having measurable activities, CYP1A2, CYP2A6, CYP2E1, and CYP3A5 were highly active in catalyzing 5-FU formation at a tegafur concentration of 100 microM. Fluorouracil 144-148 cytochrome P450 family 2 subfamily A member 6 Homo sapiens 84-90 11095583-4 2000 Kinetic analysis revealed that CYP1A2 had the highest V(max)/K(m) value and that the V(max) value of CYP2A6 was high in 5-FU formation. Fluorouracil 120-124 cytochrome P450 family 2 subfamily A member 6 Homo sapiens 101-107 11095583-9 2000 Polyclonal anti-CYP1A2 antibody, monoclonal anti-CYP2A6, and anti-CYP2C8 antibodies inhibited 5-FU formation activities to different extents in those two microsomal samples. Fluorouracil 94-98 cytochrome P450 family 2 subfamily A member 6 Homo sapiens 49-55 11095583-10 2000 These results suggest that CYP1A2, CYP2A6, and CYP2C8 have important roles in human liver microsomal 5-FU formation and that the involvement of these three P450 forms differs among individual humans. Fluorouracil 101-105 cytochrome P450 family 2 subfamily A member 6 Homo sapiens 35-41 11056019-3 2000 Indeed, MED1 acts as a mismatch-specific DNA N-glycosylase active on thymine, uracil, and 5-fluorouracil paired with guanine. Fluorouracil 90-104 mediator complex subunit 1 Homo sapiens 8-12 11106261-0 2000 Bioactivation of tegafur to 5-fluorouracil is catalyzed by cytochrome P-450 2A6 in human liver microsomes in vitro. Fluorouracil 28-42 cytochrome P450 family 2 subfamily A member 6 Homo sapiens 59-79 11106261-6 2000 In the correlation study using a panel of 10 human liver microsomes, the formation of 5-FU from tegafur showed a significant correlation (r = 0.98; P < 0.001) with coumarin 7-hydroxylation, a marker activity of CYP2A6. Fluorouracil 86-90 cytochrome P450 family 2 subfamily A member 6 Homo sapiens 214-220 11106261-7 2000 In addition, a specific substrate of CYP2A6 and anti-CYP2A6 antibody inhibited the formation of 5-FU by 90% in human liver microsomes. Fluorouracil 96-100 cytochrome P450 family 2 subfamily A member 6 Homo sapiens 37-43 11106261-7 2000 In addition, a specific substrate of CYP2A6 and anti-CYP2A6 antibody inhibited the formation of 5-FU by 90% in human liver microsomes. Fluorouracil 96-100 cytochrome P450 family 2 subfamily A member 6 Homo sapiens 53-59 11106261-8 2000 Moreover, cDNA-expressed CYP2A6 showed the highest activity for the formation of 5-FU among 10 cDNA-expressed CYPs, with a Km value similar to that found for the high-affinity component in human liver microsomes. Fluorouracil 81-85 cytochrome P450 family 2 subfamily A member 6 Homo sapiens 25-31 11106261-10 2000 However, to what extent the bioactivation of tegafur by CYP2A6 accounts for the formation of 5-FU in vivo remains unclear, because the formation of 5-FU from tegafur is also catalyzed by the soluble fraction of a 100,000 x g supernatant and also derived from spontaneous degradation of tegafur. Fluorouracil 93-97 cytochrome P450 family 2 subfamily A member 6 Homo sapiens 56-62 11029488-0 2000 Dihydropyrimidine dehydrogenase activity and mRNA expression in advanced gastric cancer analyzed in relation to effectiveness of preoperative 5-fluorouracil-based chemotherapy. Fluorouracil 142-156 dihydropyrimidine dehydrogenase Homo sapiens 0-31 12845947-1 2003 BACKGROUND/AIMS: DPD (dihydropyrimidine dehydrogenase) activity shows a correlation with 5-fluorouracil chemosensitivity. Fluorouracil 89-103 dihydropyrimidine dehydrogenase Homo sapiens 17-20 12845947-1 2003 BACKGROUND/AIMS: DPD (dihydropyrimidine dehydrogenase) activity shows a correlation with 5-fluorouracil chemosensitivity. Fluorouracil 89-103 dihydropyrimidine dehydrogenase Homo sapiens 22-53 11029488-1 2000 Dihydroxypyrimidine dehydrogenase (DPD) is an enzyme involved in degradation and inactivation of 5-fluorouracil (5-FU). Fluorouracil 97-111 dihydropyrimidine dehydrogenase Homo sapiens 0-33 11029488-1 2000 Dihydroxypyrimidine dehydrogenase (DPD) is an enzyme involved in degradation and inactivation of 5-fluorouracil (5-FU). Fluorouracil 97-111 dihydropyrimidine dehydrogenase Homo sapiens 35-38 11029488-1 2000 Dihydroxypyrimidine dehydrogenase (DPD) is an enzyme involved in degradation and inactivation of 5-fluorouracil (5-FU). Fluorouracil 113-117 dihydropyrimidine dehydrogenase Homo sapiens 0-33 11029488-1 2000 Dihydroxypyrimidine dehydrogenase (DPD) is an enzyme involved in degradation and inactivation of 5-fluorouracil (5-FU). Fluorouracil 113-117 dihydropyrimidine dehydrogenase Homo sapiens 35-38 10930409-3 2000 We show that MED1 functions as a mismatch-specific DNA N-glycosylase active on thymine, uracil, and 5-fluorouracil when these bases are opposite to guanine. Fluorouracil 100-114 mediator complex subunit 1 Homo sapiens 13-17 11098485-1 2000 Over the past decade, increasing data have emphasized both the importance of dihydropyrimidine dehydrogenase (DPD), the initial, rate-limiting enzyme in the catabolism of fluorouracil (5-FU), and its role as a control step in 5-FU metabolism, regulating the availability of 5-FU for anabolism. Fluorouracil 226-230 dihydropyrimidine dehydrogenase Homo sapiens 77-108 11098485-1 2000 Over the past decade, increasing data have emphasized both the importance of dihydropyrimidine dehydrogenase (DPD), the initial, rate-limiting enzyme in the catabolism of fluorouracil (5-FU), and its role as a control step in 5-FU metabolism, regulating the availability of 5-FU for anabolism. Fluorouracil 226-230 dihydropyrimidine dehydrogenase Homo sapiens 110-113 11098485-2 2000 It is now clear that DPD also accounts for much of the variability observed with therapeutic use of 5-FU, including variabilities in 5-FU levels over a 24-hour infusion, interindividual pharmacokinetics, bioavailability, toxicity, and drug response (resistance). Fluorouracil 100-104 dihydropyrimidine dehydrogenase Homo sapiens 21-24 11098485-2 2000 It is now clear that DPD also accounts for much of the variability observed with therapeutic use of 5-FU, including variabilities in 5-FU levels over a 24-hour infusion, interindividual pharmacokinetics, bioavailability, toxicity, and drug response (resistance). Fluorouracil 133-137 dihydropyrimidine dehydrogenase Homo sapiens 21-24 11098485-4 2000 In order to lessen this variability, and potentially improve 5-FU pharmacology, the pharmaceutical industry has made an effort to develop DPD inhibitors to modulate 5-FU metabolism, which has resulted in the creation of a new subclass of orally administered fluoropyrimidines, known as DPD-inhibiting fluoropyrimidines (DIF). Fluorouracil 165-169 dihydropyrimidine dehydrogenase Homo sapiens 138-141 12910683-9 2003 Immunohistochemical staining of ki67 showed that the ki67 label index (ki67-LI) displayed significant difference between Control group and Quercetin group, 5-Fu group, Quercetin + 5-Fu group, and so did the staining of Bcl-2. Fluorouracil 156-160 antigen identified by monoclonal antibody Ki 67 Mus musculus 32-36 12910683-9 2003 Immunohistochemical staining of ki67 showed that the ki67 label index (ki67-LI) displayed significant difference between Control group and Quercetin group, 5-Fu group, Quercetin + 5-Fu group, and so did the staining of Bcl-2. Fluorouracil 156-160 antigen identified by monoclonal antibody Ki 67 Mus musculus 53-57 12910683-9 2003 Immunohistochemical staining of ki67 showed that the ki67 label index (ki67-LI) displayed significant difference between Control group and Quercetin group, 5-Fu group, Quercetin + 5-Fu group, and so did the staining of Bcl-2. Fluorouracil 156-160 antigen identified by monoclonal antibody Ki 67 Mus musculus 53-57 12910683-9 2003 Immunohistochemical staining of ki67 showed that the ki67 label index (ki67-LI) displayed significant difference between Control group and Quercetin group, 5-Fu group, Quercetin + 5-Fu group, and so did the staining of Bcl-2. Fluorouracil 180-184 antigen identified by monoclonal antibody Ki 67 Mus musculus 32-36 12910683-9 2003 Immunohistochemical staining of ki67 showed that the ki67 label index (ki67-LI) displayed significant difference between Control group and Quercetin group, 5-Fu group, Quercetin + 5-Fu group, and so did the staining of Bcl-2. Fluorouracil 180-184 antigen identified by monoclonal antibody Ki 67 Mus musculus 53-57 12910683-9 2003 Immunohistochemical staining of ki67 showed that the ki67 label index (ki67-LI) displayed significant difference between Control group and Quercetin group, 5-Fu group, Quercetin + 5-Fu group, and so did the staining of Bcl-2. Fluorouracil 180-184 antigen identified by monoclonal antibody Ki 67 Mus musculus 53-57 10951589-5 2000 However, after treatment with the cytotoxic drug 5-fluorouracil or with gamma-radiation, the bcl-w-null animals exhibited substantially more apoptosis than their wild-type counterparts in both tissues. Fluorouracil 49-63 BCL2-like 2 Mus musculus 93-98 12829029-8 2003 In contrast to in vivo homing, both in vitro migration toward stromal-derived factor (SDF)-1 and the average CXC chemokine receptor-4 (CXCR4) expression were lower in 5-FU-treated cells. Fluorouracil 167-171 chemokine (C-X-C motif) receptor 4 Mus musculus 109-133 12829029-8 2003 In contrast to in vivo homing, both in vitro migration toward stromal-derived factor (SDF)-1 and the average CXC chemokine receptor-4 (CXCR4) expression were lower in 5-FU-treated cells. Fluorouracil 167-171 chemokine (C-X-C motif) receptor 4 Mus musculus 135-140 12851836-2 2003 DPD is also responsible for the degradation of 5-fluorouracil (5-FU), which is the most frequently prescribed anticancer drug for the treatment of malignancies of the gastrointestinal tract. Fluorouracil 63-67 dihydropyrimidine dehydrogenase Homo sapiens 0-3 12851836-3 2003 DPD could influence the antitumor effect and the adverse effects of 5-FU. Fluorouracil 68-72 dihydropyrimidine dehydrogenase Homo sapiens 0-3 12851836-4 2003 High intratumoral DPD activity markedly decreases the cytotoxic effect of 5-FU. Fluorouracil 74-78 dihydropyrimidine dehydrogenase Homo sapiens 18-21 12851836-6 2003 In 5-FU-based chemotherapy, escape from the degradation catalyzed by DPD is important. Fluorouracil 3-7 dihydropyrimidine dehydrogenase Homo sapiens 69-72 12851836-9 2003 In 5-FU-based cancer chemotherapy, severe toxicities were observed at higher rates in patients who were heterozygous for a mutant DPYD allele, compared with toxicities in patients who were homozygous for the wild DPYD allele. Fluorouracil 3-7 dihydropyrimidine dehydrogenase Homo sapiens 130-134 12851836-9 2003 In 5-FU-based cancer chemotherapy, severe toxicities were observed at higher rates in patients who were heterozygous for a mutant DPYD allele, compared with toxicities in patients who were homozygous for the wild DPYD allele. Fluorouracil 3-7 dihydropyrimidine dehydrogenase Homo sapiens 213-217 12851836-10 2003 Furthermore, the adverse effects of 5-FU are often lethal for patients homozygous for the mutant DPYD allele. Fluorouracil 36-40 dihydropyrimidine dehydrogenase Homo sapiens 97-101 10953310-1 2000 BACKGROUND: Dihydropyrimidine dehydrogenase (DPD) is the rate-limiting enzyme of 5-fluorouracil (5-FU) catabolism. Fluorouracil 81-95 dihydropyrimidine dehydrogenase Homo sapiens 12-43 12851836-11 2003 The apparently high prevalence of the DPYD mutation associated with lack of DPD activity in the normal population warrants genetic screening for the presence of these mutations in cancer patients before the administration of 5-FU. Fluorouracil 225-229 dihydropyrimidine dehydrogenase Homo sapiens 38-42 12691609-0 2003 Retroviral transduction of a mutant dihydrofolate reductase-thymidylate synthase fusion gene into murine marrow cells confers resistance to both methotrexate and 5-fluorouracil. Fluorouracil 162-176 dihydrofolate reductase Mus musculus 36-59 12691609-0 2003 Retroviral transduction of a mutant dihydrofolate reductase-thymidylate synthase fusion gene into murine marrow cells confers resistance to both methotrexate and 5-fluorouracil. Fluorouracil 162-176 thymidylate synthase Mus musculus 60-80 12691609-2 2003 Our laboratory has previously generated drug-resistant mutants of dihydrofolate reductase (DHFR F/S) and thymidylate synthase (TS G52S) for myeloprotection against methotrexate (MTX) and 5-fluorouracil (5-FU), respectively. Fluorouracil 187-201 dihydrofolate reductase Mus musculus 66-89 12691609-2 2003 Our laboratory has previously generated drug-resistant mutants of dihydrofolate reductase (DHFR F/S) and thymidylate synthase (TS G52S) for myeloprotection against methotrexate (MTX) and 5-fluorouracil (5-FU), respectively. Fluorouracil 187-201 thymidylate synthase Mus musculus 91-125 12691609-2 2003 Our laboratory has previously generated drug-resistant mutants of dihydrofolate reductase (DHFR F/S) and thymidylate synthase (TS G52S) for myeloprotection against methotrexate (MTX) and 5-fluorouracil (5-FU), respectively. Fluorouracil 203-207 dihydrofolate reductase Mus musculus 66-89 12691609-2 2003 Our laboratory has previously generated drug-resistant mutants of dihydrofolate reductase (DHFR F/S) and thymidylate synthase (TS G52S) for myeloprotection against methotrexate (MTX) and 5-fluorouracil (5-FU), respectively. Fluorouracil 203-207 thymidylate synthase Mus musculus 91-125 10953310-1 2000 BACKGROUND: Dihydropyrimidine dehydrogenase (DPD) is the rate-limiting enzyme of 5-fluorouracil (5-FU) catabolism. Fluorouracil 81-95 dihydropyrimidine dehydrogenase Homo sapiens 45-48 10953310-1 2000 BACKGROUND: Dihydropyrimidine dehydrogenase (DPD) is the rate-limiting enzyme of 5-fluorouracil (5-FU) catabolism. Fluorouracil 97-101 dihydropyrimidine dehydrogenase Homo sapiens 12-43 10953310-1 2000 BACKGROUND: Dihydropyrimidine dehydrogenase (DPD) is the rate-limiting enzyme of 5-fluorouracil (5-FU) catabolism. Fluorouracil 97-101 dihydropyrimidine dehydrogenase Homo sapiens 45-48 10953310-2 2000 Several studies have demonstrated the clinical importance of DPD in cancer patients, suggesting that the efficacy of 5-FU may be related to DPD activity in tumor tissue. Fluorouracil 117-121 dihydropyrimidine dehydrogenase Homo sapiens 61-64 10953310-2 2000 Several studies have demonstrated the clinical importance of DPD in cancer patients, suggesting that the efficacy of 5-FU may be related to DPD activity in tumor tissue. Fluorouracil 117-121 dihydropyrimidine dehydrogenase Homo sapiens 140-143 10953310-6 2000 DPD activity may be useful in determining the 5-FU sensitivity of differentiated gastric cancer. Fluorouracil 46-50 dihydropyrimidine dehydrogenase Homo sapiens 0-3 10965789-0 2000 A case of chronic myeloid leukemia with minor bcr-abl transcript following fluorouracil therapy for esophageal carcinoma. Fluorouracil 75-87 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 46-53 12820455-1 2003 BACKGROUND: The response rate of 5-FU and its clearance are due to the activity of dihydropyrimidine dehydrogenase (DPD), which is the first and rate-limiting enzyme for the catabolism of 5-FU. Fluorouracil 33-37 dihydropyrimidine dehydrogenase Homo sapiens 116-119 12820455-1 2003 BACKGROUND: The response rate of 5-FU and its clearance are due to the activity of dihydropyrimidine dehydrogenase (DPD), which is the first and rate-limiting enzyme for the catabolism of 5-FU. Fluorouracil 188-192 dihydropyrimidine dehydrogenase Homo sapiens 116-119 12820455-2 2003 Although several studies have evaluated the relationship between DPD expression and chemosensitivity to 5-FU in patients with colorectal cancer (CRC), only a few studies on DPD expression and clinicopathological features have been conducted using immunohistochemical staining since a monoclonal antibody for DPD has not been established. Fluorouracil 104-108 dihydropyrimidine dehydrogenase Homo sapiens 65-68 10965789-1 2000 We report here a very rare case of chronic myeloid leukemia (CML) with a minor bcr-abl transcript, which developed following long-term chemotherapy with fluorouracil for esophageal carcinoma. Fluorouracil 153-165 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 79-86 10910061-3 2000 In this study, we have determined the expression patterns of dUTPase in normal and neoplastic tissues and examined the association between dUTPase expression and response to 5-fluorouracil (5-FU)-based chemotherapy and overall survival in colorectal cancer. Fluorouracil 174-188 Deoxyuridine triphosphatase Drosophila melanogaster 139-146 12655443-10 2003 There was a significant correlation between DPD activity in PBMC and total body clearance of 5-FU. Fluorouracil 93-97 dihydropyrimidine dehydrogenase Homo sapiens 44-47 10910061-3 2000 In this study, we have determined the expression patterns of dUTPase in normal and neoplastic tissues and examined the association between dUTPase expression and response to 5-fluorouracil (5-FU)-based chemotherapy and overall survival in colorectal cancer. Fluorouracil 190-194 Deoxyuridine triphosphatase Drosophila melanogaster 139-146 10910061-13 2000 To examine the association between dUTPase expression and response to 5-FU-based chemotherapy and overall survival, we initiated a retrospective study including tumor specimens from 20 patients who had received protracted infusion of 5-FU and leucovorin for treatment of metastatic colon cancer. Fluorouracil 70-74 Deoxyuridine triphosphatase Drosophila melanogaster 35-42 10910061-21 2000 This study demonstrates that low intratumoral levels of nuclear dUTPase protein expression is associated with response to 5-FU-based chemotherapy, greater time to progression, and greater overall survival in colorectal cancer. Fluorouracil 122-126 Deoxyuridine triphosphatase Drosophila melanogaster 64-71 10851269-1 2000 5-Fluorouracil (5-FU), used widely for malignancies, phosphorylate mostly by uracil phosphoribosyl transferase (UPRT). Fluorouracil 0-14 uracil phosphoribosyltransferase homolog Homo sapiens 77-110 10851269-1 2000 5-Fluorouracil (5-FU), used widely for malignancies, phosphorylate mostly by uracil phosphoribosyl transferase (UPRT). Fluorouracil 0-14 uracil phosphoribosyltransferase homolog Homo sapiens 112-116 10851269-1 2000 5-Fluorouracil (5-FU), used widely for malignancies, phosphorylate mostly by uracil phosphoribosyl transferase (UPRT). Fluorouracil 16-20 uracil phosphoribosyltransferase homolog Homo sapiens 77-110 10851269-1 2000 5-Fluorouracil (5-FU), used widely for malignancies, phosphorylate mostly by uracil phosphoribosyl transferase (UPRT). Fluorouracil 16-20 uracil phosphoribosyltransferase homolog Homo sapiens 112-116 10853015-1 2000 Thymidine phosphorylase (dThdPase) is the rate-limiting enzyme that metabolizes 5"-deoxy-5-fluorouridine (5"-dFUrd, doxifluridine), an intermediate metabolite of capecitabine, to the active drug 5-fluorouracil (5-FUra), while dihydropyrimidine dehydrogenase (DPD) catabolizes 5-FUra to an inactive molecule. Fluorouracil 195-209 dihydropyrimidine dehydrogenase Homo sapiens 226-257 10853015-1 2000 Thymidine phosphorylase (dThdPase) is the rate-limiting enzyme that metabolizes 5"-deoxy-5-fluorouridine (5"-dFUrd, doxifluridine), an intermediate metabolite of capecitabine, to the active drug 5-fluorouracil (5-FUra), while dihydropyrimidine dehydrogenase (DPD) catabolizes 5-FUra to an inactive molecule. Fluorouracil 195-209 dihydropyrimidine dehydrogenase Homo sapiens 259-262 10853015-1 2000 Thymidine phosphorylase (dThdPase) is the rate-limiting enzyme that metabolizes 5"-deoxy-5-fluorouridine (5"-dFUrd, doxifluridine), an intermediate metabolite of capecitabine, to the active drug 5-fluorouracil (5-FUra), while dihydropyrimidine dehydrogenase (DPD) catabolizes 5-FUra to an inactive molecule. Fluorouracil 211-217 dihydropyrimidine dehydrogenase Homo sapiens 226-257 10853015-1 2000 Thymidine phosphorylase (dThdPase) is the rate-limiting enzyme that metabolizes 5"-deoxy-5-fluorouridine (5"-dFUrd, doxifluridine), an intermediate metabolite of capecitabine, to the active drug 5-fluorouracil (5-FUra), while dihydropyrimidine dehydrogenase (DPD) catabolizes 5-FUra to an inactive molecule. Fluorouracil 211-217 dihydropyrimidine dehydrogenase Homo sapiens 259-262 10853015-1 2000 Thymidine phosphorylase (dThdPase) is the rate-limiting enzyme that metabolizes 5"-deoxy-5-fluorouridine (5"-dFUrd, doxifluridine), an intermediate metabolite of capecitabine, to the active drug 5-fluorouracil (5-FUra), while dihydropyrimidine dehydrogenase (DPD) catabolizes 5-FUra to an inactive molecule. Fluorouracil 276-282 dihydropyrimidine dehydrogenase Homo sapiens 226-257 10853015-1 2000 Thymidine phosphorylase (dThdPase) is the rate-limiting enzyme that metabolizes 5"-deoxy-5-fluorouridine (5"-dFUrd, doxifluridine), an intermediate metabolite of capecitabine, to the active drug 5-fluorouracil (5-FUra), while dihydropyrimidine dehydrogenase (DPD) catabolizes 5-FUra to an inactive molecule. Fluorouracil 276-282 dihydropyrimidine dehydrogenase Homo sapiens 259-262 10853017-0 2000 Intratumoral expression of thymidylate synthase and dihydropyrimidine dehydrogenase in non-small cell lung cancer patients treated with 5-FU-based chemotherapy. Fluorouracil 136-140 dihydropyrimidine dehydrogenase Homo sapiens 52-83 10897217-1 2000 Dihydropyrimidine dehydrogenase (DPD) is a key enzyme in the catabolism of 5-fluorouracil (5-FU), and its expression in a tumor is thought to reduce the efficacy of 5-FU against the tumor. Fluorouracil 75-89 dihydropyrimidine dehydrogenase Homo sapiens 0-31 10897217-1 2000 Dihydropyrimidine dehydrogenase (DPD) is a key enzyme in the catabolism of 5-fluorouracil (5-FU), and its expression in a tumor is thought to reduce the efficacy of 5-FU against the tumor. Fluorouracil 75-89 dihydropyrimidine dehydrogenase Homo sapiens 33-36 10897217-1 2000 Dihydropyrimidine dehydrogenase (DPD) is a key enzyme in the catabolism of 5-fluorouracil (5-FU), and its expression in a tumor is thought to reduce the efficacy of 5-FU against the tumor. Fluorouracil 91-95 dihydropyrimidine dehydrogenase Homo sapiens 0-31 10897217-1 2000 Dihydropyrimidine dehydrogenase (DPD) is a key enzyme in the catabolism of 5-fluorouracil (5-FU), and its expression in a tumor is thought to reduce the efficacy of 5-FU against the tumor. Fluorouracil 91-95 dihydropyrimidine dehydrogenase Homo sapiens 33-36 10897217-1 2000 Dihydropyrimidine dehydrogenase (DPD) is a key enzyme in the catabolism of 5-fluorouracil (5-FU), and its expression in a tumor is thought to reduce the efficacy of 5-FU against the tumor. Fluorouracil 165-169 dihydropyrimidine dehydrogenase Homo sapiens 0-31 10897217-1 2000 Dihydropyrimidine dehydrogenase (DPD) is a key enzyme in the catabolism of 5-fluorouracil (5-FU), and its expression in a tumor is thought to reduce the efficacy of 5-FU against the tumor. Fluorouracil 165-169 dihydropyrimidine dehydrogenase Homo sapiens 33-36 10897217-3 2000 The expressed rhDPD protein was found to retain its entire molecular form and to show a high 5-FU-degrading activity equivalent to that of human liver DPD. Fluorouracil 93-97 dihydropyrimidine dehydrogenase Homo sapiens 16-19 10897217-6 2000 The DPD content in 26 tumor cells, estimated by immunoblotting, was closely related to the 5-FU-degrading activities in those cells (r = 0.874). Fluorouracil 91-95 dihydropyrimidine dehydrogenase Homo sapiens 4-7 10779805-6 2000 Moreover, pretreatment of SW480 cells with the anti-colon cancer agent, 5-fluorouracil (5-FU), led to enhanced Fas and ICAM-1 expression and triggered Ag-specific CTL-mediated lysis via Fas- and perforin-based pathways. Fluorouracil 72-86 intercellular adhesion molecule 1 Homo sapiens 119-125 10779805-6 2000 Moreover, pretreatment of SW480 cells with the anti-colon cancer agent, 5-fluorouracil (5-FU), led to enhanced Fas and ICAM-1 expression and triggered Ag-specific CTL-mediated lysis via Fas- and perforin-based pathways. Fluorouracil 88-92 intercellular adhesion molecule 1 Homo sapiens 119-125 10739677-2 2000 The multidrug-resistant FM3A/M cells overexpressing Pgp were resistant to apoptotic cell death induced either by Pgp-related drugs including vincristine and vinblastine, which are pumped out by Pgp, or by the Pgp-unrelated drugs including 5"-fluorouracil (5-FU) and bleomycin, which are not targets for Pgp, compared with the parental FM3A cells. Fluorouracil 239-254 phosphoglycolate phosphatase Mus musculus 52-55 10739677-2 2000 The multidrug-resistant FM3A/M cells overexpressing Pgp were resistant to apoptotic cell death induced either by Pgp-related drugs including vincristine and vinblastine, which are pumped out by Pgp, or by the Pgp-unrelated drugs including 5"-fluorouracil (5-FU) and bleomycin, which are not targets for Pgp, compared with the parental FM3A cells. Fluorouracil 256-260 phosphoglycolate phosphatase Mus musculus 52-55 12751387-2 2003 DPD is also the principal enzyme involved in the degradation of 5-fluorouracil (5-FU), an anticancer chemotherapeutic agent that is used clinically to treat renal cell carcinoma (RCC). Fluorouracil 64-78 dihydropyrimidine dehydrogenase Homo sapiens 0-3 10660460-1 2000 Several recent studies have reported a correlation between intratumor dihydropyrimidine dehydrogenase (DPD) messenger RNA (mRNA) levels and sensitivity to 5-fluorouracil (5-FU). Fluorouracil 155-169 dihydropyrimidine dehydrogenase Homo sapiens 70-101 12751387-2 2003 DPD is also the principal enzyme involved in the degradation of 5-fluorouracil (5-FU), an anticancer chemotherapeutic agent that is used clinically to treat renal cell carcinoma (RCC). Fluorouracil 80-84 dihydropyrimidine dehydrogenase Homo sapiens 0-3 14641294-1 2003 Pyrimidine nucleoside phosphorylase (PyNPase) converts 5"-deoxy-5-fluorouridine to 5"-fluorouracil, which exerts an anticancer effect before being catabolized by dihydropyrimidine dehydrogenase (DPD). Fluorouracil 83-98 dihydropyrimidine dehydrogenase Homo sapiens 162-193 14641294-1 2003 Pyrimidine nucleoside phosphorylase (PyNPase) converts 5"-deoxy-5-fluorouridine to 5"-fluorouracil, which exerts an anticancer effect before being catabolized by dihydropyrimidine dehydrogenase (DPD). Fluorouracil 83-98 dihydropyrimidine dehydrogenase Homo sapiens 195-198 12507543-1 2003 OBJECTIVES: Thymidine phosphorylase (TdR-Pase) and dihydropyrimidine dehydrogenase (DPD) are thought to be key enzymes in the metabolic pathway of 5-fluorouracil (5-FU). Fluorouracil 147-161 dihydropyrimidine dehydrogenase Homo sapiens 51-82 12507543-1 2003 OBJECTIVES: Thymidine phosphorylase (TdR-Pase) and dihydropyrimidine dehydrogenase (DPD) are thought to be key enzymes in the metabolic pathway of 5-fluorouracil (5-FU). Fluorouracil 147-161 dihydropyrimidine dehydrogenase Homo sapiens 84-87 12507543-1 2003 OBJECTIVES: Thymidine phosphorylase (TdR-Pase) and dihydropyrimidine dehydrogenase (DPD) are thought to be key enzymes in the metabolic pathway of 5-fluorouracil (5-FU). Fluorouracil 163-167 dihydropyrimidine dehydrogenase Homo sapiens 51-82 12507543-1 2003 OBJECTIVES: Thymidine phosphorylase (TdR-Pase) and dihydropyrimidine dehydrogenase (DPD) are thought to be key enzymes in the metabolic pathway of 5-fluorouracil (5-FU). Fluorouracil 163-167 dihydropyrimidine dehydrogenase Homo sapiens 84-87 12507543-2 2003 Theoretically, cancer cells which have high TdR-Pase activity and/or low DPD activity should be sensitive to 5-FU. Fluorouracil 109-113 dihydropyrimidine dehydrogenase Homo sapiens 73-76 12507543-12 2003 In addition, a stronger positive correlation was found between TdR-Pase / DPD ratio and 5-FU sensitivity. Fluorouracil 88-92 dihydropyrimidine dehydrogenase Homo sapiens 74-77 12775012-2 2003 S-1 is a novel oral dihydropyrimidine dehydrogenase (DPD) inhibitory fluoropyrimidine (DIF) based on a biochemical modulation of 5-fluorouracil (5-FU); S-1 contains tegafur (FF) and two types of enzyme inhibitor, 5-chloro-2,4-dihydroxypyridine (CDHP) and potassium oxonate (Oxo) in a molar ratio of 1:0.4:1. Fluorouracil 129-143 dihydropyrimidine dehydrogenase Homo sapiens 53-56 12775012-2 2003 S-1 is a novel oral dihydropyrimidine dehydrogenase (DPD) inhibitory fluoropyrimidine (DIF) based on a biochemical modulation of 5-fluorouracil (5-FU); S-1 contains tegafur (FF) and two types of enzyme inhibitor, 5-chloro-2,4-dihydroxypyridine (CDHP) and potassium oxonate (Oxo) in a molar ratio of 1:0.4:1. Fluorouracil 145-149 dihydropyrimidine dehydrogenase Homo sapiens 53-56 12469154-2 2003 On the other hand, variability of 5-FU sensitivity of the tumors is also presumed to depend on the enzymes of 5-FU metabolism (e.g. dihydropyrimidine dehydrogenase; DPD, rate limiting enzyme of catabolism) and action target (e.g. thymidylate synthase; TS). Fluorouracil 34-38 dihydropyrimidine dehydrogenase Homo sapiens 165-168 12469154-2 2003 On the other hand, variability of 5-FU sensitivity of the tumors is also presumed to depend on the enzymes of 5-FU metabolism (e.g. dihydropyrimidine dehydrogenase; DPD, rate limiting enzyme of catabolism) and action target (e.g. thymidylate synthase; TS). Fluorouracil 110-114 dihydropyrimidine dehydrogenase Homo sapiens 165-168 12406569-1 2002 Dihydropyrimidine dehydrogenase (DPD) is the initial, rate-limiting enzyme in the catabolism of 5-fluorouracil (5-FU). Fluorouracil 96-110 dihydropyrimidine dehydrogenase Homo sapiens 0-31 12406569-1 2002 Dihydropyrimidine dehydrogenase (DPD) is the initial, rate-limiting enzyme in the catabolism of 5-fluorouracil (5-FU). Fluorouracil 96-110 dihydropyrimidine dehydrogenase Homo sapiens 33-36 12406569-1 2002 Dihydropyrimidine dehydrogenase (DPD) is the initial, rate-limiting enzyme in the catabolism of 5-fluorouracil (5-FU). Fluorouracil 112-116 dihydropyrimidine dehydrogenase Homo sapiens 0-31 12406569-1 2002 Dihydropyrimidine dehydrogenase (DPD) is the initial, rate-limiting enzyme in the catabolism of 5-fluorouracil (5-FU). Fluorouracil 112-116 dihydropyrimidine dehydrogenase Homo sapiens 33-36 12406569-2 2002 DPD expression levels are believed to correlate with the 5-FU sensitivity of malignant tumors. Fluorouracil 57-61 dihydropyrimidine dehydrogenase Homo sapiens 0-3 12406569-5 2002 The objective of this study was to clarify the beneficial differences in 5-FU chemotherapy between genders in patients with the CRC based on DPD expression. Fluorouracil 73-77 dihydropyrimidine dehydrogenase Homo sapiens 141-144 12406569-10 2002 In the treatment of CRC, cases who will benefit most because of 5-FU sensitivity; i.e. cases with lower DPD expression, must be given priority. Fluorouracil 64-68 dihydropyrimidine dehydrogenase Homo sapiens 104-107 12406569-11 2002 Based on DPD expression, female gender seems to be a predictive factor for a better response to chemotherapy with 5-FU. Fluorouracil 114-118 dihydropyrimidine dehydrogenase Homo sapiens 9-12 12448660-0 2002 Biochemical modulation of 5-fluorouacil through dihydropyrimidine dehydrogenase inhibition: a Southwest Oncology Group phase II trial of eniluracil and 5-fluorouracil in advanced resistant colorectal cancer. Fluorouracil 26-39 dihydropyrimidine dehydrogenase Homo sapiens 48-79 12448660-1 2002 PURPOSE: To investigate the hypothesis that a systemic agent designed to inhibit dihydropyrimidine dehydrogenase (DPD), the first enzyme in the fluoropyrimidine degradative pathway, could improve the effective amount of 5-fluorouracil (5-FU) delivered to a tumor resulting in enhanced response. Fluorouracil 220-234 dihydropyrimidine dehydrogenase Homo sapiens 81-112 12448660-1 2002 PURPOSE: To investigate the hypothesis that a systemic agent designed to inhibit dihydropyrimidine dehydrogenase (DPD), the first enzyme in the fluoropyrimidine degradative pathway, could improve the effective amount of 5-fluorouracil (5-FU) delivered to a tumor resulting in enhanced response. Fluorouracil 220-234 dihydropyrimidine dehydrogenase Homo sapiens 114-117 12448660-1 2002 PURPOSE: To investigate the hypothesis that a systemic agent designed to inhibit dihydropyrimidine dehydrogenase (DPD), the first enzyme in the fluoropyrimidine degradative pathway, could improve the effective amount of 5-fluorouracil (5-FU) delivered to a tumor resulting in enhanced response. Fluorouracil 236-240 dihydropyrimidine dehydrogenase Homo sapiens 81-112 12448660-1 2002 PURPOSE: To investigate the hypothesis that a systemic agent designed to inhibit dihydropyrimidine dehydrogenase (DPD), the first enzyme in the fluoropyrimidine degradative pathway, could improve the effective amount of 5-fluorouracil (5-FU) delivered to a tumor resulting in enhanced response. Fluorouracil 236-240 dihydropyrimidine dehydrogenase Homo sapiens 114-117 12355409-1 2002 BACKGROUND AND OBJECTIVES: Dihydropyrimidine dehydrogenase (DPD) activity in tumor cells has been suggested to be one of the factors determining the effectiveness of 5-fluorouracil (5-FU). Fluorouracil 166-180 dihydropyrimidine dehydrogenase Homo sapiens 27-58 12355409-1 2002 BACKGROUND AND OBJECTIVES: Dihydropyrimidine dehydrogenase (DPD) activity in tumor cells has been suggested to be one of the factors determining the effectiveness of 5-fluorouracil (5-FU). Fluorouracil 166-180 dihydropyrimidine dehydrogenase Homo sapiens 60-63 12355409-1 2002 BACKGROUND AND OBJECTIVES: Dihydropyrimidine dehydrogenase (DPD) activity in tumor cells has been suggested to be one of the factors determining the effectiveness of 5-fluorouracil (5-FU). Fluorouracil 182-186 dihydropyrimidine dehydrogenase Homo sapiens 27-58 12355409-1 2002 BACKGROUND AND OBJECTIVES: Dihydropyrimidine dehydrogenase (DPD) activity in tumor cells has been suggested to be one of the factors determining the effectiveness of 5-fluorouracil (5-FU). Fluorouracil 182-186 dihydropyrimidine dehydrogenase Homo sapiens 60-63 12410361-4 2002 The activities of thymidine phosphorylase (TP) and dihydropyrimidine dehydrogenase (DPD) are reported to be correlated with cancer cell sensitivity against 5-FU in vitro. Fluorouracil 156-160 dihydropyrimidine dehydrogenase Homo sapiens 84-87 10660460-1 2000 Several recent studies have reported a correlation between intratumor dihydropyrimidine dehydrogenase (DPD) messenger RNA (mRNA) levels and sensitivity to 5-fluorouracil (5-FU). Fluorouracil 155-169 dihydropyrimidine dehydrogenase Homo sapiens 103-106 10660460-1 2000 Several recent studies have reported a correlation between intratumor dihydropyrimidine dehydrogenase (DPD) messenger RNA (mRNA) levels and sensitivity to 5-fluorouracil (5-FU). Fluorouracil 171-175 dihydropyrimidine dehydrogenase Homo sapiens 70-101 10660460-1 2000 Several recent studies have reported a correlation between intratumor dihydropyrimidine dehydrogenase (DPD) messenger RNA (mRNA) levels and sensitivity to 5-fluorouracil (5-FU). Fluorouracil 171-175 dihydropyrimidine dehydrogenase Homo sapiens 103-106 10657402-0 2000 Common DPYD mutation associated with 5-fluorouracil toxicity detected by PCR-mediated site-directed mutagenesis. Fluorouracil 37-51 dihydropyrimidine dehydrogenase Homo sapiens 7-11 10646641-2 2000 The uracil phosphoribosyltransferase (UPRT) gene, which is absent from mammalian cells, directly converts 5-fluorouracil (5-FU) to 5-fluorouridine 5"-monophosphate. Fluorouracil 106-120 uracil phosphoribosyltransferase homolog Homo sapiens 4-36 12360106-0 2002 High prevalence of the IVS14 + 1G>A mutation in the dihydropyrimidine dehydrogenase gene of patients with severe 5-fluorouracil-associated toxicity. Fluorouracil 116-130 dihydropyrimidine dehydrogenase Homo sapiens 55-86 12360106-1 2002 Dihydropyrimidine dehydrogenase (DPD) is the initial and rate-limiting enzyme in the catabolism of 5-fluorouracil (5FU) and a DPD deficiency is increasingly being recognized as an important pharmacogenetic factor in the aetiology of severe 5FU-associated toxicity. Fluorouracil 99-113 dihydropyrimidine dehydrogenase Homo sapiens 0-31 12360106-1 2002 Dihydropyrimidine dehydrogenase (DPD) is the initial and rate-limiting enzyme in the catabolism of 5-fluorouracil (5FU) and a DPD deficiency is increasingly being recognized as an important pharmacogenetic factor in the aetiology of severe 5FU-associated toxicity. Fluorouracil 99-113 dihydropyrimidine dehydrogenase Homo sapiens 33-36 12360106-1 2002 Dihydropyrimidine dehydrogenase (DPD) is the initial and rate-limiting enzyme in the catabolism of 5-fluorouracil (5FU) and a DPD deficiency is increasingly being recognized as an important pharmacogenetic factor in the aetiology of severe 5FU-associated toxicity. Fluorouracil 115-118 dihydropyrimidine dehydrogenase Homo sapiens 0-31 12360106-1 2002 Dihydropyrimidine dehydrogenase (DPD) is the initial and rate-limiting enzyme in the catabolism of 5-fluorouracil (5FU) and a DPD deficiency is increasingly being recognized as an important pharmacogenetic factor in the aetiology of severe 5FU-associated toxicity. Fluorouracil 115-118 dihydropyrimidine dehydrogenase Homo sapiens 33-36 12360106-1 2002 Dihydropyrimidine dehydrogenase (DPD) is the initial and rate-limiting enzyme in the catabolism of 5-fluorouracil (5FU) and a DPD deficiency is increasingly being recognized as an important pharmacogenetic factor in the aetiology of severe 5FU-associated toxicity. Fluorouracil 240-243 dihydropyrimidine dehydrogenase Homo sapiens 0-31 12360106-1 2002 Dihydropyrimidine dehydrogenase (DPD) is the initial and rate-limiting enzyme in the catabolism of 5-fluorouracil (5FU) and a DPD deficiency is increasingly being recognized as an important pharmacogenetic factor in the aetiology of severe 5FU-associated toxicity. Fluorouracil 240-243 dihydropyrimidine dehydrogenase Homo sapiens 33-36 12352929-1 2002 This study investigated the relationship among the pharmacokinetics of 5-fluorouracil (5-FU) and 5-fluoro-5,6-dihydrouracil (5-FDHU); the activity of dihydropyrimidine dehydrogenase (DPD) in peripheral blood mononuclear cells; and treatment-related toxicity in 26 patients with surgically resected colorectal cancer treated with short daily infusions of 5-FU adjuvant chemotherapy, each cycle consisting of 5 consecutive days every 4 weeks. Fluorouracil 354-358 dihydropyrimidine dehydrogenase Homo sapiens 150-181 12183426-1 2002 Methionine depletion in the human cell line CCRF-CEM through the action of recombinant methioninase (rMETase), a methionine-cleaving enzyme, was previously demonstrated to produce a strong cytotoxic synergistic effect with fluorouracil (FUra) throughout a broad range of concentrations of FUra and rMETase, including subcytotoxic levels of rMETase. Fluorouracil 223-235 granzyme M Rattus norvegicus 101-108 12183426-1 2002 Methionine depletion in the human cell line CCRF-CEM through the action of recombinant methioninase (rMETase), a methionine-cleaving enzyme, was previously demonstrated to produce a strong cytotoxic synergistic effect with fluorouracil (FUra) throughout a broad range of concentrations of FUra and rMETase, including subcytotoxic levels of rMETase. Fluorouracil 237-241 granzyme M Rattus norvegicus 101-108 12183426-10 2002 We hypothesize that potentiation of FUra cytotoxicity by rMETase may result from increased inhibition of thymidylate synthase, together with DNA hypomethylation and enhanced DNA repair that could be involved in cell responses to drug-induced damage. Fluorouracil 36-40 granzyme M Rattus norvegicus 57-64 12096336-0 2002 Novel gain of function activity of p53 mutants: activation of the dUTPase gene expression leading to resistance to 5-fluorouracil. Fluorouracil 115-129 Deoxyuridine triphosphatase Drosophila melanogaster 66-73 12096336-6 2002 Using tetracycline-regulated retroviral vectors for conditional expression of p53 mutants, we found that transcription of the dUTPase gene is increased within 24 h after tetracycline withdrawal, and the cells acquire higher resistance to 5-FU. Fluorouracil 238-242 Deoxyuridine triphosphatase Drosophila melanogaster 126-133 12069415-1 2002 Dihydropyrimidine dehydrogenase (DPD) is the initial, rate-limiting enzyme in the catabolism of 5-fluorouracil (5-FU). Fluorouracil 96-110 dihydropyrimidine dehydrogenase Homo sapiens 0-31 12069415-1 2002 Dihydropyrimidine dehydrogenase (DPD) is the initial, rate-limiting enzyme in the catabolism of 5-fluorouracil (5-FU). Fluorouracil 96-110 dihydropyrimidine dehydrogenase Homo sapiens 33-36 12069415-1 2002 Dihydropyrimidine dehydrogenase (DPD) is the initial, rate-limiting enzyme in the catabolism of 5-fluorouracil (5-FU). Fluorouracil 112-116 dihydropyrimidine dehydrogenase Homo sapiens 0-31 12069415-1 2002 Dihydropyrimidine dehydrogenase (DPD) is the initial, rate-limiting enzyme in the catabolism of 5-fluorouracil (5-FU). Fluorouracil 112-116 dihydropyrimidine dehydrogenase Homo sapiens 33-36 12111108-1 2002 PURPOSE: S-1 is a novel oral fluorouracil antitumor drug that combines tegafur (FT), 5-chloro-2,4-dihydroxypyridine (CDHP), which inhibits dihydropyrimidine dehydrogenase (DPD), and potassium oxonate (Oxo). Fluorouracil 29-41 cadherin 3 Homo sapiens 117-121 12111108-1 2002 PURPOSE: S-1 is a novel oral fluorouracil antitumor drug that combines tegafur (FT), 5-chloro-2,4-dihydroxypyridine (CDHP), which inhibits dihydropyrimidine dehydrogenase (DPD), and potassium oxonate (Oxo). Fluorouracil 29-41 dihydropyrimidine dehydrogenase Homo sapiens 139-170 12111108-2 2002 As 50% of CDHP is excreted in the urine, renal dysfunction may directly affect the DPD inhibitory effect and lead to increased 5-fluorouracil (5-FU) concentrations. Fluorouracil 127-141 cadherin 3 Homo sapiens 10-14 12111108-2 2002 As 50% of CDHP is excreted in the urine, renal dysfunction may directly affect the DPD inhibitory effect and lead to increased 5-fluorouracil (5-FU) concentrations. Fluorouracil 143-147 cadherin 3 Homo sapiens 10-14 12044515-0 2002 Enhancement of the antitumour activity of 5-fluorouracil (5-FU) by inhibiting dihydropyrimidine dehydrogenase activity (DPD) using 5-chloro-2,4-dihydroxypyridine (CDHP) in human tumour cells. Fluorouracil 42-56 dihydropyrimidine dehydrogenase Homo sapiens 78-109 12044515-0 2002 Enhancement of the antitumour activity of 5-fluorouracil (5-FU) by inhibiting dihydropyrimidine dehydrogenase activity (DPD) using 5-chloro-2,4-dihydroxypyridine (CDHP) in human tumour cells. Fluorouracil 42-56 dihydropyrimidine dehydrogenase Homo sapiens 120-123 12044515-0 2002 Enhancement of the antitumour activity of 5-fluorouracil (5-FU) by inhibiting dihydropyrimidine dehydrogenase activity (DPD) using 5-chloro-2,4-dihydroxypyridine (CDHP) in human tumour cells. Fluorouracil 58-62 dihydropyrimidine dehydrogenase Homo sapiens 78-109 12044515-0 2002 Enhancement of the antitumour activity of 5-fluorouracil (5-FU) by inhibiting dihydropyrimidine dehydrogenase activity (DPD) using 5-chloro-2,4-dihydroxypyridine (CDHP) in human tumour cells. Fluorouracil 58-62 dihydropyrimidine dehydrogenase Homo sapiens 120-123 12090040-1 2002 Dihydropyrimidine dehydrogenase (DPD) and thymidylate synthase (TS) in cancer are considered to play key roles in the sensitivity to 5-FU-based chemotherapy. Fluorouracil 133-137 dihydropyrimidine dehydrogenase Homo sapiens 0-31 12090040-1 2002 Dihydropyrimidine dehydrogenase (DPD) and thymidylate synthase (TS) in cancer are considered to play key roles in the sensitivity to 5-FU-based chemotherapy. Fluorouracil 133-137 dihydropyrimidine dehydrogenase Homo sapiens 33-36 12090040-6 2002 These results suggest that the reduction of DPD activity is associated with the elevation of TS content, which may be connected with the development of 5-FU resistance and the effectiveness of biochemical modulation through the stabilization of TS inhibition with folic acid in colon carcinoma. Fluorouracil 152-156 dihydropyrimidine dehydrogenase Homo sapiens 44-47 10643981-4 2000 p53 function was determined to be defective in each cell line as indicated by the lack of induction of p53-responsive genes, p21 and mdm2, following treatment with 5-fluorouracil. Fluorouracil 164-178 cyclin-dependent kinase inhibitor 1A (P21) Mus musculus 125-128 10892578-3 1999 Dihydropyrimidine dehydrogenase (DPD) is the primary catabolic enzyme of 5-FU. Fluorouracil 73-77 dihydropyrimidine dehydrogenase Homo sapiens 0-31 10892578-3 1999 Dihydropyrimidine dehydrogenase (DPD) is the primary catabolic enzyme of 5-FU. Fluorouracil 73-77 dihydropyrimidine dehydrogenase Homo sapiens 33-36 10892578-4 1999 The varying levels of DPD located in the gastrointestinal tract make the absorption of oral 5-FU and resultant plasma levels erratic. Fluorouracil 92-96 dihydropyrimidine dehydrogenase Homo sapiens 22-25 10892578-9 1999 As studies have shown so far, DPD inhibitory fluoropyrimidine can prolong exposure to 5-FU, while causing fewer toxic effects, and may have therapeutic advantage over intravenous 5-FU. Fluorouracil 86-90 dihydropyrimidine dehydrogenase Homo sapiens 30-33 10560382-6 1999 Our results suggested that the efficacy of intra-arterial infusion for metastatic liver tumor is mainly due to the fact that the high concentration of 5-FU is enough to overcome the high clearance of 5-FU, which is caused by DPD. Fluorouracil 151-155 dihydropyrimidine dehydrogenase Homo sapiens 225-228 10449194-1 1999 The biochemical basis for modulation of fluorouracil (FU) activity by leucovorin is elevation of the metabolite methylenetetrahydrofolate, which stabilizes the inhibitory ternary complex formed between thymidylate synthase and the active metabolite of FU, 5-fluorodeoxyuridylate. Fluorouracil 40-52 thymidylate synthase Mus musculus 202-222 11810506-0 1999 Pyrimidine nucleoside phosphorylase and dihydropyrimidine dehydrogenase indicate chemosensitivity of human colon cancer specimens to doxifluridine and 5-fluorouracil, respectively. Fluorouracil 151-165 dihydropyrimidine dehydrogenase Homo sapiens 40-71 12133551-18 2002 CONCLUSIONS: The CaM antagonist, EBB, has a strong anti-hepatoma effect and enhances the effect of 5-FU, induces hepatoma cell to apoptosis, promotes the P53 protein expression and decreases the amount of CaM in the cytoplasm. Fluorouracil 99-103 calmodulin 2 Mus musculus 17-20 11810506-10 1999 High PyNPase activity was associated with a high chemosensitivity to 5"-DFUR, and high DPD activity correlated with a low chemosensitivity to 5-FU. Fluorouracil 142-146 dihydropyrimidine dehydrogenase Homo sapiens 87-90 11810506-12 1999 We suggest that the activity of PyNPase and DPD represents a reliable indicator for the chemosensitivity of colon cancer to 5"-DFUR and 5-FU, respectively. Fluorouracil 136-140 dihydropyrimidine dehydrogenase Homo sapiens 44-47 10480343-1 1999 PURPOSE: We performed a phase I/II dose-escalation trial of cyclophosphamide, mitoxantrone, and 5-fluorouracil (CNF) in combination with human recombinant granulocyte-colony-stimulating factor (G-CSF, filgrastim) in patients with advanced breast cancer. Fluorouracil 96-110 NPHS1 adhesion molecule, nephrin Homo sapiens 112-115 10561307-14 1999 Treatment with eniluracil will eliminate DPD activity as a source of pharmacokinetic fluorouracil variability or resistance in human colorectal cancer. Fluorouracil 85-97 dihydropyrimidine dehydrogenase Homo sapiens 41-44 11956613-2 2002 While dihydropyrimidine dehydrogenase (DPD) catalyzes 5-FU to inactive molecules. Fluorouracil 54-58 dihydropyrimidine dehydrogenase Homo sapiens 6-37 11956613-2 2002 While dihydropyrimidine dehydrogenase (DPD) catalyzes 5-FU to inactive molecules. Fluorouracil 54-58 dihydropyrimidine dehydrogenase Homo sapiens 39-42 11953843-0 2002 Reduced 5-FU clearance in a patient with low DPD activity due to heterozygosity for a mutant allele of the DPYD gene. Fluorouracil 8-12 dihydropyrimidine dehydrogenase Homo sapiens 45-48 11953843-0 2002 Reduced 5-FU clearance in a patient with low DPD activity due to heterozygosity for a mutant allele of the DPYD gene. Fluorouracil 8-12 dihydropyrimidine dehydrogenase Homo sapiens 107-111 10362102-9 1999 The synergistic effect of CDDP and 5-FU was not specific to NA cells, since ICAM-1 was synergistically induced by CDDP and 5-FU on HSC-4 cells, a squamous cell carcinoma cell line. Fluorouracil 35-39 intercellular adhesion molecule 1 Homo sapiens 76-82 10362102-9 1999 The synergistic effect of CDDP and 5-FU was not specific to NA cells, since ICAM-1 was synergistically induced by CDDP and 5-FU on HSC-4 cells, a squamous cell carcinoma cell line. Fluorouracil 123-127 intercellular adhesion molecule 1 Homo sapiens 76-82 10362102-10 1999 These findings indicate that treatment with CDDP and 5-FU induces ICAM-1 expression by a NF-kappaB independent regulatory mechanism involving PTK. Fluorouracil 53-57 intercellular adhesion molecule 1 Homo sapiens 66-72 10424383-10 1999 The number of ED2- and CD2-expressing cells in the dental pulp was only slightly reduced by 5-FU treatment at both low and high dose, while these cells decreased in number in the oral mucosa. Fluorouracil 92-96 Cd2 molecule Rattus norvegicus 23-26 11914904-2 2002 Dihydroxypyrimidine dehydrogenase (DPD), an enzyme involved in metabolism of 5-FU, is a key factor determining the sensitivity of the tumors to 5-FU. Fluorouracil 77-81 dihydropyrimidine dehydrogenase Homo sapiens 0-33 11914904-2 2002 Dihydroxypyrimidine dehydrogenase (DPD), an enzyme involved in metabolism of 5-FU, is a key factor determining the sensitivity of the tumors to 5-FU. Fluorouracil 77-81 dihydropyrimidine dehydrogenase Homo sapiens 35-38 11914904-2 2002 Dihydroxypyrimidine dehydrogenase (DPD), an enzyme involved in metabolism of 5-FU, is a key factor determining the sensitivity of the tumors to 5-FU. Fluorouracil 144-148 dihydropyrimidine dehydrogenase Homo sapiens 0-33 11914904-2 2002 Dihydroxypyrimidine dehydrogenase (DPD), an enzyme involved in metabolism of 5-FU, is a key factor determining the sensitivity of the tumors to 5-FU. Fluorouracil 144-148 dihydropyrimidine dehydrogenase Homo sapiens 35-38 11914904-3 2002 Particularly when preoperative chemotherapy based on 5-FU is attempted, it is critical to know in advance how much DPD the tumor expresses. Fluorouracil 53-57 dihydropyrimidine dehydrogenase Homo sapiens 115-118 10190647-8 1999 The cytotoxic activities of mercaptopurine and fluorouracil are regulated by thiopurine methyltransferase (TPMT) and dihydropyrimidine dehydrogenase (DPD), respectively. Fluorouracil 47-59 dihydropyrimidine dehydrogenase Homo sapiens 117-148 10190647-8 1999 The cytotoxic activities of mercaptopurine and fluorouracil are regulated by thiopurine methyltransferase (TPMT) and dihydropyrimidine dehydrogenase (DPD), respectively. Fluorouracil 47-59 dihydropyrimidine dehydrogenase Homo sapiens 150-153 10190647-10 1999 Very low DPD activity reduces fluorouracil breakdown producing severe cytotoxicity. Fluorouracil 30-42 dihydropyrimidine dehydrogenase Homo sapiens 9-12 11977552-1 2002 Dihydropyrimidine dehydrogenase (DPD) is a rate-limiting enzyme that metabolizes 5-fluorouracil (5-FU). Fluorouracil 81-95 dihydropyrimidine dehydrogenase Homo sapiens 0-31 9830620-7 1998 The recent availability of oral formulations for 5-FU in conjunction with the capability of manipulating the metabolism of 5-FU, particularly with dihydropyrimidine dehydrogenase (DPD) inhibitors, may provide a substantial incremental improvement in these therapies by eliminating the need for parenteral administration and the use of ambulatory infusion pumps. Fluorouracil 49-53 dihydropyrimidine dehydrogenase Homo sapiens 147-178 11977552-1 2002 Dihydropyrimidine dehydrogenase (DPD) is a rate-limiting enzyme that metabolizes 5-fluorouracil (5-FU). Fluorouracil 81-95 dihydropyrimidine dehydrogenase Homo sapiens 33-36 11977552-1 2002 Dihydropyrimidine dehydrogenase (DPD) is a rate-limiting enzyme that metabolizes 5-fluorouracil (5-FU). Fluorouracil 97-101 dihydropyrimidine dehydrogenase Homo sapiens 0-31 11977552-1 2002 Dihydropyrimidine dehydrogenase (DPD) is a rate-limiting enzyme that metabolizes 5-fluorouracil (5-FU). Fluorouracil 97-101 dihydropyrimidine dehydrogenase Homo sapiens 33-36 11977552-2 2002 We report a patient with metachronous liver metastasis from rectal cancer with low expression of DPD, who demonstrated complete response to chemotherapy comprising 5-FU, Leucovorin, and UFT. Fluorouracil 164-168 dihydropyrimidine dehydrogenase Homo sapiens 97-100 11977552-9 2002 This case provides evidence that a low expression of DPD in the primary lesion is related to a favorable response of liver metastasis to 5-FU-based systemic chemotherapy. Fluorouracil 137-141 dihydropyrimidine dehydrogenase Homo sapiens 53-56 9830620-7 1998 The recent availability of oral formulations for 5-FU in conjunction with the capability of manipulating the metabolism of 5-FU, particularly with dihydropyrimidine dehydrogenase (DPD) inhibitors, may provide a substantial incremental improvement in these therapies by eliminating the need for parenteral administration and the use of ambulatory infusion pumps. Fluorouracil 49-53 dihydropyrimidine dehydrogenase Homo sapiens 180-183 9830620-7 1998 The recent availability of oral formulations for 5-FU in conjunction with the capability of manipulating the metabolism of 5-FU, particularly with dihydropyrimidine dehydrogenase (DPD) inhibitors, may provide a substantial incremental improvement in these therapies by eliminating the need for parenteral administration and the use of ambulatory infusion pumps. Fluorouracil 123-127 dihydropyrimidine dehydrogenase Homo sapiens 147-178 9830620-7 1998 The recent availability of oral formulations for 5-FU in conjunction with the capability of manipulating the metabolism of 5-FU, particularly with dihydropyrimidine dehydrogenase (DPD) inhibitors, may provide a substantial incremental improvement in these therapies by eliminating the need for parenteral administration and the use of ambulatory infusion pumps. Fluorouracil 123-127 dihydropyrimidine dehydrogenase Homo sapiens 180-183 9830621-0 1998 The role of dihydropyrimidine dehydrogenase (DPD) modulation in 5-FU pharmacology. Fluorouracil 64-68 dihydropyrimidine dehydrogenase Homo sapiens 12-43 9830621-0 1998 The role of dihydropyrimidine dehydrogenase (DPD) modulation in 5-FU pharmacology. Fluorouracil 64-68 dihydropyrimidine dehydrogenase Homo sapiens 45-48 9830621-1 1998 Over the past several years, the pyrimidine catabolic pathway and, in particular, the first enzymatic step involving dihydropyrimidine dehydrogenase (DPD) have been recognized as being critical in determining the ultimate metabolism and, in turn, the pharmacology of the antimetabolite drug 5-fluorouracil (5-FU). Fluorouracil 291-305 dihydropyrimidine dehydrogenase Homo sapiens 117-148 9830621-1 1998 Over the past several years, the pyrimidine catabolic pathway and, in particular, the first enzymatic step involving dihydropyrimidine dehydrogenase (DPD) have been recognized as being critical in determining the ultimate metabolism and, in turn, the pharmacology of the antimetabolite drug 5-fluorouracil (5-FU). Fluorouracil 291-305 dihydropyrimidine dehydrogenase Homo sapiens 150-153 9830621-1 1998 Over the past several years, the pyrimidine catabolic pathway and, in particular, the first enzymatic step involving dihydropyrimidine dehydrogenase (DPD) have been recognized as being critical in determining the ultimate metabolism and, in turn, the pharmacology of the antimetabolite drug 5-fluorouracil (5-FU). Fluorouracil 307-311 dihydropyrimidine dehydrogenase Homo sapiens 117-148 9830621-1 1998 Over the past several years, the pyrimidine catabolic pathway and, in particular, the first enzymatic step involving dihydropyrimidine dehydrogenase (DPD) have been recognized as being critical in determining the ultimate metabolism and, in turn, the pharmacology of the antimetabolite drug 5-fluorouracil (5-FU). Fluorouracil 307-311 dihydropyrimidine dehydrogenase Homo sapiens 150-153 9830621-2 1998 Variability in DPD activity in the normal population accounts for observed differences in the pharmacokinetics and oral bioavailability of 5-FU with an additional smaller percentage (< 5%) of the population having a relatively profound deficiency in DPD activity. Fluorouracil 139-143 dihydropyrimidine dehydrogenase Homo sapiens 15-18 9830621-3 1998 Diurnal variation of DPD activity is responsible for the observed variation in 5-FU levels during continuous or protracted 5-FU infusions. Fluorouracil 79-83 dihydropyrimidine dehydrogenase Homo sapiens 21-24 9830621-3 1998 Diurnal variation of DPD activity is responsible for the observed variation in 5-FU levels during continuous or protracted 5-FU infusions. Fluorouracil 123-127 dihydropyrimidine dehydrogenase Homo sapiens 21-24 9830621-4 1998 Relatively elevated levels of DPD in tumor tissue may also be partially responsible for observed 5-FU tumor resistance. Fluorouracil 97-101 dihydropyrimidine dehydrogenase Homo sapiens 30-33 9830627-1 1998 Eniluracil is a potent inactivator of dihydropyrimidine dehydrogenase (DPD), which is the first enzyme in the degradative pathway of systemically administered 5-fluorouracil (5-FU). Fluorouracil 159-173 dihydropyrimidine dehydrogenase Homo sapiens 38-69 9830627-1 1998 Eniluracil is a potent inactivator of dihydropyrimidine dehydrogenase (DPD), which is the first enzyme in the degradative pathway of systemically administered 5-fluorouracil (5-FU). Fluorouracil 159-173 dihydropyrimidine dehydrogenase Homo sapiens 71-74 9830627-1 1998 Eniluracil is a potent inactivator of dihydropyrimidine dehydrogenase (DPD), which is the first enzyme in the degradative pathway of systemically administered 5-fluorouracil (5-FU). Fluorouracil 175-179 dihydropyrimidine dehydrogenase Homo sapiens 38-69 9830627-1 1998 Eniluracil is a potent inactivator of dihydropyrimidine dehydrogenase (DPD), which is the first enzyme in the degradative pathway of systemically administered 5-fluorouracil (5-FU). Fluorouracil 175-179 dihydropyrimidine dehydrogenase Homo sapiens 71-74 9893640-3 1998 DPD activity was measured in mononuclear cells obtained prior to and after the administration of 5-FU in 20 patients with colorectal cancer. Fluorouracil 97-101 dihydropyrimidine dehydrogenase Homo sapiens 0-3 9893640-4 1998 Following the results from the human studies, DPD activity was measured in Sprague-Dawley rat liver up to 72 h after administration of 5-FU 200 mg/kg as a single injection. Fluorouracil 135-139 dihydropyrimidine dehydrogenase Homo sapiens 46-49 9893640-6 1998 Human mononuclear cell DPD activity decreased by a median of 38.7% following the administration of 5-FU (P = 0.001). Fluorouracil 99-103 dihydropyrimidine dehydrogenase Homo sapiens 23-26 9704742-5 1998 RESULTS: The uracil in UFT slows degradation of 5-FU by dihydropyrimidine dehydrogenase (DPD), which results in sustained concentrations of 5-FU in blood and tumor tissues. Fluorouracil 48-52 dihydropyrimidine dehydrogenase Homo sapiens 56-87 9704742-5 1998 RESULTS: The uracil in UFT slows degradation of 5-FU by dihydropyrimidine dehydrogenase (DPD), which results in sustained concentrations of 5-FU in blood and tumor tissues. Fluorouracil 48-52 dihydropyrimidine dehydrogenase Homo sapiens 89-92 9704742-5 1998 RESULTS: The uracil in UFT slows degradation of 5-FU by dihydropyrimidine dehydrogenase (DPD), which results in sustained concentrations of 5-FU in blood and tumor tissues. Fluorouracil 140-144 dihydropyrimidine dehydrogenase Homo sapiens 56-87 9704742-5 1998 RESULTS: The uracil in UFT slows degradation of 5-FU by dihydropyrimidine dehydrogenase (DPD), which results in sustained concentrations of 5-FU in blood and tumor tissues. Fluorouracil 140-144 dihydropyrimidine dehydrogenase Homo sapiens 89-92 9713780-3 1998 After surgery she received six 5-mg injections of subconjunctival 5-fluorouracil (5-FU) adjacent to the bleb. Fluorouracil 66-80 SIX homeobox 5 Homo sapiens 27-32 9713780-3 1998 After surgery she received six 5-mg injections of subconjunctival 5-fluorouracil (5-FU) adjacent to the bleb. Fluorouracil 82-86 SIX homeobox 5 Homo sapiens 27-32 9690942-9 1998 This drug-drug interaction of sorivudine and 5-FU further emphasizes the critical importance of DPD on the clinical pharmacology of 5-FU. Fluorouracil 45-49 dihydropyrimidine dehydrogenase Homo sapiens 96-99 9690942-9 1998 This drug-drug interaction of sorivudine and 5-FU further emphasizes the critical importance of DPD on the clinical pharmacology of 5-FU. Fluorouracil 132-136 dihydropyrimidine dehydrogenase Homo sapiens 96-99 9679577-4 1998 CDHP, inhibitor of 5-FU degradation in liver and Oxo, inhibitor of 5-FU phosphoribosylation in digestive tract, respectively. Fluorouracil 19-23 cadherin 3 Homo sapiens 0-4 9635582-10 1998 The data presented in this report thus indicate that rMETase is active alone, is synergistic in combination with 5-FU, and has negligible toxicity suggesting a novel clinical approach for effective cancer therapy. Fluorouracil 113-117 granzyme M Rattus norvegicus 53-60 9673382-5 1998 The results of the chemosensitivity assay are as follows: 5-FU seems to be the most beneficial for primary colorectal cancer; carboquone (CQ), etoposide (VP-16), 5-FU, and mitomycin-C (MMC) for nodal metastasis; CQ, cisplatin (CDDP), 5-FU, adriamycin (ADR) and VP-16 for malignant effusion; and VP-16, CDDP and CQ for liver metastasis. Fluorouracil 58-62 host cell factor C1 Homo sapiens 261-266 11875367-1 2002 A pharmacogenetic syndrome caused by molecular defects in the dihydropyrimidine dehydrogenase gene (DPYD ) results in partial to complete loss of dihydropyrimidine dehydrogenase (DPD) enzyme activity with patients exhibiting life-threatening toxicity following administration of routine doses of 5-fluorouracil. Fluorouracil 296-310 dihydropyrimidine dehydrogenase Homo sapiens 62-93 9673382-5 1998 The results of the chemosensitivity assay are as follows: 5-FU seems to be the most beneficial for primary colorectal cancer; carboquone (CQ), etoposide (VP-16), 5-FU, and mitomycin-C (MMC) for nodal metastasis; CQ, cisplatin (CDDP), 5-FU, adriamycin (ADR) and VP-16 for malignant effusion; and VP-16, CDDP and CQ for liver metastasis. Fluorouracil 58-62 host cell factor C1 Homo sapiens 261-266 11875367-1 2002 A pharmacogenetic syndrome caused by molecular defects in the dihydropyrimidine dehydrogenase gene (DPYD ) results in partial to complete loss of dihydropyrimidine dehydrogenase (DPD) enzyme activity with patients exhibiting life-threatening toxicity following administration of routine doses of 5-fluorouracil. Fluorouracil 296-310 dihydropyrimidine dehydrogenase Homo sapiens 100-104 9515799-12 1998 In stage III, adjuvant therapy with 5FU plus levamisole improved 7-year survival in patients with wild-type Ki-ras (76 versus 44%; HR, 0.4; 95% CI, 0.2-0.8) and in those without p53 overexpression (64 versus 26%; HR, 0.3; 95% CI, 0.1-0.7). Fluorouracil 36-39 KRAS proto-oncogene, GTPase Homo sapiens 108-114 11875367-1 2002 A pharmacogenetic syndrome caused by molecular defects in the dihydropyrimidine dehydrogenase gene (DPYD ) results in partial to complete loss of dihydropyrimidine dehydrogenase (DPD) enzyme activity with patients exhibiting life-threatening toxicity following administration of routine doses of 5-fluorouracil. Fluorouracil 296-310 dihydropyrimidine dehydrogenase Homo sapiens 146-177 11875367-1 2002 A pharmacogenetic syndrome caused by molecular defects in the dihydropyrimidine dehydrogenase gene (DPYD ) results in partial to complete loss of dihydropyrimidine dehydrogenase (DPD) enzyme activity with patients exhibiting life-threatening toxicity following administration of routine doses of 5-fluorouracil. Fluorouracil 296-310 dihydropyrimidine dehydrogenase Homo sapiens 179-182 11841784-7 2002 A two-reaction pathway, composed of ribokinase and phosphopentomutase, appears to be responsible of the Rib1-P formation, needed to salvage uracil to uracil-nucleotides and to activate 5-FU to cytotoxic 5-FU-ribonucleotides. Fluorouracil 185-189 ribokinase Rattus norvegicus 36-69 9515799-16 1998 Exploratory analyses suggest that patients with stage III colon cancer with wild-type Ki-ras or no p53 expression benefit from adjuvant 5FU plus levamisole, whereas those with Ki-ras mutations or p53 overexpression do not. Fluorouracil 136-139 KRAS proto-oncogene, GTPase Homo sapiens 86-92 9466662-9 1998 In addition, 5-fluorouracil could obviously inhibit AFP-induced proliferation of H-22 or EAC cells in vitro. Fluorouracil 13-27 alpha fetoprotein Mus musculus 52-55 9345027-8 1997 When lineage (Lin)-Sca-1(+) cells sorted from BMC of 5-FU-treated mice were incubated in serum-free culture, leptin synergized with SCF in the formation of blast cell colonies, which efficiently produced secondary colonies including a large proportion of multilineage colonies in the replating experiment. Fluorouracil 53-57 ataxin 1 Mus musculus 19-27 9467870-6 1997 Although nor affecting RBC and thrombocytes, treatment of pigs with uteroferrin had an initial protective effect (P < 0.05) on the 5-FU-induced leukocytopenia (63 and 64 vs 48 and 39 +/- 6% of baseline on days 3 and 5, respectively). Fluorouracil 134-138 acid phosphatase 5, tartrate resistant Sus scrofa 68-79 9467870-9 1997 Uteroferrin + rbGM-CSF also attenuated (P < 0.05) the suppression and enhanced (P < 0.05) recovery of RBC and thrombocyte numbers following 5-FU treatment. Fluorouracil 146-150 acid phosphatase 5, tartrate resistant Sus scrofa 0-11 9323539-2 1997 Dihydropyrimidine dehydrogenase (DPD) catalyzes the reduction of the naturally occurring pyrimidines, uracil and thymine, and the fluoropyrimidine anticancer drug, 5-fluorouracil (FUra) to 5,6-dihydropyrimidines. Fluorouracil 180-184 dihydropyrimidine dehydrogenase Homo sapiens 33-36 9280881-0 1997 [Determination of dihydropyrimidine dehydrogenase in the prediction of toxic side effects of 5-fluorouracil]. Fluorouracil 93-107 dihydropyrimidine dehydrogenase Homo sapiens 18-49 9262988-5 1997 Incubation with IL1+IL3+SCF caused an increase (fold expansion) in committed (28.6 +/- 8.1), immature (5.8 +/- 1.8), and primitive progenitors (4.1 +/- 0.8) among control CB MNC compared to a decrease in committed progenitors (0 +/- 0) but an increase in both immature (8.4 +/- 4.8) and primitive progenitors (7 +/- 2.9) among 5-FU resistant CB MNC. Fluorouracil 327-331 KIT ligand Homo sapiens 24-27 9189165-5 1997 At the same time SCF conferred a sensitization of these subsets after treatment with 5-FU, which indicated an enhanced proliferative activity. Fluorouracil 85-89 KIT ligand Homo sapiens 17-20 12140902-14 2002 Intratumoral DPD activity may also be assessed with high activity suggesting a poorer response to fluorouracil. Fluorouracil 98-110 dihydropyrimidine dehydrogenase Homo sapiens 13-16 11781659-0 2001 Retroviral transduction of human dihydropyrimidine dehydrogenase cDNA confers resistance to 5-fluorouracil in murine hematopoietic progenitor cells and human CD34+-enriched peripheral blood progenitor cells. Fluorouracil 92-106 dihydropyrimidine dehydrogenase Homo sapiens 33-64 11781659-1 2001 Severe 5-fluorouracil (5-FU) toxicity has been reported among patients lacking dihydropyrimidine dehydrogenase (DPD) enzymatic activity. Fluorouracil 7-21 dihydropyrimidine dehydrogenase Homo sapiens 79-110 11781659-1 2001 Severe 5-fluorouracil (5-FU) toxicity has been reported among patients lacking dihydropyrimidine dehydrogenase (DPD) enzymatic activity. Fluorouracil 7-21 dihydropyrimidine dehydrogenase Homo sapiens 112-115 11781659-1 2001 Severe 5-fluorouracil (5-FU) toxicity has been reported among patients lacking dihydropyrimidine dehydrogenase (DPD) enzymatic activity. Fluorouracil 23-27 dihydropyrimidine dehydrogenase Homo sapiens 79-110 11781659-1 2001 Severe 5-fluorouracil (5-FU) toxicity has been reported among patients lacking dihydropyrimidine dehydrogenase (DPD) enzymatic activity. Fluorouracil 23-27 dihydropyrimidine dehydrogenase Homo sapiens 112-115 11781659-2 2001 DPD is the principal enzyme involved in the degradation of 5-FU to 5"-6"-dihydrofluorouracil, which is further metabolized to fluoro-beta-alanine. Fluorouracil 59-63 dihydropyrimidine dehydrogenase Homo sapiens 0-3 11781659-3 2001 We demonstrate here that overexpression of human DPD confers resistance to 5-FU in NIH3T3 cells, mouse bone marrow cells, and in human CD34+-enriched hematopoietic progenitor cells. Fluorouracil 75-79 dihydropyrimidine dehydrogenase Homo sapiens 49-52 11781659-9 2001 Retroviral transduction of human hematopoietic progenitor cells with a cDNA-expressing human DPD conferred resistance to 5-FU in NIH3T3 cells, mouse bone marrow cells, and human CD34+-enriched cells. Fluorouracil 121-125 dihydropyrimidine dehydrogenase Homo sapiens 93-96 11745689-8 2001 These results suggest that the type of Ki-ras mutation could be a clinically useful molecular marker for the identification of CRC subgroups that are likely to benefit from 5-fluorouracil-based adjuvant chemotherapy. Fluorouracil 173-187 KRAS proto-oncogene, GTPase Homo sapiens 39-45 11714538-0 2001 Thymidylate synthase and dihydropyrimidine dehydrogenase activities in non-small cell lung cancer tissues: relationship with in vitro sensitivity to 5-fluorouracil. Fluorouracil 149-163 dihydropyrimidine dehydrogenase Homo sapiens 25-56 11714538-1 2001 We examined enzymatic activities of thymidylate synthase (TS) and dihydropyrimidine dehydrogenase (DPD) in non-small cell lung cancer (NSCLC) tissues to determine the relationship to tumor sensitivity to 5-fluorouracil (5-FU). Fluorouracil 204-218 dihydropyrimidine dehydrogenase Homo sapiens 99-102 11714538-1 2001 We examined enzymatic activities of thymidylate synthase (TS) and dihydropyrimidine dehydrogenase (DPD) in non-small cell lung cancer (NSCLC) tissues to determine the relationship to tumor sensitivity to 5-fluorouracil (5-FU). Fluorouracil 220-224 dihydropyrimidine dehydrogenase Homo sapiens 99-102 11714538-4 2001 DPD activities slightly correlated with in vitro sensitivity to 5-FU (r=0.402,P=0.013), such that tumors with higher DPD activity were more resistant to 5-FU. Fluorouracil 64-68 dihydropyrimidine dehydrogenase Homo sapiens 0-3 11714538-4 2001 DPD activities slightly correlated with in vitro sensitivity to 5-FU (r=0.402,P=0.013), such that tumors with higher DPD activity were more resistant to 5-FU. Fluorouracil 64-68 dihydropyrimidine dehydrogenase Homo sapiens 117-120 11714538-4 2001 DPD activities slightly correlated with in vitro sensitivity to 5-FU (r=0.402,P=0.013), such that tumors with higher DPD activity were more resistant to 5-FU. Fluorouracil 153-157 dihydropyrimidine dehydrogenase Homo sapiens 0-3 11714538-4 2001 DPD activities slightly correlated with in vitro sensitivity to 5-FU (r=0.402,P=0.013), such that tumors with higher DPD activity were more resistant to 5-FU. Fluorouracil 153-157 dihydropyrimidine dehydrogenase Homo sapiens 117-120 11714538-6 2001 Thus, it was suggested that only DPD activity in NSCLC tissues is a potential indicator in predicting tumor sensitivity to 5-FU. Fluorouracil 123-127 dihydropyrimidine dehydrogenase Homo sapiens 33-36 11587492-6 2001 CONCLUSIONS: It was revealed that the most important factors that determine the selective production of 5-FU in tumor tissue after capecitabine administration are tumor-specific activation by dThdPase, the nonlinear elimination of 5-FU by DPD in tumor tissue, and the blood flow rate in tumors. Fluorouracil 104-108 dihydropyrimidine dehydrogenase Homo sapiens 239-242 9189165-7 1997 These contrasting results provide an explanation for the sensitization by SCF of 5-FU-induced lethality and its converse protection against radiation-induced lethality as reported by others. Fluorouracil 81-85 KIT ligand Homo sapiens 74-77 9189165-9 1997 The number of CAFCs that remained in the bone marrow largely predicted the subsequent patterns of donor marrow engraftment in the treated BMT recipients: SCF enhanced short-term engraftment after treatment with 5-FU while it reduced the need for short-term engraftment after irradiation. Fluorouracil 211-215 KIT ligand Homo sapiens 154-157 9135003-1 1997 Deficiency of the pyrimidine catabolic enzyme, dihydropyrimidine dehydrogenase (DPD), has been shown to be responsible for a pharmacogenetic syndrome in which administration of 5-fluorouracil is associated with severe and potentially life-threatening toxicity. Fluorouracil 177-191 dihydropyrimidine dehydrogenase Homo sapiens 47-78 9135003-1 1997 Deficiency of the pyrimidine catabolic enzyme, dihydropyrimidine dehydrogenase (DPD), has been shown to be responsible for a pharmacogenetic syndrome in which administration of 5-fluorouracil is associated with severe and potentially life-threatening toxicity. Fluorouracil 177-191 dihydropyrimidine dehydrogenase Homo sapiens 80-83 9135003-6 1997 The physical map of the DPD gene should permit development of rapid assays to detect point mutations or small deletions in the DPD gene associated with 5-fluorouracil toxicity. Fluorouracil 152-166 dihydropyrimidine dehydrogenase Homo sapiens 24-27 9135003-6 1997 The physical map of the DPD gene should permit development of rapid assays to detect point mutations or small deletions in the DPD gene associated with 5-fluorouracil toxicity. Fluorouracil 152-166 dihydropyrimidine dehydrogenase Homo sapiens 127-130 9180391-1 1997 In this study 194 women with breast cancer received adjuvant CNF combination therapy (cyclophosphamide, mitoxantrone and 5-fluorouracil). Fluorouracil 121-135 NPHS1 adhesion molecule, nephrin Homo sapiens 61-64 9050858-4 1997 5-FU is a pyrimidine antimetabolite cytotoxin with multiple mechanisms of action, including inhibition of thymidylate synthase (TS), which gives rise to DNA damage, and incorporation into RNA. Fluorouracil 0-4 thymidylate synthase Mus musculus 106-126 9013973-7 1997 Leukocyte depletion with 5-fluorouracil and anti-MAC-1 Ab added to matrigel prevented the infiltration of macrophages, the synthesis of PAF and the angiogenesis induced by HGF. Fluorouracil 25-39 patchy fur Mus musculus 136-139 9013973-7 1997 Leukocyte depletion with 5-fluorouracil and anti-MAC-1 Ab added to matrigel prevented the infiltration of macrophages, the synthesis of PAF and the angiogenesis induced by HGF. Fluorouracil 25-39 hepatocyte growth factor Mus musculus 172-175 9182832-1 1997 PURPOSE: The activity of dihydropyrimidine dehydrogenase (DPD), the rate-limiting enzyme in fluorouracil catabolism, has been reported to vary according to time of day. Fluorouracil 92-104 dihydropyrimidine dehydrogenase Homo sapiens 25-56 11428679-8 2001 The 5-FU loaded microparticles approach, with PLG, might be a potential for the application of long-term delivery of hydrophilic drugs in the eye. Fluorouracil 4-8 plasminogen Oryctolagus cuniculus 46-49 11459289-11 2001 Moreover, a synergistic growth inhibition was observed when coincubating the cells with the P2Y2 receptor agonist ATP and the cytostatic drug 5-fluorouracil, which forms the basis for most currently applied chemotherapeutic regimes in colorectal cancer treatment. Fluorouracil 142-156 purinergic receptor P2Y2 Homo sapiens 92-96 11311495-4 2001 5-fluorouracil (5FU) treatment resulted in a substantial increase in the p53-positive signet-ring cell population (from 17% to 45%) and in an increased Mdm2 immunoreactivity. Fluorouracil 0-14 MDM2 proto-oncogene Homo sapiens 152-156 11311495-4 2001 5-fluorouracil (5FU) treatment resulted in a substantial increase in the p53-positive signet-ring cell population (from 17% to 45%) and in an increased Mdm2 immunoreactivity. Fluorouracil 16-19 MDM2 proto-oncogene Homo sapiens 152-156 11313250-3 2001 Next, it was determined that the majority of stem cells activated in vivo by injection of 5-fluorouracil (5-FU) or mobilized by granulocyte colony-stimulating factor are CD38(-). Fluorouracil 90-104 CD38 antigen Mus musculus 170-174 11313250-3 2001 Next, it was determined that the majority of stem cells activated in vivo by injection of 5-fluorouracil (5-FU) or mobilized by granulocyte colony-stimulating factor are CD38(-). Fluorouracil 106-110 CD38 antigen Mus musculus 170-174 11383213-9 2001 DPD is a rate-limiting enzyme in the process of degradation of 5-FU. Fluorouracil 63-67 dihydropyrimidine dehydrogenase Homo sapiens 0-3 11383213-11 2001 PyNPase/DPD suggests not only the malignant potential of the tumor but also the efficiency of chemotherapy using 5-FU, especially 5"-DFUR. Fluorouracil 113-117 dihydropyrimidine dehydrogenase Homo sapiens 8-11 11383215-0 2001 [Correlation between 5-fluorouracil (5-FU) sensitivity as measured by collagen gel droplet embedded culture drug sensitivity test (CD-DST) and expression of orotate phosphoribosyl transferase (OPRT), thymidylate synthase (TS), and dihydropyrimidine dehydrogenase (DPD) in colorectal cancer]. Fluorouracil 21-35 dihydropyrimidine dehydrogenase Homo sapiens 231-262 11383215-0 2001 [Correlation between 5-fluorouracil (5-FU) sensitivity as measured by collagen gel droplet embedded culture drug sensitivity test (CD-DST) and expression of orotate phosphoribosyl transferase (OPRT), thymidylate synthase (TS), and dihydropyrimidine dehydrogenase (DPD) in colorectal cancer]. Fluorouracil 21-35 dihydropyrimidine dehydrogenase Homo sapiens 264-267 11290431-2 2001 DPD is also the principal enzyme involved in the degradation of 5-fluorouracil (5-FU), which is one of the anticancer chemotherapeutic agents currently used in the treatment of bladder cancer. Fluorouracil 64-78 dihydropyrimidine dehydrogenase Homo sapiens 0-3 11290431-2 2001 DPD is also the principal enzyme involved in the degradation of 5-fluorouracil (5-FU), which is one of the anticancer chemotherapeutic agents currently used in the treatment of bladder cancer. Fluorouracil 80-84 dihydropyrimidine dehydrogenase Homo sapiens 0-3 11290431-4 2001 We investigated the activity of DPD in 74 bladder cancers and the relationship between the DPD activity and the sensitivity to 5-FU. Fluorouracil 127-131 dihydropyrimidine dehydrogenase Homo sapiens 91-94 11290431-5 2001 The levels of DPD activity in bladder cancer and normal bladder tissues were determined by the 5-FU degradation assay. Fluorouracil 95-99 dihydropyrimidine dehydrogenase Homo sapiens 14-17 11290431-11 2001 There was an inverse correlation between DPD activity in bladder cancer cells and their sensitivity to 5-FU. Fluorouracil 103-107 dihydropyrimidine dehydrogenase Homo sapiens 41-44 11290431-12 2001 Furthermore, 5-chloro-2,4-dihydroxypyridine (CDHP), a potent DPD inhibitor, enhanced the sensitivity to 5-FU. Fluorouracil 104-108 dihydropyrimidine dehydrogenase Homo sapiens 61-64 11290431-15 2001 In addition, it might be possible to overcome 5-FU insensitivity by using DPD inhibitors in the treatment protocols of 5-FU-based chemotherapy for bladder cancers. Fluorouracil 46-50 dihydropyrimidine dehydrogenase Homo sapiens 74-77 11290431-15 2001 In addition, it might be possible to overcome 5-FU insensitivity by using DPD inhibitors in the treatment protocols of 5-FU-based chemotherapy for bladder cancers. Fluorouracil 119-123 dihydropyrimidine dehydrogenase Homo sapiens 74-77 9182832-1 1997 PURPOSE: The activity of dihydropyrimidine dehydrogenase (DPD), the rate-limiting enzyme in fluorouracil catabolism, has been reported to vary according to time of day. Fluorouracil 92-104 dihydropyrimidine dehydrogenase Homo sapiens 58-61 1378737-3 1992 Inhibition of TSase by FUra was modulated by leucovorin (LV), and the incorporation of FUra into RNA was increased by the administration of otherwise lethal doses of FUra followed by uridine "rescue". Fluorouracil 23-27 thymidylate synthase Mus musculus 14-19 1378737-4 1992 Thymidylate synthase activity was inhibited substantially (49%) by low-dose FUra at 25 mg/kg, but was not further enhanced (48%) by repeated daily treatments at the same dose (FUra25 x 4). Fluorouracil 76-80 thymidylate synthase Mus musculus 0-20 1378737-6 1992 FUra as a single agent at the maximum tolerated weekly dose of 100 mg/kg inhibited TSase activity 66-73%. Fluorouracil 0-4 thymidylate synthase Mus musculus 83-88 1378737-10 1992 At a very-high-dose of FUra (200-225 mg/kg) followed by uridine "rescue", TSase inhibition was not further enhanced, but both (FU)RNA (4.8 nmol/mg DNA) and the therapeutic efficacy were increased. Fluorouracil 23-27 thymidylate synthase Mus musculus 74-79 1581906-0 1992 Correlation between dihydropyrimidine dehydrogenase activity in peripheral mononuclear cells and systemic clearance of fluorouracil in cancer patients. Fluorouracil 119-131 dihydropyrimidine dehydrogenase Homo sapiens 20-51 11215843-1 2001 OBJECTIVE: To briefly review the biotransformation and bioavailability of fluorouracil (5-FU); discuss the effects of dihydropyrimidine dehydrogenase (DpD) on the efficacy and toxicity profiles of 5-FU; and review a new class of drugs known collectively as the oral fluorinated pyrimidines, which inhibit or circumvent DpD activity and, when administered with 5-FU, alter its pharmacokinetic and pharmacodynamic properties. Fluorouracil 197-201 dihydropyrimidine dehydrogenase Homo sapiens 118-149 11215843-1 2001 OBJECTIVE: To briefly review the biotransformation and bioavailability of fluorouracil (5-FU); discuss the effects of dihydropyrimidine dehydrogenase (DpD) on the efficacy and toxicity profiles of 5-FU; and review a new class of drugs known collectively as the oral fluorinated pyrimidines, which inhibit or circumvent DpD activity and, when administered with 5-FU, alter its pharmacokinetic and pharmacodynamic properties. Fluorouracil 197-201 dihydropyrimidine dehydrogenase Homo sapiens 151-154 11215843-1 2001 OBJECTIVE: To briefly review the biotransformation and bioavailability of fluorouracil (5-FU); discuss the effects of dihydropyrimidine dehydrogenase (DpD) on the efficacy and toxicity profiles of 5-FU; and review a new class of drugs known collectively as the oral fluorinated pyrimidines, which inhibit or circumvent DpD activity and, when administered with 5-FU, alter its pharmacokinetic and pharmacodynamic properties. Fluorouracil 197-201 dihydropyrimidine dehydrogenase Homo sapiens 118-149 11215843-1 2001 OBJECTIVE: To briefly review the biotransformation and bioavailability of fluorouracil (5-FU); discuss the effects of dihydropyrimidine dehydrogenase (DpD) on the efficacy and toxicity profiles of 5-FU; and review a new class of drugs known collectively as the oral fluorinated pyrimidines, which inhibit or circumvent DpD activity and, when administered with 5-FU, alter its pharmacokinetic and pharmacodynamic properties. Fluorouracil 197-201 dihydropyrimidine dehydrogenase Homo sapiens 151-154 11215843-9 2001 CONCLUSIONS: The bioavailability, efficacy, and toxicity of 5-FU depend on its catabolic rate-limiting enzyme, The new oral fluorinated pyrimidines inhibit or circumvent DpD activity and, when combined with 5-FU, increase 5-FU"s bioavailability and cytotoxic effects and decrease its toxicities. Fluorouracil 60-64 dihydropyrimidine dehydrogenase Homo sapiens 170-173 1581906-1 1992 Dihydropyrimidine dehydrogenase (DPD) is the initial key enzyme in the catabolism of 5-fluorouracil (5-FU). Fluorouracil 85-99 dihydropyrimidine dehydrogenase Homo sapiens 0-31 1581906-1 1992 Dihydropyrimidine dehydrogenase (DPD) is the initial key enzyme in the catabolism of 5-fluorouracil (5-FU). Fluorouracil 85-99 dihydropyrimidine dehydrogenase Homo sapiens 33-36 1581906-1 1992 Dihydropyrimidine dehydrogenase (DPD) is the initial key enzyme in the catabolism of 5-fluorouracil (5-FU). Fluorouracil 101-105 dihydropyrimidine dehydrogenase Homo sapiens 0-31 1581906-1 1992 Dihydropyrimidine dehydrogenase (DPD) is the initial key enzyme in the catabolism of 5-fluorouracil (5-FU). Fluorouracil 101-105 dihydropyrimidine dehydrogenase Homo sapiens 33-36 1581906-5 1992 A significant linear correlation was observed between DPD activity and 5-FU clearance (r = 0.716, P less than 0.0001). Fluorouracil 71-75 dihydropyrimidine dehydrogenase Homo sapiens 54-57 1581906-10 1992 Monitoring DPD activity in lymphocytes may be useful in identifying patients at risk for altered 5-FU disposition. Fluorouracil 97-101 dihydropyrimidine dehydrogenase Homo sapiens 11-14 1580641-7 1992 Based on these results, it is suggested that measurement of F-RNA levels together with the determination of FUra concentration and the inhibition rate of thymidylate synthase should be considered as a good parameters of the evaluation of antitumor efficacy of FUra and its analogs both in experimental and clinical settings. Fluorouracil 260-264 thymidylate synthase Mus musculus 154-174 11302344-1 2001 BACKGROUND: Pyrimidine nucleoside phosphorylase (PyNPase) converts 5"-deoxy-5-fluorouridine (5"-DFUR) to 5"-fluorouracil (5-FU), which exerts an anti-cancer effect before being catabolized by dihydropyrimidine dehydrogenase (DPD). Fluorouracil 105-120 dihydropyrimidine dehydrogenase Homo sapiens 192-223 11302344-1 2001 BACKGROUND: Pyrimidine nucleoside phosphorylase (PyNPase) converts 5"-deoxy-5-fluorouridine (5"-DFUR) to 5"-fluorouracil (5-FU), which exerts an anti-cancer effect before being catabolized by dihydropyrimidine dehydrogenase (DPD). Fluorouracil 105-120 dihydropyrimidine dehydrogenase Homo sapiens 225-228 11302344-1 2001 BACKGROUND: Pyrimidine nucleoside phosphorylase (PyNPase) converts 5"-deoxy-5-fluorouridine (5"-DFUR) to 5"-fluorouracil (5-FU), which exerts an anti-cancer effect before being catabolized by dihydropyrimidine dehydrogenase (DPD). Fluorouracil 122-126 dihydropyrimidine dehydrogenase Homo sapiens 192-223 11302344-1 2001 BACKGROUND: Pyrimidine nucleoside phosphorylase (PyNPase) converts 5"-deoxy-5-fluorouridine (5"-DFUR) to 5"-fluorouracil (5-FU), which exerts an anti-cancer effect before being catabolized by dihydropyrimidine dehydrogenase (DPD). Fluorouracil 122-126 dihydropyrimidine dehydrogenase Homo sapiens 225-228 11302344-6 2001 On the other hand, the tumor/normal tissue ratio of DPD was also higher in advanced stage cases and also in the presence of vessel invasion (each p < 0.05), thus indicating a poor response to 5-FU. Fluorouracil 195-199 dihydropyrimidine dehydrogenase Homo sapiens 52-55 11564055-8 2001 The cytotoxic activities of mercaptopurine and fluorouracil are regulated by thiopurine methyltransferase (TPMT) and dihydropyrimidine dehydrogenase (DPD), respectively. Fluorouracil 47-59 dihydropyrimidine dehydrogenase Homo sapiens 117-148 11564055-8 2001 The cytotoxic activities of mercaptopurine and fluorouracil are regulated by thiopurine methyltransferase (TPMT) and dihydropyrimidine dehydrogenase (DPD), respectively. Fluorouracil 47-59 dihydropyrimidine dehydrogenase Homo sapiens 150-153 11564055-10 2001 Very low DPD activity reduces fluorouracil breakdown producing severe cytotoxicity. Fluorouracil 30-42 dihydropyrimidine dehydrogenase Homo sapiens 9-12 11104786-4 2000 Conditioning with DNA-damaging agents (ionizing irradiation, cyclophosphamide, and 5-fluorouracil) caused an increase in SDF-1 expression and in CXCR4-dependent homing and repopulation by human stem cells transplanted into NOD/SCID mice. Fluorouracil 83-97 C-X-C motif chemokine receptor 4 Homo sapiens 145-150 1373051-3 1992 Through a catheter placed in the right subclavian artery, doses of 20-30 mg of ADM were injected intermittently with MMC and 5-FU. Fluorouracil 125-129 adrenomedullin Homo sapiens 79-82 1532671-3 1992 Sufficient levels of CH2-THF enhance the inhibition of the enzyme thymidylate synthase by the 5-FU metabolite FdUMP. Fluorouracil 94-98 thymidylate synthase Mus musculus 66-86 1304835-0 1992 [Dihydropyrimidine dehydrogenase activity in lymphocytes: predictive factor for 5-fluorouracil clearance]. Fluorouracil 80-94 dihydropyrimidine dehydrogenase Homo sapiens 1-32 1304835-3 1992 Dihydropyrimidine dehydrogenase (DPD) is the initial enzyme in the catabolism of 5-FU. Fluorouracil 81-85 dihydropyrimidine dehydrogenase Homo sapiens 0-31 1304835-3 1992 Dihydropyrimidine dehydrogenase (DPD) is the initial enzyme in the catabolism of 5-FU. Fluorouracil 81-85 dihydropyrimidine dehydrogenase Homo sapiens 33-36 1304835-4 1992 DPD activity was measured in 57 head and neck cancer patients receiving CDDP (100 mg/m2, day 1) plus 5-FU (1 g/m2/day x 5, day 2-day 6). Fluorouracil 101-105 dihydropyrimidine dehydrogenase Homo sapiens 0-3 1304835-7 1992 A significant linear correlation was demonstrated between DPD activity and 5-FU clearance (Cl = 1,099 + 7,580 DPD, r2 = 0.613, P < 0.0001). Fluorouracil 75-79 dihydropyrimidine dehydrogenase Homo sapiens 58-61 1304835-7 1992 A significant linear correlation was demonstrated between DPD activity and 5-FU clearance (Cl = 1,099 + 7,580 DPD, r2 = 0.613, P < 0.0001). Fluorouracil 75-79 dihydropyrimidine dehydrogenase Homo sapiens 110-113 1304835-8 1992 In patients evaluated for more than one cycle (n = 18), variations in 5-FU clearance were associated with corresponding variations in DPD activity. Fluorouracil 70-74 dihydropyrimidine dehydrogenase Homo sapiens 134-137 1304835-9 1992 The individual determination of DPD activity measured in lymphocytes could be useful for identifying patients at risk for altered 5-FU pharmacokinetics and could be used to adjust the optimal 5-FU dose for each patient before starting the treatment. Fluorouracil 130-134 dihydropyrimidine dehydrogenase Homo sapiens 32-35 1304835-9 1992 The individual determination of DPD activity measured in lymphocytes could be useful for identifying patients at risk for altered 5-FU pharmacokinetics and could be used to adjust the optimal 5-FU dose for each patient before starting the treatment. Fluorouracil 192-196 dihydropyrimidine dehydrogenase Homo sapiens 32-35 1374741-5 1992 Proliferative responses of bone marrow cells to granulocyte/macrophage colony stimulating factor (GM-CSF) or granulocyte colony stimulating factor (G-CSF) were suppressed by 5-FU treatment and their recoveries were enhanced by SPR-901. Fluorouracil 174-178 colony stimulating factor 2 (granulocyte-macrophage) Mus musculus 48-96 1374741-5 1992 Proliferative responses of bone marrow cells to granulocyte/macrophage colony stimulating factor (GM-CSF) or granulocyte colony stimulating factor (G-CSF) were suppressed by 5-FU treatment and their recoveries were enhanced by SPR-901. Fluorouracil 174-178 colony stimulating factor 2 (granulocyte-macrophage) Mus musculus 98-104 1722409-10 1991 These results demonstrate that certain short-lived, proliferation-related enzymes are affected by FUra doses higher than those required for TSase inhibition, and this effect appears to correlate with incorporation of FUra into RNA. Fluorouracil 98-102 thymidylate synthase Mus musculus 140-145 11103235-2 2000 A recent investigation using a molecular biological method was introduced to predict the sensitivity of gastric cancer specimens to 5-fluorouracil (5-FU) by dihydropyrimidine dehydrogenase (DPD) activity and its mRNA. Fluorouracil 132-146 dihydropyrimidine dehydrogenase Homo sapiens 157-188 11103235-2 2000 A recent investigation using a molecular biological method was introduced to predict the sensitivity of gastric cancer specimens to 5-fluorouracil (5-FU) by dihydropyrimidine dehydrogenase (DPD) activity and its mRNA. Fluorouracil 132-146 dihydropyrimidine dehydrogenase Homo sapiens 190-193 11103235-2 2000 A recent investigation using a molecular biological method was introduced to predict the sensitivity of gastric cancer specimens to 5-fluorouracil (5-FU) by dihydropyrimidine dehydrogenase (DPD) activity and its mRNA. Fluorouracil 148-152 dihydropyrimidine dehydrogenase Homo sapiens 157-188 11103235-2 2000 A recent investigation using a molecular biological method was introduced to predict the sensitivity of gastric cancer specimens to 5-fluorouracil (5-FU) by dihydropyrimidine dehydrogenase (DPD) activity and its mRNA. Fluorouracil 148-152 dihydropyrimidine dehydrogenase Homo sapiens 190-193 11103235-3 2000 The low activity of DPD and DPD mRNA resulted in the low sensitivity to 5-FU, although thymidylate synthetase activity was not related to the sensitivity to 5-FU. Fluorouracil 72-76 dihydropyrimidine dehydrogenase Homo sapiens 20-23 1722409-10 1991 These results demonstrate that certain short-lived, proliferation-related enzymes are affected by FUra doses higher than those required for TSase inhibition, and this effect appears to correlate with incorporation of FUra into RNA. Fluorouracil 217-221 thymidylate synthase Mus musculus 140-145 11103235-3 2000 The low activity of DPD and DPD mRNA resulted in the low sensitivity to 5-FU, although thymidylate synthetase activity was not related to the sensitivity to 5-FU. Fluorouracil 72-76 dihydropyrimidine dehydrogenase Homo sapiens 28-31 11103235-4 2000 This method is promising, since a small amount of material obtained through gastrofiberscopy will be adequate to assess DPD mRNA to predict the sensitivity to 5-FU. Fluorouracil 159-163 dihydropyrimidine dehydrogenase Homo sapiens 120-123 1831268-6 1991 Bone marrow progenitors obtained from mice 3 days after treatment with 5-fluorouracil responded to a combination of GM-CSF and TGF-beta 1, whereas either factor alone had no effect. Fluorouracil 71-85 colony stimulating factor 2 (granulocyte-macrophage) Mus musculus 116-122 11081574-1 2000 Eniluracil (776C85, GW776) inactivates dihydropyrimidine dehydrogenase (DPD), the principal enzyme of 5-fluorouracil (5-FU) catabolism. Fluorouracil 102-116 dihydropyrimidine dehydrogenase Homo sapiens 39-70 1648430-4 1991 The activity of dihydropyrimidine dehydrogenase (DPD), the initial enzyme of pyrimidine (and FUra) catabolism, in peripheral blood mononuclear cells was measured in each subject by a specific radiometric assay using FUra as the substrate. Fluorouracil 93-97 dihydropyrimidine dehydrogenase Homo sapiens 16-47 11081574-1 2000 Eniluracil (776C85, GW776) inactivates dihydropyrimidine dehydrogenase (DPD), the principal enzyme of 5-fluorouracil (5-FU) catabolism. Fluorouracil 102-116 dihydropyrimidine dehydrogenase Homo sapiens 72-75 11081574-1 2000 Eniluracil (776C85, GW776) inactivates dihydropyrimidine dehydrogenase (DPD), the principal enzyme of 5-fluorouracil (5-FU) catabolism. Fluorouracil 118-122 dihydropyrimidine dehydrogenase Homo sapiens 39-70 11081574-1 2000 Eniluracil (776C85, GW776) inactivates dihydropyrimidine dehydrogenase (DPD), the principal enzyme of 5-fluorouracil (5-FU) catabolism. Fluorouracil 118-122 dihydropyrimidine dehydrogenase Homo sapiens 72-75 11081574-2 2000 Inactivation of DPD eliminates a potential mechanism for tumor 5-FU resistance and permits achievement of reliable and predictable pharmacokinetics following oral 5-FU administration. Fluorouracil 63-67 dihydropyrimidine dehydrogenase Homo sapiens 16-19 11081574-2 2000 Inactivation of DPD eliminates a potential mechanism for tumor 5-FU resistance and permits achievement of reliable and predictable pharmacokinetics following oral 5-FU administration. Fluorouracil 163-167 dihydropyrimidine dehydrogenase Homo sapiens 16-19 1648430-4 1991 The activity of dihydropyrimidine dehydrogenase (DPD), the initial enzyme of pyrimidine (and FUra) catabolism, in peripheral blood mononuclear cells was measured in each subject by a specific radiometric assay using FUra as the substrate. Fluorouracil 93-97 dihydropyrimidine dehydrogenase Homo sapiens 49-52 1648430-4 1991 The activity of dihydropyrimidine dehydrogenase (DPD), the initial enzyme of pyrimidine (and FUra) catabolism, in peripheral blood mononuclear cells was measured in each subject by a specific radiometric assay using FUra as the substrate. Fluorouracil 216-220 dihydropyrimidine dehydrogenase Homo sapiens 16-47 11086435-5 2000 These results indicate that: (1) degradation of 5-fluorouracil (5-FU) is enhanced in hepatic lesions more than in primary lesions, which is consistent with previous findings showing the therapeutic advantage of hepatic arterial infusion over intravenous infusion in relation to the treatment of 5-FU for liver metastases of colorectal cancer patients; and (2) predicting the effectiveness of hepatic arterial infusion of 5-FU for patients with metachronous liver metastases is difficult based on DPD determination of primary lesions alone. Fluorouracil 48-62 dihydropyrimidine dehydrogenase Homo sapiens 496-499 11086435-5 2000 These results indicate that: (1) degradation of 5-fluorouracil (5-FU) is enhanced in hepatic lesions more than in primary lesions, which is consistent with previous findings showing the therapeutic advantage of hepatic arterial infusion over intravenous infusion in relation to the treatment of 5-FU for liver metastases of colorectal cancer patients; and (2) predicting the effectiveness of hepatic arterial infusion of 5-FU for patients with metachronous liver metastases is difficult based on DPD determination of primary lesions alone. Fluorouracil 64-68 dihydropyrimidine dehydrogenase Homo sapiens 496-499 1648430-4 1991 The activity of dihydropyrimidine dehydrogenase (DPD), the initial enzyme of pyrimidine (and FUra) catabolism, in peripheral blood mononuclear cells was measured in each subject by a specific radiometric assay using FUra as the substrate. Fluorouracil 216-220 dihydropyrimidine dehydrogenase Homo sapiens 49-52 1648430-8 1991 Monitoring DPD activity may be important in the management of patients experiencing severe toxicity secondary to FUra chemotherapy. Fluorouracil 113-117 dihydropyrimidine dehydrogenase Homo sapiens 11-14 1716587-1 1991 C57BL/6 mice were established to constitutively produce multi-colony-stimulating factor (multi-CSF), granulocyte-macrophage colony-stimulating factor, or granulocyte colony-stimulating factor by transplantation with post-5-fluorouracil-treated syngeneic marrow cells infected with retroviral vectors bearing the corresponding growth factor complementary DNAs. Fluorouracil 221-235 colony stimulating factor 2 (granulocyte-macrophage) Mus musculus 101-191 10971312-1 2000 AIMS: Dihydropyrimidine dehydrogenase (DPD) reduces endogenous pyrimidines and therapeutic analogues such as the anticancer agent 5-fluorouracil (5FU). Fluorouracil 130-144 dihydropyrimidine dehydrogenase Homo sapiens 6-37 10971312-1 2000 AIMS: Dihydropyrimidine dehydrogenase (DPD) reduces endogenous pyrimidines and therapeutic analogues such as the anticancer agent 5-fluorouracil (5FU). Fluorouracil 130-144 dihydropyrimidine dehydrogenase Homo sapiens 39-42 10971312-1 2000 AIMS: Dihydropyrimidine dehydrogenase (DPD) reduces endogenous pyrimidines and therapeutic analogues such as the anticancer agent 5-fluorouracil (5FU). Fluorouracil 146-149 dihydropyrimidine dehydrogenase Homo sapiens 6-37 10971312-1 2000 AIMS: Dihydropyrimidine dehydrogenase (DPD) reduces endogenous pyrimidines and therapeutic analogues such as the anticancer agent 5-fluorouracil (5FU). Fluorouracil 146-149 dihydropyrimidine dehydrogenase Homo sapiens 39-42 10971312-4 2000 METHODS: DPD activity was determined in peripheral mononuclear cells using[14C]-5-fluorouracil and h.p.l.c. Fluorouracil 80-94 dihydropyrimidine dehydrogenase Homo sapiens 9-12 10971312-10 2000 CONCLUSIONS: The similarity in DPD activity between Caucasian, Kenyan and South-west Asian populations suggests that the incidence of 5FU-related toxicity may be comparable in these groups. Fluorouracil 134-137 dihydropyrimidine dehydrogenase Homo sapiens 31-34 10777676-2 2000 Reduced DPD activity is associated with toxicity to 5-fluorouracil (5FU) therapy in cancer patients and with neurological abnormalities in paediatric patients. Fluorouracil 52-66 dihydropyrimidine dehydrogenase Homo sapiens 8-11 10777676-2 2000 Reduced DPD activity is associated with toxicity to 5-fluorouracil (5FU) therapy in cancer patients and with neurological abnormalities in paediatric patients. Fluorouracil 68-71 dihydropyrimidine dehydrogenase Homo sapiens 8-11 10620566-1 2000 BACKGROUND: Dihydropyrimidine dehydrogenase (DPD) catalyzes the degradation of thymine, uracil, and the chemotherapeutic drug 5-fluorouracil. Fluorouracil 126-140 dihydropyrimidine dehydrogenase Homo sapiens 12-43 10620566-1 2000 BACKGROUND: Dihydropyrimidine dehydrogenase (DPD) catalyzes the degradation of thymine, uracil, and the chemotherapeutic drug 5-fluorouracil. Fluorouracil 126-140 dihydropyrimidine dehydrogenase Homo sapiens 45-48 10620566-9 2000 Low DPD activity comparable to that observed in obligate heterozygotes was initially detected in PBM cells, containing substantial amounts of myeloid cells, from a patient suffering from 5-fluorouracil toxicity. Fluorouracil 187-201 dihydropyrimidine dehydrogenase Homo sapiens 4-7 10623435-5 2000 Moreover, we have previously demonstrated that 5-fluorouracile (5-FU) resistant HSC require a combination of interleukin 12 (IL-12), IL-6 and SCF for the production of morphologically recognizable clonogenic elements at day 14 in semisolid medium. Fluorouracil 64-68 KIT ligand Homo sapiens 142-145 1913872-2 1991 The occurrence of semi-dominant mutations for 5-fluorouracil-(5FU)-resistance at this locus led us to clone and sequence the semi-dominant fur1-5 allele. Fluorouracil 46-60 uracil phosphoribosyltransferase Saccharomyces cerevisiae S288C 139-143 2019738-6 1991 Illustrative data of LAK cytotoxicity influenced by dose of the LAK response modifiers IL-2, TGF beta, TDSF and 5-FU, show different relationships between lytic units, KM and AUC. Fluorouracil 112-116 alpha kinase 1 Homo sapiens 21-24 10744051-0 2000 Dihydropyrimidine dehydrogenase and messenger RNA levels in gastric cancer: possible predictor for sensitivity to 5-fluorouracil. Fluorouracil 114-128 dihydropyrimidine dehydrogenase Homo sapiens 0-31 10744051-1 2000 We investigated the correlation between tumor sensitivity to 5-fluorouracil (5-FU) and enzymatic activities of thymidylate synthetase (TS) and dihydropyrimidine dehydrogenase (DPD) in human gastric cancer specimens. Fluorouracil 61-75 dihydropyrimidine dehydrogenase Homo sapiens 143-174 10744051-1 2000 We investigated the correlation between tumor sensitivity to 5-fluorouracil (5-FU) and enzymatic activities of thymidylate synthetase (TS) and dihydropyrimidine dehydrogenase (DPD) in human gastric cancer specimens. Fluorouracil 61-75 dihydropyrimidine dehydrogenase Homo sapiens 176-179 10744051-1 2000 We investigated the correlation between tumor sensitivity to 5-fluorouracil (5-FU) and enzymatic activities of thymidylate synthetase (TS) and dihydropyrimidine dehydrogenase (DPD) in human gastric cancer specimens. Fluorouracil 77-81 dihydropyrimidine dehydrogenase Homo sapiens 143-174 10744051-1 2000 We investigated the correlation between tumor sensitivity to 5-fluorouracil (5-FU) and enzymatic activities of thymidylate synthetase (TS) and dihydropyrimidine dehydrogenase (DPD) in human gastric cancer specimens. Fluorouracil 77-81 dihydropyrimidine dehydrogenase Homo sapiens 176-179 10744051-9 2000 DPD levels significantly correlated with 5-FU sensitivity, such that high DPD activity and high DPD mRNA levels resulted in low sensitivity to 5-FU. Fluorouracil 41-45 dihydropyrimidine dehydrogenase Homo sapiens 0-3 10744051-9 2000 DPD levels significantly correlated with 5-FU sensitivity, such that high DPD activity and high DPD mRNA levels resulted in low sensitivity to 5-FU. Fluorouracil 41-45 dihydropyrimidine dehydrogenase Homo sapiens 74-77 10744051-9 2000 DPD levels significantly correlated with 5-FU sensitivity, such that high DPD activity and high DPD mRNA levels resulted in low sensitivity to 5-FU. Fluorouracil 41-45 dihydropyrimidine dehydrogenase Homo sapiens 74-77 10744051-9 2000 DPD levels significantly correlated with 5-FU sensitivity, such that high DPD activity and high DPD mRNA levels resulted in low sensitivity to 5-FU. Fluorouracil 143-147 dihydropyrimidine dehydrogenase Homo sapiens 0-3 10744051-9 2000 DPD levels significantly correlated with 5-FU sensitivity, such that high DPD activity and high DPD mRNA levels resulted in low sensitivity to 5-FU. Fluorouracil 143-147 dihydropyrimidine dehydrogenase Homo sapiens 74-77 10744051-9 2000 DPD levels significantly correlated with 5-FU sensitivity, such that high DPD activity and high DPD mRNA levels resulted in low sensitivity to 5-FU. Fluorouracil 143-147 dihydropyrimidine dehydrogenase Homo sapiens 74-77 10744051-11 2000 We conclude that tumor DPD mRNA level, as assessed from biopsy specimens obtained by gastrofiberscopy, may be a useful indicator in predicting tumor sensitivity to 5-FU in patients with gastric cancer. Fluorouracil 164-168 dihydropyrimidine dehydrogenase Homo sapiens 23-26 10567908-9 1999 Since it has been demonstrated that dUTPase expression can mediate resistance to 5-fluorouracil, it is also possible that these MAbs may be helpful in identifying patients with colorectal carcinomas resistant to adjuvant chemotherapy using this and related compounds. Fluorouracil 81-95 Deoxyuridine triphosphatase Drosophila melanogaster 36-43 10595802-3 1999 Dihydropyrimidine dehydrogenase (DPD), a rate-limiting enzyme in the catabolism of fluorouracil, indirectly determines the drug"s anticancer efficacy by regulating the availability of fluorouracil for anabolism. Fluorouracil 83-95 dihydropyrimidine dehydrogenase Homo sapiens 0-31 10595802-3 1999 Dihydropyrimidine dehydrogenase (DPD), a rate-limiting enzyme in the catabolism of fluorouracil, indirectly determines the drug"s anticancer efficacy by regulating the availability of fluorouracil for anabolism. Fluorouracil 83-95 dihydropyrimidine dehydrogenase Homo sapiens 33-36 10595802-3 1999 Dihydropyrimidine dehydrogenase (DPD), a rate-limiting enzyme in the catabolism of fluorouracil, indirectly determines the drug"s anticancer efficacy by regulating the availability of fluorouracil for anabolism. Fluorouracil 184-196 dihydropyrimidine dehydrogenase Homo sapiens 0-31 10595802-3 1999 Dihydropyrimidine dehydrogenase (DPD), a rate-limiting enzyme in the catabolism of fluorouracil, indirectly determines the drug"s anticancer efficacy by regulating the availability of fluorouracil for anabolism. Fluorouracil 184-196 dihydropyrimidine dehydrogenase Homo sapiens 33-36 10595802-5 1999 Capecitabine, a prodrug of fluorouracil, circumvents DPD. Fluorouracil 27-39 dihydropyrimidine dehydrogenase Homo sapiens 53-56 10595802-7 1999 Fluorouracil must be administered in combination with eniluracil, an inactivator of DPD. Fluorouracil 0-12 dihydropyrimidine dehydrogenase Homo sapiens 84-87 10697632-1 1999 The measurement of thymidylate synthetase (TS) and dihydropyrimidine dehydrogenase (DPD) enzymatic activities and mRNA levels in tumors may be useful in predicting tumor sensitivity to 5-fluorouracil (5-FU). Fluorouracil 185-199 dihydropyrimidine dehydrogenase Homo sapiens 84-87 10697632-1 1999 The measurement of thymidylate synthetase (TS) and dihydropyrimidine dehydrogenase (DPD) enzymatic activities and mRNA levels in tumors may be useful in predicting tumor sensitivity to 5-fluorouracil (5-FU). Fluorouracil 201-205 dihydropyrimidine dehydrogenase Homo sapiens 84-87 10560382-1 1999 Dihydropyrimidine dehydrogenase (DPD) is the rate-limiting enzyme for 5-FU catabolism. Fluorouracil 70-74 dihydropyrimidine dehydrogenase Homo sapiens 0-31 10560382-1 1999 Dihydropyrimidine dehydrogenase (DPD) is the rate-limiting enzyme for 5-FU catabolism. Fluorouracil 70-74 dihydropyrimidine dehydrogenase Homo sapiens 33-36 10560382-2 1999 Recently, much interest has been taken in the relation between the antitumor effect of 5-FU and DPD expression in gastrointestinal cancers. Fluorouracil 87-91 dihydropyrimidine dehydrogenase Homo sapiens 96-99 10499641-6 1999 However, the increasing actions of CDDP and 5-FU on GSTpi, DPD, MRP, and TS expression varied according to the exposure time, concentration, and schedule. Fluorouracil 44-48 dihydropyrimidine dehydrogenase Homo sapiens 59-62 10499641-7 1999 A low concentration of CDDP (1 microg/ml, 30 min) followed by 5-FU (0.5 microg/ml, 72 h) was found to cause a less increased expression of DPD, MRP, GSTpi, and TS than either drug alone, thus resulting in synergistic cytotoxicity in 5-FU-resistant COLO201 and CDDP-resistant HCC-48 cells. Fluorouracil 62-66 dihydropyrimidine dehydrogenase Homo sapiens 139-142 10885904-0 1999 Modulation of 5-fluorouracil by 5-ethyl-2"-deoxyuridine on cell lines expressing different dihydropyrimidine dehydrogenase activities. Fluorouracil 14-28 dihydropyrimidine dehydrogenase Homo sapiens 91-122 10885904-1 1999 The purpose of the present study was to clarify the significance of the inhibition of dihydropyrimidine dehydrogenase (DPD) in the modulation of 5-fluorouracil (5-FU) action by 5-ethyl-2"-deoxyuridine (EUdR). Fluorouracil 145-159 dihydropyrimidine dehydrogenase Homo sapiens 86-117 10885904-1 1999 The purpose of the present study was to clarify the significance of the inhibition of dihydropyrimidine dehydrogenase (DPD) in the modulation of 5-fluorouracil (5-FU) action by 5-ethyl-2"-deoxyuridine (EUdR). Fluorouracil 145-159 dihydropyrimidine dehydrogenase Homo sapiens 119-122 10885904-1 1999 The purpose of the present study was to clarify the significance of the inhibition of dihydropyrimidine dehydrogenase (DPD) in the modulation of 5-fluorouracil (5-FU) action by 5-ethyl-2"-deoxyuridine (EUdR). Fluorouracil 161-165 dihydropyrimidine dehydrogenase Homo sapiens 86-117 10885904-1 1999 The purpose of the present study was to clarify the significance of the inhibition of dihydropyrimidine dehydrogenase (DPD) in the modulation of 5-fluorouracil (5-FU) action by 5-ethyl-2"-deoxyuridine (EUdR). Fluorouracil 161-165 dihydropyrimidine dehydrogenase Homo sapiens 119-122 10885904-8 1999 On the contrary, enhancement of the 5-FU cytotoxicity was demonstrated on COLO1 and SW620 cells with low DPD activity. Fluorouracil 36-40 dihydropyrimidine dehydrogenase Homo sapiens 105-108 2019738-6 1991 Illustrative data of LAK cytotoxicity influenced by dose of the LAK response modifiers IL-2, TGF beta, TDSF and 5-FU, show different relationships between lytic units, KM and AUC. Fluorouracil 112-116 alpha kinase 1 Homo sapiens 64-67 1958851-1 1991 We determined the effect of 1-hexylcarbamoyl-5-fluorouracil (HCFU), a masked compound of 5-fluorouracil, on the expression of heat shock protein (HSP) in heat-treated HeLa cells. Fluorouracil 45-59 heat shock protein 90 beta family member 2, pseudogene Homo sapiens 126-144 10411544-10 1999 Apo2L cooperated synergistically with the chemotherapeutic drugs 5-fluorouracil or CPT-11, causing substantial tumor regression or complete tumor ablation. Fluorouracil 65-79 tumor necrosis factor (ligand) superfamily, member 10 Mus musculus 0-5 1958851-1 1991 We determined the effect of 1-hexylcarbamoyl-5-fluorouracil (HCFU), a masked compound of 5-fluorouracil, on the expression of heat shock protein (HSP) in heat-treated HeLa cells. Fluorouracil 45-59 heat shock protein 90 beta family member 2, pseudogene Homo sapiens 146-149 1804597-6 1991 JM8 was administered alone (400 mg/m2) or in combination (300 mg/m2) with vinblastine (6 mg/m2), etoposide (100 mg/m2) or 5-fluorouracil (1,000 mg/m2). Fluorouracil 122-136 calcium voltage-gated channel subunit alpha1 F Homo sapiens 0-3 10400413-8 1999 By contrast, LTC cells or secondary colonies obtained from CML CD34+ cells without culture in the presence of 5-FU were always positive for BCR/ABL rearrangement. Fluorouracil 110-114 BCR activator of RhoGEF and GTPase Rattus norvegicus 140-147 10362102-0 1999 Synergistic induction of ICAM-1 expression by cisplatin and 5-fluorouracil in a cancer cell line via a NF-kappaB independent pathway. Fluorouracil 60-74 intercellular adhesion molecule 1 Homo sapiens 25-31 10362102-3 1999 When NA cells, a squamous cell carcinoma cell line, were exposed to CDDP and 5-FU for 18 h, the expression of intercellular adhesion molecule-1 (ICAM-1) was synergistically induced, whereas CDDP or 5-FU alone did not induce the expression of ICAM-1, as determined by flow cytometry. Fluorouracil 77-81 intercellular adhesion molecule 1 Homo sapiens 110-143 10362102-3 1999 When NA cells, a squamous cell carcinoma cell line, were exposed to CDDP and 5-FU for 18 h, the expression of intercellular adhesion molecule-1 (ICAM-1) was synergistically induced, whereas CDDP or 5-FU alone did not induce the expression of ICAM-1, as determined by flow cytometry. Fluorouracil 77-81 intercellular adhesion molecule 1 Homo sapiens 145-151 10362102-3 1999 When NA cells, a squamous cell carcinoma cell line, were exposed to CDDP and 5-FU for 18 h, the expression of intercellular adhesion molecule-1 (ICAM-1) was synergistically induced, whereas CDDP or 5-FU alone did not induce the expression of ICAM-1, as determined by flow cytometry. Fluorouracil 77-81 intercellular adhesion molecule 1 Homo sapiens 242-248 10362102-6 1999 Treatment with genistein, a protein tyrosine kinase (PTK) inhibitor, inhibited the induction of ICAM-1 on NA cells by CDDP and 5-FU, whereas staurosporin, a protein kinase C inhibitor, did not. Fluorouracil 127-131 intercellular adhesion molecule 1 Homo sapiens 96-102 10206306-0 1999 A multifactorial approach including tumoural epidermal growth factor receptor, p53, thymidylate synthase and dihydropyrimidine dehydrogenase to predict treatment outcome in head and neck cancer patients receiving 5-fluorouracil. Fluorouracil 213-227 dihydropyrimidine dehydrogenase Homo sapiens 109-140 10213225-0 1999 Dihydropyrimidine dehydrogenase activity and messenger RNA level may be related to the antitumor effect of 5-fluorouracil on human tumor xenografts in nude mice. Fluorouracil 107-121 dihydropyrimidine dehydrogenase Homo sapiens 0-31 10213225-1 1999 We investigated the correlation between tumor sensitivity to 5-fluorouracil (5-FU) and the enzymatic activity and mRNA levels of thymidylate synthetase (TS) and dihydropyrimidine dehydrogenase (DPD) using human tumor xenografts in nude mice. Fluorouracil 61-75 dihydropyrimidine dehydrogenase Homo sapiens 161-192 10213225-1 1999 We investigated the correlation between tumor sensitivity to 5-fluorouracil (5-FU) and the enzymatic activity and mRNA levels of thymidylate synthetase (TS) and dihydropyrimidine dehydrogenase (DPD) using human tumor xenografts in nude mice. Fluorouracil 61-75 dihydropyrimidine dehydrogenase Homo sapiens 194-197 1693405-0 1990 Hematologic effects of interleukin-1 beta, granulocyte colony-stimulating factor, and granulocyte-macrophage colony-stimulating factor in tumor-bearing mice treated with fluorouracil. Fluorouracil 170-182 colony stimulating factor 2 (granulocyte-macrophage) Mus musculus 86-134 1693405-5 1990 rHuIL-1 beta alone or in combination with rHuG-CSF or recombinant murine GM-CSF significantly improved tumor growth inhibition (60% vs. 90%) and survival (20% vs. 90%-100%), increased the maximally tolerated dose of 5-FU, accelerated recovery of neutrophil counts in peripheral blood, and reduced duration of significant neutropenia and loss of body weight (29% vs. 10% loss). Fluorouracil 216-220 colony stimulating factor 2 (granulocyte-macrophage) Mus musculus 73-79 2396254-4 1990 Northern blot analysis of DHFR mRNA obtained from 5-FU-sensitive and -resistant cell lines revealed four distinct bands of 1.6 kb, 1.2 kb, 1.0 kb and 0.75 kb in length. Fluorouracil 50-54 dihydrofolate reductase Mus musculus 26-30 33816278-0 2021 CMPK1 Regulated by miR-130b Attenuates Response to 5-FU Treatment in Gastric Cancer. Fluorouracil 51-55 cytidine/uridine monophosphate kinase 1 Homo sapiens 0-5 33816278-4 2021 Our bioinformatics analysis and molecular experiments demonstrated that high expression of CMPK1 was associated with prolonged survival and response to 5-FU treatment in GC samples. Fluorouracil 152-156 cytidine/uridine monophosphate kinase 1 Homo sapiens 91-96 33816278-5 2021 Further analysis demonstrated that miR-130b as a key epigenetic regulator of CMPK1, and miR-130b-mediated attenuation of CMPK1 resulted in resistance of gastric cancer cells to DNA damage and cell death after treatment with 5-FU. Fluorouracil 224-228 cytidine/uridine monophosphate kinase 1 Homo sapiens 77-82 33816278-5 2021 Further analysis demonstrated that miR-130b as a key epigenetic regulator of CMPK1, and miR-130b-mediated attenuation of CMPK1 resulted in resistance of gastric cancer cells to DNA damage and cell death after treatment with 5-FU. Fluorouracil 224-228 cytidine/uridine monophosphate kinase 1 Homo sapiens 121-126 33816278-7 2021 Thus, this newly identified miR-130b-CMPK1 axis suggests a potentially new chemotherapeutic strategy for improved response to 5-FU therapy. Fluorouracil 126-130 cytidine/uridine monophosphate kinase 1 Homo sapiens 37-42 33804148-10 2021 ANXA1 expression correlated with a sensitivity to gemcitabine, doxorubicin, and 5-fluorouracil in PC cell lines. Fluorouracil 80-94 annexin A1 Homo sapiens 0-5 33232506-3 2020 Today, there is a plethora of evidence that genetic variants in the gene encoding for the 5-FU catabolising enzyme dihydropyrimidine dehydrogenase (DPD, encoded by DPYD) are predictive of severe FP-related toxicities, and international clinical practice recommendations for DPYD genotype-guided FP dosing and therapeutic drug monitoring (TDM) are available. Fluorouracil 90-94 dihydropyrimidine dehydrogenase Homo sapiens 115-146 33232506-3 2020 Today, there is a plethora of evidence that genetic variants in the gene encoding for the 5-FU catabolising enzyme dihydropyrimidine dehydrogenase (DPD, encoded by DPYD) are predictive of severe FP-related toxicities, and international clinical practice recommendations for DPYD genotype-guided FP dosing and therapeutic drug monitoring (TDM) are available. Fluorouracil 90-94 dihydropyrimidine dehydrogenase Homo sapiens 148-151 33232506-3 2020 Today, there is a plethora of evidence that genetic variants in the gene encoding for the 5-FU catabolising enzyme dihydropyrimidine dehydrogenase (DPD, encoded by DPYD) are predictive of severe FP-related toxicities, and international clinical practice recommendations for DPYD genotype-guided FP dosing and therapeutic drug monitoring (TDM) are available. Fluorouracil 90-94 dihydropyrimidine dehydrogenase Homo sapiens 164-168 33232506-3 2020 Today, there is a plethora of evidence that genetic variants in the gene encoding for the 5-FU catabolising enzyme dihydropyrimidine dehydrogenase (DPD, encoded by DPYD) are predictive of severe FP-related toxicities, and international clinical practice recommendations for DPYD genotype-guided FP dosing and therapeutic drug monitoring (TDM) are available. Fluorouracil 90-94 dihydropyrimidine dehydrogenase Homo sapiens 274-278 33232506-9 2020 Furthermore, we recommend the use of infusional 5-FU in patients with a DPYD risk genotype in order to enable TDM-based dose escalation. Fluorouracil 48-52 dihydropyrimidine dehydrogenase Homo sapiens 72-76 23307041-10 2013 Moreover, the patients with high FAK only or combined with low JWA had significant benefit from adjuvant fluorouracil-leucovorin-oxaliplatin (FLO) therapy compared with those with surgery alone (P = 0.003); however, the cases with adjuvant fluorouracil-leucovorin-cisplatin (FLP) therapy did not show these effects. Fluorouracil 105-117 ADP ribosylation factor like GTPase 6 interacting protein 5 Homo sapiens 63-66 10217332-1 1999 Dihydropyrimidine dehydrogenase (DPD) is the major metabolic enzyme in the catabolism of 5-fluorouracil, and the activity in normal tissues shows a wide variation among individuals. Fluorouracil 89-103 dihydropyrimidine dehydrogenase Homo sapiens 0-31 10217332-1 1999 Dihydropyrimidine dehydrogenase (DPD) is the major metabolic enzyme in the catabolism of 5-fluorouracil, and the activity in normal tissues shows a wide variation among individuals. Fluorouracil 89-103 dihydropyrimidine dehydrogenase Homo sapiens 33-36 10217332-2 1999 Recent studies demonstrate the relevance of DPD in the pharmacokinetics, toxicity, and antitumor efficacy of 5-fluorouracil. Fluorouracil 109-123 dihydropyrimidine dehydrogenase Homo sapiens 44-47 10089915-0 1999 Marrow sensitization to 5-fluorouracil using the ligands for Flt-3 and c-Kit. Fluorouracil 24-38 FMS-like tyrosine kinase 3 Mus musculus 61-66 10089915-2 1999 Studies were performed to determine whether the in vivo administration of Flk-2/Flt-3 ligand (FL) is also capable of sensitizing progenitors to 5-FU. Fluorouracil 144-148 FMS-like tyrosine kinase 3 Mus musculus 74-79 10024690-0 1999 Dihydropyrimidine dehydrogenase, multidrug resistance-associated protein, and thymidylate synthase gene expression levels can predict 5-fluorouracil resistance in human gastrointestinal cancer cells. Fluorouracil 134-148 dihydropyrimidine dehydrogenase Homo sapiens 0-31 10024690-1 1999 Gene expression of dihydropyrimidine dehydrogenase (DPD) and newly multidrug resistance-associated protein (MRP) was found to correlate well with primary 5-FU resistance in 7 human gastrointestinal cancer cell lines. Fluorouracil 154-158 dihydropyrimidine dehydrogenase Homo sapiens 19-50 10024690-1 1999 Gene expression of dihydropyrimidine dehydrogenase (DPD) and newly multidrug resistance-associated protein (MRP) was found to correlate well with primary 5-FU resistance in 7 human gastrointestinal cancer cell lines. Fluorouracil 154-158 dihydropyrimidine dehydrogenase Homo sapiens 52-55 10024690-4 1999 DPD and MRP expression levels can predict primary 5-FU resistance, and TS may be a potent predictor of cellular 5-FU resistance after 5-FU treatment. Fluorouracil 50-54 dihydropyrimidine dehydrogenase Homo sapiens 0-3 34883427-2 2022 Manuka honey, alone and more in combination with 5-Fu, reduced the weight, the diameter and mass density of the spheroids and induced apoptosis through the downregulation of many apoptosis inhibitors, including IAPs (Livin, Survivin, XIAP), IGFs (IGF-I, IGF-II and IGF-IR) and HSPs (HSP-27, HSP-60 and HSP-70). Fluorouracil 49-53 baculoviral IAP repeat containing 7 Homo sapiens 217-222 10048591-5 1999 The SICs detected in our culture system were present only in Mac-1(-)CD45(-) cells, and the M-CSF treatment of 5-FU-pretreated mice actually increased the number of Mac-1(-)CD45(-) SICs. Fluorouracil 111-115 colony stimulating factor 1 (macrophage) Mus musculus 92-97 34883427-2 2022 Manuka honey, alone and more in combination with 5-Fu, reduced the weight, the diameter and mass density of the spheroids and induced apoptosis through the downregulation of many apoptosis inhibitors, including IAPs (Livin, Survivin, XIAP), IGFs (IGF-I, IGF-II and IGF-IR) and HSPs (HSP-27, HSP-60 and HSP-70). Fluorouracil 49-53 X-linked inhibitor of apoptosis Homo sapiens 234-238 34883427-2 2022 Manuka honey, alone and more in combination with 5-Fu, reduced the weight, the diameter and mass density of the spheroids and induced apoptosis through the downregulation of many apoptosis inhibitors, including IAPs (Livin, Survivin, XIAP), IGFs (IGF-I, IGF-II and IGF-IR) and HSPs (HSP-27, HSP-60 and HSP-70). Fluorouracil 49-53 insulin like growth factor 1 receptor Homo sapiens 265-271 34883427-2 2022 Manuka honey, alone and more in combination with 5-Fu, reduced the weight, the diameter and mass density of the spheroids and induced apoptosis through the downregulation of many apoptosis inhibitors, including IAPs (Livin, Survivin, XIAP), IGFs (IGF-I, IGF-II and IGF-IR) and HSPs (HSP-27, HSP-60 and HSP-70). Fluorouracil 49-53 heat shock protein family D (Hsp60) member 1 Homo sapiens 291-297 34883427-2 2022 Manuka honey, alone and more in combination with 5-Fu, reduced the weight, the diameter and mass density of the spheroids and induced apoptosis through the downregulation of many apoptosis inhibitors, including IAPs (Livin, Survivin, XIAP), IGFs (IGF-I, IGF-II and IGF-IR) and HSPs (HSP-27, HSP-60 and HSP-70). Fluorouracil 49-53 heat shock protein family A (Hsp70) member 4 Homo sapiens 302-308 10099659-4 1999 Dihydropyrimidine dehydrogenase (DPD) is the rate-limiting enzyme in the catabolism of 5-FU. Fluorouracil 87-91 dihydropyrimidine dehydrogenase Homo sapiens 0-31 34658120-0 2022 Long noncoding RNA HAGLR sponges miR-338-3p to promote 5-Fu resistance in gastric cancer through targeting the LDHA-glycolysis pathway. Fluorouracil 55-59 HOXD antisense growth-associated long non-coding RNA Homo sapiens 19-24 10099659-4 1999 Dihydropyrimidine dehydrogenase (DPD) is the rate-limiting enzyme in the catabolism of 5-FU. Fluorouracil 87-91 dihydropyrimidine dehydrogenase Homo sapiens 33-36 10099659-12 1999 Because neurologic toxicity is becoming more recognized and DPD affects the catabolism of 5-FU, we discuss management issues and the use of new DPD inhibitors. Fluorouracil 90-94 dihydropyrimidine dehydrogenase Homo sapiens 60-63 34658120-8 2022 Blocking HAGLR inhibited GC cells proliferation and sensitized GC cells to 5-Fu. Fluorouracil 75-79 HOXD antisense growth-associated long non-coding RNA Homo sapiens 9-14 9850079-4 1998 Only after the administration of 400 mg/kg 5-FU were mitotic index and DNA synthesis significantly suppressed in both small intestinal and midcolonic crypts at 24 h. This correlated with a prolonged, p53-dependent expression of p21waf-1/cip1. Fluorouracil 43-47 cyclin-dependent kinase inhibitor 1A (P21) Mus musculus 228-241 34658120-10 2022 Moreover, from the established 5-Fu resistant gastric cancer cell line (HGC27 5-Fu R), we detected significantly elevated HAGLR, downregulated miR-338-3p, and glucose metabolism compared with parental HGC27 cells. Fluorouracil 31-35 HOXD antisense growth-associated long non-coding RNA Homo sapiens 122-127 34658120-10 2022 Moreover, from the established 5-Fu resistant gastric cancer cell line (HGC27 5-Fu R), we detected significantly elevated HAGLR, downregulated miR-338-3p, and glucose metabolism compared with parental HGC27 cells. Fluorouracil 78-82 HOXD antisense growth-associated long non-coding RNA Homo sapiens 122-127 34658120-12 2022 Rescue experiments demonstrated that restoration of miR-338-3p in HAGLR-overexpressing HGC27 5-Fu R cells successfully overrode the HAGLR-promoted 5-Fu resistance through targeting LDHA. Fluorouracil 93-97 HOXD antisense growth-associated long non-coding RNA Homo sapiens 66-71 34658120-12 2022 Rescue experiments demonstrated that restoration of miR-338-3p in HAGLR-overexpressing HGC27 5-Fu R cells successfully overrode the HAGLR-promoted 5-Fu resistance through targeting LDHA. Fluorouracil 93-97 HOXD antisense growth-associated long non-coding RNA Homo sapiens 132-137 9865912-0 1998 Identification of novel mutations in the dihydropyrimidine dehydrogenase gene in a Japanese patient with 5-fluorouracil toxicity. Fluorouracil 105-119 dihydropyrimidine dehydrogenase Homo sapiens 41-72 9865912-2 1998 Dihydropyrimidine dehydrogenase (DPD) is the initial and rate-limiting enzyme in the catabolism of 5-FU. Fluorouracil 99-103 dihydropyrimidine dehydrogenase Homo sapiens 0-31 9865912-2 1998 Dihydropyrimidine dehydrogenase (DPD) is the initial and rate-limiting enzyme in the catabolism of 5-FU. Fluorouracil 99-103 dihydropyrimidine dehydrogenase Homo sapiens 33-36 34658120-12 2022 Rescue experiments demonstrated that restoration of miR-338-3p in HAGLR-overexpressing HGC27 5-Fu R cells successfully overrode the HAGLR-promoted 5-Fu resistance through targeting LDHA. Fluorouracil 147-151 HOXD antisense growth-associated long non-coding RNA Homo sapiens 66-71 9865912-4 1998 We reported recently the first Japanese case of decreased DPD activity accompanied by severe 5-FU toxicity. Fluorouracil 93-97 dihydropyrimidine dehydrogenase Homo sapiens 58-61 34658120-12 2022 Rescue experiments demonstrated that restoration of miR-338-3p in HAGLR-overexpressing HGC27 5-Fu R cells successfully overrode the HAGLR-promoted 5-Fu resistance through targeting LDHA. Fluorouracil 147-151 HOXD antisense growth-associated long non-coding RNA Homo sapiens 132-137 34658120-13 2022 Taken together, this study revealed essential roles and molecular mechanisms for the HAGLR-mediated 5-Fu resistance in GC, contributing to development of new non-coding RNA-based therapeutic strategies against chemoresistant GC. Fluorouracil 100-104 HOXD antisense growth-associated long non-coding RNA Homo sapiens 85-90 9840921-7 1998 Bak-overexpressing cells also showed greater sensitization to 5-fluorouracil and cisplatin than parent cells and MKN-neo-transfected cells. Fluorouracil 62-76 BCL2 antagonist/killer 1 Homo sapiens 0-3 34688013-4 2022 Here, compound 9d could significantly inhibit the expression of dihydropyrimidine dehydrogenase (DPD) to reverse 5-FU-resistance in HCT116DPD and SW620/5-FU cells. Fluorouracil 113-117 dihydropyrimidine dehydrogenase Homo sapiens 64-95 34688013-4 2022 Here, compound 9d could significantly inhibit the expression of dihydropyrimidine dehydrogenase (DPD) to reverse 5-FU-resistance in HCT116DPD and SW620/5-FU cells. Fluorouracil 113-117 dihydropyrimidine dehydrogenase Homo sapiens 97-100 34688013-4 2022 Here, compound 9d could significantly inhibit the expression of dihydropyrimidine dehydrogenase (DPD) to reverse 5-FU-resistance in HCT116DPD and SW620/5-FU cells. Fluorouracil 152-156 dihydropyrimidine dehydrogenase Homo sapiens 64-95 34688013-4 2022 Here, compound 9d could significantly inhibit the expression of dihydropyrimidine dehydrogenase (DPD) to reverse 5-FU-resistance in HCT116DPD and SW620/5-FU cells. Fluorouracil 152-156 dihydropyrimidine dehydrogenase Homo sapiens 97-100 34347217-0 2022 Association between ABCC2 polymorphism and hematological toxicity in patients with esophageal cancer receiving platinum plus 5-fluorouracil therapy. Fluorouracil 125-139 ATP binding cassette subfamily C member 2 Homo sapiens 20-25 9807659-23 1998 Recognition of diurnal variation in the activity of such key enzymes as DPD has led to the administration of 5FU at regulated, variable infusion rates (chronomodulation). Fluorouracil 109-112 dihydropyrimidine dehydrogenase Homo sapiens 72-75 9951876-0 1998 Dihydropyrimidine dehydrogenase but not thymidylate synthase expression is associated with resistance to 5-fluorouracil in colorectal cancer. Fluorouracil 105-119 dihydropyrimidine dehydrogenase Homo sapiens 0-31 9951876-2 1998 Thymidylate synthase (TS) and dihydropyrimidine dehydrogenase (DPD) are key enzymes involved in the biochemical functions of the antimetabolite 5-fluorouracil (5-FU). Fluorouracil 144-158 dihydropyrimidine dehydrogenase Homo sapiens 30-61 9951876-2 1998 Thymidylate synthase (TS) and dihydropyrimidine dehydrogenase (DPD) are key enzymes involved in the biochemical functions of the antimetabolite 5-fluorouracil (5-FU). Fluorouracil 144-158 dihydropyrimidine dehydrogenase Homo sapiens 63-66 9951876-2 1998 Thymidylate synthase (TS) and dihydropyrimidine dehydrogenase (DPD) are key enzymes involved in the biochemical functions of the antimetabolite 5-fluorouracil (5-FU). Fluorouracil 160-164 dihydropyrimidine dehydrogenase Homo sapiens 30-61 9951876-2 1998 Thymidylate synthase (TS) and dihydropyrimidine dehydrogenase (DPD) are key enzymes involved in the biochemical functions of the antimetabolite 5-fluorouracil (5-FU). Fluorouracil 160-164 dihydropyrimidine dehydrogenase Homo sapiens 63-66 9951876-7 1998 CaR1, which expressed the highest level of DPD and no detectable TS, showed remarkable resistance to 5-FU. Fluorouracil 101-105 nuclear receptor subfamily 1 group I member 3 Homo sapiens 0-4 9951876-8 1998 The other colorectal cancer cell lines with undetectable DPD expression were sensitive to 5-FU. Fluorouracil 90-94 dihydropyrimidine dehydrogenase Homo sapiens 57-60 9951876-11 1998 CONCLUSIONS: These data suggest that DPD, but not TS, expression predicts 5-FU sensitivity in colorectal cancer cell lines. Fluorouracil 74-78 dihydropyrimidine dehydrogenase Homo sapiens 37-40 34347217-8 2022 CONCLUSIONS: We determined that ABCC2 -24C>T is significantly associated with grade 3-4 hematological toxicity after platinum plus 5-FU therapy. Fluorouracil 131-135 ATP binding cassette subfamily C member 2 Homo sapiens 32-37 34964946-0 2022 Lactobacillus plantarum-derived metabolites sensitize the tumor-suppressive effects of butyrate by regulating the functional expression of SMCT1 in 5-FU-resistant colorectal cancer cells. Fluorouracil 148-152 solute carrier family 5 member 8 Homo sapiens 139-144 34510524-7 2022 BUP and TRAM with 5-FU synergistically increased hippocampal GFAP expression. Fluorouracil 18-22 glial fibrillary acidic protein Rattus norvegicus 61-65 34859260-0 2022 Propofol induces apoptosis and ameliorates 5-fluorouracil resistance in OSCC cells by reducing the expression and secretion of amphiregulin. Fluorouracil 43-57 amphiregulin Homo sapiens 127-139 34859260-14 2022 Moreover, the results indicated that the expression and activation of AREG was also related to 5-FU resistance, but propofol ameliorated 5-FU drug resistance. Fluorouracil 95-99 amphiregulin Homo sapiens 70-74 34859260-14 2022 Moreover, the results indicated that the expression and activation of AREG was also related to 5-FU resistance, but propofol ameliorated 5-FU drug resistance. Fluorouracil 137-141 amphiregulin Homo sapiens 70-74 34717904-4 2021 DPD accepts the common antineoplastic agent 5-fluorouracil as a substrate and so undermines the establishment of efficacious toxicity. Fluorouracil 44-58 dihydropyrimidine dehydrogenase Homo sapiens 0-3 34821902-5 2021 In addition, GA not only ameliorated the damage to hippocampal neurons and mitochondrial structure, but also significantly improved abnormal protein expression of mitochondrial biogenesis related marker PGC-1alpha, and mitochondrial dynamics related markers MFN2, DRP1 and FIS1 in the hippocampi of 5-FU-treated mice. Fluorouracil 299-303 collapsin response mediator protein 1 Mus musculus 264-268 34710829-4 2021 Here, we adopted a prodrug system that uses 5-fluorocytosine (5-FC) and a HER2-targeting scaffold protein, ZHER2:2891, fused with yeast cytosine deaminase (Fcy) to target HER2-overexpressing cancer cells and to convert 5-FC to a significantly more toxic chemotherapeutic, 5-fluorouracil (5-FU). Fluorouracil 272-286 glutamyl-tRNA(Gln) amidotransferase subunit HER2 Saccharomyces cerevisiae S288C 74-78 34710829-4 2021 Here, we adopted a prodrug system that uses 5-fluorocytosine (5-FC) and a HER2-targeting scaffold protein, ZHER2:2891, fused with yeast cytosine deaminase (Fcy) to target HER2-overexpressing cancer cells and to convert 5-FC to a significantly more toxic chemotherapeutic, 5-fluorouracil (5-FU). Fluorouracil 288-292 glutamyl-tRNA(Gln) amidotransferase subunit HER2 Saccharomyces cerevisiae S288C 74-78 34710829-4 2021 Here, we adopted a prodrug system that uses 5-fluorocytosine (5-FC) and a HER2-targeting scaffold protein, ZHER2:2891, fused with yeast cytosine deaminase (Fcy) to target HER2-overexpressing cancer cells and to convert 5-FC to a significantly more toxic chemotherapeutic, 5-fluorouracil (5-FU). Fluorouracil 288-292 glutamyl-tRNA(Gln) amidotransferase subunit HER2 Saccharomyces cerevisiae S288C 171-175 34863048-1 2022 Five-fluorouracil (5-FU) is a chemotherapeutic agent that is mainly metabolized by the rate-limiting enzyme dihydropyrimidine dehydrogenase (DPD). Fluorouracil 19-23 dihydropyrimidine dehydrogenase Homo sapiens 141-144 34863048-3 2022 Previous studies have demonstrated the effect of a DPYD single nucleotide polymorphism on 5-FU efficacy and highlighted the importance of studying such genes for cancer treatment. Fluorouracil 90-94 dihydropyrimidine dehydrogenase Homo sapiens 51-55 34530056-5 2021 We also found that compared with the control group, the 50% inhibitory concentration (IC50) values of oxaliplatin and 5-FU in the SPIB overexpression group were significantly reduced. Fluorouracil 118-122 Spi-B transcription factor Homo sapiens 130-134 34530056-10 2021 In summary, we found that SPIB is a tumor suppressor in colorectal cancer cells and that SPIB sensitizes colorectal cancer cells to oxaliplatin and 5-FU, SPIB exerts its anti-colorectal cancer effect by activating the NFkB and JNK signaling pathways through MAP4K1. Fluorouracil 148-152 Spi-B transcription factor Homo sapiens 26-30 34530056-10 2021 In summary, we found that SPIB is a tumor suppressor in colorectal cancer cells and that SPIB sensitizes colorectal cancer cells to oxaliplatin and 5-FU, SPIB exerts its anti-colorectal cancer effect by activating the NFkB and JNK signaling pathways through MAP4K1. Fluorouracil 148-152 Spi-B transcription factor Homo sapiens 89-93 34530056-10 2021 In summary, we found that SPIB is a tumor suppressor in colorectal cancer cells and that SPIB sensitizes colorectal cancer cells to oxaliplatin and 5-FU, SPIB exerts its anti-colorectal cancer effect by activating the NFkB and JNK signaling pathways through MAP4K1. Fluorouracil 148-152 Spi-B transcription factor Homo sapiens 154-158 34901834-7 2021 Conclusions: Clinical studies to date have validated four DPYD polymorphisms (DPYD*2A, DPYD*13, c.2846A>T, HapB3) associated with serious toxicities in patients treated with 5-FU. Fluorouracil 174-178 dihydropyrimidine dehydrogenase Homo sapiens 58-62 34901834-7 2021 Conclusions: Clinical studies to date have validated four DPYD polymorphisms (DPYD*2A, DPYD*13, c.2846A>T, HapB3) associated with serious toxicities in patients treated with 5-FU. Fluorouracil 174-178 dihydropyrimidine dehydrogenase Homo sapiens 87-91 34901834-9 2021 Factors other than DPYD polymorphisms (e.g., miR-27a, TYMS, ENOSF1, p53) also affect 5-FU toxicity. Fluorouracil 85-89 enolase superfamily member 1 Homo sapiens 60-66 34826159-2 2022 The results indicated that OSCC cells overexpressing GDF15 were sensitive to docetaxel, cisplatin, and 5-fluorouracil through a caspase-9-dependent pathway both in vitro and in vivo. Fluorouracil 103-117 growth differentiation factor 15 Homo sapiens 53-58 9914783-1 1998 Protein levels and gene expression of dihydropyrimidine dehydrogenase (DPD), the rate-limiting enzyme for degradation of 5-fluorouracil, were studied in two human tumor cell lines (fibrosarcoma HT-1080 and pancreatic carcinoma MIAPaCa-2) in various growth phases of the cultured cells and of tumor xenografts implanted into nude mice. Fluorouracil 121-135 dihydropyrimidine dehydrogenase Homo sapiens 38-69 9914783-1 1998 Protein levels and gene expression of dihydropyrimidine dehydrogenase (DPD), the rate-limiting enzyme for degradation of 5-fluorouracil, were studied in two human tumor cell lines (fibrosarcoma HT-1080 and pancreatic carcinoma MIAPaCa-2) in various growth phases of the cultured cells and of tumor xenografts implanted into nude mice. Fluorouracil 121-135 dihydropyrimidine dehydrogenase Homo sapiens 71-74 34596215-0 2021 Syndecan-2, negatively regulated by miR-20b-5p, contributes to 5-fluorouracil resistance of colorectal cancer cells via the JNK/ERK signaling pathway. Fluorouracil 63-77 syndecan 2 Homo sapiens 0-10 34596215-2 2021 In this study, we demonstrated the role of miR-20b-5p-regulated syndecan-2 (SDC2) in 5-FU resistance of CRC cells. Fluorouracil 85-89 syndecan 2 Homo sapiens 64-74 9781601-0 1998 Improved survival in patients with advanced colorectal carcinoma failing 5-fluorouracil who received irinotecan hydrochloride and have high intratumor C-fos expression. Fluorouracil 73-87 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 151-156 34596215-2 2021 In this study, we demonstrated the role of miR-20b-5p-regulated syndecan-2 (SDC2) in 5-FU resistance of CRC cells. Fluorouracil 85-89 syndecan 2 Homo sapiens 76-80 9781601-1 1998 This study determines the prognostic role of c-fos protein expression in patients with colon cancer who previously failed therapy with 5-fluorouracil (5-FU). Fluorouracil 135-149 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 45-50 34596215-4 2021 The results showed that SDC2 was expressed significantly higher in SW480/5-FU cells than in SW480/WT cells as revealed by quantitative real-time polymerase chain reaction and western blot analysis. Fluorouracil 73-77 syndecan 2 Homo sapiens 24-28 9781601-1 1998 This study determines the prognostic role of c-fos protein expression in patients with colon cancer who previously failed therapy with 5-fluorouracil (5-FU). Fluorouracil 151-155 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 45-50 34596215-5 2021 MTT assay and BrdU assay showed that SDC2 overexpression led to increased cell survival rate, while SDC2 knockdown reversed the drug resistance of SW480/5-FU cells. Fluorouracil 153-157 syndecan 2 Homo sapiens 37-41 9792140-11 1998 In cells containing wild-type p53 (e.g. LoVo), 5-FU-induced apoptosis was accompanied by increased expression of Bax and Bak without consistent modulation of other bcl-2 family proteins. Fluorouracil 47-51 BCL2 antagonist/killer 1 Homo sapiens 121-124 34596215-5 2021 MTT assay and BrdU assay showed that SDC2 overexpression led to increased cell survival rate, while SDC2 knockdown reversed the drug resistance of SW480/5-FU cells. Fluorouracil 153-157 syndecan 2 Homo sapiens 100-104 34596215-6 2021 Wound healing and transwell invasion assays revealed that knockdown of SDC2 inhibited the migratory and invasive ability of SW480/5-FU cells. Fluorouracil 130-134 syndecan 2 Homo sapiens 71-75 34596215-8 2021 We also confirmed that miR-20b-5p interacted with SDC2, which reversed the effect of SDC2 in SW480/5-FU cells via the c-Jun N-terminal kinase (JNK)/extracellular regulated protein kinases (ERK) signaling pathway. Fluorouracil 99-103 syndecan 2 Homo sapiens 50-54 9785450-5 1998 Furthermore, it was shown that the association of UPRT with CD facilitated the uptake of 5-FC, in the situation where the drug penetrates cells by passive diffusion as in mammalian cells, by directly channeling 5-fluorouracil, the product of CD, to 5-fluoroUMP, the product of UPRT. Fluorouracil 211-225 uracil phosphoribosyltransferase homolog Homo sapiens 50-54 9785450-5 1998 Furthermore, it was shown that the association of UPRT with CD facilitated the uptake of 5-FC, in the situation where the drug penetrates cells by passive diffusion as in mammalian cells, by directly channeling 5-fluorouracil, the product of CD, to 5-fluoroUMP, the product of UPRT. Fluorouracil 211-225 uracil phosphoribosyltransferase homolog Homo sapiens 277-281 34596215-8 2021 We also confirmed that miR-20b-5p interacted with SDC2, which reversed the effect of SDC2 in SW480/5-FU cells via the c-Jun N-terminal kinase (JNK)/extracellular regulated protein kinases (ERK) signaling pathway. Fluorouracil 99-103 syndecan 2 Homo sapiens 85-89 34596215-9 2021 These findings showed that JNK/ERK signaling pathway is involved in miR-20b-5p/SDC2 axis-mediated 5-FU resistance in SW480/5-FU cells, indicating that the miR-20b-5p/SDC2 axis is a potential target for reversing 5-FU resistance in CRC. Fluorouracil 98-102 syndecan 2 Homo sapiens 79-83 34596215-9 2021 These findings showed that JNK/ERK signaling pathway is involved in miR-20b-5p/SDC2 axis-mediated 5-FU resistance in SW480/5-FU cells, indicating that the miR-20b-5p/SDC2 axis is a potential target for reversing 5-FU resistance in CRC. Fluorouracil 98-102 syndecan 2 Homo sapiens 166-170 34596215-9 2021 These findings showed that JNK/ERK signaling pathway is involved in miR-20b-5p/SDC2 axis-mediated 5-FU resistance in SW480/5-FU cells, indicating that the miR-20b-5p/SDC2 axis is a potential target for reversing 5-FU resistance in CRC. Fluorouracil 123-127 syndecan 2 Homo sapiens 79-83 34596215-9 2021 These findings showed that JNK/ERK signaling pathway is involved in miR-20b-5p/SDC2 axis-mediated 5-FU resistance in SW480/5-FU cells, indicating that the miR-20b-5p/SDC2 axis is a potential target for reversing 5-FU resistance in CRC. Fluorouracil 123-127 syndecan 2 Homo sapiens 166-170 34596215-9 2021 These findings showed that JNK/ERK signaling pathway is involved in miR-20b-5p/SDC2 axis-mediated 5-FU resistance in SW480/5-FU cells, indicating that the miR-20b-5p/SDC2 axis is a potential target for reversing 5-FU resistance in CRC. Fluorouracil 212-216 syndecan 2 Homo sapiens 79-83 34718327-8 2021 GPER was predominantly expressed in ileal crypts, and G-1 inhibited the DNA damage induced by 5-fluorouracil in vivo and vitro, as confirmed by the decrease in the number of gammaH2AX+ cells in the crypts and the comet assay results. Fluorouracil 94-108 G protein-coupled estrogen receptor 1 Mus musculus 0-4 34414684-10 2021 Single-cell analysis showed that cell clusters with low expression of CK8/18 and ITGB4 were more sensitive to 5FU and radiotherapy (RT). Fluorouracil 110-113 keratin 8 Homo sapiens 70-76 34261152-8 2021 Indeed, the combination of allicin and 5-FU significantly decreased the expression of the P-gp and CD44 proteins (P<0.05). Fluorouracil 39-43 CD44 molecule (Indian blood group) Homo sapiens 99-103 34790374-9 2021 The miR-873-5p enhanced the sensitivity of Doxorubicin/Fluorouracil and cisplatin. Fluorouracil 55-67 microRNA 873 Homo sapiens 4-11 34396431-10 2021 Overall, isolates of the CSC population CD44+ resistant to 5FU and oxaliplatin demonstrated different expression profiles; however, the present study was able to identify overexpression of the KRT-18 gene, in most of the isolates. Fluorouracil 59-62 CD44 molecule (Indian blood group) Homo sapiens 40-44 34396431-11 2021 In conclusion, the results of the present study showed overexpression of KRT-18 in CD44+ cells is associated with chemoresistance to 5FU and oxaliplatin in CRAC. Fluorouracil 133-136 CD44 molecule (Indian blood group) Homo sapiens 83-87 2573634-4 1989 In a first step a 5-fluorouracil (5-FU)-sensitive T cell recognizes the parental bone marrow cells and stimulates a macrophage-like cell to secrete IFN-alpha/beta (recognition phase). Fluorouracil 18-32 interferon alpha Mus musculus 148-157 2573634-4 1989 In a first step a 5-fluorouracil (5-FU)-sensitive T cell recognizes the parental bone marrow cells and stimulates a macrophage-like cell to secrete IFN-alpha/beta (recognition phase). Fluorouracil 34-38 interferon alpha Mus musculus 148-157 3291980-3 1988 In cultures of BM from mice treated with 5-fluorouracil (FU) eight days before sampling, GM-CSF alone or in combination with CSF-1 stimulated the formation of large macrophage colonies with diameters greater than 0.5 mm. Fluorouracil 41-55 colony stimulating factor 2 (granulocyte-macrophage) Mus musculus 89-95 9732227-0 1998 Putative role of dihydropyrimidine dehydrogenase in the toxic side effect of 5-fluorouracil in colorectal cancer patients. Fluorouracil 77-91 dihydropyrimidine dehydrogenase Homo sapiens 17-48 9732227-1 1998 Dihydropyrimidine dehydrogenase (DPD) is the first and rate limiting enzyme in the catabolism of 5-fluorouracil (5-FU). Fluorouracil 97-111 dihydropyrimidine dehydrogenase Homo sapiens 0-31 9732227-1 1998 Dihydropyrimidine dehydrogenase (DPD) is the first and rate limiting enzyme in the catabolism of 5-fluorouracil (5-FU). Fluorouracil 97-111 dihydropyrimidine dehydrogenase Homo sapiens 33-36 9732227-1 1998 Dihydropyrimidine dehydrogenase (DPD) is the first and rate limiting enzyme in the catabolism of 5-fluorouracil (5-FU). Fluorouracil 113-117 dihydropyrimidine dehydrogenase Homo sapiens 0-31 9732227-1 1998 Dihydropyrimidine dehydrogenase (DPD) is the first and rate limiting enzyme in the catabolism of 5-fluorouracil (5-FU). Fluorouracil 113-117 dihydropyrimidine dehydrogenase Homo sapiens 33-36 9732227-2 1998 It has been reported from various laboratories that the plasma concentration of 5-FU was influenced by DPD activities in various normal human organs (e.g. liver or lymphocytes). Fluorouracil 80-84 dihydropyrimidine dehydrogenase Homo sapiens 103-106 9732227-3 1998 Since the congenital deficiency in DPD caused severe, in some cases lethal, FU-related toxicity, it was decided to collect data about the DPD activity in colorectal cancer patients in order to investigate the possible correlation between the enzyme activity and appearance of the side effects of 5-FU. Fluorouracil 296-300 dihydropyrimidine dehydrogenase Homo sapiens 35-38 9732227-4 1998 Assuming that DPD activity in lymphocytes represents the 5-FU catabolic capacity of the organism, DPD activity was determined in the lymphocytes of 48 patients with colorectal cancer after surgery during the therapeutic course with 5-FU and folinic acid. Fluorouracil 232-236 dihydropyrimidine dehydrogenase Homo sapiens 98-101 9732227-7 1998 In the low DPD activity group, 9 of 11 patients had 5-FU-related side effects (mucositis, diarrhea, myelotoxicity, angina pectoris, hypertension). Fluorouracil 52-56 dihydropyrimidine dehydrogenase Homo sapiens 11-14 9732227-12 1998 Consequently, it is recommended to measure DPD activity prior to 5-FU based chemotherapy, which might be helpful in avoiding drug-related toxicity by adjusting the dose of 5-FU individually. Fluorouracil 172-176 dihydropyrimidine dehydrogenase Homo sapiens 43-46 9723824-1 1998 AIMS: Dihydropyrimidine dehydrogenase (DPD) catalyses the reduction of pyrimidines, including the anticancer agent 5-fluorouracil (5FU). Fluorouracil 115-129 dihydropyrimidine dehydrogenase Homo sapiens 6-37 9723824-1 1998 AIMS: Dihydropyrimidine dehydrogenase (DPD) catalyses the reduction of pyrimidines, including the anticancer agent 5-fluorouracil (5FU). Fluorouracil 115-129 dihydropyrimidine dehydrogenase Homo sapiens 39-42 9723824-1 1998 AIMS: Dihydropyrimidine dehydrogenase (DPD) catalyses the reduction of pyrimidines, including the anticancer agent 5-fluorouracil (5FU). Fluorouracil 131-134 dihydropyrimidine dehydrogenase Homo sapiens 6-37 9723824-1 1998 AIMS: Dihydropyrimidine dehydrogenase (DPD) catalyses the reduction of pyrimidines, including the anticancer agent 5-fluorouracil (5FU). Fluorouracil 131-134 dihydropyrimidine dehydrogenase Homo sapiens 39-42 9723824-2 1998 Impaired 5FU degradation, through low DPD activity, has led to severe, life-threatening or fatal toxicity after administration of 5FU. Fluorouracil 9-12 dihydropyrimidine dehydrogenase Homo sapiens 38-41 9690942-8 1998 The mechanism of this interaction is mediated through inhibition of the 5-FU rate-limiting catabolizing enzyme dihydropyrmidine dehydrogenase (DPD) by the BV-araU metabolite BVU. Fluorouracil 72-76 dihydropyrimidine dehydrogenase Homo sapiens 111-141 9690942-8 1998 The mechanism of this interaction is mediated through inhibition of the 5-FU rate-limiting catabolizing enzyme dihydropyrmidine dehydrogenase (DPD) by the BV-araU metabolite BVU. Fluorouracil 72-76 dihydropyrimidine dehydrogenase Homo sapiens 143-146 9635582-9 1998 Thus, methionine depletion by rMETase potentiates the antitumor efficacy of 5-FU. Fluorouracil 76-80 granzyme M Rattus norvegicus 30-37 3291980-3 1988 In cultures of BM from mice treated with 5-fluorouracil (FU) eight days before sampling, GM-CSF alone or in combination with CSF-1 stimulated the formation of large macrophage colonies with diameters greater than 0.5 mm. Fluorouracil 41-55 colony stimulating factor 1 (macrophage) Mus musculus 125-130 3395138-0 1988 [The significance of measuring inhibition of thymidylate synthase activity as a parameter for antitumor activity of 5-fluorouracil derivatives]. Fluorouracil 116-130 thymidylate synthase Mus musculus 45-65 3395138-1 1988 We investigated the relationships between antitumor activity and the inhibition of Thymidylate Synthase (TS) activity after oral administration of 5-fluorouracil (FUra) and its derivatives, FT, UFT, HC-FU, PH-FU and 5"-DFUR, using mainly Sarcoma 180 as an experimental tumor model. Fluorouracil 147-161 thymidylate synthase Mus musculus 83-103 3395138-1 1988 We investigated the relationships between antitumor activity and the inhibition of Thymidylate Synthase (TS) activity after oral administration of 5-fluorouracil (FUra) and its derivatives, FT, UFT, HC-FU, PH-FU and 5"-DFUR, using mainly Sarcoma 180 as an experimental tumor model. Fluorouracil 147-161 thymidylate synthase Mus musculus 105-107 3395138-1 1988 We investigated the relationships between antitumor activity and the inhibition of Thymidylate Synthase (TS) activity after oral administration of 5-fluorouracil (FUra) and its derivatives, FT, UFT, HC-FU, PH-FU and 5"-DFUR, using mainly Sarcoma 180 as an experimental tumor model. Fluorouracil 163-167 thymidylate synthase Mus musculus 83-103 3395138-1 1988 We investigated the relationships between antitumor activity and the inhibition of Thymidylate Synthase (TS) activity after oral administration of 5-fluorouracil (FUra) and its derivatives, FT, UFT, HC-FU, PH-FU and 5"-DFUR, using mainly Sarcoma 180 as an experimental tumor model. Fluorouracil 163-167 thymidylate synthase Mus musculus 105-107 3395138-5 1988 However, such a correlation was not found for other FUra derivatives despite their high TS inhibiting values. Fluorouracil 52-56 thymidylate synthase Mus musculus 88-90 3665991-2 1987 5"-GDP and 5"-GMP were both equally effective in potentiating the antitumor activity of FUra without increasing toxicity. Fluorouracil 88-92 5'-nucleotidase, cytosolic II Homo sapiens 14-17 3665991-10 1987 Potentiation of the antitumor activity of FUra by 5"-GMP was reversed by the injection of cytidine. Fluorouracil 42-46 5'-nucleotidase, cytosolic II Homo sapiens 53-56 3665991-13 1987 Thus, 5"-GMP or 5"-GDP strongly enhanced the antitumor activity of FUra, and the potentiation resulted from the inhibition of RNA synthesis caused by reduction of the CTP and UTP pool sizes and increased incorporation of FUra into RNA. Fluorouracil 67-71 5'-nucleotidase, cytosolic II Homo sapiens 9-12 3665991-13 1987 Thus, 5"-GMP or 5"-GDP strongly enhanced the antitumor activity of FUra, and the potentiation resulted from the inhibition of RNA synthesis caused by reduction of the CTP and UTP pool sizes and increased incorporation of FUra into RNA. Fluorouracil 221-225 5'-nucleotidase, cytosolic II Homo sapiens 9-12 3802103-4 1987 The DNA from FUra-treated S-49 cells was purified by cesium chloride gradient centrifugation and degraded to nucleosides by DNase I and Crotalus atrox snake venom. Fluorouracil 13-17 deoxyribonuclease I Mus musculus 124-131 3752956-0 1986 Distribution and inhibition of dihydrouracil dehydrogenase activities in human tissues using 5-fluorouracil as a substrate. Fluorouracil 93-107 dihydropyrimidine dehydrogenase Homo sapiens 31-58 3752956-1 1986 Dihydrouracil dehydrogenase activity, with 5-fluorouracil used as the substrate, was measured in human tissues and leukemic cells. Fluorouracil 43-57 dihydropyrimidine dehydrogenase Homo sapiens 0-27 2427493-0 1986 The cytotoxicity of 5-fluorouracil is due to its incorporation into RNA not its inhibition of thymidylate synthase as evidenced by the use of a mouse cell mutant deficient in thymidylate synthase. Fluorouracil 20-34 thymidylate synthase Mus musculus 175-195 9552051-1 1998 PURPOSE: To determine the highest dose of fluorouracil (5-FU) that could be safely administered with Eniluracil (776C85; Glaxo Wellcome Inc, Research Triangle Park, NC), an inactivator of dihydropyrimidine dehydrogenase (DPD), on a daily schedule for 5 days, and to define the toxicities of the combination and the pharmacokinetics of 5-FU when administered with 776C85. Fluorouracil 42-54 dihydropyrimidine dehydrogenase Homo sapiens 188-219 9552051-1 1998 PURPOSE: To determine the highest dose of fluorouracil (5-FU) that could be safely administered with Eniluracil (776C85; Glaxo Wellcome Inc, Research Triangle Park, NC), an inactivator of dihydropyrimidine dehydrogenase (DPD), on a daily schedule for 5 days, and to define the toxicities of the combination and the pharmacokinetics of 5-FU when administered with 776C85. Fluorouracil 42-54 dihydropyrimidine dehydrogenase Homo sapiens 221-224 2427493-2 1986 To distinguish between these two possibilities, we took advantage of a mutant strain of the mouse mammary tumor cell line FM3A that is deficient in thymidylate synthase, which is widely believed to be the target of 5-fluorouracil. Fluorouracil 215-229 thymidylate synthase Mus musculus 148-168 6539305-4 1984 Three patterns of response were observed with the VP16 -213-resistant cells showing: marked cross-resistance to vincristine and teniposide , collateral sensitivity to 5- fluorouracil , hydroxyurea and cis-platinum, and comparable responses to the parent line for adriamycin, bleomycin, dibromodulcitol and methotrexate. Fluorouracil 167-182 host cell factor C1 Homo sapiens 50-54 6608049-0 1984 Relationship of dUMP and free FdUMP pools to inhibition of thymidylate synthase by 5-fluorouracil. Fluorouracil 83-97 thymidylate synthase Mus musculus 59-79 7206052-3 1981 In patients with prostatic carcinoma 5-fluorouracil induced an objective response as measured by a 50 per cent decrease in prostatic acid phosphatase determined in a central reference laboratory in 3 of 25 patients and objective stability by National Prostatic Cancer Project criteria in 14 of 29 patients. Fluorouracil 37-51 acid phosphatase 3 Homo sapiens 123-149 378768-1 1979 The effect of two antitumour drugs, ftorafur (Ft) and 5-fluorouracil (5-FU) on chromosomes of human tumour cells (strain CA-1) was studied in vitro. Fluorouracil 54-68 carbonic anhydrase 1 Homo sapiens 121-125 378768-1 1979 The effect of two antitumour drugs, ftorafur (Ft) and 5-fluorouracil (5-FU) on chromosomes of human tumour cells (strain CA-1) was studied in vitro. Fluorouracil 70-74 carbonic anhydrase 1 Homo sapiens 121-125 4254308-0 1970 Enzymatic determinants of responsiveness of the LPC-1 plasma cell neoplasm to fluorouracil and fluorodeoxyuridine. Fluorouracil 78-90 annexin A1 Homo sapiens 48-53 34039363-10 2021 KITENIN-overexpressing CRC cells deregulated certain microRNAs and were resistant to 5-fluorouracil, oxaliplatin, and cetuximab. Fluorouracil 85-99 VANGL planar cell polarity protein 1 Homo sapiens 0-7 34035223-0 2021 Retraction Note to: FOXM1 modulates 5-fluorouracil sensitivity in cholangiocarcinoma through thymidylate synthase (TYMS): implications of FOXM1-TYMS axis uncoupling in 5-FU resistance. Fluorouracil 36-50 forkhead box M1 Homo sapiens 20-25 33727040-0 2021 Yes associated protein 1 promotes resistance to 5-fluorouracil in gastric cancer by regulating GLUT3-dependent glycometabolism reprogramming of tumor-associated macrophages. Fluorouracil 48-62 solute carrier family 2 member 3 Homo sapiens 95-100 33990700-0 2021 The loss of SHMT2 mediates 5-fluorouracil chemoresistance in colorectal cancer by upregulating autophagy. Fluorouracil 27-41 serine hydroxymethyltransferase 2 Homo sapiens 12-17 33990700-3 2021 Here, we identified serine hydroxymethyltransferase-2 (SHMT2) as a critical regulator of 5-FU chemoresistance in CRC. Fluorouracil 89-93 serine hydroxymethyltransferase 2 Homo sapiens 20-53 33990700-3 2021 Here, we identified serine hydroxymethyltransferase-2 (SHMT2) as a critical regulator of 5-FU chemoresistance in CRC. Fluorouracil 89-93 serine hydroxymethyltransferase 2 Homo sapiens 55-60 33990700-6 2021 Under 5-FU treatment, SHMT2 depletion promotes autophagy and inhibits apoptosis. Fluorouracil 6-10 serine hydroxymethyltransferase 2 Homo sapiens 22-27 33990700-7 2021 Autophagy inhibitors decrease low SHMT2-induced 5-FU resistance in vitro and in vivo. Fluorouracil 48-52 serine hydroxymethyltransferase 2 Homo sapiens 34-39 33990700-9 2021 Taken together, our findings indicate that autophagy induced by low SHMT2 levels mediates 5-FU resistance in CRC. Fluorouracil 90-94 serine hydroxymethyltransferase 2 Homo sapiens 68-73 33667680-5 2021 The anti-cancer activity of 5-FU-loaded particles was assessed in HNSCC human cell lines (CAL27 and HSC3) and in a preclinical mouse model (AT84) utilizing cell proliferation and survival, cell motility, and autophagy endpoints. Fluorouracil 28-32 DnaJ heat shock protein family (Hsp40) member B7 Homo sapiens 100-104 9546433-6 1998 In FDCP-Mix cells expressing the ts v-abl PTK and grown at the restrictive temperature for PTK activity the cells were relatively sensitive to cytotoxic agents such as cytosine arabinoside and 5-fluorouracil but MIP-1alpha could induce growth inhibition and confer some degree of protection from these agents. Fluorouracil 193-207 c-abl oncogene 1, non-receptor tyrosine kinase Mus musculus 38-41 33996571-0 2021 NGFR Increases the Chemosensitivity of Colorectal Cancer Cells by Enhancing the Apoptotic and Autophagic Effects of 5-fluorouracil via the Activation of S100A9. Fluorouracil 116-130 S100 calcium binding protein A9 Homo sapiens 153-159 33996571-15 2021 NGFR elevated the expression of S100A9 after 5-FU treatment. Fluorouracil 45-49 S100 calcium binding protein A9 Homo sapiens 32-38 33895696-9 2021 With this approach, in France, a decreased 5-FU dose is systematically recommended at a uracil concentration of 16 ng/ml, which may lead to chemotherapy under-exposure as uracil concentration is a continuous variable and the association between uracil levels and DPD activity is not clear. Fluorouracil 43-47 dihydropyrimidine dehydrogenase Homo sapiens 263-266 9556784-0 1998 Improving 5-FU with a novel dihydropyrimidine dehydrogenase inactivator. Fluorouracil 10-14 dihydropyrimidine dehydrogenase Homo sapiens 28-59 9556784-4 1998 Finally, because tumors may theoretically become resistant to 5-FU by increased levels of DPD, the use of GW776C85 to inactivate DPD may provide a potential means by which tumor resistance can be reversed. Fluorouracil 62-66 dihydropyrimidine dehydrogenase Homo sapiens 90-93 33722958-0 2021 Exosome-mediated transfer of circ_0000338 enhances 5-FU resistance in colorectal cancer through regulating miR-217 and miR-485-3p. Fluorouracil 51-55 microRNA 217 Homo sapiens 107-114 33722958-9 2021 Treatment-sensitive cells with exosomes containing circ_0000338 reduced 5-FU response in CRC both in vitro and in vivo Besides that, exosomal circ_0000338 was higher in patients exhibiting resistance to 5-FU, and showed well diagnostic efficiency in 5-FU resistant CRC.Conclusion: The delivery of circ_0000338 via exosomes enhanced 5-FU resistance in CRC through negative regulation of miR-217 and miR-485-3p, indicating a promising diagnostic and therapeutic marker for 5-FU-based chemotherapy in CRC patients. Fluorouracil 72-76 microRNA 217 Homo sapiens 386-393 33722958-9 2021 Treatment-sensitive cells with exosomes containing circ_0000338 reduced 5-FU response in CRC both in vitro and in vivo Besides that, exosomal circ_0000338 was higher in patients exhibiting resistance to 5-FU, and showed well diagnostic efficiency in 5-FU resistant CRC.Conclusion: The delivery of circ_0000338 via exosomes enhanced 5-FU resistance in CRC through negative regulation of miR-217 and miR-485-3p, indicating a promising diagnostic and therapeutic marker for 5-FU-based chemotherapy in CRC patients. Fluorouracil 203-207 microRNA 217 Homo sapiens 386-393 33722958-9 2021 Treatment-sensitive cells with exosomes containing circ_0000338 reduced 5-FU response in CRC both in vitro and in vivo Besides that, exosomal circ_0000338 was higher in patients exhibiting resistance to 5-FU, and showed well diagnostic efficiency in 5-FU resistant CRC.Conclusion: The delivery of circ_0000338 via exosomes enhanced 5-FU resistance in CRC through negative regulation of miR-217 and miR-485-3p, indicating a promising diagnostic and therapeutic marker for 5-FU-based chemotherapy in CRC patients. Fluorouracil 203-207 microRNA 217 Homo sapiens 386-393 33722958-9 2021 Treatment-sensitive cells with exosomes containing circ_0000338 reduced 5-FU response in CRC both in vitro and in vivo Besides that, exosomal circ_0000338 was higher in patients exhibiting resistance to 5-FU, and showed well diagnostic efficiency in 5-FU resistant CRC.Conclusion: The delivery of circ_0000338 via exosomes enhanced 5-FU resistance in CRC through negative regulation of miR-217 and miR-485-3p, indicating a promising diagnostic and therapeutic marker for 5-FU-based chemotherapy in CRC patients. Fluorouracil 203-207 microRNA 217 Homo sapiens 386-393 33722958-9 2021 Treatment-sensitive cells with exosomes containing circ_0000338 reduced 5-FU response in CRC both in vitro and in vivo Besides that, exosomal circ_0000338 was higher in patients exhibiting resistance to 5-FU, and showed well diagnostic efficiency in 5-FU resistant CRC.Conclusion: The delivery of circ_0000338 via exosomes enhanced 5-FU resistance in CRC through negative regulation of miR-217 and miR-485-3p, indicating a promising diagnostic and therapeutic marker for 5-FU-based chemotherapy in CRC patients. Fluorouracil 203-207 microRNA 217 Homo sapiens 386-393 33965356-0 2021 Use of Uridine Triacetate to Reverse Severe Persistent Myelosuppression Following 5-fluorouracil Exposure in a Patient With a c.557A>G Heterozygous DPYD Variant. Fluorouracil 82-96 dihydropyrimidine dehydrogenase Homo sapiens 148-152 9516918-0 1998 Decreased dihydropyrimidine dehydrogenase activity in a population of patients with breast cancer: implication for 5-fluorouracil-based chemotherapy. Fluorouracil 115-129 dihydropyrimidine dehydrogenase Homo sapiens 10-41 9516918-1 1998 Dihydropyrimidine dehydrogenase (DPD) is the initial, rate-limiting enzyme in the catabolism of 5-fluorouracil (5-FU), one of the most widely used chemotherapeutic agents in the treatment of breast cancer. Fluorouracil 96-110 dihydropyrimidine dehydrogenase Homo sapiens 0-31 9516918-1 1998 Dihydropyrimidine dehydrogenase (DPD) is the initial, rate-limiting enzyme in the catabolism of 5-fluorouracil (5-FU), one of the most widely used chemotherapeutic agents in the treatment of breast cancer. Fluorouracil 96-110 dihydropyrimidine dehydrogenase Homo sapiens 33-36 9516918-1 1998 Dihydropyrimidine dehydrogenase (DPD) is the initial, rate-limiting enzyme in the catabolism of 5-fluorouracil (5-FU), one of the most widely used chemotherapeutic agents in the treatment of breast cancer. Fluorouracil 112-116 dihydropyrimidine dehydrogenase Homo sapiens 0-31 9516918-1 1998 Dihydropyrimidine dehydrogenase (DPD) is the initial, rate-limiting enzyme in the catabolism of 5-fluorouracil (5-FU), one of the most widely used chemotherapeutic agents in the treatment of breast cancer. Fluorouracil 112-116 dihydropyrimidine dehydrogenase Homo sapiens 33-36 9516918-6 1998 Significantly lower DPD activity in patients with breast cancer may predispose to 5-FU-associated toxicity. Fluorouracil 82-86 dihydropyrimidine dehydrogenase Homo sapiens 20-23 9598048-0 1998 Delayed hypersensitivity to 5-fluorouracil associated with reduced dihydropyrimidine dehydrogenase (DPD) activity. Fluorouracil 28-42 dihydropyrimidine dehydrogenase Homo sapiens 67-98 9598048-0 1998 Delayed hypersensitivity to 5-fluorouracil associated with reduced dihydropyrimidine dehydrogenase (DPD) activity. Fluorouracil 28-42 dihydropyrimidine dehydrogenase Homo sapiens 100-103 33471160-15 2021 A significantly higher gene expression for Bax and Bax/Bcl2 ratio was seen after 5-FU treatment. Fluorouracil 81-85 BCL2-associated X protein Mus musculus 43-46 33471160-15 2021 A significantly higher gene expression for Bax and Bax/Bcl2 ratio was seen after 5-FU treatment. Fluorouracil 81-85 BCL2-associated X protein Mus musculus 51-54 33471160-16 2021 A marked reduction in beta-catenin immunolabeling was seen in 5-FU-challenged preantral follicles. Fluorouracil 62-66 catenin (cadherin associated protein), beta 1 Mus musculus 22-34 33615510-6 2021 The IC50 of 5-Fu against colorectal cells was also declined in PTPN6 transfected cells. Fluorouracil 12-16 protein tyrosine phosphatase non-receptor type 6 Homo sapiens 63-68 9470816-1 1997 Dihydropyrimidine dehydrogenase (DPD) is responsible for the breakdown of the widely used antineoplastic agent 5-fluorouracil (5-FU), thereby limiting the efficacy of the therapy. Fluorouracil 111-125 dihydropyrimidine dehydrogenase Homo sapiens 0-31 9470816-1 1997 Dihydropyrimidine dehydrogenase (DPD) is responsible for the breakdown of the widely used antineoplastic agent 5-fluorouracil (5-FU), thereby limiting the efficacy of the therapy. Fluorouracil 111-125 dihydropyrimidine dehydrogenase Homo sapiens 33-36 9470816-1 1997 Dihydropyrimidine dehydrogenase (DPD) is responsible for the breakdown of the widely used antineoplastic agent 5-fluorouracil (5-FU), thereby limiting the efficacy of the therapy. Fluorouracil 127-131 dihydropyrimidine dehydrogenase Homo sapiens 0-31 9470816-1 1997 Dihydropyrimidine dehydrogenase (DPD) is responsible for the breakdown of the widely used antineoplastic agent 5-fluorouracil (5-FU), thereby limiting the efficacy of the therapy. Fluorouracil 127-131 dihydropyrimidine dehydrogenase Homo sapiens 33-36 9470816-2 1997 It has been suggested that patients suffering from 5-FU toxicities due to a low activity of DPD are genotypically heterozygous for a mutant allele of the gene encoding DPD. Fluorouracil 51-55 dihydropyrimidine dehydrogenase Homo sapiens 92-95 9470816-2 1997 It has been suggested that patients suffering from 5-FU toxicities due to a low activity of DPD are genotypically heterozygous for a mutant allele of the gene encoding DPD. Fluorouracil 51-55 dihydropyrimidine dehydrogenase Homo sapiens 168-171 33615510-10 2021 SP1 overexpression enhanced the drug-resistance to 5-Fu and abrogated the effects of PTPN6 upregulation on 5-Fu resistance. Fluorouracil 107-111 protein tyrosine phosphatase non-receptor type 6 Homo sapiens 85-90 33615510-16 2021 Moreover, PTPN6 overexpression not only reduced cell proliferation and viability, but decreased the resistance of colorectal cells to 5-Fu. Fluorouracil 134-138 protein tyrosine phosphatase non-receptor type 6 Homo sapiens 10-15 33460610-0 2021 Suppression of Nanog inhibited cell migration and increased the sensitivity of colorectal cancer cells to 5-fluorouracil. Fluorouracil 106-120 Nanog homeobox Homo sapiens 15-20 33460610-2 2021 Therefore, this study was aimed to evaluate the Nanog suppression effect using small interference RNA (siRNA) combined with 5-fluorouracil (5-FU) on CRC cells. Fluorouracil 124-138 Nanog homeobox Homo sapiens 48-53 33460610-2 2021 Therefore, this study was aimed to evaluate the Nanog suppression effect using small interference RNA (siRNA) combined with 5-fluorouracil (5-FU) on CRC cells. Fluorouracil 140-144 Nanog homeobox Homo sapiens 48-53 33460610-3 2021 Nanog-overexpressing SW-480 cells were transfected with Nanog si-RNA and treated with 5-FU, in combination or separately. Fluorouracil 86-90 Nanog homeobox Homo sapiens 0-5 9470816-3 1997 In this study we investigated the cDNA and a genomic region of the DPD gene of a cancer patient experiencing severe toxicity following 5-FU treatment for the presence of mutations. Fluorouracil 135-139 dihydropyrimidine dehydrogenase Homo sapiens 67-70 33460610-5 2021 Furthermore, Nanog knockdown significantly increased CRC cell sensitivity to 5-FU drug via modulating Bax and Bcl-2 mRNA expression. Fluorouracil 77-81 Nanog homeobox Homo sapiens 13-18 32647340-8 2021 The activated ATF4 upregulated RNASET2-mediated uracil generation, which impaired exogenous 5-FU uptake to blunt 5-FU therapy. Fluorouracil 92-96 activating transcription factor 4 Homo sapiens 14-18 9470816-8 1997 Considering the frequent use of 5-FU in the treatment of cancer patients, the severe 5-FU-related toxicities in patients with a low activity of DPD and the high frequency of the G-->A mutation in DPD deficient patients, analysis of the DPD activity and screening for the G-->A mutation should be routinely carried out prior to the start of the treatment with 5-FU. Fluorouracil 32-36 dihydropyrimidine dehydrogenase Homo sapiens 199-202 32647340-8 2021 The activated ATF4 upregulated RNASET2-mediated uracil generation, which impaired exogenous 5-FU uptake to blunt 5-FU therapy. Fluorouracil 113-117 activating transcription factor 4 Homo sapiens 14-18 33838628-0 2021 Upregulation of NOX-2 and Nrf-2 Promotes 5-Fluorouracil Resistance of Human Colon Carcinoma (HCT-116) Cells. Fluorouracil 41-55 cytochrome b-245 beta chain Homo sapiens 16-21 33429333-10 2021 In addition, the upregulation of miR-193-5p reduced the expression levels of CXCR4, particularly in combination with 5-FU and OX. Fluorouracil 117-121 C-X-C motif chemokine receptor 4 Homo sapiens 77-82 33650652-8 2021 The results revealed that HIPK2 depletion induced resistance to 5-FU and OXA, and that this resistance was not overcome by brusatol, an inhibitor of the antioxidant response regulator nuclear factor erythroid 2-related factor 2 (NRF2), which is frequently overexpressed in CRC. Fluorouracil 64-68 homeodomain interacting protein kinase 2 Homo sapiens 26-31 21528302-0 1997 Enhancing 5-fluorouracil cytotoxicity by inhibiting dihydropyrimidine dehydrogenase activity with uracil in human tumor cells. Fluorouracil 10-24 dihydropyrimidine dehydrogenase Homo sapiens 52-83 21528302-4 1997 Uracil inhibited both DPD activity and cell growth in a concentration-dependent manner, and exhibited maximum effect at molar ratios to 5-FU of more than 10 (DPD activity, almost complete inhibition; growth-inhibitory effect, about a 30% increase). Fluorouracil 136-140 dihydropyrimidine dehydrogenase Homo sapiens 158-161 33650652-9 2021 By contrast, cell sensitivity to 5-FU and OXA was further induced by brusatol supplementation in HIPK2-proficient cells, further supporting the contribution of HIPK2 in chemotherapy response. Fluorouracil 33-37 homeodomain interacting protein kinase 2 Homo sapiens 97-102 33650652-9 2021 By contrast, cell sensitivity to 5-FU and OXA was further induced by brusatol supplementation in HIPK2-proficient cells, further supporting the contribution of HIPK2 in chemotherapy response. Fluorouracil 33-37 homeodomain interacting protein kinase 2 Homo sapiens 160-165 33486902-12 2021 Signal transduction pathway analysis showed that after Bel-7402 cells acquired resistance to 5-Fu, CCND1, MCM2, and MCM3 gene expression was upregulated in the G1 to S cell cycle control signal transduction pathway, CDKN1C and CCNG2 gene expression was downregulated, and MCM2 and MCM3 gene expression was upregulated in the DNA replication signal transduction pathway. Fluorouracil 93-97 minichromosome maintenance complex component 2 Homo sapiens 106-110 33486902-12 2021 Signal transduction pathway analysis showed that after Bel-7402 cells acquired resistance to 5-Fu, CCND1, MCM2, and MCM3 gene expression was upregulated in the G1 to S cell cycle control signal transduction pathway, CDKN1C and CCNG2 gene expression was downregulated, and MCM2 and MCM3 gene expression was upregulated in the DNA replication signal transduction pathway. Fluorouracil 93-97 minichromosome maintenance complex component 2 Homo sapiens 272-276 9345343-0 1997 Irinotecan hydrochloride (CPT-11) resistance identified by K-ras mutation in patients with progressive colon cancer after treatment with 5-fluorouracil (5-FU). Fluorouracil 137-151 KRAS proto-oncogene, GTPase Homo sapiens 59-64 33536745-0 2021 CircNRIP1 Modulates the miR-515-5p/IL-25 Axis to Control 5-Fu and Cisplatin Resistance in Nasopharyngeal Carcinoma. Fluorouracil 57-61 interleukin 25 Homo sapiens 35-40 9345343-0 1997 Irinotecan hydrochloride (CPT-11) resistance identified by K-ras mutation in patients with progressive colon cancer after treatment with 5-fluorouracil (5-FU). Fluorouracil 153-157 KRAS proto-oncogene, GTPase Homo sapiens 59-64 9345343-9 1997 CONCLUSION: Determination of the presence of a K-ras mutation may predict survival in patients with progressive colon cancer after treatment with 5-fluorouracil who receive CPT-11. Fluorouracil 146-160 KRAS proto-oncogene, GTPase Homo sapiens 47-52 33536745-10 2021 Conclusion: These data highlight the circNRIP1/miR-515-5p/IL-25 as a novel regulator of 5-Fu and cisplatin resistance in NPC, suggesting that this pathway may be amenable to therapeutic targeting as an approach to treating this cancer type. Fluorouracil 88-92 interleukin 25 Homo sapiens 58-63 33131720-0 2021 Possible involvement of TRPM2 activation in 5-fluorouracil-induced myelosuppression in mice. Fluorouracil 44-58 transient receptor potential cation channel, subfamily M, member 2 Mus musculus 24-29 33131720-5 2021 The aim of this study was to investigate whether TRPM2 is involved in 5-FU-induced myelosuppression. Fluorouracil 70-74 transient receptor potential cation channel, subfamily M, member 2 Mus musculus 49-54 33131720-6 2021 Enhancement of H2O2-induced intracellular Ca2+ concentration ([Ca2+]i) increase by 5-FU treatment was observed in human embryonic kidney 293 (HEK) cells stably expressing TRPM2 but not in HEK cells, indicating that 5-FU stimulates TRPM2 activation. Fluorouracil 83-87 transient receptor potential cation channel subfamily M member 2 Homo sapiens 171-176 33131720-6 2021 Enhancement of H2O2-induced intracellular Ca2+ concentration ([Ca2+]i) increase by 5-FU treatment was observed in human embryonic kidney 293 (HEK) cells stably expressing TRPM2 but not in HEK cells, indicating that 5-FU stimulates TRPM2 activation. Fluorouracil 83-87 transient receptor potential cation channel subfamily M member 2 Homo sapiens 231-236 28520376-0 2012 Fluorouracil Therapy and DPYD Genotype Fluorouracil is a chemotherapy agent that belongs to the drug class of fluoropyrimidines. Fluorouracil 39-51 dihydropyrimidine dehydrogenase Homo sapiens 25-29 9327152-0 1997 Prognostic implications of c-Ki-ras2 mutations in patients with advanced colorectal cancer treated with 5-fluorouracil and interferon: a study of the eastern cooperative oncology group (EST 2292) PURPOSE: Mutations in c-Ki-ras2 (ras) occur in about 40% of patients with colorectal cancers and occur early in the pathogenesis of this disease. Fluorouracil 104-118 KRAS proto-oncogene, GTPase Homo sapiens 27-36 9327152-0 1997 Prognostic implications of c-Ki-ras2 mutations in patients with advanced colorectal cancer treated with 5-fluorouracil and interferon: a study of the eastern cooperative oncology group (EST 2292) PURPOSE: Mutations in c-Ki-ras2 (ras) occur in about 40% of patients with colorectal cancers and occur early in the pathogenesis of this disease. Fluorouracil 104-118 KRAS proto-oncogene, GTPase Homo sapiens 218-227 9323539-3 1997 Previous studies have demonstrated that cancer patients who are DPD deficient exhibit severe toxicity (including death) following treatment with FUra. Fluorouracil 145-149 dihydropyrimidine dehydrogenase Homo sapiens 64-67 9323539-8 1997 This method provides the first specific assay for DPD enzyme activity which is rapid, reproducible and sensitive enough to be used in the routine screening of cancer patients for DPD deficiency prior to treatment with FUra. Fluorouracil 218-222 dihydropyrimidine dehydrogenase Homo sapiens 50-53 9254861-1 1997 Dihydropyrimidine dehydrogenase catalyzes the first and rate-limiting step in the breakdown of thymine, uracil, and the widely used antineoplastic drug, 5-fluorouracil. Fluorouracil 153-167 dihydropyrimidine dehydrogenase Homo sapiens 0-31 28520376-3 2012 The DPYD gene encodes dihydropyrimidine dehydrogenase (DPD), an enzyme that catalyzes the rate-limiting step in fluorouracil metabolism. Fluorouracil 112-124 dihydropyrimidine dehydrogenase Homo sapiens 4-8 9238541-2 1997 In this report, we show that 5-Fluorouracil increases the Interleukin-1 expression upto 2.66 folds without significantly affecting the levels of surface expression of p55 IL-2 receptor on human Peripheral blood mononuclear cells, CD4 and CD8 T cells. Fluorouracil 29-43 CD8a molecule Homo sapiens 238-241 28520376-3 2012 The DPYD gene encodes dihydropyrimidine dehydrogenase (DPD), an enzyme that catalyzes the rate-limiting step in fluorouracil metabolism. Fluorouracil 112-124 dihydropyrimidine dehydrogenase Homo sapiens 22-53 28520376-3 2012 The DPYD gene encodes dihydropyrimidine dehydrogenase (DPD), an enzyme that catalyzes the rate-limiting step in fluorouracil metabolism. Fluorouracil 112-124 dihydropyrimidine dehydrogenase Homo sapiens 55-58 28520376-4 2012 Individuals who carry at least one copy of no function DPYD variants, such as DPYD*2A, may not be able to metabolize fluorouracil at normal rates, and are at risk of potentially life-threatening fluorouracil toxicity, such as bone marrow suppression and neurotoxicity. Fluorouracil 117-129 dihydropyrimidine dehydrogenase Homo sapiens 55-59 28520376-4 2012 Individuals who carry at least one copy of no function DPYD variants, such as DPYD*2A, may not be able to metabolize fluorouracil at normal rates, and are at risk of potentially life-threatening fluorouracil toxicity, such as bone marrow suppression and neurotoxicity. Fluorouracil 117-129 dihydropyrimidine dehydrogenase Homo sapiens 78-82 9152608-4 1997 Data obtained by in vivo and in vitro studies strongly suggested that (E)-5-(2-bromovinyl)uracil generated from SRV by gut flora was reduced in the presense of NADPH to a reactive form by hepatic dihydropyrimidine dehydrogenase (DPD), a key enzyme determining the tissue 5-FU levels, bound covalently to DPD as a suicide inhibitor, and markedly retarded the catabolism of 5-FU. Fluorouracil 271-275 dihydropyrimidine dehydrogenase Homo sapiens 196-227 28520376-4 2012 Individuals who carry at least one copy of no function DPYD variants, such as DPYD*2A, may not be able to metabolize fluorouracil at normal rates, and are at risk of potentially life-threatening fluorouracil toxicity, such as bone marrow suppression and neurotoxicity. Fluorouracil 195-207 dihydropyrimidine dehydrogenase Homo sapiens 55-59 28520376-4 2012 Individuals who carry at least one copy of no function DPYD variants, such as DPYD*2A, may not be able to metabolize fluorouracil at normal rates, and are at risk of potentially life-threatening fluorouracil toxicity, such as bone marrow suppression and neurotoxicity. Fluorouracil 195-207 dihydropyrimidine dehydrogenase Homo sapiens 78-82 9152608-4 1997 Data obtained by in vivo and in vitro studies strongly suggested that (E)-5-(2-bromovinyl)uracil generated from SRV by gut flora was reduced in the presense of NADPH to a reactive form by hepatic dihydropyrimidine dehydrogenase (DPD), a key enzyme determining the tissue 5-FU levels, bound covalently to DPD as a suicide inhibitor, and markedly retarded the catabolism of 5-FU. Fluorouracil 372-376 dihydropyrimidine dehydrogenase Homo sapiens 196-227 33461170-8 2021 We also demonstrated that treatment with fluorouracil, carboplatin, paclitaxel, and doxorubicin resulted in decreased expression of CCDC167 and suppressed growth of MCF-7 cells. Fluorouracil 41-53 coiled-coil domain containing 167 Homo sapiens 132-139 9116268-2 1997 Using the Moloney murine leukemia virus-based retroviral vector MFG-S encoding the human form of p47phox, we performed ex vivo gene transfer into Sca-1+ p47phox-/- marrow progenitor cells without conditioning of donors with 5-fluorouracil. Fluorouracil 224-238 neutrophil cytosolic factor 1 Homo sapiens 97-104 33420580-0 2021 Babao Dan () Alleviates 5-Fluorouracil-Induced Intestinal Damage via Wnt/beta-Catenin Pathway. Fluorouracil 24-38 NBL1, DAN family BMP antagonist Mus musculus 6-9 33420580-0 2021 Babao Dan () Alleviates 5-Fluorouracil-Induced Intestinal Damage via Wnt/beta-Catenin Pathway. Fluorouracil 24-38 catenin (cadherin associated protein), beta 1 Mus musculus 73-85 33420580-1 2021 OBJECTIVE: To evaluate the protective function of Babao Dan (, BBD) on 5-flurouracil (5-FU)-induced intestinal mucositis (IM) and uncover the underlying mechanism. Fluorouracil 86-90 NBL1, DAN family BMP antagonist Mus musculus 56-59 33420580-15 2021 CONCLUSIONS: BBD attenuates the adverse effects induced by 5-FU via Wnt/beta-catenin pathway, suggesting it may act as a potential agent against chemotherapy-induced intestinal mucositis. Fluorouracil 59-63 catenin (cadherin associated protein), beta 1 Mus musculus 72-84 33402109-11 2021 Overexpression of miR-383 downregulated Bcl-2, resulting in reduced survival of Fluorouracil-treated GC cells. Fluorouracil 80-92 microRNA 383 Homo sapiens 18-25 33402109-13 2021 CONCLUSION: MiR-383 reduces survival of Fluorouracil-treated GC cells through downregulating of Bcl-2. Fluorouracil 40-52 microRNA 383 Homo sapiens 12-19 33007506-3 2021 The integrated nanosystem (p122-ap1@NPC-D) was found to unleash by programmed TMEs (high level of H2O2 and low pH) to efficiently transfect miR-122 into MHCC-LM3 cells, followed by the releases of 5-FU. Fluorouracil 197-201 microRNA 122 Homo sapiens 140-147 32956680-11 2021 5-FU-treated DDIT4-/- human gastric epithelial cells had significantly increased cells entering mitosis despite DNA damage and increased proliferation in vitro and in xenografts. Fluorouracil 0-4 DNA damage inducible transcript 4 Homo sapiens 13-18 32929530-0 2021 To perform genotyping of dihydropyrimidine dehydrogenase (DPD) before starting treatment with 5-fluorouracil or related medicines: really feasible? Fluorouracil 94-108 dihydropyrimidine dehydrogenase Homo sapiens 25-56 9125688-0 1997 Myelosuppression in the pig (Sus scrofa): uteroferrin reduces the myelosuppressive effects of 5-fluorouracil in young pigs. Fluorouracil 94-108 acid phosphatase 5, tartrate resistant Sus scrofa 42-53 9125688-1 1997 The present study investigated the ability of uteroferrin to modulate the myelosuppressive effects of 5-fluorouracil (5-FU) in young pigs (Sus scrofa). Fluorouracil 102-116 acid phosphatase 5, tartrate resistant Sus scrofa 46-57 9125688-1 1997 The present study investigated the ability of uteroferrin to modulate the myelosuppressive effects of 5-fluorouracil (5-FU) in young pigs (Sus scrofa). Fluorouracil 118-122 acid phosphatase 5, tartrate resistant Sus scrofa 46-57 9125688-6 1997 Concurrent treatment of pigs with uteroferrin reduced (P < 0.05) the rate of 5-FU-induced leukocytopenia (44 vs 77 +/- 7% decline from baseline on day 3) and enhanced (P < 0.05), the recovery from 5-FU on days 10 and 12 postinfusion. Fluorouracil 80-84 acid phosphatase 5, tartrate resistant Sus scrofa 34-45 9125688-6 1997 Concurrent treatment of pigs with uteroferrin reduced (P < 0.05) the rate of 5-FU-induced leukocytopenia (44 vs 77 +/- 7% decline from baseline on day 3) and enhanced (P < 0.05), the recovery from 5-FU on days 10 and 12 postinfusion. Fluorouracil 203-207 acid phosphatase 5, tartrate resistant Sus scrofa 34-45 9125688-8 1997 In addition, uteroferrin attenuated (P < 0.05) the suppression of red blood cell numbers after 5-FU administration (6.9 vs 6.1 +/- 0.2 x 10(6) cells/microliter on day 3), an affect reflected in increased hematocrit and hemoglobin concentrations. Fluorouracil 98-102 acid phosphatase 5, tartrate resistant Sus scrofa 13-24 9125688-9 1997 The effects of uteroferrin appeared to result from enhancement of the proliferation and/or differentiation of primitive pluripotent stem cells resistant to 5-FU, as concurrent treatment of pigs with uteroferrin resulted in a protection and/or enhanced recovery (P < 0.05) of CFU-GEMM, CFU-GM and BFU-E progenitor cells in the peripheral blood. Fluorouracil 156-160 acid phosphatase 5, tartrate resistant Sus scrofa 15-26 9125688-10 1997 These results are the first to demonstrate that uteroferrin can reduce the myelosuppressive effects of 5-FU in the pig and suggest that uteroferrin has hematopoietic growth factor activity in vivo. Fluorouracil 103-107 acid phosphatase 5, tartrate resistant Sus scrofa 48-59 9815697-0 1997 Dihydropyrimidine dehydrogenase activity in hepatocellular carcinoma: implication in 5-fluorouracil-based chemotherapy. Fluorouracil 85-99 dihydropyrimidine dehydrogenase Homo sapiens 0-31 9815697-1 1997 Dihydropyrimidine dehydrogenase (DPD) is the initial, rate-limiting enzyme in the catabolism of 5-fluorouracil, one of the most widely used cancer chemotherapeutic agents. Fluorouracil 96-110 dihydropyrimidine dehydrogenase Homo sapiens 0-31 9815697-1 1997 Dihydropyrimidine dehydrogenase (DPD) is the initial, rate-limiting enzyme in the catabolism of 5-fluorouracil, one of the most widely used cancer chemotherapeutic agents. Fluorouracil 96-110 dihydropyrimidine dehydrogenase Homo sapiens 33-36 9815697-2 1997 Previous studies have demonstrated the clinical importance of determination of DPD in cancer patients, suggesting that the efficacy and toxicity of 5-fluorouracil may directly relate to the DPD activity in both tumor and host tissues. Fluorouracil 148-162 dihydropyrimidine dehydrogenase Homo sapiens 79-82 9815697-2 1997 Previous studies have demonstrated the clinical importance of determination of DPD in cancer patients, suggesting that the efficacy and toxicity of 5-fluorouracil may directly relate to the DPD activity in both tumor and host tissues. Fluorouracil 148-162 dihydropyrimidine dehydrogenase Homo sapiens 190-193 9815697-7 1997 Since high levels of DPD would be expected to metabolize 5-fluorouracil, these findings may provide an explanation for the relative 5-fluorouracil resistance of hepatoma and may have implications for designing a new therapeutic strategy such as modulation of 5-fluorouracil chemotherapy by DPD inhibitors. Fluorouracil 57-71 dihydropyrimidine dehydrogenase Homo sapiens 21-24 9815697-7 1997 Since high levels of DPD would be expected to metabolize 5-fluorouracil, these findings may provide an explanation for the relative 5-fluorouracil resistance of hepatoma and may have implications for designing a new therapeutic strategy such as modulation of 5-fluorouracil chemotherapy by DPD inhibitors. Fluorouracil 57-71 dihydropyrimidine dehydrogenase Homo sapiens 290-293 9815697-7 1997 Since high levels of DPD would be expected to metabolize 5-fluorouracil, these findings may provide an explanation for the relative 5-fluorouracil resistance of hepatoma and may have implications for designing a new therapeutic strategy such as modulation of 5-fluorouracil chemotherapy by DPD inhibitors. Fluorouracil 132-146 dihydropyrimidine dehydrogenase Homo sapiens 21-24 9815697-7 1997 Since high levels of DPD would be expected to metabolize 5-fluorouracil, these findings may provide an explanation for the relative 5-fluorouracil resistance of hepatoma and may have implications for designing a new therapeutic strategy such as modulation of 5-fluorouracil chemotherapy by DPD inhibitors. Fluorouracil 132-146 dihydropyrimidine dehydrogenase Homo sapiens 21-24 32929530-0 2021 To perform genotyping of dihydropyrimidine dehydrogenase (DPD) before starting treatment with 5-fluorouracil or related medicines: really feasible? Fluorouracil 94-108 dihydropyrimidine dehydrogenase Homo sapiens 58-61 33129983-0 2021 MTIF2 impairs 5 fluorouracil-mediated immunogenic cell death in hepatocellular carcinoma in vivo: Molecular mechanisms and therapeutic significance. Fluorouracil 14-28 mitochondrial translational initiation factor 2 Homo sapiens 0-5 33129983-6 2021 We found that down-regulation of MTIF2 impaired proliferation and migration capacity of HCC cells, chemoresistance to 5-Fluorouracil (5-FU) weakened after MTIF2 was knocked down. Fluorouracil 118-132 mitochondrial translational initiation factor 2 Homo sapiens 33-38 33129983-6 2021 We found that down-regulation of MTIF2 impaired proliferation and migration capacity of HCC cells, chemoresistance to 5-Fluorouracil (5-FU) weakened after MTIF2 was knocked down. Fluorouracil 118-132 mitochondrial translational initiation factor 2 Homo sapiens 155-160 33129983-6 2021 We found that down-regulation of MTIF2 impaired proliferation and migration capacity of HCC cells, chemoresistance to 5-Fluorouracil (5-FU) weakened after MTIF2 was knocked down. Fluorouracil 134-138 mitochondrial translational initiation factor 2 Homo sapiens 33-38 33129983-6 2021 We found that down-regulation of MTIF2 impaired proliferation and migration capacity of HCC cells, chemoresistance to 5-Fluorouracil (5-FU) weakened after MTIF2 was knocked down. Fluorouracil 134-138 mitochondrial translational initiation factor 2 Homo sapiens 155-160 33129983-9 2021 In vivo experiment also used to confirm our previously conclusion, our result indicated that MTIF2 overexpression suppresses tumor apoptosis and immune cell activity in the 5-FU therapy in vivo model, by suppression maturation of tumor-infiltrated DC. Fluorouracil 173-177 mitochondrial translational initiation factor 2 Homo sapiens 93-98 32686977-0 2021 An in vitro approach to simulate the process of 5-fluorouracil degradation with dihydropyrimidine dehydrogenase: the process in accordance to the first-order kinetic reaction. Fluorouracil 48-62 dihydropyrimidine dehydrogenase Homo sapiens 80-111 32686977-4 2021 The effects of initial 5-FU concentrations and temperatures on DPD activities were investigated as well.The degradation process followed the first-order kinetic reaction (r2>0.98). Fluorouracil 23-27 dihydropyrimidine dehydrogenase Homo sapiens 63-66 32686977-7 2021 The degradation process of 5-FU in patients" whole blood in vitro was consistent with it after mixing 5-FU with blank whole blood matrix.In conclusion, mixing 5-FU with blank matrix can simulate the process of 5-FU degradation with DPD. Fluorouracil 27-31 dihydropyrimidine dehydrogenase Homo sapiens 232-235 32686977-7 2021 The degradation process of 5-FU in patients" whole blood in vitro was consistent with it after mixing 5-FU with blank whole blood matrix.In conclusion, mixing 5-FU with blank matrix can simulate the process of 5-FU degradation with DPD. Fluorouracil 102-106 dihydropyrimidine dehydrogenase Homo sapiens 232-235 32686977-7 2021 The degradation process of 5-FU in patients" whole blood in vitro was consistent with it after mixing 5-FU with blank whole blood matrix.In conclusion, mixing 5-FU with blank matrix can simulate the process of 5-FU degradation with DPD. Fluorouracil 102-106 dihydropyrimidine dehydrogenase Homo sapiens 232-235 32686977-7 2021 The degradation process of 5-FU in patients" whole blood in vitro was consistent with it after mixing 5-FU with blank whole blood matrix.In conclusion, mixing 5-FU with blank matrix can simulate the process of 5-FU degradation with DPD. Fluorouracil 102-106 dihydropyrimidine dehydrogenase Homo sapiens 232-235 32946963-9 2020 Dihydropyrimidine dehydrogenase (DPD), the rate-limiting enzyme in 5-fluorouracil (5-FU) metabolism, was also down-regulated. Fluorouracil 67-81 dihydropyrimidine dehydrogenase Homo sapiens 0-31 32946963-9 2020 Dihydropyrimidine dehydrogenase (DPD), the rate-limiting enzyme in 5-fluorouracil (5-FU) metabolism, was also down-regulated. Fluorouracil 67-81 dihydropyrimidine dehydrogenase Homo sapiens 33-36 32946963-9 2020 Dihydropyrimidine dehydrogenase (DPD), the rate-limiting enzyme in 5-fluorouracil (5-FU) metabolism, was also down-regulated. Fluorouracil 83-87 dihydropyrimidine dehydrogenase Homo sapiens 0-31 32946963-9 2020 Dihydropyrimidine dehydrogenase (DPD), the rate-limiting enzyme in 5-fluorouracil (5-FU) metabolism, was also down-regulated. Fluorouracil 83-87 dihydropyrimidine dehydrogenase Homo sapiens 33-36 33704179-1 2020 DPYD Screening for Cancer Patients Receiving Fluorouracil. Fluorouracil 45-57 dihydropyrimidine dehydrogenase Homo sapiens 0-4 9179690-0 1997 Biochemical modulation of 5-fluorouracil with murine interferon-alpha/beta against murine renal cell carcinoma. Fluorouracil 26-40 interferon alpha Mus musculus 53-69 9179690-6 1997 Treatment with 5-FU resulted in a 2.7-fold increase in the total amount of thymidylate synthetase and an 11.6-fold increase in the thymidylate synthetase inhibition rate, while the administration of IFN-alpha/beta did not significantly reduce the 5-FU-induced increase in thymidylate synthetase. Fluorouracil 15-19 interferon alpha Mus musculus 199-208 9179690-6 1997 Treatment with 5-FU resulted in a 2.7-fold increase in the total amount of thymidylate synthetase and an 11.6-fold increase in the thymidylate synthetase inhibition rate, while the administration of IFN-alpha/beta did not significantly reduce the 5-FU-induced increase in thymidylate synthetase. Fluorouracil 247-251 interferon alpha Mus musculus 199-208 9179690-7 1997 The administration of IFN-alpha/beta decreased thymidine kinase activity to 65.5% maximally, compared with that in the control mice or the mice treated with 5-FU. Fluorouracil 157-161 interferon alpha Mus musculus 22-31 33704179-3 2020 Most 5-FU catabolism is dependent on dihydropyrimidine dehydrogenase (DPD) encoded by the DPYD gene, and DPYD variants that reduce DPD function increase 5-FU toxicity. Fluorouracil 5-9 dihydropyrimidine dehydrogenase Homo sapiens 37-68 33704179-3 2020 Most 5-FU catabolism is dependent on dihydropyrimidine dehydrogenase (DPD) encoded by the DPYD gene, and DPYD variants that reduce DPD function increase 5-FU toxicity. Fluorouracil 5-9 dihydropyrimidine dehydrogenase Homo sapiens 70-73 33704179-3 2020 Most 5-FU catabolism is dependent on dihydropyrimidine dehydrogenase (DPD) encoded by the DPYD gene, and DPYD variants that reduce DPD function increase 5-FU toxicity. Fluorouracil 5-9 dihydropyrimidine dehydrogenase Homo sapiens 90-94 33704179-3 2020 Most 5-FU catabolism is dependent on dihydropyrimidine dehydrogenase (DPD) encoded by the DPYD gene, and DPYD variants that reduce DPD function increase 5-FU toxicity. Fluorouracil 153-157 dihydropyrimidine dehydrogenase Homo sapiens 105-109 33704179-3 2020 Most 5-FU catabolism is dependent on dihydropyrimidine dehydrogenase (DPD) encoded by the DPYD gene, and DPYD variants that reduce DPD function increase 5-FU toxicity. Fluorouracil 153-157 dihydropyrimidine dehydrogenase Homo sapiens 131-134 33335403-6 2020 The expression of some apoptotic and autophagy-related genes such as Bax, Bcl2, Beclin1 and ATG7 was significantly induced by carbon-ion beam irradiation alone and was further enhanced when the beam was combined with 5-FU. Fluorouracil 217-221 beclin 1 Homo sapiens 80-87 32814111-20 2020 Knockout of SLC25A22 in CRC cells that express mutant KRAS increased their sensitivity to 5-fluorouacil. Fluorouracil 90-103 KRAS proto-oncogene, GTPase Homo sapiens 54-58 32814111-22 2020 CONCLUSIONS: In CRC cells that express activated KRAS, SLC25A22 promotes accumulation of succinate, resulting in increased DNA methylation, activation of WNT signaling to beta-catenin, increased expression of LGR5, proliferation, stem cell features, and resistance to 5-fluorouacil. Fluorouracil 268-281 KRAS proto-oncogene, GTPase Homo sapiens 49-53 33496117-8 2020 In vivo, Shuangdan Capsules combined with 5-FU inhibited the growth and prolongation of survival of Huh-7 cells in subcutaneous transplanted tumor nude mice; serum expression of CD31 and VEGF in nude mice were decreased, while caspase-3 was increased. Fluorouracil 42-46 vascular endothelial growth factor A Mus musculus 187-191 33496117-11 2020 The results showed that Shuangdan Capsules combined with 5-FU may inhibit tumor angiogenesis by inhibiting VEGF and MMP2 expressions, thereby blocking tumor growth. Fluorouracil 57-61 vascular endothelial growth factor A Mus musculus 107-111 33496117-11 2020 The results showed that Shuangdan Capsules combined with 5-FU may inhibit tumor angiogenesis by inhibiting VEGF and MMP2 expressions, thereby blocking tumor growth. Fluorouracil 57-61 matrix metallopeptidase 2 Mus musculus 116-120 33125671-0 2020 Lactobacillus-derived metabolites enhance the antitumor activity of 5-FU and inhibit metastatic behavior in 5-FU-resistant colorectal cancer cells by regulating claudin-1 expression. Fluorouracil 108-112 claudin 1 Homo sapiens 161-170 9029059-4 1997 Data obtained by in vivo and in vitro studies strongly suggested that (E)-5-(2-bromovinyl)uracil generated from SRV by gut flora was reduced in the presense of NADPH to a reactive form by hepatic dihydropyrimidine dehydrogenase (DPD), a key enzyme determining the tissue 5-FU levels, bound covalently to DPD as a suicide inhibitor, and markedly retarded the catabolism of 5-FU. Fluorouracil 271-275 dihydropyrimidine dehydrogenase Homo sapiens 196-227 9029059-4 1997 Data obtained by in vivo and in vitro studies strongly suggested that (E)-5-(2-bromovinyl)uracil generated from SRV by gut flora was reduced in the presense of NADPH to a reactive form by hepatic dihydropyrimidine dehydrogenase (DPD), a key enzyme determining the tissue 5-FU levels, bound covalently to DPD as a suicide inhibitor, and markedly retarded the catabolism of 5-FU. Fluorouracil 372-376 dihydropyrimidine dehydrogenase Homo sapiens 196-227 33125671-4 2020 The genetic silencing of CLDN-1 increased the sensitivity of HCT-116/5FUR to 5-FU and inhibited its metastatic potential by regulating the expression of epithelial-mesenchymal transition (EMT) related genes. Fluorouracil 77-81 claudin 1 Homo sapiens 25-31 33125671-5 2020 Co-treatment of HCT-116/5FUR with LDMs and 5-FU suppressed chemoresistant and metastatic behavior by downregulating CLDN-1 expression. Fluorouracil 43-47 claudin 1 Homo sapiens 116-122 8996526-9 1997 Based on allometric analysis, the estimated clearance of 5-FU (10.9 l/h) in humans with DPD deficiency was comparable to the observed values in humans lacking DPD activity due to genetic predisposition (10.1 l/h), or treatment with 776C85 (7.0 l/h) or (E)-5-(2-bromovinyl)-2"-deoxyuridine (BVdUrd, 6.6 l/h). Fluorouracil 57-61 dihydropyrimidine dehydrogenase Homo sapiens 88-91 33120790-4 2020 PATIENT CONCERNS: A 72-year-old man diagnosed with stage IV rectal adenocarcinoma (KRAS mutation) with peritoneal carcinomatosis and liver metastases developed resistance to 2 lines of treatment (bevacizumab/irinotecan/S-1 and bevacizumab/oxaliplatin/HDFL [high-dose 24-hour infusion of 5-fluorouracil and leucovorin regimen]) within 5 months. Fluorouracil 287-301 KRAS proto-oncogene, GTPase Homo sapiens 83-87 9620216-0 1997 5-fluorouracil/leucovorin-induced inhibition of thymidylate synthase in normal tissues of mouse and man. Fluorouracil 0-14 thymidylate synthase Mus musculus 48-68 32990544-13 2021 CONCLUSION: We suggest that inhibition of autophagy along with Pd(II) and 5-FU treatment has a synergistic effect in KRAS-mutant colorectal cancer cells. Fluorouracil 74-78 KRAS proto-oncogene, GTPase Homo sapiens 117-121 9007910-3 1997 DATA SYNTHESIS: Genetic deficiencies in DPD, the rate-limiting enzyme responsible for 5-FU catabolism, may occur in 3% or more of patients with cancer putting them at increased risk for unusually severe adverse reactions (e.g., diarrhea, stomatitis, mucositis, myelosuppression, neurotoxicity) to standard doses of 5-FU. Fluorouracil 86-90 dihydropyrimidine dehydrogenase Homo sapiens 40-43 9007910-3 1997 DATA SYNTHESIS: Genetic deficiencies in DPD, the rate-limiting enzyme responsible for 5-FU catabolism, may occur in 3% or more of patients with cancer putting them at increased risk for unusually severe adverse reactions (e.g., diarrhea, stomatitis, mucositis, myelosuppression, neurotoxicity) to standard doses of 5-FU. Fluorouracil 315-319 dihydropyrimidine dehydrogenase Homo sapiens 40-43 32966231-0 2020 Genetic influence of DPYD*9A polymorphism on plasma levels of 5-fluorouracil and subsequent toxicity after oral administration of capecitabine in colorectal cancer patients of South Indian origin. Fluorouracil 62-76 dihydropyrimidine dehydrogenase Homo sapiens 21-25 32966231-3 2020 Finding the phenotypic association between DPYD*9A polymorphism and 5-fluorouracil (5-FU) plasma levels will give a better prediction for toxicity susceptibility. Fluorouracil 68-82 dihydropyrimidine dehydrogenase Homo sapiens 43-47 32966231-3 2020 Finding the phenotypic association between DPYD*9A polymorphism and 5-fluorouracil (5-FU) plasma levels will give a better prediction for toxicity susceptibility. Fluorouracil 84-88 dihydropyrimidine dehydrogenase Homo sapiens 43-47 32966231-15 2020 Conclusions DPYD*9A polymorphism had a significant influence on the plasma levels of 5-FU after capecitabine administration. Fluorouracil 85-89 dihydropyrimidine dehydrogenase Homo sapiens 12-16 33042471-4 2020 The biological significance of CD44 expression in the chemoresistance response to fluorouracil, oxaliplatin or irinotecan, three major anti-cancer agents for colon cancer in the clinical setting, was examined using colon cancer cell lines. Fluorouracil 82-94 CD44 molecule (Indian blood group) Homo sapiens 31-35 33042471-8 2020 Additionally, CD44 knockdown overcame chemoresistance in response to fluorouracil and oxaliplatin with enhanced apoptosis and p27 upregulation, respectively. Fluorouracil 69-81 CD44 molecule (Indian blood group) Homo sapiens 14-18 32895407-0 2020 Activated ROCK/Akt/eNOS and ET-1/ERK pathways in 5-fluorouracil-induced cardiotoxicity: modulation by simvastatin. Fluorouracil 49-63 nitric oxide synthase 3 Rattus norvegicus 19-23 32895407-8 2020 Moreover, the cross-talk between ROCK/ NF-kappaB, ROS/COX-2/TXA2, Akt/eNOS and ET-1/ERK1/2 pathways contributes via different means to upsetting the vasoconstriction/vasodilatation equilibrium as well as endothelial cell function and finally leads to cardiomyocyte stress and death-the modulation of these trajectories offers simvastatin its potential cardio-protection against 5-FU. Fluorouracil 378-382 nitric oxide synthase 3 Rattus norvegicus 70-74 32801774-0 2020 lncRNA UCA1 Contributes to 5-Fluorouracil Resistance of Colorectal Cancer Cells Through miR-23b-3p/ZNF281 Axis. Fluorouracil 27-41 zinc finger protein 281 Homo sapiens 99-105 32801774-14 2020 MiR-23b-3p elevated the 5-FU sensitivity through down-regulating ZNF281 in CRC cells. Fluorouracil 24-28 zinc finger protein 281 Homo sapiens 65-71 32801774-15 2020 UCA1 interference enhanced the 5-FU sensitivity of CRC through miR-23b-3p/ZNF281 axis in vivo. Fluorouracil 31-35 zinc finger protein 281 Homo sapiens 74-80 32754230-0 2020 Synergistic antitumor effect of 5-fluorouracil with the novel LSD1 inhibitor ZY0511 in colorectal cancer. Fluorouracil 32-46 lysine demethylase 1A Homo sapiens 62-66 8955653-0 1996 Pharmacokinetic, oral bioavailability, and safety study of fluorouracil in patients treated with 776C85, an inactivator of dihydropyrimidine dehydrogenase. Fluorouracil 59-71 dihydropyrimidine dehydrogenase Homo sapiens 123-154 8955653-1 1996 PURPOSE: To study the absolute bioavailability and pharmacokinetics of an oral solution of fluorouracil (5-FU) in patients treated with 776C85, an oral inactivator of dihydropyrimidine dehydrogenase (DPD), and to evaluate the feasibility of administering oral 5-FU and 776C85 on a multiple-daily dosing schedule. Fluorouracil 91-103 dihydropyrimidine dehydrogenase Homo sapiens 167-198 8955653-1 1996 PURPOSE: To study the absolute bioavailability and pharmacokinetics of an oral solution of fluorouracil (5-FU) in patients treated with 776C85, an oral inactivator of dihydropyrimidine dehydrogenase (DPD), and to evaluate the feasibility of administering oral 5-FU and 776C85 on a multiple-daily dosing schedule. Fluorouracil 91-103 dihydropyrimidine dehydrogenase Homo sapiens 200-203 8955653-1 1996 PURPOSE: To study the absolute bioavailability and pharmacokinetics of an oral solution of fluorouracil (5-FU) in patients treated with 776C85, an oral inactivator of dihydropyrimidine dehydrogenase (DPD), and to evaluate the feasibility of administering oral 5-FU and 776C85 on a multiple-daily dosing schedule. Fluorouracil 105-109 dihydropyrimidine dehydrogenase Homo sapiens 167-198 8955653-11 1996 CONCLUSION: The oral DPD inactivator 776C85 enables oral administration of 5-FU and may alter conventional 5-FU administration practices. Fluorouracil 75-79 dihydropyrimidine dehydrogenase Homo sapiens 21-24 8955653-11 1996 CONCLUSION: The oral DPD inactivator 776C85 enables oral administration of 5-FU and may alter conventional 5-FU administration practices. Fluorouracil 107-111 dihydropyrimidine dehydrogenase Homo sapiens 21-24 8759880-5 1996 TPO in combination with the ligand for c-kit (SF) or interleukin-3 (IL-3) supported colony formation by marrow cells of 5-fluorouracil (5-FU)-treated mice whereas TPO alone yielded no colony. Fluorouracil 120-134 thrombopoietin Mus musculus 0-3 8759880-5 1996 TPO in combination with the ligand for c-kit (SF) or interleukin-3 (IL-3) supported colony formation by marrow cells of 5-fluorouracil (5-FU)-treated mice whereas TPO alone yielded no colony. Fluorouracil 136-140 thrombopoietin Mus musculus 0-3 32754230-2 2020 In the present study, we aimed to investigate the combined antitumor activity of a novel LSD1 inhibitor (ZY0511) with 5-fluorouracil (5-FU) and elucidate the underlying mechanism in colorectal cancer (CRC). Fluorouracil 118-132 lysine demethylase 1A Homo sapiens 89-93 32754230-2 2020 In the present study, we aimed to investigate the combined antitumor activity of a novel LSD1 inhibitor (ZY0511) with 5-fluorouracil (5-FU) and elucidate the underlying mechanism in colorectal cancer (CRC). Fluorouracil 134-138 lysine demethylase 1A Homo sapiens 89-93 32754230-3 2020 Methods: We evaluated LSD1 expression in CRC tissues from patients who received 5-FU treatment. Fluorouracil 80-84 lysine demethylase 1A Homo sapiens 22-26 32754230-6 2020 Results: Overexpression of LSD1 was observed in human CRC tissues, and correlated with CRC development and 5-FU resistance. Fluorouracil 107-111 lysine demethylase 1A Homo sapiens 27-31 32754230-11 2020 Conclusions: Our findings identify LSD1 as a potential marker for 5-FU resistance in CRC. Fluorouracil 66-70 lysine demethylase 1A Homo sapiens 35-39 33099951-9 2020 Additionally, the chemosensitivity of prostate cancer cells to 5-FU was enhanced under miR-151 overexpression. Fluorouracil 63-67 microRNA 151a Homo sapiens 87-94 32546724-2 2020 Herein we revealed a previously unrecognized mechanism of 5-fluorouracil (5-FU) resistance contributed by high SphK2-upregulated dihydropyrimidine dehydrogenase (DPD) in colorectal cancer (CRC), which is evidenced from human CRC specimens, animal models, and cancer cell lines. Fluorouracil 58-72 dihydropyrimidine dehydrogenase Homo sapiens 129-160 32546724-2 2020 Herein we revealed a previously unrecognized mechanism of 5-fluorouracil (5-FU) resistance contributed by high SphK2-upregulated dihydropyrimidine dehydrogenase (DPD) in colorectal cancer (CRC), which is evidenced from human CRC specimens, animal models, and cancer cell lines. Fluorouracil 58-72 dihydropyrimidine dehydrogenase Homo sapiens 162-165 32546724-2 2020 Herein we revealed a previously unrecognized mechanism of 5-fluorouracil (5-FU) resistance contributed by high SphK2-upregulated dihydropyrimidine dehydrogenase (DPD) in colorectal cancer (CRC), which is evidenced from human CRC specimens, animal models, and cancer cell lines. Fluorouracil 74-78 dihydropyrimidine dehydrogenase Homo sapiens 129-160 32546724-2 2020 Herein we revealed a previously unrecognized mechanism of 5-fluorouracil (5-FU) resistance contributed by high SphK2-upregulated dihydropyrimidine dehydrogenase (DPD) in colorectal cancer (CRC), which is evidenced from human CRC specimens, animal models, and cancer cell lines. Fluorouracil 74-78 dihydropyrimidine dehydrogenase Homo sapiens 162-165 32601379-12 2020 Moreover, we found that after treatment with 5-FU, TGN38 factor coimmunolocalizes with beclin-1 autophagic protein in discrete structures associated with the fragmented Golgi, suggesting that the activation of pro-survival autophagy is linked to loss of Golgi integrity. Fluorouracil 45-49 beclin 1 Homo sapiens 87-95 32541216-7 2022 RESULTS: Gastric cancer patients with high IL-10 TAM infiltration exhibited poor prognosis and inferior therapeutic responsiveness to fluorouracil-based adjuvant chemotherapy. Fluorouracil 134-146 interleukin 10 Homo sapiens 43-48 9816193-1 1996 Patients with decreased dihydropyrimidine dehydrogenase (DPD) activity are at increased risk for experiencing serious adverse reactions following 5-fluorouracil (5-FU)-based chemotherapy. Fluorouracil 146-160 dihydropyrimidine dehydrogenase Homo sapiens 24-55 9816193-1 1996 Patients with decreased dihydropyrimidine dehydrogenase (DPD) activity are at increased risk for experiencing serious adverse reactions following 5-fluorouracil (5-FU)-based chemotherapy. Fluorouracil 146-160 dihydropyrimidine dehydrogenase Homo sapiens 57-60 9816193-1 1996 Patients with decreased dihydropyrimidine dehydrogenase (DPD) activity are at increased risk for experiencing serious adverse reactions following 5-fluorouracil (5-FU)-based chemotherapy. Fluorouracil 162-166 dihydropyrimidine dehydrogenase Homo sapiens 24-55 9816193-1 1996 Patients with decreased dihydropyrimidine dehydrogenase (DPD) activity are at increased risk for experiencing serious adverse reactions following 5-fluorouracil (5-FU)-based chemotherapy. Fluorouracil 162-166 dihydropyrimidine dehydrogenase Homo sapiens 57-60 9816197-1 1996 Dihydropyrimidine dehydrogenase (DPD) is the rate-limiting enzyme of 5-fluorouracil (FU) catabolism, which occurs mainly in the liver. Fluorouracil 69-83 dihydropyrimidine dehydrogenase Homo sapiens 0-31 9816197-1 1996 Dihydropyrimidine dehydrogenase (DPD) is the rate-limiting enzyme of 5-fluorouracil (FU) catabolism, which occurs mainly in the liver. Fluorouracil 69-83 dihydropyrimidine dehydrogenase Homo sapiens 33-36 8697140-1 1996 Studies were carried out to determine whether the combination of IL-1 + M-CSF, similar to the effect of these cytokines on neutropenia, was able to reduce the duration of thrombocytopenia in the 5-fluorouracil (5-FU)-myelosuppressed mouse. Fluorouracil 195-209 colony stimulating factor 1 (macrophage) Mus musculus 72-77 8697140-1 1996 Studies were carried out to determine whether the combination of IL-1 + M-CSF, similar to the effect of these cytokines on neutropenia, was able to reduce the duration of thrombocytopenia in the 5-fluorouracil (5-FU)-myelosuppressed mouse. Fluorouracil 211-215 colony stimulating factor 1 (macrophage) Mus musculus 72-77 8697140-8 1996 Furthermore, the data presented are consistent with the hypothesis that IL-1 + M-CSF initially acts on a multilineage, 5-FU-resistant target cell and that IL-6 (and possibly IL-3 and GM-CSF) serves as a secondary cytokine further to enhance platelet production during rebound thrombopoiesis in the 5-FU-treated mouse. Fluorouracil 119-123 colony stimulating factor 1 (macrophage) Mus musculus 79-84 32541216-11 2022 CONCLUSIONS: This study revealed that IL-10 TAMs might drive an immunoevasive microenvironment and determine poor prognosis and inferior therapeutic responsiveness to fluorouracil-based adjuvant chemotherapy, indicating IL-10 TAMs could be applied as a potential target for immunotherapeutic approach in gastric cancer. Fluorouracil 167-179 interleukin 10 Homo sapiens 38-43 32541216-11 2022 CONCLUSIONS: This study revealed that IL-10 TAMs might drive an immunoevasive microenvironment and determine poor prognosis and inferior therapeutic responsiveness to fluorouracil-based adjuvant chemotherapy, indicating IL-10 TAMs could be applied as a potential target for immunotherapeutic approach in gastric cancer. Fluorouracil 167-179 interleukin 10 Homo sapiens 220-225 32044957-0 2020 Overexpressing microRNA-34a overcomes ABCG2-mediated drug resistance to 5-FU in side population cells from colon cancer via suppressing DLL1. Fluorouracil 72-76 delta like canonical Notch ligand 1 Homo sapiens 136-140 32044957-8 2020 In addition, overexpressing miR-34a overcame ABCG2-mediated resistance to 5-FU via DLL1/Notch pathway in vitro, and suppressed tumor growth under 5-FU treatment in vivo. Fluorouracil 74-78 delta like canonical Notch ligand 1 Homo sapiens 83-87 32482981-8 2022 Subgroup analysis of overall survival with respect to positive RAD51 expression indicated preoperative chemotherapy (CDDP + 5-FU or docetaxel + CDDP + 5-FU) was superior to CRT. Fluorouracil 151-155 RAD51 recombinase Homo sapiens 63-68 8603452-0 1996 Impact of different fluorouracil biochemical modulators on cellular dihydropyrimidine dehydrogenase. Fluorouracil 20-32 dihydropyrimidine dehydrogenase Homo sapiens 68-99 32478266-4 2020 The kinetic and equilibrium investigation suggested physisorption loading of 5-Fu drug in a monolayer form for MCM-48, MCM/ST, and MCM/CH (Langmuir) and in a multilayer form for MCM/CD (Freundlich). Fluorouracil 77-81 methylmalonyl-CoA mutase Homo sapiens 111-114 8612311-2 1996 Dihydropyrimidine dehydrogenase (DPD) is the initial and rate-limiting enzyme in the catabolism of 5-FU. Fluorouracil 99-103 dihydropyrimidine dehydrogenase Homo sapiens 0-31 8612311-2 1996 Dihydropyrimidine dehydrogenase (DPD) is the initial and rate-limiting enzyme in the catabolism of 5-FU. Fluorouracil 99-103 dihydropyrimidine dehydrogenase Homo sapiens 33-36 8612311-3 1996 DPD activity in peripheral blood mononuclear cells has been reported to correlate inversely with 5-FU plasma levels in patients. Fluorouracil 97-101 dihydropyrimidine dehydrogenase Homo sapiens 0-3 8541542-4 1995 Lin- Ly-6A/E+ marrow cells from 5-fluorouracil-treated mice were plated individually by micromanipulation in methylcellulose culture with steel factor (SF) and IL-11 for 8 days. Fluorouracil 32-46 lymphocyte antigen 6 complex, locus A Mus musculus 5-12 8542939-0 1995 5-Fluorouracil-resistant CD34+ cell population from peripheral blood of CML patients contains BCR-ABL-negative progenitor cells. Fluorouracil 0-14 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 94-101 32478266-4 2020 The kinetic and equilibrium investigation suggested physisorption loading of 5-Fu drug in a monolayer form for MCM-48, MCM/ST, and MCM/CH (Langmuir) and in a multilayer form for MCM/CD (Freundlich). Fluorouracil 77-81 methylmalonyl-CoA mutase Homo sapiens 119-122 32382150-0 2020 LncRNA SNORD3A specifically sensitizes breast cancer cells to 5-FU by sponging miR-185-5p to enhance UMPS expression. Fluorouracil 62-66 microRNA 185 Homo sapiens 79-86 32382150-11 2020 High SNORD3A transcript and Meis1 and UMPS protein levels predicts a better outcome, but high miR-185-5p level predicts a worse outcome in breast cancer patients receiving 5-FU-based chemotherapy. Fluorouracil 172-176 microRNA 185 Homo sapiens 94-101 32382150-12 2020 Our findings indicate that Meis1-regulated SNORD3A specifically sensitizes breast cancer cells to 5-FU via enhancing UMPS expression. Fluorouracil 98-102 Meis homeobox 1 Homo sapiens 27-32 32088343-0 2020 S1PR2 inhibitors potently reverse 5-FU resistance by downregulating DPD expression in colorectal cancer. Fluorouracil 34-38 dihydropyrimidine dehydrogenase Homo sapiens 68-71 31931052-4 2020 In this study, the effectiveness of engineered CXCR4-targeted self-assembling toxin nanoparticles has been explored in the selective killing of CXCR4+ human colon-CSCs compared to 5-Fluorouracil and Oxaliplatin, both classical CRC chemotherapeutic agents. Fluorouracil 180-194 C-X-C motif chemokine receptor 4 Homo sapiens 47-52 8591078-1 1995 PURPOSE: To evaluate FAM [5-FU (5-fluorouracil), doxorubicin, mitomycin C] chemotherapy as adjuvant therapy for patients with resected TNM stage I, II, or III gastric carcinoma. Fluorouracil 26-30 teneurin transmembrane protein 1 Homo sapiens 135-138 32019285-0 2020 CXCL-13 Regulates Resistance to 5-Fluorouracil in Colorectal Cancer. Fluorouracil 32-46 C-X-C motif chemokine ligand 13 Homo sapiens 0-7 9166490-1 1995 PURPOSE: The combination of cisplatin, 5-fluorouracil, and leucovorin (PFL) has been reported to have a 29% response rate in advanced non-small cell lung cancer. Fluorouracil 39-53 profilin 2 Homo sapiens 71-74 7586945-0 1995 Population characteristics of hepatic dihydropyrimidine dehydrogenase activity, a key metabolic enzyme in 5-fluorouracil chemotherapy. Fluorouracil 106-120 dihydropyrimidine dehydrogenase Homo sapiens 38-69 32019285-3 2020 This study is designed to reveal the important role of CXCL-13 in causing colorectal cancer resistance to 5-Fu. Fluorouracil 106-110 C-X-C motif chemokine ligand 13 Homo sapiens 55-62 7586945-1 1995 Dihydropyrimidine dehydrogenase is the initial rate-limiting enzyme in catabolism of 5-fluorouracil, one of the most widely used cancer chemotherapeutic agents. Fluorouracil 85-99 dihydropyrimidine dehydrogenase Homo sapiens 0-31 7586945-2 1995 Previous studies have shown the clinical importance of determination of dihydropyrimidine dehydrogenase in patients with cancer, particularly in those with deficiency of this enzyme who experience severe 5-fluorouracil-associated toxicity (including death) after 5-fluorouracil treatment. Fluorouracil 204-218 dihydropyrimidine dehydrogenase Homo sapiens 72-103 7586945-2 1995 Previous studies have shown the clinical importance of determination of dihydropyrimidine dehydrogenase in patients with cancer, particularly in those with deficiency of this enzyme who experience severe 5-fluorouracil-associated toxicity (including death) after 5-fluorouracil treatment. Fluorouracil 263-277 dihydropyrimidine dehydrogenase Homo sapiens 72-103 7589288-5 1995 Conversely, the effect of M-CSF depletion is seen only in G-CSF-stimulated recovery; monocyte levels in mice treated with antiserum to M-CSF after 5-FU are indistinguishable from mice given 5-FU alone. Fluorouracil 147-151 colony stimulating factor 1 (macrophage) Mus musculus 135-140 32019285-7 2020 RESULTS: In this study, we demonstrated that CXCL-13 is associated with 5-Fu resistance by culture medium exchange experiments and cytokine arrays of colorectal cancer resistant and nonresistant cells. Fluorouracil 72-76 C-X-C motif chemokine ligand 13 Homo sapiens 45-52 7575656-3 1995 DPD activity was measured in a group of human lymphocyte extracts, including an extract from a subject that actually presented toxicity to 5-fluorouracil treatment. Fluorouracil 139-153 dihydropyrimidine dehydrogenase Homo sapiens 0-3 32019285-8 2020 Clinical studies showed that CXCL-13 is highly expressed in the serum of 5-Fu-resistant patients. Fluorouracil 73-77 C-X-C motif chemokine ligand 13 Homo sapiens 29-36 32019285-10 2020 The addition of recombinant CXCL-13 cytokine resulted in 5-Fu resistance, while its antibody overcame 5-Fu resistance, and knockdown of CXCL-13 expression by siRNA also reduced 5-Fu resistance, which can be saved by added recombination CXCL-13. Fluorouracil 57-61 C-X-C motif chemokine ligand 13 Homo sapiens 28-35 32019285-11 2020 CONCLUSION: These results not only identify a CXCL-13 mediated 5-Fu resistance mechanism but also provide a novel target for 5-Fu-resistant colorectal cancer in prevention and treatment strategies. Fluorouracil 63-67 C-X-C motif chemokine ligand 13 Homo sapiens 46-53 8535028-1 1995 Dihydropyrimidine dehydrogenase (DPD) is the initial enzyme of 5-fluorouracil (5-FU) catabolism. Fluorouracil 63-77 dihydropyrimidine dehydrogenase Homo sapiens 0-31 8535028-1 1995 Dihydropyrimidine dehydrogenase (DPD) is the initial enzyme of 5-fluorouracil (5-FU) catabolism. Fluorouracil 63-77 dihydropyrimidine dehydrogenase Homo sapiens 33-36 32019285-11 2020 CONCLUSION: These results not only identify a CXCL-13 mediated 5-Fu resistance mechanism but also provide a novel target for 5-Fu-resistant colorectal cancer in prevention and treatment strategies. Fluorouracil 125-129 C-X-C motif chemokine ligand 13 Homo sapiens 46-53 31587155-0 2020 Ubiquitin-Specific Protease 22/Silent Information Regulator 1 Axis Plays a Pivotal Role in the Prognosis and 5-Fluorouracil Resistance in Hepatocellular Carcinoma. Fluorouracil 109-123 sirtuin 1 Homo sapiens 31-61 31587155-7 2020 Further experiments confirmed the role of SIRT1 in 5-FU drug resistance in vivo. Fluorouracil 51-55 sirtuin 1 Homo sapiens 42-47 31587155-11 2020 The SIRT1 inhibitor EX-527 dramatically inhibited the expression of Cyclin B1 and resistance-associated protein 3 (MRP3) to reduce 5-FU drug resistance in vivo. Fluorouracil 131-135 sirtuin 1 Homo sapiens 4-9 31587155-13 2020 The inhibition of SIRT1 in vivo could be valuable in improving 5-FU drug sensitivity and inhibiting tumor cell proliferation and inducing apoptosis. Fluorouracil 63-67 sirtuin 1 Homo sapiens 18-23 31124054-4 2020 The functional validation showed that the downregulation of ANXA1 contributes to GEM and 5-FU resistance in PDAC cells through protein kinase C/c-Jun N-terminal kinase/P-glycoprotein signaling pathway. Fluorouracil 89-93 annexin A1 Homo sapiens 60-65 31917964-9 2020 dmPGE2 treatment accelerated the recovery of 5FU-induced ISC injury via increasing expression of cyclin D1 and D2 in intestine. Fluorouracil 45-48 cyclin D1 Mus musculus 97-106 32132038-2 2020 Casein kinase 2alpha (CK2alpha) is highly expressed in 5-fluorouracil (5FU)-resistant colorectal cancer (CRC) cells. Fluorouracil 55-69 casein kinase 2 alpha 2 Homo sapiens 0-20 32132038-2 2020 Casein kinase 2alpha (CK2alpha) is highly expressed in 5-fluorouracil (5FU)-resistant colorectal cancer (CRC) cells. Fluorouracil 55-69 casein kinase 2 alpha 2 Homo sapiens 22-30 32132038-2 2020 Casein kinase 2alpha (CK2alpha) is highly expressed in 5-fluorouracil (5FU)-resistant colorectal cancer (CRC) cells. Fluorouracil 71-74 casein kinase 2 alpha 2 Homo sapiens 0-20 32132038-2 2020 Casein kinase 2alpha (CK2alpha) is highly expressed in 5-fluorouracil (5FU)-resistant colorectal cancer (CRC) cells. Fluorouracil 71-74 casein kinase 2 alpha 2 Homo sapiens 22-30 32132038-3 2020 We hypothesized that inhibition of CK2alpha might reduce CRC resistance to 5FU. Fluorouracil 75-78 casein kinase 2 alpha 2 Homo sapiens 35-43 32132038-5 2020 RESULTS: CK2alpha levels were significantly increased in 5FU-resistant CRC cells compared to those in wild-type CRC cells. Fluorouracil 57-60 casein kinase 2 alpha 2 Homo sapiens 9-17 32132038-8 2020 Combination of CK2alpha knockdown with 5FU treatment promoted apoptosis of 5FU-resistant CRC cells by inducing ER stress. Fluorouracil 75-78 casein kinase 2 alpha 2 Homo sapiens 15-23 32132038-9 2020 CONCLUSION: 5FU treatment in combination with a CK2alpha inhibitor may exert a synergistic effect against drug-resistant cancer cells. Fluorouracil 12-15 casein kinase 2 alpha 2 Homo sapiens 48-56 32355746-12 2020 Administration of SLC1A5 or GPT2 inhibitor could prohibit SRCC growth and significantly enhance the sensitivity of SRCC to the treatment of 5-fu and L-OHP. Fluorouracil 140-144 solute carrier family 1 member 5 Homo sapiens 18-24 9816071-0 1995 Dihydropyrimidine dehydrogenase: a tumoral target for fluorouracil modulation. Fluorouracil 54-66 dihydropyrimidine dehydrogenase Homo sapiens 0-31 9816071-1 1995 Dihydropyrimidine dehydrogenase (DPD) is the rate-limiting enzyme of 5-fluorouracil (FU) catabolism. Fluorouracil 69-83 dihydropyrimidine dehydrogenase Homo sapiens 0-31 9816071-1 1995 Dihydropyrimidine dehydrogenase (DPD) is the rate-limiting enzyme of 5-fluorouracil (FU) catabolism. Fluorouracil 69-83 dihydropyrimidine dehydrogenase Homo sapiens 33-36 8528101-6 1995 BM MNC of mice treated with 5-FU were separated on the basis of expression of the lineage-specific antigens (Lin), c-kit, and Ly6A/E. Fluorouracil 28-32 lymphocyte antigen 6 complex, locus A Mus musculus 126-132 7795216-2 1995 Cells expressing Sca-1 but no lineage-specific or major histocompatibility complex (MHC) class II antigens (Lin-MHC II-Sca-1+) were enriched from 5-fluorouracil-pretreated bone marrow by Ficoll density-gradient and immunomagnetic sorting. Fluorouracil 146-160 ataxin 1 Mus musculus 17-22 7795216-2 1995 Cells expressing Sca-1 but no lineage-specific or major histocompatibility complex (MHC) class II antigens (Lin-MHC II-Sca-1+) were enriched from 5-fluorouracil-pretreated bone marrow by Ficoll density-gradient and immunomagnetic sorting. Fluorouracil 146-160 ataxin 1 Mus musculus 119-124 7789895-0 1995 Modulation of 5-fluorouracil with high-dose leucovorin calcium: activity in ovarian cancer and correlation with CA-125 levels. Fluorouracil 14-28 mucin 16, cell surface associated Homo sapiens 112-118 21597737-3 1995 Expression of glutathione S-transferase-pi and thymidylate-synthase was increased after a single dose of irradiation which was accompanied by a lower sensitivity against cisplatin and 5-fluorouracil. Fluorouracil 184-198 thymidylate synthase Mus musculus 47-67 9816002-3 1995 We studied 37 patients who received chemotherapy with 5-fluorouracil and leucovorin, Exon 1 of the c-K-ras gene was PCR amplified from DNA extracted from paraffin-embedded tumor blocks. Fluorouracil 54-68 KRAS proto-oncogene, GTPase Homo sapiens 99-106 9816002-10 1995 Patients with colon cancers bearing either wild-type or mutant c-K-ras alleles are indistinguishable in overall survival and are equally likely to respond to 5-fluorouracil-based chemotherapy. Fluorouracil 158-172 KRAS proto-oncogene, GTPase Homo sapiens 63-70 7832988-2 1995 Cancer patients experiencing acute 5-fluorouracil toxicity also have lower-than-normal DPD activities. Fluorouracil 35-49 dihydropyrimidine dehydrogenase Homo sapiens 87-90 7989127-8 1994 The higher SOD2 and lower G6PD activity observed in FUra-resistant cell in comparison with parental cells at all times after sub-culture could be characteristic both of differentiative and of differentiated cells. Fluorouracil 52-56 glucose-6-phosphate dehydrogenase Homo sapiens 26-30 7964939-4 1994 Sixty-eight were head and neck patients treated by a 5-day continuous infusion of fluorouracil (FU; starting dose, 1 g/m2/d, with dose adaptation based on pharmacokinetics) for which DPD activity was measured 2 to 3 days before FU administration (94 cycles analyzed). Fluorouracil 82-94 dihydropyrimidine dehydrogenase Homo sapiens 183-186 7954335-2 1994 Elevated levels of plasma paf acetylhydrolase after rapid infusion of 5-fluorouracil in cancer patients. Fluorouracil 70-84 phospholipase A2 group VII Homo sapiens 26-45 7954335-5 1994 PAF acetylhydrolase increased in nine patients with daily bolus infusion of 0.4 g 5-FU per m2 of body surface (81.7 +/- 8.7 nmol PAF/min/ml vs. 66.6 +/- 7.0; P < 0.001 for day 5 as compared to day 1). Fluorouracil 82-86 phospholipase A2 group VII Homo sapiens 0-19 7858238-6 1994 Approximately 50% of the Ly-6A/E+ cells of both normal and 5-FU-treated mice were CD43neg-low, while the rest of the cells were CD43bright. Fluorouracil 59-63 lymphocyte antigen 6 complex, locus A Mus musculus 25-32 8064224-0 1994 Recombinant transforming growth factor beta 1 and beta 2 protect mice from acutely lethal doses of 5-fluorouracil and doxorubicin. Fluorouracil 99-113 hemoglobin, beta adult minor chain Mus musculus 50-56 32355746-12 2020 Administration of SLC1A5 or GPT2 inhibitor could prohibit SRCC growth and significantly enhance the sensitivity of SRCC to the treatment of 5-fu and L-OHP. Fluorouracil 140-144 glutamic--pyruvic transaminase 2 Homo sapiens 28-32 7519072-1 1994 Osteogenic cells were sorted from bone marrow of 5-fluorouracil (5-FU)-treated mice based on light scatter characteristics, Sca-1 expression, and their binding to wheat germ agglutinin (WGA). Fluorouracil 65-69 lymphocyte antigen 6 complex, locus A Mus musculus 124-129 32194724-2 2020 Our study showed that ribosomal protein L11 (RPL11) was a crucial factor affecting sensitivity of gastric cancer to 5-FU, implying that RPL11 expression is a potential biomarker for predicting 5-FU sensitivity. Fluorouracil 116-120 ribosomal protein L11 Homo sapiens 45-50 7908989-5 1994 The in vitro chemosensitivity of these cell lines to fluorouracil, doxorubicin, mitomycin C, cisplatin, and etoposide (VP-16) was determined using the MTT (3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyltetrazolium bromide) colorimetric assay. Fluorouracil 53-65 host cell factor C1 Homo sapiens 119-124 32194724-2 2020 Our study showed that ribosomal protein L11 (RPL11) was a crucial factor affecting sensitivity of gastric cancer to 5-FU, implying that RPL11 expression is a potential biomarker for predicting 5-FU sensitivity. Fluorouracil 116-120 ribosomal protein L11 Homo sapiens 136-141 32194724-2 2020 Our study showed that ribosomal protein L11 (RPL11) was a crucial factor affecting sensitivity of gastric cancer to 5-FU, implying that RPL11 expression is a potential biomarker for predicting 5-FU sensitivity. Fluorouracil 193-197 ribosomal protein L11 Homo sapiens 22-43 32194724-2 2020 Our study showed that ribosomal protein L11 (RPL11) was a crucial factor affecting sensitivity of gastric cancer to 5-FU, implying that RPL11 expression is a potential biomarker for predicting 5-FU sensitivity. Fluorouracil 193-197 ribosomal protein L11 Homo sapiens 45-50 32194724-2 2020 Our study showed that ribosomal protein L11 (RPL11) was a crucial factor affecting sensitivity of gastric cancer to 5-FU, implying that RPL11 expression is a potential biomarker for predicting 5-FU sensitivity. Fluorouracil 193-197 ribosomal protein L11 Homo sapiens 136-141 8059151-8 1994 5FU catabolism is governed by a key enzymatic step involving dihydropyrimidine dehydrogenase (DPD). Fluorouracil 0-3 dihydropyrimidine dehydrogenase Homo sapiens 94-97 8123839-6 1994 The physiologic relevance of NGF in early hematopoiesis was confirmed by showing that 12% to 15% of progenitor blood cells from mice treated with 5-fluorouracil expressed TrkA and that these cells could be induced to proliferate and differentiate in response to NGF in association with macrophage colony-stimulating factor. Fluorouracil 146-160 nerve growth factor Mus musculus 29-32 8123839-6 1994 The physiologic relevance of NGF in early hematopoiesis was confirmed by showing that 12% to 15% of progenitor blood cells from mice treated with 5-fluorouracil expressed TrkA and that these cells could be induced to proliferate and differentiate in response to NGF in association with macrophage colony-stimulating factor. Fluorouracil 146-160 nerve growth factor Mus musculus 262-265 7833111-0 1994 A role for dihydropyrimidine dehydrogenase and thymidylate synthase in tumour sensitivity to fluorouracil. Fluorouracil 93-105 dihydropyrimidine dehydrogenase Homo sapiens 11-42 7880618-1 1994 Interferon-alpha (IFN-alpha) enhances the activity of the 5-fluorouracil (5-FU) prodrug 5"-deoxy-5-fluorouridine (5"-dFUrd) in colorectal cancer cells in vitro by upregulating the enzyme pyrimidine nucleoside phosphorylase (PNPase), which is responsible for converting 5"-dFUrd to 5-FU. Fluorouracil 58-72 interferon alpha Mus musculus 0-16 32194724-3 2020 Kaplan-Meier survival analysis indicated that high RPL11 expression in gastric cancer patients treated with 5-FU was significantly associated with good prognosis. Fluorouracil 108-112 ribosomal protein L11 Homo sapiens 51-56 7880618-1 1994 Interferon-alpha (IFN-alpha) enhances the activity of the 5-fluorouracil (5-FU) prodrug 5"-deoxy-5-fluorouridine (5"-dFUrd) in colorectal cancer cells in vitro by upregulating the enzyme pyrimidine nucleoside phosphorylase (PNPase), which is responsible for converting 5"-dFUrd to 5-FU. Fluorouracil 58-72 interferon alpha Mus musculus 18-27 7880618-1 1994 Interferon-alpha (IFN-alpha) enhances the activity of the 5-fluorouracil (5-FU) prodrug 5"-deoxy-5-fluorouridine (5"-dFUrd) in colorectal cancer cells in vitro by upregulating the enzyme pyrimidine nucleoside phosphorylase (PNPase), which is responsible for converting 5"-dFUrd to 5-FU. Fluorouracil 74-78 interferon alpha Mus musculus 0-16 32194724-4 2020 It was therefore investigated whether RPL11 affected the sensitivity of gastric cancer against 5-FU using four human gastric cancer cell lines, MKN45 (wild-type TP53 gene), NUGC4 (wild-type), MKN7 (mutated), and KE39 cells (mutated). Fluorouracil 95-99 ribosomal protein L11 Homo sapiens 38-43 7880618-1 1994 Interferon-alpha (IFN-alpha) enhances the activity of the 5-fluorouracil (5-FU) prodrug 5"-deoxy-5-fluorouridine (5"-dFUrd) in colorectal cancer cells in vitro by upregulating the enzyme pyrimidine nucleoside phosphorylase (PNPase), which is responsible for converting 5"-dFUrd to 5-FU. Fluorouracil 74-78 interferon alpha Mus musculus 18-27 32194724-5 2020 In vitro assays demonstrated that RPL11 knockdown in gastric cancer cell lines carrying the TP53 wild-type gene attenuated 5-FU-induced cell growth suppression and activation of the P53 pathway, but not in cells carrying mutated TP53, suggesting that 5-FU suppresses tumor progression via RPL11-mediated activation of the P53 pathway in gastric cancer. Fluorouracil 123-127 ribosomal protein L11 Homo sapiens 34-39 32194724-5 2020 In vitro assays demonstrated that RPL11 knockdown in gastric cancer cell lines carrying the TP53 wild-type gene attenuated 5-FU-induced cell growth suppression and activation of the P53 pathway, but not in cells carrying mutated TP53, suggesting that 5-FU suppresses tumor progression via RPL11-mediated activation of the P53 pathway in gastric cancer. Fluorouracil 123-127 ribosomal protein L11 Homo sapiens 289-294 32194724-5 2020 In vitro assays demonstrated that RPL11 knockdown in gastric cancer cell lines carrying the TP53 wild-type gene attenuated 5-FU-induced cell growth suppression and activation of the P53 pathway, but not in cells carrying mutated TP53, suggesting that 5-FU suppresses tumor progression via RPL11-mediated activation of the P53 pathway in gastric cancer. Fluorouracil 251-255 ribosomal protein L11 Homo sapiens 34-39 32194724-6 2020 The present study provides a potential therapeutic strategy for improving 5-FU resistance in gastric cancer by elevating RPL11 expression. Fluorouracil 74-78 ribosomal protein L11 Homo sapiens 121-126 32028703-14 2020 miRNA-10b-5p and miRNA-30e-5p were associated with the 5-FU therapy resistance by targeting the related genes. Fluorouracil 55-59 microRNA 10b Homo sapiens 0-9 31871216-0 2020 Fluorouracil sensitivity in a head and neck squamous cell carcinoma with a somatic DPYD structural variant. Fluorouracil 0-12 dihydropyrimidine dehydrogenase Homo sapiens 83-87 18472919-2 1994 5-Fluoro-Uracil Induces PAF Production in Haematopoietic Organs of Rats. Fluorouracil 0-15 PCNA clamp associated factor Rattus norvegicus 24-27 18472919-4 1994 PAF was reported in thymus, spleen and femoral bone marrow of rats with or without 5-FU. Fluorouracil 83-87 PCNA clamp associated factor Rattus norvegicus 0-3 7691257-4 1993 Optimal colony formation from c-kit(low) cells from 5-FU-treated mice required the interactions of at least two factors among interleukin-3 (IL-3), IL-11 and steel factor (SF) whereas colony formation from c-kit(high) cells of normal mice was supported well by IL-3 alone. Fluorouracil 52-56 interleukin 11 Mus musculus 148-153 8242472-1 1993 1,25-Dihydroxyvitamin D3 (1,25(OH)2D3) was recently shown to promote maturation of 5-fluorouracil (5FU)-treated bone marrow cells by up-regulating macrophage-colony stimulating factor (M-CSF) receptors in the presence of interleukin 1 alpha (IL-1 alpha). Fluorouracil 99-102 colony stimulating factor 1 (macrophage) Mus musculus 147-183 8242472-1 1993 1,25-Dihydroxyvitamin D3 (1,25(OH)2D3) was recently shown to promote maturation of 5-fluorouracil (5FU)-treated bone marrow cells by up-regulating macrophage-colony stimulating factor (M-CSF) receptors in the presence of interleukin 1 alpha (IL-1 alpha). Fluorouracil 99-102 colony stimulating factor 1 (macrophage) Mus musculus 185-190 31871216-3 2020 5-FU-associated toxicity is observed in approximately 30% of treated patients and is largely caused by germline polymorphisms in DPYD which encodes dihydropyrimidine dehydrogenase (DPD), a key enzyme of 5-FU catabolism and deactivation. Fluorouracil 0-4 dihydropyrimidine dehydrogenase Homo sapiens 129-133 31871216-3 2020 5-FU-associated toxicity is observed in approximately 30% of treated patients and is largely caused by germline polymorphisms in DPYD which encodes dihydropyrimidine dehydrogenase (DPD), a key enzyme of 5-FU catabolism and deactivation. Fluorouracil 0-4 dihydropyrimidine dehydrogenase Homo sapiens 148-179 31871216-3 2020 5-FU-associated toxicity is observed in approximately 30% of treated patients and is largely caused by germline polymorphisms in DPYD which encodes dihydropyrimidine dehydrogenase (DPD), a key enzyme of 5-FU catabolism and deactivation. Fluorouracil 0-4 dihydropyrimidine dehydrogenase Homo sapiens 181-184 31871216-3 2020 5-FU-associated toxicity is observed in approximately 30% of treated patients and is largely caused by germline polymorphisms in DPYD which encodes dihydropyrimidine dehydrogenase (DPD), a key enzyme of 5-FU catabolism and deactivation. Fluorouracil 203-207 dihydropyrimidine dehydrogenase Homo sapiens 129-133 31871216-3 2020 5-FU-associated toxicity is observed in approximately 30% of treated patients and is largely caused by germline polymorphisms in DPYD which encodes dihydropyrimidine dehydrogenase (DPD), a key enzyme of 5-FU catabolism and deactivation. Fluorouracil 203-207 dihydropyrimidine dehydrogenase Homo sapiens 148-179 31871216-3 2020 5-FU-associated toxicity is observed in approximately 30% of treated patients and is largely caused by germline polymorphisms in DPYD which encodes dihydropyrimidine dehydrogenase (DPD), a key enzyme of 5-FU catabolism and deactivation. Fluorouracil 203-207 dihydropyrimidine dehydrogenase Homo sapiens 181-184 31871216-8 2020 The discovery of the novel DPYD variant led to the initiation of 5-FU treatment that resulted in a rapid response lasting 17 weeks, with subsequent relapse due to unknown resistance mechanisms. Fluorouracil 65-69 dihydropyrimidine dehydrogenase Homo sapiens 27-31 32014926-1 2020 BACKGROUND/AIM: The study aimed to test the potential for increasing the antiproliferative activity of 5-fluorouracil against breast cancer cells of various molecular subtypes by vitamin D receptor (VDR) agonists, calcitriol and tacalcitol, used at a low concentration of 10 nM. Fluorouracil 103-117 vitamin D receptor Homo sapiens 179-197 32014926-1 2020 BACKGROUND/AIM: The study aimed to test the potential for increasing the antiproliferative activity of 5-fluorouracil against breast cancer cells of various molecular subtypes by vitamin D receptor (VDR) agonists, calcitriol and tacalcitol, used at a low concentration of 10 nM. Fluorouracil 103-117 vitamin D receptor Homo sapiens 199-202 32014926-4 2020 CONCLUSION: The VDR agonist used at the relatively low concentration of 10 nM may increase the sensitivity of breast cancer cells, at least of the luminal subtype, to the antiproliferative effect of 5-fluorouracil. Fluorouracil 199-213 vitamin D receptor Homo sapiens 16-19 31313286-11 2020 Taken together, our data indicated that modification of ERRFI1 by KHSRP occurs through miR-501-5p, an essential mechanism driving CRC proliferation and 5-FU resistance. Fluorouracil 152-156 KH-type splicing regulatory protein Homo sapiens 66-71 31518438-0 2020 BTK inhibitors synergize with 5-FU to treat drug-resistant TP53-null colon cancers. Fluorouracil 30-34 Bruton tyrosine kinase Homo sapiens 0-3 31518438-6 2020 Taken together, our data demonstrated that targeting p65BTK restores the apoptotic response to chemotherapy of drug-resistant CRCs and gives a proof-of-concept for suggesting the use of BTK inhibitors in combination with 5-FU as a novel therapeutic approach in CRC patients. Fluorouracil 221-225 Bruton tyrosine kinase Homo sapiens 56-59 31835085-14 2020 Also, LDN and 5FU increased immunehistochemical staining of p21 while decreased immunostaining of Bcl2. Fluorouracil 14-17 cyclin-dependent kinase inhibitor 1A (P21) Mus musculus 60-63 31529207-0 2019 ABCC11 gene polymorphism as a potential predictive biomarker for an oral 5-fluorouracil derivative drug S-1 treatment in non-small cell lung cancer. Fluorouracil 73-87 ATP binding cassette subfamily C member 11 Homo sapiens 0-6 31549215-5 2019 Further, expression levels of BATF2- and AP-1-related genes were confirmed in vincristine-resistant SGC7901/VCR cells treated with cisplatin or 5-fluorouracil. Fluorouracil 144-158 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 41-45 31578581-9 2019 In addition, the CD55 antibody treatment synergistically enhanced the tumoricidal activity of 5-FU in colorectal cancer cells, suggesting that combined treatment may be a better strategy in colorectal cancer therapy. Fluorouracil 94-98 CD55 molecule (Cromer blood group) Homo sapiens 17-21 8401256-9 1993 The presence of SCF potentiated colony formation by 5-FU resistant PBMNC. Fluorouracil 52-56 KIT ligand Homo sapiens 16-19 1281687-11 1992 The population ratio of c-kit+Sca-1+ to c-kit+Sca-1- increased 2 and 4 days after exposure to 5-fluorouracil (5-FU). Fluorouracil 94-108 lymphocyte antigen 6 complex, locus A Mus musculus 30-35 1281687-11 1992 The population ratio of c-kit+Sca-1+ to c-kit+Sca-1- increased 2 and 4 days after exposure to 5-fluorouracil (5-FU). Fluorouracil 94-108 lymphocyte antigen 6 complex, locus A Mus musculus 46-51 1281687-11 1992 The population ratio of c-kit+Sca-1+ to c-kit+Sca-1- increased 2 and 4 days after exposure to 5-fluorouracil (5-FU). Fluorouracil 110-114 lymphocyte antigen 6 complex, locus A Mus musculus 30-35 1281687-11 1992 The population ratio of c-kit+Sca-1+ to c-kit+Sca-1- increased 2 and 4 days after exposure to 5-fluorouracil (5-FU). Fluorouracil 110-114 lymphocyte antigen 6 complex, locus A Mus musculus 46-51 1333267-1 1992 This randomized phase II study was designed to evaluate the activity of intravenous 6-thioguanine (6-TG) as a single agent and the combination of cisplatin and 5-fluorouracil (5-Fu) modulated by oral leucovorin (PFL) in patients with advanced non-small cell lung cancer (NSCLC). Fluorouracil 176-180 profilin 2 Homo sapiens 212-215 1516048-0 1992 Elevation of thymidylate synthase following 5-fluorouracil treatment is prevented by the addition of leucovorin in murine colon tumors. Fluorouracil 44-58 thymidylate synthase Mus musculus 13-33 1516048-1 1992 The inhibition of thymidylate synthase (TS) by the 5-fluorouracil (5FU) metabolite 5-fluorodeoxyuridine monophosphate can be biochemically modulated by leucovorin (LV). Fluorouracil 51-65 thymidylate synthase Mus musculus 18-38 1516048-1 1992 The inhibition of thymidylate synthase (TS) by the 5-fluorouracil (5FU) metabolite 5-fluorodeoxyuridine monophosphate can be biochemically modulated by leucovorin (LV). Fluorouracil 51-65 thymidylate synthase Mus musculus 40-42 1516048-1 1992 The inhibition of thymidylate synthase (TS) by the 5-fluorouracil (5FU) metabolite 5-fluorodeoxyuridine monophosphate can be biochemically modulated by leucovorin (LV). Fluorouracil 67-70 thymidylate synthase Mus musculus 18-38 1516048-1 1992 The inhibition of thymidylate synthase (TS) by the 5-fluorouracil (5FU) metabolite 5-fluorodeoxyuridine monophosphate can be biochemically modulated by leucovorin (LV). Fluorouracil 67-70 thymidylate synthase Mus musculus 40-42 31788043-0 2019 Claudin-1 silencing increases sensitivity of liver cancer HepG2 cells to 5-fluorouracil by inhibiting autophagy. Fluorouracil 73-87 claudin 1 Homo sapiens 0-9 31788043-5 2019 The present study investigated the effect of CLDN1 on the sensitivity of 5-fluorouracil (5-FU)-resistant liver cancer cells. Fluorouracil 73-87 claudin 1 Homo sapiens 45-50 31788043-5 2019 The present study investigated the effect of CLDN1 on the sensitivity of 5-fluorouracil (5-FU)-resistant liver cancer cells. Fluorouracil 89-93 claudin 1 Homo sapiens 45-50 31788043-10 2019 MTT and Annexin V-fluorescein isothiocyanate/propidium iodide assays demonstrated that CLDN1 silencing significantly inhibits proliferation and enhances apoptosis induced by 5-FU treatment in Hep/5FU cells, compared with non-silenced Hep/5FU cells. Fluorouracil 174-178 claudin 1 Homo sapiens 87-92 31788043-15 2019 In summary, these data indicate that CLDN1 may be a potential target for resensitizing resistant liver cancer HepG2 cells to 5-FU by regulating cell autophagy. Fluorouracil 125-129 claudin 1 Homo sapiens 37-42 31798778-14 2019 CNN3 silencing caused an increase in the SW620 colon cancer cell sensitivity to 5-fluorouracil. Fluorouracil 80-94 calponin 3 Homo sapiens 0-4 1802023-1 1991 Effects of the immunomodulator PSK on the metabolism of 1-(2-tetrahydrofuryl)-5-fluorouracil (tegafur) to 5-fluorouracil (5-FU) were examined in 10 patients with advanced gastric cancer and who had undergone curative resection. Fluorouracil 78-92 TAO kinase 2 Homo sapiens 31-34 1825140-3 1991 When tested with marrow cells harvested 2 days after injection of 5-fluorouracil at 150 mg/kg, IL-11 enhanced interleukin 3-dependent colony formation, whereas IL-11 alone supported only scant colony formation. Fluorouracil 66-80 interleukin 11 Mus musculus 95-100 31695024-7 2019 While MKK3 depletion per se affects growth and survival by induction of sustained autophagy and death in some CRC lines, it potentiates response to chemotherapeutic drug 5-fluorouracil (5-FU) in all of the tested CRC lines in vitro. Fluorouracil 170-184 mitogen-activated protein kinase kinase 3 Homo sapiens 6-10 31695024-7 2019 While MKK3 depletion per se affects growth and survival by induction of sustained autophagy and death in some CRC lines, it potentiates response to chemotherapeutic drug 5-fluorouracil (5-FU) in all of the tested CRC lines in vitro. Fluorouracil 186-190 mitogen-activated protein kinase kinase 3 Homo sapiens 6-10 31695024-8 2019 Here, we demonstrate for the first time that in CRC the MKK3 specifically activates p38delta MAPK isoform to sustain prosurvival signaling and that such effect is exacerbated upon 5-FU challenge. Fluorouracil 180-184 mitogen-activated protein kinase kinase 3 Homo sapiens 56-60 31579069-7 2019 Additionally, FOXM1 knockdown improved the cytotoxicity of 5-FU in resistant CRC. Fluorouracil 59-63 forkhead box M1 Homo sapiens 14-19 31288002-7 2019 RESULTS: combined administration of luteolin and 5-FU in SEC model increased levels of p53, p21, caspase 3, DRAM and survivability while, tumor volume, weight, thioredoxin reductase one (TR1) activity and cyclin D1 expression showed the reverse with restoration of oxidant/antioxidant indices. Fluorouracil 49-53 cyclin-dependent kinase inhibitor 1A (P21) Mus musculus 92-95 31288002-7 2019 RESULTS: combined administration of luteolin and 5-FU in SEC model increased levels of p53, p21, caspase 3, DRAM and survivability while, tumor volume, weight, thioredoxin reductase one (TR1) activity and cyclin D1 expression showed the reverse with restoration of oxidant/antioxidant indices. Fluorouracil 49-53 caspase 3 Mus musculus 97-106 31288002-7 2019 RESULTS: combined administration of luteolin and 5-FU in SEC model increased levels of p53, p21, caspase 3, DRAM and survivability while, tumor volume, weight, thioredoxin reductase one (TR1) activity and cyclin D1 expression showed the reverse with restoration of oxidant/antioxidant indices. Fluorouracil 49-53 thioredoxin reductase 1 Mus musculus 187-190 31288002-7 2019 RESULTS: combined administration of luteolin and 5-FU in SEC model increased levels of p53, p21, caspase 3, DRAM and survivability while, tumor volume, weight, thioredoxin reductase one (TR1) activity and cyclin D1 expression showed the reverse with restoration of oxidant/antioxidant indices. Fluorouracil 49-53 cyclin D1 Mus musculus 205-214 31302002-5 2019 Furthermore, IKKalpha or BRAF inhibition synergistically enhances the therapeutic potential of 5-FU and irinotecan to eradicate chemotherapy-resistant metastatic human tumors in vivo. Fluorouracil 95-99 component of inhibitor of nuclear factor kappa B kinase complex Homo sapiens 13-21 31531249-1 2019 Dihydropyrimidine dehydrogenase (DPD) is the major enzyme in the catabolism of 5-Fluorouracil (5-FU) and its prodrug capecitabine. Fluorouracil 79-93 dihydropyrimidine dehydrogenase Homo sapiens 0-31 2069321-2 1991 Normal marrow cells responsive to CSF-1; two-day post-fluorouracil cells responsive to CSF-1 plus IL-3 and IL-1 alpha; and regenerating seven-day post-fluorouracil cells responsive to CSF-1 plus IL-3, IL-1 alpha and IL-6 were all severely inhibited by TGF-beta 1; and the inhibitory effects were antagonized by increasing the concentrations of the relevant growth factors. Fluorouracil 54-66 colony stimulating factor 1 (macrophage) Mus musculus 87-92 2069321-2 1991 Normal marrow cells responsive to CSF-1; two-day post-fluorouracil cells responsive to CSF-1 plus IL-3 and IL-1 alpha; and regenerating seven-day post-fluorouracil cells responsive to CSF-1 plus IL-3, IL-1 alpha and IL-6 were all severely inhibited by TGF-beta 1; and the inhibitory effects were antagonized by increasing the concentrations of the relevant growth factors. Fluorouracil 54-66 colony stimulating factor 1 (macrophage) Mus musculus 87-92 31531249-1 2019 Dihydropyrimidine dehydrogenase (DPD) is the major enzyme in the catabolism of 5-Fluorouracil (5-FU) and its prodrug capecitabine. Fluorouracil 79-93 dihydropyrimidine dehydrogenase Homo sapiens 33-36 31531249-1 2019 Dihydropyrimidine dehydrogenase (DPD) is the major enzyme in the catabolism of 5-Fluorouracil (5-FU) and its prodrug capecitabine. Fluorouracil 95-99 dihydropyrimidine dehydrogenase Homo sapiens 0-31 31531249-1 2019 Dihydropyrimidine dehydrogenase (DPD) is the major enzyme in the catabolism of 5-Fluorouracil (5-FU) and its prodrug capecitabine. Fluorouracil 95-99 dihydropyrimidine dehydrogenase Homo sapiens 33-36 31423195-0 2019 SNHG20/miR-140-5p/NDRG3 axis contributes to 5-fluorouracil resistance in gastric cancer. Fluorouracil 44-58 NDRG family member 3 Homo sapiens 18-23 31423195-10 2019 SNHG20 was revealed to be involved in mediating resistance to 5-FU in gastric cancer cell lines via NDRG3. Fluorouracil 62-66 NDRG family member 3 Homo sapiens 100-105 31423195-11 2019 In conclusion, the results of the present study suggest that the SNHG20/miR-140-5p/NDRG3 axis may be involved in mediating resistance to 5-FU in gastric cancer. Fluorouracil 137-141 NDRG family member 3 Homo sapiens 83-88 31217433-0 2019 Docosahexaenoic acid inhibits both NLRP3 inflammasome assembly and JNK-mediated mature IL-1beta secretion in 5-fluorouracil-treated MDSC: implication in cancer treatment. Fluorouracil 109-123 mitogen-activated protein kinase 8 Mus musculus 67-70 31217433-7 2019 Treatment with 5-FU led to JNK activation through ROS production in MDSC. Fluorouracil 15-19 mitogen-activated protein kinase 8 Mus musculus 27-30 30478896-9 2019 When treated with 5-fluorouracil, the expressions of stem cell markers, including Oct4, Sox2, and CD49F, were maximally maintained in the recellularized scaffold with decreased apoptosis rates compared with monolayer cells. Fluorouracil 18-32 SRY-box transcription factor 2 Homo sapiens 88-92 30478896-9 2019 When treated with 5-fluorouracil, the expressions of stem cell markers, including Oct4, Sox2, and CD49F, were maximally maintained in the recellularized scaffold with decreased apoptosis rates compared with monolayer cells. Fluorouracil 18-32 integrin subunit alpha 6 Homo sapiens 98-103 30760080-1 2019 5-fluorouracil (5-FU) was isolated as an inhibitor of thymidylate synthase, which is important for DNA synthesis. Fluorouracil 0-14 thymidylate synthase Saccharomyces cerevisiae S288C 54-74 30760080-1 2019 5-fluorouracil (5-FU) was isolated as an inhibitor of thymidylate synthase, which is important for DNA synthesis. Fluorouracil 16-20 thymidylate synthase Saccharomyces cerevisiae S288C 54-74 30760080-5 2019 RNA profiling of synchronized 5-FU treated yeast cells and protein assays reveal that the drug specifically inhibits a set of cell cycle regulated genes involved in mitotic division, by decreasing levels of the paralogous Swi5 and Ace2 transcriptional activators. Fluorouracil 30-34 DNA-binding transcription factor SWI5 Saccharomyces cerevisiae S288C 222-226 31126331-1 2019 BACKGROUND: The 5-fluorouracil/leucovorin plus oxaliplatin (FOLFOX) regimen is the standard first-line treatment for metastatic colorectal cancer (mCRC), however, the optimal second-line regimen for KRAS wild-type mCRC patients is still investigational. Fluorouracil 16-30 KRAS proto-oncogene, GTPase Homo sapiens 199-203 30889505-6 2019 When 5-FU-treated SPF and germ-free mice were compared, 5-FU-treated germ-free mice exhibited less severe epithelial destruction with higher expression of the cell proliferation marker Ki67, coupled with lower expression levels of metalloproteinases and pro-inflammatory cytokine in the oral mucosa. Fluorouracil 5-9 antigen identified by monoclonal antibody Ki 67 Mus musculus 185-189 30889505-6 2019 When 5-FU-treated SPF and germ-free mice were compared, 5-FU-treated germ-free mice exhibited less severe epithelial destruction with higher expression of the cell proliferation marker Ki67, coupled with lower expression levels of metalloproteinases and pro-inflammatory cytokine in the oral mucosa. Fluorouracil 56-60 antigen identified by monoclonal antibody Ki 67 Mus musculus 185-189 31124962-2 2019 Dihydropyrimidine dehydrogenase (DPD) plays an important role in the 5-FU metabolism. Fluorouracil 69-73 dihydropyrimidine dehydrogenase Homo sapiens 0-31 2186922-5 1990 Experiments involving the kinetics of recovery after 5-fluorouracil treatment and generation of progenitors suggest that the GM-CSF-plus-CSF-1-responsive progenitors, and hence CFU-A, are a more mature cell type than the more primitive HPP-CFC, responsive to 5637-cell-CM plus CSF-1 or rhIL-1 plus rmIL-3 plus CSF-1. Fluorouracil 53-67 colony stimulating factor 2 (granulocyte-macrophage) Mus musculus 125-131 2186922-5 1990 Experiments involving the kinetics of recovery after 5-fluorouracil treatment and generation of progenitors suggest that the GM-CSF-plus-CSF-1-responsive progenitors, and hence CFU-A, are a more mature cell type than the more primitive HPP-CFC, responsive to 5637-cell-CM plus CSF-1 or rhIL-1 plus rmIL-3 plus CSF-1. Fluorouracil 53-67 colony stimulating factor 1 (macrophage) Mus musculus 137-142 31124962-2 2019 Dihydropyrimidine dehydrogenase (DPD) plays an important role in the 5-FU metabolism. Fluorouracil 69-73 dihydropyrimidine dehydrogenase Homo sapiens 33-36 31124962-3 2019 Dihydropyrimidine dehydrogenase gene (DPYD) is a highly polymorphic gene with several hundreds of reported genetic variants and DPD activity levels vary considerably among individuals, with different 5-FU-related efficacy and toxicity. Fluorouracil 200-204 dihydropyrimidine dehydrogenase Homo sapiens 0-31 31124962-3 2019 Dihydropyrimidine dehydrogenase gene (DPYD) is a highly polymorphic gene with several hundreds of reported genetic variants and DPD activity levels vary considerably among individuals, with different 5-FU-related efficacy and toxicity. Fluorouracil 200-204 dihydropyrimidine dehydrogenase Homo sapiens 38-42 31124962-3 2019 Dihydropyrimidine dehydrogenase gene (DPYD) is a highly polymorphic gene with several hundreds of reported genetic variants and DPD activity levels vary considerably among individuals, with different 5-FU-related efficacy and toxicity. Fluorouracil 200-204 dihydropyrimidine dehydrogenase Homo sapiens 128-131 30944635-0 2019 5-Fluorouracil-based adjuvant chemotherapy improves the clinical outcomes of patients with lymphovascular invasion of upper urinary tract cancer and low expression of dihydropyrimidine dehydrogenase. Fluorouracil 0-14 dihydropyrimidine dehydrogenase Homo sapiens 167-198 30944635-3 2019 Tegafur-uracil is an oral form of 5-fluorouracil whose efficacy is influenced by the activities of enzymes associated with its metabolism, such as dihydropyrimidine dehydrogenase (DPD), orotatephosphoribosyltransferase (OPRT) and thymidylate synthase (TS). Fluorouracil 34-48 dihydropyrimidine dehydrogenase Homo sapiens 147-178 30944635-3 2019 Tegafur-uracil is an oral form of 5-fluorouracil whose efficacy is influenced by the activities of enzymes associated with its metabolism, such as dihydropyrimidine dehydrogenase (DPD), orotatephosphoribosyltransferase (OPRT) and thymidylate synthase (TS). Fluorouracil 34-48 dihydropyrimidine dehydrogenase Homo sapiens 180-183 30944635-9 2019 Adjuvant 5-fluorouracil chemotherapy significantly improved the outcome of patients with lower DPD expression. Fluorouracil 9-23 dihydropyrimidine dehydrogenase Homo sapiens 95-98 30944635-11 2019 Adjuvant 5-fluorouracil chemotherapy appears to be effective for lymphovascular-invasive UC-UUT in patients with lower DPD expression. Fluorouracil 9-23 dihydropyrimidine dehydrogenase Homo sapiens 119-122 31014355-11 2019 Moreover, knockdown of SNHG15 increases the sensitiveness of the cells to 5-FU, while its overexpression renders them more resistant to the chemotherapeutic drug. Fluorouracil 74-78 small nucleolar RNA host gene 15 Homo sapiens 23-29 30737232-4 2019 Addition of a neutralizing antibody against the myeloid differentiation antigen GR-1 or gemcitabine/5-fluorouracil-depleted MDSCs alleviated MDSC-mediated immunosuppression and increased CD4+ and CD8+ T-cell tumor infiltration and GSK126 therapeutic efficacy. Fluorouracil 100-114 CD8a molecule Homo sapiens 196-199 31011291-13 2019 Conclusions: In light of the above findings, LATS2 downregulation could be a potential mechanism of low response to 5-FU treatment. Fluorouracil 116-120 large tumor suppressor kinase 2 Homo sapiens 45-50 31011291-14 2019 Overexpression of LATS2 to further disrupt mitochondrial function via the JNK-MIEF1 signalling pathway might be a method to optimize 5-FU-based chemotherapy. Fluorouracil 133-137 large tumor suppressor kinase 2 Homo sapiens 18-23 31011291-14 2019 Overexpression of LATS2 to further disrupt mitochondrial function via the JNK-MIEF1 signalling pathway might be a method to optimize 5-FU-based chemotherapy. Fluorouracil 133-137 mitochondrial elongation factor 1 Homo sapiens 78-83 30884222-6 2019 The DNA-modified CodA was found to retain its enzyme activity for converting prodrug 5-fluorocytosine (5-FC) to active 5-fluorouracil (5-FU) using a modified fluorescent assay. Fluorouracil 119-133 CODA Homo sapiens 17-21 1688926-2 1990 Therefore, the addition of LV to cisplatin and 5-FU (PFL) may increase the activity of that combination in head and neck cancer. Fluorouracil 47-51 profilin 2 Homo sapiens 53-56 30884222-6 2019 The DNA-modified CodA was found to retain its enzyme activity for converting prodrug 5-fluorocytosine (5-FC) to active 5-fluorouracil (5-FU) using a modified fluorescent assay. Fluorouracil 135-139 CODA Homo sapiens 17-21 30858516-2 2019 BACKGROUND: Deleterious polymorphisms in the gene encoding DPD (DPYD) may result in severe reduction of DPD enzymatic activity that causes life-threatening toxicities when the standard dose of fluorouracil is used. Fluorouracil 193-205 dihydropyrimidine dehydrogenase Homo sapiens 64-68 14701834-1 2004 We previously reported that the human Na(+)/nucleoside transporter pyrimidine-preferring 1 (hCNT1) is electrogenic and transports gemcitabine and 5"-deoxy-5-fluorouridine, a precursor of the active drug 5-fluorouracil. Fluorouracil 203-217 solute carrier family 28 member 1 Homo sapiens 92-97 30603978-0 2019 Nanoquinacrine sensitizes 5-FU-resistant cervical cancer stem-like cells by down-regulating Nectin-4 via ADAM-17 mediated NOTCH deregulation. Fluorouracil 26-30 nectin cell adhesion molecule 4 Homo sapiens 92-100 9721209-2 1998 A deficiency in human DPD is associated with congenital thymine-uraciluria in pediatric patients and severe 5-fluorouracil toxicity in cancer patients. Fluorouracil 108-122 dihydropyrimidine dehydrogenase Homo sapiens 22-25 34633539-8 2022 RESULTS: The groups with EP and treated with 5-FU or CIS showed lower percentage of bone volume in the furcation region and higher percentage of alveolar bone loss, higher number of TRAP-positive cells, and lower number of PCNA-positive cells when compared group with EP and treated with PSS (p <= 0.05). Fluorouracil 45-49 proliferating cell nuclear antigen Rattus norvegicus 223-227 34633539-9 2022 Groups with EP and treated with 5-FU or CIS showed high immunolabelling pattern of RANKL, TNF-alpha, and IL-1beta, moderate of BAX, and low of HIF-1alpha. Fluorouracil 32-36 hypoxia inducible factor 1 subunit alpha Rattus norvegicus 143-153 34592338-15 2022 AFE also efficiently regressed CT26-derived solid tumor in Balb/c mice acting alone or in synergy with 5FU through inducing autophagy as a major mechanism of action as indicated by upregulation of Beclin 1 and phospho-AMPK, and inhibition of phosphor-S6K1 levels in the tumor tissue lysates. Fluorouracil 103-106 ribosomal protein S6 kinase, polypeptide 1 Mus musculus 251-255 34411894-6 2021 The most promising compound 40 could markedly reverse the resistance in 5-FU-resistant HCT116 cells and 5-FU-resistant SW620 cells via inhibiting the expression of dihydropyrimidine dehydrogenase (DPD). Fluorouracil 72-76 dihydropyrimidine dehydrogenase Homo sapiens 164-195 34411894-6 2021 The most promising compound 40 could markedly reverse the resistance in 5-FU-resistant HCT116 cells and 5-FU-resistant SW620 cells via inhibiting the expression of dihydropyrimidine dehydrogenase (DPD). Fluorouracil 72-76 dihydropyrimidine dehydrogenase Homo sapiens 197-200 34411894-6 2021 The most promising compound 40 could markedly reverse the resistance in 5-FU-resistant HCT116 cells and 5-FU-resistant SW620 cells via inhibiting the expression of dihydropyrimidine dehydrogenase (DPD). Fluorouracil 104-108 dihydropyrimidine dehydrogenase Homo sapiens 164-195 34411894-6 2021 The most promising compound 40 could markedly reverse the resistance in 5-FU-resistant HCT116 cells and 5-FU-resistant SW620 cells via inhibiting the expression of dihydropyrimidine dehydrogenase (DPD). Fluorouracil 104-108 dihydropyrimidine dehydrogenase Homo sapiens 197-200 34411894-7 2021 The key was that compound 40 with improved pharmacokinetic properties significantly increased the inhibitory rate of 5-FU in the SW620/5-FU cells xenograft model with no observable toxicity by inhibiting the expression of DPD in tumor and liver tissues. Fluorouracil 117-121 dihydropyrimidine dehydrogenase Homo sapiens 222-225 34794098-7 2021 The most balanced potent and safe derivatives; 5i and 5q were more active than 5-fluorouracil, exhibited low mumrange MDM2 binding (KD=1.32and 1.72 mum, respectively), induced apoptosis-dependent anticancer activities up to 50%, activated p53 by 47-63%, downregulated the BCL2 gene to 59.8%, and reduced its protein level (13.75%) in the treated cancer cells. Fluorouracil 79-93 MDM2 proto-oncogene Homo sapiens 118-122 34688691-0 2021 FOXM1 inhibitor, Siomycin A, synergizes and restores 5-FU cytotoxicity in human cholangiocarcinoma cell lines via targeting thymidylate synthase. Fluorouracil 53-57 forkhead box M1 Homo sapiens 0-5 34688691-3 2021 Upregulation of Forkhead box M1 (FOXM1) and TS were shown to play a significant role in 5-FU resistance. Fluorouracil 88-92 forkhead box M1 Homo sapiens 16-31 34688691-3 2021 Upregulation of Forkhead box M1 (FOXM1) and TS were shown to play a significant role in 5-FU resistance. Fluorouracil 88-92 forkhead box M1 Homo sapiens 33-38 34688691-4 2021 In this study, the effect of Siomycin A (SioA), a FOXM1 inhibitor, on enhancing 5-FU cytotoxicity and reversing 5-FU resistance in CCA cell lines were demonstrated. Fluorouracil 80-84 forkhead box M1 Homo sapiens 50-55 34688691-4 2021 In this study, the effect of Siomycin A (SioA), a FOXM1 inhibitor, on enhancing 5-FU cytotoxicity and reversing 5-FU resistance in CCA cell lines were demonstrated. Fluorouracil 112-116 forkhead box M1 Homo sapiens 50-55 34688691-12 2021 FOXM1 and TS expression were increased in the 5-FU treated cells but were suppressed in the SioA treated cells. Fluorouracil 46-50 forkhead box M1 Homo sapiens 0-5 30603978-0 2019 Nanoquinacrine sensitizes 5-FU-resistant cervical cancer stem-like cells by down-regulating Nectin-4 via ADAM-17 mediated NOTCH deregulation. Fluorouracil 26-30 ADAM metallopeptidase domain 17 Homo sapiens 105-112 34688691-15 2021 SIGNIFICANCE: Targeting FOXM1 using SioA in combination with 5-FU might be a strategy to overcome the 5-FU resistance in CCA. Fluorouracil 61-65 forkhead box M1 Homo sapiens 24-29 34688691-15 2021 SIGNIFICANCE: Targeting FOXM1 using SioA in combination with 5-FU might be a strategy to overcome the 5-FU resistance in CCA. Fluorouracil 102-106 forkhead box M1 Homo sapiens 24-29 30603978-5 2019 This study was designed to assess the role of Nectin-4 in the acquisition of 5-FU resistance by metastatic CC cells, including its relation to the NOTCH signalling pathway. Fluorouracil 77-81 nectin cell adhesion molecule 4 Homo sapiens 46-54 30802029-4 2019 To address these issues, we reported in this study the codelivery of liver-specific miRNA-122 and anti-cancer drug 5-fluorouracil (5-Fu) using a macromolecular prodrug approach, that is, electrostatic condensation with miRNA-122 using galactosylated-chitosan-5-fluorouracil (GC-FU). Fluorouracil 115-129 microRNA 122 Homo sapiens 219-228 34506675-12 2021 IMPLICATIONS FOR PRACTICE: The syndrome of dihydropyrimidine deaminase (DPD) deficiency is an uncommon but well-described cause of severe toxicity related to fluoropyrimidine chemotherapy agents (5-fluorouracil and capecitabine). Fluorouracil 196-210 dihydropyrimidine dehydrogenase Homo sapiens 72-75 34733364-6 2021 In addition, overexpression of RNF43 increased 5-fluorouracil sensitivity and downregulation of ABC transporter genes (including ABCB1 and ABCC1 (MRP1)). Fluorouracil 47-61 ring finger protein 43 Homo sapiens 31-36 34826159-1 2022 The aim of this study was to: 1) explore the potential mechanism of cancer cell sensitivity to cisplatin, docetaxel, and 5-fluorouracil (TPF) in oral squamous cell carcinoma (OSCC) patients overexpressing growth differentiation factor 15 (GDF15); and 2) identify potential alternative agents for patients who might not benefit from inductive TPF chemotherapy. Fluorouracil 121-135 growth differentiation factor 15 Homo sapiens 205-237 34826159-1 2022 The aim of this study was to: 1) explore the potential mechanism of cancer cell sensitivity to cisplatin, docetaxel, and 5-fluorouracil (TPF) in oral squamous cell carcinoma (OSCC) patients overexpressing growth differentiation factor 15 (GDF15); and 2) identify potential alternative agents for patients who might not benefit from inductive TPF chemotherapy. Fluorouracil 121-135 growth differentiation factor 15 Homo sapiens 239-244 34826008-9 2022 Further study showed that the knockdown of NRP2 eradicated the resistance to 5-FU. Fluorouracil 77-81 neuropilin 2 Homo sapiens 43-47 34888232-8 2021 Under in vitro conditions, siRNA-mediated SPAK-knockdown in IEC-6 cells decreased cell permeability and maintained homeostasis following 5-FU treatment. Fluorouracil 137-141 serine threonine kinase 39 Rattus norvegicus 42-46 34869449-12 2021 Intriguingly, the SRI expression was negatively correlated with drug sensitivity of fluorouracil, paclitaxel, docetaxel, and isotretinoin. Fluorouracil 84-96 sorcin Homo sapiens 18-21 34773566-2 2022 This toxicity is often related to the partial or complete deficiency of the dihydropyrimidine dehydrogenase (DPD) enzyme, which causes a reduction in clearance and a longer half-life of 5-FU. Fluorouracil 186-190 dihydropyrimidine dehydrogenase Homo sapiens 109-112 34773342-11 2022 Fluorouracil increased PD-L1 and PD-L2 expression. Fluorouracil 0-12 programmed cell death 1 ligand 2 Homo sapiens 33-38 34795760-0 2021 Nrf3 Promotes 5-FU Resistance in Colorectal Cancer Cells via the NF-kappaB/BCL-2 Signaling Pathway In Vitro and In Vivo. Fluorouracil 14-18 NFE2 like bZIP transcription factor 3 Homo sapiens 0-4 34795760-3 2021 In this study, we investigated the effect and mechanism of action by which Nrf3 regulated the sensitivity of colon cancer cells to 5-fluorouracil (5-FU). Fluorouracil 131-145 NFE2 like bZIP transcription factor 3 Homo sapiens 75-79 34795760-3 2021 In this study, we investigated the effect and mechanism of action by which Nrf3 regulated the sensitivity of colon cancer cells to 5-fluorouracil (5-FU). Fluorouracil 147-151 NFE2 like bZIP transcription factor 3 Homo sapiens 75-79 34795760-5 2021 Furthermore, we observed that Nrf3 knockdown and overexpression can significantly affect the sensitivity of colon cancer cells to 5-FU in vitro and in vivo. Fluorouracil 130-134 NFE2 like bZIP transcription factor 3 Homo sapiens 30-34 34795760-7 2021 Inhibition of NF-kappaB partly reversed the effects of Nrf3 overexpression, resulting in the resistance of colon cancer cells to 5-FU. Fluorouracil 129-133 NFE2 like bZIP transcription factor 3 Homo sapiens 55-59 34795760-8 2021 Overall, the study revealed that Nrf3 was connected to the sensitivity of colon cancer cells to 5-FU, and its possible mechanism was related to the NF-kappaB signaling pathway, which provided a new target for overcoming the resistance of colon cancer cells to 5-FU. Fluorouracil 96-100 NFE2 like bZIP transcription factor 3 Homo sapiens 33-37 34795760-8 2021 Overall, the study revealed that Nrf3 was connected to the sensitivity of colon cancer cells to 5-FU, and its possible mechanism was related to the NF-kappaB signaling pathway, which provided a new target for overcoming the resistance of colon cancer cells to 5-FU. Fluorouracil 260-264 NFE2 like bZIP transcription factor 3 Homo sapiens 33-37 34588619-7 2021 Targeting LCN2 or SRC compromised the growth of CRC cells with LCN2-induced 5-FU resistance. Fluorouracil 76-80 lipocalin 2 Homo sapiens 10-14 34588619-7 2021 Targeting LCN2 or SRC compromised the growth of CRC cells with LCN2-induced 5-FU resistance. Fluorouracil 76-80 lipocalin 2 Homo sapiens 63-67 34588619-8 2021 Our findings demonstrate a novel mechanism of acquired resistance to 5-FU, suggesting that LCN2 can be used as a biomarker and/or therapeutic target for advanced CRC. Fluorouracil 69-73 lipocalin 2 Homo sapiens 91-95 34611311-7 2021 Moreover, the combination of 5-fluorouracil (5-FU) plus pladienolide B exerted synergistic effects in CRC with high RNF6 expression, leading to tumor regression in xenograft models. Fluorouracil 29-43 ring finger protein (C3H2C3 type) 6 Mus musculus 116-120 34611311-7 2021 Moreover, the combination of 5-fluorouracil (5-FU) plus pladienolide B exerted synergistic effects in CRC with high RNF6 expression, leading to tumor regression in xenograft models. Fluorouracil 45-49 ring finger protein (C3H2C3 type) 6 Mus musculus 116-120 34712612-7 2021 Furthermore, biochemical inhibition of lysine specific demethylase 1 (LSD1) restored H3k4me2, thereby reducing GS-induced chemoresistance to 5FU. Fluorouracil 141-144 lysine demethylase 1A Homo sapiens 39-68 34712612-7 2021 Furthermore, biochemical inhibition of lysine specific demethylase 1 (LSD1) restored H3k4me2, thereby reducing GS-induced chemoresistance to 5FU. Fluorouracil 141-144 lysine demethylase 1A Homo sapiens 70-74 34132895-8 2021 The highest 5-FU concentration was found in the liver, also expressing high levels of the 5-FU transporter OAT2. Fluorouracil 90-94 solute carrier family 22 member 7 Homo sapiens 107-111 34261152-9 2021 CONCLUSION: Our findings indicate that the combination of allicin with 5-FU could reverse multidrug resistance in the GC cells by reducing the expression of WNT5A, DKK1, MDR1, P-gp, and CD44 levels. Fluorouracil 71-75 CD44 molecule (Indian blood group) Homo sapiens 186-190 34551797-10 2021 Pharmacological inhibition of PTK6 using XMU-MP-2 effectively reduces the stemness property of CRC cells and improves its chemosensitivity to 5-FU/L-OHP in both nude mice subcutaneously implanted tumor model and PDX model constructed with NOD-SCID mice. Fluorouracil 142-146 PTK6 protein tyrosine kinase 6 Mus musculus 30-34 34157171-2 2021 This study aims to explore the relationship between the Annexin A1 expression and the clinical response to cisplatin, docetaxel, and 5-fluorouracil (TPF) as induction chemotherapy in patients with oral squamous cell carcinoma (OSCC). Fluorouracil 133-147 annexin A1 Homo sapiens 56-66 34157171-9 2021 In addition, downregulation of Annexin A1 promoted apoptosis induced by docetaxel, cisplatin and 5-fluorouracil, and upregulation of Annexin A1 inhibited apoptosis. Fluorouracil 97-111 annexin A1 Homo sapiens 31-41 34422665-0 2021 ARTEMIN Promotes Oncogenicity and Resistance to 5-Fluorouracil in Colorectal Carcinoma by p44/42 MAPK Dependent Expression of CDH2. Fluorouracil 48-62 cadherin 2 Homo sapiens 126-130 34214844-0 2021 Retinoblastoma tumor suppressor gene 1 enhances 5-Fluorouracil chemosensitivity through SDF-1/CXCR4 axis by regulating autophagy in gastric cancer. Fluorouracil 48-62 C-X-C motif chemokine receptor 4 Homo sapiens 94-99 34452150-3 2021 5-FU activity leads to caspase-1 activation, secretion and maturation of interleukins (IL)-1, IL-18 and reactive oxygen species (ROS) generation. Fluorouracil 0-4 interleukin 18 Homo sapiens 94-99 34452150-4 2021 Furthermore, the effects of embedding 5-FU in P.CNF were explored in order to suppress breast tumor cell growth and induce inflammasome complex activation together with extra- and intracellular ROS generation. Fluorouracil 38-42 NPHS1 adhesion molecule, nephrin Homo sapiens 48-51 34452150-5 2021 Exposure of tumor cells to P.CNF/5-FU resulted in a strong cytotoxic effect, an increased level of caspase-1 released in the culture media and ROS production-the latter directly proportional to the concentration of anti-tumor agent embedded in the scaffolds. Fluorouracil 33-37 NPHS1 adhesion molecule, nephrin Homo sapiens 29-32 34452150-7 2021 In conclusion, P.CNF/5-FU scaffolds proved to be efficient against breast tumor cells growth due to pyroptosis induction. Fluorouracil 21-25 NPHS1 adhesion molecule, nephrin Homo sapiens 17-20 34367280-0 2021 Upregulation of ECT2 Predicts Adverse Clinical Outcomes and Increases 5-Fluorouracil Resistance in Gastric Cancer Patients. Fluorouracil 70-84 epithelial cell transforming 2 Homo sapiens 16-20 34367280-2 2021 However, the effect of ECT2 on 5-fluorouracil (5-Fu) resistance in GC is unclear. Fluorouracil 31-45 epithelial cell transforming 2 Homo sapiens 23-27 30802029-4 2019 To address these issues, we reported in this study the codelivery of liver-specific miRNA-122 and anti-cancer drug 5-fluorouracil (5-Fu) using a macromolecular prodrug approach, that is, electrostatic condensation with miRNA-122 using galactosylated-chitosan-5-fluorouracil (GC-FU). Fluorouracil 131-135 microRNA 122 Homo sapiens 219-228 34367280-2 2021 However, the effect of ECT2 on 5-fluorouracil (5-Fu) resistance in GC is unclear. Fluorouracil 47-51 epithelial cell transforming 2 Homo sapiens 23-27 34367280-9 2021 More importantly, ECT2 knockdown weakened the resistance of 5-FU in GC cells. Fluorouracil 60-64 epithelial cell transforming 2 Homo sapiens 18-22 34367280-10 2021 ECT2 silencing reduced the cell migratory and invasive abilities of GC cells treated with 5-FU. Fluorouracil 90-94 epithelial cell transforming 2 Homo sapiens 0-4 28942723-3 2019 Dihydropyrimidine dehydrogenase and thymidylate synthase play a major role in fluorouracil and capecitabine activity and toxicity. Fluorouracil 78-90 dihydropyrimidine dehydrogenase Homo sapiens 0-31 34367280-11 2021 We also found that downregulation of ECT2 increased 5-FU sensitivity in GC cells by downregulating P-gp, MRP1, and Bcl-2. Fluorouracil 52-56 epithelial cell transforming 2 Homo sapiens 37-41 34367280-12 2021 Conclusion: Upregulation of ECT2 can predict adverse clinical outcomes and increase 5-FU resistance in GC patients. Fluorouracil 84-88 epithelial cell transforming 2 Homo sapiens 28-32 30803213-0 2019 Study of Thymidylate Synthase (TS) and Dihydropyrimidine Dehydrogenase (DPD) Expressions on 5-Fluorouracil in Oral Squamous Cell Carcinoma Background: The study aims to analyze Thymidylate Synthase (TS) and Dihydropyrimidine Dehydrogenase(DPD) Expressions on 5-Fluorouracil in Oral Squamous Cell Carcinoma (OSCC). Fluorouracil 92-106 dihydropyrimidine dehydrogenase Homo sapiens 39-70 30915355-7 2019 In addition, Ubenimex downregulates expression of membrane transport proteins, such as P-gp and MRP1, by inhibiting phosphorylation in the PI3K/AKT/mTOR pathway to increase intracellular accumulations of 5-fluorouracil and oxaliplatin, a process for which downregulation of CD13 expression is essential. Fluorouracil 204-218 CD9 molecule Homo sapiens 96-100 34449540-1 2021 Dihydropyrimidine dehydrogenase (DPD) is the major enzyme in the catabolism of 5-Fluorouracil (5-FU) and its prodrug capecitabine. Fluorouracil 79-93 dihydropyrimidine dehydrogenase Homo sapiens 0-31 30579838-0 2019 Schedule-dependent synergistic effects of 5-fluorouracil and selumetinib in KRAS or BRAF mutant colon cancer models. Fluorouracil 42-56 KRAS proto-oncogene, GTPase Homo sapiens 76-80 34449540-1 2021 Dihydropyrimidine dehydrogenase (DPD) is the major enzyme in the catabolism of 5-Fluorouracil (5-FU) and its prodrug capecitabine. Fluorouracil 79-93 dihydropyrimidine dehydrogenase Homo sapiens 33-36 34449540-1 2021 Dihydropyrimidine dehydrogenase (DPD) is the major enzyme in the catabolism of 5-Fluorouracil (5-FU) and its prodrug capecitabine. Fluorouracil 95-99 dihydropyrimidine dehydrogenase Homo sapiens 0-31 30579838-12 2019 Our results suggest that sequential administration of 5-FU plus selumetinib would be a promising strategy for patients having KRAS or BRAF mutant colon cancers. Fluorouracil 54-58 KRAS proto-oncogene, GTPase Homo sapiens 126-130 34449540-1 2021 Dihydropyrimidine dehydrogenase (DPD) is the major enzyme in the catabolism of 5-Fluorouracil (5-FU) and its prodrug capecitabine. Fluorouracil 95-99 dihydropyrimidine dehydrogenase Homo sapiens 33-36 34449540-3 2021 DPYD gene sequencing revealed rare different polymorphisms that prompted dose adjustments of administered 5-FU and capecitabine. Fluorouracil 106-110 dihydropyrimidine dehydrogenase Homo sapiens 0-4 34360807-7 2021 In Caco-2 cells, LMWF enhanced the suppressive effects of 5-FU on cell viability through both the c-mesenchymal-epithelial transition (MET)/Kirsten rat sarcoma virus (KRAS)/extracellular signal-regulated kinase (ERK) and the c-MET/phosphatidyl-inositol 3-kinases (PI3K)/protein kinase B (AKT) signaling pathways. Fluorouracil 58-62 KRAS proto-oncogene, GTPase Homo sapiens 167-171 30488540-0 2019 Augmented antitumor activity of 5-fluorouracil by double knockdown of MDM4 and MDM2 in colon and gastric cancer cells. Fluorouracil 32-46 MDM2 proto-oncogene Homo sapiens 79-83 30488540-5 2019 In the present study, MDM4/MDM2 double knockdown with the siRNAs enhanced 5-fluorouracil (5-FU)-induced p53 activation, arrested the cell cycle at G1 phase, and potentiated the antitumor effect of 5-FU in wtTP53/highMDM4 human colon (HCT116 and LoVo) and gastric (SNU-1 and NUGC-4) cancer cells. Fluorouracil 74-88 MDM2 proto-oncogene Homo sapiens 27-31 30488540-5 2019 In the present study, MDM4/MDM2 double knockdown with the siRNAs enhanced 5-fluorouracil (5-FU)-induced p53 activation, arrested the cell cycle at G1 phase, and potentiated the antitumor effect of 5-FU in wtTP53/highMDM4 human colon (HCT116 and LoVo) and gastric (SNU-1 and NUGC-4) cancer cells. Fluorouracil 90-94 MDM2 proto-oncogene Homo sapiens 27-31 30488540-5 2019 In the present study, MDM4/MDM2 double knockdown with the siRNAs enhanced 5-fluorouracil (5-FU)-induced p53 activation, arrested the cell cycle at G1 phase, and potentiated the antitumor effect of 5-FU in wtTP53/highMDM4 human colon (HCT116 and LoVo) and gastric (SNU-1 and NUGC-4) cancer cells. Fluorouracil 197-201 MDM2 proto-oncogene Homo sapiens 27-31 30488540-6 2019 Exposure to 5-FU alone induced MDM2 as well as p21 and PUMA by p53 activation. Fluorouracil 12-16 MDM2 proto-oncogene Homo sapiens 31-35 30488540-7 2019 As p53-MDM2 forms a negative feedback loop, enhancement of the antitumor effect of 5-FU by MDM4/MDM2 double knockdown could be attributed to blocking of the feedback mechanism in addition to direct suppression of these p53 antagonists. Fluorouracil 83-87 MDM2 proto-oncogene Homo sapiens 7-11 30488540-7 2019 As p53-MDM2 forms a negative feedback loop, enhancement of the antitumor effect of 5-FU by MDM4/MDM2 double knockdown could be attributed to blocking of the feedback mechanism in addition to direct suppression of these p53 antagonists. Fluorouracil 83-87 MDM2 proto-oncogene Homo sapiens 96-100 30488540-8 2019 Intratumor injection of the MDM4/MDM2 siRNAs suppressed in vivo tumor growth and boosted the antitumor effect of 5-FU in an athymic mouse xenograft model using HCT116 cells. Fluorouracil 113-117 transformed mouse 3T3 cell double minute 4 Mus musculus 28-32 30226808-8 2019 DPYD, a confirmed target of LINC00261, displayed a greater incidence of DNA methylation among patient"s sensitive to 5-FU. Fluorouracil 117-121 dihydropyrimidine dehydrogenase Homo sapiens 0-4 30226808-9 2019 A key finding revealed that overexpressed LINC00261 could increase the methylation of the DPYD promoter through the recruitment of DNA methyltransferase (DNMT), which, in turn, acts to decrease DPYD activity in 5-FU-resistant TE-1 cells, whereas a reversible change was recorded once the demethylation reagent 5-aza-2"-deoxyctidine was employed to treat the 5-FU-resistant TE-1 cells. Fluorouracil 211-215 dihydropyrimidine dehydrogenase Homo sapiens 90-94 30226808-9 2019 A key finding revealed that overexpressed LINC00261 could increase the methylation of the DPYD promoter through the recruitment of DNA methyltransferase (DNMT), which, in turn, acts to decrease DPYD activity in 5-FU-resistant TE-1 cells, whereas a reversible change was recorded once the demethylation reagent 5-aza-2"-deoxyctidine was employed to treat the 5-FU-resistant TE-1 cells. Fluorouracil 211-215 DNA methyltransferase 1 Homo sapiens 131-152 30226808-9 2019 A key finding revealed that overexpressed LINC00261 could increase the methylation of the DPYD promoter through the recruitment of DNA methyltransferase (DNMT), which, in turn, acts to decrease DPYD activity in 5-FU-resistant TE-1 cells, whereas a reversible change was recorded once the demethylation reagent 5-aza-2"-deoxyctidine was employed to treat the 5-FU-resistant TE-1 cells. Fluorouracil 211-215 DNA methyltransferase 1 Homo sapiens 154-158 30226808-9 2019 A key finding revealed that overexpressed LINC00261 could increase the methylation of the DPYD promoter through the recruitment of DNA methyltransferase (DNMT), which, in turn, acts to decrease DPYD activity in 5-FU-resistant TE-1 cells, whereas a reversible change was recorded once the demethylation reagent 5-aza-2"-deoxyctidine was employed to treat the 5-FU-resistant TE-1 cells. Fluorouracil 211-215 dihydropyrimidine dehydrogenase Homo sapiens 194-198 30226808-9 2019 A key finding revealed that overexpressed LINC00261 could increase the methylation of the DPYD promoter through the recruitment of DNA methyltransferase (DNMT), which, in turn, acts to decrease DPYD activity in 5-FU-resistant TE-1 cells, whereas a reversible change was recorded once the demethylation reagent 5-aza-2"-deoxyctidine was employed to treat the 5-FU-resistant TE-1 cells. Fluorouracil 358-362 dihydropyrimidine dehydrogenase Homo sapiens 90-94 30226808-9 2019 A key finding revealed that overexpressed LINC00261 could increase the methylation of the DPYD promoter through the recruitment of DNA methyltransferase (DNMT), which, in turn, acts to decrease DPYD activity in 5-FU-resistant TE-1 cells, whereas a reversible change was recorded once the demethylation reagent 5-aza-2"-deoxyctidine was employed to treat the 5-FU-resistant TE-1 cells. Fluorouracil 358-362 DNA methyltransferase 1 Homo sapiens 131-152 30226808-9 2019 A key finding revealed that overexpressed LINC00261 could increase the methylation of the DPYD promoter through the recruitment of DNA methyltransferase (DNMT), which, in turn, acts to decrease DPYD activity in 5-FU-resistant TE-1 cells, whereas a reversible change was recorded once the demethylation reagent 5-aza-2"-deoxyctidine was employed to treat the 5-FU-resistant TE-1 cells. Fluorouracil 358-362 DNA methyltransferase 1 Homo sapiens 154-158 30207288-0 2018 Early disease relapse in a patient with colorectal cancer who harbors genetic variants of DPYD, TYMS, MTHFR and DHFR after treatment with 5-fluorouracil-based chemotherapy. Fluorouracil 138-152 dihydropyrimidine dehydrogenase Homo sapiens 90-94 30207288-0 2018 Early disease relapse in a patient with colorectal cancer who harbors genetic variants of DPYD, TYMS, MTHFR and DHFR after treatment with 5-fluorouracil-based chemotherapy. Fluorouracil 138-152 methylenetetrahydrofolate reductase Homo sapiens 102-107 30339814-8 2018 However, ISL-induced p62/SQSTM1 expression also attenuated the potency of apoptosis induced by the combination of 5-FU and ISL. Fluorouracil 114-118 sequestosome 1 Homo sapiens 21-24 30339814-8 2018 However, ISL-induced p62/SQSTM1 expression also attenuated the potency of apoptosis induced by the combination of 5-FU and ISL. Fluorouracil 114-118 sequestosome 1 Homo sapiens 25-31 30538221-0 2018 FOXM1 modulates 5-fluorouracil sensitivity in cholangiocarcinoma through thymidylate synthase (TYMS): implications of FOXM1-TYMS axis uncoupling in 5-FU resistance. Fluorouracil 16-30 forkhead box M1 Homo sapiens 0-5 30538221-0 2018 FOXM1 modulates 5-fluorouracil sensitivity in cholangiocarcinoma through thymidylate synthase (TYMS): implications of FOXM1-TYMS axis uncoupling in 5-FU resistance. Fluorouracil 148-152 forkhead box M1 Homo sapiens 0-5 30538221-5 2018 In agreement, RT-qPCR and western blot analyses of four human CCA cell lines at the baseline level and in response to high doses of 5-FU revealed good correlations between FOXM1 and TYMS expression in the CCA cell lines tested, except for the highly 5-FU-resistant HuCCA cells. Fluorouracil 132-136 forkhead box M1 Homo sapiens 172-177 30539860-8 2018 Consistently, 3-MA inhibited, while rapamycin facilitated 5-FU-induced expressions of Beclin1 and LC3B. Fluorouracil 58-62 beclin 1 Homo sapiens 86-93 30539860-10 2018 Using genetic method, Beclin1 overexpression increased while Beclin1 knockdown decreased 5-FU-induced cell proliferation inhibition and apoptosis. Fluorouracil 89-93 beclin 1 Homo sapiens 61-68 30539860-11 2018 Especially, Beclin1 overexpression increased while Beclin1 knockdown decreased 5-FU-induced p53 expression. Fluorouracil 79-83 beclin 1 Homo sapiens 51-58 30274778-9 2018 Furthermore, the cellular senescence induced by Emodin and 5-FU treatment could be reverted by pcDNA-NRARP. Fluorouracil 59-63 NOTCH regulated ankyrin repeat protein Homo sapiens 101-106 30464532-0 2018 EZH2 contributes to 5-FU resistance in gastric cancer by epigenetically suppressing FBXO32 expression. Fluorouracil 20-24 F-box protein 32 Homo sapiens 84-90 30464532-8 2018 FBXO32 overexpression could mimic the functional role of downregulated EZH2 in 5-FU resistance. Fluorouracil 79-83 F-box protein 32 Homo sapiens 0-6 30464532-9 2018 FBXO32 knockdown counteracted the inductive effect of EZH2 inhibition on 5-FU sensitivity of AGS/5-FU and SGC-7901/5-FU cells. Fluorouracil 73-77 F-box protein 32 Homo sapiens 0-6 30464532-9 2018 FBXO32 knockdown counteracted the inductive effect of EZH2 inhibition on 5-FU sensitivity of AGS/5-FU and SGC-7901/5-FU cells. Fluorouracil 97-101 F-box protein 32 Homo sapiens 0-6 30464532-11 2018 Conclusion: In summary, EZH2 depletion overcame 5-FU resistance in GC by epigenetically silencing FBXO32, providing a novel therapeutic target for GC chemoresistance. Fluorouracil 48-52 F-box protein 32 Homo sapiens 98-104 30011079-8 2018 Moreover, 5-FU-upregulated ERCC1 expression was regulated by extracellular signal-regulated kinase (ERK) 1/2 and p38 signaling through activating the transcription factor c-jun/activator protein (AP)-1. Fluorouracil 10-14 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 171-201 30055226-2 2018 We developed a dual-functionalized liposomal delivery system, conjugating cell penetrating peptide penetratin to transferrin-liposomes (Tf-Pen-conjugated liposomes) to enhance the transport of an anticancer chemotherapeutic drug, 5-fluorouracil (5-FU), across the blood-brain barrier into the tumor cells. Fluorouracil 230-244 transferrin Mus musculus 113-124 30055226-2 2018 We developed a dual-functionalized liposomal delivery system, conjugating cell penetrating peptide penetratin to transferrin-liposomes (Tf-Pen-conjugated liposomes) to enhance the transport of an anticancer chemotherapeutic drug, 5-fluorouracil (5-FU), across the blood-brain barrier into the tumor cells. Fluorouracil 246-250 transferrin Mus musculus 113-124 29958141-15 2018 GSH or NAC treatment partly abolished the synergistic effects of oridonin and 5-FU on cell death. Fluorouracil 78-82 X-linked Kx blood group Homo sapiens 7-10 34336653-0 2021 Targeting Thymidylate Synthase Enhances the Chemosensitivity of Triple-Negative Breast Cancer Towards 5-FU-Based Combinatorial Therapy. Fluorouracil 102-106 thymidylate synthase Mus musculus 10-30 34336653-5 2021 We authenticated the pivotal role of thymidylate synthase (TS) in regulating the 5-FU-curcumin synergism using the TNBC pre-clinical model. Fluorouracil 81-85 thymidylate synthase Mus musculus 37-57 29769267-10 2018 Thus, the detection of rare DPYD variants might facilitate severe adverse effect prediction of 5-FU-based chemotherapy in the Japanese population. Fluorouracil 95-99 dihydropyrimidine dehydrogenase Homo sapiens 28-32 29976242-8 2018 Furthermore, downregulating DDIT4 in GC cells inhibited proliferation both in vitro and in vivo and increased 5-fluorouracil-induced apoptosis and cell cycle arrest. Fluorouracil 110-124 DNA damage inducible transcript 4 Homo sapiens 28-33 34295832-7 2021 After infection, TSf-ISPA-vaccinated and 5FU-treated mice showed a marked increase of the CD8 response, which included an increased expression of CD107a and CD44 markers in CD8+ cultured splenocytes. Fluorouracil 41-44 lysosomal-associated membrane protein 1 Mus musculus 146-152 34276810-2 2021 Genetic mutations in two major metabolizing enzymes for 5-FU; dihydropyrimidine dehydrogenase (DPYD and thymidylate synthetase (TYMS), have been associated with clinical response and toxicity. Fluorouracil 56-60 dihydropyrimidine dehydrogenase Homo sapiens 95-99 34276810-14 2021 Conclusions: Molecular testing for DPYD and TYMS genes can allow us to identify patients who are most likely to respond or face severe toxicity to 5-FU in a potentially curable cancer. Fluorouracil 147-151 dihydropyrimidine dehydrogenase Homo sapiens 35-39 31149530-2 2018 Dihydropyrimidine dehydrogenase (DPD) is an enzyme encoded by the DPYD gene, which is responsible for the rate-limiting step in pyrimidine catabolism and breaks down more than 80% of standard doses of 5-fluorouracil (5-FU) and capecitabine, an oral prodrug of 5-FU. Fluorouracil 201-215 dihydropyrimidine dehydrogenase Homo sapiens 0-31 31149530-2 2018 Dihydropyrimidine dehydrogenase (DPD) is an enzyme encoded by the DPYD gene, which is responsible for the rate-limiting step in pyrimidine catabolism and breaks down more than 80% of standard doses of 5-fluorouracil (5-FU) and capecitabine, an oral prodrug of 5-FU. Fluorouracil 201-215 dihydropyrimidine dehydrogenase Homo sapiens 33-36 31149530-2 2018 Dihydropyrimidine dehydrogenase (DPD) is an enzyme encoded by the DPYD gene, which is responsible for the rate-limiting step in pyrimidine catabolism and breaks down more than 80% of standard doses of 5-fluorouracil (5-FU) and capecitabine, an oral prodrug of 5-FU. Fluorouracil 201-215 dihydropyrimidine dehydrogenase Homo sapiens 66-70 31149530-2 2018 Dihydropyrimidine dehydrogenase (DPD) is an enzyme encoded by the DPYD gene, which is responsible for the rate-limiting step in pyrimidine catabolism and breaks down more than 80% of standard doses of 5-fluorouracil (5-FU) and capecitabine, an oral prodrug of 5-FU. Fluorouracil 217-221 dihydropyrimidine dehydrogenase Homo sapiens 0-31 31149530-2 2018 Dihydropyrimidine dehydrogenase (DPD) is an enzyme encoded by the DPYD gene, which is responsible for the rate-limiting step in pyrimidine catabolism and breaks down more than 80% of standard doses of 5-fluorouracil (5-FU) and capecitabine, an oral prodrug of 5-FU. Fluorouracil 217-221 dihydropyrimidine dehydrogenase Homo sapiens 33-36 31149530-2 2018 Dihydropyrimidine dehydrogenase (DPD) is an enzyme encoded by the DPYD gene, which is responsible for the rate-limiting step in pyrimidine catabolism and breaks down more than 80% of standard doses of 5-fluorouracil (5-FU) and capecitabine, an oral prodrug of 5-FU. Fluorouracil 217-221 dihydropyrimidine dehydrogenase Homo sapiens 66-70 31149530-2 2018 Dihydropyrimidine dehydrogenase (DPD) is an enzyme encoded by the DPYD gene, which is responsible for the rate-limiting step in pyrimidine catabolism and breaks down more than 80% of standard doses of 5-fluorouracil (5-FU) and capecitabine, an oral prodrug of 5-FU. Fluorouracil 260-264 dihydropyrimidine dehydrogenase Homo sapiens 0-31 31149530-2 2018 Dihydropyrimidine dehydrogenase (DPD) is an enzyme encoded by the DPYD gene, which is responsible for the rate-limiting step in pyrimidine catabolism and breaks down more than 80% of standard doses of 5-fluorouracil (5-FU) and capecitabine, an oral prodrug of 5-FU. Fluorouracil 260-264 dihydropyrimidine dehydrogenase Homo sapiens 33-36 31149530-2 2018 Dihydropyrimidine dehydrogenase (DPD) is an enzyme encoded by the DPYD gene, which is responsible for the rate-limiting step in pyrimidine catabolism and breaks down more than 80% of standard doses of 5-fluorouracil (5-FU) and capecitabine, an oral prodrug of 5-FU. Fluorouracil 260-264 dihydropyrimidine dehydrogenase Homo sapiens 66-70 29218650-5 2018 In vitro antitumor activity assay proved that LEP-2a could significantly enhance the inhibitory effectiveness of 5-FU on Hela cells at the concentrations of 100, 200, 300, and 400 mug/mL. Fluorouracil 113-117 late cornified envelope 1B Homo sapiens 46-51 34203267-15 2021 Overexpression of IGF2BP1 promoted the colony-forming capacity and 5-fluorouracil and etoposide resistance in CRC cells. Fluorouracil 67-81 insulin like growth factor 2 mRNA binding protein 1 Homo sapiens 18-25 34257696-12 2021 The numbers of TUNEL+ cells and the expression of Bax and caspase-3 proteins were significantly increased in the 5-FU + ETSJC groups when compared with the 5-FU group. Fluorouracil 113-117 BCL2-associated X protein Mus musculus 50-53 34257696-12 2021 The numbers of TUNEL+ cells and the expression of Bax and caspase-3 proteins were significantly increased in the 5-FU + ETSJC groups when compared with the 5-FU group. Fluorouracil 113-117 caspase 3 Mus musculus 58-67 34257696-12 2021 The numbers of TUNEL+ cells and the expression of Bax and caspase-3 proteins were significantly increased in the 5-FU + ETSJC groups when compared with the 5-FU group. Fluorouracil 156-160 BCL2-associated X protein Mus musculus 50-53 34257696-12 2021 The numbers of TUNEL+ cells and the expression of Bax and caspase-3 proteins were significantly increased in the 5-FU + ETSJC groups when compared with the 5-FU group. Fluorouracil 156-160 caspase 3 Mus musculus 58-67 34094932-0 2021 HOXA13, Negatively Regulated by miR-139-5p, Decreases the Sensitivity of Gastric Cancer to 5-Fluorouracil Possibly by Targeting ABCC4. Fluorouracil 91-105 ATP binding cassette subfamily C member 4 Homo sapiens 128-133 34094932-12 2021 Mechanistically, HOXA13, directly targeted by miR-139-5p in GC, might upregulate ABCC4 expression, thereby accentuating 5-FU resistance of GC cells. Fluorouracil 120-124 ATP binding cassette subfamily C member 4 Homo sapiens 81-86 34094932-13 2021 Conclusion: Our study suggests that HOXA13 attenuates 5-FU sensitivity of GC possibly by upregulating ABCC4. Fluorouracil 54-58 ATP binding cassette subfamily C member 4 Homo sapiens 102-107 29596542-13 2018 Finally, TS identified 8 patients with germline DPYD mutations that confer toxicity to fluorouracil chemotherapy, which could also be useful for treatment selection. Fluorouracil 87-99 dihydropyrimidine dehydrogenase Homo sapiens 48-52 34069161-4 2021 The occurrence of missense mutations in DPD protein within the general population, including those of African descent, has adverse toxicity effects due to altered 5-FU metabolism. Fluorouracil 163-167 dihydropyrimidine dehydrogenase Homo sapiens 40-43 34981469-9 2021 The expression levels of all tested genes were altered in all treatment groups compared to the control, with that of WNT1, CTNNB1, TCF, MTOR, AKT1, BIRC5, and CCND1 showing the most robust changes in the combined curcumin/berberine/5-FU treatment. Fluorouracil 232-236 baculoviral IAP repeat containing 5 Homo sapiens 148-153 35276696-3 2022 However, the role of circSAMD4A in 5-fluorouracil (5-Fu) resistance of CRC is yet to be clarified. Fluorouracil 35-49 sterile alpha motif domain containing 4A Homo sapiens 21-31 35276696-3 2022 However, the role of circSAMD4A in 5-fluorouracil (5-Fu) resistance of CRC is yet to be clarified. Fluorouracil 51-55 sterile alpha motif domain containing 4A Homo sapiens 21-31 35276696-4 2022 This study is designed to investigate the function of circSAMD4A in 5-Fu resistance of CRC and its potential molecular mechanism. Fluorouracil 68-72 sterile alpha motif domain containing 4A Homo sapiens 54-64 35276696-8 2022 Xenograft tumor model was established to confirm the biological role of circSAMD4A in 5-Fu resistance of CRC in vivo. Fluorouracil 86-90 sterile alpha motif domain containing 4A Homo sapiens 72-82 35276696-9 2022 CircSAMD4A was upregulated in 5-Fu-resistant CRC tissues and cells. Fluorouracil 30-34 sterile alpha motif domain containing 4A Homo sapiens 0-10 35276696-10 2022 Functionally, circSAMD4A knockdown inhibited the proliferation and glycolysis mechanism but promoted apoptosis in 5-Fu-resistant cells of CRC. Fluorouracil 114-118 sterile alpha motif domain containing 4A Homo sapiens 14-24 35276696-12 2022 Mechanistically, circSAMD4A knockdown-induced 5-Fu sensitivity was mediated by miR-545-3p/PFKFB3 axis. Fluorouracil 46-50 sterile alpha motif domain containing 4A Homo sapiens 17-27 35276696-13 2022 Moreover, circSAMD4A knockdown improved 5-Fu sensitivity of CRC in vivo. Fluorouracil 40-44 sterile alpha motif domain containing 4A Homo sapiens 10-20 35276696-14 2022 CircSAMD4A contributed to 5-Fu resistance of CRC cells partly through upregulating PFKFB3 expression by sponging miR-545-3p, providing a possible circRNA-targeted therapy for CRC. Fluorouracil 26-30 sterile alpha motif domain containing 4A Homo sapiens 0-10 35609368-8 2022 In addition, C3G alone or combined with 5-FU affected the expression of the tumor microenvironment-related factors Ki67, CD45, PDL1, and CD73. Fluorouracil 40-44 antigen identified by monoclonal antibody Ki 67 Mus musculus 115-119 35421356-0 2022 FAM98A promotes resistance to 5-fluorouracil in colorectal cancer by suppressing ferroptosis. Fluorouracil 30-44 family with sequence similarity 98 member A Homo sapiens 0-6 35421356-9 2022 Furthermore, we identified that metformin could reverse FAM98A-mediated 5-FU resistance in CRC cells. Fluorouracil 72-76 family with sequence similarity 98 member A Homo sapiens 56-62 35624466-16 2022 AP4-deficiency also sensitized CRC cells to 5-FU treatment, whereas ectopic AP4 conferred resistance to 5-FU in a miR-22-3p and MDC1-dependent manner. Fluorouracil 104-108 transcription factor AP4 Mus musculus 76-79 35624466-17 2022 CONCLUSIONS: In summary, AP4, miR-22-3p and MDC1 form a conserved and coherent, regulatory feed-forward loop to promote DNA repair, which suppresses DNA damage, senescence and CIN, and contributes to 5-FU resistance. Fluorouracil 200-204 transcription factor AP4 Mus musculus 25-28 35577773-13 2022 Our results indicate that the SFMBT1/HMG20A axis could be targeted to increase the resistance of CRC cells to 5-FU. Fluorouracil 110-114 high mobility group 20A Homo sapiens 37-43 35634282-9 2022 The combination of 5-FU with ICB augmented an inflammatory tumor microenvironment with markedly increased CD8+ T cell activation and upregulation of IFNgamma, TNFalpha and IL-1beta signaling. Fluorouracil 19-23 CD8a molecule Homo sapiens 106-109 35634282-10 2022 The effective anti-tumor immune response of 5-FU chemo-immunotherapy was dependent on CD8+ T cells but was unaffected when TNFalpha or IL-1beta cytokine signaling pathways were blocked. Fluorouracil 44-48 CD8a molecule Homo sapiens 86-89 29436749-0 2018 HOXA13 contributes to gastric carcinogenesis through DHRS2 interacting with MDM2 and confers 5-FU resistance by a p53-dependent pathway. Fluorouracil 93-97 dehydrogenase/reductase 2 Homo sapiens 53-58 35367196-0 2022 Synergistic antitumor activity of 5-fluorouracil and atosiban against microsatellite stable colorectal cancer through restoring GATA3. Fluorouracil 34-48 GATA binding protein 3 Homo sapiens 128-133 29738539-6 2018 We found that HMS1, LOG1 (YJL055W), HAM1, and ATR1 confer resistance to both 5-FU and HAP, whereas ADE4, DUT1 and APT2 are specific for HAP resistance, and CPA1 and CPA2 specific for 5-FU resistance. Fluorouracil 77-81 Hms1p Saccharomyces cerevisiae S288C 14-18 29739434-0 2018 Gastric cancer vaccines synthesized using a TLR7 agonist and their synergistic antitumor effects with 5-fluorouracil. Fluorouracil 102-116 toll-like receptor 7 Mus musculus 44-48 29573568-4 2018 Experimental setting include MTT assay, Annexin V/Pi method, and colony assay to assess whether silencing of LMW-PTP improves the sensitivity of A375 to dacarbazine, 5-FU, and radiotherapy. Fluorouracil 166-170 acid phosphatase 1 Homo sapiens 109-116 29573568-8 2018 We found that LMW-PTP silencing improves the effectiveness of dacarbazine, 5-FU, and radiotherapy. Fluorouracil 75-79 acid phosphatase 1 Homo sapiens 14-21 35264465-0 2022 Urushiol V Suppresses Cell Proliferation and Enhances Antitumor Activity of 5-FU in Human Colon Cancer Cells by Downregulating FoxM1. Fluorouracil 76-80 forkhead box M1 Homo sapiens 127-132 35264465-4 2022 Recent data show that FoxM1 is associated with 5-FU resistance in CRC. Fluorouracil 47-51 forkhead box M1 Homo sapiens 22-27 35264465-11 2022 The combination treatment reduced FoxM1 expression and consequently reduced cell growth and colony formation in 5-FU resistant colon cancer cells (SW480/5-FUR). Fluorouracil 112-116 forkhead box M1 Homo sapiens 34-39 29512733-8 2018 Additionally, inhibition of autophagy by either 3-MA or beclin-1 ablation increased 5-FU-induced cell death in BGC-823 cells. Fluorouracil 84-88 beclin 1 Homo sapiens 56-64 29849804-8 2018 Additionally, bufalin combined with 5-FU reduced the expression levels of anti-apoptotic proteins, such as Mcl-1, XIAP and Bcl-2 and upregulated the levels of the pro-apoptotic proteins, Bax and Bad. Fluorouracil 36-40 X-linked inhibitor of apoptosis Homo sapiens 114-118 29352327-11 2018 In addition, immunofluorescence analysis showed increased expression of active cofilin, LIMK1, LIMK2, and SSH1 in HT29 colon cancer cells resistant to 5-fluorouracil compared to parental HT29 cells. Fluorouracil 151-165 LIM domain kinase 2 Homo sapiens 95-100 35473510-7 2022 CONCLUSION: Upfront testing of DPYD variants appears to reduce the toxicity burden of Capecitabine and 5-FU in cancer patients and can lead to substantial hospital cost savings, only if the dose management of the drugs in response to variants detected is standardised and regulated. Fluorouracil 103-107 dihydropyrimidine dehydrogenase Homo sapiens 31-35 29541216-9 2018 BRAF V600E and beta-catenin T41A double mutations were identified in one cell line, and were associated with a lack of response to 5-fluorouracil, oxaliplatin and cetuximab treatment. Fluorouracil 131-145 catenin (cadherin associated protein), beta 1 Mus musculus 15-27 29872564-7 2018 Besides, in patients with TNM stage II/III disease, the rate of overall survival was higher among patients with CCL22-positive tumors who were treated with 5-fluorouracil based adjuvant chemotherapy than that among those who were not (P = 0.012, P < 0.001 and P < 0.001, in discovery, validation and combined data set). Fluorouracil 156-170 teneurin transmembrane protein 1 Homo sapiens 26-29 29535520-8 2018 Furthermore, inhibition of miR-155 by MSNs-anti-miR-155@PDA-Apt can enhance the sensitivity of SW480 to 5-fluorouracil chemotherapy. Fluorouracil 104-118 microRNA 155 Homo sapiens 27-34 29535520-8 2018 Furthermore, inhibition of miR-155 by MSNs-anti-miR-155@PDA-Apt can enhance the sensitivity of SW480 to 5-fluorouracil chemotherapy. Fluorouracil 104-118 microRNA 155 Homo sapiens 48-55 30359298-0 2018 The new 6q27 tumor suppressor DACT2, frequently silenced by CpG methylation, sensitizes nasopharyngeal cancer cells to paclitaxel and 5-FU toxicity via beta-catenin/Cdc25c signaling and G2/M arrest. Fluorouracil 134-138 dishevelled binding antagonist of beta catenin 2 Homo sapiens 30-35 30359298-14 2018 DACT2 expression also induced G2/M arrest in NPC cells through directly suppressing beta-catenin/Cdc25c signaling, which sensitized NPC cells to paclitaxel and 5-FU, but not cisplatin. Fluorouracil 160-164 dishevelled binding antagonist of beta catenin 2 Homo sapiens 0-5 29152729-1 2018 The purpose of this guideline is to provide information for the interpretation of clinical dihydropyrimidine dehydrogenase (DPYD) genotype tests so that the results can be used to guide dosing of fluoropyrimidines (5-fluorouracil and capecitabine). Fluorouracil 215-229 dihydropyrimidine dehydrogenase Homo sapiens 91-122 35460066-10 2022 Oral 5-FU followed by eribulin had a numerically longer OS1 (2.84 years) than the other sequences. Fluorouracil 5-9 frizzled related protein Homo sapiens 56-59 35422067-0 2022 SNORD1C maintains stemness and 5-FU resistance by activation of Wnt signaling pathway in colorectal cancer. Fluorouracil 31-35 small nucleolar RNA, C/D box 1C Homo sapiens 0-7 35462906-11 2022 Conclusion: Dormant CRC is associated with high glutamine metabolism and synergizes with CAFs in 5-FU resistance, and the key effectors are LMOD1, MAB21L2, and ASPN. Fluorouracil 97-101 mab-21 like 2 Homo sapiens 147-154 35133490-0 2022 Somatic nuclear auto-antigenic sperm protein sensitizes human breast cancer cells to 5-Fluorouracil. Fluorouracil 85-99 nuclear autoantigenic sperm protein Homo sapiens 8-44 35133490-1 2022 PURPOSE: To assess the potential role of nuclear auto-antigenic sperm protein (NASP) in the cellular sensitivity to 5-Fluorouracil (5-FU) in breast cancer cells. Fluorouracil 116-130 nuclear autoantigenic sperm protein Homo sapiens 41-77 35133490-1 2022 PURPOSE: To assess the potential role of nuclear auto-antigenic sperm protein (NASP) in the cellular sensitivity to 5-Fluorouracil (5-FU) in breast cancer cells. Fluorouracil 116-130 nuclear autoantigenic sperm protein Homo sapiens 79-83 35133490-1 2022 PURPOSE: To assess the potential role of nuclear auto-antigenic sperm protein (NASP) in the cellular sensitivity to 5-Fluorouracil (5-FU) in breast cancer cells. Fluorouracil 132-136 nuclear autoantigenic sperm protein Homo sapiens 41-77 35133490-1 2022 PURPOSE: To assess the potential role of nuclear auto-antigenic sperm protein (NASP) in the cellular sensitivity to 5-Fluorouracil (5-FU) in breast cancer cells. Fluorouracil 132-136 nuclear autoantigenic sperm protein Homo sapiens 79-83 35133490-2 2022 METHODS: The expression of two NASP isotypes, namely somatic NASP (sNASP) and testis NASP (tNASP) in breast cancer lines were detected under 5-FU treatment using real-time polymerase chain reaction and western blot assays. Fluorouracil 141-145 nuclear autoantigenic sperm protein Homo sapiens 31-35 35133490-2 2022 METHODS: The expression of two NASP isotypes, namely somatic NASP (sNASP) and testis NASP (tNASP) in breast cancer lines were detected under 5-FU treatment using real-time polymerase chain reaction and western blot assays. Fluorouracil 141-145 nuclear autoantigenic sperm protein Homo sapiens 61-65 35133490-2 2022 METHODS: The expression of two NASP isotypes, namely somatic NASP (sNASP) and testis NASP (tNASP) in breast cancer lines were detected under 5-FU treatment using real-time polymerase chain reaction and western blot assays. Fluorouracil 141-145 nuclear autoantigenic sperm protein Homo sapiens 85-89 35133490-3 2022 NASP effect on cellular viability and apoptosis under 5-FU treatment were evaluated. Fluorouracil 54-58 nuclear autoantigenic sperm protein Homo sapiens 0-4 35190308-7 2022 We further found that bile acid mixture (BA mix) could inhibit hOAT2-mediated uptake of cGMP, 5-fluorouracil, irinotecan and paclitaxel. Fluorouracil 94-108 solute carrier family 22 member 7 Homo sapiens 63-68 35353612-6 2022 We found that a higher level of IL-10 secreted by Kyn-induced Tregs was responsible for the 5-fluorouracil-induced resistance of gastric cancer cell lines. Fluorouracil 92-106 interleukin 10 Homo sapiens 32-37 35092904-0 2022 Long non-coding RNA HNF1A-AS1 induces 5-FU resistance of gastric cancer through miR-30b-5p/EIF5A2 pathway. Fluorouracil 38-42 eukaryotic translation initiation factor 5A2 Mus musculus 91-97 35092904-13 2022 CONCLUSIONS: The findings from the current study showed HNF1A-AS1 promoted 5-FU resistance by acting as a ceRNA of miR-30b-5p and promoting EIF5A2-induced EMT process in GC. Fluorouracil 75-79 eukaryotic translation initiation factor 5A2 Mus musculus 140-146 35448163-7 2022 Furthermore, a few lncRNAs, such as AFAP1-AS1 and LINC01014, block the efficiency of chemotherapeutic drugs, including cisplatin, 5-fluorouracil, paclitaxel, and gefitinib, used for ESCC treatment. Fluorouracil 130-144 actin filament associated protein 1 Homo sapiens 36-41 29152729-1 2018 The purpose of this guideline is to provide information for the interpretation of clinical dihydropyrimidine dehydrogenase (DPYD) genotype tests so that the results can be used to guide dosing of fluoropyrimidines (5-fluorouracil and capecitabine). Fluorouracil 215-229 dihydropyrimidine dehydrogenase Homo sapiens 124-128 35408903-9 2022 Taken together, our data suggest that kaempferol may play an important role in overcoming resistance to 5-Fu therapy by regulating the miR-326-hnRNPA1/A2/PTBP1-PKM2 axis. Fluorouracil 104-108 polypyrimidine tract binding protein 1 Homo sapiens 154-159 29239269-1 2018 AIM: Adverse drug reactions to 5-Fluorouracil(5-FU) is frequent and largely attributable to genetic variations in the DPYD gene, a rate limiting enzyme that clears 5-FU. Fluorouracil 31-45 dihydropyrimidine dehydrogenase Homo sapiens 118-122 29239269-1 2018 AIM: Adverse drug reactions to 5-Fluorouracil(5-FU) is frequent and largely attributable to genetic variations in the DPYD gene, a rate limiting enzyme that clears 5-FU. Fluorouracil 46-50 dihydropyrimidine dehydrogenase Homo sapiens 118-122 29239269-1 2018 AIM: Adverse drug reactions to 5-Fluorouracil(5-FU) is frequent and largely attributable to genetic variations in the DPYD gene, a rate limiting enzyme that clears 5-FU. Fluorouracil 164-168 dihydropyrimidine dehydrogenase Homo sapiens 118-122 29239269-6 2018 CONCLUSIONS: This is the first and largest genetic map the DPYD variants associated with adverse drug reaction to 5-FU in south Asian population. Fluorouracil 114-118 dihydropyrimidine dehydrogenase Homo sapiens 59-63 29468888-4 2018 We used the double emulsion method (water/oil/water) to prepare 5FU-encapsulated Fe3O4 magnetic nanoparticles modified with PCL-PEG-PCL copolymer. Fluorouracil 64-67 PHD finger protein 1 Homo sapiens 124-127 29468888-4 2018 We used the double emulsion method (water/oil/water) to prepare 5FU-encapsulated Fe3O4 magnetic nanoparticles modified with PCL-PEG-PCL copolymer. Fluorouracil 64-67 PHD finger protein 1 Homo sapiens 132-135 29134491-0 2018 DPYD*2A and MTHFR C677T predict toxicity and efficacy, respectively, in patients on chemotherapy with 5-fluorouracil for colorectal cancer. Fluorouracil 102-116 dihydropyrimidine dehydrogenase Homo sapiens 0-4 35306539-2 2022 Patients carrying Dihydropyrimidine Dehydrogenase (DPYD) variant alleles associated with decreased enzymatic function are at a greater risk of early/severe 5-fluorouracil/capecitabine toxicity. Fluorouracil 156-170 dihydropyrimidine dehydrogenase Homo sapiens 18-49 35306539-2 2022 Patients carrying Dihydropyrimidine Dehydrogenase (DPYD) variant alleles associated with decreased enzymatic function are at a greater risk of early/severe 5-fluorouracil/capecitabine toxicity. Fluorouracil 156-170 dihydropyrimidine dehydrogenase Homo sapiens 51-55 29134491-0 2018 DPYD*2A and MTHFR C677T predict toxicity and efficacy, respectively, in patients on chemotherapy with 5-fluorouracil for colorectal cancer. Fluorouracil 102-116 methylenetetrahydrofolate reductase Homo sapiens 12-17 29134491-6 2018 RESULTS: Multivariate analyses showed that DPYD*2A polymorphism was a predictive factor (P = 0.023) for grade 3 and grade 4 5-fluorouracil-related toxicities. Fluorouracil 124-138 dihydropyrimidine dehydrogenase Homo sapiens 43-47 29134491-7 2018 Although MTHFR C677T polymorphism might act as forecasters for grade 3 or grade 4 neutropenia, diarrhea, and mucositis, this polymorphism was found to increase significantly (P = 0.006) the response of 5-FU. Fluorouracil 202-206 methylenetetrahydrofolate reductase Homo sapiens 9-14 29134491-8 2018 CONCLUSION: DPYD*2A and MTHFR C677T polymorphisms could explain 5-FU toxicity or clinical outcome in Bangladeshi colorectal patients. Fluorouracil 64-68 dihydropyrimidine dehydrogenase Homo sapiens 12-16 29134491-8 2018 CONCLUSION: DPYD*2A and MTHFR C677T polymorphisms could explain 5-FU toxicity or clinical outcome in Bangladeshi colorectal patients. Fluorouracil 64-68 methylenetetrahydrofolate reductase Homo sapiens 24-29 29694984-0 2018 Camel Milk Ameliorates 5-Fluorouracil-Induced Renal Injury in Rats: Targeting MAPKs, NF-kappaB and PI3K/Akt/eNOS Pathways. Fluorouracil 23-37 nitric oxide synthase 3 Rattus norvegicus 108-112 29694984-8 2018 RESULTS: CM lowered 5-FU-triggered increase of creatinine, BUN, Kim-1 and NGAL renal injury biomarkers and attenuated the histopathological aberrations. Fluorouracil 20-24 hepatitis A virus cellular receptor 1 Homo sapiens 64-69 29364475-8 2018 The IC50 (inhibitory concentration 50) by 5-Fu and MMC was significantly higher in FPRL2 positive cells than those negative cells. Fluorouracil 42-46 formyl peptide receptor 3 Homo sapiens 83-88 30518710-0 2018 5-Fluorouracil inhibits neural differentiation via Mfn1/2 reduction in human induced pluripotent stem cells. Fluorouracil 0-14 mitofusin 1 Homo sapiens 51-57 30518710-5 2018 5-FU exposure reduced the expression of several neural differentiation marker genes, such as OTX2, in iPSCs. Fluorouracil 0-4 orthodenticle homeobox 2 Homo sapiens 93-97 30518710-9 2018 We found that 5-FU induced mitochondrial fragmentation and reduced the level of mitochondrial fusion proteins, mitofusin 1 and 2 (Mfn1/2). Fluorouracil 14-18 mitofusin 1 Homo sapiens 111-128 30518710-9 2018 We found that 5-FU induced mitochondrial fragmentation and reduced the level of mitochondrial fusion proteins, mitofusin 1 and 2 (Mfn1/2). Fluorouracil 14-18 mitofusin 1 Homo sapiens 130-136 27871087-0 2018 The HDM2 (MDM2) Inhibitor NVP-CGM097 Inhibits Tumor Cell Proliferation and Shows Additive Effects with 5-Fluorouracil on the p53-p21-Rb-E2F1 Cascade in the p53wild type Neuroendocrine Tumor Cell Line GOT1. Fluorouracil 103-117 MDM2 proto-oncogene Homo sapiens 4-8 27871087-0 2018 The HDM2 (MDM2) Inhibitor NVP-CGM097 Inhibits Tumor Cell Proliferation and Shows Additive Effects with 5-Fluorouracil on the p53-p21-Rb-E2F1 Cascade in the p53wild type Neuroendocrine Tumor Cell Line GOT1. Fluorouracil 103-117 MDM2 proto-oncogene Homo sapiens 10-14 29526981-7 2018 The level of DPD protein, which metabolizes 5-fluorouracil (FU), was very low (2.83U/mg). Fluorouracil 44-58 dihydropyrimidine dehydrogenase Homo sapiens 13-16 35445157-0 2022 Synergistic combination of PMBA and 5-fluorouracil (5-FU) in targeting mutant KRAS in 2D and 3D colorectal cancer cells. Fluorouracil 36-50 KRAS proto-oncogene, GTPase Homo sapiens 78-82 35445157-0 2022 Synergistic combination of PMBA and 5-fluorouracil (5-FU) in targeting mutant KRAS in 2D and 3D colorectal cancer cells. Fluorouracil 52-56 KRAS proto-oncogene, GTPase Homo sapiens 78-82 35445157-2 2022 The study has been conducted to investigate the effect and efficacy of 2-pyridin-4-yl methylene beta-boswellic acid (PMBA) and 5-Flourouracil (5-FU) in combination therapy for the treatment of KRAS mutant colon cancer. Fluorouracil 143-147 KRAS proto-oncogene, GTPase Homo sapiens 193-197 35445157-6 2022 When examined for plasma level of PMBA (20 mg) and PMBA+5-FU (20 + 40 mg), a time-dependent increase in the level of the drug (5-FU) was detected, indicating its absorption and bioavailability with excellent half-life of the PMBA for both routes of administration (IV and Oral), thereby indicating a new adjuvant therapy for KRAS mutant colon cancer. Fluorouracil 56-60 KRAS proto-oncogene, GTPase Homo sapiens 325-329 35445157-6 2022 When examined for plasma level of PMBA (20 mg) and PMBA+5-FU (20 + 40 mg), a time-dependent increase in the level of the drug (5-FU) was detected, indicating its absorption and bioavailability with excellent half-life of the PMBA for both routes of administration (IV and Oral), thereby indicating a new adjuvant therapy for KRAS mutant colon cancer. Fluorouracil 127-131 KRAS proto-oncogene, GTPase Homo sapiens 325-329 35067736-8 2022 Correlation analysis results revealed a significant correlation between 5-FU AUC, 5-FUH2 and FABL plasma concentration and adverse reactions, 5-FU AUC and clinical efficacy. Fluorouracil 72-76 EGFR long non-coding downstream RNA Homo sapiens 93-97 35232776-13 2022 Finally, we demonstrated that terbinafine, a SQLE inhibitor, could be repurposed for CRC by synergising with oxaliplatin and 5-fluorouracil to inhibit CRC growth. Fluorouracil 125-139 squalene epoxidase Mus musculus 45-49 35215344-0 2022 Xanthine Oxidase Inhibitor, Febuxostat Is Effective against 5-Fluorouracil-Induced Parotid Salivary Gland Injury in Rats Via Inhibition of Oxidative Stress, Inflammation and Targeting TRPC1/CHOP Signalling Pathway. Fluorouracil 60-74 transient receptor potential cation channel, subfamily C, member 1 Rattus norvegicus 184-189 35215344-12 2022 In conclusion, FEB pre-treatment reduced 5-FU-induced parotid salivary gland damage not only through its powerful anti-inflammatory and antioxidant effects, but also through its effect on the TRPC1/CHOP signalling pathway. Fluorouracil 41-45 transient receptor potential cation channel, subfamily C, member 1 Rattus norvegicus 192-197 35200545-1 2022 Background: 5-FU-based chemoradiotherapy (CRT) could be associated with severe treatment-related toxicities in patients harboring at-risk DPYD polymorphisms. Fluorouracil 12-16 dihydropyrimidine dehydrogenase Homo sapiens 138-142 35200545-11 2022 Upfront DPYD genotyping can identify patients in whom 5-FU-related toxicity should be avoided. Fluorouracil 54-58 dihydropyrimidine dehydrogenase Homo sapiens 8-12 35046388-7 2022 Increased SPOCK1 induced by miR-135b overexpression promoted the Warburg effect and consequently antitumour effect of 5-fluorouracil. Fluorouracil 118-132 SPARC (osteonectin), cwcv and kazal like domains proteoglycan 1 Homo sapiens 10-16 35046388-7 2022 Increased SPOCK1 induced by miR-135b overexpression promoted the Warburg effect and consequently antitumour effect of 5-fluorouracil. Fluorouracil 118-132 microRNA 135b Homo sapiens 28-36 35013311-7 2022 As a result, we find that sustained translation of IGF-1R mRNA, which encodes one of the most potent cell survival effectors, promotes the survival of 5-FU-treated colorectal cancer cells. Fluorouracil 151-155 insulin like growth factor 1 receptor Homo sapiens 51-57 35070952-0 2021 MicroRNA-155-5p Contributes to 5-Fluorouracil Resistance Through Down-Regulating TP53INP1 in Oral Squamous Cell Carcinoma. Fluorouracil 31-45 microRNA 155 Homo sapiens 0-12 35070952-2 2021 Here, in 5-FU-resistant human oral squamous cell carcinoma (OSCC) HSC3 cells (HSC3/5-FU), the levels of 21 miRNA candidates were detected using RT-PCR and miR-155-5p level increased strikingly in HSC3/5-FU cells compared to HSC3 cells. Fluorouracil 9-13 microRNA 155 Homo sapiens 155-162 35070952-2 2021 Here, in 5-FU-resistant human oral squamous cell carcinoma (OSCC) HSC3 cells (HSC3/5-FU), the levels of 21 miRNA candidates were detected using RT-PCR and miR-155-5p level increased strikingly in HSC3/5-FU cells compared to HSC3 cells. Fluorouracil 83-87 microRNA 155 Homo sapiens 155-162 35070952-3 2021 Compared with HSC3 cells, the CCK-8 assay showed that the HSC3/5-FU cells transfected with miR-155-5p inhibitors decreased 5-FU IC50. Fluorouracil 63-67 microRNA 155 Homo sapiens 91-98 35070952-3 2021 Compared with HSC3 cells, the CCK-8 assay showed that the HSC3/5-FU cells transfected with miR-155-5p inhibitors decreased 5-FU IC50. Fluorouracil 123-127 microRNA 155 Homo sapiens 91-98 35070952-4 2021 Ectopic expression of miR-155-5p in HSC3 and HSC4 cells increased 5-FU IC50 (CCK-8 assay), migration (wound-healing and transwell assays) and invasion (transwell assay) abilities. Fluorouracil 66-70 microRNA 155 Homo sapiens 22-29 35070952-8 2021 The enhancement of cell viability (CCK-8 assay), migration (wound-healing and transwell assays) and invasion (transwell assay) by miR-155-5p after 5-FU treatment was reversed by TP53INP1 overexpression. Fluorouracil 147-151 microRNA 155 Homo sapiens 130-137 35103981-11 2022 5-FU suppressed the stemness maintenance of CSCs in PANC-1 cells, as demonstrated by the inhibition of tumorsphere formation, the decrease in CD44+CD133+ cells" fraction, and downregulation of OCT4, Nanog, and SOX2 expression. Fluorouracil 0-4 CD44 molecule (Indian blood group) Homo sapiens 142-146 35103981-11 2022 5-FU suppressed the stemness maintenance of CSCs in PANC-1 cells, as demonstrated by the inhibition of tumorsphere formation, the decrease in CD44+CD133+ cells" fraction, and downregulation of OCT4, Nanog, and SOX2 expression. Fluorouracil 0-4 Nanog homeobox Homo sapiens 199-204 35103981-11 2022 5-FU suppressed the stemness maintenance of CSCs in PANC-1 cells, as demonstrated by the inhibition of tumorsphere formation, the decrease in CD44+CD133+ cells" fraction, and downregulation of OCT4, Nanog, and SOX2 expression. Fluorouracil 0-4 SRY-box transcription factor 2 Homo sapiens 210-214 35145347-4 2022 Additionally, Diac, 5-FU and their combination suppressed colonic content/gene expression of IL-6, its downstream oncogene, Kirsten rat sarcoma viral oncogene homolog (K-Ras), and consequently Notch intracellular domain and nuclear factor-kappa B (NF-kappaB) p65. Fluorouracil 20-24 KRAS proto-oncogene, GTPase Rattus norvegicus 168-173 2573634-10 1989 The 5-FU-sensitive T cell is the only target of Thy-1+CD5+CD4+CD8- suppressor cell. Fluorouracil 4-8 CD5 antigen Mus musculus 54-57 2573634-10 1989 The 5-FU-sensitive T cell is the only target of Thy-1+CD5+CD4+CD8- suppressor cell. Fluorouracil 4-8 CD4 antigen Mus musculus 58-61 2698593-0 1989 Effects of 5-fluorouracil on thymidylate synthase activity and development of bone marrow grafts in spleens of irradiated mice. Fluorouracil 11-25 thymidylate synthase Mus musculus 29-49 2698593-5 1989 The highest thymidylate synthase activity was found in spleens of mice grafted with control bone marrow and next treated with 5-FU. Fluorouracil 126-130 thymidylate synthase Mus musculus 12-32 2698593-7 1989 Thus, 5-FU prevented completely development of bone marrow grafts in spleens but increased thymidylate synthase activity in a paradoxical manner. Fluorouracil 6-10 thymidylate synthase Mus musculus 91-111 2698593-8 1989 Thymidylate synthase in myelopoietic tissue developed from bone marrow, collected in the state of hyperproduction of that enzyme induced with phenylhydrazine and 5-FU, did not show increased resistant to 5-FU. Fluorouracil 162-166 thymidylate synthase Mus musculus 0-20 28051340-0 2018 Altered tolbutamide pharmacokinetics by a decrease in hepatic expression of CYP2C6/11 in rats pretreated with 5-fluorouracil. Fluorouracil 110-124 cytochrome P450, family 2, subfamily C, polypeptide 6, variant 1 Rattus norvegicus 76-82 29487697-1 2018 Our study addresses the issue of the clinical reliability of three candidate DPYD and one UGT single nucleotide polymorphisms in predicting 5-fluorouracil- and irinotecan-related adverse events. Fluorouracil 140-154 dihydropyrimidine dehydrogenase Homo sapiens 77-81 29487697-5 2018 Present results support the preemptive screening of mentioned DPYD and UGT1A1 variants to identify patients at risk of clinically relevant 5-fluoruracil- and irinotecan-related AEs, in order to improve treatments" safety through a "genotype-guided" approach. Fluorouracil 139-152 dihydropyrimidine dehydrogenase Homo sapiens 62-66 29487697-5 2018 Present results support the preemptive screening of mentioned DPYD and UGT1A1 variants to identify patients at risk of clinically relevant 5-fluoruracil- and irinotecan-related AEs, in order to improve treatments" safety through a "genotype-guided" approach. Fluorouracil 139-152 UDP glucuronosyltransferase family 1 member A1 Homo sapiens 71-77 29373881-0 2017 The Impact of Thymidylate Synthase and Methylenetetrahydrofolate Reductase Genotypes on Sensitivity to 5-Fluorouracil Treatment in Colorectal Cancer Cells. Fluorouracil 103-117 methylenetetrahydrofolate reductase Homo sapiens 39-74 29373881-2 2017 Given the known relationship between thymidylate synthase (TS) and methylenetetrahydrofolate reductase (MTHFR) activity and 5-FU metabolism, this study investigated the impact of selected functional polymorphisms of the TS and MTHFR genes on chemotherapy resistance in 5 human CRC cell lines. Fluorouracil 124-128 methylenetetrahydrofolate reductase Homo sapiens 104-109 29373881-9 2017 HT29/219 and SW1116 cells with homozygous TS 6-bp ins/ins and heterozygous MTHFR 677 C/T and 1298 A/C genotypes had intermediate 5-FU sensitivity. Fluorouracil 129-133 methylenetetrahydrofolate reductase Homo sapiens 75-80 29373881-10 2017 The results indicate that TS 3 -UTR 6-bp insertion and MTHFR 677T and 1298C alleles increase 5-FU resistance in CRC cells. Fluorouracil 93-97 methylenetetrahydrofolate reductase Homo sapiens 55-60 29045513-7 2017 Patient safety of fluoropyrimidine treatment can be significantly improved by pre-emptive screening for DPYD genotype variants and dose reductions in heterozygous DPYD variant allele carriers, thereby normalizing 5-FU exposure. Fluorouracil 213-217 dihydropyrimidine dehydrogenase Homo sapiens 163-167 29045513-8 2017 Based on the critical appraisal of currently available data, adjusting the labels of capecitabine and 5-FU by including recommendations on pre-emptive screening for DPYD variants and DPYD genotype-guided dose adjustments should be the new standard of care. Fluorouracil 102-106 dihydropyrimidine dehydrogenase Homo sapiens 183-187 29039607-3 2017 Upregulation of miR-874-3p attenuated the chemoresistance of CRC cells to 5-fluorouracil (5-FU) in vitro and in vivo. Fluorouracil 74-88 microRNA 874 Homo sapiens 16-23 29039607-3 2017 Upregulation of miR-874-3p attenuated the chemoresistance of CRC cells to 5-fluorouracil (5-FU) in vitro and in vivo. Fluorouracil 90-94 microRNA 874 Homo sapiens 16-23 29039607-6 2017 Thus, our findings clarify a novel mechanism by which miR-874-3p restores chemotherapeutic sensitivity of CRC to 5-FU, indicating that offering miR-874-3p mimics in combination with 5-FU may serve as a new therapeutic strategy to circumvent the chemoresistance in CRC. Fluorouracil 113-117 microRNA 874 Homo sapiens 54-61 29039607-6 2017 Thus, our findings clarify a novel mechanism by which miR-874-3p restores chemotherapeutic sensitivity of CRC to 5-FU, indicating that offering miR-874-3p mimics in combination with 5-FU may serve as a new therapeutic strategy to circumvent the chemoresistance in CRC. Fluorouracil 113-117 microRNA 874 Homo sapiens 144-151 29163710-8 2017 In addition, high BRCA1 mRNA levels correlated with decreased median overall survival (mOS; P<0.001) and response rate (RR; P=0.002) in cisplatin-fluorouracil chemotherapy group and also correlated with increased mOS (P<0.001) and RR (P=0.023) in docetaxel-fluorouracil chemotherapy group. Fluorouracil 149-161 BRCA1 DNA repair associated Homo sapiens 18-23 29163710-8 2017 In addition, high BRCA1 mRNA levels correlated with decreased median overall survival (mOS; P<0.001) and response rate (RR; P=0.002) in cisplatin-fluorouracil chemotherapy group and also correlated with increased mOS (P<0.001) and RR (P=0.023) in docetaxel-fluorouracil chemotherapy group. Fluorouracil 263-275 BRCA1 DNA repair associated Homo sapiens 18-23 29170478-6 2017 In vitro experiments revealed that SGK1 overexpression promoted colonic tumor cell proliferation and migration and inhibited cell apoptosis induced by 5-fluorouracil (5-FU), while SGK1 shRNA and inhibitors showed the inverse effects. Fluorouracil 151-165 serum/glucocorticoid regulated kinase 1 Homo sapiens 35-39 29170478-6 2017 In vitro experiments revealed that SGK1 overexpression promoted colonic tumor cell proliferation and migration and inhibited cell apoptosis induced by 5-fluorouracil (5-FU), while SGK1 shRNA and inhibitors showed the inverse effects. Fluorouracil 167-171 serum/glucocorticoid regulated kinase 1 Homo sapiens 35-39 29117108-4 2017 Thus, this study was aimed to examine whether XRCC1 plays a role in the 5-FU/AMPK agonist (AICAR)-induced cytotoxic effect on CRC and the underlying mechanisms. Fluorouracil 72-76 X-ray repair cross complementing 1 Homo sapiens 46-51 29117108-6 2017 It was shown that 5-FU increases the XRCC1 expression in HCT-116 cells and then affects the cell survival through CXCR4/Akt signaling. Fluorouracil 18-22 X-ray repair cross complementing 1 Homo sapiens 37-42 29117108-6 2017 It was shown that 5-FU increases the XRCC1 expression in HCT-116 cells and then affects the cell survival through CXCR4/Akt signaling. Fluorouracil 18-22 C-X-C motif chemokine receptor 4 Homo sapiens 114-119 29117108-7 2017 Moreover, 5-FU combined with AICAR further result in more survival inhibition in HCT-116 cells, accompanied with reduced CXCR4/Akt signaling activity and XRCC1 expression. Fluorouracil 10-14 C-X-C motif chemokine receptor 4 Homo sapiens 121-126 29117108-7 2017 Moreover, 5-FU combined with AICAR further result in more survival inhibition in HCT-116 cells, accompanied with reduced CXCR4/Akt signaling activity and XRCC1 expression. Fluorouracil 10-14 X-ray repair cross complementing 1 Homo sapiens 154-159 29117108-8 2017 These results elucidate the role and mechanism of XRCC1 in the drug resistance of HCT-116 cells to 5-FU. Fluorouracil 99-103 X-ray repair cross complementing 1 Homo sapiens 50-55 28799948-8 2017 We found that 5-FU, MTX, and cisplatin significantly downregulated the expression of two genes controlled by the Hedgehog pathway (<=25-, 2.9-, and 12.5-fold, respectively, for GLI1 in UWBCC1 cells at 48 h, P<0.0001). Fluorouracil 14-18 GLI family zinc finger 1 Homo sapiens 180-184 2598178-3 1989 Treatment with either 5-FU alone or 5-FU and THF-gamma 2 resulted in restoration to normal values of Lyt1- and L3T4-positive populations in tumor-bearing mice. Fluorouracil 22-26 CD5 antigen Mus musculus 101-105 2598178-3 1989 Treatment with either 5-FU alone or 5-FU and THF-gamma 2 resulted in restoration to normal values of Lyt1- and L3T4-positive populations in tumor-bearing mice. Fluorouracil 36-40 CD5 antigen Mus musculus 101-105 28799948-12 2017 MTX, 5-FU, and cisplatin may offer particular promise through combined cytotoxicity and downregulation of Hedgehog pathway genes GLI1 and PTCH1. Fluorouracil 5-9 GLI family zinc finger 1 Homo sapiens 129-133 28886238-6 2017 Following inhibition of nucleolar function by actinomycin D or 5-fluorouracil treatment or knocking down the gene for the RNA polymerase I component UBF, SIRT7 is mobilized from the nucleolus to the nucleoplasm and promotes DDB1 deacetylation, leading to decreased DDB1-CUL4 association and CRL4 activity. Fluorouracil 63-77 sirtuin 7 Homo sapiens 154-159 28857517-0 2017 CISD2 enhances the chemosensitivity of gastric cancer through the enhancement of 5-FU-induced apoptosis and the inhibition of autophagy by AKT/mTOR pathway. Fluorouracil 81-85 CDGSH iron sulfur domain 2 Homo sapiens 0-5 3292840-0 1988 Recombinant granulocyte-macrophage colony-stimulating factor improves hematopoietic recovery after 5-fluorouracil. Fluorouracil 99-113 colony stimulating factor 2 (granulocyte-macrophage) Mus musculus 12-60 28857517-8 2017 5-FU treatment increased endogenous as well as exogenous overexpression of CISD2 in GC cells. Fluorouracil 0-4 CDGSH iron sulfur domain 2 Homo sapiens 75-80 3263749-4 1988 The 5-FU resistant BM progenitor is asialoGM1-, Thy.1+, Lyt.1- and Lyt.2-. Fluorouracil 4-8 CD5 antigen Mus musculus 56-61 28857517-9 2017 Further investigation revealed that CISD2 enhanced sensitivity to 5-FU via an increase in apoptosis and inhibition of protective autophagy through the activation of the AKT/mTOR pathway. Fluorouracil 66-70 CDGSH iron sulfur domain 2 Homo sapiens 36-41 28857517-10 2017 In conclusion, CISD2 is down-regulated in gastric cancer, and its effects on the inhibition of cellular proliferation, metastatic ability, and increased chemotherapy sensitivity are mediated by antagonism to 5-FU-induced autophagy through the AKT/mTOR pathway. Fluorouracil 208-212 CDGSH iron sulfur domain 2 Homo sapiens 15-20 29066704-1 2017 We report 2 unusual cases of Stage IV rectal cancer for which pathological complete response was achieved with neoadjuvant chemotherapy(NAC)consisting of a combination of 5-fluorouracil(5-FU), oxaliplatin, Leucovorin(mFOLFOX6)or irinotecan(FOLFIRI), and bevacizumab, without radiotherapy. Fluorouracil 171-185 X-linked Kx blood group Homo sapiens 136-139 3071089-0 1988 Effects of treatment of donor mice with phenylhydrazine and 5-fluorouracil on thymidylate synthase activity and growth of bone marrow grafts in spleens of irradiated recipients. Fluorouracil 60-74 thymidylate synthase Mus musculus 78-98 29066704-1 2017 We report 2 unusual cases of Stage IV rectal cancer for which pathological complete response was achieved with neoadjuvant chemotherapy(NAC)consisting of a combination of 5-fluorouracil(5-FU), oxaliplatin, Leucovorin(mFOLFOX6)or irinotecan(FOLFIRI), and bevacizumab, without radiotherapy. Fluorouracil 186-190 X-linked Kx blood group Homo sapiens 136-139 3498640-4 1987 Paradoxically, rG-CSF could support the colony formation of multilineage colonies as well as blast colonies from the spleen cells of 5-FU-treated mice, while r-granulocyte-macrophage colony-stimulating factor (GM-CSF) and r-erythropoietin (Ep) did not. Fluorouracil 133-137 colony stimulating factor 2 (granulocyte-macrophage) Mus musculus 18-21 28979703-13 2017 In conclusion, inhibition of miR-205-5p may reverse chemotherapeutic resistance to 5-Fu, and this may occur via the PTEN/JNK/ANXA3 pathway. Fluorouracil 83-87 annexin A3 Homo sapiens 125-130 29137307-0 2017 Reversal of 5-fluorouracil resistance by EGCG is mediate by inactivation of TFAP2A/VEGF signaling pathway and down-regulation of MDR-1 and P-gp expression in gastric cancer. Fluorouracil 12-26 transcription factor AP-2 alpha Homo sapiens 76-82 29137307-8 2017 Western blot and ELISA assay revealed that EGCG was able to inhibit VEGF secretion and expression, and its up-stream signal regulator, transcription factor activator protein 2A (TFAP2A) was also down-regulated by EGCG, our results indicated that TFAP2A/VEGF axis is one of the critical pathway inhibited by EGCG for cell proliferation and 5-FU resistance. Fluorouracil 339-343 transcription factor AP-2 alpha Homo sapiens 178-184 28711275-0 2017 Chemotherapy induced stroke mimic: 5-Fluorouracil encephalopathy fulfilling criteria for tissue plasminogen activator therapy. Fluorouracil 35-49 chromosome 20 open reading frame 181 Homo sapiens 89-117 2436576-9 1987 4) More than 3 months after 5-FU or tegafur administration, significant elevations of serum T3, T4 and TBG concentrations were demonstrated in cancer patients, compared to pre-treatment values or those within 2 months after therapy, although there were no significant changes in serum thyroglobulin and TSH levels before and after therapy. Fluorouracil 28-32 serpin family A member 7 Homo sapiens 103-106 2436576-11 1987 Long-term administration of 5-FU or tegafur caused elevations of serum T3 and T4 through high TBG concentrations. Fluorouracil 28-32 serpin family A member 7 Homo sapiens 94-97 3565050-0 1986 Increased thymidylate synthase activity in extracts of erythropoietic spleens of mice treated with 5-fluorouracil. Fluorouracil 99-113 thymidylate synthase Mus musculus 10-30 28851987-2 2017 Here we describe p53-dependent control of the rate-limiting enzyme in the pyrimidine catabolic pathway, dihydropyrimidine dehydrogenase (DPYD) and its effect on pharmacokinetics of and response to 5-fluorouracil (5-FU). Fluorouracil 197-211 dihydropyrimidine dehydrogenase Homo sapiens 104-135 28851987-2 2017 Here we describe p53-dependent control of the rate-limiting enzyme in the pyrimidine catabolic pathway, dihydropyrimidine dehydrogenase (DPYD) and its effect on pharmacokinetics of and response to 5-fluorouracil (5-FU). Fluorouracil 197-211 dihydropyrimidine dehydrogenase Homo sapiens 137-141 28851987-2 2017 Here we describe p53-dependent control of the rate-limiting enzyme in the pyrimidine catabolic pathway, dihydropyrimidine dehydrogenase (DPYD) and its effect on pharmacokinetics of and response to 5-fluorouracil (5-FU). Fluorouracil 213-217 dihydropyrimidine dehydrogenase Homo sapiens 104-135 28851987-2 2017 Here we describe p53-dependent control of the rate-limiting enzyme in the pyrimidine catabolic pathway, dihydropyrimidine dehydrogenase (DPYD) and its effect on pharmacokinetics of and response to 5-fluorouracil (5-FU). Fluorouracil 213-217 dihydropyrimidine dehydrogenase Homo sapiens 137-141 28851987-3 2017 Using in silico/chromatin-immunoprecipitation (ChIP) analysis we identify a conserved p53 DNA-binding site (p53BS) downstream of the DPYD gene with increased p53 occupancy following 5-FU treatment of cells. Fluorouracil 182-186 dihydropyrimidine dehydrogenase Homo sapiens 133-137 28465257-5 2017 Further work revealed that the degradation of p300/CBP induced by 5-FU was dependent on chaperone-mediated autophagy, mediated by heat-shock cognate protein 70 kDa (hsc70) and lysosomal-associated membrane protein 2A (LAMP2A). Fluorouracil 66-70 heat shock protein family A (Hsp70) member 8 Homo sapiens 165-170 28687498-5 2017 High PAK6 expression was associated with poor prognosis and increased chemoresistance to 5-FU/oxaliplatin chemotherapy. Fluorouracil 89-93 p21 (RAC1) activated kinase 6 Homo sapiens 5-9 28688823-0 2017 PAK6-Associated Support Vector Machine Classifier: A New Way to Evaluate Response and Survival of Gastric Cancer Treated by 5-FU/Oxaliplatin Chemotherapy. Fluorouracil 124-128 p21 (RAC1) activated kinase 6 Homo sapiens 0-4 29147601-4 2017 Patients with TNM II and III disease were used to predict response to 5-fluorouracil (5-FU)-based adjuvant chemotherapy (ACT) in both sets. Fluorouracil 70-84 teneurin transmembrane protein 1 Homo sapiens 14-17 27001120-1 2017 A missense variant (c.1637C>T, T546M) in ABCC11 encoding the MRP8 (multidrug resistance protein 8), a transporter of 5-fluorodeoxyuridine monophosphate, has been associated with an increased risk of 5-fluorouracil-related severe leukopenia. Fluorouracil 202-216 ATP binding cassette subfamily C member 11 Homo sapiens 44-50 27001120-1 2017 A missense variant (c.1637C>T, T546M) in ABCC11 encoding the MRP8 (multidrug resistance protein 8), a transporter of 5-fluorodeoxyuridine monophosphate, has been associated with an increased risk of 5-fluorouracil-related severe leukopenia. Fluorouracil 202-216 ATP binding cassette subfamily C member 11 Homo sapiens 64-68 27001120-1 2017 A missense variant (c.1637C>T, T546M) in ABCC11 encoding the MRP8 (multidrug resistance protein 8), a transporter of 5-fluorodeoxyuridine monophosphate, has been associated with an increased risk of 5-fluorouracil-related severe leukopenia. Fluorouracil 202-216 ATP binding cassette subfamily C member 11 Homo sapiens 70-100 28670884-0 2017 Low Incidence of the DPD IVS14+1G>A Polymorphism in Jordanian Breast and Colorectal Cancer patients Background: Dihydropyrimidine dehydrogenase (DPD) is a crucial enzyme in the catabolism of 5-fluorouracil(5-FU), a drug that is frequently used in cancer therapy. Fluorouracil 194-208 dihydropyrimidine dehydrogenase Homo sapiens 21-24 28670884-0 2017 Low Incidence of the DPD IVS14+1G>A Polymorphism in Jordanian Breast and Colorectal Cancer patients Background: Dihydropyrimidine dehydrogenase (DPD) is a crucial enzyme in the catabolism of 5-fluorouracil(5-FU), a drug that is frequently used in cancer therapy. Fluorouracil 194-208 dihydropyrimidine dehydrogenase Homo sapiens 115-146 28670884-0 2017 Low Incidence of the DPD IVS14+1G>A Polymorphism in Jordanian Breast and Colorectal Cancer patients Background: Dihydropyrimidine dehydrogenase (DPD) is a crucial enzyme in the catabolism of 5-fluorouracil(5-FU), a drug that is frequently used in cancer therapy. Fluorouracil 194-208 dihydropyrimidine dehydrogenase Homo sapiens 148-151 28670884-0 2017 Low Incidence of the DPD IVS14+1G>A Polymorphism in Jordanian Breast and Colorectal Cancer patients Background: Dihydropyrimidine dehydrogenase (DPD) is a crucial enzyme in the catabolism of 5-fluorouracil(5-FU), a drug that is frequently used in cancer therapy. Fluorouracil 209-213 dihydropyrimidine dehydrogenase Homo sapiens 21-24 28670884-0 2017 Low Incidence of the DPD IVS14+1G>A Polymorphism in Jordanian Breast and Colorectal Cancer patients Background: Dihydropyrimidine dehydrogenase (DPD) is a crucial enzyme in the catabolism of 5-fluorouracil(5-FU), a drug that is frequently used in cancer therapy. Fluorouracil 209-213 dihydropyrimidine dehydrogenase Homo sapiens 115-146 28670884-0 2017 Low Incidence of the DPD IVS14+1G>A Polymorphism in Jordanian Breast and Colorectal Cancer patients Background: Dihydropyrimidine dehydrogenase (DPD) is a crucial enzyme in the catabolism of 5-fluorouracil(5-FU), a drug that is frequently used in cancer therapy. Fluorouracil 209-213 dihydropyrimidine dehydrogenase Homo sapiens 148-151 28629331-2 2017 Up-regulation of CRC stem cell markers by PAK1 also contributes to the resistance of CRC to 5-fluorouracil. Fluorouracil 92-106 p21 (RAC1) activated kinase 1 Mus musculus 42-46 4044345-4 1985 Severe and prolonged anorexia, nausea, and decreased performance status occurred during and after high dose radiotherapy given twice daily in 150-170 cGy (rad) fractions when given with 5-FU. Fluorouracil 186-190 RRAD, Ras related glycolysis inhibitor and calcium channel regulator Homo sapiens 108-111 28551618-0 2017 MEK162 Enhances Antitumor Activity of 5-Fluorouracil and Trifluridine in KRAS-mutated Human Colorectal Cancer Cell Lines. Fluorouracil 38-52 KRAS proto-oncogene, GTPase Homo sapiens 73-77 6433806-3 1984 The blood level of 5-FU remained constant in 86% of patients after administration of PSK for 7 days, but decreased in 14% of patients. Fluorouracil 19-23 TAO kinase 2 Homo sapiens 85-88 28408238-7 2017 Podxl-KO also substantially heightened neutrophil levels after 5-fluorouracil myeloablation. Fluorouracil 63-77 podocalyxin-like Mus musculus 0-5 446187-3 1979 The TPP effect of transketolase enzyme activity was also increased by 5-fluorouracil in vitro. Fluorouracil 70-84 transketolase Rattus norvegicus 18-31 879810-1 1977 Topical (5-fluorouracil [5-FU]) as a 5% solution was used to treat isolated actinic keratoses of the lips as well as diffuse actinic damage of the lower lip. Fluorouracil 9-23 SMG1 nonsense mediated mRNA decay associated PI3K related kinase Homo sapiens 101-104 879810-1 1977 Topical (5-fluorouracil [5-FU]) as a 5% solution was used to treat isolated actinic keratoses of the lips as well as diffuse actinic damage of the lower lip. Fluorouracil 25-29 SMG1 nonsense mediated mRNA decay associated PI3K related kinase Homo sapiens 101-104 4599674-0 1974 Column chromatography of 5-fluorouracil on sephadex G-10. Fluorouracil 25-39 BUD31 homolog Homo sapiens 52-56 5429721-5 1970 (iii) A mutation at the locus FUR 4 gives a simultaneous resistance to 5-fluorouracil and to 5-fluorouridine by loss in the activity of the uracil-specific permease. Fluorouracil 71-85 uracil permease Saccharomyces cerevisiae S288C 30-35 6049016-0 1967 The effects of 5-fluorouracil on the storage and secretion of pancreatic lipase and zymogen granules. Fluorouracil 15-29 pancreatic lipase Homo sapiens 62-79 13896173-0 1961 Effect of 5-fluorouracil on hepatic induced increase of tryptophan-pyrrolase. Fluorouracil 10-24 tryptophan 2,3-dioxygenase Homo sapiens 56-76 33858572-6 2021 The in vitro Fluorouracil (5-FU) releasing from (Cs/AAc/AMPS) matrix was examined under the influence of pH1 and pH7.The results confirmed the hydrogels capability to release 96 % of 5-FU drug at pH 7 after 7 h. Fluorouracil 13-25 glycine-N-acyltransferase Homo sapiens 52-55 33858572-6 2021 The in vitro Fluorouracil (5-FU) releasing from (Cs/AAc/AMPS) matrix was examined under the influence of pH1 and pH7.The results confirmed the hydrogels capability to release 96 % of 5-FU drug at pH 7 after 7 h. Fluorouracil 27-31 glycine-N-acyltransferase Homo sapiens 52-55 33838133-3 2021 Human organic anion transporter 2 (hOAT2), a transporter mainly expressed in liver and kidney, is responsible for uptake of various antineoplastic drugs such as 5-fluorouracil (5-FU). Fluorouracil 161-175 solute carrier family 22 member 7 Homo sapiens 6-33 33838133-3 2021 Human organic anion transporter 2 (hOAT2), a transporter mainly expressed in liver and kidney, is responsible for uptake of various antineoplastic drugs such as 5-fluorouracil (5-FU). Fluorouracil 161-175 solute carrier family 22 member 7 Homo sapiens 35-40 33838133-3 2021 Human organic anion transporter 2 (hOAT2), a transporter mainly expressed in liver and kidney, is responsible for uptake of various antineoplastic drugs such as 5-fluorouracil (5-FU). Fluorouracil 177-181 solute carrier family 22 member 7 Homo sapiens 6-33 33838133-3 2021 Human organic anion transporter 2 (hOAT2), a transporter mainly expressed in liver and kidney, is responsible for uptake of various antineoplastic drugs such as 5-fluorouracil (5-FU). Fluorouracil 177-181 solute carrier family 22 member 7 Homo sapiens 35-40 33838133-4 2021 Among 32 pairs of human HCC samples, we preliminarily found that OAT2 was suppressed in HCC tissues compared with matched tumor-adjacent tissues at both mRNA and protein levels, which resulted in 5-FU resistance in HCC. Fluorouracil 196-200 solute carrier family 22 member 7 Homo sapiens 65-69 34035223-0 2021 Retraction Note to: FOXM1 modulates 5-fluorouracil sensitivity in cholangiocarcinoma through thymidylate synthase (TYMS): implications of FOXM1-TYMS axis uncoupling in 5-FU resistance. Fluorouracil 168-172 forkhead box M1 Homo sapiens 20-25 34003528-0 2021 Circular RNA PTGR1 regulates 5-FU resistance and development of hepatocellular carcinoma cells by modulating miR-129-5p/ABCC1 axis. Fluorouracil 29-33 microRNA 1295a Homo sapiens 109-119 34003528-10 2021 Both circPTGR1 knockdown and miR-129-5p overexpression inhibited 5-FU resistance, migration, and invasion, and induced apoptosis of HCC cells. Fluorouracil 65-69 microRNA 1295a Homo sapiens 29-39 34003528-14 2021 Our finding indicated that circPTGR1 modulated the 5-FU resistance, migration, invasion, and apoptosis of HCC cells via regulating miR-129-5p/ABCC1 axis, providing a theoretical basis for the treatment of HCC. Fluorouracil 51-55 microRNA 1295a Homo sapiens 131-141 33953165-3 2021 We found that cisplatin and 5-fluorouracil could induce fibroblast differentiation toward myofibroblasts via CCAAT/enhancer-binding protein delta (CEBPD) and consequently promote proliferation, migration, and in vitro tube formation of vascular endothelial cells and angiogenesis in vivo. Fluorouracil 28-42 CCAAT enhancer binding protein delta Homo sapiens 109-145 33953165-3 2021 We found that cisplatin and 5-fluorouracil could induce fibroblast differentiation toward myofibroblasts via CCAAT/enhancer-binding protein delta (CEBPD) and consequently promote proliferation, migration, and in vitro tube formation of vascular endothelial cells and angiogenesis in vivo. Fluorouracil 28-42 CCAAT enhancer binding protein delta Homo sapiens 147-152 33544210-3 2021 Dihydropyrimidine dehydrogenase (DPD) is the rate-limiting enzyme in the degradation of 5FU and a DPD deficiency has been shown to be a major determinant of severe fluoropyrimidine-associated toxicity. Fluorouracil 88-91 dihydropyrimidine dehydrogenase Homo sapiens 0-31 33544210-3 2021 Dihydropyrimidine dehydrogenase (DPD) is the rate-limiting enzyme in the degradation of 5FU and a DPD deficiency has been shown to be a major determinant of severe fluoropyrimidine-associated toxicity. Fluorouracil 88-91 dihydropyrimidine dehydrogenase Homo sapiens 33-36 33886055-6 2021 Also, where 5-FU is in the concentration of caspase-3 and 8-OHdG immune-positive cells and therefore causes apoptosis and DNA damage in kidney tissue cells. Fluorouracil 12-16 caspase 3 Mus musculus 44-53 33923672-12 2021 The results showed that melatonin reduced the number of p21-positive cells in the SGZ of the dentate gyrus and increased Nrf2, DCX and BDNF protein expression in rats treated with 5-FU. Fluorouracil 180-184 doublecortin Rattus norvegicus 127-130 33923672-12 2021 The results showed that melatonin reduced the number of p21-positive cells in the SGZ of the dentate gyrus and increased Nrf2, DCX and BDNF protein expression in rats treated with 5-FU. Fluorouracil 180-184 brain-derived neurotrophic factor Rattus norvegicus 135-139 28044213-0 2017 Polymorphisms of MTHFR C677T and A1298C associated with survival in patients with colorectal cancer treated with 5-fluorouracil-based chemotherapy. Fluorouracil 113-127 methylenetetrahydrofolate reductase Homo sapiens 17-22 33755421-2 2021 5-Fluorouracil (5FU) is also a substrate for DPD and a common chemotherapeutic agent used to treat numerous cancers. Fluorouracil 0-14 dihydropyrimidine dehydrogenase Homo sapiens 45-48 33837489-9 2021 RNA-seq analysis revealed 5FU + OX-pretreated CAF-derived glycoprotein 130 (gp130) as a candidate factor contributing to the increased migration of 5FU + OX-pretreated 44As3 cells. Fluorouracil 26-29 Neutrophil migration (granulocyte glycoprotein) Homo sapiens 58-74 33837489-9 2021 RNA-seq analysis revealed 5FU + OX-pretreated CAF-derived glycoprotein 130 (gp130) as a candidate factor contributing to the increased migration of 5FU + OX-pretreated 44As3 cells. Fluorouracil 26-29 Neutrophil migration (granulocyte glycoprotein) Homo sapiens 76-81 33837489-9 2021 RNA-seq analysis revealed 5FU + OX-pretreated CAF-derived glycoprotein 130 (gp130) as a candidate factor contributing to the increased migration of 5FU + OX-pretreated 44As3 cells. Fluorouracil 148-151 Neutrophil migration (granulocyte glycoprotein) Homo sapiens 58-74 33837489-9 2021 RNA-seq analysis revealed 5FU + OX-pretreated CAF-derived glycoprotein 130 (gp130) as a candidate factor contributing to the increased migration of 5FU + OX-pretreated 44As3 cells. Fluorouracil 148-151 Neutrophil migration (granulocyte glycoprotein) Homo sapiens 76-81 33837489-10 2021 Administration of the gp130 inhibitor SC144 prevented the increased migration ability of 5FU + OX-pretreated 44As3 cells owing to drug-treated CAFs. Fluorouracil 89-92 Neutrophil migration (granulocyte glycoprotein) Homo sapiens 22-27 28044213-1 2017 BACKGROUND: This study examined the association between methylenetetrahydrofolate reductase (MTHFR) polymorphisms and survival of patients with colorectal cancer (CRC) treated with 5-fluorouracil (5-FU)-based chemotherapy in Taiwan. Fluorouracil 181-195 methylenetetrahydrofolate reductase Homo sapiens 56-91 28044213-1 2017 BACKGROUND: This study examined the association between methylenetetrahydrofolate reductase (MTHFR) polymorphisms and survival of patients with colorectal cancer (CRC) treated with 5-fluorouracil (5-FU)-based chemotherapy in Taiwan. Fluorouracil 181-195 methylenetetrahydrofolate reductase Homo sapiens 93-98 28044213-1 2017 BACKGROUND: This study examined the association between methylenetetrahydrofolate reductase (MTHFR) polymorphisms and survival of patients with colorectal cancer (CRC) treated with 5-fluorouracil (5-FU)-based chemotherapy in Taiwan. Fluorouracil 197-201 methylenetetrahydrofolate reductase Homo sapiens 56-91 28044213-2 2017 METHODS: We genotyped MTHFR polymorphisms C677T (rs1801133) and A1298C (rs1801131) for 498 CRC patients treated with 5-FU-based chemotherapy after receiving surgery. Fluorouracil 117-121 methylenetetrahydrofolate reductase Homo sapiens 22-27 28044213-9 2017 CONCLUSIONS: Our findings suggest that MTHFR genotypes provide prognostic information for CRC patients treated with 5-FU-based chemotherapy. Fluorouracil 116-120 methylenetetrahydrofolate reductase Homo sapiens 39-44 28440463-5 2017 The aim of the present study was to evaluate the role of Livin in the susceptibility to popularly used chemotherapeutic drugs such as cisplatin, 5-fluorouracil (FU) and docetaxel in human HNSCC cell lines (SNU1041, PCI1 and PCI50 cells). Fluorouracil 145-159 baculoviral IAP repeat containing 7 Homo sapiens 57-62 28440463-9 2017 Livin knockdown significantly enhanced cytotoxicity to cisplatin, 5-FU and docetaxel in human HNSCC cells. Fluorouracil 66-70 baculoviral IAP repeat containing 7 Homo sapiens 0-5 28440463-10 2017 Livin knockdown induced apoptosis and enhanced chemotherapy-induced apoptosis to cisplatin, 5-FU and docetaxel. Fluorouracil 92-96 baculoviral IAP repeat containing 7 Homo sapiens 0-5 28440463-11 2017 Consistent with this, Livin-knockdown cells showed greater expression of cleaved caspases-3 and -7 and poly(ADP-ribose)polymerase compared with that in control cells after cisplatin, 5-FU, or docetaxel treatment. Fluorouracil 183-187 baculoviral IAP repeat containing 7 Homo sapiens 22-27 28440463-12 2017 In conclusion, our results suggest that siRNA-mediated Livin knockdown enhanced the chemosensitivity of the three HNSCC cell lines to cisplatin, 5-FU and docetaxel. Fluorouracil 145-149 baculoviral IAP repeat containing 7 Homo sapiens 55-60 28618970-3 2017 investigated the association between germline genetic polymorphisms in DPYD, the gene encoding dihydropyrimidine dehydrogenase, and (1) the risk of developing pediatric acute lymphoblastic leukemia and (2) outcome of acute lymphoblastic leukemia following the treatment with 5-fluorouracil plus oxaliplatin (FOLFOX). Fluorouracil 275-289 dihydropyrimidine dehydrogenase Homo sapiens 71-75 33708464-4 2021 Additionally, we found that the 5-Fluorouracil"s (5-FU) function was significantly improved when used in combination with HSP 70 inhibitor (KNK 437). Fluorouracil 32-46 heat shock protein family A (Hsp70) member 4 Homo sapiens 122-128 33708464-4 2021 Additionally, we found that the 5-Fluorouracil"s (5-FU) function was significantly improved when used in combination with HSP 70 inhibitor (KNK 437). Fluorouracil 50-54 heat shock protein family A (Hsp70) member 4 Homo sapiens 122-128 33645623-5 2021 Moreover, NEAT1 was positively associated with 5-Fu resistance. Fluorouracil 47-51 nuclear paraspeckle assembly transcript 1 Homo sapiens 10-15 33645623-6 2021 Furthermore, expression of NEAT1 was significantly upregulated in 5-Fu resistant CaSki cervical cancer cells. Fluorouracil 66-70 nuclear paraspeckle assembly transcript 1 Homo sapiens 27-32 33645623-7 2021 Knocking down NEAT1 by shRNA dramatically promoted the sensitivity of 5-Fu resistant CaSki cells. Fluorouracil 70-74 nuclear paraspeckle assembly transcript 1 Homo sapiens 14-19 33645623-15 2021 Finally, we demonstrated inhibition of NEAT1 significantly sensitized cervical cancer cells to 5-Fu through the miR-34a/LDHA pathway. Fluorouracil 95-99 nuclear paraspeckle assembly transcript 1 Homo sapiens 39-44 33645623-16 2021 In summary, this study suggests a new molecular mechanism for the NEAT1-mediated 5-Fu resistance via the miR-34a/LDHA-glycolysis axis. Fluorouracil 81-85 nuclear paraspeckle assembly transcript 1 Homo sapiens 66-71 33758608-0 2021 USP11 induce resistance to 5-Fluorouracil in Colorectal Cancer through activating autophagy by stabilizing VCP. Fluorouracil 27-41 ubiquitin specific peptidase 11 Homo sapiens 0-5 33758608-3 2021 Our study investigated the role of ubiquitin-specific protease 11 (USP11) in CRC chemotherapy and found that USP11 could induce resistance to 5-fluorouracil by activating autophagy. Fluorouracil 142-156 ubiquitin specific peptidase 11 Homo sapiens 35-65 33758608-3 2021 Our study investigated the role of ubiquitin-specific protease 11 (USP11) in CRC chemotherapy and found that USP11 could induce resistance to 5-fluorouracil by activating autophagy. Fluorouracil 142-156 ubiquitin specific peptidase 11 Homo sapiens 67-72 33758608-3 2021 Our study investigated the role of ubiquitin-specific protease 11 (USP11) in CRC chemotherapy and found that USP11 could induce resistance to 5-fluorouracil by activating autophagy. Fluorouracil 142-156 ubiquitin specific peptidase 11 Homo sapiens 109-114 33476960-6 2021 We found the combination of 5-FU and TRAIL had a greater inhibitory effect on the proliferation of gastric cancer cells than 5-FU or TRAIL alone both in vivo and in vitro. Fluorouracil 125-129 tumor necrosis factor (ligand) superfamily, member 10 Mus musculus 37-42 33476960-7 2021 5-FU enhanced TRAIL-induced gastric cancer cell apoptosis by inactivating the MAPK pathway. Fluorouracil 0-4 tumor necrosis factor (ligand) superfamily, member 10 Mus musculus 14-19 33476960-8 2021 Overall, our analysis firstly provided new insights into the role of 5-FU in increasing sensitivity to TRAIL. Fluorouracil 69-73 tumor necrosis factor (ligand) superfamily, member 10 Mus musculus 103-108 33476960-9 2021 5-FU can be used as a sensitizer for TRAIL, and its administration is a potential strategy for the treatment of gastric cancer. Fluorouracil 0-4 tumor necrosis factor (ligand) superfamily, member 10 Mus musculus 37-42 33373916-11 2021 significantly reversed 5-FU-induced loss in body weight and food intake; reversed villous atrophy; significantly suppressed myeloperoxidase, NE, and proteinase 3 activity; and reduced pro-inflammatory cytokine expression in an FUIIM mouse model. Fluorouracil 23-27 myeloperoxidase Mus musculus 124-139 33373916-11 2021 significantly reversed 5-FU-induced loss in body weight and food intake; reversed villous atrophy; significantly suppressed myeloperoxidase, NE, and proteinase 3 activity; and reduced pro-inflammatory cytokine expression in an FUIIM mouse model. Fluorouracil 23-27 proteinase 3 Mus musculus 149-161 33564301-10 2021 A tremendous rise of the CD3+/CD8+ count and a significant decrease of CD3+CD4+/CD3+CD8+ ratios were found in the 5-FU group and were both reversed by Lcr35. Fluorouracil 114-118 CD4 antigen Mus musculus 75-78 33564301-11 2021 5-FU significantly stimulated the expression of CD44 stem cells, and the expression was restored by Lcr35. Fluorouracil 0-4 CD44 antigen Mus musculus 48-52 33564301-12 2021 5-FU could increase the number of Ki67 proliferative cells. Fluorouracil 0-4 antigen identified by monoclonal antibody Ki 67 Mus musculus 34-38 33438566-11 2021 RESULTS: The results showed that the HCT-8/5-FU cells were resistant to multiple chemotherapy drugs (5-FU, ADM and DDP). Fluorouracil 43-47 adrenomedullin Homo sapiens 107-110 28618970-3 2017 investigated the association between germline genetic polymorphisms in DPYD, the gene encoding dihydropyrimidine dehydrogenase, and (1) the risk of developing pediatric acute lymphoblastic leukemia and (2) outcome of acute lymphoblastic leukemia following the treatment with 5-fluorouracil plus oxaliplatin (FOLFOX). Fluorouracil 275-289 dihydropyrimidine dehydrogenase Homo sapiens 95-126 28618970-5 2017 The authors conclude that patients carrying the c.85T>C C allele have an increased risk of developing acute lymphoblastic leukemia and have inferior outcome, and that DPYD c.85T>C can be used as a guide for individualized treatment and the decision to utilize 5-fluorouracil in acute lymphoblastic leukemia patients. Fluorouracil 266-280 dihydropyrimidine dehydrogenase Homo sapiens 170-174 28504690-6 2017 Inhibition of miR-645 reduced proliferation and enhanced sensitivity to apoptosis triggered by the chemotherapeutic drugs 5-fluorouracil and cisplatin in CRC cells, and retarded colon cancer xenograft growth. Fluorouracil 122-136 microRNA 645 Homo sapiens 14-21 33389016-6 2021 RESULTS: Gastric cancer patients with high CD47 expression exhibited poor prognosis and inferior therapeutic responsiveness to fluorouracil-based adjuvant chemotherapy (ACT). Fluorouracil 127-139 CD47 molecule Homo sapiens 43-47 33960231-0 2021 Up-regulation of KLF17 expression increases the sensitivity of gastric cancer to 5-fluorouracil. Fluorouracil 81-95 Kruppel like factor 17 Homo sapiens 17-22 33960231-4 2021 The effect of KLF17 on the sensitivity of GC cell lines to 5-fluorouracil (5-FU), and the potential mechanism were detected by MTS assay, Flow cytometry assay, and Western blot. Fluorouracil 59-73 Kruppel like factor 17 Homo sapiens 14-19 33960231-7 2021 Furthermore, through upregulating the expression of KLF17, the sensitivity of BGC-823 and SGC-7901 cell lines to 5-FU was obviously increased. Fluorouracil 113-117 Kruppel like factor 17 Homo sapiens 52-57 33935122-8 2021 CXCL1 was under expressed in HeLa cells treated with AgNPs-F (0.69-fold) and AgNPs-L (0.58-fold) and over expressed in cells treated with 5FU (4.95-fold), but the difference was not statistically significant. Fluorouracil 138-141 C-X-C motif chemokine ligand 1 Homo sapiens 0-5 33408498-6 2020 DFS and OS rates were reduced in patients with increased COX2, IL6, IL10, and TNFalpha expression with 5-FU therapy. Fluorouracil 103-107 interleukin 10 Homo sapiens 68-72 27878958-9 2017 Knockdown of Orai1 or pharmacological inhibition of SOCE enhanced 5-FU-induced inhibition of PI3K/AKT/mTOR pathway and potentiated 5-FU-activated autophagic cell death. Fluorouracil 66-70 ORAI calcium release-activated calcium modulator 1 Homo sapiens 13-18 33408498-8 2020 Moreover, smoking, 5-FU induction of IL6, TNFalpha, and IL10 expression are found to be independent prognostic factors for OS (P=0.003, 0.003, 0.002, and 0.002, respectively). Fluorouracil 19-23 interleukin 10 Homo sapiens 56-60 27878958-9 2017 Knockdown of Orai1 or pharmacological inhibition of SOCE enhanced 5-FU-induced inhibition of PI3K/AKT/mTOR pathway and potentiated 5-FU-activated autophagic cell death. Fluorouracil 131-135 ORAI calcium release-activated calcium modulator 1 Homo sapiens 13-18 27878958-10 2017 On the contrary, ectopic overexpression of Orai1 antagonizes 5-FU-induced autophagy and cell death. Fluorouracil 61-65 ORAI calcium release-activated calcium modulator 1 Homo sapiens 43-48 27878958-12 2017 5-FU can induce autophagic cell death in HepG2 hepatocarcinoma cells through inhibition of SOCE via decreasing Orai1 expression. Fluorouracil 0-4 ORAI calcium release-activated calcium modulator 1 Homo sapiens 111-116 27878958-13 2017 These findings suggest that Orai1 expression is a predictor of 5-FU sensitivity for hepatocarcinoma treatment and blockade of Orai1-mediated Ca2+ entry may be a promising strategy to sensitize hepatocarcinoma cells to 5-FU treatment. Fluorouracil 63-67 ORAI calcium release-activated calcium modulator 1 Homo sapiens 28-33 27878958-13 2017 These findings suggest that Orai1 expression is a predictor of 5-FU sensitivity for hepatocarcinoma treatment and blockade of Orai1-mediated Ca2+ entry may be a promising strategy to sensitize hepatocarcinoma cells to 5-FU treatment. Fluorouracil 218-222 ORAI calcium release-activated calcium modulator 1 Homo sapiens 126-131 28427191-12 2017 Moreover, up-regulation of RP11-708H21.4 inhibits cell migration and invasion, causes cell apoptosis, and enhances 5-FU sensitivity of CRC cells. Fluorouracil 115-119 pre-mRNA processing factor 31 Homo sapiens 27-31 32474853-5 2020 CONCLUSIONS: In this article we systematically review and update current knowledge on 5-FU pharmacogenomics related to drug uptake and activation, the expression and activity of target enzymes (DPD, TS and MTHFR) and key signaling pathways in CRC. Fluorouracil 86-90 dihydropyrimidine dehydrogenase Homo sapiens 194-197 33164645-0 2020 Matrine Inhibitory Effect on Self-renewal and Re-sensitization of 5-FU Resistant NSCLC Stem Cells were through Let-7b dependent Downregulation of CCND1. Fluorouracil 66-70 cyclin D1 Mus musculus 146-151 33164645-8 2020 And xenografts in nude mice evidenced that Matrine increased the sensitivity of lung CSCs to 5-FU and inhibited the accumulation of CCND1 in tumor tissues induced by 5-FU. Fluorouracil 166-170 cyclin D1 Mus musculus 132-137 32377978-3 2020 DFP-11207 is a novel oral cytotoxic agent that combines a 5-FU pro-drug with a reversible DPD inhibitor and a potent inhibitor of OPRT, resulting in enhanced pharmacological activity of 5-FU with decreased gastrointestinal and myelosuppressive toxicities. Fluorouracil 186-190 dihydropyrimidine dehydrogenase Homo sapiens 90-93 28638476-5 2017 Results using human HCT116 and HT29 colorectal cancer cell lines showed that miR-4260 mimic enhanced cell proliferation and migration and reduced apoptosis induced by the chemotherapeutic agent 5-fluorouracil while miR-4260 inhibitor had inverse effects. Fluorouracil 194-208 microRNA 4260 Homo sapiens 77-85 33197222-0 2020 All You Need to Know About DPYD Genetic Testing for Patients Treated With Fluorouracil and Capecitabine: A Practitioner-Friendly Guide. Fluorouracil 74-86 dihydropyrimidine dehydrogenase Homo sapiens 27-31 33035787-5 2020 After stratifying by treatment, in the 5-Fluorouracil group, the DPYD rs17376848 AG genotype was associated with hematological toxicity (OR = 2.76; p = 0.003), ABCB1 rs1045642 T-allele with the need of treatment adjustment due to toxicity (OR = 3.06; p = 0.01), and rs1045642 CC genotype with gastrointestinal toxicity (OR = 5.80; p = 0.03). Fluorouracil 39-53 dihydropyrimidine dehydrogenase Homo sapiens 65-69 28423595-0 2017 dUTPase inhibition augments replication defects of 5-Fluorouracil. Fluorouracil 51-65 Deoxyuridine triphosphatase Drosophila melanogaster 0-7 28423595-4 2017 Interestingly, these effects can be reinforced by either depletion or inhibition of the deoxyuridine triphosphatase (dUTPase, also known as DUT), highlighting the importance of (5-F)dUTP accumulation for cytotoxicity.With this study, we not only extend the current understanding of the mechanism of action of 5-FU, but also contribute to the characterization of dUTPase inhibitors. Fluorouracil 309-313 deoxyuridine triphosphatase Homo sapiens 88-115 28423595-4 2017 Interestingly, these effects can be reinforced by either depletion or inhibition of the deoxyuridine triphosphatase (dUTPase, also known as DUT), highlighting the importance of (5-F)dUTP accumulation for cytotoxicity.With this study, we not only extend the current understanding of the mechanism of action of 5-FU, but also contribute to the characterization of dUTPase inhibitors. Fluorouracil 309-313 Deoxyuridine triphosphatase Drosophila melanogaster 117-124 28423595-4 2017 Interestingly, these effects can be reinforced by either depletion or inhibition of the deoxyuridine triphosphatase (dUTPase, also known as DUT), highlighting the importance of (5-F)dUTP accumulation for cytotoxicity.With this study, we not only extend the current understanding of the mechanism of action of 5-FU, but also contribute to the characterization of dUTPase inhibitors. Fluorouracil 309-313 deoxyuridine triphosphatase Homo sapiens 140-143 28423595-4 2017 Interestingly, these effects can be reinforced by either depletion or inhibition of the deoxyuridine triphosphatase (dUTPase, also known as DUT), highlighting the importance of (5-F)dUTP accumulation for cytotoxicity.With this study, we not only extend the current understanding of the mechanism of action of 5-FU, but also contribute to the characterization of dUTPase inhibitors. Fluorouracil 309-313 Deoxyuridine triphosphatase Drosophila melanogaster 362-369 28423595-5 2017 We demonstrate that pharmacological inhibition of dUTPase is a promising approach that may improve the efficacy of 5-FU treatment in the clinic. Fluorouracil 115-119 Deoxyuridine triphosphatase Drosophila melanogaster 50-57 27780937-9 2017 More importantly, TNM II patients with higher CXCR1 expression were shown to significantly benefit from postoperative 5-fluorouracil (5-FU) based adjuvant chemotherapy (ACT). Fluorouracil 118-132 teneurin transmembrane protein 1 Homo sapiens 18-21 32390047-5 2020 We found that Rab27B expression in drug (5-fluorouracil, 5Fu)-resistant Bel7402 (Bel/5Fu) cells increased significantly compared with that in drug-sensitive Bel7402 cells. Fluorouracil 41-55 RAB27B, member RAS oncogene family Homo sapiens 14-20 32390047-5 2020 We found that Rab27B expression in drug (5-fluorouracil, 5Fu)-resistant Bel7402 (Bel/5Fu) cells increased significantly compared with that in drug-sensitive Bel7402 cells. Fluorouracil 57-60 RAB27B, member RAS oncogene family Homo sapiens 14-20 32390047-5 2020 We found that Rab27B expression in drug (5-fluorouracil, 5Fu)-resistant Bel7402 (Bel/5Fu) cells increased significantly compared with that in drug-sensitive Bel7402 cells. Fluorouracil 85-88 RAB27B, member RAS oncogene family Homo sapiens 14-20 32390047-7 2020 The number of exosomes secreted by Bel/5Fu cells significantly reduced after knocking down Rab27B, and the cellular concentration of 5Fu increased, enhancing its therapeutic effect. Fluorouracil 39-42 RAB27B, member RAS oncogene family Homo sapiens 91-97 33299409-0 2020 Retracted: Influence of DPYD Genetic Polymorphisms on 5-Fluorouracil Toxicities in Patients with Colorectal Cancer: A Meta-Analysis. Fluorouracil 54-68 dihydropyrimidine dehydrogenase Homo sapiens 24-28 27780937-9 2017 More importantly, TNM II patients with higher CXCR1 expression were shown to significantly benefit from postoperative 5-fluorouracil (5-FU) based adjuvant chemotherapy (ACT). Fluorouracil 118-132 C-X-C motif chemokine receptor 1 Homo sapiens 46-51 27780937-9 2017 More importantly, TNM II patients with higher CXCR1 expression were shown to significantly benefit from postoperative 5-fluorouracil (5-FU) based adjuvant chemotherapy (ACT). Fluorouracil 134-138 teneurin transmembrane protein 1 Homo sapiens 18-21 27780937-9 2017 More importantly, TNM II patients with higher CXCR1 expression were shown to significantly benefit from postoperative 5-fluorouracil (5-FU) based adjuvant chemotherapy (ACT). Fluorouracil 134-138 C-X-C motif chemokine receptor 1 Homo sapiens 46-51 27780937-12 2017 High expression of CXCR1 identified a subgroup of TNM stage II gastric cancer patients who appeared to benefit from 5-FU based ACT. Fluorouracil 116-120 C-X-C motif chemokine receptor 1 Homo sapiens 19-24 28278081-9 2017 Additionally, in patients with DPD activity below 3.18 before treatment, appropriate reduction of 5-FU dose could be considered to minimize the incidence of adverse events. Fluorouracil 98-102 dihydropyrimidine dehydrogenase Homo sapiens 31-34 33168814-0 2020 LncRNA NEAT1 remodels chromatin to promote the 5-Fu resistance by maintaining colorectal cancer stemness. Fluorouracil 47-51 nuclear paraspeckle assembly transcript 1 Homo sapiens 7-12 33168814-3 2020 Here we observed that lncRNA NEAT1 was associated with 5-Fu resistance in CRC. Fluorouracil 55-59 nuclear paraspeckle assembly transcript 1 Homo sapiens 29-34 33168814-4 2020 Our Functional studies showed that NEAT1 promoted 5-Fu resistance in colorectal cells. Fluorouracil 50-54 nuclear paraspeckle assembly transcript 1 Homo sapiens 35-40 33168814-6 2020 Taken together, our study suggested that NEAT1 promoted 5-Fu resistance and cancer stemness by remodeling chromatin. Fluorouracil 56-60 nuclear paraspeckle assembly transcript 1 Homo sapiens 41-46 33168814-7 2020 Our finding provides a novel role of NEAT1 and may provide a new strategy for the treatment of CRC 5-Fu resistance. Fluorouracil 99-103 nuclear paraspeckle assembly transcript 1 Homo sapiens 37-42 27865009-5 2017 We also found that melatonin synergized with 5-FU to promote the activation of the caspase/PARP-dependent apoptosis pathway and induce cell cycle arrest. Fluorouracil 45-49 poly (ADP-ribose) polymerase family, member 1 Mus musculus 91-95 33177876-0 2020 Down-Regulation of Circ_0032833 Sensitizes Colorectal Cancer to 5-Fluorouracil and Oxaliplatin Partly Depending on the Regulation of miR-125-5p and MSI1. Fluorouracil 64-78 musashi RNA-binding protein 1 Mus musculus 148-152 33177876-11 2020 Besides, miR-125-5p targeted Musashi1 (MSI1) to increase the susceptibility of 5-fluorouracil and oxaliplatin in FOLFOX-resistant CRC cells. Fluorouracil 79-93 musashi RNA-binding protein 1 Mus musculus 29-37 27912078-8 2017 Although cancer therapeutic agents 5-fluorouracil and doxorubicin could not induce a robust p53 activation in the wild-type oocytes, they induced p53 nuclear accumulation in the Mdm2 and Mdm4 double heterozygous oocytes. Fluorouracil 35-49 transformed mouse 3T3 cell double minute 4 Mus musculus 187-191 33177876-11 2020 Besides, miR-125-5p targeted Musashi1 (MSI1) to increase the susceptibility of 5-fluorouracil and oxaliplatin in FOLFOX-resistant CRC cells. Fluorouracil 79-93 musashi RNA-binding protein 1 Mus musculus 39-43 33177876-13 2020 Circ_0032833 down-regulation also promoted the 5-fluorouracil and oxaliplatin sensitivities partly through the miR-125-5p/MSI1 axis in vivo. Fluorouracil 47-61 musashi RNA-binding protein 1 Mus musculus 122-126 33177876-14 2020 Conclusion: This study illuminated an unambiguous mechanism circ_0032833/miR-125-5p/MSI1 on regulating 5-fluorouracil and oxaliplatin sensitivities in FOLFOX therapy, maybe providing a deep insight of resistance formation and developing a novel strategy to enhance chemosensitivity in CRC. Fluorouracil 103-117 musashi RNA-binding protein 1 Mus musculus 84-88 27634492-0 2017 Localization of MMP-9 in multinuclear giant cells in keloids after treatment with 5-fluorouracil with or without combination of cryotherapy and cryotherapy alone. Fluorouracil 82-96 matrix metallopeptidase 9 Homo sapiens 16-21 32436284-11 2020 CONCLUSION: This study showed that the application of PRP gel to colon anastomoses increased ABP in rats treated with HIPEC using 5-FU. Fluorouracil 130-134 proline rich protein 2-like 1 Rattus norvegicus 54-57 27856058-3 2017 TiO2 P-25 was found to be the most photoactive catalyst for the removal of 5-FU, under simulated solar irradiation. Fluorouracil 75-79 tubulin polymerization promoting protein Homo sapiens 5-9 27856058-6 2017 Scavenging experiments revealed that HO radicals and h+ were the major reactive species mediating photocatalytic degradation of 5-FU using TiO2 P-25 and N/S-doped TiO2 catalysts, under simulated solar irradiation. Fluorouracil 128-132 tubulin polymerization promoting protein Homo sapiens 144-154 28395758-0 2017 Prevention of 5-fluorouracil-induced early severe toxicity by pre-therapeutic dihydropyrimidine dehydrogenase deficiency screening: Assessment of a multiparametric approach. Fluorouracil 14-28 dihydropyrimidine dehydrogenase Homo sapiens 78-109 28025107-0 2017 Apigenin potentiates the antitumor activity of 5-FU on solid Ehrlich carcinoma: Crosstalk between apoptotic and JNK-mediated autophagic cell death platforms. Fluorouracil 47-51 mitogen-activated protein kinase 8 Mus musculus 112-115 28051999-0 2017 FOXM1 evokes 5-fluorouracil resistance in colorectal cancer depending on ABCC10. Fluorouracil 13-27 forkhead box M1 Homo sapiens 0-5 28051999-4 2017 Here we identified the upregulation of FOXM1 in 5-FU nonresponsive CRC patients by gene expression profile analysis and 5-FU-resistant CRC cells by qRT-PCR assay. Fluorouracil 48-52 forkhead box M1 Homo sapiens 39-44 28051999-5 2017 Silencing of FOXM1 promoted the sensitivity of CRC cells to 5-FU by enhancing cell apoptosis, while overexpression of FOXM1 conferred CRC cells with 5-FU resistance both in vitro and in vivo. Fluorouracil 60-64 forkhead box M1 Homo sapiens 13-18 28051999-5 2017 Silencing of FOXM1 promoted the sensitivity of CRC cells to 5-FU by enhancing cell apoptosis, while overexpression of FOXM1 conferred CRC cells with 5-FU resistance both in vitro and in vivo. Fluorouracil 149-153 forkhead box M1 Homo sapiens 118-123 28051999-6 2017 Furthermore, we showed that genetic and pharmacological inhibition of FOXM1 resensitized resistant CRC cells to 5-FU treatment. Fluorouracil 112-116 forkhead box M1 Homo sapiens 70-75 28051999-8 2017 Notably, treatment with ABCC10 inhibitor reversed FOXM1-induced resistance to 5-FU in vivo. Fluorouracil 78-82 forkhead box M1 Homo sapiens 50-55 28051999-10 2017 Therefore, FOXM1 promotes 5-FU resistance by upregulating ABCC10, suggesting that FOXM1/ABCC10 axis may serve as a potential therapeutic target for 5-FU resistance in CRC patients. Fluorouracil 26-30 forkhead box M1 Homo sapiens 11-16 28051999-10 2017 Therefore, FOXM1 promotes 5-FU resistance by upregulating ABCC10, suggesting that FOXM1/ABCC10 axis may serve as a potential therapeutic target for 5-FU resistance in CRC patients. Fluorouracil 26-30 forkhead box M1 Homo sapiens 82-87 28051999-10 2017 Therefore, FOXM1 promotes 5-FU resistance by upregulating ABCC10, suggesting that FOXM1/ABCC10 axis may serve as a potential therapeutic target for 5-FU resistance in CRC patients. Fluorouracil 148-152 forkhead box M1 Homo sapiens 11-16 28051999-10 2017 Therefore, FOXM1 promotes 5-FU resistance by upregulating ABCC10, suggesting that FOXM1/ABCC10 axis may serve as a potential therapeutic target for 5-FU resistance in CRC patients. Fluorouracil 148-152 forkhead box M1 Homo sapiens 82-87 28055019-5 2017 Notably, REP1 is highly expressed in colon cancer tissues and cell lines, and silencing of REP1 sensitizes colon cancer cells to serum starvation- and 5-FU-induced apoptosis. Fluorouracil 151-155 CHM Rab escort protein Homo sapiens 9-13 33275228-0 2020 GALNT10 promotes the proliferation and metastatic ability of gastric cancer and reduces 5-fluorouracil sensitivity by activating HOXD13. Fluorouracil 88-102 polypeptide N-acetylgalactosaminyltransferase 10 Homo sapiens 0-7 33275228-0 2020 GALNT10 promotes the proliferation and metastatic ability of gastric cancer and reduces 5-fluorouracil sensitivity by activating HOXD13. Fluorouracil 88-102 homeobox D13 Homo sapiens 129-135 33275228-7 2020 Furthermore, 5-fluorouracil (5-Fu)-resistant cells were used to detect the relationship between GALNT10 and 5-Fu sensitivity of GC cells. Fluorouracil 13-27 polypeptide N-acetylgalactosaminyltransferase 10 Homo sapiens 96-103 33275228-7 2020 Furthermore, 5-fluorouracil (5-Fu)-resistant cells were used to detect the relationship between GALNT10 and 5-Fu sensitivity of GC cells. Fluorouracil 29-33 polypeptide N-acetylgalactosaminyltransferase 10 Homo sapiens 96-103 33275228-7 2020 Furthermore, 5-fluorouracil (5-Fu)-resistant cells were used to detect the relationship between GALNT10 and 5-Fu sensitivity of GC cells. Fluorouracil 108-112 polypeptide N-acetylgalactosaminyltransferase 10 Homo sapiens 96-103 28055019-5 2017 Notably, REP1 is highly expressed in colon cancer tissues and cell lines, and silencing of REP1 sensitizes colon cancer cells to serum starvation- and 5-FU-induced apoptosis. Fluorouracil 151-155 CHM Rab escort protein Homo sapiens 91-95 29682445-0 2017 UPFRONT DPD DEFICIENCY DETECTION TO SECURE 5-FU ADMINISTRATION: PART 2- APPLICATION TO HEAD-AND-NECK CANCER PATIENTS. Fluorouracil 43-47 dihydropyrimidine dehydrogenase Homo sapiens 8-11 26715117-1 2017 BACKGROUND: Oral fluoropyrimidine S-1 contains tegafur, which is metabolized to 5-fluorouracil by cytochrome P450 2A6 (CYP2A6). Fluorouracil 80-94 cytochrome P450 family 2 subfamily A member 6 Homo sapiens 98-117 26715117-1 2017 BACKGROUND: Oral fluoropyrimidine S-1 contains tegafur, which is metabolized to 5-fluorouracil by cytochrome P450 2A6 (CYP2A6). Fluorouracil 80-94 cytochrome P450 family 2 subfamily A member 6 Homo sapiens 119-125 27130464-0 2017 Expression of BRCA1, a factor closely associated with relapse-free survival, in patients who underwent neoadjuvant chemotherapy with docetaxel, cisplatin, and fluorouracil for squamous cell carcinoma of the esophagus. Fluorouracil 159-171 BRCA1 DNA repair associated Homo sapiens 14-19 32945069-8 2020 Combined administration of 5FU and UBE significantly inhibited the tumour growth of multidrug-resistant cell lines A549/ADR in nude mice by down-regulating the mRNA and protein expression of P-gp. Fluorouracil 27-30 phosphoglycolate phosphatase Mus musculus 191-195 32945069-12 2020 The results of this study demonstrated that UBE combined with fluorouracil attenuated multiple drug resistance and inhibited the expression of P-gp in lung cancer. Fluorouracil 62-74 phosphoglycolate phosphatase Mus musculus 143-147 32738620-8 2020 Molecular docking study identified pyrocatechol (PCL) and 5-fluorouracil (FU) as potential leads of CD151-LEL. Fluorouracil 58-72 CD151 molecule (Raph blood group) Homo sapiens 100-105 33193874-0 2020 Exosomes derived from 5-fluorouracil-resistant colon cancer cells are enriched in GDF15 and can promote angiogenesis. Fluorouracil 22-36 growth differentiation factor 15 Homo sapiens 82-87 33193874-14 2020 Conclusions: Our study reveals the molecular regulation of angiogenesis in 5-FU-resistant colon cancer and suggests that the GDF15-POSTN axis may be a novel target for anti-angiogenic therapies in colon cancer. Fluorouracil 75-79 growth differentiation factor 15 Homo sapiens 125-130 27917904-6 2016 Furthermore, among TNM II and III gp130-high patients, those who were treated with 5-fluorouracil (5-FU) based adjuvant chemotherapy had better OS (P < 0.001). Fluorouracil 83-97 teneurin transmembrane protein 1 Homo sapiens 19-22 27917904-6 2016 Furthermore, among TNM II and III gp130-high patients, those who were treated with 5-fluorouracil (5-FU) based adjuvant chemotherapy had better OS (P < 0.001). Fluorouracil 99-103 teneurin transmembrane protein 1 Homo sapiens 19-22 28051262-8 2016 Knockdown of IGF1R significantly decreased IC50 of 5-FU, paclitaxel (PTX) and Doxorubicin (DOX) in Huh7 and HepG2 cells. Fluorouracil 51-55 MIR7-3 host gene Homo sapiens 99-103 28051262-10 2016 MiR-379 overexpression sensitized Huh7 and HepG2 cells to 5-FU, PTX and DOX and also enhanced DOX-induced cell apoptosis. Fluorouracil 58-62 MIR7-3 host gene Homo sapiens 34-38 27501171-9 2016 Knockdown of miR-221 in 5-FU resistant cells resulted in reduced cell proliferation, increased apoptosis, restored chemosensitivity, and led to inactivation of the Wnt/beta-catenin pathway mediated by alteration in DKK2 expression. Fluorouracil 24-28 dickkopf WNT signaling pathway inhibitor 2 Homo sapiens 215-219 27501171-12 2016 CONCLUSION: MiR-221 controls 5-FU resistance of EC partly via modulation of Wnt/beta-catenin-EMT pathways by direct targeting of DKK2 expression. Fluorouracil 29-33 dickkopf WNT signaling pathway inhibitor 2 Homo sapiens 129-133 27569869-5 2016 In addition, variants in genes of the 5-FU metabolic pathway, including TYMS, MTHFR and DPYD also influenced capecitabine efficacy and toxicity. Fluorouracil 38-42 methylenetetrahydrofolate reductase Homo sapiens 78-83 27569869-5 2016 In addition, variants in genes of the 5-FU metabolic pathway, including TYMS, MTHFR and DPYD also influenced capecitabine efficacy and toxicity. Fluorouracil 38-42 dihydropyrimidine dehydrogenase Homo sapiens 88-92 27800618-0 2016 Retracted: NEAT1 induces epithelial-mesenchymal transition and 5-FU resistance through the miR-129/ZEB2 axis in breast cancer. Fluorouracil 63-67 nuclear paraspeckle assembly transcript 1 Homo sapiens 11-16 27588398-9 2016 Partial restoration of fluorouracil sensitivity was induced by inhibiting ABCC11 in MCF7/E and MDA-MB-231/E cells. Fluorouracil 23-35 ATP binding cassette subfamily C member 11 Homo sapiens 74-80 33062674-0 2020 GDF15 Repression Contributes to 5-Fluorouracil Resistance in Human Colon Cancer by Regulating Epithelial-Mesenchymal Transition and Apoptosis. Fluorouracil 32-46 growth differentiation factor 15 Homo sapiens 0-5 33062674-6 2020 Quantitative reverse transcription-PCR and western blotting revealed that 5-FU-resistant colon cancer cells expressed lower levels of growth differentiation factor 15 (GDF15) than did 5-FU-sensitive colon cancer cells. Fluorouracil 74-78 growth differentiation factor 15 Homo sapiens 134-166 33062674-6 2020 Quantitative reverse transcription-PCR and western blotting revealed that 5-FU-resistant colon cancer cells expressed lower levels of growth differentiation factor 15 (GDF15) than did 5-FU-sensitive colon cancer cells. Fluorouracil 74-78 growth differentiation factor 15 Homo sapiens 168-173 33062674-7 2020 Moreover, the transient GDF15 overexpression resensitized 5-FU-resistant colon cells to 5-FU. Fluorouracil 58-62 growth differentiation factor 15 Homo sapiens 24-29 33062674-7 2020 Moreover, the transient GDF15 overexpression resensitized 5-FU-resistant colon cells to 5-FU. Fluorouracil 88-92 growth differentiation factor 15 Homo sapiens 24-29 27518715-3 2016 Moreover, ECL reactions were done in the presence of several solutions of 5-Fu at a fixed concentration of the G1.0 and G1.5 dendrimers at pH 6.1 and 10.0 (binding study). Fluorouracil 74-78 BUD31 homolog Homo sapiens 111-115 32929576-0 2020 Phosphorene and Na-, Ca-, and Fe-doped phosphorene as candidates for delivery of mercaptopurine and fluorouracil anticancer drugs. Fluorouracil 100-112 general transcription factor IIE subunit 1 Homo sapiens 30-32 32675286-9 2020 Cells lacking the BRCA2 were sensitive to 5-FU in the presence of ATRi. Fluorouracil 42-46 BRCA2 DNA repair associated Homo sapiens 18-23 27518715-9 2016 Graphical Abstract ECL emission for the [Ru(bpy)3](2+)/ G1.0 dendrimer reaction in the presence of the 5-Fu at pH 6.1. Fluorouracil 103-107 BUD31 homolog Homo sapiens 56-60 27544765-1 2016 PURPOSE: Dihydropyrimidine dehydrogenase (DPD) is a critical determinant of 5-fluorouracil pharmacology, and reduced activity of DPD as a result of deleterious polymorphisms in the gene encoding DPD (DPYD) can result in severe treatment-related toxicity. Fluorouracil 76-90 dihydropyrimidine dehydrogenase Homo sapiens 9-40 32927726-5 2020 Lewisx, Sox2, ALDH and CD44 expression, tumorsphere formation, resistance to 5-FU treatment and in vivo tumor growth were increased in FUT9-expressing MC38 cells compared to the control cells. Fluorouracil 77-81 fucosyltransferase 9 Mus musculus 135-139 32838518-6 2020 Western blot analysis reveals the formation of ternary complex of thymidylate synthase, which shows the intracellular conversion of tegafur into 5-FU after its release from PFL. Fluorouracil 145-149 profilin 2 Homo sapiens 173-176 27544765-1 2016 PURPOSE: Dihydropyrimidine dehydrogenase (DPD) is a critical determinant of 5-fluorouracil pharmacology, and reduced activity of DPD as a result of deleterious polymorphisms in the gene encoding DPD (DPYD) can result in severe treatment-related toxicity. Fluorouracil 76-90 dihydropyrimidine dehydrogenase Homo sapiens 42-45 27180296-0 2016 Unravelling the potential of a new uracil phosphoribosyltransferase (UPRT) from Arabidopsis thaliana in sensitizing HeLa cells towards 5-fluorouracil. Fluorouracil 135-149 uracil phosphoribosyltransferase Arabidopsis thaliana 35-67 27180296-0 2016 Unravelling the potential of a new uracil phosphoribosyltransferase (UPRT) from Arabidopsis thaliana in sensitizing HeLa cells towards 5-fluorouracil. Fluorouracil 135-149 uracil phosphoribosyltransferase Arabidopsis thaliana 69-73 27180296-1 2016 In silico studies with uracil phosphoribosyltransferase from Arabidopsis thaliana (AtUPRT) revealed its lower binding energies for uracil and 5-fluorouracil (5-FU) as compared to those of bacterial UPRT indicating the prospective of AtUPRT in gene therapy implications. Fluorouracil 142-156 uracil phosphoribosyltransferase Arabidopsis thaliana 23-55 27180296-1 2016 In silico studies with uracil phosphoribosyltransferase from Arabidopsis thaliana (AtUPRT) revealed its lower binding energies for uracil and 5-fluorouracil (5-FU) as compared to those of bacterial UPRT indicating the prospective of AtUPRT in gene therapy implications. Fluorouracil 142-156 uracil phosphoribosyltransferase Arabidopsis thaliana 85-89 27180296-1 2016 In silico studies with uracil phosphoribosyltransferase from Arabidopsis thaliana (AtUPRT) revealed its lower binding energies for uracil and 5-fluorouracil (5-FU) as compared to those of bacterial UPRT indicating the prospective of AtUPRT in gene therapy implications. Fluorouracil 158-162 uracil phosphoribosyltransferase Arabidopsis thaliana 23-55 27180296-1 2016 In silico studies with uracil phosphoribosyltransferase from Arabidopsis thaliana (AtUPRT) revealed its lower binding energies for uracil and 5-fluorouracil (5-FU) as compared to those of bacterial UPRT indicating the prospective of AtUPRT in gene therapy implications. Fluorouracil 158-162 uracil phosphoribosyltransferase Arabidopsis thaliana 85-89 27602148-6 2016 It was observed that RNAi-mediated downregulation of EGFR or MRP2 increased the sensitivity to 5-FU and cisplatin in OC2 cells. Fluorouracil 95-99 ATP binding cassette subfamily C member 2 Homo sapiens 61-65 27602148-6 2016 It was observed that RNAi-mediated downregulation of EGFR or MRP2 increased the sensitivity to 5-FU and cisplatin in OC2 cells. Fluorouracil 95-99 one cut homeobox 2 Homo sapiens 117-120 27602148-7 2016 Downregulation of EGFR resulted in significant suppression of OC2 tumor growth following 5-FU administration. Fluorouracil 89-93 one cut homeobox 2 Homo sapiens 62-65 27487151-0 2016 ABCC2-24C > T polymorphism is associated with the response to platinum/5-Fu-based neoadjuvant chemotherapy and better clinical outcomes in advanced gastric cancer patients. Fluorouracil 74-78 ATP binding cassette subfamily C member 2 Homo sapiens 0-5 27527606-7 2016 RESULTS: Upon treatment with 5-fluorouracil (5-FU), apoptosis was increased in latently infected ACH2 cells encoding competent p53 compared with uninfected parent A3.01 cells, while the apoptosis of latently infected p53 null J1.1 cells was less than that of uninfected cells. Fluorouracil 29-43 acyl-CoA thioesterase 1 Homo sapiens 97-101 27648358-5 2016 Knockdown of PCDH20 expression increases Akt phosphorylation, which leads to elevated mTOR activity and enhanced 5-fluorouracil resistance; whereas rescue of PCDH20 expression in miR-122-expressing cells decreases Akt and mTOR phosphorylation, re-sensitizing hepatocellular carcinoma cell to 5-fluorouracil induced apoptosis. Fluorouracil 113-127 microRNA 122 Homo sapiens 179-186 26392091-4 2016 The analysis of the changes in the expression of genes involved in the response to DNA damage (CDKN1A, GADD45A, MDM2), apoptosis (BAX, BCL2) and oncogenesis (MYC, JUN) showed that 5-FU, CDDP and ET upregulated the genes involved in DNA damage response, while the anti-apoptotic gene BCL2 and oncogene MYC were downregulated. Fluorouracil 180-184 MDM2 proto-oncogene Homo sapiens 112-116 27177453-7 2016 Cells combined treatment with allicin and 5-FU increased intracellular reactive oxygen species (ROS) level, reduced mitochondrial membrane potential (DeltaPsim), activated caspase-3 and PARP, and down-regulated Bcl-2 compared with DMSO, allicin and 5-FU treated alone. Fluorouracil 42-46 caspase 3 Mus musculus 172-181 27177453-7 2016 Cells combined treatment with allicin and 5-FU increased intracellular reactive oxygen species (ROS) level, reduced mitochondrial membrane potential (DeltaPsim), activated caspase-3 and PARP, and down-regulated Bcl-2 compared with DMSO, allicin and 5-FU treated alone. Fluorouracil 42-46 poly (ADP-ribose) polymerase family, member 1 Mus musculus 186-190 26883251-7 2016 Under different concentrations of 5-FU and paclitaxel in MDA-MB231 cell, E-cadherin mRNA and protein expressions increased gradually with the increase of concentrations, and Vimentin and N-cadherin mRNA and protein expressions decreased gradually with the decrease of concentrations (all P < 0.05). Fluorouracil 34-38 cadherin 2 Homo sapiens 187-197 26472729-8 2016 PRMT1 downregulation in GC cells by RNA interference inhibited cisplatin and 5-fluorouracil sensitivity. Fluorouracil 77-91 protein arginine methyltransferase 1 Homo sapiens 0-5 32863323-9 2020 5-Fu treatment was enhanced by inhibiting miR-887 and decreased by miR-887 precursor treatment. Fluorouracil 0-4 microRNA 887 Homo sapiens 42-49 32863323-9 2020 5-Fu treatment was enhanced by inhibiting miR-887 and decreased by miR-887 precursor treatment. Fluorouracil 0-4 microRNA 887 Homo sapiens 67-74 32571958-5 2020 Moreover, blockade of P38 or CREB sensitizes HCC cells to 5FU. Fluorouracil 58-61 cAMP responsive element binding protein 1 Homo sapiens 29-33 32879665-0 2020 Interleukin-1 receptor antagonist enhances chemosensitivity to fluorouracil in treatment of Kras mutant colon cancer. Fluorouracil 63-75 KRAS proto-oncogene, GTPase Homo sapiens 92-96 32922964-10 2020 Polymorphisms of the glucocorticoid receptor and variants of CCL2, YAP1, miR-21-5p and NF-kappabeta might be responsible for different responses to treatments used in keloid scars such as 5-fluorouracil. Fluorouracil 188-202 microRNA 215 Homo sapiens 73-82 32533886-5 2020 In multiple in vitro and in vivo models of PDAC, spanning human and murine PDAC cells, and orthotopic xenografts, we determined that the expression of K17 results in a more than two-fold increase in resistance to Gem and 5-fluorouracil, key components of current standard-of-care chemotherapeutic regimens. Fluorouracil 221-235 keratin 17 Mus musculus 151-154 32688344-0 2020 CTCF promotes colorectal cancer cell proliferation and chemotherapy resistance to 5-FU via the P53-Hedgehog axis. Fluorouracil 82-86 CCCTC-binding factor Homo sapiens 0-4 32688344-6 2020 CCK-8 and apoptosis assays revealed that 5-fluorouracil chemosensitivity was negatively associated with CTCF expression. Fluorouracil 41-55 CCCTC-binding factor Homo sapiens 104-108 27210058-7 2016 MTT assay and TUNEL assay revealed that metformin (4 mg/ml) and 5-FU (2.5 microg/ml) combination treatment effectively inhibited cell growth and induced apoptosis in OSCC cell lines (HSC2, HSC3 and HSC4) compared to either agent alone. Fluorouracil 64-68 DnaJ heat shock protein family (Hsp40) member B7 Homo sapiens 189-193 27334757-0 2016 Knockdown of NFBD1/MDC1 enhances chemosensitivity to cisplatin or 5-fluorouracil in nasopharyngeal carcinoma CNE1 cells. Fluorouracil 66-80 mediator of DNA damage checkpoint 1 Homo sapiens 13-18 27334757-0 2016 Knockdown of NFBD1/MDC1 enhances chemosensitivity to cisplatin or 5-fluorouracil in nasopharyngeal carcinoma CNE1 cells. Fluorouracil 66-80 mediator of DNA damage checkpoint 1 Homo sapiens 19-23 27334757-6 2016 NFBD1 expression in NPC CNE1 cell lines was depleted using lentivirus-mediated short hairpin RNA, and the elevated sensitivity of these NFBD1-inhibited NPC cells to therapeutic reagent CDDP and 5-fluorouracil (5-FU) was evaluated using MTS assays. Fluorouracil 194-208 mediator of DNA damage checkpoint 1 Homo sapiens 0-5 27334757-6 2016 NFBD1 expression in NPC CNE1 cell lines was depleted using lentivirus-mediated short hairpin RNA, and the elevated sensitivity of these NFBD1-inhibited NPC cells to therapeutic reagent CDDP and 5-fluorouracil (5-FU) was evaluated using MTS assays. Fluorouracil 194-208 mediator of DNA damage checkpoint 1 Homo sapiens 136-141 27334757-6 2016 NFBD1 expression in NPC CNE1 cell lines was depleted using lentivirus-mediated short hairpin RNA, and the elevated sensitivity of these NFBD1-inhibited NPC cells to therapeutic reagent CDDP and 5-fluorouracil (5-FU) was evaluated using MTS assays. Fluorouracil 210-214 mediator of DNA damage checkpoint 1 Homo sapiens 0-5 27334757-6 2016 NFBD1 expression in NPC CNE1 cell lines was depleted using lentivirus-mediated short hairpin RNA, and the elevated sensitivity of these NFBD1-inhibited NPC cells to therapeutic reagent CDDP and 5-fluorouracil (5-FU) was evaluated using MTS assays. Fluorouracil 210-214 mediator of DNA damage checkpoint 1 Homo sapiens 136-141 27334757-7 2016 Flow cytometry analysis also showed that NFBD1 knockdown led to an obvious induction of apoptosis in CDDP- or 5-FU-treated CNE1 cells. Fluorouracil 110-114 mediator of DNA damage checkpoint 1 Homo sapiens 41-46 27334757-8 2016 Furthermore, we implicated the involvement of NFBD1 in Rad51 and DNA-PKcs foci formation following CDDP or 5-FU chemotherapy. Fluorouracil 107-111 mediator of DNA damage checkpoint 1 Homo sapiens 46-51 27493479-0 2016 Wnt/Beta-Catenin Signal Inhibitor HC-1 Sensitizes Oral Squamous Cell Carcinoma Cells to 5-Fluorouracil through Reduction of CD44-Positive Population. Fluorouracil 88-102 CD44 molecule (Indian blood group) Homo sapiens 124-128 27493479-9 2016 In addition, HC-1 increases the cytotoxicity of HSC2 cells to 5-fluorouracil. Fluorouracil 62-76 CYCS pseudogene 39 Homo sapiens 13-17 27493479-10 2016 The combination treatment of HC-1 with 5-fluorouracil significantly increased the apoptotic cells whereas treatment by either compound did not. Fluorouracil 39-53 CYCS pseudogene 39 Homo sapiens 29-33 26967246-8 2016 Treatment of MLH1-methylated colon cancer cell lines with the demethylating agent 5"-aza-2"-deoxycytidine induces the expression of MLH1 and sensitizes cancer cells to 5-fluorouracil. Fluorouracil 168-182 mutL homolog 1 Mus musculus 13-17 27167197-6 2016 Clinically, our data reveal that overexpression of miR-363 correlates with the poor survival outcomes in patients with gastric cancer, and docetaxel + cisplatin + 5-FU (DCF) regimen response is impaired in patients with miR-363 overexpression. Fluorouracil 163-167 microRNA 363 Homo sapiens 51-58 32766276-0 2020 ZFP36 Binds With PRC1 to Inhibit Tumor Growth and Increase 5-Fu Chemosensitivity of Hepatocellular Carcinoma. Fluorouracil 59-63 zinc finger protein 36 Mus musculus 0-5 32766276-3 2020 This study aimed to investigate the underlying mechanisms by which ZFP36 inhibited HCC progression and increased fluorouracil (5-Fu) sensitivity. Fluorouracil 113-125 zinc finger protein 36 Mus musculus 67-72 32766276-3 2020 This study aimed to investigate the underlying mechanisms by which ZFP36 inhibited HCC progression and increased fluorouracil (5-Fu) sensitivity. Fluorouracil 127-131 zinc finger protein 36 Mus musculus 67-72 32766276-6 2020 Further investigations demonstrated that overexpression of ZFP36 inhibited tumor growth and promoted 5-Fu sensitivity in xenograft tumor mice model, which could be reversed when PRC1 overexpressed simultaneously. Fluorouracil 101-105 zinc finger protein 36 Mus musculus 59-64 32653028-0 2020 LncRNA HOTAIR-mediated MTHFR methylation inhibits 5-fluorouracil sensitivity in esophageal cancer cells. Fluorouracil 50-64 methylenetetrahydrofolate reductase Homo sapiens 23-28 32653028-10 2020 Interference with lncRNA HOTAIR enhanced 5-FU-induced apoptosis, exhibited anti-proliferative activity, and reduced promoter methylation of the MTHFR in EC cells. Fluorouracil 41-45 methylenetetrahydrofolate reductase Homo sapiens 144-149 32638844-13 2020 Microscopically, comparing with CT group, PRP application significantly promoted the healing of colonic anastomosis subjected to 5-FU application by improving tissue edema, necrosis, submucosal bridging and collagen formation (p<0.05). Fluorouracil 129-133 proline rich protein 2-like 1 Rattus norvegicus 42-45 32638844-16 2020 CONCLUSION: PRP administration on colonic anastomosis significantly promotes the healing process of anastomosis in rats receiving 5-FU. Fluorouracil 130-134 proline rich protein 2-like 1 Rattus norvegicus 12-15 32418739-10 2020 Furthermore, CCND1 silencing significantly increased protein level of gamma-H2AX and decreased that of RAD51 under 5-Fu exposure. Fluorouracil 115-119 RAD51 recombinase Homo sapiens 103-108 32418739-11 2020 Moreover, CCND1 silencing enhanced the sensitivity of HepG2 and SMMC-7721 cells to 5-Fu, which was effectively abrogated by RAD51 upregulation. Fluorouracil 83-87 RAD51 recombinase Homo sapiens 124-129 27268079-2 2016 However, the relationship between EGFR mutation status and dihydropyrimidine dehydrogenase (DPD), a 5-FU degrading enzyme, is unknown. Fluorouracil 100-104 dihydropyrimidine dehydrogenase Homo sapiens 59-90 27268079-2 2016 However, the relationship between EGFR mutation status and dihydropyrimidine dehydrogenase (DPD), a 5-FU degrading enzyme, is unknown. Fluorouracil 100-104 dihydropyrimidine dehydrogenase Homo sapiens 92-95 27142386-15 2016 Smaller tumor size and negative lymph node status were both associated with a higher treatment efficacy to anthracycline treatment combined with 5-FU (cT1/2 vs cT3/4, p = 0.035, cN+ vs cN-, p < 0.05). Fluorouracil 145-149 dickkopf like acrosomal protein 1 Homo sapiens 160-165 27181275-0 2016 Evaluation of clinical implementation of prospective DPYD genotyping in 5-fluorouracil- or capecitabine-treated patients. Fluorouracil 72-86 dihydropyrimidine dehydrogenase Homo sapiens 53-57 32558229-1 2020 Affibody-conjugated RALA (affi-RA) are designed for delivering oligomeric 5-fluorodeoxyuridine (FUdR, metabolite of 5-FU) strand to raise the selectivity of 5-fluorouracil (5-FU), decrease its toxicity and improve its suboptimal therapeutic efficacy. Fluorouracil 116-120 RAS like proto-oncogene A Homo sapiens 20-24 26869189-12 2016 Sca-1(high) allografts were more resistant to cisplatin/fluorouracil chemotherapy than Sca-1(negative) allografts, and overexpressed Bcl-xL. Fluorouracil 56-68 lymphocyte antigen 6 complex, locus A Mus musculus 0-5 32558229-1 2020 Affibody-conjugated RALA (affi-RA) are designed for delivering oligomeric 5-fluorodeoxyuridine (FUdR, metabolite of 5-FU) strand to raise the selectivity of 5-fluorouracil (5-FU), decrease its toxicity and improve its suboptimal therapeutic efficacy. Fluorouracil 157-171 RAS like proto-oncogene A Homo sapiens 20-24 32558229-1 2020 Affibody-conjugated RALA (affi-RA) are designed for delivering oligomeric 5-fluorodeoxyuridine (FUdR, metabolite of 5-FU) strand to raise the selectivity of 5-fluorouracil (5-FU), decrease its toxicity and improve its suboptimal therapeutic efficacy. Fluorouracil 173-177 RAS like proto-oncogene A Homo sapiens 20-24 32647090-11 2020 A 5-FU resulted in severe ileal mucositis through TNF-alpha, NF-kappaB, MMP-9, and AQP-4 disturbances. Fluorouracil 2-6 matrix metallopeptidase 9 Rattus norvegicus 72-77 32606741-6 2020 In molecular mechanisms, ELE and 5-FU in combination enhances apoptosis in both cell lines through Bl-2 family protein and caspase cascade modulation, thereby inhibiting NF-kB pathway through IKKbeta, IKKalpha, and p65 downregulation in the cytoplasm and p50 and p65 downregulation in the nucleus. Fluorouracil 33-37 component of inhibitor of nuclear factor kappa B kinase complex Homo sapiens 192-199 32606741-6 2020 In molecular mechanisms, ELE and 5-FU in combination enhances apoptosis in both cell lines through Bl-2 family protein and caspase cascade modulation, thereby inhibiting NF-kB pathway through IKKbeta, IKKalpha, and p65 downregulation in the cytoplasm and p50 and p65 downregulation in the nucleus. Fluorouracil 33-37 component of inhibitor of nuclear factor kappa B kinase complex Homo sapiens 201-209 27461651-2 2016 DPYD*2A/*5A/*9A and UGT1A1 * 6/*28 polymorphisms are related to the toxicity of fluorouracil drugs and irinotecan, respectively. Fluorouracil 80-92 UDP glucuronosyltransferase family 1 member A1 Homo sapiens 20-26 32606741-7 2020 ELE and 5-FU in combination regulated the PI3K/AKT pathway through p-AKT, P-85, p110r, p-PDK1, and p110a protein and RAF-MEK-ERK pathway inhibition through the p-c-raf and p-ERK downregulation. Fluorouracil 8-12 phosphoinositide-3-kinase regulatory subunit 2 Homo sapiens 74-85 32606741-7 2020 ELE and 5-FU in combination regulated the PI3K/AKT pathway through p-AKT, P-85, p110r, p-PDK1, and p110a protein and RAF-MEK-ERK pathway inhibition through the p-c-raf and p-ERK downregulation. Fluorouracil 8-12 pyruvate dehydrogenase kinase 1 Homo sapiens 89-93 32142918-11 2020 Drosha wild type GCSCs with SHMT2 are sensitive to 5-fluorouracil; however, Drosha low-expressing GCSCs with SHMT1 are 5-FU-resistant. Fluorouracil 51-65 serine hydroxymethyltransferase 2 Homo sapiens 28-33 32142918-11 2020 Drosha wild type GCSCs with SHMT2 are sensitive to 5-fluorouracil; however, Drosha low-expressing GCSCs with SHMT1 are 5-FU-resistant. Fluorouracil 119-123 drosha ribonuclease III Homo sapiens 76-82 32142918-12 2020 The loss of miR-6778-5p or SHMT1 notably mitigates GCSC sphere formation and increases sensitivity to 5-fluorouracil in Drosha-knockdown gastric cancer cells. Fluorouracil 102-116 drosha ribonuclease III Homo sapiens 120-126 26977021-6 2016 CCK8 viability assay indicated that inhibition of HSP70 increased the sensitivity of SK-BR-3 cells to fluorouracil treatment. Fluorouracil 102-114 heat shock protein family A (Hsp70) member 4 Homo sapiens 50-55 26634371-8 2016 The UBXN2A knockout U2OS cells revealed that UBXNA is essential for the cytotoxic effect achieved by 5-FU. Fluorouracil 101-105 UBX domain protein 2A Homo sapiens 4-10 32587773-12 2020 In vivo, HSP47 supported tumor growth despite 5-FU treatment. Fluorouracil 46-50 serpin family H member 1 Homo sapiens 9-14 32382808-2 2020 The biological activity of the 5-FU degrading enzyme, dihydropyrimidine dehydrogenase (DPD), and the target enzyme thymidylate synthase (TS), are subject to circadian rhythmicity in healthy volunteers. Fluorouracil 31-35 dihydropyrimidine dehydrogenase Homo sapiens 54-85 32382808-2 2020 The biological activity of the 5-FU degrading enzyme, dihydropyrimidine dehydrogenase (DPD), and the target enzyme thymidylate synthase (TS), are subject to circadian rhythmicity in healthy volunteers. Fluorouracil 31-35 dihydropyrimidine dehydrogenase Homo sapiens 87-90 32028241-4 2020 FAM83H-AS1 was high-expressed in chemoresistant GC tissues and cell line (SGC7901/R), and silence of FAM83H-AS1 sensitized SGC7901/R cells to cisplatin (CDDP) and 5-fluorouracil (5-FU). Fluorouracil 163-177 FAM83H antisense RNA 1 (head to head) Homo sapiens 0-10 32028241-4 2020 FAM83H-AS1 was high-expressed in chemoresistant GC tissues and cell line (SGC7901/R), and silence of FAM83H-AS1 sensitized SGC7901/R cells to cisplatin (CDDP) and 5-fluorouracil (5-FU). Fluorouracil 163-177 FAM83H antisense RNA 1 (head to head) Homo sapiens 101-111 32028241-4 2020 FAM83H-AS1 was high-expressed in chemoresistant GC tissues and cell line (SGC7901/R), and silence of FAM83H-AS1 sensitized SGC7901/R cells to cisplatin (CDDP) and 5-fluorouracil (5-FU). Fluorouracil 179-183 FAM83H antisense RNA 1 (head to head) Homo sapiens 0-10 32028241-4 2020 FAM83H-AS1 was high-expressed in chemoresistant GC tissues and cell line (SGC7901/R), and silence of FAM83H-AS1 sensitized SGC7901/R cells to cisplatin (CDDP) and 5-fluorouracil (5-FU). Fluorouracil 179-183 FAM83H antisense RNA 1 (head to head) Homo sapiens 101-111 32028241-7 2020 In conclusion, FAM83H-AS1 is related with the CDDP and 5-FU insensitivity of GC patients, silence of FAM83H-AS1 promotes chemosensitivity of GC through Wnt/beta-catenin signaling pathway. Fluorouracil 55-59 FAM83H antisense RNA 1 (head to head) Homo sapiens 15-25 32348733-2 2020 Recent findings relating to the function of the human uracil-5 methyltransferase (U5MT), TRMT2A, and its interaction with 5-FU metabolites incorporated within tRNAs, lead to an additional hypothesis that is proposed here. Fluorouracil 122-126 tRNA methyltransferase 2 homolog A Homo sapiens 89-95 32426369-10 2020 But, XRCC1 knockdown could significantly improve the sensitivity of CD133+GBC-SD cells to 5-Fluorouracil via promoting cell necrosis and apoptosis. Fluorouracil 90-104 X-ray repair cross complementing 1 Homo sapiens 5-10 32411498-5 2020 During hematopoietic regeneration, such as in response to fluorouracil (5-FU), we also found reduced frequency and number of B lymphocytes in Gpr68-/- mice compared to wild type mice. Fluorouracil 58-70 G protein-coupled receptor 68 Mus musculus 142-147 32411498-5 2020 During hematopoietic regeneration, such as in response to fluorouracil (5-FU), we also found reduced frequency and number of B lymphocytes in Gpr68-/- mice compared to wild type mice. Fluorouracil 72-76 G protein-coupled receptor 68 Mus musculus 142-147 32411498-6 2020 Mechanism studies revealed that Gpr68 expression was upregulated in B lymphocytes of BM during aging and in hematopoietic progenitor cells after treatment with 5-FU. Fluorouracil 160-164 G protein-coupled receptor 68 Mus musculus 32-37 32122395-11 2020 RESULTS: In this report it was demonstrated, using RT-PCR and ELISA assay, that members of the NF-kappaB family c-Rel, RelA, RelB, NF-kappaB1, and NF-kappaB2 were all overexpressed in the 5-FU-resistant HL-60/5FU cells and that U-332 potently reduced the activity of c-Rel, RelA and NF-kappaB1 subunits in this cell line. Fluorouracil 188-192 REL proto-oncogene, NF-kB subunit Homo sapiens 112-117 32122395-12 2020 CONCLUSIONS: This finding indicates that c-Rel, RelA and NF-kappaB1 subunits are responsible for the resistance of HL-60/5FU cells to 5-FU and that U-332 is able to reverse this resistance. Fluorouracil 134-138 REL proto-oncogene, NF-kB subunit Homo sapiens 41-46 32194724-2 2020 Our study showed that ribosomal protein L11 (RPL11) was a crucial factor affecting sensitivity of gastric cancer to 5-FU, implying that RPL11 expression is a potential biomarker for predicting 5-FU sensitivity. Fluorouracil 116-120 ribosomal protein L11 Homo sapiens 22-43 32185127-2 2020 Herein, we provide mechanistic rationale for acquired or inherent chemotherapeutic resistance to the anti-tumor effects of 5-fluorouracil (5-FU) that is linked to oncogenic GLI1 transcription activity and NBS1 overexpression. Fluorouracil 123-137 GLI family zinc finger 1 Homo sapiens 173-177 32185127-2 2020 Herein, we provide mechanistic rationale for acquired or inherent chemotherapeutic resistance to the anti-tumor effects of 5-fluorouracil (5-FU) that is linked to oncogenic GLI1 transcription activity and NBS1 overexpression. Fluorouracil 139-143 GLI family zinc finger 1 Homo sapiens 173-177 32185127-8 2020 GLI1 inhibition could therefore be a therapeutic option for 5-FU resistant and BRAFV600E variant CRC patients. Fluorouracil 60-64 GLI family zinc finger 1 Homo sapiens 0-4 31802650-0 2020 LncRNA NEAT1 knockdown attenuates autophagy to elevate 5-FU sensitivity in colorectal cancer via targeting miR-34a. Fluorouracil 55-59 nuclear paraspeckle assembly transcript 1 Homo sapiens 7-12 31802650-3 2020 In this study, we aim to investigate the effect of long noncoding RNA nuclear paraspeckle assembly transcript 1 (LncRNA NEAT1) on cell viability, sensitivity to 5-FU, and autophagy of CRC cell lines. Fluorouracil 161-165 nuclear paraspeckle assembly transcript 1 Homo sapiens 120-125 31802650-7 2020 In addition, NEAT1 knockdown noticeably inhibited the proliferation of CRC cells and enhanced 5-FU sensitivity. Fluorouracil 94-98 nuclear paraspeckle assembly transcript 1 Homo sapiens 13-18 31802650-11 2020 Inhibition of miR-34a or overexpression of HMGB1 could effectively reverse elevated 5-FU sensitivity upon NEAT1 knockdown. Fluorouracil 84-88 nuclear paraspeckle assembly transcript 1 Homo sapiens 106-111 31802650-13 2020 CONCLUSION: These findings indicate that LncRNA NEAT1 could target miR-34a and promote autophagy to facilitate 5-FU chemoresistance in CRC. Fluorouracil 111-115 nuclear paraspeckle assembly transcript 1 Homo sapiens 48-53 31811910-0 2020 FoxO3 reverses 5-fluorouracil resistance in human colorectal cancer cells by inhibiting the Nrf2/TR1 signaling pathway. Fluorouracil 15-29 thioredoxin reductase 1 Homo sapiens 97-100 31811910-5 2020 Thioredoxin reductase 1 (TR1), a pivotal target gene of Nrf2, was observed to promote 5-FU resistance by reducing intracellular ROS levels. Fluorouracil 86-90 thioredoxin reductase 1 Homo sapiens 0-23 31811910-5 2020 Thioredoxin reductase 1 (TR1), a pivotal target gene of Nrf2, was observed to promote 5-FU resistance by reducing intracellular ROS levels. Fluorouracil 86-90 thioredoxin reductase 1 Homo sapiens 25-28 31313286-0 2020 Inhibition of KHSRP sensitizes colorectal cancer to 5-fluoruracil through miR-501-5p-mediated ERRFI1 mRNA degradation. Fluorouracil 52-65 KH-type splicing regulatory protein Homo sapiens 14-19 31313286-5 2020 Manipulating KHSRP expression altered cell proliferation and 5-FU resistance in CRC cells. Fluorouracil 61-65 KH-type splicing regulatory protein Homo sapiens 13-18 31313286-7 2020 Sensitivity to 5-FU mediated by KHSRP knockdown was reversed by ERRFI1 knockdown. Fluorouracil 15-19 KH-type splicing regulatory protein Homo sapiens 32-37 31934723-7 2020 Interestingly, SPZ1 overexpressing cells were resistant to 5-FU, a drug commonly used to treat cancer. Fluorouracil 59-63 spermatogenic leucine zipper 1 Homo sapiens 15-19 31892565-9 2020 CD44+ cells also possessed stemness properties and lower sensitivity to 5-FU in vitro. Fluorouracil 72-76 CD44 antigen Mus musculus 0-4 26634371-9 2016 UBXN2A overexpression markedly increased the apoptotic response of U2OS cells to the 5-FU. Fluorouracil 85-89 UBX domain protein 2A Homo sapiens 0-6 26281864-2 2016 DPYD gene variations can potentially predict toxicity to 5-fluorouracil (FU)-based therapy and KRAS-, NRAS-, BRAF-, PIK3CA-wild type status is a known prerequisite for epidermal growth factor receptor (EGFR) inhibitor therapy. Fluorouracil 57-71 dihydropyrimidine dehydrogenase Homo sapiens 0-4 31558477-0 2020 Clinical Assessment of 5-Fluorouracil/Leucovorin, Nab-Paclitaxel, and Irinotecan (FOLFIRABRAX) in Untreated Patients with Gastrointestinal Cancer Using UGT1A1 Genotype-Guided Dosing. Fluorouracil 23-37 UDP glucuronosyltransferase family 1 member A1 Homo sapiens 152-158 32247577-7 2020 BOK, a BCL-2 family protein thought comparable to multidomain pro-apoptotic proteins BAX and BAK, has recently been identified as a key player in metabolism of and resistance to the commonly used chemotherapeutic 5-FU. Fluorouracil 213-217 BCL2 antagonist/killer 1 Homo sapiens 93-96 31881903-3 2019 To deeply investigate the MKK3 functions in cancer, taking advantage of a panel of authenticated colorectal cancer (CRC) lines and primary colonocytes, we found that MKK3 activates specifically p38delta MAPK protein, which signaling is further triggered by 5-fluorouracil (5-FU) treatments, a largely adopted chemotherapeutic drug in CRC clinical practice. Fluorouracil 257-271 mitogen-activated protein kinase kinase 3 Homo sapiens 26-30 31881903-3 2019 To deeply investigate the MKK3 functions in cancer, taking advantage of a panel of authenticated colorectal cancer (CRC) lines and primary colonocytes, we found that MKK3 activates specifically p38delta MAPK protein, which signaling is further triggered by 5-fluorouracil (5-FU) treatments, a largely adopted chemotherapeutic drug in CRC clinical practice. Fluorouracil 257-271 mitogen-activated protein kinase kinase 3 Homo sapiens 166-170 31881903-3 2019 To deeply investigate the MKK3 functions in cancer, taking advantage of a panel of authenticated colorectal cancer (CRC) lines and primary colonocytes, we found that MKK3 activates specifically p38delta MAPK protein, which signaling is further triggered by 5-fluorouracil (5-FU) treatments, a largely adopted chemotherapeutic drug in CRC clinical practice. Fluorouracil 273-277 mitogen-activated protein kinase kinase 3 Homo sapiens 26-30 31881903-3 2019 To deeply investigate the MKK3 functions in cancer, taking advantage of a panel of authenticated colorectal cancer (CRC) lines and primary colonocytes, we found that MKK3 activates specifically p38delta MAPK protein, which signaling is further triggered by 5-fluorouracil (5-FU) treatments, a largely adopted chemotherapeutic drug in CRC clinical practice. Fluorouracil 273-277 mitogen-activated protein kinase kinase 3 Homo sapiens 166-170 31881903-4 2019 The overall achieved results proposed the MKK3/p38delta MAPK as relevant molecular axis involved in abrogating efficacy to 5-FU treatments in CRC. Fluorouracil 123-127 mitogen-activated protein kinase kinase 3 Homo sapiens 42-46 32175521-11 2020 Conclusions: BRCA1 promoter methylation is predictive of improved disease outcome in patients receiving cyclophosphamide, methotrexate, and fluorouracil drug treatment. Fluorouracil 140-152 BRCA1 DNA repair associated Homo sapiens 13-18 31529207-2 2019 Since 5-fluorouracil (5-FU) is one of the substrates for ABCC11, we examined whether ABCC11 is a predictive marker for an oral 5-FU derivative drug S-1 treatment in non-small cell lung cancer (NSCLC). Fluorouracil 6-20 ATP binding cassette subfamily C member 11 Homo sapiens 57-63 26847687-3 2016 JZL184 is a MAGL inhibitor, which in the present study was administered to colorectal cancer cell lines, resulting in decreased tumor proliferation, increased apoptosis and increased tumor cell sensitivity to 5-fluorouracil. Fluorouracil 209-223 monoglyceride lipase Homo sapiens 12-16 31529207-2 2019 Since 5-fluorouracil (5-FU) is one of the substrates for ABCC11, we examined whether ABCC11 is a predictive marker for an oral 5-FU derivative drug S-1 treatment in non-small cell lung cancer (NSCLC). Fluorouracil 22-26 ATP binding cassette subfamily C member 11 Homo sapiens 57-63 31529207-6 2019 RESULTS: There was a significant correlation between dihydropyrimidine dehydrogenase (DPD) gene expression and the IC50 for 5-FU. Fluorouracil 124-128 dihydropyrimidine dehydrogenase Homo sapiens 53-84 26840457-5 2016 In addition, NgBR suppresses p53 protein levels through activation of the PI3K/Akt/MDM2 pathway, which promotes p53 degradation via the ubiquitin proteasome pathway and thus increases the resistance of human hepatocellular cancer cells to 5-FU. Fluorouracil 239-243 MDM2 proto-oncogene Homo sapiens 83-87 31529207-6 2019 RESULTS: There was a significant correlation between dihydropyrimidine dehydrogenase (DPD) gene expression and the IC50 for 5-FU. Fluorouracil 124-128 dihydropyrimidine dehydrogenase Homo sapiens 86-89 31529207-8 2019 The distribution of the IC50 for 5-FU in combination with a potent inhibitor of DPD 5-chloro-2, 4-dihydropyrimidine (CDHP), which is contained in S-1, showed a significant reduction in the A/A group compared with the combined G/G and G/A group. Fluorouracil 33-37 dihydropyrimidine dehydrogenase Homo sapiens 80-83 26864651-5 2016 Interestingly, the content of CD133 + CXCR4+ cells in HCT116 cancer cells and RKO cells treated by 5-Fu/P85 copolymer micelles was decreased. Fluorouracil 99-103 C-X-C motif chemokine receptor 4 Homo sapiens 38-43 31542354-0 2019 Inhibition of hydrogen sulfide synthesis reverses acquired resistance to 5-FU through miR-215-5p-EREG/TYMS axis in colon cancer cells. Fluorouracil 73-77 microRNA 215 Homo sapiens 86-93 26864651-6 2016 Importantly, the epithelial-mesenchymal transition (EMT) of CD133 + CXCR4+ cells, which was strongly associated with liver metastasis of colon cancer, was also suppressed by giving 5-Fu/P85 copolymer micelles. Fluorouracil 181-185 C-X-C motif chemokine receptor 4 Homo sapiens 68-73 26864651-7 2016 The results indicated that 5-Fu/P85 copolymer micelles could inhibit the growth and metastasis of colon cancer, which could be attributed to the decrease of the content of CD133 + CXCR4+ cells and suppression of EMT of CD133 + CXCR4+ cells. Fluorouracil 27-31 C-X-C motif chemokine receptor 4 Homo sapiens 180-185 26864651-7 2016 The results indicated that 5-Fu/P85 copolymer micelles could inhibit the growth and metastasis of colon cancer, which could be attributed to the decrease of the content of CD133 + CXCR4+ cells and suppression of EMT of CD133 + CXCR4+ cells. Fluorouracil 27-31 C-X-C motif chemokine receptor 4 Homo sapiens 227-232 31732877-1 2019 PURPOSE: To investigate the influence of organic cation transporter 3 (OCT3) expression on the effect of the combination regimen of 5-fluorouracil, folinic acid and oxaliplatin ((m)FOLFOX6) in colorectal cancer (CRC) patients. Fluorouracil 132-146 OCTN3 Homo sapiens 41-69 26844701-10 2016 Exposure of explant cultures to 5FU-based CT increased the percentage of cells positive for active Caspase-3 and Terminal Deoxynucleotidyl Transferase dUTP Nick end Labelling (TUNEL), but also the expression of regeneration and proliferation markers beta-Catenin and Ki-67, as well as cyclooxygenase-2 (COX-2). Fluorouracil 32-35 DNA nucleotidylexotransferase Homo sapiens 113-150 31732877-1 2019 PURPOSE: To investigate the influence of organic cation transporter 3 (OCT3) expression on the effect of the combination regimen of 5-fluorouracil, folinic acid and oxaliplatin ((m)FOLFOX6) in colorectal cancer (CRC) patients. Fluorouracil 132-146 OCTN3 Homo sapiens 71-75 31815010-4 2019 Here, we revealed that PCDH17 was more highly expressed in 5-FU-sensitive CRC tissues than in 5-FU-resistant CRC tissues, and high expression of PCDH17 was correlated with high BECN1 expression. Fluorouracil 94-98 beclin 1 Homo sapiens 177-182 26265035-2 2016 We report here the genetic and phenotypic analyses of DPD in a family related to a patient who died after a first cycle of 5-fluorouracil and in 15 additional retrospective patients having a partial DPD deficiency (as measured by plasma dihydrouracil/uracil ratio). Fluorouracil 123-137 dihydropyrimidine dehydrogenase Homo sapiens 54-57 26691280-12 2016 Results indicated that 5-FU decreased H-ras, Rho-A, p53, Stat1 and increased Bax gene expression in Tumor2 and decreased Rac1, Rho-A, NF-kappaB and increased Bax and caspase-3 protein expression in Tumor2. Fluorouracil 23-27 signal transducer and activator of transcription 1 Homo sapiens 57-62 31361898-6 2019 Our associated finding of extensive irreversible TRMT2A-tRNA crosslinking in vivo following 5-Fluorouracil exposure is also intriguing, as it suggests a tangible mechanism for a previously suspected RNA-dependent route of Fluorouracil-mediated cytotoxicity. Fluorouracil 92-106 tRNA methyltransferase 2 homolog A Homo sapiens 49-55 31361898-6 2019 Our associated finding of extensive irreversible TRMT2A-tRNA crosslinking in vivo following 5-Fluorouracil exposure is also intriguing, as it suggests a tangible mechanism for a previously suspected RNA-dependent route of Fluorouracil-mediated cytotoxicity. Fluorouracil 94-106 tRNA methyltransferase 2 homolog A Homo sapiens 49-55 31404537-8 2019 Overexpression of sox2 rescued the inhibitory effects of six1 knockdown on the stemness and 5-FU sensitivity of HCC cells. Fluorouracil 92-96 SRY-box transcription factor 2 Homo sapiens 18-22 31581233-7 2019 This link between RPL22L1 induction and 5-Fluorouracil resistance appears to be causal, because ectopic expression or knockdown of RPL22L1 in cell lines increases and decreases 5-Fluorouracil resistance, respectively, and this is associated with changes in expression of the DNA-repair genes, MGMT and MLH1. Fluorouracil 40-54 O-6-methylguanine-DNA methyltransferase Homo sapiens 293-297 26691280-12 2016 Results indicated that 5-FU decreased H-ras, Rho-A, p53, Stat1 and increased Bax gene expression in Tumor2 and decreased Rac1, Rho-A, NF-kappaB and increased Bax and caspase-3 protein expression in Tumor2. Fluorouracil 23-27 Rac family small GTPase 1 Homo sapiens 121-125 26691280-14 2016 5-FU decreased Rac1, Rho-A protein expression and increased Bax and caspase-3 protein expression in MDA-MB-231. Fluorouracil 0-4 Rac family small GTPase 1 Homo sapiens 15-19 25573703-4 2016 OBJECTIVE: Here we assessed the impact of L-citrulline (CIT) on a murine model of 5-fluorouracil (5FU)-induced mucositis. Fluorouracil 82-96 citron Mus musculus 56-59 31325706-9 2019 Furthermore, QFG inhibited the cellular apoptosis in the jejunum tissue caused by 5-FU via the increasing Bcl-2 expression and decreasing Bax expression. Fluorouracil 82-86 BCL2-associated X protein Mus musculus 138-141 25573703-4 2016 OBJECTIVE: Here we assessed the impact of L-citrulline (CIT) on a murine model of 5-fluorouracil (5FU)-induced mucositis. Fluorouracil 98-101 citron Mus musculus 56-59 25573703-12 2016 CONCLUSIONS: CIT administration attenuated 5FU-mediated damage to the mucosal architecture of the small intestine, decreasing the size of the injured areas and promoting decreased intestinal permeability. Fluorouracil 43-46 citron Mus musculus 13-16 31500586-8 2019 METHODS/DESIGN: CIFRA is a single arm, open-label, phase II study assessing the activity of cetuximab in combination with irinotecan and fluorouracile in FcgammaRIIIa V/V patients with KRAS, NRAS, BRAF wild type mCRC. Fluorouracil 137-150 Fc gamma receptor IIIa Homo sapiens 154-166 29021025-1 2016 Histone deacetylase (HDAC) inhibitors have been shown to enhance the effects of 5-fluorouracil (5-FU) against various cancer cells; however, no report has shown that an HDAC inhibitor may enhance the effects of 5-FU with radiation. Fluorouracil 80-94 histone deacetylase 9 Homo sapiens 0-19 29021025-1 2016 Histone deacetylase (HDAC) inhibitors have been shown to enhance the effects of 5-fluorouracil (5-FU) against various cancer cells; however, no report has shown that an HDAC inhibitor may enhance the effects of 5-FU with radiation. Fluorouracil 80-94 histone deacetylase 9 Homo sapiens 21-25 29021025-1 2016 Histone deacetylase (HDAC) inhibitors have been shown to enhance the effects of 5-fluorouracil (5-FU) against various cancer cells; however, no report has shown that an HDAC inhibitor may enhance the effects of 5-FU with radiation. Fluorouracil 96-100 histone deacetylase 9 Homo sapiens 0-19 31516391-9 2019 Results: SNHG6 enhanced CRC cell resistance to 5-fluorouracil (5-FU), promoted autophagy, inhibited 5-FU-induced apoptosis, and increased 5-FU resistance in vivo. Fluorouracil 47-61 small nucleolar RNA host gene 6 Homo sapiens 9-14 31516391-9 2019 Results: SNHG6 enhanced CRC cell resistance to 5-fluorouracil (5-FU), promoted autophagy, inhibited 5-FU-induced apoptosis, and increased 5-FU resistance in vivo. Fluorouracil 63-67 small nucleolar RNA host gene 6 Homo sapiens 9-14 29021025-1 2016 Histone deacetylase (HDAC) inhibitors have been shown to enhance the effects of 5-fluorouracil (5-FU) against various cancer cells; however, no report has shown that an HDAC inhibitor may enhance the effects of 5-FU with radiation. Fluorouracil 96-100 histone deacetylase 9 Homo sapiens 21-25 31516391-9 2019 Results: SNHG6 enhanced CRC cell resistance to 5-fluorouracil (5-FU), promoted autophagy, inhibited 5-FU-induced apoptosis, and increased 5-FU resistance in vivo. Fluorouracil 100-104 small nucleolar RNA host gene 6 Homo sapiens 9-14 29021025-1 2016 Histone deacetylase (HDAC) inhibitors have been shown to enhance the effects of 5-fluorouracil (5-FU) against various cancer cells; however, no report has shown that an HDAC inhibitor may enhance the effects of 5-FU with radiation. Fluorouracil 211-215 histone deacetylase 9 Homo sapiens 0-19 31516391-9 2019 Results: SNHG6 enhanced CRC cell resistance to 5-fluorouracil (5-FU), promoted autophagy, inhibited 5-FU-induced apoptosis, and increased 5-FU resistance in vivo. Fluorouracil 100-104 small nucleolar RNA host gene 6 Homo sapiens 9-14 29021025-1 2016 Histone deacetylase (HDAC) inhibitors have been shown to enhance the effects of 5-fluorouracil (5-FU) against various cancer cells; however, no report has shown that an HDAC inhibitor may enhance the effects of 5-FU with radiation. Fluorouracil 211-215 histone deacetylase 9 Homo sapiens 21-25 29021025-1 2016 Histone deacetylase (HDAC) inhibitors have been shown to enhance the effects of 5-fluorouracil (5-FU) against various cancer cells; however, no report has shown that an HDAC inhibitor may enhance the effects of 5-FU with radiation. Fluorouracil 211-215 histone deacetylase 9 Homo sapiens 169-173 26751376-5 2016 Cytotoxicity assays with inhibitors of de novo adenine synthesis (5-FU, AZA and MTX) after MTAP gene knockdown showed an increased sensitivity, mainly to 5-FU. Fluorouracil 154-158 methylthioadenosine phosphorylase Homo sapiens 91-95 31356728-0 2019 Interdomain twists of human thymidine phosphorylase and its active-inactive conformations: Binding of 5-FU and its analogues to human thymidine phosphorylase versus dihydropyrimidine dehydrogenase. Fluorouracil 102-106 dihydropyrimidine dehydrogenase Homo sapiens 165-196 26651493-1 2016 DPD is the rate-limiting enzyme involved in the metabolism of 5-fluorouracil and its prodrugs, capecitabine and tegafur. Fluorouracil 62-76 dihydropyrimidine dehydrogenase Homo sapiens 0-3 31356728-4 2019 This work compares binding of 5-FU and its analogues to hTP and DPD, and suggests strategies to reduce drug binding to DPD to decrease the required dose of 5-FU. Fluorouracil 30-34 dihydropyrimidine dehydrogenase Homo sapiens 64-67 31356728-4 2019 This work compares binding of 5-FU and its analogues to hTP and DPD, and suggests strategies to reduce drug binding to DPD to decrease the required dose of 5-FU. Fluorouracil 30-34 dihydropyrimidine dehydrogenase Homo sapiens 119-122 31356728-4 2019 This work compares binding of 5-FU and its analogues to hTP and DPD, and suggests strategies to reduce drug binding to DPD to decrease the required dose of 5-FU. Fluorouracil 156-160 dihydropyrimidine dehydrogenase Homo sapiens 119-122 31786874-17 2019 The miR-299 overexpression enhanced the chemosensitivity of the HK1 cells to 5-FU and also caused a decrease in their invasion ability. Fluorouracil 77-81 microRNA 299 Homo sapiens 4-11 31534970-6 2019 5-FU treatment increased the expressions of Oct3/4, Fbxw7, and p27 and increased the number of A549 cells at G0/G1. Fluorouracil 0-4 POU domain, class 5, transcription factor 1 Mus musculus 44-50 31534970-6 2019 5-FU treatment increased the expressions of Oct3/4, Fbxw7, and p27 and increased the number of A549 cells at G0/G1. Fluorouracil 0-4 cyclin-dependent kinase inhibitor 1B Mus musculus 63-66 31534970-7 2019 5-FU treatment triggered nuclear translocation of beta-catenin, decreased the expression levels of c-myc and Skp2, and decreased the number of A549 cells at S phase. Fluorouracil 0-4 catenin (cadherin associated protein), beta 1 Mus musculus 50-62 31534970-8 2019 Release from 5-FU decreased the expressions of Oct3/4, Fbxw7 and p27; decreased the percentage of cells in the G0/G1 phase; increased the expressions of Skp2 and c-myc; and increased the proportion of cells in S phase. Fluorouracil 13-17 POU domain, class 5, transcription factor 1 Mus musculus 47-53 31534970-8 2019 Release from 5-FU decreased the expressions of Oct3/4, Fbxw7 and p27; decreased the percentage of cells in the G0/G1 phase; increased the expressions of Skp2 and c-myc; and increased the proportion of cells in S phase. Fluorouracil 13-17 cyclin-dependent kinase inhibitor 1B Mus musculus 65-68 31534970-9 2019 5-FU treatment led to high expressions of Oct3/4, c-myc, and p27, with low expressions of Fbxw7 and Skp2. Fluorouracil 0-4 POU domain, class 5, transcription factor 1 Mus musculus 42-48 31534970-9 2019 5-FU treatment led to high expressions of Oct3/4, c-myc, and p27, with low expressions of Fbxw7 and Skp2. Fluorouracil 0-4 cyclin-dependent kinase inhibitor 1B Mus musculus 61-64 31534970-14 2019 Conclusion: 5-FU enriches the CSCs in lung adenocarcinoma cells via increasing Fbxw7 and decreasing Skp2 expression, followed by downregulation of c-myc and upregulation of p27, which switches cells to quiescence. Fluorouracil 12-16 cyclin-dependent kinase inhibitor 1B Mus musculus 173-176 31528224-0 2019 Long non-coding RNA TUG1 mediates 5-fluorouracil resistance by acting as a ceRNA of miR-197-3p in colorectal cancer. Fluorouracil 34-48 microRNA 197 Homo sapiens 84-91 31004726-14 2019 Besides, AP could significantly suppressed the 5-FU-mediated increases of the intestinal inflammatory cytokines (TNF-alpha, IFN-gamma, IL-6, IL-1beta and IL-17), while AMO or PGS only inhibited some of them after 5-FU chemotherapy. Fluorouracil 47-51 interleukin 17A Mus musculus 154-159 31360112-0 2019 TLX3 repressed SNAI1-induced epithelial-mesenchymal transition by directly constraining STAT3 phosphorylation and functionally sensitized 5-FU chemotherapy in hepatocellular carcinoma. Fluorouracil 138-142 snail family zinc finger 1 Mus musculus 15-20 26658157-5 2015 Furthermore, Fancb(-/y) BM exhibits slower recovery kinetics and less tolerance to myelotoxic stress induced by 5-fluorouracil than wild-type littermates. Fluorouracil 112-126 Fanconi anemia, complementation group B Mus musculus 13-18 31078520-8 2019 In vitro, Gain- and lose-of-function assays showed miR-567 not only weakened cells proliferative ability, but also sensitized GC cells to 5-FU and oxaliplatin. Fluorouracil 138-142 microRNA 567 Homo sapiens 51-58 26527315-4 2015 5-FU treatment-resistant cells show a de novo expression of pyruvate kinase M1 (PKM1) and repression of PKM2, correlating with repression of the pentose phosphate pathway, decrease in NADPH level and in antioxidant defenses, promoting PKM2 oxidation and acquisition of stem-like phenotype. Fluorouracil 0-4 2,4-dienoyl-CoA reductase 1 Homo sapiens 184-189 26442524-0 2015 MicroRNA-218 is a prognostic indicator in colorectal cancer and enhances 5-fluorouracil-induced apoptosis by targeting BIRC5. Fluorouracil 73-87 baculoviral IAP repeat containing 5 Homo sapiens 119-124 31191817-7 2019 Subsequent siRNA-mediated knockdown of BMMSC-CD9 in DP-HCC1806:BMMSCs resulted in an attenuation of doxorubicin and 5-fluorouracil chemoresistance associated with decreased BCRP and serum cytokine expression (CCL5, CCR5, CXCR12). Fluorouracil 116-130 CD9 molecule Homo sapiens 45-48 30590435-13 2019 Melatonin may serve as a potential therapeutic option on its own, or in conjunction with 5-FU, in the treatment of patients with advanced or chemoresistant CRC.Melatonin inhibits the growth of 5-FU resistant colorectal cancer (CRC) cells through upregulation of miR-215-5p and a concomitant downregulation of TYMS. Fluorouracil 193-197 microRNA 215 Homo sapiens 262-269 31010234-10 2019 Treatment with 5-fluorouracil (5-FU) significantly enhanced YB-1 phosphorylation in KRAS(G13D)-mutated HCT116 cells but not in KRAS wild-type SW48 cells. Fluorouracil 15-29 KRAS proto-oncogene, GTPase Homo sapiens 84-88 31010234-10 2019 Treatment with 5-fluorouracil (5-FU) significantly enhanced YB-1 phosphorylation in KRAS(G13D)-mutated HCT116 cells but not in KRAS wild-type SW48 cells. Fluorouracil 31-35 KRAS proto-oncogene, GTPase Homo sapiens 84-88 26460271-5 2015 Sorafenib and 5-FU treatment decreased growth rates in Huh7 and Huh-BAT cells; however, the treatments exerted different effects in SP cells and on the expression levels of JNK signaling molecules. Fluorouracil 14-18 MIR7-3 host gene Homo sapiens 55-59 26564107-2 2015 The MTHFR C677T polymorphism is associated with decreased risk of CRC and increased sensitivity to 5-FU treatment. Fluorouracil 99-103 methylenetetrahydrofolate reductase Homo sapiens 4-9 26598503-10 2016 Chemotherapeutic agents such as cisplatin or 5FU increase the amount of HSP70 exosomes, favoring the activation of MDSCs and hampering the development of an antitumor immune response. Fluorouracil 45-48 heat shock protein family A (Hsp70) member 4 Homo sapiens 72-77 31013771-7 2019 We therefore transplanted these cancer cells or parental cells in mice, and again, found that not only did the 5-FU-selected cancer cells generate more aggressive tumors with respect to their parental counterpart, but they also showed a different gene expression pattern as compared to what we had observed in vitro, with ID1 the top upregulated gene. Fluorouracil 111-115 inhibitor of DNA binding 1, HLH protein Mus musculus 322-325 31011291-0 2019 Large tumor suppressor kinase 2 overexpression attenuates 5-FU-resistance in colorectal cancer via activating the JNK-MIEF1-mitochondrial division pathway. Fluorouracil 58-62 large tumor suppressor kinase 2 Homo sapiens 0-31 31011291-0 2019 Large tumor suppressor kinase 2 overexpression attenuates 5-FU-resistance in colorectal cancer via activating the JNK-MIEF1-mitochondrial division pathway. Fluorouracil 58-62 mitochondrial elongation factor 1 Homo sapiens 118-123 31011291-7 2019 Results: An obvious drop in large tumor suppressor kinase 2 (LATS2) expression was observed in SW480 cells after treatment with 5-FU. Fluorouracil 128-132 large tumor suppressor kinase 2 Homo sapiens 28-59 31011291-7 2019 Results: An obvious drop in large tumor suppressor kinase 2 (LATS2) expression was observed in SW480 cells after treatment with 5-FU. Fluorouracil 128-132 large tumor suppressor kinase 2 Homo sapiens 61-66 31011291-8 2019 In addition, upregulation of LATS2 expression through infection with LATS2 adenovirus further increased the reduction of SW480 cell viability induced by 5-FU. Fluorouracil 153-157 large tumor suppressor kinase 2 Homo sapiens 29-34 31011291-8 2019 In addition, upregulation of LATS2 expression through infection with LATS2 adenovirus further increased the reduction of SW480 cell viability induced by 5-FU. Fluorouracil 153-157 large tumor suppressor kinase 2 Homo sapiens 69-74 31011291-11 2019 Mechanistically, LATS2 overexpression and 5-FU co-treatment amplified mitochondrial division by upregulating MIEF1 expression in a manner dependent on MAPK-JNK axis. Fluorouracil 42-46 mitochondrial elongation factor 1 Homo sapiens 109-114 26807186-8 2015 After inhibiting Mcl-1, the cell migration and invasion decreased (P<0.05), the resistance to VCR, DDP and 5-Fu was reversed to different extents (P<0.05), TS mRNA expression increased significantly (P<0.05), MDR1 remained unchanged (P>0.05), but DPD and TOP2A decreased significantly (P<0.05). Fluorouracil 110-114 dihydropyrimidine dehydrogenase Homo sapiens 259-262 26623034-0 2015 Association and prediction of severe 5-fluorouracil toxicity with dihydropyrimidine dehydrogenase gene polymorphisms: A meta-analysis. Fluorouracil 37-51 dihydropyrimidine dehydrogenase Homo sapiens 66-97 31167694-5 2019 After over-expression of SHMT2 in CACO2 colon cancer cells, MTT assay was used to detect cell viability, and annexin V-FITC/PI double labeling was used to detect the apoptosis of colon cancer cells induced by 5-fluorouracil (5-Fu). Fluorouracil 209-223 serine hydroxymethyltransferase 2 Homo sapiens 25-30 31167694-5 2019 After over-expression of SHMT2 in CACO2 colon cancer cells, MTT assay was used to detect cell viability, and annexin V-FITC/PI double labeling was used to detect the apoptosis of colon cancer cells induced by 5-fluorouracil (5-Fu). Fluorouracil 225-229 serine hydroxymethyltransferase 2 Homo sapiens 25-30 30898145-0 2019 Three different polymorphisms of the DPYD gene associated with severe toxicity following administration of 5-FU: a case report. Fluorouracil 107-111 dihydropyrimidine dehydrogenase Homo sapiens 37-41 30728402-0 2019 FOXM1 modulates 5-FU resistance in colorectal cancer through regulating TYMS expression. Fluorouracil 16-20 forkhead box M1 Homo sapiens 0-5 30728402-5 2019 ChIP and global ChIP-seq data also confirms that FOXM1 can also potentially regulate other 5-FU targets, such as TYMS, thymidine kinase 1 (TK-1) and thymidine phosphorylase (TYMP). Fluorouracil 91-95 forkhead box M1 Homo sapiens 49-54 30728402-10 2019 In summary, this research demonstrated that FOXM1 plays a pivotal role in 5-FU resistance at least partially through the regulation of TYMS. Fluorouracil 74-78 forkhead box M1 Homo sapiens 44-49 26623034-1 2015 The aim of the present study was to evaluate the association and prediction of dihydropyrimidine dehydrogenase gene (DPYD) polymorphisms and the risk of 5-fluorouracil (5-FU) severe toxicity in cancer patients. Fluorouracil 153-167 dihydropyrimidine dehydrogenase Homo sapiens 79-110 26623034-1 2015 The aim of the present study was to evaluate the association and prediction of dihydropyrimidine dehydrogenase gene (DPYD) polymorphisms and the risk of 5-fluorouracil (5-FU) severe toxicity in cancer patients. Fluorouracil 153-167 dihydropyrimidine dehydrogenase Homo sapiens 117-121 26623034-1 2015 The aim of the present study was to evaluate the association and prediction of dihydropyrimidine dehydrogenase gene (DPYD) polymorphisms and the risk of 5-fluorouracil (5-FU) severe toxicity in cancer patients. Fluorouracil 169-173 dihydropyrimidine dehydrogenase Homo sapiens 79-110 26623034-1 2015 The aim of the present study was to evaluate the association and prediction of dihydropyrimidine dehydrogenase gene (DPYD) polymorphisms and the risk of 5-fluorouracil (5-FU) severe toxicity in cancer patients. Fluorouracil 169-173 dihydropyrimidine dehydrogenase Homo sapiens 117-121 26623034-2 2015 A meta-analysis of the published literature was conducted to summarize evidence for DPYD gene polymorphisms associated with an increased risk of severe 5-FU toxicity in patients with cancer from an Asian population. Fluorouracil 152-156 dihydropyrimidine dehydrogenase Homo sapiens 84-88 26623034-5 2015 A total of 5 clinical studies were retrieved in the meta-analysis, including 764 cancer patients with DPYD gene polymorphisms who received 5-FU-based chemotherapy. Fluorouracil 139-143 dihydropyrimidine dehydrogenase Homo sapiens 102-106 26623034-7 2015 In conclusion, the present meta-analysis suggested that polymorphisms of several DPYD gene polymorphisms are associated with an increased risk of severe toxic response to 5-FU. Fluorouracil 171-175 dihydropyrimidine dehydrogenase Homo sapiens 81-85 26518892-6 2015 For example, overexpressing miR-34a, a master regulator of tumor suppression attenuates chemoresistance to 5-FU by downregulating silent information regulator 1 (SIRT1) and E2F3. Fluorouracil 107-111 sirtuin 1 Homo sapiens 130-160 26518892-6 2015 For example, overexpressing miR-34a, a master regulator of tumor suppression attenuates chemoresistance to 5-FU by downregulating silent information regulator 1 (SIRT1) and E2F3. Fluorouracil 107-111 sirtuin 1 Homo sapiens 162-167 26457704-0 2015 MicroRNA-302b Enhances the Sensitivity of Hepatocellular Carcinoma Cell Lines to 5-FU via Targeting Mcl-1 and DPYD. Fluorouracil 81-85 dihydropyrimidine dehydrogenase Homo sapiens 110-114 26151540-3 2015 Low expression levels of miR-197 were observed in the fluorouracil (5-FU)-resistant gastric cell line SGC7901/5-FU when compared with those in the parental gastric cell line SGC7901. Fluorouracil 54-66 microRNA 197 Homo sapiens 25-32 26151540-3 2015 Low expression levels of miR-197 were observed in the fluorouracil (5-FU)-resistant gastric cell line SGC7901/5-FU when compared with those in the parental gastric cell line SGC7901. Fluorouracil 68-72 microRNA 197 Homo sapiens 25-32 26151540-3 2015 Low expression levels of miR-197 were observed in the fluorouracil (5-FU)-resistant gastric cell line SGC7901/5-FU when compared with those in the parental gastric cell line SGC7901. Fluorouracil 110-114 microRNA 197 Homo sapiens 25-32 26151540-4 2015 Overexpression of miR-197 in SGC7901/5-FU cells was identified to partially restore 5-FU sensitivity. Fluorouracil 37-41 microRNA 197 Homo sapiens 18-25 26151540-9 2015 These results indicated that miR-197 may influence the sensitivity of 5-FU treatment in a gastric cancer cell line by targeting MAPK1. Fluorouracil 70-74 microRNA 197 Homo sapiens 29-36 26418978-6 2015 CONCLUSION MiR-21 can mediate the drug resistance to 5-FU by inhibiting its target PDCD4, which can regulate the expression of ABCC5 and CD44 genes. Fluorouracil 53-57 CD44 molecule (Indian blood group) Homo sapiens 137-141 26124179-2 2015 We determined that activation of the CCAAT/enhancer binding protein delta (CEBPD) response to Cisplatin and 5-Fluorouracil in cancer-associated macrophages and fibroblasts contributed to the metastasis, invasion, acquired chemoresistance and stemness of cancer cells by in vitro and in vivo assays. Fluorouracil 108-122 CCAAT enhancer binding protein delta Homo sapiens 37-73 30447099-2 2019 We undertook this study to investigate the association between UGT1A1 genetic polymorphisms and toxicity in patients treated with the FOLFIRINOX (comprising oxaliplatin, irinotecan, fluorouracil, and leucovorin) chemotherapy regimen in the JASPAC 06 study. Fluorouracil 182-194 UDP glucuronosyltransferase family 1 member A1 Homo sapiens 63-69 30679569-0 2019 5-Fluorouracil Induces Enteric Neuron Death and Glial Activation During Intestinal Mucositis via a S100B-RAGE-NFkappaB-Dependent Pathway. Fluorouracil 0-14 advanced glycosylation end-product specific receptor Homo sapiens 105-109 30679569-2 2019 In this report, we used an animal model to investigate the participation of the S100B/RAGE/NFkappaB pathway in intestinal mucositis and enteric neurotoxicity caused by 5-FU (450 mg/kg, IP, single dose). Fluorouracil 168-172 advanced glycosylation end-product specific receptor Homo sapiens 86-90 30679569-3 2019 5-FU induced intestinal damage observed by shortened villi, loss of crypt architecture and intense inflammatory cell infiltrate as well as increased GFAP and S100B co-expression and decreased HuC/D protein expression in the small intestine. Fluorouracil 0-4 glial fibrillary acidic protein Homo sapiens 149-153 30679569-4 2019 Furthermore, 5-FU increased RAGE and NFkappaB NLS immunostaining in enteric neurons, associated with a significant increase in the nitrite/nitrate, IL-6 and TNF-alpha levels, iNOS expression and MDA accumulation in the small intestine. Fluorouracil 13-17 advanced glycosylation end-product specific receptor Homo sapiens 28-32 30679569-5 2019 We provide evidence that 5-FU induces reactive gliosis and reduction of enteric neurons in a S100B/RAGE/NFkappaB-dependent manner, since pentamidine, a S100B inhibitor, prevented 5-FU-induced neuronal loss, enteric glia activation, intestinal inflammation, oxidative stress and histological injury. Fluorouracil 25-29 advanced glycosylation end-product specific receptor Homo sapiens 99-103 30679569-5 2019 We provide evidence that 5-FU induces reactive gliosis and reduction of enteric neurons in a S100B/RAGE/NFkappaB-dependent manner, since pentamidine, a S100B inhibitor, prevented 5-FU-induced neuronal loss, enteric glia activation, intestinal inflammation, oxidative stress and histological injury. Fluorouracil 179-183 advanced glycosylation end-product specific receptor Homo sapiens 99-103 30831507-2 2019 The reduced activity of dihydropyrimidine dehydrogenase (DPD), the key enzyme in 5-FU inactivation, increases a patient"s risk of developing severe 5-FU related toxicity. Fluorouracil 81-85 dihydropyrimidine dehydrogenase Homo sapiens 24-55 30831507-2 2019 The reduced activity of dihydropyrimidine dehydrogenase (DPD), the key enzyme in 5-FU inactivation, increases a patient"s risk of developing severe 5-FU related toxicity. Fluorouracil 81-85 dihydropyrimidine dehydrogenase Homo sapiens 57-60 30831507-2 2019 The reduced activity of dihydropyrimidine dehydrogenase (DPD), the key enzyme in 5-FU inactivation, increases a patient"s risk of developing severe 5-FU related toxicity. Fluorouracil 148-152 dihydropyrimidine dehydrogenase Homo sapiens 24-55 30831507-2 2019 The reduced activity of dihydropyrimidine dehydrogenase (DPD), the key enzyme in 5-FU inactivation, increases a patient"s risk of developing severe 5-FU related toxicity. Fluorouracil 148-152 dihydropyrimidine dehydrogenase Homo sapiens 57-60 26111049-1 2015 This study aimed to investigate the association between methylenetetrahydrofolate reductase (MTHFR) gene polymorphisms and the prognosis of colorectal cancer (CRC) patients undergoing 5-fluorouracil (5-FU)-based chemotherapy in Taiwan. Fluorouracil 184-198 methylenetetrahydrofolate reductase Homo sapiens 56-91 31210536-8 2019 The expression of Ki-67 and Lgr5 decreased and the expression of caspase-3, and the number of apoptotic cells increased 24 h after the first 5-FU administration (P < 0.05), and these responses were significantly reduced by AOS treatment (P < 0.05, at 5 or 10 mL/kg). Fluorouracil 141-145 antigen identified by monoclonal antibody Ki 67 Mus musculus 18-23 31210536-8 2019 The expression of Ki-67 and Lgr5 decreased and the expression of caspase-3, and the number of apoptotic cells increased 24 h after the first 5-FU administration (P < 0.05), and these responses were significantly reduced by AOS treatment (P < 0.05, at 5 or 10 mL/kg). Fluorouracil 141-145 leucine rich repeat containing G protein coupled receptor 5 Mus musculus 28-32 31210536-9 2019 Conclusions: AOS can alleviate 5-FU-induced mucositis in mice via increasing Lgr5 expression and suppressing apoptotic responses in the intestinal crypt cells. Fluorouracil 31-35 leucine rich repeat containing G protein coupled receptor 5 Mus musculus 77-81 30538221-8 2018 Consistently, ChIP analysis revealed that FOXM1 binds efficiently to the TYMS promoter and modulates TYMS expression at the promoter level upon 5-FU treatment in KKU-D131 but not in HuCCA cells. Fluorouracil 144-148 forkhead box M1 Homo sapiens 42-47 30538221-10 2018 In conclusion, our data show that FOXM1 regulates TYMS expression to modulate 5-FU resistance in CCA and that severe 5-FU resistance can be caused by the uncoupling of the regulation of TYMS by FOXM1. Fluorouracil 78-82 forkhead box M1 Homo sapiens 34-39 30538221-10 2018 In conclusion, our data show that FOXM1 regulates TYMS expression to modulate 5-FU resistance in CCA and that severe 5-FU resistance can be caused by the uncoupling of the regulation of TYMS by FOXM1. Fluorouracil 117-121 forkhead box M1 Homo sapiens 194-199 26111049-1 2015 This study aimed to investigate the association between methylenetetrahydrofolate reductase (MTHFR) gene polymorphisms and the prognosis of colorectal cancer (CRC) patients undergoing 5-fluorouracil (5-FU)-based chemotherapy in Taiwan. Fluorouracil 184-198 methylenetetrahydrofolate reductase Homo sapiens 93-98 26111049-1 2015 This study aimed to investigate the association between methylenetetrahydrofolate reductase (MTHFR) gene polymorphisms and the prognosis of colorectal cancer (CRC) patients undergoing 5-fluorouracil (5-FU)-based chemotherapy in Taiwan. Fluorouracil 200-204 methylenetetrahydrofolate reductase Homo sapiens 56-91 26111049-1 2015 This study aimed to investigate the association between methylenetetrahydrofolate reductase (MTHFR) gene polymorphisms and the prognosis of colorectal cancer (CRC) patients undergoing 5-fluorouracil (5-FU)-based chemotherapy in Taiwan. Fluorouracil 200-204 methylenetetrahydrofolate reductase Homo sapiens 93-98 26111049-11 2015 This study suggested that MTHFR C677T and A1298C are associated with prognosis in CRC patients undergoing 5-FU-based chemotherapy. Fluorouracil 106-110 methylenetetrahydrofolate reductase Homo sapiens 26-31 26254383-1 2015 BACKGROUND: Dihydropyrimidine dehydrogenase (DPD) degrades approximately 85% of administered 5-fluorouracil (5-FU). Fluorouracil 93-107 dihydropyrimidine dehydrogenase Homo sapiens 12-43 26254383-1 2015 BACKGROUND: Dihydropyrimidine dehydrogenase (DPD) degrades approximately 85% of administered 5-fluorouracil (5-FU). Fluorouracil 93-107 dihydropyrimidine dehydrogenase Homo sapiens 45-48 26254383-1 2015 BACKGROUND: Dihydropyrimidine dehydrogenase (DPD) degrades approximately 85% of administered 5-fluorouracil (5-FU). Fluorouracil 109-113 dihydropyrimidine dehydrogenase Homo sapiens 12-43 26254383-1 2015 BACKGROUND: Dihydropyrimidine dehydrogenase (DPD) degrades approximately 85% of administered 5-fluorouracil (5-FU). Fluorouracil 109-113 dihydropyrimidine dehydrogenase Homo sapiens 45-48 26122960-5 2015 RESULTS: Increased NECTIN-4 expression was observed in 5-FU-resistant (5-FU-R) and 5-FU-exposed HCT-116 cells. Fluorouracil 71-75 nectin cell adhesion molecule 4 Homo sapiens 19-27 26122960-7 2015 Apoptosis caused by 5-FU in 5-FU-R cells after NECTIN-4 knockdown indicates that NECTIN-4 is responsible for 5-FU resistance. Fluorouracil 20-24 nectin cell adhesion molecule 4 Homo sapiens 81-89 26122960-7 2015 Apoptosis caused by 5-FU in 5-FU-R cells after NECTIN-4 knockdown indicates that NECTIN-4 is responsible for 5-FU resistance. Fluorouracil 28-32 nectin cell adhesion molecule 4 Homo sapiens 81-89 26122960-10 2015 CONCLUSIONS: Our data suggest that NECTIN-4 is responsible for 5-FU resistance and BCNU + Resveratrol combination can be used to increase the 5-FU sensitivity. Fluorouracil 63-67 nectin cell adhesion molecule 4 Homo sapiens 35-43 26122960-10 2015 CONCLUSIONS: Our data suggest that NECTIN-4 is responsible for 5-FU resistance and BCNU + Resveratrol combination can be used to increase the 5-FU sensitivity. Fluorouracil 142-146 nectin cell adhesion molecule 4 Homo sapiens 35-43 26189067-14 2015 INTERPRETATION: Adding oxaliplatin to fluorouracil-based neoadjuvant chemoradiotherapy and adjuvant chemotherapy (at the doses and intensities used in this trial) significantly improved disease-free survival of patients with clinically staged cT3-4 or cN1-2 rectal cancer compared with our former fluorouracil-based combined modality regimen (based on CAO/ARO/AIO-94). Fluorouracil 38-50 dickkopf like acrosomal protein 1 Homo sapiens 243-248 25936796-3 2015 Co-treatment using resveratrol and 5-FU inhibited cell proliferation more efficiently compared with use of either drug alone and the antiproliferative effect coincided with changes in the expression levels of AMP-activated protein kinase (AMPK), cyclooxygenase-2, vasodilator-stimulated phosphoprotein (VASP) and vascular endothelial growth factor (VEGF). Fluorouracil 35-39 vascular endothelial growth factor A Mus musculus 313-347 25936796-3 2015 Co-treatment using resveratrol and 5-FU inhibited cell proliferation more efficiently compared with use of either drug alone and the antiproliferative effect coincided with changes in the expression levels of AMP-activated protein kinase (AMPK), cyclooxygenase-2, vasodilator-stimulated phosphoprotein (VASP) and vascular endothelial growth factor (VEGF). Fluorouracil 35-39 vascular endothelial growth factor A Mus musculus 349-353 25936796-4 2015 Furthermore, co-treatment with resveratrol and 5-FU reduced tumor growth compared with that in the control group and this growth-inhibitory effect was associated with changes in the expression levels of AMPK, VASP and VEGF. Fluorouracil 47-51 vascular endothelial growth factor A Mus musculus 218-222 26209295-0 2015 Fluorouracil induces autophagy-related gastric carcinoma cell death through Beclin-1 upregulation by miR-30 suppression. Fluorouracil 0-12 beclin 1 Homo sapiens 76-84 26209295-4 2015 Moreover, autophagy-associated protein 6 (ATG6) or Beclin-1 was dose-dependently activated by 5-FU in GC cells. Fluorouracil 94-98 beclin 1 Homo sapiens 10-40 26209295-4 2015 Moreover, autophagy-associated protein 6 (ATG6) or Beclin-1 was dose-dependently activated by 5-FU in GC cells. Fluorouracil 94-98 beclin 1 Homo sapiens 42-46 26209295-4 2015 Moreover, autophagy-associated protein 6 (ATG6) or Beclin-1 was dose-dependently activated by 5-FU in GC cells. Fluorouracil 94-98 beclin 1 Homo sapiens 51-59 26209295-6 2015 Together, these data suggest that 5-FU may suppress miR-30 to upregulate Beclin-1 to induce autophagic cell death and cell proliferation arrest in GC cells. Fluorouracil 34-38 beclin 1 Homo sapiens 73-81 26396918-0 2015 Novel 5-fluorouracil-resistant human esophageal squamous cell carcinoma cells with dihydropyrimidine dehydrogenase overexpression. Fluorouracil 6-20 dihydropyrimidine dehydrogenase Homo sapiens 83-114 26396918-6 2015 Conversely, gimeracil, a DPD inhibitor, markedly increased the intracellular 5-FU concentration, decreased the intracellular FUPA concentration, and attenuated 5-FU resistance of TE-5R cells. Fluorouracil 77-81 dihydropyrimidine dehydrogenase Homo sapiens 25-28 26396918-7 2015 These results indicate that 5-FU resistance of TE-5R cells is due to the rapid degradation of 5-FU by DPD overexpression. Fluorouracil 28-32 dihydropyrimidine dehydrogenase Homo sapiens 102-105 26396918-7 2015 These results indicate that 5-FU resistance of TE-5R cells is due to the rapid degradation of 5-FU by DPD overexpression. Fluorouracil 94-98 dihydropyrimidine dehydrogenase Homo sapiens 102-105 26396918-8 2015 The investigation of 5-FU-resistant ESCC with DPYD gene copy number amplification and consequent DPD overexpression may generate novel biological evidence to explore strategies against ESCC with 5-FU resistance. Fluorouracil 21-25 dihydropyrimidine dehydrogenase Homo sapiens 46-50 26396918-8 2015 The investigation of 5-FU-resistant ESCC with DPYD gene copy number amplification and consequent DPD overexpression may generate novel biological evidence to explore strategies against ESCC with 5-FU resistance. Fluorouracil 21-25 dihydropyrimidine dehydrogenase Homo sapiens 97-100 26396918-8 2015 The investigation of 5-FU-resistant ESCC with DPYD gene copy number amplification and consequent DPD overexpression may generate novel biological evidence to explore strategies against ESCC with 5-FU resistance. Fluorouracil 195-199 dihydropyrimidine dehydrogenase Homo sapiens 46-50 26396918-8 2015 The investigation of 5-FU-resistant ESCC with DPYD gene copy number amplification and consequent DPD overexpression may generate novel biological evidence to explore strategies against ESCC with 5-FU resistance. Fluorouracil 195-199 dihydropyrimidine dehydrogenase Homo sapiens 97-100 26276288-1 2015 OBJECTIVE: To study the effect of lipoteichoic acid (LTA) and 5-FU on the expression of caspase-3, EGFR, TGF-alpha proteins of tumor tissue of H22 cancer bearing mice and its anti-tumor mechanism. Fluorouracil 62-66 caspase 3 Mus musculus 88-97 30451549-3 2018 5-FU is mainly catabolized by dihydropyrimidine dehydrogenase (DPD), and 5-FU dosage adaptation according to DPD status at the first cycle of treatment is now recommended. Fluorouracil 0-4 dihydropyrimidine dehydrogenase Homo sapiens 30-61 26276288-9 2015 CONCLUSIONS: LTA combined with 5-FU can effectively inhibit the tumorigenesis of H22 tumor bearing mice, increase the caspase-3 protein expression, inhibit TGF-alpha and EGFR protein expression, further promote tumor cell apoptosis and play a synergistic antitumor effect. Fluorouracil 31-35 caspase 3 Mus musculus 118-127 30451549-3 2018 5-FU is mainly catabolized by dihydropyrimidine dehydrogenase (DPD), and 5-FU dosage adaptation according to DPD status at the first cycle of treatment is now recommended. Fluorouracil 0-4 dihydropyrimidine dehydrogenase Homo sapiens 63-66 30451549-3 2018 5-FU is mainly catabolized by dihydropyrimidine dehydrogenase (DPD), and 5-FU dosage adaptation according to DPD status at the first cycle of treatment is now recommended. Fluorouracil 73-77 dihydropyrimidine dehydrogenase Homo sapiens 109-112 25937522-1 2015 BACKGROUND: The OPUS study demonstrated that addition of cetuximab to 5-fluorouracil, folinic acid and oxaliplatin (FOLFOX4) significantly improved objective response and progression-free survival (PFS) in the first-line treatment of patients with KRAS exon 2 wild-type metastatic colorectal cancer (mCRC). Fluorouracil 70-84 KRAS proto-oncogene, GTPase Homo sapiens 248-252 25112781-1 2015 BACKGROUND: The efficacy of 5-fluorouracil (5FU)-based therapy, which remains the cornerstone of gastrointestinal cancer treatment, depends upon the expression of enzymes involved in pyrimidine metabolism, including thymidylate synthase (TS), dihydropyrimidine dehydrogenase (DPD), thymidine phosphorylase (TP), and orotate phosphoribosyltransferase (OPRT). Fluorouracil 44-47 dihydropyrimidine dehydrogenase Homo sapiens 276-279 25913620-5 2015 Here, we show that RAD18 is highly expressed in human 5-fluorouracil (5-FU)-resistant cancer cells after 5-FU treatment. Fluorouracil 54-68 RAD18 E3 ubiquitin protein ligase Homo sapiens 19-24 25913620-5 2015 Here, we show that RAD18 is highly expressed in human 5-fluorouracil (5-FU)-resistant cancer cells after 5-FU treatment. Fluorouracil 70-74 RAD18 E3 ubiquitin protein ligase Homo sapiens 19-24 25913620-5 2015 Here, we show that RAD18 is highly expressed in human 5-fluorouracil (5-FU)-resistant cancer cells after 5-FU treatment. Fluorouracil 105-109 RAD18 E3 ubiquitin protein ligase Homo sapiens 19-24 25913620-9 2015 Also of interest, suppression of RAD18 by miR-145 enhanced DNA damage in CRC cells after 5-FU treatment. Fluorouracil 89-93 RAD18 E3 ubiquitin protein ligase Homo sapiens 33-38 25858143-4 2015 In vivo, SOCS2 deficiency leads to unrestricted myelopoietic response to 5-fluorouracil (5-FU) and, in turn, induces exhaustion of long-term HSC function along serial bone marrow transplantations. Fluorouracil 73-87 suppressor of cytokine signaling 2 Mus musculus 9-14 25858143-4 2015 In vivo, SOCS2 deficiency leads to unrestricted myelopoietic response to 5-fluorouracil (5-FU) and, in turn, induces exhaustion of long-term HSC function along serial bone marrow transplantations. Fluorouracil 89-93 suppressor of cytokine signaling 2 Mus musculus 9-14 25858143-8 2015 Accordingly, a comparison of murine wt and Socs2(-/-) HSC gene expression in response to 5-FU revealed a significant overlap with the molecular programs that correlate with SOCS2 expression in leukemias, particularly with the oncogenic pathways and with the IKZF1/Ikaros and MEF2C-predicted targets. Fluorouracil 89-93 suppressor of cytokine signaling 2 Mus musculus 43-48 25919696-0 2015 MicroRNA-224 is associated with colorectal cancer progression and response to 5-fluorouracil-based chemotherapy by KRAS-dependent and -independent mechanisms. Fluorouracil 78-92 KRAS proto-oncogene, GTPase Homo sapiens 115-119 25919696-6 2015 5-FU chemosensitivity was significantly increased in miR-224 knockdown cells, and in NIH3T3 cells expressing KRAS and BRAF mutant proteins. Fluorouracil 0-4 microRNA 224 Homo sapiens 53-60 25906475-2 2015 Dihydropyrimidine dehydrogenase (DPD), a key enzyme in the catabolism of 5-fluorouracil, has been intensively investigated in relation to fluoropyrimidine toxicity, and several DPD gene (DPYD) polymorphisms are associated with decreased enzyme activity and increased risk of fluoropyrimidine-related toxicity. Fluorouracil 73-87 dihydropyrimidine dehydrogenase Homo sapiens 0-31 30775324-2 2018 Dihydropyrimidine dehydrogenase (DPD) catalyzes the first catabolic step of the 5-FU degradation pathway, converting 80% of 5-FU to its inactive metabolite. Fluorouracil 80-84 dihydropyrimidine dehydrogenase Homo sapiens 0-31 30775324-2 2018 Dihydropyrimidine dehydrogenase (DPD) catalyzes the first catabolic step of the 5-FU degradation pathway, converting 80% of 5-FU to its inactive metabolite. Fluorouracil 80-84 dihydropyrimidine dehydrogenase Homo sapiens 33-36 30775324-2 2018 Dihydropyrimidine dehydrogenase (DPD) catalyzes the first catabolic step of the 5-FU degradation pathway, converting 80% of 5-FU to its inactive metabolite. Fluorouracil 124-128 dihydropyrimidine dehydrogenase Homo sapiens 0-31 30775324-2 2018 Dihydropyrimidine dehydrogenase (DPD) catalyzes the first catabolic step of the 5-FU degradation pathway, converting 80% of 5-FU to its inactive metabolite. Fluorouracil 124-128 dihydropyrimidine dehydrogenase Homo sapiens 33-36 30538568-5 2018 For cases with comparably low DPD activity, advisable primary and subsequent dose adjustment of 5-fluorouracil based on plasma 5-fluorouracil levels may be a practical strategy for reducing the occurrence of adverse reactions for personalized treatment of the UGT1A1*6 or UGT1A1*28 heterozygous type. Fluorouracil 96-110 dihydropyrimidine dehydrogenase Homo sapiens 30-33 30538568-5 2018 For cases with comparably low DPD activity, advisable primary and subsequent dose adjustment of 5-fluorouracil based on plasma 5-fluorouracil levels may be a practical strategy for reducing the occurrence of adverse reactions for personalized treatment of the UGT1A1*6 or UGT1A1*28 heterozygous type. Fluorouracil 96-110 UDP glucuronosyltransferase family 1 member A1 Homo sapiens 260-266 30538568-5 2018 For cases with comparably low DPD activity, advisable primary and subsequent dose adjustment of 5-fluorouracil based on plasma 5-fluorouracil levels may be a practical strategy for reducing the occurrence of adverse reactions for personalized treatment of the UGT1A1*6 or UGT1A1*28 heterozygous type. Fluorouracil 96-110 UDP glucuronosyltransferase family 1 member A1 Homo sapiens 272-278 30538568-5 2018 For cases with comparably low DPD activity, advisable primary and subsequent dose adjustment of 5-fluorouracil based on plasma 5-fluorouracil levels may be a practical strategy for reducing the occurrence of adverse reactions for personalized treatment of the UGT1A1*6 or UGT1A1*28 heterozygous type. Fluorouracil 127-141 UDP glucuronosyltransferase family 1 member A1 Homo sapiens 260-266 30538568-5 2018 For cases with comparably low DPD activity, advisable primary and subsequent dose adjustment of 5-fluorouracil based on plasma 5-fluorouracil levels may be a practical strategy for reducing the occurrence of adverse reactions for personalized treatment of the UGT1A1*6 or UGT1A1*28 heterozygous type. Fluorouracil 127-141 UDP glucuronosyltransferase family 1 member A1 Homo sapiens 272-278 30451890-7 2018 Further, corresponding to CD44v6 knockdown cells, 5FU+ Silibinin treatment significantly decreased CD44v6, Nanog, CTNNB1 and CDKN2A expression whereas increased E-cadherin expression in HCT116 derived CD44+ cells. Fluorouracil 50-53 Nanog homeobox Homo sapiens 107-112 25906475-2 2015 Dihydropyrimidine dehydrogenase (DPD), a key enzyme in the catabolism of 5-fluorouracil, has been intensively investigated in relation to fluoropyrimidine toxicity, and several DPD gene (DPYD) polymorphisms are associated with decreased enzyme activity and increased risk of fluoropyrimidine-related toxicity. Fluorouracil 73-87 dihydropyrimidine dehydrogenase Homo sapiens 33-36 25906475-2 2015 Dihydropyrimidine dehydrogenase (DPD), a key enzyme in the catabolism of 5-fluorouracil, has been intensively investigated in relation to fluoropyrimidine toxicity, and several DPD gene (DPYD) polymorphisms are associated with decreased enzyme activity and increased risk of fluoropyrimidine-related toxicity. Fluorouracil 73-87 dihydropyrimidine dehydrogenase Homo sapiens 177-180 25906475-2 2015 Dihydropyrimidine dehydrogenase (DPD), a key enzyme in the catabolism of 5-fluorouracil, has been intensively investigated in relation to fluoropyrimidine toxicity, and several DPD gene (DPYD) polymorphisms are associated with decreased enzyme activity and increased risk of fluoropyrimidine-related toxicity. Fluorouracil 73-87 dihydropyrimidine dehydrogenase Homo sapiens 187-191 25886460-10 2015 PGE2, LTB4 synthesis and ALOX5 expression was suppressed by LA, GLA, ALA and DHA; whereas AA, EPA and 5-FU enhanced PGE2 but paradoxically AA decreased and EPA and 5-FU enhanced LTB4 synthesis in RKO cells. Fluorouracil 164-168 galactosidase alpha Homo sapiens 64-67 25855960-7 2015 PCAF was also found to sensitize HCC cells to 5-fluorouracil (5-FU) treatment by regulating GLI1/Bcl-2/BAX axis-dependent apoptosis. Fluorouracil 46-60 GLI family zinc finger 1 Homo sapiens 92-96 25855960-7 2015 PCAF was also found to sensitize HCC cells to 5-fluorouracil (5-FU) treatment by regulating GLI1/Bcl-2/BAX axis-dependent apoptosis. Fluorouracil 62-66 GLI family zinc finger 1 Homo sapiens 92-96 25855960-10 2015 Together, these results show that PCAF can induce cell apoptosis by modulating a GLI1/Bcl-2/BAX axis that in turn suppresses HCC progression, and suggest that 5-FU may exert a stronger anti-tumor effect in patients with PCAF expression in HCC tumors. Fluorouracil 159-163 GLI family zinc finger 1 Homo sapiens 81-85 24858038-5 2015 Here, we demonstrate cancer cells that overexpress Cks1 or Cks2 override the intra-S-phase checkpoint in the presence of replication stress-inducing chemotherapies such as 5-Fluorouracil (5-FU) and methotrexate (MTX) leading to enhanced sensitivity in vitro and in vivo. Fluorouracil 172-186 CDC28 protein kinase regulatory subunit 1B pseudogene 7 Homo sapiens 51-55 24858038-5 2015 Here, we demonstrate cancer cells that overexpress Cks1 or Cks2 override the intra-S-phase checkpoint in the presence of replication stress-inducing chemotherapies such as 5-Fluorouracil (5-FU) and methotrexate (MTX) leading to enhanced sensitivity in vitro and in vivo. Fluorouracil 188-192 CDC28 protein kinase regulatory subunit 1B pseudogene 7 Homo sapiens 51-55 25616574-7 2015 The recovery of platelet counts following a 5-fluorouracil challenge was delayed in Cdk2(fl/fl)Cdk4(-/-)vavCre mice revealing a critical role for Cdk2 and Cdk4 in stress hematopoiesis. Fluorouracil 44-58 cyclin-dependent kinase 2 Mus musculus 84-88 25616574-7 2015 The recovery of platelet counts following a 5-fluorouracil challenge was delayed in Cdk2(fl/fl)Cdk4(-/-)vavCre mice revealing a critical role for Cdk2 and Cdk4 in stress hematopoiesis. Fluorouracil 44-58 cyclin-dependent kinase 2 Mus musculus 146-150 25789066-0 2015 A let-7b binding site SNP in the 3"-UTR of the Bcl-xL gene enhances resistance to 5-fluorouracil and doxorubicin in breast cancer cells. Fluorouracil 82-96 microRNA let-7b Homo sapiens 2-8 25789066-4 2015 The data indicated that let-7b negatively regulates the expression of Bcl-xL and appears to sensitize MCF-7 cells to the chemotherapeutic agents 5-fluorouracil (5-FU) and doxorubicin. Fluorouracil 145-159 microRNA let-7b Homo sapiens 24-30 25789066-4 2015 The data indicated that let-7b negatively regulates the expression of Bcl-xL and appears to sensitize MCF-7 cells to the chemotherapeutic agents 5-fluorouracil (5-FU) and doxorubicin. Fluorouracil 161-165 microRNA let-7b Homo sapiens 24-30 25789066-5 2015 Furthermore, the SNP rs3208684 A>C was demonstrated to enhance Bcl-xL protein expression by disrupting the binding of let-7b to the 3"-UTR of Bcl-xL and, in MCF-7 cells, overexpression of let-7b in the presence of a mutant Bcl-xL 3"-UTR (C allele) significantly increased 5-FU and doxorubicin resistance. Fluorouracil 275-279 microRNA let-7b Homo sapiens 121-127 25789066-6 2015 Thus, the results of the present study demonstrate that the SNP rs3208684 A>C may upregulate Bcl-xL protein expression and enhance the resistance of the MCF-7 cells to 5-FU and doxorubicin by decreasing the binding of let-7b to the 3"-UTR of Bcl-xL. Fluorouracil 171-175 microRNA let-7b Homo sapiens 221-227 24943064-1 2015 BACKGROUND: Dihydropyrimidine dehydrogenase (DPYD) is an enzyme that regulates the rate-limiting step in pyrimidine metabolism, especially catabolism of fluorouracil. Fluorouracil 153-165 dihydropyrimidine dehydrogenase Homo sapiens 12-43 24943064-1 2015 BACKGROUND: Dihydropyrimidine dehydrogenase (DPYD) is an enzyme that regulates the rate-limiting step in pyrimidine metabolism, especially catabolism of fluorouracil. Fluorouracil 153-165 dihydropyrimidine dehydrogenase Homo sapiens 45-49 28123791-10 2015 Identification of the precise mechanism through which DPYD is epigenetically regulated, and underlying reasons why exactly the break (FRA1E) happens, will consequently pave the way toward preventing severe toxicity to the antineoplastic drug 5-fluorouracil (5-FU) and development of the causative therapy for the dihydropyrimidine dehydrogenase deficiency. Fluorouracil 242-256 dihydropyrimidine dehydrogenase Homo sapiens 54-58 28123791-10 2015 Identification of the precise mechanism through which DPYD is epigenetically regulated, and underlying reasons why exactly the break (FRA1E) happens, will consequently pave the way toward preventing severe toxicity to the antineoplastic drug 5-fluorouracil (5-FU) and development of the causative therapy for the dihydropyrimidine dehydrogenase deficiency. Fluorouracil 258-262 dihydropyrimidine dehydrogenase Homo sapiens 54-58 25747889-16 2015 The ratio of CD4(+)CD25(+) Treg significantly decreased and CD4(+) T cell increased in BLTA and 5-FU group (P<0.01). Fluorouracil 96-100 CD4 antigen Mus musculus 13-16 25747889-16 2015 The ratio of CD4(+)CD25(+) Treg significantly decreased and CD4(+) T cell increased in BLTA and 5-FU group (P<0.01). Fluorouracil 96-100 CD4 antigen Mus musculus 60-63 25169655-0 2015 Elevation in 5-FU-induced apoptosis in head and neck cancer stem cells by a combination of CDHP and GSK3beta inhibitors. Fluorouracil 13-17 cadherin 3 Homo sapiens 91-95 25547406-9 2015 CONCLUSIONS: CEACAM1 long cytoplasmic domain isoform dominance and HS formation are phenotypes associated with chemoresistance to 5FU. Fluorouracil 130-133 CEA cell adhesion molecule 1 Homo sapiens 13-20 25632185-16 2015 Cell fractionation assays revealed that nuclear translocation of beta-catenin was reduced by WCA and/or 5-FU treatments. Fluorouracil 104-108 catenin (cadherin associated protein), beta 1 Mus musculus 65-77 30498448-4 2018 Genetic variants resulting in decreased enzymatic activity of uridine diphosphate glucuronosyltransferase 1A1 (UGT1A1) and dihydropyrimidine dehydrogenase (DPD) are known to increase irinotecan and 5-fluorouracil-related toxicity, respectively. Fluorouracil 198-212 UDP glucuronosyltransferase family 1 member A1 Homo sapiens 62-109 30498448-4 2018 Genetic variants resulting in decreased enzymatic activity of uridine diphosphate glucuronosyltransferase 1A1 (UGT1A1) and dihydropyrimidine dehydrogenase (DPD) are known to increase irinotecan and 5-fluorouracil-related toxicity, respectively. Fluorouracil 198-212 UDP glucuronosyltransferase family 1 member A1 Homo sapiens 111-117 30498448-4 2018 Genetic variants resulting in decreased enzymatic activity of uridine diphosphate glucuronosyltransferase 1A1 (UGT1A1) and dihydropyrimidine dehydrogenase (DPD) are known to increase irinotecan and 5-fluorouracil-related toxicity, respectively. Fluorouracil 198-212 dihydropyrimidine dehydrogenase Homo sapiens 123-154 30498448-4 2018 Genetic variants resulting in decreased enzymatic activity of uridine diphosphate glucuronosyltransferase 1A1 (UGT1A1) and dihydropyrimidine dehydrogenase (DPD) are known to increase irinotecan and 5-fluorouracil-related toxicity, respectively. Fluorouracil 198-212 dihydropyrimidine dehydrogenase Homo sapiens 156-159 25561980-10 2015 Knockdown of Shp-2 in HepG2 cells resulted in upregulation of mitochondrial TERT expression and increased resistance to cisplatin (CDDP) and 5-fluorouracil (5-FU) (resistance indices, 2.094 and 1.863, respectively). Fluorouracil 141-155 protein tyrosine phosphatase non-receptor type 11 Homo sapiens 13-18 30396933-0 2018 Inhibiting xCT Improves 5-Fluorouracil Resistance of Gastric Cancer Induced by CD44 Variant 9 Expression. Fluorouracil 24-38 CD44 molecule (Indian blood group) Homo sapiens 79-83 30396941-0 2018 Dclk1 Inhibition Cancels 5-FU-induced Cell-cycle Arrest and Decreases Cell Survival in Colorectal Cancer. Fluorouracil 25-29 doublecortin like kinase 1 Homo sapiens 0-5 30396941-4 2018 RESULTS: Combined treatment with 5-FU and a Dclk1 inhibitor, LRRK2-IN-1 (LRRK), decreased 5-FU-induced phosphorylation of Chk1 and canceled 5-FU-induced cell-cycle arrest at the S phase. Fluorouracil 33-37 doublecortin like kinase 1 Homo sapiens 44-49 25561980-10 2015 Knockdown of Shp-2 in HepG2 cells resulted in upregulation of mitochondrial TERT expression and increased resistance to cisplatin (CDDP) and 5-fluorouracil (5-FU) (resistance indices, 2.094 and 1.863, respectively). Fluorouracil 157-161 protein tyrosine phosphatase non-receptor type 11 Homo sapiens 13-18 30396941-4 2018 RESULTS: Combined treatment with 5-FU and a Dclk1 inhibitor, LRRK2-IN-1 (LRRK), decreased 5-FU-induced phosphorylation of Chk1 and canceled 5-FU-induced cell-cycle arrest at the S phase. Fluorouracil 90-94 doublecortin like kinase 1 Homo sapiens 44-49 30396941-4 2018 RESULTS: Combined treatment with 5-FU and a Dclk1 inhibitor, LRRK2-IN-1 (LRRK), decreased 5-FU-induced phosphorylation of Chk1 and canceled 5-FU-induced cell-cycle arrest at the S phase. Fluorouracil 90-94 doublecortin like kinase 1 Homo sapiens 44-49 25117664-1 2015 BACKGROUND: Dihydropyrimidine dehydrogenase (DPD) encoded by DPYD gene is the major enzyme involved in metabolism of 5-flurouracil (5-FU), a pyrimidine analogue used in cancer chemotherapy. Fluorouracil 132-136 dihydropyrimidine dehydrogenase Homo sapiens 12-43 30468467-0 2018 Overexpression of miR-215-3p sensitizes colorectal cancer to 5-fluorouracil induced apoptosis through regulating CXCR1. Fluorouracil 61-75 microRNA 215 Homo sapiens 18-25 25117664-1 2015 BACKGROUND: Dihydropyrimidine dehydrogenase (DPD) encoded by DPYD gene is the major enzyme involved in metabolism of 5-flurouracil (5-FU), a pyrimidine analogue used in cancer chemotherapy. Fluorouracil 132-136 dihydropyrimidine dehydrogenase Homo sapiens 45-48 30468467-0 2018 Overexpression of miR-215-3p sensitizes colorectal cancer to 5-fluorouracil induced apoptosis through regulating CXCR1. Fluorouracil 61-75 C-X-C motif chemokine receptor 1 Homo sapiens 113-118 25117664-1 2015 BACKGROUND: Dihydropyrimidine dehydrogenase (DPD) encoded by DPYD gene is the major enzyme involved in metabolism of 5-flurouracil (5-FU), a pyrimidine analogue used in cancer chemotherapy. Fluorouracil 132-136 dihydropyrimidine dehydrogenase Homo sapiens 61-65 30468467-6 2018 RESULTS: miR-215-3p was down-expressed in the 5-FU resistant cell compared to the parent cell. Fluorouracil 46-50 microRNA 215 Homo sapiens 9-16 25117664-3 2015 Single nucleotide variants (SNVs) within DPYD that modulate DPD enzyme activity contribute to 5-FU toxicity. Fluorouracil 94-98 dihydropyrimidine dehydrogenase Homo sapiens 41-45 30468467-8 2018 Furthermore, miR-215-3p accelerated the apoptosis of colorectal cancer cell which was treated with 5-Fu. Fluorouracil 99-103 microRNA 215 Homo sapiens 13-20 25117664-3 2015 Single nucleotide variants (SNVs) within DPYD that modulate DPD enzyme activity contribute to 5-FU toxicity. Fluorouracil 94-98 dihydropyrimidine dehydrogenase Homo sapiens 60-63 30468467-9 2018 Mechanically, miR-215-3p regulated the level of endogenous CXCR1 in HCT116 cell and alternation of CXCR1 affected the 5-Fu sensibility mediated by miR-215-3p. Fluorouracil 118-122 microRNA 215 Homo sapiens 14-21 30468467-9 2018 Mechanically, miR-215-3p regulated the level of endogenous CXCR1 in HCT116 cell and alternation of CXCR1 affected the 5-Fu sensibility mediated by miR-215-3p. Fluorouracil 118-122 C-X-C motif chemokine receptor 1 Homo sapiens 99-104 30468467-9 2018 Mechanically, miR-215-3p regulated the level of endogenous CXCR1 in HCT116 cell and alternation of CXCR1 affected the 5-Fu sensibility mediated by miR-215-3p. Fluorouracil 118-122 microRNA 215 Homo sapiens 147-154 30340556-10 2018 Increased expression of osteopontin (p = 0.019) and low density of CD8-positive T-cells (p = 0.043) were significantly associated with unfavourable response to 5-FU. Fluorouracil 160-164 CD8a molecule Homo sapiens 67-70 26737503-4 2015 DPYD initiates the catabolic route of 5-FU generating metabolites such as fluoroacetate (FAC). Fluorouracil 38-42 dihydropyrimidine dehydrogenase Homo sapiens 0-4 32913994-0 2018 Temporal Dynamics of Genomic Alterations in a BRCA1 Germline-Mutated Pancreatic Cancer With Low Genomic Instability Burden but Exceptional Response to Fluorouracil, Oxaliplatin, Leucovorin, and Irinotecan. Fluorouracil 151-163 BRCA1 DNA repair associated Homo sapiens 46-51 24999837-0 2015 Exogenous IL-1Ra attenuates intestinal mucositis induced by oxaliplatin and 5-fluorouracil through suppression of p53-dependent apoptosis. Fluorouracil 76-90 interleukin 1 receptor antagonist Mus musculus 10-16 30056083-8 2018 MH also influenced the anti-metastasis effects of 5-FU by decreasing migration ability, suppressing the expression of MMP-2, MMP-9 and increasing N-cadherin and E-cadherin. Fluorouracil 50-54 matrix metallopeptidase 9 Homo sapiens 125-130 25241082-9 2015 After 5-FU treatment, the expression of CD133 was 6.7 +- 1.6% relative to the untreated mice 2.6 +- 0.96% by nude mice tumor xenograft model. Fluorouracil 6-10 prominin 1 Mus musculus 40-45 30056083-8 2018 MH also influenced the anti-metastasis effects of 5-FU by decreasing migration ability, suppressing the expression of MMP-2, MMP-9 and increasing N-cadherin and E-cadherin. Fluorouracil 50-54 cadherin 2 Homo sapiens 146-156 31949552-0 2018 Integrin beta1 mediates 5-fluorouracil chemoresistance under translational control of eIF4E in colorectal cancer. Fluorouracil 24-38 integrin subunit beta 1 Homo sapiens 0-14 31949552-5 2018 Cell transfection techniques of small interfering RNA (siRNA) and cDNA expression plasmid were applied to investigate the molecular relationship of integrin beta1 and eIF4E and their biological effects on 5FU resistance in SW480 and LoVo cell lines. Fluorouracil 205-208 integrin subunit beta 1 Homo sapiens 148-162 31949552-7 2018 Integrin beta1 could contribute to 5-fluorouracil (5FU) resistance in colorectal cancer cell lines. Fluorouracil 35-49 integrin subunit beta 1 Homo sapiens 0-14 31949552-7 2018 Integrin beta1 could contribute to 5-fluorouracil (5FU) resistance in colorectal cancer cell lines. Fluorouracil 51-54 integrin subunit beta 1 Homo sapiens 0-14 31949552-9 2018 Significantly, Hoechst/PI double staining and an MTT assay proved integrin beta1 could contribute to cellular survival and 5FU resistance under translational control of eIF4E in these cells. Fluorouracil 123-126 integrin subunit beta 1 Homo sapiens 66-80 31949552-10 2018 CONCLUSION: We conclude that integrin beta1 mediated 5FU chemo resistance in colorectal cancer could be translationally regulated by eIF4E. Fluorouracil 53-56 integrin subunit beta 1 Homo sapiens 29-43 30510992-8 2019 The 3D organoid formation capability and 5-fluorouracil resistance were accounted for by cancer cells with high CD44 expression and autophagy, respectively. Fluorouracil 41-55 CD44 molecule (Indian blood group) Homo sapiens 112-116 30096914-11 2018 Administration with both AA and 5-FU in prevention and throughout was able to prevent decreases in Notch1 SOX2, nestin, DCX, and Nrf2 caused by 5-FU. Fluorouracil 144-148 doublecortin Rattus norvegicus 120-123 29769267-1 2018 Dihydropyrimidine dehydrogenase (DPD, EC 1.3.1.2), encoded by the DPYD gene, is the rate-limiting enzyme in the degradation pathway of endogenous pyrimidine and fluoropyrimidine drugs such as 5-fluorouracil (5-FU). Fluorouracil 192-206 dihydropyrimidine dehydrogenase Homo sapiens 0-31 29769267-1 2018 Dihydropyrimidine dehydrogenase (DPD, EC 1.3.1.2), encoded by the DPYD gene, is the rate-limiting enzyme in the degradation pathway of endogenous pyrimidine and fluoropyrimidine drugs such as 5-fluorouracil (5-FU). Fluorouracil 192-206 dihydropyrimidine dehydrogenase Homo sapiens 33-36 29769267-1 2018 Dihydropyrimidine dehydrogenase (DPD, EC 1.3.1.2), encoded by the DPYD gene, is the rate-limiting enzyme in the degradation pathway of endogenous pyrimidine and fluoropyrimidine drugs such as 5-fluorouracil (5-FU). Fluorouracil 192-206 dihydropyrimidine dehydrogenase Homo sapiens 66-70 29769267-1 2018 Dihydropyrimidine dehydrogenase (DPD, EC 1.3.1.2), encoded by the DPYD gene, is the rate-limiting enzyme in the degradation pathway of endogenous pyrimidine and fluoropyrimidine drugs such as 5-fluorouracil (5-FU). Fluorouracil 208-212 dihydropyrimidine dehydrogenase Homo sapiens 0-31 29769267-1 2018 Dihydropyrimidine dehydrogenase (DPD, EC 1.3.1.2), encoded by the DPYD gene, is the rate-limiting enzyme in the degradation pathway of endogenous pyrimidine and fluoropyrimidine drugs such as 5-fluorouracil (5-FU). Fluorouracil 208-212 dihydropyrimidine dehydrogenase Homo sapiens 33-36 29769267-1 2018 Dihydropyrimidine dehydrogenase (DPD, EC 1.3.1.2), encoded by the DPYD gene, is the rate-limiting enzyme in the degradation pathway of endogenous pyrimidine and fluoropyrimidine drugs such as 5-fluorouracil (5-FU). Fluorouracil 208-212 dihydropyrimidine dehydrogenase Homo sapiens 66-70 29769267-2 2018 DPD catalyzes the reduction of uracil, thymine, and 5-FU. Fluorouracil 52-56 dihydropyrimidine dehydrogenase Homo sapiens 0-3 29769267-3 2018 In Caucasians, DPYD mutations, including DPYD*2A, DPYD*13, c.2846A>T, and c.1129-5923C>G/hapB3, are known to contribute to interindividual variations in the toxicity of 5-FU; however, none of these DPYD polymorphisms has been identified in the Asian population. Fluorouracil 175-179 dihydropyrimidine dehydrogenase Homo sapiens 15-19 29769267-5 2018 In this study, in vitro analysis was performed on 22 DPD allelic variants by transiently expressing wild-type DPD and 21 DPD variants in 293FT cells and characterizing their enzymatic activities using 5-FU as a substrate. Fluorouracil 201-205 dihydropyrimidine dehydrogenase Homo sapiens 53-56 30087856-2 2018 Dihydropyrimidine dehydrogenase (DPD) is the crucial enzyme in the catabolism of 5-FU. Fluorouracil 81-85 dihydropyrimidine dehydrogenase Homo sapiens 0-31 30087856-2 2018 Dihydropyrimidine dehydrogenase (DPD) is the crucial enzyme in the catabolism of 5-FU. Fluorouracil 81-85 dihydropyrimidine dehydrogenase Homo sapiens 33-36 29643149-7 2018 Moreover, the administration of a neutrophil-depleting antibody or a Cxcr2 antagonist, SB225002, significantly attenuated 5-FU-mediated enhanced lung metastasis with depressed neutrophil infiltration. Fluorouracil 122-126 chemokine (C-X-C motif) receptor 2 Mus musculus 69-74 30034629-0 2018 MACROD2 expression predicts response to 5-FU-based chemotherapy in stage III colon cancer. Fluorouracil 40-44 mono-ADP ribosylhydrolase 2 Homo sapiens 0-7 30034629-6 2018 Results: Loss of nuclear MACROD2 protein expression in epithelial neoplastic cells of stage III microsatellite stable (MSS) colon cancers was associated with poor DFS within the subgroup of 59 patients who received 5-fluorouracil (5-FU)-based adjuvant chemotherapy (p=0.005; HR=3.8, 95% CI 1.4-10.0). Fluorouracil 215-229 mono-ADP ribosylhydrolase 2 Homo sapiens 25-32 30034629-6 2018 Results: Loss of nuclear MACROD2 protein expression in epithelial neoplastic cells of stage III microsatellite stable (MSS) colon cancers was associated with poor DFS within the subgroup of 59 patients who received 5-fluorouracil (5-FU)-based adjuvant chemotherapy (p=0.005; HR=3.8, 95% CI 1.4-10.0). Fluorouracil 231-235 mono-ADP ribosylhydrolase 2 Homo sapiens 25-32 30034629-7 2018 Conclusion: These data indicate that low nuclear expression of MACROD2 is associated with poor prognosis of patients with stage III MSS primary colon cancer who were treated with 5-FU-based adjuvant chemotherapy. Fluorouracil 179-183 mono-ADP ribosylhydrolase 2 Homo sapiens 63-70 26557771-4 2015 Reg IV treatment inhibits 5-fluorouracil induced apoptosis, at least two mechanisms are involved in inhibition of apoptosis by Reg IV, including Bcl-2 and dihydropyrimidine dehydrogenase (DPD). Fluorouracil 26-40 dihydropyrimidine dehydrogenase Homo sapiens 188-191 25452783-12 2015 The expression levels of HIF-2, ABCG2 and Oct-4 mRNA and protein were high in the blank control group, and were further increased in the 5-Fu group. Fluorouracil 137-141 POU domain, class 5, transcription factor 1 Mus musculus 42-47 25755712-8 2015 Treatment of BA-responsive RMS-13 cells with 5-FU and BA combination resulted in inhibition of GLI1, GLI2, PTCH1, and IGF2 genes. Fluorouracil 45-49 GLI family zinc finger 1 Homo sapiens 95-99 25444672-1 2015 Complement regulatory proteins (CD55 and CD59) were known to be expressed in many tumors and tumor cell lines including colorectal carcinoma, and were proposed as immunotherapy targets, however whether knocking down of CD55 and CD59 will affect the sensitivity of HT-29 cells to chemotherapy drugs for example, 5-Fluorouracil and Oxaliplatin and their possible mechanisms haven"t been studied. Fluorouracil 311-325 CD55 molecule (Cromer blood group) Homo sapiens 32-36 25444672-1 2015 Complement regulatory proteins (CD55 and CD59) were known to be expressed in many tumors and tumor cell lines including colorectal carcinoma, and were proposed as immunotherapy targets, however whether knocking down of CD55 and CD59 will affect the sensitivity of HT-29 cells to chemotherapy drugs for example, 5-Fluorouracil and Oxaliplatin and their possible mechanisms haven"t been studied. Fluorouracil 311-325 CD55 molecule (Cromer blood group) Homo sapiens 219-223 25426562-0 2015 PAK6 increase chemoresistance and is a prognostic marker for stage II and III colon cancer patients undergoing 5-FU based chemotherapy. Fluorouracil 111-115 p21 (RAC1) activated kinase 6 Homo sapiens 0-4 25426562-2 2015 We have further evaluated PAK6 as a predictor of 5-fluorouracil (5-FU) treatment response in colon cancer. Fluorouracil 49-63 p21 (RAC1) activated kinase 6 Homo sapiens 26-30 25426562-2 2015 We have further evaluated PAK6 as a predictor of 5-fluorouracil (5-FU) treatment response in colon cancer. Fluorouracil 65-69 p21 (RAC1) activated kinase 6 Homo sapiens 26-30 25426562-4 2015 In the clinical analysis, PAK6 was overexpressed in 104 of 147 (70.75%) stage II and III patients who received 5-FU based chemotherapy after surgery. Fluorouracil 111-115 p21 (RAC1) activated kinase 6 Homo sapiens 26-30 25426562-6 2015 Colon cancer cell lines showed increased PAK6 expression upon 5-FU treatment. Fluorouracil 62-66 p21 (RAC1) activated kinase 6 Homo sapiens 41-45 25426562-7 2015 In PAK6-knockdown cells treated with 5-FU, cell viability and phosphorylation of BAD decreased, and the number of apoptotic cells, levels of cleaved caspase 3 and PARP increased compared to control cells. Fluorouracil 37-41 p21 (RAC1) activated kinase 6 Homo sapiens 3-7 25426562-11 2015 This study demonstrates that PAK6 is an independent prognostic factor for adjuvant 5-FU-based chemotherapy in patients with stage II and stage III colon cancer. Fluorouracil 83-87 p21 (RAC1) activated kinase 6 Homo sapiens 29-33 25628941-4 2015 The influence of overexpression of CDX2 on MDR was assessed by measuring IC50 of SGC7901/DDP and BGC823/5-FU cells to cisplatin, doxorubicin, and 5-fluorouracil, rate of doxorubicin efflux, apoptosis, and cell cycle progression detected by flow cytometry. Fluorouracil 146-160 caudal type homeobox 2 Homo sapiens 35-39 29996281-2 2018 Tegafur is the major active prodrug, which is metabolized to 5-Fu by cytochrome P4502A6 (CYP2A6). Fluorouracil 61-65 cytochrome P450 family 2 subfamily A member 6 Homo sapiens 89-95 29720580-9 2018 Notably, AZD8055, but not everolimus, synergistically enhanced the efficacy of 5-FU via reversing 5-FU-induced upregulation of P-glycoprotein (P-gp). Fluorouracil 79-83 phosphoglycolate phosphatase Mus musculus 127-141 29720580-9 2018 Notably, AZD8055, but not everolimus, synergistically enhanced the efficacy of 5-FU via reversing 5-FU-induced upregulation of P-glycoprotein (P-gp). Fluorouracil 79-83 phosphoglycolate phosphatase Mus musculus 143-147 29720580-9 2018 Notably, AZD8055, but not everolimus, synergistically enhanced the efficacy of 5-FU via reversing 5-FU-induced upregulation of P-glycoprotein (P-gp). Fluorouracil 98-102 phosphoglycolate phosphatase Mus musculus 127-141 29720580-9 2018 Notably, AZD8055, but not everolimus, synergistically enhanced the efficacy of 5-FU via reversing 5-FU-induced upregulation of P-glycoprotein (P-gp). Fluorouracil 98-102 phosphoglycolate phosphatase Mus musculus 143-147 25664120-0 2014 Correlation analysis of peripheral DPYD gene polymorphism with 5-fluorouracil susceptibility and side effects in colon cancer patients. Fluorouracil 63-77 dihydropyrimidine dehydrogenase Homo sapiens 35-39 29508026-14 2018 CONCLUSIONS: Fluorouracil monotherapy combined with panitumumab was safely administered to patients with KRAS WT mCRC intolerant to oxaliplatin and irinotecan. Fluorouracil 13-25 KRAS proto-oncogene, GTPase Homo sapiens 105-109 31938347-0 2018 CD44high/ESAlow squamous cell carcinoma cell-derived prostaglandin E2 confers resistance to 5-fluorouracil-induced apoptosis in CD44high/ESAhigh cells. Fluorouracil 92-106 CD44 molecule (Indian blood group) Homo sapiens 0-4 31938347-0 2018 CD44high/ESAlow squamous cell carcinoma cell-derived prostaglandin E2 confers resistance to 5-fluorouracil-induced apoptosis in CD44high/ESAhigh cells. Fluorouracil 92-106 CD44 molecule (Indian blood group) Homo sapiens 128-132 31938347-1 2018 We previously found that CD44high/ESAlow head and neck squamous cell carcinoma (HNSCC) cells harboring high dihydropyrimidine dehydrogenase (DPD) expression exhibited potent resistance to 5-fluorouracil (5-FU)-induced apoptosis. Fluorouracil 188-202 CD44 molecule (Indian blood group) Homo sapiens 25-29 31938347-1 2018 We previously found that CD44high/ESAlow head and neck squamous cell carcinoma (HNSCC) cells harboring high dihydropyrimidine dehydrogenase (DPD) expression exhibited potent resistance to 5-fluorouracil (5-FU)-induced apoptosis. Fluorouracil 188-202 dihydropyrimidine dehydrogenase Homo sapiens 141-144 31938347-1 2018 We previously found that CD44high/ESAlow head and neck squamous cell carcinoma (HNSCC) cells harboring high dihydropyrimidine dehydrogenase (DPD) expression exhibited potent resistance to 5-fluorouracil (5-FU)-induced apoptosis. Fluorouracil 204-208 CD44 molecule (Indian blood group) Homo sapiens 25-29 31938347-1 2018 We previously found that CD44high/ESAlow head and neck squamous cell carcinoma (HNSCC) cells harboring high dihydropyrimidine dehydrogenase (DPD) expression exhibited potent resistance to 5-fluorouracil (5-FU)-induced apoptosis. Fluorouracil 204-208 dihydropyrimidine dehydrogenase Homo sapiens 141-144 31938347-3 2018 In this study, we examined 5-FU-induced apoptosis in sorted cell populations (i.e., CD44high/ESAlow, CD44high/ESAhigh, and CD44low cells from the HNSCC cell line A-253) to clarify the anti-apoptotic effect of PGE2 on CD44high cells. Fluorouracil 27-31 CD44 molecule (Indian blood group) Homo sapiens 84-88 31938347-7 2018 Furthermore, 5-FU-induced apoptosis of CD44high/ESAhigh cells was significantly increased in the presence of an inhibitor of the PGE2 receptors (EP1/EP2) when CD44high/ESAhigh cells were co-cultured with CD44high/ESAlow cells. Fluorouracil 13-17 CD44 molecule (Indian blood group) Homo sapiens 39-43 31938347-7 2018 Furthermore, 5-FU-induced apoptosis of CD44high/ESAhigh cells was significantly increased in the presence of an inhibitor of the PGE2 receptors (EP1/EP2) when CD44high/ESAhigh cells were co-cultured with CD44high/ESAlow cells. Fluorouracil 13-17 CD44 molecule (Indian blood group) Homo sapiens 159-163 31938347-8 2018 These results suggest that CD44high/ESAlow cell-derived PGE2 may contribute to the inhibition of 5-FU-induced apoptosis in CD44high/ESAhigh cells. Fluorouracil 97-101 CD44 molecule (Indian blood group) Homo sapiens 27-31 31938347-9 2018 Additionally, NR4A2 knockdown enhances 5-FU-induced apoptosis in CD44high/ESAhigh cells, suggesting that PGE2 attenuates 5-FU-induced apoptosis in an NR4A2-dependent manner in CD44high/ESAhigh cells. Fluorouracil 39-43 nuclear receptor subfamily 4 group A member 2 Homo sapiens 14-19 31938347-9 2018 Additionally, NR4A2 knockdown enhances 5-FU-induced apoptosis in CD44high/ESAhigh cells, suggesting that PGE2 attenuates 5-FU-induced apoptosis in an NR4A2-dependent manner in CD44high/ESAhigh cells. Fluorouracil 121-125 nuclear receptor subfamily 4 group A member 2 Homo sapiens 150-155 31938347-10 2018 In conclusion, CD44high/ESAlow cells contribute to induction of resistance to 5-FU in CD44high/ESAhigh cells through provision of PGE2. Fluorouracil 78-82 CD44 molecule (Indian blood group) Homo sapiens 15-19 29512753-11 2018 Additionally, a Cell Counting Kit-8 assay demonstrated that specific inhibitors of NOS3 and BDNF/neurotrophic receptor tyrosine kinase, type 2 signaling reduced the IC50 of MCF-7/MDR cells in response to various anticancer drugs, including adriamycin, cisplatin and 5-fluorouracil. Fluorouracil 266-280 brain derived neurotrophic factor Homo sapiens 92-96 29681787-9 2018 We have also identified that DPYD, the main degradation enzyme of 5-FU, was overexpressed in NR, as well as several ribosomal and mitochondrial proteins also overexpressed in NR. Fluorouracil 66-70 dihydropyrimidine dehydrogenase Homo sapiens 29-33 29556386-5 2018 For example, miR-34a attenuates the chemoresistance of colon cancer to 5-FU by inhibiting E2F3 and SIRT1. Fluorouracil 71-75 sirtuin 1 Homo sapiens 99-104 29155481-7 2018 The RGZ reduced leukocyte infiltration, preserved tissue structure, and dampened the 5-FU-induced expression of p53 and matrix metalloproteinase (Mmp)-2 after 5 days, and of Mmp-2 and interleukin (Il-1beta after 15 days. Fluorouracil 85-89 matrix metallopeptidase 2 Mus musculus 120-152 29155481-7 2018 The RGZ reduced leukocyte infiltration, preserved tissue structure, and dampened the 5-FU-induced expression of p53 and matrix metalloproteinase (Mmp)-2 after 5 days, and of Mmp-2 and interleukin (Il-1beta after 15 days. Fluorouracil 85-89 matrix metallopeptidase 2 Mus musculus 174-179 29581785-0 2018 A Meta-Analysis: Methylenetetrahydrofolate Reductase C677T Polymorphism in Gastric Cancer Patients Treated with 5-Fu Based Chemotherapy Predicts Serious Hematologic Toxicity but Not Prognosis. Fluorouracil 112-116 methylenetetrahydrofolate reductase Homo sapiens 17-52 29581785-1 2018 5-fluorouracil (5-Fu) metabolism associated enzyme, methylenetetrahydrofolate reductase (MTHFR)"s polymorphism C677T can affect enzyme activity and a series of studies have been performed to examine the association of this MTHFR polymorphism with the clinical outcomes of gastric cancer (GC) patients treated with 5-Fu based chemotherapies. Fluorouracil 0-14 methylenetetrahydrofolate reductase Homo sapiens 52-87 29581785-1 2018 5-fluorouracil (5-Fu) metabolism associated enzyme, methylenetetrahydrofolate reductase (MTHFR)"s polymorphism C677T can affect enzyme activity and a series of studies have been performed to examine the association of this MTHFR polymorphism with the clinical outcomes of gastric cancer (GC) patients treated with 5-Fu based chemotherapies. Fluorouracil 0-14 methylenetetrahydrofolate reductase Homo sapiens 89-94 29581785-1 2018 5-fluorouracil (5-Fu) metabolism associated enzyme, methylenetetrahydrofolate reductase (MTHFR)"s polymorphism C677T can affect enzyme activity and a series of studies have been performed to examine the association of this MTHFR polymorphism with the clinical outcomes of gastric cancer (GC) patients treated with 5-Fu based chemotherapies. Fluorouracil 0-14 methylenetetrahydrofolate reductase Homo sapiens 223-228 29581785-1 2018 5-fluorouracil (5-Fu) metabolism associated enzyme, methylenetetrahydrofolate reductase (MTHFR)"s polymorphism C677T can affect enzyme activity and a series of studies have been performed to examine the association of this MTHFR polymorphism with the clinical outcomes of gastric cancer (GC) patients treated with 5-Fu based chemotherapies. Fluorouracil 16-20 methylenetetrahydrofolate reductase Homo sapiens 52-87 29581785-1 2018 5-fluorouracil (5-Fu) metabolism associated enzyme, methylenetetrahydrofolate reductase (MTHFR)"s polymorphism C677T can affect enzyme activity and a series of studies have been performed to examine the association of this MTHFR polymorphism with the clinical outcomes of gastric cancer (GC) patients treated with 5-Fu based chemotherapies. Fluorouracil 16-20 methylenetetrahydrofolate reductase Homo sapiens 89-94 29581785-1 2018 5-fluorouracil (5-Fu) metabolism associated enzyme, methylenetetrahydrofolate reductase (MTHFR)"s polymorphism C677T can affect enzyme activity and a series of studies have been performed to examine the association of this MTHFR polymorphism with the clinical outcomes of gastric cancer (GC) patients treated with 5-Fu based chemotherapies. Fluorouracil 16-20 methylenetetrahydrofolate reductase Homo sapiens 223-228 29581785-1 2018 5-fluorouracil (5-Fu) metabolism associated enzyme, methylenetetrahydrofolate reductase (MTHFR)"s polymorphism C677T can affect enzyme activity and a series of studies have been performed to examine the association of this MTHFR polymorphism with the clinical outcomes of gastric cancer (GC) patients treated with 5-Fu based chemotherapies. Fluorouracil 314-318 methylenetetrahydrofolate reductase Homo sapiens 52-87 29581785-1 2018 5-fluorouracil (5-Fu) metabolism associated enzyme, methylenetetrahydrofolate reductase (MTHFR)"s polymorphism C677T can affect enzyme activity and a series of studies have been performed to examine the association of this MTHFR polymorphism with the clinical outcomes of gastric cancer (GC) patients treated with 5-Fu based chemotherapies. Fluorouracil 314-318 methylenetetrahydrofolate reductase Homo sapiens 89-94 29581785-1 2018 5-fluorouracil (5-Fu) metabolism associated enzyme, methylenetetrahydrofolate reductase (MTHFR)"s polymorphism C677T can affect enzyme activity and a series of studies have been performed to examine the association of this MTHFR polymorphism with the clinical outcomes of gastric cancer (GC) patients treated with 5-Fu based chemotherapies. Fluorouracil 314-318 methylenetetrahydrofolate reductase Homo sapiens 223-228 29581785-5 2018 Researches exploring MTHFR polymorphisms C677T"s relationship with the clinical outcomes (response rate, overall survival and toxicity) of GC patients treated with 5-Fu based chemotherapy were included. Fluorouracil 164-168 methylenetetrahydrofolate reductase Homo sapiens 21-26 29581785-11 2018 In conclusion, MTHFR C677T polymorphism predicts severe hematologic toxicity in GC patients receiving 5-Fu based chemotherapy, but not the efficiency. Fluorouracil 102-106 methylenetetrahydrofolate reductase Homo sapiens 15-20 29371412-0 2018 Loss of ABCB4 attenuates the caspase-dependent apoptosis regulating resistance to 5-Fu in colorectal cancer. Fluorouracil 82-86 ATP binding cassette subfamily B member 4 Homo sapiens 8-13 29371412-3 2018 The present study is aimed to investigate the putative mechanism of ABCB4 in 5-fluorouracil (5-Fu) resistance. Fluorouracil 77-91 ATP binding cassette subfamily B member 4 Homo sapiens 68-73 29371412-3 2018 The present study is aimed to investigate the putative mechanism of ABCB4 in 5-fluorouracil (5-Fu) resistance. Fluorouracil 93-97 ATP binding cassette subfamily B member 4 Homo sapiens 68-73 29371412-5 2018 The knockdown of ABCB4 by small interfering RNA decreased the apoptosis by 5-Fu in resistant HCT8R cell lines without influencing the proliferation. Fluorouracil 75-79 ATP binding cassette subfamily B member 4 Homo sapiens 17-22 29371412-8 2018 Furthermore, the histological detection of ABCB4 mRNA level in human colorectal cancer tissues and even in the recurrent tissues after 5-Fu single-agent chemotherapy was employed to provide more concrete evidence that ABCB4 may be a tumor suppressor gene to regulate chemoresistance in colorectal cancer. Fluorouracil 135-139 ATP binding cassette subfamily B member 4 Homo sapiens 218-223 29374697-4 2018 RESULTS: Under pretreatment with HGF for 96 h, 5 muM and 10 muM of 5-FU mediated significant growth inhibition by 72.5+-3.9% and 76.2+-2.4%, respectively, compared to HGF alone, and by 105.1+-2.8% and 103.5+-2.9%, respectively, without HGF. Fluorouracil 67-71 hepatocyte growth factor Mus musculus 33-36 29374697-4 2018 RESULTS: Under pretreatment with HGF for 96 h, 5 muM and 10 muM of 5-FU mediated significant growth inhibition by 72.5+-3.9% and 76.2+-2.4%, respectively, compared to HGF alone, and by 105.1+-2.8% and 103.5+-2.9%, respectively, without HGF. Fluorouracil 67-71 hepatocyte growth factor Mus musculus 167-170 29374697-4 2018 RESULTS: Under pretreatment with HGF for 96 h, 5 muM and 10 muM of 5-FU mediated significant growth inhibition by 72.5+-3.9% and 76.2+-2.4%, respectively, compared to HGF alone, and by 105.1+-2.8% and 103.5+-2.9%, respectively, without HGF. Fluorouracil 67-71 hepatocyte growth factor Mus musculus 167-170 29374697-6 2018 Thymidylate synthase was also decreased in a time-dependent manner to 80.6+-2.0% after 24 h and to 52.7+-1.5% after 96 h. CONCLUSION: The presence of HGF was found to increase the 5-FU-induced death signal, JNK pathway, and inhibition of cell growth. Fluorouracil 180-184 thymidylate synthase Mus musculus 0-20 29374697-6 2018 Thymidylate synthase was also decreased in a time-dependent manner to 80.6+-2.0% after 24 h and to 52.7+-1.5% after 96 h. CONCLUSION: The presence of HGF was found to increase the 5-FU-induced death signal, JNK pathway, and inhibition of cell growth. Fluorouracil 180-184 hepatocyte growth factor Mus musculus 150-153 29374697-8 2018 The chemotherapeutic effect of 5-FU was increased in HGF- but not TGF-beta-induced EMT. Fluorouracil 31-35 hepatocyte growth factor Mus musculus 53-56 25664120-1 2014 OBJECTIVE: To investigate the correlation of peripheral DPYD gene polymorphism with 5-fluorouracil (5-FU) susceptibility and side effect in patients with colon cancer. Fluorouracil 84-98 dihydropyrimidine dehydrogenase Homo sapiens 56-60 25664120-1 2014 OBJECTIVE: To investigate the correlation of peripheral DPYD gene polymorphism with 5-fluorouracil (5-FU) susceptibility and side effect in patients with colon cancer. Fluorouracil 100-104 dihydropyrimidine dehydrogenase Homo sapiens 56-60 25664120-7 2014 CONCLUSION: DPYD gene polymorphism plays a guiding role in predicting efficacy and toxicity of 5-FU, which can be used as an important reference index of 5-FU individualized administration scheme. Fluorouracil 95-99 dihydropyrimidine dehydrogenase Homo sapiens 12-16 25664120-7 2014 CONCLUSION: DPYD gene polymorphism plays a guiding role in predicting efficacy and toxicity of 5-FU, which can be used as an important reference index of 5-FU individualized administration scheme. Fluorouracil 154-158 dihydropyrimidine dehydrogenase Homo sapiens 12-16 25124805-0 2014 Assessment of 5-fluorouracil and 4-nitroquinoline-1-oxide in vivo genotoxicity with Pig-a mutation and micronucleus endpoints. Fluorouracil 14-28 phosphatidylinositol glycan anchor biosynthesis class A Sus scrofa 84-89 25520862-8 2014 In gastric cancer patients treated with 5-FU and cisplatin, the five-year survival rates are higher in DACT2 methylated cases. Fluorouracil 40-44 dishevelled binding antagonist of beta catenin 2 Homo sapiens 103-108 25520862-11 2014 Restoration of DACT2 expression sensitized gastric cancer cells to paclitaxel and 5-FU. Fluorouracil 82-86 dishevelled binding antagonist of beta catenin 2 Homo sapiens 15-20 25401795-4 2014 Elimination of hepatic MDSC in EL4 tumor-bearing mice using low dose 5-fluorouracil (5-FU) treatment reversed transaminase elevation and adoptive transfer of hepatic MDSC from B16 tumor-bearing mice caused transaminase elevation indicating a direct MDSC mediated effect. Fluorouracil 69-83 epilepsy 4 Mus musculus 31-34 29398868-0 2018 Overexpression of CREPT confers colorectal cancer sensitivity to fluorouracil. Fluorouracil 65-77 regulation of nuclear pre-mRNA domain containing 1B Homo sapiens 18-23 29398868-1 2018 AIM: To investigate expression of cell cycle-related and expression-elevated protein in tumor (CREPT) in colorectal cancer (CRC) and determine its prognostic value in response to 5-fluorouracil (5-FU). Fluorouracil 179-193 regulation of nuclear pre-mRNA domain containing 1B Homo sapiens 95-100 29398868-1 2018 AIM: To investigate expression of cell cycle-related and expression-elevated protein in tumor (CREPT) in colorectal cancer (CRC) and determine its prognostic value in response to 5-fluorouracil (5-FU). Fluorouracil 195-199 regulation of nuclear pre-mRNA domain containing 1B Homo sapiens 95-100 29398868-9 2018 More importantly, high expression of CREPT sensitized CRC cells to 5-FU treatment. Fluorouracil 67-71 regulation of nuclear pre-mRNA domain containing 1B Homo sapiens 37-42 29398868-10 2018 Furthermore, we demonstrated that 5-FU elicited significant apoptosis in CREPT-positive cells. Fluorouracil 34-38 regulation of nuclear pre-mRNA domain containing 1B Homo sapiens 73-78 29398868-11 2018 CONCLUSION: Aberrant overexpression of CREPT contributes to tumorigenesis of CRC by promoting cell proliferation and accelerating the cell cycle, and confers sensitivity to 5-FU. Fluorouracil 173-177 regulation of nuclear pre-mRNA domain containing 1B Homo sapiens 39-44 29398868-12 2018 CREPT is a potential prognostic biomarker for 5-FU in CRC. Fluorouracil 46-50 regulation of nuclear pre-mRNA domain containing 1B Homo sapiens 0-5 29515783-6 2018 Taken together, our data suggest that HMGA2 enhances the chemoresistance to 5-FU in CRC via activating the Dvl2/Wnt pathway. Fluorouracil 76-80 dishevelled segment polarity protein 2 Homo sapiens 107-111 25401795-4 2014 Elimination of hepatic MDSC in EL4 tumor-bearing mice using low dose 5-fluorouracil (5-FU) treatment reversed transaminase elevation and adoptive transfer of hepatic MDSC from B16 tumor-bearing mice caused transaminase elevation indicating a direct MDSC mediated effect. Fluorouracil 85-89 epilepsy 4 Mus musculus 31-34 25381393-11 2014 CONCLUSION: In the largest study to date, statistically significant associations were found between DPYD variants (DPYD*2A and D949V) and increased incidence of grade 3 or greater 5FU-AEs in patients treated with adjuvant 5-FU-based combination chemotherapy. Fluorouracil 222-226 dihydropyrimidine dehydrogenase Homo sapiens 100-104 25381393-11 2014 CONCLUSION: In the largest study to date, statistically significant associations were found between DPYD variants (DPYD*2A and D949V) and increased incidence of grade 3 or greater 5FU-AEs in patients treated with adjuvant 5-FU-based combination chemotherapy. Fluorouracil 222-226 dihydropyrimidine dehydrogenase Homo sapiens 115-119 25381394-0 2014 DPYD variants to predict 5-FU toxicity: the ultimate proof. Fluorouracil 25-29 dihydropyrimidine dehydrogenase Homo sapiens 0-4 25088576-5 2014 The effect of MRP3 down-regulation on cell proliferation and apoptosis in response to 5-fluorouracil and/or irradiation were examined in vitro and in xenograft mouse models, respectively. Fluorouracil 86-100 ATP-binding cassette, sub-family C (CFTR/MRP), member 3 Mus musculus 14-18 25272957-6 2014 The benefit on DFS in AREG-/EREG- patients was even stronger in the group that received 5-FU/FA/irinotecan as adjuvant treatment (p=0.002). Fluorouracil 88-92 amphiregulin Homo sapiens 22-26 25272957-9 2014 Patients with negative VEGF-D expression had a trend to live longer when treated with 5-FU/FA (p=0.106). Fluorouracil 86-90 vascular endothelial growth factor D Homo sapiens 23-29 24583265-4 2014 We show that both ORAI1 and STIM1 play pro-survival anti-apoptotic role in pancreatic adenocarcinoma cell lines, as siRNA-mediated knockdown of ORAI1 and/or STIM1 increases apoptosis induced by chemotherapy drugs 5-fluorouracil (5-FU) or gemcitabine. Fluorouracil 213-227 ORAI calcium release-activated calcium modulator 1 Homo sapiens 18-23 24583265-4 2014 We show that both ORAI1 and STIM1 play pro-survival anti-apoptotic role in pancreatic adenocarcinoma cell lines, as siRNA-mediated knockdown of ORAI1 and/or STIM1 increases apoptosis induced by chemotherapy drugs 5-fluorouracil (5-FU) or gemcitabine. Fluorouracil 213-227 ORAI calcium release-activated calcium modulator 1 Homo sapiens 144-149 24583265-4 2014 We show that both ORAI1 and STIM1 play pro-survival anti-apoptotic role in pancreatic adenocarcinoma cell lines, as siRNA-mediated knockdown of ORAI1 and/or STIM1 increases apoptosis induced by chemotherapy drugs 5-fluorouracil (5-FU) or gemcitabine. Fluorouracil 229-233 ORAI calcium release-activated calcium modulator 1 Homo sapiens 18-23 24583265-4 2014 We show that both ORAI1 and STIM1 play pro-survival anti-apoptotic role in pancreatic adenocarcinoma cell lines, as siRNA-mediated knockdown of ORAI1 and/or STIM1 increases apoptosis induced by chemotherapy drugs 5-fluorouracil (5-FU) or gemcitabine. Fluorouracil 229-233 ORAI calcium release-activated calcium modulator 1 Homo sapiens 144-149 25063444-5 2014 In CRC cells, IL-22 was able to attenuate the cytotoxic and apoptosis-inducing effects of 5-FU and OXA by activating the STAT3 pathway and subsequently increasing the expression of anti-apoptotic genes. Fluorouracil 90-94 interleukin 22 Homo sapiens 14-19 25063444-6 2014 In addition, IL-22 conferred resistance to 5-FU and OXA by inducing IL-8 autocrine expression through STAT3 activation. Fluorouracil 43-47 interleukin 22 Homo sapiens 13-18 25050539-8 2014 Among these, collapsin response mediator protein 2 (CRMP-2), DNA replication complex GINS protein PSF2 (PSF-2) and selenium-binding protein 1 (SBP-1) were notable not only for their differential expression but also for decreased expression following 5-FU exposure, indicating their possible roles as novel biomarkers for sensitivity (CRMP-2, PSF-2) as well as resistance (SBP-1) to 5-FU. Fluorouracil 250-254 GINS complex subunit 2 Homo sapiens 104-109 25050539-8 2014 Among these, collapsin response mediator protein 2 (CRMP-2), DNA replication complex GINS protein PSF2 (PSF-2) and selenium-binding protein 1 (SBP-1) were notable not only for their differential expression but also for decreased expression following 5-FU exposure, indicating their possible roles as novel biomarkers for sensitivity (CRMP-2, PSF-2) as well as resistance (SBP-1) to 5-FU. Fluorouracil 382-386 GINS complex subunit 2 Homo sapiens 104-109 25216706-6 2014 The expression of some K-ras mutations resulted in a reduced sensitivity to gefitinib, 5-FU, docetaxel and gemcitabine, while showed no effects on erlotinib or cisplatin. Fluorouracil 87-91 KRAS proto-oncogene, GTPase Homo sapiens 23-28 30686002-0 2018 Synergic and comparative effect of 5-fluorouracil and leucoverin on breast and colon cancer cells through TRPM2 channels. Fluorouracil 35-49 transient receptor potential cation channel subfamily M member 2 Homo sapiens 106-111 25218240-1 2014 BACKGROUND: Recently, it has been shown that 5-fluorouracil (5-FU) with a strong dihydropyrimidine dehydrogenase (DPD) inhibitor elicits a significant response in bladder cancer with a high level of DPD. Fluorouracil 45-59 dihydropyrimidine dehydrogenase Homo sapiens 81-112 29362333-8 2018 DISCUSSION: It is known that S-1 not only achieves a high anticancer effect via dihydropyrimidine dehydrogenase(DPD)inhibition, which is a major metabolic pathway of 5-FU, but also increases the radiation susceptibility of malignancies. Fluorouracil 166-170 dihydropyrimidine dehydrogenase Homo sapiens 112-115 25218240-1 2014 BACKGROUND: Recently, it has been shown that 5-fluorouracil (5-FU) with a strong dihydropyrimidine dehydrogenase (DPD) inhibitor elicits a significant response in bladder cancer with a high level of DPD. Fluorouracil 45-59 dihydropyrimidine dehydrogenase Homo sapiens 114-117 25218240-1 2014 BACKGROUND: Recently, it has been shown that 5-fluorouracil (5-FU) with a strong dihydropyrimidine dehydrogenase (DPD) inhibitor elicits a significant response in bladder cancer with a high level of DPD. Fluorouracil 45-59 dihydropyrimidine dehydrogenase Homo sapiens 199-202 25218240-1 2014 BACKGROUND: Recently, it has been shown that 5-fluorouracil (5-FU) with a strong dihydropyrimidine dehydrogenase (DPD) inhibitor elicits a significant response in bladder cancer with a high level of DPD. Fluorouracil 61-65 dihydropyrimidine dehydrogenase Homo sapiens 81-112 29593202-2 2018 S-1, an oral dihydropyrimidine dehydrogenase (DPD)-inhibitory 5-fluorouracil, is a more potent DPD inhibitor than UFT;therefore, we hypothesized that postoperative adjuvant chemotherapy with S-1 would be effective for advanced non-small cell lung cancer (NSCLC). Fluorouracil 62-76 dihydropyrimidine dehydrogenase Homo sapiens 46-49 25218240-1 2014 BACKGROUND: Recently, it has been shown that 5-fluorouracil (5-FU) with a strong dihydropyrimidine dehydrogenase (DPD) inhibitor elicits a significant response in bladder cancer with a high level of DPD. Fluorouracil 61-65 dihydropyrimidine dehydrogenase Homo sapiens 114-117 25218240-1 2014 BACKGROUND: Recently, it has been shown that 5-fluorouracil (5-FU) with a strong dihydropyrimidine dehydrogenase (DPD) inhibitor elicits a significant response in bladder cancer with a high level of DPD. Fluorouracil 61-65 dihydropyrimidine dehydrogenase Homo sapiens 199-202 25222248-8 2014 We found that the XPF rs6498486 and XPF rs2276465 polymorphisms are mark-ers of response to oxaliplatin/5-fluorouracil-based chemotherapy in gastric cancer patients. Fluorouracil 104-118 ERCC excision repair 4, endonuclease catalytic subunit Homo sapiens 18-21 28968593-10 2018 Moreover, AR-A014418 displayed promising chemosensitizing effects on 5-FU in QGP1 and slight radiosensitizing properties in BON1 and QGP1 cells. Fluorouracil 69-73 p21 (RAC1) activated kinase 3 Homo sapiens 10-14 29371950-0 2017 Overexpression of miR-489 enhances efficacy of 5-fluorouracil-based treatment in breast cancer stem cells by targeting XIAP. Fluorouracil 47-61 X-linked inhibitor of apoptosis Homo sapiens 119-123 25222248-8 2014 We found that the XPF rs6498486 and XPF rs2276465 polymorphisms are mark-ers of response to oxaliplatin/5-fluorouracil-based chemotherapy in gastric cancer patients. Fluorouracil 104-118 ERCC excision repair 4, endonuclease catalytic subunit Homo sapiens 36-39 29371950-9 2017 We found that enforced expression of XIAP through its recombinant expression vector abolished the effect of miR-489 on reversing the 5-fluorouracil resistance. Fluorouracil 133-147 X-linked inhibitor of apoptosis Homo sapiens 37-41 25232494-2 2014 Organic anion transporter 2 (OAT2) and organic cation transporter 2 (OCT2) are critical determinants in uptake of 5-FU and oxaliplatin, respectively. Fluorouracil 114-118 solute carrier family 22 member 7 Homo sapiens 0-27 25232494-2 2014 Organic anion transporter 2 (OAT2) and organic cation transporter 2 (OCT2) are critical determinants in uptake of 5-FU and oxaliplatin, respectively. Fluorouracil 114-118 solute carrier family 22 member 7 Homo sapiens 29-33 25002745-0 2014 Effect of CYP2A6 genetic polymorphism on the metabolic conversion of tegafur to 5-fluorouracil and its enantioselectivity. Fluorouracil 80-94 cytochrome P450 family 2 subfamily A member 6 Homo sapiens 10-16 25002745-1 2014 Tegafur (FT), a prodrug of 5-fluorouracil, is a chiral molecule, a racemate of R- and S-isomers, and CYP2A6 plays an important role in the enantioselective metabolism of FT in human liver microsomes (R-FT >> S-FT). Fluorouracil 27-41 cytochrome P450 family 2 subfamily A member 6 Homo sapiens 101-107 24867971-4 2014 Fur4p specifically transports uracil and 5-fluorouracil. Fluorouracil 41-55 uracil permease Saccharomyces cerevisiae S288C 0-5 28379040-2 2017 5-FU is a time-dependent drug but is rapidly degraded in plasma by dihydropyrimidine dehydrogenase (DPD). Fluorouracil 0-4 dihydropyrimidine dehydrogenase Homo sapiens 67-98 28379040-2 2017 5-FU is a time-dependent drug but is rapidly degraded in plasma by dihydropyrimidine dehydrogenase (DPD). Fluorouracil 0-4 dihydropyrimidine dehydrogenase Homo sapiens 100-103 28379040-6 2017 However, the efficacy of 5-FU can be further improved by its combination with DPD inhibitors and biochemical modulators, such as uracil and leucovorin, in addition to modifying administration schedules. Fluorouracil 25-29 dihydropyrimidine dehydrogenase Homo sapiens 78-81 29344221-8 2017 It was also revealed that knockdown of livin by siRNA increased the apoptotic rate, suppressed invasion of LoVo cells, and decreased the half-maximal inhibitory concentration of oxaliplatin and 5-fluorouracil by ~50% in LoVo cells significantly compared with control groups. Fluorouracil 194-208 baculoviral IAP repeat containing 7 Homo sapiens 39-44 24867971-6 2014 Deletion of the FUR4 gene confers resistance to 5-fluorouracil as well as cross-resistance to triazoles and imidazole antifungals when they are used simultaneously with 5-fluorouracil. Fluorouracil 48-62 uracil permease Saccharomyces cerevisiae S288C 16-20 24867971-6 2014 Deletion of the FUR4 gene confers resistance to 5-fluorouracil as well as cross-resistance to triazoles and imidazole antifungals when they are used simultaneously with 5-fluorouracil. Fluorouracil 169-183 uracil permease Saccharomyces cerevisiae S288C 16-20 24684961-5 2014 The CD44(+)CD117(+)CSCs also exhibited high chemoresistance to anticancer drugs when the cells were incubated with 5-fluorouracil, cisplatin and carboplatin, respectively in 3D versus 2D environment. Fluorouracil 115-129 CD44 molecule (Indian blood group) Homo sapiens 4-8 28903131-2 2017 In gastric cancer, existing studies on this topic are limited and the association between MGMT and fluorouracil-based adjuvant chemotherapy remains obscure. Fluorouracil 99-111 O-6-methylguanine-DNA methyltransferase Homo sapiens 90-94 28903131-3 2017 Objective: To investigate the postoperative prognostic significance of MGMT in patients with resectable gastric cancer and its responsiveness to fluorouracil-based adjuvant chemotherapy. Fluorouracil 145-157 O-6-methylguanine-DNA methyltransferase Homo sapiens 71-75 28903131-14 2017 In stage II disease, the benefit from fluorouracil-based adjuvant chemotherapy was superior among MGMT-positive patients (HR, 0.35; 95% CI, 0.13-0.95; P = .007 for interaction) compared with MGMT-negative patients. Fluorouracil 38-50 O-6-methylguanine-DNA methyltransferase Homo sapiens 98-102 28903131-14 2017 In stage II disease, the benefit from fluorouracil-based adjuvant chemotherapy was superior among MGMT-positive patients (HR, 0.35; 95% CI, 0.13-0.95; P = .007 for interaction) compared with MGMT-negative patients. Fluorouracil 38-50 O-6-methylguanine-DNA methyltransferase Homo sapiens 191-195 28911246-6 2017 With 5-fluorouracil-loaded LC-PLGA NPs, we were able to demonstrate significant increases in the uptake efficiency and cytotoxicity in colon cancer cells that were positive for OCTN2 and ATB0,+. Fluorouracil 5-19 solute carrier family 1 member 5 Homo sapiens 187-191 29113268-0 2017 JAB1-STAT3 activation loop is associated with recurrence following 5-fluorouracil-based adjuvant chemotherapy in human colorectal cancer. Fluorouracil 67-81 COP9 signalosome subunit 5 Homo sapiens 0-4 29113268-7 2017 In the present study, it was found that high JAB1 expression in primary colorectal cancer tissues is an independent predictor of recurrence following 5-fluorouracil (5-FU)-based adjuvant chemotherapy in colorectal cancer patients, and that high expression of both JAB1 and STAT3 in primary colorectal cancer tissues is associated with a lower recurrence-free survival rate following 5-FU-based adjuvant chemotherapy compared to high expression of only JAB1 or STAT3. Fluorouracil 150-164 COP9 signalosome subunit 5 Homo sapiens 45-49 29113268-7 2017 In the present study, it was found that high JAB1 expression in primary colorectal cancer tissues is an independent predictor of recurrence following 5-fluorouracil (5-FU)-based adjuvant chemotherapy in colorectal cancer patients, and that high expression of both JAB1 and STAT3 in primary colorectal cancer tissues is associated with a lower recurrence-free survival rate following 5-FU-based adjuvant chemotherapy compared to high expression of only JAB1 or STAT3. Fluorouracil 166-170 COP9 signalosome subunit 5 Homo sapiens 45-49 29113268-7 2017 In the present study, it was found that high JAB1 expression in primary colorectal cancer tissues is an independent predictor of recurrence following 5-fluorouracil (5-FU)-based adjuvant chemotherapy in colorectal cancer patients, and that high expression of both JAB1 and STAT3 in primary colorectal cancer tissues is associated with a lower recurrence-free survival rate following 5-FU-based adjuvant chemotherapy compared to high expression of only JAB1 or STAT3. Fluorouracil 166-170 COP9 signalosome subunit 5 Homo sapiens 264-268 29113268-7 2017 In the present study, it was found that high JAB1 expression in primary colorectal cancer tissues is an independent predictor of recurrence following 5-fluorouracil (5-FU)-based adjuvant chemotherapy in colorectal cancer patients, and that high expression of both JAB1 and STAT3 in primary colorectal cancer tissues is associated with a lower recurrence-free survival rate following 5-FU-based adjuvant chemotherapy compared to high expression of only JAB1 or STAT3. Fluorouracil 166-170 COP9 signalosome subunit 5 Homo sapiens 264-268 29113268-7 2017 In the present study, it was found that high JAB1 expression in primary colorectal cancer tissues is an independent predictor of recurrence following 5-fluorouracil (5-FU)-based adjuvant chemotherapy in colorectal cancer patients, and that high expression of both JAB1 and STAT3 in primary colorectal cancer tissues is associated with a lower recurrence-free survival rate following 5-FU-based adjuvant chemotherapy compared to high expression of only JAB1 or STAT3. Fluorouracil 383-387 COP9 signalosome subunit 5 Homo sapiens 45-49 29113268-8 2017 Overall, these results suggest that JAB1 is a novel predictive marker of recurrence following 5-FU-based adjuvant chemotherapy in colorectal cancer patients, and that the JAB1-STAT3 activation loop may be a potential therapeutic target in recurrent colorectal cancer following 5-FU-based adjuvant chemotherapy. Fluorouracil 94-98 COP9 signalosome subunit 5 Homo sapiens 36-40 29113268-8 2017 Overall, these results suggest that JAB1 is a novel predictive marker of recurrence following 5-FU-based adjuvant chemotherapy in colorectal cancer patients, and that the JAB1-STAT3 activation loop may be a potential therapeutic target in recurrent colorectal cancer following 5-FU-based adjuvant chemotherapy. Fluorouracil 277-281 COP9 signalosome subunit 5 Homo sapiens 36-40 29113268-8 2017 Overall, these results suggest that JAB1 is a novel predictive marker of recurrence following 5-FU-based adjuvant chemotherapy in colorectal cancer patients, and that the JAB1-STAT3 activation loop may be a potential therapeutic target in recurrent colorectal cancer following 5-FU-based adjuvant chemotherapy. Fluorouracil 277-281 COP9 signalosome subunit 5 Homo sapiens 171-175 29442040-0 2017 Lidocaine sensitizes the cytotoxicity of 5-fluorouacil in melanoma cells via upregulation of microRNA-493. Fluorouracil 41-54 microRNA 493 Homo sapiens 93-105 29442040-10 2017 Moreover, we verified that Sox4 was a target of miR-493, and Sox4 overexpression decreased the sensitivity to 5-FU. Fluorouracil 110-114 SRY-box transcription factor 4 Homo sapiens 27-31 29442040-10 2017 Moreover, we verified that Sox4 was a target of miR-493, and Sox4 overexpression decreased the sensitivity to 5-FU. Fluorouracil 110-114 microRNA 493 Homo sapiens 48-55 29442040-10 2017 Moreover, we verified that Sox4 was a target of miR-493, and Sox4 overexpression decreased the sensitivity to 5-FU. Fluorouracil 110-114 SRY-box transcription factor 4 Homo sapiens 61-65 29442040-12 2017 Our results suggest that lidocaine sensitizes the cytotoxicity of 5-FU in melanoma cells via upregulation of miR-493, which might be involved in SOX4-mediated PI3K/AKT and Smad pathways. Fluorouracil 66-70 microRNA 493 Homo sapiens 109-116 29442040-12 2017 Our results suggest that lidocaine sensitizes the cytotoxicity of 5-FU in melanoma cells via upregulation of miR-493, which might be involved in SOX4-mediated PI3K/AKT and Smad pathways. Fluorouracil 66-70 SRY-box transcription factor 4 Homo sapiens 145-149 28640389-0 2017 Efficacy and safety of recombinant human lymphotoxin-alpha derivative with cisplatin and fluorouracil in patients with metastatic esophageal squamous cell carcinoma: A randomized, multicenter, open-label, controlled, phase 2b trial. Fluorouracil 89-101 lymphotoxin alpha Homo sapiens 41-58 28713943-2 2017 In order to investigate whether the c-Jun N-terminal kinase (JNK) signaling pathway is involved in the mechanism underlying ASIV-induced downregulated the expression of mdr1, the present study used 5-fluorouracil-resistant Bel-7402/FU human hepatic cancer cells as target cells. Fluorouracil 198-212 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 36-41 28927087-1 2017 Gimeracil or 5-chloro-2,4-dihydroxypyridine (CDHP) enhances the antitumor effects of 5-fluorouracil (5-FU) by inhibiting dihydropyrimidine dehydrogenase (DPD), which is involved in the degradation of 5-FU. Fluorouracil 85-99 dihydropyrimidine dehydrogenase Homo sapiens 121-152 28927087-1 2017 Gimeracil or 5-chloro-2,4-dihydroxypyridine (CDHP) enhances the antitumor effects of 5-fluorouracil (5-FU) by inhibiting dihydropyrimidine dehydrogenase (DPD), which is involved in the degradation of 5-FU. Fluorouracil 85-99 dihydropyrimidine dehydrogenase Homo sapiens 154-157 28927087-1 2017 Gimeracil or 5-chloro-2,4-dihydroxypyridine (CDHP) enhances the antitumor effects of 5-fluorouracil (5-FU) by inhibiting dihydropyrimidine dehydrogenase (DPD), which is involved in the degradation of 5-FU. Fluorouracil 101-105 dihydropyrimidine dehydrogenase Homo sapiens 121-152 28927087-1 2017 Gimeracil or 5-chloro-2,4-dihydroxypyridine (CDHP) enhances the antitumor effects of 5-fluorouracil (5-FU) by inhibiting dihydropyrimidine dehydrogenase (DPD), which is involved in the degradation of 5-FU. Fluorouracil 101-105 dihydropyrimidine dehydrogenase Homo sapiens 154-157 24919507-4 2014 In HT-29 tumors and in cells from in vitro culture, we observed increased vitamin D receptor (VDR) expression after treatment with either PRI-2205 or 5-FU alone, or in combination. Fluorouracil 150-154 vitamin D receptor Homo sapiens 74-92 24919507-4 2014 In HT-29 tumors and in cells from in vitro culture, we observed increased vitamin D receptor (VDR) expression after treatment with either PRI-2205 or 5-FU alone, or in combination. Fluorouracil 150-154 vitamin D receptor Homo sapiens 94-97 24919507-6 2014 Increased VDR expression was also observed after combined treatment of mice with 5-FU and PRI-2191. Fluorouracil 81-85 vitamin D (1,25-dihydroxyvitamin D3) receptor Mus musculus 10-13 24869908-8 2014 PDZK1 overexpression was associated with resistance to paclitaxel/5-fluorouracil/etoposide only at low concentrations. Fluorouracil 66-80 PDZ domain containing 1 Homo sapiens 0-5 23376192-10 2014 Overall, we present examples of how Pharmaco-miR provides possible explanations for previously published observations, including how the cisplatin and 5-fluorouracil resistance induced by miR-148a may be caused by miR-148a targeting of the gene KIT. Fluorouracil 151-165 membrane associated ring-CH-type finger 8 Homo sapiens 45-48 24940508-2 2014 UDP-N-acetyl-alpha-D-galactosamine:polypeptide N-acetyl-galactosaminyltransferase 14 (GALNT14) genotype was previously identified as a prognostic marker for HCC patients receiving 5-fluorouracil, mitoxantrone and cisplatin (FMP) combination chemotherapy. Fluorouracil 180-194 polypeptide N-acetylgalactosaminyltransferase 14 Homo sapiens 47-84 24940508-2 2014 UDP-N-acetyl-alpha-D-galactosamine:polypeptide N-acetyl-galactosaminyltransferase 14 (GALNT14) genotype was previously identified as a prognostic marker for HCC patients receiving 5-fluorouracil, mitoxantrone and cisplatin (FMP) combination chemotherapy. Fluorouracil 180-194 polypeptide N-acetylgalactosaminyltransferase 14 Homo sapiens 86-93 24961587-1 2014 F10 is an oligonucleotide based on the thymidylate synthase (TS) inhibitory 5-fluorouracil (5-FU) metabolite, 5-fluoro-2"-deoxyuridine-5"-O-monophosphate. Fluorouracil 76-90 thymidylate synthase Mus musculus 39-59 28554763-7 2017 After treatment of 5-FU, the intestinal mucous were damaged, although the number of msi-1 positive cells has a little decrease, there was no statistical difference among the mice at different time after injection (P>0.05). Fluorouracil 19-23 musashi RNA-binding protein 1 Mus musculus 84-89 28554763-9 2017 There was significant positive correction between the percentage of msi-1 positive cells and the percentage of Rho low staining cell fraction (r=0.867, p<0.01) after 5-FU injection. Fluorouracil 169-173 musashi RNA-binding protein 1 Mus musculus 68-73 28624221-0 2017 miR-1290 Is a Biomarker in DNA-Mismatch-Repair-Deficient Colon Cancer and Promotes Resistance to 5-Fluorouracil by Directly Targeting hMSH2. Fluorouracil 97-111 microRNA 1290 Homo sapiens 0-8 28624221-6 2017 We identified that miR-1290 was one of the most upregulated miRNAs in both dMMR colon cancer tissues and 5-FU-resistant cells. Fluorouracil 105-109 microRNA 1290 Homo sapiens 19-27 28624221-7 2017 We also found that miR-1290 was positively correlated with dMMR status and predicted poor prognosis in stage II and III colon cancer patients who received 5-FU-based chemotherapy. Fluorouracil 155-159 microRNA 1290 Homo sapiens 19-27 28624221-8 2017 Furthermore, we demonstrated that inhibition of the expression of miR-1290 enhanced sensitivity to 5-FU treatment in vitro and in tumor xenografts in vivo by direct targeting hMSH2. Fluorouracil 99-103 microRNA 1290 Homo sapiens 66-74 28624221-9 2017 Our study indicates that miR-1290 may become a promising biomarker of dMMR colon cancer and predicts the prognosis of stage II and III patients who receive 5-FU-based adjuvant therapy. Fluorouracil 156-160 microRNA 1290 Homo sapiens 25-33 27836590-5 2017 However, the addition of CA125 induced obvious NIR PL recovery, which was ascribed to the strong binding affinity of CA125 with its aptamer, and the separation of aptamer/5-Fu complex from the surface of QDs. Fluorouracil 171-175 mucin 16, cell surface associated Homo sapiens 25-30 28481246-8 2017 Moreover, CMP in combination with 5-FU alleviated severe liver injury induced by 5-FU via reducing the levels of ROS, IL-1beta, and IL-6, decreasing expression of p-IkappaB-alpha, NF-kappaB, p-NF-kappaB, pp38 and Bax, and elevating levels of Nrf2, GCL, HO-1 and Bcl-2. Fluorouracil 34-38 BCL2-associated X protein Mus musculus 213-216 28428709-9 2017 5-FU-induced expression of IL-13, IL-17A, TNF-alpha, and IFN-gamma in the ileum was Fn14 dependent. Fluorouracil 0-4 interleukin 17A Mus musculus 34-40 28262261-3 2017 This review presents the usefulness of pharmacogenetic tests for some key applications: dihydropyrimidine dehydrogenase (DPYD) genotyping for fluoropyrimidine (5-fluorouracil, capecitabine), UDP glucuronosylstransferase (UGT1A1) for irinotecan and thiopurine S-methyltransferase (TPMT) for thiopurine drugs. Fluorouracil 160-174 dihydropyrimidine dehydrogenase Homo sapiens 88-119 28381190-10 2017 Furthermore, CD133 promotes chemoresistance by arresting transition of the cell cycle and reducing apoptosis, which results in inhibition of tumor growth in 5-FU- or cisplatin-injected mouse tumor model. Fluorouracil 157-161 prominin 1 Mus musculus 13-18 28435470-0 2017 Downregulation of SIRT7 by 5-fluorouracil induces radiosensitivity in human colorectal cancer. Fluorouracil 27-41 sirtuin 7 Homo sapiens 18-23 28435470-2 2017 Here, we report that NAD+-dependent deacetylase sirtuin-7 (SIRT7) protein levels were decreased due to 5-FU exposure rendering colorectal cancer cells sensitive to radiation. Fluorouracil 103-107 sirtuin 7 Homo sapiens 21-57 28435470-2 2017 Here, we report that NAD+-dependent deacetylase sirtuin-7 (SIRT7) protein levels were decreased due to 5-FU exposure rendering colorectal cancer cells sensitive to radiation. Fluorouracil 103-107 sirtuin 7 Homo sapiens 59-64 28435470-6 2017 Interestingly, decreased levels of SIRT7 mediated by 5-FU correlated well with improved therapeutic effect in patients with rectal cancer and with inhibited tumor growth in immune-compromised mice post-irradiation. Fluorouracil 53-57 sirtuin 7 Homo sapiens 35-40 28435470-7 2017 Taken together, these data suggest that 5-FU induces radiosensitivity via SIRT7 degradation to favor a cell death pathway in targeted cancer cells. Fluorouracil 40-44 sirtuin 7 Homo sapiens 74-79 28024938-1 2017 Dihydropyrimidine dehydrogenase (DPD) is the initial and rate-limiting enzyme in the catabolism of 5-fluorouracil (5FU). Fluorouracil 99-113 dihydropyrimidine dehydrogenase Homo sapiens 0-31 28024938-1 2017 Dihydropyrimidine dehydrogenase (DPD) is the initial and rate-limiting enzyme in the catabolism of 5-fluorouracil (5FU). Fluorouracil 99-113 dihydropyrimidine dehydrogenase Homo sapiens 33-36 28024938-1 2017 Dihydropyrimidine dehydrogenase (DPD) is the initial and rate-limiting enzyme in the catabolism of 5-fluorouracil (5FU). Fluorouracil 115-118 dihydropyrimidine dehydrogenase Homo sapiens 0-31 28024938-1 2017 Dihydropyrimidine dehydrogenase (DPD) is the initial and rate-limiting enzyme in the catabolism of 5-fluorouracil (5FU). Fluorouracil 115-118 dihydropyrimidine dehydrogenase Homo sapiens 33-36 27727460-0 2017 Novel Deleterious Dihydropyrimidine Dehydrogenase Variants May Contribute to 5-Fluorouracil Sensitivity in an East African Population. Fluorouracil 77-91 dihydropyrimidine dehydrogenase Homo sapiens 18-49 27727460-1 2017 Clinical studies have identified specific genetic variants in dihydropyrimidine dehydrogenase (DPD; DPYD gene) as predictors of severe adverse toxicity to the commonly used chemotherapeutic 5-fluorouracil (5-FU); however, these studies have focused on European and European-American populations. Fluorouracil 190-204 dihydropyrimidine dehydrogenase Homo sapiens 62-93 27727460-1 2017 Clinical studies have identified specific genetic variants in dihydropyrimidine dehydrogenase (DPD; DPYD gene) as predictors of severe adverse toxicity to the commonly used chemotherapeutic 5-fluorouracil (5-FU); however, these studies have focused on European and European-American populations. Fluorouracil 190-204 dihydropyrimidine dehydrogenase Homo sapiens 95-98 27727460-1 2017 Clinical studies have identified specific genetic variants in dihydropyrimidine dehydrogenase (DPD; DPYD gene) as predictors of severe adverse toxicity to the commonly used chemotherapeutic 5-fluorouracil (5-FU); however, these studies have focused on European and European-American populations. Fluorouracil 190-204 dihydropyrimidine dehydrogenase Homo sapiens 100-104 27727460-1 2017 Clinical studies have identified specific genetic variants in dihydropyrimidine dehydrogenase (DPD; DPYD gene) as predictors of severe adverse toxicity to the commonly used chemotherapeutic 5-fluorouracil (5-FU); however, these studies have focused on European and European-American populations. Fluorouracil 206-210 dihydropyrimidine dehydrogenase Homo sapiens 62-93 27727460-1 2017 Clinical studies have identified specific genetic variants in dihydropyrimidine dehydrogenase (DPD; DPYD gene) as predictors of severe adverse toxicity to the commonly used chemotherapeutic 5-fluorouracil (5-FU); however, these studies have focused on European and European-American populations. Fluorouracil 206-210 dihydropyrimidine dehydrogenase Homo sapiens 95-98 27727460-1 2017 Clinical studies have identified specific genetic variants in dihydropyrimidine dehydrogenase (DPD; DPYD gene) as predictors of severe adverse toxicity to the commonly used chemotherapeutic 5-fluorouracil (5-FU); however, these studies have focused on European and European-American populations. Fluorouracil 206-210 dihydropyrimidine dehydrogenase Homo sapiens 100-104 28351306-7 2017 The results showed that MTA3 promoted cancer cell proliferation, invasion, migration, and cell cycle progression, and inhibited 5-fluorouracil-induced apoptosis in LoVo cell line. Fluorouracil 128-142 metastasis associated 1 family member 3 Homo sapiens 24-28 28176874-0 2017 CXCL12/CXCR4 axis induced miR-125b promotes invasion and confers 5-fluorouracil resistance through enhancing autophagy in colorectal cancer. Fluorouracil 65-79 C-X-C motif chemokine receptor 4 Homo sapiens 7-12 28176874-9 2017 MiR-125b functions as an important downstream mediator upon the activation of CXCL12/CXCR4 axis that involved in EMT, invasion and 5-FU resistance of CRC. Fluorouracil 131-135 C-X-C motif chemokine receptor 4 Homo sapiens 85-90 27993681-10 2017 In contrast, the cell motile activity enhanced by 5-FU treatment was suppressed by LPA1 knockdown. Fluorouracil 50-54 lysophosphatidic acid receptor 1 Homo sapiens 83-87 27993681-11 2017 These results suggest that LPA signaling via LPA4 and LPA6 negatively regulates the cell motile activities of DLD1 and HCT116 cells as well as long-term 5-FU treated cells. Fluorouracil 153-157 lysophosphatidic acid receptor 6 Homo sapiens 54-58 24961587-1 2014 F10 is an oligonucleotide based on the thymidylate synthase (TS) inhibitory 5-fluorouracil (5-FU) metabolite, 5-fluoro-2"-deoxyuridine-5"-O-monophosphate. Fluorouracil 92-96 thymidylate synthase Mus musculus 39-59 25320405-2 2014 Multidrug-resistance protein 8 (ABCC11/MRP8) is also involved in 5-fluorouracil (5-FU) metabolism. Fluorouracil 65-79 ATP binding cassette subfamily C member 11 Homo sapiens 32-38 27682136-7 2017 The 5-FU group showed an increase in IP and MPO activity (CTL vs. 5-FU: P < 0.05). Fluorouracil 4-8 myeloperoxidase Mus musculus 44-47 27682136-8 2017 Additionally, increased levels of IP and MPO were observed in CLA 5-FU group compared to those in the test groups (P < 0.05). Fluorouracil 66-70 myeloperoxidase Mus musculus 34-44 25320405-2 2014 Multidrug-resistance protein 8 (ABCC11/MRP8) is also involved in 5-fluorouracil (5-FU) metabolism. Fluorouracil 65-79 ATP binding cassette subfamily C member 11 Homo sapiens 39-43 25320405-2 2014 Multidrug-resistance protein 8 (ABCC11/MRP8) is also involved in 5-fluorouracil (5-FU) metabolism. Fluorouracil 81-85 ATP binding cassette subfamily C member 11 Homo sapiens 32-38 25320405-2 2014 Multidrug-resistance protein 8 (ABCC11/MRP8) is also involved in 5-fluorouracil (5-FU) metabolism. Fluorouracil 81-85 ATP binding cassette subfamily C member 11 Homo sapiens 39-43 25320405-10 2014 Thus, low expression of ABCC11/MRP8 is consistent with chemotherapeutic regimens using 5-FU and its derivatives in gastrointestinal tract cancers. Fluorouracil 87-91 ATP binding cassette subfamily C member 11 Homo sapiens 24-30 25320405-10 2014 Thus, low expression of ABCC11/MRP8 is consistent with chemotherapeutic regimens using 5-FU and its derivatives in gastrointestinal tract cancers. Fluorouracil 87-91 ATP binding cassette subfamily C member 11 Homo sapiens 31-35 24618665-0 2014 dCK expression correlates with 5-fluorouracil efficacy and HuR cytoplasmic expression in pancreatic cancer: a dual-institutional follow-up with the RTOG 9704 trial. Fluorouracil 31-45 Calcium/calmodulin-dependent protein kinase II Drosophila melanogaster 0-3 24728989-5 2014 Notably, we discovered that RACK1, a protein mediating cell survival and apoptosis, is a component of 5-fluorouracil-induced stress granules. Fluorouracil 102-116 receptor for activated C kinase 1 Homo sapiens 28-33 27840982-0 2017 Annexin A1 is involved in resistance to 5-FU in colon cancer cells. Fluorouracil 40-44 annexin A1 Homo sapiens 0-10 27840982-7 2017 Overexpression of ANXA1 induced a significant increase of cell viability to 5-FU, whereas ANXA1 knockdown induced a significant decrease of cell viability to 5-FU. Fluorouracil 76-80 annexin A1 Homo sapiens 18-23 27840982-7 2017 Overexpression of ANXA1 induced a significant increase of cell viability to 5-FU, whereas ANXA1 knockdown induced a significant decrease of cell viability to 5-FU. Fluorouracil 158-162 annexin A1 Homo sapiens 90-95 27840982-9 2017 These results suggest that ANXA1 expression may play a critical role in 5-FU resistance and may be induced by hypoxia during cancer progression. Fluorouracil 72-76 annexin A1 Homo sapiens 27-32 27840982-10 2017 Our results provide a possible strategy to overcome 5-FU resistance by modulating ANXA1 expression. Fluorouracil 52-56 annexin A1 Homo sapiens 82-87 27840990-7 2017 Then, we designed siRNA against IGF-1R and found that si-IGF-1R resembled the effect of miR-302a on 5-FU treatment. Fluorouracil 100-104 insulin like growth factor 1 receptor Homo sapiens 32-38 27840990-7 2017 Then, we designed siRNA against IGF-1R and found that si-IGF-1R resembled the effect of miR-302a on 5-FU treatment. Fluorouracil 100-104 insulin like growth factor 1 receptor Homo sapiens 57-63 28149883-5 2016 The reviewed paper by Sebio and colleagues report a study that links polymorphisms in the DNA repair gene XRCC1 with response to neoadjuvant 5-Fluorouracil treatment in rectal cancer patients. Fluorouracil 141-155 X-ray repair cross complementing 1 Homo sapiens 106-111 28101205-8 2016 Cytoplasmic KRAS levels decreased whereas nuclear MutS protein homolog 2 (MSH2) levels increased slightly in CRC HCT116 cells that were microsatellite instable, following treatment with 76.9 microM 5-FU for 2 days. Fluorouracil 198-202 KRAS proto-oncogene, GTPase Homo sapiens 12-16 27942212-11 2016 Furthermore, tumor growth in CT26 tumor-bearing mice given the oral OXA/DCK- and 5-FU-loaded nanoemulsion was maximally inhibited by 73.9%, 48.5%, and 38.1%, compared with tumor volumes in the control group and the oral OXA and 5-FU groups, respectively. Fluorouracil 228-232 deoxycytidine kinase Mus musculus 72-75 27589829-3 2016 Activity of the main 5-fluorouracil (5-FU) metabolic enzyme, dihydropyrimidine dehydrogenase (DPD), is the key determinant of 5-FU pharmacology, and accounts for around 80% of 5-FU catabolism. Fluorouracil 21-35 dihydropyrimidine dehydrogenase Homo sapiens 61-92 27589829-3 2016 Activity of the main 5-fluorouracil (5-FU) metabolic enzyme, dihydropyrimidine dehydrogenase (DPD), is the key determinant of 5-FU pharmacology, and accounts for around 80% of 5-FU catabolism. Fluorouracil 21-35 dihydropyrimidine dehydrogenase Homo sapiens 94-97 27589829-3 2016 Activity of the main 5-fluorouracil (5-FU) metabolic enzyme, dihydropyrimidine dehydrogenase (DPD), is the key determinant of 5-FU pharmacology, and accounts for around 80% of 5-FU catabolism. Fluorouracil 37-41 dihydropyrimidine dehydrogenase Homo sapiens 61-92 27589829-3 2016 Activity of the main 5-fluorouracil (5-FU) metabolic enzyme, dihydropyrimidine dehydrogenase (DPD), is the key determinant of 5-FU pharmacology, and accounts for around 80% of 5-FU catabolism. Fluorouracil 37-41 dihydropyrimidine dehydrogenase Homo sapiens 94-97 27589829-3 2016 Activity of the main 5-fluorouracil (5-FU) metabolic enzyme, dihydropyrimidine dehydrogenase (DPD), is the key determinant of 5-FU pharmacology, and accounts for around 80% of 5-FU catabolism. Fluorouracil 126-130 dihydropyrimidine dehydrogenase Homo sapiens 61-92 27589829-3 2016 Activity of the main 5-fluorouracil (5-FU) metabolic enzyme, dihydropyrimidine dehydrogenase (DPD), is the key determinant of 5-FU pharmacology, and accounts for around 80% of 5-FU catabolism. Fluorouracil 126-130 dihydropyrimidine dehydrogenase Homo sapiens 94-97 27589829-3 2016 Activity of the main 5-fluorouracil (5-FU) metabolic enzyme, dihydropyrimidine dehydrogenase (DPD), is the key determinant of 5-FU pharmacology, and accounts for around 80% of 5-FU catabolism. Fluorouracil 126-130 dihydropyrimidine dehydrogenase Homo sapiens 61-92 27589829-3 2016 Activity of the main 5-fluorouracil (5-FU) metabolic enzyme, dihydropyrimidine dehydrogenase (DPD), is the key determinant of 5-FU pharmacology, and accounts for around 80% of 5-FU catabolism. Fluorouracil 126-130 dihydropyrimidine dehydrogenase Homo sapiens 94-97 27589829-4 2016 There is a consistent relationship between DPD activity and 5-FU exposure on the one hand, and risk of severe and potentially lethal fluoropyrimidine-associated toxicity on the other hand. Fluorouracil 60-64 dihydropyrimidine dehydrogenase Homo sapiens 43-46 27566562-5 2016 (4) After overexpressing each candidate in ESCC cells, miR-23a induced significant chemoresistance to both 5-fluorouracil and cisplatin, and miR-223 to cisplatin in vitro. Fluorouracil 107-121 microRNA 23a Homo sapiens 55-62 27752409-0 2016 The First Case of Severe Takotsubo Cardiomyopathy Associated with 5-Fluorouracil in a Patient with Abnormalities of Both Dihydropyrimidine Dehydrogenase (DPYD) and Thymidylate Synthase (TYMS) Genes. Fluorouracil 66-80 dihydropyrimidine dehydrogenase Homo sapiens 154-158 24800948-7 2014 CONCLUSIONS: Present data suggesting that both TS and DPD are overexpressed in dMMR tumours as compared with pMMR tumours provide a strong rationale that may explain the resistance of dMMR tumours to 5FU-based therapy. Fluorouracil 200-203 dihydropyrimidine dehydrogenase Homo sapiens 54-57 24452635-7 2014 Western blot analysis showed downregulated E-cadherin, and upregulated N-cadherin and Twist in the 5-FU-resistant OSCC cell lines. Fluorouracil 99-103 cadherin 2 Homo sapiens 71-81 24602180-8 2014 RESULTS: We identified mitochondrial phosphoenolpyruvate carboxykinase (mPEPCK) as a candidate predictor of 5-FU resistance. Fluorouracil 108-112 phosphoenolpyruvate carboxykinase 1, cytosolic Mus musculus 72-78 24602180-11 2014 Suppression of mPEPCK led to a decrease in both the cellular level of phosphoenolpyruvate and the susceptibility to 5-FU and radiation. Fluorouracil 116-120 phosphoenolpyruvate carboxykinase 1, cytosolic Mus musculus 15-21 24602180-14 2014 Downregulation of total PEPCK was observed in tissues from patients with rectal cancer who displayed poor responses to preoperative 5-FU-based radiation therapy. Fluorouracil 132-136 phosphoenolpyruvate carboxykinase 2, mitochondrial Homo sapiens 24-29 24362470-4 2014 Here, we found that colorectal cancer (CRC) cells treated with oxaliplatin (OXA) and/or 5-fluorouracil (5-Fu) released high levels of high-mobility group box 1 (HMGB1) and heat shock protein 70 (HSP70). Fluorouracil 104-108 heat shock protein family A (Hsp70) member 4 Homo sapiens 172-193 24362470-4 2014 Here, we found that colorectal cancer (CRC) cells treated with oxaliplatin (OXA) and/or 5-fluorouracil (5-Fu) released high levels of high-mobility group box 1 (HMGB1) and heat shock protein 70 (HSP70). Fluorouracil 104-108 heat shock protein family A (Hsp70) member 4 Homo sapiens 195-200 24362470-5 2014 After OXA/5-Fu therapy, the sera of CRC patients also exhibited increased levels of HMGB1 and HSP70, both of which are well-known DAMPs. Fluorouracil 10-14 heat shock protein family A (Hsp70) member 4 Homo sapiens 94-99 24405586-0 2014 High expression of dihydropyrimidine dehydrogenase in lung adenocarcinoma is associated with mutations in epidermal growth factor receptor: implications for the treatment of non--small-cell lung cancer using 5-fluorouracil. Fluorouracil 208-222 dihydropyrimidine dehydrogenase Homo sapiens 19-50 24495286-2 2014 We tested whether SGLT-1 engagement might protect the intestinal mucosa from doxorubicin (DXR)- and 5-fluorouracil (5-FU)-induced injury in animal models mimicking acute or chronic mucositis. Fluorouracil 100-114 solute carrier family 5 (sodium/glucose cotransporter), member 1 Mus musculus 18-24 24495286-2 2014 We tested whether SGLT-1 engagement might protect the intestinal mucosa from doxorubicin (DXR)- and 5-fluorouracil (5-FU)-induced injury in animal models mimicking acute or chronic mucositis. Fluorouracil 116-120 solute carrier family 5 (sodium/glucose cotransporter), member 1 Mus musculus 18-24 24037119-0 2014 A case of 5-FU-related severe toxicity associated with the p.Y186C DPYD variant. Fluorouracil 10-14 dihydropyrimidine dehydrogenase Homo sapiens 67-71 27349874-2 2016 In this study, the effect of PSPH on 5-fluorouracil (5-FU) efficacy was evaluated. Fluorouracil 37-51 phosphoserine phosphatase Homo sapiens 29-33 27349874-2 2016 In this study, the effect of PSPH on 5-fluorouracil (5-FU) efficacy was evaluated. Fluorouracil 53-57 phosphoserine phosphatase Homo sapiens 29-33 27349874-3 2016 CRC cells exposed to 5-FU acquire metabolic remodeling, resulting in increased glucose flux for PSPH-mediated serine synthesis. Fluorouracil 21-25 phosphoserine phosphatase Homo sapiens 96-100 27349874-5 2016 Consequently, repression of PSPH by the use of shRNAs for PSPH impaired the defense against drug-induced oxidative stress, thereby sensitizing cells to 5-FU. Fluorouracil 152-156 phosphoserine phosphatase Homo sapiens 28-32 27349874-5 2016 Consequently, repression of PSPH by the use of shRNAs for PSPH impaired the defense against drug-induced oxidative stress, thereby sensitizing cells to 5-FU. Fluorouracil 152-156 phosphoserine phosphatase Homo sapiens 58-62 27349874-6 2016 The importance of the PSPH in supporting tumor growth during 5-FU treatment was also demonstrated in an in vivo tumor model of CRC. Fluorouracil 61-65 phosphoserine phosphatase Homo sapiens 22-26 27602102-1 2016 The current study aimed to determine the association between protein kinase Calpha (PKCalpha) and Kirsten rat sarcoma viral oncogene homolog (KRAS) expression and the response to folinic acid, 5-fluorouracil and oxaliplatin (FOLFOX regimen) in patients with colorectal cancer (CRC). Fluorouracil 193-207 protein kinase C, alpha Rattus norvegicus 61-82 27602102-1 2016 The current study aimed to determine the association between protein kinase Calpha (PKCalpha) and Kirsten rat sarcoma viral oncogene homolog (KRAS) expression and the response to folinic acid, 5-fluorouracil and oxaliplatin (FOLFOX regimen) in patients with colorectal cancer (CRC). Fluorouracil 193-207 protein kinase C, alpha Rattus norvegicus 84-92 27602102-1 2016 The current study aimed to determine the association between protein kinase Calpha (PKCalpha) and Kirsten rat sarcoma viral oncogene homolog (KRAS) expression and the response to folinic acid, 5-fluorouracil and oxaliplatin (FOLFOX regimen) in patients with colorectal cancer (CRC). Fluorouracil 193-207 KRAS proto-oncogene, GTPase Rattus norvegicus 142-146 27602108-7 2016 In addition, MTS assays demonstrated that SYK(L) and SYK(S) increased the cellular sensitivity to 5-fluorouracil (5-FU), suggesting that SYK(L) and 5-FU produce a significant synergistic effect on CRC cell proliferation, while SYK(S) has an effect on modulating CRC 5-FU sensitivity. Fluorouracil 98-112 spleen associated tyrosine kinase Homo sapiens 42-45 27602108-7 2016 In addition, MTS assays demonstrated that SYK(L) and SYK(S) increased the cellular sensitivity to 5-fluorouracil (5-FU), suggesting that SYK(L) and 5-FU produce a significant synergistic effect on CRC cell proliferation, while SYK(S) has an effect on modulating CRC 5-FU sensitivity. Fluorouracil 98-112 spleen associated tyrosine kinase Homo sapiens 53-59 27602108-7 2016 In addition, MTS assays demonstrated that SYK(L) and SYK(S) increased the cellular sensitivity to 5-fluorouracil (5-FU), suggesting that SYK(L) and 5-FU produce a significant synergistic effect on CRC cell proliferation, while SYK(S) has an effect on modulating CRC 5-FU sensitivity. Fluorouracil 98-112 spleen associated tyrosine kinase Homo sapiens 53-56 27602108-7 2016 In addition, MTS assays demonstrated that SYK(L) and SYK(S) increased the cellular sensitivity to 5-fluorouracil (5-FU), suggesting that SYK(L) and 5-FU produce a significant synergistic effect on CRC cell proliferation, while SYK(S) has an effect on modulating CRC 5-FU sensitivity. Fluorouracil 98-112 spleen associated tyrosine kinase Homo sapiens 227-233 27602108-7 2016 In addition, MTS assays demonstrated that SYK(L) and SYK(S) increased the cellular sensitivity to 5-fluorouracil (5-FU), suggesting that SYK(L) and 5-FU produce a significant synergistic effect on CRC cell proliferation, while SYK(S) has an effect on modulating CRC 5-FU sensitivity. Fluorouracil 114-118 spleen associated tyrosine kinase Homo sapiens 42-45 27602108-7 2016 In addition, MTS assays demonstrated that SYK(L) and SYK(S) increased the cellular sensitivity to 5-fluorouracil (5-FU), suggesting that SYK(L) and 5-FU produce a significant synergistic effect on CRC cell proliferation, while SYK(S) has an effect on modulating CRC 5-FU sensitivity. Fluorouracil 114-118 spleen associated tyrosine kinase Homo sapiens 53-59 27602108-7 2016 In addition, MTS assays demonstrated that SYK(L) and SYK(S) increased the cellular sensitivity to 5-fluorouracil (5-FU), suggesting that SYK(L) and 5-FU produce a significant synergistic effect on CRC cell proliferation, while SYK(S) has an effect on modulating CRC 5-FU sensitivity. Fluorouracil 114-118 spleen associated tyrosine kinase Homo sapiens 53-56 27602108-7 2016 In addition, MTS assays demonstrated that SYK(L) and SYK(S) increased the cellular sensitivity to 5-fluorouracil (5-FU), suggesting that SYK(L) and 5-FU produce a significant synergistic effect on CRC cell proliferation, while SYK(S) has an effect on modulating CRC 5-FU sensitivity. Fluorouracil 114-118 spleen associated tyrosine kinase Homo sapiens 227-233 27602108-7 2016 In addition, MTS assays demonstrated that SYK(L) and SYK(S) increased the cellular sensitivity to 5-fluorouracil (5-FU), suggesting that SYK(L) and 5-FU produce a significant synergistic effect on CRC cell proliferation, while SYK(S) has an effect on modulating CRC 5-FU sensitivity. Fluorouracil 148-152 spleen associated tyrosine kinase Homo sapiens 42-45 27602108-7 2016 In addition, MTS assays demonstrated that SYK(L) and SYK(S) increased the cellular sensitivity to 5-fluorouracil (5-FU), suggesting that SYK(L) and 5-FU produce a significant synergistic effect on CRC cell proliferation, while SYK(S) has an effect on modulating CRC 5-FU sensitivity. Fluorouracil 148-152 spleen associated tyrosine kinase Homo sapiens 53-59 27602108-7 2016 In addition, MTS assays demonstrated that SYK(L) and SYK(S) increased the cellular sensitivity to 5-fluorouracil (5-FU), suggesting that SYK(L) and 5-FU produce a significant synergistic effect on CRC cell proliferation, while SYK(S) has an effect on modulating CRC 5-FU sensitivity. Fluorouracil 148-152 spleen associated tyrosine kinase Homo sapiens 53-56 27602108-7 2016 In addition, MTS assays demonstrated that SYK(L) and SYK(S) increased the cellular sensitivity to 5-fluorouracil (5-FU), suggesting that SYK(L) and 5-FU produce a significant synergistic effect on CRC cell proliferation, while SYK(S) has an effect on modulating CRC 5-FU sensitivity. Fluorouracil 148-152 spleen associated tyrosine kinase Homo sapiens 227-233 27602108-7 2016 In addition, MTS assays demonstrated that SYK(L) and SYK(S) increased the cellular sensitivity to 5-fluorouracil (5-FU), suggesting that SYK(L) and 5-FU produce a significant synergistic effect on CRC cell proliferation, while SYK(S) has an effect on modulating CRC 5-FU sensitivity. Fluorouracil 148-152 spleen associated tyrosine kinase Homo sapiens 42-45 27385218-0 2016 SEP enhanced the antitumor activity of 5-fluorouracil by up-regulating NKG2D/MICA and reversed immune suppression via inhibiting ROS and caspase-3 in mice. Fluorouracil 39-53 epoxide hydrolase 2, cytoplasmic Mus musculus 0-3 27385218-0 2016 SEP enhanced the antitumor activity of 5-fluorouracil by up-regulating NKG2D/MICA and reversed immune suppression via inhibiting ROS and caspase-3 in mice. Fluorouracil 39-53 caspase 3 Mus musculus 137-146 27385218-8 2016 Moreover, in H22- or Lewis lung cancer (LLC)-bearing mouse models, SEP reversed 5-FU-induced atrophy and apoptosis in both the spleen and bone marrow in vivo by suppressing ROS generation and caspase-3 activation. Fluorouracil 80-84 epoxide hydrolase 2, cytoplasmic Mus musculus 67-70 27385218-8 2016 Moreover, in H22- or Lewis lung cancer (LLC)-bearing mouse models, SEP reversed 5-FU-induced atrophy and apoptosis in both the spleen and bone marrow in vivo by suppressing ROS generation and caspase-3 activation. Fluorouracil 80-84 caspase 3 Mus musculus 192-201 27273130-3 2016 S100A4 expression was analyzed by immunohistochemistry in primary colorectal carcinomas from a consecutively collected, population-representative cohort and a randomized phase III study on adjuvant 5-fluorouracil/levamisole. Fluorouracil 198-213 S100 calcium binding protein A4 Homo sapiens 0-6 27273130-4 2016 Sensitivity to treatment with 5-fluorouracil in S100A4 knockdown cells was investigated using 2D and 3D cell culture assays. Fluorouracil 30-44 S100 calcium binding protein A4 Homo sapiens 48-54 27278667-5 2016 PATIENTS AND METHODS: We identified two patients with advanced pancreatic cancer who were referred to us for testing of DPYD status following severe toxicity associated with 5-FU administered at a dose of 1400 mg/m(2) weekly bolus high-dose 5-FU followed by oral uridine triacetate as a part of a clinical trail. Fluorouracil 174-178 dihydropyrimidine dehydrogenase Homo sapiens 120-124 27278667-5 2016 PATIENTS AND METHODS: We identified two patients with advanced pancreatic cancer who were referred to us for testing of DPYD status following severe toxicity associated with 5-FU administered at a dose of 1400 mg/m(2) weekly bolus high-dose 5-FU followed by oral uridine triacetate as a part of a clinical trail. Fluorouracil 241-245 dihydropyrimidine dehydrogenase Homo sapiens 120-124 26511802-1 2016 PURPOSE: We evaluated the usefulness of the in vitro adenosine triphosphate-based chemotherapy response assay (ATP-CRA) for prediction of clinical response to fluorouracil-based adjuvant chemotherapy in stage II colorectal cancer. Fluorouracil 159-171 myotubularin related protein 11 Homo sapiens 115-118 26511802-7 2016 CONCLUSION: In stage II colorectal cancer, the in vitro ATP-CRA may be useful in identifying patients likely to benefit from fluorouracil-based adjuvant chemotherapy. Fluorouracil 125-137 myotubularin related protein 11 Homo sapiens 60-63 27431628-2 2016 By taking advantage of the metabolism of 5-FU, researchers have made efforts to develop prodrugs, combination drug products, and combination therapy regimens via biochemical modulation(BCM)with alteration of the drug metabolism. Fluorouracil 41-45 TNF receptor superfamily member 17 Homo sapiens 185-188 24107927-0 2014 Response to "A case of 5-FU-related severe toxicity associated with the P.Y186C DPYD variant". Fluorouracil 23-27 dihydropyrimidine dehydrogenase Homo sapiens 80-84 27121324-5 2016 In our results, ANRIL was highly expressed in gastric cancer tissues of cisplatin-resistant and 5-fluorouracil (5-FU)-resistant patients, and the same upregulation trends were observed in cisplatin-resistant cells (BGC823/DDP) and 5-FU-resistant cells (BGC823/5-FU). Fluorouracil 96-110 CDKN2B antisense RNA 1 Homo sapiens 16-21 27121324-5 2016 In our results, ANRIL was highly expressed in gastric cancer tissues of cisplatin-resistant and 5-fluorouracil (5-FU)-resistant patients, and the same upregulation trends were observed in cisplatin-resistant cells (BGC823/DDP) and 5-FU-resistant cells (BGC823/5-FU). Fluorouracil 112-116 CDKN2B antisense RNA 1 Homo sapiens 16-21 23852449-6 2014 In Caco-2 and SW620 cells, compared to controls, PROM1 (CD133)(+) CD44(+) cells were significantly decreased by indomethacin treatment, and increased by 5-fluorouracil (5-FU) treatment. Fluorouracil 153-167 CD44 molecule (Indian blood group) Homo sapiens 66-70 27121324-5 2016 In our results, ANRIL was highly expressed in gastric cancer tissues of cisplatin-resistant and 5-fluorouracil (5-FU)-resistant patients, and the same upregulation trends were observed in cisplatin-resistant cells (BGC823/DDP) and 5-FU-resistant cells (BGC823/5-FU). Fluorouracil 231-235 CDKN2B antisense RNA 1 Homo sapiens 16-21 27121324-6 2016 In addition, BGC823/DDP and BGC823/5-FU cells transfected with ANRIL siRNA and treated with cisplatin or 5-FU, respectively, exhibited significant lower survival rate, decreased invasion capability, and high percentage of apoptotic tumor cells. Fluorouracil 35-39 CDKN2B antisense RNA 1 Homo sapiens 63-68 27121324-7 2016 The influence of ANRIL knockdown on MDR was assessed by measuring IC50 of BGC823/DDP and BGC823/5-FU cells to cisplatin and 5-FU, the result showed that silencing ANRIL decreased the IC50 values in gastric cancer cells. Fluorouracil 96-100 CDKN2B antisense RNA 1 Homo sapiens 17-22 23852449-6 2014 In Caco-2 and SW620 cells, compared to controls, PROM1 (CD133)(+) CD44(+) cells were significantly decreased by indomethacin treatment, and increased by 5-fluorouracil (5-FU) treatment. Fluorouracil 169-173 CD44 molecule (Indian blood group) Homo sapiens 66-70 23852449-7 2014 This 5-FU-induced increase of PROM1 (CD133)(+) CD44(+) cells was significantly attenuated by combination with indomethacin. Fluorouracil 5-9 CD44 molecule (Indian blood group) Homo sapiens 47-51 23852449-11 2014 In addition, treatment of indomethacin alone or combination of 5-FU and indomethacin decreased the expressions of PROM1 (CD133), CD44, PTGS2 (cyclooxygenase 2) and HES1, and increased PPARG expression. Fluorouracil 63-67 CD44 molecule (Indian blood group) Homo sapiens 129-133 27221209-8 2016 Functional assays revealed that restoration of miR-874 inhibited proliferation, reduced colony formation, enhanced apoptosis, as well as decreased the 5-fluorouracil (5-FU) resistance of the CRC cells. Fluorouracil 151-165 microRNA 874 Homo sapiens 47-54 27221209-8 2016 Functional assays revealed that restoration of miR-874 inhibited proliferation, reduced colony formation, enhanced apoptosis, as well as decreased the 5-fluorouracil (5-FU) resistance of the CRC cells. Fluorouracil 167-171 microRNA 874 Homo sapiens 47-54 24337061-0 2014 TWEAK/Fn14 signaling mediates gastric cancer cell resistance to 5-fluorouracil via NF-kappaB activation. Fluorouracil 64-78 TNF superfamily member 12 Homo sapiens 0-5 27144434-4 2016 In colon cancer cells, 5-FU exposure impaired endogenous KRAS/MEK5/ERK5 expression and/or activation. Fluorouracil 23-27 KRAS proto-oncogene, GTPase Homo sapiens 57-61 24337061-4 2014 In contrast, Fn14 overexpression or TWEAK treatment promoted resistance to 5-FU. Fluorouracil 75-79 TNF superfamily member 12 Homo sapiens 36-41 24100087-1 2014 BACKGROUND: 5-Fluorouracil (5-FU) is a cornerstone of chemotherapy for colorectal cancer (CRC), and the major targets of 5-FU are thymidylate synthase (TS), methylenetetrahydrofolate reductase (MTHFR), and reduced folate carrier 1 (RFC1). Fluorouracil 12-26 methylenetetrahydrofolate reductase Homo sapiens 157-192 24100087-1 2014 BACKGROUND: 5-Fluorouracil (5-FU) is a cornerstone of chemotherapy for colorectal cancer (CRC), and the major targets of 5-FU are thymidylate synthase (TS), methylenetetrahydrofolate reductase (MTHFR), and reduced folate carrier 1 (RFC1). Fluorouracil 12-26 methylenetetrahydrofolate reductase Homo sapiens 194-199 24100087-1 2014 BACKGROUND: 5-Fluorouracil (5-FU) is a cornerstone of chemotherapy for colorectal cancer (CRC), and the major targets of 5-FU are thymidylate synthase (TS), methylenetetrahydrofolate reductase (MTHFR), and reduced folate carrier 1 (RFC1). Fluorouracil 28-32 methylenetetrahydrofolate reductase Homo sapiens 157-192 24100087-1 2014 BACKGROUND: 5-Fluorouracil (5-FU) is a cornerstone of chemotherapy for colorectal cancer (CRC), and the major targets of 5-FU are thymidylate synthase (TS), methylenetetrahydrofolate reductase (MTHFR), and reduced folate carrier 1 (RFC1). Fluorouracil 28-32 methylenetetrahydrofolate reductase Homo sapiens 194-199 26872725-5 2016 LSD1 depletion via siRNA-mediated knockdown in OSCC cells resulted in impaired cell proliferation, migration/invasion, tumorsphere formation and reduced xenograft growth while inducing cell apoptosis and enhancing chemosensitivity to 5-FU. Fluorouracil 234-238 lysine demethylase 1A Homo sapiens 0-4 26967565-2 2016 The efforts to establish pretreatment tools for toxicity prediction, led to the development of various pharmacogenetic and biochemical assays, mainly targeted to assess the activity level of dihydropyrimidine dehydrogenase (DPD), the main metabolizing enzyme for 5-fluorouracil. Fluorouracil 263-277 dihydropyrimidine dehydrogenase Homo sapiens 191-222 24100087-1 2014 BACKGROUND: 5-Fluorouracil (5-FU) is a cornerstone of chemotherapy for colorectal cancer (CRC), and the major targets of 5-FU are thymidylate synthase (TS), methylenetetrahydrofolate reductase (MTHFR), and reduced folate carrier 1 (RFC1). Fluorouracil 121-125 methylenetetrahydrofolate reductase Homo sapiens 157-192 26967565-2 2016 The efforts to establish pretreatment tools for toxicity prediction, led to the development of various pharmacogenetic and biochemical assays, mainly targeted to assess the activity level of dihydropyrimidine dehydrogenase (DPD), the main metabolizing enzyme for 5-fluorouracil. Fluorouracil 263-277 dihydropyrimidine dehydrogenase Homo sapiens 224-227 24100087-1 2014 BACKGROUND: 5-Fluorouracil (5-FU) is a cornerstone of chemotherapy for colorectal cancer (CRC), and the major targets of 5-FU are thymidylate synthase (TS), methylenetetrahydrofolate reductase (MTHFR), and reduced folate carrier 1 (RFC1). Fluorouracil 121-125 methylenetetrahydrofolate reductase Homo sapiens 194-199 26967565-6 2016 Patient stratification depending on the individual 5-fluorouracil degradation rate allows to identify a 10% of the overall population at high risk of developing severe toxicity, compared to the 1.3% (as assessed in the Italian population) identified by the most commonly employed pharmacogenetic test, including the DPD polymorphism IVS14+1G>A. Fluorouracil 51-65 dihydropyrimidine dehydrogenase Homo sapiens 316-319 24520224-0 2014 Combination of TRAP1 and ERCC1 Expression Predicts Clinical Outcomes in Metastatic Colorectal Cancer Treated with Oxaliplatin/5-Fluorouracil. Fluorouracil 126-140 TNF receptor associated protein 1 Homo sapiens 15-20 27274438-7 2016 We examined the protein levels of 5-FU metabolism-related enzymes (TS, DPD, OPRT, and thymidine phosphorylase [TP]) in 14 cases RESULTS: High TS, DPD, OPRT, and TP expressions were seen in 28.6%, 71.4%, 85.7%, and 35.7% of patients, respectively. Fluorouracil 34-38 dihydropyrimidine dehydrogenase Homo sapiens 71-74 24520224-12 2014 CONCLUSION: The present study demonstrates that the combination of TRAP1 and ERCC1 expression predicts the survival of metastatic CRC patients who were treated with oxaliplatin/5-fluorouracil. Fluorouracil 177-191 TNF receptor associated protein 1 Homo sapiens 67-72 25316230-0 2014 Polymorphism of methylenetetrahydrofolate reductase gene is associated with response to fluorouracil-based chemotherapy in Chinese patients with gastric cancer. Fluorouracil 88-100 methylenetetrahydrofolate reductase Homo sapiens 16-51 25896536-1 2016 Multidrug resistance protein 8 (ABCC11) is an efflux transporter for anionic lipophilic compounds, conferring resistance to antiviral and anticancer agents like 5-fluorouracil (5-FU). Fluorouracil 161-175 ATP binding cassette subfamily C member 11 Homo sapiens 32-38 25896536-1 2016 Multidrug resistance protein 8 (ABCC11) is an efflux transporter for anionic lipophilic compounds, conferring resistance to antiviral and anticancer agents like 5-fluorouracil (5-FU). Fluorouracil 177-181 ATP binding cassette subfamily C member 11 Homo sapiens 32-38 25896536-4 2016 We identified c.1637C>T (T546M), previously associated with 5-FU-related toxicity, as a novel functionally damaging ABCC11 variant exhibiting markedly reduced transport function of 5-FdUMP, the active cytotoxic metabolite of 5-FU. Fluorouracil 63-67 ATP binding cassette subfamily C member 11 Homo sapiens 119-125 25896536-4 2016 We identified c.1637C>T (T546M), previously associated with 5-FU-related toxicity, as a novel functionally damaging ABCC11 variant exhibiting markedly reduced transport function of 5-FdUMP, the active cytotoxic metabolite of 5-FU. Fluorouracil 228-232 ATP binding cassette subfamily C member 11 Homo sapiens 119-125 25316230-1 2014 BACKGROUND: The importance of polymorphisms in the methylenetetrahydrofolate reductase (MTHFR) gene for the prediction of the response to fluorouracil-based adjuvant chemotherapy in gastric cancer patients remains unclear. Fluorouracil 138-150 methylenetetrahydrofolate reductase Homo sapiens 51-86 25316230-1 2014 BACKGROUND: The importance of polymorphisms in the methylenetetrahydrofolate reductase (MTHFR) gene for the prediction of the response to fluorouracil-based adjuvant chemotherapy in gastric cancer patients remains unclear. Fluorouracil 138-150 methylenetetrahydrofolate reductase Homo sapiens 88-93 25316230-2 2014 The aim of this study is to assess the predictive value of several polymorphisms of the MTHFR gene for clinical outcomes of gastric cancer patients treated with fluorouracil-based adjuvant chemotherapy in Chinese population. Fluorouracil 161-173 methylenetetrahydrofolate reductase Homo sapiens 88-93 25317816-2 2014 Dihydropyrimidine dehydrogenase (DPD) is the rate-limiting enzyme in the catabolism of 5-FU, and DPD enzymatic activities are usually varied dramatically from individual to individual, including both the intrapatient differences and the interpatient variability. Fluorouracil 87-91 dihydropyrimidine dehydrogenase Homo sapiens 0-31 26658227-0 2016 Association between DPYD c.1129-5923 C>G/hapB3 and severe toxicity to 5-fluorouracil-based chemotherapy in stage III colon cancer patients: NCCTG N0147 (Alliance). Fluorouracil 73-87 dihydropyrimidine dehydrogenase Homo sapiens 20-24 26658227-4 2016 Logistic regression was used to assess multivariable associations between DPYD variant status and AEs common to 5-FU (5FU-AEs). Fluorouracil 112-116 dihydropyrimidine dehydrogenase Homo sapiens 74-78 26840027-2 2016 In this study, using gene expression profiles for a panel of cell lines with drug sensitivity data and two cohorts of patients, we extracted a signature consisting of two gene pairs (KCNE2 and API5, KCNE2 and PRPF3) whose within-sample relative expression orderings (REOs) could robustly predict prognoses of gastric cancer patients treated with 5-FU-based chemotherapy. Fluorouracil 346-350 pre-mRNA processing factor 3 Homo sapiens 209-214 26716512-6 2016 Treatment of breast cancer cells with 5-fluorouracil (5-FU) increased the expression of pro-apoptotic and anti-proliferative factor, BAX and p21 protein through phosphorylation of p53 and p38. Fluorouracil 38-52 BCL2-associated X protein Mus musculus 133-136 26716512-6 2016 Treatment of breast cancer cells with 5-fluorouracil (5-FU) increased the expression of pro-apoptotic and anti-proliferative factor, BAX and p21 protein through phosphorylation of p53 and p38. Fluorouracil 38-52 cyclin-dependent kinase inhibitor 1A (P21) Mus musculus 141-144 26716512-6 2016 Treatment of breast cancer cells with 5-fluorouracil (5-FU) increased the expression of pro-apoptotic and anti-proliferative factor, BAX and p21 protein through phosphorylation of p53 and p38. Fluorouracil 54-58 BCL2-associated X protein Mus musculus 133-136 26716512-6 2016 Treatment of breast cancer cells with 5-fluorouracil (5-FU) increased the expression of pro-apoptotic and anti-proliferative factor, BAX and p21 protein through phosphorylation of p53 and p38. Fluorouracil 54-58 cyclin-dependent kinase inhibitor 1A (P21) Mus musculus 141-144 26801910-3 2016 The objective of this study was to develop a novel targeted enzyme-prodrug system using 5-fluorocytosine (5-FC) and an NGR-containing peptide fused with yeast cytosine deaminase (yCD), i.e. CNGRC-yCD fusion protein, to target APN-expressing cells within the tumor tissues and to convert 5-FC into 5-fluorouracil (5-FU) to kill tumors. Fluorouracil 297-311 reticulon 4 receptor Homo sapiens 119-122 26801910-3 2016 The objective of this study was to develop a novel targeted enzyme-prodrug system using 5-fluorocytosine (5-FC) and an NGR-containing peptide fused with yeast cytosine deaminase (yCD), i.e. CNGRC-yCD fusion protein, to target APN-expressing cells within the tumor tissues and to convert 5-FC into 5-fluorouracil (5-FU) to kill tumors. Fluorouracil 313-317 reticulon 4 receptor Homo sapiens 119-122 26801910-9 2016 Systematic experiments demonstrated that the CNGRC-yCD protein retained both the APN-binding affinity of NGR and the enzyme activity of yCD to convert 5-FC into 5-FU. Fluorouracil 161-165 reticulon 4 receptor Homo sapiens 46-49 26768731-10 2016 Moreover, they showed reduced apoptosis, increased proliferation and different response to 5-fluorouracil and oxaliplatin upon CRY1 and CRY2 ectopic expression. Fluorouracil 91-105 cryptochrome circadian regulator 2 Homo sapiens 136-140 26722024-3 2016 Various approaches have been used to improve the efficacy of 5-FU including inhibition of its degradation enzyme dihydropyrimidine dehydrogenase (DPD) such as S1, UTF, use of 5-FU pro-drug capecitabine to exploit thymidine phosphorylase (TP) and supplementation of reduced folate acid to increase cytotoxicity. Fluorouracil 61-65 dihydropyrimidine dehydrogenase Homo sapiens 113-144 25317816-2 2014 Dihydropyrimidine dehydrogenase (DPD) is the rate-limiting enzyme in the catabolism of 5-FU, and DPD enzymatic activities are usually varied dramatically from individual to individual, including both the intrapatient differences and the interpatient variability. Fluorouracil 87-91 dihydropyrimidine dehydrogenase Homo sapiens 33-36 26722024-3 2016 Various approaches have been used to improve the efficacy of 5-FU including inhibition of its degradation enzyme dihydropyrimidine dehydrogenase (DPD) such as S1, UTF, use of 5-FU pro-drug capecitabine to exploit thymidine phosphorylase (TP) and supplementation of reduced folate acid to increase cytotoxicity. Fluorouracil 61-65 dihydropyrimidine dehydrogenase Homo sapiens 146-149 26722024-4 2016 TAS-102 is a newly-developed anti-folate drug containing the 5-FU analogue trifluridine (TFD) and tipiracil hydrochloride (TPI). Fluorouracil 61-65 THAS Homo sapiens 0-3 25614737-0 2014 Influence of DPYD Genetic Polymorphisms on 5-Fluorouracil Toxicities in Patients with Colorectal Cancer: A Meta-Analysis. Fluorouracil 43-57 dihydropyrimidine dehydrogenase Homo sapiens 13-17 25614737-1 2014 Our meta-analysis aggregated existing results from relevant studies to comprehensively investigate the correlations between genetic polymorphisms in dihydropyrimidine dehydrogenase (DPYD) gene and 5-fluorouracil (5-FU) toxicities in patients with colorectal cancer (CRC). Fluorouracil 197-211 dihydropyrimidine dehydrogenase Homo sapiens 149-180 25614737-1 2014 Our meta-analysis aggregated existing results from relevant studies to comprehensively investigate the correlations between genetic polymorphisms in dihydropyrimidine dehydrogenase (DPYD) gene and 5-fluorouracil (5-FU) toxicities in patients with colorectal cancer (CRC). Fluorouracil 197-211 dihydropyrimidine dehydrogenase Homo sapiens 182-186 25614737-1 2014 Our meta-analysis aggregated existing results from relevant studies to comprehensively investigate the correlations between genetic polymorphisms in dihydropyrimidine dehydrogenase (DPYD) gene and 5-fluorouracil (5-FU) toxicities in patients with colorectal cancer (CRC). Fluorouracil 213-217 dihydropyrimidine dehydrogenase Homo sapiens 149-180 25614737-1 2014 Our meta-analysis aggregated existing results from relevant studies to comprehensively investigate the correlations between genetic polymorphisms in dihydropyrimidine dehydrogenase (DPYD) gene and 5-fluorouracil (5-FU) toxicities in patients with colorectal cancer (CRC). Fluorouracil 213-217 dihydropyrimidine dehydrogenase Homo sapiens 182-186 25614737-5 2014 Our findings showed that DPYD genetic polymorphisms were significantly correlated with high incidences of 5-FU-related toxicity in CRC patients. Fluorouracil 106-110 dihydropyrimidine dehydrogenase Homo sapiens 25-29 25614737-9 2014 The present meta-analysis suggests that DPYD genetic polymorphisms may be correlated with the incidence of 5-FU-related toxicity in CRC patients. Fluorouracil 107-111 dihydropyrimidine dehydrogenase Homo sapiens 40-44 25030435-8 2014 Besides, we also found that suppression of BDNF in Raji cells increased their sensitivity to chemotherapeutic drug, 5-Fluorouracil (5-FU). Fluorouracil 116-130 brain derived neurotrophic factor Homo sapiens 43-47 26392323-0 2016 Beating the odds: efficacy and toxicity of dihydropyrimidine dehydrogenase-driven adaptive dosing of 5-FU in patients with digestive cancer. Fluorouracil 101-105 dihydropyrimidine dehydrogenase Homo sapiens 43-74 26392323-3 2016 Dihydropyrimidine dehydrogenase (DPD) deficiency is a pharmacogenetic syndrome responsible for most cases of life-threatening toxicities upon 5-FU intake, and pre-treatment checking for DPD status should help to reduce both incidence and severity of side effects through adaptive dosing strategies. Fluorouracil 142-146 dihydropyrimidine dehydrogenase Homo sapiens 33-36 26392323-4 2016 METHODS: We have used a simple method for rapidly establishing the DPD phenotype of patients with cancer and used it prospectively in 59 routine patients treated with 5-FU-based therapy for digestive cancers. Fluorouracil 167-171 dihydropyrimidine dehydrogenase Homo sapiens 67-70 27415661-0 2016 MicroRNA-149 Increases the Sensitivity of Colorectal Cancer Cells to 5-Fluorouracil by Targeting Forkhead Box Transcription Factor FOXM1. Fluorouracil 69-83 forkhead box M1 Homo sapiens 131-136 27415661-3 2016 The aim of this study is to investigate whether miR-149 targets FOXM1 to regulate the 5-FU resistance of CRC. Fluorouracil 86-90 forkhead box M1 Homo sapiens 64-69 27415661-10 2016 The silencing of FOXM1 could mimic the effect of miR-149 upregulation on the 5-FU resistance of 5-FU-resistant CRC cells. Fluorouracil 77-81 forkhead box M1 Homo sapiens 17-22 25030435-8 2014 Besides, we also found that suppression of BDNF in Raji cells increased their sensitivity to chemotherapeutic drug, 5-Fluorouracil (5-FU). Fluorouracil 132-136 brain derived neurotrophic factor Homo sapiens 43-47 27415661-10 2016 The silencing of FOXM1 could mimic the effect of miR-149 upregulation on the 5-FU resistance of 5-FU-resistant CRC cells. Fluorouracil 96-100 forkhead box M1 Homo sapiens 17-22 27415661-11 2016 Furthermore, the expression of miR-149 in the 5-FU-responding CRC tissues was significantly higher than that in the non-responding tissues and inversely correlated with FOXM1 mRNA level. Fluorouracil 46-50 forkhead box M1 Homo sapiens 169-174 24854104-0 2014 The novel HDAC inhibitor OBP-801/YM753 enhances the effects of 5-fluorouracil with radiation on esophageal squamous carcinoma cells. Fluorouracil 63-77 histone deacetylase 9 Homo sapiens 10-14 27415661-12 2016 CONCLUSIONS: MiR-149 reverses the resistance of CRC cells to 5-FU by directly targeting FOXM1. Fluorouracil 61-65 forkhead box M1 Homo sapiens 88-93 27415661-13 2016 Thus, targeting miR-149/FOXM1 signaling will be a potential strategy in the treatment of 5-FU-chemoresistant CRC. Fluorouracil 89-93 forkhead box M1 Homo sapiens 24-29 24854104-1 2014 Histone deacetylase (HDAC) inhibitors have been shown to enhance the effects of 5-fluorouracil (5-FU) against various cancer cells; however, no report has shown that an HDAC inhibitor may enhance the effects of 5-FU with radiation. Fluorouracil 80-94 histone deacetylase 9 Homo sapiens 0-19 24854104-1 2014 Histone deacetylase (HDAC) inhibitors have been shown to enhance the effects of 5-fluorouracil (5-FU) against various cancer cells; however, no report has shown that an HDAC inhibitor may enhance the effects of 5-FU with radiation. Fluorouracil 80-94 histone deacetylase 9 Homo sapiens 21-25 26546214-3 2015 Especially, compounds 8c and 8e presented obviously selective cytotoxic activities against Huh-7 in vitro (8c, IC50=7.74+-2.18mug/mL; 8e, IC50=4.46+-1.05mug/mL) compared to 5-FU (IC50=10.41+-3.41mug/mL). Fluorouracil 173-177 MIR7-3 host gene Homo sapiens 91-96 26552750-4 2015 RESULTS: 5-Fluorouracil, oxaliplatin and SN-38 (the active metabolite of irinotecan), as well as cisplatin, methotrexate and vinblastine, each caused decreases in cell-surface CXCR4 and concomitant increases in CD26 on HT-29, T84, HRT-18, SW480 and SW620 CRC cell lines. Fluorouracil 9-23 C-X-C motif chemokine receptor 4 Homo sapiens 176-181 26552750-9 2015 Analysis of cancer-initiating cell CD44 and CD133 subsets revealed drug-dependent responses of CD26/CD44/CD133 populations, suggesting that the benefits of combining standard chemotherapies 5-fluoruracil and oxaliplatin may be derived from their complementary elimination of cell populations. Fluorouracil 190-203 CD44 molecule (Indian blood group) Homo sapiens 100-104 24854104-1 2014 Histone deacetylase (HDAC) inhibitors have been shown to enhance the effects of 5-fluorouracil (5-FU) against various cancer cells; however, no report has shown that an HDAC inhibitor may enhance the effects of 5-FU with radiation. Fluorouracil 96-100 histone deacetylase 9 Homo sapiens 0-19 26055341-2 2015 The down-regulation of miR-197 in colorectal cancer cells after exposure to 5-fluorouracil might be related to the mechanism of resistance to fluoropyrimidine-based chemotherapy. Fluorouracil 76-90 microRNA 197 Homo sapiens 23-30 24854104-1 2014 Histone deacetylase (HDAC) inhibitors have been shown to enhance the effects of 5-fluorouracil (5-FU) against various cancer cells; however, no report has shown that an HDAC inhibitor may enhance the effects of 5-FU with radiation. Fluorouracil 96-100 histone deacetylase 9 Homo sapiens 21-25 26055341-3 2015 So we investigated the regulatory mechanism of miR-197 on 5-FU sensitivity. Fluorouracil 58-62 microRNA 197 Homo sapiens 47-54 24854104-1 2014 Histone deacetylase (HDAC) inhibitors have been shown to enhance the effects of 5-fluorouracil (5-FU) against various cancer cells; however, no report has shown that an HDAC inhibitor may enhance the effects of 5-FU with radiation. Fluorouracil 211-215 histone deacetylase 9 Homo sapiens 0-19 26055341-9 2015 Overexpressing miR-197 could increase the sensitivity of colorectal cancer cells to 5-fluorouracil (5-FU). Fluorouracil 84-98 microRNA 197 Homo sapiens 15-22 26055341-9 2015 Overexpressing miR-197 could increase the sensitivity of colorectal cancer cells to 5-fluorouracil (5-FU). Fluorouracil 100-104 microRNA 197 Homo sapiens 15-22 24854104-1 2014 Histone deacetylase (HDAC) inhibitors have been shown to enhance the effects of 5-fluorouracil (5-FU) against various cancer cells; however, no report has shown that an HDAC inhibitor may enhance the effects of 5-FU with radiation. Fluorouracil 211-215 histone deacetylase 9 Homo sapiens 21-25 24854104-1 2014 Histone deacetylase (HDAC) inhibitors have been shown to enhance the effects of 5-fluorouracil (5-FU) against various cancer cells; however, no report has shown that an HDAC inhibitor may enhance the effects of 5-FU with radiation. Fluorouracil 211-215 histone deacetylase 9 Homo sapiens 169-173 26636535-5 2015 MATERIALS AND METHODS: A systematic literature search of the MEDLINE, EMBASE, and Cochrane databases was conducted to identify all clinical studies of any association between DPYD and 5-FU correlated to allelic status of 6 validated polymorphisms in five genes Dihydropyrimidine Dehydrogenase (DPYD), Thymidylate Synthase (TYMS), Glutathione S-Transferase (GSTP1), and DNA-repair genes (ERCC2 and XRCC1). Fluorouracil 184-188 dihydropyrimidine dehydrogenase Homo sapiens 175-179 26130327-0 2015 5-Fluorouracil preferentially sensitizes mutant KRAS non-small cell lung carcinoma cells to TRAIL-induced apoptosis. Fluorouracil 0-14 KRAS proto-oncogene, GTPase Homo sapiens 48-52 26130327-5 2015 In the current study, we found that NSCLC cells with a KRAS mutation were highly sensitive to treatment with TRAIL and 5-fluorouracil (5FU). Fluorouracil 119-133 KRAS proto-oncogene, GTPase Homo sapiens 55-59 26130327-5 2015 In the current study, we found that NSCLC cells with a KRAS mutation were highly sensitive to treatment with TRAIL and 5-fluorouracil (5FU). Fluorouracil 135-138 KRAS proto-oncogene, GTPase Homo sapiens 55-59 28959548-10 2016 The formulation also modulated inflammatory response triggered by 5-FU through reduction of 68% of myeloperoxidase activity and a 4-fold increase in anti-inflammatory IL-10 levels. Fluorouracil 66-70 myeloperoxidase Mus musculus 99-114 26290450-6 2015 In accord with this observation, PHD1 knockdown greatly sensitizes CRC to 5-FU in mice. Fluorouracil 74-78 egl-9 family hypoxia-inducible factor 2 Mus musculus 33-37 26099525-21 2015 Alternatively, expression of ATOH8 in PLC8024 and Huh7 cells significantly reduced the numbers of cells expressing CD133, and increased the chemo-sensitivity of Huh7 cells to 5-fluorouracil (5-FU) and cisplatin, in vitro and in mice. Fluorouracil 175-189 MIR7-3 host gene Homo sapiens 50-54 26099525-21 2015 Alternatively, expression of ATOH8 in PLC8024 and Huh7 cells significantly reduced the numbers of cells expressing CD133, and increased the chemo-sensitivity of Huh7 cells to 5-fluorouracil (5-FU) and cisplatin, in vitro and in mice. Fluorouracil 175-189 MIR7-3 host gene Homo sapiens 161-165 26099525-21 2015 Alternatively, expression of ATOH8 in PLC8024 and Huh7 cells significantly reduced the numbers of cells expressing CD133, and increased the chemo-sensitivity of Huh7 cells to 5-fluorouracil (5-FU) and cisplatin, in vitro and in mice. Fluorouracil 191-195 MIR7-3 host gene Homo sapiens 50-54 26099525-21 2015 Alternatively, expression of ATOH8 in PLC8024 and Huh7 cells significantly reduced the numbers of cells expressing CD133, and increased the chemo-sensitivity of Huh7 cells to 5-fluorouracil (5-FU) and cisplatin, in vitro and in mice. Fluorouracil 191-195 MIR7-3 host gene Homo sapiens 161-165 26722420-0 2015 Correlations between expression levels of thymidylate synthase, thymidine phosphorylase and dihydropyrimidine dehydrogenase, and efficacy of 5-fluorouracil-based chemotherapy for advanced colorectal cancer. Fluorouracil 141-155 dihydropyrimidine dehydrogenase Homo sapiens 92-123 26722420-6 2015 Therefore, TS, TP, and DPD mRNA levels appear to be suitable indicators of the efficacy of 5-FU-based chemotherapy and prognosis of CRC. Fluorouracil 91-95 dihydropyrimidine dehydrogenase Homo sapiens 23-26 25665511-1 2015 We recently found variants in cancer stem cell genes (CD44, ALCAM and LGR5) significantly associated with increased time to recurrence (TTR) in patients with stage III and high-risk stage II colon cancer treated with 5-fluorouracil (5-FU)-based chemotherapy. Fluorouracil 217-231 CD44 molecule (Indian blood group) Homo sapiens 54-58 25665511-1 2015 We recently found variants in cancer stem cell genes (CD44, ALCAM and LGR5) significantly associated with increased time to recurrence (TTR) in patients with stage III and high-risk stage II colon cancer treated with 5-fluorouracil (5-FU)-based chemotherapy. Fluorouracil 233-237 CD44 molecule (Indian blood group) Homo sapiens 54-58 26317793-5 2015 We showed that EIF5A2 overexpression in ESCC cells resulted in increased chemoresistance to 5-fluorouracil (5-FU), docetaxel and taxol. Fluorouracil 92-106 eukaryotic translation initiation factor 5A2 Mus musculus 15-21 26317793-5 2015 We showed that EIF5A2 overexpression in ESCC cells resulted in increased chemoresistance to 5-fluorouracil (5-FU), docetaxel and taxol. Fluorouracil 108-112 eukaryotic translation initiation factor 5A2 Mus musculus 15-21 26242737-6 2015 5-Fluorouracil-resistant TYMS T51S, G52S (TYMS(SS)) is resistant to MTX and improves MTX resistance of DHFR(FS) in primary T cells. Fluorouracil 0-14 thymidylate synthase Mus musculus 25-29 26242737-6 2015 5-Fluorouracil-resistant TYMS T51S, G52S (TYMS(SS)) is resistant to MTX and improves MTX resistance of DHFR(FS) in primary T cells. Fluorouracil 0-14 thymidylate synthase Mus musculus 42-46 26242737-6 2015 5-Fluorouracil-resistant TYMS T51S, G52S (TYMS(SS)) is resistant to MTX and improves MTX resistance of DHFR(FS) in primary T cells. Fluorouracil 0-14 dihydrofolate reductase Mus musculus 103-107 26124179-2 2015 We determined that activation of the CCAAT/enhancer binding protein delta (CEBPD) response to Cisplatin and 5-Fluorouracil in cancer-associated macrophages and fibroblasts contributed to the metastasis, invasion, acquired chemoresistance and stemness of cancer cells by in vitro and in vivo assays. Fluorouracil 108-122 CCAAT enhancer binding protein delta Homo sapiens 75-80 26242620-2 2015 In this work, acquired 5-FU resistance in the colorectal cancer cell line SW480 was obtained with the up-regulation of dihydropyrimidine dehydrogenase (DPYD) gene expression which can convert 5-FU to its inactive metabolite. Fluorouracil 23-27 dihydropyrimidine dehydrogenase Homo sapiens 119-150 26242620-2 2015 In this work, acquired 5-FU resistance in the colorectal cancer cell line SW480 was obtained with the up-regulation of dihydropyrimidine dehydrogenase (DPYD) gene expression which can convert 5-FU to its inactive metabolite. Fluorouracil 23-27 dihydropyrimidine dehydrogenase Homo sapiens 152-156 26242620-2 2015 In this work, acquired 5-FU resistance in the colorectal cancer cell line SW480 was obtained with the up-regulation of dihydropyrimidine dehydrogenase (DPYD) gene expression which can convert 5-FU to its inactive metabolite. Fluorouracil 192-196 dihydropyrimidine dehydrogenase Homo sapiens 119-150 26242620-2 2015 In this work, acquired 5-FU resistance in the colorectal cancer cell line SW480 was obtained with the up-regulation of dihydropyrimidine dehydrogenase (DPYD) gene expression which can convert 5-FU to its inactive metabolite. Fluorouracil 192-196 dihydropyrimidine dehydrogenase Homo sapiens 152-156 26330892-1 2015 BACKGROUND: Dihydropyrimidine dehydrogenase (DPD) is the initial and rate-limiting enzyme of the metabolic pathway of 5-fluorouracil (5-FU) and other fluoropyrimidines to inactive compounds. Fluorouracil 118-132 dihydropyrimidine dehydrogenase Homo sapiens 12-43 26330892-1 2015 BACKGROUND: Dihydropyrimidine dehydrogenase (DPD) is the initial and rate-limiting enzyme of the metabolic pathway of 5-fluorouracil (5-FU) and other fluoropyrimidines to inactive compounds. Fluorouracil 118-132 dihydropyrimidine dehydrogenase Homo sapiens 45-48 26330892-1 2015 BACKGROUND: Dihydropyrimidine dehydrogenase (DPD) is the initial and rate-limiting enzyme of the metabolic pathway of 5-fluorouracil (5-FU) and other fluoropyrimidines to inactive compounds. Fluorouracil 134-138 dihydropyrimidine dehydrogenase Homo sapiens 12-43 26330892-1 2015 BACKGROUND: Dihydropyrimidine dehydrogenase (DPD) is the initial and rate-limiting enzyme of the metabolic pathway of 5-fluorouracil (5-FU) and other fluoropyrimidines to inactive compounds. Fluorouracil 134-138 dihydropyrimidine dehydrogenase Homo sapiens 45-48 26122960-0 2015 NECTIN-4 increased the 5-FU resistance in colon cancer cells by inducing the PI3K-AKT cascade. Fluorouracil 23-27 nectin cell adhesion molecule 4 Homo sapiens 0-8 26122960-5 2015 RESULTS: Increased NECTIN-4 expression was observed in 5-FU-resistant (5-FU-R) and 5-FU-exposed HCT-116 cells. Fluorouracil 55-59 nectin cell adhesion molecule 4 Homo sapiens 19-27 26122960-5 2015 RESULTS: Increased NECTIN-4 expression was observed in 5-FU-resistant (5-FU-R) and 5-FU-exposed HCT-116 cells. Fluorouracil 71-75 nectin cell adhesion molecule 4 Homo sapiens 19-27 26063742-0 2015 Suppression of Reserve MCM Complexes Chemosensitizes to Gemcitabine and 5-Fluorouracil. Fluorouracil 72-86 methylmalonyl-CoA mutase Homo sapiens 23-26 26063742-7 2015 The current study provides definitive evidence that cosuppression of the excess/backup MCM complexes sensitizes PDAC tumor lines to both gemcitabine and 5-FU, leading to increased loss of proliferative capacity compared with drugs alone. Fluorouracil 153-157 methylmalonyl-CoA mutase Homo sapiens 87-90 26349992-0 2015 Low-dose all-trans retinoic acid enhances cytotoxicity of cisplatin and 5-fluorouracil on CD44(+) cancer stem cells. Fluorouracil 72-86 CD44 molecule (Indian blood group) Homo sapiens 90-94 26349992-6 2015 We allowed the CD44(+-) cells to grow 6 days at a subtoxic concentration of ATRA and then treated with different concentration of CDDP and 5-FU for 24h. Fluorouracil 139-143 CD44 molecule (Indian blood group) Homo sapiens 15-19 26017781-8 2015 Atoh1 protein also enriched cancer stem cells with upregulated Lgr5 expression and cells in G0/G1 cell cycle phase, resulting in both the chemoresistance to 5-fluorouracil and oxaliplatin and the promotion of cell migration. Fluorouracil 157-171 atonal bHLH transcription factor 1 Homo sapiens 0-5 26048344-3 2015 We investigated the effects of oral supplementation with ED on mucin in 5-fluorouracil (5-FU)-induced intestinal mucositis. Fluorouracil 72-86 solute carrier family 13 member 2 Rattus norvegicus 63-68 26181717-6 2015 For this purpose, we focused on the anticancer prodrug tegafur, which is converted to its active metabolite 5-fluorouracil (5-FU) mainly by CYP2A6. Fluorouracil 108-122 cytochrome P450 family 2 subfamily A member 6 Homo sapiens 140-146 26181717-6 2015 For this purpose, we focused on the anticancer prodrug tegafur, which is converted to its active metabolite 5-fluorouracil (5-FU) mainly by CYP2A6. Fluorouracil 124-128 cytochrome P450 family 2 subfamily A member 6 Homo sapiens 140-146 25112781-1 2015 BACKGROUND: The efficacy of 5-fluorouracil (5FU)-based therapy, which remains the cornerstone of gastrointestinal cancer treatment, depends upon the expression of enzymes involved in pyrimidine metabolism, including thymidylate synthase (TS), dihydropyrimidine dehydrogenase (DPD), thymidine phosphorylase (TP), and orotate phosphoribosyltransferase (OPRT). Fluorouracil 28-42 dihydropyrimidine dehydrogenase Homo sapiens 243-274 25112781-1 2015 BACKGROUND: The efficacy of 5-fluorouracil (5FU)-based therapy, which remains the cornerstone of gastrointestinal cancer treatment, depends upon the expression of enzymes involved in pyrimidine metabolism, including thymidylate synthase (TS), dihydropyrimidine dehydrogenase (DPD), thymidine phosphorylase (TP), and orotate phosphoribosyltransferase (OPRT). Fluorouracil 28-42 dihydropyrimidine dehydrogenase Homo sapiens 276-279 25112781-1 2015 BACKGROUND: The efficacy of 5-fluorouracil (5FU)-based therapy, which remains the cornerstone of gastrointestinal cancer treatment, depends upon the expression of enzymes involved in pyrimidine metabolism, including thymidylate synthase (TS), dihydropyrimidine dehydrogenase (DPD), thymidine phosphorylase (TP), and orotate phosphoribosyltransferase (OPRT). Fluorouracil 44-47 dihydropyrimidine dehydrogenase Homo sapiens 243-274 25963746-12 2015 5-FU increased the IFN-beta/receptor 2 (IFNAR2) and BXA levels, indicating that 5-FU increased sensitivity of endometrial cancer cells to IFN-beta, leading to apoptosis of cancer cells. Fluorouracil 0-4 interferon alpha and beta receptor subunit 2 Homo sapiens 19-38 25963746-12 2015 5-FU increased the IFN-beta/receptor 2 (IFNAR2) and BXA levels, indicating that 5-FU increased sensitivity of endometrial cancer cells to IFN-beta, leading to apoptosis of cancer cells. Fluorouracil 0-4 interferon alpha and beta receptor subunit 2 Homo sapiens 40-46 25963746-12 2015 5-FU increased the IFN-beta/receptor 2 (IFNAR2) and BXA levels, indicating that 5-FU increased sensitivity of endometrial cancer cells to IFN-beta, leading to apoptosis of cancer cells. Fluorouracil 80-84 interferon alpha and beta receptor subunit 2 Homo sapiens 19-38 25963746-12 2015 5-FU increased the IFN-beta/receptor 2 (IFNAR2) and BXA levels, indicating that 5-FU increased sensitivity of endometrial cancer cells to IFN-beta, leading to apoptosis of cancer cells. Fluorouracil 80-84 interferon alpha and beta receptor subunit 2 Homo sapiens 40-46 25348620-1 2015 Dihydropyrimidine dehydrogenase is a crucial enzyme for the degradation of 5-fluorouracil (5FU). Fluorouracil 75-89 dihydropyrimidine dehydrogenase Homo sapiens 0-31 25348620-1 2015 Dihydropyrimidine dehydrogenase is a crucial enzyme for the degradation of 5-fluorouracil (5FU). Fluorouracil 91-94 dihydropyrimidine dehydrogenase Homo sapiens 0-31 25951903-10 2015 Transfection of let-7b or let-7c combined with 5-FU inhibited proliferation and potentiated the antitumor efficacies of 5-FU at tolerated concentration. Fluorouracil 120-124 microRNA let-7b Homo sapiens 16-22 25951903-12 2015 Overexpression of let-7b and let-7c reduced Akt2 expression, and Akt2 inhibition enhanced the sensitivity to 5-FU by affecting apoptotic pathway. Fluorouracil 109-113 microRNA let-7b Homo sapiens 18-24 25951903-14 2015 The dysregulation of let-7b and let-7c may be involved in chemoresistance of RCC cells to 5-FU by down-regulating Akt2. Fluorouracil 90-94 microRNA let-7b Homo sapiens 21-27 25724180-7 2015 TRIM24 overxpression also induced chemoresistance to 5-FU in gastric cancer cells. Fluorouracil 53-57 tripartite motif containing 24 Homo sapiens 0-6 25811796-5 2015 Furthermore, downregulation of LMWPTP in CRC leads to a reduced migration ability in both 2D- and 3D-migration assays, and sensitizes tumor cells to the chemotherapeutic agent 5-FU. Fluorouracil 176-180 acid phosphatase 1 Homo sapiens 31-37 25860483-0 2015 Slug-dependent upregulation of L1CAM is responsible for the increased invasion potential of pancreatic cancer cells following long-term 5-FU treatment. Fluorouracil 136-140 snail family transcriptional repressor 2 Homo sapiens 0-4 25744244-2 2015 This work aimed to investigate the alterations in chemosensitivity of A549 lung cancer cells for 5-Fluorouracil (5-FU) and irinotecan by silencing ABCE1 using specific small interfering RNAs (siRNA). Fluorouracil 97-111 ATP binding cassette subfamily E member 1 Homo sapiens 147-152 25744244-2 2015 This work aimed to investigate the alterations in chemosensitivity of A549 lung cancer cells for 5-Fluorouracil (5-FU) and irinotecan by silencing ABCE1 using specific small interfering RNAs (siRNA). Fluorouracil 113-117 ATP binding cassette subfamily E member 1 Homo sapiens 147-152 25744244-7 2015 Downregulation of ABCE1 improved the anticancer effects of 5-FU in inducing cell viability/proliferation inhibition and apoptosis/necrosis, whereas interestingly, almost did not change or slightly reduced the anticancer effects of irinotecan. Fluorouracil 59-63 ATP binding cassette subfamily E member 1 Homo sapiens 18-23 25744244-11 2015 Our findings demonstrate that the strategy of downregulation of ABCE1 may be included in conventional 5-FU chemotherapy for lung cancer, minimizing the usage of 5-FU at high dosages. Fluorouracil 102-106 ATP binding cassette subfamily E member 1 Homo sapiens 64-69 25744244-11 2015 Our findings demonstrate that the strategy of downregulation of ABCE1 may be included in conventional 5-FU chemotherapy for lung cancer, minimizing the usage of 5-FU at high dosages. Fluorouracil 161-165 ATP binding cassette subfamily E member 1 Homo sapiens 64-69 25861418-10 2015 Compared to mice treated with 5-FU, mice treated with AHCC plus 5-FU had higher thymus index, percentages of CD3(+), CD4(+), and NK cells (P < 0.01), and ratio of CD4(+)/CD8(+) (P < 0.01) in peripheral blood. Fluorouracil 64-68 CD4 antigen Mus musculus 117-120 25861418-10 2015 Compared to mice treated with 5-FU, mice treated with AHCC plus 5-FU had higher thymus index, percentages of CD3(+), CD4(+), and NK cells (P < 0.01), and ratio of CD4(+)/CD8(+) (P < 0.01) in peripheral blood. Fluorouracil 64-68 CD4 antigen Mus musculus 166-169 25861418-13 2015 In addition, the combination of AHCC and 5-FU further up-regulated the expression of Bcl-2 associated X protein (Bax) (P < 0.01), while it down-regulated the expression of B cell lymphoma 2 (Bcl-2) (P < 0.01). Fluorouracil 41-45 BCL2-associated X protein Mus musculus 113-116 25870609-5 2015 In this study, we propose to analyze the different clinical outcomes and disease prognosis of patients with stage IV CRC treated with FOLFOX chemotherapy (fluorouracil, leucovorin, oxaliplatin) based on different Kirsten ras (KRAS) mutation patterns. Fluorouracil 155-167 KRAS proto-oncogene, GTPase Homo sapiens 213-224 25742476-8 2015 Besides, we identified the frequencies of CD3(+) lymphocytes, effCD8(+) T cells and NK cells in the peripheral blood of the patients, and IL-10 amount in serum, to be predictive values for 5FU-based chemotherapy. Fluorouracil 189-192 interleukin 10 Homo sapiens 138-143 24434920-0 2015 Dihydropyrimidine dehydrogenase 85T>C mutation is associated with ocular toxicity of 5-fluorouracil: a case report. Fluorouracil 88-102 dihydropyrimidine dehydrogenase Homo sapiens 0-31 24434920-1 2015 5-Fluorouracil (5-FU), the mainstay of solid tumor chemotherapy over the past 40 years, induces grade III-IV toxicities in up to 15% of patients with polymorphisms in the dihydropyrimidine dehydrogenase (DPYD), thymidylate synthase (TYMS), and methylenetetrahydrofolate reductase (MTHFR) genes. Fluorouracil 0-14 dihydropyrimidine dehydrogenase Homo sapiens 171-202 24434920-1 2015 5-Fluorouracil (5-FU), the mainstay of solid tumor chemotherapy over the past 40 years, induces grade III-IV toxicities in up to 15% of patients with polymorphisms in the dihydropyrimidine dehydrogenase (DPYD), thymidylate synthase (TYMS), and methylenetetrahydrofolate reductase (MTHFR) genes. Fluorouracil 0-14 dihydropyrimidine dehydrogenase Homo sapiens 204-208 24434920-1 2015 5-Fluorouracil (5-FU), the mainstay of solid tumor chemotherapy over the past 40 years, induces grade III-IV toxicities in up to 15% of patients with polymorphisms in the dihydropyrimidine dehydrogenase (DPYD), thymidylate synthase (TYMS), and methylenetetrahydrofolate reductase (MTHFR) genes. Fluorouracil 0-14 methylenetetrahydrofolate reductase Homo sapiens 244-279 24434920-1 2015 5-Fluorouracil (5-FU), the mainstay of solid tumor chemotherapy over the past 40 years, induces grade III-IV toxicities in up to 15% of patients with polymorphisms in the dihydropyrimidine dehydrogenase (DPYD), thymidylate synthase (TYMS), and methylenetetrahydrofolate reductase (MTHFR) genes. Fluorouracil 0-14 methylenetetrahydrofolate reductase Homo sapiens 281-286 24434920-1 2015 5-Fluorouracil (5-FU), the mainstay of solid tumor chemotherapy over the past 40 years, induces grade III-IV toxicities in up to 15% of patients with polymorphisms in the dihydropyrimidine dehydrogenase (DPYD), thymidylate synthase (TYMS), and methylenetetrahydrofolate reductase (MTHFR) genes. Fluorouracil 16-20 dihydropyrimidine dehydrogenase Homo sapiens 171-202 24434920-1 2015 5-Fluorouracil (5-FU), the mainstay of solid tumor chemotherapy over the past 40 years, induces grade III-IV toxicities in up to 15% of patients with polymorphisms in the dihydropyrimidine dehydrogenase (DPYD), thymidylate synthase (TYMS), and methylenetetrahydrofolate reductase (MTHFR) genes. Fluorouracil 16-20 dihydropyrimidine dehydrogenase Homo sapiens 204-208 24434920-1 2015 5-Fluorouracil (5-FU), the mainstay of solid tumor chemotherapy over the past 40 years, induces grade III-IV toxicities in up to 15% of patients with polymorphisms in the dihydropyrimidine dehydrogenase (DPYD), thymidylate synthase (TYMS), and methylenetetrahydrofolate reductase (MTHFR) genes. Fluorouracil 16-20 methylenetetrahydrofolate reductase Homo sapiens 244-279 24434920-1 2015 5-Fluorouracil (5-FU), the mainstay of solid tumor chemotherapy over the past 40 years, induces grade III-IV toxicities in up to 15% of patients with polymorphisms in the dihydropyrimidine dehydrogenase (DPYD), thymidylate synthase (TYMS), and methylenetetrahydrofolate reductase (MTHFR) genes. Fluorouracil 16-20 methylenetetrahydrofolate reductase Homo sapiens 281-286 25873402-0 2015 MicroRNA-494 sensitizes colon cancer cells to fluorouracil through regulation of DPYD. Fluorouracil 46-58 dihydropyrimidine dehydrogenase Homo sapiens 81-85 25873402-8 2015 Overexpression or knockdown of DPYD could attenuate miR-494 mediated 5-Fu sensitivity regulation, suggesting the dependence of DPYD regulation in miR-494 activity. Fluorouracil 69-73 dihydropyrimidine dehydrogenase Homo sapiens 31-35 25873402-10 2015 Thus, we concluded that in colon cancer cells, tumor suppressor miR-494 enhanced 5-Fu sensitivity via regulation of DPYD expression. Fluorouracil 81-85 dihydropyrimidine dehydrogenase Homo sapiens 116-120 25605843-1 2015 PURPOSE: The phase III CRYSTAL study demonstrated that addition of cetuximab to fluorouracil, leucovorin, and irinotecan (FOLFIRI) significantly improved overall survival, progression-free survival, and objective response in the first-line treatment of patients with KRAS codon 12/13 (exon 2) wild-type metastatic colorectal cancer (mCRC). Fluorouracil 80-92 KRAS proto-oncogene, GTPase Homo sapiens 267-271 25169655-7 2015 RESULTS: CD44(high) /ESA(low) cells exhibited marked resistance to 5-FU-induced apoptosis and had high expression of dihydropyrimidine dehydrogenase (DPD). Fluorouracil 67-71 CD44 molecule (Indian blood group) Homo sapiens 9-13 25169655-8 2015 The DPD inhibitor, 5-chloro-2, 4-dihydroxypyridine (CDHP) significantly enhanced 5-FU-induced apoptosis of CD44(high)/ESA(low) cells. Fluorouracil 81-85 dihydropyrimidine dehydrogenase Homo sapiens 4-7 25169655-8 2015 The DPD inhibitor, 5-chloro-2, 4-dihydroxypyridine (CDHP) significantly enhanced 5-FU-induced apoptosis of CD44(high)/ESA(low) cells. Fluorouracil 81-85 cadherin 3 Homo sapiens 52-56 25169655-8 2015 The DPD inhibitor, 5-chloro-2, 4-dihydroxypyridine (CDHP) significantly enhanced 5-FU-induced apoptosis of CD44(high)/ESA(low) cells. Fluorouracil 81-85 CD44 molecule (Indian blood group) Homo sapiens 107-111 25169655-11 2015 Combination of both CDHP and GSK3beta inhibitors markedly enhanced 5-FU-induced apoptosis of CD44(high) /ESA(low) cells. Fluorouracil 67-71 cadherin 3 Homo sapiens 20-24 25169655-11 2015 Combination of both CDHP and GSK3beta inhibitors markedly enhanced 5-FU-induced apoptosis of CD44(high) /ESA(low) cells. Fluorouracil 67-71 CD44 molecule (Indian blood group) Homo sapiens 93-97 25783977-5 2015 The evidence to support broad utilization of uridine 5"-diphospho-glucuronosyltransferase 1A1 (UGT1A1) and dihydropyrimidine dehydrogenase (DPD) testing to guide irinotecan and fluorouracil dosing remains limited. Fluorouracil 177-189 dihydropyrimidine dehydrogenase Homo sapiens 140-143 25744837-9 2015 Compared with HT-29 cells, HT-29/5-FU cells showed remarkable reduction of cell proliferation and colony formation, higher expressions of TS and DPD, higher percentage of cells in the S phase, and stronger ability of resistance to apoptosis induced by 5-FU. Fluorouracil 33-37 dihydropyrimidine dehydrogenase Homo sapiens 145-148 25325304-3 2015 We aimed to investigate the effect of silencing both mutant and wild-type Kristen Rous sarcoma (k-ras) on the response of human colorectal tumor 116 (HCT-116) as a colon cancer cell line to the cytotoxic effect of 5-flurouracil (5-FU). Fluorouracil 229-233 KRAS proto-oncogene, GTPase Homo sapiens 96-101 25325304-12 2015 In conclusion, silencing mutant and wild-type k-ras would increase the resistance of HCT-116 cell line as a model of colorectal cancer to 5-FU. Fluorouracil 138-142 KRAS proto-oncogene, GTPase Homo sapiens 46-51 25325304-14 2015 Therefore, both mutant and wild-type k-ras may play a role in sensitizing colorectal cancer cells to 5-FU as a common chemotherapeutic drug. Fluorouracil 101-105 KRAS proto-oncogene, GTPase Homo sapiens 37-42 25502560-5 2015 When the level of miR-96 increased, the expression of the anti-apoptotic regulator XIAP and p53 stability regulator UBE2N decreased, resulting in increased apoptosis and growth inhibition following 5-FU exposure. Fluorouracil 198-202 X-linked inhibitor of apoptosis Homo sapiens 83-87 25547406-0 2015 CEACAM1 and hollow spheroid formation modulate the chemosensitivity of colorectal cancer to 5-fluorouracil. Fluorouracil 92-106 CEA cell adhesion molecule 1 Homo sapiens 0-7 25547406-2 2015 The aim of the present study was to clarify whether CEACAM1 cytoplasmic domain isoform balance and HS are associated with resistance to 5-fluorouracil (5FU). Fluorouracil 136-150 CEA cell adhesion molecule 1 Homo sapiens 52-59 25547406-2 2015 The aim of the present study was to clarify whether CEACAM1 cytoplasmic domain isoform balance and HS are associated with resistance to 5-fluorouracil (5FU). Fluorouracil 152-155 CEA cell adhesion molecule 1 Homo sapiens 52-59 25449431-4 2015 Thus, miR-22 may function as an important switch between autophagy and apoptosis to regulate 5-FU sensitivity through post-transcriptional silencing of BTG1. Fluorouracil 93-97 BTG anti-proliferation factor 1 Homo sapiens 152-156 25449437-8 2015 Furthermore, miR-BART20-5p increased chemoresistance to 5-fluorouracil and docetaxel. Fluorouracil 56-70 membrane associated ring-CH-type finger 8 Homo sapiens 13-16 24889488-2 2015 The purpose of this study was to assess the prognostic impact of KRAS and BRAF mutation in patients treated with adjuvant 5-fluorouracil/leucovorin/oxaliplatin (FOLFOX). Fluorouracil 122-136 KRAS proto-oncogene, GTPase Homo sapiens 65-69 25929864-9 2015 Inversely, downregulation of miR-23a reduced viability in and promoted cell apoptosis in MSI CRC cells treated with 5-FU. Fluorouracil 116-120 microRNA 23a Homo sapiens 29-36 25929864-12 2015 Interestingly, repressing ABCF1 expression by either miR-23a overexpression or siABCF1 led to recovery of 5-FU sensitivity in MSI CRC cells. Fluorouracil 106-110 ATP binding cassette subfamily F member 1 Homo sapiens 26-31 25929864-13 2015 These data demonstrated that miR-23a enhances 5-FU resistance in MSI CRC cells through targeting ABCF1 and thus provided important implications for therapeutic approaches aiming to overcome MSI CRC resistance to 5-FU. Fluorouracil 46-50 microRNA 23a Homo sapiens 29-36 25929864-13 2015 These data demonstrated that miR-23a enhances 5-FU resistance in MSI CRC cells through targeting ABCF1 and thus provided important implications for therapeutic approaches aiming to overcome MSI CRC resistance to 5-FU. Fluorouracil 46-50 ATP binding cassette subfamily F member 1 Homo sapiens 97-102 25929864-13 2015 These data demonstrated that miR-23a enhances 5-FU resistance in MSI CRC cells through targeting ABCF1 and thus provided important implications for therapeutic approaches aiming to overcome MSI CRC resistance to 5-FU. Fluorouracil 212-216 microRNA 23a Homo sapiens 29-36 24647007-3 2015 The few proven genetic biomarkers of 5-FU toxicity are rare variants and polymorphisms, respectively, at candidate loci dihydropyrimidine dehydrogenase (DPYD) and thymidylate synthase (TYMS). Fluorouracil 37-41 dihydropyrimidine dehydrogenase Homo sapiens 120-151 24647007-3 2015 The few proven genetic biomarkers of 5-FU toxicity are rare variants and polymorphisms, respectively, at candidate loci dihydropyrimidine dehydrogenase (DPYD) and thymidylate synthase (TYMS). Fluorouracil 37-41 dihydropyrimidine dehydrogenase Homo sapiens 153-157 24512327-9 2015 The results demonstrated that 5-FU treatment significantly inhibited G-CSF, GM-CSF, and M-CSF expression in all three sites at all timepoints from 6-72 h post 5-FU. Fluorouracil 30-34 colony stimulating factor 2 (granulocyte-macrophage) Mus musculus 76-82 24512327-9 2015 The results demonstrated that 5-FU treatment significantly inhibited G-CSF, GM-CSF, and M-CSF expression in all three sites at all timepoints from 6-72 h post 5-FU. Fluorouracil 30-34 colony stimulating factor 1 (macrophage) Mus musculus 77-82 25333670-8 2015 From this, it was concluded that let-7b increased 5-FU sensitivity by repressing Bcl-xl expression in HCC cells. Fluorouracil 50-54 microRNA let-7b Homo sapiens 33-39 25351906-4 2015 For this purpose, we examined cell proliferation and the SP cell ratio following treatment of Huh7 cells with the anticancer drugs 5-fluorouracil (5-FU) and paclitaxel. Fluorouracil 131-145 MIR7-3 host gene Homo sapiens 94-98 25351906-4 2015 For this purpose, we examined cell proliferation and the SP cell ratio following treatment of Huh7 cells with the anticancer drugs 5-fluorouracil (5-FU) and paclitaxel. Fluorouracil 147-151 MIR7-3 host gene Homo sapiens 94-98 25269761-0 2014 Knockdown of beta3GnT8 reverses 5-fluorouracil resistance in human colorectal cancer cells via inhibition the biosynthesis of polylactosamine-type N-glycans. Fluorouracil 32-46 UDP-GlcNAc:betaGal beta-1,3-N-acetylglucosaminyltransferase 8 Homo sapiens 13-22 25269761-10 2014 Further studies showed that beta3GnT8 expression was also upregulated in 5-FU-resistant cancer cells, and knockdown of beta3GnT8 by RNA interference reversed 5-FU resistance through, at least partly, by suppressing the formation of polylactosamine. Fluorouracil 73-77 UDP-GlcNAc:betaGal beta-1,3-N-acetylglucosaminyltransferase 8 Homo sapiens 28-37 25269761-10 2014 Further studies showed that beta3GnT8 expression was also upregulated in 5-FU-resistant cancer cells, and knockdown of beta3GnT8 by RNA interference reversed 5-FU resistance through, at least partly, by suppressing the formation of polylactosamine. Fluorouracil 158-162 UDP-GlcNAc:betaGal beta-1,3-N-acetylglucosaminyltransferase 8 Homo sapiens 119-128 25360167-10 2014 Due to the results obtained in the current study, we hypothesize that CDHP enhanced the antitumor efficacy of 5-FU by inhibiting the excess DPD protein produced by the tumor. Fluorouracil 110-114 dihydropyrimidine dehydrogenase Homo sapiens 140-143 25381393-0 2014 DPYD variants as predictors of 5-fluorouracil toxicity in adjuvant colon cancer treatment (NCCTG N0147). Fluorouracil 31-45 dihydropyrimidine dehydrogenase Homo sapiens 0-4 25381393-1 2014 BACKGROUND: Previous studies have suggested the potential importance of three DPYD variants (DPYD*2A, D949V, and I560S) with increased 5-FU toxicity. Fluorouracil 135-139 dihydropyrimidine dehydrogenase Homo sapiens 78-82 25381393-1 2014 BACKGROUND: Previous studies have suggested the potential importance of three DPYD variants (DPYD*2A, D949V, and I560S) with increased 5-FU toxicity. Fluorouracil 135-139 dihydropyrimidine dehydrogenase Homo sapiens 93-97 22038671-13 2014 DPD is the main enzyme involved in the catabolism of 5-FU. Fluorouracil 53-57 dihydropyrimidine dehydrogenase Homo sapiens 0-3 24898807-5 2014 In this study, we generated 5-FU-resistant colon cancer cell lines from which we found that miR-122 was downregulated in 5-FU-resistant cells compared with sensitive cells. Fluorouracil 28-32 microRNA 122 Homo sapiens 92-99 24898807-5 2014 In this study, we generated 5-FU-resistant colon cancer cell lines from which we found that miR-122 was downregulated in 5-FU-resistant cells compared with sensitive cells. Fluorouracil 121-125 microRNA 122 Homo sapiens 92-99 24898807-8 2014 Importantly, overexpression of miR-122 in 5-FU-resistant cells resensitizes 5-FU resistance through the inhibition of PKM2 both in vitro and in vivo. Fluorouracil 42-46 microRNA 122 Homo sapiens 31-38 24898807-8 2014 Importantly, overexpression of miR-122 in 5-FU-resistant cells resensitizes 5-FU resistance through the inhibition of PKM2 both in vitro and in vivo. Fluorouracil 76-80 microRNA 122 Homo sapiens 31-38 24898807-9 2014 In summary, these findings reveal that the dysregulated glucose metabolism contributes to 5-FU resistance, and glycolysis inhibition by miR-122 might be a promising therapeutic strategy to overcome 5-FU resistance. Fluorouracil 198-202 microRNA 122 Homo sapiens 136-143 25249558-0 2014 SNAI2 modulates colorectal cancer 5-fluorouracil sensitivity through miR145 repression. Fluorouracil 34-48 snail family transcriptional repressor 2 Homo sapiens 0-5 25249558-2 2014 Therefore, we hypothesized that SNAI2 (Slug) may mediate 5-fluorouracil (5FU) chemotherapy resistance through inhibition of miR145 in colorectal cancer and thus represents a novel therapeutic target to enhance current colorectal cancer treatment strategies. Fluorouracil 57-71 snail family transcriptional repressor 2 Homo sapiens 32-37 25249558-2 2014 Therefore, we hypothesized that SNAI2 (Slug) may mediate 5-fluorouracil (5FU) chemotherapy resistance through inhibition of miR145 in colorectal cancer and thus represents a novel therapeutic target to enhance current colorectal cancer treatment strategies. Fluorouracil 57-71 snail family transcriptional repressor 2 Homo sapiens 39-43 25249558-2 2014 Therefore, we hypothesized that SNAI2 (Slug) may mediate 5-fluorouracil (5FU) chemotherapy resistance through inhibition of miR145 in colorectal cancer and thus represents a novel therapeutic target to enhance current colorectal cancer treatment strategies. Fluorouracil 73-76 snail family transcriptional repressor 2 Homo sapiens 32-37 25249558-2 2014 Therefore, we hypothesized that SNAI2 (Slug) may mediate 5-fluorouracil (5FU) chemotherapy resistance through inhibition of miR145 in colorectal cancer and thus represents a novel therapeutic target to enhance current colorectal cancer treatment strategies. Fluorouracil 73-76 snail family transcriptional repressor 2 Homo sapiens 39-43 24583265-5 2014 We also demonstrate that both 5-FU and gemcitabine treatments increase SOCE in Panc1 pancreatic adenocarcinoma cell line via upregulation of ORAI1 and STIM1. Fluorouracil 30-34 ORAI calcium release-activated calcium modulator 1 Homo sapiens 141-146 25102934-1 2014 PURPOSE: 5-fluorouracil (5-FU) competes with uracil (Ura) as a substrate for dihydropyrimidine dehydrogenase (DPD). Fluorouracil 9-23 dihydropyrimidine dehydrogenase Homo sapiens 77-108 25102934-1 2014 PURPOSE: 5-fluorouracil (5-FU) competes with uracil (Ura) as a substrate for dihydropyrimidine dehydrogenase (DPD). Fluorouracil 9-23 dihydropyrimidine dehydrogenase Homo sapiens 110-113 25102934-1 2014 PURPOSE: 5-fluorouracil (5-FU) competes with uracil (Ura) as a substrate for dihydropyrimidine dehydrogenase (DPD). Fluorouracil 25-29 dihydropyrimidine dehydrogenase Homo sapiens 77-108 25102934-1 2014 PURPOSE: 5-fluorouracil (5-FU) competes with uracil (Ura) as a substrate for dihydropyrimidine dehydrogenase (DPD). Fluorouracil 25-29 dihydropyrimidine dehydrogenase Homo sapiens 110-113 25102934-2 2014 Low DPD activity impairs breakdown of Ura to dihydrouracil (UH2) and is associated with toxicity during 5-FU-based chemotherapy. Fluorouracil 104-108 dihydropyrimidine dehydrogenase Homo sapiens 4-7 25253112-2 2014 Dihydropyrimidine dehydrogenase plays an important role in catabolism and clearance of 5-FU. Fluorouracil 87-91 dihydropyrimidine dehydrogenase Homo sapiens 0-31 25209093-5 2014 In general, participants agreed that 5-fluorouracil (5-FU) infusion regimens in doublets can be substituted with UFT (capecitabine, tegafur-uracil) and S1 (tegafur, 5-chloro-2,4-dihydroxypyridine and oxonic acid), and that the monoclonal antibodies cetuximab and panitumumab are recommended for KRAS wild type tumors. Fluorouracil 37-51 KRAS proto-oncogene, GTPase Homo sapiens 295-299 25209093-5 2014 In general, participants agreed that 5-fluorouracil (5-FU) infusion regimens in doublets can be substituted with UFT (capecitabine, tegafur-uracil) and S1 (tegafur, 5-chloro-2,4-dihydroxypyridine and oxonic acid), and that the monoclonal antibodies cetuximab and panitumumab are recommended for KRAS wild type tumors. Fluorouracil 53-57 KRAS proto-oncogene, GTPase Homo sapiens 295-299 24994673-2 2014 Since 5-FU is converted into active or inactive forms by orotate phosphoribosyltransferase (OPRT) or dihydropyrimidine dehydrogenase (DPD), a correlation between these enzymes and response to 5-FU has been suggested. Fluorouracil 6-10 dihydropyrimidine dehydrogenase Homo sapiens 101-132 24994673-2 2014 Since 5-FU is converted into active or inactive forms by orotate phosphoribosyltransferase (OPRT) or dihydropyrimidine dehydrogenase (DPD), a correlation between these enzymes and response to 5-FU has been suggested. Fluorouracil 6-10 dihydropyrimidine dehydrogenase Homo sapiens 134-137 24994673-2 2014 Since 5-FU is converted into active or inactive forms by orotate phosphoribosyltransferase (OPRT) or dihydropyrimidine dehydrogenase (DPD), a correlation between these enzymes and response to 5-FU has been suggested. Fluorouracil 192-196 dihydropyrimidine dehydrogenase Homo sapiens 101-132 24994673-2 2014 Since 5-FU is converted into active or inactive forms by orotate phosphoribosyltransferase (OPRT) or dihydropyrimidine dehydrogenase (DPD), a correlation between these enzymes and response to 5-FU has been suggested. Fluorouracil 192-196 dihydropyrimidine dehydrogenase Homo sapiens 134-137 24994673-4 2014 Therefore, in the present study, we aimed to prospectively evaluate whether OPRT and DPD were predictive factors of the response to 5-FU treatment in patients with resectable CRC. Fluorouracil 132-136 dihydropyrimidine dehydrogenase Homo sapiens 85-88 24994673-15 2014 In conclusion, our results suggest that the OPRT/DPD ratio could be a predictive factor for response to 5-FU/LV adjuvant chemotherapy. Fluorouracil 104-108 dihydropyrimidine dehydrogenase Homo sapiens 49-52 24972040-9 2014 Administration of 5-FU induced diarrhea and decreased the expression levels of AQP 4 and 8 in the colon. Fluorouracil 18-22 aquaporin 4 Mus musculus 79-84 24972040-13 2014 These findings provide evidence that neutrophil recruitment and neutrophil elastase may decrease the levels of AQP 4 and 8 in the colon of mice treated with 5-FU and contribute to the pathophysiology of 5-FU-induced body weight loss and diarrhea. Fluorouracil 157-161 aquaporin 4 Mus musculus 111-116 24972040-13 2014 These findings provide evidence that neutrophil recruitment and neutrophil elastase may decrease the levels of AQP 4 and 8 in the colon of mice treated with 5-FU and contribute to the pathophysiology of 5-FU-induced body weight loss and diarrhea. Fluorouracil 203-207 aquaporin 4 Mus musculus 111-116 25410891-0 2014 Predicting 5-fluorouracil toxicity: DPD genotype and 5,6-dihydrouracil:uracil ratio. Fluorouracil 11-25 dihydropyrimidine dehydrogenase Homo sapiens 36-39 25410891-1 2014 AIM: Decreased DPD activity is a major cause of 5-fluorouracil (5-FU) toxicity, but known reduced-function variants in the DPD gene (DPYD) explain only a part of DPD-related 5-FU toxicities. Fluorouracil 48-62 dihydropyrimidine dehydrogenase Homo sapiens 15-18 25410891-1 2014 AIM: Decreased DPD activity is a major cause of 5-fluorouracil (5-FU) toxicity, but known reduced-function variants in the DPD gene (DPYD) explain only a part of DPD-related 5-FU toxicities. Fluorouracil 48-62 dihydropyrimidine dehydrogenase Homo sapiens 123-126 25410891-1 2014 AIM: Decreased DPD activity is a major cause of 5-fluorouracil (5-FU) toxicity, but known reduced-function variants in the DPD gene (DPYD) explain only a part of DPD-related 5-FU toxicities. Fluorouracil 48-62 dihydropyrimidine dehydrogenase Homo sapiens 123-126 25410891-1 2014 AIM: Decreased DPD activity is a major cause of 5-fluorouracil (5-FU) toxicity, but known reduced-function variants in the DPD gene (DPYD) explain only a part of DPD-related 5-FU toxicities. Fluorouracil 64-68 dihydropyrimidine dehydrogenase Homo sapiens 15-18 25410891-1 2014 AIM: Decreased DPD activity is a major cause of 5-fluorouracil (5-FU) toxicity, but known reduced-function variants in the DPD gene (DPYD) explain only a part of DPD-related 5-FU toxicities. Fluorouracil 174-178 dihydropyrimidine dehydrogenase Homo sapiens 123-126 25410891-1 2014 AIM: Decreased DPD activity is a major cause of 5-fluorouracil (5-FU) toxicity, but known reduced-function variants in the DPD gene (DPYD) explain only a part of DPD-related 5-FU toxicities. Fluorouracil 174-178 dihydropyrimidine dehydrogenase Homo sapiens 133-137 25410891-1 2014 AIM: Decreased DPD activity is a major cause of 5-fluorouracil (5-FU) toxicity, but known reduced-function variants in the DPD gene (DPYD) explain only a part of DPD-related 5-FU toxicities. Fluorouracil 174-178 dihydropyrimidine dehydrogenase Homo sapiens 123-126 25162958-1 2014 Cholesterol-conjugated 5-fluorouracil prodrugs were designed to be carried in vivo via low density lipoproteins (LDL) and subsequently undergo LDL-receptor-mediated internalisation into cancer cells. Fluorouracil 23-37 low density lipoprotein receptor Mus musculus 143-155 24800927-8 2014 Mechanistically, CXCL4mab reduced the apoptosis of the crypt epithelia by suppression of the 5-FU-induced expression of p53 and Bax through its receptor CXCR3. Fluorouracil 93-97 BCL2-associated X protein Mus musculus 128-131 24947926-7 2014 CD44(+) cells, compared with unselected cells, were also resistant to 5-fluorouracil and cisplatin chemotherapy, and this resistance was reversed in vitro and in xenografts with Smo shRNA or VIS. Fluorouracil 70-84 CD44 molecule (Indian blood group) Homo sapiens 0-4 25464567-4 2014 CCK-8 assay had been used to test the sensitivity of Hep-2 cells to 5-FU and PTX after silencing SOX2 expression. Fluorouracil 68-72 SRY-box transcription factor 2 Homo sapiens 97-101 25464567-5 2014 Hoechst staining had been used to exam the changes of Hep-2 cells apoptosis treatment by 5-FU and PTX after silencing SOX2 expression. Fluorouracil 89-93 SRY-box transcription factor 2 Homo sapiens 118-122 25464567-8 2014 After reducing SOX2 expression, the sensitivity of Hep-2 cells to 5-FU and PTX were increased and the IC50 values for 48 h were decreased to 8.12 mug/ml and 5.16 mug/ml. Fluorouracil 66-70 SRY-box transcription factor 2 Homo sapiens 15-19 25464567-10 2014 CONCLUSION: Down-regulating the protein expression of SOX2 by RNAi will significantly enhance the sensitivity of human laryngeal epithelial cells Hep-2 to 5-FU and PTX. Fluorouracil 155-159 SRY-box transcription factor 2 Homo sapiens 54-58 24981311-0 2014 VEGFR-3 and CXCR4 as predictive markers for treatment with fluorouracil, leucovorin plus either oxaliplatin or cisplatin in patients with advanced esophagogastric cancer: a comparative study of the Arbeitsgemeinschaft Internistische Onkologie (AIO). Fluorouracil 59-71 fms related receptor tyrosine kinase 4 Homo sapiens 0-7 25199288-9 2014 According to the results of Immunohistochemistry and Real-time PCR, the expressions of PCNA protein, P53, Cyclin D1 and CDK4 proteins and mRNAs of the medication administration groups are decreased obviously compared with negative control group (P < 0.05), expressions of P21 proteins are higher than negative control group (P < 0.05), the expressions of related genes mRNA and proteins changes are more remarkable in high dose of 5-FU combined SJAMP group (P < 0.05). Fluorouracil 437-441 proliferating cell nuclear antigen Mus musculus 87-91 25199288-10 2014 CONCLUSION: SJAMP and 5-FU can via decrease the expressions of PCNA protein, P53, Cyclin D1 and CDK4 proteins and mRNAs, increase the expressions of P21 proteins and mRNAs, to inhibit the growth of H22 tumor in mice. Fluorouracil 22-26 proliferating cell nuclear antigen Mus musculus 63-67 25199288-10 2014 CONCLUSION: SJAMP and 5-FU can via decrease the expressions of PCNA protein, P53, Cyclin D1 and CDK4 proteins and mRNAs, increase the expressions of P21 proteins and mRNAs, to inhibit the growth of H22 tumor in mice. Fluorouracil 22-26 cyclin D1 Mus musculus 82-91 25199288-10 2014 CONCLUSION: SJAMP and 5-FU can via decrease the expressions of PCNA protein, P53, Cyclin D1 and CDK4 proteins and mRNAs, increase the expressions of P21 proteins and mRNAs, to inhibit the growth of H22 tumor in mice. Fluorouracil 22-26 cyclin-dependent kinase inhibitor 1A (P21) Mus musculus 149-152 24751000-3 2014 METHODS: To elucidate the mechanisms of variations to 5-FU outcome, the authors investigated MTHFR, DHFR, TYMS and SLC19A1 folate genes expression for 5-FU response in laryngeal cancer cell line (Hep-2). Fluorouracil 151-155 methylenetetrahydrofolate reductase Homo sapiens 93-98 24618665-2 2014 The present study investigates the prognostic and predictive value of dCK and HuR expression levels for sensitivity to gemcitabine and 5-fluorouracil (5-FU) in a large phase III adjuvant trial with chemoradiation backbone in pancreatic ductal adenocarcinoma (PDA). Fluorouracil 135-149 Calcium/calmodulin-dependent protein kinase II Drosophila melanogaster 70-73 24618665-2 2014 The present study investigates the prognostic and predictive value of dCK and HuR expression levels for sensitivity to gemcitabine and 5-fluorouracil (5-FU) in a large phase III adjuvant trial with chemoradiation backbone in pancreatic ductal adenocarcinoma (PDA). Fluorouracil 151-155 Calcium/calmodulin-dependent protein kinase II Drosophila melanogaster 70-73 24618665-8 2014 Studies in cultured cells confirmed that dCK expression rendered cells more sensitive to 5-FU. Fluorouracil 89-93 Calcium/calmodulin-dependent protein kinase II Drosophila melanogaster 41-44 24618665-13 2014 This dual-institutional follow up study, in a multi-institutional PDA randomized clinical trial, observed that dCK expression levels were prognostic and had predictive value for sensitivity to 5-FU. Fluorouracil 193-197 Calcium/calmodulin-dependent protein kinase II Drosophila melanogaster 111-114 24992758-8 2014 Serum levels of TNF-alpha, IL-2, and IFN-gamma, frequencies of CD4 + and CD8+ T cells in the spleen, and splenic NK and CTL activities were also significantly increased in mice treated with 5-FU+PL or 5-FU+PTM compared with mice treated with 5-FU alone (P < 0.05). Fluorouracil 190-194 CD4 antigen Mus musculus 63-66 24648345-1 2014 Dihydropyrimidine dehydrogenase (DPD) is the initial and rate-limiting enzyme of the uracil catabolic pathway, being critically important for inactivation of the commonly prescribed anti-cancer drug 5-fluorouracil (5-FU). Fluorouracil 199-213 dihydropyrimidine dehydrogenase Homo sapiens 0-31 24648345-1 2014 Dihydropyrimidine dehydrogenase (DPD) is the initial and rate-limiting enzyme of the uracil catabolic pathway, being critically important for inactivation of the commonly prescribed anti-cancer drug 5-fluorouracil (5-FU). Fluorouracil 199-213 dihydropyrimidine dehydrogenase Homo sapiens 33-36 24648345-1 2014 Dihydropyrimidine dehydrogenase (DPD) is the initial and rate-limiting enzyme of the uracil catabolic pathway, being critically important for inactivation of the commonly prescribed anti-cancer drug 5-fluorouracil (5-FU). Fluorouracil 215-219 dihydropyrimidine dehydrogenase Homo sapiens 0-31 24648345-1 2014 Dihydropyrimidine dehydrogenase (DPD) is the initial and rate-limiting enzyme of the uracil catabolic pathway, being critically important for inactivation of the commonly prescribed anti-cancer drug 5-fluorouracil (5-FU). Fluorouracil 215-219 dihydropyrimidine dehydrogenase Homo sapiens 33-36 24648345-2 2014 DPD impairment leads to increased exposure to 5-FU and, in turn, increased anabolism of 5-FU to cytotoxic nucleotides, resulting in more severe clinical adverse effects. Fluorouracil 46-50 dihydropyrimidine dehydrogenase Homo sapiens 0-3 24648345-2 2014 DPD impairment leads to increased exposure to 5-FU and, in turn, increased anabolism of 5-FU to cytotoxic nucleotides, resulting in more severe clinical adverse effects. Fluorouracil 88-92 dihydropyrimidine dehydrogenase Homo sapiens 0-3 24648345-4 2014 To identify DPYD variants that alter enzyme function, we expressed 80 protein-coding variants in an isogenic mammalian system and measured their capacities to convert 5-FU to dihydro-fluorouracil, the product of DPD catabolism. Fluorouracil 167-171 dihydropyrimidine dehydrogenase Homo sapiens 12-16 24648345-10 2014 These data strongly suggest that testing for the reported deficient DPYD variations could dramatically improve predictive genetic tests for 5-FU sensitivity, especially in individuals of non-European descent. Fluorouracil 140-144 dihydropyrimidine dehydrogenase Homo sapiens 68-72 24604396-9 2014 Furthermore, pretreatment of the SW620 cells with 5-FU inhibited the expression of beta1,3-N-acetylglucosaminyltransferase-8 (beta3Gn-T8) and cluster of differentiation (CD)147 in a time-dependent manner. Fluorouracil 50-54 UDP-GlcNAc:betaGal beta-1,3-N-acetylglucosaminyltransferase 8 Homo sapiens 83-124 24604396-9 2014 Furthermore, pretreatment of the SW620 cells with 5-FU inhibited the expression of beta1,3-N-acetylglucosaminyltransferase-8 (beta3Gn-T8) and cluster of differentiation (CD)147 in a time-dependent manner. Fluorouracil 50-54 UDP-GlcNAc:betaGal beta-1,3-N-acetylglucosaminyltransferase 8 Homo sapiens 126-136 24772313-2 2014 In order to reveal the effects of smoking and alcohol consumption on the 5-fluorouracil (5-FU)-related metabolic enzymes, namely thymidylate synthase, dihydropyrimidine dehydrogenase (DPD; a sole catabolic enzyme of 5-FU), orotate phosphoribosyl transferase (OPRT) and thymidine phosphorylase, in oral squamous cell carcinomas, the mRNA expression of these enzymes was investigated in 29 surgical specimens and compared by the Brinkman index and drinking years. Fluorouracil 89-93 dihydropyrimidine dehydrogenase Homo sapiens 151-182 24772313-2 2014 In order to reveal the effects of smoking and alcohol consumption on the 5-fluorouracil (5-FU)-related metabolic enzymes, namely thymidylate synthase, dihydropyrimidine dehydrogenase (DPD; a sole catabolic enzyme of 5-FU), orotate phosphoribosyl transferase (OPRT) and thymidine phosphorylase, in oral squamous cell carcinomas, the mRNA expression of these enzymes was investigated in 29 surgical specimens and compared by the Brinkman index and drinking years. Fluorouracil 89-93 dihydropyrimidine dehydrogenase Homo sapiens 184-187 24772313-6 2014 DPD is the initial and rate-limiting enzyme in the catabolic pathway of 5-FU. Fluorouracil 72-76 dihydropyrimidine dehydrogenase Homo sapiens 0-3 24772313-7 2014 Therefore, smoking and alcohol consumption may reduce the anticancer activity of 5-FU, possibly through the induction of DPD activity. Fluorouracil 81-85 dihydropyrimidine dehydrogenase Homo sapiens 121-124 24627042-0 2014 The BRCA2 gene is a potential molecular target during 5-fluorouracil therapy in human oral cancer cells. Fluorouracil 54-68 BRCA2 DNA repair associated Homo sapiens 4-9 24627042-7 2014 It was found that BRCA2 was involved in such repair, and may be effectively targeted to inhibit the repair of 5-FU-induced damage. Fluorouracil 110-114 BRCA2 DNA repair associated Homo sapiens 18-23 24627042-8 2014 Observations showed that knockdown of BRCA2 using small interference RNA suppression increased the sensitivity to 5-FU of human oral cancer cell lines (SAS and HSC3). Fluorouracil 114-118 BRCA2 DNA repair associated Homo sapiens 38-43 24627042-9 2014 These findings suggest that downregulation of BRCA2 may be useful for sensitizing tumor cells during 5-FU chemotherapy. Fluorouracil 101-105 BRCA2 DNA repair associated Homo sapiens 46-51 24764659-5 2014 The CRYSTAL study showed that adding cetuximab to FOLFIRI (regimen of irinotecan, infusional fluorouracil and leucovorin) significantly improved results in the first-line treatment of KRAS wild-type mCRC. Fluorouracil 93-105 KRAS proto-oncogene, GTPase Homo sapiens 184-188 24700034-3 2014 The patient was found to be heterozygous for a mutation, DPD IVS14+1G>A, leading to the severe toxicity exhibited following this regimen caused by delayed metabolism of 5-FU. Fluorouracil 172-176 dihydropyrimidine dehydrogenase Homo sapiens 57-60 24692733-0 2014 Multicenter phase II study of second-line cetuximab plus folinic acid/5-fluorouracil/irinotecan (FOLFIRI) in KRAS wild-type metastatic colorectal cancer: the FLIER study. Fluorouracil 70-84 KRAS proto-oncogene, GTPase Homo sapiens 109-113 24692733-1 2014 BACKGROUND: This study was the first multicenter phase II study of cetuximab plus folinic acid/5-fluorouracil/irinotecan (FOLFIRI) in KRAS wild-type mCRC as a second-line treatment in Japan including BRAF and PIK3CA genotyping. Fluorouracil 95-109 KRAS proto-oncogene, GTPase Homo sapiens 134-138 24535229-10 2014 Following treatment with the COX-2 inhibitor and 5-FU, the OPRT expression was upregulated and the DPD expression was downregulated in the resistant cells. Fluorouracil 49-53 dihydropyrimidine dehydrogenase Homo sapiens 99-102 24249161-0 2014 MicroRNA-23a antisense enhances 5-fluorouracil chemosensitivity through APAF-1/caspase-9 apoptotic pathway in colorectal cancer cells. Fluorouracil 32-46 microRNA 23a Homo sapiens 0-12 24249161-2 2014 The microRNA-23a (miR-23a)-regulated apoptosis in response to the 5-fluorouracil (5-FU)-induced mitochondria-mediated apoptotic pathway was determined in this study. Fluorouracil 66-80 microRNA 23a Homo sapiens 4-16 24249161-2 2014 The microRNA-23a (miR-23a)-regulated apoptosis in response to the 5-fluorouracil (5-FU)-induced mitochondria-mediated apoptotic pathway was determined in this study. Fluorouracil 66-80 microRNA 23a Homo sapiens 18-25 24249161-2 2014 The microRNA-23a (miR-23a)-regulated apoptosis in response to the 5-fluorouracil (5-FU)-induced mitochondria-mediated apoptotic pathway was determined in this study. Fluorouracil 82-86 microRNA 23a Homo sapiens 4-16 24249161-2 2014 The microRNA-23a (miR-23a)-regulated apoptosis in response to the 5-fluorouracil (5-FU)-induced mitochondria-mediated apoptotic pathway was determined in this study. Fluorouracil 82-86 microRNA 23a Homo sapiens 18-25 24249161-3 2014 The miR-23a expression in 5-FU-treated and untreated colon cancer cells and tissues was assessed using real-time PCR analysis. Fluorouracil 26-30 microRNA 23a Homo sapiens 4-11 24249161-4 2014 To determine the function of miR-23a in the regulation of 5-FU-induced apoptosis, cell-proliferation, cytotoxicity, and apoptosis analyses were performed. Fluorouracil 58-62 microRNA 23a Homo sapiens 29-36 24249161-7 2014 A xenograft tumor model was established to evaluate the biological relevance of altered miR-23a expression to the 5-FU-based chemotherapy in vivo. Fluorouracil 114-118 microRNA 23a Homo sapiens 88-95 24249161-8 2014 We found that the expression of miR-23a was increased and the level of apoptosis-activating factor-1 (APAF-1) was decreased in 5-FU-treated colon cancer cells compared to untreated cells. Fluorouracil 127-131 microRNA 23a Homo sapiens 32-39 24249161-11 2014 The overexpression of miR-23a antisense up-regulated the 5-FU induced apoptosis in colon cancer cells. Fluorouracil 57-61 microRNA 23a Homo sapiens 22-29 24249161-13 2014 This study shows that miR-23a antisense enhanced 5-FU-induced apoptosis in colorectal cancer cells through the APAF-1/caspase-9 apoptotic pathway. Fluorouracil 49-53 microRNA 23a Homo sapiens 22-29 23529007-8 2014 In subgroup meta-analysis, the higher incidence of diarrhoea in UGT1A1*28/*28 patients was limited to studies where when IRI was given at higher doses (OR=2.37, 95% CI: 1.39-4.04; P=0.002) or combined with 5-fluorouracil (FU or analogue) (OR=1.78, 95% CI: 1.16-2.75; P=0.009). Fluorouracil 206-220 UDP glucuronosyltransferase family 1 member A1 Homo sapiens 64-70 23529007-10 2014 IRI-combined 5-FU (or analogue) and a high-dose IRI therapy enhance IRI-induced diarrhoea among patients bearing the UGT1A1*28 allele. Fluorouracil 13-17 UDP glucuronosyltransferase family 1 member A1 Homo sapiens 117-123 24362470-4 2014 Here, we found that colorectal cancer (CRC) cells treated with oxaliplatin (OXA) and/or 5-fluorouracil (5-Fu) released high levels of high-mobility group box 1 (HMGB1) and heat shock protein 70 (HSP70). Fluorouracil 88-102 heat shock protein family A (Hsp70) member 4 Homo sapiens 172-193 24362470-4 2014 Here, we found that colorectal cancer (CRC) cells treated with oxaliplatin (OXA) and/or 5-fluorouracil (5-Fu) released high levels of high-mobility group box 1 (HMGB1) and heat shock protein 70 (HSP70). Fluorouracil 88-102 heat shock protein family A (Hsp70) member 4 Homo sapiens 195-200 24401318-1 2014 Dihydropyrimidine dehydrogenase (DPD, encoded by DPYD) is the rate-limiting enzyme in the uracil catabolic pathway and has a pivotal role in the pharmacokinetics of the commonly prescribed anticancer drug 5-fluorouracil (5-FU). Fluorouracil 205-219 dihydropyrimidine dehydrogenase Homo sapiens 0-31 24401318-1 2014 Dihydropyrimidine dehydrogenase (DPD, encoded by DPYD) is the rate-limiting enzyme in the uracil catabolic pathway and has a pivotal role in the pharmacokinetics of the commonly prescribed anticancer drug 5-fluorouracil (5-FU). Fluorouracil 205-219 dihydropyrimidine dehydrogenase Homo sapiens 33-36 24401318-1 2014 Dihydropyrimidine dehydrogenase (DPD, encoded by DPYD) is the rate-limiting enzyme in the uracil catabolic pathway and has a pivotal role in the pharmacokinetics of the commonly prescribed anticancer drug 5-fluorouracil (5-FU). Fluorouracil 205-219 dihydropyrimidine dehydrogenase Homo sapiens 49-53 24401318-1 2014 Dihydropyrimidine dehydrogenase (DPD, encoded by DPYD) is the rate-limiting enzyme in the uracil catabolic pathway and has a pivotal role in the pharmacokinetics of the commonly prescribed anticancer drug 5-fluorouracil (5-FU). Fluorouracil 221-225 dihydropyrimidine dehydrogenase Homo sapiens 0-31 24401318-1 2014 Dihydropyrimidine dehydrogenase (DPD, encoded by DPYD) is the rate-limiting enzyme in the uracil catabolic pathway and has a pivotal role in the pharmacokinetics of the commonly prescribed anticancer drug 5-fluorouracil (5-FU). Fluorouracil 221-225 dihydropyrimidine dehydrogenase Homo sapiens 33-36 24401318-1 2014 Dihydropyrimidine dehydrogenase (DPD, encoded by DPYD) is the rate-limiting enzyme in the uracil catabolic pathway and has a pivotal role in the pharmacokinetics of the commonly prescribed anticancer drug 5-fluorouracil (5-FU). Fluorouracil 221-225 dihydropyrimidine dehydrogenase Homo sapiens 49-53 24401318-2 2014 Deficiency of DPD, whether due to inadequate expression or deleterious variants in DPYD, has been linked to severe toxic responses to 5-FU. Fluorouracil 134-138 dihydropyrimidine dehydrogenase Homo sapiens 83-87 24329577-6 2014 In conclusion, we show that nuclear-targeted 30 nm gold nanoparticles enhance 5-Fluorouracil drug efficacy in HSC-3 cells via regulation of the cell cycle, a chemosensitization technique that could potentially be expanded to different cell lines and different chemotherapies. Fluorouracil 78-92 DnaJ heat shock protein family (Hsp40) member B7 Homo sapiens 110-115 24342832-2 2014 The expression profiles of hypoxia-inducible factor-1alpha (HIF-1alpha) and pyruvate dehydrogenase kinase-1 (PDK-1) were analyzed in tissues from 10 patients with gastric cancer who had different responses to adjuvant 5-FU treatment. Fluorouracil 218-222 pyruvate dehydrogenase kinase 1 Homo sapiens 109-114 24342832-4 2014 The expression levels of HIF-1alpha and PDK-1 were both elevated in the tumor tissues relative to the normal gastric tissues of most patients who showed recurrence after adjuvant 5-FU treatment. Fluorouracil 179-183 pyruvate dehydrogenase kinase 1 Homo sapiens 40-45 24342832-6 2014 Moreover, the addition of 20mM DCA only increased the sensitivity of these cells to 5-FU under hypoxic conditions, and the resistance to 5-FU under hypoxia was also attenuated in PDK1 knockdown cell lines. Fluorouracil 137-141 pyruvate dehydrogenase kinase 1 Homo sapiens 179-183 24490800-1 2014 BACKGROUND: Methylentetrahydrofolate reductase (MTHFR) plays a major role in folate metabolism and consequently could be an important factor for the efficacy of a treatment with 5-fluorouracil. Fluorouracil 178-192 methylenetetrahydrofolate reductase Homo sapiens 12-46 24490800-1 2014 BACKGROUND: Methylentetrahydrofolate reductase (MTHFR) plays a major role in folate metabolism and consequently could be an important factor for the efficacy of a treatment with 5-fluorouracil. Fluorouracil 178-192 methylenetetrahydrofolate reductase Homo sapiens 48-53 24255072-11 2014 Compared with controls, CXCR4 cells showed increased sensitivity against 5-FU, whereas CXCR7 cells were more chemoresistant. Fluorouracil 73-77 C-X-C motif chemokine receptor 4 Homo sapiens 24-29 24396484-3 2014 The present study revealed that the expression levels of the three antitumor miRNAs, miR-122a, miR-145 and miR-205, were significantly elevated in MDA-MB-453 LAR-type TNBC tumor cells treated with 5-fluorouracil together with ixabepilone. Fluorouracil 197-211 microRNA 122 Homo sapiens 85-93 25227787-0 2014 Overcoming 5-Fu resistance of colon cells through inhibition of Glut1 by the specific inhibitor WZB117. Fluorouracil 11-15 solute carrier family 2 member 1 Homo sapiens 64-69 25227787-7 2014 RESULTS: We found that 5-Fu resistance was associated with the overexpression of Glut1 in colon cancer cells. Fluorouracil 23-27 solute carrier family 2 member 1 Homo sapiens 81-86 25227787-8 2014 5-Fu treatment at low toxic concentration induced Glut1 expression. Fluorouracil 0-4 solute carrier family 2 member 1 Homo sapiens 50-55 25227787-10 2014 Importantly, inhibition of Glut1 by a specific inhibitor, WZB117, significantly increased the sensitivity of 5-Fu resistant cells to the drug. Fluorouracil 109-113 solute carrier family 2 member 1 Homo sapiens 27-32 25227787-12 2014 In particular it demonstrated that Glut1 inhibitors such as WZB117 may be considered an additional treatment options for patients with 5-Fu resistant colon cancers. Fluorouracil 135-139 solute carrier family 2 member 1 Homo sapiens 35-40 26330092-1 2014 Dihydropyrimidine dehydrogenase (DPD) is a metabolic enzyme that is crucial in 5-fluorouracil (5-FU) degradation. Fluorouracil 79-93 dihydropyrimidine dehydrogenase Homo sapiens 0-31 26330092-1 2014 Dihydropyrimidine dehydrogenase (DPD) is a metabolic enzyme that is crucial in 5-fluorouracil (5-FU) degradation. Fluorouracil 79-93 dihydropyrimidine dehydrogenase Homo sapiens 33-36 26330092-1 2014 Dihydropyrimidine dehydrogenase (DPD) is a metabolic enzyme that is crucial in 5-fluorouracil (5-FU) degradation. Fluorouracil 95-99 dihydropyrimidine dehydrogenase Homo sapiens 0-31 26330092-1 2014 Dihydropyrimidine dehydrogenase (DPD) is a metabolic enzyme that is crucial in 5-fluorouracil (5-FU) degradation. Fluorouracil 95-99 dihydropyrimidine dehydrogenase Homo sapiens 33-36 25316230-10 2014 CONCLUSIONS: These results suggest that polymorphisms of the MTHFR gene may be used as predictors of the response to fluorouracil-based chemotherapy for gastric cancer patients in Chinese population. Fluorouracil 117-129 methylenetetrahydrofolate reductase Homo sapiens 61-66 25316230-11 2014 Well-designed, comprehensive, and prospective studies on determining these polymorphisms of MTHFR gene as clinical markers for predicting the response to fluorouracil-based therapy in gastric cancer patients is warranted. Fluorouracil 154-166 methylenetetrahydrofolate reductase Homo sapiens 92-97 24817302-1 2014 AIM: We retrospectively investigated the relationship between IVS14+1 G > A genotype of the dihydropyrimidine dehydrogenase (DPD) gene with plasma concentration of 5-fluorouracil (5-FU) as well as adverse reactions in 80 patients with locally advanced or metastatic colorectal cancer. Fluorouracil 167-181 dihydropyrimidine dehydrogenase Homo sapiens 95-126 24817302-1 2014 AIM: We retrospectively investigated the relationship between IVS14+1 G > A genotype of the dihydropyrimidine dehydrogenase (DPD) gene with plasma concentration of 5-fluorouracil (5-FU) as well as adverse reactions in 80 patients with locally advanced or metastatic colorectal cancer. Fluorouracil 167-181 dihydropyrimidine dehydrogenase Homo sapiens 128-131 24817302-1 2014 AIM: We retrospectively investigated the relationship between IVS14+1 G > A genotype of the dihydropyrimidine dehydrogenase (DPD) gene with plasma concentration of 5-fluorouracil (5-FU) as well as adverse reactions in 80 patients with locally advanced or metastatic colorectal cancer. Fluorouracil 183-187 dihydropyrimidine dehydrogenase Homo sapiens 95-126 24817302-1 2014 AIM: We retrospectively investigated the relationship between IVS14+1 G > A genotype of the dihydropyrimidine dehydrogenase (DPD) gene with plasma concentration of 5-fluorouracil (5-FU) as well as adverse reactions in 80 patients with locally advanced or metastatic colorectal cancer. Fluorouracil 183-187 dihydropyrimidine dehydrogenase Homo sapiens 128-131 24817302-7 2014 Stepwise regression analysis showed that the plasma concentration of fluorouracil was associated with myelosuppression, hand-foot syndrome, diarrhea, overall survival (OS) and DPD genotype. Fluorouracil 69-81 dihydropyrimidine dehydrogenase Homo sapiens 176-179 24817302-9 2014 CONCLUSIONS: Among the advanced colorectal cancer patients receiving fluorouracil-based chemotherapy, those with plasma concentration of 5-FU above 26.83 mg/L can obtain better survival; for patients with heterozygous DPD IVS14+1 mutation, 5-FU dose should be appropriately reduced according to last plasma concentration to reduce adverse reactions, while the homozygous ones should avoid application of 5-FU and its derivatives. Fluorouracil 69-81 dihydropyrimidine dehydrogenase Homo sapiens 218-221 24817302-9 2014 CONCLUSIONS: Among the advanced colorectal cancer patients receiving fluorouracil-based chemotherapy, those with plasma concentration of 5-FU above 26.83 mg/L can obtain better survival; for patients with heterozygous DPD IVS14+1 mutation, 5-FU dose should be appropriately reduced according to last plasma concentration to reduce adverse reactions, while the homozygous ones should avoid application of 5-FU and its derivatives. Fluorouracil 137-141 dihydropyrimidine dehydrogenase Homo sapiens 218-221 24817302-9 2014 CONCLUSIONS: Among the advanced colorectal cancer patients receiving fluorouracil-based chemotherapy, those with plasma concentration of 5-FU above 26.83 mg/L can obtain better survival; for patients with heterozygous DPD IVS14+1 mutation, 5-FU dose should be appropriately reduced according to last plasma concentration to reduce adverse reactions, while the homozygous ones should avoid application of 5-FU and its derivatives. Fluorouracil 240-244 dihydropyrimidine dehydrogenase Homo sapiens 218-221 24817302-9 2014 CONCLUSIONS: Among the advanced colorectal cancer patients receiving fluorouracil-based chemotherapy, those with plasma concentration of 5-FU above 26.83 mg/L can obtain better survival; for patients with heterozygous DPD IVS14+1 mutation, 5-FU dose should be appropriately reduced according to last plasma concentration to reduce adverse reactions, while the homozygous ones should avoid application of 5-FU and its derivatives. Fluorouracil 240-244 dihydropyrimidine dehydrogenase Homo sapiens 218-221 24122835-6 2014 Knockdown of MAP3K3 expression in MAP3K3-amplified breast cancer cells sensitized breast cancer cells to apoptotic induction by TNFalpha and TRAIL, as well as doxorubicin, VP-16 and fluorouracil, three commonly used chemotherapeutic drugs for treating breast cancer. Fluorouracil 182-194 mitogen-activated protein kinase kinase kinase 3 Homo sapiens 13-19 24122835-6 2014 Knockdown of MAP3K3 expression in MAP3K3-amplified breast cancer cells sensitized breast cancer cells to apoptotic induction by TNFalpha and TRAIL, as well as doxorubicin, VP-16 and fluorouracil, three commonly used chemotherapeutic drugs for treating breast cancer. Fluorouracil 182-194 mitogen-activated protein kinase kinase kinase 3 Homo sapiens 34-40 24388031-0 2014 A DPYD variant (Y186C) specific to individuals of African descent in a patient with life-threatening 5-FU toxic effects: potential for an individualized medicine approach. Fluorouracil 101-105 dihydropyrimidine dehydrogenase Homo sapiens 2-6 24388031-2 2014 Severe toxic reactions to 5-FU have been associated with decreased levels of dihydropyrimidine dehydrogenase (DPD) enzyme activity. Fluorouracil 26-30 dihydropyrimidine dehydrogenase Homo sapiens 77-108 24388031-2 2014 Severe toxic reactions to 5-FU have been associated with decreased levels of dihydropyrimidine dehydrogenase (DPD) enzyme activity. Fluorouracil 26-30 dihydropyrimidine dehydrogenase Homo sapiens 110-113 24388031-4 2014 A variety of genetic variations in DPYD, the gene encoding DPD, are known to result in decreased DPD enzyme activity and to contribute to 5-FU toxic effects. Fluorouracil 138-142 dihydropyrimidine dehydrogenase Homo sapiens 35-39 24388031-4 2014 A variety of genetic variations in DPYD, the gene encoding DPD, are known to result in decreased DPD enzyme activity and to contribute to 5-FU toxic effects. Fluorouracil 138-142 dihydropyrimidine dehydrogenase Homo sapiens 59-62 24391839-9 2013 The elevated resistance of U87-MCSF cells towards 5-FU was due to the increase in the expressions (10.2 and 6 fold) of ABCB1 and mdm2, respectively. Fluorouracil 50-54 MDM2 proto-oncogene Homo sapiens 129-133 24391839-10 2013 Furthermore, increase in expressions of ABCG1, mdm2 and CD24 was also observed in U87MG cells after prolonged incubation with 5-FU. Fluorouracil 126-130 MDM2 proto-oncogene Homo sapiens 47-51 27478804-10 2016 Decreased proportions of autophagy and apoptosis were also observed in 5-FU treated SW742- and CHO-CEA transfectants. Fluorouracil 71-75 CEA cell adhesion molecule 3 Homo sapiens 99-102 24126887-7 2013 Western blot analysis showed that FGFR4 expression was weak in the 5-Fu-treated groups when compared with the control. Fluorouracil 67-71 fibroblast growth factor receptor 4 Homo sapiens 34-39 24126887-10 2013 Inhibition of the activity of FGFR4 may be the main mechanisms of PD effect while 5-Fu reduced FGFR4 expression. Fluorouracil 82-86 fibroblast growth factor receptor 4 Homo sapiens 95-100 23864195-0 2013 Knockdown of inhibitor of growth protein 2 inhibits cell invasion and enhances chemosensitivity to 5-FU in human gastric cancer cells. Fluorouracil 99-103 inhibitor of growth family member 2 Homo sapiens 13-42 23864195-2 2013 AIM: To investigate the effects of ING2 gene knockdown on chemosensitivity to 5-fluorouracil (5-FU) in human gastric cancer cells and its possible mechanisms. Fluorouracil 78-92 inhibitor of growth family member 2 Homo sapiens 35-39 23864195-2 2013 AIM: To investigate the effects of ING2 gene knockdown on chemosensitivity to 5-fluorouracil (5-FU) in human gastric cancer cells and its possible mechanisms. Fluorouracil 94-98 inhibitor of growth family member 2 Homo sapiens 35-39 23864195-8 2013 Furthermore, the suppression of ING2 could enhance the chemosensitivity of gastric cancer cells to 5-FU significantly. Fluorouracil 99-103 inhibitor of growth family member 2 Homo sapiens 32-36 23784051-0 2013 Overexpression of Lgr5 correlates with resistance to 5-FU-based chemotherapy in colorectal cancer. Fluorouracil 53-57 leucine rich repeat containing G protein-coupled receptor 5 Homo sapiens 18-22 23955475-4 2013 The codA-encoded enzyme converts nontoxic FC to toxic 5-fluorouracil, which is channeled into the metabolism by the uracil phosphoribosyltransferase, encoded by the chromosomal upp gene of Gluconobacter. Fluorouracil 54-68 plasmid maintenance protein CcdA Escherichia coli 4-8 23420533-7 2013 5-FU treatment resulted in a significant upregulation of NKG2D activating molecules (Rae-1 and H60) and DNAM-1 ligands (CD112 and CD155) on MC38 cells, but alpha-GalCer did not. Fluorouracil 0-4 killer cell lectin-like receptor subfamily K, member 1 Mus musculus 57-62 23420533-9 2013 The increase of the cytolytic activity induced by 5-FU partially depended on NKG2D-Rae-1 or H60 signals. Fluorouracil 50-54 killer cell lectin like receptor K1 Homo sapiens 77-88 23810214-7 2013 The modulation of Col-1, VEGF, TGF-beta1 and MMP-2 expression by triamcinolone and 5-fluorouracil alone or their combination varied between individual cell lines; the trend is to promote a reduction in Col-1 and TGF-beta1 but up-regulation of MMP-2 expression. Fluorouracil 83-97 matrix metallopeptidase 2 Homo sapiens 45-50 23810214-7 2013 The modulation of Col-1, VEGF, TGF-beta1 and MMP-2 expression by triamcinolone and 5-fluorouracil alone or their combination varied between individual cell lines; the trend is to promote a reduction in Col-1 and TGF-beta1 but up-regulation of MMP-2 expression. Fluorouracil 83-97 matrix metallopeptidase 2 Homo sapiens 243-248 23810214-8 2013 5-Fluorouracil played a predominant role in the combined treatment leading to more significant cell proliferation inhibition, apoptosis, Col-1 suppression and MMP-2 induction (p < 0.05). Fluorouracil 0-14 matrix metallopeptidase 2 Homo sapiens 159-164 23817620-0 2013 Histone deacetylase 4 mediates SMAD family member 4 deacetylation and induces 5-fluorouracil resistance in breast cancer cells. Fluorouracil 78-92 SMAD family member 4 Homo sapiens 31-35 23817620-12 2013 In addition, SMAD4 knockdown in MCF-7 cells increased 5-FU resistance. Fluorouracil 54-58 SMAD family member 4 Homo sapiens 13-18 23817620-13 2013 In summary, our data suggest that HDAC4-mediated deacetylation of the SMAD4 promoter may lead to 5-FU resistance in breast cancer cells. Fluorouracil 97-101 SMAD family member 4 Homo sapiens 70-75 24009080-6 2013 Furthermore, ectopic expression of c-Kit conferred resistance of colorectal cancer (CRC) cells to treatment with 5-fluorouracil (5-FU), whereas ectopic miR-34a sensitized the cells to 5-FU. Fluorouracil 184-188 microRNA 34a Homo sapiens 152-159 23908588-6 2013 In contrast, cisplatin and 5-fluorouracil (5-FU) treatment altered anti-DR5 binding only marginally. Fluorouracil 27-41 tumor necrosis factor receptor superfamily, member 10b Mus musculus 72-75 23908588-6 2013 In contrast, cisplatin and 5-fluorouracil (5-FU) treatment altered anti-DR5 binding only marginally. Fluorouracil 43-47 tumor necrosis factor receptor superfamily, member 10b Mus musculus 72-75 23729362-8 2013 Cell death of 5-fluorouracil (5FU)-treated p53-null GSK3B-silenced colon carcinoma cells occurred via PARP1-dependent and AIF-mediated but RIP1-independent necroptosis. Fluorouracil 30-33 glycogen synthase kinase 3 beta Homo sapiens 52-57 23861589-0 2013 Clinical significance of the thymidylate synthase, dihydropyrimidine dehydrogenase, and thymidine phosphorylase mRNA expressions in hepatocellular carcinoma patients receiving 5-fluorouracil-based transarterial chemoembolization treatment. Fluorouracil 176-190 thymidine phosphorylase Homo sapiens 88-111 23861589-1 2013 PURPOSE: To determine whether 5-fluorouracil (5-FU) sensitivity is associated with the mRNA expressions of thymidylate synthase (TS), dihydropyrimidine dehydrogenase (DPD), and thymidine phosphorylase (TP) in patients with hepatocellular carcinoma (HCC) treated with 5-FU-based transarterial chemoembolization (TACE). Fluorouracil 30-44 thymidine phosphorylase Homo sapiens 177-200 23435877-8 2013 Sorafenib (1 mumol/L) enhanced inhibitory efficacy of 5-FU on HCC cells in vitro, dropping IC50 of 5-FU from 167.7 +- 12.1 to 105.4 +- 8.4 mumol/L for PLC/PRF/5 and 115 +- 10.2 to 82 +- 7.4 mumol/L for SK-HEP-1 (both p < 0.01). Fluorouracil 54-58 perlecan (heparan sulfate proteoglycan 2) Mus musculus 151-154 22623155-11 2013 Furthermore, the treatment combining miR-34a with 5-FU significantly showed more efficient anti-tumor effects than single treatment of miR-34a or 5-FU. Fluorouracil 50-54 microRNA 34a Homo sapiens 135-142 23678290-0 2013 A novel aurora-A inhibitor, BPR1K0609S1, sensitizes colorectal tumor cells to 5-fluorofracil (5-FU) treatment. Fluorouracil 94-98 aurora kinase A Homo sapiens 8-16 23678290-8 2013 Significantly, 5-FU (5-fluorouracil) treatment further induces apoptosis of BP-resistant HCT116 deficient for Chk2 or Puma. Fluorouracil 15-19 checkpoint kinase 2 Homo sapiens 110-114 23678290-8 2013 Significantly, 5-FU (5-fluorouracil) treatment further induces apoptosis of BP-resistant HCT116 deficient for Chk2 or Puma. Fluorouracil 21-35 checkpoint kinase 2 Homo sapiens 110-114 23440340-9 2013 Cell cultures treated with 5-fluoro-uracil and cisplatin exhibited higher numbers of ALDH(high) cells. Fluorouracil 27-42 aldehyde dehydrogenase family 3, subfamily A1 Mus musculus 85-89 23386248-0 2013 Refining the UGT1A haplotype associated with irinotecan-induced hematological toxicity in metastatic colorectal cancer patients treated with 5-fluorouracil/irinotecan-based regimens. Fluorouracil 141-155 UDP glucuronosyltransferase family 1 member A complex locus Homo sapiens 13-18 22231565-2 2013 We hypothesized that gene expression levels and germline variations in CD133 will predict clinical outcome in patients with metastatic colorectal cancer (mCRC), treated in first-line setting with 5-fluorouracil, oxaliplatin and bevacizumab (BV), and we investigated whether there is a correlation with gene expression levels of CD133, vascular endothelial growth factor (VEGF) and its receptors. Fluorouracil 196-210 prominin 1 Homo sapiens 71-76 23608802-5 2013 The volumes of 5-FU converted from 5"-DFUR in media, where TP-transfected and parental LOVO were cultured, were detected by HPLC. Fluorouracil 15-19 thymidine phosphorylase Homo sapiens 59-61 23608802-10 2013 CONCLUSION: TP cDNA transfection into LOVO can up-regulate the TP mRNA and protein expressions, increase the 5-FU converted from 5"-DFUR, and enhance the cytotoxic effect of 5"-DFUR on the LOVO cells. Fluorouracil 109-113 thymidine phosphorylase Homo sapiens 12-14 23452395-10 2013 At the cytological level, SSX2IP stimulates the wound healing, metastasis and invasion of hepatoma cells, and reduces the sensitivity of hepatoma cells to 5-Fu and CDDP. Fluorouracil 155-159 synovial sarcoma, X 2 interacting protein Mus musculus 26-32 23253900-0 2013 SMUG1 but not UNG DNA glycosylase contributes to the cellular response to recovery from 5-fluorouracil induced replication stress. Fluorouracil 88-102 single-strand-selective monofunctional uracil-DNA glycosylase 1 Homo sapiens 0-5 23253900-5 2013 UNG and SMUG1 are the two human UDGs most likely to combat the genomic incorporation of uracil and 5-FU during replication. Fluorouracil 99-103 single-strand-selective monofunctional uracil-DNA glycosylase 1 Homo sapiens 8-13 23253900-8 2013 Loss of SMUG1 corresponded with >2-fold increase in sensitivity to 5-FU, but only with a 24h treatment followed by recovery. Fluorouracil 70-74 single-strand-selective monofunctional uracil-DNA glycosylase 1 Homo sapiens 8-13 23253900-11 2013 However, SMUG1-depleted cells showed a prolonged S-phase arrest, a transient increase in DNA double-strand breaks following 5-FU treatment and an altered phosphorylation of CHK1 following removal of drug. Fluorouracil 124-128 single-strand-selective monofunctional uracil-DNA glycosylase 1 Homo sapiens 9-14 23253900-12 2013 Collectively, the results suggest that SMUG1 has a role in the resumption of replication following 5-FU treatment. Fluorouracil 99-103 single-strand-selective monofunctional uracil-DNA glycosylase 1 Homo sapiens 39-44 23232555-2 2013 Various antimetabolites such as 5-fluorouracil often increase ENT1 activity and [(18)F]FLT uptake (flare) in spite of cell death. Fluorouracil 32-46 solute carrier family 29 member 1 (Augustine blood group) Homo sapiens 62-66 22370641-9 2013 In GC patients, WNT6 expression was positively associated with the tumor stage and the nodal status, and inversely correlated with the response to ECF (Epi, cisplatin, 5-fluorouracil) chemotherapy. Fluorouracil 168-182 Wnt family member 6 Homo sapiens 16-20 23457527-6 2013 Adenovirus-mediated transfer of TGFBR2 and EXT1 enhanced IFN-alpha/5-FU-induced cytotoxicity as well as 5-FU, although the overexpression of these genes in the absence of IFN-alpha/5-FU did not induce cell death. Fluorouracil 67-71 transforming growth factor beta receptor 2 Homo sapiens 32-38 23457527-6 2013 Adenovirus-mediated transfer of TGFBR2 and EXT1 enhanced IFN-alpha/5-FU-induced cytotoxicity as well as 5-FU, although the overexpression of these genes in the absence of IFN-alpha/5-FU did not induce cell death. Fluorouracil 67-71 exostosin glycosyltransferase 1 Homo sapiens 43-47 23457527-6 2013 Adenovirus-mediated transfer of TGFBR2 and EXT1 enhanced IFN-alpha/5-FU-induced cytotoxicity as well as 5-FU, although the overexpression of these genes in the absence of IFN-alpha/5-FU did not induce cell death. Fluorouracil 104-108 transforming growth factor beta receptor 2 Homo sapiens 32-38 23457527-6 2013 Adenovirus-mediated transfer of TGFBR2 and EXT1 enhanced IFN-alpha/5-FU-induced cytotoxicity as well as 5-FU, although the overexpression of these genes in the absence of IFN-alpha/5-FU did not induce cell death. Fluorouracil 104-108 exostosin glycosyltransferase 1 Homo sapiens 43-47 23457527-6 2013 Adenovirus-mediated transfer of TGFBR2 and EXT1 enhanced IFN-alpha/5-FU-induced cytotoxicity as well as 5-FU, although the overexpression of these genes in the absence of IFN-alpha/5-FU did not induce cell death. Fluorouracil 104-108 transforming growth factor beta receptor 2 Homo sapiens 32-38 23457527-6 2013 Adenovirus-mediated transfer of TGFBR2 and EXT1 enhanced IFN-alpha/5-FU-induced cytotoxicity as well as 5-FU, although the overexpression of these genes in the absence of IFN-alpha/5-FU did not induce cell death. Fluorouracil 104-108 exostosin glycosyltransferase 1 Homo sapiens 43-47 23099809-1 2012 BACKGROUND: The aim of this study was to investigate the value of the cyclin D1 isoforms D1a and D1b as prognostic factors and their relevance as predictors of response to adjuvant chemotherapy with 5-fluorouracil and levamisole (5-FU/LEV) in colorectal cancer (CRC). Fluorouracil 230-234 cyclin D1 Homo sapiens 70-79 23239440-8 2012 SCF/TGF-beta ratio increased in both the young and aged mice after 5-FU treatment. Fluorouracil 67-71 transforming growth factor, beta 1 Mus musculus 4-12 23160694-1 2012 BACKGROUND: Thymidine phosphorylase (TYMP) is an angiogenic factor that has potent chemotactic activity for endothelial cells and is involved in 5-fluorouracil (5-FU) metabolism. Fluorouracil 145-159 thymidine phosphorylase Homo sapiens 12-35 23160694-1 2012 BACKGROUND: Thymidine phosphorylase (TYMP) is an angiogenic factor that has potent chemotactic activity for endothelial cells and is involved in 5-fluorouracil (5-FU) metabolism. Fluorouracil 145-159 thymidine phosphorylase Homo sapiens 37-41 23160694-1 2012 BACKGROUND: Thymidine phosphorylase (TYMP) is an angiogenic factor that has potent chemotactic activity for endothelial cells and is involved in 5-fluorouracil (5-FU) metabolism. Fluorouracil 161-165 thymidine phosphorylase Homo sapiens 12-35 23160694-1 2012 BACKGROUND: Thymidine phosphorylase (TYMP) is an angiogenic factor that has potent chemotactic activity for endothelial cells and is involved in 5-fluorouracil (5-FU) metabolism. Fluorouracil 161-165 thymidine phosphorylase Homo sapiens 37-41 22989419-6 2012 Knockdown of PTK6 enhances apoptosis in HCT116 cells with wild-type p53, following treatment of cells with gamma-radiation, doxorubicin, or 5-fluorouracil. Fluorouracil 140-154 protein tyrosine kinase 6 Homo sapiens 13-17 22955854-7 2012 Pre-miR144 treatment and the resultant repression of ZFX in GC cell lines moderately upregulated their susceptibility to 5-fluorouracil chemotherapy. Fluorouracil 121-135 zinc finger protein X-linked Homo sapiens 53-56 22252525-8 2012 In conclusion, our results demonstrate that knockdown of PAK1 could enhance the chemosensitivity of CRCs to 5-fluorouracil through G1 arrest. Fluorouracil 108-122 p21 (RAC1) activated kinase 1 Homo sapiens 57-61 22261621-5 2012 An in vivo nude mouse xenograft assay was performed to assess the effects of Survivin knockdown on regulation of the sensitivity of SGC7901 cells to irradiation, cisplatin or 5-FU treatment. Fluorouracil 175-179 baculoviral IAP repeat-containing 5 Mus musculus 77-85 22261621-7 2012 The same is true for cisplatin- and 5-FU-treated tumor cells, ie, colony formation and cell viability of the survivin-knocked down SGC7901 cells were reduced, while apoptosis was induced compared with the control cells. Fluorouracil 36-40 baculoviral IAP repeat-containing 5 Mus musculus 109-117 22261621-9 2012 CONCLUSIONS: Knockdown of survivin expression enhanced sensitivity of gastric cancer cells to radiation, cisplatin and 5-FU treatment in vitro and in nude mice. Fluorouracil 119-123 baculoviral IAP repeat-containing 5 Mus musculus 26-34 22716215-11 2012 The combination of 5-FU and chloroquine induced G1 arrest, up-regulation of p27 and p53, and down-regulation of CDK2 and cyclin D1. Fluorouracil 19-23 cyclin dependent kinase 2 Homo sapiens 112-116 22716215-11 2012 The combination of 5-FU and chloroquine induced G1 arrest, up-regulation of p27 and p53, and down-regulation of CDK2 and cyclin D1. Fluorouracil 19-23 cyclin D1 Homo sapiens 121-130 21601882-0 2012 CD133(-) cells, derived from a single human colon cancer cell line, are more resistant to 5-fluorouracil (FU) than CD133(+) cells, dependent on the beta1-integrin signaling. Fluorouracil 90-104 prominin 1 Homo sapiens 0-5 21601882-4 2012 On the other hand, CD133(-) cells were more resistant to 5-fluorouracil (FU) treatment than CD133(+) cells, and it was found to be dependent on the higher expression of ss1-integrins, and consequently, higher ability to bind collagen. Fluorouracil 57-71 prominin 1 Homo sapiens 19-24 22611193-5 2012 Instead, hematopoietic Cx43 (H-Cx43) deficiency delays hematopoietic recovery after myeloablation with 5-fluorouracil (5-FU). Fluorouracil 103-117 gap junction protein alpha 1 Homo sapiens 23-27 22611193-5 2012 Instead, hematopoietic Cx43 (H-Cx43) deficiency delays hematopoietic recovery after myeloablation with 5-fluorouracil (5-FU). Fluorouracil 119-123 gap junction protein alpha 1 Homo sapiens 23-27 22611193-6 2012 5-FU-treated H-Cx43-deficient HSC and progenitors (HSC/P) cells display decreased survival and fail to enter the cell cycle to proliferate. Fluorouracil 0-4 gap junction protein alpha 1 Homo sapiens 15-19 21487682-7 2012 RESULTS: Under normoxic conditions, clusterin overexpressing cells were more sensitive to FOLFOX treatment (p = 0.01); under 3% and 1% hypoxic conditions, overexpressing clusterin cells were more sensitive to 5-FU, oxaliplatin and FOLFOX, p values <0.05 for all conditions. Fluorouracil 209-213 clusterin Homo sapiens 170-179 22403796-0 2012 Potential role of the NADPH oxidase NOX1 in the pathogenesis of 5-fluorouracil-induced intestinal mucositis in mice. Fluorouracil 64-78 NADPH oxidase 1 Mus musculus 36-40 22403796-2 2012 In the present study, we investigated the role of NOX1 in the pathogenesis of intestinal mucositis induced by the cancer chemotherapeutic agent 5-fluorouracil (5-FU) in mice. Fluorouracil 144-158 NADPH oxidase 1 Mus musculus 50-54 22403796-7 2012 Furthermore, the 5-FU-mediated upregulation of TNF-alpha, IL-1beta, and NOX1 and the production of reactive oxygen species were significantly attenuated in Nox1KO mice compared with that in WT mice. Fluorouracil 17-21 NADPH oxidase 1 Mus musculus 72-76 22403796-8 2012 These findings suggest that NOX1 plays an important role in the pathogenesis of 5-FU-induced intestinal mucositis. Fluorouracil 80-84 NADPH oxidase 1 Mus musculus 28-32 22403796-9 2012 NOX1-derived ROS production following administration of 5-FU may promote the apoptotic response through upregulation of inflammatory cytokines. Fluorouracil 56-60 NADPH oxidase 1 Mus musculus 0-4 22421942-0 2012 5-Fluorouracil and interferon-alpha immunochemotherapy enhances immunogenicity of murine pancreatic cancer through upregulation of NKG2D ligands and MHC class I. Pancreatic cancer has the poorest prognosis of all gastrointestinal cancers, driving the need for new therapeutic approaches. Fluorouracil 0-14 killer cell lectin-like receptor subfamily K, member 1 Mus musculus 131-136 22189143-0 2012 Treatment of prostate carcinoma with (galectin-3)-targeted HPMA copolymer-(G3-C12)-5-Fluorouracil conjugates. Fluorouracil 83-97 galectin 3 Homo sapiens 38-48 22189143-5 2012 Compared with non-targeted conjugates (P-Fu), Gal-3-targeted HPMA copolymer-(G3-C12)-5-Fu conjugates (P-(G3-C12)-Fu) displayed a superior intracellular internalization followed by enhanced cytotoxicity and apoptosis-induction. Fluorouracil 85-89 galectin 3 Homo sapiens 46-51 22076044-1 2012 Yeast cytosine deaminase (yCD) is a well-characterized prodrug/enzyme system that converts 5-fluorocytosine (5-FC) to 5-fluorouracil (5-FU), and has been combined with oncolytic viruses. Fluorouracil 118-132 cytosine deaminase Saccharomyces cerevisiae S288C 6-24 22076044-1 2012 Yeast cytosine deaminase (yCD) is a well-characterized prodrug/enzyme system that converts 5-fluorocytosine (5-FC) to 5-fluorouracil (5-FU), and has been combined with oncolytic viruses. Fluorouracil 134-138 cytosine deaminase Saccharomyces cerevisiae S288C 6-24 22780970-5 2012 The cells were treated with chemotherapeutic agent 5-Fu to observe whether Bcl-w protein-silecing affects the pro-apoptotic effect of 5-Fu. Fluorouracil 134-138 BCL2 like 2 Homo sapiens 75-80 22780970-10 2012 However, compared with the 5-Fu group, the apoptosis in HuTu-80 cells was effectively enhanced after combination treatment with Bcl-w siRNA and 5-Fu (45.7+-2.1)% vs. (71.6+-3.2)% (P<0.05). Fluorouracil 27-31 BCL2 like 2 Homo sapiens 128-133 22780970-12 2012 Down-regulation of Bcl-w protein in small intestine adenocarcinoma HuTu-80 cells leads them susceptible to 5-Fu. Fluorouracil 107-111 BCL2 like 2 Homo sapiens 19-24 22117060-0 2012 DNA methylation-regulated miR-193a-3p dictates resistance of hepatocellular carcinoma to 5-fluorouracil via repression of SRSF2 expression. Fluorouracil 89-103 serine and arginine rich splicing factor 2 Homo sapiens 122-127 22117060-4 2012 In turn, SRSF2 preferentially up-regulates the proapoptotic splicing form of caspase 2 (CASP2L) and sensitizes HCC cells to 5-FU. Fluorouracil 124-128 serine and arginine rich splicing factor 2 Homo sapiens 9-14 22117060-7 2012 This newly identified miR-193a-3p-SRSF2 axis highlights a new set of companion diagnostics required for optimal 5-FU therapy of HCC, which involve assaying both the DNA methylation state of the miR-193a gene and the expression of miR-193a-3p and SRSF2 and the relative level of the proapoptotic versus antiapoptotic splicing forms of caspase 2 in clinical samples. Fluorouracil 112-116 serine and arginine rich splicing factor 2 Homo sapiens 34-39 22117060-7 2012 This newly identified miR-193a-3p-SRSF2 axis highlights a new set of companion diagnostics required for optimal 5-FU therapy of HCC, which involve assaying both the DNA methylation state of the miR-193a gene and the expression of miR-193a-3p and SRSF2 and the relative level of the proapoptotic versus antiapoptotic splicing forms of caspase 2 in clinical samples. Fluorouracil 112-116 serine and arginine rich splicing factor 2 Homo sapiens 246-251 22186294-6 2012 Immunohistochemistry, RT-PCR and TUNEL assay showed that p65 siRNA downregulated the expression of p65 and enhanced the sensitivity of EC9706 cells to 5-FU treatment in vivo. Fluorouracil 151-155 RELA proto-oncogene, NF-kB subunit Homo sapiens 57-60 22208667-1 2012 Yeast cytosine deaminase (yCD) catalyzes the hydrolytic deamination of cytosine to uracil as well as the deamination of the prodrug 5-fluorocytosine (5FC) to the anticancer drug 5-fluorouracil. Fluorouracil 178-192 cytosine deaminase Saccharomyces cerevisiae S288C 6-24 21947305-0 2012 miRNA-195 sensitizes human hepatocellular carcinoma cells to 5-FU by targeting BCL-w. Fluorouracil 61-65 BCL2 like 2 Homo sapiens 91-96 22590561-4 2012 RESULTS: Administration of 5-FU but not pemetrexed potentiated CXCL8 secretion and increased CXCR1 and CXCR2 gene expression in metastatic PC3 cells. Fluorouracil 27-31 C-X-C motif chemokine receptor 2 Homo sapiens 103-108 22590561-5 2012 Consistent with this, the inhibition of CXCL8 signaling using a CXCR2 antagonist, AZ10397767, increased the cytotoxicity of 5-FU by 4-fold (P<0.001), and increased 5-FU-induced apoptosis in PC3 cells (P<0.01). Fluorouracil 124-128 C-X-C motif chemokine receptor 2 Homo sapiens 64-69 22590561-5 2012 Consistent with this, the inhibition of CXCL8 signaling using a CXCR2 antagonist, AZ10397767, increased the cytotoxicity of 5-FU by 4-fold (P<0.001), and increased 5-FU-induced apoptosis in PC3 cells (P<0.01). Fluorouracil 167-171 C-X-C motif chemokine receptor 2 Homo sapiens 64-69 22479651-8 2012 We show that treatment of HeLa and HepG2 cells with MMS, Cisplatin and Doxorubicin lead to rapid proteolysis of Cdt1, whereas treatment with 5-Fluorouracil and Tamoxifen leave Cdt1 expression unaffected. Fluorouracil 141-155 chromatin licensing and DNA replication factor 1 Homo sapiens 176-180 21855639-1 2011 Uridine phosphorylase (UPP) catalyzes the reversible conversion of uridine to uracil and ribose-1-phosphate and plays an important pharmacological role in activating fluoropyrimidine nucleoside chemotherapeutic agents such as 5-fluorouracil and capecitabine. Fluorouracil 226-240 uridine phosphorylase 1 Homo sapiens 23-26 21836633-0 2011 An oncolytic adenovirus defective in pRb-binding (dl922-947) can efficiently eliminate pancreatic cancer cells and tumors in vivo in combination with 5-FU or gemcitabine. Fluorouracil 150-154 RB transcriptional corepressor 1 Homo sapiens 37-40 21707510-10 2011 Furthermore, treatment with 5-FU chemotherapy combined with INT2-31 resulted in a synergistic increase in apoptosis and decrease in tumor growth compared to 5-FU or INT2-31 alone. Fluorouracil 28-32 fibroblast growth factor 3 Homo sapiens 165-169 21707510-10 2011 Furthermore, treatment with 5-FU chemotherapy combined with INT2-31 resulted in a synergistic increase in apoptosis and decrease in tumor growth compared to 5-FU or INT2-31 alone. Fluorouracil 157-161 fibroblast growth factor 3 Homo sapiens 60-64 21116627-2 2011 Recent studies have suggested that MRP5 conferred resistance to first-line drugs 5-fluorouracil and gemcitabine by active efflux of drugs from the cell. Fluorouracil 81-95 ATP binding cassette subfamily C member 5 Homo sapiens 35-39 21116627-8 2011 In the proliferation assays, curcumin caused a concentration-dependant increase in the sensitivity to the cytotoxic drug 5-fluorouracil in HEK293/MRP5 cells, PANC-1 and MiaPaCa-2 pancreatic cancer cells, but not in parental HEK293 cells. Fluorouracil 121-135 ATP binding cassette subfamily C member 5 Homo sapiens 146-150 21674128-3 2011 The pattern of DNA damage checkpoint activation in bolus 5-FU-treated HT29 (TP53-deficient/MMR-proficient) cultures suggested SSB formation (CHEK1 activation) followed by DSB formation (CHEK2 activation and increased phospho-H2AX levels), but no cell death suggested that DNA repair capacity was not overwhelmed. Fluorouracil 57-61 checkpoint kinase 2 Homo sapiens 186-191 21674128-3 2011 The pattern of DNA damage checkpoint activation in bolus 5-FU-treated HT29 (TP53-deficient/MMR-proficient) cultures suggested SSB formation (CHEK1 activation) followed by DSB formation (CHEK2 activation and increased phospho-H2AX levels), but no cell death suggested that DNA repair capacity was not overwhelmed. Fluorouracil 57-61 H2A.X variant histone Homo sapiens 225-229 21674128-4 2011 High-dose 5-FU treatment led to activation of ATM/CHEK2/TP53 (not CHEK1) in TP53-proficient and TP53-depleted HCT116 (later CHEK2 activation relative to TP53-proficient) cultures; HCT15 cultures had ATM activation only. Fluorouracil 10-14 checkpoint kinase 2 Homo sapiens 50-55 21674128-4 2011 High-dose 5-FU treatment led to activation of ATM/CHEK2/TP53 (not CHEK1) in TP53-proficient and TP53-depleted HCT116 (later CHEK2 activation relative to TP53-proficient) cultures; HCT15 cultures had ATM activation only. Fluorouracil 10-14 checkpoint kinase 2 Homo sapiens 124-129 21674128-8 2011 Overall, activation of ATM, CHEK1 and/or CHEK2 and phospho-H2AX levels reflected the nature of 5-FU-induced DNA damage and indi-cated when DNA damage was significant (5-FU-dose-dependent). Fluorouracil 95-99 checkpoint kinase 2 Homo sapiens 41-46 21674128-8 2011 Overall, activation of ATM, CHEK1 and/or CHEK2 and phospho-H2AX levels reflected the nature of 5-FU-induced DNA damage and indi-cated when DNA damage was significant (5-FU-dose-dependent). Fluorouracil 95-99 H2A.X variant histone Homo sapiens 59-63 21674128-8 2011 Overall, activation of ATM, CHEK1 and/or CHEK2 and phospho-H2AX levels reflected the nature of 5-FU-induced DNA damage and indi-cated when DNA damage was significant (5-FU-dose-dependent). Fluorouracil 167-171 H2A.X variant histone Homo sapiens 59-63 21596996-3 2011 The present investigation was undertaken to examine whether Slfn-3 plays a role in regulating differentiation of FOLFOX-resistant (5-fluorouracil + oxaliplatin) colon cancer cells that are highly enriched in cancer stem cells (CSCs). Fluorouracil 131-145 schlafen family member 12 Homo sapiens 60-66 21624362-5 2011 There was a correlation between the expression of ZNF689 and an anticancer drug 5-fluorouracil (5-FU) resistance of HCC cells. Fluorouracil 80-94 zinc finger protein 689 Homo sapiens 50-56 21624362-5 2011 There was a correlation between the expression of ZNF689 and an anticancer drug 5-fluorouracil (5-FU) resistance of HCC cells. Fluorouracil 96-100 zinc finger protein 689 Homo sapiens 50-56 21624362-8 2011 Taken together, our results indicate that ZNF689 blocks pro-apoptotic signaling by suppressing the Bak/Bax/Bid pathway, resulting in the progression of liver cancer and resistance to 5-FU. Fluorouracil 183-187 zinc finger protein 689 Homo sapiens 42-48 21709442-4 2011 DR5, Fas, Bax, Bad, Puma and Bnip3L were induced by 5-FU and adriamycin (ADR) in HCT116 cells in a p53-dependent manner. Fluorouracil 52-56 tumor necrosis factor receptor superfamily, member 10b Mus musculus 0-3 21555373-2 2011 Previously we showed that Par-4-overexpressing colon cancer cells responded more readily to 5-fluorouracil (5-FU) than their wild-type counterparts. Fluorouracil 92-106 PRKC, apoptosis, WT1, regulator Mus musculus 26-31 21555373-2 2011 Previously we showed that Par-4-overexpressing colon cancer cells responded more readily to 5-fluorouracil (5-FU) than their wild-type counterparts. Fluorouracil 108-112 PRKC, apoptosis, WT1, regulator Mus musculus 26-31 21444628-8 2011 Combined treatment with 5-FU could decrease cisplatin-induced ERK1/2 activation and the induction of TS and TP, which subsequently resulted in synergistic cytotoxic effects. Fluorouracil 24-28 thymidine phosphorylase Homo sapiens 108-110 21444628-9 2011 Enforced expression of constitutive active MKK1/2 vectors rescued the protein levels of phospho-ERK1/2, TS, and TP, and the cell viability that were decreased by cisplatin and 5-FU combination. Fluorouracil 176-180 thymidine phosphorylase Homo sapiens 112-114 21737644-8 2011 On 5-FU treatment, phosphorylation of Akt and Erk1/2 was suppressed in CT26/NK4 less than in mock-transfected cells. Fluorouracil 3-7 mitogen-activated protein kinase 3 Mus musculus 46-52 21455575-4 2011 Furthermore, 5-FU inhibited the phosphorylation of Akt and p70 S6K, while the knockdown of IGFBP3 reduced the levels of poly (ADP-ribose) polymerase cleaved by 5-FU in PC3 cells. Fluorouracil 160-164 keratin 6A Homo sapiens 168-171 21455575-5 2011 Therefore, the up-regulation of IGFBP3 by 5-FU not only inhibits cell growth by reducing the IGF1 signal but also induces apoptosis in PC3 cells. Fluorouracil 42-46 keratin 6A Homo sapiens 135-138 21605422-10 2011 Allopurinol, an inhibitor of xanthine oxidoreductase that converts xanthine to uric acid, blocked uric acid production, MICA/B expression, and sensitivity to NK-92 cell killing toward a PANC-1 cancer cell line exposed to radiation and two genotoxic drugs, gemcitabine and 5-fluorouracil. Fluorouracil 272-286 xanthine dehydrogenase Homo sapiens 29-52 21350194-6 2011 Elf4-null mice exhibited enhanced recovery of bone marrow CD45- CD31+ endothelial cells and sinusoidal blood vessels following administration of 5-fluorouracil. Fluorouracil 145-159 E74-like factor 4 (ets domain transcription factor) Mus musculus 0-4 21325880-4 2011 Specific inhibition of early autophagy induction with siRNA targeted to Beclin 1 and ATG7 significantly enhanced the effect of 5-FU and reduced the recovery of drug-treated cells. Fluorouracil 127-131 autophagy related 7 Homo sapiens 85-89 21415167-7 2011 Most interestingly, orexin-A also promoted robust apoptosis in cells that are resistant to the most commonly used drug in colon cancer chemotherapy, 5-fluorouracil. Fluorouracil 149-163 hypocretin Mus musculus 20-28 21756828-1 2011 OBJECTIVE: To investigate the relationship between the expression of thymidine phosphorylase (TP) and the sensitivity of gastric carcinoma to 5-fluorouracil (5-FU) and its prodrugs. Fluorouracil 142-156 thymidine phosphorylase Homo sapiens 69-92 21756828-1 2011 OBJECTIVE: To investigate the relationship between the expression of thymidine phosphorylase (TP) and the sensitivity of gastric carcinoma to 5-fluorouracil (5-FU) and its prodrugs. Fluorouracil 142-156 thymidine phosphorylase Homo sapiens 94-96 21756828-1 2011 OBJECTIVE: To investigate the relationship between the expression of thymidine phosphorylase (TP) and the sensitivity of gastric carcinoma to 5-fluorouracil (5-FU) and its prodrugs. Fluorouracil 158-162 thymidine phosphorylase Homo sapiens 69-92 21756828-1 2011 OBJECTIVE: To investigate the relationship between the expression of thymidine phosphorylase (TP) and the sensitivity of gastric carcinoma to 5-fluorouracil (5-FU) and its prodrugs. Fluorouracil 158-162 thymidine phosphorylase Homo sapiens 94-96 21544729-7 2011 Immunofluorescence assay and Western blot showed that 5-FU induced the expression of EBV-lytic genes including BZLF1, BRLF1, BMRF1 and BHRF1. Fluorouracil 54-58 BMRF1 Human gammaherpesvirus 4 125-130 21068133-12 2011 Furthermore, an adenoviral vector containing short hairpin RNAs against CHD1L (CHD1L-shRNAs) could suppress cell growth, clonogenicity and chemoresistance to 5-FU. Fluorouracil 158-162 chromodomain helicase DNA binding protein 1 like Homo sapiens 72-77 21161336-5 2011 RESULTS: We observed that CDF together with 5-FU + Ox were more potent than curcumin in reducing CD44 and CD166 in chemo-resistant colon cancer cells, accompanied by inhibition of growth, induction of apoptosis and disintegration of colonospheres. Fluorouracil 44-48 activated leukocyte cell adhesion molecule Homo sapiens 106-111 21661452-0 2011 PinX1 gene transfection enhances the sensitivity of gastric carcinoma cell line to 5-fluorouracil. Fluorouracil 83-97 PIN2 (TERF1) interacting telomerase inhibitor 1 Homo sapiens 0-5 21661452-8 2011 PinX1 gene transfection enhanced the sensitivity of MKN28 cells to 5-fluorouracil (p<0.05). Fluorouracil 67-81 PIN2 (TERF1) interacting telomerase inhibitor 1 Homo sapiens 0-5 20597995-8 2010 These results support the idea that isolating survivin and MRP5+ CTCs may help in the selection of metastatic colorectal cancer patients resistant to standard 5-FU and L-OHP based chemotherapy, for which alternative regimens may be appropriate. Fluorouracil 159-163 ATP binding cassette subfamily C member 5 Homo sapiens 59-63 20367642-6 2010 We found that the DNA-damaging reagent 5-fluorouracil (5-FU) increased TLR3 mRNA expression and potentiated poly I:C-induced apoptosis in HCT116 p53(+/+) cells but had only minimal effect in p53(-/-) cells, indicating a p53-dependent pathway. Fluorouracil 39-53 toll like receptor 3 Homo sapiens 71-75 20367642-6 2010 We found that the DNA-damaging reagent 5-fluorouracil (5-FU) increased TLR3 mRNA expression and potentiated poly I:C-induced apoptosis in HCT116 p53(+/+) cells but had only minimal effect in p53(-/-) cells, indicating a p53-dependent pathway. Fluorouracil 55-59 toll like receptor 3 Homo sapiens 71-75 19904749-0 2010 The effect of focal adhesion kinase gene silencing on 5-fluorouracil chemosensitivity involves an Akt/NF-kappaB signaling pathway in colorectal carcinomas. Fluorouracil 54-68 protein tyrosine kinase 2 Homo sapiens 14-35 19904749-9 2010 Knockdown of FAK reversed the formation and aggregation of MCSs, significantly decreased the 50% inhibitory concentration of 5-FU, and markedly increased MCS culture cells apoptosis. Fluorouracil 125-129 protein tyrosine kinase 2 Homo sapiens 13-16 19904749-11 2010 These results indicate that suppressing FAK expression potentiated 5-FU-induced cytotoxicity and contributed to its chemosensitizing effect by suppressing Akt/NF-kappaB signaling in colon carcinoma MCS culture cells. Fluorouracil 67-71 protein tyrosine kinase 2 Homo sapiens 40-43 20482226-9 2010 The experimental results demonstrated that FAM46A, IL18, CCL28, TNF, CXCL2, PLEKHA8, HRAS, FDXR, and CHI3L1 genes showed statistically significant differential expression between primary breast cancer culture cells that respond and nonrespond to 5-FU. Fluorouracil 246-250 terminal nucleotidyltransferase 5A Homo sapiens 43-49 20226755-2 2010 The human UP type 1 (hUP1) is a molecular target for the design of inhibitors intended to boost endogenous uridine levels to rescue normal tissues from the toxicity of fluoropyrimidine nucleoside chemotherapeutic agents, such as capecitabine and 5-fluorouracil. Fluorouracil 246-260 heterogeneous nuclear ribonucleoprotein A1 Homo sapiens 21-25 20031193-3 2010 Recent studies showed that the thymidylate synthase inhibitor 5-fluorouracil (5-FU) affects polyamine metabolism in colon carcinoma cells through the induction of the key catabolic enzyme spermidine/spermine N1-acetyltransferase (SSAT). Fluorouracil 62-76 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 230-234 20031193-3 2010 Recent studies showed that the thymidylate synthase inhibitor 5-fluorouracil (5-FU) affects polyamine metabolism in colon carcinoma cells through the induction of the key catabolic enzyme spermidine/spermine N1-acetyltransferase (SSAT). Fluorouracil 78-82 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 188-228 20031193-3 2010 Recent studies showed that the thymidylate synthase inhibitor 5-fluorouracil (5-FU) affects polyamine metabolism in colon carcinoma cells through the induction of the key catabolic enzyme spermidine/spermine N1-acetyltransferase (SSAT). Fluorouracil 78-82 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 230-234 20433755-0 2010 Prostate apoptosis response protein 4 sensitizes human colon cancer cells to chemotherapeutic 5-FU through mediation of an NF kappaB and microRNA network. Fluorouracil 94-98 pro-apoptotic WT1 regulator Homo sapiens 0-37 20433755-5 2010 Overexpression augmented the interaction of Par-4 with NF kappaB in the cytosol but not nucleus, and facilitated apoptosis in the presence of 5-fluorouracil (5-FU). Fluorouracil 142-156 pro-apoptotic WT1 regulator Homo sapiens 44-49 20433755-5 2010 Overexpression augmented the interaction of Par-4 with NF kappaB in the cytosol but not nucleus, and facilitated apoptosis in the presence of 5-fluorouracil (5-FU). Fluorouracil 158-162 pro-apoptotic WT1 regulator Homo sapiens 44-49 20433755-15 2010 Treating Par-4-overexpressing HT29 cells with a miR-34a antagomir functionally reversed both BCL2 down-regulation and apoptosis by 5-FU. Fluorouracil 131-135 pro-apoptotic WT1 regulator Homo sapiens 9-14 20433755-15 2010 Treating Par-4-overexpressing HT29 cells with a miR-34a antagomir functionally reversed both BCL2 down-regulation and apoptosis by 5-FU. Fluorouracil 131-135 microRNA 34a Homo sapiens 48-55 20433755-16 2010 Conversely, bypassing Par-4 overexpression by direct knockdown of DROSHA expression in native HT29 cells increased miR-34a expression and 5-FU sensitivity. Fluorouracil 138-142 pro-apoptotic WT1 regulator Homo sapiens 22-27 20355241-6 2010 siRNA also reduced the ability of TP to resist hypoxia-induced apoptosis, while suppression of TP reduced the sensitivity of KKU-M139 to 5-fluorouracil. Fluorouracil 137-151 thymidine phosphorylase Homo sapiens 95-97 20355241-7 2010 CONCLUSION: Inhibition of TP may be beneficial in decreasing angiogenesis-dependent growth and migration of cholangiocarcinoma but may diminish the response to 5-fluorouracil chemotherapy. Fluorouracil 160-174 thymidine phosphorylase Homo sapiens 26-28 22966291-3 2010 We focused on thymidine phosphorylase (TP), an enzyme metabolizing 5"-DFUR, an intermediate of capecitabine, to 5-fluorouracil in order to investigate the application of well-known therapeutics for TNBC. Fluorouracil 112-126 thymidine phosphorylase Homo sapiens 14-37 22966291-3 2010 We focused on thymidine phosphorylase (TP), an enzyme metabolizing 5"-DFUR, an intermediate of capecitabine, to 5-fluorouracil in order to investigate the application of well-known therapeutics for TNBC. Fluorouracil 112-126 thymidine phosphorylase Homo sapiens 39-41 22966307-0 2010 Influence of 5-fluorouracil on ferredoxin reductase mRNA splice variants in colorectal carcinomas. Fluorouracil 13-27 ferredoxin reductase Homo sapiens 31-51 22966307-2 2010 Recently, it has been shown that mRNA and protein levels of the ferredoxin reductase gene (gene, FDXR; protein, FR) increase drastically after 5-FU treatment in various cell lines including colorectal cancer. Fluorouracil 143-147 ferredoxin reductase Homo sapiens 64-84 22966307-2 2010 Recently, it has been shown that mRNA and protein levels of the ferredoxin reductase gene (gene, FDXR; protein, FR) increase drastically after 5-FU treatment in various cell lines including colorectal cancer. Fluorouracil 143-147 ferredoxin reductase Homo sapiens 97-101 19845688-5 2010 After treatment with 5-FU, the normally proliferating tracheal epithelium desquamated and only a few cells in G0 phase of the cell cycle were left on the basement membrane and Oct3/4, Nanog and Sox2 could be observed at this time. Fluorouracil 21-25 Nanog homeobox Rattus norvegicus 184-189 19845688-8 2010 CONCLUSIONS: G0 phase cells with resistance to 5-FU damage expressed Oct3/4, Nanog and Sox2. Fluorouracil 47-51 Nanog homeobox Rattus norvegicus 77-82 20159707-0 2010 [Survivin antisense oligodeoxynucleotides inhibits the proliferation of hepatocellular carcinoma cells and enhances 5-FU sensitivity]. Fluorouracil 116-120 baculoviral IAP repeat-containing 5 Mus musculus 1-9 20159707-1 2010 OBJECTIVE: To investigate the inhibitory effect of survivin antisense oligodeoxynuleotides (ASODN) mediated by polyethylenimine (PEI) on hepatocelluar carcinoma SMMC-7721 cell proliferation and its effect on chemosensitivity to 5-FU in tumor-bearing mice. Fluorouracil 228-232 baculoviral IAP repeat-containing 5 Mus musculus 51-59 20356498-8 2010 5-FU (10 mg/L, 48 h) and bleomycin (100 mg/L, 48 h) also induced BIC RNA up-regulation (5.2 +/- 1.1 vs 1.7 +/- 0.7, 11.5 +/- 0.7 vs 1.7 +/- 0.7, both P < 0.05). Fluorouracil 0-4 MIR155 host gene Homo sapiens 65-68 19879751-8 2010 IFN-lambda1 produced combinatory anti-tumour effects with chemotherapeutic agents, cisplatin (CDDP) and 5-fluorouracil (5-FU), in IFN-lambda1-sensitive oesophageal carcinoma cells but not in normal or Het-1A cells, while IFN-alpha achieved the combinatory suppressive effects to normal cells. Fluorouracil 104-118 interferon lambda 1 Homo sapiens 0-11 19879751-8 2010 IFN-lambda1 produced combinatory anti-tumour effects with chemotherapeutic agents, cisplatin (CDDP) and 5-fluorouracil (5-FU), in IFN-lambda1-sensitive oesophageal carcinoma cells but not in normal or Het-1A cells, while IFN-alpha achieved the combinatory suppressive effects to normal cells. Fluorouracil 104-118 interferon lambda 1 Homo sapiens 130-141 19948396-7 2010 And indeed, different miRNAs have been found to predict sensitivity to anticancer treatment: miR-30c, miR-130a and miR-335 are downregulated in various chemoresistant cell lines, hsa-Let-7g and hsa-miR-181b are strongly associated with response to 5-fluorouracil-based antimetabolite S-1. Fluorouracil 248-262 microRNA 30c-1 Homo sapiens 93-100 19948396-7 2010 And indeed, different miRNAs have been found to predict sensitivity to anticancer treatment: miR-30c, miR-130a and miR-335 are downregulated in various chemoresistant cell lines, hsa-Let-7g and hsa-miR-181b are strongly associated with response to 5-fluorouracil-based antimetabolite S-1. Fluorouracil 248-262 microRNA 130a Homo sapiens 102-110 19948396-7 2010 And indeed, different miRNAs have been found to predict sensitivity to anticancer treatment: miR-30c, miR-130a and miR-335 are downregulated in various chemoresistant cell lines, hsa-Let-7g and hsa-miR-181b are strongly associated with response to 5-fluorouracil-based antimetabolite S-1. Fluorouracil 248-262 microRNA 335 Homo sapiens 115-122 19928967-4 2009 The combinatory use of AE and 5-fluorouracil (5-Fu) achieved significantly more cell death in A431 and SCC25 cells than only the use of AE or 5-Fu, likely via regulation of caspase-8, -9, and -3 expressions. Fluorouracil 30-44 caspase 8 Homo sapiens 173-194 19928967-4 2009 The combinatory use of AE and 5-fluorouracil (5-Fu) achieved significantly more cell death in A431 and SCC25 cells than only the use of AE or 5-Fu, likely via regulation of caspase-8, -9, and -3 expressions. Fluorouracil 46-50 caspase 8 Homo sapiens 173-194 19731257-3 2009 The dependence of p53-mediated chemosensitivity on pRb status was first investigated in a prospective study on the prognostic relevance of p53 in breast cancer patients treated with adjuvant chemotherapy (5-fluorouracil, methotrexate and cyclophosphamide). Fluorouracil 205-219 RB transcriptional corepressor 1 Homo sapiens 51-54 19731257-6 2009 We then studied the role of pRb status in the p53-mediated response to 5-fluorouracil and methotrexate or doxorubicin treatment in three human cancer cell lines. Fluorouracil 71-85 RB transcriptional corepressor 1 Homo sapiens 28-31 19846930-0 2009 Effects of 5-FU on DNA synthesis and cytotoxicity of human lymphocytes induced by IL-2, TGF-beta3 and PGE2. Fluorouracil 11-15 transforming growth factor beta 3 Homo sapiens 88-97 19846930-2 2009 MATERIALS AND METHODS: We explored 2.5 microM 5-FU-induced DNA synthesis by testing 5-FU activity in hypoxanthine-aminopterin-thymidine (HAT)-containing medium, and its effect on thymidylate synthase (TS) activity and CD25 expression in interleukin (IL)-2-activated human peripheral blood mononuclear cells (PBMCs) and the combined effects with prostaglandin E(2) (PGE(2)) and transforming growth factor (TGF)-beta3. Fluorouracil 46-50 interleukin 2 receptor subunit alpha Homo sapiens 218-222 19846930-2 2009 MATERIALS AND METHODS: We explored 2.5 microM 5-FU-induced DNA synthesis by testing 5-FU activity in hypoxanthine-aminopterin-thymidine (HAT)-containing medium, and its effect on thymidylate synthase (TS) activity and CD25 expression in interleukin (IL)-2-activated human peripheral blood mononuclear cells (PBMCs) and the combined effects with prostaglandin E(2) (PGE(2)) and transforming growth factor (TGF)-beta3. Fluorouracil 46-50 transforming growth factor beta 3 Homo sapiens 377-415 19846936-9 2009 Moreover, the addition of either of the GSH modulators to 5-FU produced an increase of nearly 40% in the 5-FU activity in the case of HGF or VEGF, and a 25% increase in the case of EGF. Fluorouracil 58-62 hepatocyte growth factor Homo sapiens 134-137 19846936-9 2009 Moreover, the addition of either of the GSH modulators to 5-FU produced an increase of nearly 40% in the 5-FU activity in the case of HGF or VEGF, and a 25% increase in the case of EGF. Fluorouracil 105-109 hepatocyte growth factor Homo sapiens 134-137 19605487-0 2009 Hepatitis C virus core protein and cellular protein HAX-1 promote 5-fluorouracil-mediated hepatocyte growth inhibition. Fluorouracil 66-80 HCLS1 associated protein X-1 Homo sapiens 52-57 19605487-9 2009 Further, 5-FU-mediated p53 expression was reduced with concurrent HAX-1 suppression in core- or polyprotein-expressing cells compared to control HepG2 cells, and caspase-2 and -7 activities were diminished. Fluorouracil 9-13 HCLS1 associated protein X-1 Homo sapiens 66-71 19605487-11 2009 These observations underscore an association between HCV core and HAX-1, which promotes 5-FU mediated p53-dependent caspase-7 activation and hepatocyte growth inhibition. Fluorouracil 88-92 HCLS1 associated protein X-1 Homo sapiens 66-71 19542220-7 2009 Treatment of p53 mutant colon cancer cells with 5-FU led to an elongated G1 in a Mirk-dependent manner, as G1 was shortened by ectopic overexpression of cyclin D1 mutated at the Mirk phosphorylation site (T288A), but not by wild-type cyclin D1. Fluorouracil 48-52 cyclin D1 Homo sapiens 153-162 19542220-7 2009 Treatment of p53 mutant colon cancer cells with 5-FU led to an elongated G1 in a Mirk-dependent manner, as G1 was shortened by ectopic overexpression of cyclin D1 mutated at the Mirk phosphorylation site (T288A), but not by wild-type cyclin D1. Fluorouracil 48-52 cyclin D1 Homo sapiens 234-243 19698236-4 2009 In cultured cell lines, hormone or its inhibitor such as corticosteroid, tamoxifen, forskolin, phenylephrine, inflammatory factors such as IFNgamma and TNFalpha, and chemotherapeutics 5-fluorouracil could down-regulate the lrp16 gene expression as compared with absent ones. Fluorouracil 184-198 mono-ADP ribosylhydrolase 1 Homo sapiens 223-228 18820913-0 2009 Role of BCRP as a biomarker for predicting resistance to 5-fluorouracil in breast cancer. Fluorouracil 57-71 ATP binding cassette subfamily G member 2 (Junior blood group) Mus musculus 8-12 18820913-6 2009 The suspicious substrate [5-fluorouracil (5-Fu)] was further confirmed in PA317 and breast cancer cell MCF-7 by HLCP, apoptosis assay (staining and FACS) and RNAi technique. Fluorouracil 26-40 acyl-CoA synthetase long-chain family member 1 Mus musculus 148-152 18820913-6 2009 The suspicious substrate [5-fluorouracil (5-Fu)] was further confirmed in PA317 and breast cancer cell MCF-7 by HLCP, apoptosis assay (staining and FACS) and RNAi technique. Fluorouracil 42-46 acyl-CoA synthetase long-chain family member 1 Mus musculus 148-152 18820913-7 2009 RESULTS: Mitoxantrone, 5-Fu, adriamycin, Methotrexate, Pirarubicin, and Etoposide were identified as substrates of BCRP. Fluorouracil 23-27 ATP binding cassette subfamily G member 2 (Junior blood group) Mus musculus 115-119 18820913-9 2009 5-Fu was identified as substrate of BCRP for the first time. Fluorouracil 0-4 ATP binding cassette subfamily G member 2 (Junior blood group) Mus musculus 36-40 18820913-10 2009 The further study showed that the intracellular retention dose of 5-Fu and the 5-Fu induced cellular apoptosis all decreased when BCRP highly expressed. Fluorouracil 66-70 ATP binding cassette subfamily G member 2 (Junior blood group) Mus musculus 130-134 18820913-10 2009 The further study showed that the intracellular retention dose of 5-Fu and the 5-Fu induced cellular apoptosis all decreased when BCRP highly expressed. Fluorouracil 79-83 ATP binding cassette subfamily G member 2 (Junior blood group) Mus musculus 130-134 18820913-11 2009 Furthermore, 5-Fu accumulation and 5-Fu induced DNA damage increased when BCRP was silenced by RNAi in breast cancer cells. Fluorouracil 13-17 ATP binding cassette subfamily G member 2 (Junior blood group) Mus musculus 74-78 18820913-11 2009 Furthermore, 5-Fu accumulation and 5-Fu induced DNA damage increased when BCRP was silenced by RNAi in breast cancer cells. Fluorouracil 35-39 ATP binding cassette subfamily G member 2 (Junior blood group) Mus musculus 74-78 18820913-12 2009 CONCLUSIONS: 5-Fluorouracil may be a specific substrate which can be bound by BCRP. Fluorouracil 13-27 ATP binding cassette subfamily G member 2 (Junior blood group) Mus musculus 78-82 18820913-13 2009 BCRP can predict the sensitivity of breast cancer to 5-Fu. Fluorouracil 53-57 ATP binding cassette subfamily G member 2 (Junior blood group) Mus musculus 0-4 18820913-14 2009 And BCRP-targeted therapy will reverse the resistance of breast cancer to 5-Fu. Fluorouracil 74-78 ATP binding cassette subfamily G member 2 (Junior blood group) Mus musculus 4-8 19383845-6 2009 Moreover, treatment of nude mice bearing a 5-FU-resistant tumor, characterized by decreased levels of UMP kinase (UMPK), with DAC overcame resistance to bolus 5-FU. Fluorouracil 43-47 uridine-cytidine kinase 1 Mus musculus 102-112 19383845-6 2009 Moreover, treatment of nude mice bearing a 5-FU-resistant tumor, characterized by decreased levels of UMP kinase (UMPK), with DAC overcame resistance to bolus 5-FU. Fluorouracil 43-47 uridine-cytidine kinase 1 Mus musculus 114-118 19383845-6 2009 Moreover, treatment of nude mice bearing a 5-FU-resistant tumor, characterized by decreased levels of UMP kinase (UMPK), with DAC overcame resistance to bolus 5-FU. Fluorouracil 159-163 uridine-cytidine kinase 1 Mus musculus 114-118 19383845-7 2009 DAC-mediated restoration of 5-FU sensitivity was associated with increases in UMPK levels. Fluorouracil 28-32 uridine-cytidine kinase 1 Mus musculus 78-82 19402749-6 2009 Hence, excision of 5-FU by TDG, but not by other UDGs (UNG2 and SMUG1), prevents efficient downstream processing of the repair intermediate, thereby mediating DNA-directed cytotoxicity. Fluorouracil 19-23 single-strand-selective monofunctional uracil-DNA glycosylase 1 Homo sapiens 64-69 19097688-0 2009 Andrographolide enhances 5-fluorouracil-induced apoptosis via caspase-8-dependent mitochondrial pathway involving p53 participation in hepatocellular carcinoma (SMMC-7721) cells. Fluorouracil 25-39 caspase 8 Homo sapiens 62-71 19097688-8 2009 Surprisingly, the addition of ANDRO to 5-FU induces synergistic apoptosis, which could be corroborated to the increased caspase-8, p53 activity and the significant changes of Bax conformation in these cells, resulting in increased losses of mitochondrial membrane potential, increased release of cytochrome c, and activation of caspase-9 and caspase-3. Fluorouracil 39-43 caspase 8 Homo sapiens 120-129 19097688-9 2009 Suppression of caspase-8 with the specific inhibitor z-IETD-fmk abrogates largely ANDRO/5-FU biological activity by preventing mitochondrial membrane potential disappearance, caspase-3,9 activation and subsequent apoptosis. Fluorouracil 88-92 caspase 8 Homo sapiens 15-24 19147571-3 2009 We then report that chemotherapy induces Notch-1, as oxaliplatin, 5-fluorouracil (5-FU), or SN-38 (the active metabolite of irinotecan) induced Notch-1 intracellular domain (NICD) protein and activated Hes-1. Fluorouracil 66-80 hes family bHLH transcription factor 1 Homo sapiens 202-207 17063488-2 2007 In the present study, we explored the involvement of p53 in the promoter activation of Gadd45alpha as well as the role of Gadd45alpha in carboplatin (Carb) or 5-fluorouracil (5-FU)-induced apoptosis in human papillomavirus virus (HPV)-positive HEp-2 and HeLa cells. Fluorouracil 175-179 growth arrest and DNA damage inducible alpha Homo sapiens 122-133 17063488-3 2007 We report that Carb or 5-FU upregulate Gadd45alpha and p53 in both these cells. Fluorouracil 23-27 growth arrest and DNA damage inducible alpha Homo sapiens 39-50 17159505-3 2007 Using the SNU-719 gastric cancer cell line, which is naturally infected with Epstein-Barr virus, we found that the chemotherapeutic agents, such as 5-fluorouracil, cis-platinum and taxol, induced the expressions of BMRF1, BZLF1 and BRLF1 proteins that are usually found in the lytic form of the virus. Fluorouracil 148-162 BMRF1 Human gammaherpesvirus 4 215-220 17237273-3 2007 SSAT was shown to be inducible in response to 5-fluorouracil (5-FU) or oxaliplatin in parental and drug-resistant HCT116 cell lines. Fluorouracil 46-60 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 0-4 17237273-3 2007 SSAT was shown to be inducible in response to 5-fluorouracil (5-FU) or oxaliplatin in parental and drug-resistant HCT116 cell lines. Fluorouracil 62-66 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 0-4 16528528-0 2006 Gene expression of ferredoxin reductase predicts outcome in patients with metastatic colorectal cancer treated by 5-fluorouracil plus leucovorin. Fluorouracil 114-128 ferredoxin reductase Homo sapiens 19-39 16528528-1 2006 PURPOSE: Ferredoxin reductase (FDXR) is a putative contributor to p53-mediated apoptosis from 5-fluorouracil (5-FU) through the generation of oxidative stress in the mitochondria. Fluorouracil 94-108 ferredoxin reductase Homo sapiens 9-29 16528528-1 2006 PURPOSE: Ferredoxin reductase (FDXR) is a putative contributor to p53-mediated apoptosis from 5-fluorouracil (5-FU) through the generation of oxidative stress in the mitochondria. Fluorouracil 94-108 ferredoxin reductase Homo sapiens 31-35 16528528-1 2006 PURPOSE: Ferredoxin reductase (FDXR) is a putative contributor to p53-mediated apoptosis from 5-fluorouracil (5-FU) through the generation of oxidative stress in the mitochondria. Fluorouracil 110-114 ferredoxin reductase Homo sapiens 9-29 16528528-1 2006 PURPOSE: Ferredoxin reductase (FDXR) is a putative contributor to p53-mediated apoptosis from 5-fluorouracil (5-FU) through the generation of oxidative stress in the mitochondria. Fluorouracil 110-114 ferredoxin reductase Homo sapiens 31-35 16528528-3 2006 The aim of this study is to investigate the association between FDXR gene expressions and the clinical outcome when treated by 5-FU chemotherapy, as well as the correlation of FDXR gene expressions and p53 mutation. Fluorouracil 127-131 ferredoxin reductase Homo sapiens 64-68 16528528-10 2006 FDXR gene expression, which is regulated at least in part by p53, is associated with both response and survival when metastatic colorectal cancer is treated with 5-FU plus LV. Fluorouracil 162-166 ferredoxin reductase Homo sapiens 0-4 16528528-11 2006 In addition, analysis of p53 mutation combined with FDXR gene expression might be useful in estimating the outcome in 5-FU-treated patients. Fluorouracil 118-122 ferredoxin reductase Homo sapiens 52-56 17197759-7 2006 Although systemic combination chemotherapy of 5-FU and IFN-alpha induced the bone marrow suppression, it was effective for lung metastases and palliates symptoms and signs in our case of HCC. Fluorouracil 46-50 HCC Homo sapiens 187-190 17054996-6 2006 5-FU induced apoptosis primarily via a caspase-8-dependent pathway, and ADM and GEM via caspase-9. Fluorouracil 0-4 caspase 8 Homo sapiens 39-48 17207318-13 2006 We found that 5-FU increased pRb and p21WAF1/CIP1 expression in both p53-transfected and vector-transfected cells without the significant accumulation of p53. Fluorouracil 14-18 RB transcriptional corepressor 1 Homo sapiens 29-32 17016659-0 2006 Combination of 5-FU and IFNalpha enhances IFN signaling pathway and caspase-8 activity, resulting in marked apoptosis in hepatoma cell lines. Fluorouracil 15-19 caspase 8 Homo sapiens 68-77 17016659-7 2006 Caspase-3, -9, and especially caspase-8 activity was higher with IFN alpha plus 5-FU than IFN or 5-FU alone. Fluorouracil 80-84 caspase 8 Homo sapiens 30-39 17016659-7 2006 Caspase-3, -9, and especially caspase-8 activity was higher with IFN alpha plus 5-FU than IFN or 5-FU alone. Fluorouracil 97-101 caspase 8 Homo sapiens 30-39 17016659-10 2006 In conclusion, caspase-8 is the most important factor that controls IFN and 5-FU-induced apoptosis in hepatoma cell lines. Fluorouracil 76-80 caspase 8 Homo sapiens 15-24 16945912-7 2006 To induce hematopoietic stress and a subsequent response from HSCs, we treated Hmgb3(-/Y) mice with 5-fluorouracil. Fluorouracil 100-114 high mobility group box 3 Mus musculus 79-88 16945912-8 2006 Hmgb3(-/Y) mice exhibit a faster recovery of functional HSCs after administration of 5-fluorouracil compared with wild-type mice, which may be due to the increased Wnt signaling. Fluorouracil 85-99 high mobility group box 3 Mus musculus 0-10 16732331-5 2006 The recovery of the BM myeloid compartment following 5-Fluorouracil-induced myelo-ablation was much slower in gadd45a-/- and gadd45b-/- mice compared to wt controls. Fluorouracil 53-67 growth arrest and DNA-damage-inducible 45 beta Mus musculus 125-132 16568206-3 2006 METHODS: RIF-1 and HT29 cells were treated with the TS inhibitors 5-fluorouracil (5-FU) and AG337 (nolatrexed dihydrochloride), as well as cisplatin as control. Fluorouracil 66-80 replication timing regulatory factor 1 Homo sapiens 9-14 16720348-2 2006 Upon availability of ribose-1-phosphate, UPase can also catalyze the formation of nucleosides from uracil as well as from 5-fluorouracil, therefore involved in fluoropyrimidine metabolism. Fluorouracil 122-136 uridine phosphorylase 1 Homo sapiens 41-46 16872266-2 2006 The final requisite enzyme, thymidine phosphorylase, is present at consistently higher levels in tumours compared with normal tissues, thereby suggesting that 5-fluorouracil that is delivered in this way may benefit from an element of tumour targeting and thus enhanced selectivity and better tolerability. Fluorouracil 159-173 thymidine phosphorylase Homo sapiens 28-51 16680372-9 2006 Finally, small interfering RNA of p65 decreased the expression of p65, and the viability of cells transfected with p65 small interfering RNA was significantly suppressed at the same concentration of 5-fluorouracil (P < 0.05) compared to untransfected cells. Fluorouracil 199-213 RELA proto-oncogene, NF-kB subunit Homo sapiens 34-37 16680372-11 2006 RNA interference targeting at p65 increased the sensitivity of the ESCC cell lines to 5-fluorouracil, suggesting that NF-kappaB might be a good target for cancer treatment. Fluorouracil 86-100 RELA proto-oncogene, NF-kB subunit Homo sapiens 30-33 16552801-12 2006 Meanwhile, the expression rate of PD-ECGF was significantly lower in 5"-DFUR group (4/18,28.6%) than in CF+5-FU group(9/16,56.3%)and control group (13/20,65.0%) (chi2=7.542, P=0.023). Fluorouracil 107-111 thymidine phosphorylase Homo sapiens 34-41 16608732-0 2006 Enhanced liver targeting of 5-fluorouracil using galactosylated human serum albumin as a carrier molecule. Fluorouracil 28-42 albumin Mus musculus 70-83 16608732-2 2006 The galactosylated human serum albumin 5-fluorouracil conjugate (GHSA-5-FU) was prepared and tested for its chemical characteristic, biodistribution and primary cytotoxicity. Fluorouracil 39-53 albumin Mus musculus 25-38 17216005-5 2006 The main mechanisms of the resistance against 5-fluorouracil are due to the overexpression of dihydropyrimidine dehydrogenase, MRP8, thymidylate synthase, and NFkB p65. Fluorouracil 46-60 ATP binding cassette subfamily C member 8 Homo sapiens 127-131 17179731-0 2006 Predictive role of thymidylate synthase, dihydropyrimidine dehydrogenase and thymidine phosphorylase expression in colorectal cancer patients receiving adjuvant 5-fluorouracil. Fluorouracil 161-175 thymidine phosphorylase Homo sapiens 77-100 17179731-13 2006 The role of TP as a predictor for 5-FU-based therapy needs further investigations. Fluorouracil 34-38 thymidine phosphorylase Homo sapiens 12-14 16160472-2 2005 Thymidylate synthase (TS), thymidine phosphorylase (TP), and dihydropyrimidine dehydrogenase (DPD) are known to be important biomarkers to predict tumor response to 5-FU-based therapy. Fluorouracil 165-169 thymidine phosphorylase Homo sapiens 27-50 16315867-4 2005 Although OK-432 also enhanced the expression of the genes encoding SOCS-1 and SOCS-3, which are negative regulators for cytokine signaling, this was reduced by 5-FU or X-irradiation. Fluorouracil 160-164 suppressor of cytokine signaling 3 Homo sapiens 78-84 16101138-5 2005 Among them, three IFN-related genes, an IFN receptor gene (IFNAR2) and two IFN-stimulated genes (ISG15K, ISG-54K), that were up-regulated following addition of 5-FU, were investigated. Fluorouracil 160-164 interferon induced protein with tetratricopeptide repeats 2 Homo sapiens 105-112 16144935-4 2005 In this study, we evaluate the prognostic value of SMAD4 in patients treated with surgery and 5-FU-based adjuvant therapy. Fluorouracil 94-98 SMAD family member 4 Homo sapiens 51-56 16144935-10 2005 In conclusion, low SMAD4 tumor levels identified a subset of patients with poor prognosis following surgery and 5-FU-based adjuvant therapy; therefore, these patients could be good candidates to receive combined treatment with additional chemotherapeutic agents such as CPT-11 and/or oxaliplatin. Fluorouracil 112-116 SMAD family member 4 Homo sapiens 19-24 15896711-0 2005 Combination of 5-fluorouracil and genistein induces apoptosis synergistically in chemo-resistant cancer cells through the modulation of AMPK and COX-2 signaling pathways. Fluorouracil 15-29 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 136-140 15896711-5 2005 The present study focused on the correlation of AMPK and COX-2 in combined cytotoxicity of 5-FU and genistein, since AMPK is known as a primary cellular homeostasis regulator and a possible target molecule of cancer treatment, and COX-2 as cell proliferation and anti-apoptotic molecule. Fluorouracil 91-95 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 48-52 15896711-5 2005 The present study focused on the correlation of AMPK and COX-2 in combined cytotoxicity of 5-FU and genistein, since AMPK is known as a primary cellular homeostasis regulator and a possible target molecule of cancer treatment, and COX-2 as cell proliferation and anti-apoptotic molecule. Fluorouracil 91-95 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 117-121 15890238-0 2005 Silencing of the p53R2 gene by RNA interference inhibits growth and enhances 5-fluorouracil sensitivity of oral cancer cells. Fluorouracil 77-91 ribonucleotide reductase regulatory TP53 inducible subunit M2B Homo sapiens 17-22 15890238-9 2005 The cancer cell lines with higher p53R2 expression were more resistant to 5-FU. Fluorouracil 74-78 ribonucleotide reductase regulatory TP53 inducible subunit M2B Homo sapiens 34-39 15890242-1 2005 Thymidylate synthase (TS), Dihydropyrimidine dehydrogenase (DPD) and Thymidine Phosphorylase (TP) gene expressions are reported to be predictive markers for 5-fluorouracil (5-FU) sensitivity in gastrointestinal cancer. Fluorouracil 157-171 thymidine phosphorylase Homo sapiens 69-92 15890242-1 2005 Thymidylate synthase (TS), Dihydropyrimidine dehydrogenase (DPD) and Thymidine Phosphorylase (TP) gene expressions are reported to be predictive markers for 5-fluorouracil (5-FU) sensitivity in gastrointestinal cancer. Fluorouracil 157-171 thymidine phosphorylase Homo sapiens 94-96 15890242-1 2005 Thymidylate synthase (TS), Dihydropyrimidine dehydrogenase (DPD) and Thymidine Phosphorylase (TP) gene expressions are reported to be predictive markers for 5-fluorouracil (5-FU) sensitivity in gastrointestinal cancer. Fluorouracil 173-177 thymidine phosphorylase Homo sapiens 69-92 15890242-1 2005 Thymidylate synthase (TS), Dihydropyrimidine dehydrogenase (DPD) and Thymidine Phosphorylase (TP) gene expressions are reported to be predictive markers for 5-fluorouracil (5-FU) sensitivity in gastrointestinal cancer. Fluorouracil 173-177 thymidine phosphorylase Homo sapiens 94-96 15687373-2 2005 A three-step in vivo-targeted activation process requiring carboxylesterases, cytidine deaminase, and thymidine phosphorylase converts capecitabine to 5-fluorouracil. Fluorouracil 151-165 cytidine deaminase Homo sapiens 78-96 15750632-0 2005 YB-1 facilitates basal and 5-fluorouracil-inducible expression of the human major vault protein (MVP) gene. Fluorouracil 27-41 major vault protein Homo sapiens 76-95 15750632-0 2005 YB-1 facilitates basal and 5-fluorouracil-inducible expression of the human major vault protein (MVP) gene. Fluorouracil 27-41 major vault protein Homo sapiens 97-100 15750632-3 2005 Here, we demonstrate that besides MDR-related cytostatics, also the non-MDR-related drug 5-fluorouracil (5-FU) was able to induce MVP mRNA and protein expression. Fluorouracil 89-103 major vault protein Homo sapiens 130-133 15750632-3 2005 Here, we demonstrate that besides MDR-related cytostatics, also the non-MDR-related drug 5-fluorouracil (5-FU) was able to induce MVP mRNA and protein expression. Fluorouracil 105-109 major vault protein Homo sapiens 130-133 15750632-4 2005 Treatment with 5-FU amplified the binding activity and interaction of the transcription factor Y-box binding protein-1 (YB-1) with the Y-box of the human MVP gene promoter in a time-dependent manner. Fluorouracil 15-19 major vault protein Homo sapiens 154-157 15750632-5 2005 5-FU also induced reporter expressions driven by a panel of newly generated MVP promoter deletion mutants. Fluorouracil 0-4 major vault protein Homo sapiens 76-79 15750632-6 2005 Interestingly, stably YB-1 overexpressing cell clones showed enhanced binding of YB-1 to the Y-box motif, associated with enhanced basal as well as 5-FU-inducible MVP promoter-driven reporter expressions. Fluorouracil 148-152 major vault protein Homo sapiens 163-166 15750632-9 2005 In summary, our data demonstrate a direct involvement of YB-1 in controlling basal and 5-FU-induced MVP promoter activity. Fluorouracil 87-91 major vault protein Homo sapiens 100-103 15611052-4 2005 Analyses of ATPase activation suggested that the hMSH2-hMSH6 heterodimer only recognized FdUrd moieties (as the base 5-fluorouracil (FU) in DNA) when mispaired with guanine, but not paired with adenine. Fluorouracil 117-131 mutS homolog 2 Homo sapiens 49-54 15608676-7 2005 5-FU confers S-phase arrest through Chk1-mediated Cdc25A proteolysis leading to inhibition of Cdk2. Fluorouracil 0-4 cyclin dependent kinase 2 Homo sapiens 94-98 15608676-14 2005 Additionally, we show that Chk1 deficiency potentiates 5-FU efficacy through the preferential induction of the caspase-8 pathway and subsequent caspase-3 activation. Fluorouracil 55-59 caspase 8 Homo sapiens 111-120 15709212-4 2005 There exist several clinically relevant examples of the utility of pharmacogenomics that associate specific genetic polymorphisms in drug metabolizing enzymes (e.g., TPMT, UGT1A1, DPD), drug transporters (MDR1), and drug target enzymes (TS) with clinical outcomes in patients treated with commonly prescribed chemotherapy drugs, such as 5-fluorouracil and irinotecan (Camptosar; Pfizer Pharmaceuticals; New York, NY http://www.pfizer.com). Fluorouracil 337-351 thiopurine S-methyltransferase Homo sapiens 166-170 15711100-4 2005 METHODS: Two human RCC cell lines (ACHN and SN12K1) and renal tubular epithelial cells (HK2) were treated with 5-fluorouracil (0.2-20 microg/ml) or cisplatin (1-100 microM). Fluorouracil 111-125 hexokinase 2 Homo sapiens 88-91 15548681-8 2004 Cotransfection of NFkappaB p50 and p65 cDNA induced 5-FU resistance in MCF-7 cells. Fluorouracil 52-56 RELA proto-oncogene, NF-kB subunit Homo sapiens 35-38 15470036-5 2004 Our results show that methotrexate and 5-fluorouracil prevent the acquisition of effector functions, such as IFN-gamma, granzyme B expression, and cytotoxic function following antigenic stimulation of naive cells. Fluorouracil 39-53 granzyme B Mus musculus 120-130 15369444-5 2004 Agents such as luteinizing hormone releasing hormone (LHRH) agonists can suppress ovarian function in premenopausal patients and have been shown to be as effective and even better than chemotherapy (CMF--cyclophosphamide, methotrexate, fluorouracil-containing regimens) in certain patient populations. Fluorouracil 236-248 gonadotropin releasing hormone 1 Homo sapiens 15-52 15369444-5 2004 Agents such as luteinizing hormone releasing hormone (LHRH) agonists can suppress ovarian function in premenopausal patients and have been shown to be as effective and even better than chemotherapy (CMF--cyclophosphamide, methotrexate, fluorouracil-containing regimens) in certain patient populations. Fluorouracil 236-248 gonadotropin releasing hormone 1 Homo sapiens 54-58 15260847-4 2004 We immunohistochemically evaluated the relationship between the expression of TS, p16(INK4a), CDK4 and cyclin D1 and the effect of 5-FU-based chemotherapy in colorectal cancers. Fluorouracil 131-135 cyclin dependent kinase 4 Homo sapiens 94-98 15105837-9 2004 Thus, a potential mechanism for TRAIL sensitisation by 5-FU is the increased effectiveness of caspase-8 recruitment to and activation at the DISC facilitated by the downregulation of cFLIP and the consequent shift in the ratio of caspase-8 to cFLIP at the DISC. Fluorouracil 55-59 caspase 8 Homo sapiens 94-103 15105837-9 2004 Thus, a potential mechanism for TRAIL sensitisation by 5-FU is the increased effectiveness of caspase-8 recruitment to and activation at the DISC facilitated by the downregulation of cFLIP and the consequent shift in the ratio of caspase-8 to cFLIP at the DISC. Fluorouracil 55-59 caspase 8 Homo sapiens 230-239 15130763-6 2004 Treatment with Doxorubicin, Paclitaxel or 5-Fluorouracil induced a breakdown of the mitochondrial membrane potential and apoptotic cell death in p56/Lck expressing Jurkat and the retransfected JCaM1.6/Lck cells within 48h of treatment. Fluorouracil 42-56 cyclin dependent kinase like 2 Homo sapiens 145-148 15130763-11 2004 In conclusion, the tyrosine kinase p56/Lck is essential for apoptosis induction by Doxorubicin, Paclitaxel and 5-Fluorouracil regulating early steps of the mitochondrial apoptosis signaling cascade, including alteration of mitochondrial functions and caspase-activation. Fluorouracil 111-125 cyclin dependent kinase like 2 Homo sapiens 35-38 15130763-11 2004 In conclusion, the tyrosine kinase p56/Lck is essential for apoptosis induction by Doxorubicin, Paclitaxel and 5-Fluorouracil regulating early steps of the mitochondrial apoptosis signaling cascade, including alteration of mitochondrial functions and caspase-activation. Fluorouracil 111-125 caspase 8 Homo sapiens 251-258 15124184-0 2004 5-Fluorouracil enhances apoptosis sensitivity of T lymphocytes mediated by CD3 epsilon. Fluorouracil 0-14 CD3 antigen, epsilon polypeptide Mus musculus 75-78 15319798-2 2004 Upon the availability of substrates, UPase can also catalyze the formation of nucleosides from uracil or 5-fluorouracil (5-FU) and ribose-1-phosphate (Rib-1-P). Fluorouracil 105-119 uridine phosphorylase 1 Homo sapiens 37-42 15152939-4 2004 RESULTS: We identified several novel 5-FU-inducible target genes that have not previously been linked to 5-FU response, including spermine/spermidine acetyl transferase (SSAT) and annexin II. Fluorouracil 37-41 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 130-168 15152939-4 2004 RESULTS: We identified several novel 5-FU-inducible target genes that have not previously been linked to 5-FU response, including spermine/spermidine acetyl transferase (SSAT) and annexin II. Fluorouracil 37-41 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 170-174 15152939-4 2004 RESULTS: We identified several novel 5-FU-inducible target genes that have not previously been linked to 5-FU response, including spermine/spermidine acetyl transferase (SSAT) and annexin II. Fluorouracil 105-109 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 130-168 15152939-4 2004 RESULTS: We identified several novel 5-FU-inducible target genes that have not previously been linked to 5-FU response, including spermine/spermidine acetyl transferase (SSAT) and annexin II. Fluorouracil 105-109 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 170-174 15152939-6 2004 Inactivation of wild-type p53 abrogated the 5-FU-mediated induction of SSAT and annexin II. Fluorouracil 44-48 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 71-75 15152939-8 2004 Furthermore, basal expression of SSAT and annexin II was elevated in cells resistant to 5-FU. Fluorouracil 88-92 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 33-37 15095856-2 2004 The aim of this study was to determine whether exogenously administered growth hormone modified the effect of 5-fluorouracil on the gut and an implanted colon adenocarcinoma in the rat METHODS: An adenocarcinoma was implanted into rats that had been treated with 5-fluorouracil and growth hormone 3 days previously. Fluorouracil 110-124 gonadotropin releasing hormone receptor Rattus norvegicus 72-86 15095856-4 2004 RESULTS: Growth hormone protected the intestines against 5-fluorouracil by increasing proliferation and mucosal length, and decreasing apoptosis and p53 expression. Fluorouracil 57-71 gonadotropin releasing hormone receptor Rattus norvegicus 9-23 15095856-6 2004 CONCLUSIONS: Growth hormone protects the intestines from the deleterious effects of 5-fluorouracil while preserving its antitumoural action on the adenocarcinoma in the short term. Fluorouracil 84-98 gonadotropin releasing hormone receptor Rattus norvegicus 13-27 15449204-10 2004 As compared with SGC7901, SGC7901-CacyBP cells exhibited significantly increased ( P < 0.01) IC(50) values for vincristine, adriamycin, and 5-fluorouracil. Fluorouracil 143-157 calcyclin binding protein Homo sapiens 34-40 15604581-8 2004 Thymidine phosphorylase (TP), the enzyme that converts 5"-DFUR into 5-FU and 5-FU into FdUMP, was estimated by ELISA. Fluorouracil 68-72 thymidine phosphorylase Homo sapiens 0-23 15604581-8 2004 Thymidine phosphorylase (TP), the enzyme that converts 5"-DFUR into 5-FU and 5-FU into FdUMP, was estimated by ELISA. Fluorouracil 68-72 thymidine phosphorylase Homo sapiens 25-27 15604581-8 2004 Thymidine phosphorylase (TP), the enzyme that converts 5"-DFUR into 5-FU and 5-FU into FdUMP, was estimated by ELISA. Fluorouracil 77-81 thymidine phosphorylase Homo sapiens 0-23 15604581-8 2004 Thymidine phosphorylase (TP), the enzyme that converts 5"-DFUR into 5-FU and 5-FU into FdUMP, was estimated by ELISA. Fluorouracil 77-81 thymidine phosphorylase Homo sapiens 25-27 15604581-11 2004 On the other hand, in the high TP expression group, TP expression was enhanced by IFNalpha in 5 out of 6 cell lines, and antitumor effects were enhanced by IFNalpha in 5 out of 6 cell lines for 5-FU and in all 6 cell lines for 5"-DFUR. Fluorouracil 194-198 thymidine phosphorylase Homo sapiens 31-33 15604581-13 2004 CONCLUSIONS: These results suggested that TP may be useful as a predictive factor in combination therapy with IFNalpha and 5-FU or 5"-DFUR, which may be a promising treatment for advanced RCC. Fluorouracil 123-127 thymidine phosphorylase Homo sapiens 42-44 14723346-6 2003 Compared with 5-Fu injection, a study on the distribution of 5-FuS-SLN in mice showed that 5-FuS-SLN could double 5-Fu concentration in mice livers. Fluorouracil 61-65 fused in sarcoma Mus musculus 93-96 12920208-4 2003 In addition, 5-FU inhibits both SMAD3/4-specific transcription and formation of SMAD/DNA complexes induced by TGF-beta. Fluorouracil 13-17 SMAD family member 3 Homo sapiens 32-37 12907638-7 2003 The 5-FU-induced activation of MAT-8, thymosin-beta-10, and chaperonin-10 was abrogated by inactivation of p53 in MCF-7 cells, whereas induction of SSAT and annexin II was significantly reduced in the absence of p53. Fluorouracil 4-8 heat shock protein family E (Hsp10) member 1 Homo sapiens 60-73 12907638-7 2003 The 5-FU-induced activation of MAT-8, thymosin-beta-10, and chaperonin-10 was abrogated by inactivation of p53 in MCF-7 cells, whereas induction of SSAT and annexin II was significantly reduced in the absence of p53. Fluorouracil 4-8 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 148-152 12761490-4 2003 Transfection of HER2 in MCF7 breast cancer cells that express HER3 caused a phosphoinoside-3 kinase (PI-3K)-dependent activation of Akt, and was associated with an increased resistance of the cells to multiple chemotherapeutic agents (paclitaxel, doxorubicin, 5-fluorouracil, etoposide, and camptothecin). Fluorouracil 260-274 erb-b2 receptor tyrosine kinase 3 Homo sapiens 62-66 12777821-1 2003 Cytosine deaminase is an attractive candidate for anticancer gene therapy through its catalysis of the deamination of the prodrug 5-fluorocytosine to 5-fluorouracil. Fluorouracil 150-164 cytosine deaminase Saccharomyces cerevisiae S288C 0-18 12717833-8 2003 Expression levels of c-jun and p53 were found to be elevated for the tumors from mice treated with nimesulide and 5-FU comparing to those with either of them, but a reduced PGE(2) level was observed only for the treatment with nimesulide. Fluorouracil 114-118 jun proto-oncogene Mus musculus 21-26 12692863-0 2003 5-Fluorouracil efficiently enhanced apoptosis induced by adenovirus-mediated transfer of caspase-8 in DLD-1 colon cancer cells. Fluorouracil 0-14 caspase 8 Homo sapiens 89-98 12692863-9 2003 A potentiating effect of adenoviral treatment was also seen when 5-FU treatment was substituted by the overexpression of cyclin-dependent kinase inhibitors, p21(WAF1/CIP1) and p27(KIP1), suggesting that the cytostatic effect of 5-FU augmented apoptosis induced by caspase-8 gene transduction by inhibiting the dilution of gene products associated with cell division. Fluorouracil 65-69 caspase 8 Homo sapiens 264-273 12566311-2 2003 In this study, we investigated the use of an enhanced human carcinoembryonic antigen (CEA) promoter for yeast cytosine deaminase (yCD), which converts 5-fluorocytosine to 5-fluorouracil, to increase targeting while maintaining activity both in cell culture and in nude rats bearing intrahepatic xenografts. Fluorouracil 171-185 carcinoembryonic antigen gene family 4 Rattus norvegicus 86-89 12566311-2 2003 In this study, we investigated the use of an enhanced human carcinoembryonic antigen (CEA) promoter for yeast cytosine deaminase (yCD), which converts 5-fluorocytosine to 5-fluorouracil, to increase targeting while maintaining activity both in cell culture and in nude rats bearing intrahepatic xenografts. Fluorouracil 171-185 cytosine deaminase Saccharomyces cerevisiae S288C 110-128 12566311-7 2003 Moreover, the efficiency of 5-fluorocytosine conversion into 5-fluorouracil in tumors was significantly higher than that in normal liver ( approximately 3-fold) in rats receiving portal venous viral infusion of CEA-yCD and subsequent 5FC treatment. Fluorouracil 61-75 carcinoembryonic antigen gene family 4 Rattus norvegicus 211-214 12680199-6 2003 However, FRNK overexpression did sensitize cells to the cytotoxic effect of 5-fluorouracil and led to a decrease in haptotactic mobility. Fluorouracil 76-90 protein tyrosine kinase 2 Homo sapiens 9-13 12497203-1 2003 PURPOSE: Thymidine phosphorylase (TdR-Pase) and dihydropyrimidine dehydrogenase (DPD) are thought to be key enzymes in the metabolic pathways of 5-fluorouracil (5-FU). Fluorouracil 145-159 thymidine phosphorylase Homo sapiens 34-42 12497203-1 2003 PURPOSE: Thymidine phosphorylase (TdR-Pase) and dihydropyrimidine dehydrogenase (DPD) are thought to be key enzymes in the metabolic pathways of 5-fluorouracil (5-FU). Fluorouracil 161-165 thymidine phosphorylase Homo sapiens 34-42 12497203-2 2003 Theoretically, tumors which have low DPD and/or high TdR-Pase expression should be 5-FU-sensitive. Fluorouracil 83-87 thymidine phosphorylase Homo sapiens 53-61 12743424-2 2003 This report addressed the time-dependent dynamic alterations in the expression of three tumor-associated antigens: carcinoembryonic antigen (CEA), colon-specific antigen (CSAp) and mucin-1 (MUC-1) following chemotherapy with 5-fluorouracil (5-FU) or radioimmunotherapy (RAIT; (131)I-labeled anti-CEA IgG) in human colonic tumor xenografts. Fluorouracil 225-239 mucin 1, cell surface associated Homo sapiens 190-195 12414664-7 2002 NSAIDs and 5-FU induced the mitochondrial release of cytochrome c as well as caspase-3 and -9 activation, and to a much lesser extent, caspase-8. Fluorouracil 11-15 caspase 8 Homo sapiens 135-144 12185618-8 2002 CONCLUSIONS: We have obtained in our study very good results using subconjunctival 5-FU injections, associated in complicated or refractory cases to needling revision, in eyes with encapsulated blebs after glaucoma drainage device surgery, with no major complications (Arch Soc Esp Oftalmol 2002; 77: 429-434). Fluorouracil 83-87 protein tyrosine phosphatase receptor type V, pseudogene Homo sapiens 278-281 12396726-4 2002 In this report, we characterized the viability of various human tumor cells in vitro after combination treatment with IFN-beta protein and the chemotherapeutic drugs, cis-platinum (II) diamine dichloride (cisplatin), 5-fluorouracil (5-FU), paclitaxel (Taxol) and gemcitabine. Fluorouracil 217-231 interferon beta 1 Homo sapiens 118-126 12396726-4 2002 In this report, we characterized the viability of various human tumor cells in vitro after combination treatment with IFN-beta protein and the chemotherapeutic drugs, cis-platinum (II) diamine dichloride (cisplatin), 5-fluorouracil (5-FU), paclitaxel (Taxol) and gemcitabine. Fluorouracil 233-237 interferon beta 1 Homo sapiens 118-126 12173327-1 2002 BACKGROUND: The objective of this study was to determine the response rate and toxicity of gemcitabine and continuous-infusion 5-fluorouracil (5-FU) in combination with subcutaneous interleukin-2 (IL2) and interferon-alpha (IFNA) in patients with metastatic renal cell carcinoma. Fluorouracil 127-141 interferon alpha 2 Homo sapiens 224-228 12168834-7 2002 When the esophageal cancer cells were treated with 5-fluorouracil (5-FU) in the presence of a low concentration of liposome-entrapped-gene, the rate of growth inhibition of these cells increased over that caused by either 5-FU or hIFN-beta gene entrapped in the liposomes alone. Fluorouracil 51-65 interferon beta 1 Homo sapiens 230-239 12168834-7 2002 When the esophageal cancer cells were treated with 5-fluorouracil (5-FU) in the presence of a low concentration of liposome-entrapped-gene, the rate of growth inhibition of these cells increased over that caused by either 5-FU or hIFN-beta gene entrapped in the liposomes alone. Fluorouracil 67-71 interferon beta 1 Homo sapiens 230-239 11986258-0 2002 CD8 alpha-deficient mice are highly susceptible to 5-fluorouracil-induced lethality. Fluorouracil 51-65 CD8 antigen, alpha chain Mus musculus 0-9 11986258-2 2002 We found that mice rendered deficient in CD8 alpha molecules by homologous recombination were susceptible to 5-fluorouracil (5-FU)-induced lethality accompanied by translocation of members of the enterobacteria. Fluorouracil 109-123 CD8 antigen, alpha chain Mus musculus 41-50 12020396-2 2002 Thymidine phosphorylase (TP) converts 5"-deoxy-5-fluorouridine (5"-DFUR), an intermediate metabolite of capecitabine, to 5-FU. Fluorouracil 121-125 thymidine phosphorylase Homo sapiens 0-23 12020396-2 2002 Thymidine phosphorylase (TP) converts 5"-deoxy-5-fluorouridine (5"-DFUR), an intermediate metabolite of capecitabine, to 5-FU. Fluorouracil 121-125 thymidine phosphorylase Homo sapiens 25-27 11812172-10 2002 CAF chemotherapy (cyclophosphamide, adriamycin, and 5-fluorouracil) is predicted to be more effective than CMF (cyclophosphamide, methotrexate, and 5-fluorouracil). Fluorouracil 52-66 lysine acetyltransferase 2B Homo sapiens 0-3 11812172-10 2002 CAF chemotherapy (cyclophosphamide, adriamycin, and 5-fluorouracil) is predicted to be more effective than CMF (cyclophosphamide, methotrexate, and 5-fluorouracil). Fluorouracil 148-162 lysine acetyltransferase 2B Homo sapiens 0-3 11868789-3 2002 Synergistic effects of interferon-alpha-2b on 5-fluorouracil or cisplatin were demonstrated in Huh7 cells. Fluorouracil 46-60 interferon alpha 2 Homo sapiens 23-42 11454690-0 2001 Multimodality therapy with a replication-conditional herpes simplex virus 1 mutant that expresses yeast cytosine deaminase for intratumoral conversion of 5-fluorocytosine to 5-fluorouracil. Fluorouracil 174-188 cytosine deaminase Saccharomyces cerevisiae S288C 104-122 11454690-2 2001 In this study, an HSV-1 mutant (HSV1yCD) was engineered such that the viral ribonucleotide reductase gene is disrupted by sequences encoding yeast cytosine deaminase, which efficiently metabolizes the prodrug 5-fluorocytosine (5-FC) to 5-fluorouracil (5-FU). Fluorouracil 236-250 cytosine deaminase Saccharomyces cerevisiae S288C 147-165 11454690-2 2001 In this study, an HSV-1 mutant (HSV1yCD) was engineered such that the viral ribonucleotide reductase gene is disrupted by sequences encoding yeast cytosine deaminase, which efficiently metabolizes the prodrug 5-fluorocytosine (5-FC) to 5-fluorouracil (5-FU). Fluorouracil 252-256 cytosine deaminase Saccharomyces cerevisiae S288C 147-165 11353746-3 2001 Of 12 cDNA-expressed rat P450 enzymes tested, CYP1A2, CYP3A1, and CYP2C11 had high 5-FU formation rates from 100 microM and 1.0 mM tegafur concentrations. Fluorouracil 83-87 cytochrome P450, family 3, subfamily a, polypeptide 23-polypeptide 1 Rattus norvegicus 54-60 11391857-2 2001 In the present study, the distribution and clinical significance of TdRPase in IDCs and benign diseases of the pancreas were assessed, especially in relation to the efficacy of chemotherapy with 5-FU or its derivatives. Fluorouracil 195-199 thymidine phosphorylase Homo sapiens 68-75 11286326-8 2001 The tumour-preferential activation of capecitabine to fluorouracil is explained by tissue differences in the activity of cytidine deaminase and thymidine phosphorylase, key enzymes in the conversion process. Fluorouracil 54-66 cytidine deaminase Homo sapiens 121-139 11092985-6 2000 5-FU sensitivity of tumor cells increased in the presence of EGF or TGF-alpha. Fluorouracil 0-4 transforming growth factor alpha Homo sapiens 68-77 11092985-8 2000 The tumor environmental factors, EGF and TGF-alpha, may act as intrinsic regulators of DPD and PyNPase activities that affect the 5-FU sensitivity of individual tumors. Fluorouracil 130-134 transforming growth factor alpha Homo sapiens 41-50 11062731-8 2000 These findings suggested that 5-FU induced apoptosis was mediated by the activation of a caspase cascade involving caspase 1, 3 and 8. Fluorouracil 30-34 caspase 8 Homo sapiens 115-133 10891390-5 2000 In addition, the expression of TRAF-2 and cIAP-1, which are transcriptionally regulated by NF-kappaB and function as anti-apoptotic molecules through the interruption of caspase pathway, was also inhibited by 5-FU. Fluorouracil 209-213 baculoviral IAP repeat containing 2 Homo sapiens 42-48 10891390-5 2000 In addition, the expression of TRAF-2 and cIAP-1, which are transcriptionally regulated by NF-kappaB and function as anti-apoptotic molecules through the interruption of caspase pathway, was also inhibited by 5-FU. Fluorouracil 209-213 caspase 8 Homo sapiens 170-177 10891390-6 2000 Finally, the activity of caspase-8 and caspase-3 showed a significant increase in response to 5-FU. Fluorouracil 94-98 caspase 8 Homo sapiens 25-34 10853031-1 2000 We have previously reported that HT29 human colon cancer cells selected by adaptation to 5-fluorouracil (5FU) (HT29-5FU cells) express increased levels of a major intestinal mucin MUC2 mRNA compared with parental HT29 cells. Fluorouracil 89-103 LOC100508689 Homo sapiens 174-179 10853031-1 2000 We have previously reported that HT29 human colon cancer cells selected by adaptation to 5-fluorouracil (5FU) (HT29-5FU cells) express increased levels of a major intestinal mucin MUC2 mRNA compared with parental HT29 cells. Fluorouracil 105-108 LOC100508689 Homo sapiens 174-179 10778957-0 2000 Colorectal tumors responding to 5-fluorouracil have low gene expression levels of dihydropyrimidine dehydrogenase, thymidylate synthase, and thymidine phosphorylase. Fluorouracil 32-46 thymidine phosphorylase Homo sapiens 141-164 10883892-5 2000 We examined the apoptotic tendencies of HeLa and WISH cell lines caused by one of the drugs used, 5-FU. Fluorouracil 98-102 NCK interacting protein with SH3 domain Homo sapiens 49-53 10606256-3 1999 In phase II trials in patients with colorectal cancer that was recurrent or refractory to 5-Ruorouracil (5-FU)based front-line therapy, response rates of 14% to 22% and median survival times of 8 to 10 months have been consistently reported by groups from Japan, Europe, and the United States using avariety of drug administration schedules Two recently reported phase III trials comparing CPT-II against infusional 5-FU or best supportive care demonstrated that CPT-II confers a survival advantage over either of the two other approaches. Fluorouracil 105-109 carnitine palmitoyltransferase 2 Homo sapiens 390-396 10606256-3 1999 In phase II trials in patients with colorectal cancer that was recurrent or refractory to 5-Ruorouracil (5-FU)based front-line therapy, response rates of 14% to 22% and median survival times of 8 to 10 months have been consistently reported by groups from Japan, Europe, and the United States using avariety of drug administration schedules Two recently reported phase III trials comparing CPT-II against infusional 5-FU or best supportive care demonstrated that CPT-II confers a survival advantage over either of the two other approaches. Fluorouracil 105-109 carnitine palmitoyltransferase 2 Homo sapiens 463-469 10606256-4 1999 In front-line treatment of colorectal cancer, CPT-II produces response rates of 19% to 32% and median survival times of 11 to 12 months, figures quite similar to those achievable with bolus 5-FU and leucovorin. Fluorouracil 190-194 carnitine palmitoyltransferase 2 Homo sapiens 46-52 10606256-13 1999 To date, only one topoisomerase I inhibitor, CPT-II, has demonstrated a level of activity sufficient for it to become an integral component of treatment for patients with 5-FU-refractory colorectal cancer. Fluorouracil 171-175 carnitine palmitoyltransferase 2 Homo sapiens 45-51 10606259-1 1999 Interferons (IFN)-alpha, -beta, and -gamma enhance the activity of 5-fluorouracil (5-FU) in vitro and in vivo. Fluorouracil 67-81 interferon beta 1 Homo sapiens 0-42 10606259-1 1999 Interferons (IFN)-alpha, -beta, and -gamma enhance the activity of 5-fluorouracil (5-FU) in vitro and in vivo. Fluorouracil 83-87 interferon beta 1 Homo sapiens 0-42 10766293-2 1999 This review firstly discusses the biological role of TP/PD-ECGF and its importance in the activation of 5-fluorouracil and its prodrugs. Fluorouracil 104-118 thymidine phosphorylase Homo sapiens 56-63 10507772-3 1999 The expression of nm23-H1 protein was examined immunohistochemically in 32 eligible patients with OSCC who underwent adjuvant chemotherapy with cisplatin, etoposide, and 5-fluorouracil after tumour resection. Fluorouracil 170-184 NME/NM23 nucleoside diphosphate kinase 1 Homo sapiens 18-25 10507772-10 1999 MTT (3-(4,5-dimethyl-2-thiazol)-2,5-diphenyl-2H tetrazolium bromide) assay showed that reduced expression of the nm23-H1 protein in AS clones was consistent with the degree of increased resistance to cisplatin but not etoposide or 5-fluorouracil. Fluorouracil 231-245 NME/NM23 nucleoside diphosphate kinase 1 Homo sapiens 113-120 10507774-0 1999 The expression of thymidine phosphorylase correlates with angiogenesis and the efficacy of chemotherapy using fluorouracil derivatives in advanced gastric carcinoma. Fluorouracil 110-122 thymidine phosphorylase Homo sapiens 18-41 10507774-5 1999 In patients treated with fluorouracil derivatives (FUs), the expression of TP significantly correlated with favourable prognosis and with unfavourable prognosis in those not treated with FUs. Fluorouracil 25-37 thymidine phosphorylase Homo sapiens 75-77 10468288-0 1999 Increased cytotoxicity and bystander effect of 5-fluorouracil and 5-deoxy-5-fluorouridine in human colorectal cancer cells transfected with thymidine phosphorylase. Fluorouracil 47-61 thymidine phosphorylase Homo sapiens 140-163 10468288-1 1999 5-Fluorouracil (5-FU) and 5"-deoxy-5-fluorouridine (5"-DFUR), a prodrug of 5-FU, are anticancer agents activated by thymidine phosphorylase (TP). Fluorouracil 0-14 thymidine phosphorylase Homo sapiens 116-139 10468288-1 1999 5-Fluorouracil (5-FU) and 5"-deoxy-5-fluorouridine (5"-DFUR), a prodrug of 5-FU, are anticancer agents activated by thymidine phosphorylase (TP). Fluorouracil 0-14 thymidine phosphorylase Homo sapiens 141-143 10468288-1 1999 5-Fluorouracil (5-FU) and 5"-deoxy-5-fluorouridine (5"-DFUR), a prodrug of 5-FU, are anticancer agents activated by thymidine phosphorylase (TP). Fluorouracil 16-20 thymidine phosphorylase Homo sapiens 116-139 10468288-1 1999 5-Fluorouracil (5-FU) and 5"-deoxy-5-fluorouridine (5"-DFUR), a prodrug of 5-FU, are anticancer agents activated by thymidine phosphorylase (TP). Fluorouracil 16-20 thymidine phosphorylase Homo sapiens 141-143 10468288-1 1999 5-Fluorouracil (5-FU) and 5"-deoxy-5-fluorouridine (5"-DFUR), a prodrug of 5-FU, are anticancer agents activated by thymidine phosphorylase (TP). Fluorouracil 75-79 thymidine phosphorylase Homo sapiens 116-139 10468288-1 1999 5-Fluorouracil (5-FU) and 5"-deoxy-5-fluorouridine (5"-DFUR), a prodrug of 5-FU, are anticancer agents activated by thymidine phosphorylase (TP). Fluorouracil 75-79 thymidine phosphorylase Homo sapiens 141-143 10468288-5 1999 The cytotoxic effects of 5-FU and 5"-DFUR were higher in TP-transfected cells as compared to wild-type cells. Fluorouracil 25-29 thymidine phosphorylase Homo sapiens 57-59 11367342-0 1999 Topical 5-FU reduces CIN recurrence. Fluorouracil 8-12 pyridoxal phosphatase Homo sapiens 21-24 10083888-3 1998 Nevertheless 5-FU efficiency is limited, this is due to the rapidity of its metabolism (T1/2 10 min). Fluorouracil 13-17 interleukin 1 receptor like 1 Homo sapiens 88-99 9725052-0 1998 [The in vitro combination-effect of toremifene with CAF (cyclophosphamide, adriamycin, 5-fluorouracil) on growth of various human mammary carcinomas]. Fluorouracil 87-101 lysine acetyltransferase 2B Homo sapiens 52-55 9282825-1 1997 Interleukin-1alpha (IL-1), by itself, accelerates both granulopoietic and thrombopoietic recovery in the 5-fluorouracil (5-FU) myelosuppressed mouse (FUM). Fluorouracil 105-119 interleukin 1 complex Mus musculus 20-24 9282825-1 1997 Interleukin-1alpha (IL-1), by itself, accelerates both granulopoietic and thrombopoietic recovery in the 5-fluorouracil (5-FU) myelosuppressed mouse (FUM). Fluorouracil 121-125 interleukin 1 complex Mus musculus 20-24 9070485-0 1997 Bimonthly high dose leucovorin and 5-fluorouracil 48-hour infusion with interferon-alpha-2a in patients with advanced colorectal carcinoma. Fluorouracil 35-49 interferon alpha 2 Homo sapiens 72-91 9268987-5 1997 In these cells, 5-FU pretreatment progressively inhibited mRNA expression of both ERCC1 and gamma-GCS after removal of 5-FU, without affecting glyceraldehyde-3-phosphate dehydrogenase (GAPDH) mRNA. Fluorouracil 16-20 glutamate-cysteine ligase catalytic subunit Homo sapiens 92-101 9268987-5 1997 In these cells, 5-FU pretreatment progressively inhibited mRNA expression of both ERCC1 and gamma-GCS after removal of 5-FU, without affecting glyceraldehyde-3-phosphate dehydrogenase (GAPDH) mRNA. Fluorouracil 119-123 glutamate-cysteine ligase catalytic subunit Homo sapiens 92-101 9268987-9 1997 Although not convinced, our data suggest that 5-FU, when incorporated into RNA, may inhibit both GSH synthesis and repair of platinum-DNA adducts by downregulating the ERCC1 and gamma-GCS genes, thereby enhancing antitumor activity of CDDP and reversing resistance to CDDP in HST-1/CP0.2 cells. Fluorouracil 46-50 glutamate-cysteine ligase catalytic subunit Homo sapiens 178-187 9229325-1 1996 To improve the therapeutic ratio of palliative chemotherapy in patients with metastatic colorectal and gastric cancer 5-fluorouracil (5-FU) was administered as weekly high-dose 24-hour continuous infusion in combination with leucovorin (LV) and interferon-alpha-2b (IFN) as biomodulating agents: Chemotherapy consisted of a weekly schedule of 500 mg/m2 leucovorin as a 2-hour infusion, followed by a 24-hour continuous infusion of 2500 mg/m2 5-FU. Fluorouracil 134-138 interferon alpha 2 Homo sapiens 245-264 8639415-6 1996 In addition, PF4-preincubated CD34+ cells exhibited a higher potential in MK colony formation in the presence of 5-fluorouracil (5FU). Fluorouracil 113-127 platelet factor 4 Homo sapiens 13-16 8639415-6 1996 In addition, PF4-preincubated CD34+ cells exhibited a higher potential in MK colony formation in the presence of 5-fluorouracil (5FU). Fluorouracil 129-132 platelet factor 4 Homo sapiens 13-16 8820949-3 1996 Methenyltetrahydrofolate synthetase (MTHFS) catalyzes the transformation of 5-formyl-tetrahydrofolate to methenylH4folate, which is the obligatory initial metabolic step prior to the intracellular conversion of 5-formylH4folate to other reduced folates and the increase in intracellular folate pools required for 5-FU potentiation. Fluorouracil 313-317 methenyltetrahydrofolate synthetase Homo sapiens 0-35 8820949-3 1996 Methenyltetrahydrofolate synthetase (MTHFS) catalyzes the transformation of 5-formyl-tetrahydrofolate to methenylH4folate, which is the obligatory initial metabolic step prior to the intracellular conversion of 5-formylH4folate to other reduced folates and the increase in intracellular folate pools required for 5-FU potentiation. Fluorouracil 313-317 methenyltetrahydrofolate synthetase Homo sapiens 37-42 8746791-1 1995 We investigated the dual modulation by l-leucovorin (LV) and recombinant human interferon-alpha 2a (IFN-alpha 2a) of 5-fluorouracil (5-FU) antitumor activity against human colon carcinoma cells (Co-4) using a nude mouse system. Fluorouracil 117-131 interferon alpha 2 Homo sapiens 79-98 8746791-1 1995 We investigated the dual modulation by l-leucovorin (LV) and recombinant human interferon-alpha 2a (IFN-alpha 2a) of 5-fluorouracil (5-FU) antitumor activity against human colon carcinoma cells (Co-4) using a nude mouse system. Fluorouracil 133-137 interferon alpha 2 Homo sapiens 79-98 8717183-4 1995 Moreover, incubation of CD34+ cells with PF4 in liquid culture caused an increase in the number of both stem cell factor (SCF)-binding cells and CD34 antigen-bearing cells, and exhibited greater capacity to form MK colonies than control after the treatment of 5-FU. Fluorouracil 260-264 platelet factor 4 Homo sapiens 41-44 8717183-8 1995 These results demonstrate that PF4 and TGF beta 1 inhibit MK development from CD34+ CB cells by different mechanisms and suggest that PF4, unlike TGF beta 1, exerts its inhibitory effect on cell growth in a reversible and S phase-specific manner by which it protects stem cells and MK progenitor cells from 5-FU cytotoxicity. Fluorouracil 307-311 platelet factor 4 Homo sapiens 134-137 7474606-3 1995 Experimental data suggest that PC-3, a human hormone refractory prostate cancer cell line, showed a 2-fold increase in 5-Fluorouracil (5FU) sensitivity in the presence of alpha-2a Interferon (IFN alpha 2a) at 100 IU/ml, compared to that without IFN alpha 2a. Fluorouracil 119-133 interferon alpha 2 Homo sapiens 171-190 7474606-3 1995 Experimental data suggest that PC-3, a human hormone refractory prostate cancer cell line, showed a 2-fold increase in 5-Fluorouracil (5FU) sensitivity in the presence of alpha-2a Interferon (IFN alpha 2a) at 100 IU/ml, compared to that without IFN alpha 2a. Fluorouracil 119-133 interferon alpha 2 Homo sapiens 192-203 7474606-3 1995 Experimental data suggest that PC-3, a human hormone refractory prostate cancer cell line, showed a 2-fold increase in 5-Fluorouracil (5FU) sensitivity in the presence of alpha-2a Interferon (IFN alpha 2a) at 100 IU/ml, compared to that without IFN alpha 2a. Fluorouracil 119-133 interferon alpha 2 Homo sapiens 245-256 7474606-3 1995 Experimental data suggest that PC-3, a human hormone refractory prostate cancer cell line, showed a 2-fold increase in 5-Fluorouracil (5FU) sensitivity in the presence of alpha-2a Interferon (IFN alpha 2a) at 100 IU/ml, compared to that without IFN alpha 2a. Fluorouracil 135-138 interferon alpha 2 Homo sapiens 171-190 7627962-0 1995 5-Ethoxy-2"-deoxyuridine, a novel substrate for thymidine phosphorylase, potentiates the antitumor activity of 5-fluorouracil when used in combination with interferon, an inducer of thymidine phosphorylase expression. Fluorouracil 111-125 thymidine phosphorylase Homo sapiens 48-71 7627962-0 1995 5-Ethoxy-2"-deoxyuridine, a novel substrate for thymidine phosphorylase, potentiates the antitumor activity of 5-fluorouracil when used in combination with interferon, an inducer of thymidine phosphorylase expression. Fluorouracil 111-125 thymidine phosphorylase Homo sapiens 182-205 7627962-3 1995 Since TP catalyzes the first step in the direct conversion of FUra to deoxyribonucleotides, its induction by IFN is a potential biochemical mechanism for the modulation of the antitumor activity of FUra. Fluorouracil 62-66 thymidine phosphorylase Homo sapiens 6-8 7627962-3 1995 Since TP catalyzes the first step in the direct conversion of FUra to deoxyribonucleotides, its induction by IFN is a potential biochemical mechanism for the modulation of the antitumor activity of FUra. Fluorouracil 198-202 thymidine phosphorylase Homo sapiens 6-8 7627962-4 1995 In contrast to the activity measured in cell extracts, however, thymine utilization by intact cells was increased less than 2-fold by IFN, suggesting that the metabolic activation of FUra by TP in the IFN-treated cells was similarly suboptimal. Fluorouracil 183-187 thymidine phosphorylase Homo sapiens 191-193 7627962-6 1995 One of the compounds, the novel pyrimidine analogue 5-ethoxy-2"-deoxyuridine (EOdU), was found to be a substrate for the transferase reaction of TP, to have little or no direct cytotoxicity, to selectively increase the cellular levels of 5-fluoro-dUMP, to enhance the inhibitory effect of FUra on thymidylate synthase activity, and to potentiate the cytotoxicity of FUra and IFN in human colon carcinoma cells. Fluorouracil 289-293 thymidine phosphorylase Homo sapiens 145-147 7642571-0 1995 Thymidine phosphorylase mediates the sensitivity of human colon carcinoma cells to 5-fluorouracil. Fluorouracil 83-97 thymidine phosphorylase Homo sapiens 0-23 7642571-2 1995 A likely mechanism for this action is the induction by IFN alpha of thymidine phosphorylase (TP), the first enzyme in one pathway for the metabolic activation of FUra to fluorodeoxyribonucleotides. Fluorouracil 162-166 thymidine phosphorylase Homo sapiens 68-91 7819023-1 1995 Interferon alpha-2a (IFN-alpha) and folinic acid (FA) have been shown to modulate the cytotoxic effects of 5-fluorouracil (5-FU) in the treatment of cancer. Fluorouracil 107-121 interferon alpha 2 Homo sapiens 0-19 7819023-1 1995 Interferon alpha-2a (IFN-alpha) and folinic acid (FA) have been shown to modulate the cytotoxic effects of 5-fluorouracil (5-FU) in the treatment of cancer. Fluorouracil 107-121 interferon alpha 2 Homo sapiens 21-30 7819023-1 1995 Interferon alpha-2a (IFN-alpha) and folinic acid (FA) have been shown to modulate the cytotoxic effects of 5-fluorouracil (5-FU) in the treatment of cancer. Fluorouracil 123-127 interferon alpha 2 Homo sapiens 0-19 7819023-1 1995 Interferon alpha-2a (IFN-alpha) and folinic acid (FA) have been shown to modulate the cytotoxic effects of 5-fluorouracil (5-FU) in the treatment of cancer. Fluorouracil 123-127 interferon alpha 2 Homo sapiens 21-30 7819023-11 1995 These data suggest that biochemical modulation of 5-FU with FA and IFN-alpha has some positive effects in the treatment of pancreatic cancer of moderate toxicity. Fluorouracil 50-54 interferon alpha 2 Homo sapiens 67-76 7882458-1 1995 To determine the maximum tolerated dose (MTD) of escalating doses of interferon-alpha-2b (IFN, Intron A) with 5-fluorouracil (5-FU) and cisplatin (DDP) in patients with advanced cancer, 15 patients were accrued between May 1990 and July 1991. Fluorouracil 110-124 interferon alpha 2 Homo sapiens 69-88 9815884-0 1995 Potentiation of 5-fluorouracil-leucovorin activity by alpha2a-interferon in colon adenocarcinoma xenografts. Fluorouracil 16-30 interferon alpha 2 Homo sapiens 54-72 8085859-0 1994 [Feasibility of adjuvant high-dose CAF (cyclophosphamide, adriamycin, 5-FU) therapy for primary breast cancer patients]. Fluorouracil 70-74 lysine acetyltransferase 2B Homo sapiens 35-38 21607436-0 1994 Double alternate modulation of high-dose 5-Fluorouracil by interferon-alpha-2b and phosphonacetyl-L-aspartic Acid in patients with advanced colorectal-cancer. Fluorouracil 41-55 interferon alpha 2 Homo sapiens 59-78 8186170-10 1994 26/32 patients (81%) with SD or PR after the first chemotherapy again obtained SD or PR on high-dose 5-FU/FA but only 8/18 (44%) of those with PD after first chemotherapy did so. Fluorouracil 101-105 caveolae associated protein 2 Homo sapiens 32-34 8186170-10 1994 26/32 patients (81%) with SD or PR after the first chemotherapy again obtained SD or PR on high-dose 5-FU/FA but only 8/18 (44%) of those with PD after first chemotherapy did so. Fluorouracil 101-105 caveolae associated protein 2 Homo sapiens 85-87 8186170-13 1994 CONCLUSION: Pretreated patients with metastatic colorectal carcinoma, notably those with a primary PR or SD, can probably benefit from weekly high-dose 5-FU/FA. Fluorouracil 152-156 caveolae associated protein 2 Homo sapiens 99-101 8374869-2 1993 BACKGROUND: 5-Fluorouracil (5-FU), when combined with leucovorin (LV) or interferon-alpha (IFN-alpha), may result in improved response rates compared with 5-FU alone in patients with advanced colorectal cancer. Fluorouracil 12-26 interferon alpha 2 Homo sapiens 91-100 8374869-9 1993 The addition of IFN-alpha produced more 5-FU-related toxicity compared with a previous study in which the same dosage and schedule of 5-FU plus LV was used. Fluorouracil 40-44 interferon alpha 2 Homo sapiens 16-25 8374869-9 1993 The addition of IFN-alpha produced more 5-FU-related toxicity compared with a previous study in which the same dosage and schedule of 5-FU plus LV was used. Fluorouracil 134-138 interferon alpha 2 Homo sapiens 16-25 8374869-11 1993 However, this schedule of 5-FU combined with LV and IFN-alpha produces less toxicity compared with previous trials using bolus 5-FU plus IFN-alpha. Fluorouracil 26-30 interferon alpha 2 Homo sapiens 137-146 8339255-2 1993 Preclinical evidence suggests a similar potential role for IFN-alpha combined with cyclophosphamide, doxorubicin (Adriamycin, Adria Laboratories, Columbus, OH), and 5-fluorouracil (CAF) in advanced adenocarcinoma of the breast. Fluorouracil 165-179 lysine acetyltransferase 2B Homo sapiens 181-184 8339382-4 1993 The increased susceptibility would be a result of the induction of thymidine phosphorylase (TdR Pase), which is the essential enzyme for the conversion of 5"-dFUrd to 5-FUra. Fluorouracil 167-173 thymidine phosphorylase Homo sapiens 92-100 19920524-7 1993 This study shows that (a) interferon-alpha-2b, in the doses used, is well-tolerated by the human eye, and (b) interferon-alpha-2b may reduce the risk of failure of glaucoma filtration surgery with fewer corneal complications than are seen with 5-fluorouracil. Fluorouracil 244-258 interferon alpha 2 Homo sapiens 26-45 19920524-7 1993 This study shows that (a) interferon-alpha-2b, in the doses used, is well-tolerated by the human eye, and (b) interferon-alpha-2b may reduce the risk of failure of glaucoma filtration surgery with fewer corneal complications than are seen with 5-fluorouracil. Fluorouracil 244-258 interferon alpha 2 Homo sapiens 110-129 1435214-7 1992 25, 45 (1992) have been implemented to obtain absolute phosphate metabolite concentrations in subcutaneous RIF-1 tumors during untreated growth and following treatment with 5-fluorouracil. Fluorouracil 173-187 replication timing regulatory factor 1 Homo sapiens 107-112 1394037-1 1992 BACKGROUND: Based on initial encouraging results of the combination of 5-fluorouracil (5-FU) with recombinant alpha-2a-interferon (r alpha-2a-IFN) in the treatment of advanced colorectal carcinomas, a clinical trial was conducted using 5-FU with r alpha-2a-IFN in 49 patients with advanced pancreatic adenocarcinoma. Fluorouracil 236-240 interferon alpha 2 Homo sapiens 110-129 1657205-5 1991 Treatment based on combinations of fluorouracil, methotrexate, doxorubicin, etoposide, and cisplatin have shown high response rates (FAMTX [fluorouracil, doxorubicin, and methotrexate], EAP [etoposide, doxorubicin, and cisplatin], ELF [etoposide, leucovorin, and fluorouracil]) and a survival benefit (FAMTX). Fluorouracil 35-47 glutamyl aminopeptidase Homo sapiens 186-189 1867955-0 1991 Interaction between 5-fluorouracil, [6RS]leucovorin, and recombinant human interferon-alpha 2a in cultured colon adenocarcinoma cells. Fluorouracil 20-34 interferon alpha 2 Homo sapiens 75-94 1867955-1 1991 Recombinant human interferon-alpha 2a (rIFN-alpha 2a; 500 or 5,000 IU/mL) or [6RS] leucovorin ([6RS]LV; 1 microM) each potentiated the cytotoxic activity of 5-fluorouracil (FUra) by 2.6- to 3.2-fold during 72 hr exposures in two human colon adenocarcinoma cell lines (GC3/c1; VRC5/c1). Fluorouracil 157-171 interferon alpha 2 Homo sapiens 18-37 1867955-1 1991 Recombinant human interferon-alpha 2a (rIFN-alpha 2a; 500 or 5,000 IU/mL) or [6RS] leucovorin ([6RS]LV; 1 microM) each potentiated the cytotoxic activity of 5-fluorouracil (FUra) by 2.6- to 3.2-fold during 72 hr exposures in two human colon adenocarcinoma cell lines (GC3/c1; VRC5/c1). Fluorouracil 173-177 interferon alpha 2 Homo sapiens 18-37 33794252-11 2021 The propolis combined with 5FU reduced the expression of Cox-2, iNOS, and beta-catenin proteins. Fluorouracil 27-30 prostaglandin-endoperoxide synthase 2 Mus musculus 57-62 34665902-10 2022 The immunoblotting analysis also showed that thymol significantly inhibited the 5-FU-induced expression of nuclear factor-kappaB, tumor necrosis factor-alpha, and transforming growth factor beta-1 (TGF-beta1), in addition to the suppression of p38 and phosphorylated c-Jun N-terminal kinases (p-JNK) mitogen-activated protein kinase proteins" expressions. Fluorouracil 80-84 mitogen activated protein kinase 14 Rattus norvegicus 244-247 34927777-6 2022 Loss- and gain-function assays were performed to ascertain the effect of SOX4, miR-17, and CYLD on biological cellular processes and drug resistance to 5-FU. Fluorouracil 152-156 microRNA 17 Homo sapiens 79-85 34927777-10 2022 Functionally, SOX4 triggered drug resistance of CRC cells to 5-FU through the miR-17/CYLD axis. Fluorouracil 61-65 microRNA 17 Homo sapiens 78-84 34332405-4 2022 In this study, the 5Fu/CaPO-NH2 particles could be efficiently uptaken by cancer cells, and then decompose into Ca2+ and release 5Fu drug in the cytoplasm; therefore calcium overload and reactive oxygen species (ROS) accumulation were found in PSN1 cells that could induce cell membrane damage and elicit cell apoptosis through a series of biochemical reactions including endoplasmic reticulum stress, lipid peroxidation and mitochondrial apoptosis. Fluorouracil 19-22 5'-nucleotidase, cytosolic IIIA Homo sapiens 244-248 34332405-4 2022 In this study, the 5Fu/CaPO-NH2 particles could be efficiently uptaken by cancer cells, and then decompose into Ca2+ and release 5Fu drug in the cytoplasm; therefore calcium overload and reactive oxygen species (ROS) accumulation were found in PSN1 cells that could induce cell membrane damage and elicit cell apoptosis through a series of biochemical reactions including endoplasmic reticulum stress, lipid peroxidation and mitochondrial apoptosis. Fluorouracil 129-132 5'-nucleotidase, cytosolic IIIA Homo sapiens 244-248 34791507-13 2022 Knockdown of CD133 expression in the resistant cell lines, KOA-1/5-FU and KOA-1/PYM, decreased the survival rate and invasive ability. Fluorouracil 65-69 prominin 1 Homo sapiens 13-18 34845374-6 2022 In vivo, we observed that combined 5-FU with Thiamet-G (O-GlcNAcase (OGA) inhibitor) treatment had a synergistic inhibitory effect on grade and tumor progression. Fluorouracil 35-39 O-GlcNAcase Homo sapiens 56-67 34845374-6 2022 In vivo, we observed that combined 5-FU with Thiamet-G (O-GlcNAcase (OGA) inhibitor) treatment had a synergistic inhibitory effect on grade and tumor progression. Fluorouracil 35-39 O-GlcNAcase Homo sapiens 69-72 34966683-13 2021 The enhanced 5-FU chemosensitivity by circPVT1 knockdown was reversed with miR-30a-5p inhibitor. Fluorouracil 13-17 microRNA 30a Homo sapiens 75-82 34966683-14 2021 Besides, the increased 5-FU chemosensitivity by miR-30a-5p mimics was reversed with FZD3 overexpression. Fluorouracil 23-27 microRNA 30a Homo sapiens 48-55 34966683-14 2021 Besides, the increased 5-FU chemosensitivity by miR-30a-5p mimics was reversed with FZD3 overexpression. Fluorouracil 23-27 frizzled class receptor 3 Homo sapiens 84-88 34966683-16 2021 Conclusions: These results suggested a key role for circPVT1 in ESCC 5-FU-chemosensitivity in regulating the Wnt/beta-catenin pathway and ferroptosis via miR-30a-5p/FZD3 axis, which might be a potential target in ESCC therapy. Fluorouracil 69-73 microRNA 30a Homo sapiens 154-161 34966683-16 2021 Conclusions: These results suggested a key role for circPVT1 in ESCC 5-FU-chemosensitivity in regulating the Wnt/beta-catenin pathway and ferroptosis via miR-30a-5p/FZD3 axis, which might be a potential target in ESCC therapy. Fluorouracil 69-73 frizzled class receptor 3 Homo sapiens 165-169 34605863-2 2021 In this study, we determined the effects of FOXD3-AS1-enriched exosomes derived from lung cancer cells on the proliferation, invasion, and 5-FU resistance of lung cancer cells. Fluorouracil 139-143 prostaglandin D2 receptor Homo sapiens 50-53 34605863-7 2021 Moreover, exosome-incubated A549 cells were co-transfected with si-FOXD3-AS1 and pcDNA-ELAVL1, showing the same cell proliferation, invasion, and 5-FU resistance as those of A549 cells treated with lung cancer cell-derived exosomes alone. Fluorouracil 146-150 prostaglandin D2 receptor Homo sapiens 73-76 34747284-6 2021 5-FU injection caused marked elevation of MDA, NO, TNF-alpha, IL-1beta, IL-6, PAF, histamine, myeloperoxidase, caspase-3, and NF-kappaB expressions. Fluorouracil 0-4 caspase 3 Rattus norvegicus 111-120 34508993-11 2021 In addition, CD73high tumours indicated better chemotherapeutic responsiveness to fluorouracil yet a worse objective response rate to pembrolizumab in GC. Fluorouracil 82-94 5'-nucleotidase ecto Homo sapiens 13-17 34686918-10 2022 The imbalance in bone turnover was observed by the lower number of BMP2/4-, RUNX2-, and OCN-positive cells/mm2 and the higher number of TRAP-positive cells/mm in groups CIS and 5-FU as compared with PSS in all time points. Fluorouracil 177-181 bone morphogenetic protein 2 Homo sapiens 67-73 34683888-6 2021 The expression levels of E2F2 and Bcl-2 genes were found to be suppressed after treatment with both WO3-Cys and WO3-Trp NPs more than 5-FU-treated cells. Fluorouracil 134-138 E2F transcription factor 2 Homo sapiens 25-29 34589618-10 2021 These findings suggest that miR-30a in OSCC may be a novel biomarker of 5-FU-resistant tumors, as well as a therapeutic target for combating resistance. Fluorouracil 72-76 microRNA 30a Homo sapiens 28-35 34659563-12 2021 More importantly, advanced GAC patients with low dysbindin expression were likely to benefit from fluorouracil-based PACT. Fluorouracil 98-110 dystrobrevin binding protein 1 Homo sapiens 49-58 34659563-14 2021 Advanced GAC patients with low dysbindin expression revealed better response of fluorouracil-based adjuvant chemotherapy. Fluorouracil 80-92 dystrobrevin binding protein 1 Homo sapiens 31-40 34535128-0 2021 LncRNA LBX2-AS1 promotes colorectal cancer progression and 5-fluorouracil resistance. Fluorouracil 59-73 prostaglandin D2 receptor Homo sapiens 12-15 34535128-6 2021 In vitro and PDX models were used to determine if LBX2-AS1 promotes 5-fluorouracil resistance. Fluorouracil 68-82 prostaglandin D2 receptor Homo sapiens 55-58 34535128-11 2021 Ex vivo analysis of patient-derived CRC xenografts showed that low LBX2-AS1 expression cases exhibited 5-FU responsiveness and clinical investigations confirmed that low LBX2-AS1 expression was associated with improved clinical benefits from 5-FU therapy. Fluorouracil 242-246 prostaglandin D2 receptor Homo sapiens 175-178 34535128-12 2021 CONCLUSIONS: Together these results suggest that LBX2-AS1 may serve as a therapeutic target and predictor of 5-FU benefit in CRC patients. Fluorouracil 109-113 prostaglandin D2 receptor Homo sapiens 54-57 34507320-0 2021 Pro-pigmentary action of 5-fluorouracil through the stimulated secretion of CXCL12 by dermal fibroblasts. Fluorouracil 25-39 chemokine (C-X-C motif) ligand 12 Mus musculus 76-82 34507320-5 2021 Quantitative real-time polymerase chain reaction and Western blotting analyses were performed to detect the expression levels of CXCL12 mRNA and protein in primary mouse dermal fibroblasts treated with or without 5-FU. Fluorouracil 213-217 chemokine (C-X-C motif) ligand 12 Mus musculus 129-135 34507320-8 2021 Meanwhile, CXCL12 immunostaining was significantly increased in the dermal compartment of wounds treated with 5-FU (control vs. 5-FU, 22.47 +- 8.85 vs. 44.69 +- 5.97, P < 0.05). Fluorouracil 110-114 chemokine (C-X-C motif) ligand 12 Mus musculus 11-17 34507320-8 2021 Meanwhile, CXCL12 immunostaining was significantly increased in the dermal compartment of wounds treated with 5-FU (control vs. 5-FU, 22.47 +- 8.85 vs. 44.69 +- 5.97, P < 0.05). Fluorouracil 128-132 chemokine (C-X-C motif) ligand 12 Mus musculus 11-17 34507320-9 2021 Moreover, 5-FU significantly upregulated the expression levels of CXCL12 mRNA (control vs. 5-FU, 1.00 +- 0.08 vs. 1.54 +- 0.06, P < 0.05) and protein (control vs. 5-FU, 1.00 +- 0.06 vs. 2.93 +- 0.10, P < 0.05) in cultured fibroblasts. Fluorouracil 10-14 chemokine (C-X-C motif) ligand 12 Mus musculus 66-72 34507320-9 2021 Moreover, 5-FU significantly upregulated the expression levels of CXCL12 mRNA (control vs. 5-FU, 1.00 +- 0.08 vs. 1.54 +- 0.06, P < 0.05) and protein (control vs. 5-FU, 1.00 +- 0.06 vs. 2.93 +- 0.10, P < 0.05) in cultured fibroblasts. Fluorouracil 91-95 chemokine (C-X-C motif) ligand 12 Mus musculus 66-72 34507320-11 2021 CONCLUSION: 5-FU possesses a pro-pigmentary activity through activation of the CXCL12/CXCR4 axis to drive the chemotactic migration of melanocytes. Fluorouracil 12-16 chemokine (C-X-C motif) ligand 12 Mus musculus 79-85 34572508-0 2021 Curcumin Reverses NNMT-Induced 5-Fluorouracil Resistance via Increasing ROS and Cell Cycle Arrest in Colorectal Cancer Cells. Fluorouracil 31-45 nicotinamide N-methyltransferase Homo sapiens 18-22 34472291-7 2021 The latest research showed that the combination of 5-fluorouracil and CD13 inhibitors could inhibit the proliferation of CD13+ LCSCs, thereby reducing overall tumor burden. Fluorouracil 51-65 alanyl aminopeptidase, membrane Homo sapiens 121-125 34416072-0 2022 The clinical and pathological effectiveness of microneedling and topical 5-fluorouracil in vitiligo treatment: An association with matrix metalloproteinase 2 immunohistochemical expression. Fluorouracil 73-87 matrix metallopeptidase 2 Homo sapiens 131-157 34489705-14 2021 Compared with untreated group and 5-FU group, CHB-II-F also enhanced the expression of OX1R, GHSR, NPY, and AgRP protein and gene and decreased the expression of Ob-R, POMC, and CART protein and gene in hypothalamus of mice, and the gene expression was consistent with the protein expression. Fluorouracil 34-38 neuropeptide Y Mus musculus 99-102 34489705-14 2021 Compared with untreated group and 5-FU group, CHB-II-F also enhanced the expression of OX1R, GHSR, NPY, and AgRP protein and gene and decreased the expression of Ob-R, POMC, and CART protein and gene in hypothalamus of mice, and the gene expression was consistent with the protein expression. Fluorouracil 34-38 pro-opiomelanocortin-alpha Mus musculus 168-172 34485154-6 2021 ASP alleviated 5-FU-induced the increase in alanine aminotransferase (ALT), triglyceride (TG), and aspartate aminotransferase (AST) content; hepatic steatosis; and liver fibrosis. Fluorouracil 15-19 glutamic--pyruvic transaminase Homo sapiens 44-68 34351910-7 2021 A different stimulus (5-fluorouracil (5FU)) also showed Delta40p53:WTp53-specific changes in mRNA induction; however, other transcription factors (TFs; e.g., E2F2) could then drive the response, yielding similar outcomes vs. WTp53. Fluorouracil 22-36 E2F transcription factor 2 Homo sapiens 158-162 34351910-7 2021 A different stimulus (5-fluorouracil (5FU)) also showed Delta40p53:WTp53-specific changes in mRNA induction; however, other transcription factors (TFs; e.g., E2F2) could then drive the response, yielding similar outcomes vs. WTp53. Fluorouracil 38-41 E2F transcription factor 2 Homo sapiens 158-162 34062410-10 2021 The influence of colossolactone-G alone or in combination with GCB or 5-FU on the apoptosis and autophagy were confirmed by qPCR analysis for the expression of several key apoptosis and autophagy genes such as, TRAIL, TP53INP1, BNIP3, hp62, ATG5, ATG7, Lamp2A and the golden standard for autophagy (LC3-II). Fluorouracil 70-74 autophagy related 7 Homo sapiens 247-251 34214844-10 2021 The results showed that RB1 expressions were downregulated in GC cell lines and had significant differences between 5-FU resistance cell lines (SNU-620/5-FU and NUGC-3/5-FU) and non-resistance cell lines (SNU-620 and NUGC-3). Fluorouracil 168-172 RB transcriptional corepressor 1 Homo sapiens 24-27 34214844-11 2021 Overexpression of RB1 enhanced 5-FU sensitivity of GC cells and caused cell cycle arrest in the S phase. Fluorouracil 31-35 RB transcriptional corepressor 1 Homo sapiens 18-21 34214844-14 2021 Autophagy activator, SDF-1 treatment and CXCR4 activation reversed the promoted effects of RB1 on 5-FU sensitivity in GC cells. Fluorouracil 98-102 C-X-C motif chemokine ligand 12 Homo sapiens 21-26 34214844-14 2021 Autophagy activator, SDF-1 treatment and CXCR4 activation reversed the promoted effects of RB1 on 5-FU sensitivity in GC cells. Fluorouracil 98-102 RB transcriptional corepressor 1 Homo sapiens 91-94 34214844-16 2021 RB1 overexpression enhanced 5-FU chemosensitivity in GC cells by regulating cell autophagy via SDF-1/CXCR4 pathway. Fluorouracil 28-32 RB transcriptional corepressor 1 Homo sapiens 0-3 34236032-0 2021 (Knockdown of hexokinase 2 (HK2) inhibits breast cancer cell proliferation and reduces their resistance to fluorouracil). Fluorouracil 107-119 hexokinase 2 Homo sapiens 14-26 34236032-0 2021 (Knockdown of hexokinase 2 (HK2) inhibits breast cancer cell proliferation and reduces their resistance to fluorouracil). Fluorouracil 107-119 hexokinase 2 Homo sapiens 28-31 34236032-5 2021 Knockdown of HK2 significantly inhibited the proliferation of breast cancer cells and enhanced the killing effect of 5-FU on them. Fluorouracil 117-121 hexokinase 2 Homo sapiens 13-16 34236032-7 2021 Conclusion Knockdown of HK2 inhibits the proliferation of MDA-MB-231 breast cancer cells and reduce their resistance to 5-FU. Fluorouracil 120-124 hexokinase 2 Homo sapiens 24-27 34440086-5 2021 Based on the genetic status of adenomatous polyposis coli (APC), the most frequent mutated gene found in CRC, we found that combining a MEK inhibitor with 5-FU exhibited synergism effects on CRC cells with APC truncations. Fluorouracil 155-159 APC regulator of WNT signaling pathway Homo sapiens 31-57 34440086-5 2021 Based on the genetic status of adenomatous polyposis coli (APC), the most frequent mutated gene found in CRC, we found that combining a MEK inhibitor with 5-FU exhibited synergism effects on CRC cells with APC truncations. Fluorouracil 155-159 APC regulator of WNT signaling pathway Homo sapiens 59-62 34440086-5 2021 Based on the genetic status of adenomatous polyposis coli (APC), the most frequent mutated gene found in CRC, we found that combining a MEK inhibitor with 5-FU exhibited synergism effects on CRC cells with APC truncations. Fluorouracil 155-159 APC regulator of WNT signaling pathway Homo sapiens 206-209 34440086-6 2021 While considering the gene expression in 5-FU resistant cells, we demonstrated that targeting ROCK is a potential avenue to restore 5-FU response to resistant cells with wild-type APC background. Fluorouracil 132-136 APC regulator of WNT signaling pathway Homo sapiens 180-183 34440086-7 2021 Our results reveal MEK signaling plays a pivotal role in loss-of-function, APC-mediated 5-FU resistance, and ROCK activation serves as a signature in APC-independent 5-FU resistance. Fluorouracil 88-92 APC regulator of WNT signaling pathway Homo sapiens 75-78 34440086-7 2021 Our results reveal MEK signaling plays a pivotal role in loss-of-function, APC-mediated 5-FU resistance, and ROCK activation serves as a signature in APC-independent 5-FU resistance. Fluorouracil 166-170 APC regulator of WNT signaling pathway Homo sapiens 150-153 34589581-10 2021 Finally, in vitro and in vivo xenograft experiments consistently demonstrated that inhibition of EGFR by the specific inhibitor erlotinib effectively enhanced the anti-tumor toxicity of 5-Fu by targeting the EGFR-FGD5-AS1-miR-330-3p-HK2 pathway. Fluorouracil 186-190 FYVE, RhoGEF and PH domain containing 5 Homo sapiens 213-217 34589581-10 2021 Finally, in vitro and in vivo xenograft experiments consistently demonstrated that inhibition of EGFR by the specific inhibitor erlotinib effectively enhanced the anti-tumor toxicity of 5-Fu by targeting the EGFR-FGD5-AS1-miR-330-3p-HK2 pathway. Fluorouracil 186-190 prostaglandin D2 receptor Homo sapiens 218-221 34589581-10 2021 Finally, in vitro and in vivo xenograft experiments consistently demonstrated that inhibition of EGFR by the specific inhibitor erlotinib effectively enhanced the anti-tumor toxicity of 5-Fu by targeting the EGFR-FGD5-AS1-miR-330-3p-HK2 pathway. Fluorouracil 186-190 hexokinase 2 Homo sapiens 233-236 34279763-0 2021 The role of SIRT5 and p53 proteins in the sensitivity of colon cancer cells to chemotherapeutic agent 5-Fluorouracil. Fluorouracil 102-116 sirtuin 5 Homo sapiens 12-17 34257696-14 2021 In conclusion, the findings of the study showed that ETSJC improved the chemosensitivity of 5-FU by blocking Notch1/Hes1 signaling pathway in gastric cancer-bearing mice. Fluorouracil 92-96 hes family bHLH transcription factor 1 Mus musculus 116-120 34078881-5 2021 During adult life, the Gata2-L359V heterozygous mice exhibited a notable decrease in bone marrow (BM) recovery under stress induction with cytotoxic drug 5-fluorouracil. Fluorouracil 154-168 GATA binding protein 2 Mus musculus 23-28 34380920-6 2021 The mRNA expressions of the CYP2B6 and ATP-binding cassette transporter genes were decreased after 5-FU treatment. Fluorouracil 99-103 cytochrome P450 family 2 subfamily B member 6 Homo sapiens 28-34 35621145-3 2022 The results of cell proliferation assay revealed that the conditioned medium (CM) collected from CAFs further increased resistance to 5-fluorouracil (5-FU) in GC cell lines. Fluorouracil 134-148 T-box transcription factor 1 Homo sapiens 97-101 35621145-3 2022 The results of cell proliferation assay revealed that the conditioned medium (CM) collected from CAFs further increased resistance to 5-fluorouracil (5-FU) in GC cell lines. Fluorouracil 150-154 T-box transcription factor 1 Homo sapiens 97-101 35462329-10 2022 Furthermore, LINC00963 is associated with drug resistance in oral squamous cell carcinoma (cisplatin and 5-fluorouracil) and gastric cancer (oxaliplatin) and predicts neoadjuvant efficacy of taxane-anthracyclines in breast cancer. Fluorouracil 105-119 long intergenic non-protein coding RNA 963 Homo sapiens 13-22 35506454-0 2022 Visfatin inhibits colon cancer cell apoptosis and decreases chemosensitivity to 5-FU by promoting the SDF-1/CXCR4/Akt axis. Fluorouracil 80-84 nicotinamide phosphoribosyltransferase Homo sapiens 0-8 35506454-0 2022 Visfatin inhibits colon cancer cell apoptosis and decreases chemosensitivity to 5-FU by promoting the SDF-1/CXCR4/Akt axis. Fluorouracil 80-84 C-X-C motif chemokine ligand 12 Homo sapiens 102-107 35506454-3 2022 The present study aimed to verify the effects of visfatin on the sensitivity of colon cancer cells to 5-FU and to elucidate the potential mechanisms involved. Fluorouracil 102-106 nicotinamide phosphoribosyltransferase Homo sapiens 49-57 35506454-5 2022 Cell Counting Kit-8, clone formation, caspase-3/7 activity assays, as well as other analyses were used to verify the effects of visfatin on sensitivity to 5-FU. Fluorouracil 155-159 nicotinamide phosphoribosyltransferase Homo sapiens 128-136 35506454-7 2022 Rescue experiments and PI3K/Akt inhibitors were used to verify the role of the visfatin/SDF-1/Akt axis in the sensitivity of colon cancer cells to 5-FU. Fluorouracil 147-151 nicotinamide phosphoribosyltransferase Homo sapiens 79-87 35506454-9 2022 Moreover, visfatin knockdown increased apoptosis, reduced cell proliferation and enhanced the chemosensitivity of DLD-1 and SW48 cells to 5-FU. Fluorouracil 138-142 nicotinamide phosphoribosyltransferase Homo sapiens 10-18 35506454-10 2022 A positive correlation between visfatin and SDF-1 was observed, with the knockdown of visfatin enhancing cell sensitivity to 5-FU chemotherapy by targeting the SDF-1/C-X-C chemokine receptor type 4 (CXCR4) axis. Fluorouracil 125-129 C-X-C motif chemokine ligand 12 Homo sapiens 44-49 35506454-10 2022 A positive correlation between visfatin and SDF-1 was observed, with the knockdown of visfatin enhancing cell sensitivity to 5-FU chemotherapy by targeting the SDF-1/C-X-C chemokine receptor type 4 (CXCR4) axis. Fluorouracil 125-129 nicotinamide phosphoribosyltransferase Homo sapiens 86-94 35506454-10 2022 A positive correlation between visfatin and SDF-1 was observed, with the knockdown of visfatin enhancing cell sensitivity to 5-FU chemotherapy by targeting the SDF-1/C-X-C chemokine receptor type 4 (CXCR4) axis. Fluorouracil 125-129 C-X-C motif chemokine ligand 12 Homo sapiens 160-165 35506454-11 2022 Furthermore, the Akt signalling pathway downstream of SDF-1/CXCR4 proved to be critical in the decreased sensitisation of colon cancer cells to 5-FU induced by visfatin. Fluorouracil 144-148 C-X-C motif chemokine ligand 12 Homo sapiens 54-59 35506454-11 2022 Furthermore, the Akt signalling pathway downstream of SDF-1/CXCR4 proved to be critical in the decreased sensitisation of colon cancer cells to 5-FU induced by visfatin. Fluorouracil 144-148 nicotinamide phosphoribosyltransferase Homo sapiens 160-168 35506454-12 2022 On the whole, the present study demonstrates that visatin can potentially decrease colon cancer cell apoptosis, promote proliferation and decrease colon cancer cell sensitivity to 5-FU via the visfatin/SDF-1/Akt axis. Fluorouracil 180-184 nicotinamide phosphoribosyltransferase Homo sapiens 193-201 35506454-12 2022 On the whole, the present study demonstrates that visatin can potentially decrease colon cancer cell apoptosis, promote proliferation and decrease colon cancer cell sensitivity to 5-FU via the visfatin/SDF-1/Akt axis. Fluorouracil 180-184 C-X-C motif chemokine ligand 12 Homo sapiens 202-207 35193822-3 2022 Therefore, inhibition of TP is an attractive anticancer strategy; however, an alternative approach that exploits the catalytic activity of TP to activate 5-fluorouracil (5-FU) prodrugs has been clinically successful. Fluorouracil 154-168 thymidine phosphorylase Homo sapiens 25-27 35193822-3 2022 Therefore, inhibition of TP is an attractive anticancer strategy; however, an alternative approach that exploits the catalytic activity of TP to activate 5-fluorouracil (5-FU) prodrugs has been clinically successful. Fluorouracil 154-168 thymidine phosphorylase Homo sapiens 139-141 35193822-3 2022 Therefore, inhibition of TP is an attractive anticancer strategy; however, an alternative approach that exploits the catalytic activity of TP to activate 5-fluorouracil (5-FU) prodrugs has been clinically successful. Fluorouracil 170-174 thymidine phosphorylase Homo sapiens 25-27 35193822-3 2022 Therefore, inhibition of TP is an attractive anticancer strategy; however, an alternative approach that exploits the catalytic activity of TP to activate 5-fluorouracil (5-FU) prodrugs has been clinically successful. Fluorouracil 170-174 thymidine phosphorylase Homo sapiens 139-141 35606482-8 2022 5-FU resulted in significant cardiotoxicity represented by an increase in malondialdehyde (MDA) levels, cyclooxygenase-2 (COX-2) and tumor necrosis factor-alpha (TNF-alpha) expression, cardiac enzyme levels, and histopathological degenerations. Fluorouracil 0-4 prostaglandin-endoperoxide synthase 2 Rattus norvegicus 104-120 35606482-8 2022 5-FU resulted in significant cardiotoxicity represented by an increase in malondialdehyde (MDA) levels, cyclooxygenase-2 (COX-2) and tumor necrosis factor-alpha (TNF-alpha) expression, cardiac enzyme levels, and histopathological degenerations. Fluorouracil 0-4 prostaglandin-endoperoxide synthase 2 Rattus norvegicus 122-127 35367196-3 2022 Since the sensitivity of 5-Fu is negatively correlated with oxytocin receptor (OXTR) expression in MSS CRC cell lines, our current study aimed to investigate the synergistic antitumor activity of 5-Fu combined with atosiban, an antagonist of OXTR. Fluorouracil 196-200 oxytocin receptor Homo sapiens 60-77 35367196-3 2022 Since the sensitivity of 5-Fu is negatively correlated with oxytocin receptor (OXTR) expression in MSS CRC cell lines, our current study aimed to investigate the synergistic antitumor activity of 5-Fu combined with atosiban, an antagonist of OXTR. Fluorouracil 196-200 oxytocin receptor Homo sapiens 79-83 35394639-11 2022 CD133+ SW480 and SW620 cells were more resistant to 5-fluorouracil (5-FU) than CD133- cells. Fluorouracil 52-66 prominin 1 Homo sapiens 0-5 35394639-11 2022 CD133+ SW480 and SW620 cells were more resistant to 5-fluorouracil (5-FU) than CD133- cells. Fluorouracil 68-72 prominin 1 Homo sapiens 0-5 35394639-12 2022 In vitro and in vivo experiments showed that 5-FU and MR combined therapy further inhibited CD133+ cell activity and ATP binding cassette subfamily G member 2 (ABCG2) expression, and reduced tumor volume compared with drug administration alone. Fluorouracil 45-49 prominin 1 Homo sapiens 92-97 35149588-7 2022 Deletion of DR5 in cancer cells in vitro and in vivo abrogated the potentiating effects of CDK4/6 inhibitors on immune cytokine TNF-related apoptosis-inducing ligand (TRAIL), 5-fluorouracil (5-FU) chemotherapy, and anti-PD-1 immunotherapy. Fluorouracil 175-189 cyclin dependent kinase 4 Homo sapiens 91-97 35149588-7 2022 Deletion of DR5 in cancer cells in vitro and in vivo abrogated the potentiating effects of CDK4/6 inhibitors on immune cytokine TNF-related apoptosis-inducing ligand (TRAIL), 5-fluorouracil (5-FU) chemotherapy, and anti-PD-1 immunotherapy. Fluorouracil 191-195 cyclin dependent kinase 4 Homo sapiens 91-97 35402237-5 2022 TRPV1 overexpression induced cisplatin (DDP) and fluorouracil (5-FU) resistance in A549 cells independent of its channel function. Fluorouracil 49-61 transient receptor potential cation channel subfamily V member 1 Homo sapiens 0-5 35402237-5 2022 TRPV1 overexpression induced cisplatin (DDP) and fluorouracil (5-FU) resistance in A549 cells independent of its channel function. Fluorouracil 63-67 transient receptor potential cation channel subfamily V member 1 Homo sapiens 0-5 35402237-6 2022 TRPV1 expression was upregulated in A549-DDP/5-FU resistant cells, and DDP/5-FU sensitivity was restored by TRPV1 knockdown. Fluorouracil 45-49 transient receptor potential cation channel subfamily V member 1 Homo sapiens 0-5 35402237-6 2022 TRPV1 expression was upregulated in A549-DDP/5-FU resistant cells, and DDP/5-FU sensitivity was restored by TRPV1 knockdown. Fluorouracil 75-79 transient receptor potential cation channel subfamily V member 1 Homo sapiens 0-5 35402237-6 2022 TRPV1 expression was upregulated in A549-DDP/5-FU resistant cells, and DDP/5-FU sensitivity was restored by TRPV1 knockdown. Fluorouracil 75-79 transient receptor potential cation channel subfamily V member 1 Homo sapiens 108-113 35402237-7 2022 TRPV1 overexpression mediated DDP and 5-FU resistance by upregulation of ABCA5 drug transporter gene expression, thereby increasing drug efflux, enhancing homologous recombination (HR) DNA repair pathway to alleviate apoptosis and activating IL-8 signaling to promote cell survival. Fluorouracil 38-42 transient receptor potential cation channel subfamily V member 1 Homo sapiens 0-5 35402237-7 2022 TRPV1 overexpression mediated DDP and 5-FU resistance by upregulation of ABCA5 drug transporter gene expression, thereby increasing drug efflux, enhancing homologous recombination (HR) DNA repair pathway to alleviate apoptosis and activating IL-8 signaling to promote cell survival. Fluorouracil 38-42 ATP binding cassette subfamily A member 5 Homo sapiens 73-78 35326689-11 2022 Moreover, 5-FU/VD3/Met revealed maximal inhibitions of cell cycle inducers (CCND1/CCND3), cell survival (BCL2), and the PI3K/Akt/mTOR molecules alongside the highest expression of cell cycle inhibitors (p21/p27), proapoptotic markers (BAX/cytochrome C/caspase-3), and PTEN in both cell lines. Fluorouracil 10-14 cyclin D1 Homo sapiens 76-81 35252200-4 2022 Results: A total of 3,175 differentially expressed mRNAs (DEGs), lncRNAs (DELs), and miRNAs (DEMs) related to 5-FU resistance were identified, including significantly upregulated IL33, H19, and miR-17-5p; the downregulated AKR1B10, LINC01012, and miR-125b-5p; and chromatin modifiers such as INO80C, HDAC6, and KDM5A. Fluorouracil 110-114 interleukin 33 Homo sapiens 179-183 35252200-4 2022 Results: A total of 3,175 differentially expressed mRNAs (DEGs), lncRNAs (DELs), and miRNAs (DEMs) related to 5-FU resistance were identified, including significantly upregulated IL33, H19, and miR-17-5p; the downregulated AKR1B10, LINC01012, and miR-125b-5p; and chromatin modifiers such as INO80C, HDAC6, and KDM5A. Fluorouracil 110-114 microRNA 17 Homo sapiens 194-203 35252200-4 2022 Results: A total of 3,175 differentially expressed mRNAs (DEGs), lncRNAs (DELs), and miRNAs (DEMs) related to 5-FU resistance were identified, including significantly upregulated IL33, H19, and miR-17-5p; the downregulated AKR1B10, LINC01012, and miR-125b-5p; and chromatin modifiers such as INO80C, HDAC6, and KDM5A. Fluorouracil 110-114 aldo-keto reductase family 1 member B10 Homo sapiens 223-230 35252200-4 2022 Results: A total of 3,175 differentially expressed mRNAs (DEGs), lncRNAs (DELs), and miRNAs (DEMs) related to 5-FU resistance were identified, including significantly upregulated IL33, H19, and miR-17-5p; the downregulated AKR1B10, LINC01012, and miR-125b-5p; and chromatin modifiers such as INO80C, HDAC6, and KDM5A. Fluorouracil 110-114 long intergenic non-protein coding RNA 1012 Homo sapiens 232-241 35151311-0 2022 UHMK1-dependent phosphorylation of Cajal body protein coilin alters 5-FU sensitivity in colon cancer cells. Fluorouracil 68-72 coilin Homo sapiens 54-60 35131032-4 2022 Our results also reveal that cells depleted of KChIP3 are four times more resistant (measured as cell viability and DNA damage) to chemotherapeutics 5-Fluorouracil plus Irinotecan (5-FU+iri.) Fluorouracil 149-163 potassium voltage-gated channel interacting protein 3 Homo sapiens 47-53 35131032-4 2022 Our results also reveal that cells depleted of KChIP3 are four times more resistant (measured as cell viability and DNA damage) to chemotherapeutics 5-Fluorouracil plus Irinotecan (5-FU+iri.) Fluorouracil 181-185 potassium voltage-gated channel interacting protein 3 Homo sapiens 47-53 35131032-7 2022 Finally, sensitivity of CRC patient-derived organoids to 5-FU+iri increases 40-fold upon mucin secretion inhibition. Fluorouracil 57-61 LOC100508689 Homo sapiens 89-94 35093881-0 2022 Effect of Thymidine Phosphorylase Gene Demethylation on Sensitivity to 5-Fluorouracil in Colorectal Cancer Cells. Fluorouracil 71-85 thymidine phosphorylase Homo sapiens 10-33 35093881-2 2022 We hypothesized that thymidine phosphorylase (TYMP) expression, a rate-limiting activating enzyme of 5-FU, is regulated by methylation of the gene promoter region, and demethylation of TYMP would increase sensitivity to 5-FU. Fluorouracil 101-105 thymidine phosphorylase Homo sapiens 21-44 35093881-2 2022 We hypothesized that thymidine phosphorylase (TYMP) expression, a rate-limiting activating enzyme of 5-FU, is regulated by methylation of the gene promoter region, and demethylation of TYMP would increase sensitivity to 5-FU. Fluorouracil 101-105 thymidine phosphorylase Homo sapiens 46-50 35093881-2 2022 We hypothesized that thymidine phosphorylase (TYMP) expression, a rate-limiting activating enzyme of 5-FU, is regulated by methylation of the gene promoter region, and demethylation of TYMP would increase sensitivity to 5-FU. Fluorouracil 101-105 thymidine phosphorylase Homo sapiens 185-189 35093881-2 2022 We hypothesized that thymidine phosphorylase (TYMP) expression, a rate-limiting activating enzyme of 5-FU, is regulated by methylation of the gene promoter region, and demethylation of TYMP would increase sensitivity to 5-FU. Fluorouracil 220-224 thymidine phosphorylase Homo sapiens 21-44 35093881-2 2022 We hypothesized that thymidine phosphorylase (TYMP) expression, a rate-limiting activating enzyme of 5-FU, is regulated by methylation of the gene promoter region, and demethylation of TYMP would increase sensitivity to 5-FU. Fluorouracil 220-224 thymidine phosphorylase Homo sapiens 46-50 35093881-2 2022 We hypothesized that thymidine phosphorylase (TYMP) expression, a rate-limiting activating enzyme of 5-FU, is regulated by methylation of the gene promoter region, and demethylation of TYMP would increase sensitivity to 5-FU. Fluorouracil 220-224 thymidine phosphorylase Homo sapiens 185-189 35093881-3 2022 MATERIALS AND METHODS: HCT116 colon cancer cells were treated with 5-aza-2"-deoxycytidine, a demethylating agent, and changes in TYMP transcription and sensitivity to 5-FU were evaluated. Fluorouracil 167-171 thymidine phosphorylase Homo sapiens 129-133 35014676-0 2022 N6-methyladenosine upregulates miR-181d-5p in exosomes derived from cancer-associated fibroblasts to inhibit 5-FU sensitivity by targeting NCALD in colorectal cancer. Fluorouracil 109-113 neurocalcin delta Homo sapiens 139-144 35014676-12 2022 A mechanistic study revealed that miR-181d-5p directly targeted neurocalcin delta (NCALD) to inhibit the 5-FU sensitivity of CRC cells. Fluorouracil 105-109 neurocalcin delta Homo sapiens 64-81 35014676-12 2022 A mechanistic study revealed that miR-181d-5p directly targeted neurocalcin delta (NCALD) to inhibit the 5-FU sensitivity of CRC cells. Fluorouracil 105-109 neurocalcin delta Homo sapiens 83-88 35014676-15 2022 This led to increased miR-181d-5p expression, which inhibited the 5-FU sensitivity of CRC cells by targeting NCALD. Fluorouracil 66-70 neurocalcin delta Homo sapiens 109-114 35126817-12 2022 5-Fluorouracil resulted in significant cardiotoxicity represented by an increase in cardiac enzymes, malondialdehyde levels, cyclooxygenase-2 and tumor necrosis factor-alpha expression, cardiac enzymes, and histopathological degenerations. Fluorouracil 0-14 prostaglandin-endoperoxide synthase 2 Rattus norvegicus 125-141 34988975-3 2022 OTR-CSCC chemoprevention with topical AK treatments has not been investigated in randomised controlled trials (RCT), although there is evidence that 5% 5-fluorouracil (5-FU) maybe chemoprotective in immunocompetent patients. Fluorouracil 152-166 oxytocin receptor Homo sapiens 0-3 34988975-3 2022 OTR-CSCC chemoprevention with topical AK treatments has not been investigated in randomised controlled trials (RCT), although there is evidence that 5% 5-fluorouracil (5-FU) maybe chemoprotective in immunocompetent patients. Fluorouracil 168-172 oxytocin receptor Homo sapiens 0-3 34983557-6 2022 More importantly, Iacs-miR-30c potently suppressed the Wnt signaling pathway in vitro and in vivo, and effectively sensitized both potency of 5-Fu in PDX model of colon cancer and Anti-PD1 in B16F10 homograft model of melanoma. Fluorouracil 142-146 microRNA 30c-1 Homo sapiens 23-30 35154904-1 2022 DNA damage by genotoxic drugs such as gemcitabine and 5-fluorouracil (5-FU) activates the ataxia telangiectasia, mutated (ATM)-Chk pathway and induces the expression of NKG2D ligands such as the MHC class I-related chain A and B (MICA/B). Fluorouracil 54-68 ataxia telangiectasia mutated Mus musculus 122-125 35154904-1 2022 DNA damage by genotoxic drugs such as gemcitabine and 5-fluorouracil (5-FU) activates the ataxia telangiectasia, mutated (ATM)-Chk pathway and induces the expression of NKG2D ligands such as the MHC class I-related chain A and B (MICA/B). Fluorouracil 54-68 killer cell lectin-like receptor subfamily K, member 1 Mus musculus 169-174 35154904-1 2022 DNA damage by genotoxic drugs such as gemcitabine and 5-fluorouracil (5-FU) activates the ataxia telangiectasia, mutated (ATM)-Chk pathway and induces the expression of NKG2D ligands such as the MHC class I-related chain A and B (MICA/B). Fluorouracil 70-74 ataxia telangiectasia mutated Mus musculus 122-125 35154904-1 2022 DNA damage by genotoxic drugs such as gemcitabine and 5-fluorouracil (5-FU) activates the ataxia telangiectasia, mutated (ATM)-Chk pathway and induces the expression of NKG2D ligands such as the MHC class I-related chain A and B (MICA/B). Fluorouracil 70-74 killer cell lectin-like receptor subfamily K, member 1 Mus musculus 169-174 35075806-14 2022 CONCLUSION: Our results reveal that circCPM has a crucial role in regulating GC autophagy and 5-FU resistance by targeting PRKAA2. Fluorouracil 94-98 protein kinase AMP-activated catalytic subunit alpha 2 Homo sapiens 123-129 35071747-5 2022 Functionally, the transgenic expression of XRCC5 promoted HCC progression and 5-fluorouracil resistance, whereas short hairpin RNA knockdown of XRCC5 had converse effects in vitro and in vivo. Fluorouracil 78-92 X-ray repair cross complementing 5 Homo sapiens 43-48 35071747-5 2022 Functionally, the transgenic expression of XRCC5 promoted HCC progression and 5-fluorouracil resistance, whereas short hairpin RNA knockdown of XRCC5 had converse effects in vitro and in vivo. Fluorouracil 78-92 X-ray repair cross complementing 5 Homo sapiens 144-149 2669999-3 1989 When spleen cells from mice pretreated in vivo with 5-FU were cultured in the presence of methylcellulose medium containing recombinant interleukin-3 (rIL-3), small colonies consisting of blast cells with little sign of differentiation developed on day 7 of culture. Fluorouracil 52-56 interleukin 3 Rattus norvegicus 151-156 2484306-7 1989 IL-1 administered alone or in combination with other colony stimulating factors to spontaneous breast tumor bearing mice following 5-FU therapy resulted in a rapid recovery of neutrophils, improved survival, and markedly reduced the tumor mass. Fluorouracil 131-135 interleukin 1 complex Mus musculus 0-4 3136700-6 1988 These results indicate that the combination therapy of 5-FU and fluoropyrimidine derivatives with IFN alpha-A/D would be useful. Fluorouracil 55-59 interferon alpha 2 Homo sapiens 98-111 2453060-7 1988 In cultures of day-2 post-5-fluorouracil bone marrow cells, G-CSF in concentrations as low as 1 unit/ml revealed synergism with interleukin 3 in supporting the proliferation of multipotential progenitors. Fluorouracil 26-40 colony stimulating factor 3 (granulocyte) Mus musculus 60-65 2455481-12 1988 When mice were treated with 5-fluorouracil, cyclophosphamide or irradiation, the period of granulocytopenia was significantly shortened by subcutaneous injection of Re Hu G-CSF. Fluorouracil 28-42 colony stimulating factor 3 (granulocyte) Mus musculus 171-176 6084319-0 1984 Disappearance of antibodies to Factor VIII in a patient with acquired haemophilia and carcinoma of the pancreas during cytotoxic therapy with fluorouracil and CCNU. Fluorouracil 142-154 cytochrome c oxidase subunit 8A Homo sapiens 38-42 6438379-3 1984 Cytochrome P-450, NADPH-cytochrome P-450 reductase and NADPH were required for 5-FU production. Fluorouracil 79-83 cytochrome P450 family 2 subfamily B member 6 Homo sapiens 11-16 7407333-1 1980 Fluorouracil in human plasma of a concentration as low as 2 ng ml-1 can be assayed with the use of gas-liquid chromatography and a multiple ion detector. Fluorouracil 0-12 interleukin 17F Homo sapiens 63-67 34022544-9 2021 IL-8 and 5-FU increased MMP-2 and MMP-3 expression, while IL-6 and MTX augmented MMP-2 expression. Fluorouracil 9-13 matrix metallopeptidase 2 Homo sapiens 24-29 33978826-13 2022 We demonstrated that intratumoral Foxp3+RORgammat+ T cell infiltration was a prognostic biomarker for overall survival and the identification of patients might benefit from post-gastrectomy 5-fluorouracil. Fluorouracil 190-204 forkhead box P3 Homo sapiens 34-39 34045966-3 2021 We show that the drug of fluorouracil (5FU), epirubicin (EPI) and gemcitabine (GEM) can induce ROS generation, activate Ets2 and promote CD13 expression. Fluorouracil 25-37 alanyl aminopeptidase, membrane Homo sapiens 137-141 34045966-3 2021 We show that the drug of fluorouracil (5FU), epirubicin (EPI) and gemcitabine (GEM) can induce ROS generation, activate Ets2 and promote CD13 expression. Fluorouracil 39-42 alanyl aminopeptidase, membrane Homo sapiens 137-141 33662352-5 2021 The use of 5-FU and L-OHP, either alone or in combination, strongly suppressed Akt activation, Survivin, Bcl-2, and Bcl-xL expression, and enhanced Puma, phospho-p53, and p53 expression in Caco-2 cells than in DLD-1 cells. Fluorouracil 11-15 BCL2 binding component 3 Homo sapiens 148-152 33961855-12 2021 UCA1 enhanced cell proliferation, migration/invasion, angiogenesis, epithelial-mesenchymal transition, and resistance to 5-FU in CRC cell lines. Fluorouracil 121-125 urothelial cancer associated 1 Homo sapiens 0-4 33780262-10 2021 The inactivation of the Wnt/beta-catenin axis resulted in the reduction of resistance to 5-FU in CRC cells; while activation of the Wnt/beta-catenin axis reversed the reduced resistance to 5-FU in CRC cells caused by PITX2 knockout. Fluorouracil 89-93 Wnt family member 3A Homo sapiens 24-27 33780262-10 2021 The inactivation of the Wnt/beta-catenin axis resulted in the reduction of resistance to 5-FU in CRC cells; while activation of the Wnt/beta-catenin axis reversed the reduced resistance to 5-FU in CRC cells caused by PITX2 knockout. Fluorouracil 189-193 Wnt family member 3A Homo sapiens 132-135 33780262-12 2021 This study clarified that PITX2 enhanced resistance to 5-FU in CRC upregulating the Wnt/beta-catenin axis. Fluorouracil 55-59 Wnt family member 3A Homo sapiens 84-87 33927358-8 2021 Co-administration of GA also retarded the 5-FU-induced central fatigue-like behavior accompanied by down-regulating the expression of IL-6, iNOS and COX2 in the hippocampus through inhibiting TLR4/Myd88/NF-kappaB pathway. Fluorouracil 42-46 cytochrome c oxidase II, mitochondrial Mus musculus 149-153 33886055-5 2021 Also, 5-FU-induced kidney damage, increased levels of malondialdehyde (MDA), decreased superoxide dismutase (SOD), catalase (CAT), glutathione reductase (GR) activity, and glutathione (GSH) level have been demonstrated. Fluorouracil 6-10 glutathione reductase Mus musculus 131-152 33886055-5 2021 Also, 5-FU-induced kidney damage, increased levels of malondialdehyde (MDA), decreased superoxide dismutase (SOD), catalase (CAT), glutathione reductase (GR) activity, and glutathione (GSH) level have been demonstrated. Fluorouracil 6-10 glutathione reductase Mus musculus 154-156 33648930-4 2021 Overall survival of patients with PDAC who had undergone 5-FU-based chemotherapy was shorter in high TUG1 group than in low TUG1 group. Fluorouracil 57-61 taurine up-regulated 1 Homo sapiens 101-105 33648930-4 2021 Overall survival of patients with PDAC who had undergone 5-FU-based chemotherapy was shorter in high TUG1 group than in low TUG1 group. Fluorouracil 57-61 taurine up-regulated 1 Homo sapiens 124-128 33648930-6 2021 TUG1 depletion induced susceptibility to 5-FU in BxPC-3 and PK-9 pancreatic cell lines. Fluorouracil 41-45 taurine up-regulated 1 Homo sapiens 0-4 33648930-7 2021 Consistently, the cellular concentration of 5-FU was significantly higher under TUG1-depleted conditions. Fluorouracil 44-48 taurine up-regulated 1 Homo sapiens 80-84 33648930-8 2021 In PDAC xenograft models, intravenous treatment with a cancer-specific drug delivery system (TUG1-DDS) and 5-FU significantly suppressed PDAC tumor growth compared with 5-FU treatment alone. Fluorouracil 169-173 taurine up-regulated 1 Homo sapiens 93-97 33648930-9 2021 This novel approach using TUG1-DDS in combination with 5-FU may serve as an effective therapeutic option to attenuate DPD activity and meet appropriate 5-FU dosage requirements in targeted PDAC cells, which can reduce the systemic adverse effects of chemotherapy. Fluorouracil 152-156 taurine up-regulated 1 Homo sapiens 26-30 33648930-10 2021 SIGNIFICANCE: Targeting TUG1 coupled with a cancer-specific drug delivery system effectively modulates 5-FU catabolism in TUG1-overexpressing PDAC cells, thus contributing to a new combinatorial strategy for cancer treatment. Fluorouracil 103-107 taurine up-regulated 1 Homo sapiens 24-28 33648930-10 2021 SIGNIFICANCE: Targeting TUG1 coupled with a cancer-specific drug delivery system effectively modulates 5-FU catabolism in TUG1-overexpressing PDAC cells, thus contributing to a new combinatorial strategy for cancer treatment. Fluorouracil 103-107 taurine up-regulated 1 Homo sapiens 122-126 33472949-0 2021 Crosstalk between YAP and RAR-RXR drives expression of stemness genes to promote 5-FU resistance and self-renewal in colorectal cancer cells. Fluorouracil 81-85 Yes1 associated transcriptional regulator Homo sapiens 18-21 33472949-2 2021 We previously showed that in 5FU-resistant colorectal cancer (CRC) cells the transcriptional co-activator YAP is differentially regulated at critical transitions connected with reversible quiescence/dormancy to promote metastasis. Fluorouracil 29-32 Yes1 associated transcriptional regulator Homo sapiens 106-109 33472949-3 2021 Here we found that experimental YAP activation in 5FU-sensitive and 5FU-resistant HT29 CRC cells enhanced nuclear YAP localization and the transcript levels of the retinoic acid (RA) receptors RARalpha/gamma and RAR target genes CYP26A1, ALDH1A3 and LGR5 through RA Response Elements (RAREs). Fluorouracil 50-53 Yes1 associated transcriptional regulator Homo sapiens 32-35 33472949-3 2021 Here we found that experimental YAP activation in 5FU-sensitive and 5FU-resistant HT29 CRC cells enhanced nuclear YAP localization and the transcript levels of the retinoic acid (RA) receptors RARalpha/gamma and RAR target genes CYP26A1, ALDH1A3 and LGR5 through RA Response Elements (RAREs). Fluorouracil 50-53 Yes1 associated transcriptional regulator Homo sapiens 114-117 33472949-3 2021 Here we found that experimental YAP activation in 5FU-sensitive and 5FU-resistant HT29 CRC cells enhanced nuclear YAP localization and the transcript levels of the retinoic acid (RA) receptors RARalpha/gamma and RAR target genes CYP26A1, ALDH1A3 and LGR5 through RA Response Elements (RAREs). Fluorouracil 50-53 leucine rich repeat containing G protein-coupled receptor 5 Homo sapiens 250-254 33472949-3 2021 Here we found that experimental YAP activation in 5FU-sensitive and 5FU-resistant HT29 CRC cells enhanced nuclear YAP localization and the transcript levels of the retinoic acid (RA) receptors RARalpha/gamma and RAR target genes CYP26A1, ALDH1A3 and LGR5 through RA Response Elements (RAREs). Fluorouracil 68-71 Yes1 associated transcriptional regulator Homo sapiens 32-35 33472949-3 2021 Here we found that experimental YAP activation in 5FU-sensitive and 5FU-resistant HT29 CRC cells enhanced nuclear YAP localization and the transcript levels of the retinoic acid (RA) receptors RARalpha/gamma and RAR target genes CYP26A1, ALDH1A3 and LGR5 through RA Response Elements (RAREs). Fluorouracil 68-71 Yes1 associated transcriptional regulator Homo sapiens 114-117 33472949-3 2021 Here we found that experimental YAP activation in 5FU-sensitive and 5FU-resistant HT29 CRC cells enhanced nuclear YAP localization and the transcript levels of the retinoic acid (RA) receptors RARalpha/gamma and RAR target genes CYP26A1, ALDH1A3 and LGR5 through RA Response Elements (RAREs). Fluorouracil 68-71 leucine rich repeat containing G protein-coupled receptor 5 Homo sapiens 250-254 33674443-10 2021 Human peripheral blood monocytes co-cultured with ESCC cells treated with 5-FU/CDDP increased the expression of CD163, which was attenuated by the treatment with CSF-1R inhibitors. Fluorouracil 74-78 colony stimulating factor 1 receptor Homo sapiens 162-168 33426680-1 2021 Equilibrative nucleoside transporters (ENTs) 1 and 2 reportedly accept fluorouracil as a substrate. Fluorouracil 71-83 solute carrier family 29 member 1 (Augustine blood group) Homo sapiens 0-52 33426680-2 2021 Here, we evaluated ENT1/2 expression at the mRNA, protein and functional levels in a panel of four triple-negative breast cancer (TNBC) cell lines, BT-549, Hs578T, MDA-MB-231, and MDA-MB-435, and we examined the relationship of the observed profiles to fluorouracil sensitivity. Fluorouracil 253-265 solute carrier family 29 member 1 (Augustine blood group) Homo sapiens 19-25 33645623-16 2021 In summary, this study suggests a new molecular mechanism for the NEAT1-mediated 5-Fu resistance via the miR-34a/LDHA-glycolysis axis. Fluorouracil 81-85 microRNA 34a Homo sapiens 105-112 33392922-10 2021 Interestingly, the use of FO alongwith 5-FU also significantly declined the expression of drug transporters (ABCB1,ABCC5) and consequently resulted in an increased cellular uptake of 5-FU and its metabolite, 5-FdUMP at target site (colon). Fluorouracil 39-43 ATP-binding cassette, sub-family C (CFTR/MRP), member 5 Mus musculus 115-120 33658858-0 2021 The Combination Therapy of Fluorouracil and Oxaliplatin Suppress the Progression of Colon Cancer Through miR-183-5p/SOCS3 Axis and Downregulating PD-L1. Fluorouracil 27-39 suppressor of cytokine signaling 3 Homo sapiens 116-121 33658858-1 2021 Purpose: The purpose of this study was to investigate the mechanism of combination of fluorouracil (FU) and oxaliplatin (OXA) on the progression of colon cancer via miR-183-5p/SOCS3 axis and regulating PD-L1. Fluorouracil 86-98 suppressor of cytokine signaling 3 Homo sapiens 176-181 33462372-11 2021 Finally, CAF elimination by CAFs-PIT in vivo demonstrated that the combination of 5-FU and NIR-PIT succeeded in producing 70.9% tumor reduction, while 5-FU alone achieved only 13.3% reduction, suggesting the recovery of 5-FU sensitivity in CAF-rich tumors. Fluorouracil 82-86 lysine acetyltransferase 2B Homo sapiens 9-12 33489876-8 2020 E2F7 silencing reduced the production of ALDH1+ and CD133+ colon cancer stem cells and antagonized the effects of 5-fluorouracil (5-FU) treatment. Fluorouracil 114-128 E2F transcription factor 7 Homo sapiens 0-4 33489876-8 2020 E2F7 silencing reduced the production of ALDH1+ and CD133+ colon cancer stem cells and antagonized the effects of 5-fluorouracil (5-FU) treatment. Fluorouracil 130-134 E2F transcription factor 7 Homo sapiens 0-4 33310186-4 2021 Whether the FDA-approved clinical drug 5-fluorouracil (5-FU) that is used to target the enzyme thymidylate synthase for anticancer therapy can also bind to SSBs remains unknown. Fluorouracil 39-53 thymidylate synthase Staphylococcus aureus 95-115 33310186-4 2021 Whether the FDA-approved clinical drug 5-fluorouracil (5-FU) that is used to target the enzyme thymidylate synthase for anticancer therapy can also bind to SSBs remains unknown. Fluorouracil 55-59 thymidylate synthase Staphylococcus aureus 95-115 33500737-7 2021 5-FU and miR-34a(m) were loaded into TCP1-CD-QD nanocarriers, which were used to treat CRC in vitro and in vivo. Fluorouracil 0-4 t-complex 1 Homo sapiens 37-41 33500737-9 2021 Results: 5-FU and miR-34a(m) can be efficiently encapsulated into TCP1-CD-QD nanocarriers and delivered into CRC cells, which led to the inhibition of the proliferation and migration of CRC cells in vitro and suppression of tumor growth in a CRC cell-derived tumor xenograft model. Fluorouracil 9-13 t-complex 1 Homo sapiens 66-70 33091827-3 2021 Therefore, we identified the expression of eight genes closely associated with platinum and fluorouracil metabolism (RRM1, RRM2, RRM2B, POLH, DUT, TYMS, TYMP, MKI67) in the discovery cohort (N=291). Fluorouracil 92-104 ribonucleotide reductase catalytic subunit M1 Homo sapiens 117-121 33091827-3 2021 Therefore, we identified the expression of eight genes closely associated with platinum and fluorouracil metabolism (RRM1, RRM2, RRM2B, POLH, DUT, TYMS, TYMP, MKI67) in the discovery cohort (N=291). Fluorouracil 92-104 ribonucleotide reductase regulatory TP53 inducible subunit M2B Homo sapiens 129-134 33377131-6 2020 Susceptible tumors are characterized by a stemness signature, an activated interferon pathway, and suppression of PD-1 ligands in response to 5-FU+irinotecan. Fluorouracil 142-146 programmed cell death 1 Homo sapiens 114-118 33051247-12 2020 In particular, let-7c enhances 5-FU exposure (via suppressing ABCC5/MRP5 expression) and co-targets thymidylate synthase with 5-FU (let-7c reduces protein expression while 5-FU irreversibly inactivates enzyme). Fluorouracil 126-130 ATP binding cassette subfamily C member 5 Homo sapiens 62-67 33051247-12 2020 In particular, let-7c enhances 5-FU exposure (via suppressing ABCC5/MRP5 expression) and co-targets thymidylate synthase with 5-FU (let-7c reduces protein expression while 5-FU irreversibly inactivates enzyme). Fluorouracil 126-130 ATP binding cassette subfamily C member 5 Homo sapiens 68-72 33046798-0 2020 Molecular biological analysis of 5-FU-resistant gastric cancer organoids; KHDRBS3 contributes to the attainment of features of cancer stem cell. Fluorouracil 33-37 KH RNA binding domain containing, signal transduction associated 3 Homo sapiens 74-81 33046798-8 2020 We found KHDRBS3 to be an independent prognostic factor in GC patients, especially in GC patients treated with 5-FU chemotherapy. Fluorouracil 111-115 KH RNA binding domain containing, signal transduction associated 3 Homo sapiens 9-16 33256074-0 2020 SAHA Overcomes 5-FU Resistance in IFIT2-Depleted Oral Squamous Cell Carcinoma Cells. Fluorouracil 15-19 interferon induced protein with tetratricopeptide repeats 2 Homo sapiens 34-39 33256074-3 2020 In this study, we found that IFIT2-knockdown cells displayed higher resistance to 5-fluorouracil (5-FU) than control cells. Fluorouracil 82-96 interferon induced protein with tetratricopeptide repeats 2 Homo sapiens 29-34 33256074-3 2020 In this study, we found that IFIT2-knockdown cells displayed higher resistance to 5-fluorouracil (5-FU) than control cells. Fluorouracil 98-102 interferon induced protein with tetratricopeptide repeats 2 Homo sapiens 29-34 33256074-4 2020 The comet assay and annexin V analysis showed decreased DNA damage and cell death in IFIT2-knockdown cells compared to control cells treated with 5-FU. Fluorouracil 146-150 interferon induced protein with tetratricopeptide repeats 2 Homo sapiens 85-90 33256074-5 2020 Cell cycle progression was also perturbed by 5-FU treatment, with the accumulation of IFIT2-depleted cells in S phase in a time-dependent manner. Fluorouracil 45-49 interferon induced protein with tetratricopeptide repeats 2 Homo sapiens 86-91 33256074-7 2020 Inhibition of TS alone or double inhibition of TS and TK1 using the siRNA technique increased susceptibility to 5-FU in IFIT2-knockdown cells. Fluorouracil 112-116 interferon induced protein with tetratricopeptide repeats 2 Homo sapiens 120-125 33256074-8 2020 We further identified that suberanilohydroxamic acid (SAHA) treatment decreased the expression of TS in IFIT2-knockdown cells and demonstrated that pretreatment with SAHA sensitized IFIT2-knockdown cells to 5-FU in vitro and in vivo. Fluorouracil 207-211 interferon induced protein with tetratricopeptide repeats 2 Homo sapiens 182-187 33256074-9 2020 In conclusion, IFIT2 knockdown enhances TS expression, which mediates 5-FU resistance, and SAHA pretreatment suppresses TS expression and hence sensitizes cells to 5-FU. Fluorouracil 70-74 interferon induced protein with tetratricopeptide repeats 2 Homo sapiens 15-20 32561283-6 2020 Further mechanistic studies indicated that the 5-Fu + SATP group showed a decrease in hepatotoxicity caused by 5-Fu via a reduction in the levels of interleukin-1beta (IL-1beta), an increase in the expression of Bcl-2 and decreases in the expression of p-p38, p-JNK and Bax. Fluorouracil 47-51 mitogen-activated protein kinase 14 Mus musculus 255-258 33177877-13 2020 Our research suggested that CDK1 may be used to predict 5-Fu efficacy and as a therapeutic target for CRC. Fluorouracil 56-60 cyclin-dependent kinase 1 Mus musculus 28-32 32907836-6 2020 UPP1 facilitated the conversion of 5-FU to its active compound, thereby enhancing the inhibition of thymidylate synthase. Fluorouracil 35-39 uridine phosphorylase 1 Homo sapiens 0-4 32907836-7 2020 Consistently, knockout of UPP1 abrogated the tumor inhibitory effect of combined CB-839 and 5-FU administration. Fluorouracil 92-96 uridine phosphorylase 1 Homo sapiens 26-30 32785986-1 2020 Intralesional 5- fluorouracil (IL5-FU) has been used off-label for warts treatment; however its use was limited by intense pain. Fluorouracil 14-29 interleukin 5 Homo sapiens 31-34 32864839-3 2020 Here, we comprehensively studied the influence of ATP levels on the functional state of the human enzyme, uridine phosphorylase I (hUP1), which is responsible for activating the chemotherapeutic pro-drug, 5-fluorouracil. Fluorouracil 205-219 heterogeneous nuclear ribonucleoprotein A1 Homo sapiens 131-135 32483624-3 2020 Deletion of Yap1 and Taz induces a loss of HSC quiescence, symmetric self-renewal ability and renders HSC more vulnerable to serial myeloablative 5-fluorouracil treatment. Fluorouracil 146-160 Yes1 associated transcriptional regulator Homo sapiens 12-16 33016107-0 2020 CAVIN2 is frequently silenced by CpG methylation and sensitizes lung cancer cells to paclitaxel and 5-FU. Fluorouracil 100-104 caveolae associated protein 2 Homo sapiens 0-6 33016107-6 2020 Furthermore, ectopic expression of CAVIN2 inhibits cell proliferation in vivo and in vitro by inducing G2/M cell cycle arrest, which sensitizes the chemosensitivity of lung cancer cells to paclitaxel and 5-fluorouracil, but not cisplatin. Fluorouracil 204-218 caveolae associated protein 2 Homo sapiens 35-41 33016107-7 2020 Conclusion: CAVIN2 is a tumor suppressor in non-small-cell lung cancer and can sensitize lung cancer cells to paclitaxel and 5-fluorouracil. Fluorouracil 125-139 caveolae associated protein 2 Homo sapiens 12-18 32945504-7 2020 We also found that combined treatment of Rg3 and 5-FU significantly enhanced the apoptosis of colon cancer cells by activating the Apaf1/caspase 9/caspase 3 pathway and arrested the cell cycle of the colon cancer cells in G0/G1 by promoting the expression of Cyclin D1, CDK2 and CDK4. Fluorouracil 49-53 cyclin dependent kinase 2 Homo sapiens 270-274 32945504-7 2020 We also found that combined treatment of Rg3 and 5-FU significantly enhanced the apoptosis of colon cancer cells by activating the Apaf1/caspase 9/caspase 3 pathway and arrested the cell cycle of the colon cancer cells in G0/G1 by promoting the expression of Cyclin D1, CDK2 and CDK4. Fluorouracil 49-53 cyclin dependent kinase 4 Homo sapiens 279-283 32888127-2 2020 In this study, we explored the relationship between silencing SEMA4D expression and 5-fluorouracil (5-FU) response in the colorectal cancer cell line. Fluorouracil 84-98 semaphorin 4D Homo sapiens 62-68 32888127-2 2020 In this study, we explored the relationship between silencing SEMA4D expression and 5-fluorouracil (5-FU) response in the colorectal cancer cell line. Fluorouracil 100-104 semaphorin 4D Homo sapiens 62-68 32888127-3 2020 SW48 cells were transfected with a short interfering RNA (siRNA) in order to silence SEMA4D gene expression and then exposed to 5-FU for 48 h. The down-regulation of SEMA4D expression was confirmed by qRT-PCR and the particular concentration of 5-FU was acquired using MTT assay. Fluorouracil 128-132 semaphorin 4D Homo sapiens 166-172 32888127-3 2020 SW48 cells were transfected with a short interfering RNA (siRNA) in order to silence SEMA4D gene expression and then exposed to 5-FU for 48 h. The down-regulation of SEMA4D expression was confirmed by qRT-PCR and the particular concentration of 5-FU was acquired using MTT assay. Fluorouracil 245-249 semaphorin 4D Homo sapiens 166-172 32888127-7 2020 Our data demonstrate that SEMA4D silencing results in strikingly elevated apoptosis in response to 5-FU treatment and leads to down-regulation of Bcl-2 and overexpression of Bax, P53, and caspase-3 in protein levels. Fluorouracil 99-103 semaphorin 4D Homo sapiens 26-32 32888127-10 2020 This study implicates that the silencing of SEMA4D by siRNA promotes the chemosensitivity of SW48 cells to 5-FU and it may be a potential therapeutic agent for colon cancer therapy. Fluorouracil 107-111 semaphorin 4D Homo sapiens 44-50 32729895-7 2020 Additionally, CD133+CD44+ cells presented significant chemoresistance compared with corresponding nontumorigenic CD133-CD44- cells following exposure to oxaliplatin or 5-FU. Fluorouracil 168-172 prominin 1 Homo sapiens 14-19 32847597-8 2020 NPTXR silencing promoted caspase-mediated apoptosis and attenuated GC cell proliferation, cell cycle progression, migration, invasion, adhesion, stem cell-like properties, and resistance to 5-fluorouracil in vitro, and also inhibited the tumorigenicity of GC cells in vivo. Fluorouracil 190-204 neuronal pentraxin receptor Homo sapiens 0-5 32339641-5 2020 Moreover, RHBDD2 expression is induced by 5Fu. Fluorouracil 42-45 rhomboid domain containing 2 Homo sapiens 10-16 32339641-6 2020 In this study, we demonstrate that the overexpression of RHBDD2 in CACO2 cell line confers resistance to 5Fu, favors cell migration, adhesion and proliferation and has a profound impact on the expression of both, the UPR genes BiP, PERK and CHOP, and on the cell adhesion genes FAK and PXN. Fluorouracil 105-108 rhomboid domain containing 2 Homo sapiens 57-63 32497621-0 2020 Roles of a TMPO-AS1/microRNA-200c/TMEFF2 ceRNA network in the malignant behaviors and 5-FU resistance of ovarian cancer cells. Fluorouracil 86-90 microRNA 200c Homo sapiens 20-33 32497621-9 2020 Silenced TMPO-AS1 and over-expressed miR-200c inhibited epithelial-mesenchymal transition (EMT), invasion, migration and 5-FU resistance of OC cells. Fluorouracil 121-125 TMPO antisense RNA 1 Homo sapiens 9-17 32497621-9 2020 Silenced TMPO-AS1 and over-expressed miR-200c inhibited epithelial-mesenchymal transition (EMT), invasion, migration and 5-FU resistance of OC cells. Fluorouracil 121-125 microRNA 200c Homo sapiens 37-45 32975155-3 2020 Results: Combination treatment with 5-FU and radiation had a stronger effect on decreasing Bcl-2 expression and increasing expression of Bax, cleaved caspase-9, cleaved caspase-3, cleaved PARP compared with each treatment alone. Fluorouracil 36-40 collagen type XI alpha 2 chain Homo sapiens 188-192 32760222-16 2020 Exogenous increase in miR-203 in the EC cell lines significantly inhibited Snail-1 mediated in vitro pro-metastatic function of invasion, wound-healing, and increased chemosensitivity to 5-FU. Fluorouracil 187-191 microRNA 203a Homo sapiens 22-29 32742490-0 2020 Combinational inhibition of EGFR and YAP reverses 5-Fu resistance in colorectal cancer. Fluorouracil 50-54 Yes1 associated transcriptional regulator Homo sapiens 37-40 32253228-12 2020 CONCLUSIONS: The combination of trametinib with 5FU-CRT is safe and well-tolerated, and may warrant additional study in a phase II trial, perhaps in a RAS/RAF-mutant selected population. Fluorouracil 48-51 zinc fingers and homeoboxes 2 Homo sapiens 155-158 32247004-12 2020 Besides, Andro markedly down-regulated the 5-Fu-induced protein expression of caspase8/3, Bax and the phosphorylation of p38. Fluorouracil 43-47 caspase 8 Homo sapiens 78-88 32627138-0 2020 Expression profile of stem cell markers and ABC transporters in 5-fluorouracil resistant Hep-2 cells. Fluorouracil 64-78 ATP binding cassette subfamily B member 6 (Langereis blood group) Homo sapiens 44-47 32627138-2 2020 In this study, we aimed at investigating the expression profiles of ATP-binding cassette (ABC) transporters and stem cell markers in 5-fluorouracil (5-FU) resistant laryngeal Hep-2 cells. Fluorouracil 133-147 ATP binding cassette subfamily B member 6 (Langereis blood group) Homo sapiens 68-88 32627138-2 2020 In this study, we aimed at investigating the expression profiles of ATP-binding cassette (ABC) transporters and stem cell markers in 5-fluorouracil (5-FU) resistant laryngeal Hep-2 cells. Fluorouracil 133-147 ATP binding cassette subfamily B member 6 (Langereis blood group) Homo sapiens 90-93 32627138-2 2020 In this study, we aimed at investigating the expression profiles of ATP-binding cassette (ABC) transporters and stem cell markers in 5-fluorouracil (5-FU) resistant laryngeal Hep-2 cells. Fluorouracil 149-153 ATP binding cassette subfamily B member 6 (Langereis blood group) Homo sapiens 68-88 32627138-2 2020 In this study, we aimed at investigating the expression profiles of ATP-binding cassette (ABC) transporters and stem cell markers in 5-fluorouracil (5-FU) resistant laryngeal Hep-2 cells. Fluorouracil 149-153 ATP binding cassette subfamily B member 6 (Langereis blood group) Homo sapiens 90-93 32627138-7 2020 Expressions of tested ABC transporters (ABCA5, ABCB1, ABCB6, ABCC1, ABCC2, ABCC3, ABCC5, ABCC10 and ABCF2, and ABCG2) were also deregulated in 5-FU resistant Hep-2 cells. Fluorouracil 143-147 ATP binding cassette subfamily B member 6 (Langereis blood group) Homo sapiens 22-25 32627138-7 2020 Expressions of tested ABC transporters (ABCA5, ABCB1, ABCB6, ABCC1, ABCC2, ABCC3, ABCC5, ABCC10 and ABCF2, and ABCG2) were also deregulated in 5-FU resistant Hep-2 cells. Fluorouracil 143-147 ATP binding cassette subfamily A member 5 Homo sapiens 40-45 32627138-7 2020 Expressions of tested ABC transporters (ABCA5, ABCB1, ABCB6, ABCC1, ABCC2, ABCC3, ABCC5, ABCC10 and ABCF2, and ABCG2) were also deregulated in 5-FU resistant Hep-2 cells. Fluorouracil 143-147 ATP binding cassette subfamily B member 6 (Langereis blood group) Homo sapiens 54-59 32627138-7 2020 Expressions of tested ABC transporters (ABCA5, ABCB1, ABCB6, ABCC1, ABCC2, ABCC3, ABCC5, ABCC10 and ABCF2, and ABCG2) were also deregulated in 5-FU resistant Hep-2 cells. Fluorouracil 143-147 ATP binding cassette subfamily C member 3 Homo sapiens 75-80 32627138-7 2020 Expressions of tested ABC transporters (ABCA5, ABCB1, ABCB6, ABCC1, ABCC2, ABCC3, ABCC5, ABCC10 and ABCF2, and ABCG2) were also deregulated in 5-FU resistant Hep-2 cells. Fluorouracil 143-147 ATP binding cassette subfamily C member 5 Homo sapiens 82-87 32627138-8 2020 Although their expressions remained unaltered at the beginning of acquisition of resistance, expressions of ABC transporters except from ABCB6 increased significantly when cells became resistant to higher doses of 5-FU. Fluorouracil 214-218 ATP binding cassette subfamily B member 6 (Langereis blood group) Homo sapiens 108-111 32627138-8 2020 Although their expressions remained unaltered at the beginning of acquisition of resistance, expressions of ABC transporters except from ABCB6 increased significantly when cells became resistant to higher doses of 5-FU. Fluorouracil 214-218 ATP binding cassette subfamily B member 6 (Langereis blood group) Homo sapiens 137-142 32753880-0 2020 Helicobacter pylori CagA Protein Attenuates 5-Fu Sensitivity of Gastric Cancer Cells Through Upregulating Cellular Glucose Metabolism. Fluorouracil 44-48 S100 calcium binding protein A8 Homo sapiens 20-24 32753880-5 2020 The 5-Fu resistant gastric cancer cell line was generated from MKN45-CagA cells which was transfected with CagA overexpression vector. Fluorouracil 4-8 S100 calcium binding protein A8 Homo sapiens 69-73 32753880-5 2020 The 5-Fu resistant gastric cancer cell line was generated from MKN45-CagA cells which was transfected with CagA overexpression vector. Fluorouracil 4-8 S100 calcium binding protein A8 Homo sapiens 107-111 32753880-7 2020 Results: We report that the Helicobacter pylori (H. pylori)-secreted Cytotoxin-associated gene A (CagA) oncoprotein is positively correlated with 5-Fu resistance of gastric cancer. Fluorouracil 146-150 S100 calcium binding protein A8 Homo sapiens 98-102 32753880-8 2020 From totally 72 CagA-positive gastric cancer patients, CagA high-expressed patients showed more resistance to 5-Fu than CagA low-expressed patients. Fluorouracil 110-114 S100 calcium binding protein A8 Homo sapiens 16-20 32753880-8 2020 From totally 72 CagA-positive gastric cancer patients, CagA high-expressed patients showed more resistance to 5-Fu than CagA low-expressed patients. Fluorouracil 110-114 S100 calcium binding protein A8 Homo sapiens 55-59 32753880-8 2020 From totally 72 CagA-positive gastric cancer patients, CagA high-expressed patients showed more resistance to 5-Fu than CagA low-expressed patients. Fluorouracil 110-114 S100 calcium binding protein A8 Homo sapiens 55-59 32753880-9 2020 Moreover, statistical analysis revealed that CagA mRNA and protein expressions were significantly upregulated in 5-Fu resistant gastric cancer patients. Fluorouracil 113-117 S100 calcium binding protein A8 Homo sapiens 45-49 32753880-10 2020 We observed that CagA protein is upregulated in 5-Fu resistant gastric cancer cells compared with sensitive cells. Fluorouracil 48-52 S100 calcium binding protein A8 Homo sapiens 17-21 32753880-12 2020 The Akt phosphorylation and expressions of glycolysis key enzymes, Hexokinase 2 and LDHA, were significantly upregulated in 5-Fu resistant gastric cancer cells. Fluorouracil 124-128 hexokinase 2 Homo sapiens 67-79 32753880-14 2020 Finally, we report that the combination of Akt or glycolysis inhibitor with 5-Fu could synergistically enhance the cytotoxicity of 5-Fu to CagA-overexpressed gastric cancer cells. Fluorouracil 76-80 S100 calcium binding protein A8 Homo sapiens 139-143 32753880-14 2020 Finally, we report that the combination of Akt or glycolysis inhibitor with 5-Fu could synergistically enhance the cytotoxicity of 5-Fu to CagA-overexpressed gastric cancer cells. Fluorouracil 131-135 S100 calcium binding protein A8 Homo sapiens 139-143 32753880-15 2020 Discussion: In summary, our study demonstrated a CagA-Akt-glycolysis-5-Fu resistance axis, contributing to the development of new therapeutic agents against chemoresistant human gastric cancer. Fluorouracil 69-73 S100 calcium binding protein A8 Homo sapiens 49-53 32460371-4 2020 In this study, we assessed the auxiliary antitumor effects of immunomodulatory fungal proteins from Hericium erinaceus (HEP) administered with the chemotherapy drug 5-Fluorouracil (5-Fu), and we attempted to identify new potential prebiotic bacteria for auxiliary antitumor treatment. Fluorouracil 181-185 histocompatibility 51 Mus musculus 120-123 32460371-6 2020 In a xenografted mouse model of cancer, HEP with 5-Fu significantly suppressed tumor growth, inhibited inflammatory markers such as interferon (IFN)-gamma, interleukin (IL)-1beta, IL-2, IL-6, tumor necrosis factor (TNF)-alpha, and lipopolysaccharide (LPS), and regulated the expression of Akt, CCDN1, CKD4, FOXM1, MMP7, MYC, PPAR-alpha, and PPAR-gamma. Fluorouracil 49-53 histocompatibility 51 Mus musculus 40-43 32460371-6 2020 In a xenografted mouse model of cancer, HEP with 5-Fu significantly suppressed tumor growth, inhibited inflammatory markers such as interferon (IFN)-gamma, interleukin (IL)-1beta, IL-2, IL-6, tumor necrosis factor (TNF)-alpha, and lipopolysaccharide (LPS), and regulated the expression of Akt, CCDN1, CKD4, FOXM1, MMP7, MYC, PPAR-alpha, and PPAR-gamma. Fluorouracil 49-53 myelocytomatosis oncogene Mus musculus 320-323 32460371-6 2020 In a xenografted mouse model of cancer, HEP with 5-Fu significantly suppressed tumor growth, inhibited inflammatory markers such as interferon (IFN)-gamma, interleukin (IL)-1beta, IL-2, IL-6, tumor necrosis factor (TNF)-alpha, and lipopolysaccharide (LPS), and regulated the expression of Akt, CCDN1, CKD4, FOXM1, MMP7, MYC, PPAR-alpha, and PPAR-gamma. Fluorouracil 49-53 peroxisome proliferator activated receptor gamma Mus musculus 341-351 32460371-8 2020 This demonstrates that HEP could promote the antitumor efficacy of 5-Fu by improving the microbiota composition, the immune inflammatory response, and homeostasis. Fluorouracil 67-71 histocompatibility 51 Mus musculus 23-26 32427870-9 2020 miR-21 targets PDCD4, TPM1 and PTEN were down-regulated by exosomes and silencing of PDCD4 mimicked miR-21 functional effects, even the induced resistance against 5-FU. Fluorouracil 163-167 programmed cell death 4 Homo sapiens 15-20 32427870-9 2020 miR-21 targets PDCD4, TPM1 and PTEN were down-regulated by exosomes and silencing of PDCD4 mimicked miR-21 functional effects, even the induced resistance against 5-FU. Fluorouracil 163-167 programmed cell death 4 Homo sapiens 85-90 32370786-11 2020 Furthermore, downregulation of GLYR1 decreased the sensitivity to 5-fluorouracil (5-FU) by inhibiting the mitochondrial apoptosis pathway in CRC cells. Fluorouracil 66-80 glyoxylate reductase 1 homolog Homo sapiens 31-36 32370786-11 2020 Furthermore, downregulation of GLYR1 decreased the sensitivity to 5-fluorouracil (5-FU) by inhibiting the mitochondrial apoptosis pathway in CRC cells. Fluorouracil 82-86 glyoxylate reductase 1 homolog Homo sapiens 31-36 32370786-13 2020 CONCLUSIONS: Ours is the first study to elucidate the role of GLYR1 in tumors and provide evidence for GLYR1 as a biological marker that reflects the degree of malignancy and sensitivity to 5-FU in MSI CRC. Fluorouracil 190-194 glyoxylate reductase 1 homolog Homo sapiens 62-67 32370786-13 2020 CONCLUSIONS: Ours is the first study to elucidate the role of GLYR1 in tumors and provide evidence for GLYR1 as a biological marker that reflects the degree of malignancy and sensitivity to 5-FU in MSI CRC. Fluorouracil 190-194 glyoxylate reductase 1 homolog Homo sapiens 103-108 32426273-8 2020 Then, the anti-cancer drug 5-fluorouracil was used to stimulate the NCI-H460 cells; the mRNA levels of miR-93, miR-373, and miR-17-5p were decreased, and the level of TBP-2 mRNA and protein was increased. Fluorouracil 27-41 microRNA 373 Homo sapiens 111-118 32426273-8 2020 Then, the anti-cancer drug 5-fluorouracil was used to stimulate the NCI-H460 cells; the mRNA levels of miR-93, miR-373, and miR-17-5p were decreased, and the level of TBP-2 mRNA and protein was increased. Fluorouracil 27-41 microRNA 17 Homo sapiens 124-133 32426273-8 2020 Then, the anti-cancer drug 5-fluorouracil was used to stimulate the NCI-H460 cells; the mRNA levels of miR-93, miR-373, and miR-17-5p were decreased, and the level of TBP-2 mRNA and protein was increased. Fluorouracil 27-41 TATA-box binding protein like 2 Homo sapiens 167-172 31102118-9 2020 Additionally, the combination of cardamonin and 5-FU might result in the apoptosis and cell cycle arrest of BGC-823/5-FU cells, accompanied by the downregulated expression levels of P-glycoprotein, beta-catenin and TCF4. Fluorouracil 48-52 transcription factor 4 Homo sapiens 215-219 32144252-8 2020 Further investigation showed that NOD2 exerted its anti-tumor effect through activating adenosine 5"-monophosphate (AMP) -activated protein kinase (AMPK) signaling pathway, and NOD2 significantly enhanced the sensitivity of HCC cells to sorafenib, lenvatinib and 5-FU treatment through activating AMPK pathway induced apoptosis. Fluorouracil 263-267 nucleotide-binding oligomerization domain containing 2 Mus musculus 34-38 32144252-8 2020 Further investigation showed that NOD2 exerted its anti-tumor effect through activating adenosine 5"-monophosphate (AMP) -activated protein kinase (AMPK) signaling pathway, and NOD2 significantly enhanced the sensitivity of HCC cells to sorafenib, lenvatinib and 5-FU treatment through activating AMPK pathway induced apoptosis. Fluorouracil 263-267 nucleotide-binding oligomerization domain containing 2 Mus musculus 177-181 32195170-9 2020 Loss of HK2 in HNSCC cells resulted in reduced cell (in vitro) and tumor (in vivo) growth, as well as decreased epithelial-mesenchymal transition-mediated cell movement; in contrast, HK2-deficient HNSCC cells exhibited greater sensitivity to chemotherapeutic drugs cisplatin and 5-fluorouracil but are more resistant to photodynamic therapy, indicating that HK2 expression could selectively define treatment sensitivity in HNSCC cells. Fluorouracil 279-293 hexokinase 2 Homo sapiens 8-11 32066801-1 2020 Capecitabine is selectively converted from 5"-DFUR to 5-fluorouracil (5-FU) in tumours by thymidine phosphorylase (TP). Fluorouracil 54-68 thymidine phosphorylase Homo sapiens 90-113 32066801-1 2020 Capecitabine is selectively converted from 5"-DFUR to 5-fluorouracil (5-FU) in tumours by thymidine phosphorylase (TP). Fluorouracil 54-68 thymidine phosphorylase Homo sapiens 115-117 32066801-1 2020 Capecitabine is selectively converted from 5"-DFUR to 5-fluorouracil (5-FU) in tumours by thymidine phosphorylase (TP). Fluorouracil 70-74 thymidine phosphorylase Homo sapiens 90-113 32066801-1 2020 Capecitabine is selectively converted from 5"-DFUR to 5-fluorouracil (5-FU) in tumours by thymidine phosphorylase (TP). Fluorouracil 70-74 thymidine phosphorylase Homo sapiens 115-117 32127943-6 2020 We found that B7-H3 could effectively enhance the resistance to a chemotherapeutic drug (oxaliplatin or 5-fluorouracil) via CDC25A. Fluorouracil 104-118 CD276 molecule Homo sapiens 14-19 31778273-1 2020 The high expression of human equilibrative nucleoside transporter-1 (hENT1) and the low expression of dihydropyrimidine dehydrogenase (DPD) are reported to predict a favorable prognosis in patients treated with gemcitabine (GEM) and 5-fluorouracil (5FU) as the adjuvant setting, respectively. Fluorouracil 233-247 solute carrier family 29 member 1 (Augustine blood group) Homo sapiens 29-67 31778273-1 2020 The high expression of human equilibrative nucleoside transporter-1 (hENT1) and the low expression of dihydropyrimidine dehydrogenase (DPD) are reported to predict a favorable prognosis in patients treated with gemcitabine (GEM) and 5-fluorouracil (5FU) as the adjuvant setting, respectively. Fluorouracil 233-247 solute carrier family 29 member 1 (Augustine blood group) Homo sapiens 69-74 31778273-1 2020 The high expression of human equilibrative nucleoside transporter-1 (hENT1) and the low expression of dihydropyrimidine dehydrogenase (DPD) are reported to predict a favorable prognosis in patients treated with gemcitabine (GEM) and 5-fluorouracil (5FU) as the adjuvant setting, respectively. Fluorouracil 249-252 solute carrier family 29 member 1 (Augustine blood group) Homo sapiens 29-67 31778273-1 2020 The high expression of human equilibrative nucleoside transporter-1 (hENT1) and the low expression of dihydropyrimidine dehydrogenase (DPD) are reported to predict a favorable prognosis in patients treated with gemcitabine (GEM) and 5-fluorouracil (5FU) as the adjuvant setting, respectively. Fluorouracil 249-252 solute carrier family 29 member 1 (Augustine blood group) Homo sapiens 69-74 31760170-0 2020 LncRNA HAND2-AS1 inhibits 5-fluorouracil resistance by modulating miR-20a/PDCD4 axis in colorectal cancer. Fluorouracil 26-40 prostaglandin D2 receptor Homo sapiens 13-16 31760170-0 2020 LncRNA HAND2-AS1 inhibits 5-fluorouracil resistance by modulating miR-20a/PDCD4 axis in colorectal cancer. Fluorouracil 26-40 programmed cell death 4 Homo sapiens 74-79 31760170-15 2020 Moreover, HAND2-AS1 suppressed cell progression and 5-FU resistance by upregulating PDCD4 via sponging miR-20a in 5-FU-resistant CRC cells. Fluorouracil 114-118 programmed cell death 4 Homo sapiens 84-89 31760170-17 2020 CONCLUSION: HAND2-AS1/miR-20a/PDCD4 axis inhibited cell progression and 5-FU resistance in 5-FU-resistant CRC cells. Fluorouracil 72-76 programmed cell death 4 Homo sapiens 30-35 31760170-17 2020 CONCLUSION: HAND2-AS1/miR-20a/PDCD4 axis inhibited cell progression and 5-FU resistance in 5-FU-resistant CRC cells. Fluorouracil 91-95 programmed cell death 4 Homo sapiens 30-35 31864766-0 2020 Corrigendum to "5-Fluorouracil causes severe CNS demyelination by disruption of TCF7L2/HDAC1/HDAC2 complex in adolescent mice" [Toxicology 325 (2014) 144-150]. Fluorouracil 16-30 transcription factor 7 like 2, T cell specific, HMG box Mus musculus 80-86 31936203-11 2020 Our findings suggest that TRX at a concentration of 100 mg/kg had chemopreventive effects on 5-FU-induced intestinal mucositis via COX-2 pathway. Fluorouracil 93-97 prostaglandin-endoperoxide synthase 2 Mus musculus 131-136 31906589-7 2020 Clusterin (CLU), a marker of the revival stem cell population, was significantly enriched following 5-FU treatment and expression correlated with the level of drug resistance. Fluorouracil 100-104 clusterin Homo sapiens 0-9 31906589-7 2020 Clusterin (CLU), a marker of the revival stem cell population, was significantly enriched following 5-FU treatment and expression correlated with the level of drug resistance. Fluorouracil 100-104 clusterin Homo sapiens 11-14 32304779-12 2020 5-FU resistance of CRC cells was mediated by CpG-methylation of miR-34a and the resulting elevated expression of CSF1R. Fluorouracil 0-4 microRNA 34a Homo sapiens 64-71 32304779-12 2020 5-FU resistance of CRC cells was mediated by CpG-methylation of miR-34a and the resulting elevated expression of CSF1R. Fluorouracil 0-4 colony stimulating factor 1 receptor Homo sapiens 113-118 31401369-0 2020 Modulation of 5-fluorouracil activation of toll-like/MyD88/NF-kappaB/MAPK pathway by Saccharomyces boulardii CNCM I-745 probiotic. Fluorouracil 14-28 MYD88 innate immune signal transduction adaptor Homo sapiens 53-58 31702387-5 2020 Functionally, knockdown of UCA1 remarkably inhibited proliferation and sensitized retinoblastoma cells to multiple chemotherapy drugs, including vincristine (VCR), carboplatin (CBP), cisplatin (DDP), VP-16 (etoposide), and 5-fluorouracil (5-Fu). Fluorouracil 223-237 urothelial cancer associated 1 Homo sapiens 27-31 31702387-5 2020 Functionally, knockdown of UCA1 remarkably inhibited proliferation and sensitized retinoblastoma cells to multiple chemotherapy drugs, including vincristine (VCR), carboplatin (CBP), cisplatin (DDP), VP-16 (etoposide), and 5-fluorouracil (5-Fu). Fluorouracil 239-243 urothelial cancer associated 1 Homo sapiens 27-31 33097678-1 2020 Cancer stem cells (CSCs) from colorectal cancer (CRC), characterized by CD133 expression, have been associated with 5-fluorouracile (5-FU) chemoresistance. Fluorouracil 133-137 prominin 1 Homo sapiens 72-77 33097678-3 2020 The aim of this study was to evaluate the modulation of CD133 and MGMT in MMRproficient and MMR-deficient CRC cells under 5-FU treatment and the effect of this drug in CSCs. Fluorouracil 122-126 prominin 1 Homo sapiens 56-61 33097678-8 2020 5-FU treatment increased CD133 expression independently to MMR status in SW480 and RKO and was able to increase hMLH1 expression in RKO, a MMR-deficient cell line. Fluorouracil 0-4 prominin 1 Homo sapiens 25-30 31897166-6 2020 The combination of oxymatrine and 5-FU reduced the protein expression of snail family transcriptional repressor 2 and vimentin, phosphorylated p65 and induced the expression of E-cadherin, by inhibiting the nuclear factor kappaB (NF-kappaB) signaling pathway. Fluorouracil 34-38 RELA proto-oncogene, NF-kB subunit Homo sapiens 143-146 31835445-0 2019 Pharmacological Inhibition of TFF3 Enhances Sensitivity of CMS4 Colorectal Carcinoma to 5-Fluorouracil through Inhibition of p44/42 MAPK. Fluorouracil 88-102 mitogen-activated protein kinase 3 Mus musculus 125-128 31646712-5 2019 On the other hand, miR-338-5p-knockdown induced 5-FU resistance in chemosensitive esophageal cell lines, while knockdown of both miR-338-5p and Id-1 re-sensitized the cells to 5-FU. Fluorouracil 176-180 inhibitor of DNA binding 1, HLH protein Homo sapiens 144-148 30362384-5 2019 SLC-0111 also increases breast cancer cell response to Doxorubicin and enhances 5-Fluorouracil cytostatic activity on colon cancer cells. Fluorouracil 80-94 C-C motif chemokine ligand 21 Homo sapiens 0-3 31582208-0 2019 H1, a derivative of tetrandrine, enhances the efficacy of 5-FU in Bel7402/5-FU cells via suppressing STAT3/MCL-1 and inducing PUMA. Fluorouracil 58-62 BCL2 binding component 3 Homo sapiens 126-130 31582208-9 2019 Taken together, H1 effectively improve the cytotoxic effect of 5-FU against Bel7402/5-FU cells via blocking STAT3/MCL-1 pathway and inducing PUMA. Fluorouracil 63-67 BCL2 binding component 3 Homo sapiens 141-145 31685921-7 2019 Inhibition of MYD88 reduced antagonistic cytotoxic effects between CKI and 5-Fu, indicating that MYD88 is an important gene in the DDI mechanism between CKI and chemotherapy drugs. Fluorouracil 75-79 MYD88 innate immune signal transduction adaptor Homo sapiens 14-19 31685921-7 2019 Inhibition of MYD88 reduced antagonistic cytotoxic effects between CKI and 5-Fu, indicating that MYD88 is an important gene in the DDI mechanism between CKI and chemotherapy drugs. Fluorouracil 75-79 MYD88 innate immune signal transduction adaptor Homo sapiens 97-102 31704837-8 2019 These results indicated that the simultaneous expression of APEX1 and Jagged-1 might be associated with chemoresistance toward 5-FU, oxaliplatin, and irinotecan. Fluorouracil 127-131 apurinic/apyrimidinic endodeoxyribonuclease 1 Homo sapiens 60-65 31444231-6 2019 Here, we show that loss of LGR5 in colon cancer cells enhanced resistance to irinotecan and 5-fluorouracil and increased expression of adhesion G-protein-coupled receptor, GPR56. Fluorouracil 92-106 leucine rich repeat containing G protein-coupled receptor 5 Homo sapiens 27-31 31579069-0 2019 miR-361 enhances sensitivity to 5-fluorouracil by targeting the FOXM1-ABCC5/10 signaling pathway in colorectal cancer. Fluorouracil 32-46 microRNA 361 Homo sapiens 0-7 31579069-0 2019 miR-361 enhances sensitivity to 5-fluorouracil by targeting the FOXM1-ABCC5/10 signaling pathway in colorectal cancer. Fluorouracil 32-46 ATP binding cassette subfamily C member 5 Homo sapiens 70-75 31579069-3 2019 The present study investigated several candidate microRNAs (miRs) in parental and 5-FU-resistant HCT116 and HT29 cells, and identified miR-361 as a novel regulator of chemosensitivity. Fluorouracil 82-86 microRNA 361 Homo sapiens 135-142 31454556-16 2019 Furthermore, knockdown of PLCbeta3, PKCdelta and SRC increased the susceptibility of Bel/5-Fu cells to 5-Fu. Fluorouracil 89-93 phospholipase C beta 3 Homo sapiens 26-34 31454556-16 2019 Furthermore, knockdown of PLCbeta3, PKCdelta and SRC increased the susceptibility of Bel/5-Fu cells to 5-Fu. Fluorouracil 89-93 protein kinase C delta Homo sapiens 36-44 31454556-16 2019 Furthermore, knockdown of PLCbeta3, PKCdelta and SRC increased the susceptibility of Bel/5-Fu cells to 5-Fu. Fluorouracil 103-107 phospholipase C beta 3 Homo sapiens 26-34 31454556-16 2019 Furthermore, knockdown of PLCbeta3, PKCdelta and SRC increased the susceptibility of Bel/5-Fu cells to 5-Fu. Fluorouracil 103-107 protein kinase C delta Homo sapiens 36-44 31686841-0 2019 MAP3K1 rs889312 genotypes influence survival outcomes of Chinese gastric cancer patients who received adjuvant chemotherapy based on platinum and fluorouracil regimes. Fluorouracil 146-158 mitogen-activated protein kinase kinase kinase 1 Homo sapiens 0-6 31395078-8 2019 Among the drugs in Folfox chemotherapy, we confirmed that 5-FU increased the expression of CCL20 in CRC. Fluorouracil 58-62 C-C motif chemokine ligand 20 Homo sapiens 91-96 31395078-9 2019 Moreover, CCL20 derived from 5-FU-resistant CRC cells promoted recruitment of Tregs. Fluorouracil 29-33 C-C motif chemokine ligand 20 Homo sapiens 10-15 31395078-11 2019 FOXO1/CEBPB/NF-kappaB signaling was activated in CRC cells after 5-FU treatment and was required for CCL20 upregulation mediated by 5-FU. Fluorouracil 65-69 CCAAT enhancer binding protein beta Homo sapiens 6-11 31395078-11 2019 FOXO1/CEBPB/NF-kappaB signaling was activated in CRC cells after 5-FU treatment and was required for CCL20 upregulation mediated by 5-FU. Fluorouracil 132-136 CCAAT enhancer binding protein beta Homo sapiens 6-11 31395078-11 2019 FOXO1/CEBPB/NF-kappaB signaling was activated in CRC cells after 5-FU treatment and was required for CCL20 upregulation mediated by 5-FU. Fluorouracil 132-136 C-C motif chemokine ligand 20 Homo sapiens 101-106 31395078-12 2019 Furthermore, CCL20 blockade suppressed tumor progression and restored 5-FU sensitivity in CRC. Fluorouracil 70-74 C-C motif chemokine ligand 20 Homo sapiens 13-18 30536714-5 2019 Blood monocytes depletion by 5-fluorouracil (5-FU) significantly limited the neuroprotection of RIPC or G-CSF treatment. Fluorouracil 29-43 colony stimulating factor 3 (granulocyte) Mus musculus 104-109 30536714-5 2019 Blood monocytes depletion by 5-fluorouracil (5-FU) significantly limited the neuroprotection of RIPC or G-CSF treatment. Fluorouracil 45-49 colony stimulating factor 3 (granulocyte) Mus musculus 104-109 31189612-6 2019 Mechanistically, vorinostat reverted 5FU/CDDP-induced EGFR phosphorylation and nuclear translocation, leading to the impairment of nuclear EGFR noncanonical induction of genes such as thymidylate synthase and cyclin D1. Fluorouracil 37-40 cyclin D1 Homo sapiens 209-218 31341363-9 2019 Also, RA decreased protein expression of Wee1, while the combinational effect of RA and 5-Fu decreased protein expressions of cyclooxygenase-2, B cell lymphoma 2, and Wee1 but increased protein levels of Bax, cyclin D1, and cyclin E. CONCLUSION: Taken together, the results suggest that RA acts as an anti-cancer agent and enhancer of 5-Fu in bile duct cancer cells via regulating multiple cell cycle and apoptosis-related proteins. Fluorouracil 88-92 cyclin D1 Homo sapiens 209-218 31217433-9 2019 The repression of 5-FU-induced caspase-1 activity by DHA supplementation is partially due to beta-arrestin-2-dependent inhibition of NLRP3 inflammasome activity but was independent of JNK pathway. Fluorouracil 18-22 caspase 1 Mus musculus 31-40 31033216-7 2019 Furthermore, a xenograft nude mouse model showed that silencing RAD18 significantly slowed tumor growth after irradiation or/and 5-Fu in vivo. Fluorouracil 129-133 RAD18 E3 ubiquitin protein ligase Mus musculus 64-69 31042625-3 2019 Unlike other acetyltransferases and deacetylases, we found that the expression of acetyltransferase P300/CBP-associated factor (PCAF) is consistently decreased in three 5-FU resistant CRC cell lines. Fluorouracil 169-173 lysine acetyltransferase 2B Homo sapiens 128-132 31042625-4 2019 Similarly, knockdown of PCAF in HCT116 CRC parental cell line also increases the resistance to 5-FU and attenuates 5-FU-induced apoptosis. Fluorouracil 95-99 lysine acetyltransferase 2B Homo sapiens 24-28 31042625-4 2019 Similarly, knockdown of PCAF in HCT116 CRC parental cell line also increases the resistance to 5-FU and attenuates 5-FU-induced apoptosis. Fluorouracil 115-119 lysine acetyltransferase 2B Homo sapiens 24-28 31042625-5 2019 Mechanistically, we demonstrated that increased binding of trimethylated histone H3K27 in the promoter region of PCAF attenuated its transcription in 5-FU resistant HCT116/5-FU cells. Fluorouracil 150-154 lysine acetyltransferase 2B Homo sapiens 113-117 31042625-5 2019 Mechanistically, we demonstrated that increased binding of trimethylated histone H3K27 in the promoter region of PCAF attenuated its transcription in 5-FU resistant HCT116/5-FU cells. Fluorouracil 172-176 lysine acetyltransferase 2B Homo sapiens 113-117 31042625-7 2019 Conversely, overexpression of PCAF in CRC cell lines increases p21 and their susceptibility to 5-FU in vitro and in vivo. Fluorouracil 95-99 lysine acetyltransferase 2B Homo sapiens 30-34 31042625-8 2019 However, knockdown of p21 abolishes the beneficial effects of PCAF overexpression on increasing the sensitivity of HCT116/5-FU cells to 5-FU. Fluorouracil 122-126 lysine acetyltransferase 2B Homo sapiens 62-66 30150027-0 2019 SCID/NOD mice model for 5-FU induced intestinal mucositis: Safety and effects of probiotics as therapy. Fluorouracil 24-28 protein kinase, DNA activated, catalytic polypeptide Mus musculus 0-4 30150027-11 2019 Average VH significantly decreased and CD significantly increased in SCID mice given 5-FU. Fluorouracil 85-89 protein kinase, DNA activated, catalytic polypeptide Mus musculus 69-73 30150027-13 2019 Besides IL-13, all cytokine levels increased in 5-FU SCID mice. Fluorouracil 48-52 protein kinase, DNA activated, catalytic polypeptide Mus musculus 53-57 30150027-16 2019 CONCLUSION: Using SCID/NOD mice as a novel model for 5-FU induced intestinal mucositis, we find that probiotics Lcr35 and LaBi do not lead to bacteremia, can improve diarrhea and body weight, can restore jejunal crypt depth, and significantly inhibit cytokines TNF-alpha, IL-1beta, IFNgamma, IL-6, IL-4, IL-10, and IL-17. Fluorouracil 53-57 protein kinase, DNA activated, catalytic polypeptide Mus musculus 18-22 30582240-1 2019 BACKGROUND: To evaluate the expression of programmed death-1 (PD-1) and programmed death-ligand 1 (PD-L1) by using immunohistochemistry analysis in locoregionally advanced nasopharyngeal carcinoma (NPC) patients receiving cisplatin, fluorouracil, and docetaxel followed by concurrent chemoradiotherapy. Fluorouracil 233-245 programmed cell death 1 Homo sapiens 42-60 30884120-0 2019 Inhibition of circular RNA CDR1as increases chemosensitivity of 5-FU-resistant BC cells through up-regulating miR-7. Fluorouracil 64-68 cerebellar degeneration related antigen 1 Mus musculus 27-31 30884120-9 2019 In comparison to si-CDR1as group, CCNE1 was increased and chemosensitivity to 5-Fu was suppressed in si-CDR1as + miR-7 inhibitor group. Fluorouracil 78-82 cerebellar degeneration related antigen 1 Mus musculus 20-24 30944308-0 2019 VPS33B interacts with NESG1 to modulate EGFR/PI3K/AKT/c-Myc/P53/miR-133a-3p signaling and induce 5-fluorouracil sensitivity in nasopharyngeal carcinoma. Fluorouracil 97-111 VPS33B late endosome and lysosome associated Homo sapiens 0-6 30944308-2 2019 In this research, we demonstrated that overexpression of VPS33B inhibited proliferation and chemoresistance to fluorouracil (5-FU) in nasopharyngeal carcinoma (NPC) in vivo and in vitro. Fluorouracil 111-123 VPS33B late endosome and lysosome associated Homo sapiens 57-63 30944308-2 2019 In this research, we demonstrated that overexpression of VPS33B inhibited proliferation and chemoresistance to fluorouracil (5-FU) in nasopharyngeal carcinoma (NPC) in vivo and in vitro. Fluorouracil 125-129 VPS33B late endosome and lysosome associated Homo sapiens 57-63 30213181-8 2019 5-Fluorouracil treatment also accelerated the expression of the pro-apoptotic protein BAX and decelerated the expression of the anti-apoptotic protein Bcl-xL on melanoma cell line. Fluorouracil 0-14 BCL2-like 1 Mus musculus 151-157 30587545-11 2019 Among patients receiving 5-fluorouracil (5-FU)-based systemic chemotherapy, those with SMAD4 loss had a median RFS of 3.8 years compared with 13 years for patients with SMAD4 retained. Fluorouracil 25-39 SMAD family member 4 Homo sapiens 87-92 30587545-11 2019 Among patients receiving 5-fluorouracil (5-FU)-based systemic chemotherapy, those with SMAD4 loss had a median RFS of 3.8 years compared with 13 years for patients with SMAD4 retained. Fluorouracil 25-39 SMAD family member 4 Homo sapiens 169-174 30587545-11 2019 Among patients receiving 5-fluorouracil (5-FU)-based systemic chemotherapy, those with SMAD4 loss had a median RFS of 3.8 years compared with 13 years for patients with SMAD4 retained. Fluorouracil 41-45 SMAD family member 4 Homo sapiens 87-92 30587545-11 2019 Among patients receiving 5-fluorouracil (5-FU)-based systemic chemotherapy, those with SMAD4 loss had a median RFS of 3.8 years compared with 13 years for patients with SMAD4 retained. Fluorouracil 41-45 SMAD family member 4 Homo sapiens 169-174 30770552-5 2019 After combination treatment of 5-FU and LEP-2a, Ras/Raf/MEK/ERK and PI3K/AKT/mTOR pathway were inactivated. Fluorouracil 31-35 zinc fingers and homeoboxes 2 Homo sapiens 52-55 31582661-8 2019 Methotrexate slightly increased dipeptidyl peptidase IV (DPP-4) mRNA expression, whereas 5-fluorouracil significantly increased DPP-4 mRNA expression. Fluorouracil 89-103 dipeptidylpeptidase 4 Rattus norvegicus 128-133 30662539-1 2019 Purpose: The aim of the preliminary study was to evaluate the efficacy and safety of 4-week chemotherapy with 5-Fluorouracil and leucovorin (LV5FU2) during the resting periods between preoperative CRT and surgery in patients with LARC. Fluorouracil 110-124 C-C motif chemokine ligand 20 Homo sapiens 230-234 29495973-8 2018 The recovered CCND1 expression counteracted the effects of miR-623 on GC cell proliferation, chemosensitivity, and 5-FU-induced apoptosis. Fluorouracil 115-119 cyclin D1 Homo sapiens 14-19 30205014-0 2018 Vitamin D potentiates anti-tumor activity of 5-fluorouracil via modulating caspase-3 and TGF-beta1 expression in hepatocellular carcinoma-induced in rats. Fluorouracil 45-59 caspase 3 Rattus norvegicus 75-84 30205014-6 2018 Treatment with 5-FU + Vit D significantly decreased gene expression of nuclear factor erythroid 2-related factor 2 (NrF2) and transforming growth factor beta1 (TGF-beta1) at both the gene and protein level and serum AFP concentrations in comparison with their corresponding monotherapy. Fluorouracil 15-19 alpha-fetoprotein Rattus norvegicus 216-219 30205014-7 2018 Moreover, 5-FU + Vit D treatment enhanced apoptosis by increasing caspase-3 gene and protein expression. Fluorouracil 10-14 caspase 3 Rattus norvegicus 66-75 30564297-11 2018 Notably, losartan, an angiotensin receptor blocker, inhibited intracellular angiotensin-II production and AGTR2 nuclear localization to enhance the antitumoral effect of 5-FU in an OSCC tumor model. Fluorouracil 170-174 angiotensin II receptor type 2 Homo sapiens 106-111 30464507-0 2018 RGS17 inhibits tumorigenesis and improves 5-fluorouracil sensitivity in nasopharyngeal carcinoma. Fluorouracil 42-56 regulator of G protein signaling 17 Homo sapiens 0-5 30464507-8 2018 In addition, RGS17 could significantly improve the sensitivity of NPC cells to 5-FU. Fluorouracil 79-83 regulator of G protein signaling 17 Homo sapiens 13-18 29991529-5 2018 Brk was robustly induced following exposure of TNBC model systems to chemotherapeutic agents (Taxol or 5-fluorouracil) and growth in suspension [ultra-low attachment (ULA)]. Fluorouracil 103-117 protein tyrosine kinase 6 Homo sapiens 0-3 30304835-0 2018 Cytoplasmic p21 Mediates 5-Fluorouracil Resistance by Inhibiting Pro-Apoptotic Chk2. Fluorouracil 25-39 checkpoint kinase 2 Homo sapiens 79-83 30304835-3 2018 Here, we show for the first time that cytoplasmic p21 mediates 5-Fluorouracil (5FU) resistance by shuttling p-Chk2 out of the nucleus to protect the tumor cells from its pro-apoptotic functions. Fluorouracil 63-77 checkpoint kinase 2 Homo sapiens 110-114 30304835-3 2018 Here, we show for the first time that cytoplasmic p21 mediates 5-Fluorouracil (5FU) resistance by shuttling p-Chk2 out of the nucleus to protect the tumor cells from its pro-apoptotic functions. Fluorouracil 79-82 checkpoint kinase 2 Homo sapiens 110-114 30250581-0 2018 MiR-1260b inhibitor enhances the chemosensitivity of colorectal cancer cells to fluorouracil by targeting PDCD4/IGF1. Fluorouracil 80-92 programmed cell death 4 Homo sapiens 106-111 29890207-8 2018 Of particular importance, HDAC1 inhibitor vorinostat restored ASPP2 transcription and produced a synergistic effect with 5-FU in elevating ASPP2, promoting apoptosis and inhibiting EMT in both in vitro and in vivo RCC models. Fluorouracil 121-125 tumor protein p53 binding protein 2 Homo sapiens 139-144 29959920-9 2018 Our work demonstrates that eIF4E inhibition using inhibitor or siRNA, either as single agent or in combination, could sensitize chemoresistant cancer cells to paclitaxel or 5-FU treatment and thereby improving the efficacy of chemodrug. Fluorouracil 173-177 eukaryotic translation initiation factor 4E Homo sapiens 27-32 30220130-0 2018 [MiR--210 promotes 5--fluorouracil resistance in breast cancer cells by increasing the antioxidant activity mediated by GPX1]. Fluorouracil 22-34 microRNA 210 Homo sapiens 1-9 29953965-10 2018 Moreover, inhibition of miR-17 reduced resistance to cisplatin- or 5-Fu in GC cells and induced cisplatin- or 5-Fu-treated GC cell apoptosis, which evaluated by using CCK-8 and flow cytometry assays. Fluorouracil 67-71 microRNA 17 Homo sapiens 24-30 29953965-10 2018 Moreover, inhibition of miR-17 reduced resistance to cisplatin- or 5-Fu in GC cells and induced cisplatin- or 5-Fu-treated GC cell apoptosis, which evaluated by using CCK-8 and flow cytometry assays. Fluorouracil 110-114 microRNA 17 Homo sapiens 24-30 31949859-0 2018 c-Jun and Camk2a contribute to the drug resistance of induction docetaxel/cisplatin/5-fluorouracil in hypopharyngeal carcinoma. Fluorouracil 84-98 calcium/calmodulin dependent protein kinase II alpha Homo sapiens 10-16 30127965-0 2018 miR-329 regulates the sensitivity of 5-FU in chemotherapy of colorectal cancer by targeting E2F1. Fluorouracil 37-41 E2F transcription factor 1 L homeolog Xenopus laevis 92-96 30127965-15 2018 miR-329 expression is reduced in CRC, and overexpression of miR-329 promotes the sensitivity of 5-FU in the chemotherapy of CRC by degrading the target gene E2F1. Fluorouracil 96-100 E2F transcription factor 1 L homeolog Xenopus laevis 157-161 30214243-11 2018 Conclusion: Our results indicate that STARD13 could enhances 5-FU sensitivity by suppressing cancer stemness in hepatocellular carcinoma cells via attenuating YAP transcriptional activity. Fluorouracil 61-65 Yes1 associated transcriptional regulator Homo sapiens 159-162 29772441-0 2018 Six2 is negatively correlated with good prognosis and decreases 5-FU sensitivity via suppressing E-cadherin expression in hepatocellular carcinoma cells. Fluorouracil 64-68 SIX homeobox 2 Homo sapiens 0-4 29772441-1 2018 This work aims to study the roles and related mechanisms of six2 in 5-FU sensitivity of hepatocellular carcinoma (HCC) cells. Fluorouracil 68-72 SIX homeobox 2 Homo sapiens 60-64 29772441-4 2018 Additionally, six2 overexpression decreased the sensitivity of HCC cells to 5-Fu, characterized as attenuating 5-FU-induced cell apoptosis and downregulation of cell viability, and promoted HCC cells stemness. Fluorouracil 76-80 SIX homeobox 2 Homo sapiens 14-18 29772441-4 2018 Additionally, six2 overexpression decreased the sensitivity of HCC cells to 5-Fu, characterized as attenuating 5-FU-induced cell apoptosis and downregulation of cell viability, and promoted HCC cells stemness. Fluorouracil 111-115 SIX homeobox 2 Homo sapiens 14-18 29772441-6 2018 And E-cadherin overexpression rescued six2-induced decrease of 5-FU sensitivity and promotion on HCC cells stemness. Fluorouracil 63-67 SIX homeobox 2 Homo sapiens 38-42 29772441-7 2018 Therefore, our results suggest that Six2 is negatively correlated with good prognosis and decreases 5-FU sensitivity via suppressing E-cadherin expression in HCC cells. Fluorouracil 100-104 SIX homeobox 2 Homo sapiens 36-40 30011263-0 2018 miR-106a Reduces 5-Fluorouracil (5-FU) Sensitivity of Colorectal Cancer by Targeting Dual-Specificity Phosphatases 2 (DUSP2). Fluorouracil 17-31 dual specificity phosphatase 2 Homo sapiens 85-116 30011263-0 2018 miR-106a Reduces 5-Fluorouracil (5-FU) Sensitivity of Colorectal Cancer by Targeting Dual-Specificity Phosphatases 2 (DUSP2). Fluorouracil 17-31 dual specificity phosphatase 2 Homo sapiens 118-123 30011263-0 2018 miR-106a Reduces 5-Fluorouracil (5-FU) Sensitivity of Colorectal Cancer by Targeting Dual-Specificity Phosphatases 2 (DUSP2). Fluorouracil 33-37 dual specificity phosphatase 2 Homo sapiens 85-116 30011263-0 2018 miR-106a Reduces 5-Fluorouracil (5-FU) Sensitivity of Colorectal Cancer by Targeting Dual-Specificity Phosphatases 2 (DUSP2). Fluorouracil 33-37 dual specificity phosphatase 2 Homo sapiens 118-123 30011263-15 2018 Silencing of DUSP2 reversed elevated 5-FU sensitivity induced by miR-106a antagonist in HCT116 cells. Fluorouracil 37-41 dual specificity phosphatase 2 Homo sapiens 13-18 29789423-1 2018 ABC member B5 (ABCB5) mediates multidrug resistance (MDR) in diverse malignancies and confers clinically relevant 5-fluorouracil resistance to CD133-expressing cancer stem cells in human colorectal cancer (CRC). Fluorouracil 114-128 ATP binding cassette subfamily B member 5 Homo sapiens 0-13 29789423-1 2018 ABC member B5 (ABCB5) mediates multidrug resistance (MDR) in diverse malignancies and confers clinically relevant 5-fluorouracil resistance to CD133-expressing cancer stem cells in human colorectal cancer (CRC). Fluorouracil 114-128 ATP binding cassette subfamily B member 5 Homo sapiens 15-20 28934847-0 2018 Participation of CCL1 in Snail-Positive Fibroblasts in Colorectal Cancer Contribute to 5-Fluorouracil/Paclitaxel Chemoresistance. Fluorouracil 87-101 chemokine (C-C motif) ligand 1 Mus musculus 17-21 29620211-8 2018 Furthermore, MORC2 regulated apoptosis and its expression level had an effect on the sensitivity of liver cancer cells to doxorubicin, 5-fluorouracil and cisplatin. Fluorouracil 135-149 MORC family CW-type zinc finger 2 Homo sapiens 13-18 29637602-8 2018 HES1 silencing increased viability of HCT116 and its chemoresistant sublines after 5-FU or OxaPt treatment. Fluorouracil 83-87 hes family bHLH transcription factor 1 Homo sapiens 0-4 29098557-10 2018 By targeting LOC285629, the viability, proliferative abilities, invasiveness and resistance of colorectal cancer cells towards 5-fluorouracil were reduced. Fluorouracil 127-141 long intergenic non-protein coding RNA 2159 Homo sapiens 13-22 29870276-13 2018 Furthermore, HOXA10 knockdown significantly increased sensitivity to 5-FU chemotherapy in vitro and in vivo. Fluorouracil 69-73 homeobox A10 Homo sapiens 13-19 29870276-14 2018 CONCLUSIONS: Significant HOXA10 overexpression in CRC may be a potential biomarker indicating poor prognosis and 5-FU resistance. Fluorouracil 113-117 homeobox A10 Homo sapiens 25-31 29771440-0 2018 MiR-519d reduces the 5-fluorouracil resistance in colorectal cancer cells by down-regulating the expression of CCND1. Fluorouracil 21-35 microRNA 519d Homo sapiens 0-8 29771440-0 2018 MiR-519d reduces the 5-fluorouracil resistance in colorectal cancer cells by down-regulating the expression of CCND1. Fluorouracil 21-35 cyclin D1 Homo sapiens 111-116 29771440-1 2018 OBJECTIVE: To investigate the effects of miR-519d on the 5-fluorouracil resistance in colorectal cancer cells and to explore the mechanism. Fluorouracil 57-71 microRNA 519d Homo sapiens 41-49 29771440-4 2018 Dual luciferase assay was used to examine the effect of CCND1 on the sensitivity of cells to 5-Fu mediated by miR-519d. Fluorouracil 93-97 cyclin D1 Homo sapiens 56-61 29771440-4 2018 Dual luciferase assay was used to examine the effect of CCND1 on the sensitivity of cells to 5-Fu mediated by miR-519d. Fluorouracil 93-97 microRNA 519d Homo sapiens 110-118 29771440-6 2018 Overexpression of miR-519d increased the sensitivity of colorectal cancer cells to 5-Fu. Fluorouracil 83-87 microRNA 519d Homo sapiens 18-26 29771440-9 2018 si-CCND1 increased the sensitivity of colorectal cancer cells to 5-Fu. Fluorouracil 65-69 cyclin D1 Homo sapiens 3-8 29771440-10 2018 CONCLUSIONS: miR-519d inhibits the expression of CCND1 and then plays a role in alleviating 5-Fu resistance in colorectal cancer cells. Fluorouracil 92-96 microRNA 519d Homo sapiens 13-21 29701074-3 2018 Thymidine phosphorylase (TP) is a nucleoside-metabolizing enzyme involved in 5-fluorouracil pharmacokinetics, as well as inflammatory responses, neoangiogenesis and apoptosis. Fluorouracil 77-91 thymidine phosphorylase Homo sapiens 0-23 29701074-3 2018 Thymidine phosphorylase (TP) is a nucleoside-metabolizing enzyme involved in 5-fluorouracil pharmacokinetics, as well as inflammatory responses, neoangiogenesis and apoptosis. Fluorouracil 77-91 thymidine phosphorylase Homo sapiens 25-27 29921390-9 2018 The percentage of cell apoptosis increased, and the Western blot showed that the expression of caspase-3, caspase-8, and c-myc, respectively, in the semi-combination group, the 5-Fluorouracil group, and the combination group increased successively and that the successive increasing of c-myc was the most significant. Fluorouracil 177-191 caspase 8 Homo sapiens 106-115 29755597-6 2018 The results indicated that, compared with parental cells, proteins associated with the Wnt/beta-catenin signaling pathway and aldehyde dehydrogenase 1 were overexpressed, the number and size of spheres in the 5-FU-resistant cells were increased, the ratio of CD44+/CD24-/low cells was increased and the migratory ability was improved in vitro compared with the 5-FU-susceptible cells. Fluorouracil 209-213 CD44 molecule Canis lupus familiaris 259-263 29695684-8 2018 5-Fluorouracil enhanced circularly permuted tumor necrosis factor-related apoptosis-inducing ligand-induced apoptosis by increasing death receptor 4 and 5 levels in HCT116 cells, but only of death receptor 4 in SW480 cells. Fluorouracil 0-14 TNF receptor superfamily member 10a Homo sapiens 132-154 29695684-8 2018 5-Fluorouracil enhanced circularly permuted tumor necrosis factor-related apoptosis-inducing ligand-induced apoptosis by increasing death receptor 4 and 5 levels in HCT116 cells, but only of death receptor 4 in SW480 cells. Fluorouracil 0-14 TNF receptor superfamily member 10a Homo sapiens 132-148 29695684-9 2018 Moreover, 5-fluorouracil plus circularly permuted tumor necrosis factor-related apoptosis-inducing ligand increased apoptosis-related protein levels such as cleaved caspase-3, caspase-8, and poly-ADP-ribose polymerase and downregulated that of the survival protein B-cell lymphoma-extra-large. Fluorouracil 10-24 caspase 8 Homo sapiens 176-185 29560281-7 2018 5-FU inhibited the phosphorylation of SMAD2 and reduced the total protein levels of SMAD2, SMAD4, and pINK4b. Fluorouracil 0-4 SMAD family member 2 Homo sapiens 38-43 29560281-7 2018 5-FU inhibited the phosphorylation of SMAD2 and reduced the total protein levels of SMAD2, SMAD4, and pINK4b. Fluorouracil 0-4 SMAD family member 2 Homo sapiens 84-89 29560281-7 2018 5-FU inhibited the phosphorylation of SMAD2 and reduced the total protein levels of SMAD2, SMAD4, and pINK4b. Fluorouracil 0-4 SMAD family member 4 Homo sapiens 91-96 29560281-11 2018 Interestingly, the phosphorylated protein levels of SMAD2 and the total protein levels of E-cadherin and p15INK4b were increased in 5-FU-stimulated HuH-7 cells, but not in Hep G2 cells. Fluorouracil 132-136 SMAD family member 2 Homo sapiens 52-57 28795251-0 2018 5-Fluorouracil-induced mitochondrial oxidative cytotoxicity and apoptosis are increased in MCF-7 human breast cancer cells by TRPV1 channel activation but not Hypericum perforatum treatment. Fluorouracil 0-14 transient receptor potential cation channel subfamily V member 1 Homo sapiens 126-131 28795251-4 2018 Therefore, we investigated the apoptotic and antioxidant properties of 5-FU with/without HPer through activation of TRPV1 in MCF-7 cells. Fluorouracil 71-75 transient receptor potential cation channel subfamily V member 1 Homo sapiens 116-121 28795251-10 2018 In conclusion, antitumor and apoptosis effects of 5-FU are up-regulated by activation of TRPV1 channels, but its action was down-regulated by HPer treatment. Fluorouracil 50-54 transient receptor potential cation channel subfamily V member 1 Homo sapiens 89-94 29167315-5 2018 Furthermore, CA3, combined with 5-FU, synergistically inhibits esophageal adenocarcinoma cell growth especially in YAP1 high esophageal adenocarcinoma cells. Fluorouracil 32-36 Yes1 associated transcriptional regulator Homo sapiens 115-119 29635244-13 2018 CONCLUSIONS: MTDH-stimulated cancer resistance to 5-FU may be mediated through autophagy activated by the AMPK/ATG5 pathway in GC. Fluorouracil 50-54 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 106-110 29689552-4 2018 Moreover, knockdown of RBFOX3 improved the inhibitory effect of 5-fluorouracil (5-FU) on cell proliferation, migration and invasion, and enhanced the apoptosis induced by 5-FU. Fluorouracil 80-84 RNA binding protein, fox-1 homolog (C. elegans) 3 Mus musculus 23-29 29689552-4 2018 Moreover, knockdown of RBFOX3 improved the inhibitory effect of 5-fluorouracil (5-FU) on cell proliferation, migration and invasion, and enhanced the apoptosis induced by 5-FU. Fluorouracil 171-175 RNA binding protein, fox-1 homolog (C. elegans) 3 Mus musculus 23-29 29689552-5 2018 However, overexpression of RBFOX3 reduced the inhibitory effect of 5-fluorouracil (5-FU) on cell proliferation, migration and invasion, and decreased the apoptosis induced by 5-FU. Fluorouracil 67-81 RNA binding protein, fox-1 homolog (C. elegans) 3 Mus musculus 27-33 29689552-5 2018 However, overexpression of RBFOX3 reduced the inhibitory effect of 5-fluorouracil (5-FU) on cell proliferation, migration and invasion, and decreased the apoptosis induced by 5-FU. Fluorouracil 83-87 RNA binding protein, fox-1 homolog (C. elegans) 3 Mus musculus 27-33 29689552-5 2018 However, overexpression of RBFOX3 reduced the inhibitory effect of 5-fluorouracil (5-FU) on cell proliferation, migration and invasion, and decreased the apoptosis induced by 5-FU. Fluorouracil 175-179 RNA binding protein, fox-1 homolog (C. elegans) 3 Mus musculus 27-33 29689552-6 2018 We further elucidated that RBFOX3 knockdown synergized with 5-FU to inhibit the growth and invasion of HCC cells through PI3K/AKT and epithelial-mesenchymal transition (EMT) signaling, and promote apoptosis by activating the cytochrome-c/caspase signaling pathway. Fluorouracil 60-64 RNA binding protein, fox-1 homolog (C. elegans) 3 Mus musculus 27-33 29689552-7 2018 Finally, we validated that RBFOX3 regulated 5-FU-mediated cytotoxicity in HCC in mouse xenograft models. Fluorouracil 44-48 RNA binding protein, fox-1 homolog (C. elegans) 3 Mus musculus 27-33 29689552-8 2018 CONCLUSIONS: The findings from this study indicate that RBFOX3 regulates the chemosensitivity of HCC to 5-FU in vitro and in vivo. Fluorouracil 104-108 RNA binding protein, fox-1 homolog (C. elegans) 3 Mus musculus 56-62 29689552-9 2018 Therefore, targeting RBFOX3 may improve the inhibition of HCC growth and progression by 5-FU, and provide a novel potential therapeutic strategy for HCC. Fluorouracil 88-92 RNA binding protein, fox-1 homolog (C. elegans) 3 Mus musculus 21-27 29940566-0 2018 Sensitization of Gastric Cancer Cells to 5-FU by MicroRNA-204 Through Targeting the TGFBR2-Mediated Epithelial to Mesenchymal Transition. Fluorouracil 41-45 transforming growth factor beta receptor 2 Homo sapiens 84-90 29940566-17 2018 Eventually, we illustrated the restoration of TGFBR2 in miR-204 overexpression GC cells, which recovered resistance to 5-FU treatments compared with miR-204 overexpression GC cells. Fluorouracil 119-123 transforming growth factor beta receptor 2 Homo sapiens 46-52 28411308-0 2018 The Effect of miR-200c Inhibition on Chemosensitivity (5- FluoroUracil) in Colorectal Cancer. Fluorouracil 55-70 microRNA 200c Homo sapiens 14-22 28411308-4 2018 In this study, we examined the effect of inhibition of miR-200c on the sensitivity of HCT-116 cells to 5-FU. Fluorouracil 103-107 microRNA 200c Homo sapiens 55-63 28411308-10 2018 LNA-anti-miR-200c reduced the 5-FU-induced apoptosis and caspase 3 activity. Fluorouracil 30-34 microRNA 200c Homo sapiens 9-17 28411308-11 2018 miR-200c, as a novel prognostic marker in CRC, can be a potential therapeutic approach to overcome chemoresistance during 5-FU chemotherapy. Fluorouracil 122-126 microRNA 200c Homo sapiens 0-8 28127745-9 2017 Furthermore, 5FU up-regulated VCAM1 and TYMP (encodes enzyme activating capecitabine and 5FU), and sVCAM-1 and CD146 concentrations were higher after than before capecitabine chemotherapy. Fluorouracil 13-16 thymidine phosphorylase Homo sapiens 40-44 29048661-7 2017 The single agent treatment and combinations of 5-FU and Blu9931 arrest cell cycle (P<0.05), increased p27kip1 expression and reduced cyclin D1 expression. Fluorouracil 47-51 cyclin D1 Homo sapiens 136-145 28970092-5 2017 A targeted therapy for improvement of the therapeutic efficacy of 5-FU and vascular function was performed through administration of TCP-1/TNFalpha fusion protein in this model. Fluorouracil 66-70 t-complex protein 1 Mus musculus 133-138 28734226-6 2017 We investigated the status of phosphorylation of pRB along esophageal tumorigenesis stages, as well as whether hyperphosphorylation of pRB could suppress apoptosis induced by cisplatin, 5-FU, or TNF-alpha in esophageal cancer cells. Fluorouracil 186-190 RB transcriptional corepressor 1 Homo sapiens 135-138 28734226-8 2017 When RB-1 was knocked down or CDK inhibitors reduced the levels of phosphorylated pRB, opposite apoptotic effects were observed, depending on the combination of drugs tested: whereas TNF-alpha- and cisplatin-induced apoptosis increased, 5-FU-induced apoptosis decreased. Fluorouracil 237-241 RB transcriptional corepressor 1 Homo sapiens 5-9 28734226-8 2017 When RB-1 was knocked down or CDK inhibitors reduced the levels of phosphorylated pRB, opposite apoptotic effects were observed, depending on the combination of drugs tested: whereas TNF-alpha- and cisplatin-induced apoptosis increased, 5-FU-induced apoptosis decreased. Fluorouracil 237-241 RB transcriptional corepressor 1 Homo sapiens 82-85 28928869-0 2017 HES1 Promotes Colorectal Cancer Cell Resistance To 5-Fu by Inducing Of EMT and ABC Transporter Proteins. Fluorouracil 51-55 hes family bHLH transcription factor 1 Homo sapiens 0-4 28928869-8 2017 Colon cancer cell lines which over-expressed HES1 were more resistant to 5-Fu treatment in vitro. Fluorouracil 73-77 hes family bHLH transcription factor 1 Homo sapiens 45-49 28928869-12 2017 Conclusions: HES1 promotes chemoresistance to 5-Fu by prompting EMT and inducing of several ABC transporter genes. Fluorouracil 46-50 hes family bHLH transcription factor 1 Homo sapiens 13-17 29416616-3 2018 In our study, we indicated that overexpression of miR-761 promoted the sensitivity of colorectal cancer cells to 5-Fluorouracil (5-FU). Fluorouracil 113-127 microRNA 761 Homo sapiens 50-57 29416616-3 2018 In our study, we indicated that overexpression of miR-761 promoted the sensitivity of colorectal cancer cells to 5-Fluorouracil (5-FU). Fluorouracil 129-133 microRNA 761 Homo sapiens 50-57 29416616-10 2018 Elevated expression of FOXM1 suppressed the sensitivity of miR-761-overexpressing HT29 cells to 5-FU. Fluorouracil 96-100 microRNA 761 Homo sapiens 59-66 29416616-12 2018 These data suggested that miR-761 played a tumor suppressor miRNA in colorectal cancer progression and reduced miR-761 expression might be a major mechanism for 5-FU resistance in colorectal cancer cell. Fluorouracil 161-165 microRNA 761 Homo sapiens 26-33 29416616-12 2018 These data suggested that miR-761 played a tumor suppressor miRNA in colorectal cancer progression and reduced miR-761 expression might be a major mechanism for 5-FU resistance in colorectal cancer cell. Fluorouracil 161-165 microRNA 761 Homo sapiens 111-118 28791524-7 2017 These findings suggest that the 5-FU@FACS-Mn:ZnS composite has a superior role during the induction of apoptosis in the 4T1 cells as compared to the free 5-FU drug treated groups. Fluorouracil 32-36 acyl-CoA synthetase long-chain family member 1 Mus musculus 37-41 28791524-7 2017 These findings suggest that the 5-FU@FACS-Mn:ZnS composite has a superior role during the induction of apoptosis in the 4T1 cells as compared to the free 5-FU drug treated groups. Fluorouracil 154-158 acyl-CoA synthetase long-chain family member 1 Mus musculus 37-41 28791524-8 2017 The results of the study therefore suggest that the impregnation of 5-FU anti-cancer drug within the FACS-Mn:ZnS system significantly improves its selective targeting efficacy, in addition to improving the anti-proliferative properties and attenuate possible tumor resistances to the 5-FU drug. Fluorouracil 68-72 acyl-CoA synthetase long-chain family member 1 Mus musculus 101-105 28791524-8 2017 The results of the study therefore suggest that the impregnation of 5-FU anti-cancer drug within the FACS-Mn:ZnS system significantly improves its selective targeting efficacy, in addition to improving the anti-proliferative properties and attenuate possible tumor resistances to the 5-FU drug. Fluorouracil 284-288 acyl-CoA synthetase long-chain family member 1 Mus musculus 101-105 28696813-2 2017 Therefore, to enhance the 5-FU antitumor activity, the present research used a novel tumor-targeted therapy based on the co-administration of 5-FU encapsulated in long-circulating liposomes (LCL-5-FU) together with liposomal prednisolone phosphate (LCL-PLP), a formulation with known anti-angiogenic actions on C26 murine colon carcinoma cells. Fluorouracil 142-146 proteolipid protein (myelin) 1 Mus musculus 253-256 28591704-7 2017 Our results further demonstrate that miR-196b-5p promotes stemness and chemoresistance of CRC cells to 5-fluorouracil via targeting negative regulators SOCS1 and SOCS3 of STAT3 signaling pathway, giving rise to activation of STAT3 signaling. Fluorouracil 103-117 suppressor of cytokine signaling 3 Homo sapiens 162-167 29100320-0 2017 Suppression of pancreatic adenocarcinoma upregulated factor (PAUF) increases the sensitivity of pancreatic cancer to gemcitabine and 5FU, and inhibits the formation of pancreatic cancer stem like cells. Fluorouracil 133-136 zymogen granule protein 16B Homo sapiens 15-59 29100320-0 2017 Suppression of pancreatic adenocarcinoma upregulated factor (PAUF) increases the sensitivity of pancreatic cancer to gemcitabine and 5FU, and inhibits the formation of pancreatic cancer stem like cells. Fluorouracil 133-136 zymogen granule protein 16B Homo sapiens 61-65 29100320-6 2017 In addition, siPAUF CFPAC-1 decreased the mRNA expression of multidrug resistant protein 5 (MRP5) and ribonucleotide reductase M2 (RRM2) and were more vulnerable to gemcitabine and 5-FU than negative control (p<0.05). Fluorouracil 181-185 ATP binding cassette subfamily C member 5 Homo sapiens 61-90 29100320-6 2017 In addition, siPAUF CFPAC-1 decreased the mRNA expression of multidrug resistant protein 5 (MRP5) and ribonucleotide reductase M2 (RRM2) and were more vulnerable to gemcitabine and 5-FU than negative control (p<0.05). Fluorouracil 181-185 ATP binding cassette subfamily C member 5 Homo sapiens 92-96 28693221-5 2017 The expression of the stem cell markers CD133 and nucleostemin (NS) increased in all three cell lines treated concurrently with 5-FU and either LA or EA when compared with cells treated with 5-FU alone. Fluorouracil 128-132 guanine nucleotide binding protein-like 3 (nucleolar) Mus musculus 50-62 27836590-0 2017 Aptamer and 5-fluorouracil dual-loading Ag2S quantum dots used as a sensitive label-free probe for near-infrared photoluminescence turn-on detection of CA125 antigen. Fluorouracil 12-26 angiotensin II receptor type 1 Homo sapiens 40-44 27836590-3 2017 The surface of as-prepared Ag2S QDs was modified with polyethylenimine, followed by combination with the aptamer/5-Fu complex to form Ag2S QDs/aptamer/5-Fu hybrids. Fluorouracil 113-117 angiotensin II receptor type 1 Homo sapiens 27-31 27836590-3 2017 The surface of as-prepared Ag2S QDs was modified with polyethylenimine, followed by combination with the aptamer/5-Fu complex to form Ag2S QDs/aptamer/5-Fu hybrids. Fluorouracil 113-117 angiotensin II receptor type 1 Homo sapiens 134-138 27836590-3 2017 The surface of as-prepared Ag2S QDs was modified with polyethylenimine, followed by combination with the aptamer/5-Fu complex to form Ag2S QDs/aptamer/5-Fu hybrids. Fluorouracil 151-155 angiotensin II receptor type 1 Homo sapiens 27-31 28404976-8 2017 Furthermore, we identified that ERbeta exerted an inhibitory effect on CRC tumor proliferation in vitro and in vivo, combined with 5-FU, through up-regulation of MLH1 expression. Fluorouracil 131-135 estrogen receptor 2 Homo sapiens 32-38 28433634-6 2017 Additional Western blot analyses have shown that possible mechanisms underlying enhanced sensitivity to 5-FU induced by dual Sphk 1/2 inhibition could include abrogation of FAK-regulated IGF-1R activity and down-regulation of osteopontin expression culminating in the inhibition of NF-kappaB activity and its downstream signalling mediated by sirtuin 1 and p38 MAPK. Fluorouracil 104-108 protein tyrosine kinase 2 Homo sapiens 173-176 28969100-2 2017 Overexpression of lncRNA UCA1 correlates with resistance to chemotherapeutics such as cisplatin, gemcitabine, 5-FU, tamoxifen, imatinib and EGFR-TKIs, whereas lncRNA UCA1 knockdown restores drug sensitivity. Fluorouracil 110-114 urothelial cancer associated 1 Homo sapiens 25-29 28314603-11 2017 Knockdown of MSK1 in CRC cells suppressed cell proliferation, anchorage-independent growth, migration and invasion, and promoted 5-fluorouracil chemosensitivity and intracellular NADP+/NADPH ratio. Fluorouracil 129-143 ribosomal protein S6 kinase A5 Homo sapiens 13-17 28496200-8 2017 We also showed that dual-specificity phosphatase 6 (DUSP6) is a novel target of miR-200a-3p and regulates resistance to 5-FU. Fluorouracil 120-124 dual specificity phosphatase 6 Homo sapiens 20-50 28496200-8 2017 We also showed that dual-specificity phosphatase 6 (DUSP6) is a novel target of miR-200a-3p and regulates resistance to 5-FU. Fluorouracil 120-124 dual specificity phosphatase 6 Homo sapiens 52-57 28881782-0 2017 miR-106b regulates the 5-fluorouracil resistance by targeting Zbtb7a in cholangiocarcinoma. Fluorouracil 23-37 zinc finger and BTB domain containing 7A Homo sapiens 62-68 28881782-9 2017 Instead, over-expression of miR-106b could re-sensitize resistant CCA cells to 5-FU through down-regulation of Zbtb7a. Fluorouracil 79-83 zinc finger and BTB domain containing 7A Homo sapiens 111-117 28881782-11 2017 CONCLUSION: Our study demonstrates that miR-106b can reverse 5-FU resistance via Zbtb7a suppression, thus offer a novel and powerful strategy for CCA chemotherapy. Fluorouracil 61-65 zinc finger and BTB domain containing 7A Homo sapiens 81-87 28402255-7 2017 We found that 5-fluorouracil-based chemotherapy regimens significantly increased plasma levels of leptin and adiponectin and decreased plasma levels of resistin and visfatin in PR and SD patients, whereas the plasma levels of these molecules were not affected in PD patients. Fluorouracil 14-28 nicotinamide phosphoribosyltransferase Homo sapiens 165-173 29871302-8 2017 The combination of metformin and 5-fluorouracil produced an antagonism action in Hep-2 cells.Western blot assay showed that metformin, cisplatin, 5-fluorouracil could have caused the increase of expression level of AMPK-alpha, P21 and Cyclin D1 in Hep-2 cells while Paclitaxel could have cause the decrease of expression level of Cyclin D1. Fluorouracil 33-47 cyclin D1 Homo sapiens 235-244 29871302-8 2017 The combination of metformin and 5-fluorouracil produced an antagonism action in Hep-2 cells.Western blot assay showed that metformin, cisplatin, 5-fluorouracil could have caused the increase of expression level of AMPK-alpha, P21 and Cyclin D1 in Hep-2 cells while Paclitaxel could have cause the decrease of expression level of Cyclin D1. Fluorouracil 33-47 cyclin D1 Homo sapiens 330-339 27641154-7 2017 Polymorphisms in DPYD, TPMT, and UGT1A1 have been described that have a major impact on the pharmacokinetics of 5-fluorouracil, mercaptopurine, and irinotecan, respectively. Fluorouracil 112-126 thiopurine S-methyltransferase Homo sapiens 23-27 27838786-0 2017 53BP1 loss induces chemoresistance of colorectal cancer cells to 5-fluorouracil by inhibiting the ATM-CHK2-P53 pathway. Fluorouracil 65-79 checkpoint kinase 2 Homo sapiens 102-106 28351329-8 2017 Furthermore, Crocetin decreased Beclin-1 levels but increased ATG1 levels in fluorouracil-treated breast cancer cells. Fluorouracil 77-89 unc-51 like autophagy activating kinase 1 Homo sapiens 62-66 28351329-9 2017 Together, these data suggest that Crocetin may shift autophagic cell survival to autophagic cell death in fluorouracil-treated breast cancer cells, possibly through modulation of the expression of ATG1 and Beclin-1. Fluorouracil 106-118 unc-51 like autophagy activating kinase 1 Homo sapiens 197-201 28255248-8 2017 We also found that miR-320 mimic downregulated chemoresistance and cell survival of gastric cancer cells when treated with 5-fluorouracil. Fluorouracil 123-137 microRNA 320a Homo sapiens 19-26 28028695-0 2017 5-Fluorouracil inhibits cell migration by induction of Sestrin2 in colon cancer cells. Fluorouracil 0-14 sestrin 2 Homo sapiens 55-63 28028695-2 2017 In this study, we investigated whether 5-FU induces Sestrin2 (SESN2), an antioxidant enzyme, and the role of SESN2 in 5-FU action in colon cancer cells. Fluorouracil 39-43 sestrin 2 Homo sapiens 52-60 28028695-3 2017 We found that 5-FU upregulated SESN2 protein expression in both HCT116 and HT29 cells. Fluorouracil 14-18 sestrin 2 Homo sapiens 31-36 28028695-5 2017 Furthermore, we investigated whether production of reactive oxygen species (ROS) was involved in 5-FU-induced SESN2 expression. Fluorouracil 97-101 sestrin 2 Homo sapiens 110-115 28028695-7 2017 Moreover, SESN2 upregulation by 5-FU was not prevented by pretreatment with antioxidants. Fluorouracil 32-36 sestrin 2 Homo sapiens 10-15 28028695-8 2017 Next, we investigated p53 levels after 5-FU treatment to elucidate the regulation of SESN2 by 5-FU. Fluorouracil 94-98 sestrin 2 Homo sapiens 85-90 28510612-0 2017 Suppression of ID1 expression in colon cancer cells increases sensitivity to 5-fluorouracil. Fluorouracil 77-91 inhibitor of DNA binding 1, HLH protein Homo sapiens 15-18 28510612-3 2017 Here we examined the impact of ID1 silencing on the sensitivity of CRC cells to 5-FU. Fluorouracil 80-84 inhibitor of DNA binding 1, HLH protein Homo sapiens 31-34 28510612-6 2017 HCT-116 cells with suppressed ID1 became sensitized to 5-FU and this was not observed in HT-29 cells. Fluorouracil 55-59 inhibitor of DNA binding 1, HLH protein Homo sapiens 30-33 28510612-7 2017 Silencing ID1 resulted in altered expression of genes encoding enzymes metabolizing 5-FU. Fluorouracil 84-88 inhibitor of DNA binding 1, HLH protein Homo sapiens 10-13 28090501-5 2017 RESULTS: The result of MTT assay after APEX1 knockdown showed that strong coexpression of APEX1 and Jagged1 cell line (SNU-245, SNU-1079, and SNU-1196) showed a greater decrease in IC50 of chemotherapeutic agent (5-fluorouracil, gemcitabine and cisplatin). Fluorouracil 213-227 apurinic/apyrimidinic endodeoxyribonuclease 1 Homo sapiens 90-95 27188205-3 2017 MATERIALS AND METHODS: CD can convert a prodrug, 5-fluorocytosine (5-FC), to active 5-fluorouracil, which inhibits tumor growth through the inhibition of DNA synthesis,while IFN-beta also strongly inhibits tumor growth by inducing the apoptotic process. Fluorouracil 84-98 interferon beta 1 Homo sapiens 174-182 27878272-0 2017 miR-20b reduces 5-FU resistance by suppressing the ADAM9/EGFR signaling pathway in colon cancer. Fluorouracil 16-20 microRNA 20b Homo sapiens 0-7 27878272-8 2017 Finally, 5-FU resistance in HCT116 and HCT116-R cells was compared after transfection with miR-20b. Fluorouracil 9-13 microRNA 20b Homo sapiens 91-98 27878272-9 2017 Our results showed that miR-20b was expressed at lower levels in the 5-FU-resistant tissues and cells than in the 5-FU-sensitive tissues and cells. Fluorouracil 69-73 microRNA 20b Homo sapiens 24-31 27878272-9 2017 Our results showed that miR-20b was expressed at lower levels in the 5-FU-resistant tissues and cells than in the 5-FU-sensitive tissues and cells. Fluorouracil 114-118 microRNA 20b Homo sapiens 24-31 27878272-11 2017 In addition, we demonstrated that ADAM9 is a direct target of miR-20b and that miR-20b decreased the 5-FU resistance of HCT116-R cells. Fluorouracil 101-105 microRNA 20b Homo sapiens 79-86 27878272-12 2017 Our findings suggest that miR-20b reduces 5-FU resistance to induce apoptosis in vitro by suppressing ADAM9/EGFR in CC cells. Fluorouracil 42-46 microRNA 20b Homo sapiens 26-33 28105142-8 2016 In the rAd/p53 + 5-Fu group, the tumor necrosis ratio, and Smad4 and Brca1 expression levels also significantly increased at various time points (P<0.05). Fluorouracil 17-21 SMAD family member 4 Homo sapiens 59-64 27942222-0 2016 CTGF enhances resistance to 5-FU-mediating cell apoptosis through FAK/MEK/ERK signal pathway in colorectal cancer. Fluorouracil 28-32 cellular communication network factor 2 Homo sapiens 0-4 27942222-0 2016 CTGF enhances resistance to 5-FU-mediating cell apoptosis through FAK/MEK/ERK signal pathway in colorectal cancer. Fluorouracil 28-32 protein tyrosine kinase 2 Homo sapiens 66-69 27942222-5 2016 Overexpression of CTGF enhanced the resistance to 5-FU-induced cell apoptosis. Fluorouracil 50-54 cellular communication network factor 2 Homo sapiens 18-22 27942222-7 2016 We also found that CTGF facilitated resistance to 5-FU-induced apoptosis by increasing the expression of B-cell lymphoma-extra large (Bcl-xL) and survivin. Fluorouracil 50-54 cellular communication network factor 2 Homo sapiens 19-23 27942222-9 2016 Our current results indicate that the expression of phosphorylated forms of MEK/ERK increased in high CTGF expression cells and MEK inhibited increases in 5-FU-mediated apoptosis of resistant CRC cells. Fluorouracil 155-159 cellular communication network factor 2 Homo sapiens 102-106 27942222-10 2016 Therefore, our data suggest that MEK/ERK signaling contributes to 5-FU resistance through upstream of CTGF, and supports CRC cell growth. Fluorouracil 66-70 cellular communication network factor 2 Homo sapiens 102-106 27659530-10 2016 Consequently, CD133+CD24lo cells exhibit decreased sensitivity to 5-FU. Fluorouracil 66-70 prominin 1 Homo sapiens 14-19 27793037-8 2016 Chronic hypoxia suppressed the expression of cyclinD1, CDK4, and CDK6, inducing G1 phase block and 5-flurouracil (5-FU) chemoresistance. Fluorouracil 114-118 cyclin D1 Homo sapiens 45-53 27793037-9 2016 Overexpression of c-Myc reversed the inhibition of cyclinD1, CDK4, and CDK6, which accelerated the G1/S phase transition under hypoxia and enhanced sensitivity to 5-FU. Fluorouracil 163-167 cyclin D1 Homo sapiens 51-59 27793037-9 2016 Overexpression of c-Myc reversed the inhibition of cyclinD1, CDK4, and CDK6, which accelerated the G1/S phase transition under hypoxia and enhanced sensitivity to 5-FU. Fluorouracil 163-167 cyclin dependent kinase 4 Homo sapiens 61-65 27245475-10 2016 CONCLUSIONS: Because hENT1 and OAT2 are crucial for the uptake of gemcitabine and 5-fluorouracil, respectively, our results suggest that patients with AFP-producing GC could potentially benefit from gemcitabine/fluoropyrimidine combination chemotherapy. Fluorouracil 82-96 solute carrier family 29 member 1 (Augustine blood group) Homo sapiens 21-26 27514455-4 2016 Noteworthily, either pharmacological or genetic blockage of ornithine decarboxylase (ODC) prevented TAMs-induced chemoresistance to 5-FU in vitro and in vivo. Fluorouracil 132-136 ornithine decarboxylase 1 Homo sapiens 60-83 27514455-4 2016 Noteworthily, either pharmacological or genetic blockage of ornithine decarboxylase (ODC) prevented TAMs-induced chemoresistance to 5-FU in vitro and in vivo. Fluorouracil 132-136 ornithine decarboxylase 1 Homo sapiens 85-88 27612427-0 2016 DCTPP1 attenuates the sensitivity of human gastric cancer cells to 5-fluorouracil by up-regulating MDR1 expression epigenetically. Fluorouracil 67-81 dCTP pyrophosphatase 1 Homo sapiens 0-6 27612427-4 2016 In the present study, we reported that DCTPP1-knockdown GC cell line BGC-823 exhibited more sensitivity to 5-fluorouracil (5-FU), demonstrated by the retardation of cell proliferation, the increase in cell apoptosis, cell cycle arrest at S phase and more DNA damages. Fluorouracil 107-121 dCTP pyrophosphatase 1 Homo sapiens 39-45 27612427-4 2016 In the present study, we reported that DCTPP1-knockdown GC cell line BGC-823 exhibited more sensitivity to 5-fluorouracil (5-FU), demonstrated by the retardation of cell proliferation, the increase in cell apoptosis, cell cycle arrest at S phase and more DNA damages. Fluorouracil 123-127 dCTP pyrophosphatase 1 Homo sapiens 39-45 27612427-5 2016 Multidrug resistance 1 (MDR1) expression was unexpectedly down-regulated in DCTPP1-knockdown BGC-823 cells together with more intracellular 5-FU accumulation. Fluorouracil 140-144 dCTP pyrophosphatase 1 Homo sapiens 76-82 27509880-7 2016 Furthermore, our global analysis of gene expression, which was focused on genes involved in the molecular regulation of MHC class II genes, showed enhancement of pro-apoptotic PCAF and CIITA after the combination of 5-FU and depsipeptide. Fluorouracil 216-220 lysine acetyltransferase 2B Homo sapiens 176-180 27613840-6 2016 After 5-fluorouracil (5-Fu) treatment, the reduction in the proportion of cell apoptosis, CD133 and TERT expression levels in SW620 were lower than that in SW480 cells. Fluorouracil 6-20 prominin 1 Homo sapiens 90-95 27613840-6 2016 After 5-fluorouracil (5-Fu) treatment, the reduction in the proportion of cell apoptosis, CD133 and TERT expression levels in SW620 were lower than that in SW480 cells. Fluorouracil 22-26 prominin 1 Homo sapiens 90-95 27299503-8 2016 Similar to the in vitro coculture stress, in vivo genotoxic stress in 5-FU-treated Sfrp2(-) (/) (-) mice increased cell cycle activity of LSK cells with higher levels of BrdU incorporation, increased expression of Ki-67, and canonical Wnt signaling. Fluorouracil 70-74 lymphocyte protein tyrosine kinase Mus musculus 138-141 27527859-1 2016 Our aim was to decipher the role and clinical relevance of the YAP/TAZ transcriptional coactivators in the regulation of the proliferation/quiescence balance in human colon cancer cells (CCC) and survival after 5FU-based chemotherapy. Fluorouracil 211-214 Yes1 associated transcriptional regulator Homo sapiens 63-66 27527606-8 2016 Treatment with 5-FU increased the levels of cleaved caspase-3 and PARP in ACH2 cells compared with uninfected and latently infected p53 null J1.1 cells. Fluorouracil 15-19 collagen type XI alpha 2 chain Homo sapiens 66-70 27145382-8 2016 Similarly to 5-FU, targeting tumor-derived MIF conferred a survival advantage to tumor-bearing animals and increased the cytotoxic T cell response within the tumor. Fluorouracil 13-17 macrophage migration inhibitory factor Homo sapiens 43-46 27323852-7 2016 These observations suggest that NNMT and the 1-MNA it produces inhibit the ASK1-p38 MAPK pathway, resulting in increased CRC cell resistance to 5-FU. Fluorouracil 144-148 nicotinamide N-methyltransferase Homo sapiens 32-36 27468227-9 2016 Mechanistically, 5-FU and TQ remarkably cooperated to repress the expression of procancerous Wnt, beta-catenin, NF-kappaB, COX-2, iNOS, VEGF, and TBRAS and upregulate the expression of anti-tumorigenesis DKK-1, CDNK-1A, TGF-beta1, TGF-betaRII, Smad4, and GPx. Fluorouracil 17-21 cytochrome c oxidase II, mitochondrial Rattus norvegicus 123-128 27468227-9 2016 Mechanistically, 5-FU and TQ remarkably cooperated to repress the expression of procancerous Wnt, beta-catenin, NF-kappaB, COX-2, iNOS, VEGF, and TBRAS and upregulate the expression of anti-tumorigenesis DKK-1, CDNK-1A, TGF-beta1, TGF-betaRII, Smad4, and GPx. Fluorouracil 17-21 dickkopf WNT signaling pathway inhibitor 1 Rattus norvegicus 204-209 27236157-9 2016 5-FU treatment at various concentrations induced the expressions of T?10 and ABC transporters (ABCB1, ABCG2 ABCA3) in two CCA cell lines, KKU-M055 and KKU-M214. Fluorouracil 0-4 ATP binding cassette subfamily B member 6 (Langereis blood group) Homo sapiens 77-80 27236157-10 2016 M214-5FUR, a 5-FU-resistant cell line, exhibited a 5-FU resistant phenotype with a 16-fold extremely high expression of T?10 and ABC transporters, as compared to the parental cells, KKU-M214. Fluorouracil 13-17 ATP binding cassette subfamily B member 6 (Langereis blood group) Homo sapiens 129-132 27236157-10 2016 M214-5FUR, a 5-FU-resistant cell line, exhibited a 5-FU resistant phenotype with a 16-fold extremely high expression of T?10 and ABC transporters, as compared to the parental cells, KKU-M214. Fluorouracil 51-55 ATP binding cassette subfamily B member 6 (Langereis blood group) Homo sapiens 129-132 27175567-4 2016 DNA comet assay results indicate an inverse correlation between the extent of 5-Fu-induced DNA damage and the expression level of B7-H3 in both SW480- and HCT-8-based cell lines. Fluorouracil 78-82 CD276 molecule Homo sapiens 130-135 27175567-5 2016 In SW480 cells that overexpress B7-H3, knockdown of BRCC3 similarly permitted greater 5-Fu-induced DNA damage. Fluorouracil 86-90 CD276 molecule Homo sapiens 32-37 27175567-6 2016 Altogether, results suggest that BRCC3 may play a role in B7-H3-induced 5-Fu resistance, such that B7-H3 upregulates BRCC3 expression, enhancing DNA repair in colorectal cancer cells. Fluorouracil 72-76 CD276 molecule Homo sapiens 58-63 27175567-6 2016 Altogether, results suggest that BRCC3 may play a role in B7-H3-induced 5-Fu resistance, such that B7-H3 upregulates BRCC3 expression, enhancing DNA repair in colorectal cancer cells. Fluorouracil 72-76 CD276 molecule Homo sapiens 99-104 27259240-0 2016 Interaction of DNA demethylase and histone methyltransferase upregulates Nrf2 in 5-fluorouracil-resistant colon cancer cells. Fluorouracil 81-95 PR/SET domain 9 Homo sapiens 35-60 26755331-6 2016 Furthermore, we demonstrated that SSRP1-modulated apoptosis process and its knockdown increased the sensitivity of HCC cells to doxorubicin, 5-Fluorouracil, and cisplatin. Fluorouracil 141-155 structure specific recognition protein 1 Homo sapiens 34-39 26808144-0 2016 Distinct TRPV1- and TRPA1-based mechanisms underlying enhancement of oral ulcerative mucositis-induced pain by 5-fluorouracil. Fluorouracil 111-125 transient receptor potential cation channel, subfamily V, member 1 Rattus norvegicus 9-14 27111450-13 2016 Microarray analyses of primitive erythroid progenitors from 5-FU-treated WT and ESAM-KO mice revealed that various signaling pathways, including the GATA1 system, were impaired in ESAM-KO mice. Fluorouracil 60-64 GATA binding protein 1 Mus musculus 149-154 26956045-4 2016 5-Fluorouracil (5FU) was able to stimulate the activation of SMAD3 and the transcription of specific genes such as ACVRL1, FN1 and TGFB1. Fluorouracil 0-14 SMAD family member 3 Homo sapiens 61-66 26956045-4 2016 5-Fluorouracil (5FU) was able to stimulate the activation of SMAD3 and the transcription of specific genes such as ACVRL1, FN1 and TGFB1. Fluorouracil 16-19 SMAD family member 3 Homo sapiens 61-66 24336083-12 2013 Indeed, knockdown of PATZ1 in p53-null osteosarcoma cells upregulates BAX expression and decreases survival of 5FU-treated cells, then suggesting an anti-apoptotic role of PATZ1 in p53-null cancer cells. Fluorouracil 111-114 transformation related protein 53, pseudogene Mus musculus 30-33 24336083-12 2013 Indeed, knockdown of PATZ1 in p53-null osteosarcoma cells upregulates BAX expression and decreases survival of 5FU-treated cells, then suggesting an anti-apoptotic role of PATZ1 in p53-null cancer cells. Fluorouracil 111-114 transformation related protein 53, pseudogene Mus musculus 181-184 24363520-9 2013 Annexin V/PI staining and Hoechst 33258 staining both indicated that the percentage of apoptotic cells induced by SIN and 5-FU combined or alone were significantly different from the control (P < 0.05). Fluorouracil 122-126 annexin A5 Homo sapiens 0-9 23695873-0 2013 Increased expression of 5-HT3 and NK 1 receptors in 5-fluorouracil-induced mucositis in mouse jejunum. Fluorouracil 52-66 tachykinin 1 Mus musculus 34-38 23695873-10 2013 The numbers of NK1 receptor cells in mucosa and immunopositive expression of NK1 receptors in deep muscular plexus were dramatically increased in 5-FU-treated mice. Fluorouracil 146-150 tachykinin 1 Mus musculus 15-18 23695873-10 2013 The numbers of NK1 receptor cells in mucosa and immunopositive expression of NK1 receptors in deep muscular plexus were dramatically increased in 5-FU-treated mice. Fluorouracil 146-150 tachykinin 1 Mus musculus 77-80 23695873-11 2013 Real-time PCR demonstrated that 5-FU treatment significantly increased mRNA levels of 5-HT3A, 5-HT3B, and NK1 receptors. Fluorouracil 32-36 tachykinin 1 Mus musculus 106-109 23695873-12 2013 The amounts of 5-HT and substance P increased after 5-FU treatment. Fluorouracil 52-56 tachykinin 1 Mus musculus 24-35 24095863-8 2013 Moreover, P-ERK/ERK ratio was modified by nicotine addition to 5-FU and CPT treated cells in an opposite manner. Fluorouracil 63-67 eukaryotic translation initiation factor 2 alpha kinase 3 Homo sapiens 10-15 24037775-1 2013 BACKGROUND: Weekly or daily cisplatin and 5-fluorouracil (5-FU)-based chemoradiation was evaluated for patients with locally advanced squamous cell carcinoma (SCC) of the anal canal treated at a single institution over a 20-year period. Fluorouracil 42-56 serpin family B member 3 Homo sapiens 159-162 24037775-1 2013 BACKGROUND: Weekly or daily cisplatin and 5-fluorouracil (5-FU)-based chemoradiation was evaluated for patients with locally advanced squamous cell carcinoma (SCC) of the anal canal treated at a single institution over a 20-year period. Fluorouracil 58-62 serpin family B member 3 Homo sapiens 159-162 24037775-2 2013 METHODS: A retrospective, single-institution analysis was conducted of patients receiving concurrent 5-FU/cisplatin and radiotherapy for locally advanced SCC from 1989 to 2009. Fluorouracil 101-105 serpin family B member 3 Homo sapiens 154-157 24037775-14 2013 CONCLUSIONS: The combination of weekly/daily cisplatin and 5-FU-based chemotherapy with concurrent radiotherapy is an effective regimen, and our long-term results indicate that cisplatin is an alternative to mitomycin C and may be considered for the treatment of locally advanced SCC of the anal canal. Fluorouracil 59-63 serpin family B member 3 Homo sapiens 280-283 23962907-0 2013 ERCC1 C8092A (rs3212986) polymorphism as a predictive marker in esophageal cancer patients treated with cisplatin/5-FU-based neoadjuvant therapy. Fluorouracil 114-118 ERCC excision repair 1, endonuclease non-catalytic subunit Homo sapiens 0-5 23962907-4 2013 RESULTS: We found that the ERCC1 rs3212986, although not associated with therapeutic response, is an independent predictive marker of better outcome in a cisplatin/5-FU-based neoadjuvant setting (hazard ratio: 0.38, 95% confidence interval: 0.2-0.73, P=0.008). Fluorouracil 164-168 ERCC excision repair 1, endonuclease non-catalytic subunit Homo sapiens 27-32 23962907-6 2013 CONCLUSION: Our study indicates the ERCC1 rs3212986 as a predictive marker in the cisplatin/5-FU-based neoadjuvant setting, and also suggests its use as a marker to select the appropriate therapeutic approach in esophageal cancer patients. Fluorouracil 92-96 ERCC excision repair 1, endonuclease non-catalytic subunit Homo sapiens 36-41 24447479-0 2013 [Effects of 5-Aza-dC on 5-Fu chemosensitivity by modulating TIP30 gene expression in human colorectal cancer cells]. Fluorouracil 24-28 HIV-1 Tat interactive protein 2 Homo sapiens 60-65 23836081-1 2013 The relationship between the plasma ratio of dihydrouracil/uracil (UH2/Ura) and hepatic dihydropyrimidine dehydrogenase (DPD) activity after repeated 5-fluorouracil (5-FU) treatment in rats with colorectal cancer (CRC) was investigated. Fluorouracil 166-170 dihydropyrimidine dehydrogenase Rattus norvegicus 121-124 23836081-3 2013 Furthermore, the hepatic DPD levels and the plasma ratio of UH2/Ura decreased significantly and lost their circadian rhythms in CRC rats treated repeatedly with 5-FU, although significant circadian variation in the two parameters was observed in the control CRC rats. Fluorouracil 161-165 dihydropyrimidine dehydrogenase Rattus norvegicus 25-28 23836081-4 2013 Moreover, a significant correlation was found between the plasma ratio of UH2/Ura and hepatic DPD activity in CRC rats untreated and treated with single or repeated 5-FU administration (r(2) = 0.865, p < 0.01). Fluorouracil 165-169 dihydropyrimidine dehydrogenase Rattus norvegicus 94-97 23836081-5 2013 The ratio of UH2/Ura in plasma could be a predictive biomarker of the suppression of hepatic DPD levels during repeated 5-FU-based treatment. Fluorouracil 120-124 dihydropyrimidine dehydrogenase Rattus norvegicus 93-96 23836081-6 2013 Furthermore, by plotting the observed pharmacokinetic parameters of 5-FU against hepatic DPD activity levels predicted by the ratio of UH2/Ura in plasma, AUC0- , CLtot and half-life (t1/2 ) were closely linked to predicted hepatic DPD activity levels. Fluorouracil 68-72 dihydropyrimidine dehydrogenase Rattus norvegicus 232-235 23836081-7 2013 These observations suggest that the factor that significantly influences the AUC0- , CLtot and t1/2 of 5-FU after single or repeated administration of 5-FU is the hepatic DPD activity and it could be assessed by the ratio of UH2/Ura in plasma. Fluorouracil 104-108 dihydropyrimidine dehydrogenase Rattus norvegicus 172-175 23836081-7 2013 These observations suggest that the factor that significantly influences the AUC0- , CLtot and t1/2 of 5-FU after single or repeated administration of 5-FU is the hepatic DPD activity and it could be assessed by the ratio of UH2/Ura in plasma. Fluorouracil 152-156 dihydropyrimidine dehydrogenase Rattus norvegicus 172-175 23444104-3 2013 We have previously reported on the efficacy of AxE1CAUP, an oncolytic adenovirus (OAd) expressing uracil phosphoribosyltransferase (UPRT), an enzyme that markedly enhanced the toxicity of 5-fluorouracil (5-FU), in immunodeficient, Ad-nonpermissive nude mice. Fluorouracil 188-202 uracil phosphoribosyltransferase Mus musculus 98-130 24040364-6 2013 Furthermore, we demonstrated that 53BP1 regulated the sensitivity to 5-Fu through thymidylate synthase (TS) and dihydropyrimidine dehydrogenase (DPYD). Fluorouracil 69-73 dihydropyrimidine dehydrogenase Mus musculus 112-143 24040364-6 2013 Furthermore, we demonstrated that 53BP1 regulated the sensitivity to 5-Fu through thymidylate synthase (TS) and dihydropyrimidine dehydrogenase (DPYD). Fluorouracil 69-73 dihydropyrimidine dehydrogenase Mus musculus 145-149 23197286-5 2013 These results suggest that the decrease of hepatic availability in CRC rats is brought about by the increase in intrinsic clearance induced by the increase in DPD activity, resulting in a decrease in AUC and t 1/2 and an increase in CLtot after 5-FU IV bolus injection. Fluorouracil 245-249 dihydropyrimidine dehydrogenase Rattus norvegicus 159-162 23420533-7 2013 5-FU treatment resulted in a significant upregulation of NKG2D activating molecules (Rae-1 and H60) and DNAM-1 ligands (CD112 and CD155) on MC38 cells, but alpha-GalCer did not. Fluorouracil 0-4 histocompatibility 60a Mus musculus 95-98 23420533-7 2013 5-FU treatment resulted in a significant upregulation of NKG2D activating molecules (Rae-1 and H60) and DNAM-1 ligands (CD112 and CD155) on MC38 cells, but alpha-GalCer did not. Fluorouracil 0-4 nectin cell adhesion molecule 2 Mus musculus 120-125 23420533-9 2013 The increase of the cytolytic activity induced by 5-FU partially depended on NKG2D-Rae-1 or H60 signals. Fluorouracil 50-54 histocompatibility 60a Mus musculus 92-95 23997940-7 2013 EGFR inhibitors have exhibited single agent activity, and seem to synergize very well with standard chemotherapy except for cetuximab and 5-fluorouracil, leucovorin, oxaliplatin (FOLFOX). Fluorouracil 138-152 epidermal growth factor Homo sapiens 0-4 23810214-6 2013 By contrast, 5-fluorouracil induced G2 cell-cycle arrest and apoptosis that may be associated with p53 activation and p21 up-regulation. Fluorouracil 13-27 H3 histone pseudogene 16 Homo sapiens 118-121 23817620-0 2013 Histone deacetylase 4 mediates SMAD family member 4 deacetylation and induces 5-fluorouracil resistance in breast cancer cells. Fluorouracil 78-92 histone deacetylase 4 Homo sapiens 0-21 23817620-5 2013 We found that increased HDAC4 expression in MDA-MB-231 cells was associated with resistance to the anticancer drug 5-fluorouracil (5-FU). Fluorouracil 115-129 histone deacetylase 4 Homo sapiens 24-29 23817620-5 2013 We found that increased HDAC4 expression in MDA-MB-231 cells was associated with resistance to the anticancer drug 5-fluorouracil (5-FU). Fluorouracil 131-135 histone deacetylase 4 Homo sapiens 24-29 23817620-7 2013 This cell line displayed increased 5-FU resistance, and HDAC4 knockdown in HDAC4OE cells restored 5-FU sensitivity. Fluorouracil 98-102 histone deacetylase 4 Homo sapiens 56-61 23817620-7 2013 This cell line displayed increased 5-FU resistance, and HDAC4 knockdown in HDAC4OE cells restored 5-FU sensitivity. Fluorouracil 98-102 histone deacetylase 4 Homo sapiens 75-80 23817620-13 2013 In summary, our data suggest that HDAC4-mediated deacetylation of the SMAD4 promoter may lead to 5-FU resistance in breast cancer cells. Fluorouracil 97-101 histone deacetylase 4 Homo sapiens 34-39 24137384-11 2013 GSTP1-105 and GSTM1 genotypes may be useful markers of severe peripheral neuropathy in MCRC patients treated with 5-FU/oxaliplatin as first-line chemotherapy. Fluorouracil 114-118 glutathione S-transferase pi 1 Homo sapiens 0-5 24156021-1 2013 Thymidylate synthase (TS), a target enzyme of 5-fluorouracil (5-FU), is significantly associated with prognosis in various cancers. Fluorouracil 46-60 thymidylate synthetase Homo sapiens 0-20 24156021-1 2013 Thymidylate synthase (TS), a target enzyme of 5-fluorouracil (5-FU), is significantly associated with prognosis in various cancers. Fluorouracil 46-60 thymidylate synthetase Homo sapiens 22-24 24156021-1 2013 Thymidylate synthase (TS), a target enzyme of 5-fluorouracil (5-FU), is significantly associated with prognosis in various cancers. Fluorouracil 62-66 thymidylate synthetase Homo sapiens 0-20 24156021-1 2013 Thymidylate synthase (TS), a target enzyme of 5-fluorouracil (5-FU), is significantly associated with prognosis in various cancers. Fluorouracil 62-66 thymidylate synthetase Homo sapiens 22-24 24156021-9 2013 The 5-FU treatment in KU-19-19 cells transfected with siRNA for TS gene (TYMS) inhibited cell growth more significantly than that for nontargeting control. Fluorouracil 4-8 thymidylate synthetase Homo sapiens 64-66 24156021-9 2013 The 5-FU treatment in KU-19-19 cells transfected with siRNA for TS gene (TYMS) inhibited cell growth more significantly than that for nontargeting control. Fluorouracil 4-8 thymidylate synthetase Homo sapiens 73-77 23894404-0 2013 Tumor site- and stage-specific associations between allelic variants of glutathione S-transferase and DNA-repair genes and overall survival in colorectal cancer patients receiving 5-fluorouracil-based chemotherapy. Fluorouracil 180-194 glutathione S-transferase kappa 1 Homo sapiens 72-97 23894404-1 2013 INTRODUCTION: Our retrospective cohort study investigated the effect of tumor site and stage on the associations between the allelic variants of glutathione S-transferase (GST) and DNA-repair genes and overall survival (OS) in CRC patients treated with 5-fluorouracil (5-FU)-based adjuvant chemotherapy. Fluorouracil 253-267 glutathione S-transferase kappa 1 Homo sapiens 145-170 23894404-1 2013 INTRODUCTION: Our retrospective cohort study investigated the effect of tumor site and stage on the associations between the allelic variants of glutathione S-transferase (GST) and DNA-repair genes and overall survival (OS) in CRC patients treated with 5-fluorouracil (5-FU)-based adjuvant chemotherapy. Fluorouracil 269-273 glutathione S-transferase kappa 1 Homo sapiens 145-170 23729362-8 2013 Cell death of 5-fluorouracil (5FU)-treated p53-null GSK3B-silenced colon carcinoma cells occurred via PARP1-dependent and AIF-mediated but RIP1-independent necroptosis. Fluorouracil 30-33 receptor interacting serine/threonine kinase 1 Homo sapiens 139-143 23861589-0 2013 Clinical significance of the thymidylate synthase, dihydropyrimidine dehydrogenase, and thymidine phosphorylase mRNA expressions in hepatocellular carcinoma patients receiving 5-fluorouracil-based transarterial chemoembolization treatment. Fluorouracil 176-190 thymidylate synthetase Homo sapiens 29-49 23861589-1 2013 PURPOSE: To determine whether 5-fluorouracil (5-FU) sensitivity is associated with the mRNA expressions of thymidylate synthase (TS), dihydropyrimidine dehydrogenase (DPD), and thymidine phosphorylase (TP) in patients with hepatocellular carcinoma (HCC) treated with 5-FU-based transarterial chemoembolization (TACE). Fluorouracil 30-44 thymidylate synthetase Homo sapiens 107-127 23861589-1 2013 PURPOSE: To determine whether 5-fluorouracil (5-FU) sensitivity is associated with the mRNA expressions of thymidylate synthase (TS), dihydropyrimidine dehydrogenase (DPD), and thymidine phosphorylase (TP) in patients with hepatocellular carcinoma (HCC) treated with 5-FU-based transarterial chemoembolization (TACE). Fluorouracil 30-44 thymidylate synthetase Homo sapiens 129-131 22968820-14 2013 CONCLUSION: These results strongly suggest that the decrease in FANCJ caused by 5FU treatment leads to an increase in sensitivity to oxaliplatin, thus indicating that the FANCJ protein plays an important role in the synergism of the combination of 5FU and oxaliplatin. Fluorouracil 80-83 BRCA1 interacting helicase 1 Homo sapiens 64-69 22968820-14 2013 CONCLUSION: These results strongly suggest that the decrease in FANCJ caused by 5FU treatment leads to an increase in sensitivity to oxaliplatin, thus indicating that the FANCJ protein plays an important role in the synergism of the combination of 5FU and oxaliplatin. Fluorouracil 80-83 BRCA1 interacting helicase 1 Homo sapiens 171-176 23946796-7 2013 Functional assays demonstrated that HuR and FOXO1 expression levels were markedly enhanced upon 5-fluorouracil (5-FU) stimulation in MDA-MB-231 cells. Fluorouracil 96-110 ELAV like RNA binding protein 1 Homo sapiens 36-39 23946796-7 2013 Functional assays demonstrated that HuR and FOXO1 expression levels were markedly enhanced upon 5-fluorouracil (5-FU) stimulation in MDA-MB-231 cells. Fluorouracil 112-116 ELAV like RNA binding protein 1 Homo sapiens 36-39 23946796-8 2013 Knockdown of HuR apparently abrogated 5-FU-induced apoptosis detected by caspase-3 activities. Fluorouracil 38-42 ELAV like RNA binding protein 1 Homo sapiens 13-16 23946796-9 2013 Furthermore, in HuR knockdown cells, additional overexpression of FOXO1 moderately recovered 5-FU-induced apoptosis, which verified that HuR-modulated apoptosis upon 5-FU treatment was partially mediated by its post-transcriptional regulation of FOXO1. Fluorouracil 93-97 ELAV like RNA binding protein 1 Homo sapiens 16-19 23946796-9 2013 Furthermore, in HuR knockdown cells, additional overexpression of FOXO1 moderately recovered 5-FU-induced apoptosis, which verified that HuR-modulated apoptosis upon 5-FU treatment was partially mediated by its post-transcriptional regulation of FOXO1. Fluorouracil 93-97 ELAV like RNA binding protein 1 Homo sapiens 137-140 23946796-9 2013 Furthermore, in HuR knockdown cells, additional overexpression of FOXO1 moderately recovered 5-FU-induced apoptosis, which verified that HuR-modulated apoptosis upon 5-FU treatment was partially mediated by its post-transcriptional regulation of FOXO1. Fluorouracil 166-170 ELAV like RNA binding protein 1 Homo sapiens 16-19 23946796-9 2013 Furthermore, in HuR knockdown cells, additional overexpression of FOXO1 moderately recovered 5-FU-induced apoptosis, which verified that HuR-modulated apoptosis upon 5-FU treatment was partially mediated by its post-transcriptional regulation of FOXO1. Fluorouracil 166-170 ELAV like RNA binding protein 1 Homo sapiens 137-140 23762305-11 2013 CONCLUSION: PPI and EVO both could inhibit the activity of freshly-removed gastric tumor, and they could enhance the anticancer effect of Pt and 5-FU by reducing the mRNA expression levels of ERCC1 and TS. Fluorouracil 145-149 ERCC excision repair 1, endonuclease non-catalytic subunit Homo sapiens 192-197 23332421-11 2013 TS and ERCC1 expression was inversely related to response to 5-FU-and/or oxaliplatin-containing regimens. Fluorouracil 61-65 ERCC excision repair 1, endonuclease non-catalytic subunit Homo sapiens 7-12 23724141-8 2013 In contrast, suppression of MLH1 attenuated the cytotoxic effect of 5-FU, but did not alter sensitivity to SN-38 or oxaliplatin. Fluorouracil 68-72 mutL homolog 1 Homo sapiens 28-32 23313143-0 2013 The upregulation of dihydropyrimidine dehydrogenase in liver is involved in acquired resistance to 5-fluorouracil. Fluorouracil 99-113 dihydropyrimidine dehydrogenase Mus musculus 20-51 23313143-2 2013 The upregulation of dihydropyrimidine dehydrogenase (DPD) in tumours was reported as an important factor for acquired 5-FU resistance. Fluorouracil 118-122 dihydropyrimidine dehydrogenase Mus musculus 20-51 23313143-2 2013 The upregulation of dihydropyrimidine dehydrogenase (DPD) in tumours was reported as an important factor for acquired 5-FU resistance. Fluorouracil 118-122 dihydropyrimidine dehydrogenase Mus musculus 53-56 23313143-10 2013 Furthermore, the upregulation of DPD expression in livers led to accelerated metabolism of 5-FU. Fluorouracil 91-95 dihydropyrimidine dehydrogenase Mus musculus 33-36 23313143-13 2013 CONCLUSION: Our study suggested that the upregulation of DPD in liver may be involved in acquired resistance to 5-FU, and DPD inhibitors or increasing 5-FU dosage may have potential application in overcoming 5-FU acquired resistance. Fluorouracil 112-116 dihydropyrimidine dehydrogenase Mus musculus 57-60 23313143-13 2013 CONCLUSION: Our study suggested that the upregulation of DPD in liver may be involved in acquired resistance to 5-FU, and DPD inhibitors or increasing 5-FU dosage may have potential application in overcoming 5-FU acquired resistance. Fluorouracil 151-155 dihydropyrimidine dehydrogenase Mus musculus 57-60 23313143-13 2013 CONCLUSION: Our study suggested that the upregulation of DPD in liver may be involved in acquired resistance to 5-FU, and DPD inhibitors or increasing 5-FU dosage may have potential application in overcoming 5-FU acquired resistance. Fluorouracil 151-155 dihydropyrimidine dehydrogenase Mus musculus 57-60 24649191-8 2013 Findings of this study demonstrated that OPRT expression positively correlated with fewer side-effects of 5-FU-based chemotherapy and longer patient survival. Fluorouracil 106-110 uridine monophosphate synthetase Homo sapiens 41-45 22963136-6 2013 Most of the p53 negative cases with Maspin nuclear predominance, which seems to respond to 5-Fluorouracil, were microsatellite instability (MSI) cases. Fluorouracil 91-105 serpin family B member 5 Homo sapiens 36-42 22963136-10 2013 CONCLUSIONS: Maspin nuclear expression, associated with p53 ones, might be used either to select the high-risk microsatellite stable (MSS) colorectal carcinomas diagnosed in Stage II or those MSI cases which can respond to 5-Fluorouracil. Fluorouracil 223-237 serpin family B member 5 Homo sapiens 13-19 23481186-9 2013 CONCLUSION: Excision repair cross-complementation group 1 status is highly predictive of which patients will benefit from the addition of OX to 5-FU for stage III colon cancer. Fluorouracil 144-148 ERCC excision repair 1, endonuclease non-catalytic subunit Homo sapiens 12-57 22958523-2 2013 Thymidylate synthase (TS) is the most important target of 5-fluorouracil; three main genetic polymorphisms of TS have been described. Fluorouracil 58-72 thymidylate synthetase Homo sapiens 0-20 22958523-2 2013 Thymidylate synthase (TS) is the most important target of 5-fluorouracil; three main genetic polymorphisms of TS have been described. Fluorouracil 58-72 thymidylate synthetase Homo sapiens 22-24 22958523-2 2013 Thymidylate synthase (TS) is the most important target of 5-fluorouracil; three main genetic polymorphisms of TS have been described. Fluorouracil 58-72 thymidylate synthetase Homo sapiens 110-112 22249354-2 2013 The gene uridine monophosphate synthetase (UMPS) is thought to be primarily responsible for conversion of 5-FU to active anticancer metabolites in tumor cells. Fluorouracil 106-110 uridine monophosphate synthetase Homo sapiens 9-41 22249354-2 2013 The gene uridine monophosphate synthetase (UMPS) is thought to be primarily responsible for conversion of 5-FU to active anticancer metabolites in tumor cells. Fluorouracil 106-110 uridine monophosphate synthetase Homo sapiens 43-47 22249354-3 2013 Mutation or aberrant expression of UMPS may contribute to 5-FU resistance during treatment. Fluorouracil 58-62 uridine monophosphate synthetase Homo sapiens 35-39 22249354-5 2013 We observed reciprocal differential expression of two UMPS isoforms in a colorectal cancer cell line with acquired 5-FU resistance relative to the 5-FU-sensitive cell line from which it was derived. Fluorouracil 115-119 uridine monophosphate synthetase Homo sapiens 54-58 22249354-5 2013 We observed reciprocal differential expression of two UMPS isoforms in a colorectal cancer cell line with acquired 5-FU resistance relative to the 5-FU-sensitive cell line from which it was derived. Fluorouracil 147-151 uridine monophosphate synthetase Homo sapiens 54-58 22249354-8 2013 We developed sequencing and expression assays to specifically detect alternative UMPS isoforms and used these to determine that UMPS was recurrently disrupted by mutations and aberrant splicing in additional 5-FU-resistant colorectal cancer cell lines and colorectal tumors. Fluorouracil 208-212 uridine monophosphate synthetase Homo sapiens 128-132 22249354-9 2013 The observed mutations, aberrant splicing and downregulation of UMPS represent novel mechanisms for acquired 5-FU resistance in colorectal cancer. Fluorouracil 109-113 uridine monophosphate synthetase Homo sapiens 64-68 23072534-9 2013 The number of apoptotic, caspase-3- and caspase-8-activated cells increased 24 h after the first 5-FU administration, and these responses were reduced by ramosetron. Fluorouracil 97-101 caspase 8 Mus musculus 40-49 23076534-5 2013 Compared to empty vector-transfected cells, overexpression of periostin rendered SGC-7901 cells more resistant to cisplatin or 5-fluorouracil (5-FU)-induced apoptosis, accompanying with less release of cytochrome c from mitochondria and diminished cleavage of caspase-3 and poly (ADP-ribose) polymerase. Fluorouracil 127-141 periostin Homo sapiens 62-71 23076534-5 2013 Compared to empty vector-transfected cells, overexpression of periostin rendered SGC-7901 cells more resistant to cisplatin or 5-fluorouracil (5-FU)-induced apoptosis, accompanying with less release of cytochrome c from mitochondria and diminished cleavage of caspase-3 and poly (ADP-ribose) polymerase. Fluorouracil 143-147 periostin Homo sapiens 62-71 23076534-6 2013 Periostin-overexpressing cells treated with cisplatin or 5-FU showed significantly (p < 0.05) decreased expression of Bax and p53 proteins and increased expression of Bcl-2 protein, when compared to drug-treated mock counterparts. Fluorouracil 57-61 periostin Homo sapiens 0-9 23076534-10 2013 Taken together, our data indicate that periostin confers protection against cisplatin or 5-FU-induced apoptosis in SGC-7901 cells, likely through modulating the Akt/p53 pathway, and thus represents a potential therapeutic target in gastric cancer. Fluorouracil 89-93 periostin Homo sapiens 39-48 23449328-0 2013 Effect of rice cell-derived human granulocyte-macrophage colony-stimulating factor on 5-fluorouracil-induced mucositis in hamsters. Fluorouracil 86-100 colony stimulating factor 2 Homo sapiens 34-82 23575271-2 2013 5-FU pharmacokinetic and pharmacodynamic studies were performed using DPD circadian variation in rats with 1,2-dimethylhydrazine-induced CRC. Fluorouracil 0-4 dihydropyrimidine dehydrogenase Rattus norvegicus 70-73 23575271-4 2013 5-FU concentration fluctuations induced by DPD activity variation affected tumor volume. Fluorouracil 0-4 dihydropyrimidine dehydrogenase Rattus norvegicus 43-46 23155336-18 2012 CONCLUSION: GC/5-FU nanoparticles can significantly inhibit the growth of liver cancer in mice via the p53 apoptosis pathway, and relieve the side effects and immunosuppression of 5-FU. Fluorouracil 15-19 transformation related protein 53, pseudogene Mus musculus 103-106 23239440-8 2012 SCF/TGF-beta ratio increased in both the young and aged mice after 5-FU treatment. Fluorouracil 67-71 kit ligand Mus musculus 0-3 23084747-3 2012 We report an in vivo gain-of-function screen and the identification of miR-150 as an inhibitor of hematopoietic recovery upon 5-fluorouracil-induced injury. Fluorouracil 126-140 microRNA 150 Mus musculus 71-78 23170110-12 2012 The combination of a relatively low expression of TS and high expression of OPRT suggests an improved antitumor effect of 5-FU drugs in thymic carcinoma compared to in lung carcinoma. Fluorouracil 122-126 thymidylate synthetase Homo sapiens 50-52 23170110-12 2012 The combination of a relatively low expression of TS and high expression of OPRT suggests an improved antitumor effect of 5-FU drugs in thymic carcinoma compared to in lung carcinoma. Fluorouracil 122-126 uridine monophosphate synthetase Homo sapiens 76-80 22866897-8 2012 In addition, down-regulation of the selected siRNA target, choline kinase (Chk), and the conversion of the nontoxic prodrug 5-fluorocytosine (5-FC) to cytotoxic 5-fluorouracil (5-FU) were also demonstrated with noninvasive imaging. Fluorouracil 177-181 choline kinase alpha Homo sapiens 75-78 22998564-2 2012 High levels of thymidylate synthase (TS), the target enzyme of 5-FU and DPD which degrades the majority of 5-FU, are associated with poor prognosis in some cancers. Fluorouracil 107-111 thymidylate synthetase Homo sapiens 15-35 22998564-2 2012 High levels of thymidylate synthase (TS), the target enzyme of 5-FU and DPD which degrades the majority of 5-FU, are associated with poor prognosis in some cancers. Fluorouracil 107-111 thymidylate synthetase Homo sapiens 37-39 22998564-7 2012 Furthermore, the association between their levels and the sensitivity to 5-FU was examined using the small interfering RNA (siRNA) specific for TS and DPD. Fluorouracil 73-77 thymidylate synthetase Homo sapiens 144-146 22963400-9 2012 Concurrent ATO and 5-FU treatment of HepG2 cells was synergistic, leading to increased cytotoxicity due in part to modulation of thymidylate synthase levels by ATO. Fluorouracil 19-23 thymidylate synthetase Homo sapiens 129-149 22766915-5 2012 To understand the mechanisms underlying the enhanced growth inhibitory effect of the administration sequence, DOC followed by 5-FU, we examined the expression of 5-FU metabolic enzymes such as thymidylate synthase (TS), dihydropyrimidine dehydrogenase (DPD) and orotate phosphoribosyl transferase (OPRT), which were known to regulate the antitumor effect of 5-FU, by real-time RT-PCR and western blot analysis. Fluorouracil 162-166 thymidylate synthetase Homo sapiens 193-213 22766915-5 2012 To understand the mechanisms underlying the enhanced growth inhibitory effect of the administration sequence, DOC followed by 5-FU, we examined the expression of 5-FU metabolic enzymes such as thymidylate synthase (TS), dihydropyrimidine dehydrogenase (DPD) and orotate phosphoribosyl transferase (OPRT), which were known to regulate the antitumor effect of 5-FU, by real-time RT-PCR and western blot analysis. Fluorouracil 162-166 thymidylate synthetase Homo sapiens 193-213 22766915-6 2012 Downregulation of TS and DPD expression and upregulation of OPRT expression were induced by DOC treatment, suggesting that DOC enhanced the efficacy of 5-FU by altering the expression of its metabolic enzymes. Fluorouracil 152-156 thymidylate synthetase Homo sapiens 18-20 22766915-6 2012 Downregulation of TS and DPD expression and upregulation of OPRT expression were induced by DOC treatment, suggesting that DOC enhanced the efficacy of 5-FU by altering the expression of its metabolic enzymes. Fluorouracil 152-156 uridine monophosphate synthetase Homo sapiens 60-64 22797697-8 2012 Moreover, activation of VEGFR-3 increased platelet counts in thrombopoietin-treated mice significantly and modulated 5-fluorouracil-induced thrombocytosis strongly, suggesting a regulatory role for VEGFR-3 in megakaryopoiesis. Fluorouracil 117-131 FMS-like tyrosine kinase 4 Mus musculus 24-31 22797697-8 2012 Moreover, activation of VEGFR-3 increased platelet counts in thrombopoietin-treated mice significantly and modulated 5-fluorouracil-induced thrombocytosis strongly, suggesting a regulatory role for VEGFR-3 in megakaryopoiesis. Fluorouracil 117-131 FMS-like tyrosine kinase 4 Mus musculus 198-205 22382630-0 2012 Role of miR-19b and its target mRNAs in 5-fluorouracil resistance in colon cancer cells. Fluorouracil 40-54 microRNA 19b-1 Homo sapiens 8-15 22382630-6 2012 RESULTS: In response to 5-FU, miR-19b and miR-21 were over-expressed in 5-FU-resistant cells. Fluorouracil 24-28 microRNA 19b-1 Homo sapiens 30-37 22382630-6 2012 RESULTS: In response to 5-FU, miR-19b and miR-21 were over-expressed in 5-FU-resistant cells. Fluorouracil 24-28 microRNA 21 Homo sapiens 42-48 22382630-6 2012 RESULTS: In response to 5-FU, miR-19b and miR-21 were over-expressed in 5-FU-resistant cells. Fluorouracil 72-76 microRNA 19b-1 Homo sapiens 30-37 22382630-6 2012 RESULTS: In response to 5-FU, miR-19b and miR-21 were over-expressed in 5-FU-resistant cells. Fluorouracil 72-76 microRNA 21 Homo sapiens 42-48 22382630-7 2012 Of note, miR-19b was up-regulated 3.47-fold in the DLD-1 resistant cells, which exhibited no alteration in cell cycle profiles despite exposure to 5-FU. Fluorouracil 147-151 microRNA 19b-1 Homo sapiens 9-16 22382630-12 2012 CONCLUSIONS: We revealed up-regulation of miR-19b in response to 5-FU and potential targets of miR-19b mediating the cell cycle under treatment with 5-FU. Fluorouracil 65-69 microRNA 19b-1 Homo sapiens 42-49 22382630-12 2012 CONCLUSIONS: We revealed up-regulation of miR-19b in response to 5-FU and potential targets of miR-19b mediating the cell cycle under treatment with 5-FU. Fluorouracil 149-153 microRNA 19b-1 Homo sapiens 42-49 22382630-12 2012 CONCLUSIONS: We revealed up-regulation of miR-19b in response to 5-FU and potential targets of miR-19b mediating the cell cycle under treatment with 5-FU. Fluorouracil 149-153 microRNA 19b-1 Homo sapiens 95-102 22716215-11 2012 The combination of 5-FU and chloroquine induced G1 arrest, up-regulation of p27 and p53, and down-regulation of CDK2 and cyclin D1. Fluorouracil 19-23 interferon alpha inducible protein 27 Homo sapiens 76-79 22133572-2 2012 The aim of this trial was to determine the value of thymidylate synthase (TS), a key enzyme of DNA synthesis and target of 5-FU, to predict response to chemotherapy of mCRC. Fluorouracil 123-127 thymidylate synthetase Homo sapiens 52-72 22133572-2 2012 The aim of this trial was to determine the value of thymidylate synthase (TS), a key enzyme of DNA synthesis and target of 5-FU, to predict response to chemotherapy of mCRC. Fluorouracil 123-127 thymidylate synthetase Homo sapiens 74-76 22552693-7 2012 The cells treated with combination of p65 siRNA or curcumin and 5-FU revealed a lower cell viability and higher apoptosis compared to those treated with 5-FU alone. Fluorouracil 153-157 v-rel reticuloendotheliosis viral oncogene homolog A (avian) Mus musculus 38-41 22552693-10 2012 Overall, our results indicate that the constitutively activated NF-kappaB signaling pathway plays a crucial role in these two ESCC cell lines and both p65siRNA and curcumin can promote ESCC cell apoptosis and enhance the sensitivity to 5-FU through suppression of the NF-kappaB signaling pathway. Fluorouracil 236-240 v-rel reticuloendotheliosis viral oncogene homolog A (avian) Mus musculus 151-154 22824673-6 2012 By immunoblot assay, the FTS antibody specifically recognizes modified TS in a dose-dependent manner in 5FU-treated cells, in cancer xenograft tissues of 5FU-treated mice, and in the murine tissues. Fluorouracil 104-107 AKT interacting protein Mus musculus 25-28 22824673-6 2012 By immunoblot assay, the FTS antibody specifically recognizes modified TS in a dose-dependent manner in 5FU-treated cells, in cancer xenograft tissues of 5FU-treated mice, and in the murine tissues. Fluorouracil 154-157 AKT interacting protein Mus musculus 25-28 22611193-6 2012 5-FU-treated H-Cx43-deficient HSC and progenitors (HSC/P) cells display decreased survival and fail to enter the cell cycle to proliferate. Fluorouracil 0-4 fucosyltransferase 1 (H blood group) Homo sapiens 30-33 22611193-6 2012 5-FU-treated H-Cx43-deficient HSC and progenitors (HSC/P) cells display decreased survival and fail to enter the cell cycle to proliferate. Fluorouracil 0-4 fucosyltransferase 1 (H blood group) Homo sapiens 51-54 22270332-1 2012 PURPOSE: Thymidylate synthase (TS) and dihydropyrimidine dehydrogenase (DPD) are important enzymes in the metabolism of 5-fluorouracil, which have been examined as possible predictive markers. Fluorouracil 120-134 thymidylate synthetase Homo sapiens 9-29 22270332-1 2012 PURPOSE: Thymidylate synthase (TS) and dihydropyrimidine dehydrogenase (DPD) are important enzymes in the metabolism of 5-fluorouracil, which have been examined as possible predictive markers. Fluorouracil 120-134 thymidylate synthetase Homo sapiens 31-33 22474250-2 2012 This paper reports our observation that the expression of the chemokine monokine induced by IFN-gamma (Mig) and its receptor CXCR3 was significantly activated in mice after treatment with the chemotherapeutic agent 5-fluorouracil (5-FU). Fluorouracil 215-229 chemokine (C-X-C motif) ligand 9 Mus musculus 72-101 22474250-2 2012 This paper reports our observation that the expression of the chemokine monokine induced by IFN-gamma (Mig) and its receptor CXCR3 was significantly activated in mice after treatment with the chemotherapeutic agent 5-fluorouracil (5-FU). Fluorouracil 215-229 chemokine (C-X-C motif) ligand 9 Mus musculus 103-106 22474250-2 2012 This paper reports our observation that the expression of the chemokine monokine induced by IFN-gamma (Mig) and its receptor CXCR3 was significantly activated in mice after treatment with the chemotherapeutic agent 5-fluorouracil (5-FU). Fluorouracil 215-229 chemokine (C-X-C motif) receptor 3 Mus musculus 125-130 22474250-2 2012 This paper reports our observation that the expression of the chemokine monokine induced by IFN-gamma (Mig) and its receptor CXCR3 was significantly activated in mice after treatment with the chemotherapeutic agent 5-fluorouracil (5-FU). Fluorouracil 231-235 chemokine (C-X-C motif) ligand 9 Mus musculus 72-101 22474250-2 2012 This paper reports our observation that the expression of the chemokine monokine induced by IFN-gamma (Mig) and its receptor CXCR3 was significantly activated in mice after treatment with the chemotherapeutic agent 5-fluorouracil (5-FU). Fluorouracil 231-235 chemokine (C-X-C motif) ligand 9 Mus musculus 103-106 22474250-2 2012 This paper reports our observation that the expression of the chemokine monokine induced by IFN-gamma (Mig) and its receptor CXCR3 was significantly activated in mice after treatment with the chemotherapeutic agent 5-fluorouracil (5-FU). Fluorouracil 231-235 chemokine (C-X-C motif) receptor 3 Mus musculus 125-130 22474250-4 2012 In addition, elevation of Mig plasma levels after 5-FU treatment corresponded with increased mortality. Fluorouracil 50-54 chemokine (C-X-C motif) ligand 9 Mus musculus 26-29 22474250-9 2012 Our results strongly suggest that Mig contributes to the acute lethal toxicity arising from 5-FU administration. Fluorouracil 92-96 chemokine (C-X-C motif) ligand 9 Mus musculus 34-37 22621392-9 2012 GKN1 expression also enhanced tumor cell sensitivity to 5-FU treatment. Fluorouracil 56-60 gastrokine 1 Homo sapiens 0-4 22621392-11 2012 CONCLUSIONS: Expression of GKN1 is progressively lost from normal mucosa, precancerous to cancerous gastric tissues, while restoration of GKN1 expression induces gastric cancer cells to undergo apoptosis, and enhances sensitivity of gastric cancer cells to 5-FU-induced apoptosis. Fluorouracil 257-261 gastrokine 1 Homo sapiens 27-31 22403796-6 2012 The numbers of apoptotic caspase-3- and caspase-8-activated cells in the intestinal crypt increased 24 h after the first 5-FU administration but were overall significantly lower in Nox1KO than in WT mice. Fluorouracil 121-125 caspase 8 Mus musculus 40-49 22564307-5 2012 RESULTS: We show here that a strain with the mcm2 allele lacking DDK phosphorylation sites (mcm2AA) is also sensitive to the ribonucleotide reductase inhibitor, hydroxyurea (HU) and to the base analogue 5-fluorouracil (5-FU) but not the radiomimetic drug, phleomycin. Fluorouracil 203-217 MCM DNA helicase complex subunit MCM2 Saccharomyces cerevisiae S288C 45-49 22564307-5 2012 RESULTS: We show here that a strain with the mcm2 allele lacking DDK phosphorylation sites (mcm2AA) is also sensitive to the ribonucleotide reductase inhibitor, hydroxyurea (HU) and to the base analogue 5-fluorouracil (5-FU) but not the radiomimetic drug, phleomycin. Fluorouracil 219-223 MCM DNA helicase complex subunit MCM2 Saccharomyces cerevisiae S288C 45-49 22320227-1 2012 The purpose of the present study was to investigate the association of glutathione S-transferase P1 (GSTP1) expression with resistance to neoadjuvant paclitaxel followed by 5-fluorouracil/epirubicin/cyclophosphamide (P-FEC) in human breast cancers. Fluorouracil 173-187 glutathione S-transferase pi 1 Homo sapiens 71-99 22071131-1 2012 BACKGROUND: Microsatellite instability (MSI) is a distinct molecular phenotype of colorectal cancer related to prognosis and tumour response to 5-fluorouracil (5-FU)-based chemotherapy. Fluorouracil 144-158 RB binding protein 4, chromatin remodeling factor Homo sapiens 40-43 22071131-1 2012 BACKGROUND: Microsatellite instability (MSI) is a distinct molecular phenotype of colorectal cancer related to prognosis and tumour response to 5-fluorouracil (5-FU)-based chemotherapy. Fluorouracil 160-164 RB binding protein 4, chromatin remodeling factor Homo sapiens 40-43 22071131-9 2012 CONCLUSION: These results support the use of MSI status as a marker of prognosis and response to 5-FU-based chemotherapy in patients with colon cancers. Fluorouracil 97-101 RB binding protein 4, chromatin remodeling factor Homo sapiens 45-48 22006578-8 2012 CONCLUSIONS: High TS and DPD mRNA levels on FFPE specimens may predict distant recurrence of rectal cancer treated with 5-FU-based preoperative CRT followed by surgery. Fluorouracil 120-124 thymidylate synthetase Homo sapiens 18-20 22367509-0 2012 STAT5a-targeting miRNA enhances chemosensitivity to cisplatin and 5-fluorouracil in human colorectal cancer cells. Fluorouracil 66-80 signal transducer and activator of transcription 5A Homo sapiens 0-6 22367509-7 2012 However, we found that inhibition of STAT5a restored the sensitivity of SW1116 cells to CDDP and 5-Fu. Fluorouracil 97-101 signal transducer and activator of transcription 5A Homo sapiens 37-43 22367509-8 2012 In additional experiments, we found that inhibition of STAT5a significantly promoted CRC cell apoptosis by CDDP and 5-Fu. Fluorouracil 116-120 signal transducer and activator of transcription 5A Homo sapiens 55-61 22367509-9 2012 In the present study, we found that inhibition of STAT5a promotes apoptosis of CRC cells induced by chemotherapy drugs, such as CDDP or 5-Fu. Fluorouracil 136-140 signal transducer and activator of transcription 5A Homo sapiens 50-56 22179686-4 2012 First, two 5-FU-resistant cell lines, HLF-R4 and HLF-R10, were established from the HLF undifferentiated human HCC cell line. Fluorouracil 11-15 HLF transcription factor, PAR bZIP family member Homo sapiens 50-53 22179686-4 2012 First, two 5-FU-resistant cell lines, HLF-R4 and HLF-R10, were established from the HLF undifferentiated human HCC cell line. Fluorouracil 11-15 HLF transcription factor, PAR bZIP family member Homo sapiens 61-64 22179686-4 2012 First, two 5-FU-resistant cell lines, HLF-R4 and HLF-R10, were established from the HLF undifferentiated human HCC cell line. Fluorouracil 11-15 HLF transcription factor, PAR bZIP family member Homo sapiens 61-64 22179686-6 2012 The terminal deoxyribonucleotidyl transferase-mediated dUTP nick end labeling assay also showed a dramatically decreased number of apoptotic cells in the HLF-Rs after treatment with 5-FU. Fluorouracil 218-222 HLF transcription factor, PAR bZIP family member Homo sapiens 178-181 22179686-11 2012 Our results suggested that the metabolism of EMT and 5-FU has important roles in 5-FU chemoresistance in the HLF-R cells, and that the HLF-R cells would be useful in vitro models for understanding the 5-FU-resistant mechanisms in HCC. Fluorouracil 53-57 HLF transcription factor, PAR bZIP family member Homo sapiens 121-124 22179686-11 2012 Our results suggested that the metabolism of EMT and 5-FU has important roles in 5-FU chemoresistance in the HLF-R cells, and that the HLF-R cells would be useful in vitro models for understanding the 5-FU-resistant mechanisms in HCC. Fluorouracil 93-97 HLF transcription factor, PAR bZIP family member Homo sapiens 121-124 22543147-0 2012 [Effect of 1,25-dihydroxyvitamin D(3) combined with 5-fluorouracil on IGFBP-3 expression in human esophageal carcinoma 109 cell xenograft in nude mice]. Fluorouracil 52-66 insulin like growth factor binding protein 3 Homo sapiens 70-77 22303938-3 2012 Their mode of action probably involves their ability to act as acceptors in a Michael-addition mechanism, while it was revealed that 5- fluorouracil nucleosides represent novel prodrugs of 5-fluorouracil targeting thymidylate synthase. Fluorouracil 189-203 thymidylate synthetase Homo sapiens 214-234 22117060-7 2012 This newly identified miR-193a-3p-SRSF2 axis highlights a new set of companion diagnostics required for optimal 5-FU therapy of HCC, which involve assaying both the DNA methylation state of the miR-193a gene and the expression of miR-193a-3p and SRSF2 and the relative level of the proapoptotic versus antiapoptotic splicing forms of caspase 2 in clinical samples. Fluorouracil 112-116 caspase 2 Homo sapiens 334-343 21351099-5 2012 The CRPC specimens and C4-2 cells exhibited significantly lower thymidylate synthase (TS) expression, a target of 5-FU, than the ADPC specimens and LNCaP cells. Fluorouracil 114-118 thymidylate synthetase Homo sapiens 64-84 22186294-4 2012 5-FU was used to investigate whether knockdown NF-kappaB p65 can potentiate 5-FU"s antitumor effect. Fluorouracil 0-4 v-rel reticuloendotheliosis viral oncogene homolog A (avian) Mus musculus 57-60 22186294-4 2012 5-FU was used to investigate whether knockdown NF-kappaB p65 can potentiate 5-FU"s antitumor effect. Fluorouracil 76-80 v-rel reticuloendotheliosis viral oncogene homolog A (avian) Mus musculus 57-60 22186294-5 2012 Animal results indicated that tumor growth was inhibited in p65 siRNA and p65 siRNA+5-FU groups as compared with the control group. Fluorouracil 84-88 v-rel reticuloendotheliosis viral oncogene homolog A (avian) Mus musculus 74-77 22186294-7 2012 Overall, our work indicates that downregulation of p65 can increase tumor apoptosis and potentiates the effects of 5-FU by suppressing NF-kappaB signaling pathway. Fluorouracil 115-119 v-rel reticuloendotheliosis viral oncogene homolog A (avian) Mus musculus 51-54 22041582-3 2012 In the present study we dissect the mechanism of a more drastic inhibition of PARN by novel glucopyranosyl analogues bearing uracil, 5-fluorouracil or thymine as the base moiety. Fluorouracil 133-147 poly(A)-specific ribonuclease Homo sapiens 78-82 22336586-2 2012 Here, we tested the hypothesis that the dual PI3K/mTOR inhibitor, PI103, could synergize with the chemotherapeutic agent, 5-fluorouracil (5-FU) by inhibiting E2F1, thymidylate synthase (TS) and enhancing DNA damage. Fluorouracil 122-136 E2F transcription factor 1 Homo sapiens 158-162 22336586-2 2012 Here, we tested the hypothesis that the dual PI3K/mTOR inhibitor, PI103, could synergize with the chemotherapeutic agent, 5-fluorouracil (5-FU) by inhibiting E2F1, thymidylate synthase (TS) and enhancing DNA damage. Fluorouracil 138-142 E2F transcription factor 1 Homo sapiens 158-162 22336586-8 2012 E2F1 siRNA enhanced sensitivity to 5-FU only in cells displaying synergy. Fluorouracil 35-39 E2F transcription factor 1 Homo sapiens 0-4 21167658-10 2012 Germline thymidylate synthase and XRCC1 polymorphisms might be useful as predictive markers of rectal tumor response to neoadjuvant chemoradiotherapy with 5-fluorouracil. Fluorouracil 155-169 thymidylate synthetase Homo sapiens 9-29 22213823-9 2012 Furthermore, a significant correlation between baseline uPAR expression and sensitivity toward 5-fluorouracil was revealed, thus illustrating the possible potentials of uPAR PET in a clinical setting. Fluorouracil 95-109 plasminogen activator, urokinase receptor Homo sapiens 56-60 22213823-9 2012 Furthermore, a significant correlation between baseline uPAR expression and sensitivity toward 5-fluorouracil was revealed, thus illustrating the possible potentials of uPAR PET in a clinical setting. Fluorouracil 95-109 plasminogen activator, urokinase receptor Homo sapiens 169-173 23077553-0 2012 5-Fluorouracil nanoparticles inhibit hepatocellular carcinoma via activation of the p53 pathway in the orthotopic transplant mouse model. Fluorouracil 0-14 transformation related protein 53, pseudogene Mus musculus 84-87 22496803-3 2012 Clinical associations between 5FU-related toxicity and the TYMS VNTR were reported, however, results were inconsistent, suggesting that additional genetic variation in the TYMS gene might influence Tyms expression. Fluorouracil 30-33 thymidylate synthetase Homo sapiens 172-176 22143355-1 2012 PURPOSE: Thymidylate synthase (TS) and dihydropyrimidine dehydrogenase (DPD) are important enzymes in the metabolism of 5-fluorouracil and possible predictive markers. Fluorouracil 120-134 thymidylate synthetase Homo sapiens 9-29 21775092-4 2011 The chemokine (C-X-C motif) ligand 9 (CXCL9) was one of the candidates identified that presented a characteristic gene expression profile; its temporal expression pattern was correlated with the damage and regeneration phases of the small intestine upon 5-FU chemotherapy. Fluorouracil 254-258 chemokine (C-X-C motif) ligand 9 Mus musculus 4-36 21775092-4 2011 The chemokine (C-X-C motif) ligand 9 (CXCL9) was one of the candidates identified that presented a characteristic gene expression profile; its temporal expression pattern was correlated with the damage and regeneration phases of the small intestine upon 5-FU chemotherapy. Fluorouracil 254-258 chemokine (C-X-C motif) ligand 9 Mus musculus 38-43 21775092-7 2011 Moreover, we demonstrated that CXCL9 was able to promote the proliferation and regeneration of intestinal cells by inhibiting the proliferation of normal intestinal mucosal cells prior to chemotherapy and by reducing the 5-FU-induced apoptosis in intestinal crypts. Fluorouracil 221-225 chemokine (C-X-C motif) ligand 9 Mus musculus 31-36 21374737-6 2011 siRNAs targeting TS or survivin or both could mimic the effect of CaSR activation in promoting sensitivity to 5-FU. Fluorouracil 110-114 thymidylate synthetase Homo sapiens 17-19 22384554-11 2011 RESULTS: Compared with the model control group, the tumor volume was markedly reduced in the small, medium, large dose RKY groups, and the medium dose RKY +5-FU group, the expressions of VEGF-C and VEGFR-3 were significantly down-regulated and LMVD were obviously lowered, showing statistical difference (P < 0.05, P < 0.01). Fluorouracil 156-160 FMS-like tyrosine kinase 4 Mus musculus 198-205 22110208-1 2011 AIM: The aim of this study was to determine whether the relative mRNA expressions of the thymidylate synthase (TYMS) and the excision repair cross-complementing 1 (ERCC1) genes are associated with in vitro chemosensitivity to 5-fluorouracil (5-FU) and oxaliplatin in colorectal cancer, respectively. Fluorouracil 226-240 thymidylate synthetase Homo sapiens 89-109 22110208-1 2011 AIM: The aim of this study was to determine whether the relative mRNA expressions of the thymidylate synthase (TYMS) and the excision repair cross-complementing 1 (ERCC1) genes are associated with in vitro chemosensitivity to 5-fluorouracil (5-FU) and oxaliplatin in colorectal cancer, respectively. Fluorouracil 226-240 thymidylate synthetase Homo sapiens 111-115 22110208-1 2011 AIM: The aim of this study was to determine whether the relative mRNA expressions of the thymidylate synthase (TYMS) and the excision repair cross-complementing 1 (ERCC1) genes are associated with in vitro chemosensitivity to 5-fluorouracil (5-FU) and oxaliplatin in colorectal cancer, respectively. Fluorouracil 226-240 ERCC excision repair 1, endonuclease non-catalytic subunit Homo sapiens 125-162 22110208-1 2011 AIM: The aim of this study was to determine whether the relative mRNA expressions of the thymidylate synthase (TYMS) and the excision repair cross-complementing 1 (ERCC1) genes are associated with in vitro chemosensitivity to 5-fluorouracil (5-FU) and oxaliplatin in colorectal cancer, respectively. Fluorouracil 226-240 ERCC excision repair 1, endonuclease non-catalytic subunit Homo sapiens 164-169 22110208-1 2011 AIM: The aim of this study was to determine whether the relative mRNA expressions of the thymidylate synthase (TYMS) and the excision repair cross-complementing 1 (ERCC1) genes are associated with in vitro chemosensitivity to 5-fluorouracil (5-FU) and oxaliplatin in colorectal cancer, respectively. Fluorouracil 242-246 thymidylate synthetase Homo sapiens 89-109 22110208-1 2011 AIM: The aim of this study was to determine whether the relative mRNA expressions of the thymidylate synthase (TYMS) and the excision repair cross-complementing 1 (ERCC1) genes are associated with in vitro chemosensitivity to 5-fluorouracil (5-FU) and oxaliplatin in colorectal cancer, respectively. Fluorouracil 242-246 thymidylate synthetase Homo sapiens 111-115 22110208-1 2011 AIM: The aim of this study was to determine whether the relative mRNA expressions of the thymidylate synthase (TYMS) and the excision repair cross-complementing 1 (ERCC1) genes are associated with in vitro chemosensitivity to 5-fluorouracil (5-FU) and oxaliplatin in colorectal cancer, respectively. Fluorouracil 242-246 ERCC excision repair 1, endonuclease non-catalytic subunit Homo sapiens 125-162 22110208-1 2011 AIM: The aim of this study was to determine whether the relative mRNA expressions of the thymidylate synthase (TYMS) and the excision repair cross-complementing 1 (ERCC1) genes are associated with in vitro chemosensitivity to 5-fluorouracil (5-FU) and oxaliplatin in colorectal cancer, respectively. Fluorouracil 242-246 ERCC excision repair 1, endonuclease non-catalytic subunit Homo sapiens 164-169 22110208-6 2011 RESULTS: The mean level of TYMS mRNA expression in the groups with low and high response to 5-FU was 2.35x10(-3) +- 2.16x10(-3) 2(-(DeltaCt)) and 4.54x10(-3) +- 2.46x10(-3) 2(-(DeltaCt)), respectively. Fluorouracil 92-96 thymidylate synthetase Homo sapiens 27-31 22110208-8 2011 Groups with high response to 5-FU and oxaliplatin had significantly higher expression of TYMS and ERCC1 mRNA, respectively (p<0.01 and p=0.01, respectively). Fluorouracil 29-33 thymidylate synthetase Homo sapiens 89-93 22110208-8 2011 Groups with high response to 5-FU and oxaliplatin had significantly higher expression of TYMS and ERCC1 mRNA, respectively (p<0.01 and p=0.01, respectively). Fluorouracil 29-33 ERCC excision repair 1, endonuclease non-catalytic subunit Homo sapiens 98-103 22110208-9 2011 CONCLUSION: High expression of TYMS and ERCC1 mRNA was associated with better in vitro chemosensitivity to 5-FU and oxaliplatin, respectively, in patients with colorectal cancer. Fluorouracil 107-111 thymidylate synthetase Homo sapiens 31-35 22110208-9 2011 CONCLUSION: High expression of TYMS and ERCC1 mRNA was associated with better in vitro chemosensitivity to 5-FU and oxaliplatin, respectively, in patients with colorectal cancer. Fluorouracil 107-111 ERCC excision repair 1, endonuclease non-catalytic subunit Homo sapiens 40-45 20932673-0 2011 Thymidylate synthase gene polymorphism affects the response to preoperative 5-fluorouracil chemoradiation therapy in patients with rectal cancer. Fluorouracil 76-90 thymidylate synthetase Homo sapiens 0-20 20932673-1 2011 PURPOSE: This study aims to correlate thymidylate synthase (TS) gene polymorphisms with the tumor response to preoperative 5-fluorouracil (5-FU)-based chemoradiation therapy (CRT) in patients with rectal cancer. Fluorouracil 123-137 thymidylate synthetase Homo sapiens 38-58 20932673-1 2011 PURPOSE: This study aims to correlate thymidylate synthase (TS) gene polymorphisms with the tumor response to preoperative 5-fluorouracil (5-FU)-based chemoradiation therapy (CRT) in patients with rectal cancer. Fluorouracil 123-137 thymidylate synthetase Homo sapiens 60-62 20932673-1 2011 PURPOSE: This study aims to correlate thymidylate synthase (TS) gene polymorphisms with the tumor response to preoperative 5-fluorouracil (5-FU)-based chemoradiation therapy (CRT) in patients with rectal cancer. Fluorouracil 139-143 thymidylate synthetase Homo sapiens 38-58 20932673-1 2011 PURPOSE: This study aims to correlate thymidylate synthase (TS) gene polymorphisms with the tumor response to preoperative 5-fluorouracil (5-FU)-based chemoradiation therapy (CRT) in patients with rectal cancer. Fluorouracil 139-143 thymidylate synthetase Homo sapiens 60-62 20932673-11 2011 CONCLUSIONS: This study suggests that SNPs within the TS enhancer region affect the tumor response to preoperative 5-FU-based CRT in rectal cancer. Fluorouracil 115-119 thymidylate synthetase Homo sapiens 54-56 21965773-1 2011 Thymidylate synthase (TS) and dihydropyrimidine dehydrogenase (DPD) are 5-fluorouracil (5-FU) metabolizing enzymes and are involved in the sensitivity of carcinoma patients to 5-FU. Fluorouracil 72-86 thymidylate synthetase Homo sapiens 0-20 21965773-1 2011 Thymidylate synthase (TS) and dihydropyrimidine dehydrogenase (DPD) are 5-fluorouracil (5-FU) metabolizing enzymes and are involved in the sensitivity of carcinoma patients to 5-FU. Fluorouracil 88-92 thymidylate synthetase Homo sapiens 0-20 21965773-1 2011 Thymidylate synthase (TS) and dihydropyrimidine dehydrogenase (DPD) are 5-fluorouracil (5-FU) metabolizing enzymes and are involved in the sensitivity of carcinoma patients to 5-FU. Fluorouracil 176-180 thymidylate synthetase Homo sapiens 0-20 21229356-1 2011 PURPOSE: The aim of this study was to evaluate the feasibility and toxicity of concurrent chemoradiotherapy (CCRT) with docetaxel, cisplatin (CDDP) and 5-fluorouracil (5-FU) (TPF regimen) or with CDDP, 5-FU, methotrexate and leucovorin (PFML regimen) in previously untreated patients with advanced oropharyngeal squamous cell carcinoma (SCC). Fluorouracil 152-166 serpin family B member 3 Homo sapiens 337-340 21868535-9 2011 CONCLUSION: We demonstrate for the first time an important inhibitory effect of etodolac on TS expression leading to sensitization to 5-FU in 5-FU-resistant cells. Fluorouracil 134-138 thymidylate synthetase Homo sapiens 92-94 21868535-9 2011 CONCLUSION: We demonstrate for the first time an important inhibitory effect of etodolac on TS expression leading to sensitization to 5-FU in 5-FU-resistant cells. Fluorouracil 142-146 thymidylate synthetase Homo sapiens 92-94 21868535-10 2011 Our data suggest that TS inhibition can be accomplished by this routinely used nonsteroidal anti-inflammatory drug, and this may have a role as novel effective cancer treatment for 5-FU-resistant cancer. Fluorouracil 181-185 thymidylate synthetase Homo sapiens 22-24 21674128-4 2011 High-dose 5-FU treatment led to activation of ATM/CHEK2/TP53 (not CHEK1) in TP53-proficient and TP53-depleted HCT116 (later CHEK2 activation relative to TP53-proficient) cultures; HCT15 cultures had ATM activation only. Fluorouracil 10-14 ATM serine/threonine kinase Homo sapiens 46-49 21674128-4 2011 High-dose 5-FU treatment led to activation of ATM/CHEK2/TP53 (not CHEK1) in TP53-proficient and TP53-depleted HCT116 (later CHEK2 activation relative to TP53-proficient) cultures; HCT15 cultures had ATM activation only. Fluorouracil 10-14 ATM serine/threonine kinase Homo sapiens 199-202 21674128-8 2011 Overall, activation of ATM, CHEK1 and/or CHEK2 and phospho-H2AX levels reflected the nature of 5-FU-induced DNA damage and indi-cated when DNA damage was significant (5-FU-dose-dependent). Fluorouracil 95-99 ATM serine/threonine kinase Homo sapiens 23-26 21561529-0 2011 Calpain regulates thymidylate synthase-5-fluoro-dUMP complex levels associated with response to 5-fluorouracil in gastric cancer cells. Fluorouracil 96-110 thymidylate synthetase Homo sapiens 18-38 21561529-1 2011 Thymidylate synthase (TS) plays a major role in the response to 5-fluorouracil (5-FU) by binding directly to the 5-FU metabolite, 5-fluoro-dUMP (FdUMP). Fluorouracil 64-78 thymidylate synthetase Homo sapiens 0-20 21561529-1 2011 Thymidylate synthase (TS) plays a major role in the response to 5-fluorouracil (5-FU) by binding directly to the 5-FU metabolite, 5-fluoro-dUMP (FdUMP). Fluorouracil 80-84 thymidylate synthetase Homo sapiens 0-20 21561529-1 2011 Thymidylate synthase (TS) plays a major role in the response to 5-fluorouracil (5-FU) by binding directly to the 5-FU metabolite, 5-fluoro-dUMP (FdUMP). Fluorouracil 113-117 thymidylate synthetase Homo sapiens 0-20 21741827-1 2011 BACKGROUND: The aim of this study was to investigate whether c-myc amplification in human breast cancer is associated with response to neoadjuvant chemotherapy comprising paclitaxel followed by 5-FU/epirubicin/cyclophosphamide (P-FEC). Fluorouracil 194-198 MYC proto-oncogene, bHLH transcription factor Homo sapiens 61-66 21828290-3 2011 T-DNA insertions in UKL1 and UKL2 reduced transcript expression and increased plant tolerance to toxic analogs 5-fluorouridine and 5-fluorouracil. Fluorouracil 131-145 uridine kinase-like 2 Arabidopsis thaliana 29-33 21444628-9 2011 Enforced expression of constitutive active MKK1/2 vectors rescued the protein levels of phospho-ERK1/2, TS, and TP, and the cell viability that were decreased by cisplatin and 5-FU combination. Fluorouracil 176-180 mitogen-activated protein kinase kinase 1 Homo sapiens 43-49 21737644-10 2011 CONCLUSION: 5-FU exerts an additional effect on apoptosis of NK4-expressing CT26 cells by down-regulating intracellular signaling of the HGF/c-Met pathway. Fluorouracil 12-16 met proto-oncogene Mus musculus 141-146 21677485-11 2011 Moreover, we evaluated immunohistochemical expressions of thymidylate synthase (TS), dihydropyrimidine dehydrogenase(DPD), and orotate phosphoribosyl transferase(OPRT)which are associated with chemosensitivity to 5-FU-based therapies. Fluorouracil 213-217 uridine monophosphate synthetase Homo sapiens 162-166 21455575-3 2011 We assessed the expression changes of certain growth factor receptors and regulating proteins when treated with 5-FU, and found that 5-FU increased the expression of the IGF-binding protein 3 (IGFBP3). Fluorouracil 112-116 insulin like growth factor binding protein 3 Homo sapiens 170-191 21455575-3 2011 We assessed the expression changes of certain growth factor receptors and regulating proteins when treated with 5-FU, and found that 5-FU increased the expression of the IGF-binding protein 3 (IGFBP3). Fluorouracil 112-116 insulin like growth factor binding protein 3 Homo sapiens 193-199 21455575-3 2011 We assessed the expression changes of certain growth factor receptors and regulating proteins when treated with 5-FU, and found that 5-FU increased the expression of the IGF-binding protein 3 (IGFBP3). Fluorouracil 133-137 insulin like growth factor binding protein 3 Homo sapiens 170-191 21455575-3 2011 We assessed the expression changes of certain growth factor receptors and regulating proteins when treated with 5-FU, and found that 5-FU increased the expression of the IGF-binding protein 3 (IGFBP3). Fluorouracil 133-137 insulin like growth factor binding protein 3 Homo sapiens 193-199 21455575-4 2011 Furthermore, 5-FU inhibited the phosphorylation of Akt and p70 S6K, while the knockdown of IGFBP3 reduced the levels of poly (ADP-ribose) polymerase cleaved by 5-FU in PC3 cells. Fluorouracil 13-17 ribosomal protein S6 kinase B1 Homo sapiens 59-66 21455575-4 2011 Furthermore, 5-FU inhibited the phosphorylation of Akt and p70 S6K, while the knockdown of IGFBP3 reduced the levels of poly (ADP-ribose) polymerase cleaved by 5-FU in PC3 cells. Fluorouracil 160-164 insulin like growth factor binding protein 3 Homo sapiens 91-97 21455575-5 2011 Therefore, the up-regulation of IGFBP3 by 5-FU not only inhibits cell growth by reducing the IGF1 signal but also induces apoptosis in PC3 cells. Fluorouracil 42-46 insulin like growth factor binding protein 3 Homo sapiens 32-38 21455575-6 2011 The synergistic effect of bicalutamide and 5-FU on 22Rv1 cells was reduced by IGFBP3 gene silencing using small-interfering RNA. Fluorouracil 43-47 insulin like growth factor binding protein 3 Homo sapiens 78-84 21455575-7 2011 These results suggest that the up-regulation of IGFBP3 induced by 5-FU plays an important role in the potent anti-tumor effect of 5-FU combined with anti-androgens on CRPC. Fluorouracil 66-70 insulin like growth factor binding protein 3 Homo sapiens 48-54 21455575-7 2011 These results suggest that the up-regulation of IGFBP3 induced by 5-FU plays an important role in the potent anti-tumor effect of 5-FU combined with anti-androgens on CRPC. Fluorouracil 130-134 insulin like growth factor binding protein 3 Homo sapiens 48-54 21742238-4 2011 Intratumoral expression of TS mRNA has been shown to be associated with prognosis and with the response to 5-FU therapy in patients with breast, colorectal, head and neck cancer types. Fluorouracil 107-111 thymidylate synthetase Homo sapiens 27-29 21447833-7 2011 Moreover, TIP110(+/-) bone marrow HPCs responded more effectively, and TIP110(TG) HPCs less effectively, than those of wild-type control mice to recovery from the cell-cycle-active drug 5-fluorouracil (5-FU). Fluorouracil 186-200 spliceosome associated factor 3, U4/U6 recycling protein Homo sapiens 10-16 21447833-7 2011 Moreover, TIP110(+/-) bone marrow HPCs responded more effectively, and TIP110(TG) HPCs less effectively, than those of wild-type control mice to recovery from the cell-cycle-active drug 5-fluorouracil (5-FU). Fluorouracil 202-206 spliceosome associated factor 3, U4/U6 recycling protein Homo sapiens 10-16 21464406-1 2011 PURPOSE: PTK787/ZK 222584 (PTK/ZK; vatalanib), an orally active, multitargeted angiogenesis inhibitor, has shown tolerability and promising activity in early-phase studies, which led to a phase III trial in combination with oxaliplatin, fluorouracil, and leucovorin (FOLFOX4). Fluorouracil 237-249 protein tyrosine kinase 2 beta Homo sapiens 27-33 21544729-7 2011 Immunofluorescence assay and Western blot showed that 5-FU induced the expression of EBV-lytic genes including BZLF1, BRLF1, BMRF1 and BHRF1. Fluorouracil 54-58 protein Zta Human gammaherpesvirus 4 111-116 21243325-0 2011 Hydroxyflutamide enhances cellular sensitivity to 5-fluorouracil by suppressing thymidylate synthase expression in bicalutamide-resistant human prostate cancer cells. Fluorouracil 50-64 thymidylate synthetase Homo sapiens 80-100 21133646-0 2011 Clinicopathologic significance of ERCC1, thymidylate synthase and glutathione S-transferase P1 expression for advanced gastric cancer patients receiving adjuvant 5-FU and cisplatin chemotherapy. Fluorouracil 162-166 glutathione S-transferase pi 1 Homo sapiens 66-94 21210725-6 2011 mRNA levels of TS and OPRT correlated significantly with the chemosensitivity of 5-FU. Fluorouracil 81-85 uridine monophosphate synthetase Homo sapiens 22-26 20714440-3 2010 In this study, CD34(+)CD38(-)stem-like cell subsets in human KG-1a leukemic cell line were enriched by cytotoxic agent 5-fluorouracil (5-FU). Fluorouracil 119-133 CD38 molecule Homo sapiens 22-26 20714440-3 2010 In this study, CD34(+)CD38(-)stem-like cell subsets in human KG-1a leukemic cell line were enriched by cytotoxic agent 5-fluorouracil (5-FU). Fluorouracil 135-139 CD38 molecule Homo sapiens 22-26 20714440-4 2010 After 4 days incubation of KG-1a cell line with 5-FU (50 microg/ml), the CD34(+)CD38(-) subpopulation of cell lines was enriched more than 10 times. Fluorouracil 48-52 CD38 molecule Homo sapiens 80-84 20735209-6 2010 CONCLUSIONS: As telomerase is reactivated in a broad spectrum of tumors and prodrug 5-FC is much safe than its metabolized 5-fluorouracil, a chemotherapeutic agent in the treatment of many malignancies, Ad.hTERT-E1A/CMV-CD in combination with 5-FC may be a potential strategy for the treatment of a wide range of solid tumors. Fluorouracil 123-137 telomerase reverse transcriptase Homo sapiens 206-211 20647341-2 2010 TYMS expression levels have been identified as predictive biomarkers for 5-fluoruracil (FU) response in colorectal cancer, but their clinical utility remains controversial. Fluorouracil 73-86 thymidylate synthetase Homo sapiens 0-4 20689797-1 2010 OBJECTIVE: To evaluate the efficacy and risks of complications of pulse dosing of topical 5-fluorouracil (5-FU) in the treatment of corneal intraepithelial neoplasia (CIN), and conjunctival squamous cell carcinoma (SCC). Fluorouracil 90-104 serpin family B member 3 Homo sapiens 215-218 20689797-12 2010 CONCLUSIONS: Adjuvant 1% topical 5-FU appears to be effective in the prevention of recurrence of conjunctival or corneal CIN and SCC after excision biopsy. Fluorouracil 33-37 serpin family B member 3 Homo sapiens 129-132 20706620-15 2010 TYMS has been reported as being associated with resistance to the anti-cancer drug 5-fluorouracil, and we observed a copy number increase for this gene. Fluorouracil 83-97 thymidylate synthetase Homo sapiens 0-4 20162308-11 2010 Down regulation of CYP2C9 and CYP2C19 synthesis by 5FU therapies may explain the adverse effect of 5FU on the clinical disposition of warfarin and phenytoin. Fluorouracil 51-54 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 19-25 20562578-8 2010 SMAD4/DPC4 transfection restored PSN1 resistance to the effects of combined 5-FU and alpha-TOS effects. Fluorouracil 76-80 SMAD family member 4 Mus musculus 0-5 20562578-8 2010 SMAD4/DPC4 transfection restored PSN1 resistance to the effects of combined 5-FU and alpha-TOS effects. Fluorouracil 76-80 SMAD family member 4 Mus musculus 6-10 20368736-4 2010 We found that BNIP3 protein levels are upregulated in a MLH1 (MMR(+))-dependent manner following 6-TG and 5-FU treatment. Fluorouracil 106-110 mutL homolog 1 Homo sapiens 56-60 20463601-7 2010 MC38 cells pretreated with 5-FU exhibited enhanced expression of procaspase 8 and efficiently underwent apoptosis by TNF-alpha with activation of caspase 8. Fluorouracil 27-31 caspase 8 Mus musculus 68-77 19415536-0 2010 Overexpression of FADD enhances 5-fluorouracil-induced apoptosis in colorectal adenocarcinoma cells. Fluorouracil 32-46 Fas associated via death domain Homo sapiens 18-22 19415536-1 2010 To investigate the mechanism of enhancing apoptosis-inducing effects of 5-fluorouracil on human colorectal adenocarcinoma cells by stable transfection of extrinsic Fas-associated death domain protein (FADD) gene, both in vitro and in vivo. Fluorouracil 72-86 Fas associated via death domain Homo sapiens 164-199 19415536-1 2010 To investigate the mechanism of enhancing apoptosis-inducing effects of 5-fluorouracil on human colorectal adenocarcinoma cells by stable transfection of extrinsic Fas-associated death domain protein (FADD) gene, both in vitro and in vivo. Fluorouracil 72-86 Fas associated via death domain Homo sapiens 201-205 19415536-7 2010 Chemosensitivity and apoptosis rates of SW480/FADD cells were remarkably higher than SW480 and SW480/neo cells when treated with 5-fluorouracil. Fluorouracil 129-143 Fas associated via death domain Homo sapiens 46-50 19415536-8 2010 In in vivo study, overexpression of FADD increased the efficacy of 5-fluorouracil-induced inhibition of tumor growth in nude mice. Fluorouracil 67-81 Fas (TNFRSF6)-associated via death domain Mus musculus 36-40 19415536-9 2010 Stable overexpression of extrinsic FADD gene can conspicuously ameliorate apoptosis-inducing effects of 5-fluorouracil on colorectal adenocarcinoma cells, which is a novel strategy to improve chemotherapeutic effects on colorectal cancer. Fluorouracil 104-118 Fas associated via death domain Homo sapiens 35-39 20202824-4 2010 RESULTS: While both cleaved and total CK-18 levels were intrinsically elevated in tumour patients, they were further increased during 5-fluorouracil (5-FU)-based therapy. Fluorouracil 150-154 keratin 18 Homo sapiens 38-43 19697054-1 2010 Thymidylate synthase (TS) is a major target of 5-fluorouracil (5-FU) and dihydropyrimidine dehydrogenase (DPD) is a rate-limiting enzyme in the degradation of 5-FU. Fluorouracil 47-61 thymidylate synthetase Homo sapiens 0-20 19697054-1 2010 Thymidylate synthase (TS) is a major target of 5-fluorouracil (5-FU) and dihydropyrimidine dehydrogenase (DPD) is a rate-limiting enzyme in the degradation of 5-FU. Fluorouracil 47-61 thymidylate synthetase Homo sapiens 22-24 19697054-1 2010 Thymidylate synthase (TS) is a major target of 5-fluorouracil (5-FU) and dihydropyrimidine dehydrogenase (DPD) is a rate-limiting enzyme in the degradation of 5-FU. Fluorouracil 63-67 thymidylate synthetase Homo sapiens 0-20 19697054-1 2010 Thymidylate synthase (TS) is a major target of 5-fluorouracil (5-FU) and dihydropyrimidine dehydrogenase (DPD) is a rate-limiting enzyme in the degradation of 5-FU. Fluorouracil 63-67 thymidylate synthetase Homo sapiens 22-24 19697054-1 2010 Thymidylate synthase (TS) is a major target of 5-fluorouracil (5-FU) and dihydropyrimidine dehydrogenase (DPD) is a rate-limiting enzyme in the degradation of 5-FU. Fluorouracil 159-163 thymidylate synthetase Homo sapiens 0-20 19697054-1 2010 Thymidylate synthase (TS) is a major target of 5-fluorouracil (5-FU) and dihydropyrimidine dehydrogenase (DPD) is a rate-limiting enzyme in the degradation of 5-FU. Fluorouracil 159-163 thymidylate synthetase Homo sapiens 22-24 19697054-3 2010 In addition, increased interest has been focused on the biological roles of TS and DPD as the independent prognostic factors as well as responsive determinants for cancer patients with 5-FU based therapy. Fluorouracil 185-189 thymidylate synthetase Homo sapiens 76-78 20332484-7 2010 Patients with the highest level of TS expression (grade 3) had an improved clinical outcome following adjuvant 5-FU-based chemotherapy. Fluorouracil 111-115 thymidylate synthetase Homo sapiens 35-37 19616374-5 2010 In cancer cells, a subtoxic concentration of 5-fluorouracil also enhanced resveratrol-evoked caspase-6 activation. Fluorouracil 45-59 caspase 6 Homo sapiens 93-102 19652968-0 2010 Dynamic monitoring the TCR CDR3 spectratypes in patients with metastatic CRC treated with a combination of bevacizumab, irinotecan, fluorouracil, and leucovorin. Fluorouracil 132-144 T cell receptor beta variable 20/OR9-2 (non-functional) Homo sapiens 23-26 19845688-5 2010 After treatment with 5-FU, the normally proliferating tracheal epithelium desquamated and only a few cells in G0 phase of the cell cycle were left on the basement membrane and Oct3/4, Nanog and Sox2 could be observed at this time. Fluorouracil 21-25 solute carrier family 22 member 8 Rattus norvegicus 176-182 19845688-5 2010 After treatment with 5-FU, the normally proliferating tracheal epithelium desquamated and only a few cells in G0 phase of the cell cycle were left on the basement membrane and Oct3/4, Nanog and Sox2 could be observed at this time. Fluorouracil 21-25 SRY-box transcription factor 2 Rattus norvegicus 194-198 19845688-8 2010 CONCLUSIONS: G0 phase cells with resistance to 5-FU damage expressed Oct3/4, Nanog and Sox2. Fluorouracil 47-51 solute carrier family 22 member 8 Rattus norvegicus 69-75 19845688-8 2010 CONCLUSIONS: G0 phase cells with resistance to 5-FU damage expressed Oct3/4, Nanog and Sox2. Fluorouracil 47-51 SRY-box transcription factor 2 Rattus norvegicus 87-91 20966539-2 2010 With this study, we aimed to elucidate the role of TS gene polymorphisms genotyping in therapy response in stage III colon carcinoma patients treated with 5-FU adjuvant chemotherapy. Fluorouracil 155-159 thymidylate synthetase Homo sapiens 51-53 20714149-2 2010 Toxicity from fluorouracil therapy is known to be associated with the individual genetic background of the enzymes, thymidylate synthase and dihydropyrimidine dehydrogenase. Fluorouracil 14-26 thymidylate synthetase Homo sapiens 116-136 20714149-4 2010 To evaluate the genetic background of the fluorouracil-associated hyperammonemic encephalopathy, analysis of the polymorphisms of the TYMS, DPYD and MTHFR genes was performed. Fluorouracil 42-54 thymidylate synthetase Homo sapiens 134-138 20714149-6 2010 CONCLUSION: Genetic polymorphisms of the TYMS gene would contribute to the 5-fluorouracil-associated hyperammonemic encephalopathy. Fluorouracil 75-89 thymidylate synthetase Homo sapiens 41-45 20205661-5 2010 Increased 5FU toxicity is associated with variations in the DPYD gene, TYMS gene and MTHFR gene. Fluorouracil 10-13 thymidylate synthetase Homo sapiens 71-75 19948396-7 2010 And indeed, different miRNAs have been found to predict sensitivity to anticancer treatment: miR-30c, miR-130a and miR-335 are downregulated in various chemoresistant cell lines, hsa-Let-7g and hsa-miR-181b are strongly associated with response to 5-fluorouracil-based antimetabolite S-1. Fluorouracil 248-262 microRNA let-7g Homo sapiens 179-189 20014456-8 2009 Apoptosis resistance towards TRAIL could be considerably reduced by adding the chemotherapeutic drugs 5-fluorouracil and doxorubicin as well as the kinase inhibitors LY294002 [inhibition of phosphoinositol-3-kinase (PI3K)], AG1478 (epidermal growth factor receptor kinase), PD98059 (MEK1), rapamycin (mammalian target of rapamycin) and the multi-kinase inhibitor Sorafenib. Fluorouracil 102-116 mitogen-activated protein kinase kinase 1 Homo sapiens 283-287 19622348-7 2009 For instance, 5-FU significantly suppressed ATP7B and human organic cation transporter 2 and increased multidrug resistance-associated protein (MRP) 2 mRNA expression (5.8-fold). Fluorouracil 14-18 solute carrier family 22 member 2 Homo sapiens 60-88 19722231-9 2009 CONCLUSION: TS genotyping on paraffin-embedded fixed tissues proved to be the most useful method for prediction of outcome of 5-FU treatment in patients with colorectal adenocarcinoma. Fluorouracil 126-130 thymidylate synthetase Homo sapiens 12-14 19885579-8 2009 The E-selectin mRNA level increased in cells exposed to 5-FU, DXR, or CDDP, but the addition of cimetidine had no effect on the E-selectin mRNA level. Fluorouracil 56-60 selectin E Homo sapiens 4-14 19885579-9 2009 The expression of E-selectin protein was also significantly higher after the addition of 5-FU, DXR, or CDDP, compared with that of a negative control. Fluorouracil 89-93 selectin E Homo sapiens 18-28 19885579-10 2009 However, when cimetidine was added prior to the addition of 5-FU, DXR, or CDDP, the expression of E-selectin was significantly suppressed. Fluorouracil 60-64 selectin E Homo sapiens 98-108 19734943-2 2009 Tumor cells ectopically transfected with miR-140 were more resistant to methotrexate and 5-fluorouracil (5-FU). Fluorouracil 89-103 microRNA 140 Homo sapiens 41-48 19734943-2 2009 Tumor cells ectopically transfected with miR-140 were more resistant to methotrexate and 5-fluorouracil (5-FU). Fluorouracil 105-109 microRNA 140 Homo sapiens 41-48 19734943-7 2009 Blocking endogenous miR-140 by locked nucleic acid-modified anti-miR partially sensitized resistant colon cancer stem-like cells to 5-FU treatment. Fluorouracil 132-136 microRNA 140 Homo sapiens 20-27 19306093-2 2009 TYMS is a key target of the 5-fluorouracil (5-FU)-based class of drugs, frequently considered in combination therapies in advanced RCC. Fluorouracil 28-42 thymidylate synthetase Homo sapiens 0-4 19306093-2 2009 TYMS is a key target of the 5-fluorouracil (5-FU)-based class of drugs, frequently considered in combination therapies in advanced RCC. Fluorouracil 44-48 thymidylate synthetase Homo sapiens 0-4 19306093-3 2009 TYMS variants, such as the TYMS polymorphic 5"-untranslated region variable number tandem repeat sequence (VNTR), are under investigation to guide 5-FU treatment. Fluorouracil 147-151 thymidylate synthetase Homo sapiens 0-4 19306093-3 2009 TYMS variants, such as the TYMS polymorphic 5"-untranslated region variable number tandem repeat sequence (VNTR), are under investigation to guide 5-FU treatment. Fluorouracil 147-151 thymidylate synthetase Homo sapiens 27-31 19901540-0 2009 Inhibition of Hsp27 and Hsp40 potentiates 5-fluorouracil and carboplatin mediated cell killing in hepatoma cells. Fluorouracil 42-56 heat shock protein family B (small) member 1 Homo sapiens 14-19 19901540-4 2009 We for the first time report that 5-fluorouracil (5-FU) and carboplatin specifically induce expression of Hsp40 in addition to Hsp27 in Hep3B and HepG2 cells. Fluorouracil 34-48 heat shock protein family B (small) member 1 Homo sapiens 127-132 19901540-4 2009 We for the first time report that 5-fluorouracil (5-FU) and carboplatin specifically induce expression of Hsp40 in addition to Hsp27 in Hep3B and HepG2 cells. Fluorouracil 50-54 heat shock protein family B (small) member 1 Homo sapiens 127-132 19749785-10 2009 Silencing of dbpA also suppressed cell invasion and colony formation of SGC7901 cells, and enhanced their chemosensitivity to 5-fluorouracil. Fluorouracil 126-140 Y-box binding protein 3 Homo sapiens 13-17 19749785-12 2009 Silencing of dbpA might be a novel therapeutic strategy for increasing chemosensitivity to 5-fluorouracil in gastric cancer. Fluorouracil 91-105 Y-box binding protein 3 Homo sapiens 13-17 19846930-2 2009 MATERIALS AND METHODS: We explored 2.5 microM 5-FU-induced DNA synthesis by testing 5-FU activity in hypoxanthine-aminopterin-thymidine (HAT)-containing medium, and its effect on thymidylate synthase (TS) activity and CD25 expression in interleukin (IL)-2-activated human peripheral blood mononuclear cells (PBMCs) and the combined effects with prostaglandin E(2) (PGE(2)) and transforming growth factor (TGF)-beta3. Fluorouracil 46-50 thymidylate synthetase Homo sapiens 179-199 19822515-0 2009 Toxicity and efficacy of 5-fluorouracil and capecitabine in a patient with TYMS gene polymorphism: A challenge or a dilemma? Fluorouracil 25-39 thymidylate synthetase Homo sapiens 75-79 19822515-12 2009 Pharmacogenetic testing revealed 2R/2R genotype of TYMS gene, which is associated with up to a 2.5-fold risk of toxicity to 5-FU therapy. Fluorouracil 124-128 thymidylate synthetase Homo sapiens 51-55 19822515-15 2009 Genetic variations such as polymorphic abnormality of TYMS are potential causative factors for a significant portion of serious adverse reactions to 5-FU-based therapy. Fluorouracil 149-153 thymidylate synthetase Homo sapiens 54-58 19638344-6 2009 GAS1 suppression resulted in significant epirubicin resistance and cross-resistance to 5-fluorouracil and cisplatin in various gastric cancer cell lines. Fluorouracil 87-101 growth arrest specific 1 Homo sapiens 0-4 19638344-11 2009 BCRP down-regulation could partially reverse 5-fluorouracil but not cisplatin resistance induced by GAS1 suppression, suggesting 5-fluorouracil but not cisplatin was a BCRP substrate. Fluorouracil 129-143 growth arrest specific 1 Homo sapiens 100-104 19598290-3 2009 The in-vitro stability trial showed 5-FU-cholic acid conjugates could be completely hydrolyzed by heating at 70 degrees C in an acidic solution, pH = 1, for 5 min. Fluorouracil 36-40 formamidase 5 Mus musculus 153-158 19698189-12 2009 Resistance to 5-FU was also significantly associated with basal pERK expression in these HCC cell lines (Spearman r = 0.7832, P = 0.0026). Fluorouracil 14-18 eukaryotic translation initiation factor 2 alpha kinase 3 Homo sapiens 64-68 20641233-17 2004 The CDy part of the recombinant fusion protein deaminates 5-fluorocytosine (5-FC), the prodrug, to produce cytotoxic 5-fluorouracil after the A33scFv part binds to the A33 antigen on the cell surface. Fluorouracil 117-131 glycoprotein A33 Homo sapiens 142-145 19661313-1 2009 BACKGROUND: We have reported that resveratrol (RSV) and 5-fluorouracil (5-FU) evoked apoptosis through caspase-6 activation in wild-type (p53+/+) and knockout (p53(-/-)) HCT116 human colon cancer cells. Fluorouracil 56-70 caspase 6 Homo sapiens 103-112 19661313-1 2009 BACKGROUND: We have reported that resveratrol (RSV) and 5-fluorouracil (5-FU) evoked apoptosis through caspase-6 activation in wild-type (p53+/+) and knockout (p53(-/-)) HCT116 human colon cancer cells. Fluorouracil 72-76 caspase 6 Homo sapiens 103-112 19661313-5 2009 RSV- and 5-FU-elicited caspase-6 activation was promoted by SC in a time-dependent manner. Fluorouracil 9-13 caspase 6 Homo sapiens 23-32 19661313-7 2009 CONCLUSION: SC is a novel sensitizing agent for both RSV- and 5-FU-evoked apoptosis, through the enhancement of caspase-6 activation in a p53-dependent manner. Fluorouracil 62-66 caspase 6 Homo sapiens 112-121 19486256-5 2009 We then used hMSC in which a gene expressed the prodrug-activating enzyme CD, which can convert the prodrug 5-FC into the cytotoxic agent 5-fluorouracil (5-FU), and further investigated the potential of these cells to deliver the CD gene and to reduce tumor growth in nude mice. Fluorouracil 138-152 musculin Homo sapiens 13-17 19486256-5 2009 We then used hMSC in which a gene expressed the prodrug-activating enzyme CD, which can convert the prodrug 5-FC into the cytotoxic agent 5-fluorouracil (5-FU), and further investigated the potential of these cells to deliver the CD gene and to reduce tumor growth in nude mice. Fluorouracil 154-158 musculin Homo sapiens 13-17 19486256-8 2009 Effective conversion of 5-FC to 5-FU by hMSC transfected with the CD gene (CD-hMSC) showed therapeutic anticancer potential in a MKN45 cell co-culture system, as confirmed by thin layer chromatography. Fluorouracil 32-36 musculin Homo sapiens 40-44 19486256-8 2009 Effective conversion of 5-FC to 5-FU by hMSC transfected with the CD gene (CD-hMSC) showed therapeutic anticancer potential in a MKN45 cell co-culture system, as confirmed by thin layer chromatography. Fluorouracil 32-36 musculin Homo sapiens 78-82 19486256-12 2009 CONCLUSION: The CD-hMSC system showed anticancer therapeutic potential, and minimized the side-effects of 5-FU. Fluorouracil 106-110 musculin Homo sapiens 19-23 19628084-4 2009 We hypothesized that DPD has a circadian expression pattern, accounting for the reduced GI side effects of chrono-modulated 5FU therapy. Fluorouracil 124-127 dihydropyrimidine dehydrogenase Rattus norvegicus 21-24 19384949-2 2009 Previous studies have demonstrated that overexpression of thymidylate synthase (TS) is a key determinant of resistance to 5-FU-based chemotherapy. Fluorouracil 122-126 thymidylate synthetase Homo sapiens 58-78 19384949-2 2009 Previous studies have demonstrated that overexpression of thymidylate synthase (TS) is a key determinant of resistance to 5-FU-based chemotherapy. Fluorouracil 122-126 thymidylate synthetase Homo sapiens 80-82 19384949-9 2009 These data demonstrate that HDACi repress TS expression at the level of transcription and provides the first evidence suggesting a direct mechanistic link between TS downregulation and the synergistic interaction observed between HDACi and 5-FU. Fluorouracil 240-244 thymidylate synthetase Homo sapiens 42-44 19384949-10 2009 This study provides rationale for the continued clinical evaluation of HDACi in combination with 5-FU-based therapies as a strategy to overcome TS-mediated resistance. Fluorouracil 97-101 thymidylate synthetase Homo sapiens 144-146 19528468-9 2009 CONCLUSION: The sequence dependency between SN-38 and 5-FU against colon cancer cells may be related to the dual action on cell cycle regulation by 5-FU and to the down-regulation of TS level by SN-38. Fluorouracil 54-58 thymidylate synthetase Homo sapiens 183-185 19528421-7 2009 RESULTS: One day after the final fluorouracil treatment, gene expression of the effectors of epidermal injury (keratin 16), inflammation (interleukin 1beta), and extracellular matrix degradation (matrix metalloproteinases 1 and 3) was significantly increased. Fluorouracil 33-45 matrix metallopeptidase 1 Homo sapiens 162-229 19582719-9 2009 In particular, the level of PK-M2, a key enzyme in the glycolytic pathway, showed an increasing tendency in both sera and tissues from CRC patients displaying no response to 5-FU-based chemotherapy (progressive and stable disease cases), compared with that in complete or partial responders to 5-FU-based chemotherapy; however, it did not reach the statistical significance. Fluorouracil 174-178 pyruvate kinase M1/2 Homo sapiens 28-33 19582719-9 2009 In particular, the level of PK-M2, a key enzyme in the glycolytic pathway, showed an increasing tendency in both sera and tissues from CRC patients displaying no response to 5-FU-based chemotherapy (progressive and stable disease cases), compared with that in complete or partial responders to 5-FU-based chemotherapy; however, it did not reach the statistical significance. Fluorouracil 294-298 pyruvate kinase M1/2 Homo sapiens 28-33 19582719-10 2009 In conclusion, increasing pattern of PK-M2 observed with 5-FU resistance induced in vitro and in sera and tissues from CRC patients displaying poor response to 5-FU-based chemotherapy suggest the relevance of dysregulated glycolysis and 5-FU-resistant CRC. Fluorouracil 57-61 pyruvate kinase M1/2 Homo sapiens 37-42 19582719-10 2009 In conclusion, increasing pattern of PK-M2 observed with 5-FU resistance induced in vitro and in sera and tissues from CRC patients displaying poor response to 5-FU-based chemotherapy suggest the relevance of dysregulated glycolysis and 5-FU-resistant CRC. Fluorouracil 160-164 pyruvate kinase M1/2 Homo sapiens 37-42 19582719-10 2009 In conclusion, increasing pattern of PK-M2 observed with 5-FU resistance induced in vitro and in sera and tissues from CRC patients displaying poor response to 5-FU-based chemotherapy suggest the relevance of dysregulated glycolysis and 5-FU-resistant CRC. Fluorouracil 160-164 pyruvate kinase M1/2 Homo sapiens 37-42 19147506-1 2009 5-Fluorouracil (5-FU) represents the basis of chemotherapy for colorectal carcinoma, inhibiting thymidylate synthase (TS), an essential enzyme for DNA replication. Fluorouracil 0-14 thymidylate synthetase Homo sapiens 96-116 19147506-1 2009 5-Fluorouracil (5-FU) represents the basis of chemotherapy for colorectal carcinoma, inhibiting thymidylate synthase (TS), an essential enzyme for DNA replication. Fluorouracil 0-14 thymidylate synthetase Homo sapiens 118-120 19147506-1 2009 5-Fluorouracil (5-FU) represents the basis of chemotherapy for colorectal carcinoma, inhibiting thymidylate synthase (TS), an essential enzyme for DNA replication. Fluorouracil 16-20 thymidylate synthetase Homo sapiens 96-116 19147506-1 2009 5-Fluorouracil (5-FU) represents the basis of chemotherapy for colorectal carcinoma, inhibiting thymidylate synthase (TS), an essential enzyme for DNA replication. Fluorouracil 16-20 thymidylate synthetase Homo sapiens 118-120 19147506-7 2009 This result possibly reflects a complex tumor response to 5-FU therapy, where TS is just one of the involved proteins. Fluorouracil 58-62 thymidylate synthetase Homo sapiens 78-80 19444465-2 2009 Thymidylate synthase (TS) is a major target of 5-fluorouracil-based chemotherapy for CRC and high expression of this enzyme in tumor cells can influence the effect of therapy. Fluorouracil 47-61 thymidylate synthetase Homo sapiens 0-20 19444465-2 2009 Thymidylate synthase (TS) is a major target of 5-fluorouracil-based chemotherapy for CRC and high expression of this enzyme in tumor cells can influence the effect of therapy. Fluorouracil 47-61 thymidylate synthetase Homo sapiens 22-24 19401692-0 2009 Activation of Wnt/beta-catenin signalling pathway induces chemoresistance to interferon-alpha/5-fluorouracil combination therapy for hepatocellular carcinoma. Fluorouracil 94-108 catenin beta 1 Homo sapiens 18-30 19401692-10 2009 The results indicate that activation of Wnt/beta-catenin signalling pathway induces chemoresistance to IFN-alpha/5-FU therapy and suggest that Ep-CAM is a potentially useful marker for resistance to such therapy, especially in IFNAR2-positive cases. Fluorouracil 113-117 catenin beta 1 Homo sapiens 44-56 19426394-0 2009 Polymorphism of thymidylate synthase gene and chemosensitivity of 5-fluorouracil regimen in metastatic gastrointestinal cancer. Fluorouracil 66-80 thymidylate synthetase Homo sapiens 16-36 19426394-1 2009 OBJECTIVE: To explore the polymorphism of thymidylate synthase (TS) gene and chemosensitivity of a 5-fluorouracil (5-FU)-containing regimen in metastatic colorectal and gastric cancer. Fluorouracil 99-113 thymidylate synthetase Homo sapiens 42-62 19426394-1 2009 OBJECTIVE: To explore the polymorphism of thymidylate synthase (TS) gene and chemosensitivity of a 5-fluorouracil (5-FU)-containing regimen in metastatic colorectal and gastric cancer. Fluorouracil 99-113 thymidylate synthetase Homo sapiens 64-66 19426394-1 2009 OBJECTIVE: To explore the polymorphism of thymidylate synthase (TS) gene and chemosensitivity of a 5-fluorouracil (5-FU)-containing regimen in metastatic colorectal and gastric cancer. Fluorouracil 115-119 thymidylate synthetase Homo sapiens 42-62 19426394-1 2009 OBJECTIVE: To explore the polymorphism of thymidylate synthase (TS) gene and chemosensitivity of a 5-fluorouracil (5-FU)-containing regimen in metastatic colorectal and gastric cancer. Fluorouracil 115-119 thymidylate synthetase Homo sapiens 64-66 19426394-12 2009 Patients with a TS polymorphism expressed as 2R/3R might be more sensitive to 5-FU regimen than those with a polymorphism expressed as 3R/3R. Fluorouracil 78-82 thymidylate synthetase Homo sapiens 16-18 19383851-4 2009 Although conflicting results have been reported, higher thymidylate synthase (TS) protein and mRNA expression levels in tumors have generally been associated with poor clinical outcome in patients treated with 5-FU-based chemotherapy regimens. Fluorouracil 210-214 thymidylate synthetase Homo sapiens 56-76 19383851-4 2009 Although conflicting results have been reported, higher thymidylate synthase (TS) protein and mRNA expression levels in tumors have generally been associated with poor clinical outcome in patients treated with 5-FU-based chemotherapy regimens. Fluorouracil 210-214 thymidylate synthetase Homo sapiens 78-80 19383851-5 2009 However, the cause of the variability in TS expression still remains not fully understood, although several germ-line polymorphisms seem to affect the expression of TS, some of which have been found to have an effect on prognosis and the probability of response to 5-FU-based chemotherapy. Fluorouracil 265-269 thymidylate synthetase Homo sapiens 165-167 21475840-6 2009 This resulted in the formation of much higher levels of the ternary complex with thymidylate synthase (TS) and 5-fluoro-2"-deoxyuridine 5"-monophosphate (FdUMP) derived from 5-FU, leading to a prolonged inhibition of TS activity in combined administration with oral S-1. Fluorouracil 174-178 thymidylate synthetase Homo sapiens 81-101 19097686-7 2009 Additionally, chemo-sensitivity to 5-fluorouracil of KB/V was increased by CD147 silencing as measured by MTT colorimetric assay. Fluorouracil 35-49 basigin (Ok blood group) Homo sapiens 75-80 19097688-8 2009 Surprisingly, the addition of ANDRO to 5-FU induces synergistic apoptosis, which could be corroborated to the increased caspase-8, p53 activity and the significant changes of Bax conformation in these cells, resulting in increased losses of mitochondrial membrane potential, increased release of cytochrome c, and activation of caspase-9 and caspase-3. Fluorouracil 39-43 caspase 9 Homo sapiens 328-337 19414338-5 2009 RESULTS: A significant positive correlation between OPRT activity level and the sensitivity of BUC to 5-FU was identified. Fluorouracil 102-106 uridine monophosphate synthetase Homo sapiens 52-56 19414338-7 2009 CONCLUSION: OPRT was the most important enzyme in predicting sensitivity to 5-FU in BUC. Fluorouracil 76-80 uridine monophosphate synthetase Homo sapiens 12-16 19372549-6 2009 PK-M2 mRNA levels were measured by real-time quantitative PCR in 41 tumors treated with oxaliplatin/5-fluorouracil. Fluorouracil 100-114 pyruvate kinase M1/2 Homo sapiens 0-5 19051292-10 2009 Gene panels assessing pretreatment TP, DPD, ERCC1, dihydrofolate reductase and thymidylate synthase gene expression may help improve the therapeutic potential of 5-FU- or other novel antifolate-based regimens. Fluorouracil 162-166 dihydrofolate reductase Homo sapiens 51-74 19051292-10 2009 Gene panels assessing pretreatment TP, DPD, ERCC1, dihydrofolate reductase and thymidylate synthase gene expression may help improve the therapeutic potential of 5-FU- or other novel antifolate-based regimens. Fluorouracil 162-166 thymidylate synthetase Homo sapiens 79-99 19544707-5 2009 Patients who needed NAC underwent a preoperative regimen consisting of cisplatin and fluouracil. Fluorouracil 85-95 synuclein alpha Homo sapiens 20-23 19212626-10 2009 DDP facilitated the induction of expression of DR4 and DR5 significantly in cell line (P<0.05), but 5-FU influenced only the expression of DR5 significantly. Fluorouracil 103-107 TNF receptor superfamily member 10b Homo sapiens 142-145 19261089-6 2009 Regenerating islet-derived family, member 4 (Reg IV) participated in 5-fluorouracil (5-FU) resistance and peritoneal metastasis, and its expression was associated with an intestinal phenotype of gastric cancer and with endocrine differentiation. Fluorouracil 69-83 regenerating family member 4 Homo sapiens 45-51 19261089-6 2009 Regenerating islet-derived family, member 4 (Reg IV) participated in 5-fluorouracil (5-FU) resistance and peritoneal metastasis, and its expression was associated with an intestinal phenotype of gastric cancer and with endocrine differentiation. Fluorouracil 85-89 regenerating family member 4 Homo sapiens 45-51 19293370-9 2009 Mutants expressing the Arabidopsis enzyme or the homolog from rice (Oryza sativa) exhibit resistance toward toxic fluorouridine, fluorouracil, and fluoroorotic acid, providing clear evidence for a pivotal function of URH1 as regulative in pyrimidine degradation. Fluorouracil 129-141 uridine-ribohydrolase 1 Arabidopsis thaliana 217-221 18986760-3 2009 In this study, we determined the expression levels of 5-FU metabolism-related enzymes like thymidylate synthase (TS), dihydropyrimidine dehydrogenase (DPD), thymidine phosphorylate (TP) and orotate phosphoribosyl transferase (OPRT) using reverse transcription-polymerase chain reaction (RT-PCR) combined with laser capture microdissection (LCM). Fluorouracil 54-58 thymidylate synthetase Homo sapiens 91-111 18986760-3 2009 In this study, we determined the expression levels of 5-FU metabolism-related enzymes like thymidylate synthase (TS), dihydropyrimidine dehydrogenase (DPD), thymidine phosphorylate (TP) and orotate phosphoribosyl transferase (OPRT) using reverse transcription-polymerase chain reaction (RT-PCR) combined with laser capture microdissection (LCM). Fluorouracil 54-58 thymidylate synthetase Homo sapiens 113-115 18986760-3 2009 In this study, we determined the expression levels of 5-FU metabolism-related enzymes like thymidylate synthase (TS), dihydropyrimidine dehydrogenase (DPD), thymidine phosphorylate (TP) and orotate phosphoribosyl transferase (OPRT) using reverse transcription-polymerase chain reaction (RT-PCR) combined with laser capture microdissection (LCM). Fluorouracil 54-58 uridine monophosphate synthetase Homo sapiens 190-224 18986760-3 2009 In this study, we determined the expression levels of 5-FU metabolism-related enzymes like thymidylate synthase (TS), dihydropyrimidine dehydrogenase (DPD), thymidine phosphorylate (TP) and orotate phosphoribosyl transferase (OPRT) using reverse transcription-polymerase chain reaction (RT-PCR) combined with laser capture microdissection (LCM). Fluorouracil 54-58 uridine monophosphate synthetase Homo sapiens 226-230 19194123-1 2009 BACKGROUND: The aim of this study was to determine whether the expression of the excision repair cross-complementing 1 (ERCC1), thymidylate synthase (TS) and glutathione S-transferase pi (GSTpi) predict clinical outcome in patients with advanced colorectal cancer treated with fluorouracil (5-FU)/oxaliplatin chemotherapy. Fluorouracil 291-295 ERCC excision repair 1, endonuclease non-catalytic subunit Homo sapiens 81-118 19194123-1 2009 BACKGROUND: The aim of this study was to determine whether the expression of the excision repair cross-complementing 1 (ERCC1), thymidylate synthase (TS) and glutathione S-transferase pi (GSTpi) predict clinical outcome in patients with advanced colorectal cancer treated with fluorouracil (5-FU)/oxaliplatin chemotherapy. Fluorouracil 291-295 ERCC excision repair 1, endonuclease non-catalytic subunit Homo sapiens 120-125 19194123-1 2009 BACKGROUND: The aim of this study was to determine whether the expression of the excision repair cross-complementing 1 (ERCC1), thymidylate synthase (TS) and glutathione S-transferase pi (GSTpi) predict clinical outcome in patients with advanced colorectal cancer treated with fluorouracil (5-FU)/oxaliplatin chemotherapy. Fluorouracil 291-295 thymidylate synthetase Homo sapiens 128-148 19194123-12 2009 CONCLUSION: Immunohistochemical study of ERCC1 and TS may be useful for the prediction of clinical outcome in patients with advanced colorectal cancer treated with 5-FU and oxaliplatin. Fluorouracil 164-168 ERCC excision repair 1, endonuclease non-catalytic subunit Homo sapiens 41-46 19194123-12 2009 CONCLUSION: Immunohistochemical study of ERCC1 and TS may be useful for the prediction of clinical outcome in patients with advanced colorectal cancer treated with 5-FU and oxaliplatin. Fluorouracil 164-168 thymidylate synthetase Homo sapiens 51-53 17504194-3 2007 Since modulation of alpha-tubulin and human leukocyte antigen (HLA) class I expression has been detected during malignant transformation, we analyzed in this study the expression pattern of both kinds of proteins after the treatment with 5-FU derivatives in the human RMS RD cell line. Fluorouracil 238-242 tubulin alpha 1b Homo sapiens 20-33 17290426-8 2007 We modulated checkpoint-related gene expression in testis using the anti-metabolite, 5-fluorouracil, resulting in increased apoptosis and upregulation of Chk1 (P<0.0001) and Cdc2 (P<0.02) mRNA. Fluorouracil 85-99 cyclin dependent kinase 1 Homo sapiens 177-181 17425594-5 2007 Among these regions, 18p11.32 at the location of the thymidylate synthase gene (TYMS) was strongly associated with resistance to 5-FU-based drugs. Fluorouracil 129-133 thymidylate synthetase Homo sapiens 53-73 17425594-5 2007 Among these regions, 18p11.32 at the location of the thymidylate synthase gene (TYMS) was strongly associated with resistance to 5-FU-based drugs. Fluorouracil 129-133 thymidylate synthetase Homo sapiens 80-84 17425594-6 2007 A change in copy number of the TYMS gene was reflected in the TYMS expression level, and showed a significant negative correlation with sensitivity against 5-FU-based drugs. Fluorouracil 156-160 thymidylate synthetase Homo sapiens 31-35 17425594-6 2007 A change in copy number of the TYMS gene was reflected in the TYMS expression level, and showed a significant negative correlation with sensitivity against 5-FU-based drugs. Fluorouracil 156-160 thymidylate synthetase Homo sapiens 62-66 17275316-1 2007 Thymidylate synthase (TS) is a target enzyme for a number of anticancer agents including the 5-fluorouracil metabolite, FdUMP. Fluorouracil 93-107 thymidylate synthetase Homo sapiens 0-20 17322540-1 2007 BACKGROUND: The aim of this study was to determine whether expressions of the excision repair cross-complementing (ERCC1), thymidylate synthase (TS), and glutathione S-transferase P1 (GSTP1) predict clinical outcome in patients with advanced gastric cancer treated with fluorouracil (5-fluorouracil)/oxaliplatin chemotherapy. Fluorouracil 284-298 glutathione S-transferase pi 1 Homo sapiens 184-189 17322540-12 2007 CONCLUSION: Immunohistochemical studies for ERCC1 may be useful in prediction of the clinical outcome in advanced gastric cancer patients treated with 5-FU and oxaliplatin. Fluorouracil 151-155 ERCC excision repair 1, endonuclease non-catalytic subunit Homo sapiens 44-49 17273745-4 2007 In the OXA + 5-FU group, patients with the TS 5" single nucleotide polymorphism and/or XRCC1 genotypes favourable to treatment had a better TTP (log-rank p=0.02). Fluorouracil 13-17 thymidylate synthetase Homo sapiens 43-45 17453364-2 2007 A toxicity-based dosing schedule for individually tailored treatment with granulocyte colony-stimulating factor (G-CSF) supported 5-fluorouracil (F), epirubicin (E) and cyclophosphamide (C) (dFEC) was developed and studied in patients with metastatic breast cancer with the purpose to determine its efficiency and toxicity. Fluorouracil 130-144 colony stimulating factor 3 Homo sapiens 74-111 17453364-2 2007 A toxicity-based dosing schedule for individually tailored treatment with granulocyte colony-stimulating factor (G-CSF) supported 5-fluorouracil (F), epirubicin (E) and cyclophosphamide (C) (dFEC) was developed and studied in patients with metastatic breast cancer with the purpose to determine its efficiency and toxicity. Fluorouracil 130-144 colony stimulating factor 3 Homo sapiens 113-118 17361317-4 2007 Treatment of these preneoplastic Apc mutant cells with a combination of celecoxib and 5-fluorouracil at clinically achievable low concentrations produced a 2.1 fold to 5.5 fold higher efficacy for cytostatic growth arrest and a 40.2% to 52.4% higher efficacy for inhibition of carcinogenic risk, relative to that obtained by these agents used individually. Fluorouracil 86-100 APC, WNT signaling pathway regulator Mus musculus 33-36 17159505-3 2007 Using the SNU-719 gastric cancer cell line, which is naturally infected with Epstein-Barr virus, we found that the chemotherapeutic agents, such as 5-fluorouracil, cis-platinum and taxol, induced the expressions of BMRF1, BZLF1 and BRLF1 proteins that are usually found in the lytic form of the virus. Fluorouracil 148-162 protein Zta Human gammaherpesvirus 4 222-227 17220568-1 2006 Forty genetic variations including 14 novel ones were found in the human TYMS gene, which encodes thymidylate synthase, in 263 Japanese cancer patients who received 5-fluorouracil (FU)-based chemotherapy. Fluorouracil 165-179 thymidylate synthetase Homo sapiens 73-77 17220568-1 2006 Forty genetic variations including 14 novel ones were found in the human TYMS gene, which encodes thymidylate synthase, in 263 Japanese cancer patients who received 5-fluorouracil (FU)-based chemotherapy. Fluorouracil 165-179 thymidylate synthetase Homo sapiens 98-118 17172411-0 2006 Histone deacetylase inhibitor enhances 5-fluorouracil cytotoxicity by down-regulating thymidylate synthase in human cancer cells. Fluorouracil 39-53 thymidylate synthetase Homo sapiens 86-106 17172411-1 2006 Thymidylate synthase (TS) overexpression is a key determinant of 5-fluorouracil (5-FU) resistance in human cancer cells. Fluorouracil 65-79 thymidylate synthetase Homo sapiens 0-20 17172411-1 2006 Thymidylate synthase (TS) overexpression is a key determinant of 5-fluorouracil (5-FU) resistance in human cancer cells. Fluorouracil 65-79 thymidylate synthetase Homo sapiens 22-24 17172411-1 2006 Thymidylate synthase (TS) overexpression is a key determinant of 5-fluorouracil (5-FU) resistance in human cancer cells. Fluorouracil 81-85 thymidylate synthetase Homo sapiens 0-20 17172411-1 2006 Thymidylate synthase (TS) overexpression is a key determinant of 5-fluorouracil (5-FU) resistance in human cancer cells. Fluorouracil 81-85 thymidylate synthetase Homo sapiens 22-24 17172411-2 2006 TS is also acutely up-regulated with 5-FU treatment, and, thus, novel strategies targeting TS down-regulation seem to be promising in terms of modulating 5-FU resistance. Fluorouracil 37-41 thymidylate synthetase Homo sapiens 0-2 17172411-2 2006 TS is also acutely up-regulated with 5-FU treatment, and, thus, novel strategies targeting TS down-regulation seem to be promising in terms of modulating 5-FU resistance. Fluorouracil 154-158 thymidylate synthetase Homo sapiens 0-2 17172411-2 2006 TS is also acutely up-regulated with 5-FU treatment, and, thus, novel strategies targeting TS down-regulation seem to be promising in terms of modulating 5-FU resistance. Fluorouracil 154-158 thymidylate synthetase Homo sapiens 91-93 17172411-3 2006 Here, we report that histone deacetylase inhibitors can reverse 5-FU resistance by down-regulating TS. Fluorouracil 64-68 thymidylate synthetase Homo sapiens 99-101 17172411-8 2006 Of note, combined treatment with low-dose trichostatin A and 5-FU enhanced 5-FU-mediated cytotoxicity in 5-FU-resistant cancer cells in accordance with TS protein down-regulation. Fluorouracil 61-65 thymidylate synthetase Homo sapiens 152-154 17172411-8 2006 Of note, combined treatment with low-dose trichostatin A and 5-FU enhanced 5-FU-mediated cytotoxicity in 5-FU-resistant cancer cells in accordance with TS protein down-regulation. Fluorouracil 75-79 thymidylate synthetase Homo sapiens 152-154 17172411-8 2006 Of note, combined treatment with low-dose trichostatin A and 5-FU enhanced 5-FU-mediated cytotoxicity in 5-FU-resistant cancer cells in accordance with TS protein down-regulation. Fluorouracil 75-79 thymidylate synthetase Homo sapiens 152-154 17089033-1 2006 Orotate phosphoribosyltransferase (OPRT) is an enzyme that causes the activation of 5-fluorouracil (5-FU). Fluorouracil 84-98 uridine monophosphate synthetase Homo sapiens 0-33 17089033-1 2006 Orotate phosphoribosyltransferase (OPRT) is an enzyme that causes the activation of 5-fluorouracil (5-FU). Fluorouracil 84-98 uridine monophosphate synthetase Homo sapiens 35-39 17089033-1 2006 Orotate phosphoribosyltransferase (OPRT) is an enzyme that causes the activation of 5-fluorouracil (5-FU). Fluorouracil 100-104 uridine monophosphate synthetase Homo sapiens 0-33 17089033-1 2006 Orotate phosphoribosyltransferase (OPRT) is an enzyme that causes the activation of 5-fluorouracil (5-FU). Fluorouracil 100-104 uridine monophosphate synthetase Homo sapiens 35-39 17214322-2 2006 Thymidylate synthase (TS) is the target enzyme of 5-FU. Fluorouracil 50-54 thymidylate synthetase Homo sapiens 0-20 17214322-2 2006 Thymidylate synthase (TS) is the target enzyme of 5-FU. Fluorouracil 50-54 thymidylate synthetase Homo sapiens 22-24 17214322-3 2006 In addition, activation of 5-FU to form various nucleotides via three pathways requires phosphorylation by orotate phosphoribosyltransferase, thymidine phosphorylase and uridine phosphorylase, respectively. Fluorouracil 27-31 uridine monophosphate synthetase Homo sapiens 107-140 16757204-1 2006 In this study, we investigated whether orotate phosphoribosyl transferase (OPRT) correlates with the clinicopathological features and effect of 5-fluorouracil (5-FU) in human oral carcinoma. Fluorouracil 144-158 uridine monophosphate synthetase Homo sapiens 39-73 16757204-1 2006 In this study, we investigated whether orotate phosphoribosyl transferase (OPRT) correlates with the clinicopathological features and effect of 5-fluorouracil (5-FU) in human oral carcinoma. Fluorouracil 144-158 uridine monophosphate synthetase Homo sapiens 75-79 16757204-1 2006 In this study, we investigated whether orotate phosphoribosyl transferase (OPRT) correlates with the clinicopathological features and effect of 5-fluorouracil (5-FU) in human oral carcinoma. Fluorouracil 160-164 uridine monophosphate synthetase Homo sapiens 39-73 16757204-5 2006 The expression of OPRT mRNA showed correlation with effect of 5-FU for oral carcinoma in either in vivo or in vitro. Fluorouracil 62-66 uridine monophosphate synthetase Homo sapiens 18-22 16757204-6 2006 These results suggest that the OPRT expressions may therefore be a prognostic factor of 5-FU efficacy in patients with oral squamous cell carcinoma. Fluorouracil 88-92 uridine monophosphate synthetase Homo sapiens 31-35 17217824-5 2006 RESULTS: The mutant exogenous P27(kip1) gene was expressed effectively in the cells, and the expression enhanced the apoptosis and growth inhibition of QBC(939) inducted by 5-FU, MMC and CTX. Fluorouracil 173-177 cyclin dependent kinase inhibitor 1B Homo sapiens 30-38 16652156-11 2006 As suppression of caspase-2 expression in 5-FU-treated cells also affects the level of the p53 protein, possibilities of a reciprocal interaction between these proteins are discussed. Fluorouracil 42-46 caspase 2 Homo sapiens 18-27 16572420-1 2006 Gene expression levels of thymidylate synthase (TS), dihydropyrimidine dehydrogenase (DPD), thymidine phosphorylase (TP) and orotate phosphoribosyl transferase (OPRT) have been shown to be associated with response to 5-fluorouracil-based therapies. Fluorouracil 217-231 thymidylate synthetase Homo sapiens 26-46 16572420-1 2006 Gene expression levels of thymidylate synthase (TS), dihydropyrimidine dehydrogenase (DPD), thymidine phosphorylase (TP) and orotate phosphoribosyl transferase (OPRT) have been shown to be associated with response to 5-fluorouracil-based therapies. Fluorouracil 217-231 uridine monophosphate synthetase Homo sapiens 125-159 16477629-3 2006 In this study, the mRNA expression levels of these 81 selected genes and the genes of 5-FU-related enzymes, including thymidylate synthase (TS), dihydropyrimidine dehydrogenase (DPD) and orotate phosphoribosyltransferase (OPRT), were measured using real-time quantitative RT-PCR assays of surgically resected materials from primary colorectal tumors in 22 patients. Fluorouracil 86-90 thymidylate synthetase Homo sapiens 118-138 16477629-3 2006 In this study, the mRNA expression levels of these 81 selected genes and the genes of 5-FU-related enzymes, including thymidylate synthase (TS), dihydropyrimidine dehydrogenase (DPD) and orotate phosphoribosyltransferase (OPRT), were measured using real-time quantitative RT-PCR assays of surgically resected materials from primary colorectal tumors in 22 patients. Fluorouracil 86-90 thymidylate synthetase Homo sapiens 140-142 16477629-3 2006 In this study, the mRNA expression levels of these 81 selected genes and the genes of 5-FU-related enzymes, including thymidylate synthase (TS), dihydropyrimidine dehydrogenase (DPD) and orotate phosphoribosyltransferase (OPRT), were measured using real-time quantitative RT-PCR assays of surgically resected materials from primary colorectal tumors in 22 patients. Fluorouracil 86-90 uridine monophosphate synthetase Homo sapiens 187-220 16477629-3 2006 In this study, the mRNA expression levels of these 81 selected genes and the genes of 5-FU-related enzymes, including thymidylate synthase (TS), dihydropyrimidine dehydrogenase (DPD) and orotate phosphoribosyltransferase (OPRT), were measured using real-time quantitative RT-PCR assays of surgically resected materials from primary colorectal tumors in 22 patients. Fluorouracil 86-90 uridine monophosphate synthetase Homo sapiens 222-226 16477629-5 2006 Four genes (TNFRSF1B, SLC35F5, NAG-1 and OPRT) had significantly different expression profiles in 5-FU-nonresponding and responding tumors (p < 0.05). Fluorouracil 98-102 uridine monophosphate synthetase Homo sapiens 41-45 16477629-8 2006 Our "Response Index" system, consisting of TNFRSF1B, SLC35F5 and OPRT, has great potential for predicting the efficacy of 5-FU-based chemotherapy against liver metastases from colorectal cancer. Fluorouracil 122-126 uridine monophosphate synthetase Homo sapiens 65-69 16804527-0 2006 Regional localisation of p53-independent apoptosis determines toxicity to 5-fluorouracil and pyrrolidinedithiocarbamate in the murine gut. Fluorouracil 74-88 transformation related protein 53, pseudogene Mus musculus 25-28 16804527-7 2006 Large intestinal crypts affect apoptosis purely by p53-dependent mechanisms, whereas small intestinal crypts are able to initiate both p53-dependent and -independent pathways following treatment with 5-FU. Fluorouracil 200-204 transformation related protein 53, pseudogene Mus musculus 135-138 16818689-0 2006 Orotate phosphoribosyltransferase gene polymorphism predicts toxicity in patients treated with bolus 5-fluorouracil regimen. Fluorouracil 101-115 uridine monophosphate synthetase Homo sapiens 0-33 16818689-1 2006 PURPOSE: We investigated whether the determination of orotate phosphoribosyltransferase (OPRT) and thymidylate synthase (TYMS) polymorphisms could predict the toxicity of 5-fluorouracil (5-FU) in colorectal cancer patients. Fluorouracil 187-191 uridine monophosphate synthetase Homo sapiens 54-87 16818689-7 2006 CONCLUSION: OPRT Gly213Ala polymorphism seems to be a useful marker for predicting toxicity to bolus 5-FU chemotherapy. Fluorouracil 101-105 uridine monophosphate synthetase Homo sapiens 12-16 16788943-1 2006 BACKGROUND AND OBJECTIVES: Phosphoribosylation of 5-fluorouracil (5-FU) is an essential step which leads to tumor growth inhibition and orotate phosphoribosyl transferase (OPRT) is the main enzyme that involves in this conversion of 5-FU to 5-fluorouridine monophosphate. Fluorouracil 50-64 uridine monophosphate synthetase Homo sapiens 172-176 16788943-1 2006 BACKGROUND AND OBJECTIVES: Phosphoribosylation of 5-fluorouracil (5-FU) is an essential step which leads to tumor growth inhibition and orotate phosphoribosyl transferase (OPRT) is the main enzyme that involves in this conversion of 5-FU to 5-fluorouridine monophosphate. Fluorouracil 66-70 uridine monophosphate synthetase Homo sapiens 172-176 16788943-2 2006 This retrospective study was aimed to evaluate the correlation between tumor OPRT activity and the clinical outcome in colorectal cancer (CRC) patients treated by oral 5-FU-based adjuvant chemotherapy. Fluorouracil 168-172 uridine monophosphate synthetase Homo sapiens 77-81 16788943-9 2006 CONCLUSIONS: This study demonstrated that an assay of tumor OPRT contributes to the determination of 5-FU-based adjuvant chemotherapy outcome and application in clinical practice should be included in tumor analysis prior to 5-FU-based adjuvant chemotherapy. Fluorouracil 101-105 uridine monophosphate synthetase Homo sapiens 60-64 16838650-4 2006 Concerning the mechanism of FAIT, we reported the synergistic effects of IFNalpha and 5-FU, in terms of the influence to cell cycle progression leading into the S phase via p27Kip1, an apoptosis-inducing effect through a reduction of Bcl-xl, and an immuno-modulatory effect via the TRAIL/TRAIL-receptor pathway. Fluorouracil 86-90 cyclin dependent kinase inhibitor 1B Homo sapiens 173-180 16187112-2 2006 Methylenetetrahydrofolate reductase (MTHFR) may play a central role in the action of 5-FU, an inhibitor of thymidylate synthase, by converting 5,10-methylenetetrahydrofolate to 5-methyltetrahydrofolate. Fluorouracil 85-89 thymidylate synthetase Homo sapiens 107-127 16897978-12 2006 The expressions of thymidylate synthase (TS) and dihydropyrimidine dehydrogenase (DPD) were decreased and that of orotate phosphorybosyl transferase (OPRT) was increased in mRNA, protein level and activity assay after the treatment with docetaxel and 5-FU in the TMK-1 gastric cancer cell. Fluorouracil 251-255 uridine monophosphate synthetase Homo sapiens 114-148 16897978-12 2006 The expressions of thymidylate synthase (TS) and dihydropyrimidine dehydrogenase (DPD) were decreased and that of orotate phosphorybosyl transferase (OPRT) was increased in mRNA, protein level and activity assay after the treatment with docetaxel and 5-FU in the TMK-1 gastric cancer cell. Fluorouracil 251-255 uridine monophosphate synthetase Homo sapiens 150-154 16331619-0 2006 Nuclear Maspin expression is associated with response to adjuvant 5-fluorouracil based chemotherapy in patients with stage III colon cancer. Fluorouracil 66-80 serpin family B member 5 Homo sapiens 8-14 16331619-6 2006 However, patients with primary tumors expressing Maspin in the nucleus showed a significant treatment benefit from 5-FU chemotherapy (hazard ratio 0.384; 95% CI, 0.188-0.784; p = 0.009) compared to adjuvantly treated patients whose tumors did not express this molecule. Fluorouracil 115-119 serpin family B member 5 Homo sapiens 49-55 16331619-7 2006 Nuclear Maspin expression is highly predictive of 5-FU chemotherapy response in patients with advanced stage colon cancer. Fluorouracil 50-54 serpin family B member 5 Homo sapiens 8-14 16596248-0 2006 Thymidylate synthase expression pattern, expression level and single nucleotide polymorphism are predictors for disease-free survival in patients of colorectal cancer treated with 5-fluorouracil. Fluorouracil 180-194 thymidylate synthetase Homo sapiens 0-20 16596248-7 2006 Low TS expression levels, cytoplasmic expression pattern and C SNP arose as variables associated to longer progression-free survival (PFS) in patients treated with 5FU. Fluorouracil 164-167 thymidylate synthetase Homo sapiens 4-6 16609021-1 2006 PURPOSE: Thymidylate synthase (TS), a critical target in fluorouracil-based chemotherapy, is a prognostic marker in colon carcinomas and a predictor of response to treatment. Fluorouracil 57-69 thymidylate synthetase Homo sapiens 9-29 16609021-1 2006 PURPOSE: Thymidylate synthase (TS), a critical target in fluorouracil-based chemotherapy, is a prognostic marker in colon carcinomas and a predictor of response to treatment. Fluorouracil 57-69 thymidylate synthetase Homo sapiens 31-33 16612157-3 2006 Determination of the thymidylate synthase (TS) demonstrated a higher inhibition of the enzyme by adding CDDP to 5-FU, suggesting biochemical modulation. Fluorouracil 112-116 thymidylate synthetase Homo sapiens 21-41 16612158-1 2006 Orotate phosphoribosyltransferase (OPRT EC 2.4.2.10) is a key enzyme related to the first-step phosphorylation process of 5-fluorouracil. Fluorouracil 122-136 uridine monophosphate synthetase Homo sapiens 0-33 16612158-1 2006 Orotate phosphoribosyltransferase (OPRT EC 2.4.2.10) is a key enzyme related to the first-step phosphorylation process of 5-fluorouracil. Fluorouracil 122-136 uridine monophosphate synthetase Homo sapiens 35-39 16438929-2 2006 5-Fluorouracil is inactivated by dihydropyrimidine dehydrogenase and targets thymidylate synthase. Fluorouracil 0-14 thymidylate synthetase Homo sapiens 77-97 16520664-14 2006 Thus, in metastatic breast cancer patients pre-treated with anthracyclines, the weekly administration of paclitaxel, 5-FU and folinic acid with G-CSF support seems to be extremely tolerable and active. Fluorouracil 117-121 colony stimulating factor 3 Homo sapiens 144-149 16540728-1 2006 Thymidylate synthase (TS) is a key regulatory enzyme in the cellular pathway of de novo pyrimidine synthesis and a target enzyme for 5-fluorouracil (5-FU). Fluorouracil 133-147 thymidylate synthetase Homo sapiens 0-20 16540728-1 2006 Thymidylate synthase (TS) is a key regulatory enzyme in the cellular pathway of de novo pyrimidine synthesis and a target enzyme for 5-fluorouracil (5-FU). Fluorouracil 133-147 thymidylate synthetase Homo sapiens 22-24 16540728-1 2006 Thymidylate synthase (TS) is a key regulatory enzyme in the cellular pathway of de novo pyrimidine synthesis and a target enzyme for 5-fluorouracil (5-FU). Fluorouracil 149-153 thymidylate synthetase Homo sapiens 0-20 16540728-1 2006 Thymidylate synthase (TS) is a key regulatory enzyme in the cellular pathway of de novo pyrimidine synthesis and a target enzyme for 5-fluorouracil (5-FU). Fluorouracil 149-153 thymidylate synthetase Homo sapiens 22-24 16540728-2 2006 Most clinical studies have shown that high levels of TS in tumors are associated with decreased sensitivity to 5-FU treatment. Fluorouracil 111-115 thymidylate synthetase Homo sapiens 53-55 16540728-11 2006 The results indicate that clinical studies of the significance of TS with regard to 5-FU-based chemotherapy should be based on assessment of TS activity at DNA, RNA, and protein levels. Fluorouracil 84-88 thymidylate synthetase Homo sapiens 66-68 16361227-6 2006 Similarly, su(r) mutants are hypersensitive to dietary 5-fluorouracil, CRMP mutants are less sensitive, and pyd3 mutants exhibit wild-type sensitivity. Fluorouracil 55-69 Sulfonylurea receptor Drosophila melanogaster 11-16 16511603-3 2006 In mice expressing a phosphotyrosine-null (PY-null) Epo receptor allele (EpoR-HM), severe and persistent anemia was induced by hemolysis or 5-fluorouracil. Fluorouracil 140-154 erythropoietin receptor Mus musculus 73-77 16445595-0 2006 Inhibitory effect of 5-fluorouracil on cytochrome P450 2C9 activity in cancer patients. Fluorouracil 21-35 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 39-58 16445595-1 2006 Drug interactions have been reported between 5-fluorouracil and cytochrome P450 2C9 (CYP2C9) substrates, S-warfarin and phenytoin. Fluorouracil 45-59 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 64-83 16445595-1 2006 Drug interactions have been reported between 5-fluorouracil and cytochrome P450 2C9 (CYP2C9) substrates, S-warfarin and phenytoin. Fluorouracil 45-59 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 85-91 16445595-2 2006 This study was performed to determine the influence of 5-fluorouracil on cytochrome P450 2C9 (CYP2C9) activity in colorectal cancer patients (n=17) receiving 5-fluorouracil. Fluorouracil 55-69 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 73-92 16445595-2 2006 This study was performed to determine the influence of 5-fluorouracil on cytochrome P450 2C9 (CYP2C9) activity in colorectal cancer patients (n=17) receiving 5-fluorouracil. Fluorouracil 55-69 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 94-100 16445595-2 2006 This study was performed to determine the influence of 5-fluorouracil on cytochrome P450 2C9 (CYP2C9) activity in colorectal cancer patients (n=17) receiving 5-fluorouracil. Fluorouracil 158-172 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 73-92 16445595-2 2006 This study was performed to determine the influence of 5-fluorouracil on cytochrome P450 2C9 (CYP2C9) activity in colorectal cancer patients (n=17) receiving 5-fluorouracil. Fluorouracil 158-172 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 94-100 16445595-9 2006 The results suggest that in most patients 5-fluorouracil inhibited CYP2C9 activity. Fluorouracil 42-56 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 67-73 16445595-11 2006 This finding may help explain the mechanism of interaction between 5-fluorouracil and CYP2C9 substrates. Fluorouracil 67-81 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 86-92 16075279-11 2006 Interestingly, Mad2 protein expression with PXL treatment followed by 5-FU gradually increased after the PXL removal and 5-FU exposure. Fluorouracil 70-74 mitotic arrest deficient 2 like 1 Homo sapiens 15-19 16075279-11 2006 Interestingly, Mad2 protein expression with PXL treatment followed by 5-FU gradually increased after the PXL removal and 5-FU exposure. Fluorouracil 121-125 mitotic arrest deficient 2 like 1 Homo sapiens 15-19 16455633-5 2006 Transfected cells were treated with 5-fluorouracil, a chemotherapeutic that decreases hTERT gene expression, and treatment-induced changes in hTERT promoter activity were imaged. Fluorouracil 36-50 telomerase reverse transcriptase Homo sapiens 86-91 16455633-8 2006 Decreases in hTERT gene expression caused by 5-fluorouracil treatment could be visualized in living 293T cells by both fluorescent microscopy and bioluminescent imaging. Fluorouracil 45-59 telomerase reverse transcriptase Homo sapiens 13-18 16407331-4 2006 A strain lacking the major abasic site endonuclease of Saccharomyces cerevisiae (Apn1) showed significantly increased sensitivity to 5-FU with G2/M arrest. Fluorouracil 133-137 DNA-(apurinic or apyrimidinic site) lyase APN1 Saccharomyces cerevisiae S288C 81-85 17216005-5 2006 The main mechanisms of the resistance against 5-fluorouracil are due to the overexpression of dihydropyrimidine dehydrogenase, MRP8, thymidylate synthase, and NFkB p65. Fluorouracil 46-60 thymidylate synthetase Homo sapiens 133-153 17216011-10 2006 Pharmacogenomic studies on the role of polymorphism of the serine-hydroxymethyl-transferase (SHMT) gene in the efficacy of 5-FU and FOLFIRI protocols of colorectal cancer patients revealed a significant effect resulting in altered overall survival as well. Fluorouracil 123-127 serine hydroxymethyltransferase 1 Homo sapiens 59-91 17216011-10 2006 Pharmacogenomic studies on the role of polymorphism of the serine-hydroxymethyl-transferase (SHMT) gene in the efficacy of 5-FU and FOLFIRI protocols of colorectal cancer patients revealed a significant effect resulting in altered overall survival as well. Fluorouracil 123-127 serine hydroxymethyltransferase 1 Homo sapiens 93-97 17065089-4 2006 TS is the main target of 5-fluorouracil (5-FU) activity, and its overexpression is one of the mechanisms of 5-FU drug resistance; however, in some studies its absence is responsible for a worse response to 5-FU. Fluorouracil 41-45 thymidylate synthetase Homo sapiens 0-2 17065089-4 2006 TS is the main target of 5-fluorouracil (5-FU) activity, and its overexpression is one of the mechanisms of 5-FU drug resistance; however, in some studies its absence is responsible for a worse response to 5-FU. Fluorouracil 108-112 thymidylate synthetase Homo sapiens 0-2 17065089-4 2006 TS is the main target of 5-fluorouracil (5-FU) activity, and its overexpression is one of the mechanisms of 5-FU drug resistance; however, in some studies its absence is responsible for a worse response to 5-FU. Fluorouracil 108-112 thymidylate synthetase Homo sapiens 0-2 16328050-0 2006 The relationship between 5-fluorouracil sensitivity and single nucleotide polymorphisms of the orotate phosphoribosyl transferase gene in colorectal cancer. Fluorouracil 25-39 uridine monophosphate synthetase Homo sapiens 95-129 16328050-1 2006 Orotate phosphoribosyl transferase (OPRT) is an enzyme playing an important role in exertion of the effect of 5-fluorouracil (5-FU). Fluorouracil 110-124 uridine monophosphate synthetase Homo sapiens 0-34 16328050-1 2006 Orotate phosphoribosyl transferase (OPRT) is an enzyme playing an important role in exertion of the effect of 5-fluorouracil (5-FU). Fluorouracil 110-124 uridine monophosphate synthetase Homo sapiens 36-40 16328050-1 2006 Orotate phosphoribosyl transferase (OPRT) is an enzyme playing an important role in exertion of the effect of 5-fluorouracil (5-FU). Fluorouracil 126-130 uridine monophosphate synthetase Homo sapiens 0-34 16328050-1 2006 Orotate phosphoribosyl transferase (OPRT) is an enzyme playing an important role in exertion of the effect of 5-fluorouracil (5-FU). Fluorouracil 126-130 uridine monophosphate synthetase Homo sapiens 36-40 16328050-3 2006 We investigated the correlation between SNP of OPRT and 5-FU sensitivity in colon and rectal cancers. Fluorouracil 56-60 uridine monophosphate synthetase Homo sapiens 47-51 16328050-9 2006 However, there are many unknown factors in the relationship between SNP of OPRT and 5-FU sensitivity, and SNP analysis of other regions is necessary. Fluorouracil 84-88 uridine monophosphate synthetase Homo sapiens 75-79 17179731-0 2006 Predictive role of thymidylate synthase, dihydropyrimidine dehydrogenase and thymidine phosphorylase expression in colorectal cancer patients receiving adjuvant 5-fluorouracil. Fluorouracil 161-175 thymidylate synthetase Homo sapiens 19-39 16322293-2 2005 The aim of this study was to analyze the prognostic significance of high levels of MSI (MSI-H) in CRC patients in relation to fluorouracil-based chemotherapy. Fluorouracil 126-138 RB binding protein 4, chromatin remodeling factor Homo sapiens 83-86 16267625-1 2005 Thymidylate synthase (TYMS) is an important target for chemotherapy drugs, such as 5-fluorouracil (5FU) and methotrexate. Fluorouracil 83-97 thymidylate synthetase Homo sapiens 0-20 16267625-1 2005 Thymidylate synthase (TYMS) is an important target for chemotherapy drugs, such as 5-fluorouracil (5FU) and methotrexate. Fluorouracil 83-97 thymidylate synthetase Homo sapiens 22-26 16267625-1 2005 Thymidylate synthase (TYMS) is an important target for chemotherapy drugs, such as 5-fluorouracil (5FU) and methotrexate. Fluorouracil 99-102 thymidylate synthetase Homo sapiens 0-20 16267625-1 2005 Thymidylate synthase (TYMS) is an important target for chemotherapy drugs, such as 5-fluorouracil (5FU) and methotrexate. Fluorouracil 99-102 thymidylate synthetase Homo sapiens 22-26 16838911-1 2005 The normal Raman and SERS spectra of 5-fluorouracil (5-FU) in water solution and attached to a biological artificial model (a silver colloid) at different pH values were recorded and discussed. Fluorouracil 37-51 seryl-tRNA synthetase 2, mitochondrial Homo sapiens 21-25 16838911-1 2005 The normal Raman and SERS spectra of 5-fluorouracil (5-FU) in water solution and attached to a biological artificial model (a silver colloid) at different pH values were recorded and discussed. Fluorouracil 53-57 seryl-tRNA synthetase 2, mitochondrial Homo sapiens 21-25 16160472-2 2005 Thymidylate synthase (TS), thymidine phosphorylase (TP), and dihydropyrimidine dehydrogenase (DPD) are known to be important biomarkers to predict tumor response to 5-FU-based therapy. Fluorouracil 165-169 thymidylate synthetase Homo sapiens 0-20 16160472-2 2005 Thymidylate synthase (TS), thymidine phosphorylase (TP), and dihydropyrimidine dehydrogenase (DPD) are known to be important biomarkers to predict tumor response to 5-FU-based therapy. Fluorouracil 165-169 thymidylate synthetase Homo sapiens 22-24 16315867-4 2005 Although OK-432 also enhanced the expression of the genes encoding SOCS-1 and SOCS-3, which are negative regulators for cytokine signaling, this was reduced by 5-FU or X-irradiation. Fluorouracil 160-164 suppressor of cytokine signaling 1 Homo sapiens 67-73 16141798-0 2005 Influence of thymidylate synthase gene polymorphisms on the survival of colorectal cancer patients receiving adjuvant 5-fluorouracil. Fluorouracil 118-132 thymidylate synthetase Homo sapiens 13-33 16251801-3 2005 By treating fresh human colonic explants with 5-Fluorouracil (200 microg/ml), CPT-11 (100 microg/ml) and/or TRAIL (100 ng/ml) we readily detected a signal in situ using FITC-VAD-FMK at different time points, whereas labeling of colonic explants with EGFP-conjugated Annexin V proved less specific. Fluorouracil 46-60 annexin A5 Homo sapiens 266-275 16270533-2 2005 Metabolizing enzymes such as thymidylate synthase (TS) and dihydropyrimidine dehydrogenase (DPD) have long been known to be useful for predicting response and outcome in patients receiving 5-fluorouracil (5-FU). Fluorouracil 189-203 thymidylate synthetase Homo sapiens 29-49 16270533-2 2005 Metabolizing enzymes such as thymidylate synthase (TS) and dihydropyrimidine dehydrogenase (DPD) have long been known to be useful for predicting response and outcome in patients receiving 5-fluorouracil (5-FU). Fluorouracil 189-203 thymidylate synthetase Homo sapiens 51-53 16270533-2 2005 Metabolizing enzymes such as thymidylate synthase (TS) and dihydropyrimidine dehydrogenase (DPD) have long been known to be useful for predicting response and outcome in patients receiving 5-fluorouracil (5-FU). Fluorouracil 205-209 thymidylate synthetase Homo sapiens 29-49 16270533-2 2005 Metabolizing enzymes such as thymidylate synthase (TS) and dihydropyrimidine dehydrogenase (DPD) have long been known to be useful for predicting response and outcome in patients receiving 5-fluorouracil (5-FU). Fluorouracil 205-209 thymidylate synthetase Homo sapiens 51-53 15993511-0 2005 The role of thymidylate synthase and dihydropyrimidine dehydrogenase in resistance to 5-fluorouracil in human lung cancer cells. Fluorouracil 86-100 thymidylate synthetase Homo sapiens 12-32 15993511-1 2005 The expressions of thymidylate synthase (TS) and intracellular metabolic enzymes have been reported to be associated with the sensitivity and/or resistance to 5-fluorouracil (5-FU). Fluorouracil 159-173 thymidylate synthetase Homo sapiens 19-39 15993511-1 2005 The expressions of thymidylate synthase (TS) and intracellular metabolic enzymes have been reported to be associated with the sensitivity and/or resistance to 5-fluorouracil (5-FU). Fluorouracil 159-173 thymidylate synthetase Homo sapiens 41-43 15993511-1 2005 The expressions of thymidylate synthase (TS) and intracellular metabolic enzymes have been reported to be associated with the sensitivity and/or resistance to 5-fluorouracil (5-FU). Fluorouracil 175-179 thymidylate synthetase Homo sapiens 19-39 15993511-1 2005 The expressions of thymidylate synthase (TS) and intracellular metabolic enzymes have been reported to be associated with the sensitivity and/or resistance to 5-fluorouracil (5-FU). Fluorouracil 175-179 thymidylate synthetase Homo sapiens 41-43 15993511-2 2005 However, since the role of these enzymes in the mechanism of resistance to 5-FU has not been fully examined in lung cancer, in the present study we measured the expression levels of TS, dihydropyrimidine dehydrogenase (DPD), thymidine phosphorylase (TP), and orotate phosphoribosyltransferase (OPRT) genes in lung cancer cell lines by real-time PCR, and the sensitivity to 5-FU using the MTS assay. Fluorouracil 75-79 thymidylate synthetase Homo sapiens 182-184 15993511-5 2005 In contrast, TS expression was dramatically higher in a 5-FU-resistant small-cell lung cancer cell line than in the parent cell line, whereas the expressions of DPD, TP, and OPRT genes were not markedly different. Fluorouracil 56-60 thymidylate synthetase Homo sapiens 13-15 16055198-3 2005 Humoral immune response to TYMS is induced by chemotherapy using TYMS inhibitors, such as 5-fluorouracil (5-FU), and may be associated with tumor burden. Fluorouracil 90-104 thymidylate synthetase Homo sapiens 27-31 16055198-3 2005 Humoral immune response to TYMS is induced by chemotherapy using TYMS inhibitors, such as 5-fluorouracil (5-FU), and may be associated with tumor burden. Fluorouracil 90-104 thymidylate synthetase Homo sapiens 65-69 16055198-3 2005 Humoral immune response to TYMS is induced by chemotherapy using TYMS inhibitors, such as 5-fluorouracil (5-FU), and may be associated with tumor burden. Fluorouracil 106-110 thymidylate synthetase Homo sapiens 27-31 16055198-3 2005 Humoral immune response to TYMS is induced by chemotherapy using TYMS inhibitors, such as 5-fluorouracil (5-FU), and may be associated with tumor burden. Fluorouracil 106-110 thymidylate synthetase Homo sapiens 65-69 15944938-1 2005 Thymidylate synthase (TS) is a major target of 5-fluorouracil (5-FU) and dihydropyrimidine dehydrogenase (DPD) is a rate-limiting enzyme in the degradation of 5-FU. Fluorouracil 47-61 thymidylate synthetase Homo sapiens 0-20 15944938-1 2005 Thymidylate synthase (TS) is a major target of 5-fluorouracil (5-FU) and dihydropyrimidine dehydrogenase (DPD) is a rate-limiting enzyme in the degradation of 5-FU. Fluorouracil 47-61 thymidylate synthetase Homo sapiens 22-24 15944938-1 2005 Thymidylate synthase (TS) is a major target of 5-fluorouracil (5-FU) and dihydropyrimidine dehydrogenase (DPD) is a rate-limiting enzyme in the degradation of 5-FU. Fluorouracil 63-67 thymidylate synthetase Homo sapiens 0-20 15944938-1 2005 Thymidylate synthase (TS) is a major target of 5-fluorouracil (5-FU) and dihydropyrimidine dehydrogenase (DPD) is a rate-limiting enzyme in the degradation of 5-FU. Fluorouracil 63-67 thymidylate synthetase Homo sapiens 22-24 15944938-1 2005 Thymidylate synthase (TS) is a major target of 5-fluorouracil (5-FU) and dihydropyrimidine dehydrogenase (DPD) is a rate-limiting enzyme in the degradation of 5-FU. Fluorouracil 159-163 thymidylate synthetase Homo sapiens 0-20 15944938-1 2005 Thymidylate synthase (TS) is a major target of 5-fluorouracil (5-FU) and dihydropyrimidine dehydrogenase (DPD) is a rate-limiting enzyme in the degradation of 5-FU. Fluorouracil 159-163 thymidylate synthetase Homo sapiens 22-24 15944938-11 2005 The current study demonstrated that TS but not DPD expression was associated with both progression and prognosis in breast cancer receiving 5-FU-based chemotherapy. Fluorouracil 140-144 thymidylate synthetase Homo sapiens 36-38 15944938-12 2005 TS expression in the primary tumor might be useful as a predictive parameter for the efficacy of 5-FU-based chemotherapy for breast cancer. Fluorouracil 97-101 thymidylate synthetase Homo sapiens 0-2 15856030-8 2005 In contrast, we showed that Ras interferes with 5-FU-induced expression of gelsolin, a protein with known antiapoptotic activity. Fluorouracil 48-52 gelsolin Homo sapiens 75-83 15856030-9 2005 We ascertained the role of gelsolin in 5-FU-induced apoptosis by demonstrating that silencing of gelsolin expression through RNAi sensitized cells to 5-FU-induced apoptosis and that re-expression of gelsolin in cells harboring mutant Ras protected cells from 5-FU-induced apoptosis. Fluorouracil 39-43 gelsolin Homo sapiens 27-35 15890242-0 2005 Thymidylate synthase and dihydropyrimidine dehydrogenase gene expression in breast cancer predicts 5-FU sensitivity by a histocultural drug sensitivity test. Fluorouracil 99-103 thymidylate synthetase Homo sapiens 0-20 15890242-1 2005 Thymidylate synthase (TS), Dihydropyrimidine dehydrogenase (DPD) and Thymidine Phosphorylase (TP) gene expressions are reported to be predictive markers for 5-fluorouracil (5-FU) sensitivity in gastrointestinal cancer. Fluorouracil 157-171 thymidylate synthetase Homo sapiens 0-20 15890242-1 2005 Thymidylate synthase (TS), Dihydropyrimidine dehydrogenase (DPD) and Thymidine Phosphorylase (TP) gene expressions are reported to be predictive markers for 5-fluorouracil (5-FU) sensitivity in gastrointestinal cancer. Fluorouracil 157-171 thymidylate synthetase Homo sapiens 22-24 15890242-1 2005 Thymidylate synthase (TS), Dihydropyrimidine dehydrogenase (DPD) and Thymidine Phosphorylase (TP) gene expressions are reported to be predictive markers for 5-fluorouracil (5-FU) sensitivity in gastrointestinal cancer. Fluorouracil 173-177 thymidylate synthetase Homo sapiens 0-20 15890242-7 2005 The group of high TS and high DPD gene expression in Ca was resistant to 5-FU, and the group of low TS and low DPD gene expression in Ca was sensitive to 5-FU (P=0.048 chi-square test). Fluorouracil 73-77 thymidylate synthetase Homo sapiens 18-20 15890242-7 2005 The group of high TS and high DPD gene expression in Ca was resistant to 5-FU, and the group of low TS and low DPD gene expression in Ca was sensitive to 5-FU (P=0.048 chi-square test). Fluorouracil 154-158 thymidylate synthetase Homo sapiens 100-102 15890242-8 2005 TS and DPD mRNA expressions measured using LCM+RT-PCR might be useful predictive markers for 5-FU sensitivity in human breast cancer. Fluorouracil 93-97 thymidylate synthetase Homo sapiens 0-2 15958060-6 2005 The protein expressions of TS, FPGS, and RFC1 were significantly associated with IC50 for 5-fluorouracil, but no such association was found for pemetrexed chemosensitivity. Fluorouracil 90-104 folylpolyglutamate synthase Homo sapiens 31-35 15867226-6 2005 EXPERIMENTAL DESIGN: We examined Drg1 expression by immunohistochemistry in 131 patients with metastatic colorectal cancer enrolled in a clinical trial of adjuvant fluorouracil-based therapy from 1991 to 1995. Fluorouracil 164-176 developmentally regulated GTP binding protein 1 Homo sapiens 33-37 15616154-1 2005 Dihydropyrimidine dehydrogenase (DPD), the first enzyme in the sequential metabolism of pyrimidine, regulates blood concentrations of 5-fluorouracil and is deeply involved in its toxicity. Fluorouracil 134-148 dihydropyrimidine dehydrogenase Canis lupus familiaris 0-31 15616154-1 2005 Dihydropyrimidine dehydrogenase (DPD), the first enzyme in the sequential metabolism of pyrimidine, regulates blood concentrations of 5-fluorouracil and is deeply involved in its toxicity. Fluorouracil 134-148 dihydropyrimidine dehydrogenase Canis lupus familiaris 33-36 15611052-4 2005 Analyses of ATPase activation suggested that the hMSH2-hMSH6 heterodimer only recognized FdUrd moieties (as the base 5-fluorouracil (FU) in DNA) when mispaired with guanine, but not paired with adenine. Fluorouracil 117-131 mutS homolog 6 Homo sapiens 55-60 15727486-7 2005 Several studies confirm the influence of the activity of thymidylate synthase, thymidine phosphorylase and dihydropyrimidine dehydrogenase on the outcome of fluorouracil therapy for colorectal cancer, with higher enzyme activities predicting lower treatment efficacy. Fluorouracil 157-169 thymidylate synthetase Homo sapiens 57-77 15727486-8 2005 Although fewer studies are available regarding therapy of hepatic metastases, the same relationship between thymidylate synthase activity and outcome of fluorouracil therapy observed for primary colorectal cancer was found. Fluorouracil 153-165 thymidylate synthetase Homo sapiens 108-128 15365767-9 2005 DHA markedly increased the inhibitory effect of 5-FU on the expression of the antiapoptotic proteins BCL-2 and BCL-XL, and induced overexpression of c-MYC which has recently been shown to drive apoptosis and, when overexpressed, to sensitize cancer cells to the action of proapoptotic agents, including 5-FU. Fluorouracil 303-307 MYC proto-oncogene, bHLH transcription factor Homo sapiens 149-154 15604591-1 2005 This paper reports on an early stopped prospective randomized phase III trial comparing cisplatin, ifosfamide and 5-fluorouracil (PIF) with cisplatin monotherapy in the treatment of recurrent cervical cancer. Fluorouracil 114-128 PIF1 5'-to-3' DNA helicase Homo sapiens 130-133 15359285-3 2004 Mutants of two of these enzymes, dihydrofolate reductase (DHFR F/S) and thymidylate synthase (TS G52S), were previously shown to confer resistance to methotrexate and 5-FU, respectively, and recently a fusion cDNA of both mutant enzymes (DHFR F/S-TS G52S) was shown to confer dual resistance to both antimetabolites. Fluorouracil 167-171 dihydrofolate reductase Homo sapiens 33-56 15359285-3 2004 Mutants of two of these enzymes, dihydrofolate reductase (DHFR F/S) and thymidylate synthase (TS G52S), were previously shown to confer resistance to methotrexate and 5-FU, respectively, and recently a fusion cDNA of both mutant enzymes (DHFR F/S-TS G52S) was shown to confer dual resistance to both antimetabolites. Fluorouracil 167-171 thymidylate synthetase Homo sapiens 58-92 15359285-3 2004 Mutants of two of these enzymes, dihydrofolate reductase (DHFR F/S) and thymidylate synthase (TS G52S), were previously shown to confer resistance to methotrexate and 5-FU, respectively, and recently a fusion cDNA of both mutant enzymes (DHFR F/S-TS G52S) was shown to confer dual resistance to both antimetabolites. Fluorouracil 167-171 dihydrofolate reductase Homo sapiens 58-62 15542523-4 2004 AIM: We investigated the effects of FPGS modulation on the chemosensitivity of colon cancer cells to 5-FU and MTX. Fluorouracil 101-105 folylpolyglutamate synthase Homo sapiens 36-40 15542523-8 2004 FPGS overexpression significantly enhanced, whereas FPGS inhibition decreased, chemosensitivity to 5-FU. Fluorouracil 99-103 folylpolyglutamate synthase Homo sapiens 0-4 15542523-8 2004 FPGS overexpression significantly enhanced, whereas FPGS inhibition decreased, chemosensitivity to 5-FU. Fluorouracil 99-103 folylpolyglutamate synthase Homo sapiens 52-56 15542523-10 2004 CONCLUSIONS: These data provide functional evidence that FPGS overexpression and inhibition modulate chemosensitivity of colon cancer cells to 5-FU by altering intracellular folate polyglutamylation, providing proof of principle. Fluorouracil 143-147 folylpolyglutamate synthase Homo sapiens 57-61 15542523-11 2004 Thus FPGS status may be an important predictor of chemosensitivity of colon cancer cells to 5-FU based chemotherapy, and FPGS gene transfer may increase the sensitivity of colon cancer cells to 5-FU-based chemotherapy. Fluorouracil 92-96 folylpolyglutamate synthase Homo sapiens 5-9 15640503-0 2004 Prognostic implications of the expression of erbB2, topoisomerase II alpha and thymidylate synthase in metastatic gastric cancer after fluorouracil-based therapy. Fluorouracil 135-147 thymidylate synthetase Homo sapiens 79-99 15480428-9 2004 Consistent with these data, RTKN-expressing cells showed increased chemoresistance to 5-fluorouracil and paclitaxol, and the resistance was greatly attenuated by NF-kappaB inhibitor. Fluorouracil 86-100 rhotekin Homo sapiens 28-32 15549590-0 2004 Prognostic significance of thymidylate synthase in patients with metastatic colorectal cancer who receive protracted venous infusions of 5-fluorouracil. Fluorouracil 137-151 thymidylate synthetase Homo sapiens 27-47 15549590-1 2004 BACKGROUND: This study was conducted to evaluate the prognostic significance of thymidylate synthase (TS) expression in the tumor tissue of patients with metastatic colorectal cancer (CRC) who received protracted venous infusions of 5-fluorouracil (5-FU). Fluorouracil 233-247 thymidylate synthetase Homo sapiens 80-100 15549590-1 2004 BACKGROUND: This study was conducted to evaluate the prognostic significance of thymidylate synthase (TS) expression in the tumor tissue of patients with metastatic colorectal cancer (CRC) who received protracted venous infusions of 5-fluorouracil (5-FU). Fluorouracil 233-247 thymidylate synthetase Homo sapiens 102-104 15549590-1 2004 BACKGROUND: This study was conducted to evaluate the prognostic significance of thymidylate synthase (TS) expression in the tumor tissue of patients with metastatic colorectal cancer (CRC) who received protracted venous infusions of 5-fluorouracil (5-FU). Fluorouracil 249-253 thymidylate synthetase Homo sapiens 102-104 15549590-5 2004 CONCLUSION: In patients with metastatic CRC who received protracted venous infusions of 5-FU, TS expression was related to survival independently of other established clinical prognostic factors. Fluorouracil 88-92 thymidylate synthetase Homo sapiens 94-96 15500737-1 2004 OBJECTIVE: To study the relationship between the expression of thymidylate synthase (TS) gene and the prognosis of colorectal carcinoma and between the TS expression and the effect of 5-fluorouracil (5-Fu) on advanced colorectal carcinoma. Fluorouracil 184-198 thymidylate synthetase Homo sapiens 152-154 15500737-1 2004 OBJECTIVE: To study the relationship between the expression of thymidylate synthase (TS) gene and the prognosis of colorectal carcinoma and between the TS expression and the effect of 5-fluorouracil (5-Fu) on advanced colorectal carcinoma. Fluorouracil 200-204 thymidylate synthetase Homo sapiens 152-154 15353299-6 2004 Thymidylate synthase (TS) continues to be a critical target for 5-fluorouracil (5-FU) and its prodrugs, UFT/LV (Orzel), capecitabine (Xeloda), and S-1, primarily because this enzyme is essential for the synthesis of 2-deoxythymidine-5-monophosphate, a precursor for DNA synthesis. Fluorouracil 64-78 thymidylate synthetase Homo sapiens 0-20 15353299-6 2004 Thymidylate synthase (TS) continues to be a critical target for 5-fluorouracil (5-FU) and its prodrugs, UFT/LV (Orzel), capecitabine (Xeloda), and S-1, primarily because this enzyme is essential for the synthesis of 2-deoxythymidine-5-monophosphate, a precursor for DNA synthesis. Fluorouracil 64-78 thymidylate synthetase Homo sapiens 22-24 15353299-6 2004 Thymidylate synthase (TS) continues to be a critical target for 5-fluorouracil (5-FU) and its prodrugs, UFT/LV (Orzel), capecitabine (Xeloda), and S-1, primarily because this enzyme is essential for the synthesis of 2-deoxythymidine-5-monophosphate, a precursor for DNA synthesis. Fluorouracil 80-84 thymidylate synthetase Homo sapiens 0-20 15353299-6 2004 Thymidylate synthase (TS) continues to be a critical target for 5-fluorouracil (5-FU) and its prodrugs, UFT/LV (Orzel), capecitabine (Xeloda), and S-1, primarily because this enzyme is essential for the synthesis of 2-deoxythymidine-5-monophosphate, a precursor for DNA synthesis. Fluorouracil 80-84 thymidylate synthetase Homo sapiens 22-24 15446554-1 2004 Thymidylate synthase (TS) is a target enzyme of 5-fluorouracil (5-FU), and the TS expression level of cancer tissues is a potential predictor of the response to 5-FU-based chemotherapy. Fluorouracil 48-62 thymidylate synthetase Homo sapiens 0-20 15446554-1 2004 Thymidylate synthase (TS) is a target enzyme of 5-fluorouracil (5-FU), and the TS expression level of cancer tissues is a potential predictor of the response to 5-FU-based chemotherapy. Fluorouracil 48-62 thymidylate synthetase Homo sapiens 22-24 15446554-1 2004 Thymidylate synthase (TS) is a target enzyme of 5-fluorouracil (5-FU), and the TS expression level of cancer tissues is a potential predictor of the response to 5-FU-based chemotherapy. Fluorouracil 48-62 thymidylate synthetase Homo sapiens 79-81 15446554-1 2004 Thymidylate synthase (TS) is a target enzyme of 5-fluorouracil (5-FU), and the TS expression level of cancer tissues is a potential predictor of the response to 5-FU-based chemotherapy. Fluorouracil 64-68 thymidylate synthetase Homo sapiens 0-20 15446554-1 2004 Thymidylate synthase (TS) is a target enzyme of 5-fluorouracil (5-FU), and the TS expression level of cancer tissues is a potential predictor of the response to 5-FU-based chemotherapy. Fluorouracil 64-68 thymidylate synthetase Homo sapiens 22-24 15446554-1 2004 Thymidylate synthase (TS) is a target enzyme of 5-fluorouracil (5-FU), and the TS expression level of cancer tissues is a potential predictor of the response to 5-FU-based chemotherapy. Fluorouracil 64-68 thymidylate synthetase Homo sapiens 79-81 15446554-1 2004 Thymidylate synthase (TS) is a target enzyme of 5-fluorouracil (5-FU), and the TS expression level of cancer tissues is a potential predictor of the response to 5-FU-based chemotherapy. Fluorouracil 161-165 thymidylate synthetase Homo sapiens 0-20 15446554-1 2004 Thymidylate synthase (TS) is a target enzyme of 5-fluorouracil (5-FU), and the TS expression level of cancer tissues is a potential predictor of the response to 5-FU-based chemotherapy. Fluorouracil 161-165 thymidylate synthetase Homo sapiens 22-24 15446554-1 2004 Thymidylate synthase (TS) is a target enzyme of 5-fluorouracil (5-FU), and the TS expression level of cancer tissues is a potential predictor of the response to 5-FU-based chemotherapy. Fluorouracil 161-165 thymidylate synthetase Homo sapiens 79-81 15446554-3 2004 Therefore, the TS polymorphism may also be a predictor of the response to 5-FU-based chemotherapy. Fluorouracil 74-78 thymidylate synthetase Homo sapiens 15-17 15446554-11 2004 These results suggest that the TS gene polymorphism and TS protein level may be independent predictors for 5-FU-based chemotherapy. Fluorouracil 107-111 thymidylate synthetase Homo sapiens 31-33 15446554-11 2004 These results suggest that the TS gene polymorphism and TS protein level may be independent predictors for 5-FU-based chemotherapy. Fluorouracil 107-111 thymidylate synthetase Homo sapiens 56-58 15446572-2 2004 Orotate phosphoribosyl transferase (OPRT) is one of the key enzymes in metabolic pathways of 5-FU. Fluorouracil 93-97 uridine monophosphate synthetase Homo sapiens 0-34 15446572-2 2004 Orotate phosphoribosyl transferase (OPRT) is one of the key enzymes in metabolic pathways of 5-FU. Fluorouracil 93-97 uridine monophosphate synthetase Homo sapiens 36-40 15446572-10 2004 There was a significant correlation between OPRT activity and 5-FU sensitivity (r=0.571, p<0.01) in 19 cases whose OPRT activities and 5-FU sensitivities were assessed simultaneously. Fluorouracil 62-66 uridine monophosphate synthetase Homo sapiens 44-48 15289866-7 2004 The level of caspase activity induced by 5-fluorouracil (5-FU) was higher in Hep3B than in PLC/PRF/5 and a significant increase in the activity occurred at a rather late stage, after 48 h of the treatment. Fluorouracil 41-55 heparan sulfate proteoglycan 2 Homo sapiens 91-94 15289866-7 2004 The level of caspase activity induced by 5-fluorouracil (5-FU) was higher in Hep3B than in PLC/PRF/5 and a significant increase in the activity occurred at a rather late stage, after 48 h of the treatment. Fluorouracil 57-61 heparan sulfate proteoglycan 2 Homo sapiens 91-94 15260847-1 2004 High expression of thymidylate synthase (TS) is allegedly associated with the chemoresistance to 5-fluorouracil (5-FU) in colorectal cancers. Fluorouracil 97-111 thymidylate synthetase Homo sapiens 19-39 15260847-1 2004 High expression of thymidylate synthase (TS) is allegedly associated with the chemoresistance to 5-fluorouracil (5-FU) in colorectal cancers. Fluorouracil 97-111 thymidylate synthetase Homo sapiens 41-43 15260847-1 2004 High expression of thymidylate synthase (TS) is allegedly associated with the chemoresistance to 5-fluorouracil (5-FU) in colorectal cancers. Fluorouracil 113-117 thymidylate synthetase Homo sapiens 19-39 15260847-1 2004 High expression of thymidylate synthase (TS) is allegedly associated with the chemoresistance to 5-fluorouracil (5-FU) in colorectal cancers. Fluorouracil 113-117 thymidylate synthetase Homo sapiens 41-43 15260847-4 2004 We immunohistochemically evaluated the relationship between the expression of TS, p16(INK4a), CDK4 and cyclin D1 and the effect of 5-FU-based chemotherapy in colorectal cancers. Fluorouracil 131-135 thymidylate synthetase Homo sapiens 78-80 15260847-12 2004 In conclusion, the combination of low expression of TS and induction of p16(INK4a) after chemotherapy can be important indicators of the sensitivity to 5-FU-based chemotherapy in colorectal cancers. Fluorouracil 152-156 thymidylate synthetase Homo sapiens 52-54 15213713-2 2004 Functional polymorphisms in DNA-repair genes XPD, ERCC1, XRCC1, XPA, and metabolising genes glutathione S-transferase GSTP1, GSTT1, GSTM1, and thymidylate synthase (TS) were assessed retrospectively in 106 patients with refractory stage IV disease who received 5-FU/oxaliplatin combination chemotherapy, using a polymerase chain reaction-based RFLP technique. Fluorouracil 261-265 glutathione S-transferase pi 1 Homo sapiens 118-123 15213713-2 2004 Functional polymorphisms in DNA-repair genes XPD, ERCC1, XRCC1, XPA, and metabolising genes glutathione S-transferase GSTP1, GSTT1, GSTM1, and thymidylate synthase (TS) were assessed retrospectively in 106 patients with refractory stage IV disease who received 5-FU/oxaliplatin combination chemotherapy, using a polymerase chain reaction-based RFLP technique. Fluorouracil 261-265 thymidylate synthetase Homo sapiens 143-163 15222106-1 2004 Thymidylate synthase (TS) and dihydropyrimidine dehydrogenase (DPD) have been identified as a predictor of response to 5-fluorouracil (5-FU). Fluorouracil 119-133 thymidylate synthetase Homo sapiens 0-20 15222106-1 2004 Thymidylate synthase (TS) and dihydropyrimidine dehydrogenase (DPD) have been identified as a predictor of response to 5-fluorouracil (5-FU). Fluorouracil 135-139 thymidylate synthetase Homo sapiens 0-20 15130763-6 2004 Treatment with Doxorubicin, Paclitaxel or 5-Fluorouracil induced a breakdown of the mitochondrial membrane potential and apoptotic cell death in p56/Lck expressing Jurkat and the retransfected JCaM1.6/Lck cells within 48h of treatment. Fluorouracil 42-56 LCK proto-oncogene, Src family tyrosine kinase Homo sapiens 149-152 15130763-6 2004 Treatment with Doxorubicin, Paclitaxel or 5-Fluorouracil induced a breakdown of the mitochondrial membrane potential and apoptotic cell death in p56/Lck expressing Jurkat and the retransfected JCaM1.6/Lck cells within 48h of treatment. Fluorouracil 42-56 LCK proto-oncogene, Src family tyrosine kinase Homo sapiens 201-204 15130763-11 2004 In conclusion, the tyrosine kinase p56/Lck is essential for apoptosis induction by Doxorubicin, Paclitaxel and 5-Fluorouracil regulating early steps of the mitochondrial apoptosis signaling cascade, including alteration of mitochondrial functions and caspase-activation. Fluorouracil 111-125 LCK proto-oncogene, Src family tyrosine kinase Homo sapiens 39-42 15132128-2 2004 5-FU interferes with DNA synthesis by blocking thymidylate synthase (TS) but is inactivated by dihydropyrimidine dehydrogenase (DPD). Fluorouracil 0-4 thymidylate synthetase Homo sapiens 47-67 15132128-2 2004 5-FU interferes with DNA synthesis by blocking thymidylate synthase (TS) but is inactivated by dihydropyrimidine dehydrogenase (DPD). Fluorouracil 0-4 thymidylate synthetase Homo sapiens 69-71 15132128-3 2004 Favorable enzyme profiles (high TP and low DPD) generate high intratumor levels of 5-FU that are effective against many tumors, especially those with low TS. Fluorouracil 83-87 thymidylate synthetase Homo sapiens 154-156 15138115-11 2004 When 5-FU or carboplatin was added, there was a significant difference in growth suppression rate between FasL positive and controlled cancer cells (t=9.02, t=11.93, P<0.01). Fluorouracil 5-9 Fas ligand Homo sapiens 106-110 15067352-9 2004 5-FU metabolism-associated genes (e.g., TYMS, DTYMK, UP) and DNA repair genes (e.g., FEN1, FANCG, RAD23B) were also up-regulated in one or both resistant derivatives, suggesting that the resistant derivatives might be able to overcome both 5-FU inhibition of thymidylate synthase and the DNA damage caused by 5-FU, respectively. Fluorouracil 0-4 thymidylate synthetase Homo sapiens 40-44 15067352-9 2004 5-FU metabolism-associated genes (e.g., TYMS, DTYMK, UP) and DNA repair genes (e.g., FEN1, FANCG, RAD23B) were also up-regulated in one or both resistant derivatives, suggesting that the resistant derivatives might be able to overcome both 5-FU inhibition of thymidylate synthase and the DNA damage caused by 5-FU, respectively. Fluorouracil 0-4 flap structure-specific endonuclease 1 Homo sapiens 85-89 15067352-9 2004 5-FU metabolism-associated genes (e.g., TYMS, DTYMK, UP) and DNA repair genes (e.g., FEN1, FANCG, RAD23B) were also up-regulated in one or both resistant derivatives, suggesting that the resistant derivatives might be able to overcome both 5-FU inhibition of thymidylate synthase and the DNA damage caused by 5-FU, respectively. Fluorouracil 0-4 FA complementation group G Homo sapiens 91-96 15067352-9 2004 5-FU metabolism-associated genes (e.g., TYMS, DTYMK, UP) and DNA repair genes (e.g., FEN1, FANCG, RAD23B) were also up-regulated in one or both resistant derivatives, suggesting that the resistant derivatives might be able to overcome both 5-FU inhibition of thymidylate synthase and the DNA damage caused by 5-FU, respectively. Fluorouracil 0-4 RAD23 homolog B, nucleotide excision repair protein Homo sapiens 98-104 15067352-9 2004 5-FU metabolism-associated genes (e.g., TYMS, DTYMK, UP) and DNA repair genes (e.g., FEN1, FANCG, RAD23B) were also up-regulated in one or both resistant derivatives, suggesting that the resistant derivatives might be able to overcome both 5-FU inhibition of thymidylate synthase and the DNA damage caused by 5-FU, respectively. Fluorouracil 0-4 thymidylate synthetase Homo sapiens 259-279 14689231-2 2004 Thymidylate synthase (TS), the target enzyme of FUra, and dihydropyrimidine dehydrogenase (DPD), the rate-limiting catabolic enzyme of pyrimidines, have both been reported to be predictors of the response to FUra-based chemotherapies. Fluorouracil 48-52 thymidylate synthetase Homo sapiens 0-20 14689231-2 2004 Thymidylate synthase (TS), the target enzyme of FUra, and dihydropyrimidine dehydrogenase (DPD), the rate-limiting catabolic enzyme of pyrimidines, have both been reported to be predictors of the response to FUra-based chemotherapies. Fluorouracil 48-52 thymidylate synthetase Homo sapiens 22-24 14689231-2 2004 Thymidylate synthase (TS), the target enzyme of FUra, and dihydropyrimidine dehydrogenase (DPD), the rate-limiting catabolic enzyme of pyrimidines, have both been reported to be predictors of the response to FUra-based chemotherapies. Fluorouracil 208-212 thymidylate synthetase Homo sapiens 0-20 14689231-2 2004 Thymidylate synthase (TS), the target enzyme of FUra, and dihydropyrimidine dehydrogenase (DPD), the rate-limiting catabolic enzyme of pyrimidines, have both been reported to be predictors of the response to FUra-based chemotherapies. Fluorouracil 208-212 thymidylate synthetase Homo sapiens 22-24 15044053-0 2004 The combination of metformin and a dipeptidyl peptidase IV inhibitor prevents 5-fluorouracil-induced reduction of small intestine weight. Fluorouracil 78-92 dipeptidylpeptidase 4 Mus musculus 35-58 14970324-0 2004 Digital karyotyping identifies thymidylate synthase amplification as a mechanism of resistance to 5-fluorouracil in metastatic colorectal cancer patients. Fluorouracil 98-112 thymidylate synthetase Homo sapiens 31-51 14970324-4 2004 Analysis of TYMS by fluorescence in situ hybridization identified TYMS gene amplification in 23% of 31 5-FU-treated cancers, whereas no amplification was observed in metastases of patients that had not been treated with 5-FU. Fluorouracil 103-107 thymidylate synthetase Homo sapiens 66-70 14970324-6 2004 These data suggest that genetic amplification of TYMS is a major mechanism of 5-FU resistance in vivo and have important implications for the management of colorectal cancer patients with recurrent disease. Fluorouracil 78-82 thymidylate synthetase Homo sapiens 49-53 15025949-1 2004 BACKGROUND & OBJECTIVE: Anti-cancer effect of 5-Fluorouracil (5-FU) is mediated mainly by inhibition of the thymidylate synthase (TS), while dihydropyrimidine dehydrogenase (DPD) is an initial and a rate-limiting catabolic enzyme of 5-FU. Fluorouracil 50-64 dihydropyrimidine dehydrogenase Mus musculus 145-176 15025949-1 2004 BACKGROUND & OBJECTIVE: Anti-cancer effect of 5-Fluorouracil (5-FU) is mediated mainly by inhibition of the thymidylate synthase (TS), while dihydropyrimidine dehydrogenase (DPD) is an initial and a rate-limiting catabolic enzyme of 5-FU. Fluorouracil 50-64 dihydropyrimidine dehydrogenase Mus musculus 178-181 15025949-1 2004 BACKGROUND & OBJECTIVE: Anti-cancer effect of 5-Fluorouracil (5-FU) is mediated mainly by inhibition of the thymidylate synthase (TS), while dihydropyrimidine dehydrogenase (DPD) is an initial and a rate-limiting catabolic enzyme of 5-FU. Fluorouracil 66-70 dihydropyrimidine dehydrogenase Mus musculus 145-176 15025949-1 2004 BACKGROUND & OBJECTIVE: Anti-cancer effect of 5-Fluorouracil (5-FU) is mediated mainly by inhibition of the thymidylate synthase (TS), while dihydropyrimidine dehydrogenase (DPD) is an initial and a rate-limiting catabolic enzyme of 5-FU. Fluorouracil 66-70 dihydropyrimidine dehydrogenase Mus musculus 178-181 15025949-1 2004 BACKGROUND & OBJECTIVE: Anti-cancer effect of 5-Fluorouracil (5-FU) is mediated mainly by inhibition of the thymidylate synthase (TS), while dihydropyrimidine dehydrogenase (DPD) is an initial and a rate-limiting catabolic enzyme of 5-FU. Fluorouracil 237-241 dihydropyrimidine dehydrogenase Mus musculus 145-176 15152939-4 2004 RESULTS: We identified several novel 5-FU-inducible target genes that have not previously been linked to 5-FU response, including spermine/spermidine acetyl transferase (SSAT) and annexin II. Fluorouracil 37-41 annexin A2 Homo sapiens 180-190 15152939-4 2004 RESULTS: We identified several novel 5-FU-inducible target genes that have not previously been linked to 5-FU response, including spermine/spermidine acetyl transferase (SSAT) and annexin II. Fluorouracil 105-109 annexin A2 Homo sapiens 180-190 15152939-6 2004 Inactivation of wild-type p53 abrogated the 5-FU-mediated induction of SSAT and annexin II. Fluorouracil 44-48 annexin A2 Homo sapiens 80-90 15152939-8 2004 Furthermore, basal expression of SSAT and annexin II was elevated in cells resistant to 5-FU. Fluorouracil 88-92 annexin A2 Homo sapiens 42-52 14993808-1 2004 We evaluated the features of cell death induced by CDF (cyclophosphamide [CPA], doxorubicin [DOX], 5-fluorouracil [5-FU]) multi-drug administration in vitro using the human breast cancer cell line MCF-7. Fluorouracil 115-119 LIF interleukin 6 family cytokine Homo sapiens 51-54 15025795-0 2004 Dihydropyrimidine dehydrogenase and thymidylate synthase polymorphisms and their association with 5-fluorouracil/leucovorin chemotherapy in colorectal cancer. Fluorouracil 98-112 thymidylate synthetase Homo sapiens 36-56 14760062-1 2004 Thymidylate synthase (TS), the target enzyme of the fluoropyrimidine class of drugs, has a 28-bp repeat polymorphism in the promoter region that has been associated with response of tumors to 5-fluorouracil-based therapy. Fluorouracil 192-206 thymidylate synthetase Homo sapiens 0-20 14760062-1 2004 Thymidylate synthase (TS), the target enzyme of the fluoropyrimidine class of drugs, has a 28-bp repeat polymorphism in the promoter region that has been associated with response of tumors to 5-fluorouracil-based therapy. Fluorouracil 192-206 thymidylate synthetase Homo sapiens 22-24 14726200-1 2004 Thymidylate synthase (TS) is the target in colon cancer therapeutic protocols utilizing such drugs as 5-fluorouracil and raltitrexed. Fluorouracil 102-116 thymidylate synthetase Homo sapiens 0-20 15095856-7 2004 Within the crypt, p53 expression is likely to be modulated by growth hormone after 5-fluorouracil treatment. Fluorouracil 83-97 Wistar clone pR53P1 p53 pseudogene Rattus norvegicus 18-21 15224198-1 2004 BACKGROUND: Although 5-fluorouracil (5-FU) and cis-diamminedichloroplatinum (cisplatin) in combination have synergistic cytotoxicity against both murine and human neoplasms, the precise mechanism of the synergism, and the effects on thymidylate synthase and its percent inhibition, and the effects on dihydropyrimidine dehydrogenase (DPD) remained to be elucidated. Fluorouracil 21-35 thymidylate synthetase Homo sapiens 233-253 15224198-1 2004 BACKGROUND: Although 5-fluorouracil (5-FU) and cis-diamminedichloroplatinum (cisplatin) in combination have synergistic cytotoxicity against both murine and human neoplasms, the precise mechanism of the synergism, and the effects on thymidylate synthase and its percent inhibition, and the effects on dihydropyrimidine dehydrogenase (DPD) remained to be elucidated. Fluorouracil 37-41 thymidylate synthetase Homo sapiens 233-253 15224198-8 2004 The short-term administration of 5-FU significantly decreased DPD. Fluorouracil 33-37 dihydropyrimidine dehydrogenase Mus musculus 62-65 15224198-11 2004 Changes in DPD after the administration of 5-FU may provide an insight into tumor sensitivity and resistance to 5-FU. Fluorouracil 43-47 dihydropyrimidine dehydrogenase Mus musculus 11-14 15224198-11 2004 Changes in DPD after the administration of 5-FU may provide an insight into tumor sensitivity and resistance to 5-FU. Fluorouracil 112-116 dihydropyrimidine dehydrogenase Mus musculus 11-14 15254665-0 2004 Expression of p65 gene in experimental colon cancer under the influence of 5-fluorouracil given alone and in combination with hormonal modulation. Fluorouracil 75-89 v-rel reticuloendotheliosis viral oncogene homolog A (avian) Mus musculus 14-17 15254665-1 2004 The effect of tamoxifen (TAM), lanreotide (LAN) and 5-fluorouracil (5-FU), given separately or together, on p65 gene expression in murine Colon 38 cancer was investigated by RT-PCR method. Fluorouracil 52-66 v-rel reticuloendotheliosis viral oncogene homolog A (avian) Mus musculus 108-111 15254665-1 2004 The effect of tamoxifen (TAM), lanreotide (LAN) and 5-fluorouracil (5-FU), given separately or together, on p65 gene expression in murine Colon 38 cancer was investigated by RT-PCR method. Fluorouracil 68-72 v-rel reticuloendotheliosis viral oncogene homolog A (avian) Mus musculus 108-111 15254665-11 2004 In the group with 5-FU alone the expression of p65 was present in about 80% of samples. Fluorouracil 18-22 v-rel reticuloendotheliosis viral oncogene homolog A (avian) Mus musculus 47-50 15254665-13 2004 In the group treated with a combination of TAM and 5-FU all analyzed cases showed the presence of p65 gene expression. Fluorouracil 51-55 v-rel reticuloendotheliosis viral oncogene homolog A (avian) Mus musculus 98-101 15254665-15 2004 Based on these findings we conclude that p65 gene expression in murine Colon 38 cancer tissues can be modulated via chemotherapy (5-FU) and also via hormonal modulation (TAM and LAN). Fluorouracil 130-134 v-rel reticuloendotheliosis viral oncogene homolog A (avian) Mus musculus 41-44 14654475-6 2003 As for IFN-alpha, synergistic effects were observed when combined with 5-FU and DOX on PLC/PRF/5 cells only, whereas IFN-beta showed synergistic effects with 5-FU and CDDP on HuH7 and PLC/PRF/5 cell lines. Fluorouracil 71-75 heparan sulfate proteoglycan 2 Homo sapiens 87-90 14751837-6 2003 The antisense oligonucleotides also potentiated the effects of p53 activation and p21 induction by chemotherapeutic agents 10-hydroxycamptothecin, adriamycin, 5-fluorouracil, and paclitaxel. Fluorouracil 159-173 H3 histone pseudogene 16 Homo sapiens 82-85 14612954-1 2003 Thymidylate synthase (TS) and dihydropyrimidine dehydrogenase (DPD) has been suggested to be sensitivity-limiting factors of 5-fluorouracil therapy in cancer patients. Fluorouracil 125-139 thymidylate synthetase Homo sapiens 0-20 14672398-0 2003 E2F1 expression is related with the poor survival of lymph node-positive breast cancer patients treated with fluorouracil, doxorubicin and cyclophosphamide. Fluorouracil 109-121 E2F transcription factor 1 Homo sapiens 0-4 14641346-1 2003 BACKGROUND: 5-Fluorouracil (5-FU) has been used topically and intralesionally to treat lesions related to squamous cell carcinoma (SCC) such as actinic keratosis, Bowen"s disease, and keratoacanthoma. Fluorouracil 12-26 serpin family B member 3 Homo sapiens 131-134 14641346-1 2003 BACKGROUND: 5-Fluorouracil (5-FU) has been used topically and intralesionally to treat lesions related to squamous cell carcinoma (SCC) such as actinic keratosis, Bowen"s disease, and keratoacanthoma. Fluorouracil 28-32 serpin family B member 3 Homo sapiens 131-134 14641346-2 2003 OBJECTIVE: We sought to determine whether intralesional 5-FU might be effective in treating a patient with SCC. Fluorouracil 56-60 serpin family B member 3 Homo sapiens 107-110 14641346-3 2003 METHODS: A patient with SCC at the junction of the right alar crease and right nasolabial fold was treated with eight weekly injections of 5-FU, with doses ranging from 0.8 to 2.4 mL. Fluorouracil 139-143 serpin family B member 3 Homo sapiens 24-27 14562021-1 2003 Activation of 5-fluorouracil into its nucleotides requires phosphorylation by three pathways involving orotate phosphoribosyl-transferase (OPRT), uridine phosphorylase (UP), or thymidine phosphorylase (TP). Fluorouracil 14-28 uridine monophosphate synthetase Homo sapiens 103-137 14562021-1 2003 Activation of 5-fluorouracil into its nucleotides requires phosphorylation by three pathways involving orotate phosphoribosyl-transferase (OPRT), uridine phosphorylase (UP), or thymidine phosphorylase (TP). Fluorouracil 14-28 uridine monophosphate synthetase Homo sapiens 139-143 14632965-1 2003 Various studies suggested that cytotoxicity induced by 5-fluorouracil (5-FU) is an apoptotic mechanism possibly mediated by the Fas/FasL system. Fluorouracil 55-69 Fas ligand Homo sapiens 132-136 14632965-1 2003 Various studies suggested that cytotoxicity induced by 5-fluorouracil (5-FU) is an apoptotic mechanism possibly mediated by the Fas/FasL system. Fluorouracil 71-75 Fas ligand Homo sapiens 132-136 14519641-10 2003 This difference in survival among patients with low- and high-TS-expressing tumors became more significant when the analysis was restricted to the 73 patients receiving 5-FU-based adjuvant therapy (RR = 0.37; 95% CI = 0.16-0.86; P = 0.0006). Fluorouracil 169-173 thymidylate synthetase Homo sapiens 62-64 14522928-1 2003 The variable number of tandem repeat (VNTR) of thymidylate synthase (TS) gene, mainly 2 repeat (2R) and 3 repeat (3R), is one of the genetic variations that can potentially predict the effectiveness of 5-fluorouracil-based chemotherapy. Fluorouracil 202-216 thymidylate synthetase Homo sapiens 47-67 14522928-1 2003 The variable number of tandem repeat (VNTR) of thymidylate synthase (TS) gene, mainly 2 repeat (2R) and 3 repeat (3R), is one of the genetic variations that can potentially predict the effectiveness of 5-fluorouracil-based chemotherapy. Fluorouracil 202-216 thymidylate synthetase Homo sapiens 69-71 14522928-12 2003 These results suggest that the double polymorphism in the TS tandem repeat sequence, the SNP and the VNTR, may provide a potential for more effective prediction of the clinical outcome of 5-fluorouracil-based chemotherapy. Fluorouracil 188-202 thymidylate synthetase Homo sapiens 58-60 12907638-7 2003 The 5-FU-induced activation of MAT-8, thymosin-beta-10, and chaperonin-10 was abrogated by inactivation of p53 in MCF-7 cells, whereas induction of SSAT and annexin II was significantly reduced in the absence of p53. Fluorouracil 4-8 thymosin beta 10 Homo sapiens 38-54 12907638-7 2003 The 5-FU-induced activation of MAT-8, thymosin-beta-10, and chaperonin-10 was abrogated by inactivation of p53 in MCF-7 cells, whereas induction of SSAT and annexin II was significantly reduced in the absence of p53. Fluorouracil 4-8 annexin A2 Homo sapiens 157-167 12739060-10 2003 In a biopsy of an esophageal adenocarcinoma metastasis that had regressed, thymidylate synthase, the target of 5-FU, was inhibited 50%, but increased four- to tenfold after relapse in subsequent biopsies. Fluorouracil 111-115 thymidylate synthetase Homo sapiens 75-95 12842708-11 2003 bcl-2 overexpression also prevents the dramatic changes in HSC following 5-FU treatment (downregulation of c-kit, upregulation of Lin, less efficient long-term reconstitution). Fluorouracil 73-77 KIT proto-oncogene receptor tyrosine kinase Mus musculus 107-112 12802789-1 2003 Thymidylate synthase (TS) is a chemotherapeutic target for the fluoropyrimidine 5-fluorouracil (5-FU) and antifolate tomudex (TDX). Fluorouracil 96-100 thymidylate synthetase Homo sapiens 0-20 12684658-2 2003 Overexpression of TS has been correlated to 5-fluorouracil (5FU)-resistance. Fluorouracil 44-58 thymidylate synthetase Homo sapiens 18-20 12684658-2 2003 Overexpression of TS has been correlated to 5-fluorouracil (5FU)-resistance. Fluorouracil 60-63 thymidylate synthetase Homo sapiens 18-20 12870370-0 2003 Intratumoural thymidylate synthase and dihydropyrimidine dehydrogenase activities are good predictors of 5-fluorouracil sensitivity in colorectal cancer. Fluorouracil 105-119 thymidylate synthetase Homo sapiens 14-34 12870370-3 2003 The activities of TS and DPD were significantly lower in the tumours sensitive to 5-FU compared with those that were not sensitive to 5-FU. Fluorouracil 82-86 thymidylate synthetase Homo sapiens 18-20 12870370-3 2003 The activities of TS and DPD were significantly lower in the tumours sensitive to 5-FU compared with those that were not sensitive to 5-FU. Fluorouracil 134-138 thymidylate synthetase Homo sapiens 18-20 12870370-6 2003 Tumour sensitivity to 5-FU can be more precisely predicted by taking the activities of both TS and DPD into consideration than by using either alone. Fluorouracil 22-26 thymidylate synthetase Homo sapiens 92-94 12717833-8 2003 Expression levels of c-jun and p53 were found to be elevated for the tumors from mice treated with nimesulide and 5-FU comparing to those with either of them, but a reduced PGE(2) level was observed only for the treatment with nimesulide. Fluorouracil 114-118 transformation related protein 53, pseudogene Mus musculus 31-34 12703987-1 2003 BACKGROUND & OBJECTIVE: The aim of this study was to investigate the influence of low dosage (131)I-labeled anti-carcinoembryonic antigen (CEA) monoclonal antibody C50 ((131)I-C50) on tumor growth and the therapeutic efficacy of combination of low dosage (131)I-C50 with chemotherapy using 5-fluorouracil (5-FU) on human colorectal cancer xenografts in nude mice. Fluorouracil 294-308 CEA cell adhesion molecule 5 Homo sapiens 143-146 12703987-1 2003 BACKGROUND & OBJECTIVE: The aim of this study was to investigate the influence of low dosage (131)I-labeled anti-carcinoembryonic antigen (CEA) monoclonal antibody C50 ((131)I-C50) on tumor growth and the therapeutic efficacy of combination of low dosage (131)I-C50 with chemotherapy using 5-fluorouracil (5-FU) on human colorectal cancer xenografts in nude mice. Fluorouracil 310-314 CEA cell adhesion molecule 5 Homo sapiens 143-146 12649104-2 2003 Phase II trials have shown that gemcitabine can be successfully combined with thymidylate synthase (TS) inhibitors such as continuous-infusion 5-fluorouracil (5-FU). Fluorouracil 143-157 thymidylate synthetase Homo sapiens 78-98 12649104-2 2003 Phase II trials have shown that gemcitabine can be successfully combined with thymidylate synthase (TS) inhibitors such as continuous-infusion 5-fluorouracil (5-FU). Fluorouracil 143-157 thymidylate synthetase Homo sapiens 100-102 12649104-2 2003 Phase II trials have shown that gemcitabine can be successfully combined with thymidylate synthase (TS) inhibitors such as continuous-infusion 5-fluorouracil (5-FU). Fluorouracil 159-163 thymidylate synthetase Homo sapiens 78-98 12649104-2 2003 Phase II trials have shown that gemcitabine can be successfully combined with thymidylate synthase (TS) inhibitors such as continuous-infusion 5-fluorouracil (5-FU). Fluorouracil 159-163 thymidylate synthetase Homo sapiens 100-102 12684419-2 2003 5-FU inhibits thymidylate synthase (TS) and blocks DNA synthesis. Fluorouracil 0-4 thymidylate synthetase Homo sapiens 14-34 12684419-2 2003 5-FU inhibits thymidylate synthase (TS) and blocks DNA synthesis. Fluorouracil 0-4 thymidylate synthetase Homo sapiens 36-38 12684419-5 2003 We investigated the activity of TS in 68 RCCs and the association with dihydropyrimidine dehydrogenase (DPD) activities, which is a principal enzyme in the degradation of 5-FU and pyrimidine nucleotides. Fluorouracil 171-175 thymidylate synthetase Homo sapiens 32-34 12684419-7 2003 EXPERIMENTAL DESIGN: The levels of TS and DPD activities in nonfixed fresh-frozen RCC and normal kidney were determined biochemically by the 5-fluoro-2"-deoxyuridine 5"-monophosphate binding assay and the 5-FU degradation assay, respectively. Fluorouracil 205-209 thymidylate synthetase Homo sapiens 35-37 12684419-17 2003 TS activity in primary cultured RCC cells was positively correlated with their sensitivity to 5-FU. Fluorouracil 94-98 thymidylate synthetase Homo sapiens 0-2 12684419-18 2003 Furthermore, RCC cells with both high TS activity and low DPD activity were more sensitive to 5-FU, compared with those with either low TS activity or high DPD activity. Fluorouracil 94-98 thymidylate synthetase Homo sapiens 38-40 12684419-19 2003 CONCLUSIONS: The present study is the first study to demonstrate that the level of TS activity was correlated with both the progression of the stage and the increase of the grade of RCC, and that higher TS activity in primary cultured RCC predicted higher sensitivity to 5-FU. Fluorouracil 271-275 thymidylate synthetase Homo sapiens 203-205 12684419-20 2003 These results suggest that high TS activity may be associated with malignant potential of RCC, and that it may be possible to use 5-FU for RCC with high TS activity. Fluorouracil 130-134 thymidylate synthetase Homo sapiens 153-155 12720098-0 2003 Relationships between the expression of thymidylate synthase, dihydropyrimidine dehydrogenase, and orotate phosphoribosyltransferase and cell proliferative activity and 5-fluorouracil sensitivity in colorectal carcinoma. Fluorouracil 169-183 thymidylate synthetase Homo sapiens 40-60 12720098-6 2003 Assays of thymidylate synthase (TS), dihydropyrimidine dehydrogenase (DPD), and orotate phosphoribosyltransferase (OPRT) activities in colorectal carcinoma tissue and assays of 5-FU sensitivity by the collagen gel droplet embedded culture drug sensitivity test (CD-DST) were conducted to investigate the relationships between each enzyme activity and 5-FU sensitivity. Fluorouracil 177-181 uridine monophosphate synthetase Homo sapiens 115-119 12720098-6 2003 Assays of thymidylate synthase (TS), dihydropyrimidine dehydrogenase (DPD), and orotate phosphoribosyltransferase (OPRT) activities in colorectal carcinoma tissue and assays of 5-FU sensitivity by the collagen gel droplet embedded culture drug sensitivity test (CD-DST) were conducted to investigate the relationships between each enzyme activity and 5-FU sensitivity. Fluorouracil 351-355 uridine monophosphate synthetase Homo sapiens 115-119 12720098-8 2003 RESULTS: 5-FU sensitivity was high in the low-TS-activity group and in the high-OPRT-activity group. Fluorouracil 9-13 thymidylate synthetase Homo sapiens 5-7 12720098-8 2003 RESULTS: 5-FU sensitivity was high in the low-TS-activity group and in the high-OPRT-activity group. Fluorouracil 9-13 uridine monophosphate synthetase Homo sapiens 80-84 12720098-10 2003 CONCLUSION: The results suggest that OPRT activity can predict sensitivity to 5-FU, and high OPRT activity may cause good 5-FU sensitivity in cancers with high cell proliferative activity. Fluorouracil 78-82 uridine monophosphate synthetase Homo sapiens 37-41 12720098-10 2003 CONCLUSION: The results suggest that OPRT activity can predict sensitivity to 5-FU, and high OPRT activity may cause good 5-FU sensitivity in cancers with high cell proliferative activity. Fluorouracil 122-126 uridine monophosphate synthetase Homo sapiens 93-97 12610179-1 2003 PURPOSE: The aim of this study was to investigate the utility of quantitating thymidylate synthase (TS) in the primary tumor as a surrogate for metastatic disease sites to predict the likelihood of response and outcome to fluorouracil (FU) treatment in patients with metastatic colorectal cancer. Fluorouracil 222-234 thymidylate synthetase Homo sapiens 78-98 12610179-1 2003 PURPOSE: The aim of this study was to investigate the utility of quantitating thymidylate synthase (TS) in the primary tumor as a surrogate for metastatic disease sites to predict the likelihood of response and outcome to fluorouracil (FU) treatment in patients with metastatic colorectal cancer. Fluorouracil 222-234 thymidylate synthetase Homo sapiens 100-102 12518324-7 2003 The antisense oligonucleotide also potentiated the effects of p53 activation and p21 induction by chemotherapeutic agents 10-hydroxycamptothecin, adriamycin, 5-fluorouracil, and paclitaxel. Fluorouracil 158-172 H3 histone pseudogene 16 Homo sapiens 81-84 12569298-2 2003 The cytotoxic activity of the metabolized 5-FU depends on thymidylate synthase (TS) inhibition, leading to defective DNA synthesis. Fluorouracil 42-46 thymidylate synthetase Homo sapiens 58-78 12527935-2 2003 The administered 5-FU is degraded mainly in the liver by dihydropyrimidine dehydrogenase (DPD), which is the initial rate-limiting enzyme in the catabolic pathway of pyrimidine. Fluorouracil 17-21 dihydropyrimidine dehydrogenase Mus musculus 57-88 12527935-2 2003 The administered 5-FU is degraded mainly in the liver by dihydropyrimidine dehydrogenase (DPD), which is the initial rate-limiting enzyme in the catabolic pathway of pyrimidine. Fluorouracil 17-21 dihydropyrimidine dehydrogenase Mus musculus 90-93 12557715-0 2003 [A case of advanced gastric adenocarcinoma with mild elevation of serum SCC that responded remarkably to adjuvant chemotherapy of ADM, CDDP, ETP and 5-FU (ACVF)]. Fluorouracil 149-153 serpin family B member 3 Homo sapiens 72-75 12451472-1 2002 PURPOSE: Combinations of vinorelbine (VRB) and drugs targeting thymidylate synthase (TS) such as 5-fluorouracil (5-FU) have proven clinical efficacy in the management of advanced breast cancer. Fluorouracil 97-111 thymidylate synthetase Homo sapiens 63-83 12451472-1 2002 PURPOSE: Combinations of vinorelbine (VRB) and drugs targeting thymidylate synthase (TS) such as 5-fluorouracil (5-FU) have proven clinical efficacy in the management of advanced breast cancer. Fluorouracil 113-117 thymidylate synthetase Homo sapiens 63-83 12437479-3 2002 There is compelling evidence that TS gene transcripts and TS polymorphisms could be used to decide which patients can best benefit from adjuvant chemotherapy approaches, especially in colorectal cancer, and not less importantly, to tailor chemotherapy in metastatic NSCLC when using drugs akin to fluorouracil, such as pemetrexed. Fluorouracil 297-309 thymidylate synthetase Homo sapiens 34-36 12487851-1 2002 OBJECTIVE: To study target killing of 5-FU drug-fast cancer cells with thymidylate synthase (TS) and p16 gene promoters inducting TK gene expression. Fluorouracil 38-42 thymidylate synthetase Homo sapiens 71-91 12530000-1 2002 Thymidylate synthase (TS) is a target enzyme of 5-fluorouracil (5-FU). Fluorouracil 48-62 thymidylate synthetase Homo sapiens 22-24 12530000-1 2002 Thymidylate synthase (TS) is a target enzyme of 5-fluorouracil (5-FU). Fluorouracil 64-68 thymidylate synthetase Homo sapiens 0-20 12530000-1 2002 Thymidylate synthase (TS) is a target enzyme of 5-fluorouracil (5-FU). Fluorouracil 64-68 thymidylate synthetase Homo sapiens 22-24 12530000-3 2002 TS polymorphism has been reported to link with the efficacy of 5-FU-based chemotherapy in colorectal cancer. Fluorouracil 63-67 thymidylate synthetase Homo sapiens 0-2 12530000-12 2002 These results warrant further large-scale clinical study of the role of the TS genotyping for the prediction of efficacy using 5-FU-based chemotherapy and prognosis in gastric cancer. Fluorouracil 127-131 thymidylate synthetase Homo sapiens 76-78 12703544-13 2002 The antitumor effect of 5FU is enhanced by augmenting 5-fluorodeoxyuridine monophosphate (FdUMP) converted from FUMP, which inhibits Thymidylate Synthetase (TS). Fluorouracil 24-27 thymidylate synthetase Homo sapiens 133-155 12102601-2 2002 As a consequence, TS is a target for anticancer chemotherapy by several drugs, including 5-fluorouracil (5-FU) and raltitrexed (Tomudex), in treatment of colorectal and other tumors. Fluorouracil 89-103 thymidylate synthetase Homo sapiens 18-20 12102601-2 2002 As a consequence, TS is a target for anticancer chemotherapy by several drugs, including 5-fluorouracil (5-FU) and raltitrexed (Tomudex), in treatment of colorectal and other tumors. Fluorouracil 105-109 thymidylate synthetase Homo sapiens 18-20 12102601-7 2002 These studies have revealed that targeting the 3" end of human TS mRNA downregulates TS mRNA and protein, inhibits cell proliferation, and sensitizes HeLa cells to raltitrexed, 5-FU, and 5-fluorodeoxyuridine (5-FUdR) in vitro (Ferguson et al., Br. Fluorouracil 177-181 thymidylate synthetase Homo sapiens 63-65 12084458-14 2002 We have also generated mutants of both DHFR and TS that confer resistance to MTX as well as 5-FU by random as well as site-directed mutagenesis. Fluorouracil 92-96 thymidylate synthetase Homo sapiens 48-50 12084461-0 2002 Induction of thymidylate synthase as a 5-fluorouracil resistance mechanism. Fluorouracil 39-53 thymidylate synthetase Homo sapiens 13-33 12084461-2 2002 TS is an important target for chemotherapy; it is inhibited by folate and nucleotide analogs, such as by 5-fluoro-dUMP (FdUMP), the active metabolite of 5-fluorouracil (5FU). Fluorouracil 153-167 thymidylate synthetase Homo sapiens 0-2 12084461-2 2002 TS is an important target for chemotherapy; it is inhibited by folate and nucleotide analogs, such as by 5-fluoro-dUMP (FdUMP), the active metabolite of 5-fluorouracil (5FU). Fluorouracil 169-172 thymidylate synthetase Homo sapiens 0-2 12084461-13 2002 Treatment with 5FU or RTX rapidly induced TS levels two- to five-fold. Fluorouracil 15-18 thymidylate synthetase Homo sapiens 42-44 12072547-4 2002 In a retrospective study, we investigated associations between common polymorphisms in genes for several GST subclasses (GSTP1, GSTT1, GSTM1) and survival of patients with metastatic colorectal cancer receiving 5-fluorouracil (5-FU)/oxaliplatin chemotherapy. Fluorouracil 211-225 glutathione S-transferase kappa 1 Homo sapiens 105-108 12072547-4 2002 In a retrospective study, we investigated associations between common polymorphisms in genes for several GST subclasses (GSTP1, GSTT1, GSTM1) and survival of patients with metastatic colorectal cancer receiving 5-fluorouracil (5-FU)/oxaliplatin chemotherapy. Fluorouracil 211-225 glutathione S-transferase pi 1 Homo sapiens 121-126 12072547-4 2002 In a retrospective study, we investigated associations between common polymorphisms in genes for several GST subclasses (GSTP1, GSTT1, GSTM1) and survival of patients with metastatic colorectal cancer receiving 5-fluorouracil (5-FU)/oxaliplatin chemotherapy. Fluorouracil 227-231 glutathione S-transferase kappa 1 Homo sapiens 105-108 12072547-13 2002 CONCLUSIONS: The GSTP1 Ile(105)Val polymorphism is associated in a dose-dependent fashion with increased survival of patients with advanced colorectal cancer receiving 5-FU/oxaliplatin chemotherapy. Fluorouracil 168-172 glutathione S-transferase pi 1 Homo sapiens 17-22 12123334-2 2002 Theoretically, this approach could be hazardous with infusional 5-fluorouracil (5-FU) chemotherapy, since G-CSF-stimulated neutrophil proliferation would be occurring in the face of continuous S-phase active 5-FU. Fluorouracil 64-78 colony stimulating factor 3 Homo sapiens 106-111 12123334-2 2002 Theoretically, this approach could be hazardous with infusional 5-fluorouracil (5-FU) chemotherapy, since G-CSF-stimulated neutrophil proliferation would be occurring in the face of continuous S-phase active 5-FU. Fluorouracil 80-84 colony stimulating factor 3 Homo sapiens 106-111 12022983-2 2002 High levels of thymidylate synthase (TS) and dihydropyrimidine dehydrogenase (DPD) have been associated with resistance to 5-FU in advanced colorectal cancer. Fluorouracil 123-127 thymidylate synthetase Homo sapiens 15-35 12022983-2 2002 High levels of thymidylate synthase (TS) and dihydropyrimidine dehydrogenase (DPD) have been associated with resistance to 5-FU in advanced colorectal cancer. Fluorouracil 123-127 thymidylate synthetase Homo sapiens 37-39 12022983-3 2002 The aim of this study was to investigate the association of TS and DPD mRNA levels with recurrence-free survival in patients with colorectal cancer who are receiving adjuvant 5-FU-based chemotherapy. Fluorouracil 175-179 thymidylate synthetase Homo sapiens 60-62 12022983-8 2002 The TS mRNA level may be a useful marker to predict the time to recurrence in patients with colorectal cancer who are receiving adjuvant 5-FU treatment. Fluorouracil 137-141 thymidylate synthetase Homo sapiens 4-6 11953901-0 2002 Thymidylate synthase polymorphism and survival of colorectal cancer patients treated with 5-fluorouracil. Fluorouracil 90-104 thymidylate synthetase Homo sapiens 0-20 11841993-7 2002 To corroborate the findings in transgenic mice, ICR mice were treated with exogenous EGF after receiving fluorouracil. Fluorouracil 105-117 epidermal growth factor Mus musculus 85-88 11734334-3 2002 Exposure to 5-FU also reduced the level of the anti-apoptotic protein, protein kinase B, in the MDR cells, but not in the control cells. Fluorouracil 12-16 protein tyrosine kinase 2 beta Homo sapiens 71-87 12017314-6 2002 Furthermore, neoadjuvant chemotherapy using the 5-fluorouracil derivative UFT demonstrates a stronger suppression of increased activities of thymidylate synthase in the tumorous tissues than in the non-tumorous mucosa. Fluorouracil 48-62 thymidylate synthetase Homo sapiens 141-161 12018454-1 2002 Thymidylate synthase is a target enzyme for chemotherapeutic agents such as 5-fluorouracil and capecitabine, its oral prodrug. Fluorouracil 76-90 thymidylate synthetase Homo sapiens 0-20 11754376-9 2002 TE-9 cells exposed to 5-FU showed a diminished telomerase activity preceded by a time-dependent decrease in the mRNA expression of hTERT. Fluorouracil 22-26 telomerase reverse transcriptase Homo sapiens 131-136 12138244-7 2002 RNase protection assay showed a negative correlation between bcl-x(L) and mcl-1 mRNA expression levels and the sensitivity to 5-FU and gemcitabine after 5-FU and gemcitabine treatment. Fluorouracil 126-130 MCL1 apoptosis regulator, BCL2 family member Homo sapiens 74-79 12138244-7 2002 RNase protection assay showed a negative correlation between bcl-x(L) and mcl-1 mRNA expression levels and the sensitivity to 5-FU and gemcitabine after 5-FU and gemcitabine treatment. Fluorouracil 153-157 MCL1 apoptosis regulator, BCL2 family member Homo sapiens 74-79 12138244-10 2002 The bax/bcl-2 ratio is predictive of chemotherapy sensitivity, whereas bcl-x(L) and mcl-1 mRNA levels following repeated exposure to 5-FU or gemcitabine are associated with resistance to these drugs. Fluorouracil 133-137 MCL1 apoptosis regulator, BCL2 family member Homo sapiens 84-89 11751507-1 2001 PURPOSE: Thymidylate synthase (TS) is a target enzyme of 5-fluorouracil. Fluorouracil 57-71 thymidylate synthetase Homo sapiens 9-29 11751507-1 2001 PURPOSE: Thymidylate synthase (TS) is a target enzyme of 5-fluorouracil. Fluorouracil 57-71 thymidylate synthetase Homo sapiens 31-33 11751507-11 2001 The results provide the rationale for comprehensive usage of TS genotyping with quantitation of TS mRNA or TS protein to predict the patient"s response to 5-fluorouracil-based chemotherapy. Fluorouracil 155-169 thymidylate synthetase Homo sapiens 61-63 11751507-11 2001 The results provide the rationale for comprehensive usage of TS genotyping with quantitation of TS mRNA or TS protein to predict the patient"s response to 5-fluorouracil-based chemotherapy. Fluorouracil 155-169 thymidylate synthetase Homo sapiens 96-98 11751507-11 2001 The results provide the rationale for comprehensive usage of TS genotyping with quantitation of TS mRNA or TS protein to predict the patient"s response to 5-fluorouracil-based chemotherapy. Fluorouracil 155-169 thymidylate synthetase Homo sapiens 96-98 11705873-1 2001 Thymidylate synthase (TS) is responsible for the de novo synthesis of thymidylate, which is required for DNA synthesis and repair and which is an important target for fluoropyrimidines such as 5-fluorouracil (5-FU), and antifolates such as Tomudex (TDX), ZD9331, and multitargeted antifolate (MTA). Fluorouracil 193-207 thymidylate synthetase Homo sapiens 0-20 11705873-1 2001 Thymidylate synthase (TS) is responsible for the de novo synthesis of thymidylate, which is required for DNA synthesis and repair and which is an important target for fluoropyrimidines such as 5-fluorouracil (5-FU), and antifolates such as Tomudex (TDX), ZD9331, and multitargeted antifolate (MTA). Fluorouracil 193-207 thymidylate synthetase Homo sapiens 22-24 11705873-1 2001 Thymidylate synthase (TS) is responsible for the de novo synthesis of thymidylate, which is required for DNA synthesis and repair and which is an important target for fluoropyrimidines such as 5-fluorouracil (5-FU), and antifolates such as Tomudex (TDX), ZD9331, and multitargeted antifolate (MTA). Fluorouracil 209-213 thymidylate synthetase Homo sapiens 0-20 11705873-1 2001 Thymidylate synthase (TS) is responsible for the de novo synthesis of thymidylate, which is required for DNA synthesis and repair and which is an important target for fluoropyrimidines such as 5-fluorouracil (5-FU), and antifolates such as Tomudex (TDX), ZD9331, and multitargeted antifolate (MTA). Fluorouracil 209-213 thymidylate synthetase Homo sapiens 22-24 11791891-4 2001 METHODS: The inhibitory effect of 5-FU on MPO was studied in rat tissue, human leukocytes, and leukocytes from cancer patients under 5-FU therapy. Fluorouracil 34-38 myeloperoxidase Rattus norvegicus 42-45 11878102-1 2001 A prospective study was done to test the efficacy of 5-fluorouracil (topical and systemic) in multiple and unresectable histologically proven facial squamous cell carcinomas (SCC) secondary to XP. Fluorouracil 53-67 serpin family B member 3 Homo sapiens 175-178 11878102-11 2001 Despite a dissociation between a good cosmetic result and a relatively superficial effect, topical 5-FU represents a useful therapeutic option in multiple unresectable facial SCC in patients with XP. Fluorouracil 99-103 serpin family B member 3 Homo sapiens 175-178 11760216-2 2001 Over-expression or mutation of thymidylate synthase (TS), the target enzyme of the 5-FU metabolite, 5-fluorodeoxyuridine monophosphate, is strictly correlated with cancer cell resistance to 5-FU. Fluorouracil 83-87 thymidylate synthetase Homo sapiens 31-51 11760216-2 2001 Over-expression or mutation of thymidylate synthase (TS), the target enzyme of the 5-FU metabolite, 5-fluorodeoxyuridine monophosphate, is strictly correlated with cancer cell resistance to 5-FU. Fluorouracil 83-87 thymidylate synthetase Homo sapiens 53-55 11760216-2 2001 Over-expression or mutation of thymidylate synthase (TS), the target enzyme of the 5-FU metabolite, 5-fluorodeoxyuridine monophosphate, is strictly correlated with cancer cell resistance to 5-FU. Fluorouracil 190-194 thymidylate synthetase Homo sapiens 31-51 11760216-2 2001 Over-expression or mutation of thymidylate synthase (TS), the target enzyme of the 5-FU metabolite, 5-fluorodeoxyuridine monophosphate, is strictly correlated with cancer cell resistance to 5-FU. Fluorouracil 190-194 thymidylate synthetase Homo sapiens 53-55 11760216-3 2001 On this basis we investigated whether TS is a potential target for active specific immunotherapy of human colon carcinoma, which acquires resistance to 5-FU. Fluorouracil 152-156 thymidylate synthetase Homo sapiens 38-40 11760216-6 2001 Specific CTL lines showed HLA-A2.1-restricted cytotoxicity in vitro to HLA-A2.1+ target cells pulsed with the specific TS peptide and to HLA-class I matching colon carcinoma target cells over-expressing TS enzyme after exposure to 5-FU. Fluorouracil 231-235 thymidylate synthetase Homo sapiens 119-121 11760216-7 2001 Recognition by CTL lines suggests that these TS peptides may be potential candidates for use in a peptide-based vaccine against 5-FU resistant colon carcinoma. Fluorouracil 128-132 thymidylate synthetase Homo sapiens 45-47 11527696-0 2001 Thymidylate synthase (TS) and ribonucleotide reductase (RNR) may be involved in acquired resistance to 5-fluorouracil (5-FU) in human cancer xenografts in vivo. Fluorouracil 103-117 thymidylate synthetase Homo sapiens 0-20 11527696-0 2001 Thymidylate synthase (TS) and ribonucleotide reductase (RNR) may be involved in acquired resistance to 5-fluorouracil (5-FU) in human cancer xenografts in vivo. Fluorouracil 103-117 thymidylate synthetase Homo sapiens 22-24 11527696-0 2001 Thymidylate synthase (TS) and ribonucleotide reductase (RNR) may be involved in acquired resistance to 5-fluorouracil (5-FU) in human cancer xenografts in vivo. Fluorouracil 119-123 thymidylate synthetase Homo sapiens 0-20 11527696-0 2001 Thymidylate synthase (TS) and ribonucleotide reductase (RNR) may be involved in acquired resistance to 5-fluorouracil (5-FU) in human cancer xenografts in vivo. Fluorouracil 119-123 thymidylate synthetase Homo sapiens 22-24 11527696-4 2001 A 2- to 3-fold increase in thymidylate synthase (TS) activity and 4- to 5-fold decrease in ribonucleotide reductase (RNR) activity were observed in 5-FU-resistant KM12C tumours, while the activities of orotate phosphoribosyltransferase (OPRT) thymidine and uridine phosphorylases (TP,UP) and thymidine kinase (TK) were not markedly changed as a consequence of repeated treatment of KM12C tumours with 5-FU. Fluorouracil 148-152 thymidylate synthetase Homo sapiens 27-47 11527696-4 2001 A 2- to 3-fold increase in thymidylate synthase (TS) activity and 4- to 5-fold decrease in ribonucleotide reductase (RNR) activity were observed in 5-FU-resistant KM12C tumours, while the activities of orotate phosphoribosyltransferase (OPRT) thymidine and uridine phosphorylases (TP,UP) and thymidine kinase (TK) were not markedly changed as a consequence of repeated treatment of KM12C tumours with 5-FU. Fluorouracil 148-152 thymidylate synthetase Homo sapiens 49-51 11527696-4 2001 A 2- to 3-fold increase in thymidylate synthase (TS) activity and 4- to 5-fold decrease in ribonucleotide reductase (RNR) activity were observed in 5-FU-resistant KM12C tumours, while the activities of orotate phosphoribosyltransferase (OPRT) thymidine and uridine phosphorylases (TP,UP) and thymidine kinase (TK) were not markedly changed as a consequence of repeated treatment of KM12C tumours with 5-FU. Fluorouracil 148-152 uridine monophosphate synthetase Homo sapiens 202-235 11527696-4 2001 A 2- to 3-fold increase in thymidylate synthase (TS) activity and 4- to 5-fold decrease in ribonucleotide reductase (RNR) activity were observed in 5-FU-resistant KM12C tumours, while the activities of orotate phosphoribosyltransferase (OPRT) thymidine and uridine phosphorylases (TP,UP) and thymidine kinase (TK) were not markedly changed as a consequence of repeated treatment of KM12C tumours with 5-FU. Fluorouracil 148-152 uridine monophosphate synthetase Homo sapiens 237-241 11527696-5 2001 The expression of TS mRNA was also amplified in accordance with the increased TS activity in a 5-FU-treated tumour sub-line (KM12C/5-FU) compared with that in parental tumours, but changed expressions of both RNR-R1 and RNA-R2 mRNA could not be detected in the 5-FU-resistant tumour sub-line compared with the parental tumours, suggesting possible post-transcriptional regulation of RNR. Fluorouracil 95-99 thymidylate synthetase Homo sapiens 18-20 11527696-5 2001 The expression of TS mRNA was also amplified in accordance with the increased TS activity in a 5-FU-treated tumour sub-line (KM12C/5-FU) compared with that in parental tumours, but changed expressions of both RNR-R1 and RNA-R2 mRNA could not be detected in the 5-FU-resistant tumour sub-line compared with the parental tumours, suggesting possible post-transcriptional regulation of RNR. Fluorouracil 131-135 thymidylate synthetase Homo sapiens 18-20 11527696-7 2001 From these results, it may be concluded that RNR activity is one of the acquired or inherent resistant factors, including TS, to 5-FU in human cancer xenografts in vivo. Fluorouracil 129-133 thymidylate synthetase Homo sapiens 122-124 11686531-1 2001 The enzyme thymidylate synthase (TS) is an important target of 5-fluorouracil (FUra) that is utilized for the treatment of disseminated colorectal cancer. Fluorouracil 63-77 thymidylate synthetase Homo sapiens 11-31 11686531-1 2001 The enzyme thymidylate synthase (TS) is an important target of 5-fluorouracil (FUra) that is utilized for the treatment of disseminated colorectal cancer. Fluorouracil 63-77 thymidylate synthetase Homo sapiens 33-35 11686531-1 2001 The enzyme thymidylate synthase (TS) is an important target of 5-fluorouracil (FUra) that is utilized for the treatment of disseminated colorectal cancer. Fluorouracil 79-83 thymidylate synthetase Homo sapiens 11-31 11686531-1 2001 The enzyme thymidylate synthase (TS) is an important target of 5-fluorouracil (FUra) that is utilized for the treatment of disseminated colorectal cancer. Fluorouracil 79-83 thymidylate synthetase Homo sapiens 33-35 11686531-2 2001 One determinant of clinical response to FUra-based therapy is TS expression. Fluorouracil 40-44 thymidylate synthetase Homo sapiens 62-64 11686531-8 2001 Two metastases with high TS expression were obtained from patients who received adjuvant therapy with FUra. Fluorouracil 102-106 thymidylate synthetase Homo sapiens 25-27 11511236-7 2001 Folate receptor alpha (FRalpha) mRNA was shown by RT-PCR to be overexpressed 26.3-fold in 5-FU-resistant H630-10 cells relative to H630 cells. Fluorouracil 90-94 folate receptor alpha Homo sapiens 0-21 11511236-7 2001 Folate receptor alpha (FRalpha) mRNA was shown by RT-PCR to be overexpressed 26.3-fold in 5-FU-resistant H630-10 cells relative to H630 cells. Fluorouracil 90-94 FOS like 1, AP-1 transcription factor subunit Homo sapiens 23-30 11505394-2 2001 5-FU inhibits thymidylate synthase (TS) and blocks DNA synthesis. Fluorouracil 0-4 thymidylate synthetase Homo sapiens 14-34 11505394-2 2001 5-FU inhibits thymidylate synthase (TS) and blocks DNA synthesis. Fluorouracil 0-4 thymidylate synthetase Homo sapiens 36-38 11406570-6 2001 Finally, the in vitro data predicted that only patients with both amplified c-myc and wild-type p53 in their primary tumors would be responsive to 5FU-based therapy, which was borne out by analysis of tumors from 135 patients entered into a Phase III clinical trial of 5FU-based adjuvant therapy. Fluorouracil 269-272 MYC proto-oncogene, bHLH transcription factor Homo sapiens 76-81 11442593-7 2001 RESULTS: We treated these five patients with a combination of a local immune therapy, imiquimod cream, and a topical chemotherapeutic agent, 5% 5-fluorouracil (5-FU), with clearing of the areas of SCC in situ. Fluorouracil 160-164 serpin family B member 3 Homo sapiens 197-200 11442593-9 2001 In addition, there is evidence that cytokines induced by imiquimod may improve the therapeutic efficacy of topical 5% 5-FU in the treatment of SCC in situ. Fluorouracil 118-122 serpin family B member 3 Homo sapiens 143-146 11353746-3 2001 Of 12 cDNA-expressed rat P450 enzymes tested, CYP1A2, CYP3A1, and CYP2C11 had high 5-FU formation rates from 100 microM and 1.0 mM tegafur concentrations. Fluorouracil 83-87 cytochrome P450, subfamily 2, polypeptide 11 Rattus norvegicus 66-73 11325838-1 2001 Plasma levels of folates and thymidine in mice are about 10-fold higher than in humans and may influence the therapeutic efficacy of thymidylate synthase (TS) inhibitors, such as 5-fluorouracil (5FU) and the antifolates pemetrexed (MTA) and raltitrexed (RTX). Fluorouracil 179-193 thymidylate synthetase Homo sapiens 133-153 11383215-5 2001 The coefficients of correlation of tumor sensitivity to 5-FU and OPRT activity were A: 0.8246, B: 0.7670, and C: 0.7856, and to DPD activity were A: 0.2525, B: 0.3928, and C: 0.4337, while the coefficients of correlation to TS enzyme levels were A: -0.5240, B: -0.4770, and C: -0.6131. Fluorouracil 56-60 uridine monophosphate synthetase Homo sapiens 65-69 11383215-6 2001 These findings demonstrate a high degree of correlation between OPRT activity at the tumor site and tumor sensitivity to 5-FU under a variety of conditions, suggesting that OPRT activity can be a useful indicator in predicting the anti-tumor effectiveness of 5-FU for a specific tumor. Fluorouracil 121-125 uridine monophosphate synthetase Homo sapiens 64-68 11383215-6 2001 These findings demonstrate a high degree of correlation between OPRT activity at the tumor site and tumor sensitivity to 5-FU under a variety of conditions, suggesting that OPRT activity can be a useful indicator in predicting the anti-tumor effectiveness of 5-FU for a specific tumor. Fluorouracil 121-125 uridine monophosphate synthetase Homo sapiens 173-177 11383215-6 2001 These findings demonstrate a high degree of correlation between OPRT activity at the tumor site and tumor sensitivity to 5-FU under a variety of conditions, suggesting that OPRT activity can be a useful indicator in predicting the anti-tumor effectiveness of 5-FU for a specific tumor. Fluorouracil 259-263 uridine monophosphate synthetase Homo sapiens 64-68 11383215-6 2001 These findings demonstrate a high degree of correlation between OPRT activity at the tumor site and tumor sensitivity to 5-FU under a variety of conditions, suggesting that OPRT activity can be a useful indicator in predicting the anti-tumor effectiveness of 5-FU for a specific tumor. Fluorouracil 259-263 uridine monophosphate synthetase Homo sapiens 173-177 11304774-1 2001 PURPOSE: To evaluate whether an accelerated-intensified cyclophosphamide, epirubicin, and fluorouracil (CEF) chemotherapy regimen with the support of granulocyte colony-stimulating factor (G-CSF) induces a higher activity and efficacy compared with standard CEF in metastatic breast cancer patients. Fluorouracil 90-102 colony stimulating factor 3 Homo sapiens 150-187 11283924-3 2001 Leucovorin (LV) is another biochemical modulator of 5-FU that potentiates inhibition of thymidylate synthase, the primary target of 5-FU. Fluorouracil 52-56 thymidylate synthetase Homo sapiens 88-108 11283924-3 2001 Leucovorin (LV) is another biochemical modulator of 5-FU that potentiates inhibition of thymidylate synthase, the primary target of 5-FU. Fluorouracil 132-136 thymidylate synthetase Homo sapiens 88-108 11320669-6 2001 However, (E)-5-(2)-(bromovinyl)uracil (BVU), a DPD inhibitor, significantly increased the half-life and area under the curve of 5-FU to 238.1% and 323.2%, respectively, of the control values. Fluorouracil 128-132 dihydropyrimidine dehydrogenase Rattus norvegicus 47-50 11221829-10 2001 Nuclear cyclin B1 expression was markedly induced with exposure to 100 ng/ml of 5-FU in SW480 and COLO320DM; and expression of 14-3-3sigma protein, a cell cycle inhibitor in the GG phase, was induced in SW480. Fluorouracil 80-84 cyclin B1 Homo sapiens 8-17 11161374-0 2001 Expression of thymidylate synthase in gastric cancer patients treated with 5-fluorouracil and doxorubicin-based adjuvant chemotherapy after curative resection. Fluorouracil 75-89 thymidylate synthetase Homo sapiens 14-34 11161374-2 2001 TS expression was evaluated by immunohistochemical staining using TS106 monoclonal antibody in 103 locally advanced gastric cancer patients (stage IB-IV) who underwent 5-fluorouracil (5-FU) and doxorubicin-based adjuvant chemotherapy after curative resection. Fluorouracil 168-182 thymidylate synthetase Homo sapiens 0-2 11161374-2 2001 TS expression was evaluated by immunohistochemical staining using TS106 monoclonal antibody in 103 locally advanced gastric cancer patients (stage IB-IV) who underwent 5-fluorouracil (5-FU) and doxorubicin-based adjuvant chemotherapy after curative resection. Fluorouracil 184-188 thymidylate synthetase Homo sapiens 0-2 11078920-4 2000 After 5-fluorouracil application for 4 days, HSP 27 and 70 expression was increased in HT29 colon tumours. Fluorouracil 6-20 heat shock protein family B (small) member 1 Homo sapiens 45-51 11076661-0 2000 Prolonged and enhanced suppression of thymidylate synthase by weekly 24-h infusion of high-dose 5-fluorouracil. Fluorouracil 96-110 thymidylate synthetase Homo sapiens 38-58 11142481-10 2000 CONCLUSIONS: Alternating, schedule-specific biochemical modulation of FU is more active than MTX --> 5-FU as first-line treatment of advanced colorectal cancer. Fluorouracil 104-108 metaxin 1 Homo sapiens 93-96 11205269-6 2000 Now we report on the use of RT-PCR techniques to see if that variant TS form could be present in human samples from patients who underwent surgery for primary colorectal cancer and been previously untreated and to try to find relationships between that hypothetical variant TS form and the 5-Fluorouracil treatment. Fluorouracil 290-304 thymidylate synthetase Homo sapiens 69-71 11205269-6 2000 Now we report on the use of RT-PCR techniques to see if that variant TS form could be present in human samples from patients who underwent surgery for primary colorectal cancer and been previously untreated and to try to find relationships between that hypothetical variant TS form and the 5-Fluorouracil treatment. Fluorouracil 290-304 thymidylate synthetase Homo sapiens 274-276 11054680-0 2000 Circadian organization of thymidylate synthase activity in normal tissues: a possible basis for 5-fluorouracil chronotherapeutic advantage. Fluorouracil 96-110 thymidylate synthetase Homo sapiens 26-46 11092985-6 2000 5-FU sensitivity of tumor cells increased in the presence of EGF or TGF-alpha. Fluorouracil 0-4 epidermal growth factor Homo sapiens 61-64 11092985-8 2000 The tumor environmental factors, EGF and TGF-alpha, may act as intrinsic regulators of DPD and PyNPase activities that affect the 5-FU sensitivity of individual tumors. Fluorouracil 130-134 epidermal growth factor Homo sapiens 33-36 11092986-0 2000 UCN-01 (7-hydroxystaurosporine) enhances 5-fluorouracil cytotoxicity through down-regulation of thymidylate synthetase messenger RNA. Fluorouracil 41-55 thymidylate synthetase Homo sapiens 96-118 11092986-5 2000 Although treatment with UCN-01 alone, 5-FU alone, and 5-FU/UCN-01 inhibited CRL 1420 growth in a concentration-dependent manner, treatment with UCN-01/5-FU inhibited the growth of CRL 1420 synergistically at less than 1 microg/ml drug concentration. Fluorouracil 38-42 interleukin 31 receptor A Homo sapiens 76-79 11092986-5 2000 Although treatment with UCN-01 alone, 5-FU alone, and 5-FU/UCN-01 inhibited CRL 1420 growth in a concentration-dependent manner, treatment with UCN-01/5-FU inhibited the growth of CRL 1420 synergistically at less than 1 microg/ml drug concentration. Fluorouracil 54-58 interleukin 31 receptor A Homo sapiens 76-79 11092986-5 2000 Although treatment with UCN-01 alone, 5-FU alone, and 5-FU/UCN-01 inhibited CRL 1420 growth in a concentration-dependent manner, treatment with UCN-01/5-FU inhibited the growth of CRL 1420 synergistically at less than 1 microg/ml drug concentration. Fluorouracil 54-58 interleukin 31 receptor A Homo sapiens 76-79 11092986-8 2000 The suppression of TS mRNA and TS activity by UCN-01 may lead to higher sensitivity of tumor cells to 5-FU and may explain the synergistic antitumor effect of UCN-01/5-FU. Fluorouracil 102-106 thymidylate synthetase Homo sapiens 19-21 11000583-3 2000 From analyses on the amount of 5-FU incorporated into cellular RNA and the activity of thymidylate synthase (TS), suppression of TS and depletion of dTTP, a possible consequence of the former, was considered to be the major action of 5-FU in these cells. Fluorouracil 234-238 thymidylate synthetase Homo sapiens 87-107 11057323-1 2000 We studied dihydropyrimidine dehydrogenase (DPD) and thymidylate synthase (TS), key enzymes in regulating the pharmacokinetics and chemosensitivity to 5-FU, in 36 breast cancer patients as a control group and 18 patients as a 5-FU group, in which 5-FU was given orally for 2 weeks before surgery at a dose of 200 mg/day. Fluorouracil 151-155 thymidylate synthetase Homo sapiens 53-73 10995874-2 2000 Many reports have demonstrated that thymidylate synthase (TS) and dihydropyrimidine dehydrogenase (DPD) are biomarkers for the response and prognosis of patients treated with 5-fluorouracil (5-FU)-based chemotherapy. Fluorouracil 175-189 thymidylate synthetase Homo sapiens 36-56 10995874-2 2000 Many reports have demonstrated that thymidylate synthase (TS) and dihydropyrimidine dehydrogenase (DPD) are biomarkers for the response and prognosis of patients treated with 5-fluorouracil (5-FU)-based chemotherapy. Fluorouracil 191-195 thymidylate synthetase Homo sapiens 36-56 11098484-3 2000 The more downstream events of 5-FU action and their implication in 5-FU resistance, with the possible involvement of the Fas/FasL system and the proteins associated with apoptosis regulation, are highlighted. Fluorouracil 30-34 Fas ligand Homo sapiens 125-129 10927027-10 2000 In addition, the increase in plasma uridine concentration induced by PSAU as well as the catabolism of FUra by the high dihydrouracil dehydrogenase activity in the liver also may have circumvented any residual FUra toxic effects against the host. Fluorouracil 103-107 dihydropyrimidine dehydrogenase Mus musculus 120-147 10927027-10 2000 In addition, the increase in plasma uridine concentration induced by PSAU as well as the catabolism of FUra by the high dihydrouracil dehydrogenase activity in the liver also may have circumvented any residual FUra toxic effects against the host. Fluorouracil 210-214 dihydropyrimidine dehydrogenase Mus musculus 120-147 10975677-6 2000 A combination of IL-2 gene therapy with 5-fluorouracil treatment increased the antitumoral efficacy and survival of mice bearing primary and metastatic Renca tumors (42% survival with IL-2:lipid compared with 94% survival with IL-2:lipid plus 5-fluorouracil). Fluorouracil 40-54 interleukin 2 Mus musculus 184-188 10975677-6 2000 A combination of IL-2 gene therapy with 5-fluorouracil treatment increased the antitumoral efficacy and survival of mice bearing primary and metastatic Renca tumors (42% survival with IL-2:lipid compared with 94% survival with IL-2:lipid plus 5-fluorouracil). Fluorouracil 40-54 interleukin 2 Mus musculus 184-188 10975677-6 2000 A combination of IL-2 gene therapy with 5-fluorouracil treatment increased the antitumoral efficacy and survival of mice bearing primary and metastatic Renca tumors (42% survival with IL-2:lipid compared with 94% survival with IL-2:lipid plus 5-fluorouracil). Fluorouracil 243-257 interleukin 2 Mus musculus 17-21 10891536-1 2000 5-Fluorouracil (5-FU), 5-fluoro-2"-deoxyuridine (FdUrd) and 5-trifluorothymidine (F3(d)Thd) are antimetabolites which are metabolized to their corresponding active forms which inhibit DNA synthesis via inhibition of thymidylate synthase (TS). Fluorouracil 0-14 thymidylate synthetase Homo sapiens 216-236 10891536-1 2000 5-Fluorouracil (5-FU), 5-fluoro-2"-deoxyuridine (FdUrd) and 5-trifluorothymidine (F3(d)Thd) are antimetabolites which are metabolized to their corresponding active forms which inhibit DNA synthesis via inhibition of thymidylate synthase (TS). Fluorouracil 0-14 thymidylate synthetase Homo sapiens 238-240 11038143-1 2000 PURPOSE: Resistance to 5-fluorouracil (5-FU) has been associated with thymidylate synthase (TS) gene amplification and increased TS protein levels. Fluorouracil 23-37 thymidylate synthetase Homo sapiens 70-90 11038143-1 2000 PURPOSE: Resistance to 5-fluorouracil (5-FU) has been associated with thymidylate synthase (TS) gene amplification and increased TS protein levels. Fluorouracil 23-37 thymidylate synthetase Homo sapiens 92-94 11038143-1 2000 PURPOSE: Resistance to 5-fluorouracil (5-FU) has been associated with thymidylate synthase (TS) gene amplification and increased TS protein levels. Fluorouracil 23-37 thymidylate synthetase Homo sapiens 129-131 11038143-1 2000 PURPOSE: Resistance to 5-fluorouracil (5-FU) has been associated with thymidylate synthase (TS) gene amplification and increased TS protein levels. Fluorouracil 39-43 thymidylate synthetase Homo sapiens 70-90 11038143-1 2000 PURPOSE: Resistance to 5-fluorouracil (5-FU) has been associated with thymidylate synthase (TS) gene amplification and increased TS protein levels. Fluorouracil 39-43 thymidylate synthetase Homo sapiens 92-94 11038143-1 2000 PURPOSE: Resistance to 5-fluorouracil (5-FU) has been associated with thymidylate synthase (TS) gene amplification and increased TS protein levels. Fluorouracil 39-43 thymidylate synthetase Homo sapiens 129-131 11038143-2 2000 Increased TS protein expression has also been found to be a significant independent prognostic factor for disease-free survival and overall survival in patients treated with adjuvant 5-FU-based chemotherapy. Fluorouracil 183-187 thymidylate synthetase Homo sapiens 10-12 11038143-5 2000 The influence of increased TS levels on cell cycle progression may provide insight into methods to overcome 5-FU resistance. Fluorouracil 108-112 thymidylate synthetase Homo sapiens 27-29 10914738-5 2000 IFN-alpha significantly enhanced the growth inhibitory effect of 5-FU in PLC/PRF/5 cells but not in HuH7 cells, and the isobolographic analysis indicated that this effect was synergistic. Fluorouracil 65-69 heparan sulfate proteoglycan 2 Homo sapiens 73-76 10914738-10 2000 Our results suggest that the synergistic effects of 5-FU and IFN-alpha may in part be attributable to alterations in cell cycle progression via up-regulation of p27Kip1. Fluorouracil 52-56 cyclin dependent kinase inhibitor 1B Homo sapiens 161-168 10853017-1 2000 5-fluorouracil (5-FU) has been used widely, including in gastrointestinal cancer, breast cancer, and non-small cell lung cancer (NSCLC), and its efficacy has been reported to be associated with intratumoral expression of thymidylate synthase (TS) and dihydropyrimidine dehydrogenase (DPD). Fluorouracil 0-14 thymidylate synthetase Homo sapiens 221-241 10853017-1 2000 5-fluorouracil (5-FU) has been used widely, including in gastrointestinal cancer, breast cancer, and non-small cell lung cancer (NSCLC), and its efficacy has been reported to be associated with intratumoral expression of thymidylate synthase (TS) and dihydropyrimidine dehydrogenase (DPD). Fluorouracil 0-14 thymidylate synthetase Homo sapiens 243-245 10853017-1 2000 5-fluorouracil (5-FU) has been used widely, including in gastrointestinal cancer, breast cancer, and non-small cell lung cancer (NSCLC), and its efficacy has been reported to be associated with intratumoral expression of thymidylate synthase (TS) and dihydropyrimidine dehydrogenase (DPD). Fluorouracil 16-20 thymidylate synthetase Homo sapiens 221-241 10853017-1 2000 5-fluorouracil (5-FU) has been used widely, including in gastrointestinal cancer, breast cancer, and non-small cell lung cancer (NSCLC), and its efficacy has been reported to be associated with intratumoral expression of thymidylate synthase (TS) and dihydropyrimidine dehydrogenase (DPD). Fluorouracil 16-20 thymidylate synthetase Homo sapiens 243-245 10853017-6 2000 The Cox regression analysis of prognostic variables for NSCLC patients treated with 5-FU demonstrated that the simultaneous evaluation for both TS and DPD expression was found to be a significant indicator of a poor prognosis (P=0.0043). Fluorouracil 84-88 thymidylate synthetase Homo sapiens 144-146 10853017-7 2000 Our results demonstrated that the evaluation of intratumoral TS and DPD activity can be used to accurately predict responsiveness to 5-FU-based chemotherapy in NSCLC patients. Fluorouracil 133-137 thymidylate synthetase Homo sapiens 61-63 11294501-5 2000 However, it exhibited comparable activities as IL-1alpha to down-regulate serum glucose and to improve the recovery of peripheral white blood cells from myelosuppression in 5-fluorouracil-treated mice. Fluorouracil 173-187 interleukin 1 alpha Mus musculus 47-56 10879745-0 2000 Over-expression of TSC-22 (TGF-beta stimulated clone-22) markedly enhances 5-fluorouracil-induced apoptosis in a human salivary gland cancer cell line. Fluorouracil 75-89 TSC22 domain family member 1 Homo sapiens 19-25 10879745-0 2000 Over-expression of TSC-22 (TGF-beta stimulated clone-22) markedly enhances 5-fluorouracil-induced apoptosis in a human salivary gland cancer cell line. Fluorouracil 75-89 TSC22 domain family member 1 Homo sapiens 27-55 10879745-7 2000 Furthermore, over-expression of the TSC-22-GFP fusion protein markedly enhanced 5-fluorouracil-induced apoptosis. Fluorouracil 80-94 TSC22 domain family member 1 Homo sapiens 36-42 10785598-0 2000 Molecular downstream events and induction of thymidylate synthase in mutant and wild-type p53 colon cancer cell lines after treatment with 5-fluorouracil and the thymidylate synthase inhibitor raltitrexed. Fluorouracil 139-153 thymidylate synthetase Homo sapiens 45-65 10744679-1 2000 Cell death due to thymine (dThd) deficiency, associated with the cytotoxic action of 5-fluorouracil in colon cancer, is regulated in thymidylate synthase-deficient (TS(-)) human colon carcinoma cells via the Fas (CD95, APO-1) death receptor. Fluorouracil 85-99 Fas cell surface death receptor Homo sapiens 213-217 10847455-2 2000 TS has been used as a target for cancer chemotherapy in the development of fluoropyrimidines such as 5-fluorouracil (5-FU) and 5-fluorodeoxyuridine and of novel folate-based TS inhibitors such as ZD1694 (Tomudex, Raltitrexed), ZD9331, LY231514 (ALIMTA, Pemetrexed), AG337 (Thymitaq, Nolatrexed) and AG331. Fluorouracil 101-115 thymidylate synthetase Homo sapiens 0-2 10847455-2 2000 TS has been used as a target for cancer chemotherapy in the development of fluoropyrimidines such as 5-fluorouracil (5-FU) and 5-fluorodeoxyuridine and of novel folate-based TS inhibitors such as ZD1694 (Tomudex, Raltitrexed), ZD9331, LY231514 (ALIMTA, Pemetrexed), AG337 (Thymitaq, Nolatrexed) and AG331. Fluorouracil 117-121 thymidylate synthetase Homo sapiens 0-2 10847455-8 2000 TS inhibition by either 5-FU or antifolates can also result in a depression of TS protein mediated inhibition of TS mRNA translation leading to induction of more TS protein synthesis, and p53 protein may further deregulate this process. Fluorouracil 24-28 thymidylate synthetase Homo sapiens 0-2 10847455-8 2000 TS inhibition by either 5-FU or antifolates can also result in a depression of TS protein mediated inhibition of TS mRNA translation leading to induction of more TS protein synthesis, and p53 protein may further deregulate this process. Fluorouracil 24-28 thymidylate synthetase Homo sapiens 79-81 10847455-8 2000 TS inhibition by either 5-FU or antifolates can also result in a depression of TS protein mediated inhibition of TS mRNA translation leading to induction of more TS protein synthesis, and p53 protein may further deregulate this process. Fluorouracil 24-28 thymidylate synthetase Homo sapiens 79-81 10847455-8 2000 TS inhibition by either 5-FU or antifolates can also result in a depression of TS protein mediated inhibition of TS mRNA translation leading to induction of more TS protein synthesis, and p53 protein may further deregulate this process. Fluorouracil 24-28 thymidylate synthetase Homo sapiens 79-81 10811483-1 2000 Uracil phosphoribosyltransferase (UPRT) of Escherichia coli origin can convert 5-fluorouracil (5-FU), a chemotherapeutic agent widely used for solid tumors, to an active intermediate, 5-fluorouridine-5"-monophosphate, as mammalian orotate phosphoribosyltransferase does. Fluorouracil 79-93 uracil phosphoribosyltransferase Mus musculus 34-38 10811483-1 2000 Uracil phosphoribosyltransferase (UPRT) of Escherichia coli origin can convert 5-fluorouracil (5-FU), a chemotherapeutic agent widely used for solid tumors, to an active intermediate, 5-fluorouridine-5"-monophosphate, as mammalian orotate phosphoribosyltransferase does. Fluorouracil 95-99 uracil phosphoribosyltransferase Mus musculus 34-38 10811483-2 2000 To examine whether the E. coli UPRT gene expressed in tumor cells can confer increased sensitivity to 5-FU, we retrovirally transduced Colon 26 cells, a murine colon carcinoma cell line, with the UPRT gene (Colon 26/UPRT cells) and tested the in vivo antitumoral effect of 5-FU in syngeneic immunocompetent mice. Fluorouracil 102-106 uracil phosphoribosyltransferase Mus musculus 31-35 10811483-3 2000 After 5-FU administration, tumors of Colon 26/UPRT cells regressed, whereas those of wild-type cells were unaffected. Fluorouracil 6-10 uracil phosphoribosyltransferase Mus musculus 46-50 10811483-7 2000 Therefore, expression of the UPRT gene in tumor cells followed by 5-FU administration is a possible strategy for cancer gene therapy, but potentiation of the bystander effect is required for its therapeutic application. Fluorouracil 66-70 uracil phosphoribosyltransferase Mus musculus 29-33 10778957-0 2000 Colorectal tumors responding to 5-fluorouracil have low gene expression levels of dihydropyrimidine dehydrogenase, thymidylate synthase, and thymidine phosphorylase. Fluorouracil 32-46 thymidylate synthetase Homo sapiens 115-135 10796062-5 2000 The most promising agents were further studied by assessment of their ability to modulate intracellular activation of FUra to enhance thymidylate synthase (TS) inhibition by FUra and to increase the subsequent induction of apoptosis. Fluorouracil 118-122 thymidylate synthetase Homo sapiens 134-154 10796062-5 2000 The most promising agents were further studied by assessment of their ability to modulate intracellular activation of FUra to enhance thymidylate synthase (TS) inhibition by FUra and to increase the subsequent induction of apoptosis. Fluorouracil 174-178 thymidylate synthetase Homo sapiens 134-154 10791219-7 2000 Both thymidylate synthase and thymidine kinase activities were significantly inhibited in tumor tissue when the combination of 5-fluorouracil and IL-2 was administered. Fluorouracil 127-141 thymidylate synthetase Homo sapiens 5-25 10791219-8 2000 CONCLUSIONS: IL-2 increases 5-fluorouracil cytotoxicity through the inhibition of thymidylate synthase/thymidine kinase activities in the hepatic arterial infusion. Fluorouracil 28-42 thymidylate synthetase Homo sapiens 82-102 10660804-1 2000 Thymidylate synthase (TS) is the target enzyme for 5-fluorouracil (5-FU). Fluorouracil 51-65 thymidylate synthetase Homo sapiens 0-20 10660804-1 2000 Thymidylate synthase (TS) is the target enzyme for 5-fluorouracil (5-FU). Fluorouracil 51-65 thymidylate synthetase Homo sapiens 22-24 10660804-1 2000 Thymidylate synthase (TS) is the target enzyme for 5-fluorouracil (5-FU). Fluorouracil 67-71 thymidylate synthetase Homo sapiens 0-20 10660804-1 2000 Thymidylate synthase (TS) is the target enzyme for 5-fluorouracil (5-FU). Fluorouracil 67-71 thymidylate synthetase Homo sapiens 22-24 10660804-2 2000 TS mRNA and protein levels in colorectal tumours are among the most important determinants for tumour response to 5-FU. Fluorouracil 114-118 thymidylate synthetase Homo sapiens 0-2 10660804-3 2000 TS mRNA levels in blood leukocytes may give information on pharmacokinetic and pharmacodynamic actions of 5-FU on TS as it has previously been shown that inhibition of TS levels by 5-FU in bone marrow leukocytes resembles the degree of TS inhibition in colorectal tumours. Fluorouracil 106-110 thymidylate synthetase Homo sapiens 0-2 10660804-3 2000 TS mRNA levels in blood leukocytes may give information on pharmacokinetic and pharmacodynamic actions of 5-FU on TS as it has previously been shown that inhibition of TS levels by 5-FU in bone marrow leukocytes resembles the degree of TS inhibition in colorectal tumours. Fluorouracil 106-110 thymidylate synthetase Homo sapiens 114-116 10660804-3 2000 TS mRNA levels in blood leukocytes may give information on pharmacokinetic and pharmacodynamic actions of 5-FU on TS as it has previously been shown that inhibition of TS levels by 5-FU in bone marrow leukocytes resembles the degree of TS inhibition in colorectal tumours. Fluorouracil 106-110 thymidylate synthetase Homo sapiens 114-116 10660804-3 2000 TS mRNA levels in blood leukocytes may give information on pharmacokinetic and pharmacodynamic actions of 5-FU on TS as it has previously been shown that inhibition of TS levels by 5-FU in bone marrow leukocytes resembles the degree of TS inhibition in colorectal tumours. Fluorouracil 106-110 thymidylate synthetase Homo sapiens 114-116 10660804-3 2000 TS mRNA levels in blood leukocytes may give information on pharmacokinetic and pharmacodynamic actions of 5-FU on TS as it has previously been shown that inhibition of TS levels by 5-FU in bone marrow leukocytes resembles the degree of TS inhibition in colorectal tumours. Fluorouracil 181-185 thymidylate synthetase Homo sapiens 0-2 10644554-12 2000 Nevertheless, p53 is an important determinant of the histopathological damage induced by 5-fluorouracil in murine intestinal epithelium. Fluorouracil 89-103 transformation related protein 53, pseudogene Mus musculus 14-17 10674003-6 1999 The differential responses to 5-FU alone were possibly determined by differences in substrate affinity and conversion rate of thymidylate synthase (K(m) of approximately 7.5, 5.0 and 2.5 microM and V0 of approximately 800, 200 and 2400 microM/h, respectively). Fluorouracil 30-34 thymidylate synthetase Homo sapiens 126-146 10766580-0 1999 [Dihydropyrimidine dehydrogenase and thymidylate synthase activities in colonic cancer tissue and sensitivity to 5-fluorouracil]. Fluorouracil 113-127 thymidylate synthetase Homo sapiens 37-57 10606255-2 1999 TS is the primary target of 5-fluorouracil (5-FU), which has been used for cancer treatment for more than 40 years. Fluorouracil 28-42 thymidylate synthetase Homo sapiens 0-2 10606255-2 1999 TS is the primary target of 5-fluorouracil (5-FU), which has been used for cancer treatment for more than 40 years. Fluorouracil 44-48 thymidylate synthetase Homo sapiens 0-2 10606259-4 1999 Second, IFN treatment leads to abrogation of an 5-FU-associated increase in the enzyme thymidylate synthase (TS), thus increasing tumor sensitivity to 5-FU. Fluorouracil 48-52 thymidylate synthetase Homo sapiens 87-107 10606259-4 1999 Second, IFN treatment leads to abrogation of an 5-FU-associated increase in the enzyme thymidylate synthase (TS), thus increasing tumor sensitivity to 5-FU. Fluorouracil 151-155 thymidylate synthetase Homo sapiens 87-107 10584579-6 1999 Thymidylate synthase (TS) and dihydropyrimidine dehydrogenase (DPD), which are enzymes in 5-FU metabolism, and the labeling index (ID) of DNA fragmentation in the tumor were estimated before and after UFT. Fluorouracil 90-94 thymidylate synthetase Homo sapiens 22-24 10622537-1 1999 5-Fluorouracil (5-FU) has been used worldwide, and the correlation between its effects and thymidylate synthase (TS) expression has been reported in gastrointestinal malignancy. Fluorouracil 0-14 thymidylate synthetase Homo sapiens 91-111 10622537-1 1999 5-Fluorouracil (5-FU) has been used worldwide, and the correlation between its effects and thymidylate synthase (TS) expression has been reported in gastrointestinal malignancy. Fluorouracil 16-20 thymidylate synthetase Homo sapiens 91-111 10564261-2 1999 In suspension cultures of lineage-negative (Lin(-)), 5-fluorouracil-resistant bone marrow cells of the transgenic mice, a combination of hGM-CSF and stem cell factor (SCF) induced exponential expansions of mixed colony-forming unit. Fluorouracil 53-67 colony stimulating factor 2 Homo sapiens 137-144 10564261-2 1999 In suspension cultures of lineage-negative (Lin(-)), 5-fluorouracil-resistant bone marrow cells of the transgenic mice, a combination of hGM-CSF and stem cell factor (SCF) induced exponential expansions of mixed colony-forming unit. Fluorouracil 53-67 kit ligand Mus musculus 149-165 10564261-2 1999 In suspension cultures of lineage-negative (Lin(-)), 5-fluorouracil-resistant bone marrow cells of the transgenic mice, a combination of hGM-CSF and stem cell factor (SCF) induced exponential expansions of mixed colony-forming unit. Fluorouracil 53-67 kit ligand Mus musculus 167-170 10473927-4 1999 Although the mechanism of the interaction is unclear, it has been postulated that 5-FU interferes with the synthesis of hepatic cytochrome P-450 2C9. Fluorouracil 82-86 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 128-148 10382961-6 1999 Despite surgery and adjuvant chemotherapy with 5-fluorouracil (5-FU) the patient died 1 year after the diagnosis of SCC. Fluorouracil 63-67 serpin family B member 3 Homo sapiens 116-119 10097740-3 1999 It has been determined that leucovorin (LV) potentiates the cytotoxic effect of 5-FU through prolonged inhibition of thymidylate synthase. Fluorouracil 80-84 thymidylate synthetase Homo sapiens 117-137 10051538-2 1999 The host-cell system used was phytohemagglutinin-stimulated peripheral blood mononuclear cells; dTMP and dTTP depletion were induced by single exposures to a low level of the thymidylate synthase inhibitor 5-fluorouracil (5-FU) or its deoxynucleoside, 2"-deoxy-5-fluorouridine. Fluorouracil 206-220 thymidylate synthetase Homo sapiens 175-195 10037193-8 1999 The cytotoxic activity of FUra/LV was inhibited by dThd in HT29 cells and also, in part, by NOK-1+NOK-2 MoAbs that prevent Fas/FasL interactions. Fluorouracil 26-30 Fas ligand Homo sapiens 127-131 10397478-9 1998 L-CAV-treated cells were also significantly more sensitive to cisplatin, 5-fluorouracil, mitoxantrone and bleomycin than were untreated controls. Fluorouracil 73-87 caveolin 2 Homo sapiens 2-5 9893640-7 1998 5-FU-induced alterations in rat liver DPD were also observed, with the lowest activity occurring 48 h after injection (50% of control activity; P = 0.009). Fluorouracil 0-4 dihydropyrimidine dehydrogenase Rattus norvegicus 38-41 9893640-10 1998 Thus, 5-FU demonstrates autoregulation of its metabolism through inhibition of DPD activity. Fluorouracil 6-10 dihydropyrimidine dehydrogenase Rattus norvegicus 79-82 9726090-3 1998 This trial demonstrated that intratumoral TS/beta-actin messenger RNA (mRNA) ratio can accurately predict which metastatic colorectal tumors will be resistant to a leucovorin-modulated 5-FU infusion and which have a high likelihood of responding to such a regimen. Fluorouracil 185-189 thymidylate synthetase Homo sapiens 42-44 9726090-4 1998 Results of other studies of adjuvant therapy in gastric cancer and colorectal cancer also indicated that TS expression within the tumor is predictive of response of 5-FU-based therapy. Fluorouracil 165-169 thymidylate synthetase Homo sapiens 105-107 9662268-6 1998 We evaluated 5-FU-treated human CD34+ PBSC proliferation in cultures with Epo, G-CSF, and IL-3, in the presence or absence of IL-12. Fluorouracil 13-17 colony stimulating factor 3 Homo sapiens 79-84 9662268-6 1998 We evaluated 5-FU-treated human CD34+ PBSC proliferation in cultures with Epo, G-CSF, and IL-3, in the presence or absence of IL-12. Fluorouracil 13-17 interleukin 3 Homo sapiens 90-94 9662268-8 1998 However, in cultures of 5-FU-treated human CD34+ cells, the most efficient combination was IL-3 + Epo + G-CSF + Accessory cells (CD34-). Fluorouracil 24-28 interleukin 3 Homo sapiens 91-95 9662268-8 1998 However, in cultures of 5-FU-treated human CD34+ cells, the most efficient combination was IL-3 + Epo + G-CSF + Accessory cells (CD34-). Fluorouracil 24-28 colony stimulating factor 3 Homo sapiens 104-109 9663808-7 1998 The combination of 5-fluorouracil plus folinic acid results in more efficient inhibition of thymidylate synthase, a finding which is now utilized routinely in the treatment of colorectal cancer. Fluorouracil 19-33 thymidylate synthetase Homo sapiens 92-112 9581837-3 1998 The present study demonstrates that adenovirus-mediated transduction of E. coli UPRT gene results in marked sensitization of colon, gastric, liver, and pancreas cancer cell lines to low concentration of 5-FU in vitro. Fluorouracil 203-207 uracil phosphoribosyltransferase Mus musculus 80-84 9581837-5 1998 In addition, 5-FU treatment of human hepatoma or gastric cancer xenografts in nude mice transduced with UPRT was demonstrated to result in significant in vivo antitumor effects. Fluorouracil 13-17 uracil phosphoribosyltransferase Mus musculus 104-108 9531612-5 1998 In post-5-FU recovering BMCs, the percentage of HSC-enriched Lin- Sca-1(+) c-Kit+ cells was about threefold higher in p53-/- than in p53+/+ cells. Fluorouracil 8-12 fucosyltransferase 1 (H blood group) Homo sapiens 48-51 9636831-4 1998 The first 89 consecutive patients who have received nine courses q three weeks of individually dose-escalated and G-CSF (filgrastim)-supported FEC (5-fluorouracil (5-FU), epirubicin, and cyclophosphamide) therapy given with ciprofloxacin prophylaxis were included in this analysis. Fluorouracil 148-162 colony stimulating factor 3 Homo sapiens 114-119 9500453-4 1998 Using multiple-dose 5-fluorouracil, methotrexate, and radiation in combination and total body radiation alone models, KGF increased survival by 55% or greater. Fluorouracil 20-34 fibroblast growth factor 7 Mus musculus 118-121 9500453-6 1998 The basis of these systemic benefits appears to be due in part to the trophic effects of the growth factor on the intestinal epithelium because KGF pretreatment caused an increase in measures of mucosal thickness (villus height and crypt depth) that persisted during the course of 5-fluorouracil chemotherapy. Fluorouracil 281-295 fibroblast growth factor 7 Mus musculus 144-147 9520026-2 1998 OBJECTIVE: To assess the safety and efficacy, we conducted an open-label pilot study of 5-FU/epi gel in 25 patients with biopsy-proven SCC lesions on the face, head, neck, trunk, arms, and hands. Fluorouracil 88-92 serpin family B member 3 Homo sapiens 135-138 9520026-8 1998 CONCLUSION: Treatment of superficial SCC with 5-FU/epi injectable gel results in a high rate of histologically confirmed complete tumor responses and may provide a nonsurgical treatment alternative in selected patients. Fluorouracil 46-50 serpin family B member 3 Homo sapiens 37-40 9463483-7 1998 Thymidylate synthase catalytic activity was reduced to 28% and 24% of control with FUra with or without IFN-alpha + gamma, suggesting that the enhanced dTTP depletion must be due to another mechanism. Fluorouracil 83-87 thymidylate synthetase Homo sapiens 0-20 9743457-7 1998 Addition of 5-FU to CDDP decreased the expression of weel and promoted cdc25C-activation. Fluorouracil 12-16 cell division cycle 25C Homo sapiens 71-77 9399677-0 1997 5-Fluorouracil-resistant colonic tumors are highly responsive to sodium butyrate/interleukin-2 bitherapy in rats. Fluorouracil 0-14 interleukin 2 Rattus norvegicus 81-94 9399677-12 1997 Our results suggest that NaBut/rIL-2 treatment is efficient against 5-FU-chemoresistant rat colon cancer. Fluorouracil 68-72 interleukin 2 Rattus norvegicus 31-36 10851489-8 1997 In the phase I trial, increments in neopterin and beta 2 microglobulin levels differed significantly between patients treated with lower and higher doses of 5-fluorouracil. Fluorouracil 157-171 beta-2-microglobulin Homo sapiens 50-70 9282825-1 1997 Interleukin-1alpha (IL-1), by itself, accelerates both granulopoietic and thrombopoietic recovery in the 5-fluorouracil (5-FU) myelosuppressed mouse (FUM). Fluorouracil 105-119 interleukin 1 alpha Mus musculus 0-18 9282825-1 1997 Interleukin-1alpha (IL-1), by itself, accelerates both granulopoietic and thrombopoietic recovery in the 5-fluorouracil (5-FU) myelosuppressed mouse (FUM). Fluorouracil 121-125 interleukin 1 alpha Mus musculus 0-18 9186496-1 1997 Fluorinated pyrimidines, such as 5-fluorouracil (FUra) and 5-fluoro-2"-deoxyuridine (FdUrd), are cytotoxic to cells as a consequence of generation of 5-fluoro-2"-deoxyuridylate (FdUMP), which is a mechanism-based inhibitor of the enzyme thymidylate synthase (TS). Fluorouracil 33-47 thymidylate synthetase Homo sapiens 237-257 9186496-1 1997 Fluorinated pyrimidines, such as 5-fluorouracil (FUra) and 5-fluoro-2"-deoxyuridine (FdUrd), are cytotoxic to cells as a consequence of generation of 5-fluoro-2"-deoxyuridylate (FdUMP), which is a mechanism-based inhibitor of the enzyme thymidylate synthase (TS). Fluorouracil 33-47 thymidylate synthetase Homo sapiens 259-261 9186496-1 1997 Fluorinated pyrimidines, such as 5-fluorouracil (FUra) and 5-fluoro-2"-deoxyuridine (FdUrd), are cytotoxic to cells as a consequence of generation of 5-fluoro-2"-deoxyuridylate (FdUMP), which is a mechanism-based inhibitor of the enzyme thymidylate synthase (TS). Fluorouracil 49-53 thymidylate synthetase Homo sapiens 237-257 9186496-1 1997 Fluorinated pyrimidines, such as 5-fluorouracil (FUra) and 5-fluoro-2"-deoxyuridine (FdUrd), are cytotoxic to cells as a consequence of generation of 5-fluoro-2"-deoxyuridylate (FdUMP), which is a mechanism-based inhibitor of the enzyme thymidylate synthase (TS). Fluorouracil 49-53 thymidylate synthetase Homo sapiens 259-261 9256160-6 1997 Resistance factors for TS inhibitors were: 2.4 and 0.4 for 5-fluorouracil (5FU), 18.8 and 8.8 for ZD1694, 17 and 0.7 for AG337, and 40 and 8.3 for BW1843U89 in SW-1573/2R160 and SW-1573/2R120, respectively. Fluorouracil 59-73 thymidylate synthetase Homo sapiens 23-25 9256160-6 1997 Resistance factors for TS inhibitors were: 2.4 and 0.4 for 5-fluorouracil (5FU), 18.8 and 8.8 for ZD1694, 17 and 0.7 for AG337, and 40 and 8.3 for BW1843U89 in SW-1573/2R160 and SW-1573/2R120, respectively. Fluorouracil 75-78 thymidylate synthetase Homo sapiens 23-25 9212806-8 1997 The TS inhibition rate correlated with the 5-FU concentration in the tumor tissue (r = 0.527, p = 0.047). Fluorouracil 43-47 thymidylate synthetase Homo sapiens 4-6 9143391-1 1997 Interleukin-1 alpha (IL-1 alpha) is myeloprotective in a variety of animal models of cancer chemotherapy and is similarly beneficial in adults treated with carboplatin, 5-fluorouracil, and after autologous bone marrow transplantation. Fluorouracil 169-183 interleukin 1 alpha Homo sapiens 0-19 9143391-1 1997 Interleukin-1 alpha (IL-1 alpha) is myeloprotective in a variety of animal models of cancer chemotherapy and is similarly beneficial in adults treated with carboplatin, 5-fluorouracil, and after autologous bone marrow transplantation. Fluorouracil 169-183 interleukin 1 alpha Homo sapiens 21-31 9291820-4 1997 5-FU sensitivity (IC50 range 0.6-25.4 microM) was not related to the basal intracellular folate concentration, whereas, significantly, it was linked to FPGS activity (range 2.5-11.1 pmol/min/mg protein): the higher the FPGS activity, the greater the 5-FU sensitivity. Fluorouracil 0-4 folylpolyglutamate synthase Homo sapiens 219-223 9291820-8 1997 In the presence of [l-FA]90, 5-FU sensitivity remained significantly correlated to the basal FPGS activity. Fluorouracil 29-33 folylpolyglutamate synthase Homo sapiens 93-97 9291820-11 1997 Above all, these data establish the relevance of FPGS activity for predicting the efficacy of 5-FU modulated by FA or not and point to the potential clinical interest of FPGS determination in human tumours. Fluorouracil 94-98 folylpolyglutamate synthase Homo sapiens 49-53 9126308-0 1997 [The correlation between thymidylate synthase expression and cytotoxicity of 5-fluorouracil in human cancer cell lines: study using polyclonal antibody against recombinant human thymidylate synthase]. Fluorouracil 77-91 thymidylate synthetase Homo sapiens 25-45 9126308-0 1997 [The correlation between thymidylate synthase expression and cytotoxicity of 5-fluorouracil in human cancer cell lines: study using polyclonal antibody against recombinant human thymidylate synthase]. Fluorouracil 77-91 thymidylate synthetase Homo sapiens 178-198 9126308-1 1997 To estimate the relationship between the expression of thymidylate synthase (TS) in tumors and clinical response and prognosis in cancer patients treated with 5-fluorouracil (5-FU), the anti-TS polyclonal antibody against recombinant human TS (rhTS) was prepared and purified. Fluorouracil 159-173 thymidylate synthetase Homo sapiens 55-75 9126308-1 1997 To estimate the relationship between the expression of thymidylate synthase (TS) in tumors and clinical response and prognosis in cancer patients treated with 5-fluorouracil (5-FU), the anti-TS polyclonal antibody against recombinant human TS (rhTS) was prepared and purified. Fluorouracil 159-173 thymidylate synthetase Homo sapiens 77-79 9126308-1 1997 To estimate the relationship between the expression of thymidylate synthase (TS) in tumors and clinical response and prognosis in cancer patients treated with 5-fluorouracil (5-FU), the anti-TS polyclonal antibody against recombinant human TS (rhTS) was prepared and purified. Fluorouracil 175-179 thymidylate synthetase Homo sapiens 55-75 9126308-1 1997 To estimate the relationship between the expression of thymidylate synthase (TS) in tumors and clinical response and prognosis in cancer patients treated with 5-fluorouracil (5-FU), the anti-TS polyclonal antibody against recombinant human TS (rhTS) was prepared and purified. Fluorouracil 175-179 thymidylate synthetase Homo sapiens 77-79 9126308-2 1997 At the initial stage, we attempted to clarify the relationships between the expression of TS protein and the cytotoxicity of 5-FU in established human cancer cells in vitro. Fluorouracil 125-129 thymidylate synthetase Homo sapiens 90-92 9126308-4 1997 Furthermore, it was revealed that the expression of TS proteins correlated with cytotoxicity (IC50 value) of 5-FU against human colorectal tumor cells, both sensitive and those with acquired resistance to 5-fluoropyrimidines, and other cancer cell lines as well. Fluorouracil 109-113 thymidylate synthetase Homo sapiens 52-54 9111585-3 1997 We assessed whether glioma cell killing is synergistically enhanced by cotreatment with CD95 ligand and chemotherapeutic agents, including doxorubicin, carmustine, vincristine, etoposide, teniposide, 5-fluorouracil and cytarabine. Fluorouracil 200-214 Fas cell surface death receptor Homo sapiens 88-92 9155534-3 1997 IFN-alpha may elevate the levels of the active 5-FU metabolite 5-fluoro-2"-deoxyuridine-5"-monophosphate (FdUMP) in the cell, possibly leading to increased inhibition of the target enzyme thymidylate synthase (TS), which might enhance DNA damage. Fluorouracil 47-51 thymidylate synthetase Homo sapiens 188-208 9155534-13 1997 Expression of TS protein, analysed by ELISA, was increased after 5-FU exposure of SW948 cells, but this increase was not affected by addition of either IFN-alpha or IFN-gamma. Fluorouracil 65-69 thymidylate synthetase Homo sapiens 14-16 9062414-1 1997 The increasing interest in 5-fluorouracil (5-FU) modulation and the development of new antifolates has focused attention in recent studies on the expression of the target enzyme thymidylate synthase (TS) as a determinant of drug sensitivity and resistance. Fluorouracil 27-41 thymidylate synthetase Homo sapiens 178-198 9062414-1 1997 The increasing interest in 5-fluorouracil (5-FU) modulation and the development of new antifolates has focused attention in recent studies on the expression of the target enzyme thymidylate synthase (TS) as a determinant of drug sensitivity and resistance. Fluorouracil 27-41 thymidylate synthetase Homo sapiens 200-202 9062414-1 1997 The increasing interest in 5-fluorouracil (5-FU) modulation and the development of new antifolates has focused attention in recent studies on the expression of the target enzyme thymidylate synthase (TS) as a determinant of drug sensitivity and resistance. Fluorouracil 43-47 thymidylate synthetase Homo sapiens 178-198 9062414-1 1997 The increasing interest in 5-fluorouracil (5-FU) modulation and the development of new antifolates has focused attention in recent studies on the expression of the target enzyme thymidylate synthase (TS) as a determinant of drug sensitivity and resistance. Fluorouracil 43-47 thymidylate synthetase Homo sapiens 200-202 9268987-3 1997 We therefore examined the effect of 5-FU on the steady-state levels of messenger RNA (mRNA) of a human excision repair gene ERCC1 and gamma-glutamylcysteine synthetase (gamma-GCS) gene coding for a rate-limiting enzyme for GSH synthesis. Fluorouracil 36-40 ERCC excision repair 1, endonuclease non-catalytic subunit Homo sapiens 124-129 9268987-5 1997 In these cells, 5-FU pretreatment progressively inhibited mRNA expression of both ERCC1 and gamma-GCS after removal of 5-FU, without affecting glyceraldehyde-3-phosphate dehydrogenase (GAPDH) mRNA. Fluorouracil 16-20 ERCC excision repair 1, endonuclease non-catalytic subunit Homo sapiens 82-87 9268987-5 1997 In these cells, 5-FU pretreatment progressively inhibited mRNA expression of both ERCC1 and gamma-GCS after removal of 5-FU, without affecting glyceraldehyde-3-phosphate dehydrogenase (GAPDH) mRNA. Fluorouracil 119-123 ERCC excision repair 1, endonuclease non-catalytic subunit Homo sapiens 82-87 9268987-9 1997 Although not convinced, our data suggest that 5-FU, when incorporated into RNA, may inhibit both GSH synthesis and repair of platinum-DNA adducts by downregulating the ERCC1 and gamma-GCS genes, thereby enhancing antitumor activity of CDDP and reversing resistance to CDDP in HST-1/CP0.2 cells. Fluorouracil 46-50 ERCC excision repair 1, endonuclease non-catalytic subunit Homo sapiens 168-173 8639826-12 1996 In contrast, 40% and 100% of mice that received SCF + IL-11 before the first dose of 5-FU, survived a second dose of 5-FU given respectively after 7 or 10 days. Fluorouracil 85-89 kit ligand Mus musculus 48-51 8639826-12 1996 In contrast, 40% and 100% of mice that received SCF + IL-11 before the first dose of 5-FU, survived a second dose of 5-FU given respectively after 7 or 10 days. Fluorouracil 117-121 kit ligand Mus musculus 48-51 8645024-2 1996 We used two inhibitors which regulate the anabolism of 5-FU for the purpose of elucidation of its pathways; one is oxonic acid (Oxo), an inhibitor of orotate phosphoribosyltransferase (OPRTase), catalizing a formation of FUMP from 5-FU, and another is 2, 6-dihydroxypyridine (DP), an inhibitor of uracil ribosyltransferase which catalizes a conversion of 5-FU to 5-fluorouridine. Fluorouracil 55-59 uridine monophosphate synthetase Homo sapiens 150-183 8645024-2 1996 We used two inhibitors which regulate the anabolism of 5-FU for the purpose of elucidation of its pathways; one is oxonic acid (Oxo), an inhibitor of orotate phosphoribosyltransferase (OPRTase), catalizing a formation of FUMP from 5-FU, and another is 2, 6-dihydroxypyridine (DP), an inhibitor of uracil ribosyltransferase which catalizes a conversion of 5-FU to 5-fluorouridine. Fluorouracil 55-59 uridine monophosphate synthetase Homo sapiens 185-192 8645024-2 1996 We used two inhibitors which regulate the anabolism of 5-FU for the purpose of elucidation of its pathways; one is oxonic acid (Oxo), an inhibitor of orotate phosphoribosyltransferase (OPRTase), catalizing a formation of FUMP from 5-FU, and another is 2, 6-dihydroxypyridine (DP), an inhibitor of uracil ribosyltransferase which catalizes a conversion of 5-FU to 5-fluorouridine. Fluorouracil 231-235 uridine monophosphate synthetase Homo sapiens 150-183 8645024-2 1996 We used two inhibitors which regulate the anabolism of 5-FU for the purpose of elucidation of its pathways; one is oxonic acid (Oxo), an inhibitor of orotate phosphoribosyltransferase (OPRTase), catalizing a formation of FUMP from 5-FU, and another is 2, 6-dihydroxypyridine (DP), an inhibitor of uracil ribosyltransferase which catalizes a conversion of 5-FU to 5-fluorouridine. Fluorouracil 231-235 uridine monophosphate synthetase Homo sapiens 150-183 8645024-3 1996 Although the pathway of 5-FU phosphorylation in murine tumor cells was varied, about 80% of human cancer cells tested were found to utilize the first pathway in which 5-FU was converted to FUMP by OPRTase. Fluorouracil 167-171 uridine monophosphate synthetase Homo sapiens 197-204 8809659-0 1996 Treatment of metastatic breast cancer by navelbine, mitoxantrone and continuous infusion 5-fluorouracil (FMN regimen): results of a pilot study. Fluorouracil 89-103 formin 1 Homo sapiens 105-108 8630380-1 1996 We conducted a prospective randomized trial to evaluate the ability of the interleukin-3/granulocyte-macrophage colony-stimulating factor (GM-CSF) fusion protein, PIXY321, to ameliorate cumulative thrombocytopenia after multiple cycles of 5-fluorouracil, leucovorin, doxorubicin, cyclophosphamide (FLAC) chemotherapy compared with GM-CSF in patients with advanced breast cancer. Fluorouracil 239-253 colony stimulating factor 2 Homo sapiens 75-137 8630380-1 1996 We conducted a prospective randomized trial to evaluate the ability of the interleukin-3/granulocyte-macrophage colony-stimulating factor (GM-CSF) fusion protein, PIXY321, to ameliorate cumulative thrombocytopenia after multiple cycles of 5-fluorouracil, leucovorin, doxorubicin, cyclophosphamide (FLAC) chemotherapy compared with GM-CSF in patients with advanced breast cancer. Fluorouracil 239-253 colony stimulating factor 2 Homo sapiens 139-145 8599970-5 1996 Furthermore, when lentinan administration was followed by administration of erythropoietin (Epo) in 5-FU-treated mice, increases in femoral marrow and splenic CFU-E formation and augmentation of reticulocyte counts were observed beyond the level observed in mice treated with Epo alone. Fluorouracil 100-104 erythropoietin Mus musculus 76-90 8599970-5 1996 Furthermore, when lentinan administration was followed by administration of erythropoietin (Epo) in 5-FU-treated mice, increases in femoral marrow and splenic CFU-E formation and augmentation of reticulocyte counts were observed beyond the level observed in mice treated with Epo alone. Fluorouracil 100-104 erythropoietin Mus musculus 92-95 8599970-5 1996 Furthermore, when lentinan administration was followed by administration of erythropoietin (Epo) in 5-FU-treated mice, increases in femoral marrow and splenic CFU-E formation and augmentation of reticulocyte counts were observed beyond the level observed in mice treated with Epo alone. Fluorouracil 100-104 erythropoietin Mus musculus 276-279 8609072-4 1996 On the other hand, NUGC-3/5/5FU/L also showed resistance to in situ thymidylate synthase (TS) inhibition by 5-FU. Fluorouracil 108-112 thymidylate synthetase Homo sapiens 68-88 8695163-1 1996 Knowledge of population thymidylate synthase (TS) levels in malignant tumors and normal tissues is essential for the use of TS as a predictor for 5-fluorouracil treatment. Fluorouracil 146-160 thymidylate synthetase Homo sapiens 24-44 8695163-1 1996 Knowledge of population thymidylate synthase (TS) levels in malignant tumors and normal tissues is essential for the use of TS as a predictor for 5-fluorouracil treatment. Fluorouracil 146-160 thymidylate synthetase Homo sapiens 46-48 8695163-1 1996 Knowledge of population thymidylate synthase (TS) levels in malignant tumors and normal tissues is essential for the use of TS as a predictor for 5-fluorouracil treatment. Fluorouracil 146-160 thymidylate synthetase Homo sapiens 124-126 8742097-1 1996 It was our intention to verify if increases of granulocyte colony stimulating factor (G-CSF) dose were able to reduce treatment delays due to leukopenia in our weekly regimen of cisplatin (40 mg/m2), epidoxorubicin (35 mg/m2), 6S-leucovorin (250 mg/m2) and 5-fluorouracil (500 mg/m2), usually supported by G-CSF at a dose of 5 mu g/kg. Fluorouracil 257-271 colony stimulating factor 3 Homo sapiens 47-84 8742097-1 1996 It was our intention to verify if increases of granulocyte colony stimulating factor (G-CSF) dose were able to reduce treatment delays due to leukopenia in our weekly regimen of cisplatin (40 mg/m2), epidoxorubicin (35 mg/m2), 6S-leucovorin (250 mg/m2) and 5-fluorouracil (500 mg/m2), usually supported by G-CSF at a dose of 5 mu g/kg. Fluorouracil 257-271 colony stimulating factor 3 Homo sapiens 86-91 8823488-0 1996 Erythropoietin and granulocyte-macrophage colony-stimulating factor allow acceleration and dose escalation of cyclophosphamide/epidoxorubicin/5-fluorouracil chemotherapy: a dose-finding study in patients with advanced breast cancer. Fluorouracil 142-156 colony stimulating factor 2 Homo sapiens 19-67 8823488-1 1996 To verify whether the association of granulocyte-macrophage colony-stimulating factor (GM-CSF) and erythropoietin (EPO) would allow both the acceleration and the dose escalation of the cyclophosphamide/epidoxorubicin/5-fluorouracil (CEF) regimen as first-line therapy in advanced breast cancer patients, we conducted a dose-finding study. Fluorouracil 217-231 colony stimulating factor 2 Homo sapiens 37-85 8823488-1 1996 To verify whether the association of granulocyte-macrophage colony-stimulating factor (GM-CSF) and erythropoietin (EPO) would allow both the acceleration and the dose escalation of the cyclophosphamide/epidoxorubicin/5-fluorouracil (CEF) regimen as first-line therapy in advanced breast cancer patients, we conducted a dose-finding study. Fluorouracil 217-231 colony stimulating factor 2 Homo sapiens 87-93 8823488-11 1996 Increasing the doses of Ctx and Epidx while maintaining a fixed dose of 5-Fu with the support of both EPO and GM-CSF allows safe acceleration and dose escalation of CEF chemotherapy. Fluorouracil 72-76 colony stimulating factor 2 Homo sapiens 110-116 8884811-1 1996 5-fluorouracil (5-FU), an inhibitor of thymidylate synthase (EC 2.1.1.45), is clinically used in the treatment of several solid tumors, including colorectal, head and neck, gastric, and pancreatic cancer. Fluorouracil 0-14 thymidylate synthetase Homo sapiens 39-59 8884811-1 1996 5-fluorouracil (5-FU), an inhibitor of thymidylate synthase (EC 2.1.1.45), is clinically used in the treatment of several solid tumors, including colorectal, head and neck, gastric, and pancreatic cancer. Fluorouracil 16-20 thymidylate synthetase Homo sapiens 39-59 21594312-2 1996 In the present study, it is demonstrated that MTX enhanced the chemosensitivity of 5-FU, especially, in the tumor cells with less than 70% inhibition ratio by the MTT assay. Fluorouracil 83-87 metaxin 1 Homo sapiens 46-49 21594312-3 1996 It has been reported that MTX/5-FU sequential chemotherapy was one of the effective chemotherapies against gastric cancer and colon cancer, and it is possible to anticipate the efficacy of MTX/5-FU sequential chemotherapy by the MTT assays. Fluorouracil 30-34 metaxin 1 Homo sapiens 26-29 21594312-3 1996 It has been reported that MTX/5-FU sequential chemotherapy was one of the effective chemotherapies against gastric cancer and colon cancer, and it is possible to anticipate the efficacy of MTX/5-FU sequential chemotherapy by the MTT assays. Fluorouracil 30-34 metaxin 1 Homo sapiens 189-192 21594312-3 1996 It has been reported that MTX/5-FU sequential chemotherapy was one of the effective chemotherapies against gastric cancer and colon cancer, and it is possible to anticipate the efficacy of MTX/5-FU sequential chemotherapy by the MTT assays. Fluorouracil 193-197 metaxin 1 Homo sapiens 26-29 8820950-5 1996 One of the critical mechanisms of resistance to 5-FU appears to be the acute induction in thymidylate synthase (TS) levels following therapy with inhibitors of this enzyme. Fluorouracil 48-52 thymidylate synthetase Homo sapiens 90-110 8820950-5 1996 One of the critical mechanisms of resistance to 5-FU appears to be the acute induction in thymidylate synthase (TS) levels following therapy with inhibitors of this enzyme. Fluorouracil 48-52 thymidylate synthetase Homo sapiens 112-114 8746791-8 1995 LV augmented the antitumor activity of 5-FU through increment of thymidylate synthetase (TS) inhibition, and IFN-alpha 2a showed a modulatory effect in elevating the intratumoral concentration of fluorouridine without change in TS inhibition. Fluorouracil 39-43 thymidylate synthetase Homo sapiens 65-87 7474606-3 1995 Experimental data suggest that PC-3, a human hormone refractory prostate cancer cell line, showed a 2-fold increase in 5-Fluorouracil (5FU) sensitivity in the presence of alpha-2a Interferon (IFN alpha 2a) at 100 IU/ml, compared to that without IFN alpha 2a. Fluorouracil 119-133 chromobox 8 Homo sapiens 31-35 7474606-3 1995 Experimental data suggest that PC-3, a human hormone refractory prostate cancer cell line, showed a 2-fold increase in 5-Fluorouracil (5FU) sensitivity in the presence of alpha-2a Interferon (IFN alpha 2a) at 100 IU/ml, compared to that without IFN alpha 2a. Fluorouracil 135-138 chromobox 8 Homo sapiens 31-35 7641209-1 1995 Thymidylate synthase (TS) is a target enzyme of 5-fluorouracil and is inhibited by 5-fluoro-dUMP (FdUMP) to form an inactive ternary complex. Fluorouracil 48-62 thymidylate synthetase Homo sapiens 0-20 7641209-1 1995 Thymidylate synthase (TS) is a target enzyme of 5-fluorouracil and is inhibited by 5-fluoro-dUMP (FdUMP) to form an inactive ternary complex. Fluorouracil 48-62 thymidylate synthetase Homo sapiens 22-24 7574773-6 1995 After intrapleural instillation of a combination of 5-FU 250 mg and leucovorin 3 mg, the total amount and the catalytic activity of TS could be measured. Fluorouracil 52-56 thymidylate synthetase Homo sapiens 132-134 8528944-6 1995 However, the glycosylated IL-1 alpha possessed the same potency as untreated IL-1 alpha in reduction of serum levels of glucose and triglyceride and in recovery of peripheral white blood cells in 5-fluorouracil-treated mice. Fluorouracil 198-210 interleukin 1 alpha Mus musculus 26-36 9816038-1 1995 In colon cancers induction of a thymineless state following inhibition of thymidylate synthase (TS) by 5-fluorouracil combined with leucovorin can initiate a cytotoxic response. Fluorouracil 103-117 thymidylate synthetase Homo sapiens 74-94 7577040-2 1995 Resistance to 5-fluorouracil (5FU) can be related to insufficient inhibition of thymidylate synthase. Fluorouracil 14-28 thymidylate synthetase Homo sapiens 80-100 7577040-2 1995 Resistance to 5-fluorouracil (5FU) can be related to insufficient inhibition of thymidylate synthase. Fluorouracil 30-33 thymidylate synthetase Homo sapiens 80-100 7577041-0 1995 Quantitation of intratumoral thymidylate synthase expression predicts for resistance to protracted infusion of 5-fluorouracil and weekly leucovorin in disseminated colorectal cancers: preliminary report from an ongoing trial. Fluorouracil 111-125 thymidylate synthetase Homo sapiens 29-49 7577041-1 1995 A clinical trial for patients with measurable, disseminated colorectal cancer is being conducted to determine: (1) if intratumoral expression of thymidylate synthase (TS) affects response to protracted-infusion 5-fluorouracil (5FU); and (2) whether intratumoral expression of TS increases when clinical resistance is found after response to 5-FU. Fluorouracil 211-225 thymidylate synthetase Homo sapiens 145-165 7577041-1 1995 A clinical trial for patients with measurable, disseminated colorectal cancer is being conducted to determine: (1) if intratumoral expression of thymidylate synthase (TS) affects response to protracted-infusion 5-fluorouracil (5FU); and (2) whether intratumoral expression of TS increases when clinical resistance is found after response to 5-FU. Fluorouracil 211-225 thymidylate synthetase Homo sapiens 167-169 7577041-1 1995 A clinical trial for patients with measurable, disseminated colorectal cancer is being conducted to determine: (1) if intratumoral expression of thymidylate synthase (TS) affects response to protracted-infusion 5-fluorouracil (5FU); and (2) whether intratumoral expression of TS increases when clinical resistance is found after response to 5-FU. Fluorouracil 227-230 thymidylate synthetase Homo sapiens 167-169 7577041-1 1995 A clinical trial for patients with measurable, disseminated colorectal cancer is being conducted to determine: (1) if intratumoral expression of thymidylate synthase (TS) affects response to protracted-infusion 5-fluorouracil (5FU); and (2) whether intratumoral expression of TS increases when clinical resistance is found after response to 5-FU. Fluorouracil 341-345 thymidylate synthetase Homo sapiens 167-169 7577041-8 1995 On average, patients previously treated with 5-FU have slightly higher levels of TS expression in their measurable tumours (P = 0.4). Fluorouracil 45-49 thymidylate synthetase Homo sapiens 81-83 7779703-0 1995 The effect of dose and interval between 5-fluorouracil and leucovorin on the formation of thymidylate synthase ternary complex in human cancer cells. Fluorouracil 40-54 thymidylate synthetase Homo sapiens 90-110 7779703-1 1995 We examined the importance of dosing interval between leucovorin (LCV) and 5-fluorouracil (5-FU) on intracellular thymidylate synthase (TS) ternary complex, free TS and total TS protein levels in human MCF-7 breast and NCI H630 colon cancer cell lines. Fluorouracil 91-95 thymidylate synthetase Homo sapiens 114-134 7779703-2 1995 A 2- to 3-fold increase in total TS was noted when either cell line was exposed to 5-FU 10 microM plus LCV (0.01-10 microM) compared with a 1.4- to 1.6-fold increase in total TS due to 5-FU 10 microM alone. Fluorouracil 83-87 thymidylate synthetase Homo sapiens 33-35 7779703-2 1995 A 2- to 3-fold increase in total TS was noted when either cell line was exposed to 5-FU 10 microM plus LCV (0.01-10 microM) compared with a 1.4- to 1.6-fold increase in total TS due to 5-FU 10 microM alone. Fluorouracil 185-189 thymidylate synthetase Homo sapiens 33-35 7779703-5 1995 In MCF-7 cells, the maximal increase in total TS protein and TS ternary complex formation was observed when 5-FU was delayed for 4 h after the start of LCV exposure. Fluorouracil 108-112 thymidylate synthetase Homo sapiens 46-48 7779703-5 1995 In MCF-7 cells, the maximal increase in total TS protein and TS ternary complex formation was observed when 5-FU was delayed for 4 h after the start of LCV exposure. Fluorouracil 108-112 thymidylate synthetase Homo sapiens 61-63 7779703-6 1995 In NCI H630 cells, maximal total TS protein and ternary complex formation occurred when 5-FU was delayed for 18 h after the start of LCV exposure. Fluorouracil 88-92 thymidylate synthetase Homo sapiens 33-35 7779703-8 1995 In these human carcinoma cell lines, the LCV dose and interval between 5-FU and LCV play a role in increased TS total protein and TS ternary complex; however, the amount of free TS is independent of the interval between 5-FU and LCV. Fluorouracil 71-75 thymidylate synthetase Homo sapiens 109-111 7611790-0 1995 [Effect of low dose CDDP/5-fluorouracil therapy on PCNA labeling index and TS inhibition rate of gastric cancer]. Fluorouracil 25-39 proliferating cell nuclear antigen Homo sapiens 51-55 7611790-1 1995 The response of gastric cancer to intravenous application of low-dose CDDP plus 5-fluorouracil (FP) was assessed by changes in DNA indices (DIs) and PCNA labeling indices (LIs) by flow cytometry, and by the thymidylate synthetase inhibition rate (TSIR). Fluorouracil 80-94 proliferating cell nuclear antigen Homo sapiens 149-153 7534710-2 1995 We found a significant increase in the proportion of CD34+ cells in the PBSC fraction resistant to 25 micrograms/mL 5-FU after 7-day incubation with IL-1 plus IL-3 plus SCF as compared with the untreated fraction (p = 0.011). Fluorouracil 116-120 interleukin 1 alpha Homo sapiens 149-153 7534710-2 1995 We found a significant increase in the proportion of CD34+ cells in the PBSC fraction resistant to 25 micrograms/mL 5-FU after 7-day incubation with IL-1 plus IL-3 plus SCF as compared with the untreated fraction (p = 0.011). Fluorouracil 116-120 interleukin 3 Homo sapiens 159-163 7534710-3 1995 We also showed that 5-FU-resistant PBSC have a greater capacity for expansion of IL-1/IL-3/SCF-responsive immature progenitors (p = 0.05), amplification of IL-3 plus GM-CSF responsive progenitors (p = 0.01), and production of committed single growth factor-responsive (granulocyte-macrophage colony-stimulating factor [GM-CSF]) precursors (p = 0.01) than the untreated PBSC. Fluorouracil 20-24 interleukin 1 alpha Homo sapiens 81-85 7534710-3 1995 We also showed that 5-FU-resistant PBSC have a greater capacity for expansion of IL-1/IL-3/SCF-responsive immature progenitors (p = 0.05), amplification of IL-3 plus GM-CSF responsive progenitors (p = 0.01), and production of committed single growth factor-responsive (granulocyte-macrophage colony-stimulating factor [GM-CSF]) precursors (p = 0.01) than the untreated PBSC. Fluorouracil 20-24 interleukin 3 Homo sapiens 86-90 7534710-3 1995 We also showed that 5-FU-resistant PBSC have a greater capacity for expansion of IL-1/IL-3/SCF-responsive immature progenitors (p = 0.05), amplification of IL-3 plus GM-CSF responsive progenitors (p = 0.01), and production of committed single growth factor-responsive (granulocyte-macrophage colony-stimulating factor [GM-CSF]) precursors (p = 0.01) than the untreated PBSC. Fluorouracil 20-24 interleukin 3 Homo sapiens 156-160 7534710-3 1995 We also showed that 5-FU-resistant PBSC have a greater capacity for expansion of IL-1/IL-3/SCF-responsive immature progenitors (p = 0.05), amplification of IL-3 plus GM-CSF responsive progenitors (p = 0.01), and production of committed single growth factor-responsive (granulocyte-macrophage colony-stimulating factor [GM-CSF]) precursors (p = 0.01) than the untreated PBSC. Fluorouracil 20-24 colony stimulating factor 2 Homo sapiens 166-172 7534710-3 1995 We also showed that 5-FU-resistant PBSC have a greater capacity for expansion of IL-1/IL-3/SCF-responsive immature progenitors (p = 0.05), amplification of IL-3 plus GM-CSF responsive progenitors (p = 0.01), and production of committed single growth factor-responsive (granulocyte-macrophage colony-stimulating factor [GM-CSF]) precursors (p = 0.01) than the untreated PBSC. Fluorouracil 20-24 colony stimulating factor 2 Homo sapiens 269-317 7534710-3 1995 We also showed that 5-FU-resistant PBSC have a greater capacity for expansion of IL-1/IL-3/SCF-responsive immature progenitors (p = 0.05), amplification of IL-3 plus GM-CSF responsive progenitors (p = 0.01), and production of committed single growth factor-responsive (granulocyte-macrophage colony-stimulating factor [GM-CSF]) precursors (p = 0.01) than the untreated PBSC. Fluorouracil 20-24 colony stimulating factor 2 Homo sapiens 319-325 7597304-7 1995 Moreover, IFN can reverse resistance against 5-FU by inhibiting the overexpression of thymidylate synthase. Fluorouracil 45-49 thymidylate synthetase Homo sapiens 86-106 7989939-10 1994 Adjuvant fluorouracil (5-FU)-based chemotherapy demonstrated significant improvement in disease-free and overall survival for patients with high TS levels. Fluorouracil 9-21 thymidylate synthetase Homo sapiens 145-147 7989939-10 1994 Adjuvant fluorouracil (5-FU)-based chemotherapy demonstrated significant improvement in disease-free and overall survival for patients with high TS levels. Fluorouracil 23-27 thymidylate synthetase Homo sapiens 145-147 7872700-1 1994 Catalytic activity and FdUMP binding characteristics of thymidylate synthase (TS) were determined in 22 tumor biopsies of patients to be treated (15) or just treated (7) for colorectal cancer with 5-fluorouracil and leucovorin. Fluorouracil 197-211 thymidylate synthetase Homo sapiens 56-76 7872700-1 1994 Catalytic activity and FdUMP binding characteristics of thymidylate synthase (TS) were determined in 22 tumor biopsies of patients to be treated (15) or just treated (7) for colorectal cancer with 5-fluorouracil and leucovorin. Fluorouracil 197-211 thymidylate synthetase Homo sapiens 78-80 7949162-2 1994 The small coding region of the human cell surface antigen CD24 (approximately 240 bp) was introduced into a myeloproliferative sarcoma virus (MPSV)-based retroviral vector, which was then used to infect day 4 5-fluorouracil (5-FU)-treated murine bone marrow cells. Fluorouracil 209-223 CD24a antigen Mus musculus 58-62 7949162-2 1994 The small coding region of the human cell surface antigen CD24 (approximately 240 bp) was introduced into a myeloproliferative sarcoma virus (MPSV)-based retroviral vector, which was then used to infect day 4 5-fluorouracil (5-FU)-treated murine bone marrow cells. Fluorouracil 225-229 CD24a antigen Mus musculus 58-62 7826903-13 1994 A modest increase in FLAC dose intensity over the starting doses was achievable with the addition of GM-CSF. Fluorouracil 21-25 colony stimulating factor 2 Homo sapiens 101-107 7961162-5 1994 CNG prevented reduction of the production of interleukin-2, 3 and 6 in cultured supernatants of spleen cells taken from mice given 5-fluorouracil. Fluorouracil 131-145 interleukin 2 Mus musculus 45-67 7931471-0 1994 Thymidylate synthase inhibition after administration of fluorouracil with or without leucovorin in colon cancer patients: implications for treatment with fluorouracil. Fluorouracil 56-68 thymidylate synthetase Homo sapiens 0-20 7931471-0 1994 Thymidylate synthase inhibition after administration of fluorouracil with or without leucovorin in colon cancer patients: implications for treatment with fluorouracil. Fluorouracil 154-166 thymidylate synthetase Homo sapiens 0-20 7931471-1 1994 PURPOSE: To determine the time-dependence of fluorouracil (5FU)-induced thymidylate synthase (TS) inhibition in colon cancer patients, the effect of leucovorin (LV), and the relation to response. Fluorouracil 45-57 thymidylate synthetase Homo sapiens 72-92 7931471-1 1994 PURPOSE: To determine the time-dependence of fluorouracil (5FU)-induced thymidylate synthase (TS) inhibition in colon cancer patients, the effect of leucovorin (LV), and the relation to response. Fluorouracil 59-62 thymidylate synthetase Homo sapiens 72-92 8080451-4 1994 In the opposite direction, DPDase catalyzed the reduction of 5-fluorouracil (FU) with a Km of 0.70 microM and a kcat of 3 sec-1 at a saturating concentration of NADPH. Fluorouracil 61-75 secretory blood group 1 Rattus norvegicus 122-127 8060136-0 1994 [Detection of thymidylate synthase mRNA in 5-fluorouracil resistant human colon adenocarcinoma cells]. Fluorouracil 43-57 thymidylate synthetase Homo sapiens 14-34 7522897-2 1994 The resulting 5-FU-resistant cells were evaluated for (1) the production of GM-CSF-responsive clonogenic elements (CE), (2) the production of IL-3+GM-CSF-responsive CE, and (3) their self-renewal capacity (production of IL-1+IL-3+SCF-responsive CE). Fluorouracil 14-18 colony stimulating factor 2 Homo sapiens 76-82 7522897-2 1994 The resulting 5-FU-resistant cells were evaluated for (1) the production of GM-CSF-responsive clonogenic elements (CE), (2) the production of IL-3+GM-CSF-responsive CE, and (3) their self-renewal capacity (production of IL-1+IL-3+SCF-responsive CE). Fluorouracil 14-18 interleukin 3 Homo sapiens 142-146 7522897-2 1994 The resulting 5-FU-resistant cells were evaluated for (1) the production of GM-CSF-responsive clonogenic elements (CE), (2) the production of IL-3+GM-CSF-responsive CE, and (3) their self-renewal capacity (production of IL-1+IL-3+SCF-responsive CE). Fluorouracil 14-18 interleukin 1 alpha Homo sapiens 220-229 7522897-6 1994 We also showed that 5-FU-resistant PBSC have a greater capacity for self-renewal, amplification of IL-3+GM-CSF-responsive progenitors, and the production of committed GM-CSF-responsive progenitors as compared with BM cells, but this did not reach statistical significant. Fluorouracil 20-24 interleukin 3 Homo sapiens 99-103 7522897-6 1994 We also showed that 5-FU-resistant PBSC have a greater capacity for self-renewal, amplification of IL-3+GM-CSF-responsive progenitors, and the production of committed GM-CSF-responsive progenitors as compared with BM cells, but this did not reach statistical significant. Fluorouracil 20-24 colony stimulating factor 2 Homo sapiens 104-110 7522897-6 1994 We also showed that 5-FU-resistant PBSC have a greater capacity for self-renewal, amplification of IL-3+GM-CSF-responsive progenitors, and the production of committed GM-CSF-responsive progenitors as compared with BM cells, but this did not reach statistical significant. Fluorouracil 20-24 colony stimulating factor 2 Homo sapiens 167-173 7515714-2 1994 When polyethylene glycolated (PEG-ylated) SCF was administered to mice before 5-FU, it had a significant sensitizing effect on primitive bone marrow cells. Fluorouracil 78-82 kit ligand Mus musculus 42-45 7515714-3 1994 Examination of the hematopoietic status of these mice showed that the damage caused by 5-FU to both bone marrow and spleen hematopoiesis was exaggerated when it was preceded by SCF. Fluorouracil 87-91 kit ligand Mus musculus 177-180 7515714-10 1994 Examination of hematopoiesis in mice treated concurrently with SCF and TGF-beta 3 showed that the degree of marrow and spleen damage had reverted to that caused by 5-FU alone. Fluorouracil 164-168 kit ligand Mus musculus 63-66 7515714-10 1994 Examination of hematopoiesis in mice treated concurrently with SCF and TGF-beta 3 showed that the degree of marrow and spleen damage had reverted to that caused by 5-FU alone. Fluorouracil 164-168 transforming growth factor, beta 3 Mus musculus 71-81 7515714-12 1994 These data indicate that PEG-ylated SCF can sensitize normally resistant hematopoietic and gut stem cells to the effects of 5-FU. Fluorouracil 124-128 kit ligand Mus musculus 36-39 8206932-2 1994 Human TS cDNA was transcribed in the presence of Ura-, FUra-, or BrUTP to obtain 100% substituted mRNA. Fluorouracil 55-60 thymidylate synthetase Homo sapiens 6-8 8206932-5 1994 Time courses of TS formation revealed a characteristic peak which occurred at 45 min for the Ura- and FUra-RNAs and at 2 h for the BrUra-RNA. Fluorouracil 102-106 thymidylate synthetase Homo sapiens 16-18 8194879-0 1994 Anti-tumor effect of combined treatment with thymosin alpha 1 and interleukin-2 after 5-fluorouracil in liver metastases from colorectal cancer in rats. Fluorouracil 86-100 interleukin 2 Rattus norvegicus 66-79 7941467-1 1994 As shown on the experimental model of rat acute pancreatitis, an intensive 5-fluorouracil electrophoresis course in combination with magnetotherapy significantly reduces the activity of blood trypsin, amylase, lipase and corticosterone. Fluorouracil 75-89 lipase G, endothelial type Rattus norvegicus 210-216 8049506-0 1994 Interleukin-2 in neoadjuvant therapy potentiates inhibitory activity of 5-fluorouracil and interferon in experimental liver metastases. Fluorouracil 72-86 interleukin 2 Mus musculus 0-13 8049506-5 1994 IL-2 was found to be equally effective, if not superior, to IFN as a neoadjuvant in inhibiting liver and lung metastases with 5-FU + IFN. Fluorouracil 126-130 interleukin 2 Mus musculus 0-4 8168119-7 1994 In bulk cultures containing IL-2 (1000 CU/ml, 3-4 days), both 5-FU and CY reduced LAK activity of euthymic mice splenocytes for up to 6 days after chemotherapy, which was followed on day 9 by full recovery. Fluorouracil 62-66 interleukin 2 Mus musculus 28-32 8168119-7 1994 In bulk cultures containing IL-2 (1000 CU/ml, 3-4 days), both 5-FU and CY reduced LAK activity of euthymic mice splenocytes for up to 6 days after chemotherapy, which was followed on day 9 by full recovery. Fluorouracil 62-66 alpha-kinase 1 Mus musculus 82-85 8168119-9 1994 In athymic mice, 5-FU markedly augmented the total number of LAK-p/spleen (up to 30-fold, days 3-9), as determined by limiting-dilution cultures with IL-2 (for 7-8 days). Fluorouracil 17-21 alpha-kinase 1 Mus musculus 61-64 8168119-9 1994 In athymic mice, 5-FU markedly augmented the total number of LAK-p/spleen (up to 30-fold, days 3-9), as determined by limiting-dilution cultures with IL-2 (for 7-8 days). Fluorouracil 17-21 interleukin 2 Mus musculus 150-154 8168119-10 1994 In euthymic mice, in contrast, LAK-p levels decreased for up to 6-9 days after treatment with 5-FU, Adriamycin or decarbazine, later recovering to pretreatment levels, whereas CY markedly increased LAK-p (up to 15-fold) when administered 6-12 days before limiting-dilution culture initiation. Fluorouracil 94-98 alpha-kinase 1 Mus musculus 31-34 8168119-12 1994 In other experiments, a subset of asialoGM1- LAK-p was found in the spleens of 5-FU-treated mice, but not in untreated mice. Fluorouracil 79-83 alpha-kinase 1 Mus musculus 45-48 8120554-2 1994 PATIENTS AND METHODS: Thirty-seven patients received escalating doses of 5-FU/LCV on days 1 to 5 with subcutaneous GM-CSF either 5 or 10 micrograms/kg/d starting on day 6 or 3 micrograms/kg/d starting on day 1. Fluorouracil 73-77 colony stimulating factor 2 Homo sapiens 115-121 8181904-6 1994 LAK activity of spleen cells from mice treated with both SPR-901 and 5-FU was higher than that from the untreated control group and either the SPR-901 or 5-FU treated group. Fluorouracil 69-73 alpha-kinase 1 Mus musculus 0-3 8181904-6 1994 LAK activity of spleen cells from mice treated with both SPR-901 and 5-FU was higher than that from the untreated control group and either the SPR-901 or 5-FU treated group. Fluorouracil 154-158 alpha-kinase 1 Mus musculus 0-3 8181904-8 1994 Furthermore, spleen cells from both the SPR-901- and 5-FU-treated groups exhibited higher growth responses to IL-2 than that from the untreated control group and either of the SPR-901- or 5-FU-treated groups. Fluorouracil 53-57 interleukin 2 Mus musculus 110-114 8028610-1 1994 5-Fluorouracil (5FU), an antimetabolite often used for the treatment of breast cancer, binds to and inactivates the enzyme thymidylate synthase (TS). Fluorouracil 0-14 thymidylate synthetase Homo sapiens 123-143 8028610-1 1994 5-Fluorouracil (5FU), an antimetabolite often used for the treatment of breast cancer, binds to and inactivates the enzyme thymidylate synthase (TS). Fluorouracil 0-14 thymidylate synthetase Homo sapiens 145-147 8028610-1 1994 5-Fluorouracil (5FU), an antimetabolite often used for the treatment of breast cancer, binds to and inactivates the enzyme thymidylate synthase (TS). Fluorouracil 16-19 thymidylate synthetase Homo sapiens 123-143 8028610-1 1994 5-Fluorouracil (5FU), an antimetabolite often used for the treatment of breast cancer, binds to and inactivates the enzyme thymidylate synthase (TS). Fluorouracil 16-19 thymidylate synthetase Homo sapiens 145-147 7506084-5 1994 When tested on marrow cells from 5-fluorouracil (5-FU)-treated mice, the combination of IL-12 and SF, but not the single factors, was effective in support of formation of various types of colonies. Fluorouracil 33-47 kit ligand Mus musculus 98-100 7506084-5 1994 When tested on marrow cells from 5-fluorouracil (5-FU)-treated mice, the combination of IL-12 and SF, but not the single factors, was effective in support of formation of various types of colonies. Fluorouracil 49-53 kit ligand Mus musculus 98-100 7987994-1 1994 Fluorodeoxyuridine (FUdR), the deoxynucleoside metabolite of 5-fluorouracil (5-FU), can be converted in a single step to fluorodeoxyuridine monophosphate (FdUMP), which binds covalently to thymidylate synthase (TS). Fluorouracil 61-75 thymidylate synthetase Homo sapiens 189-209 7987994-1 1994 Fluorodeoxyuridine (FUdR), the deoxynucleoside metabolite of 5-fluorouracil (5-FU), can be converted in a single step to fluorodeoxyuridine monophosphate (FdUMP), which binds covalently to thymidylate synthase (TS). Fluorouracil 77-81 thymidylate synthetase Homo sapiens 189-209 7787251-1 1994 Recombinant human interleukin-1 alpha (rIL-1 alpha), at concentrations that were not growth-inhibitory when given alone (100-10,000 U/ml), enhanced the growth inhibition resulting from a 72-h fluorouracil (FUra) exposure in HCT116 colon cancer cells. Fluorouracil 192-204 interleukin 1 alpha Homo sapiens 18-37 7787251-1 1994 Recombinant human interleukin-1 alpha (rIL-1 alpha), at concentrations that were not growth-inhibitory when given alone (100-10,000 U/ml), enhanced the growth inhibition resulting from a 72-h fluorouracil (FUra) exposure in HCT116 colon cancer cells. Fluorouracil 206-210 interleukin 1 alpha Homo sapiens 18-37 8142915-1 1994 In vivo, recombinant human interleukin 1 alpha (rHuIL-1 alpha) + recombinant human macrophage colony-stimulating factor (rHuM-CSF) (IL-1 + M-CSF) effectively serves as a rescue agent for myelosuppression by enhancing the recovery of hematopoietic stem cell (HSC) subpopulations following treatment with 5-fluorouracil (5-FU). Fluorouracil 303-317 interleukin 1 alpha Homo sapiens 27-46 8142915-1 1994 In vivo, recombinant human interleukin 1 alpha (rHuIL-1 alpha) + recombinant human macrophage colony-stimulating factor (rHuM-CSF) (IL-1 + M-CSF) effectively serves as a rescue agent for myelosuppression by enhancing the recovery of hematopoietic stem cell (HSC) subpopulations following treatment with 5-fluorouracil (5-FU). Fluorouracil 319-323 interleukin 1 alpha Homo sapiens 27-46 8054813-0 1994 Augmentation of 5-fluorouracil cytotoxicity by epidermal growth factor in a newly established human signet-ring cell carcinoma of the stomach in culture. Fluorouracil 16-30 epidermal growth factor Homo sapiens 47-70 8054813-6 1994 The simultaneous treatment with EGF and 5-fluorouracil (5-FU) produced a nearly 2.4-fold enhancement of 5-FU cytotoxicity against TSG6 cells. Fluorouracil 56-60 epidermal growth factor Homo sapiens 32-35 8054813-6 1994 The simultaneous treatment with EGF and 5-fluorouracil (5-FU) produced a nearly 2.4-fold enhancement of 5-FU cytotoxicity against TSG6 cells. Fluorouracil 104-108 epidermal growth factor Homo sapiens 32-35 8054813-7 1994 A bromodeoxyuridine/DNA flow cytometry analysis revealed that EGF augmented 5-FU cytotoxicity by inducing the accumulation of S phase cells which might be more susceptible to 5-FU. Fluorouracil 76-80 epidermal growth factor Homo sapiens 62-65 8054813-7 1994 A bromodeoxyuridine/DNA flow cytometry analysis revealed that EGF augmented 5-FU cytotoxicity by inducing the accumulation of S phase cells which might be more susceptible to 5-FU. Fluorouracil 175-179 epidermal growth factor Homo sapiens 62-65 8054813-8 1994 Moreover, we found that the incorporation of 5-FU into the TSG6 cells was increased with the addition of EGF. Fluorouracil 45-49 epidermal growth factor Homo sapiens 105-108 8054813-9 1994 These data indicate that EGF may be a potent agent as a biological response modifier for 5-FU against the tumors which express the EGF/EGFR autocrine mechanism, and that the TSG6 cell line is useful in furthering our understanding of the interaction between anticancer drugs and EGF. Fluorouracil 89-93 epidermal growth factor Homo sapiens 25-28 8054813-9 1994 These data indicate that EGF may be a potent agent as a biological response modifier for 5-FU against the tumors which express the EGF/EGFR autocrine mechanism, and that the TSG6 cell line is useful in furthering our understanding of the interaction between anticancer drugs and EGF. Fluorouracil 89-93 epidermal growth factor Homo sapiens 131-134 8054813-9 1994 These data indicate that EGF may be a potent agent as a biological response modifier for 5-FU against the tumors which express the EGF/EGFR autocrine mechanism, and that the TSG6 cell line is useful in furthering our understanding of the interaction between anticancer drugs and EGF. Fluorouracil 89-93 epidermal growth factor Homo sapiens 131-134 8138551-1 1993 3-Cyano-2,6-dihydroxypyridine (CNDP) was identified as a potent inhibitor (IC50 value, 4.4 nM) of dihydrouracil dehydrogenase (DHUDase) [EC 1.3.1.2], a rate-limiting enzyme in 5-fluorouracil (5-FU) degradation. Fluorouracil 176-190 dihydropyrimidine dehydrogenase Rattus norvegicus 98-125 8138551-1 1993 3-Cyano-2,6-dihydroxypyridine (CNDP) was identified as a potent inhibitor (IC50 value, 4.4 nM) of dihydrouracil dehydrogenase (DHUDase) [EC 1.3.1.2], a rate-limiting enzyme in 5-fluorouracil (5-FU) degradation. Fluorouracil 176-190 dihydropyrimidine dehydrogenase Rattus norvegicus 127-134 8138551-1 1993 3-Cyano-2,6-dihydroxypyridine (CNDP) was identified as a potent inhibitor (IC50 value, 4.4 nM) of dihydrouracil dehydrogenase (DHUDase) [EC 1.3.1.2], a rate-limiting enzyme in 5-fluorouracil (5-FU) degradation. Fluorouracil 192-196 dihydropyrimidine dehydrogenase Rattus norvegicus 98-125 8138551-1 1993 3-Cyano-2,6-dihydroxypyridine (CNDP) was identified as a potent inhibitor (IC50 value, 4.4 nM) of dihydrouracil dehydrogenase (DHUDase) [EC 1.3.1.2], a rate-limiting enzyme in 5-fluorouracil (5-FU) degradation. Fluorouracil 192-196 dihydropyrimidine dehydrogenase Rattus norvegicus 127-134 8240657-10 1993 The differential effects of DPM on the potentiation of 5-FU cytotoxicity might be closely related to the cellular levels of FdUMP and its target enzyme, thymidylate synthase in three human maxillary cancer cell lines. Fluorouracil 55-59 thymidylate synthetase Homo sapiens 153-173 8398636-3 1993 Leucovorin, which is metabolized intracellularly to polyglutamated 5,10-methylenetetrahydrofolate, modulates the cellular cytotoxicity of fluorouracil by increasing TS inhibition in vitro and in vivo. Fluorouracil 138-150 thymidylate synthetase Homo sapiens 165-167 8481510-8 1993 In 8 of 10 patients whose marrow was studied before and after 5-FU treatment, the numbers of CFU-C responsive to the combination of GM-CSF and IL-3 was increased 6.15-fold by 5-FU pretreatment. Fluorouracil 62-66 colony stimulating factor 2 Homo sapiens 132-138 8481510-8 1993 In 8 of 10 patients whose marrow was studied before and after 5-FU treatment, the numbers of CFU-C responsive to the combination of GM-CSF and IL-3 was increased 6.15-fold by 5-FU pretreatment. Fluorouracil 62-66 interleukin 3 Homo sapiens 143-147 8481510-8 1993 In 8 of 10 patients whose marrow was studied before and after 5-FU treatment, the numbers of CFU-C responsive to the combination of GM-CSF and IL-3 was increased 6.15-fold by 5-FU pretreatment. Fluorouracil 175-179 colony stimulating factor 2 Homo sapiens 132-138 8481510-8 1993 In 8 of 10 patients whose marrow was studied before and after 5-FU treatment, the numbers of CFU-C responsive to the combination of GM-CSF and IL-3 was increased 6.15-fold by 5-FU pretreatment. Fluorouracil 175-179 interleukin 3 Homo sapiens 143-147 8474431-0 1993 Regulation of thymidylate synthase in human colon cancer cells treated with 5-fluorouracil and interferon-gamma. Fluorouracil 76-90 thymidylate synthetase Homo sapiens 14-34 8474431-1 1993 The effects of fluorouracil (5-FU) and interferon-gamma (IFN-gamma) on the regulation of thymidylate synthase (TS) gene expression were investigated in the human colon cancer H630 cell line. Fluorouracil 15-27 thymidylate synthetase Homo sapiens 89-109 8474431-1 1993 The effects of fluorouracil (5-FU) and interferon-gamma (IFN-gamma) on the regulation of thymidylate synthase (TS) gene expression were investigated in the human colon cancer H630 cell line. Fluorouracil 15-27 thymidylate synthetase Homo sapiens 111-113 8474431-1 1993 The effects of fluorouracil (5-FU) and interferon-gamma (IFN-gamma) on the regulation of thymidylate synthase (TS) gene expression were investigated in the human colon cancer H630 cell line. Fluorouracil 29-33 thymidylate synthetase Homo sapiens 89-109 8474431-1 1993 The effects of fluorouracil (5-FU) and interferon-gamma (IFN-gamma) on the regulation of thymidylate synthase (TS) gene expression were investigated in the human colon cancer H630 cell line. Fluorouracil 29-33 thymidylate synthetase Homo sapiens 111-113 8474431-4 1993 A 24-hr exposure to 1 microM 5-FU resulted in a 4.5-fold increase in the level of TS protein, whereas in 5-FU/IFN-gamma-treated cells TS protein was increased by only 1.8-fold, compared with control cells. Fluorouracil 29-33 thymidylate synthetase Homo sapiens 82-84 8474431-8 1993 Pulse-chase studies revealed that the half-lives of TS protein in control and 5-FU-treated cells were equivalent. Fluorouracil 78-82 thymidylate synthetase Homo sapiens 52-54 8474431-9 1993 These findings demonstrate that the increase in TS protein after 5-FU exposure and the subsequent inhibitory effect of IFN-gamma on TS protein expression are both regulated at the post-transcriptional level. Fluorouracil 65-69 thymidylate synthetase Homo sapiens 48-50 8453096-6 1993 However, the MIP-1 alpha protocol used here did substantially decrease the number of more mature hematopoietic progenitors (granulocyte-macrophage colony-forming cells [CFC], burst-forming unit-erythroid, CFCmulti, and preCFCmulti) recovered in the bone marrow shortly after a single 5-FU injection. Fluorouracil 284-288 C-C motif chemokine ligand 3 Homo sapiens 13-24 8452386-3 1993 And in normal FdUMP, an active metabolite of 5-FU, binds tightly to thymidylate synthase in the presence of cofactor, 5, 10-methylene tetrahydrofolate. Fluorouracil 45-49 thymidylate synthetase Homo sapiens 68-88 8452386-4 1993 This interaction leads to potentiate the cytotoxic effect of 5-FU by prolonged inhibition of thymidylate synthase. Fluorouracil 61-65 thymidylate synthetase Homo sapiens 93-113 21573550-1 1993 Thymidylate synthase (TS) is an essential enzyme for DNA biosynthesis that is an important target of fluoropyrimidine anti-cancer drugs such as 5-fluorouracil (5-FU), which is frequently used against human colon adenocarcinomas. Fluorouracil 144-158 thymidylate synthetase Homo sapiens 0-20 21573550-1 1993 Thymidylate synthase (TS) is an essential enzyme for DNA biosynthesis that is an important target of fluoropyrimidine anti-cancer drugs such as 5-fluorouracil (5-FU), which is frequently used against human colon adenocarcinomas. Fluorouracil 160-164 thymidylate synthetase Homo sapiens 0-20 8304192-0 1993 Potentiation of 5-fluorouracil induced inhibition of thymidylate synthase in human colon tumors by leucovorin is dose dependent. Fluorouracil 16-30 thymidylate synthetase Homo sapiens 53-73 8178713-0 1993 Regulation of thymidylate synthase in human colon cancer cells treated with 5-fluorouracil and interferon-gamma. Fluorouracil 76-90 thymidylate synthetase Homo sapiens 14-34 8178733-0 1993 Comparison of continuous infusions and bolus injections of 5-fluorouracil with or without leucovorin: implications for inhibition of thymidylate synthase. Fluorouracil 59-73 thymidylate synthetase Homo sapiens 133-153 8339382-1 1993 The present study shows that various cytokines such as tumor necrosis factor (TNF alpha), interleukin-1 alpha (IL-1 alpha), and interferon-gamma (IFN gamma) make tumor cells much more susceptible to the cytostatic 5"-deoxy-5-fluorouridine (5"-dFUrd) than to 5-fluorouracil (5-FUra) and other cytostatics. Fluorouracil 258-272 interleukin 1 alpha Homo sapiens 90-109 8339382-1 1993 The present study shows that various cytokines such as tumor necrosis factor (TNF alpha), interleukin-1 alpha (IL-1 alpha), and interferon-gamma (IFN gamma) make tumor cells much more susceptible to the cytostatic 5"-deoxy-5-fluorouridine (5"-dFUrd) than to 5-fluorouracil (5-FUra) and other cytostatics. Fluorouracil 258-272 interleukin 1 alpha Homo sapiens 111-121 8339382-1 1993 The present study shows that various cytokines such as tumor necrosis factor (TNF alpha), interleukin-1 alpha (IL-1 alpha), and interferon-gamma (IFN gamma) make tumor cells much more susceptible to the cytostatic 5"-deoxy-5-fluorouridine (5"-dFUrd) than to 5-fluorouracil (5-FUra) and other cytostatics. Fluorouracil 274-280 interleukin 1 alpha Homo sapiens 90-109 8339382-1 1993 The present study shows that various cytokines such as tumor necrosis factor (TNF alpha), interleukin-1 alpha (IL-1 alpha), and interferon-gamma (IFN gamma) make tumor cells much more susceptible to the cytostatic 5"-deoxy-5-fluorouridine (5"-dFUrd) than to 5-fluorouracil (5-FUra) and other cytostatics. Fluorouracil 274-280 interleukin 1 alpha Homo sapiens 111-121 8500227-2 1993 Leucovorin is metabolized to methylene tetrahydrofolate, which potentiates the antitumor actions of 5-FU by forming a ternary complex of thymidylate synthase, fluorodeoxyuridine and methylene tetrahydrofolate. Fluorouracil 100-104 thymidylate synthetase Homo sapiens 137-157 8432620-2 1993 Bone marrow precursor cells, from mice treated with 5-fluorouracil (FUBM), when cultured with IL-2, generated mature NK cells. Fluorouracil 52-66 interleukin 2 Mus musculus 94-98 1449107-1 1992 A Phase I study was conducted to determine whether the addition of recombinant human granulocyte-macrophage colony-stimulating factor (rhGM-CSF) to a combined 5-fluorouracil (5-FU) and folinic acid (FA) regimen would allow an escalated starting dose of 5-FU. Fluorouracil 175-179 colony stimulating factor 2 Homo sapiens 85-133 1449107-1 1992 A Phase I study was conducted to determine whether the addition of recombinant human granulocyte-macrophage colony-stimulating factor (rhGM-CSF) to a combined 5-fluorouracil (5-FU) and folinic acid (FA) regimen would allow an escalated starting dose of 5-FU. Fluorouracil 253-257 colony stimulating factor 2 Homo sapiens 85-133 1382702-4 1992 The stimulatory effect of SCF was approximately three to four times as high as that of IL-6 on the primitive progenitors capable of megakaryocytic-lineage expression derived from 5-FU-treated mice. Fluorouracil 179-183 kit ligand Mus musculus 26-29 1519926-7 1992 Comparing the 5-FU levels and TS activity according to the histological effects (i.e.: "grade-0" vs "grade-1"), the 5-FU levels in the tumors achieved grade-1 were significantly higher than in the tumors showed "grade 0" (p less than 0.01), and TSIR in the former were relatively greater than in the latter (p = 0.053). Fluorouracil 116-120 thymidylate synthetase Homo sapiens 30-32 1520312-0 1992 Effect of 5-fluorouracil on interleukin-2 expression. Fluorouracil 10-24 interleukin 2 Rattus norvegicus 28-41 1520312-1 1992 The effect of 5-fluorouracil on the expression of IL-2 gene and the production of IL-2 protein has been studied using spleenic lymphocytes of rats. Fluorouracil 14-28 interleukin 2 Rattus norvegicus 50-54 1520312-1 1992 The effect of 5-fluorouracil on the expression of IL-2 gene and the production of IL-2 protein has been studied using spleenic lymphocytes of rats. Fluorouracil 14-28 interleukin 2 Rattus norvegicus 82-86 1520312-3 1992 The results show that there is up to 3.75 fold increase in the production of IL-2 message in 5-fluorouracil treated lymphocytes over Con A treated controls. Fluorouracil 93-107 interleukin 2 Rattus norvegicus 77-81 1520312-4 1992 There is also a concomitant increase in IL-2 protein production upon 5-fluorouracil treatment in rat lymphocytes. Fluorouracil 69-83 interleukin 2 Rattus norvegicus 40-44 1379852-0 1992 Evidence that stem cell factor is involved in the rebound thrombocytosis that follows 5-fluorouracil treatment. Fluorouracil 86-100 kit ligand Mus musculus 14-30 1379852-3 1992 Recent reports by several groups that the SI locus encodes a protein known variably as stem cell factor (SCF), mast cell growth factor, or kit ligand, suggests the possibility that the lack of wild-type SCF in SI/SI(d) mice is responsible for their defective response to 5FU-induced thrombocytopenia. Fluorouracil 271-274 kit ligand Mus musculus 87-103 1643628-0 1992 Immunological quantitation of thymidylate synthase using the monoclonal antibody TS 106 in 5-fluorouracil-sensitive and -resistant human cancer cell lines. Fluorouracil 91-105 thymidylate synthetase Homo sapiens 30-50 1643628-0 1992 Immunological quantitation of thymidylate synthase using the monoclonal antibody TS 106 in 5-fluorouracil-sensitive and -resistant human cancer cell lines. Fluorouracil 91-105 thymidylate synthetase Homo sapiens 81-83 1643628-3 1992 Densitometric quantitation of TS 106-labeled Western immunoblot analysis of cell lysates from two 5-FU-resistant colon carcinoma cell lines, NCI H630R1 and NCI H630R10, revealed 12.8- and 16-fold increases in TS, respectively, compared to the parent 5-FU-sensitive NCI H630 colon cell line. Fluorouracil 250-254 thymidylate synthetase Homo sapiens 30-32 1643628-11 1992 This revealed a 26-fold increase in TS in the 5-FU-resistant NCI H630R10 line compared to the parent NCI H630 line and a 3.5-fold increase in TS compared to the 5-FU-resistant MCF-Ad10 breast cell line. Fluorouracil 46-50 thymidylate synthetase Homo sapiens 36-38 1643628-12 1992 The 5-FU-resistant MCF-Ad10 breast cell line, in turn, displayed a 7.7-fold increase in TS, compared to the 5-FU-sensitive NCI H630 cell lines. Fluorouracil 4-8 thymidylate synthetase Homo sapiens 88-90 1638519-2 1992 The results presented herein demonstrate that the pretreatment of mice with recombinant human interleukin 1 alpha (rhIL-1 alpha) protects mice from the lethal effects of several myelotoxic chemotherapeutic drugs, including 5-fluorouracil (5FUra), cyclophosphamide, cis-diammine(1,1-cyclobutanedicarboxylato)platinum(II), and 1,3-bis-(2-chloroethyl)-1-nitrosourea. Fluorouracil 223-237 interleukin 1 alpha Homo sapiens 94-113 1634917-1 1992 PURPOSE: The use of leucovorin (LV) to modulate fluorouracil (FU)-mediated inhibition of thymidylate synthase has been shown both in vitro and in vivo to improve the antitumor activity of this drug. Fluorouracil 48-60 thymidylate synthetase Homo sapiens 89-109 1626951-2 1992 FdUMP which is an active metabolite of 5-FU binds tightly to thymidylate synthase in the presence of the cofactor 5, 10-methylene tetrahydrofolate. Fluorouracil 39-43 thymidylate synthetase Homo sapiens 61-81 1626951-3 1992 This interaction leads to potentiate the cytotoxic effect of 5-FU by prolonged inhibition of thymidylate synthase. Fluorouracil 61-65 thymidylate synthetase Homo sapiens 93-113 1904428-6 1991 HCFU was effective against both strains and 5-FU was effective against Co-4, although the other agents were ineffective against either strain. Fluorouracil 44-48 complement C4A (Rodgers blood group) Homo sapiens 71-75 2148086-1 1990 Lysyl-tRNA synthetase isolated from rat liver cleaves glycosidic bond of 5-Fluorouridine and 5-Fluoro-2"-deoxyuridine to generate 5-Fluorouracil. Fluorouracil 130-144 lysyl-tRNA synthetase 1 Rattus norvegicus 0-21 2239803-1 1990 It has been suggested that the addition of weekly low-dose cisplatin (DDP) may potentiate the efficacy of continuous infusion 5-fluorouracil (5-FU) without adding significant toxicity. Fluorouracil 126-140 translocase of inner mitochondrial membrane 8A Homo sapiens 70-73 2239803-1 1990 It has been suggested that the addition of weekly low-dose cisplatin (DDP) may potentiate the efficacy of continuous infusion 5-fluorouracil (5-FU) without adding significant toxicity. Fluorouracil 142-146 translocase of inner mitochondrial membrane 8A Homo sapiens 70-73 2239803-6 1990 Compared with historical toxicity patterns when 5-FU infusion is administered alone, the addition of DDP has resulted in significant increases in nausea and vomiting, anorexia, diarrhea, stomatitis, and myelosuppression. Fluorouracil 48-52 translocase of inner mitochondrial membrane 8A Homo sapiens 101-104 2239803-7 1990 The addition of low-dose weekly DDP adds significant toxicity and morbidity to the continuous 5-FU infusion regimen. Fluorouracil 94-98 translocase of inner mitochondrial membrane 8A Homo sapiens 32-35 2092280-1 1990 Modulation of 5-FU cytotoxicity by GM-CSF. Fluorouracil 14-18 colony stimulating factor 2 Homo sapiens 35-41 2092282-0 1990 [Modulation of the biochemical effect of 5-fluorouracil (5-FU) by leucovorin measured by thymidylate synthase activity and nucleoside incorporation into DNA]. Fluorouracil 41-55 thymidylate synthetase Homo sapiens 89-109 2092282-0 1990 [Modulation of the biochemical effect of 5-fluorouracil (5-FU) by leucovorin measured by thymidylate synthase activity and nucleoside incorporation into DNA]. Fluorouracil 57-61 thymidylate synthetase Homo sapiens 89-109 2092282-7 1990 Neither with sequential nor with simultaneous application of both substances was it possible to demonstrate a significantly increased substances was it possible to demonstrate a significantly increased inhibition of TS as compared with 5-FU alone. Fluorouracil 236-240 thymidylate synthetase Homo sapiens 216-218 2128782-7 1990 The decreases in the ER and PgR levels in responsive tumors after treatment were considerably greater in the groups greated with TAM alone and the combination of 5-FU and TAM than in the group treated with 5-FU alone. Fluorouracil 162-166 progesterone receptor Rattus norvegicus 28-31 2128782-7 1990 The decreases in the ER and PgR levels in responsive tumors after treatment were considerably greater in the groups greated with TAM alone and the combination of 5-FU and TAM than in the group treated with 5-FU alone. Fluorouracil 206-210 estrogen receptor 1 Rattus norvegicus 21-23 2128782-7 1990 The decreases in the ER and PgR levels in responsive tumors after treatment were considerably greater in the groups greated with TAM alone and the combination of 5-FU and TAM than in the group treated with 5-FU alone. Fluorouracil 206-210 progesterone receptor Rattus norvegicus 28-31 1697502-8 1990 Moreover, we found that free thymidylate synthase in the 5-FU/IFN-gamma-treated cells was significantly decreased, as compared to the cells treated with 5-FU alone. Fluorouracil 57-61 thymidylate synthetase Homo sapiens 29-49 1697502-8 1990 Moreover, we found that free thymidylate synthase in the 5-FU/IFN-gamma-treated cells was significantly decreased, as compared to the cells treated with 5-FU alone. Fluorouracil 153-157 thymidylate synthetase Homo sapiens 29-49 2344373-9 1990 Also in these cells, at concentrations of FUra less than 100 microM, FUra cytotoxicity appeared to be mediated via the inhibition of thymidylate synthase. Fluorouracil 69-73 thymidylate synthetase Homo sapiens 133-153 33798029-0 2021 Characterization of the binding between anti-tumor drug 5-fluorouracil and human alpha-2-macroglobulin: spectroscopic and molecular docking analyses. Fluorouracil 56-70 alpha-2-macroglobulin Homo sapiens 81-102 33798029-3 2021 Present work investigates the interaction between 5-FU and human major antiproteinase-alpha-2-macroglobulin (alpha2M) by multi-spectroscopic, calorimetric and molecular docking techniques. Fluorouracil 50-54 alpha-2-macroglobulin Homo sapiens 109-116 33798029-4 2021 UV/Visible absorption, intrinsic fluorescence and circular dichroism (CD) spectroscopic methods have been employed to unveil the mode and mechanism of 5-FU-alpha2M interaction. Fluorouracil 151-155 alpha-2-macroglobulin Homo sapiens 156-163 33798029-6 2021 Far UV-CD spectra suggest slight alterations in the secondary structure of alpha2M by 5-FU. Fluorouracil 86-90 alpha-2-macroglobulin Homo sapiens 75-82 33798029-10 2021 Molecular dynamics simulation studies suggested that 5-FU was stabilizing the alpha2M structure and forming a stable complex. Fluorouracil 53-57 alpha-2-macroglobulin Homo sapiens 78-85 33798029-11 2021 It was concluded that 5-FU lower the antiproteolytic activity of alpha2M significantly and causes disruption in the native structure and conformation of alpha2M.Communicated by Ramaswamy H. Sarma. Fluorouracil 22-26 alpha-2-macroglobulin Homo sapiens 65-72 33798029-11 2021 It was concluded that 5-FU lower the antiproteolytic activity of alpha2M significantly and causes disruption in the native structure and conformation of alpha2M.Communicated by Ramaswamy H. Sarma. Fluorouracil 22-26 alpha-2-macroglobulin Homo sapiens 153-160 33805673-8 2021 Interestingly, HCT116RF10 cells were regulated by the function of thymidylate synthase (TS), a 5-FU active metabolite 5-fluorodeoxyuridine monophosphate (FdUMP) inhibiting enzyme. Fluorouracil 95-99 thymidylate synthetase Homo sapiens 66-86 33805673-8 2021 Interestingly, HCT116RF10 cells were regulated by the function of thymidylate synthase (TS), a 5-FU active metabolite 5-fluorodeoxyuridine monophosphate (FdUMP) inhibiting enzyme. Fluorouracil 95-99 thymidylate synthetase Homo sapiens 88-90 33805673-10 2021 This finding indicates that 5-FU-resistant cells exhibited increased TS expression, and the TS enzyme is used to trap FdUMP, resulting in resistance to 5-FU and its analogs. Fluorouracil 28-32 thymidylate synthetase Homo sapiens 69-71 33805673-10 2021 This finding indicates that 5-FU-resistant cells exhibited increased TS expression, and the TS enzyme is used to trap FdUMP, resulting in resistance to 5-FU and its analogs. Fluorouracil 152-156 thymidylate synthetase Homo sapiens 92-94 34749259-3 2022 The fluorescence data indicated both Fe3O4 NPs and 5-FU could quench the intrinsic fluorescence of beta-CN. Fluorouracil 51-55 apoptotic chromatin condensation inducer 1 Homo sapiens 99-106 34749259-4 2022 Fluorescence measurements showed that the single interaction of beta-CN with 5-FU or Fe3O4 NPs was static, while reacted beta-CN with both 5-FU and Fe3O4 NPs simultaneously showed a dynamic quenching. Fluorouracil 77-81 apoptotic chromatin condensation inducer 1 Homo sapiens 64-71 34749259-4 2022 Fluorescence measurements showed that the single interaction of beta-CN with 5-FU or Fe3O4 NPs was static, while reacted beta-CN with both 5-FU and Fe3O4 NPs simultaneously showed a dynamic quenching. Fluorouracil 139-143 apoptotic chromatin condensation inducer 1 Homo sapiens 121-128 34749259-5 2022 Synchronous fluorescence data in both tests revealed that the tryptophan (Trp) residue of beta-CN had a dominant role in quenching and the polarity of its microenvironment more than tyrosine (Tyr) increased in interaction with 5-FU. Fluorouracil 227-231 apoptotic chromatin condensation inducer 1 Homo sapiens 90-97 34749259-7 2022 The CD spectra in the region of far-UV and thermal denaturation study indicated minor changes in the secondary structure of beta-CN in the presence of various concentrations of Fe3O4 NPs and 5-FU. Fluorouracil 191-195 apoptotic chromatin condensation inducer 1 Homo sapiens 124-131 34749259-9 2022 The outcomes highlighted that beta-CN protein could form a great bind with 5-FU and Fe3O4 NPs ligands (supporting the zeta potential assay results) by independent binding sites. Fluorouracil 75-79 apoptotic chromatin condensation inducer 1 Homo sapiens 30-37 34749259-10 2022 These results would be helpful insight to construct a potential magnetic nanocarrier beta-CN base for 5-FU drug delivery. Fluorouracil 102-106 apoptotic chromatin condensation inducer 1 Homo sapiens 85-92 34952246-3 2022 In this study, we aimed to investigate the interaction between MLH1 and the autophagy marker LC3, which facilitated nucleophagy induction, and its potential role in determining sensitivity to 5-Fluorouracil (5-FU) induced cell death. Fluorouracil 192-206 microtubule-associated protein 1 light chain 3 alpha Mus musculus 93-96 34952246-3 2022 In this study, we aimed to investigate the interaction between MLH1 and the autophagy marker LC3, which facilitated nucleophagy induction, and its potential role in determining sensitivity to 5-Fluorouracil (5-FU) induced cell death. Fluorouracil 208-212 microtubule-associated protein 1 light chain 3 alpha Mus musculus 93-96 34952246-7 2022 The 5-FU induced DNA damage led to LC3 up-regulation, which was dependent on MLH1 overexpression. Fluorouracil 4-8 microtubule-associated protein 1 light chain 3 alpha Mus musculus 35-38 34665902-10 2022 The immunoblotting analysis also showed that thymol significantly inhibited the 5-FU-induced expression of nuclear factor-kappaB, tumor necrosis factor-alpha, and transforming growth factor beta-1 (TGF-beta1), in addition to the suppression of p38 and phosphorylated c-Jun N-terminal kinases (p-JNK) mitogen-activated protein kinase proteins" expressions. Fluorouracil 80-84 mitogen-activated protein kinase 8 Rattus norvegicus 295-298 34845374-0 2022 Thymidylate synthase O-GlcNAcylation: a molecular mechanism of 5-FU sensitization in colorectal cancer. Fluorouracil 63-67 thymidylate synthetase Homo sapiens 0-20 34845374-3 2022 Standard treatment for colorectal cancer (CRC), 5-fluorouracil (5-FU), mainly targets Thymidylate Synthase (TS). Fluorouracil 48-62 thymidylate synthetase Homo sapiens 86-106 34845374-3 2022 Standard treatment for colorectal cancer (CRC), 5-fluorouracil (5-FU), mainly targets Thymidylate Synthase (TS). Fluorouracil 64-68 thymidylate synthetase Homo sapiens 86-106 34845374-8 2022 In vitro in non-cancerous and cancerous colon cells, we showed that 5-FU impacts O-GlcNAcylation by decreasing O-GlcNAc Transferase (OGT) expression both at mRNA and protein levels. Fluorouracil 68-72 O-linked N-acetylglucosamine (GlcNAc) transferase Homo sapiens 111-131 34845374-8 2022 In vitro in non-cancerous and cancerous colon cells, we showed that 5-FU impacts O-GlcNAcylation by decreasing O-GlcNAc Transferase (OGT) expression both at mRNA and protein levels. Fluorouracil 68-72 O-linked N-acetylglucosamine (GlcNAc) transferase Homo sapiens 133-136 34845374-9 2022 Reciprocally, OGT knockdown decreased 5-FU-induced cancer cell apoptosis by reducing TS protein level and activity. Fluorouracil 38-42 O-linked N-acetylglucosamine (GlcNAc) transferase Homo sapiens 14-17 34966683-0 2021 Circular RNA CircPVT1 Inhibits 5-Fluorouracil Chemosensitivity by Regulating Ferroptosis Through MiR-30a-5p/FZD3 Axis in Esophageal Cancer Cells. Fluorouracil 31-45 Pvt1 oncogene Homo sapiens 13-21 34966683-2 2021 However, the role and potential functional mechanisms of circPVT1 in regulating 5-fluorouracil (5-FU) chemosensitivity remain largely unknown. Fluorouracil 80-94 Pvt1 oncogene Homo sapiens 57-65 34966683-2 2021 However, the role and potential functional mechanisms of circPVT1 in regulating 5-fluorouracil (5-FU) chemosensitivity remain largely unknown. Fluorouracil 96-100 Pvt1 oncogene Homo sapiens 57-65 34966683-10 2021 Results: CircPVT1 was significantly upregulated in ESCC cells resistant to 5-FU. Fluorouracil 75-79 Pvt1 oncogene Homo sapiens 9-17 34966683-11 2021 Knockdown of circPVT1 enhanced the 5-FU chemosensitivity of ESCC cells resistant to 5-FU by increasing cytotoxicity and downregulating multidrug-resistant associated proteins, including P-gp and MRP1. Fluorouracil 35-39 Pvt1 oncogene Homo sapiens 13-21 34966683-11 2021 Knockdown of circPVT1 enhanced the 5-FU chemosensitivity of ESCC cells resistant to 5-FU by increasing cytotoxicity and downregulating multidrug-resistant associated proteins, including P-gp and MRP1. Fluorouracil 35-39 phosphoglycolate phosphatase Homo sapiens 186-190 34966683-11 2021 Knockdown of circPVT1 enhanced the 5-FU chemosensitivity of ESCC cells resistant to 5-FU by increasing cytotoxicity and downregulating multidrug-resistant associated proteins, including P-gp and MRP1. Fluorouracil 35-39 MDM4 regulator of p53 Homo sapiens 195-199 34966683-11 2021 Knockdown of circPVT1 enhanced the 5-FU chemosensitivity of ESCC cells resistant to 5-FU by increasing cytotoxicity and downregulating multidrug-resistant associated proteins, including P-gp and MRP1. Fluorouracil 84-88 Pvt1 oncogene Homo sapiens 13-21 34966683-11 2021 Knockdown of circPVT1 enhanced the 5-FU chemosensitivity of ESCC cells resistant to 5-FU by increasing cytotoxicity and downregulating multidrug-resistant associated proteins, including P-gp and MRP1. Fluorouracil 84-88 phosphoglycolate phosphatase Homo sapiens 186-190 34966683-11 2021 Knockdown of circPVT1 enhanced the 5-FU chemosensitivity of ESCC cells resistant to 5-FU by increasing cytotoxicity and downregulating multidrug-resistant associated proteins, including P-gp and MRP1. Fluorouracil 84-88 MDM4 regulator of p53 Homo sapiens 195-199 34966683-13 2021 The enhanced 5-FU chemosensitivity by circPVT1 knockdown was reversed with miR-30a-5p inhibitor. Fluorouracil 13-17 Pvt1 oncogene Homo sapiens 38-46 34966683-16 2021 Conclusions: These results suggested a key role for circPVT1 in ESCC 5-FU-chemosensitivity in regulating the Wnt/beta-catenin pathway and ferroptosis via miR-30a-5p/FZD3 axis, which might be a potential target in ESCC therapy. Fluorouracil 69-73 Pvt1 oncogene Homo sapiens 52-60 34966683-16 2021 Conclusions: These results suggested a key role for circPVT1 in ESCC 5-FU-chemosensitivity in regulating the Wnt/beta-catenin pathway and ferroptosis via miR-30a-5p/FZD3 axis, which might be a potential target in ESCC therapy. Fluorouracil 69-73 catenin beta 1 Homo sapiens 113-125 34773342-5 2022 We investigated the influence of chemotherapeutic drugs (cisplatin and fluorouracil) on PD-L1/L2 expression and PD-L1/L2-related pathways in vitro. Fluorouracil 71-83 CD274 molecule Homo sapiens 88-93 34605863-7 2021 Moreover, exosome-incubated A549 cells were co-transfected with si-FOXD3-AS1 and pcDNA-ELAVL1, showing the same cell proliferation, invasion, and 5-FU resistance as those of A549 cells treated with lung cancer cell-derived exosomes alone. Fluorouracil 146-150 ELAV like RNA binding protein 1 Homo sapiens 87-93 34747284-6 2021 5-FU injection caused marked elevation of MDA, NO, TNF-alpha, IL-1beta, IL-6, PAF, histamine, myeloperoxidase, caspase-3, and NF-kappaB expressions. Fluorouracil 0-4 myeloperoxidase Rattus norvegicus 94-109 34790580-10 2021 Restoration of the expression of HOXD10 in 5-fluorouracil (5-FU)-resistant cells significantly upregulates the expressions of miR-7 and IGFBP3 and enhances chemosensitivity to 5-FU. Fluorouracil 43-57 insulin like growth factor binding protein 3 Homo sapiens 136-142 34790580-10 2021 Restoration of the expression of HOXD10 in 5-fluorouracil (5-FU)-resistant cells significantly upregulates the expressions of miR-7 and IGFBP3 and enhances chemosensitivity to 5-FU. Fluorouracil 59-63 insulin like growth factor binding protein 3 Homo sapiens 136-142 34562873-0 2021 Apigenin enhances apoptosis induction by 5-fluorouracil through regulation of thymidylate synthase in colorectal cancer cells. Fluorouracil 41-55 thymidylate synthetase Homo sapiens 78-98 34562873-2 2021 Thymidylate synthase (TS) is a target protein of 5-FU, and elevated TS lowers the 5-FU sensitivity of CRC cells. Fluorouracil 49-53 thymidylate synthetase Homo sapiens 0-20 34562873-2 2021 Thymidylate synthase (TS) is a target protein of 5-FU, and elevated TS lowers the 5-FU sensitivity of CRC cells. Fluorouracil 49-53 thymidylate synthetase Homo sapiens 22-24 34562873-2 2021 Thymidylate synthase (TS) is a target protein of 5-FU, and elevated TS lowers the 5-FU sensitivity of CRC cells. Fluorouracil 49-53 thymidylate synthetase Homo sapiens 68-70 34562873-2 2021 Thymidylate synthase (TS) is a target protein of 5-FU, and elevated TS lowers the 5-FU sensitivity of CRC cells. Fluorouracil 82-86 thymidylate synthetase Homo sapiens 0-20 34562873-2 2021 Thymidylate synthase (TS) is a target protein of 5-FU, and elevated TS lowers the 5-FU sensitivity of CRC cells. Fluorouracil 82-86 thymidylate synthetase Homo sapiens 22-24 34562873-2 2021 Thymidylate synthase (TS) is a target protein of 5-FU, and elevated TS lowers the 5-FU sensitivity of CRC cells. Fluorouracil 82-86 thymidylate synthetase Homo sapiens 68-70 34562873-5 2021 In addition, apigenin inhibited the upregulation of TS induced by 5-FU. Fluorouracil 66-70 thymidylate synthetase Homo sapiens 52-54 34562873-10 2021 Therefore, apigenin may improve the therapeutic efficacy of 5-FU against CRC by suppressing TS, but apoptosis induction is mainly dependent on functional P53. Fluorouracil 60-64 thymidylate synthetase Homo sapiens 92-94 34531676-5 2021 A recent study showed that HSPB1 could be a new therapeutic target for colorectal cancer with 5-fluorouracil-acquired resistance. Fluorouracil 94-108 heat shock protein family B (small) member 1 Homo sapiens 27-32 34373709-0 2021 mRNA expression level of CDH2, LEP, POSTN, TIMP1 and VEGFC modulates 5-fluorouracil resistance in colon cancer cells. Fluorouracil 69-83 leptin Homo sapiens 31-34 34373709-0 2021 mRNA expression level of CDH2, LEP, POSTN, TIMP1 and VEGFC modulates 5-fluorouracil resistance in colon cancer cells. Fluorouracil 69-83 periostin Homo sapiens 36-41 34373709-13 2021 Taken together, the results suggested that CDH2, LEP, POSTN, TIMP1 and VEGFC might play a role in chemotherapeutic resistance in colon cancer and represent potential targets for overcoming 5-FU resistance in colon cancer. Fluorouracil 189-193 leptin Homo sapiens 49-52 34373709-13 2021 Taken together, the results suggested that CDH2, LEP, POSTN, TIMP1 and VEGFC might play a role in chemotherapeutic resistance in colon cancer and represent potential targets for overcoming 5-FU resistance in colon cancer. Fluorouracil 189-193 periostin Homo sapiens 54-59 34571731-5 2021 Certain resistance mechanisms that are 5-FU-specific have also been ascertained to include the upregulation of thymidylate synthase, dihydropyrimidine dehydrogenase, methylenetetrahydrofolate reductase, and the downregulation of thymidine phosphorylase. Fluorouracil 39-43 thymidylate synthetase Homo sapiens 111-131 34489705-14 2021 Compared with untreated group and 5-FU group, CHB-II-F also enhanced the expression of OX1R, GHSR, NPY, and AgRP protein and gene and decreased the expression of Ob-R, POMC, and CART protein and gene in hypothalamus of mice, and the gene expression was consistent with the protein expression. Fluorouracil 34-38 growth hormone secretagogue receptor Mus musculus 93-97 34489705-14 2021 Compared with untreated group and 5-FU group, CHB-II-F also enhanced the expression of OX1R, GHSR, NPY, and AgRP protein and gene and decreased the expression of Ob-R, POMC, and CART protein and gene in hypothalamus of mice, and the gene expression was consistent with the protein expression. Fluorouracil 34-38 leptin receptor Mus musculus 162-166 34485154-8 2021 5-FU promoted the expression of Keap1 and increased the binding to NF-E2-related factor 2 (Nrf2) to reduce the nuclear translocation of Nrf2, thereby weakening the transcriptional activity of Nrf2 to inhibit the expression of HO-1; reducing the activity of GSH, SOD, and CAT to increase ROS content; and aggravating DNA damage (indicated by the increase in 8-OHdG). Fluorouracil 0-4 heme oxygenase 1 Homo sapiens 226-230 34389726-6 2021 Mice lacking PD-L1+ and XCR1+ DC have a proinflammatory gut milieu associated with an increase in Th1/Th17 cells and a decrease in Treg cells and have exacerbated disease in the models of 5-FU-induced mucositis and DSS-induced colitis. Fluorouracil 188-192 chemokine (C motif) receptor 1 Mus musculus 24-28 34382859-9 2021 GA inhibited the activation of protein kinase B/nuclear factor signaling; this effect was potentiated with GA and 5-fluorouracil (5-FU), which also enhanced 5-FU-induced apoptosis. Fluorouracil 114-128 protein tyrosine kinase 2 beta Homo sapiens 31-47 34382859-9 2021 GA inhibited the activation of protein kinase B/nuclear factor signaling; this effect was potentiated with GA and 5-fluorouracil (5-FU), which also enhanced 5-FU-induced apoptosis. Fluorouracil 130-134 protein tyrosine kinase 2 beta Homo sapiens 31-47 34382859-9 2021 GA inhibited the activation of protein kinase B/nuclear factor signaling; this effect was potentiated with GA and 5-fluorouracil (5-FU), which also enhanced 5-FU-induced apoptosis. Fluorouracil 157-161 protein tyrosine kinase 2 beta Homo sapiens 31-47 34440086-2 2021 As an antimetabolite, 5-FU inhibits thymidylate synthase to disrupt the synthesis and repair of DNA and RNA. Fluorouracil 22-26 thymidylate synthetase Homo sapiens 36-56 34589581-10 2021 Finally, in vitro and in vivo xenograft experiments consistently demonstrated that inhibition of EGFR by the specific inhibitor erlotinib effectively enhanced the anti-tumor toxicity of 5-Fu by targeting the EGFR-FGD5-AS1-miR-330-3p-HK2 pathway. Fluorouracil 186-190 microRNA 330 Homo sapiens 222-229 34185243-8 2021 Furthermore, the 5FU group showed toxic histopathological changes including marked cardiac damage and a significant decrease in reduced glutathione (GSH), total antioxidant capacity (TAC), and peroxisome proliferator-activated receptor alpha (PPARalpha) expression. Fluorouracil 17-20 peroxisome proliferator activated receptor alpha Homo sapiens 193-241 34185243-8 2021 Furthermore, the 5FU group showed toxic histopathological changes including marked cardiac damage and a significant decrease in reduced glutathione (GSH), total antioxidant capacity (TAC), and peroxisome proliferator-activated receptor alpha (PPARalpha) expression. Fluorouracil 17-20 peroxisome proliferator activated receptor alpha Homo sapiens 243-252 34185243-9 2021 FEN reversed 5FU-induced cardiotoxicity by various mechanisms including upregulation of PPARalpha, inhibition of the IL-6/STAT signaling pathway, and anti-inflammatory, antiapoptotic, and antioxidant properties. Fluorouracil 13-16 peroxisome proliferator activated receptor alpha Homo sapiens 88-97 34168463-3 2021 The expressions of OCT3/4 and Nanog in cells treated with 5-Fu or CDDP were measured by immunofluorescence, Western blot and qPCR. Fluorouracil 58-62 POU class 5 homeobox 1 Homo sapiens 19-25 34268937-13 2021 CONCLUSIONS: The overexpression of miR-183 can inhibit the drug resistance of the human primary laryngeal cancer cells to 5-Fu, promote cancer cell apoptosis and inhibit their invasive and migratory abilities at the same time, whose mechanism may be associated with the targeted regulation of the TBX3/PTEN signaling pathway by miR-183. Fluorouracil 122-126 T-box transcription factor 3 Homo sapiens 297-301 34268937-13 2021 CONCLUSIONS: The overexpression of miR-183 can inhibit the drug resistance of the human primary laryngeal cancer cells to 5-Fu, promote cancer cell apoptosis and inhibit their invasive and migratory abilities at the same time, whose mechanism may be associated with the targeted regulation of the TBX3/PTEN signaling pathway by miR-183. Fluorouracil 122-126 phosphatase and tensin homolog Homo sapiens 302-306 34631487-5 2021 Further, Annexin-V Flow cytometry was used for determining the effects of melatonin and 5-FU on the apoptosis of SW-480 cell lines. Fluorouracil 88-92 annexin A5 Homo sapiens 9-18 34185773-12 2021 5-FU treatment caused an increase in BCKDH activity that appears to result mainly from increased dephosphorylation of the complex and is associated with an increase of PPM1K mRNA level and reduction of BDK and E1 mRNA levels. Fluorouracil 0-4 protein phosphatase, Mg2+/Mn2+ dependent, 1K Rattus norvegicus 168-173 35606881-9 2022 Moreover, through CRISPR library screening, ZEB2 was found to be a critical driver gene that mediates fluorouracil resistance, which is associated with histone modifier expression patterns. Fluorouracil 102-114 zinc finger E-box binding homeobox 2 Homo sapiens 44-48 35436101-6 2022 Subtle differences among AcK analogues are revealed with 5-FU in single-stranded DNA. Fluorouracil 57-61 tyrosine kinase non receptor 2 Homo sapiens 25-28 35609416-4 2022 Notably, ectopic expression of miR-330-5p restrained tumor cell proliferation, migration, and enhance the sensitivity of CRC cells to 5-FU. Fluorouracil 134-138 microRNA 330 Homo sapiens 31-38 35538714-3 2022 Repurposing FDA drugs against human thymidylate synthase revealed a number of FDA drugs that have a potential to be further developed for the treatment of various cancers for which 5-fluorouracil and analogs have been used for chemotherapy. Fluorouracil 181-195 thymidylate synthetase Homo sapiens 36-56 35522902-8 2022 Subsequently, we prove that blocking beta-catenin inhibits DCLK1-mediated 5-fluorouracil resistance in CRC cells. Fluorouracil 74-88 catenin beta 1 Homo sapiens 37-49 35288979-11 2022 Similarly, overexpression of PFKFB3 can regulate CRC cell behavior and 5-FU resistance caused by miR-197-3p. Fluorouracil 71-75 6-phosphofructo-2-kinase/fructose-2,6-biphosphatase 3 Homo sapiens 29-35 35288979-13 2022 Circ_0014130 modulates 5-FU resistance in colorectal cancer by modulating the miR-197-3p/PFKFB3 axis, which is helpful for drug chemotherapy in colorectal cancer. Fluorouracil 23-27 6-phosphofructo-2-kinase/fructose-2,6-biphosphatase 3 Homo sapiens 89-95 35245520-3 2022 KEY FINDINGS: TQ monotherapy had greater anticancer effects to active VD3 or 5-FU, revealing higher expression of p21/p27/PTEN/BAX/Cyto-C/Casp-3 and increased levels of total glutathione, with inhibitions in CCND1/CCND3/BCL-2 and PI3K/AKT/mTOR molecules, alongside higher rates of apoptosis in HT29, SW480 and SW620 cells (P < 0.005 for all markers). Fluorouracil 77-81 H3 histone pseudogene 16 Homo sapiens 114-117 35245520-3 2022 KEY FINDINGS: TQ monotherapy had greater anticancer effects to active VD3 or 5-FU, revealing higher expression of p21/p27/PTEN/BAX/Cyto-C/Casp-3 and increased levels of total glutathione, with inhibitions in CCND1/CCND3/BCL-2 and PI3K/AKT/mTOR molecules, alongside higher rates of apoptosis in HT29, SW480 and SW620 cells (P < 0.005 for all markers). Fluorouracil 77-81 phosphatase and tensin homolog Homo sapiens 122-126 35558437-0 2022 BDNF Val66Met Polymorphism Reduces the Fatigue-Like Effects of 5-Fluorouracil on Voluntary Wheel-Running Activity in Mice. Fluorouracil 63-77 brain derived neurotrophic factor Mus musculus 0-4 35558437-8 2022 In contrast, during the second week after 5FU treatment, the fatigue-like phenotype was unrelated to the BDNF genotype but was more severe in middle aged mice compared to young mice. Fluorouracil 42-45 brain derived neurotrophic factor Mus musculus 105-109 35448938-6 2022 In our results, the three SCFAs could inhibit ROS expressions, NLRP3, Caspase-1, IL-1beta, IL-6, IL-18, Beclin-1 and LC3-II, when induced by 5-FU. Fluorouracil 141-145 interleukin 1 alpha Homo sapiens 81-89 35448938-7 2022 In a 5-FU-induced chemoentermuctis mouse model, Lactobacillus rhamnoides can increase the concentrations of three SCFAs in faeces and increase the concentrations of IL-1beta, IL-6 and IgA in serum, and decrease the expressions of NLRP3 and IL-17 in spleen cells. Fluorouracil 5-9 interleukin 1 alpha Mus musculus 165-173 35453647-3 2022 Investigation of the role of Hsp27 in the resistance of various cancer cell types against doxorubicin, herceptin/trastuzumab, gemcitabine, 5-FU, temozolomide, and paclitaxel suggested that Hsp27 overexpression promotes cancer cell survival against the above-mentioned chemotherapeutic agents. Fluorouracil 139-143 heat shock protein family B (small) member 1 Homo sapiens 29-34 35133703-5 2022 Importantly, mechanistic studies highlight the PP2A obtrusion in FUDR/5-fluorouracil (5-FU) therapy and underscore the importance of its inhibition to harbor therapeutic potential. Fluorouracil 70-84 protein phosphatase 2 phosphatase activator Homo sapiens 47-51 35133703-5 2022 Importantly, mechanistic studies highlight the PP2A obtrusion in FUDR/5-fluorouracil (5-FU) therapy and underscore the importance of its inhibition to harbor therapeutic potential. Fluorouracil 86-90 protein phosphatase 2 phosphatase activator Homo sapiens 47-51 35394639-13 2022 Interference with miR-320d or overexpression of c-Myc reversed the increased chemotherapeutic sensitivity of CRC-SCs induced by synergistic therapy with 5-FU and MR. miR-320d can target and regulate c-Myc. Fluorouracil 153-157 MYC proto-oncogene, bHLH transcription factor Homo sapiens 48-53 35394639-13 2022 Interference with miR-320d or overexpression of c-Myc reversed the increased chemotherapeutic sensitivity of CRC-SCs induced by synergistic therapy with 5-FU and MR. miR-320d can target and regulate c-Myc. Fluorouracil 153-157 MYC proto-oncogene, bHLH transcription factor Homo sapiens 199-204 35149588-7 2022 Deletion of DR5 in cancer cells in vitro and in vivo abrogated the potentiating effects of CDK4/6 inhibitors on immune cytokine TNF-related apoptosis-inducing ligand (TRAIL), 5-fluorouracil (5-FU) chemotherapy, and anti-PD-1 immunotherapy. Fluorouracil 175-189 TNF receptor superfamily member 10b Homo sapiens 12-15 35149588-7 2022 Deletion of DR5 in cancer cells in vitro and in vivo abrogated the potentiating effects of CDK4/6 inhibitors on immune cytokine TNF-related apoptosis-inducing ligand (TRAIL), 5-fluorouracil (5-FU) chemotherapy, and anti-PD-1 immunotherapy. Fluorouracil 191-195 TNF receptor superfamily member 10b Homo sapiens 12-15 35235860-8 2022 RESULTS: Valsartan suppressed CRC cell-growth and synergistically enhanced the anti-tumor-activities of 5-FU by induction of apoptosis, BAX, BCL2, P53 and modulation of the cell cycle. Fluorouracil 104-108 transformation related protein 53, pseudogene Mus musculus 147-150 35326689-0 2022 In Vivo and In Vitro Enhanced Tumoricidal Effects of Metformin, Active Vitamin D3, and 5-Fluorouracil Triple Therapy against Colon Cancer by Modulating the PI3K/Akt/PTEN/mTOR Network. Fluorouracil 87-101 phosphatase and tensin homolog Homo sapiens 165-169 35326689-11 2022 Moreover, 5-FU/VD3/Met revealed maximal inhibitions of cell cycle inducers (CCND1/CCND3), cell survival (BCL2), and the PI3K/Akt/mTOR molecules alongside the highest expression of cell cycle inhibitors (p21/p27), proapoptotic markers (BAX/cytochrome C/caspase-3), and PTEN in both cell lines. Fluorouracil 10-14 H3 histone pseudogene 16 Homo sapiens 203-206 35326689-11 2022 Moreover, 5-FU/VD3/Met revealed maximal inhibitions of cell cycle inducers (CCND1/CCND3), cell survival (BCL2), and the PI3K/Akt/mTOR molecules alongside the highest expression of cell cycle inhibitors (p21/p27), proapoptotic markers (BAX/cytochrome C/caspase-3), and PTEN in both cell lines. Fluorouracil 10-14 phosphatase and tensin homolog Homo sapiens 268-272 35326689-13 2022 However, the 5-FU/VD3/Met approach displayed the best in vivo and in vitro tumoricidal effects related to cell cycle arrest and apoptosis, justifiably by enhanced modulations of the PI3K/PTEN/Akt/mTOR pathway. Fluorouracil 13-17 phosphatase and tensin homolog Homo sapiens 187-191 35399709-10 2022 These findings indicate that hinokitiol could enhance 5-Fluorouracil therapeutic effects in murine B16F10 and CT26 tumor cells via downregulation of the AKT/mTOR pathway. Fluorouracil 54-68 mechanistic target of rapamycin kinase Mus musculus 157-161 35170195-9 2022 The 5-Fu-resistant MCF-7/5-Fu and MDA-MB-231/5-Fu cells were treated with CCAT2 overexpression/knockdown or CCI-779 (the mTOR pathway inhibitor). Fluorouracil 4-8 colon cancer associated transcript 2 Homo sapiens 74-79 35170195-14 2022 p-mTOR/mTOR in 5-Fu-resistant BC cells with inhibited CCAT2 was decreased, while CCAT2 overexpression activated the mTOR pathway. Fluorouracil 15-19 colon cancer associated transcript 2 Homo sapiens 54-59 35170195-17 2022 CCAT2 may reduce BC cell chemosensitivity to 5-Fu by activating the mTOR pathway. Fluorouracil 45-49 colon cancer associated transcript 2 Homo sapiens 0-5 35252200-4 2022 Results: A total of 3,175 differentially expressed mRNAs (DEGs), lncRNAs (DELs), and miRNAs (DEMs) related to 5-FU resistance were identified, including significantly upregulated IL33, H19, and miR-17-5p; the downregulated AKR1B10, LINC01012, and miR-125b-5p; and chromatin modifiers such as INO80C, HDAC6, and KDM5A. Fluorouracil 110-114 H19 imprinted maternally expressed transcript Homo sapiens 185-188 35252200-5 2022 The construction of the ceRNA regulatory network revealed that H19, HOXA11-AS, and NEAT1 might function as ceRNAs associated with 5-FU resistance in HCT15 cells. Fluorouracil 130-134 H19 imprinted maternally expressed transcript Homo sapiens 63-66 35252200-5 2022 The construction of the ceRNA regulatory network revealed that H19, HOXA11-AS, and NEAT1 might function as ceRNAs associated with 5-FU resistance in HCT15 cells. Fluorouracil 130-134 homeobox A11 Homo sapiens 68-74 35252200-9 2022 Finally, we obtained several critical TFs and their potential targets associated with DARs and 5-FU resistance, including FOXA1 and KLF3. Fluorouracil 95-99 forkhead box A1 Homo sapiens 122-127 35224365-0 2022 Trapping of 5-Fluorodeoxyuridine Monophosphate by Thymidylate Synthase Confers Resistance to 5-Fluorouracil. Fluorouracil 93-107 thymidylate synthetase Homo sapiens 50-70 35224365-1 2022 The major metabolite of the anticancer agent 5-fluorouracil (5-FU) is 5-fluorodeoxyuridine monophosphate (FdUMP), which is a potent inhibitor of thymidylate synthase (TS). Fluorouracil 45-59 thymidylate synthetase Homo sapiens 145-165 35224365-1 2022 The major metabolite of the anticancer agent 5-fluorouracil (5-FU) is 5-fluorodeoxyuridine monophosphate (FdUMP), which is a potent inhibitor of thymidylate synthase (TS). Fluorouracil 45-59 thymidylate synthetase Homo sapiens 167-169 35224365-1 2022 The major metabolite of the anticancer agent 5-fluorouracil (5-FU) is 5-fluorodeoxyuridine monophosphate (FdUMP), which is a potent inhibitor of thymidylate synthase (TS). Fluorouracil 61-65 thymidylate synthetase Homo sapiens 145-165 35224365-1 2022 The major metabolite of the anticancer agent 5-fluorouracil (5-FU) is 5-fluorodeoxyuridine monophosphate (FdUMP), which is a potent inhibitor of thymidylate synthase (TS). Fluorouracil 61-65 thymidylate synthetase Homo sapiens 167-169 35224365-2 2022 Recently, we hypothesized that 5-FU-resistant colorectal cancer (CRC) cells have increased levels of TS protein relative to 5-FU-sensitive CRC cells and use a fraction of their TS to trap FdUMP, which results in resistance to 5-FU. Fluorouracil 31-35 thymidylate synthetase Homo sapiens 101-103 35224365-2 2022 Recently, we hypothesized that 5-FU-resistant colorectal cancer (CRC) cells have increased levels of TS protein relative to 5-FU-sensitive CRC cells and use a fraction of their TS to trap FdUMP, which results in resistance to 5-FU. Fluorouracil 31-35 thymidylate synthetase Homo sapiens 177-179 35224365-2 2022 Recently, we hypothesized that 5-FU-resistant colorectal cancer (CRC) cells have increased levels of TS protein relative to 5-FU-sensitive CRC cells and use a fraction of their TS to trap FdUMP, which results in resistance to 5-FU. Fluorouracil 226-230 thymidylate synthetase Homo sapiens 177-179 35224365-3 2022 In this study, we analyzed the difference between the regulation of the balance of the free, active form of TS and the inactive FdUMP-TS form in 5-FU-resistant HCT116 cells and parental HCT116 cells. Fluorouracil 145-149 thymidylate synthetase Homo sapiens 108-110 35224365-3 2022 In this study, we analyzed the difference between the regulation of the balance of the free, active form of TS and the inactive FdUMP-TS form in 5-FU-resistant HCT116 cells and parental HCT116 cells. Fluorouracil 145-149 thymidylate synthetase Homo sapiens 134-136 35224365-4 2022 Silencing of TYMS, the gene that encodes TS, resulted in greater enhancement of the anticancer effect of 5-FU in the 5-FU-resistant HCT116RF10 cells than in the parental HCT116 cells. Fluorouracil 105-109 thymidylate synthetase Homo sapiens 13-17 35224365-4 2022 Silencing of TYMS, the gene that encodes TS, resulted in greater enhancement of the anticancer effect of 5-FU in the 5-FU-resistant HCT116RF10 cells than in the parental HCT116 cells. Fluorouracil 105-109 thymidylate synthetase Homo sapiens 41-43 35224365-4 2022 Silencing of TYMS, the gene that encodes TS, resulted in greater enhancement of the anticancer effect of 5-FU in the 5-FU-resistant HCT116RF10 cells than in the parental HCT116 cells. Fluorouracil 117-121 thymidylate synthetase Homo sapiens 13-17 35224365-4 2022 Silencing of TYMS, the gene that encodes TS, resulted in greater enhancement of the anticancer effect of 5-FU in the 5-FU-resistant HCT116RF10 cells than in the parental HCT116 cells. Fluorouracil 117-121 thymidylate synthetase Homo sapiens 41-43 35224365-6 2022 Our observations suggest that the regulation of the balance between the storage of the active TS form and the accumulation of FdUMP-TS is responsible for direct resistance to 5-FU. Fluorouracil 175-179 thymidylate synthetase Homo sapiens 94-96 35224365-6 2022 Our observations suggest that the regulation of the balance between the storage of the active TS form and the accumulation of FdUMP-TS is responsible for direct resistance to 5-FU. Fluorouracil 175-179 thymidylate synthetase Homo sapiens 132-134 35014676-0 2022 N6-methyladenosine upregulates miR-181d-5p in exosomes derived from cancer-associated fibroblasts to inhibit 5-FU sensitivity by targeting NCALD in colorectal cancer. Fluorouracil 109-113 microRNA 181d Homo sapiens 31-39 35014676-6 2022 Exosomal miR-181d-5p was identified as a miRNA associated with 5-FU sensitivity. Fluorouracil 63-67 microRNA 181d Homo sapiens 9-17 35014676-11 2022 CAFs-derived exosomes inhibited 5-FU sensitivity in CRC cells through the METTL3/miR-181d-5p axis. Fluorouracil 32-36 methyltransferase 3, N6-adenosine-methyltransferase complex catalytic subunit Homo sapiens 74-80 35014676-11 2022 CAFs-derived exosomes inhibited 5-FU sensitivity in CRC cells through the METTL3/miR-181d-5p axis. Fluorouracil 32-36 microRNA 181d Homo sapiens 81-89 35014676-15 2022 This led to increased miR-181d-5p expression, which inhibited the 5-FU sensitivity of CRC cells by targeting NCALD. Fluorouracil 66-70 microRNA 181d Homo sapiens 22-30 35098910-5 2022 Mechanistically, 5-FU exerts its effect through incorporating the active metabolites into nucleic acids directly, or inhibiting thymidylate synthase to disrupt the function of DNA and RNA, leading to profound effects on cellular metabolism and viability. Fluorouracil 17-21 thymidylate synthetase Homo sapiens 128-148 35093082-13 2022 TYMS knockdown reversed the 5-FU resistance caused by FOXM1 overexpression and re-sensitized HCC cells to 5-FU treatment. Fluorouracil 28-32 thymidylate synthetase Homo sapiens 0-4 35093082-13 2022 TYMS knockdown reversed the 5-FU resistance caused by FOXM1 overexpression and re-sensitized HCC cells to 5-FU treatment. Fluorouracil 106-110 thymidylate synthetase Homo sapiens 0-4 35115838-0 2022 MiR-145 Regulates the Chemoresistance of Hepatic Carcinoma Cells Against 5-Fluorouracil by Targeting Toll-Like Receptor 4 (Expression of Concern). Fluorouracil 73-87 microRNA 145 Homo sapiens 0-7 35115838-0 2022 MiR-145 Regulates the Chemoresistance of Hepatic Carcinoma Cells Against 5-Fluorouracil by Targeting Toll-Like Receptor 4 (Expression of Concern). Fluorouracil 73-87 toll like receptor 4 Homo sapiens 101-121 35207462-7 2022 Our findings demonstrate that down-regulation of C1GALT1 in CCA increases the expression of immature core 1 O-glycan, enhancing CCA progression, including growth and 5-fluorouracil resistance via the activation of the AKT/ERK signaling pathway. Fluorouracil 166-180 core 1 synthase, glycoprotein-N-acetylgalactosamine 3-beta-galactosyltransferase 1 Homo sapiens 49-56 35096810-6 2021 Moreover, combination of HAUS6 knockdown and 5-FU treatment further enhanced the suppression of cell proliferation of CRC cells by increasing activation of the p53/p21 pathway. Fluorouracil 45-49 H3 histone pseudogene 16 Homo sapiens 164-167 35154904-1 2022 DNA damage by genotoxic drugs such as gemcitabine and 5-fluorouracil (5-FU) activates the ataxia telangiectasia, mutated (ATM)-Chk pathway and induces the expression of NKG2D ligands such as the MHC class I-related chain A and B (MICA/B). Fluorouracil 54-68 megakaryocyte-associated tyrosine kinase Mus musculus 127-130 35154904-1 2022 DNA damage by genotoxic drugs such as gemcitabine and 5-fluorouracil (5-FU) activates the ataxia telangiectasia, mutated (ATM)-Chk pathway and induces the expression of NKG2D ligands such as the MHC class I-related chain A and B (MICA/B). Fluorouracil 70-74 megakaryocyte-associated tyrosine kinase Mus musculus 127-130 34976591-15 2022 CD44-Apt1 when conjugated with inhibitor 5-FU showed efficient guidance of 5-FU into HCC cells that significantly enhanced drug toxicity by more than thousands-fold. Fluorouracil 41-45 Fas cell surface death receptor Homo sapiens 5-9 34976591-15 2022 CD44-Apt1 when conjugated with inhibitor 5-FU showed efficient guidance of 5-FU into HCC cells that significantly enhanced drug toxicity by more than thousands-fold. Fluorouracil 75-79 Fas cell surface death receptor Homo sapiens 5-9 35071747-6 2022 Moreover, hTERT overexpression reversed XRCC5 knockdown- or 5-fluorouracil (5-Fu)-mediated HCC inhibition. Fluorouracil 60-74 telomerase reverse transcriptase Homo sapiens 10-15 35071747-6 2022 Moreover, hTERT overexpression reversed XRCC5 knockdown- or 5-fluorouracil (5-Fu)-mediated HCC inhibition. Fluorouracil 76-80 telomerase reverse transcriptase Homo sapiens 10-15 2592384-0 1989 5-Fluorouracil inhibits dihydrofolate reductase precursor mRNA processing and/or nuclear mRNA stability in methotrexate-resistant KB cells. Fluorouracil 0-14 dihydrofolate reductase Homo sapiens 24-47 2592384-1 1989 This laboratory previously reported that 5-fluorouracil (FUra) increases dihydrofolate reductase (DHFR) precursor mRNA (pre-mRNA) levels relative to DHFR mRNA levels in a methotrexate-resistant KB cell line; these data suggested that incorporation of FUra into RNA may, in part, lead to cell death through the inhibition of mRNA processing (Will, C. L., and Dolnick, B.J. Fluorouracil 41-55 dihydrofolate reductase Homo sapiens 73-96 2592384-1 1989 This laboratory previously reported that 5-fluorouracil (FUra) increases dihydrofolate reductase (DHFR) precursor mRNA (pre-mRNA) levels relative to DHFR mRNA levels in a methotrexate-resistant KB cell line; these data suggested that incorporation of FUra into RNA may, in part, lead to cell death through the inhibition of mRNA processing (Will, C. L., and Dolnick, B.J. Fluorouracil 41-55 dihydrofolate reductase Homo sapiens 98-102 2592384-1 1989 This laboratory previously reported that 5-fluorouracil (FUra) increases dihydrofolate reductase (DHFR) precursor mRNA (pre-mRNA) levels relative to DHFR mRNA levels in a methotrexate-resistant KB cell line; these data suggested that incorporation of FUra into RNA may, in part, lead to cell death through the inhibition of mRNA processing (Will, C. L., and Dolnick, B.J. Fluorouracil 57-61 dihydrofolate reductase Homo sapiens 73-96 2592384-1 1989 This laboratory previously reported that 5-fluorouracil (FUra) increases dihydrofolate reductase (DHFR) precursor mRNA (pre-mRNA) levels relative to DHFR mRNA levels in a methotrexate-resistant KB cell line; these data suggested that incorporation of FUra into RNA may, in part, lead to cell death through the inhibition of mRNA processing (Will, C. L., and Dolnick, B.J. Fluorouracil 57-61 dihydrofolate reductase Homo sapiens 98-102 2592384-5 1989 Utilizing a methotrexate-resistant KB cell line designated 1BT, we now report the kinetic basis for altered levels of DHFR RNA observed in FUra-treated cells. Fluorouracil 139-143 dihydrofolate reductase Homo sapiens 118-122 2592384-7 1989 However, steady-state levels of total DHFR mRNA decreased 2.0-fold on a per cell basis in cells exposed to 1.0 microM FUra. Fluorouracil 118-122 dihydrofolate reductase Homo sapiens 38-42 2592384-9 1989 Nuclear/cytoplasmic RNA labeling experiments demonstrated that the rate of nuclear DHFR RNA conversion to cytoplasmic DHFR mRNA decreased approximately 1.8-fold in FUra-treated cells. Fluorouracil 164-168 dihydrofolate reductase Homo sapiens 83-87 2592384-9 1989 Nuclear/cytoplasmic RNA labeling experiments demonstrated that the rate of nuclear DHFR RNA conversion to cytoplasmic DHFR mRNA decreased approximately 1.8-fold in FUra-treated cells. Fluorouracil 164-168 dihydrofolate reductase Homo sapiens 118-122 2592384-10 1989 These results provide further evidence the FUra may inhibit processing of mRNA precursors and/or affect the stability of nuclear DHFR mRNA. Fluorouracil 43-47 dihydrofolate reductase Homo sapiens 129-133 2805072-7 1989 It was noted that the residual immature marrow cells from 5-FU-treated mice showed little NK activity even after the culture with high concentrations of IL 2. Fluorouracil 58-62 interleukin 2 Mus musculus 153-157 2805072-8 1989 Importantly, IL 3 could induce the generation of NK activity from 5-FU-treated marrow cells in the presence of IL 2. Fluorouracil 66-70 interleukin 2 Mus musculus 111-115 2805072-9 1989 Kinetic studies indicated that NK activity was appreciably generated from 5-FU-treated marrow cells when preincubated with IL 3 at least for 12 hr and subsequently cultured with IL 2. Fluorouracil 74-78 interleukin 2 Mus musculus 178-182 2805072-10 1989 The cells bearing IL 2 receptors appeared in 5-FU-treated marrow cells, even though cultured only with IL 3, which implied that IL 3 could support the development of very primitive NK cells from IL 2-unresponsive to IL 2-responsive states. Fluorouracil 45-49 interleukin 2 Mus musculus 18-22 2805072-10 1989 The cells bearing IL 2 receptors appeared in 5-FU-treated marrow cells, even though cultured only with IL 3, which implied that IL 3 could support the development of very primitive NK cells from IL 2-unresponsive to IL 2-responsive states. Fluorouracil 45-49 interleukin 2 Mus musculus 195-199 2805072-10 1989 The cells bearing IL 2 receptors appeared in 5-FU-treated marrow cells, even though cultured only with IL 3, which implied that IL 3 could support the development of very primitive NK cells from IL 2-unresponsive to IL 2-responsive states. Fluorouracil 45-49 interleukin 2 Mus musculus 195-199 2910504-11 1989 Thus, the 5-FU-resistant NK/LAK progenitors were asialo GM1 negative but became asialo GM1+ after induction by IL-2. Fluorouracil 10-14 interleukin 2 Rattus norvegicus 111-115 3593415-0 1987 Determination of thymidylate synthase activity in colon tumor tissues after treatment with 5-fluorouracil. Fluorouracil 91-105 thymidylate synthetase Homo sapiens 17-37 3108221-3 1987 The effect which BVdUrd has on the antitumor potency of FT is apparently due to inhibitory action by bromovinyluracil, the phosphorolytic product of BVdUrd, on the degradation of 5-fluorouracil, the oxidative product of FT, by dihydrothymine dehydrogenase. Fluorouracil 179-193 dihydropyrimidine dehydrogenase Mus musculus 227-255 3491641-0 1987 Effect of human recombinant granulocyte colony-stimulating factor on hematopoietic injury in mice induced by 5-fluorouracil. Fluorouracil 109-123 colony stimulating factor 3 Homo sapiens 28-65 2944259-9 1986 These results suggest that the unresponsiveness to alloantigens in CMC and MLR was induced through a clonal deletion mechanism, and there may exist a 5-FU-resistant--thus less-proliferative--cell population that can produce IL-2 even after the tolerance induction. Fluorouracil 150-154 interleukin 2 Mus musculus 224-228 3525762-7 1986 Like LAK, both HAK and D-LAK were able to compensate for the immunosuppressive effect of the cytotoxic drugs dianhydrogalactitol, vincristine, and 5-fluorouracil, which all have different mechanisms of action, provided that combined treatment by polypeptide and drug was applied repeatedly before the SRBC immunization. Fluorouracil 147-161 alpha-kinase 1 Mus musculus 25-28 2994597-4 1985 Chemotherapy with streptozotocin and 5-fluorouracil was highly effective in ameliorating clinical symptoms, diminishing serum levels of gastrin and VIP, and greatly reducing the bulk of metastatic disease in this case. Fluorouracil 37-51 gastrin Homo sapiens 136-143 4038469-3 1985 Superior complete response rate in the group receiving three courses of 120-hour 5-FU infusion + cisplatin was 54% versus 29% for COB and 19% for two-course 96-hour 5-FU infusion + cisplatin (P = 0.04). Fluorouracil 81-85 metabolism of cobalamin associated B Homo sapiens 130-133 6426399-6 1984 2) The level of 5-FU concentration in CSF had been kept highly very longer time, compared with that of in plasma. Fluorouracil 16-20 colony stimulating factor 2 Homo sapiens 38-41 6426399-8 1984 3) About 0,05 mcg/ml of 5-FU in CSF would be maintained for 24 hours in patients following administration of FT-207 suppository (1 g, daily) for 3 days or more. Fluorouracil 24-28 colony stimulating factor 2 Homo sapiens 32-35 6720373-4 1984 These increased levels of orotate would be expected to compete more effectively with 5-fluorouracil for conversion to a nucleotide by orotate phosphoribosyltransferase. Fluorouracil 85-99 uridine monophosphate synthetase Homo sapiens 134-167 6191988-7 1983 Group 2 tumors demonstrated a lower enzyme ratio (1-2), higher endogenous levels of PRPP, a lower R-1-P/PRPP ratio (1) and appeared to metabolize FUra predominantly by the activity of OPRTase. Fluorouracil 146-150 uridine monophosphate synthetase Homo sapiens 184-191 7084423-0 1982 Erythropoietin formation during hypoxia in mice with impaired responsiveness to erythropoietin induced by irradiation or 5-fluorouracil injection. Fluorouracil 121-135 erythropoietin Mus musculus 0-14 7084423-0 1982 Erythropoietin formation during hypoxia in mice with impaired responsiveness to erythropoietin induced by irradiation or 5-fluorouracil injection. Fluorouracil 121-135 erythropoietin Mus musculus 80-94 7084423-1 1982 Plasma erythropoietin levels during continuous exposure to hypobaric hypoxia in mice with marrow aplasia induced by whole body X-irradiation of 5-fluorouracil injection were higher than in control mice similarly exposed. Fluorouracil 144-158 erythropoietin Mus musculus 7-21 6175442-1 1982 The elevation in the serum level of CEA in cancer patients undergoing treatment with 5-FU and other antitumor drugs has been reported. Fluorouracil 85-89 pregnancy specific beta-1-glycoprotein 2 Homo sapiens 36-39 6756336-4 1982 At present mostly combinations containing fluorouracil + doxorubicin as FAM or FAMe are recommended. Fluorouracil 42-54 benign adult familial myoclonic epilepsy 1 Homo sapiens 79-83 83561-5 1978 By combination of fluorouracil with other drugs remission rates were improved and in responders survival was prolonged (mitomycin C and/or adriamycin in gastric cancer, methyl-CCNU in colorectal cancer). Fluorouracil 18-30 cyclin O Homo sapiens 176-180 623430-3 1978 5-Fluorouracil (5-FU) administered on a Q7DX3 schedule starting on Day 21 post tumor implantation elicited significant retardation in the growth rate of CX-2 tumor. Fluorouracil 0-14 interleukin 17C Homo sapiens 153-157 623430-3 1978 5-Fluorouracil (5-FU) administered on a Q7DX3 schedule starting on Day 21 post tumor implantation elicited significant retardation in the growth rate of CX-2 tumor. Fluorouracil 16-20 interleukin 17C Homo sapiens 153-157 1212650-8 1975 It was also found that in a group of 55 patients treated with 5-fluorouracil, all of the 13 patients that showed objective response to therapy had activities of arylsulfatase B in the tumor tissue within the normal range for large bowel mucosa. Fluorouracil 62-76 arylsulfatase B Homo sapiens 161-176 33636290-10 2021 As a main target of 5-FU, overexpressed TYMS promoted the resistance of 5-FU. Fluorouracil 20-24 thymidylate synthetase Homo sapiens 40-44 33636290-10 2021 As a main target of 5-FU, overexpressed TYMS promoted the resistance of 5-FU. Fluorouracil 72-76 thymidylate synthetase Homo sapiens 40-44 34045966-3 2021 We show that the drug of fluorouracil (5FU), epirubicin (EPI) and gemcitabine (GEM) can induce ROS generation, activate Ets2 and promote CD13 expression. Fluorouracil 25-37 ETS proto-oncogene 2, transcription factor Homo sapiens 120-124 34045966-3 2021 We show that the drug of fluorouracil (5FU), epirubicin (EPI) and gemcitabine (GEM) can induce ROS generation, activate Ets2 and promote CD13 expression. Fluorouracil 39-42 ETS proto-oncogene 2, transcription factor Homo sapiens 120-124 33951601-0 2021 DNA damage response- and JAK-dependent regulation of PD-L1 expression in head and neck squamous cell carcinoma (HNSCC) cells exposed to 5-fluorouracil (5-FU). Fluorouracil 136-150 CD274 molecule Homo sapiens 53-58 33951601-0 2021 DNA damage response- and JAK-dependent regulation of PD-L1 expression in head and neck squamous cell carcinoma (HNSCC) cells exposed to 5-fluorouracil (5-FU). Fluorouracil 152-156 CD274 molecule Homo sapiens 53-58 33951601-5 2021 RESULTS: 5-Fluorouracil (5-FU) increased the expression of PD-L1 with high efficacy in HNSCC cells. Fluorouracil 9-23 CD274 molecule Homo sapiens 59-64 33951601-5 2021 RESULTS: 5-Fluorouracil (5-FU) increased the expression of PD-L1 with high efficacy in HNSCC cells. Fluorouracil 25-29 CD274 molecule Homo sapiens 59-64 33951601-7 2021 The effect of 5-FU on PD-L1 expression was related to its genotoxic effect and was prevented by extracellular application of thymidine or using a chemical inhibitor of the DNA damage Response kinases ATM/ATR. Fluorouracil 14-18 CD274 molecule Homo sapiens 22-27 33951601-7 2021 The effect of 5-FU on PD-L1 expression was related to its genotoxic effect and was prevented by extracellular application of thymidine or using a chemical inhibitor of the DNA damage Response kinases ATM/ATR. Fluorouracil 14-18 ATM serine/threonine kinase Homo sapiens 200-203 33951601-8 2021 We found that the effect of 5-FU was additive or synergistic with IFN-gamma, the canonical inducer of PD-L1 in epithelial cells. Fluorouracil 28-32 CD274 molecule Homo sapiens 102-107 33951601-10 2021 The induction of PD-L1 by 5-FU was partially prevented by Epidermal Growth Factor Receptor (EGFR) inhibition with cetuximab. Fluorouracil 26-30 CD274 molecule Homo sapiens 17-22 33951601-11 2021 CONCLUSION: Our study highlights the specific DNA Damage Response- and JAK- dependent induction of PD-L1 by 5-FU in HNSCC cells. Fluorouracil 108-112 CD274 molecule Homo sapiens 99-104 33780262-10 2021 The inactivation of the Wnt/beta-catenin axis resulted in the reduction of resistance to 5-FU in CRC cells; while activation of the Wnt/beta-catenin axis reversed the reduced resistance to 5-FU in CRC cells caused by PITX2 knockout. Fluorouracil 89-93 catenin beta 1 Homo sapiens 28-40 33780262-10 2021 The inactivation of the Wnt/beta-catenin axis resulted in the reduction of resistance to 5-FU in CRC cells; while activation of the Wnt/beta-catenin axis reversed the reduced resistance to 5-FU in CRC cells caused by PITX2 knockout. Fluorouracil 189-193 catenin beta 1 Homo sapiens 136-148 33780262-12 2021 This study clarified that PITX2 enhanced resistance to 5-FU in CRC upregulating the Wnt/beta-catenin axis. Fluorouracil 55-59 catenin beta 1 Homo sapiens 88-100 33795573-0 2021 Rate and Proportion of Malignant Skin Biopsies for Basal Cell and Squamous Cell Carcinoma on the Face and Ears After a Single Course of Topical 5-Fluorouracil: The Veterans Affairs Keratinocyte Carcinoma Chemoprevention Trial. Fluorouracil 144-158 FA complementation group E Homo sapiens 97-101 33472949-0 2021 Crosstalk between YAP and RAR-RXR drives expression of stemness genes to promote 5-FU resistance and self-renewal in colorectal cancer cells. Fluorouracil 81-85 retinoic acid receptor alpha Homo sapiens 26-29 33472949-3 2021 Here we found that experimental YAP activation in 5FU-sensitive and 5FU-resistant HT29 CRC cells enhanced nuclear YAP localization and the transcript levels of the retinoic acid (RA) receptors RARalpha/gamma and RAR target genes CYP26A1, ALDH1A3 and LGR5 through RA Response Elements (RAREs). Fluorouracil 50-53 retinoic acid receptor alpha Homo sapiens 193-196 33472949-3 2021 Here we found that experimental YAP activation in 5FU-sensitive and 5FU-resistant HT29 CRC cells enhanced nuclear YAP localization and the transcript levels of the retinoic acid (RA) receptors RARalpha/gamma and RAR target genes CYP26A1, ALDH1A3 and LGR5 through RA Response Elements (RAREs). Fluorouracil 50-53 aldehyde dehydrogenase 1 family member A3 Homo sapiens 238-245 33472949-3 2021 Here we found that experimental YAP activation in 5FU-sensitive and 5FU-resistant HT29 CRC cells enhanced nuclear YAP localization and the transcript levels of the retinoic acid (RA) receptors RARalpha/gamma and RAR target genes CYP26A1, ALDH1A3 and LGR5 through RA Response Elements (RAREs). Fluorouracil 68-71 retinoic acid receptor alpha Homo sapiens 193-196 33472949-3 2021 Here we found that experimental YAP activation in 5FU-sensitive and 5FU-resistant HT29 CRC cells enhanced nuclear YAP localization and the transcript levels of the retinoic acid (RA) receptors RARalpha/gamma and RAR target genes CYP26A1, ALDH1A3 and LGR5 through RA Response Elements (RAREs). Fluorouracil 68-71 aldehyde dehydrogenase 1 family member A3 Homo sapiens 238-245 33593942-1 2021 CF10 is a 2nd generation polymeric fluoropyrimidine (FP) that targets both thymidylate synthase (TS), the target of 5-fluorouracil (5-FU), and DNA topoisomerase 1 (Top1), the target of irinotecan, two drugs that are key components of FOLFIRNOX, a standard of care regimen for pancreatic ductal adenocarcinoma (PDAC). Fluorouracil 116-130 thymidylate synthetase Homo sapiens 75-95 33593942-1 2021 CF10 is a 2nd generation polymeric fluoropyrimidine (FP) that targets both thymidylate synthase (TS), the target of 5-fluorouracil (5-FU), and DNA topoisomerase 1 (Top1), the target of irinotecan, two drugs that are key components of FOLFIRNOX, a standard of care regimen for pancreatic ductal adenocarcinoma (PDAC). Fluorouracil 116-130 thymidylate synthetase Homo sapiens 97-99 33593942-1 2021 CF10 is a 2nd generation polymeric fluoropyrimidine (FP) that targets both thymidylate synthase (TS), the target of 5-fluorouracil (5-FU), and DNA topoisomerase 1 (Top1), the target of irinotecan, two drugs that are key components of FOLFIRNOX, a standard of care regimen for pancreatic ductal adenocarcinoma (PDAC). Fluorouracil 132-136 thymidylate synthetase Homo sapiens 75-95 33593942-1 2021 CF10 is a 2nd generation polymeric fluoropyrimidine (FP) that targets both thymidylate synthase (TS), the target of 5-fluorouracil (5-FU), and DNA topoisomerase 1 (Top1), the target of irinotecan, two drugs that are key components of FOLFIRNOX, a standard of care regimen for pancreatic ductal adenocarcinoma (PDAC). Fluorouracil 132-136 thymidylate synthetase Homo sapiens 97-99 33593942-3 2021 The increased potency of CF10 relative to 5-FU correlated with enhanced TS inhibition and strong Top1 cleavage complex formation. Fluorouracil 42-46 thymidylate synthetase Homo sapiens 72-74 33785559-10 2022 Knockdown of ARID1A in GAC cell lines increased pS6 and nuclear SOX9 and increased sensitivity to an mTOR inhibitor which was further amplified by its combination with fluorouracil both in vitro and in vivo in PDXs. Fluorouracil 168-180 AT rich interactive domain 1A (SWI-like) Mus musculus 13-19 33785559-10 2022 Knockdown of ARID1A in GAC cell lines increased pS6 and nuclear SOX9 and increased sensitivity to an mTOR inhibitor which was further amplified by its combination with fluorouracil both in vitro and in vivo in PDXs. Fluorouracil 168-180 mechanistic target of rapamycin kinase Mus musculus 101-105 33788719-0 2021 Inhibition of Heat-shock Protein 27 Reduces 5-Fluorouracil-acquired Resistance in Human Colon Cancer Cells. Fluorouracil 44-58 heat shock protein family B (small) member 1 Homo sapiens 14-35 33788719-1 2021 BACKGROUND/AIM: In previous work we showed that expression of heat-shock protein 27 (HSP27; encoded by HSPB1) was associated with inherent resistance to 5-fluorouracil (5-FU). Fluorouracil 153-167 heat shock protein family B (small) member 1 Homo sapiens 62-83 33658858-0 2021 The Combination Therapy of Fluorouracil and Oxaliplatin Suppress the Progression of Colon Cancer Through miR-183-5p/SOCS3 Axis and Downregulating PD-L1. Fluorouracil 27-39 CD274 molecule Homo sapiens 146-151 33658858-1 2021 Purpose: The purpose of this study was to investigate the mechanism of combination of fluorouracil (FU) and oxaliplatin (OXA) on the progression of colon cancer via miR-183-5p/SOCS3 axis and regulating PD-L1. Fluorouracil 86-98 CD274 molecule Homo sapiens 202-207 33580870-7 2021 Moreover, inhibition of PIN1 enhanced the inhibitory effect of 5-FU on SW-48 cell proliferation. Fluorouracil 63-67 peptidylprolyl cis/trans isomerase, NIMA-interacting 1 Homo sapiens 24-28 33604188-7 2021 To get the mechanisms more clear, the transcriptional silencing of mapk10 was reversed by pharmacological demethylation, and ectopic expression of mapk10 in silenced HCC cell lines significantly inhibited the colony formation ability, induced apoptosis, or enhanced the chemosensitivity of HCC cells to 5-fluorouracil. Fluorouracil 303-317 mitogen-activated protein kinase 10 Homo sapiens 147-153 33613849-3 2021 5-Fluorouracil (5FU) seems to act differently depending on administration method: elastomer-mediated continuous infusion better inhibits Thymidylate Synthase (TS), an enzyme playing a pivotal role in DNA synthetic pathway. Fluorouracil 0-14 thymidylate synthetase Homo sapiens 137-157 33613849-3 2021 5-Fluorouracil (5FU) seems to act differently depending on administration method: elastomer-mediated continuous infusion better inhibits Thymidylate Synthase (TS), an enzyme playing a pivotal role in DNA synthetic pathway. Fluorouracil 16-19 thymidylate synthetase Homo sapiens 137-157 33168448-7 2021 The role of miR-766 on 5-fluorouracil-induced apoptosis in MCF-7 and T47D cells was determined using the Caspase-Glo3/7 assay. Fluorouracil 23-37 microRNA 766 Homo sapiens 12-19 33168448-10 2021 Furthermore, miR-766 reduced the sensitivity of MCF-7 and T47D cells to 5-fluorouracil treatment. Fluorouracil 72-86 microRNA 766 Homo sapiens 13-20 33321421-0 2021 Discovery of a potent beta-catenin destabilizer for overcoming the resistance of 5-fluorouracil in colorectal cancer. Fluorouracil 81-95 catenin beta 1 Homo sapiens 22-34 33140501-2 2021 5-Fluorouracil (5-FU) is an anticancer nucleoside analog that both inhibits thymidylate synthase (TS) and causes DNA damage via the misincorporation of FdUTP and dUTP into DNA under the conditions of dTTP depletion. Fluorouracil 16-20 thymidylate synthetase Homo sapiens 76-96 32507687-5 2021 RESULTS: We observed the time-dependent upregulation of GBA1 expression and enzyme activity in multiple gastric cancer cell lines in response to prolonged exposure of 5-FU. Fluorouracil 167-171 glucosylceramidase beta Homo sapiens 56-60 32507687-9 2021 Functional analysis demonstrated that GBA1 inhibition suppressed gastric cancer growth and survival without affecting migration, and augmented 5-FU"s efficacy. Fluorouracil 143-147 glucosylceramidase beta Homo sapiens 38-42 32507687-10 2021 Consistently, GBA1 inhibition was active against 5-FU-resistant gastric cancer cells. Fluorouracil 49-53 glucosylceramidase beta Homo sapiens 14-18 32507687-11 2021 Mechanism studies showed that GBA1 inhibition led to loss of lysosomal integrity and function in 5-FU-resistant gastric cancer cells. Fluorouracil 97-101 glucosylceramidase beta Homo sapiens 30-34 33325631-7 2021 A study of transcriptional regulation allowed identifying a decrease in ATF3 expression, as an explanation of sortilin overexpression following 5-FU treatment. Fluorouracil 144-148 activating transcription factor 3 Homo sapiens 72-76 33091827-3 2021 Therefore, we identified the expression of eight genes closely associated with platinum and fluorouracil metabolism (RRM1, RRM2, RRM2B, POLH, DUT, TYMS, TYMP, MKI67) in the discovery cohort (N=291). Fluorouracil 92-104 ribonucleotide reductase regulatory subunit M2 Homo sapiens 123-127 33318473-9 2020 We further found that disrupting the miR-21/VMP1 feedback loop will decrease the expression of miR-21, reduce the malignancy, and increase their sensitivity to 5-fluorouracil in colorectal cancer cells. Fluorouracil 160-174 vacuole membrane protein 1 Homo sapiens 44-48 33079995-5 2020 Moreover, DJ-1 overexpression conferred the MDR phenotype to SGC7901 cells, while DJ-1 knockdown in SGC7901/VCR cells induced re-sensitization to adriamycin, vincristine, cisplatin, and 5-fluorouracil. Fluorouracil 186-200 Parkinsonism associated deglycase Homo sapiens 10-14 33079995-5 2020 Moreover, DJ-1 overexpression conferred the MDR phenotype to SGC7901 cells, while DJ-1 knockdown in SGC7901/VCR cells induced re-sensitization to adriamycin, vincristine, cisplatin, and 5-fluorouracil. Fluorouracil 186-200 Parkinsonism associated deglycase Homo sapiens 82-86 33051247-12 2020 In particular, let-7c enhances 5-FU exposure (via suppressing ABCC5/MRP5 expression) and co-targets thymidylate synthase with 5-FU (let-7c reduces protein expression while 5-FU irreversibly inactivates enzyme). Fluorouracil 126-130 thymidylate synthetase Homo sapiens 100-120 33051247-12 2020 In particular, let-7c enhances 5-FU exposure (via suppressing ABCC5/MRP5 expression) and co-targets thymidylate synthase with 5-FU (let-7c reduces protein expression while 5-FU irreversibly inactivates enzyme). Fluorouracil 126-130 microRNA let-7c Homo sapiens 132-138 33178338-0 2020 Paroxetine combined with fluorouracil plays a therapeutic role in mouse models of colorectal cancer with depression through inhibiting IL-22 expression to regulate the MAPK signaling pathway. Fluorouracil 25-37 interleukin 22 Mus musculus 135-140 32805281-10 2020 RESULTS: High expression of CCAT2 induced CIN in CRC cell lines and increased resistance to 5-fluorouracil and oxaliplatin. Fluorouracil 92-106 colon cancer associated transcript 2 Homo sapiens 28-33 33154782-0 2020 Halofuginone inhibits tumorigenic progression of 5-FU-resistant human colorectal cancer HCT-15/FU cells by targeting miR-132-3p in vitro. Fluorouracil 49-53 microRNA 1323 Homo sapiens 117-127 33154782-11 2020 Therefore, miR-132-3p may serve as a molecular marker, which may be used to predict CRC resistance to 5-FU, and HF may serve as a novel clinical treatment for 5-FU-resistant CRC. Fluorouracil 102-106 microRNA 1323 Homo sapiens 11-21 33243730-6 2020 In the cells with BIRC6 silencing, treatment with 12.5, 25, 50, 100 and 200 mug/mL 5-FU resulted in significantly higher proliferation inhibition rates than in the cells transfected with the control siRNA (P < 0.01). Fluorouracil 83-87 baculoviral IAP repeat containing 6 Homo sapiens 18-23 33243730-7 2020 BIRC6 silencing also significantly increased the apoptosis rate of 786-O cells following 5-FU treatment (P < 0.01). Fluorouracil 89-93 baculoviral IAP repeat containing 6 Homo sapiens 0-5 33243730-9 2020 CONCLUSIONS: Interference of BIRC6 mediated by siRNA can inhibit autophagy and promote 5-FU-induced apoptosis to enhance the sensitivity of 786-O cells to 5-FU. Fluorouracil 87-91 baculoviral IAP repeat containing 6 Homo sapiens 29-34 33243730-9 2020 CONCLUSIONS: Interference of BIRC6 mediated by siRNA can inhibit autophagy and promote 5-FU-induced apoptosis to enhance the sensitivity of 786-O cells to 5-FU. Fluorouracil 155-159 baculoviral IAP repeat containing 6 Homo sapiens 29-34 33256074-7 2020 Inhibition of TS alone or double inhibition of TS and TK1 using the siRNA technique increased susceptibility to 5-FU in IFIT2-knockdown cells. Fluorouracil 112-116 thymidylate synthetase Homo sapiens 14-16 33256074-7 2020 Inhibition of TS alone or double inhibition of TS and TK1 using the siRNA technique increased susceptibility to 5-FU in IFIT2-knockdown cells. Fluorouracil 112-116 thymidylate synthetase Homo sapiens 47-49 33205649-8 2020 Remarkably, the combination of CE and 5-FU treatment attenuated beta-catenin, MDR1, and ABCC1 expressions, while TFAP4 overexpression reversed their expressions by 2.68 +- 0.46-, 0.72 +- 0.44-, and 0.93 +- 0.21-fold, respectively. Fluorouracil 38-42 catenin beta 1 Homo sapiens 64-76 32898694-5 2020 The tumor vascular targeted and ultrasound-responsive microbubbles of 5-FU@DLL4-MBs were prepared by the thin-film dispersion method. Fluorouracil 70-74 delta like canonical Notch ligand 4 Homo sapiens 75-79 32898694-6 2020 The size and zeta potential of 5-FU@DLL4-MBs was about 1248 nm and -9.1 mV. Fluorouracil 31-35 delta like canonical Notch ligand 4 Homo sapiens 36-40 32898694-7 2020 5-FU@DLL4-MBs released 5-FU showed an ultrasound-responsive manner, and had better vascular-targeting ability. Fluorouracil 0-4 delta like canonical Notch ligand 4 Homo sapiens 5-9 32898694-7 2020 5-FU@DLL4-MBs released 5-FU showed an ultrasound-responsive manner, and had better vascular-targeting ability. Fluorouracil 23-27 delta like canonical Notch ligand 4 Homo sapiens 5-9 32898694-8 2020 Furthermore, the 5-FU@DLL4-MBs showed the strongest cytotoxic effect on HUVECs or HepG-2 cells and can be effectively internalized into the HUVECs cells. Fluorouracil 17-21 delta like canonical Notch ligand 4 Homo sapiens 22-26 32898694-9 2020 Thus, 5-FU@DLL4-MBs combined with HIFU can be considered as a potential method for antitumor angiogenesis in the future. Fluorouracil 6-10 delta like canonical Notch ligand 4 Homo sapiens 11-15 32561283-4 2020 The results indicated that compared to the 5-Fu group, the 5-Fu + SATP group showed effective amelioration of the liver, kidney and small intestine injury caused by 5-Fu and decreases in the levels of related biochemical indicators, such as aspartate aminotransferase (AST), alanine aminotransferase (ALT) and urea nitrogen (BUN). Fluorouracil 59-63 solute carrier family 17 (anion/sugar transporter), member 5 Mus musculus 241-267 32561283-4 2020 The results indicated that compared to the 5-Fu group, the 5-Fu + SATP group showed effective amelioration of the liver, kidney and small intestine injury caused by 5-Fu and decreases in the levels of related biochemical indicators, such as aspartate aminotransferase (AST), alanine aminotransferase (ALT) and urea nitrogen (BUN). Fluorouracil 59-63 solute carrier family 17 (anion/sugar transporter), member 5 Mus musculus 269-272 32561283-4 2020 The results indicated that compared to the 5-Fu group, the 5-Fu + SATP group showed effective amelioration of the liver, kidney and small intestine injury caused by 5-Fu and decreases in the levels of related biochemical indicators, such as aspartate aminotransferase (AST), alanine aminotransferase (ALT) and urea nitrogen (BUN). Fluorouracil 59-63 glutamic pyruvic transaminase, soluble Mus musculus 275-299 32561283-4 2020 The results indicated that compared to the 5-Fu group, the 5-Fu + SATP group showed effective amelioration of the liver, kidney and small intestine injury caused by 5-Fu and decreases in the levels of related biochemical indicators, such as aspartate aminotransferase (AST), alanine aminotransferase (ALT) and urea nitrogen (BUN). Fluorouracil 59-63 glutamic pyruvic transaminase, soluble Mus musculus 301-304 32561283-4 2020 The results indicated that compared to the 5-Fu group, the 5-Fu + SATP group showed effective amelioration of the liver, kidney and small intestine injury caused by 5-Fu and decreases in the levels of related biochemical indicators, such as aspartate aminotransferase (AST), alanine aminotransferase (ALT) and urea nitrogen (BUN). Fluorouracil 59-63 solute carrier family 17 (anion/sugar transporter), member 5 Mus musculus 241-267 32561283-4 2020 The results indicated that compared to the 5-Fu group, the 5-Fu + SATP group showed effective amelioration of the liver, kidney and small intestine injury caused by 5-Fu and decreases in the levels of related biochemical indicators, such as aspartate aminotransferase (AST), alanine aminotransferase (ALT) and urea nitrogen (BUN). Fluorouracil 59-63 solute carrier family 17 (anion/sugar transporter), member 5 Mus musculus 269-272 32561283-4 2020 The results indicated that compared to the 5-Fu group, the 5-Fu + SATP group showed effective amelioration of the liver, kidney and small intestine injury caused by 5-Fu and decreases in the levels of related biochemical indicators, such as aspartate aminotransferase (AST), alanine aminotransferase (ALT) and urea nitrogen (BUN). Fluorouracil 59-63 glutamic pyruvic transaminase, soluble Mus musculus 275-299 32561283-4 2020 The results indicated that compared to the 5-Fu group, the 5-Fu + SATP group showed effective amelioration of the liver, kidney and small intestine injury caused by 5-Fu and decreases in the levels of related biochemical indicators, such as aspartate aminotransferase (AST), alanine aminotransferase (ALT) and urea nitrogen (BUN). Fluorouracil 59-63 glutamic pyruvic transaminase, soluble Mus musculus 301-304 32561283-6 2020 Further mechanistic studies indicated that the 5-Fu + SATP group showed a decrease in hepatotoxicity caused by 5-Fu via a reduction in the levels of interleukin-1beta (IL-1beta), an increase in the expression of Bcl-2 and decreases in the expression of p-p38, p-JNK and Bax. Fluorouracil 47-51 interleukin 1 alpha Mus musculus 168-176 32561283-6 2020 Further mechanistic studies indicated that the 5-Fu + SATP group showed a decrease in hepatotoxicity caused by 5-Fu via a reduction in the levels of interleukin-1beta (IL-1beta), an increase in the expression of Bcl-2 and decreases in the expression of p-p38, p-JNK and Bax. Fluorouracil 111-115 interleukin 1 alpha Mus musculus 168-176 32977944-0 2020 miR-149 contributes to resistance of 5-FU in gastric cancer via targeting TREM2 and regulating beta-catenin pathway. Fluorouracil 37-41 microRNA 149 Homo sapiens 0-7 32977944-0 2020 miR-149 contributes to resistance of 5-FU in gastric cancer via targeting TREM2 and regulating beta-catenin pathway. Fluorouracil 37-41 catenin beta 1 Homo sapiens 95-107 32977944-3 2020 The relationship between miR-149 and 5-fluorouracil (5-FU) resistance in GC remains unclear. Fluorouracil 37-51 microRNA 149 Homo sapiens 25-32 32977944-3 2020 The relationship between miR-149 and 5-fluorouracil (5-FU) resistance in GC remains unclear. Fluorouracil 53-57 microRNA 149 Homo sapiens 25-32 32977944-4 2020 Here we detected miR-149 expression in 5-FU resistance tumor tissues and cell lines, and found that miR-149 expression is upregulated in AGS/5-FU cells compared with AGS cells. Fluorouracil 39-43 microRNA 149 Homo sapiens 17-24 32977944-4 2020 Here we detected miR-149 expression in 5-FU resistance tumor tissues and cell lines, and found that miR-149 expression is upregulated in AGS/5-FU cells compared with AGS cells. Fluorouracil 141-145 microRNA 149 Homo sapiens 100-107 32977944-5 2020 Further experiments indicated that overexpression of miR-149 can alleviate 5-FU-induced apoptosis and proliferation inhibition by targeting TREM2. Fluorouracil 75-79 microRNA 149 Homo sapiens 53-60 32977944-6 2020 It was also confirmed that TREM2 regulated 5-FU resistance through beta-catenin pathway. Fluorouracil 43-47 catenin beta 1 Homo sapiens 67-79 32907836-6 2020 UPP1 facilitated the conversion of 5-FU to its active compound, thereby enhancing the inhibition of thymidylate synthase. Fluorouracil 35-39 thymidylate synthetase Homo sapiens 100-120 32652867-2 2020 The present study aimed to investigate the role of dbpA in 5-Fluorouracil (5-FU)-resistant and Oxaliplatin (L-OHP)-resistant colorectal cancer (CRC) cells. Fluorouracil 59-73 Y-box binding protein 3 Homo sapiens 51-55 32652867-2 2020 The present study aimed to investigate the role of dbpA in 5-Fluorouracil (5-FU)-resistant and Oxaliplatin (L-OHP)-resistant colorectal cancer (CRC) cells. Fluorouracil 75-79 Y-box binding protein 3 Homo sapiens 51-55 32652867-3 2020 We found that 5-FU and L-OPH treatment promoted the expression of dbpA. Fluorouracil 14-18 Y-box binding protein 3 Homo sapiens 66-70 32652867-4 2020 Enhanced dbpA promoted the drug resistance of SW620 cells to 5-FU and L-OHP. Fluorouracil 61-65 Y-box binding protein 3 Homo sapiens 9-13 32652867-6 2020 Besides, dbpA shRNA enhanced the cytotoxicity of 5-FU and L-OHP to SW620/5-FU and SW620/L-OHP cells. Fluorouracil 49-53 Y-box binding protein 3 Homo sapiens 9-13 32652867-6 2020 Besides, dbpA shRNA enhanced the cytotoxicity of 5-FU and L-OHP to SW620/5-FU and SW620/L-OHP cells. Fluorouracil 73-77 Y-box binding protein 3 Homo sapiens 9-13 32652867-7 2020 Meanwhile, dbpA shRNA inhibited the activation of the Wnt/beta-catenin pathway that induced by 5-FU stimulation in SW620/5-FU cells. Fluorouracil 95-99 Y-box binding protein 3 Homo sapiens 11-15 32652867-7 2020 Meanwhile, dbpA shRNA inhibited the activation of the Wnt/beta-catenin pathway that induced by 5-FU stimulation in SW620/5-FU cells. Fluorouracil 95-99 catenin beta 1 Homo sapiens 58-70 32652867-7 2020 Meanwhile, dbpA shRNA inhibited the activation of the Wnt/beta-catenin pathway that induced by 5-FU stimulation in SW620/5-FU cells. Fluorouracil 121-125 Y-box binding protein 3 Homo sapiens 11-15 32652867-7 2020 Meanwhile, dbpA shRNA inhibited the activation of the Wnt/beta-catenin pathway that induced by 5-FU stimulation in SW620/5-FU cells. Fluorouracil 121-125 catenin beta 1 Homo sapiens 58-70 32652867-8 2020 Activation of the Wnt/beta-catenin pathway or overexpression of Chk1 abrogated the promoting effect of dbpA downregulation on 5-FU sensitivity of CRC cells. Fluorouracil 126-130 catenin beta 1 Homo sapiens 22-34 32652867-8 2020 Activation of the Wnt/beta-catenin pathway or overexpression of Chk1 abrogated the promoting effect of dbpA downregulation on 5-FU sensitivity of CRC cells. Fluorouracil 126-130 Y-box binding protein 3 Homo sapiens 103-107 32652867-9 2020 Importantly, downregulation of dbpA suppressed tumor growth and promoted CRC cells sensitivity to 5-FU in vivo. Fluorouracil 98-102 Y-box binding protein 3 Homo sapiens 31-35 32652867-10 2020 Our study indicated that knockdown of dbpA enhanced the sensitivity of colorectal cancer cells to 5-FU via Wnt/beta-catenin/Chk1 pathway, and DbpA may be a potential therapeutic target to sensitize drug resistance colorectal cancer to 5-FU and L-OHP. Fluorouracil 98-102 Y-box binding protein 3 Homo sapiens 38-42 32652867-10 2020 Our study indicated that knockdown of dbpA enhanced the sensitivity of colorectal cancer cells to 5-FU via Wnt/beta-catenin/Chk1 pathway, and DbpA may be a potential therapeutic target to sensitize drug resistance colorectal cancer to 5-FU and L-OHP. Fluorouracil 98-102 catenin beta 1 Homo sapiens 111-123 32652867-10 2020 Our study indicated that knockdown of dbpA enhanced the sensitivity of colorectal cancer cells to 5-FU via Wnt/beta-catenin/Chk1 pathway, and DbpA may be a potential therapeutic target to sensitize drug resistance colorectal cancer to 5-FU and L-OHP. Fluorouracil 235-239 Y-box binding protein 3 Homo sapiens 38-42 32652867-10 2020 Our study indicated that knockdown of dbpA enhanced the sensitivity of colorectal cancer cells to 5-FU via Wnt/beta-catenin/Chk1 pathway, and DbpA may be a potential therapeutic target to sensitize drug resistance colorectal cancer to 5-FU and L-OHP. Fluorouracil 235-239 catenin beta 1 Homo sapiens 111-123 32474153-6 2020 Increases in thymidylate synthase and active beta-catenin were also observed in the 5-FU-R-cells. Fluorouracil 84-88 thymidylate synthetase Homo sapiens 13-33 32474153-6 2020 Increases in thymidylate synthase and active beta-catenin were also observed in the 5-FU-R-cells. Fluorouracil 84-88 catenin beta 1 Homo sapiens 45-57 33005290-4 2020 Different mechanisms including microsatellite instability, increased expression level of key enzyme thymidylate synthase and its polymorphism, increased level of 5-FU-activating enzymes and mutation of TP53 are proposed as the main determinants of resistance to 5-FU in CRC cells. Fluorouracil 262-266 thymidylate synthetase Homo sapiens 100-120 32819569-11 2020 Finally, we found that TAGLN knockdown could improve the sensitivity of NSCLC cells to sorafenib (SFB) and 5-FU treatment, further suppressing the proliferation, migration and invasion of NSCLC cells. Fluorouracil 107-111 transgelin Mus musculus 23-28 32819569-12 2020 Consistently, TAGLN deletion attenuated tumor xenografts growth and metastasis of NSCLC in mouse models by enhancing the anti-cancer effects of SFB and 5-FU. Fluorouracil 152-156 transgelin Mus musculus 14-19 32559627-0 2020 Hydrazinocurcumin and 5-fluorouracil enhance apoptosis and restrain tumorigenicity of HepG2 cells via disrupting the PTEN-mediated PI3K/Akt signaling pathway. Fluorouracil 22-36 phosphatase and tensin homolog Homo sapiens 117-121 32559627-6 2020 We found that HZC or 5-Fu induced apoptosis and repressed proliferation of HepG2 cells by upregulating the expression of PTEN and disrupting the PI3K/Akt signaling pathway activation. Fluorouracil 21-25 phosphatase and tensin homolog Homo sapiens 121-125 32559627-9 2020 Inhibition of PTEN expression activated the PI3K/Akt signaling pathway and reversed the protective effects of HZC or 5-Fu. Fluorouracil 117-121 phosphatase and tensin homolog Homo sapiens 14-18 32559627-10 2020 Thus, HZC and 5-Fu increase PTEN, which blocks the PI3K/Akt signaling pathway, ultimately inducing HepG2 cell apoptosis. Fluorouracil 14-18 phosphatase and tensin homolog Homo sapiens 28-32 31863486-4 2020 SOX17 expression in human CCA cells (EGI-1 and TFK-1) selectively potentiated cytotoxicity of SN-38, 5-fluorouracil (5-FU) and mitoxantrone, but not that of gemcitabine, capecitabine, cisplatin or oxaliplatin. Fluorouracil 101-115 SRY-box transcription factor 17 Homo sapiens 0-5 31863486-4 2020 SOX17 expression in human CCA cells (EGI-1 and TFK-1) selectively potentiated cytotoxicity of SN-38, 5-fluorouracil (5-FU) and mitoxantrone, but not that of gemcitabine, capecitabine, cisplatin or oxaliplatin. Fluorouracil 117-121 SRY-box transcription factor 17 Homo sapiens 0-5 33463109-8 2020 It was also concluded that LPS in combination with 5-FU increased TLR-4 expression and down-regulated gene expression in NF-kappaB, ERK, and AKT pathways (p=0.001). Fluorouracil 51-55 toll like receptor 4 Homo sapiens 66-71 33463109-8 2020 It was also concluded that LPS in combination with 5-FU increased TLR-4 expression and down-regulated gene expression in NF-kappaB, ERK, and AKT pathways (p=0.001). Fluorouracil 51-55 EPH receptor B2 Homo sapiens 132-135 32922531-10 2020 The levels of HSP90 were inversely associated with short-term efficacy in GC patients who had received fluorouracil/platinum-based advanced first-line treatment. Fluorouracil 103-115 heat shock protein 90 alpha family class A member 1 Homo sapiens 14-19 32784600-6 2020 To further exploit the therapeutic potentials of miR-489 in TNBC models, we chemically modified the guide strand of miR-489 (CMM489) by replacing Uracil with 5-fluorouracil (5-FU) so that tumor suppressor (miR-489) and DNA damaging (5-FU) components are combined into a single agent as a novel drug candidate for TNBCs. Fluorouracil 158-172 microRNA 489 Homo sapiens 116-123 32784600-6 2020 To further exploit the therapeutic potentials of miR-489 in TNBC models, we chemically modified the guide strand of miR-489 (CMM489) by replacing Uracil with 5-fluorouracil (5-FU) so that tumor suppressor (miR-489) and DNA damaging (5-FU) components are combined into a single agent as a novel drug candidate for TNBCs. Fluorouracil 158-172 microRNA 489 Homo sapiens 116-123 32784600-6 2020 To further exploit the therapeutic potentials of miR-489 in TNBC models, we chemically modified the guide strand of miR-489 (CMM489) by replacing Uracil with 5-fluorouracil (5-FU) so that tumor suppressor (miR-489) and DNA damaging (5-FU) components are combined into a single agent as a novel drug candidate for TNBCs. Fluorouracil 174-178 microRNA 489 Homo sapiens 116-123 32784600-6 2020 To further exploit the therapeutic potentials of miR-489 in TNBC models, we chemically modified the guide strand of miR-489 (CMM489) by replacing Uracil with 5-fluorouracil (5-FU) so that tumor suppressor (miR-489) and DNA damaging (5-FU) components are combined into a single agent as a novel drug candidate for TNBCs. Fluorouracil 174-178 microRNA 489 Homo sapiens 116-123 32784600-6 2020 To further exploit the therapeutic potentials of miR-489 in TNBC models, we chemically modified the guide strand of miR-489 (CMM489) by replacing Uracil with 5-fluorouracil (5-FU) so that tumor suppressor (miR-489) and DNA damaging (5-FU) components are combined into a single agent as a novel drug candidate for TNBCs. Fluorouracil 233-237 microRNA 489 Homo sapiens 116-123 32784600-6 2020 To further exploit the therapeutic potentials of miR-489 in TNBC models, we chemically modified the guide strand of miR-489 (CMM489) by replacing Uracil with 5-fluorouracil (5-FU) so that tumor suppressor (miR-489) and DNA damaging (5-FU) components are combined into a single agent as a novel drug candidate for TNBCs. Fluorouracil 233-237 microRNA 489 Homo sapiens 116-123 32975155-3 2020 Results: Combination treatment with 5-FU and radiation had a stronger effect on decreasing Bcl-2 expression and increasing expression of Bax, cleaved caspase-9, cleaved caspase-3, cleaved PARP compared with each treatment alone. Fluorouracil 36-40 caspase 9 Homo sapiens 150-159 32801865-0 2020 MiR-145 Regulates the Chemoresistance of Hepatic Carcinoma Cells Against 5-Fluorouracil by Targeting Toll-Like Receptor 4. Fluorouracil 73-87 microRNA 145 Homo sapiens 0-7 32801865-0 2020 MiR-145 Regulates the Chemoresistance of Hepatic Carcinoma Cells Against 5-Fluorouracil by Targeting Toll-Like Receptor 4. Fluorouracil 73-87 toll like receptor 4 Homo sapiens 101-121 32801865-3 2020 Objective: To explore the prognostic value of miR-145 in HCC and its molecular mechanism in 5-FU-resistant HCC cells. Fluorouracil 92-96 microRNA 145 Homo sapiens 46-53 32801865-10 2020 In contrast, miR-145 overexpression improved the sensitivity of HCC cells to 5-FU and enhanced the inhibition of 5-FU on tumor growth. Fluorouracil 77-81 microRNA 145 Homo sapiens 13-20 32801865-10 2020 In contrast, miR-145 overexpression improved the sensitivity of HCC cells to 5-FU and enhanced the inhibition of 5-FU on tumor growth. Fluorouracil 113-117 microRNA 145 Homo sapiens 13-20 32689938-7 2020 Our results further showed that melatonin can downregulate the expression levels of 5-FU resistance-related genes, such as thymidylate synthase in GC and ATR, CHEK1, BAX and MYC in CRC. Fluorouracil 84-88 thymidylate synthetase Homo sapiens 123-143 32689938-7 2020 Our results further showed that melatonin can downregulate the expression levels of 5-FU resistance-related genes, such as thymidylate synthase in GC and ATR, CHEK1, BAX and MYC in CRC. Fluorouracil 84-88 MYC proto-oncogene, bHLH transcription factor Homo sapiens 174-177 32627138-7 2020 Expressions of tested ABC transporters (ABCA5, ABCB1, ABCB6, ABCC1, ABCC2, ABCC3, ABCC5, ABCC10 and ABCF2, and ABCG2) were also deregulated in 5-FU resistant Hep-2 cells. Fluorouracil 143-147 ATP binding cassette subfamily C member 10 Homo sapiens 89-95 32627138-7 2020 Expressions of tested ABC transporters (ABCA5, ABCB1, ABCB6, ABCC1, ABCC2, ABCC3, ABCC5, ABCC10 and ABCF2, and ABCG2) were also deregulated in 5-FU resistant Hep-2 cells. Fluorouracil 143-147 ATP binding cassette subfamily F member 2 Homo sapiens 100-105 32665777-10 2020 Moreover, qPCR analyses showed that CASP3 and CASP9 mRNA levels significantly increased after pre-treatment with Pxd followed by 5-Fu and 1-OHP treatments, compared to 5-Fu with 1-OHP alone. Fluorouracil 168-172 caspase 9 Homo sapiens 46-51 32656396-1 2020 5-Fluorouracil-nicotinamide (5-FU-NCM), a co-crystal with a 2D layer structure formed by hydrogen bonds, was synthesized by solvent evaporation and liquid phase-assisted grinding at room temperature. Fluorouracil 0-14 CWC22 spliceosome associated protein homolog Homo sapiens 34-37 32585842-2 2020 Preclinical and clinical studies have demonstrated a strong association between development of Pt-drug resistance and increased thymidylate synthase (hTS) expression, and the consequent cross-resistance to the hTS inhibitors 5-fluorouracil (5-FU) and raltitrexed (RTX). Fluorouracil 225-239 thymidylate synthetase Homo sapiens 128-148 32585842-2 2020 Preclinical and clinical studies have demonstrated a strong association between development of Pt-drug resistance and increased thymidylate synthase (hTS) expression, and the consequent cross-resistance to the hTS inhibitors 5-fluorouracil (5-FU) and raltitrexed (RTX). Fluorouracil 241-245 thymidylate synthetase Homo sapiens 128-148 32606803-0 2020 Circ-PRKDC Contributes to 5-Fluorouracil Resistance of Colorectal Cancer Cells by Regulating miR-375/FOXM1 Axis and Wnt/beta-Catenin Pathway. Fluorouracil 26-40 catenin beta 1 Homo sapiens 120-132 32606803-16 2020 Conclusion: Circ-PRKDC enhanced 5-FU resistance in CRC by regulating FOXM1/miR-375 axis and wnt/beta-catenin pathway. Fluorouracil 32-36 catenin beta 1 Homo sapiens 96-108 32606759-9 2020 Results: We verified that PTEN was involved in noscapine-induced apoptosis in HT29/5-FU and LoVo/5-FU cells. Fluorouracil 83-87 phosphatase and tensin homolog Homo sapiens 26-30 32606759-9 2020 Results: We verified that PTEN was involved in noscapine-induced apoptosis in HT29/5-FU and LoVo/5-FU cells. Fluorouracil 97-101 phosphatase and tensin homolog Homo sapiens 26-30 32606759-12 2020 However, PTEN interference counteracted the effect of noscapine on mitochondrial damage and the Warburg effect in HT29/5-FU and LoVo/5-FU cells by decreasing the activation of PI3K/mTOR signaling. Fluorouracil 119-123 phosphatase and tensin homolog Homo sapiens 9-13 32606759-12 2020 However, PTEN interference counteracted the effect of noscapine on mitochondrial damage and the Warburg effect in HT29/5-FU and LoVo/5-FU cells by decreasing the activation of PI3K/mTOR signaling. Fluorouracil 133-137 phosphatase and tensin homolog Homo sapiens 9-13 32078695-8 2020 Cisplatin, 5-fluorouracil and carboplatin induced dose-dependent apoptosis in primary lines of iNKT cells and inhibited CD1d-dependent interferon-gamma production and cytolytic degranulation by viable iNKT cells. Fluorouracil 11-25 CD1d molecule Homo sapiens 120-124 31479512-7 2020 Based on concurrent biomarker expression, combinations of immunotherapy with platinum (ERCC1 negativity) or with doxorubicin, epirubicin, or etoposide (TOP2A positivity), have a higher probability of response while combinations with irinotecan or topotecan (TOPO1 positivity), with gemcitabine (RRM1 negativity), and fluorouracil, pemetrexed, or capecitabine (TS negativity) may be of less benefit. Fluorouracil 317-329 ERCC excision repair 1, endonuclease non-catalytic subunit Homo sapiens 87-92 31479512-7 2020 Based on concurrent biomarker expression, combinations of immunotherapy with platinum (ERCC1 negativity) or with doxorubicin, epirubicin, or etoposide (TOP2A positivity), have a higher probability of response while combinations with irinotecan or topotecan (TOPO1 positivity), with gemcitabine (RRM1 negativity), and fluorouracil, pemetrexed, or capecitabine (TS negativity) may be of less benefit. Fluorouracil 317-329 DNA topoisomerase II alpha Homo sapiens 152-157 32460371-6 2020 In a xenografted mouse model of cancer, HEP with 5-Fu significantly suppressed tumor growth, inhibited inflammatory markers such as interferon (IFN)-gamma, interleukin (IL)-1beta, IL-2, IL-6, tumor necrosis factor (TNF)-alpha, and lipopolysaccharide (LPS), and regulated the expression of Akt, CCDN1, CKD4, FOXM1, MMP7, MYC, PPAR-alpha, and PPAR-gamma. Fluorouracil 49-53 interleukin 1 alpha Mus musculus 156-178 32427870-9 2020 miR-21 targets PDCD4, TPM1 and PTEN were down-regulated by exosomes and silencing of PDCD4 mimicked miR-21 functional effects, even the induced resistance against 5-FU. Fluorouracil 163-167 microRNA 21 Homo sapiens 0-6 32427870-9 2020 miR-21 targets PDCD4, TPM1 and PTEN were down-regulated by exosomes and silencing of PDCD4 mimicked miR-21 functional effects, even the induced resistance against 5-FU. Fluorouracil 163-167 phosphatase and tensin homolog Homo sapiens 31-35 32457882-9 2020 Determine the role of Cyclin-related protein Cyclin D3 in beta-elemene reversing the resistance of HCT116p53-/- to 5-fluorouracil was detected by overexpression of Cyclin D3. Fluorouracil 115-129 proliferating cell nuclear antigen Homo sapiens 22-28 32269616-5 2020 Moreover, GAS5 knockdown sensitized CSCs to the chemotherapeutic agents 5-fluorouracil and doxorubicin by inducing apoptosis detected by Annexin V-FITC/PI double staining. Fluorouracil 72-86 annexin A5 Homo sapiens 137-146 32426273-8 2020 Then, the anti-cancer drug 5-fluorouracil was used to stimulate the NCI-H460 cells; the mRNA levels of miR-93, miR-373, and miR-17-5p were decreased, and the level of TBP-2 mRNA and protein was increased. Fluorouracil 27-41 microRNA 9-3 Homo sapiens 103-109 33194315-4 2020 In cell experiments, slow-releasing poly(EDP-NAC) rescued H9C2 cardiomyocytes more effectively than EDP-NAC when cells were treated with 5-fluorouricil (5-FU), which induces sustained production of ROS. Fluorouracil 153-157 synuclein alpha Homo sapiens 45-48 33194315-4 2020 In cell experiments, slow-releasing poly(EDP-NAC) rescued H9C2 cardiomyocytes more effectively than EDP-NAC when cells were treated with 5-fluorouricil (5-FU), which induces sustained production of ROS. Fluorouracil 153-157 synuclein alpha Homo sapiens 104-107 31102118-8 2020 Results Our data provided the first demonstration that cardamonin significantly enhanced the chemosensitivity of 5-FU in GC cells via suppression of Wnt/beta-catenin signaling pathway. Fluorouracil 113-117 catenin beta 1 Homo sapiens 153-165 31102118-9 2020 Additionally, the combination of cardamonin and 5-FU might result in the apoptosis and cell cycle arrest of BGC-823/5-FU cells, accompanied by the downregulated expression levels of P-glycoprotein, beta-catenin and TCF4. Fluorouracil 48-52 catenin beta 1 Homo sapiens 198-210 32256983-6 2020 METHODS: This review discusses the effects of FPGS and GGH on chemosensitivity to cancer chemotherapeutic agents such as antifolates, such as methotrexate, and 5-fluorouracil. Fluorouracil 160-174 folylpolyglutamate synthase Homo sapiens 46-50 32256983-6 2020 METHODS: This review discusses the effects of FPGS and GGH on chemosensitivity to cancer chemotherapeutic agents such as antifolates, such as methotrexate, and 5-fluorouracil. Fluorouracil 160-174 gamma-glutamyl hydrolase Homo sapiens 55-58 32256983-9 2020 Therefore, FPGS and GGH affect chemosensitivity to antifolates and 5-fluorouracil by altering intracellular retention status of antifolates and folate cofactors such as 5,10-methylenetetrahydrofolate, subsequently influencing the cytotoxic effects of 5-fluorouracil, respectively. Fluorouracil 67-81 folylpolyglutamate synthase Homo sapiens 11-15 32256983-9 2020 Therefore, FPGS and GGH affect chemosensitivity to antifolates and 5-fluorouracil by altering intracellular retention status of antifolates and folate cofactors such as 5,10-methylenetetrahydrofolate, subsequently influencing the cytotoxic effects of 5-fluorouracil, respectively. Fluorouracil 67-81 gamma-glutamyl hydrolase Homo sapiens 20-23 32256983-9 2020 Therefore, FPGS and GGH affect chemosensitivity to antifolates and 5-fluorouracil by altering intracellular retention status of antifolates and folate cofactors such as 5,10-methylenetetrahydrofolate, subsequently influencing the cytotoxic effects of 5-fluorouracil, respectively. Fluorouracil 251-265 folylpolyglutamate synthase Homo sapiens 11-15 32266094-12 2020 These data supported an important role of the ER stress-mediated GRP78/OCT4/lncRNA MIAT/AKT pathway in BC cell resistance to 5-FU, highlighting potential molecular targets for combating 5-FU resistance in BC. Fluorouracil 125-129 POU class 5 homeobox 1 Homo sapiens 71-75 32266094-12 2020 These data supported an important role of the ER stress-mediated GRP78/OCT4/lncRNA MIAT/AKT pathway in BC cell resistance to 5-FU, highlighting potential molecular targets for combating 5-FU resistance in BC. Fluorouracil 186-190 POU class 5 homeobox 1 Homo sapiens 71-75 31960523-7 2020 ALDH1A3 was selectively overexpressed among the ALDH isozymes after treatment with 5-FU or SN38, a DNA topoisomerase I inhibitor. Fluorouracil 83-87 aldehyde dehydrogenase 1 family member A3 Homo sapiens 0-7 31960523-7 2020 ALDH1A3 was selectively overexpressed among the ALDH isozymes after treatment with 5-FU or SN38, a DNA topoisomerase I inhibitor. Fluorouracil 83-87 aldehyde dehydrogenase 1 family member A3 Homo sapiens 0-4 32158231-9 2020 Meanwhile, downregulation of miR-486-5p markedly enhanced the anti-tumor effect of 5-Fu in PANC-1 cells via upregulation of the level of PTEN, and downregulation of the expressions of p-ERK and p-Akt. Fluorouracil 83-87 phosphatase and tensin homolog Homo sapiens 137-141 32158231-9 2020 Meanwhile, downregulation of miR-486-5p markedly enhanced the anti-tumor effect of 5-Fu in PANC-1 cells via upregulation of the level of PTEN, and downregulation of the expressions of p-ERK and p-Akt. Fluorouracil 83-87 eukaryotic translation initiation factor 2 alpha kinase 3 Homo sapiens 184-189 31760170-12 2020 RESULTS: HAND2-AS1 and PDCD4 were downregulated and miR-20a was upregulated in 5-FU-resistant CRC tissues and cells. Fluorouracil 79-83 heart and neural crest derivatives expressed 2 Mus musculus 9-14 31760170-13 2020 HAND2-AS1 suppressed 5-FU resistance, cell proliferation, migration and invasion and promoted cell apoptosis in 5-FU-resistant CRC cells. Fluorouracil 21-25 heart and neural crest derivatives expressed 2 Mus musculus 0-5 31760170-13 2020 HAND2-AS1 suppressed 5-FU resistance, cell proliferation, migration and invasion and promoted cell apoptosis in 5-FU-resistant CRC cells. Fluorouracil 112-116 heart and neural crest derivatives expressed 2 Mus musculus 0-5 31760170-15 2020 Moreover, HAND2-AS1 suppressed cell progression and 5-FU resistance by upregulating PDCD4 via sponging miR-20a in 5-FU-resistant CRC cells. Fluorouracil 52-56 heart and neural crest derivatives expressed 2 Mus musculus 10-15 31760170-15 2020 Moreover, HAND2-AS1 suppressed cell progression and 5-FU resistance by upregulating PDCD4 via sponging miR-20a in 5-FU-resistant CRC cells. Fluorouracil 114-118 heart and neural crest derivatives expressed 2 Mus musculus 10-15 31760170-17 2020 CONCLUSION: HAND2-AS1/miR-20a/PDCD4 axis inhibited cell progression and 5-FU resistance in 5-FU-resistant CRC cells. Fluorouracil 72-76 heart and neural crest derivatives expressed 2 Mus musculus 12-17 31760170-17 2020 CONCLUSION: HAND2-AS1/miR-20a/PDCD4 axis inhibited cell progression and 5-FU resistance in 5-FU-resistant CRC cells. Fluorouracil 91-95 heart and neural crest derivatives expressed 2 Mus musculus 12-17 31898732-7 2020 Additionally, SRPK2 had no association with mutant p53 (mtp53) in SW480 and SW620 cells, but negatively regulated Numb and wild-type p53 (wtp53) in response to 5-fluorouracil or cisplatin treatment in HCT116 cells. Fluorouracil 160-174 SRSF protein kinase 2 Homo sapiens 14-19 31898732-8 2020 Moreover, SRPK2, Numb and p53 coimmunoprecipitated into a triple complex without or with the treatment of 5-fluorouracil in HCT116 cells, and p53 knockdown reversed the upregulation of wtp53 induced by SRPK2 silencing with chemical agent treatment. Fluorouracil 106-120 SRSF protein kinase 2 Homo sapiens 10-15 31898732-9 2020 Furthermore, overexpression of SRPK2 increased cell migration and invasion and decreased chemosensitivity to 5-fluorouracil or cisplatin in HCT116 cells. Fluorouracil 109-123 SRSF protein kinase 2 Homo sapiens 31-36 31898732-10 2020 Conversely, SRPK2 silencing decreased cell migration and invasion and increased chemosensitivity to 5-fluorouracil or cisplatin, yet these effects could be reversed by p53 knockdown under chemical agent treatment. Fluorouracil 100-114 SRSF protein kinase 2 Homo sapiens 12-17 31864766-0 2020 Corrigendum to "5-Fluorouracil causes severe CNS demyelination by disruption of TCF7L2/HDAC1/HDAC2 complex in adolescent mice" [Toxicology 325 (2014) 144-150]. Fluorouracil 16-30 histone deacetylase 1 Mus musculus 87-92 32426701-1 2020 Objective: To investigate the expressions of MAPK10, c-Jun and Itga6 in laryngeal carcinoma and its influence on the sensitivity to docetaxel, cisplatin and 5-fluorouracil (TPF) chemotherapy. Fluorouracil 157-171 mitogen-activated protein kinase 10 Homo sapiens 45-51 32021282-10 2020 Additionally, RNF38/LDB1 axis was involved in the drug sensitivity of 5-FU to CRC cells. Fluorouracil 70-74 ring finger protein 38 Homo sapiens 14-19 32021282-10 2020 Additionally, RNF38/LDB1 axis was involved in the drug sensitivity of 5-FU to CRC cells. Fluorouracil 70-74 LIM domain binding 1 Homo sapiens 20-24 31704613-9 2020 Importantly, we were able to overcome the resistance to 5-FU seen in CRC cells carrying short APC by tankyrase inhibitor, XAV939, thereby inhibiting Wnt/beta-catenin signaling cascade. Fluorouracil 56-60 catenin beta 1 Homo sapiens 153-165 31754833-2 2020 High GGH expression affects 5-FU thymidylate synthase (TS) inhibition and is a risk factor for various malignancies. Fluorouracil 28-32 gamma-glutamyl hydrolase Homo sapiens 5-8 31754833-2 2020 High GGH expression affects 5-FU thymidylate synthase (TS) inhibition and is a risk factor for various malignancies. Fluorouracil 28-32 thymidylate synthetase Homo sapiens 33-53 31754833-2 2020 High GGH expression affects 5-FU thymidylate synthase (TS) inhibition and is a risk factor for various malignancies. Fluorouracil 28-32 thymidylate synthetase Homo sapiens 55-57 33097678-8 2020 5-FU treatment increased CD133 expression independently to MMR status in SW480 and RKO and was able to increase hMLH1 expression in RKO, a MMR-deficient cell line. Fluorouracil 0-4 mutL homolog 1 Homo sapiens 112-117 33097678-10 2020 Thus, although CSCs 5-FU chemoresistance appears to be independently to MMR status, hMLH1 might play a key role in CSC response to 5-FU. Fluorouracil 131-135 mutL homolog 1 Homo sapiens 84-89 32694681-7 2020 Inhibition of SRR suppresses growth of colorectal tumours in mice and augments the efficacy of 5-fluorouracil treatment. Fluorouracil 95-109 serine racemase Mus musculus 14-17 31897166-6 2020 The combination of oxymatrine and 5-FU reduced the protein expression of snail family transcriptional repressor 2 and vimentin, phosphorylated p65 and induced the expression of E-cadherin, by inhibiting the nuclear factor kappaB (NF-kappaB) signaling pathway. Fluorouracil 34-38 vimentin Homo sapiens 118-126 31582208-0 2019 H1, a derivative of tetrandrine, enhances the efficacy of 5-FU in Bel7402/5-FU cells via suppressing STAT3/MCL-1 and inducing PUMA. Fluorouracil 58-62 MCL1 apoptosis regulator, BCL2 family member Homo sapiens 107-112 31582208-9 2019 Taken together, H1 effectively improve the cytotoxic effect of 5-FU against Bel7402/5-FU cells via blocking STAT3/MCL-1 pathway and inducing PUMA. Fluorouracil 63-67 MCL1 apoptosis regulator, BCL2 family member Homo sapiens 114-119 31806933-1 2019 Purpose: A previous study has identified that XRCC4-like factor (XLF) is a potential target to overcome resistance to 5-fluorouracil (5-Fu) and oxaliplatin (OXA) in colorectal cancer (CRC). Fluorouracil 118-132 non-homologous end joining factor 1 Homo sapiens 46-63 31806933-1 2019 Purpose: A previous study has identified that XRCC4-like factor (XLF) is a potential target to overcome resistance to 5-fluorouracil (5-Fu) and oxaliplatin (OXA) in colorectal cancer (CRC). Fluorouracil 118-132 non-homologous end joining factor 1 Homo sapiens 65-68 31806933-1 2019 Purpose: A previous study has identified that XRCC4-like factor (XLF) is a potential target to overcome resistance to 5-fluorouracil (5-Fu) and oxaliplatin (OXA) in colorectal cancer (CRC). Fluorouracil 134-138 non-homologous end joining factor 1 Homo sapiens 46-63 31806933-1 2019 Purpose: A previous study has identified that XRCC4-like factor (XLF) is a potential target to overcome resistance to 5-fluorouracil (5-Fu) and oxaliplatin (OXA) in colorectal cancer (CRC). Fluorouracil 134-138 non-homologous end joining factor 1 Homo sapiens 65-68 31704837-8 2019 These results indicated that the simultaneous expression of APEX1 and Jagged-1 might be associated with chemoresistance toward 5-FU, oxaliplatin, and irinotecan. Fluorouracil 127-131 jagged canonical Notch ligand 1 Homo sapiens 70-78 31477270-6 2019 Furthermore, DJ-1 overexpressed gastric cancer cell line SGC7901/LV-DJ-1 led to the increase of cell survival rate, the IC50 of chemotherapeutic drugs and number of cell clones as well as decrease of cell cycle G0/G1 phase ratio compared with its parental cells under the treatment of VCR, adriamycin (ADR), 5-Fluorouracil (5-FU) and cisplatin (DDP). Fluorouracil 308-322 Parkinsonism associated deglycase Homo sapiens 13-17 31477270-6 2019 Furthermore, DJ-1 overexpressed gastric cancer cell line SGC7901/LV-DJ-1 led to the increase of cell survival rate, the IC50 of chemotherapeutic drugs and number of cell clones as well as decrease of cell cycle G0/G1 phase ratio compared with its parental cells under the treatment of VCR, adriamycin (ADR), 5-Fluorouracil (5-FU) and cisplatin (DDP). Fluorouracil 308-322 Parkinsonism associated deglycase Homo sapiens 68-72 31477270-6 2019 Furthermore, DJ-1 overexpressed gastric cancer cell line SGC7901/LV-DJ-1 led to the increase of cell survival rate, the IC50 of chemotherapeutic drugs and number of cell clones as well as decrease of cell cycle G0/G1 phase ratio compared with its parental cells under the treatment of VCR, adriamycin (ADR), 5-Fluorouracil (5-FU) and cisplatin (DDP). Fluorouracil 324-328 Parkinsonism associated deglycase Homo sapiens 13-17 31477270-6 2019 Furthermore, DJ-1 overexpressed gastric cancer cell line SGC7901/LV-DJ-1 led to the increase of cell survival rate, the IC50 of chemotherapeutic drugs and number of cell clones as well as decrease of cell cycle G0/G1 phase ratio compared with its parental cells under the treatment of VCR, adriamycin (ADR), 5-Fluorouracil (5-FU) and cisplatin (DDP). Fluorouracil 324-328 Parkinsonism associated deglycase Homo sapiens 68-72 31802939-8 2019 Moreover, ANO1 prevent colon cancer apoptosis from oxaliplatin and 5-FU. Fluorouracil 67-71 anoctamin 1 Homo sapiens 10-14 31802939-9 2019 Additionally, knockdown ANO1 expression could block F. nucleatum protective effects and increase the apoptosis effects induced by oxaliplatin and 5-FU. Fluorouracil 146-150 anoctamin 1 Homo sapiens 24-28 31081972-5 2019 Viabilities and apoptosis of choriocarcinoma JEG-3 and JAR cells after lidocaine and/or 5-Fu treatment were detected using Cell Counting Kit-8 assay, annexin V-FITC/PI (fluorescein isothiocyanate/propidium iodide) staining and Western blot analysis, respectively. Fluorouracil 88-92 annexin A5 Homo sapiens 150-159 31206244-2 2019 The aim of our study was to determine the prognostic and predictive relevance of these subgroups in the context of platinum/5-fluorouracil (5-FU) based preoperative chemotherapy (CTx). Fluorouracil 124-138 cytochrome P450 family 27 subfamily A member 1 Homo sapiens 179-182 31206244-2 2019 The aim of our study was to determine the prognostic and predictive relevance of these subgroups in the context of platinum/5-fluorouracil (5-FU) based preoperative chemotherapy (CTx). Fluorouracil 140-144 cytochrome P450 family 27 subfamily A member 1 Homo sapiens 179-182 31497531-0 2019 LINC00957 Acted as Prognostic Marker Was Associated With Fluorouracil Resistance in Human Colorectal Cancer. Fluorouracil 57-69 long intergenic non-protein coding RNA 957 Homo sapiens 0-9 31592435-3 2019 Combined effects of rutin with the widely used anti-cancer drug, 5-fluorouracil (5-FU), on prostate cancer cell line (PC3) was investigated herein. Fluorouracil 65-79 chromobox 8 Homo sapiens 118-121 31592435-3 2019 Combined effects of rutin with the widely used anti-cancer drug, 5-fluorouracil (5-FU), on prostate cancer cell line (PC3) was investigated herein. Fluorouracil 81-85 chromobox 8 Homo sapiens 118-121 31592435-4 2019 Methods: Different concentrations of combined 5-FU and rutin were applied to PC3 cells compared to separate treatment for 48 hours. Fluorouracil 46-50 chromobox 8 Homo sapiens 77-80 31592435-9 2019 Combination of 5-FU/rutin enhanced apoptosis and p53 gene expression in PC3 cells. Fluorouracil 15-19 chromobox 8 Homo sapiens 72-75 31592435-10 2019 PC3 cell colony counts and Bcl-2 signaling protein were decreased by 5-FU/rutin combination. Fluorouracil 69-73 chromobox 8 Homo sapiens 0-3 31592435-11 2019 Conclusion: Synergistic effects of 5-FU/rutin combination on PC3 cells line enhanced apoptosis, p53 gene expression, and down-regulation of Bcl-2 protein, compared to control separate application. Fluorouracil 35-39 chromobox 8 Homo sapiens 61-64 31423282-11 2019 In conclusion, the multifactorial predictive biomarker model of alpha-SMA, p-AKT, p-ERK and survivin expression for patients with aCRC to predict intrinsic resistance to oxaliplatin plus 5-FU regimens is of great efficiency and accuracy. Fluorouracil 187-191 eukaryotic translation initiation factor 2 alpha kinase 3 Homo sapiens 82-87 31184647-0 2019 Theragnosis by a miR-141-3p molecular beacon: simultaneous detection and sensitization of 5-fluorouracil resistant colorectal cancer cells through the activation of the TRIM13-associated apoptotic pathway. Fluorouracil 90-104 tripartite motif containing 13 Homo sapiens 169-175 31217433-9 2019 The repression of 5-FU-induced caspase-1 activity by DHA supplementation is partially due to beta-arrestin-2-dependent inhibition of NLRP3 inflammasome activity but was independent of JNK pathway. Fluorouracil 18-22 arrestin, beta 2 Mus musculus 93-108 31217433-9 2019 The repression of 5-FU-induced caspase-1 activity by DHA supplementation is partially due to beta-arrestin-2-dependent inhibition of NLRP3 inflammasome activity but was independent of JNK pathway. Fluorouracil 18-22 NLR family, pyrin domain containing 3 Mus musculus 133-138 31217433-10 2019 Interestingly, we showed that DHA, through beta-arrestin-2-mediated inhibition of JNK pathway, reduces V5-tagged mature IL-1beta release induced by 5-FU, in MDSC stably overexpressing a V5-tagged mature IL-1beta form. Fluorouracil 148-152 arrestin, beta 2 Mus musculus 43-58 31217433-10 2019 Interestingly, we showed that DHA, through beta-arrestin-2-mediated inhibition of JNK pathway, reduces V5-tagged mature IL-1beta release induced by 5-FU, in MDSC stably overexpressing a V5-tagged mature IL-1beta form. Fluorouracil 148-152 interleukin 1 alpha Mus musculus 120-128 31000196-4 2019 eIF4E inhibition thus significantly sensitizes NPC cell response to 5-FU. Fluorouracil 68-72 eukaryotic translation initiation factor 4E Mus musculus 0-5 31000196-9 2019 Our findings provide the better understanding on the role of eIF4E in NPC in response to 5-FU and preclinical rationale to explore ribavirin as a sensitizing strategy to treat NPC, particularly in those who develop 5-FU resistance. Fluorouracil 89-93 eukaryotic translation initiation factor 4E Mus musculus 61-66 30484020-11 2019 The mRNA levels of P-gp (0.28+-0.02) and HSP-27 (0.28+-0.09) in HCT-8/5-FU cells treated with combination drugs were lower than cells treated with 5-FU alone (P-gp, 0.48+-0.07, P=0.009; HSP-27, 0.57+-0.10, P=0.007). Fluorouracil 70-74 heat shock protein family B (small) member 1 Homo sapiens 41-47 30484020-11 2019 The mRNA levels of P-gp (0.28+-0.02) and HSP-27 (0.28+-0.09) in HCT-8/5-FU cells treated with combination drugs were lower than cells treated with 5-FU alone (P-gp, 0.48+-0.07, P=0.009; HSP-27, 0.57+-0.10, P=0.007). Fluorouracil 70-74 heat shock protein family B (small) member 1 Homo sapiens 186-192 30484020-12 2019 The protein levels of P-gp (0.25+-0.06) and HSP-27 (0.09+-0.02) in HCT-8/5-FU cells treated with combination drugs were decreased when compared to 5-FU alone (P-gp, 0.46+-0.02, P=0.005; HSP-27, 0.43+-0.01, P=0.000). Fluorouracil 73-77 heat shock protein family B (small) member 1 Homo sapiens 44-50 30484020-15 2019 Down-regulation of P-gp and HSP-27 may be the mechanism of curcumin reversing the drug resistance of HCT-8/5-FU to 5-FU. Fluorouracil 107-111 heat shock protein family B (small) member 1 Homo sapiens 28-34 30484020-15 2019 Down-regulation of P-gp and HSP-27 may be the mechanism of curcumin reversing the drug resistance of HCT-8/5-FU to 5-FU. Fluorouracil 115-119 heat shock protein family B (small) member 1 Homo sapiens 28-34 31934061-0 2019 MiR-21/PTEN signaling modulates the chemo-sensitivity to 5-fluorouracil in human lung adenocarcinoma A549 cells. Fluorouracil 57-71 microRNA 21 Homo sapiens 0-6 31934061-0 2019 MiR-21/PTEN signaling modulates the chemo-sensitivity to 5-fluorouracil in human lung adenocarcinoma A549 cells. Fluorouracil 57-71 phosphatase and tensin homolog Homo sapiens 7-11 31934061-2 2019 Our work aims at investigating the role of miR-21 in human lung adenocarcinoma A549 cells and cells treated with 5-fluorouracil and their potential molecular mechanisms. Fluorouracil 113-127 microRNA 21 Homo sapiens 43-49 31934061-8 2019 Our findings demonstrated that the overexpression of miR-21 decreased 5-fluorouracil-induced apoptosis and necrosis, and the opposite effects were obtained by the suppression of miR-21. Fluorouracil 70-84 microRNA 21 Homo sapiens 53-59 31934061-9 2019 Further, we found that the phosphatase and tensin homologue (PTEN) was regulated by the alteration of miR-21 in A549 cells treated with 5-fluorouracil. Fluorouracil 136-150 phosphatase and tensin homolog Homo sapiens 27-59 31934061-9 2019 Further, we found that the phosphatase and tensin homologue (PTEN) was regulated by the alteration of miR-21 in A549 cells treated with 5-fluorouracil. Fluorouracil 136-150 phosphatase and tensin homolog Homo sapiens 61-65 31934061-9 2019 Further, we found that the phosphatase and tensin homologue (PTEN) was regulated by the alteration of miR-21 in A549 cells treated with 5-fluorouracil. Fluorouracil 136-150 microRNA 21 Homo sapiens 102-108 31934061-11 2019 Our present work indicated the involvement of the miR-21/PTEN axis in the 5-fluorouracil-induced cell apoptosis of NSCLC. Fluorouracil 74-88 microRNA 21 Homo sapiens 50-56 31934061-11 2019 Our present work indicated the involvement of the miR-21/PTEN axis in the 5-fluorouracil-induced cell apoptosis of NSCLC. Fluorouracil 74-88 phosphatase and tensin homolog Homo sapiens 57-61 31934061-12 2019 Therefore, the inhibition of the miRNA-21/PTEN pathway may be a novel therapeutic target to block 5-fluorouracil-induced chemotherapy resistance in NSCLC. Fluorouracil 98-112 microRNA 21 Homo sapiens 33-41 31934061-12 2019 Therefore, the inhibition of the miRNA-21/PTEN pathway may be a novel therapeutic target to block 5-fluorouracil-induced chemotherapy resistance in NSCLC. Fluorouracil 98-112 phosphatase and tensin homolog Homo sapiens 42-46 30923017-0 2019 Tacalcitol increases the sensitivity of colorectal cancer cells to 5-fluorouracil by downregulating the thymidylate synthase. Fluorouracil 67-81 thymidylate synthetase Homo sapiens 104-124 30923017-7 2019 5-FU significantly increased TYMS (gene encoding thymidylate synthase (TS)) and BIRC5 (gene encoding survivin) level in HT-29 cells with silenced VDR. Fluorouracil 0-4 thymidylate synthetase Homo sapiens 29-33 30923017-7 2019 5-FU significantly increased TYMS (gene encoding thymidylate synthase (TS)) and BIRC5 (gene encoding survivin) level in HT-29 cells with silenced VDR. Fluorouracil 0-4 thymidylate synthetase Homo sapiens 49-69 31120863-5 2019 We now demonstrate that simultaneous deletion of P110alpha and P110delta in double knockout (DKO) HSCs uncovers their redundant requirement in HSC cycling after 5-fluorouracil (5-FU) chemotherapy administration. Fluorouracil 177-181 phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit delta Homo sapiens 63-72 31120863-7 2019 We found that DKO HSCs and progenitors have impaired sensing of inflammatory signals ex vivo, and that levels of IL1-beta and MIG are higher in the bone marrow after LPS than after 5-FU administration. Fluorouracil 181-185 interleukin 1 alpha Homo sapiens 113-121 31139044-0 2019 Co-treatment With BGP-15 Exacerbates 5-Fluorouracil-Induced Gastrointestinal Dysfunction. Fluorouracil 37-51 carcinoembryonic antigen-related cell adhesion molecule 1 Mus musculus 18-21 31139044-5 2019 In this study, we investigated whether the cytoprotectant, BGP-15, has a neuroprotective effect during 5-FU treatment. Fluorouracil 103-107 carcinoembryonic antigen-related cell adhesion molecule 1 Mus musculus 59-62 31139044-10 2019 BGP-15 co-administration significantly increased mitochondrial superoxide production, mitochondrial depolarization and cytochrome c release in myenteric plexus and exacerbated 5-FU-induced colonic inflammation. Fluorouracil 176-180 carcinoembryonic antigen-related cell adhesion molecule 1 Mus musculus 0-3 31139044-11 2019 BGP-15 exacerbated 5-FU-induced colonic dysmotility by reducing the number and proportion of colonic migrating motor complexes and increasing the number and proportion of fragmented contractions and increased fecal water content indicative of diarrhea. Fluorouracil 19-23 carcinoembryonic antigen-related cell adhesion molecule 1 Mus musculus 0-3 31139044-12 2019 Taken together, BGP-15 co-treatment aggravates 5-FU-induced GI side-effects, in contrast with our previous findings that BGP-15 alleviates GI side-effects of oxaliplatin. Fluorouracil 47-51 carcinoembryonic antigen-related cell adhesion molecule 1 Mus musculus 16-19 31205469-0 2019 LncRNA PVT1 Mediates Antiapoptosis and 5-Fluorouracil Resistance via Increasing Bcl2 Expression in Gastric Cancer. Fluorouracil 39-53 Pvt1 oncogene Homo sapiens 7-11 31205469-6 2019 The resistance to 5- Fluorouracil (5-Fu) caused by PVT1 was evaluated using cell viability assay. Fluorouracil 18-33 Pvt1 oncogene Homo sapiens 51-55 31205469-6 2019 The resistance to 5- Fluorouracil (5-Fu) caused by PVT1 was evaluated using cell viability assay. Fluorouracil 35-39 Pvt1 oncogene Homo sapiens 51-55 31205469-10 2019 We confirmed that PVT1 can regulate the expression of Bcl2 and enhance drug-resistance of gastric cancer to 5-Fu. Fluorouracil 108-112 Pvt1 oncogene Homo sapiens 18-22 31205469-12 2019 Conclusion: Our results showed that PVT1 can inhibit the apoptosis and enhance the 5-Fu resistance of gastric cancer through the activation of Bcl2. Fluorouracil 83-87 Pvt1 oncogene Homo sapiens 36-40 31205469-13 2019 PVT1 has the potential to serve as an indicator to predict 5-Fu treatment resistance. Fluorouracil 59-63 Pvt1 oncogene Homo sapiens 0-4 30582240-1 2019 BACKGROUND: To evaluate the expression of programmed death-1 (PD-1) and programmed death-ligand 1 (PD-L1) by using immunohistochemistry analysis in locoregionally advanced nasopharyngeal carcinoma (NPC) patients receiving cisplatin, fluorouracil, and docetaxel followed by concurrent chemoradiotherapy. Fluorouracil 233-245 CD274 molecule Homo sapiens 99-104 30651398-1 2019 LESSONS LEARNED: The upregulation of dihydropyrimidine dehydrogenase (DPD) and thymidylate synthase (TS) are important mechanisms of resistance to 5-fluorouracil (5-FU) in metastatic colorectal cancer (mCRC) after long exposure to 5-FU.S-1 (containing a DPD inhibitor) combined with raltitrexed (a TS inhibitor) showed a moderate effect, which needs further study as a third- or later-line therapy in mCRC. Fluorouracil 147-161 thymidylate synthetase Homo sapiens 79-99 30651398-1 2019 LESSONS LEARNED: The upregulation of dihydropyrimidine dehydrogenase (DPD) and thymidylate synthase (TS) are important mechanisms of resistance to 5-fluorouracil (5-FU) in metastatic colorectal cancer (mCRC) after long exposure to 5-FU.S-1 (containing a DPD inhibitor) combined with raltitrexed (a TS inhibitor) showed a moderate effect, which needs further study as a third- or later-line therapy in mCRC. Fluorouracil 163-167 thymidylate synthetase Homo sapiens 79-99 30651398-1 2019 LESSONS LEARNED: The upregulation of dihydropyrimidine dehydrogenase (DPD) and thymidylate synthase (TS) are important mechanisms of resistance to 5-fluorouracil (5-FU) in metastatic colorectal cancer (mCRC) after long exposure to 5-FU.S-1 (containing a DPD inhibitor) combined with raltitrexed (a TS inhibitor) showed a moderate effect, which needs further study as a third- or later-line therapy in mCRC. Fluorouracil 231-235 thymidylate synthetase Homo sapiens 79-99 30651398-4 2019 The upregulation of dihydropyrimidine dehydrogenase (DPD) and/or thymidylate synthase (TS) are important mechanisms of resistance of 5-FU. Fluorouracil 133-137 thymidylate synthetase Homo sapiens 65-85 31118569-9 2019 Conclusion: This is the first report of the angiographic characteristics of OSSN and its response to subconjunctival/perilesional 5-fluorouracil injections by simultaneous conjunctival angiography and AS-OCT. Fluorouracil 130-144 plexin A2 Homo sapiens 204-207 30742943-6 2019 SMURF2 is negatively regulated by USP47, and USP47 depletion sensitizes colon cancer cells to 5-FU treatment-induced apoptosis. Fluorouracil 94-98 ubiquitin specific peptidase 47 Mus musculus 45-50 30965636-3 2019 We showed the expression levels of both beta-catenin and RAS were significantly increased and correlated in tissues of 756 gastric cancer (GC) patients and tissues of primary- and acquired-resistance patient-derived xenograft tumors treated with 5-fluorouracil and oxaliplatin modulated with leucovorin (FOLFOX). Fluorouracil 246-260 catenin beta 1 Homo sapiens 40-52 30875351-4 2019 TYMS gene encodes for the human thymidylate synthase, and is considered a candid factor for toxicity and efficacy of 5-FU and capecitabine. Fluorouracil 117-121 thymidylate synthetase Homo sapiens 0-4 30875351-4 2019 TYMS gene encodes for the human thymidylate synthase, and is considered a candid factor for toxicity and efficacy of 5-FU and capecitabine. Fluorouracil 117-121 thymidylate synthetase Homo sapiens 32-52 30842340-0 2019 Down-regulation of miR-543 expression increases the sensitivity of colorectal cancer cells to 5-Fluorouracil through the PTEN/PI3K/AKT pathway. Fluorouracil 94-108 microRNA 543 Homo sapiens 19-26 30842340-0 2019 Down-regulation of miR-543 expression increases the sensitivity of colorectal cancer cells to 5-Fluorouracil through the PTEN/PI3K/AKT pathway. Fluorouracil 94-108 phosphatase and tensin homolog Homo sapiens 121-125 30842340-4 2019 This study investigated whether the down-regulation of miR-543 expression enhanced 5-fluorouracil (5-FU)-induced apoptosis in HCT8/FU colon cancer cells. Fluorouracil 83-97 microRNA 543 Homo sapiens 55-62 30842340-4 2019 This study investigated whether the down-regulation of miR-543 expression enhanced 5-fluorouracil (5-FU)-induced apoptosis in HCT8/FU colon cancer cells. Fluorouracil 99-103 microRNA 543 Homo sapiens 55-62 30842340-6 2019 An miR-543 inhibitor or mimic was transfected, followed by MTT assay to detect 5-FU sensitivity in HCT8 and HCT8/FU cell lines, which showed that IC50 of 5-FU was positively correlated with miR-543 expression. Fluorouracil 154-158 microRNA 543 Homo sapiens 3-10 30842340-8 2019 Additionally, an elevated expression of PTEN reversed the chemoresistance of miR-543-overexpressing HCT8 cells to 5-FU. Fluorouracil 114-118 phosphatase and tensin homolog Homo sapiens 40-44 30842340-8 2019 Additionally, an elevated expression of PTEN reversed the chemoresistance of miR-543-overexpressing HCT8 cells to 5-FU. Fluorouracil 114-118 microRNA 543 Homo sapiens 77-84 30842340-9 2019 These results indicate that miR-543 might be a target to increase the sensitivity of CRC cells to 5-FU through the PTEN/PI3K/AKT pathway. Fluorouracil 98-102 microRNA 543 Homo sapiens 28-35 30842340-9 2019 These results indicate that miR-543 might be a target to increase the sensitivity of CRC cells to 5-FU through the PTEN/PI3K/AKT pathway. Fluorouracil 98-102 phosphatase and tensin homolog Homo sapiens 115-119 30587545-12 2019 In xenografted mice, the SMAD4-lost tumors displayed resistance to 5-FU. Fluorouracil 67-71 SMAD family member 4 Mus musculus 25-30 30677405-8 2019 Moreover, miR-31 overexpression also enhanced the chemosensitivity of miR-31 to the anticancer drug 5-fluorouracil. Fluorouracil 100-114 microRNA 31 Homo sapiens 10-16 30677405-8 2019 Moreover, miR-31 overexpression also enhanced the chemosensitivity of miR-31 to the anticancer drug 5-fluorouracil. Fluorouracil 100-114 microRNA 31 Homo sapiens 70-76 30858358-5 2019 Importantly, depletion of NAA40 inhibits cell proliferation and survival of CRC cell lines and increases their sensitivity to 5-Fluorouracil (5-FU) treatment. Fluorouracil 126-140 N-alpha-acetyltransferase 40, NatD catalytic subunit Homo sapiens 26-31 30858358-5 2019 Importantly, depletion of NAA40 inhibits cell proliferation and survival of CRC cell lines and increases their sensitivity to 5-Fluorouracil (5-FU) treatment. Fluorouracil 142-146 N-alpha-acetyltransferase 40, NatD catalytic subunit Homo sapiens 26-31 30316684-1 2019 BACKGROUND: Treatment of advanced anal squamous cell cancer (SCC) is usually with the combination of cisplatin and 5-fluorouracil, which is associated with heterogeneous responses across patients and significant toxicity. Fluorouracil 115-129 serpin family B member 3 Homo sapiens 61-64 31933924-0 2019 SREBP1 promotes 5-FU resistance in colorectal cancer cells by inhibiting the expression of caspase7. Fluorouracil 16-20 sterol regulatory element binding transcription factor 1 Homo sapiens 0-6 31933924-0 2019 SREBP1 promotes 5-FU resistance in colorectal cancer cells by inhibiting the expression of caspase7. Fluorouracil 16-20 caspase 7 Homo sapiens 91-99 31933924-8 2019 We found that over-expression of SREBP1 through SREBP1 gene transfection enhances the resistant of CRC cell lines to 5-FU, and SREBP1 silencing through SREBP1 shRNA transfection can promote apoptosis in 5-FU treated SW620 cells. Fluorouracil 117-121 sterol regulatory element binding transcription factor 1 Homo sapiens 33-39 31933924-8 2019 We found that over-expression of SREBP1 through SREBP1 gene transfection enhances the resistant of CRC cell lines to 5-FU, and SREBP1 silencing through SREBP1 shRNA transfection can promote apoptosis in 5-FU treated SW620 cells. Fluorouracil 203-207 sterol regulatory element binding transcription factor 1 Homo sapiens 33-39 31933924-10 2019 CONCLUSION: Our results suggest that SREBP1 protect the 5-FU treated CRC cells through caspase7 dependent PARP1 cleavage in apoptosis pathway and potentially provide a new target in the treatment of CRC. Fluorouracil 56-60 sterol regulatory element binding transcription factor 1 Homo sapiens 37-43 31933924-10 2019 CONCLUSION: Our results suggest that SREBP1 protect the 5-FU treated CRC cells through caspase7 dependent PARP1 cleavage in apoptosis pathway and potentially provide a new target in the treatment of CRC. Fluorouracil 56-60 caspase 7 Homo sapiens 87-95 30824833-4 2019 In this study, we discovered that activation of the PERK branch of the unfolded protein response (UPR) pathways is required for colon cancer cells to survive treatment of 5-Fluorouracil (5-FU), one of the first-line chemotherapeutics for late-stage colon cancer patients. Fluorouracil 171-185 eukaryotic translation initiation factor 2 alpha kinase 3 Homo sapiens 52-56 30824833-4 2019 In this study, we discovered that activation of the PERK branch of the unfolded protein response (UPR) pathways is required for colon cancer cells to survive treatment of 5-Fluorouracil (5-FU), one of the first-line chemotherapeutics for late-stage colon cancer patients. Fluorouracil 187-191 eukaryotic translation initiation factor 2 alpha kinase 3 Homo sapiens 52-56 30824833-5 2019 Genetic and pharmacological inhibition of PERK or its downstream factors greatly sensitize colon cancer cells to 5-FU. Fluorouracil 113-117 eukaryotic translation initiation factor 2 alpha kinase 3 Homo sapiens 42-46 30703870-0 2019 The MicroRNA-551a/MEF2C Axis Regulates the Survival and Sphere Formation of Cancer Cells in Response to 5-Fluorouracil. Fluorouracil 104-118 myocyte enhancer factor 2C Homo sapiens 18-23 31205515-7 2019 Higher expression levels of both c-Myb and COX-2 were significantly associated with shorter overall survival for stage II and stage III patients with 5-Fu based chemotherapy. Fluorouracil 150-154 MYB proto-oncogene, transcription factor Homo sapiens 33-38 30527814-3 2019 In addition, the MSI status would also be a biomarker able to predict the lack of efficacy of adjuvant 5-fluorouracil (5FU) chemotherapy. Fluorouracil 103-117 RB binding protein 4, chromatin remodeling factor Homo sapiens 17-20 30527814-3 2019 In addition, the MSI status would also be a biomarker able to predict the lack of efficacy of adjuvant 5-fluorouracil (5FU) chemotherapy. Fluorouracil 119-122 RB binding protein 4, chromatin remodeling factor Homo sapiens 17-20 30226808-0 2019 Long noncoding RNA LINC00261 induces chemosensitization to 5-fluorouracil by mediating methylation-dependent repression of DPYD in human esophageal cancer. Fluorouracil 59-73 long intergenic non-protein coding RNA 261 Homo sapiens 19-28 30226808-3 2019 Hence, the aim of the present study was to evaluate the prevailing hypothesis which suggests that overexpression of LINC00261 possesses the ability to modulate the methylation-dependent repression of DPYD, ultimately resulting in an elevation of the sensitivity of human esophageal cancer cells to 5-FU. Fluorouracil 298-302 long intergenic non-protein coding RNA 261 Homo sapiens 116-125 30226808-5 2019 In an attempt to determine the levels of LINC00261 related to the esophageal cancer cell resistance to 5-FU and to identify the interaction between the levels of LINC00261 and methylation of the DYPD promoter, esophageal cancer cells TE-1 and -5 were prepared, in which LINC00261 and the 5-FU-resistant TE-1 and -5 cells were overexpressed. Fluorouracil 103-107 long intergenic non-protein coding RNA 261 Homo sapiens 41-50 30535504-0 2019 MEK inhibitor enhanced the antitumor effect of oxaliplatin and 5-fluorouracil in MEK1 Q56P-mutant colorectal cancer cells. Fluorouracil 63-77 mitogen-activated protein kinase kinase 1 Homo sapiens 81-85 30535504-4 2019 In addition, U0126 increased the sensitivity of SW48 cells to 5-fluorouracil (5-FU) and oxaliplatin by producing more gammaH2AX foci and decreasing the expression of excision repair cross-complementation group 1 and thymidylate synthase. Fluorouracil 78-82 thymidylate synthetase Homo sapiens 216-236 30525581-5 2019 This novel structural data explains the basis of the AC inhibition, provides insights into the enzymatic properties of the protein, and is a great aid toward the structure-based drug design of potent inhibitors for AC, providing the detailed mechanism, which has eluded the scientific community for more than 30 years, of carmofur"s mysterious 5-fluorouracil-independent antitumor activity. Fluorouracil 344-358 N-acylsphingosine amidohydrolase 1 Homo sapiens 53-55 30525581-5 2019 This novel structural data explains the basis of the AC inhibition, provides insights into the enzymatic properties of the protein, and is a great aid toward the structure-based drug design of potent inhibitors for AC, providing the detailed mechanism, which has eluded the scientific community for more than 30 years, of carmofur"s mysterious 5-fluorouracil-independent antitumor activity. Fluorouracil 344-358 N-acylsphingosine amidohydrolase 1 Homo sapiens 215-217 30551491-0 2019 Rosmarinic acid reduces the resistance of gastric carcinoma cells to 5-fluorouracil by downregulating FOXO4-targeting miR-6785-5p. Fluorouracil 69-83 forkhead box O4 Homo sapiens 102-107 30551491-0 2019 Rosmarinic acid reduces the resistance of gastric carcinoma cells to 5-fluorouracil by downregulating FOXO4-targeting miR-6785-5p. Fluorouracil 69-83 microRNA 6785 Homo sapiens 118-126 30551491-14 2019 Down- or up-regulation of miR-6785-5p increased or reduced chemosensitivity of gastric carcinoma cells to 5-Fu, respectively. Fluorouracil 106-110 microRNA 6785 Homo sapiens 26-34 31582661-7 2019 In contrast, 5-fluorouracil significantly inhibited proglucagon, GLP-2 receptor, IGF-1, and TGF-beta2 mRNA expression as well as the number of anti-GLP-2 antibody-positive cells. Fluorouracil 13-27 insulin-like growth factor 1 Rattus norvegicus 81-86 31582661-7 2019 In contrast, 5-fluorouracil significantly inhibited proglucagon, GLP-2 receptor, IGF-1, and TGF-beta2 mRNA expression as well as the number of anti-GLP-2 antibody-positive cells. Fluorouracil 13-27 transforming growth factor, beta 2 Rattus norvegicus 92-101 30685990-0 2019 Induction of miR-31 causes increased sensitivity to 5-FU and decreased migration and cell invasion in gastric adenocarcinoma. Fluorouracil 52-56 microRNA 31 Homo sapiens 13-19 30685990-5 2019 MKN-45-miR-31 showed an increased sensitivity to 5-FU, decreased migration and cell invasion compared to the control groups (p = 0.0001, p = 0.01 and p = 0.01, respectively). Fluorouracil 49-53 microRNA 31 Homo sapiens 7-13 31372308-13 2019 Gene expression of casp-3, casp-4, and casp-10 were significantly inhibited in the DCLK1+ cells after 5-Fu treatment compared to the WT cells (p=7.616e-08, 1.575e-05 and 5.307e-08, respectively). Fluorouracil 102-106 caspase 10 Homo sapiens 39-46 30643421-9 2019 Results: DDX27 is upregulated in CRC tissues and downregulation of DDX27 inhibits proliferation of colorectal cancer cell and promotes sensitivity to 5-fluorouracil. Fluorouracil 150-164 DEAD-box helicase 27 Homo sapiens 67-72 30662808-0 2018 MiR-26b regulates 5-FU-resistance in human colorectal cancer via down-regulation of Pgp. Fluorouracil 18-22 microRNA 26b Homo sapiens 0-7 30662808-4 2018 Meanwhile, we showed that miR-26b improved sensibility of colorectal cancer cells to 5-FU in vitro and enhanced the potency of 5-FU in the inhibition of tumor growth in vivo. Fluorouracil 85-89 microRNA 26b Homo sapiens 26-33 30662808-4 2018 Meanwhile, we showed that miR-26b improved sensibility of colorectal cancer cells to 5-FU in vitro and enhanced the potency of 5-FU in the inhibition of tumor growth in vivo. Fluorouracil 127-131 microRNA 26b Homo sapiens 26-33 30662808-7 2018 Importantly, we found that CpG islands in the miR-26b promoter region were hypermethylated in 5-FU resistant cells. Fluorouracil 94-98 microRNA 26b Homo sapiens 46-53 30155759-10 2018 Furthermore, the enhanced efficacy of 5-FU by simultaneous inhibition of PKM2 was demonstrated in an in vivo HCT116 CRC model. Fluorouracil 38-42 pyruvate kinase M1/2 Homo sapiens 73-77 31949649-0 2018 MiR-106a-5p promotes 5-FU resistance and the metastasis of colorectal cancer by targeting TGFbetaR2. Fluorouracil 21-25 microRNA 106a Homo sapiens 0-8 31949649-4 2018 The aim of this study was to elucidate the molecular mechanisms of 5-FU resistance through miR-106a-5p in CRC. Fluorouracil 67-71 microRNA 106a Homo sapiens 91-99 31949649-11 2018 RESULTS: MiR-106a-5p was up-regulated and TGFbetaR2 was down-regulated in 5-FU resistant CRC tissues and HT-29 cells. Fluorouracil 74-78 microRNA 106a Homo sapiens 9-17 31949649-13 2018 Additionally, cell invasion was promoted by miR-106a-5p overexpression in the HT-29 cells and was inhibited by miR-106a-5p knockdown in the 5-FU resistant HT-29 cells; miR-106a-5p overexpression contributed to migration by increasing vimentin expression and by decreasing E-cadherin expression in the HT-29 cells; miR-106a-5p functioned by directly binding to TGFbetaR2. Fluorouracil 140-144 microRNA 106a Homo sapiens 111-119 31949649-13 2018 Additionally, cell invasion was promoted by miR-106a-5p overexpression in the HT-29 cells and was inhibited by miR-106a-5p knockdown in the 5-FU resistant HT-29 cells; miR-106a-5p overexpression contributed to migration by increasing vimentin expression and by decreasing E-cadherin expression in the HT-29 cells; miR-106a-5p functioned by directly binding to TGFbetaR2. Fluorouracil 140-144 microRNA 106a Homo sapiens 111-119 31949649-13 2018 Additionally, cell invasion was promoted by miR-106a-5p overexpression in the HT-29 cells and was inhibited by miR-106a-5p knockdown in the 5-FU resistant HT-29 cells; miR-106a-5p overexpression contributed to migration by increasing vimentin expression and by decreasing E-cadherin expression in the HT-29 cells; miR-106a-5p functioned by directly binding to TGFbetaR2. Fluorouracil 140-144 vimentin Homo sapiens 234-242 30485509-8 2018 Furthermore, enhanced chemosensitivity mediated by DEC2 can be reversed by STAT5A which confer GC cells resistance to apoptosis induced by 5-Fu. Fluorouracil 139-143 signal transducer and activator of transcription 5A Homo sapiens 75-81 30485509-9 2018 Together, our results suggest that through inhibiting activation of STAT5A, DEC2 enhances 5-Fu-induced apoptosis and suppression of proliferation in GC cells. Fluorouracil 90-94 signal transducer and activator of transcription 5A Homo sapiens 68-74 30451820-0 2018 Long non-coding RNA H19 confers 5-Fu resistance in colorectal cancer by promoting SIRT1-mediated autophagy. Fluorouracil 32-36 H19 imprinted maternally expressed transcript Homo sapiens 20-23 30451820-3 2018 Here, we observed lncRNA H19 was associated with the 5-Fu resistance in CRC. Fluorouracil 53-57 H19 imprinted maternally expressed transcript Homo sapiens 25-28 30451820-6 2018 Our functional studies demonstrated that H19 promoted colorectal cells 5-Fu resistance. Fluorouracil 71-75 H19 imprinted maternally expressed transcript Homo sapiens 41-44 30451820-11 2018 Our finding provides a novel mechanistic role of H19 in CRC chemoresistance, suggesting that H19 may function as a marker for prediction of chemotherapeutic response to 5-Fu. Fluorouracil 169-173 H19 imprinted maternally expressed transcript Homo sapiens 93-96 30269739-9 2018 Overexpression of miR-301b promoted cell proliferation in TNBC cells, while inhibited the apoptosis induced by 5-FU. Fluorouracil 111-115 microRNA 301b Homo sapiens 18-26 30333885-7 2018 Oteracil, a UMPS inhibitor, decreased the cytotoxicity of 5-FU in MDA468 cells, but not in MDA468/FU cells. Fluorouracil 58-62 uridine monophosphate synthetase Homo sapiens 12-16 30304835-0 2018 Cytoplasmic p21 Mediates 5-Fluorouracil Resistance by Inhibiting Pro-Apoptotic Chk2. Fluorouracil 25-39 H3 histone pseudogene 16 Homo sapiens 12-15 30304835-3 2018 Here, we show for the first time that cytoplasmic p21 mediates 5-Fluorouracil (5FU) resistance by shuttling p-Chk2 out of the nucleus to protect the tumor cells from its pro-apoptotic functions. Fluorouracil 63-77 H3 histone pseudogene 16 Homo sapiens 50-53 30304835-3 2018 Here, we show for the first time that cytoplasmic p21 mediates 5-Fluorouracil (5FU) resistance by shuttling p-Chk2 out of the nucleus to protect the tumor cells from its pro-apoptotic functions. Fluorouracil 79-82 H3 histone pseudogene 16 Homo sapiens 50-53 29852230-6 2018 In 5-FU-resistant cells, expression of miR-195-5p, P-gp and ABCG2 was decreased. Fluorouracil 3-7 phosphoglycolate phosphatase Homo sapiens 51-55 30250581-0 2018 MiR-1260b inhibitor enhances the chemosensitivity of colorectal cancer cells to fluorouracil by targeting PDCD4/IGF1. Fluorouracil 80-92 microRNA 1260b Homo sapiens 0-9 29890207-8 2018 Of particular importance, HDAC1 inhibitor vorinostat restored ASPP2 transcription and produced a synergistic effect with 5-FU in elevating ASPP2, promoting apoptosis and inhibiting EMT in both in vitro and in vivo RCC models. Fluorouracil 121-125 IL2 inducible T cell kinase Homo sapiens 181-184 29959920-8 2018 Cell cycle analysis indicate that ribavirin enhances the anti-proliferative effect of 5-FU by additionally arresting cells at G2/M phase via increasing cyclin B1, p-histone H3(Ser10) and Mad2 levels. Fluorouracil 86-90 cyclin B1 Homo sapiens 152-161 29959920-8 2018 Cell cycle analysis indicate that ribavirin enhances the anti-proliferative effect of 5-FU by additionally arresting cells at G2/M phase via increasing cyclin B1, p-histone H3(Ser10) and Mad2 levels. Fluorouracil 86-90 mitotic arrest deficient 2 like 1 Homo sapiens 187-191 30195757-9 2018 Meanwhile, analysis based on the miRNA-drug relationships demonstrated that drugs 5-fluorouracil, ascorbate, and trastuzumab targeting miR-1246 could serve as potential supplements for the standard therapy. Fluorouracil 82-96 microRNA 1246 Homo sapiens 135-143 29683214-12 2018 Decreased PIEZO1 enhanced the sensitivity of Cisplatin or 5-FU treatment. Fluorouracil 58-62 piezo type mechanosensitive ion channel component 1 Homo sapiens 10-16 30214237-0 2018 Eukaryotic translation initiation factor 3 subunit G (EIF3G) resensitized HCT116/5-Fu to 5-fluorouracil (5-Fu) via inhibition of MRP and MDR1. Fluorouracil 105-109 MARCKS like 1 Homo sapiens 129-132 30096914-9 2018 Treatment with 5-FU caused significant reductions in Notch1, sex determining region Y-box 2 (SOX2), nestin, doublecortin (DCX), and nuclear factor erythroid 2-related factor 2 (Nrf2) levels within the hippocampus. Fluorouracil 15-19 notch receptor 1 Rattus norvegicus 53-59 30096914-9 2018 Treatment with 5-FU caused significant reductions in Notch1, sex determining region Y-box 2 (SOX2), nestin, doublecortin (DCX), and nuclear factor erythroid 2-related factor 2 (Nrf2) levels within the hippocampus. Fluorouracil 15-19 SRY-box transcription factor 2 Rattus norvegicus 61-91 30096914-9 2018 Treatment with 5-FU caused significant reductions in Notch1, sex determining region Y-box 2 (SOX2), nestin, doublecortin (DCX), and nuclear factor erythroid 2-related factor 2 (Nrf2) levels within the hippocampus. Fluorouracil 15-19 SRY-box transcription factor 2 Rattus norvegicus 93-97 30096914-11 2018 Administration with both AA and 5-FU in prevention and throughout was able to prevent decreases in Notch1 SOX2, nestin, DCX, and Nrf2 caused by 5-FU. Fluorouracil 32-36 notch receptor 1 Rattus norvegicus 99-105 30096914-11 2018 Administration with both AA and 5-FU in prevention and throughout was able to prevent decreases in Notch1 SOX2, nestin, DCX, and Nrf2 caused by 5-FU. Fluorouracil 32-36 SRY-box transcription factor 2 Rattus norvegicus 106-110 29800725-0 2018 MEL-pep, an analog of melittin, disrupts cell membranes and reverses 5-fluorouracil resistance in human hepatocellular carcinoma cells. Fluorouracil 69-83 progestagen associated endometrial protein Homo sapiens 4-7 29800725-2 2018 The purpose of this study was to investigate the anti-cancer effect of MEL-pep, a novel analog of the natural antibacterial peptide melittin (MEL), on human 5-fluorouracil-resistant HCC cells (BEL-7402/5-FU) and to clarify the molecular mechanisms involved in these effects. Fluorouracil 157-171 progestagen associated endometrial protein Homo sapiens 75-78 29800725-3 2018 We found that MEL-pep inhibited the proliferation of BEL-7402/5-FU cells and reversed 5-FU resistance in vitro. Fluorouracil 62-66 progestagen associated endometrial protein Homo sapiens 18-21 29748212-4 2018 In addition, TAS-114 had moderate and reversible inhibitory activity on dihydropyrimidine dehydrogenase (DPD), a catabolizing enzyme of 5-FU. Fluorouracil 136-140 dihydropyrimidine dehydrogenase Mus musculus 72-103 29748212-4 2018 In addition, TAS-114 had moderate and reversible inhibitory activity on dihydropyrimidine dehydrogenase (DPD), a catabolizing enzyme of 5-FU. Fluorouracil 136-140 dihydropyrimidine dehydrogenase Mus musculus 105-108 30011263-0 2018 miR-106a Reduces 5-Fluorouracil (5-FU) Sensitivity of Colorectal Cancer by Targeting Dual-Specificity Phosphatases 2 (DUSP2). Fluorouracil 17-31 microRNA 106a Homo sapiens 0-8 30011263-0 2018 miR-106a Reduces 5-Fluorouracil (5-FU) Sensitivity of Colorectal Cancer by Targeting Dual-Specificity Phosphatases 2 (DUSP2). Fluorouracil 33-37 microRNA 106a Homo sapiens 0-8 30011263-10 2018 RESULTS miR-106a level was associated with 5-FU sensitivity in CRC cells. Fluorouracil 43-47 microRNA 106a Homo sapiens 8-16 30011263-11 2018 Overexpression of miR-106a reduced 5-FU sensitivity of HCT116 and SW620 cells, and antagonist of miR-106a sensitized HCT116 and SW620 towards 5-FU. Fluorouracil 35-39 microRNA 106a Homo sapiens 18-26 30011263-11 2018 Overexpression of miR-106a reduced 5-FU sensitivity of HCT116 and SW620 cells, and antagonist of miR-106a sensitized HCT116 and SW620 towards 5-FU. Fluorouracil 142-146 microRNA 106a Homo sapiens 97-105 30011263-15 2018 Silencing of DUSP2 reversed elevated 5-FU sensitivity induced by miR-106a antagonist in HCT116 cells. Fluorouracil 37-41 microRNA 106a Homo sapiens 65-73 30011263-17 2018 CONCLUSIONS miR-106a plays an important role in mediating response to 5-FU-based chemotherapy in CRC and could serve as a potential target for CRC patients. Fluorouracil 70-74 microRNA 106a Homo sapiens 12-20 29604392-6 2018 Furthermore, in vivo experiments demonstrated that IGF2-neutralizing antibody enhanced the sensitivity of tumor xenografts in nude mice to 5-fluorouracil treatment. Fluorouracil 139-153 insulin-like growth factor 2 Mus musculus 51-55 29977534-0 2018 Thymidylate synthase expression in primary colorectal cancer as a predictive marker for the response to 5-fluorouracil- and oxaliplatin-based preoperative chemotherapy for liver metastases. Fluorouracil 104-118 thymidylate synthetase Homo sapiens 0-20 29963136-4 2018 The present study describes the effect of gene knockdown of the aquaglyceroporin AQP3 on MDA-MB-231 breast cancer cell proliferation, migration, invasion, adherence and response to the chemotherapeutic agent 5-fluorouracil. Fluorouracil 208-222 aquaporin 3 (Gill blood group) Homo sapiens 81-85 29963136-5 2018 shRNA mediated AQP3 gene knockdown induced a 28% reduction in cellular proliferation (P<0.01), a 39% decrease in migration (P<0.0001), a 24% reduction in invasion (P<0.05) and a 25% increase in cell death at 100 microM 5-FU (P<0.01). Fluorouracil 228-232 aquaporin 3 (Gill blood group) Homo sapiens 15-19 29715584-5 2018 First, we showed that 5-FU-resistant SNUC5 colon cancer cells (SNUC5/FUR cells) undergo EMT by analyzing the expression of EMT markers such as N-cadherin, vimentin and E-cadherin. Fluorouracil 22-26 vimentin Homo sapiens 155-163 29715584-9 2018 Importantly, silencing of TET1 reversed the effects of 5-FU on the cells. Fluorouracil 55-59 tet methylcytosine dioxygenase 1 Homo sapiens 26-30 29922087-0 2018 Influence of TS (rs34743033) and RUNX1 (rs2014300) gene polymorphisms on survival outcomes of fluorouracil-based chemotherapy in Chinese advanced gastric cancer patients. Fluorouracil 94-106 RUNX family transcription factor 1 Homo sapiens 33-38 29855486-3 2018 High levels of GCNT3 are associated with increased sensibility to 5-fluoracil in metastatic cells. Fluorouracil 66-77 glucosaminyl (N-acetyl) transferase 3, mucin type Homo sapiens 15-20 29921390-9 2018 The percentage of cell apoptosis increased, and the Western blot showed that the expression of caspase-3, caspase-8, and c-myc, respectively, in the semi-combination group, the 5-Fluorouracil group, and the combination group increased successively and that the successive increasing of c-myc was the most significant. Fluorouracil 177-191 MYC proto-oncogene, bHLH transcription factor Homo sapiens 121-126 29808164-15 2018 Importantly, overexpression of MEG3 suppressed the growth of xenograft tumor and improved chemotherapy sensitivity of A375 cells to cisplatin and 5-FU treatment. Fluorouracil 146-150 maternally expressed 3 Homo sapiens 31-35 29599307-10 2018 Irinotecan, 5-FU and 50 mg/kg EEG significantly decreased the protein expression of beta-catenin and MMP-7. Fluorouracil 12-16 catenin beta 1 Homo sapiens 84-96 29599307-10 2018 Irinotecan, 5-FU and 50 mg/kg EEG significantly decreased the protein expression of beta-catenin and MMP-7. Fluorouracil 12-16 matrix metallopeptidase 7 Homo sapiens 101-106 29061341-6 2018 There was a significant increase in the expression of the drug-metabolizing cytochrome P450 enzymes CYP1A2 and CYP2A6 in 5-FU-resistant cells. Fluorouracil 121-125 cytochrome P450 family 1 subfamily A member 2 Homo sapiens 100-106 29328475-0 2018 Heat shock protein 27 knockdown using nucleotide-based therapies enhances sensitivity to 5-FU chemotherapy in SW480 human colon cancer cells. Fluorouracil 89-93 heat shock protein family B (small) member 1 Homo sapiens 0-21 29328475-2 2018 In the present study we found that there is a strong correlation between sensitivity to 5-fluorouracil (5-FU) and the expression of Hsp27 in colorectal cancer. Fluorouracil 88-102 heat shock protein family B (small) member 1 Homo sapiens 132-137 29328475-2 2018 In the present study we found that there is a strong correlation between sensitivity to 5-fluorouracil (5-FU) and the expression of Hsp27 in colorectal cancer. Fluorouracil 104-108 heat shock protein family B (small) member 1 Homo sapiens 132-137 29328475-5 2018 In the present study, we examined the impact of Hsp27 downregulation (via apatorsen) on 5-FU sensitivity in colon cancer both in vitro and in vivo. Fluorouracil 88-92 heat shock protein family B (small) member 1 Homo sapiens 48-53 29328475-9 2018 Although further research is warranted, the present study confirmed that concurrent treatment with Hsp27 knockdown using apatorsen and 5-FU could be a promising therapy for colon cancer. Fluorouracil 135-139 heat shock protein family B (small) member 1 Homo sapiens 99-104 29016350-9 2018 METase supplementation promoted the inhibition effect of 5-Fu on thymidylate synthetase (TS), as well as cell apoptosis. Fluorouracil 57-61 thymidylate synthetase Homo sapiens 65-87 29463243-13 2018 Interestingly, 5-Fluorouracil and Gemcitabine also induced an increase in Chmp1A protein level, suggesting that Chmp1A might mediate the cytotoxic action of chemotherapeutics. Fluorouracil 15-29 charged multivesicular body protein 1A Homo sapiens 74-80 29463243-13 2018 Interestingly, 5-Fluorouracil and Gemcitabine also induced an increase in Chmp1A protein level, suggesting that Chmp1A might mediate the cytotoxic action of chemotherapeutics. Fluorouracil 15-29 charged multivesicular body protein 1A Homo sapiens 112-118 29439714-8 2018 Furthermore, upregulating TFAP2C enhances spheroids formation ability, the fraction of SP cells, expression of stem cell factors and the mitochondrial potential, and reduces the apoptosis induced by 5-fluorouracil in colorectal cancer cells in vitro, and promotes stemness and chemoresistance of CRC cells in vivo; while silencing TFAP2C yields an opposite effect. Fluorouracil 199-213 transcription factor AP-2 gamma Homo sapiens 26-32 29439714-9 2018 Importantly, downregulation of TFAP2C dramatically restores chemotherapeutic sensitivity of CRC cells to 5-FU in vivo. Fluorouracil 105-109 transcription factor AP-2 gamma Homo sapiens 31-37 29439714-10 2018 Our results further demonstrate that TFAP2C promotes stemness and chemoresistance of CRC cells to 5-FU by inhibiting Hippo signaling via transcriptionally upregulating ROCK1 and ROCK2 in CRC cells. Fluorouracil 98-102 transcription factor AP-2 gamma Homo sapiens 37-43 29568368-0 2018 Trifluridine/tipiracil overcomes the resistance of human gastric 5-fluorouracil-refractory cells with high thymidylate synthase expression. Fluorouracil 65-79 thymidylate synthetase Homo sapiens 107-127 29293402-7 2018 Furthermore, LINP1 was upregulated in doxorubicin- and 5-fluorouracil-resistant cells and induced chemoresistance. Fluorouracil 55-69 lncRNA in non-homologous end joining pathway 1 Homo sapiens 13-18 29345285-6 2018 Although morphologic and proliferative changes were unaffected, METTL3-depleted cells showed higher sensitivity to anticancer reagents such as gemcitabine, 5-fluorouracil, cisplatin and irradiation. Fluorouracil 156-170 methyltransferase 3, N6-adenosine-methyltransferase complex catalytic subunit Homo sapiens 64-70 29556329-4 2018 Caffeine, a known ligand for T2R10, rendered the tumor cells more susceptible to two standard chemotherapeutics, Gemcitabine and 5-Fluoruracil. Fluorouracil 129-142 taste 2 receptor member 10 Homo sapiens 29-34 29117941-1 2018 Thymidylate synthase (TS) inhibitors including fluoropyrimidines [e.g., 5-Fluorouracil (5-FU) and 5-Fluorodeoxyuridine (5-FdU, floxuridine)] and antifolates (e.g., pemetrexed) are widely used against solid tumors. Fluorouracil 72-86 thymidylate synthetase Homo sapiens 0-20 29086459-4 2018 Following 5-fluorouracil (5-FU), EGF accelerated hematopoietic stem cell regeneration and prolonged survival compared with saline-treated mice. Fluorouracil 10-24 epidermal growth factor Mus musculus 33-36 29086459-4 2018 Following 5-fluorouracil (5-FU), EGF accelerated hematopoietic stem cell regeneration and prolonged survival compared with saline-treated mice. Fluorouracil 26-30 epidermal growth factor Mus musculus 33-36 29086459-9 2018 EGF increased G-CSF receptor (G-CSFR) expression following 5-FU. Fluorouracil 59-63 epidermal growth factor Mus musculus 0-3 29086459-9 2018 EGF increased G-CSF receptor (G-CSFR) expression following 5-FU. Fluorouracil 59-63 colony stimulating factor 3 Homo sapiens 14-19 29086459-9 2018 EGF increased G-CSF receptor (G-CSFR) expression following 5-FU. Fluorouracil 59-63 colony stimulating factor 3 receptor Homo sapiens 30-36 29054700-8 2018 This is in contrast to 5-FU-induced suppression of Akt and mTOR activation, Bcl-2 and Bcl-xL expressions, and the enhanced expression of Bax and Bim. Fluorouracil 23-27 BCL2 like 11 Homo sapiens 145-148 29364834-2 2018 Therefore, we examined the effects of flavones against CYR61-overexpressing human gastric adenocarcinoma AGS (AGS-cyr61) cells, which show remarkable resistance to 5-fluorouracil (5-FU), adriamycin (ADR), tamoxifen (TAM), paclitaxel (PAC), and docetaxel (DOC). Fluorouracil 164-178 cellular communication network factor 1 Homo sapiens 55-60 29364834-2 2018 Therefore, we examined the effects of flavones against CYR61-overexpressing human gastric adenocarcinoma AGS (AGS-cyr61) cells, which show remarkable resistance to 5-fluorouracil (5-FU), adriamycin (ADR), tamoxifen (TAM), paclitaxel (PAC), and docetaxel (DOC). Fluorouracil 180-184 cellular communication network factor 1 Homo sapiens 55-60 29364834-5 2018 Moreover, AGS-cyr61 cells treated with quercetin concentrations close to the IC50 and simultaneously treated with 5-FU or ADR in the sub-lethal range showed strong synergism between quercetin and these two drugs. Fluorouracil 114-118 cellular communication network factor 1 Homo sapiens 14-19 29344407-2 2018 Whether induction docetaxel, platinum and fluorouracil (TPF) modifies PD-L1 expression or tumour immune infiltrates is unknown. Fluorouracil 42-54 CD274 molecule Homo sapiens 70-75 29066414-9 2018 Our results demonstrate that Z-505 ameliorates cisplatin- and 5-FU-induced anorexia through the activation of the ghrelin receptor, GHSR1a, suggesting its usefulness in the preventive treatment of anorexia during chemotherapy. Fluorouracil 62-66 growth hormone secretagogue receptor Mus musculus 132-138 29189182-5 2018 CONCLUSION: The newly synthesized compounds showed good activity against PC-3 and MCF-7 cell lines in comparison with 5-fluorouracil. Fluorouracil 118-132 chromobox 8 Homo sapiens 73-77 29183726-7 2018 The release of LDH and the percentage of PI and APC Annexin-V double positive cells after 5-FU treatment were elevated compared to control group. Fluorouracil 90-94 annexin A5 Homo sapiens 52-61 29794421-13 2018 Notably, cobimetinib appeared to enhance the efficacy of 5-fluorouracil (5-FU) by decreasing TYMS expression, high expression of which is responsible for 5-FU resistance in colorectal cancer. Fluorouracil 57-71 thymidylate synthetase Homo sapiens 93-97 29794421-13 2018 Notably, cobimetinib appeared to enhance the efficacy of 5-fluorouracil (5-FU) by decreasing TYMS expression, high expression of which is responsible for 5-FU resistance in colorectal cancer. Fluorouracil 73-77 thymidylate synthetase Homo sapiens 93-97 29794421-13 2018 Notably, cobimetinib appeared to enhance the efficacy of 5-fluorouracil (5-FU) by decreasing TYMS expression, high expression of which is responsible for 5-FU resistance in colorectal cancer. Fluorouracil 154-158 thymidylate synthetase Homo sapiens 93-97 29940566-12 2018 It is noteworthy that 5-FU treatments induced miR-204 expression and suppressed TGF-beta pathway. Fluorouracil 22-26 microRNA 204 Homo sapiens 46-53 29940566-13 2018 By establishment of 5-FU resistant GC cell line, it was revealed that miR-204 was significantly downregulated in 5-FU resistant GC cells, representing mesenchymal features with downregulation of epithelial marker, while mesenchymal markers were upregulated. Fluorouracil 20-24 microRNA 204 Homo sapiens 70-77 29940566-13 2018 By establishment of 5-FU resistant GC cell line, it was revealed that miR-204 was significantly downregulated in 5-FU resistant GC cells, representing mesenchymal features with downregulation of epithelial marker, while mesenchymal markers were upregulated. Fluorouracil 113-117 microRNA 204 Homo sapiens 70-77 29940566-15 2018 In addition, overexpression of miR-204 sensitized GC cells to 5-FU in vitro. Fluorouracil 62-66 microRNA 204 Homo sapiens 31-38 29940566-17 2018 Eventually, we illustrated the restoration of TGFBR2 in miR-204 overexpression GC cells, which recovered resistance to 5-FU treatments compared with miR-204 overexpression GC cells. Fluorouracil 119-123 microRNA 204 Homo sapiens 56-63 29115590-3 2018 Thus, the aim of the present study was to elucidate the influence of LMNB1 upregulation on colon cancer cell line after treatment with 5-FU. Fluorouracil 135-139 lamin B1 Homo sapiens 69-74 28051340-8 2018 The expression level of mRNAs for hepatic CYP2C6 and CYP2C11 was significantly lower than in the control group when the rats were pretreated with 5-FU. Fluorouracil 146-150 cytochrome P450, subfamily 2, polypeptide 11 Rattus norvegicus 53-60 29435169-10 2018 Combined treatment of colon cancer cells with miR-340 and 5-FU enhanced the inhibitory effects of 5-FU. Fluorouracil 98-102 microRNA 340 Homo sapiens 46-53 29258566-0 2017 5-FU resistant EMT-like pancreatic cancer cells are hypersensitive to photochemical internalization of the novel endoglin-targeting immunotoxin CD105-saporin. Fluorouracil 0-4 endoglin Homo sapiens 113-121 29311921-5 2017 Co-administration of clinical doses of PPIs protected kidney function in patients receiving cisplatin and fluorouracil, presumably by decreasing accumulation of cisplatin in the kidney via OCT2 inhibition. Fluorouracil 106-118 solute carrier family 22 member 2 Homo sapiens 189-193 28849584-2 2017 This study aimed to investigate quantitatively the effect of 5-FU-induced intestinal damage on the expression of intestinal transporters: P-glycoprotein (P-gp), breast cancer resistance protein (BCRP) and peptide transporter 1 (PEPT1) in rats. Fluorouracil 61-65 solute carrier family 15 member 1 Rattus norvegicus 205-226 28849584-2 2017 This study aimed to investigate quantitatively the effect of 5-FU-induced intestinal damage on the expression of intestinal transporters: P-glycoprotein (P-gp), breast cancer resistance protein (BCRP) and peptide transporter 1 (PEPT1) in rats. Fluorouracil 61-65 solute carrier family 15 member 1 Rattus norvegicus 228-233 28849584-7 2017 Pept1 expression was increased by 5-FU in almost all segments. Fluorouracil 34-38 solute carrier family 15 member 1 Rattus norvegicus 0-5 28720546-8 2017 LncRNA NEAT1 induced EMT and 5-FU resistance through the miR-211/HMGA2 axis. Fluorouracil 29-33 high mobility group AT-hook 2 Homo sapiens 65-70 29184703-8 2017 Rats administered 5-FU significantly increased jejunal and ileal MPO levels (1048%; P < 0.001 and 409%; P < 0.001), compared to healthy controls. Fluorouracil 18-22 myeloperoxidase Rattus norvegicus 65-68 29048661-7 2017 The single agent treatment and combinations of 5-FU and Blu9931 arrest cell cycle (P<0.05), increased p27kip1 expression and reduced cyclin D1 expression. Fluorouracil 47-51 cyclin dependent kinase inhibitor 1B Homo sapiens 105-112 29048661-8 2017 The single agent treatment and combinations of 5-FU and Blu9931 inhibited EMT. Fluorouracil 47-51 IL2 inducible T cell kinase Homo sapiens 74-77 29137332-0 2017 Long noncoding RNA XIST is a prognostic factor in colorectal cancer and inhibits 5-fluorouracil-induced cell cytotoxicity through promoting thymidylate synthase expression. Fluorouracil 81-95 X inactive specific transcript Homo sapiens 19-23 29137332-0 2017 Long noncoding RNA XIST is a prognostic factor in colorectal cancer and inhibits 5-fluorouracil-induced cell cytotoxicity through promoting thymidylate synthase expression. Fluorouracil 81-95 thymidylate synthetase Homo sapiens 140-160 29137332-5 2017 In addition, increased serum XIST level was associated with poor response and lower survival rate in CRC patients receiving 5FU-based treatment. Fluorouracil 124-127 X inactive specific transcript Homo sapiens 29-33 27838412-4 2017 However, expression of intratumor thymidylate synthase (TS), a significant gene in cellular proliferation, is associated with poor outcome to 5-FU-based chemotherapeutic regimens. Fluorouracil 142-146 thymidylate synthetase Homo sapiens 34-54 28759561-0 2017 Regenerating Family Member 4 (Reg4) Enhances 5-Fluorouracil Resistance of Gastric Cancer Through Activating MAPK/Erk/Bim Signaling Pathway. Fluorouracil 45-59 regenerating family member 4 Homo sapiens 30-34 28759561-0 2017 Regenerating Family Member 4 (Reg4) Enhances 5-Fluorouracil Resistance of Gastric Cancer Through Activating MAPK/Erk/Bim Signaling Pathway. Fluorouracil 45-59 BCL2 like 11 Homo sapiens 117-120 28759561-2 2017 The enhanced expression of Reg4 is associated with the resistance of GC to 5-fluorouracil (5-FU), while the underlying mechanism is not clear. Fluorouracil 75-89 regenerating family member 4 Homo sapiens 27-31 28759561-2 2017 The enhanced expression of Reg4 is associated with the resistance of GC to 5-fluorouracil (5-FU), while the underlying mechanism is not clear. Fluorouracil 91-95 regenerating family member 4 Homo sapiens 27-31 28759561-11 2017 Over-expression of flag-Reg4 in SGC-7901 led to an increase in cell viability and lower apoptosis with 5-FU treatment. Fluorouracil 103-107 regenerating family member 4 Homo sapiens 24-28 28759561-12 2017 In contrast, siRNA knockdown of Reg4 enhanced 5-FU induced apoptosis. Fluorouracil 46-50 regenerating family member 4 Homo sapiens 32-36 28759561-15 2017 CONCLUSIONS Reg4 inhibited apoptosis through regulating MAPK/Erk/Bim signaling pathway and thereby enhanced the resistance of GC to 5-FU. Fluorouracil 132-136 regenerating family member 4 Homo sapiens 12-16 28591704-7 2017 Our results further demonstrate that miR-196b-5p promotes stemness and chemoresistance of CRC cells to 5-fluorouracil via targeting negative regulators SOCS1 and SOCS3 of STAT3 signaling pathway, giving rise to activation of STAT3 signaling. Fluorouracil 103-117 suppressor of cytokine signaling 1 Homo sapiens 152-157 29100320-6 2017 In addition, siPAUF CFPAC-1 decreased the mRNA expression of multidrug resistant protein 5 (MRP5) and ribonucleotide reductase M2 (RRM2) and were more vulnerable to gemcitabine and 5-FU than negative control (p<0.05). Fluorouracil 181-185 ribonucleotide reductase regulatory subunit M2 Homo sapiens 131-135 28696828-6 2017 And our results reveal that chemotherapeutics, Cisplatin (CDDP) and 5-Fluoracil (5-FU), result in the greater decrease of protein level of Bcl-2 and Mcl-1 in NPC cells than those in NPE cells. Fluorouracil 68-79 MCL1 apoptosis regulator, BCL2 family member Homo sapiens 149-154 28696828-6 2017 And our results reveal that chemotherapeutics, Cisplatin (CDDP) and 5-Fluoracil (5-FU), result in the greater decrease of protein level of Bcl-2 and Mcl-1 in NPC cells than those in NPE cells. Fluorouracil 81-85 MCL1 apoptosis regulator, BCL2 family member Homo sapiens 149-154 28515355-8 2017 Among these genes, we showed that 5-FU increases the mRNA translation of HIVEP2, which encodes a transcription factor whose translation in normal condition is known to be inhibited by mir-155. Fluorouracil 34-38 HIVEP zinc finger 2 Homo sapiens 73-79 28515355-9 2017 In response to 5-FU, the expression of mir-155 decreases thus stimulating the translation of HIVEP2 mRNA. Fluorouracil 15-19 HIVEP zinc finger 2 Homo sapiens 93-99 28693221-1 2017 The present study investigated the effects of two major dietary fatty acid components, linoleic acid (LA) and elaidic acid (EA), on the antitumor effects of 5-fluorouracil (5-FU) in the LL2, CT26 and CMT93 mouse cancer cell lines. Fluorouracil 157-171 peroxiredoxin 2, pseudogene 1 Mus musculus 186-189 28693221-1 2017 The present study investigated the effects of two major dietary fatty acid components, linoleic acid (LA) and elaidic acid (EA), on the antitumor effects of 5-fluorouracil (5-FU) in the LL2, CT26 and CMT93 mouse cancer cell lines. Fluorouracil 173-177 peroxiredoxin 2, pseudogene 1 Mus musculus 186-189 29296753-5 2017 Importantly, the miR-26a aptamer effectively repressed tumor growth in vivo and synergized with 5-FU or carboplatin in cancer therapy in the mouse breast cancer models. Fluorouracil 96-100 microRNA 26a-1 Mus musculus 17-24 28637493-0 2017 The role of NLRP3 inflammasome in 5-fluorouracil resistance of oral squamous cell carcinoma. Fluorouracil 34-48 NLR family, pyrin domain containing 3 Mus musculus 12-17 28637493-3 2017 In this study, we explored the role of NLRP3 inflammasome in 5-FU resistance of oral squamous cell carcinoma (OSCC). Fluorouracil 61-65 NLR family, pyrin domain containing 3 Mus musculus 39-44 28637493-6 2017 The correlation between 5-FU treatment and the expression and activation of NLRP3 inflammasome was further examined by evaluating NLRP3 and IL-1beta expression in OSCC cell lines without or with NLRP3 knocked down. Fluorouracil 24-28 NLR family, pyrin domain containing 3 Mus musculus 76-81 28637493-6 2017 The correlation between 5-FU treatment and the expression and activation of NLRP3 inflammasome was further examined by evaluating NLRP3 and IL-1beta expression in OSCC cell lines without or with NLRP3 knocked down. Fluorouracil 24-28 NLR family, pyrin domain containing 3 Mus musculus 130-135 28637493-6 2017 The correlation between 5-FU treatment and the expression and activation of NLRP3 inflammasome was further examined by evaluating NLRP3 and IL-1beta expression in OSCC cell lines without or with NLRP3 knocked down. Fluorouracil 24-28 NLR family, pyrin domain containing 3 Mus musculus 130-135 28637493-13 2017 Moreover, 5-FU treatment increased expression and activation of NLRP3 inflammasome in OSCC cells in a cell culture system and xenograft mouse model. Fluorouracil 10-14 NLR family, pyrin domain containing 3 Mus musculus 64-69 28637493-14 2017 Silencing of NLRP3 expression significantly inhibited OSCC cell proliferation and enhanced 5-FU-induced apoptosis of OSCC cells. Fluorouracil 91-95 NLR family, pyrin domain containing 3 Mus musculus 13-18 28637493-15 2017 Further investigation showed that intracellular ROS induced by 5-FU promoted the expression and activation of NLRP3 inflammasome and increased the production of interleukin (IL)-1beta, which then mediated the chemoresistance. Fluorouracil 63-67 NLR family, pyrin domain containing 3 Mus musculus 110-115 28637493-18 2017 CONCLUSIONS: Our findings suggest that NLRP3 inflammasome promoted 5-FU resistance of OSCC both in vitro and in vivo, and targeting the ROS/NLRP3 inflammasome/IL-1beta signaling pathway may help 5-FU-based adjuvant chemotherapy of OSCC. Fluorouracil 67-71 NLR family, pyrin domain containing 3 Mus musculus 39-44 28637493-18 2017 CONCLUSIONS: Our findings suggest that NLRP3 inflammasome promoted 5-FU resistance of OSCC both in vitro and in vivo, and targeting the ROS/NLRP3 inflammasome/IL-1beta signaling pathway may help 5-FU-based adjuvant chemotherapy of OSCC. Fluorouracil 195-199 NLR family, pyrin domain containing 3 Mus musculus 39-44 28637493-18 2017 CONCLUSIONS: Our findings suggest that NLRP3 inflammasome promoted 5-FU resistance of OSCC both in vitro and in vivo, and targeting the ROS/NLRP3 inflammasome/IL-1beta signaling pathway may help 5-FU-based adjuvant chemotherapy of OSCC. Fluorouracil 195-199 NLR family, pyrin domain containing 3 Mus musculus 140-145 28404976-8 2017 Furthermore, we identified that ERbeta exerted an inhibitory effect on CRC tumor proliferation in vitro and in vivo, combined with 5-FU, through up-regulation of MLH1 expression. Fluorouracil 131-135 mutL homolog 1 Homo sapiens 162-166 28433634-6 2017 Additional Western blot analyses have shown that possible mechanisms underlying enhanced sensitivity to 5-FU induced by dual Sphk 1/2 inhibition could include abrogation of FAK-regulated IGF-1R activity and down-regulation of osteopontin expression culminating in the inhibition of NF-kappaB activity and its downstream signalling mediated by sirtuin 1 and p38 MAPK. Fluorouracil 104-108 sphingosine kinase 1 Homo sapiens 125-131 28433634-6 2017 Additional Western blot analyses have shown that possible mechanisms underlying enhanced sensitivity to 5-FU induced by dual Sphk 1/2 inhibition could include abrogation of FAK-regulated IGF-1R activity and down-regulation of osteopontin expression culminating in the inhibition of NF-kappaB activity and its downstream signalling mediated by sirtuin 1 and p38 MAPK. Fluorouracil 104-108 secreted phosphoprotein 1 Homo sapiens 226-237 28433634-7 2017 Our results clearly show that pharmacological blockade of both Sphk isoforms represents a promising strategy to boost the anti-tumour efficacy of 5-FU and provide a rationale for further in vivo studies into the possible use of SKI-II inhibitor as an adjunct to 5-FU treatment in HCC. Fluorouracil 146-150 sphingosine kinase 1 Homo sapiens 63-67 28433634-7 2017 Our results clearly show that pharmacological blockade of both Sphk isoforms represents a promising strategy to boost the anti-tumour efficacy of 5-FU and provide a rationale for further in vivo studies into the possible use of SKI-II inhibitor as an adjunct to 5-FU treatment in HCC. Fluorouracil 262-266 sphingosine kinase 1 Homo sapiens 63-67 28670496-6 2017 For example, resistance to 5-fluorouracil is mediated by alterations in miR-21, miR-27a/b, and miR-155; the sensitivity to Docetaxel is influenced by miR-98, miR-192, miR-194, miR-200b, miR-212, and miR-424; and the resistance to Cisplatin is mediated by miR-let-7, miR-15, miR-16 miR-21 and miR-214. Fluorouracil 27-41 microRNA 21 Homo sapiens 72-78 28588704-0 2017 Ell3 stimulates 5-FU resistance in a breast cancer cell line. Fluorouracil 16-20 elongation factor for RNA polymerase II 3 Homo sapiens 0-4 28588704-2 2017 Recent studies by our group have demonstrated that ectopic expression of Ell3 in breast cancer cell lines enhances cell proliferation, potentiates cancer stem cell properties, and promotes 5-Fluorouracil (5-FU) resistance. Fluorouracil 189-203 elongation factor for RNA polymerase II 3 Homo sapiens 73-77 28588704-2 2017 Recent studies by our group have demonstrated that ectopic expression of Ell3 in breast cancer cell lines enhances cell proliferation, potentiates cancer stem cell properties, and promotes 5-Fluorouracil (5-FU) resistance. Fluorouracil 205-209 elongation factor for RNA polymerase II 3 Homo sapiens 73-77 28588704-3 2017 In the present study, the underlying mechanism for the induction of 5-FU resistance was investigated in Ell3 over-expressing MCF-7 cells (Ell3 OE cells). Fluorouracil 68-72 elongation factor for RNA polymerase II 3 Homo sapiens 104-108 28588704-3 2017 In the present study, the underlying mechanism for the induction of 5-FU resistance was investigated in Ell3 over-expressing MCF-7 cells (Ell3 OE cells). Fluorouracil 68-72 elongation factor for RNA polymerase II 3 Homo sapiens 138-142 28588704-4 2017 By comparing the gene expression profiles of Ell3 OE cells with control cells, the present data revealed that Lipocalin2 (LCN2) and Wnt signaling activity are associated with 5-FU resistance of Ell3 OE. Fluorouracil 175-179 elongation factor for RNA polymerase II 3 Homo sapiens 45-49 28588704-4 2017 By comparing the gene expression profiles of Ell3 OE cells with control cells, the present data revealed that Lipocalin2 (LCN2) and Wnt signaling activity are associated with 5-FU resistance of Ell3 OE. Fluorouracil 175-179 elongation factor for RNA polymerase II 3 Homo sapiens 194-198 28588704-5 2017 siRNA-mediated suppression of LCN2 reversed 5-FU resistance in Ell3 OE cells. Fluorouracil 44-48 elongation factor for RNA polymerase II 3 Homo sapiens 63-67 28588704-6 2017 Chemical inhibition of Wnt signaling also reversed 5-FU resistance in Ell3 OE cells. Fluorouracil 51-55 elongation factor for RNA polymerase II 3 Homo sapiens 70-74 28588704-7 2017 Furthermore, the expression levels of survivin, which is a direct transcriptional target of Wnt/beta-catenin and an inhibitor of apoptosis, were markedly elevated when Ell3 OE cells were treated with 5-FU, as detected by western blot analysis. Fluorouracil 200-204 catenin beta 1 Homo sapiens 96-108 28588704-8 2017 These findings suggest that enhanced expression of LCN2 and activation of the Wnt signaling pathway may induce 5-FU resistance in Ell3 OE cells as a means of evading apoptosis. Fluorouracil 111-115 elongation factor for RNA polymerase II 3 Homo sapiens 130-134 28599477-0 2017 Novel proapoptotic agent SM-1 enhances the inhibitory effect of 5-fluorouracil on colorectal cancer cells in vitro and in vivo. Fluorouracil 64-78 SM1 Homo sapiens 25-29 28599477-7 2017 SM-1 significantly decreased the half-maximal inhibitory concentration of 5-FU from 8.07+-0.49 to 2.55+-0.41 micromol/l in HCT116 cells, and from 7.90+-0.98 to 3.14+-0.81 micromol/l in LoVo cells. Fluorouracil 74-78 SM1 Homo sapiens 0-4 28599477-13 2017 SM-1 significantly enhanced the antitumor activity of 5-FU in colorectal cancer. Fluorouracil 54-58 SM1 Homo sapiens 0-4 27911869-0 2017 Paclitaxel/oxaliplatin/fluorouracil (TOF) regimen versus S-1/oxaliplatin (SOX) regimen for metastatic gastric cancer patients. Fluorouracil 23-35 FEZ family zinc finger 2 Homo sapiens 37-40 28417458-6 2017 Interestingly, we observe that resistin-exposed cells survive 5-fluorouracil treatment because of a decrease in drug uptake due to the arrest of cells in G1 phase. Fluorouracil 62-76 resistin Homo sapiens 31-39 28243729-8 2017 In addition, overexpression of Rab5a induced resistance to 5-FU and gemcitabine while its knockdown reduced resistance to 5-FU and gemcitabine. Fluorouracil 59-63 RAB5A, member RAS oncogene family Homo sapiens 31-36 28243729-8 2017 In addition, overexpression of Rab5a induced resistance to 5-FU and gemcitabine while its knockdown reduced resistance to 5-FU and gemcitabine. Fluorouracil 122-126 RAB5A, member RAS oncogene family Homo sapiens 31-36 28402255-7 2017 We found that 5-fluorouracil-based chemotherapy regimens significantly increased plasma levels of leptin and adiponectin and decreased plasma levels of resistin and visfatin in PR and SD patients, whereas the plasma levels of these molecules were not affected in PD patients. Fluorouracil 14-28 leptin Homo sapiens 98-104 28402255-7 2017 We found that 5-fluorouracil-based chemotherapy regimens significantly increased plasma levels of leptin and adiponectin and decreased plasma levels of resistin and visfatin in PR and SD patients, whereas the plasma levels of these molecules were not affected in PD patients. Fluorouracil 14-28 resistin Homo sapiens 152-160 28373425-11 2017 CONCLUSION: ME-143 alone and in combination with 5FU and oxaliplatin effectively inhibits the WNT/beta-catenin pathway in colorectal cancer cells of diverse genetic background. Fluorouracil 49-52 catenin beta 1 Homo sapiens 98-110 28314989-0 2017 Inhibition of GOT1 sensitizes colorectal cancer cells to 5-fluorouracil. Fluorouracil 57-71 glutamic-oxaloacetic transaminase 1 Homo sapiens 14-18 28314989-2 2017 In our study, the role of GOT1 in the anticancer efficacy of 5-fluorouracil (5-FU) was examined. Fluorouracil 61-75 glutamic-oxaloacetic transaminase 1 Homo sapiens 26-30 28314989-2 2017 In our study, the role of GOT1 in the anticancer efficacy of 5-fluorouracil (5-FU) was examined. Fluorouracil 77-81 glutamic-oxaloacetic transaminase 1 Homo sapiens 26-30 28314989-5 2017 A CRC subcutaneous tumor model was performed to determine the impact of GOT1 inhibition on 5-FU efficacy in vivo. Fluorouracil 91-95 glutamic-oxaloacetic transaminase 1 Homo sapiens 72-76 28314989-8 2017 The GOT1-mediated metabolic process is able to maintain the NADP+/NADPH ratio, which counteracts 5-FU-induced oxidative stress. Fluorouracil 97-101 glutamic-oxaloacetic transaminase 1 Homo sapiens 4-8 28314989-9 2017 Inhibition of GOT1 impaired the defense against 5-FU-induced ROS, thereby sensitizing cells to 5-FU. Fluorouracil 48-52 glutamic-oxaloacetic transaminase 1 Homo sapiens 14-18 28314989-9 2017 Inhibition of GOT1 impaired the defense against 5-FU-induced ROS, thereby sensitizing cells to 5-FU. Fluorouracil 95-99 glutamic-oxaloacetic transaminase 1 Homo sapiens 14-18 28314989-10 2017 The importance of GOT1 in supporting tumor growth during 5-FU treatment was also indicated in an in vivo tumor model of CRC. Fluorouracil 57-61 glutamic-oxaloacetic transaminase 1 Homo sapiens 18-22 28182993-7 2017 RESULTS: 5-FU or epirubicin treatment resulted in the generation of CD90+ and CD105+ cells in vitro in HuH1 and HuH7 cells, which originally contain no CD90+ or CD105+ cells. Fluorouracil 9-13 Thy-1 cell surface antigen Homo sapiens 68-72 28314255-11 2017 Expression of VEGF-D and VEGFR-3 in the 5-FU-treated group was not significantly increased (p>0.05). Fluorouracil 40-44 FMS-like tyrosine kinase 4 Mus musculus 25-32 28011190-5 2017 This cytotoxic theranostic agent, containing four carboxyl-modified 5-FU molecules, has several desirable advantages: i) the ability to self-assemble into nanoparticles; ii) enhanced cytotoxicity with high drug loading capacity (16%) and a specific receptor-targeted interaction with NK1R through the SP moiety; and iii) a high NIR squaraine fluorescence efficiency due to the specific dendron isolation, avoiding aggregation-mediated quenching. Fluorouracil 68-72 tachykinin receptor 1 Homo sapiens 284-288 27838786-0 2017 53BP1 loss induces chemoresistance of colorectal cancer cells to 5-fluorouracil by inhibiting the ATM-CHK2-P53 pathway. Fluorouracil 65-79 tumor protein p53 binding protein 1 Homo sapiens 0-5 27838786-0 2017 53BP1 loss induces chemoresistance of colorectal cancer cells to 5-fluorouracil by inhibiting the ATM-CHK2-P53 pathway. Fluorouracil 65-79 ATM serine/threonine kinase Homo sapiens 98-101 27838786-3 2017 This study aimed to examine the association of 53BP1 expression with chemosensitivity of colorectal cancer cells to 5-FU. Fluorouracil 116-120 tumor protein p53 binding protein 1 Homo sapiens 47-52 27838786-11 2017 In addition, 53BP1 silencing increased proliferation, inhibited apoptosis and induced S phase arrest in HCT116 and HT29 cells after 5-FU treatment. Fluorouracil 132-136 tumor protein p53 binding protein 1 Homo sapiens 13-18 27838786-14 2017 CONCLUSIONS: These findings confirmed that 53BP1 loss might be a negative factor for chemotherapy efficacy, promoting cell proliferation and inhibiting apoptosis by suppressing ATM-CHK2-P53 signaling, and finally inducing 5-FU resistance. Fluorouracil 222-226 tumor protein p53 binding protein 1 Homo sapiens 43-48 27865009-7 2017 Melatonin in combination with 5-FU markedly suppressed the phosphorylation of PI3K, AKT, IKKalpha, IkappaBalpha, and p65 proteins, promoted the translocation of NF-kappaB p50/p65 from the nuclei to cytoplasm, abrogated their binding to the iNOS promoter, and thereby enhanced the inhibition of iNOS signaling. Fluorouracil 30-34 conserved helix-loop-helix ubiquitous kinase Mus musculus 89-97 27865009-7 2017 Melatonin in combination with 5-FU markedly suppressed the phosphorylation of PI3K, AKT, IKKalpha, IkappaBalpha, and p65 proteins, promoted the translocation of NF-kappaB p50/p65 from the nuclei to cytoplasm, abrogated their binding to the iNOS promoter, and thereby enhanced the inhibition of iNOS signaling. Fluorouracil 30-34 v-rel reticuloendotheliosis viral oncogene homolog A (avian) Mus musculus 117-120 27865009-7 2017 Melatonin in combination with 5-FU markedly suppressed the phosphorylation of PI3K, AKT, IKKalpha, IkappaBalpha, and p65 proteins, promoted the translocation of NF-kappaB p50/p65 from the nuclei to cytoplasm, abrogated their binding to the iNOS promoter, and thereby enhanced the inhibition of iNOS signaling. Fluorouracil 30-34 v-rel reticuloendotheliosis viral oncogene homolog A (avian) Mus musculus 175-178 28184917-0 2017 [Corrigendum] Loss of Runt-related transcription factor 3 induces resistance to 5-fluorouracil and cisplatin in hepatocellular carcinoma. Fluorouracil 80-94 RUNX family transcription factor 3 Homo sapiens 22-57 28184917-7 2017 RUNX3 expression enhanced 5-FU sensitivity in both cell lines; the cell viability with 5-FU (100 nM) decreased from 66.3+-4.6 to 34.3+-5.0%, and from 71.0+-4.7% to 27.0+-5.5% in the Hep3B and Huh7 cells, respectively (Fig. Fluorouracil 26-30 RUNX family transcription factor 3 Homo sapiens 0-5 28184917-7 2017 RUNX3 expression enhanced 5-FU sensitivity in both cell lines; the cell viability with 5-FU (100 nM) decreased from 66.3+-4.6 to 34.3+-5.0%, and from 71.0+-4.7% to 27.0+-5.5% in the Hep3B and Huh7 cells, respectively (Fig. Fluorouracil 87-91 RUNX family transcription factor 3 Homo sapiens 0-5 28055957-5 2017 The latter is known to generate reactive oxygen species, and consequently, expression of the antioxidant enzyme heme oxygenase 1 (HMOX1) was significantly upregulated in 5-FU-treated cells, indicative for oxidative stress. Fluorouracil 170-174 heme oxygenase 1 Homo sapiens 112-128 28055957-5 2017 The latter is known to generate reactive oxygen species, and consequently, expression of the antioxidant enzyme heme oxygenase 1 (HMOX1) was significantly upregulated in 5-FU-treated cells, indicative for oxidative stress. Fluorouracil 170-174 heme oxygenase 1 Homo sapiens 130-135 28055957-7 2017 Also in vivo, 5-FU significantly induced hepatic ACOX1 and HMOX1 expression as well as JNK-activation, pro-inflammatory gene expression and immune cell infiltration. Fluorouracil 14-18 heme oxygenase 1 Homo sapiens 59-64 28143584-0 2017 Translationally controlled tumour protein TCTP is induced early in human colorectal tumours and contributes to the resistance of HCT116 colon cancer cells to 5-FU and oxaliplatin. Fluorouracil 158-162 tumor protein, translationally-controlled 1 Homo sapiens 42-46 28143584-3 2017 Here we study the early increase of TCTP levels in human colorectal cancer (CRC) and the regulation of TCTP expression in HCT116 colon cancer cells, in response to treatment with the anti-cancer drugs 5-FU and oxaliplatin. Fluorouracil 201-205 tumor protein, translationally-controlled 1 Homo sapiens 36-40 28143584-3 2017 Here we study the early increase of TCTP levels in human colorectal cancer (CRC) and the regulation of TCTP expression in HCT116 colon cancer cells, in response to treatment with the anti-cancer drugs 5-FU and oxaliplatin. Fluorouracil 201-205 tumor protein, translationally-controlled 1 Homo sapiens 103-107 28143584-5 2017 We also studied the regulation of TCTP in HCT116 colon cancer cells in response to 5-FU and oxaliplatin by western blotting. Fluorouracil 83-87 tumor protein, translationally-controlled 1 Homo sapiens 34-38 28143584-8 2017 Employing the Real-Time Cell Analysis (RTCA) System and the MTS assay, we investigated the effect of TCTP-knockdown on the sensitivity of HCT116 cells to the anti-cancer drugs 5-FU and oxaliplatin. Fluorouracil 176-180 tumor protein, translationally-controlled 1 Homo sapiens 101-105 28143584-12 2017 TCTP protein levels are about 4-fold upregulated in HCT116 colon cancer cells, in response to 5-FU and oxaliplatin treatment, whereas TCTP mRNA levels are down regulated. Fluorouracil 94-98 tumor protein, translationally-controlled 1 Homo sapiens 0-4 28143584-16 2017 Using two cellular assay systems, we demonstrated that TCTP-knockdown sensitises HCT116 cells to the cytotoxicity caused by 5-FU and oxaliplatin. Fluorouracil 124-128 tumor protein, translationally-controlled 1 Homo sapiens 55-59 27864056-6 2017 5-FU loaded lactoferrin nanoparticles (5-FU-LfNPs) were prepared by sol-oil method with a narrow size distribution of 150+-20nm 5-FU-LfNPs exhibits high encapsulation efficiency (64+-2.3%) and increased storage stability at 4 C. Competitive ligand binding and lysosomal colocalization studies suggested a receptor mediated uptake for LfNPs internalization in B16F10 cells. Fluorouracil 0-4 lactotransferrin Mus musculus 12-23 27864056-6 2017 5-FU loaded lactoferrin nanoparticles (5-FU-LfNPs) were prepared by sol-oil method with a narrow size distribution of 150+-20nm 5-FU-LfNPs exhibits high encapsulation efficiency (64+-2.3%) and increased storage stability at 4 C. Competitive ligand binding and lysosomal colocalization studies suggested a receptor mediated uptake for LfNPs internalization in B16F10 cells. Fluorouracil 39-43 lactotransferrin Mus musculus 12-23 27864056-6 2017 5-FU loaded lactoferrin nanoparticles (5-FU-LfNPs) were prepared by sol-oil method with a narrow size distribution of 150+-20nm 5-FU-LfNPs exhibits high encapsulation efficiency (64+-2.3%) and increased storage stability at 4 C. Competitive ligand binding and lysosomal colocalization studies suggested a receptor mediated uptake for LfNPs internalization in B16F10 cells. Fluorouracil 39-43 lactotransferrin Mus musculus 12-23 28000878-4 2017 The upregulation of the Ca2+-permeable transient receptor potential channel 5 (TrpC5) activates the Wnt/beta-catenin signaling pathway in 5-fluorouracil (5-Fu)-resistant human colorectal cancer (CRC) HCT-8 (HCT-8/5-Fu) cells. Fluorouracil 138-152 catenin beta 1 Homo sapiens 104-116 28000878-4 2017 The upregulation of the Ca2+-permeable transient receptor potential channel 5 (TrpC5) activates the Wnt/beta-catenin signaling pathway in 5-fluorouracil (5-Fu)-resistant human colorectal cancer (CRC) HCT-8 (HCT-8/5-Fu) cells. Fluorouracil 154-158 catenin beta 1 Homo sapiens 104-116 28052098-0 2017 IDH1 R132H Mutation Enhances Cell Migration by Activating AKT-mTOR Signaling Pathway, but Sensitizes Cells to 5-FU Treatment as NADPH and GSH Are Reduced. Fluorouracil 110-114 isocitrate dehydrogenase (NADP(+)) 1 Homo sapiens 0-4 28052098-9 2017 The reduced antioxidants (NADPH and GSH) sensitized U87MG cells with IDH R132H mutant to 5-FU treatment. Fluorouracil 89-93 isocitrate dehydrogenase (NADP(+)) 1 Homo sapiens 69-72 28011495-8 2017 Granulocyte colony-stimulating factor (G-CSF) in serum was elevated at 5.6 pg/ml, which further raised to 43 pg/ml one week after FOLFIRINOX chemotherapy (oxaliplatin, irinotecan, 5-fluorouracil), while WBC decreased from 103.3 G/l to 59.3 G/l. Fluorouracil 180-194 colony stimulating factor 3 Homo sapiens 0-37 28011495-8 2017 Granulocyte colony-stimulating factor (G-CSF) in serum was elevated at 5.6 pg/ml, which further raised to 43 pg/ml one week after FOLFIRINOX chemotherapy (oxaliplatin, irinotecan, 5-fluorouracil), while WBC decreased from 103.3 G/l to 59.3 G/l. Fluorouracil 180-194 colony stimulating factor 3 Homo sapiens 39-44 28090501-5 2017 RESULTS: The result of MTT assay after APEX1 knockdown showed that strong coexpression of APEX1 and Jagged1 cell line (SNU-245, SNU-1079, and SNU-1196) showed a greater decrease in IC50 of chemotherapeutic agent (5-fluorouracil, gemcitabine and cisplatin). Fluorouracil 213-227 jagged canonical Notch ligand 1 Homo sapiens 100-107 29199237-14 2017 Under such experimental condition, CXCL1 gene, protein levels of neutrophil elastase and myeloperoxidase upregulation induced by 5-FU in the colon was attenuated by HST. Fluorouracil 129-133 elastase, neutrophil expressed Mus musculus 65-84 28948165-0 2017 Expression and Role of Oct3/4 in Injury-Repair Process of Rat Alveolar Epithelium after 5-Fu Treatment. Fluorouracil 88-92 solute carrier family 22 member 8 Rattus norvegicus 23-29 28948165-1 2017 OBJECTIVE: We aimed to investigate how the embryonic stem cell-related gene Oct3/4 changes during the injury-repair process of distal pulmonary epithelium induced by 5-fluorouracil (5-Fu). Fluorouracil 166-180 solute carrier family 22 member 8 Rattus norvegicus 76-82 28948165-1 2017 OBJECTIVE: We aimed to investigate how the embryonic stem cell-related gene Oct3/4 changes during the injury-repair process of distal pulmonary epithelium induced by 5-fluorouracil (5-Fu). Fluorouracil 182-186 solute carrier family 22 member 8 Rattus norvegicus 76-82 28948165-5 2017 However, after treatment with 5-Fu, Oct3/4(+) cells appeared at 12 h, reached the peak at 24 h, then decreased at 48 h, and eventually disappeared at 72 h. Oct3/4 was localized in the nucleus. Fluorouracil 30-34 solute carrier family 22 member 8 Rattus norvegicus 36-42 28948165-5 2017 However, after treatment with 5-Fu, Oct3/4(+) cells appeared at 12 h, reached the peak at 24 h, then decreased at 48 h, and eventually disappeared at 72 h. Oct3/4 was localized in the nucleus. Fluorouracil 30-34 solute carrier family 22 member 8 Rattus norvegicus 156-162 28948165-7 2017 CONCLUSIONS: Our results revealed that, in rat alveolar epithelium, expression of Oct3/4 could be induced after treatment with 5-Fu, then decreased gradually, and was silenced following the alveolar epithelial differentiation. Fluorouracil 127-131 solute carrier family 22 member 8 Rattus norvegicus 82-88 27891816-10 2017 DLL4 knockdown also blocked the Notch-1 pathway, weakening invasion ability and resistance to 5-FU chemotherapy. Fluorouracil 94-98 delta like canonical Notch ligand 4 Homo sapiens 0-4 27878272-0 2017 miR-20b reduces 5-FU resistance by suppressing the ADAM9/EGFR signaling pathway in colon cancer. Fluorouracil 16-20 ADAM metallopeptidase domain 9 Homo sapiens 51-56 27878272-11 2017 In addition, we demonstrated that ADAM9 is a direct target of miR-20b and that miR-20b decreased the 5-FU resistance of HCT116-R cells. Fluorouracil 101-105 ADAM metallopeptidase domain 9 Homo sapiens 34-39 27878272-12 2017 Our findings suggest that miR-20b reduces 5-FU resistance to induce apoptosis in vitro by suppressing ADAM9/EGFR in CC cells. Fluorouracil 42-46 ADAM metallopeptidase domain 9 Homo sapiens 102-107 27821793-1 2017 PURPOSE: Tumor levels of thymidylate synthase (TS), a target of 5-fluorouracil (5-FU)-based chemotherapy for colorectal cancer, have been studied as a predictive or prognostic biomarker with mixed results. Fluorouracil 64-78 thymidylate synthetase Homo sapiens 25-45 27821793-1 2017 PURPOSE: Tumor levels of thymidylate synthase (TS), a target of 5-fluorouracil (5-FU)-based chemotherapy for colorectal cancer, have been studied as a predictive or prognostic biomarker with mixed results. Fluorouracil 64-78 thymidylate synthetase Homo sapiens 47-49 27821793-1 2017 PURPOSE: Tumor levels of thymidylate synthase (TS), a target of 5-fluorouracil (5-FU)-based chemotherapy for colorectal cancer, have been studied as a predictive or prognostic biomarker with mixed results. Fluorouracil 80-84 thymidylate synthetase Homo sapiens 25-45 27821793-1 2017 PURPOSE: Tumor levels of thymidylate synthase (TS), a target of 5-fluorouracil (5-FU)-based chemotherapy for colorectal cancer, have been studied as a predictive or prognostic biomarker with mixed results. Fluorouracil 80-84 thymidylate synthetase Homo sapiens 47-49 28027897-0 2017 Relevance of dihydropyrimidine-dehydrogenase and thymidylate-synthase in patients with pancreatic neuroendocrine neoplasms treated with 5-FU-based chemotherapy. Fluorouracil 136-140 thymidylate synthetase Homo sapiens 49-69 29324220-2 2017 The main mechanisms of 5-FU action are thymidylate synthase (TS) inhibition which can be abrogated by thymidine and strengthened by calciumfolinate (CF) and incorporation of fluorouridinetriphosphate into RNA which can be abrogated by uridine. Fluorouracil 23-27 thymidylate synthetase Homo sapiens 39-59 27929535-7 2016 Dual inhibition with BPTES and thymidylate synthase inhibitor, 5-fluorouracil (5-FU), elicits cell death synergistically through cell cycle arrest in NSCLC. Fluorouracil 63-77 thymidylate synthetase Homo sapiens 31-51 27929535-7 2016 Dual inhibition with BPTES and thymidylate synthase inhibitor, 5-fluorouracil (5-FU), elicits cell death synergistically through cell cycle arrest in NSCLC. Fluorouracil 79-83 thymidylate synthetase Homo sapiens 31-51 27793037-0 2016 c-Myc is regulated by HIF-2alpha in chronic hypoxia and influences sensitivity to 5-FU in colon cancer. Fluorouracil 82-86 MYC proto-oncogene, bHLH transcription factor Homo sapiens 0-5 27793037-0 2016 c-Myc is regulated by HIF-2alpha in chronic hypoxia and influences sensitivity to 5-FU in colon cancer. Fluorouracil 82-86 endothelial PAS domain protein 1 Homo sapiens 22-32 27793037-9 2016 Overexpression of c-Myc reversed the inhibition of cyclinD1, CDK4, and CDK6, which accelerated the G1/S phase transition under hypoxia and enhanced sensitivity to 5-FU. Fluorouracil 163-167 MYC proto-oncogene, bHLH transcription factor Homo sapiens 18-23 27793037-11 2016 In summary, HIF-2alpha plays an important role in regulating the expression of c-Myc in chronic hypoxia, and consequently controls the sensitivity of colon cancer cells to 5-FU treatment in this environment. Fluorouracil 172-176 endothelial PAS domain protein 1 Homo sapiens 12-22 27793037-11 2016 In summary, HIF-2alpha plays an important role in regulating the expression of c-Myc in chronic hypoxia, and consequently controls the sensitivity of colon cancer cells to 5-FU treatment in this environment. Fluorouracil 172-176 MYC proto-oncogene, bHLH transcription factor Homo sapiens 79-84 27835895-0 2016 Enhancement of 5-FU sensitivity by the proapoptotic rpL3 gene in p53 null colon cancer cells through combined polymer nanoparticles. Fluorouracil 15-19 ribosomal protein L3 Homo sapiens 52-56 27835895-2 2016 Recently, we have demonstrated that nucleolar stress upon 5-FU treatment leads to the activation of ribosome-free rpL3 (L3) as proapoptotic factor. Fluorouracil 58-62 ribosomal protein L3 Homo sapiens 114-118 27586268-8 2016 Further studies demonstrated that the combined administration of 5-FU and beta-carotene significantly down-regulated the protein levels of Cav-1, p-AKT, p-NF-kappaB, p-mTOR and p-p70S6K in Eca109 cells more effectively than did 5-FU alone. Fluorouracil 65-69 ribosomal protein S6 kinase B1 Homo sapiens 179-185 27500968-6 2016 In addition, the clinical chemotherapeutic drug 5-fluorouracil was used to investigate the impact of GGCT silencing on drug sensitivity by an Annexin V/7-AAD double-staining assay. Fluorouracil 48-62 annexin A5 Homo sapiens 142-151 27501171-9 2016 Knockdown of miR-221 in 5-FU resistant cells resulted in reduced cell proliferation, increased apoptosis, restored chemosensitivity, and led to inactivation of the Wnt/beta-catenin pathway mediated by alteration in DKK2 expression. Fluorouracil 24-28 microRNA 221 Homo sapiens 13-20 27501171-9 2016 Knockdown of miR-221 in 5-FU resistant cells resulted in reduced cell proliferation, increased apoptosis, restored chemosensitivity, and led to inactivation of the Wnt/beta-catenin pathway mediated by alteration in DKK2 expression. Fluorouracil 24-28 catenin beta 1 Homo sapiens 168-180 27578004-0 2016 Histone H3K27 Trimethylation Modulates 5-Fluorouracil Resistance by Inhibiting PU.1 Binding to the DPYD Promoter. Fluorouracil 39-53 Spi-1 proto-oncogene Homo sapiens 79-83 27578004-4 2016 Here, we report that H3K27 trimethylation (H3K27me3) at the DPYD promoter regulated by Ezh2 and UTX suppresses DPYD expression by inhibiting transcription factor PU.1 binding, leading to increased resistance to 5-FU. Fluorouracil 211-215 Spi-1 proto-oncogene Homo sapiens 162-166 27669502-6 2016 RESULTS: Global RNA expression profiling and subsequent correlation studies of gene expression level and drug response has identified that elevated expression of cyclin A1 (CCNA1) was significantly associated with cellular resistance to paclitaxel, doxorubicin and 5-fluorouracil. Fluorouracil 265-279 cyclin A1 Homo sapiens 162-171 27669502-6 2016 RESULTS: Global RNA expression profiling and subsequent correlation studies of gene expression level and drug response has identified that elevated expression of cyclin A1 (CCNA1) was significantly associated with cellular resistance to paclitaxel, doxorubicin and 5-fluorouracil. Fluorouracil 265-279 cyclin A1 Homo sapiens 173-178 27423551-4 2016 Genetic polymorphisms affect the activity of thymidylate synthase, an enzyme involved in 5-Fluorouracil metabolism, which may account for observed differences in response to neoadjuvant treatment between patients. Fluorouracil 89-103 thymidylate synthetase Homo sapiens 45-65 27423551-12 2016 RESULTS: Patients with at least 1 thymidylate synthase 3G allele were more likely to have a complete or partial pathologic response to 5-Fluorouracil neoadjuvant therapy (odds ratio 10.4; 95% confidence interval, 1.3-81.6; P = .01) than those without at least one 3G allele. Fluorouracil 135-149 thymidylate synthetase Homo sapiens 34-54 27651161-12 2016 Additionally, functional studies indicated that over-expression of RAD51B promoted cell proliferation, aneuploidy, and drug resistance, while RAD51B knockdown led to G1 arrest and sensitized cells to 5-fluorouracil (5-FU). Fluorouracil 200-214 RAD51 paralog B Mus musculus 142-148 27729739-8 2016 Rats administered 5-FU significantly increased intestinal MPO levels (>= 307%; P < 0.001), compared to healthy controls. Fluorouracil 18-22 myeloperoxidase Rattus norvegicus 58-61 27729739-9 2016 However, LDR attenuated this effect in 5-FU treated rats, significantly decreasing ileal MPO activity (by 45%; P < 0.05), as compared to 5-FU controls. Fluorouracil 39-43 myeloperoxidase Rattus norvegicus 89-92 27322756-1 2016 We designed and synthesized a novel mutual prodrug, named BC-01 (3), by integrating ubenimex and Fluorouracil (5-FU) into one molecule based on prior research results that showed that a combination of the aminopeptidase N (CD13) inhibitor, ubenimex, and the cytotoxic antitumor agent, 5-FU, exhibited improved in vitro and in vivo antitumor efficiency. Fluorouracil 111-115 alanyl (membrane) aminopeptidase Mus musculus 205-221 27509880-0 2016 Combination of the histone deacetylase inhibitor depsipeptide and 5-fluorouracil upregulates major histocompatibility complex class II and p21 genes and activates caspase-3/7 in human colon cancer HCT-116 cells. Fluorouracil 66-80 H3 histone pseudogene 16 Homo sapiens 139-142 27509880-7 2016 Furthermore, our global analysis of gene expression, which was focused on genes involved in the molecular regulation of MHC class II genes, showed enhancement of pro-apoptotic PCAF and CIITA after the combination of 5-FU and depsipeptide. Fluorouracil 216-220 class II major histocompatibility complex transactivator Homo sapiens 185-190 27509921-4 2016 Furthermore, knockdown of NEK2 inhibited drug resistance of HCC cells, as shown by the promoted suppression of cell viability in 5-fluorouracil (5-FU)-treated HCC cells. Fluorouracil 129-143 NIMA related kinase 2 Homo sapiens 26-30 27509921-4 2016 Furthermore, knockdown of NEK2 inhibited drug resistance of HCC cells, as shown by the promoted suppression of cell viability in 5-fluorouracil (5-FU)-treated HCC cells. Fluorouracil 145-149 NIMA related kinase 2 Homo sapiens 26-30 27613840-6 2016 After 5-fluorouracil (5-Fu) treatment, the reduction in the proportion of cell apoptosis, CD133 and TERT expression levels in SW620 were lower than that in SW480 cells. Fluorouracil 6-20 telomerase reverse transcriptase Homo sapiens 100-104 27613840-6 2016 After 5-fluorouracil (5-Fu) treatment, the reduction in the proportion of cell apoptosis, CD133 and TERT expression levels in SW620 were lower than that in SW480 cells. Fluorouracil 22-26 telomerase reverse transcriptase Homo sapiens 100-104 27774364-0 2016 Pancytopenia and Severe Gastrointestinal Toxicities Associated with 5-Fluorouracil in a Patient with Thymidylate Synthase (TYMS) Polymorphism. Fluorouracil 68-82 thymidylate synthetase Homo sapiens 101-121 27774364-0 2016 Pancytopenia and Severe Gastrointestinal Toxicities Associated with 5-Fluorouracil in a Patient with Thymidylate Synthase (TYMS) Polymorphism. Fluorouracil 68-82 thymidylate synthetase Homo sapiens 123-127 27774364-10 2016 Our case report further underlines the fact that TYMS polymorphism not only predicts response to 5-FU by relating to intratumoral-TYMS mRNA expression but also the toxicity in these patients receiving fluoropyrimidines. Fluorouracil 97-101 thymidylate synthetase Homo sapiens 49-53 27774364-10 2016 Our case report further underlines the fact that TYMS polymorphism not only predicts response to 5-FU by relating to intratumoral-TYMS mRNA expression but also the toxicity in these patients receiving fluoropyrimidines. Fluorouracil 97-101 thymidylate synthetase Homo sapiens 130-134 27774364-11 2016 In brief, TYMS genotype variations present a dilemma in 5-FU-driven cancer therapy- overexpression leads to decreased drug sensitivity and poor prognosis, while underexpression leads to the manifestation of toxic drug effects that may halt therapy altogether. Fluorouracil 56-60 thymidylate synthetase Homo sapiens 10-14 27506940-4 2016 DR5, which is essential for 5-FU-induced apoptosis, accumulated in lysosomes and autophagosomes upon chloroquine treatment. Fluorouracil 28-32 TNF receptor superfamily member 10b Homo sapiens 0-3 27468921-2 2016 METHODS: Protein content of ABCC10 and ABCC11 was assessed in tumor tissue blocks of 140 colorectal cancer patients and associated with survival of patients with regard to 5-fluorouracil-based therapy. Fluorouracil 172-186 ATP binding cassette subfamily C member 10 Homo sapiens 28-34 27449036-6 2016 The data shows the role of stem cell marker Oct4 in the resistance of primary colorectal cancer tumor cells to 5-fluorouracil. Fluorouracil 111-125 POU class 5 homeobox 1 Homo sapiens 44-48 27385096-0 2016 5-FU targets rpL3 to induce mitochondrial apoptosis via cystathionine-beta-synthase in colon cancer cells lacking p53. Fluorouracil 0-4 ribosomal protein L3 Homo sapiens 13-17 27385096-3 2016 Here, we demonstrate that nucleolar stress induced by 5-fluorouracil (5-FU) in colon cancer cells devoid of p53 leads to the activation of ribosomal protein L3 (rpL3) as proapoptotic factor. Fluorouracil 54-68 ribosomal protein L3 Homo sapiens 139-159 27385096-3 2016 Here, we demonstrate that nucleolar stress induced by 5-fluorouracil (5-FU) in colon cancer cells devoid of p53 leads to the activation of ribosomal protein L3 (rpL3) as proapoptotic factor. Fluorouracil 54-68 ribosomal protein L3 Homo sapiens 161-165 27385096-3 2016 Here, we demonstrate that nucleolar stress induced by 5-fluorouracil (5-FU) in colon cancer cells devoid of p53 leads to the activation of ribosomal protein L3 (rpL3) as proapoptotic factor. Fluorouracil 70-74 ribosomal protein L3 Homo sapiens 139-159 27385096-3 2016 Here, we demonstrate that nucleolar stress induced by 5-fluorouracil (5-FU) in colon cancer cells devoid of p53 leads to the activation of ribosomal protein L3 (rpL3) as proapoptotic factor. Fluorouracil 70-74 ribosomal protein L3 Homo sapiens 161-165 27118047-7 2016 MAIN FINDINGS: CRT with mitomycin C (MMC) and 5-fluorouracil (5-FU) has been proven to have effective results in the treatment of anal SCC. Fluorouracil 46-60 serpin family B member 3 Homo sapiens 135-138 27118047-7 2016 MAIN FINDINGS: CRT with mitomycin C (MMC) and 5-fluorouracil (5-FU) has been proven to have effective results in the treatment of anal SCC. Fluorouracil 62-66 serpin family B member 3 Homo sapiens 135-138 27118047-10 2016 CONCLUSIONS: Primary CRT with MMC and 5-FU is the current standard treatment for anal SCC. Fluorouracil 38-42 serpin family B member 3 Homo sapiens 86-89 26886287-9 2016 LY294002 inhibits the proliferation and invasion of MHCC97H-derived CD90+ LCCs and sensitized CD90+ LCCs-derived tumors to 5-FU in the current study which may provide insight into the association between the LY294002 combined 5-FU and liver cancer stem cell (LCSCs). Fluorouracil 123-127 Thy-1 cell surface antigen Homo sapiens 94-98 27323852-5 2016 The reduction in ROS leads to inactivation of the ASK1-p38 mitogen-activated protein kinase (MAPK) pathway, which reduces 5-FU-induced apoptosis. Fluorouracil 122-126 mitogen-activated protein kinase kinase kinase 5 Homo sapiens 50-54 27323852-7 2016 These observations suggest that NNMT and the 1-MNA it produces inhibit the ASK1-p38 MAPK pathway, resulting in increased CRC cell resistance to 5-FU. Fluorouracil 144-148 mitogen-activated protein kinase kinase kinase 5 Homo sapiens 75-79 27468227-9 2016 Mechanistically, 5-FU and TQ remarkably cooperated to repress the expression of procancerous Wnt, beta-catenin, NF-kappaB, COX-2, iNOS, VEGF, and TBRAS and upregulate the expression of anti-tumorigenesis DKK-1, CDNK-1A, TGF-beta1, TGF-betaRII, Smad4, and GPx. Fluorouracil 17-21 catenin beta 1 Rattus norvegicus 98-110 27468227-9 2016 Mechanistically, 5-FU and TQ remarkably cooperated to repress the expression of procancerous Wnt, beta-catenin, NF-kappaB, COX-2, iNOS, VEGF, and TBRAS and upregulate the expression of anti-tumorigenesis DKK-1, CDNK-1A, TGF-beta1, TGF-betaRII, Smad4, and GPx. Fluorouracil 17-21 vascular endothelial growth factor A Rattus norvegicus 136-140 27468227-9 2016 Mechanistically, 5-FU and TQ remarkably cooperated to repress the expression of procancerous Wnt, beta-catenin, NF-kappaB, COX-2, iNOS, VEGF, and TBRAS and upregulate the expression of anti-tumorigenesis DKK-1, CDNK-1A, TGF-beta1, TGF-betaRII, Smad4, and GPx. Fluorouracil 17-21 SMAD family member 4 Rattus norvegicus 244-249 27236157-0 2016 Thymosin beta10 as a predictive biomarker of response to 5-fluorouracil chemotherapy in cholangiocarcinoma. Fluorouracil 57-71 thymosin beta 10 Homo sapiens 0-15 27236157-9 2016 5-FU treatment at various concentrations induced the expressions of T?10 and ABC transporters (ABCB1, ABCG2 ABCA3) in two CCA cell lines, KKU-M055 and KKU-M214. Fluorouracil 0-4 ATP binding cassette subfamily A member 3 Homo sapiens 108-113 26522725-0 2016 Inhibition of caspases primes colon cancer cells for 5-fluorouracil-induced TNF-alpha-dependent necroptosis driven by RIP1 kinase and NF-kappaB. Fluorouracil 53-67 receptor interacting serine/threonine kinase 1 Homo sapiens 118-122 27259240-1 2016 We recently reported that DNA demethylase ten-eleven translocation 1 (TET1) upregulates nuclear factor erythroid 2-related factor 2 (Nrf2) in 5-fluorouracil-resistant colon cancer cells (SNUC5/5-FUR). Fluorouracil 142-156 tet methylcytosine dioxygenase 1 Homo sapiens 70-74 27163731-5 2016 SNUC5/FUR cells transfected with siRNA against GRP78, ATF6, ERK, or AKT were more sensitive to 5-FU than siControl RNA-transfected cells. Fluorouracil 95-99 activating transcription factor 6 Homo sapiens 54-58 27284361-13 2016 In addition, when the level of Mus81 was low, GEN1 expression was increased under a low concentration of 5-FU. Fluorouracil 105-109 MUS81 structure-specific endonuclease subunit Homo sapiens 31-36 27095441-0 2016 MicroRNA-204 modulates colorectal cancer cell sensitivity in response to 5-fluorouracil-based treatment by targeting high mobility group protein A2. Fluorouracil 73-87 high mobility group AT-hook 2 Homo sapiens 117-147 27095441-3 2016 However, whether miR-204 modulates chemosensitivity to 5-fluorouracil (5-Fu) in colorectal cancer is still unclear. Fluorouracil 55-69 microRNA 204 Homo sapiens 17-24 27095441-3 2016 However, whether miR-204 modulates chemosensitivity to 5-fluorouracil (5-Fu) in colorectal cancer is still unclear. Fluorouracil 71-75 microRNA 204 Homo sapiens 17-24 27095441-7 2016 Moreover, the miR-204/HMGA2 axis modulated the resistance of tumor cells to 5-Fu in HCT-116 and SW480 colon cancer cells via activation of the PI3K/AKT pathway. Fluorouracil 76-80 microRNA 204 Homo sapiens 14-21 27095441-7 2016 Moreover, the miR-204/HMGA2 axis modulated the resistance of tumor cells to 5-Fu in HCT-116 and SW480 colon cancer cells via activation of the PI3K/AKT pathway. Fluorouracil 76-80 high mobility group AT-hook 2 Homo sapiens 22-27 27095441-8 2016 These results demonstrate that the miR-204/HMGA2 axis could play a vital role in the 5-Fu resistance of colon cancer cells. Fluorouracil 85-89 microRNA 204 Homo sapiens 35-42 27095441-8 2016 These results demonstrate that the miR-204/HMGA2 axis could play a vital role in the 5-Fu resistance of colon cancer cells. Fluorouracil 85-89 high mobility group AT-hook 2 Homo sapiens 43-48 27095441-9 2016 Taken together, our present study elucidated that miR-204 upregulated 5-Fu chemosensitivity via the downregulation of HMGA2 in colorectal cancer and provided significant insight into the mechanism of 5-Fu resistance in colorectal cancer patients. Fluorouracil 70-74 microRNA 204 Homo sapiens 50-57 27095441-9 2016 Taken together, our present study elucidated that miR-204 upregulated 5-Fu chemosensitivity via the downregulation of HMGA2 in colorectal cancer and provided significant insight into the mechanism of 5-Fu resistance in colorectal cancer patients. Fluorouracil 70-74 high mobility group AT-hook 2 Homo sapiens 118-123 27095441-9 2016 Taken together, our present study elucidated that miR-204 upregulated 5-Fu chemosensitivity via the downregulation of HMGA2 in colorectal cancer and provided significant insight into the mechanism of 5-Fu resistance in colorectal cancer patients. Fluorouracil 200-204 microRNA 204 Homo sapiens 50-57 27095441-9 2016 Taken together, our present study elucidated that miR-204 upregulated 5-Fu chemosensitivity via the downregulation of HMGA2 in colorectal cancer and provided significant insight into the mechanism of 5-Fu resistance in colorectal cancer patients. Fluorouracil 200-204 high mobility group AT-hook 2 Homo sapiens 118-123 27095441-10 2016 More importantly, our present study suggested that miR-204 has potential as a therapeutic strategy for 5-Fu-resistant colorectal cancer. Fluorouracil 103-107 microRNA 204 Homo sapiens 51-58 27748284-1 2016 BACKGROUND & OBJECTIVES: The two key aspects associated with the microsatellite instability (MSI) as genetic phenomenon in colorectal cancer (CRC) are better survival prognosis, and the varying response to 5-fluorouracil (5-FU)-based chemotherapy. Fluorouracil 210-224 RB binding protein 4, chromatin remodeling factor Homo sapiens 97-100 27748284-1 2016 BACKGROUND & OBJECTIVES: The two key aspects associated with the microsatellite instability (MSI) as genetic phenomenon in colorectal cancer (CRC) are better survival prognosis, and the varying response to 5-fluorouracil (5-FU)-based chemotherapy. Fluorouracil 226-230 RB binding protein 4, chromatin remodeling factor Homo sapiens 97-100 26956045-4 2016 5-Fluorouracil (5FU) was able to stimulate the activation of SMAD3 and the transcription of specific genes such as ACVRL1, FN1 and TGFB1. Fluorouracil 0-14 activin A receptor like type 1 Homo sapiens 115-121 26956045-4 2016 5-Fluorouracil (5FU) was able to stimulate the activation of SMAD3 and the transcription of specific genes such as ACVRL1, FN1 and TGFB1. Fluorouracil 16-19 activin A receptor like type 1 Homo sapiens 115-121 27027355-0 2016 5-Fluorouracil targets thymidylate synthase in the selective suppression of TH17 cell differentiation. Fluorouracil 0-14 thymidylate synthetase Homo sapiens 23-43 27027355-2 2016 We found that low dose 5-FU selectively suppresses TH17 and TH1 cell differentiation without apparent effect on Treg, TH2, and significantly suppresses thymidylate synthase (TS) expression in TH17 and TH1 cells but has a lesser effect in tumor cells and macrophages. Fluorouracil 23-27 thymidylate synthetase Homo sapiens 152-172 27069140-9 2016 The efficacy of MAP3K8 inhibition in our model potentially uncovers a new mechanism to circumvent 5-FU resistance. Fluorouracil 98-102 mitogen-activated protein kinase kinase kinase 8 Homo sapiens 16-22 24336083-12 2013 Indeed, knockdown of PATZ1 in p53-null osteosarcoma cells upregulates BAX expression and decreases survival of 5FU-treated cells, then suggesting an anti-apoptotic role of PATZ1 in p53-null cancer cells. Fluorouracil 111-114 BCL2-associated X protein Mus musculus 70-73 23695873-3 2013 The current study was designed to investigate peripheral alterations due to the 5-FU-induced mucositis of neuronal and non-neuronal 5-HT3 and NK1 receptor expression by immunohistochemical analysis. Fluorouracil 80-84 tachykinin receptor 1 Mus musculus 142-154 23952905-10 2013 The physical and functional interactions between SIRT1 and TDG may mediate DNA repair, gene expression and FU (5-fluorouracil)-mediated cytotoxicity. Fluorouracil 111-125 sirtuin 1 Homo sapiens 49-54 23809767-11 2013 High NR4A2 expression specifically predicted a shorter DSS of colon cancer patients (dichotomisation, HR=2.55, log-rank test P=0.011), especially for those who received postoperative 5-fluorouracil/leucovorin plus oxaliplatin (FOLFOX) chemotherapy (3-score range, HR=1.86, log-rank test P=0.020). Fluorouracil 183-197 nuclear receptor subfamily 4 group A member 2 Homo sapiens 5-10 24649282-2 2013 The aim of this study was to determine whether the expression of thymidylate synthase (TS), thymidine phosphorylase (TP) and dihydropyrimidine dehydrogenase (DPD) predict clinical outcome in BTC patients treated with adjuvant 5-fluorouracil (5-FU)-based chemotherapy. Fluorouracil 226-240 dihydropyrimidine dehydrogenase Homo sapiens 158-161 24649282-2 2013 The aim of this study was to determine whether the expression of thymidylate synthase (TS), thymidine phosphorylase (TP) and dihydropyrimidine dehydrogenase (DPD) predict clinical outcome in BTC patients treated with adjuvant 5-fluorouracil (5-FU)-based chemotherapy. Fluorouracil 242-246 dihydropyrimidine dehydrogenase Homo sapiens 158-161 24104963-1 2013 BACKGROUND: Genomic rearrangements at the fragile site FRA1E may disrupt the dihydropyrimidine dehydrogenase gene (DPYD) which is involved in 5-fluorouracil (5-FU) catabolism. Fluorouracil 142-156 dihydropyrimidine dehydrogenase Homo sapiens 77-108 24104963-1 2013 BACKGROUND: Genomic rearrangements at the fragile site FRA1E may disrupt the dihydropyrimidine dehydrogenase gene (DPYD) which is involved in 5-fluorouracil (5-FU) catabolism. Fluorouracil 142-156 dihydropyrimidine dehydrogenase Homo sapiens 115-119 24104963-1 2013 BACKGROUND: Genomic rearrangements at the fragile site FRA1E may disrupt the dihydropyrimidine dehydrogenase gene (DPYD) which is involved in 5-fluorouracil (5-FU) catabolism. Fluorouracil 158-162 dihydropyrimidine dehydrogenase Homo sapiens 77-108 24104963-1 2013 BACKGROUND: Genomic rearrangements at the fragile site FRA1E may disrupt the dihydropyrimidine dehydrogenase gene (DPYD) which is involved in 5-fluorouracil (5-FU) catabolism. Fluorouracil 158-162 dihydropyrimidine dehydrogenase Homo sapiens 115-119 25505563-6 2013 Based on the evaluation using cDNA-expressed enzymes, CYP2A6 showed the highest activity for 5-FU formation from R-FT with the K m value similar to that of the high-affinity component in microsomes. Fluorouracil 93-97 cytochrome P450 family 2 subfamily A member 6 Homo sapiens 54-60 25505563-8 2013 These results suggest that the enantioselectivity in the bioactivation of FT to 5-FU in humans is mainly due to the large difference of the catalytic activity of CYP2A6 between R- and S-FT. Fluorouracil 80-84 cytochrome P450 family 2 subfamily A member 6 Homo sapiens 162-168 23942539-0 2013 Potential of dihydropyrimidine dehydrogenase genotypes in personalizing 5-fluorouracil therapy among colorectal cancer patients. Fluorouracil 72-86 dihydropyrimidine dehydrogenase Homo sapiens 13-44 23942539-1 2013 BACKGROUND: Dihydropyrimidine dehydrogenase (DPD) is a pyrimidine catabolic enzyme involved in the initial and rate-limiting step of the catabolic pathway of toxic metabolites of 5-fluorouracil (5-FU). Fluorouracil 179-193 dihydropyrimidine dehydrogenase Homo sapiens 12-43 23942539-1 2013 BACKGROUND: Dihydropyrimidine dehydrogenase (DPD) is a pyrimidine catabolic enzyme involved in the initial and rate-limiting step of the catabolic pathway of toxic metabolites of 5-fluorouracil (5-FU). Fluorouracil 179-193 dihydropyrimidine dehydrogenase Homo sapiens 45-48 23942539-1 2013 BACKGROUND: Dihydropyrimidine dehydrogenase (DPD) is a pyrimidine catabolic enzyme involved in the initial and rate-limiting step of the catabolic pathway of toxic metabolites of 5-fluorouracil (5-FU). Fluorouracil 195-199 dihydropyrimidine dehydrogenase Homo sapiens 12-43 23942539-1 2013 BACKGROUND: Dihydropyrimidine dehydrogenase (DPD) is a pyrimidine catabolic enzyme involved in the initial and rate-limiting step of the catabolic pathway of toxic metabolites of 5-fluorouracil (5-FU). Fluorouracil 195-199 dihydropyrimidine dehydrogenase Homo sapiens 45-48 23942539-4 2013 Hence, this study aims to understand the role of DPYD variants in serum level of 5-FU and the risk of developing toxicity to prevent adverse reactions and maximize therapy outcome for personalized medicine. Fluorouracil 81-85 dihydropyrimidine dehydrogenase Homo sapiens 49-53 23942539-8 2013 RESULTS: Patients with DPYD genotypes of deficient enzyme activity had higher median serum levels of 5-FU compared with normal DPD group (median, 11.51 mcg/mL; 95% confidence interval, 10.18-16.11 versus median, 0.83 mcg/mL; 95% confidence interval, 0.55-5.90, Mann-Whitney U test; P = 0.010). Fluorouracil 101-105 dihydropyrimidine dehydrogenase Homo sapiens 23-27 23942539-10 2013 Combined regression analysis showed that the predictive power of DPYD*5 (rs1801159) and 1896 T>C (rs17376848) for serum concentrations of 5-FU in the studied group was 36.6% (P = 0.04). Fluorouracil 141-145 dihydropyrimidine dehydrogenase Homo sapiens 65-69 24040364-6 2013 Furthermore, we demonstrated that 53BP1 regulated the sensitivity to 5-Fu through thymidylate synthase (TS) and dihydropyrimidine dehydrogenase (DPYD). Fluorouracil 69-73 thymidylate synthase Mus musculus 82-102 23197286-1 2013 To investigate the hepatic dihydropyrimidine dehydrogenase (DPD) activity in colorectal cancer (CRC), which is critically important to create a patient-specific dosing regimen, we performed 5-FU pharmacokinetic studies in 1,2-dimethylhydrazine-induced CRC model rats (CRC rats). Fluorouracil 190-194 dihydropyrimidine dehydrogenase Homo sapiens 60-63 23623394-6 2013 Retrovirus VSV-Betv1-GFP was generated to transduce 5-FU-mobilized BALB/c hematopoietic cells to express membrane-bound Bet v 1 (VSV-GFP virus was used as control). Fluorouracil 52-56 delta/notch-like EGF repeat containing Mus musculus 15-18 23420533-7 2013 5-FU treatment resulted in a significant upregulation of NKG2D activating molecules (Rae-1 and H60) and DNAM-1 ligands (CD112 and CD155) on MC38 cells, but alpha-GalCer did not. Fluorouracil 0-4 ribonucleic acid export 1 Mus musculus 85-90 23420533-7 2013 5-FU treatment resulted in a significant upregulation of NKG2D activating molecules (Rae-1 and H60) and DNAM-1 ligands (CD112 and CD155) on MC38 cells, but alpha-GalCer did not. Fluorouracil 0-4 CD226 antigen Mus musculus 104-110 23420533-7 2013 5-FU treatment resulted in a significant upregulation of NKG2D activating molecules (Rae-1 and H60) and DNAM-1 ligands (CD112 and CD155) on MC38 cells, but alpha-GalCer did not. Fluorouracil 0-4 poliovirus receptor Mus musculus 130-135 23585145-1 2013 Dihydropyrimidine dehydrogenase (DPD) is a key enzyme in the metabolic catabolism of 5-fluorouracil (5-FU) and its derivatives (capecitabine and tegafur). Fluorouracil 85-99 dihydropyrimidine dehydrogenase Homo sapiens 0-31 23585145-1 2013 Dihydropyrimidine dehydrogenase (DPD) is a key enzyme in the metabolic catabolism of 5-fluorouracil (5-FU) and its derivatives (capecitabine and tegafur). Fluorouracil 85-99 dihydropyrimidine dehydrogenase Homo sapiens 33-36 23585145-1 2013 Dihydropyrimidine dehydrogenase (DPD) is a key enzyme in the metabolic catabolism of 5-fluorouracil (5-FU) and its derivatives (capecitabine and tegafur). Fluorouracil 101-105 dihydropyrimidine dehydrogenase Homo sapiens 0-31 23585145-1 2013 Dihydropyrimidine dehydrogenase (DPD) is a key enzyme in the metabolic catabolism of 5-fluorouracil (5-FU) and its derivatives (capecitabine and tegafur). Fluorouracil 101-105 dihydropyrimidine dehydrogenase Homo sapiens 33-36 23768762-8 2013 Double-positive cells for CD44 and SSEA-4 exhibited preferential expression of some stemness genes and were more resistant to the anticancer drugs, cisplatin and 5-fluorouracil (5-FU). Fluorouracil 162-176 CD44 molecule (Indian blood group) Homo sapiens 26-30 23768762-8 2013 Double-positive cells for CD44 and SSEA-4 exhibited preferential expression of some stemness genes and were more resistant to the anticancer drugs, cisplatin and 5-fluorouracil (5-FU). Fluorouracil 178-182 CD44 molecule (Indian blood group) Homo sapiens 26-30 23861589-0 2013 Clinical significance of the thymidylate synthase, dihydropyrimidine dehydrogenase, and thymidine phosphorylase mRNA expressions in hepatocellular carcinoma patients receiving 5-fluorouracil-based transarterial chemoembolization treatment. Fluorouracil 176-190 dihydropyrimidine dehydrogenase Homo sapiens 51-82 23861589-1 2013 PURPOSE: To determine whether 5-fluorouracil (5-FU) sensitivity is associated with the mRNA expressions of thymidylate synthase (TS), dihydropyrimidine dehydrogenase (DPD), and thymidine phosphorylase (TP) in patients with hepatocellular carcinoma (HCC) treated with 5-FU-based transarterial chemoembolization (TACE). Fluorouracil 30-44 dihydropyrimidine dehydrogenase Homo sapiens 134-165 23861589-1 2013 PURPOSE: To determine whether 5-fluorouracil (5-FU) sensitivity is associated with the mRNA expressions of thymidylate synthase (TS), dihydropyrimidine dehydrogenase (DPD), and thymidine phosphorylase (TP) in patients with hepatocellular carcinoma (HCC) treated with 5-FU-based transarterial chemoembolization (TACE). Fluorouracil 30-44 dihydropyrimidine dehydrogenase Homo sapiens 167-170 23814490-8 2013 Importantly, this also antagonizes a 5-FU-triggered Pim-1 up-regulation, which is mediated by decreased levels of miR-15b, a microRNA we newly identify to regulate Pim-1. Fluorouracil 37-41 microRNA 15b Homo sapiens 114-121 23786757-4 2013 The aim of this study was to investigate Annexin A1 expression in pre-treatment biopsies from a cohort of OSCC patients treated with surgery and post-operative radiotherapy or docetaxel, cisplatin and 5-fluorouracil (TPF) induction chemotherapy followed by surgery and post-operative radiotherapy. Fluorouracil 201-215 annexin A1 Homo sapiens 41-51 23338779-1 2013 The present study investigated whether a water-soluble extract from the culture medium of Ganoderma lucidum mycelia (Japanese: Reishi or Mannentake) (designated as MAK) exerted a protective effect against induction of aberrant crypt foci (ACF) by azoxymethane (AOM) and small-intestinal damage induced by the anticancer drug 5-FU. Fluorouracil 325-329 male germ cell-associated kinase Rattus norvegicus 164-167 23338779-9 2013 The present results indicate that MAK ameliorates the colon precancerous lesions induced by AOM and the small-intestinal injury caused by 5-FU, suggesting that MAK could have potential as a preventive agent against colonic precancer, which is a common adverse effect of chemotherapy. Fluorouracil 138-142 male germ cell-associated kinase Rattus norvegicus 34-37 23338779-9 2013 The present results indicate that MAK ameliorates the colon precancerous lesions induced by AOM and the small-intestinal injury caused by 5-FU, suggesting that MAK could have potential as a preventive agent against colonic precancer, which is a common adverse effect of chemotherapy. Fluorouracil 138-142 male germ cell-associated kinase Rattus norvegicus 160-163 23781135-0 2013 Evaluation of clinical value of single nucleotide polymorphisms of dihydropyrimidine dehydrogenase gene to predict 5-fluorouracil toxicity in 60 colorectal cancer patients in China. Fluorouracil 115-129 dihydropyrimidine dehydrogenase Homo sapiens 67-98 23781135-2 2013 To evaluate if SNPs of DPD can be used to predict 5-FU toxicity, we evaluated five SNPs of DPD (14G1A, G1156T, G2194A, T85C and T464A) by TaqMan real time PCR in 60 colorectal cancer patients. Fluorouracil 50-54 dihydropyrimidine dehydrogenase Homo sapiens 23-26 23781135-3 2013 Clinical data demonstrated that there was higher correlation between DPD activity and toxic effects of 5-FU (p<0.05). Fluorouracil 103-107 dihydropyrimidine dehydrogenase Homo sapiens 69-72 23175232-11 2013 CONCLUSION: SALL4"s expression is an indicator of stem cells, a prognostic marker in liver cancers, correlates with cell and tumor growth, with resistance to 5-FU, and its suppression results in differentiation and slowed tumor growth. Fluorouracil 158-162 spalt like transcription factor 4 Homo sapiens 12-17 23054116-7 2013 RESULTS: Our clinical results showed that FoxM1 overexpression was significantly associated with resistance in chemotherapy of docetaxel in addition to 5-fluorouracil (5-FU) plus S-1 plus cisplatin (CDDP) and was not significant in chemotherapy of 5-FU plus CDDP for patients with advanced gastric cancer. Fluorouracil 152-166 forkhead box M1 Homo sapiens 42-47 23054116-7 2013 RESULTS: Our clinical results showed that FoxM1 overexpression was significantly associated with resistance in chemotherapy of docetaxel in addition to 5-fluorouracil (5-FU) plus S-1 plus cisplatin (CDDP) and was not significant in chemotherapy of 5-FU plus CDDP for patients with advanced gastric cancer. Fluorouracil 168-172 forkhead box M1 Homo sapiens 42-47 23054116-7 2013 RESULTS: Our clinical results showed that FoxM1 overexpression was significantly associated with resistance in chemotherapy of docetaxel in addition to 5-fluorouracil (5-FU) plus S-1 plus cisplatin (CDDP) and was not significant in chemotherapy of 5-FU plus CDDP for patients with advanced gastric cancer. Fluorouracil 248-252 forkhead box M1 Homo sapiens 42-47 23603345-0 2013 Dihydropyrimidine dehydrogenase gene (DPYD) polymorphism among Caucasian and non-Caucasian patients with 5-FU- and capecitabine-related toxicity using full sequencing of DPYD. Fluorouracil 105-109 dihydropyrimidine dehydrogenase Homo sapiens 0-31 23603345-0 2013 Dihydropyrimidine dehydrogenase gene (DPYD) polymorphism among Caucasian and non-Caucasian patients with 5-FU- and capecitabine-related toxicity using full sequencing of DPYD. Fluorouracil 105-109 dihydropyrimidine dehydrogenase Homo sapiens 38-42 23603345-1 2013 BACKGROUND: Dihydropyrimidine dehydrogenase (DPD) is the rate-limiting enzyme of the degradation of pyrimidine base, and plays a pivotal role in the pharmacogenetic syndrome of 5-fluorouracil (5-FU). Fluorouracil 177-191 dihydropyrimidine dehydrogenase Homo sapiens 12-43 23603345-1 2013 BACKGROUND: Dihydropyrimidine dehydrogenase (DPD) is the rate-limiting enzyme of the degradation of pyrimidine base, and plays a pivotal role in the pharmacogenetic syndrome of 5-fluorouracil (5-FU). Fluorouracil 177-191 dihydropyrimidine dehydrogenase Homo sapiens 45-48 23603345-1 2013 BACKGROUND: Dihydropyrimidine dehydrogenase (DPD) is the rate-limiting enzyme of the degradation of pyrimidine base, and plays a pivotal role in the pharmacogenetic syndrome of 5-fluorouracil (5-FU). Fluorouracil 193-197 dihydropyrimidine dehydrogenase Homo sapiens 12-43 23603345-1 2013 BACKGROUND: Dihydropyrimidine dehydrogenase (DPD) is the rate-limiting enzyme of the degradation of pyrimidine base, and plays a pivotal role in the pharmacogenetic syndrome of 5-fluorouracil (5-FU). Fluorouracil 193-197 dihydropyrimidine dehydrogenase Homo sapiens 45-48 23603345-10 2013 CONCLUSION: Mutated DPYD is frequently observed in Caucasian patients who experience toxicities while receiving 5-FU/capecitabine. Fluorouracil 112-116 dihydropyrimidine dehydrogenase Homo sapiens 20-24 23603345-11 2013 Screening of patients for DPYD mutations prior to administration of 5-FU/capecitabine using new pharmacogenetic testing methods, may help for identify those patients who are at greatest risk for adverse effects, allowing a more individualized approach to their chemotherapy management. Fluorouracil 68-72 dihydropyrimidine dehydrogenase Homo sapiens 26-30 23139054-1 2013 BACKGROUND: This study was initiated to assess the quantitative impact of patient anthropometrics and dihydropyrimidine dehydrogenase (DPYD) mutations on the pharmacokinetics (PK) of 5-fluorouracil (5FU) and to explore limited sampling strategies of 5FU. Fluorouracil 183-197 dihydropyrimidine dehydrogenase Homo sapiens 102-133 23139054-1 2013 BACKGROUND: This study was initiated to assess the quantitative impact of patient anthropometrics and dihydropyrimidine dehydrogenase (DPYD) mutations on the pharmacokinetics (PK) of 5-fluorouracil (5FU) and to explore limited sampling strategies of 5FU. Fluorouracil 183-197 dihydropyrimidine dehydrogenase Homo sapiens 135-139 23139054-1 2013 BACKGROUND: This study was initiated to assess the quantitative impact of patient anthropometrics and dihydropyrimidine dehydrogenase (DPYD) mutations on the pharmacokinetics (PK) of 5-fluorouracil (5FU) and to explore limited sampling strategies of 5FU. Fluorouracil 199-202 dihydropyrimidine dehydrogenase Homo sapiens 102-133 23139054-1 2013 BACKGROUND: This study was initiated to assess the quantitative impact of patient anthropometrics and dihydropyrimidine dehydrogenase (DPYD) mutations on the pharmacokinetics (PK) of 5-fluorouracil (5FU) and to explore limited sampling strategies of 5FU. Fluorouracil 199-202 dihydropyrimidine dehydrogenase Homo sapiens 135-139 23368632-4 2013 Anticancer drugs 5FU, docetaxel, cisplatin, and carboplatin were seen to inhibit growth of the CD44+CD117+ cells by 50% in the 2D culture with IC50 concentration, whereas, in the 3D culture, the four drugs inhibited the cell growth by only 34.4%, 40.8%, 34.8% and 21.9% at 3D one, respectively. Fluorouracil 17-20 CD44 molecule (Indian blood group) Homo sapiens 95-99 25026750-0 2013 [Dihydropirymidine dehydrogenase (DPD)--a toxicity marker for 5-fluorouracil?]. Fluorouracil 62-76 dihydropyrimidine dehydrogenase Homo sapiens 34-37 25026750-10 2013 Detection of reduced DPD activity in patients with planned chemotherapy will allow a lower dosage of 5-FU or alternative treatment without exposing them to adverse reactions. Fluorouracil 101-105 dihydropyrimidine dehydrogenase Homo sapiens 21-24 23457527-10 2013 In conclusion, we identified three genes that chemosensitize the effects of 5-FU and IFN-alpha/5-FU on HCC cells and demonstrated that PRKAG2 mRNA can serve as a prognostic marker for IFN-alpha/5-FU therapy. Fluorouracil 76-80 protein kinase AMP-activated non-catalytic subunit gamma 2 Homo sapiens 135-141 22935545-0 2012 A new DPYD genotyping assay for improving the safety of 5-fluorouracil therapy. Fluorouracil 56-70 dihydropyrimidine dehydrogenase Homo sapiens 6-10 22935545-2 2012 Recently described genetic variation in dihydropyrimidine dehydrogenase (DPYD) has been shown to be a major predictor of 5FU toxicity. Fluorouracil 121-124 dihydropyrimidine dehydrogenase Homo sapiens 73-77 22286760-3 2012 The MTA1 promoter contains two putative p53 response elements (p53REs), which were repressed by the p53-inducing drug 5-fluorouracil (5-FU). Fluorouracil 118-132 metastasis associated 1 Homo sapiens 4-8 22286760-3 2012 The MTA1 promoter contains two putative p53 response elements (p53REs), which were repressed by the p53-inducing drug 5-fluorouracil (5-FU). Fluorouracil 134-138 metastasis associated 1 Homo sapiens 4-8 22286760-4 2012 Notably, 5-FU treatment decreased MTA1 expression only in p53 wild-type cells. Fluorouracil 9-13 metastasis associated 1 Homo sapiens 34-38 22895071-0 2012 Genetic disruption of USP9X sensitizes colorectal cancer cells to 5-fluorouracil. Fluorouracil 66-80 ubiquitin specific peptidase 9 X-linked Homo sapiens 22-27 22895071-4 2012 The resulting USP9X-deficient cancer cells exhibited increased activation of apoptotic pathways and markedly decreased clonogenic survival in response to 5-fluorouracil, a chemotherapeutic drug that is widely used for treatment of gastrointestinal malignancies. Fluorouracil 154-168 ubiquitin specific peptidase 9 X-linked Homo sapiens 14-19 22998775-9 2012 Finally, in contrast to PTGR2-overexpressing cells, PTGR2-knockdown cells were more sensitive to cisplatin and 5-fluorouracil. Fluorouracil 111-125 prostaglandin reductase 2 Homo sapiens 52-57 23064073-5 2012 Dihydropyrimidine dehydrogenase(DPD)is the rate-limiting enzyme in the degradation of 5-FU, and S-1 contains the inhibitor of DPD. Fluorouracil 86-90 dihydropyrimidine dehydrogenase Homo sapiens 32-35 23020798-9 2012 CONCLUSION: Polymorphisms of ERCC1, GSTs, TS and MTHFR were closely associated with clinical outcomes of GC patients treated with platinum/5-Fu-based chemotherapy. Fluorouracil 139-143 methylenetetrahydrofolate reductase Homo sapiens 49-54 22998564-2 2012 High levels of thymidylate synthase (TS), the target enzyme of 5-FU and DPD which degrades the majority of 5-FU, are associated with poor prognosis in some cancers. Fluorouracil 107-111 dihydropyrimidine dehydrogenase Homo sapiens 72-75 22998564-7 2012 Furthermore, the association between their levels and the sensitivity to 5-FU was examined using the small interfering RNA (siRNA) specific for TS and DPD. Fluorouracil 73-77 dihydropyrimidine dehydrogenase Homo sapiens 151-154 22998564-11 2012 In in vitro study using UC cell lines, high levels of TS and DPD were associated with low response to 5-FU and these associations were confirmed with siRNA specific for TS and DPD. Fluorouracil 102-106 dihydropyrimidine dehydrogenase Homo sapiens 54-64 22998564-11 2012 In in vitro study using UC cell lines, high levels of TS and DPD were associated with low response to 5-FU and these associations were confirmed with siRNA specific for TS and DPD. Fluorouracil 102-106 dihydropyrimidine dehydrogenase Homo sapiens 169-179 22825330-0 2012 Increasing the therapeutic index of 5-fluorouracil and 6-thioguanine by targeting loss of MTAP in tumor cells. Fluorouracil 36-50 methylthioadenosine phosphorylase Homo sapiens 90-94 22766915-6 2012 Downregulation of TS and DPD expression and upregulation of OPRT expression were induced by DOC treatment, suggesting that DOC enhanced the efficacy of 5-FU by altering the expression of its metabolic enzymes. Fluorouracil 152-156 dihydropyrimidine dehydrogenase Homo sapiens 25-28 22876791-1 2012 BACKGROUND: TS-1 is an oral anticancer drug containing a 5-fluorouracil derivative (Tegafur) that is widely used in Japan for the treatment of cancer, especially gastrointestinal tumors. Fluorouracil 57-71 Trichinella spiralis resistance 1 Mus musculus 12-16 22716215-9 2012 LC3-II protein increased after treatment with 5-FU, and chloroquine potentiated the cytotoxicity of 5-FU. Fluorouracil 46-50 microtubule associated protein 1 light chain 3 alpha Homo sapiens 0-3 22716215-9 2012 LC3-II protein increased after treatment with 5-FU, and chloroquine potentiated the cytotoxicity of 5-FU. Fluorouracil 100-104 microtubule associated protein 1 light chain 3 alpha Homo sapiens 0-3 22824673-1 2012 5-Fluorouracil (5FU) and similar fluoropyrimidines induce covalent modification of thymidylate synthase (TS) and inhibit its activity. Fluorouracil 0-14 thymidylate synthase Mus musculus 83-103 22824673-1 2012 5-Fluorouracil (5FU) and similar fluoropyrimidines induce covalent modification of thymidylate synthase (TS) and inhibit its activity. Fluorouracil 0-14 thymidylate synthase Mus musculus 105-107 22824673-1 2012 5-Fluorouracil (5FU) and similar fluoropyrimidines induce covalent modification of thymidylate synthase (TS) and inhibit its activity. Fluorouracil 16-19 thymidylate synthase Mus musculus 83-103 22824673-1 2012 5-Fluorouracil (5FU) and similar fluoropyrimidines induce covalent modification of thymidylate synthase (TS) and inhibit its activity. Fluorouracil 16-19 thymidylate synthase Mus musculus 105-107 22824673-6 2012 By immunoblot assay, the FTS antibody specifically recognizes modified TS in a dose-dependent manner in 5FU-treated cells, in cancer xenograft tissues of 5FU-treated mice, and in the murine tissues. Fluorouracil 104-107 thymidylate synthase Mus musculus 26-28 22824673-6 2012 By immunoblot assay, the FTS antibody specifically recognizes modified TS in a dose-dependent manner in 5FU-treated cells, in cancer xenograft tissues of 5FU-treated mice, and in the murine tissues. Fluorouracil 154-157 thymidylate synthase Mus musculus 26-28 22824673-8 2012 Speculatively, a high-throughput assay could be enabled by pairing anti-TS antibodies of two specificities, one recognizing only modified TS and another recognizing both forms, to structurally quantify the TS-inhibiting effect of fluorouracil at a cellular or tissue level without requiring prior protein separation. Fluorouracil 230-242 thymidylate synthase Mus musculus 72-74 22736919-10 2012 XIAP shRNA also inhibited the growth of pancreatic cancer cells in vitro and in vivo, enhanced drug-induced apoptosis and increased chemosensitivity to 5-FU and gemcitabine. Fluorouracil 152-156 X-linked inhibitor of apoptosis Homo sapiens 0-4 21601882-0 2012 CD133(-) cells, derived from a single human colon cancer cell line, are more resistant to 5-fluorouracil (FU) than CD133(+) cells, dependent on the beta1-integrin signaling. Fluorouracil 90-104 integrin subunit beta 1 Homo sapiens 148-162 22270332-1 2012 PURPOSE: Thymidylate synthase (TS) and dihydropyrimidine dehydrogenase (DPD) are important enzymes in the metabolism of 5-fluorouracil, which have been examined as possible predictive markers. Fluorouracil 120-134 dihydropyrimidine dehydrogenase Homo sapiens 39-70 22270332-1 2012 PURPOSE: Thymidylate synthase (TS) and dihydropyrimidine dehydrogenase (DPD) are important enzymes in the metabolism of 5-fluorouracil, which have been examined as possible predictive markers. Fluorouracil 120-134 dihydropyrimidine dehydrogenase Homo sapiens 72-75 22403796-6 2012 The numbers of apoptotic caspase-3- and caspase-8-activated cells in the intestinal crypt increased 24 h after the first 5-FU administration but were overall significantly lower in Nox1KO than in WT mice. Fluorouracil 121-125 caspase 3 Mus musculus 25-34 21822560-8 2012 CONCLUSION: Neoadjuvant chemotherapy utilizing 5-fluorouracil and cisplatin in esophageal squamous cell carcinoma is useful to induce CD4 and CD8 T lymphocytes in the tumor microenvironment and to maintain HLA class I expression levels in combination with its direct cytotoxic effects. Fluorouracil 47-61 CD8a molecule Homo sapiens 142-145 22006578-8 2012 CONCLUSIONS: High TS and DPD mRNA levels on FFPE specimens may predict distant recurrence of rectal cancer treated with 5-FU-based preoperative CRT followed by surgery. Fluorouracil 120-124 dihydropyrimidine dehydrogenase Homo sapiens 25-28 22322240-2 2012 Cytochrome P450 2A6 (CYP2A6) is the principal enzyme responsible for bioconversion of tegafur to 5-FU. Fluorouracil 109-113 cytochrome P450 family 2 subfamily A member 6 Homo sapiens 0-19 22322240-2 2012 Cytochrome P450 2A6 (CYP2A6) is the principal enzyme responsible for bioconversion of tegafur to 5-FU. Fluorouracil 109-113 cytochrome P450 family 2 subfamily A member 6 Homo sapiens 21-27 22322240-13 2012 Thus, the reduced efficacy of standard chemotherapy dosage in Chinese cancer patients may be explained by the lack of CYP2A6-mediated S-1 bioconversion to 5-FU. Fluorouracil 179-183 cytochrome P450 family 2 subfamily A member 6 Homo sapiens 130-136 21706156-0 2012 MDM2 SNP309 and TP53 R72P associated with severe and febrile neutropenia in breast cancer patients treated with 5-FU/epirubicin/cyclophosphamide. Fluorouracil 112-116 MDM2 proto-oncogene Homo sapiens 0-4 21706156-1 2012 The aim of this study was to investigate the association of two genetic polymorphisms, MDM2 SNP309 and TP53 R72P, with incidence of neutropenia in breast cancer patients treated with 5-FU/epirubicin/cyclophosphamide (FEC). Fluorouracil 183-187 MDM2 proto-oncogene Homo sapiens 87-91 22421942-5 2012 Tumors of mice treated with 5-FU+IFN-alpha harbored higher numbers of infiltrating NK cells in comparison with control mice. Fluorouracil 28-32 interferon alpha Mus musculus 33-42 22419291-2 2012 Apart from surgery - which remains the mainstay of treatment for resectable primary tumours - postoperative (i.e., adjuvant) chemotherapy with 5-fluorouracil (5-FU) based regimens is now the standard treatment in Dukes" C (TNM stage III) colon tumours i.e. tumours with metastases in the regional lymph nodes but no distant metastases. Fluorouracil 159-163 teneurin transmembrane protein 1 Homo sapiens 223-226 22076043-5 2012 CD/UPRT converts 5-fluorocytosine (5-FC) into the chemotherapeutic 5-FU, a mainstay of HNSCC chemotherapy. Fluorouracil 67-71 uracil phosphoribosyltransferase homolog Homo sapiens 0-7 22151662-9 2012 HuH-7 cells were the most sensitive to 5-FU and KYN-2 cells were the most resistant. Fluorouracil 39-43 MIR7-3 host gene Homo sapiens 0-5 22490566-0 2012 Polymorphisms of dihydropyrimidine dehydrogenase gene and clinical outcomes of gastric cancer patients treated with fluorouracil-based adjuvant chemotherapy in Chinese population. Fluorouracil 116-128 dihydropyrimidine dehydrogenase Homo sapiens 17-48 22490566-1 2012 BACKGROUND: Dihydropyrimidine dehydrogenase (DPD), a key enzyme involved in the catabolism of 5-fluorouracil (5-FU), is the attractive candidate for pharmacogenetic research on efficacies and toxicities of 5-FU. Fluorouracil 94-108 dihydropyrimidine dehydrogenase Homo sapiens 12-43 22490566-1 2012 BACKGROUND: Dihydropyrimidine dehydrogenase (DPD), a key enzyme involved in the catabolism of 5-fluorouracil (5-FU), is the attractive candidate for pharmacogenetic research on efficacies and toxicities of 5-FU. Fluorouracil 94-108 dihydropyrimidine dehydrogenase Homo sapiens 45-48 22490566-1 2012 BACKGROUND: Dihydropyrimidine dehydrogenase (DPD), a key enzyme involved in the catabolism of 5-fluorouracil (5-FU), is the attractive candidate for pharmacogenetic research on efficacies and toxicities of 5-FU. Fluorouracil 110-114 dihydropyrimidine dehydrogenase Homo sapiens 12-43 22490566-1 2012 BACKGROUND: Dihydropyrimidine dehydrogenase (DPD), a key enzyme involved in the catabolism of 5-fluorouracil (5-FU), is the attractive candidate for pharmacogenetic research on efficacies and toxicities of 5-FU. Fluorouracil 110-114 dihydropyrimidine dehydrogenase Homo sapiens 45-48 22490566-1 2012 BACKGROUND: Dihydropyrimidine dehydrogenase (DPD), a key enzyme involved in the catabolism of 5-fluorouracil (5-FU), is the attractive candidate for pharmacogenetic research on efficacies and toxicities of 5-FU. Fluorouracil 206-210 dihydropyrimidine dehydrogenase Homo sapiens 12-43 22490566-1 2012 BACKGROUND: Dihydropyrimidine dehydrogenase (DPD), a key enzyme involved in the catabolism of 5-fluorouracil (5-FU), is the attractive candidate for pharmacogenetic research on efficacies and toxicities of 5-FU. Fluorouracil 206-210 dihydropyrimidine dehydrogenase Homo sapiens 45-48 22490566-2 2012 The aim of this study is to explore the association between polymorphisms of dihydropyrimidine dehydrogenase gene (DPYD) and clinical outcomes of gastric cancer patients treated with fluorouracil-based adjuvant chemotherapy in the Chinese population. Fluorouracil 183-195 dihydropyrimidine dehydrogenase Homo sapiens 77-108 22490566-2 2012 The aim of this study is to explore the association between polymorphisms of dihydropyrimidine dehydrogenase gene (DPYD) and clinical outcomes of gastric cancer patients treated with fluorouracil-based adjuvant chemotherapy in the Chinese population. Fluorouracil 183-195 dihydropyrimidine dehydrogenase Homo sapiens 115-119 22490566-10 2012 CONCLUSIONS: These results suggest that polymorphisms of rs1801159 in DPYD may be used as valuable predictors of the response to fluorouracil-based chemotherapy for gastric cancer patients in the Chinese population. Fluorouracil 129-141 dihydropyrimidine dehydrogenase Homo sapiens 70-74 22490566-11 2012 Well-designed, comprehensive, and prospective studies on determining these polymorphisms of DPYD as predictive markers for gastric cancer in response to fluorouracil-based therapies are warranted. Fluorouracil 153-165 dihydropyrimidine dehydrogenase Homo sapiens 92-96 22294766-15 2012 In conclusion, ABCC11 may be a promising candidate marker for a validation study on 5-FU therapy outcome. Fluorouracil 84-88 ATP binding cassette subfamily C member 11 Homo sapiens 15-21 21841826-5 2012 Activation of p38MAPK by 5-FU was dependent on canonical MAP2K, MAPK kinase (MKK)-3 and MKK6. Fluorouracil 25-29 mitogen-activated protein kinase kinase 3 Homo sapiens 64-83 22740893-0 2012 Good response to leucovorin and fluorouracil plus oxaliplatin and cetuximab therapy in a patient with metastatic ascending colon cancer harboring a KRAS p.G13D mutation. Fluorouracil 32-44 KRAS proto-oncogene, GTPase Homo sapiens 148-152 21167658-10 2012 Germline thymidylate synthase and XRCC1 polymorphisms might be useful as predictive markers of rectal tumor response to neoadjuvant chemoradiotherapy with 5-fluorouracil. Fluorouracil 155-169 X-ray repair cross complementing 1 Homo sapiens 34-39 22213823-9 2012 Furthermore, a significant correlation between baseline uPAR expression and sensitivity toward 5-fluorouracil was revealed, thus illustrating the possible potentials of uPAR PET in a clinical setting. Fluorouracil 95-109 thyroid stimulating hormone receptor Mus musculus 174-177 22590561-4 2012 RESULTS: Administration of 5-FU but not pemetrexed potentiated CXCL8 secretion and increased CXCR1 and CXCR2 gene expression in metastatic PC3 cells. Fluorouracil 27-31 C-X-C motif chemokine receptor 1 Homo sapiens 93-98 23401991-3 2012 In 39-61% of the cases severe toxicity of 5-FU is caused by decreased DPD acivity. Fluorouracil 42-46 dihydropyrimidine dehydrogenase Homo sapiens 70-73 23401991-5 2012 80-90% of the administered 5-FU is catabolised by DPD. Fluorouracil 27-31 dihydropyrimidine dehydrogenase Homo sapiens 50-53 22143355-1 2012 PURPOSE: Thymidylate synthase (TS) and dihydropyrimidine dehydrogenase (DPD) are important enzymes in the metabolism of 5-fluorouracil and possible predictive markers. Fluorouracil 120-134 dihydropyrimidine dehydrogenase Homo sapiens 39-70 22143355-1 2012 PURPOSE: Thymidylate synthase (TS) and dihydropyrimidine dehydrogenase (DPD) are important enzymes in the metabolism of 5-fluorouracil and possible predictive markers. Fluorouracil 120-134 dihydropyrimidine dehydrogenase Homo sapiens 72-75 22199347-0 2011 Low dihydropyrimidine dehydrogenase correlates with prolonged survival in patients with lung adenocarcinoma treated with 5-fluorouracil. Fluorouracil 121-135 dihydropyrimidine dehydrogenase Homo sapiens 4-35 22199347-1 2011 BACKGROUND: The enzyme dihydropyrimidine dehydrogenase (DPD) is involved in the metabolism of 5-fluorouracil (5-FU). Fluorouracil 94-108 dihydropyrimidine dehydrogenase Homo sapiens 23-54 22199347-1 2011 BACKGROUND: The enzyme dihydropyrimidine dehydrogenase (DPD) is involved in the metabolism of 5-fluorouracil (5-FU). Fluorouracil 94-108 dihydropyrimidine dehydrogenase Homo sapiens 56-59 22199347-1 2011 BACKGROUND: The enzyme dihydropyrimidine dehydrogenase (DPD) is involved in the metabolism of 5-fluorouracil (5-FU). Fluorouracil 110-114 dihydropyrimidine dehydrogenase Homo sapiens 23-54 22199347-1 2011 BACKGROUND: The enzyme dihydropyrimidine dehydrogenase (DPD) is involved in the metabolism of 5-fluorouracil (5-FU). Fluorouracil 110-114 dihydropyrimidine dehydrogenase Homo sapiens 56-59 22199347-2 2011 The aim of this study was to clarify the correlation between the expression of DPD and the efficacy of 5-FU therapy in patients with lung adenocarcinoma (AD). Fluorouracil 103-107 dihydropyrimidine dehydrogenase Homo sapiens 79-82 22199347-4 2011 RESULTS: Administration of 5-FU improved the prognosis of patients with low DPD-expressing tumors, whereas it did not do so for patients with high DPD expressing tumors. Fluorouracil 27-31 dihydropyrimidine dehydrogenase Homo sapiens 76-79 22199347-5 2011 Patients with low DPD-expressing tumors administered with 5-FU had a significantly better prognosis than those who underwent surgery alone. Fluorouracil 58-62 dihydropyrimidine dehydrogenase Homo sapiens 18-21 22199347-6 2011 A Cox proportional hazards regression model revealed that administration of 5-FU was an independent variable to predict prognosis in patients with low DPD-expressing tumors. Fluorouracil 76-80 dihydropyrimidine dehydrogenase Homo sapiens 151-154 21781197-4 2011 Mutant plants that are deficient in ARP grow normally but are hypersensitive to 5-fluorouracil, a compound that favours mis-incorporation of uracil into DNA. Fluorouracil 80-94 apurinic endonuclease-redox protein Arabidopsis thaliana 36-39 21965773-1 2011 Thymidylate synthase (TS) and dihydropyrimidine dehydrogenase (DPD) are 5-fluorouracil (5-FU) metabolizing enzymes and are involved in the sensitivity of carcinoma patients to 5-FU. Fluorouracil 72-86 dihydropyrimidine dehydrogenase Homo sapiens 63-66 21965773-1 2011 Thymidylate synthase (TS) and dihydropyrimidine dehydrogenase (DPD) are 5-fluorouracil (5-FU) metabolizing enzymes and are involved in the sensitivity of carcinoma patients to 5-FU. Fluorouracil 88-92 dihydropyrimidine dehydrogenase Homo sapiens 63-66 21965773-1 2011 Thymidylate synthase (TS) and dihydropyrimidine dehydrogenase (DPD) are 5-fluorouracil (5-FU) metabolizing enzymes and are involved in the sensitivity of carcinoma patients to 5-FU. Fluorouracil 176-180 dihydropyrimidine dehydrogenase Homo sapiens 63-66 21975339-11 2011 Neither c-FOS nor SERPINE-1 gene expression was induced by 5-FU treatment or gamma irradiation in vitro, but MUC 18 was up-regulated by 5-FU treatment. Fluorouracil 136-140 melanoma cell adhesion molecule Homo sapiens 109-115 21668582-1 2011 Gimeracil (5-chloro-2, 4-dihydroxypyridine) is an inhibitor of dihydropyrimidine dehydrogenase (DPYD), which degrades pyrimidine including 5-fluorouracil in the blood. Fluorouracil 139-153 dihydropyrimidine dehydrogenase Homo sapiens 63-94 21668582-1 2011 Gimeracil (5-chloro-2, 4-dihydroxypyridine) is an inhibitor of dihydropyrimidine dehydrogenase (DPYD), which degrades pyrimidine including 5-fluorouracil in the blood. Fluorouracil 139-153 dihydropyrimidine dehydrogenase Homo sapiens 96-100 21107571-10 2011 CONCLUSION: The measurements of 5-FU, FUH2, and especially their ratio (FUH2/5-FU) by the modified LC-MS/MS method could be used to determine DHPDH enzyme activity. Fluorouracil 32-36 dihydropyrimidine dehydrogenase Homo sapiens 142-147 21107571-10 2011 CONCLUSION: The measurements of 5-FU, FUH2, and especially their ratio (FUH2/5-FU) by the modified LC-MS/MS method could be used to determine DHPDH enzyme activity. Fluorouracil 77-81 dihydropyrimidine dehydrogenase Homo sapiens 142-147 21458988-4 2011 PATIENTS AND METHODS: DNMT1/3b expression was analysed immunohistochemically in 127 pretherapeutic biopsies of neoadjuvant (platinum/5-fluorouracil)-treated GC patients and correlated with response and overall survival (OS). Fluorouracil 133-147 DNA methyltransferase 1 Homo sapiens 22-30 21458988-11 2011 CONCLUSION: Low DNMT1 expression defines a subgroup of GC patients with better outcomes following platinum/5FU-based neoadjuvant chemotherapy. Fluorouracil 107-110 DNA methyltransferase 1 Homo sapiens 16-21 21737644-6 2011 NK4 gene expression enhanced 5-FU-induced caspase-3 and -7 activation of CT26. Fluorouracil 29-33 caspase 3 Mus musculus 42-58 21737644-10 2011 CONCLUSION: 5-FU exerts an additional effect on apoptosis of NK4-expressing CT26 cells by down-regulating intracellular signaling of the HGF/c-Met pathway. Fluorouracil 12-16 hepatocyte growth factor Mus musculus 137-140 21677502-6 2011 Three of four cell lines showed an increasing sensitivity to 5-FU with the combination of uracilor CDHP. Fluorouracil 61-65 cadherin 3 Homo sapiens 99-103 21325880-4 2011 Specific inhibition of early autophagy induction with siRNA targeted to Beclin 1 and ATG7 significantly enhanced the effect of 5-FU and reduced the recovery of drug-treated cells. Fluorouracil 127-131 beclin 1 Homo sapiens 72-80 21544729-7 2011 Immunofluorescence assay and Western blot showed that 5-FU induced the expression of EBV-lytic genes including BZLF1, BRLF1, BMRF1 and BHRF1. Fluorouracil 54-58 BRLF1 Human gammaherpesvirus 4 118-123 21635994-6 2011 RESULTS: For the metastatic colorectal cancer LLD population with K-ras wild-type genotype, mean overall survival estimates were 37.7 months for first-line treatment with cetuximab plus FOLFIRI (irinotecan, leucovorin, fluorouracil) and 30.4 months for bevacizumab plus FOLFOX (oxaliplatin, leucovorin, fluorouracil). Fluorouracil 219-231 KRAS proto-oncogene, GTPase Homo sapiens 66-71 21635994-6 2011 RESULTS: For the metastatic colorectal cancer LLD population with K-ras wild-type genotype, mean overall survival estimates were 37.7 months for first-line treatment with cetuximab plus FOLFIRI (irinotecan, leucovorin, fluorouracil) and 30.4 months for bevacizumab plus FOLFOX (oxaliplatin, leucovorin, fluorouracil). Fluorouracil 303-315 KRAS proto-oncogene, GTPase Homo sapiens 66-71 21161336-5 2011 RESULTS: We observed that CDF together with 5-FU + Ox were more potent than curcumin in reducing CD44 and CD166 in chemo-resistant colon cancer cells, accompanied by inhibition of growth, induction of apoptosis and disintegration of colonospheres. Fluorouracil 44-48 CD44 molecule (Indian blood group) Homo sapiens 97-101 21410976-1 2011 BACKGROUND: Considerable variation in intravenous 5-fluorouracil (5-FU) metabolism can occur due to the wide range of dihydropyrimidine dehydrogenase (DPD) enzyme activity, which can affect both tolerability and efficacy. Fluorouracil 50-64 dihydropyrimidine dehydrogenase Homo sapiens 118-149 21410976-1 2011 BACKGROUND: Considerable variation in intravenous 5-fluorouracil (5-FU) metabolism can occur due to the wide range of dihydropyrimidine dehydrogenase (DPD) enzyme activity, which can affect both tolerability and efficacy. Fluorouracil 50-64 dihydropyrimidine dehydrogenase Homo sapiens 151-154 21410976-1 2011 BACKGROUND: Considerable variation in intravenous 5-fluorouracil (5-FU) metabolism can occur due to the wide range of dihydropyrimidine dehydrogenase (DPD) enzyme activity, which can affect both tolerability and efficacy. Fluorouracil 66-70 dihydropyrimidine dehydrogenase Homo sapiens 118-149 21410976-1 2011 BACKGROUND: Considerable variation in intravenous 5-fluorouracil (5-FU) metabolism can occur due to the wide range of dihydropyrimidine dehydrogenase (DPD) enzyme activity, which can affect both tolerability and efficacy. Fluorouracil 66-70 dihydropyrimidine dehydrogenase Homo sapiens 151-154 21228350-8 2011 Interestingly, APE2-deficient mice show a delay in recovery of B lymphocyte progenitors following bone marrow depletion by 5-fluorouracil, with the pro-B and pre-B cell pools still markedly decreased 2 wk after a single treatment. Fluorouracil 123-137 apurinic/apyrimidinic endonuclease 2 Mus musculus 15-19 21378348-0 2011 A phase I study evaluating the effect of CDHP as a component of S-1 on the pharmacokinetics of 5-fluorouracil. Fluorouracil 95-109 cadherin 3 Homo sapiens 41-45 21378348-1 2011 UNLABELLED: The purpose of this study was to investigate the effect of gimeracil (CDHP), a reversible dihydropyrimidine dehydrogenase (DPD) inhibitor, on the pharmacokinetics of 5-fluorouracil (5-FU) and other related metabolites by comparing the pharmacokinetic (PK) profile of S-1 (tegafur [FT] + CDHP + oteracil potassium [Oxo]) to that of FT alone. Fluorouracil 178-192 cadherin 3 Homo sapiens 82-86 21378348-1 2011 UNLABELLED: The purpose of this study was to investigate the effect of gimeracil (CDHP), a reversible dihydropyrimidine dehydrogenase (DPD) inhibitor, on the pharmacokinetics of 5-fluorouracil (5-FU) and other related metabolites by comparing the pharmacokinetic (PK) profile of S-1 (tegafur [FT] + CDHP + oteracil potassium [Oxo]) to that of FT alone. Fluorouracil 178-192 dihydropyrimidine dehydrogenase Homo sapiens 102-133 21378348-1 2011 UNLABELLED: The purpose of this study was to investigate the effect of gimeracil (CDHP), a reversible dihydropyrimidine dehydrogenase (DPD) inhibitor, on the pharmacokinetics of 5-fluorouracil (5-FU) and other related metabolites by comparing the pharmacokinetic (PK) profile of S-1 (tegafur [FT] + CDHP + oteracil potassium [Oxo]) to that of FT alone. Fluorouracil 178-192 dihydropyrimidine dehydrogenase Homo sapiens 135-138 21378348-1 2011 UNLABELLED: The purpose of this study was to investigate the effect of gimeracil (CDHP), a reversible dihydropyrimidine dehydrogenase (DPD) inhibitor, on the pharmacokinetics of 5-fluorouracil (5-FU) and other related metabolites by comparing the pharmacokinetic (PK) profile of S-1 (tegafur [FT] + CDHP + oteracil potassium [Oxo]) to that of FT alone. Fluorouracil 178-192 cadherin 3 Homo sapiens 299-303 21378348-1 2011 UNLABELLED: The purpose of this study was to investigate the effect of gimeracil (CDHP), a reversible dihydropyrimidine dehydrogenase (DPD) inhibitor, on the pharmacokinetics of 5-fluorouracil (5-FU) and other related metabolites by comparing the pharmacokinetic (PK) profile of S-1 (tegafur [FT] + CDHP + oteracil potassium [Oxo]) to that of FT alone. Fluorouracil 194-198 cadherin 3 Homo sapiens 82-86 20653680-1 2010 WHAT IS ALREADY KNOWN ABOUT THIS SUBJECT * Dihydropyrimidine dehydrogenase (DPD) is the enzyme responsible for the elimination of approximately 80% of the administered dose of 5-fluorouracil (5-FU). Fluorouracil 176-190 dihydropyrimidine dehydrogenase Homo sapiens 43-74 20653680-1 2010 WHAT IS ALREADY KNOWN ABOUT THIS SUBJECT * Dihydropyrimidine dehydrogenase (DPD) is the enzyme responsible for the elimination of approximately 80% of the administered dose of 5-fluorouracil (5-FU). Fluorouracil 176-190 dihydropyrimidine dehydrogenase Homo sapiens 76-79 20653680-1 2010 WHAT IS ALREADY KNOWN ABOUT THIS SUBJECT * Dihydropyrimidine dehydrogenase (DPD) is the enzyme responsible for the elimination of approximately 80% of the administered dose of 5-fluorouracil (5-FU). Fluorouracil 192-196 dihydropyrimidine dehydrogenase Homo sapiens 43-74 20653680-1 2010 WHAT IS ALREADY KNOWN ABOUT THIS SUBJECT * Dihydropyrimidine dehydrogenase (DPD) is the enzyme responsible for the elimination of approximately 80% of the administered dose of 5-fluorouracil (5-FU). Fluorouracil 192-196 dihydropyrimidine dehydrogenase Homo sapiens 76-79 20653680-2 2010 * Mutations in the DPD-coding gene have been shown to increase the risk of severe toxicity in 5-FU treated patients. Fluorouracil 94-98 dihydropyrimidine dehydrogenase Homo sapiens 19-22 20653680-4 2010 WHAT THIS STUDY ADDS * The intragenic rearrangements of DPYD using multiplex ligation-dependent probe amplification (MLPA) were studied for the first time in a large series of 234 colorectal cancer patients treated with 5-FU-containing chemotherapy. Fluorouracil 220-224 dihydropyrimidine dehydrogenase Homo sapiens 56-60 20653680-8 2010 AIMS To study the relationship between the toxicity associated with a 5-FU-based therapy and the presence of (i) the large intragenic rearrangements in the DPYD gene and (ii) the IVS14+1G>A mutation. Fluorouracil 70-74 dihydropyrimidine dehydrogenase Homo sapiens 156-160 20653683-0 2010 Lethal outcome of 5-fluorouracil infusion in a patient with a total DPD deficiency and a double DPYD and UTG1A1 gene mutation. Fluorouracil 18-32 dihydropyrimidine dehydrogenase Homo sapiens 96-100 20647341-0 2010 miR-192/miR-215 influence 5-fluorouracil resistance through cell cycle-mediated mechanisms complementary to its post-transcriptional thymidilate synthase regulation. Fluorouracil 26-40 microRNA 215 Homo sapiens 8-15 19830428-10 2010 Downregulation of DPD was observed after 5-FU monotherapy, but the combined effect of NSAIDs and 5-FU on DPD mRNA expression, and enzyme activity was superior to the effect of 5-FU alone. Fluorouracil 97-101 dihydropyrimidine dehydrogenase Homo sapiens 105-108 19830428-11 2010 CONCLUSIONS: Since 5-FU + NSAID treatment can alter the DPD enzyme activity resulting in an enhanced cytotoxic effect, further studies in clinical practice are warranted. Fluorouracil 19-23 dihydropyrimidine dehydrogenase Homo sapiens 56-59 20162308-0 2010 Do 5-fluorouracil therapies alter CYP2C19 metaboliser status? Fluorouracil 3-17 cytochrome P450 family 2 subfamily C member 19 Homo sapiens 34-41 20162308-1 2010 PURPOSE: To report a case of altered CYP2C19 metaboliser status following 5-fluorouracil treatment. Fluorouracil 74-88 cytochrome P450 family 2 subfamily C member 19 Homo sapiens 37-44 20162308-9 2010 CONCLUSIONS: Although 5FU is not a substrate for hepatic drug metabolising CYP enzymes, it may interfere with the synthesis of CYP2C19. Fluorouracil 22-25 cytochrome P450 family 2 subfamily C member 19 Homo sapiens 127-134 20162308-11 2010 Down regulation of CYP2C9 and CYP2C19 synthesis by 5FU therapies may explain the adverse effect of 5FU on the clinical disposition of warfarin and phenytoin. Fluorouracil 51-54 cytochrome P450 family 2 subfamily C member 19 Homo sapiens 30-37 20591220-0 2010 Low dosage 5-fluorouracil increases the transfection efficiency of Ad/VEGF-A in mouse lung carcinoma cell line LA795 and inhibits tumor growth. Fluorouracil 11-25 vascular endothelial growth factor A Mus musculus 70-76 20591220-7 2010 Real-time PCR and ELISA were applied to measure the expression level of VEGF-A after LA795 cells were infected by Ad/siVEGF-A and treated with 5-FU. Fluorouracil 143-147 vascular endothelial growth factor A Mus musculus 72-78 20591220-9 2010 RESULTS: Low dose of 5-FU elevated the Ad/EGFP infection in LA795 cells significantly, and also enhanced the effect of Ad/siVEGF-A in down-regulating VEGF-A mRNA and protein levels in tumor cells. Fluorouracil 21-25 vascular endothelial growth factor A Mus musculus 124-130 20570921-7 2010 RESULTS: Chemotherapy (5-fluorouracil) treatment resulted in acute increases in transforming growth factor-alpha, amphiregulin, and heregulin ligand shedding in vitro and in vivo that correlated with significantly increased ADAM-17 activity. Fluorouracil 23-37 amphiregulin Homo sapiens 114-126 20570921-7 2010 RESULTS: Chemotherapy (5-fluorouracil) treatment resulted in acute increases in transforming growth factor-alpha, amphiregulin, and heregulin ligand shedding in vitro and in vivo that correlated with significantly increased ADAM-17 activity. Fluorouracil 23-37 ADAM metallopeptidase domain 17 Homo sapiens 224-231 20570578-1 2010 The efficacy of the chemotherapeutic drug 5"-fluorouracil is reduced by catabolism to 2"-fluoro-beta-alanine (FBAL), a three-step reaction in which dihydropyrimidine dehydrogenase (DPD) catalyzes the rate-limiting step. Fluorouracil 42-57 dihydropyrimidine dehydrogenase Homo sapiens 148-179 20570578-1 2010 The efficacy of the chemotherapeutic drug 5"-fluorouracil is reduced by catabolism to 2"-fluoro-beta-alanine (FBAL), a three-step reaction in which dihydropyrimidine dehydrogenase (DPD) catalyzes the rate-limiting step. Fluorouracil 42-57 dihydropyrimidine dehydrogenase Homo sapiens 181-184 20562578-7 2010 Only PSN1 cells were sensitive to nontoxic 5-FU and alpha-TOS combination. Fluorouracil 43-47 5'-nucleotidase, cytosolic III Mus musculus 5-9 20562578-8 2010 SMAD4/DPC4 transfection restored PSN1 resistance to the effects of combined 5-FU and alpha-TOS effects. Fluorouracil 76-80 5'-nucleotidase, cytosolic III Mus musculus 33-37 20460542-6 2010 5-Fluorouracil- and methotrexate-resistant HT-29 cells expressing an invasive phenotype in collagen type I and a metastatic behavior in immunodeficient mice exhibited high expression of the chemokine receptor CXCR4. Fluorouracil 0-14 chemokine (C-X-C motif) receptor 4 Mus musculus 209-214 20622967-1 2010 Patients with reduced dihydropyrimidine dehydrogenase (DPD) activity are at risk for experiencing serious adverse effects following 5-fluorouracil (5-FU) based chemotherapy. Fluorouracil 132-146 dihydropyrimidine dehydrogenase Homo sapiens 22-53 20622967-1 2010 Patients with reduced dihydropyrimidine dehydrogenase (DPD) activity are at risk for experiencing serious adverse effects following 5-fluorouracil (5-FU) based chemotherapy. Fluorouracil 132-146 dihydropyrimidine dehydrogenase Homo sapiens 55-58 20622967-1 2010 Patients with reduced dihydropyrimidine dehydrogenase (DPD) activity are at risk for experiencing serious adverse effects following 5-fluorouracil (5-FU) based chemotherapy. Fluorouracil 148-152 dihydropyrimidine dehydrogenase Homo sapiens 22-53 20622967-1 2010 Patients with reduced dihydropyrimidine dehydrogenase (DPD) activity are at risk for experiencing serious adverse effects following 5-fluorouracil (5-FU) based chemotherapy. Fluorouracil 148-152 dihydropyrimidine dehydrogenase Homo sapiens 55-58 20463601-8 2010 Although treatment with 5-FU upregulated Rae-1 expression on MC38 cells, the NK-cell-mediated cytotoxic activity was not suppressed by treatment with an anti-Rae-1 mAb or an antinatural killer group 2D mAb or both. Fluorouracil 24-28 ribonucleic acid export 1 Mus musculus 41-46 20740189-4 2010 Case Reports: Here we describe the cases of 2 patients with metastatic KRAS wild-type colorectal cancer who received a fourth-line monotherapy with panitumumab after failure of 5-fluorouracil, irinotecan, oxaliplatin, and bevacizumab. Fluorouracil 177-191 KRAS proto-oncogene, GTPase Homo sapiens 71-75 20507294-0 2010 Investigation of IVS14 + 1G > A polymorphism of DPYD gene in a group of Bosnian patients treated with 5-Fluorouracil and capecitabine. Fluorouracil 105-119 dihydropyrimidine dehydrogenase Homo sapiens 51-55 20507294-2 2010 Dihydropyrimidine dehydrogenase (DPD) is an enzyme that regulates 5-FU quantities available for anabolic processes and hence affects its pharmacokinetics, toxicity and efficacy. Fluorouracil 66-70 dihydropyrimidine dehydrogenase Homo sapiens 0-31 20507294-2 2010 Dihydropyrimidine dehydrogenase (DPD) is an enzyme that regulates 5-FU quantities available for anabolic processes and hence affects its pharmacokinetics, toxicity and efficacy. Fluorouracil 66-70 dihydropyrimidine dehydrogenase Homo sapiens 33-36 20507294-3 2010 There are several studies describing a hereditary (pharmacogenetic) disorder in which individuals with absent or significantly reduced DPD activity may even develop a life-threatening toxicity following exposure to 5-FU. Fluorouracil 215-219 dihydropyrimidine dehydrogenase Homo sapiens 135-138 20171199-5 2010 Knocking down of Livin expression in HCT-8/V cells by specific RNAi facilitated the apoptosis of HCT-8/V cells in response to vincristine (VCR), etoposide (VP-16), and 5-flourouracil (5-FU). Fluorouracil 184-188 baculoviral IAP repeat containing 7 Homo sapiens 17-22 20448262-0 2010 Specific effect of 5-fluorouracil on alpha-fetoprotein gene expression during the in vitro mouse embryonic stem cell differentiation. Fluorouracil 19-33 alpha fetoprotein Mus musculus 37-54 20448262-5 2010 At lower concentrations, 5-FU led to decrease in the expression of the alpha-fetoprotein gene, a marker of the visceral endoderm, in the EBs. Fluorouracil 25-29 alpha fetoprotein Mus musculus 71-88 20128868-8 2010 Platelet recovery after 5-FU-induced thrombocytopenia was significantly delayed in bim KO mice. Fluorouracil 24-28 BCL2-like 11 (apoptosis facilitator) Mus musculus 83-86 20501401-7 2010 The expression of apoptotic protein Bcl-6 and Bim were significantly higher in PI3K p85alpha/RNAi-LoVo cells treated with 5-FU than LoVo cells (P=0.000). Fluorouracil 122-126 BCL6 transcription repressor Homo sapiens 36-41 20433755-16 2010 Conversely, bypassing Par-4 overexpression by direct knockdown of DROSHA expression in native HT29 cells increased miR-34a expression and 5-FU sensitivity. Fluorouracil 138-142 drosha ribonuclease III Homo sapiens 66-72 20723428-5 2010 RESULTS: Among the 10 genes, only genes IGFBP6 and FOXL2 displayed differential DNA methylation pattern between the 5-Fu-resistant and 5-Fu-sensitive cell lines. Fluorouracil 116-120 insulin like growth factor binding protein 6 Homo sapiens 40-46 20723428-5 2010 RESULTS: Among the 10 genes, only genes IGFBP6 and FOXL2 displayed differential DNA methylation pattern between the 5-Fu-resistant and 5-Fu-sensitive cell lines. Fluorouracil 116-120 forkhead box L2 Homo sapiens 51-56 20723428-5 2010 RESULTS: Among the 10 genes, only genes IGFBP6 and FOXL2 displayed differential DNA methylation pattern between the 5-Fu-resistant and 5-Fu-sensitive cell lines. Fluorouracil 135-139 insulin like growth factor binding protein 6 Homo sapiens 40-46 20723428-5 2010 RESULTS: Among the 10 genes, only genes IGFBP6 and FOXL2 displayed differential DNA methylation pattern between the 5-Fu-resistant and 5-Fu-sensitive cell lines. Fluorouracil 135-139 forkhead box L2 Homo sapiens 51-56 20354524-5 2010 A multiplexed RT-PCR assay was used to identify KRAS-controlled apoptosis regulators after exposure to 5-FU or oxaliplatin. Fluorouracil 103-107 KRAS proto-oncogene, GTPase Homo sapiens 48-52 20354524-7 2010 RESULTS: Oncogenic KRAS sensitised colorectal tumour cells to oxaliplatin and 5-FU in a p53-dependent manner and promoted p53 phosphorylation at Ser37 and Ser392, without affecting p53 stabilisation, p21 induction, or cell-cycle arrest. Fluorouracil 78-82 KRAS proto-oncogene, GTPase Homo sapiens 19-23 20354524-11 2010 CONCLUSION: Oncogenic KRAS determines the cellular response to p53 activation by oxaliplatin or 5-FU, by facilitating apoptosis induction through Noxa. Fluorouracil 96-100 KRAS proto-oncogene, GTPase Homo sapiens 22-26 19697054-1 2010 Thymidylate synthase (TS) is a major target of 5-fluorouracil (5-FU) and dihydropyrimidine dehydrogenase (DPD) is a rate-limiting enzyme in the degradation of 5-FU. Fluorouracil 47-61 dihydropyrimidine dehydrogenase Homo sapiens 106-109 19697054-1 2010 Thymidylate synthase (TS) is a major target of 5-fluorouracil (5-FU) and dihydropyrimidine dehydrogenase (DPD) is a rate-limiting enzyme in the degradation of 5-FU. Fluorouracil 159-163 dihydropyrimidine dehydrogenase Homo sapiens 73-104 19697054-1 2010 Thymidylate synthase (TS) is a major target of 5-fluorouracil (5-FU) and dihydropyrimidine dehydrogenase (DPD) is a rate-limiting enzyme in the degradation of 5-FU. Fluorouracil 159-163 dihydropyrimidine dehydrogenase Homo sapiens 106-109 19697054-3 2010 In addition, increased interest has been focused on the biological roles of TS and DPD as the independent prognostic factors as well as responsive determinants for cancer patients with 5-FU based therapy. Fluorouracil 185-189 dihydropyrimidine dehydrogenase Homo sapiens 83-86 19739116-2 2010 Here, we report on the elevated expression of claudin-1 in nasopharyngeal carcinoma (NPC) cell lines under serum deprivation or fluorouracil (5-FU) treatment. Fluorouracil 128-140 claudin 1 Homo sapiens 46-55 19739116-2 2010 Here, we report on the elevated expression of claudin-1 in nasopharyngeal carcinoma (NPC) cell lines under serum deprivation or fluorouracil (5-FU) treatment. Fluorouracil 142-146 claudin 1 Homo sapiens 46-55 19822137-0 2010 Two cases of 5-fluorouracil toxicity linked with gene variants in the DPYD gene. Fluorouracil 13-27 dihydropyrimidine dehydrogenase Homo sapiens 70-74 19822137-1 2010 OBJECTIVES: Dihydropyrimidine dehydrogenase (DPD) is the initial rate-limiting enzyme in endogenous pyrimidine catabolism and is responsible for the reduction of the pyrimidine analog 5-fluorouracil (5-FU). Fluorouracil 184-198 dihydropyrimidine dehydrogenase Homo sapiens 12-43 19822137-1 2010 OBJECTIVES: Dihydropyrimidine dehydrogenase (DPD) is the initial rate-limiting enzyme in endogenous pyrimidine catabolism and is responsible for the reduction of the pyrimidine analog 5-fluorouracil (5-FU). Fluorouracil 184-198 dihydropyrimidine dehydrogenase Homo sapiens 45-48 19822137-1 2010 OBJECTIVES: Dihydropyrimidine dehydrogenase (DPD) is the initial rate-limiting enzyme in endogenous pyrimidine catabolism and is responsible for the reduction of the pyrimidine analog 5-fluorouracil (5-FU). Fluorouracil 200-204 dihydropyrimidine dehydrogenase Homo sapiens 12-43 19822137-1 2010 OBJECTIVES: Dihydropyrimidine dehydrogenase (DPD) is the initial rate-limiting enzyme in endogenous pyrimidine catabolism and is responsible for the reduction of the pyrimidine analog 5-fluorouracil (5-FU). Fluorouracil 200-204 dihydropyrimidine dehydrogenase Homo sapiens 45-48 19822137-5 2010 RESULTS: In 400 patients that were diagnosed with cancer and were eligible for 5-FU treatment, 14 patients were found to be heterozygous for the splice-site mutation DPYD IVS14+1G>A, which corresponds to a population frequency of 3.5%. Fluorouracil 79-83 dihydropyrimidine dehydrogenase Homo sapiens 166-170 20072795-9 2010 CONCLUSIONS: The efficacy of 5-FU may be lower in pancreatic cancer tissue than in normal tissue because DPD activity is upregulated in pancreatic cancer tissue compared to normal pancreatic tissue. Fluorouracil 29-33 dihydropyrimidine dehydrogenase Homo sapiens 105-108 19409643-1 2010 INTRODUCTION: The feasibility of using S-1, a novel oral dihydropyrimidine dehydrogenase (DPD)-inhibitory 5-fluorouracil, as postoperative adjuvant chemotherapy for completely resected non-small cell lung cancer (NSCLC) was analyzed. Fluorouracil 106-120 dihydropyrimidine dehydrogenase Homo sapiens 90-93 20714149-2 2010 Toxicity from fluorouracil therapy is known to be associated with the individual genetic background of the enzymes, thymidylate synthase and dihydropyrimidine dehydrogenase. Fluorouracil 14-26 dihydropyrimidine dehydrogenase Homo sapiens 141-172 20714149-4 2010 To evaluate the genetic background of the fluorouracil-associated hyperammonemic encephalopathy, analysis of the polymorphisms of the TYMS, DPYD and MTHFR genes was performed. Fluorouracil 42-54 methylenetetrahydrofolate reductase Homo sapiens 149-154 20205661-5 2010 Increased 5FU toxicity is associated with variations in the DPYD gene, TYMS gene and MTHFR gene. Fluorouracil 10-13 dihydropyrimidine dehydrogenase Homo sapiens 60-64 20205661-5 2010 Increased 5FU toxicity is associated with variations in the DPYD gene, TYMS gene and MTHFR gene. Fluorouracil 10-13 methylenetetrahydrofolate reductase Homo sapiens 85-90 20058135-1 2010 UFT and S-1 are oral 5-fluorouracil (5-FU) derivative drugs containing an inhibitor of dihydropyrimidine dehydrogenase (DPD); they are defined as DPD-inhibitory fluoropyrimidine (DIF). Fluorouracil 37-41 dihydropyrimidine dehydrogenase Homo sapiens 87-118 19622348-7 2009 For instance, 5-FU significantly suppressed ATP7B and human organic cation transporter 2 and increased multidrug resistance-associated protein (MRP) 2 mRNA expression (5.8-fold). Fluorouracil 14-18 ATPase copper transporting beta Homo sapiens 44-49 19622348-7 2009 For instance, 5-FU significantly suppressed ATP7B and human organic cation transporter 2 and increased multidrug resistance-associated protein (MRP) 2 mRNA expression (5.8-fold). Fluorouracil 14-18 ATP binding cassette subfamily C member 2 Homo sapiens 103-150 19622348-12 2009 In conclusion, we propose as one mechanism for FOLFOX synergism the 5-FU mediated suppression of ATP7B, the over-expression of glutathione exporters such as MRP2/ABCC2 and the decrease of glutathione levels by oxalate. Fluorouracil 68-72 ATPase copper transporting beta Homo sapiens 97-102 20037295-6 2009 In addition, when cells were incubated with different concentrations of 5-FU and docetaxel in the presence of PSK at the dose of 5 microg/mL showing no growth suppression, cytotoxicity induced by 5-FU and docetaxel was significantly enhanced. Fluorouracil 72-76 TAO kinase 2 Homo sapiens 110-113 20037295-6 2009 In addition, when cells were incubated with different concentrations of 5-FU and docetaxel in the presence of PSK at the dose of 5 microg/mL showing no growth suppression, cytotoxicity induced by 5-FU and docetaxel was significantly enhanced. Fluorouracil 196-200 TAO kinase 2 Homo sapiens 110-113 20037295-7 2009 These results indicate that PSK not only shows tumor growth suppression by apoptosis induction, but also enhances 5-FU and docetaxel-induced cytotoxicity. Fluorouracil 114-118 TAO kinase 2 Homo sapiens 28-31 20037380-0 2009 [Expression of dihydropyrimidine dehydrogenase in primary colorectal cancer and liver metastasis--a relationship between mRNA levels in cancer cells and protein levels in cancerous tissue and effect of 5-fluorouracil]. Fluorouracil 202-216 dihydropyrimidine dehydrogenase Homo sapiens 15-46 19816189-8 2009 Gemcitabine with 5-fluorouracil or oxaliplatin, but not alone, increased IL-18 and free IL-18 levels statistically significantly, without affecting IL-18BPa. Fluorouracil 17-31 interleukin 18 Homo sapiens 73-78 19816189-8 2009 Gemcitabine with 5-fluorouracil or oxaliplatin, but not alone, increased IL-18 and free IL-18 levels statistically significantly, without affecting IL-18BPa. Fluorouracil 17-31 interleukin 18 Homo sapiens 88-93 19465420-1 2009 BACKGROUND: Methylenetetrahydrofolate reductase is a pivotal enzyme in folate metabolism and 5-fluorouracil (5-FU) cytotoxicity. Fluorouracil 109-113 methylenetetrahydrofolate reductase Homo sapiens 12-47 19796232-9 2009 However, when soluble VEGFR-1, a decoy receptor for VEGF-A and PlGF, was injected after 5-FU, both angiogenic remodeling and regeneration of megakaryopoiesis were delayed. Fluorouracil 88-92 FMS-like tyrosine kinase 1 Mus musculus 22-29 19575748-10 2009 Moreover, 5-fluorouracil combined with 2-OX significantly inhibited tumor growth in this model, which was accompanied by reduction of Vegf gene expression and inhibited angiogenesis in tumor tissues. Fluorouracil 10-24 vascular endothelial growth factor A Mus musculus 134-138 19464156-9 2009 Recent studies revealed an increased locoregional control and a slight toxicity when radiotherapy was given concurrently with cyclophosphamide, mitoxantrone and fluorouracil (CNF). Fluorouracil 161-173 NPHS1 adhesion molecule, nephrin Homo sapiens 175-178 19671192-4 2009 RESULTS: The expression of CXCR4 was examined using 3 different chemotherapeutic agents; 5-fluorouracil, cisplatin, and vesnarinone (3,4-dihydro-6-[4-(3,4-dimethoxybenzoyl)-1-piperazinyl]-2-(1H)-quinolinone) in B88, a line of oral cancer cells that exhibits high levels of CXCR4 and lymph node metastatic potential. Fluorouracil 89-103 C-X-C motif chemokine receptor 4 Homo sapiens 27-32 19661321-3 2009 It was demonstrated that elevated dihydropyrimidine dehydrogenase (DPD) and COX-2 activities influence the response to 5-fluorouracil (5-FU). Fluorouracil 119-133 dihydropyrimidine dehydrogenase Homo sapiens 34-65 19661321-3 2009 It was demonstrated that elevated dihydropyrimidine dehydrogenase (DPD) and COX-2 activities influence the response to 5-fluorouracil (5-FU). Fluorouracil 119-133 dihydropyrimidine dehydrogenase Homo sapiens 67-70 19661321-3 2009 It was demonstrated that elevated dihydropyrimidine dehydrogenase (DPD) and COX-2 activities influence the response to 5-fluorouracil (5-FU). Fluorouracil 135-139 dihydropyrimidine dehydrogenase Homo sapiens 34-65 19661321-3 2009 It was demonstrated that elevated dihydropyrimidine dehydrogenase (DPD) and COX-2 activities influence the response to 5-fluorouracil (5-FU). Fluorouracil 135-139 dihydropyrimidine dehydrogenase Homo sapiens 67-70 19663673-1 2009 AIMS: Pharmacogenetic studies investigating the relationship between MTHFR gene polymorphisms and response to fluorouracil-based chemotherapy in patients with colorectal cancer have produced inconclusive results. Fluorouracil 110-122 methylenetetrahydrofolate reductase Homo sapiens 69-74 19604090-1 2009 AIMS: S-1, an oral fluoropyrimidine, contains tegafur, which is converted to 5-fluorouracil mainly by CYP2A6. Fluorouracil 77-91 cytochrome P450 family 2 subfamily A member 6 Homo sapiens 102-108 19530960-1 2009 AIMS: The importance of polymorphisms in the dihydropyrimidine dehydrogenase gene (DPYD) for the prediction of severe toxicity in 5-fluorouracil (5-FU)-based chemotherapy is still unclear. Fluorouracil 130-144 dihydropyrimidine dehydrogenase Homo sapiens 45-76 19530960-1 2009 AIMS: The importance of polymorphisms in the dihydropyrimidine dehydrogenase gene (DPYD) for the prediction of severe toxicity in 5-fluorouracil (5-FU)-based chemotherapy is still unclear. Fluorouracil 130-144 dihydropyrimidine dehydrogenase Homo sapiens 83-87 19530960-1 2009 AIMS: The importance of polymorphisms in the dihydropyrimidine dehydrogenase gene (DPYD) for the prediction of severe toxicity in 5-fluorouracil (5-FU)-based chemotherapy is still unclear. Fluorouracil 146-150 dihydropyrimidine dehydrogenase Homo sapiens 45-76 19530960-1 2009 AIMS: The importance of polymorphisms in the dihydropyrimidine dehydrogenase gene (DPYD) for the prediction of severe toxicity in 5-fluorouracil (5-FU)-based chemotherapy is still unclear. Fluorouracil 146-150 dihydropyrimidine dehydrogenase Homo sapiens 83-87 19530960-2 2009 This study aims to assess the predictive value of DPYD variation with respect to previously described DPYD variants for 5-FU toxicity. Fluorouracil 120-124 dihydropyrimidine dehydrogenase Homo sapiens 50-54 19252138-6 2009 More modest enhancement of platelet recovery after 5-fluorouracil or bone marrow transplantation was also evident in p300(Plt6/+) animals. Fluorouracil 51-65 E1A binding protein p300 Mus musculus 117-121 19401692-1 2009 Type I IFN receptor type 2 (IFNAR2) expression correlates significantly with clinical response to interferon (IFN)-alpha/5-fluorouracil (5-FU) combination therapy for hepatocellular carcinoma (HCC). Fluorouracil 121-135 interferon alpha and beta receptor subunit 2 Homo sapiens 28-34 19401692-1 2009 Type I IFN receptor type 2 (IFNAR2) expression correlates significantly with clinical response to interferon (IFN)-alpha/5-fluorouracil (5-FU) combination therapy for hepatocellular carcinoma (HCC). Fluorouracil 137-141 interferon alpha and beta receptor subunit 2 Homo sapiens 28-34 19101922-1 2009 Main inborn errors of metabolism diagnosable through uracil (Ura) analysis and the therapeutic monitoring of toxic 5-fluorouracil (5FU) in dihydro pyrimidine dehydrogenase (DPD) deficient patients require a sensitive, reproducible, selective and accurate method. Fluorouracil 115-129 dihydropyrimidine dehydrogenase Homo sapiens 173-176 19101922-1 2009 Main inborn errors of metabolism diagnosable through uracil (Ura) analysis and the therapeutic monitoring of toxic 5-fluorouracil (5FU) in dihydro pyrimidine dehydrogenase (DPD) deficient patients require a sensitive, reproducible, selective and accurate method. Fluorouracil 131-134 dihydropyrimidine dehydrogenase Homo sapiens 173-176 19270508-0 2009 Modulation of thymidilate synthase and p53 expression by HDAC inhibitor vorinostat resulted in synergistic antitumor effect in combination with 5FU or raltitrexed. Fluorouracil 144-147 histone deacetylase 9 Homo sapiens 57-61 19402749-4 2009 Using genetic and biochemical tools, we found that inactivation of TDG significantly increases resistance of both mouse and human cancer cells towards 5-FU. Fluorouracil 151-155 thymine DNA glycosylase Mus musculus 67-70 19212321-9 2009 Although dormant HSCs are resistant to the anti-proliferative chemotherapeutic agent 5-fluoro-uracil, HSCs pre-treated (primed) with IFNalpha and thus induced to proliferate are efficiently eliminated by 5-fluoro-uracil exposure in vivo. Fluorouracil 204-219 interferon alpha Mus musculus 133-141 19414338-6 2009 Moreover, the combination of 5-FU and 5-chloro-2,4-dihydroxypyrimidine significantly enhanced 5-FU sensitivity in BUC, particularly in cases showing higher DPD activity. Fluorouracil 29-33 dihydropyrimidine dehydrogenase Homo sapiens 156-159 19414338-6 2009 Moreover, the combination of 5-FU and 5-chloro-2,4-dihydroxypyrimidine significantly enhanced 5-FU sensitivity in BUC, particularly in cases showing higher DPD activity. Fluorouracil 94-98 dihydropyrimidine dehydrogenase Homo sapiens 156-159 19176868-4 2009 The aim of this study was to investigate changes in mucin secretion and microflora following treatment with 5-FU. Fluorouracil 108-112 solute carrier family 13 member 2 Rattus norvegicus 52-57 19176868-23 2009 In conclusion, 5-FU treatment causes significant changes in intestinal flora and mucin secretion in rats. Fluorouracil 15-19 solute carrier family 13 member 2 Rattus norvegicus 81-86 19381049-1 2009 Individual differences in 5-FU metabolism are mainly attributed to individual differences in the activity of DPD, an enzyme that can metabolize more than 85% of 5-FU. Fluorouracil 26-30 dihydropyrimidine dehydrogenase Homo sapiens 109-112 19381049-1 2009 Individual differences in 5-FU metabolism are mainly attributed to individual differences in the activity of DPD, an enzyme that can metabolize more than 85% of 5-FU. Fluorouracil 161-165 dihydropyrimidine dehydrogenase Homo sapiens 109-112 19052026-6 2009 RESULTS: Of the six 5-FU-related enzymes, the numbers of patients with expression of dUTPase (54% versus 15%; p = 0.005), TK (26% versus 0%; p = 0.019) and DPD (17% versus 45%; p = 0.033) were significantly different in those with primary tumours with metastasis compared with those with non-metastasis, respectively. Fluorouracil 20-24 Deoxyuridine triphosphatase Drosophila melanogaster 85-92 19052026-6 2009 RESULTS: Of the six 5-FU-related enzymes, the numbers of patients with expression of dUTPase (54% versus 15%; p = 0.005), TK (26% versus 0%; p = 0.019) and DPD (17% versus 45%; p = 0.033) were significantly different in those with primary tumours with metastasis compared with those with non-metastasis, respectively. Fluorouracil 20-24 dihydropyrimidine dehydrogenase Homo sapiens 156-159 19052026-9 2009 CONCLUSIONS: From this comparative study of the six 5-FU-related enzymes in colorectal cancer, the expression of dUTPase was most significantly different between primary tumours and their corresponding metastatic tumour. Fluorouracil 52-56 Deoxyuridine triphosphatase Drosophila melanogaster 113-120 19180589-1 2009 BACKGROUND: DPD and TS expression have been shown to correlate with response of 5-FU based chemotherapy in colorectal cancer tissue. Fluorouracil 80-84 dihydropyrimidine dehydrogenase Homo sapiens 12-15 18553083-7 2009 The PKR inhibitor potentiated the cytotoxicity of both 5-fluorouracil and gemcitabine to MAC16 cells in vitro. Fluorouracil 55-69 eukaryotic translation initiation factor 2-alpha kinase 2 Mus musculus 4-7 19051292-10 2009 Gene panels assessing pretreatment TP, DPD, ERCC1, dihydrofolate reductase and thymidylate synthase gene expression may help improve the therapeutic potential of 5-FU- or other novel antifolate-based regimens. Fluorouracil 162-166 dihydropyrimidine dehydrogenase Homo sapiens 39-42 18986760-0 2009 Combined evaluation of dihydropyrimidine dehydrogenase and thymidine phosphorylate mRNA levels in tumor predicts the histopathological effect of 5-fluorouracil-based chemoradiotherapy. Fluorouracil 145-159 dihydropyrimidine dehydrogenase Homo sapiens 23-54 18986760-3 2009 In this study, we determined the expression levels of 5-FU metabolism-related enzymes like thymidylate synthase (TS), dihydropyrimidine dehydrogenase (DPD), thymidine phosphorylate (TP) and orotate phosphoribosyl transferase (OPRT) using reverse transcription-polymerase chain reaction (RT-PCR) combined with laser capture microdissection (LCM). Fluorouracil 54-58 dihydropyrimidine dehydrogenase Homo sapiens 118-149 18986760-3 2009 In this study, we determined the expression levels of 5-FU metabolism-related enzymes like thymidylate synthase (TS), dihydropyrimidine dehydrogenase (DPD), thymidine phosphorylate (TP) and orotate phosphoribosyl transferase (OPRT) using reverse transcription-polymerase chain reaction (RT-PCR) combined with laser capture microdissection (LCM). Fluorouracil 54-58 dihydropyrimidine dehydrogenase Homo sapiens 151-154 18986760-8 2009 Our results suggest that the combined evaluation of TP and DPD mRNA expression in tumor cells using LCM and RT-PCR may be a useful predictor of the efficacy of 5-FU-based chemotherapy combined with radiotherapy in patients with OSCC. Fluorouracil 160-164 dihydropyrimidine dehydrogenase Homo sapiens 59-62 19155291-1 2009 The major determinants of 5-flurouracil (5-FU) response would seem, based on accumulated literature, to be thymidylate synthase (TYMS, TS) expression levels, TS gene modifications, and TP53 status. Fluorouracil 41-45 thymidylate synthase Saccharomyces cerevisiae S288C 107-127 19155291-1 2009 The major determinants of 5-flurouracil (5-FU) response would seem, based on accumulated literature, to be thymidylate synthase (TYMS, TS) expression levels, TS gene modifications, and TP53 status. Fluorouracil 41-45 thymidylate synthase Saccharomyces cerevisiae S288C 129-133 19155291-8 2009 Additionally, a TS (CDC21) knockout yeast strain, obviating any potential role for TS protein as a target, was hypersensitive to 5-FU. Fluorouracil 129-133 thymidylate synthase Saccharomyces cerevisiae S288C 20-25 19309276-1 2009 AIMS: The purpose of this study was to investigate the association of methylation in the promoter regions of adenomatous polyposis coli (APC) and O(6)-methylguanine-DNA methyltransferase (MGMT) and the survival of Taiwanese colorectal cancer (CRC) subjects who received 5-fluorouracil (5-FU) adjuvant chemotherapy. Fluorouracil 270-284 O-6-methylguanine-DNA methyltransferase Homo sapiens 146-186 19309276-1 2009 AIMS: The purpose of this study was to investigate the association of methylation in the promoter regions of adenomatous polyposis coli (APC) and O(6)-methylguanine-DNA methyltransferase (MGMT) and the survival of Taiwanese colorectal cancer (CRC) subjects who received 5-fluorouracil (5-FU) adjuvant chemotherapy. Fluorouracil 270-284 O-6-methylguanine-DNA methyltransferase Homo sapiens 188-192 19309276-1 2009 AIMS: The purpose of this study was to investigate the association of methylation in the promoter regions of adenomatous polyposis coli (APC) and O(6)-methylguanine-DNA methyltransferase (MGMT) and the survival of Taiwanese colorectal cancer (CRC) subjects who received 5-fluorouracil (5-FU) adjuvant chemotherapy. Fluorouracil 286-290 O-6-methylguanine-DNA methyltransferase Homo sapiens 146-186 19309276-1 2009 AIMS: The purpose of this study was to investigate the association of methylation in the promoter regions of adenomatous polyposis coli (APC) and O(6)-methylguanine-DNA methyltransferase (MGMT) and the survival of Taiwanese colorectal cancer (CRC) subjects who received 5-fluorouracil (5-FU) adjuvant chemotherapy. Fluorouracil 286-290 O-6-methylguanine-DNA methyltransferase Homo sapiens 188-192 17350823-1 2007 Dihydropyrimidine dehydrogenase (DPD) is a key enzyme in the metabolic catabolism of chemotherapeutic agent 5-fluorouracil (5FU) and its derivatives, including capecitabine. Fluorouracil 124-127 dihydropyrimidine dehydrogenase Homo sapiens 33-36 17350823-3 2007 Deficiencies in DPD activity have been shown to cause 5FU-treated cancer patients to experience severe drug-related toxicities, often requiring extensive medical intervention. Fluorouracil 54-57 dihydropyrimidine dehydrogenase Homo sapiens 16-19 17254767-0 2007 Changes to the dihydropyrimidine dehydrogenase gene copy number influence the susceptibility of cancers to 5-FU-based drugs: Data mining of the NCI-DTP data sets and validation with human tumour xenografts. Fluorouracil 107-111 dihydropyrimidine dehydrogenase Homo sapiens 15-46 17273745-0 2007 Combined analysis of genetic polymorphisms in thymidylate synthase, uridine diphosphate glucoronosyltransferase and X-ray cross complementing factor 1 genes as a prognostic factor in advanced colorectal cancer patients treated with 5-fluorouracil plus oxaliplatin or irinotecan. Fluorouracil 232-246 X-ray repair cross complementing 1 Homo sapiens 116-150 17273745-1 2007 The aim of this study was to investigate the influence of combining thymidylate synthase (TS), X-ray cross complementing factor 1 (XRCC1) and uridine diphosphate glucoronosyltransferase (UGT1A1 *28) polymorphism genotypes in response rate and time to progression (TTP) in metastatic colorectal cancer patients treated with 5-fluorouracil (5-FU) plus irinotecan or oxaliplatin (OXA). Fluorouracil 323-337 UDP glucuronosyltransferase family 1 member A1 Homo sapiens 187-193 17273745-1 2007 The aim of this study was to investigate the influence of combining thymidylate synthase (TS), X-ray cross complementing factor 1 (XRCC1) and uridine diphosphate glucoronosyltransferase (UGT1A1 *28) polymorphism genotypes in response rate and time to progression (TTP) in metastatic colorectal cancer patients treated with 5-fluorouracil (5-FU) plus irinotecan or oxaliplatin (OXA). Fluorouracil 339-343 UDP glucuronosyltransferase family 1 member A1 Homo sapiens 187-193 17273745-4 2007 In the OXA + 5-FU group, patients with the TS 5" single nucleotide polymorphism and/or XRCC1 genotypes favourable to treatment had a better TTP (log-rank p=0.02). Fluorouracil 13-17 X-ray repair cross complementing 1 Homo sapiens 87-92 16556484-7 2007 Deficiency in human DPD is associated with autosomal recessive disease, thymine-uraciluria, and with severe 5-fluorouracil toxicity in cancer patients. Fluorouracil 108-122 dihydropyrimidine dehydrogenase Homo sapiens 20-23 17159505-3 2007 Using the SNU-719 gastric cancer cell line, which is naturally infected with Epstein-Barr virus, we found that the chemotherapeutic agents, such as 5-fluorouracil, cis-platinum and taxol, induced the expressions of BMRF1, BZLF1 and BRLF1 proteins that are usually found in the lytic form of the virus. Fluorouracil 148-162 BRLF1 Human gammaherpesvirus 4 232-237 17828463-1 2007 Dihydropyrimidine dehydrogenase (DPD) is an inactivating and rate-limiting enzyme for 5-fluorouracil (5-FU), and its deficiency is associated with a risk for developing a severe or fatal toxicity to 5-FU. Fluorouracil 86-100 dihydropyrimidine dehydrogenase Homo sapiens 0-31 17828463-1 2007 Dihydropyrimidine dehydrogenase (DPD) is an inactivating and rate-limiting enzyme for 5-fluorouracil (5-FU), and its deficiency is associated with a risk for developing a severe or fatal toxicity to 5-FU. Fluorouracil 86-100 dihydropyrimidine dehydrogenase Homo sapiens 33-36 17828463-1 2007 Dihydropyrimidine dehydrogenase (DPD) is an inactivating and rate-limiting enzyme for 5-fluorouracil (5-FU), and its deficiency is associated with a risk for developing a severe or fatal toxicity to 5-FU. Fluorouracil 102-106 dihydropyrimidine dehydrogenase Homo sapiens 0-31 17828463-1 2007 Dihydropyrimidine dehydrogenase (DPD) is an inactivating and rate-limiting enzyme for 5-fluorouracil (5-FU), and its deficiency is associated with a risk for developing a severe or fatal toxicity to 5-FU. Fluorouracil 102-106 dihydropyrimidine dehydrogenase Homo sapiens 33-36 17828463-1 2007 Dihydropyrimidine dehydrogenase (DPD) is an inactivating and rate-limiting enzyme for 5-fluorouracil (5-FU), and its deficiency is associated with a risk for developing a severe or fatal toxicity to 5-FU. Fluorouracil 199-203 dihydropyrimidine dehydrogenase Homo sapiens 0-31 17828463-1 2007 Dihydropyrimidine dehydrogenase (DPD) is an inactivating and rate-limiting enzyme for 5-fluorouracil (5-FU), and its deficiency is associated with a risk for developing a severe or fatal toxicity to 5-FU. Fluorouracil 199-203 dihydropyrimidine dehydrogenase Homo sapiens 33-36 17660867-1 2007 The cytotoxic effect of 5-fluorouracil (5-FU) is mediated by the inhibition of thymidylate synthase (TS), however, at the same time 5-FU is catabolized by dihydropyrimidine dehydrogenase (DPD). Fluorouracil 40-44 dihydropyrimidine dehydrogenase Homo sapiens 155-186 17660867-1 2007 The cytotoxic effect of 5-fluorouracil (5-FU) is mediated by the inhibition of thymidylate synthase (TS), however, at the same time 5-FU is catabolized by dihydropyrimidine dehydrogenase (DPD). Fluorouracil 40-44 dihydropyrimidine dehydrogenase Homo sapiens 188-191 17660867-1 2007 The cytotoxic effect of 5-fluorouracil (5-FU) is mediated by the inhibition of thymidylate synthase (TS), however, at the same time 5-FU is catabolized by dihydropyrimidine dehydrogenase (DPD). Fluorouracil 132-136 dihydropyrimidine dehydrogenase Homo sapiens 155-186 17660867-1 2007 The cytotoxic effect of 5-fluorouracil (5-FU) is mediated by the inhibition of thymidylate synthase (TS), however, at the same time 5-FU is catabolized by dihydropyrimidine dehydrogenase (DPD). Fluorouracil 132-136 dihydropyrimidine dehydrogenase Homo sapiens 188-191 17660867-2 2007 Efficacy of 5-FU may therefore depend on the TS and DPD activity and on pharmacogenetic factors influencing these enzymes. Fluorouracil 12-16 dihydropyrimidine dehydrogenase Homo sapiens 52-55 17660867-15 2007 The determination of DPD activity proved to be a more valuable parameter in the evaluation of serious 5-FU-related toxicity compared to the IVS14+1G>A mutation analysis. Fluorouracil 102-106 dihydropyrimidine dehydrogenase Homo sapiens 21-24 17660867-16 2007 According to the Cox multivariate analysis the combination of germline TS polymorphisms and DPD activity is/an independent prognostic marker of survival in CRC patients treated with adjuvant 5-FU therapy. Fluorouracil 191-195 dihydropyrimidine dehydrogenase Homo sapiens 92-95 17848752-0 2007 DPYD*5 gene mutation contributes to the reduced DPYD enzyme activity and chemotherapeutic toxicity of 5-FU: results from genotyping study on 75 gastric carcinoma and colon carcinoma patients. Fluorouracil 102-106 dihydropyrimidine dehydrogenase Homo sapiens 0-4 17848752-1 2007 BACKGROUND: Dihydropyrimidine dehydrogenase (DPYD) plays an important role in the metabolism of 5-FU, which can directly influence the pharmacokinetics and toxicity of 5-FU in patients undergoing chemotherapy. Fluorouracil 96-100 dihydropyrimidine dehydrogenase Homo sapiens 12-43 17848752-1 2007 BACKGROUND: Dihydropyrimidine dehydrogenase (DPYD) plays an important role in the metabolism of 5-FU, which can directly influence the pharmacokinetics and toxicity of 5-FU in patients undergoing chemotherapy. Fluorouracil 96-100 dihydropyrimidine dehydrogenase Homo sapiens 45-49 17848752-1 2007 BACKGROUND: Dihydropyrimidine dehydrogenase (DPYD) plays an important role in the metabolism of 5-FU, which can directly influence the pharmacokinetics and toxicity of 5-FU in patients undergoing chemotherapy. Fluorouracil 168-172 dihydropyrimidine dehydrogenase Homo sapiens 12-43 17848752-1 2007 BACKGROUND: Dihydropyrimidine dehydrogenase (DPYD) plays an important role in the metabolism of 5-FU, which can directly influence the pharmacokinetics and toxicity of 5-FU in patients undergoing chemotherapy. Fluorouracil 168-172 dihydropyrimidine dehydrogenase Homo sapiens 45-49 17237272-0 2007 MRP8/ABCC11 directly confers resistance to 5-fluorouracil. Fluorouracil 43-57 ATP binding cassette subfamily C member 11 Homo sapiens 0-4 17237272-0 2007 MRP8/ABCC11 directly confers resistance to 5-fluorouracil. Fluorouracil 43-57 ATP binding cassette subfamily C member 11 Homo sapiens 5-11 17237272-4 2007 These findings suggest that ABCC11 confers 5-FU resistance in the sublines by enhancing the efflux for the active metabolite FdUMP. Fluorouracil 43-47 ATP binding cassette subfamily C member 11 Homo sapiens 28-34 17237272-6 2007 To confirm our hypothesis, we examined whether decreasing the expression of ABCC11 in PC-6/FU23-26 cells by small interfering RNA altered the cytotoxicity to 5-FU and methotrexate and found that this enhanced 5-FU and methotrexate cytotoxicity in PC-6/FU23-26 cells. Fluorouracil 158-162 ATP binding cassette subfamily C member 11 Homo sapiens 76-82 17237272-6 2007 To confirm our hypothesis, we examined whether decreasing the expression of ABCC11 in PC-6/FU23-26 cells by small interfering RNA altered the cytotoxicity to 5-FU and methotrexate and found that this enhanced 5-FU and methotrexate cytotoxicity in PC-6/FU23-26 cells. Fluorouracil 209-213 ATP binding cassette subfamily C member 11 Homo sapiens 76-82 17237272-7 2007 These data indicate that expression of the ABCC11 gene is induced by 5-FU, and that ABCC11 is directly involved in 5-FU resistance by the efflux transport of the active metabolite FdUMP. Fluorouracil 69-73 ATP binding cassette subfamily C member 11 Homo sapiens 43-49 17237272-7 2007 These data indicate that expression of the ABCC11 gene is induced by 5-FU, and that ABCC11 is directly involved in 5-FU resistance by the efflux transport of the active metabolite FdUMP. Fluorouracil 69-73 ATP binding cassette subfamily C member 11 Homo sapiens 84-90 17237272-7 2007 These data indicate that expression of the ABCC11 gene is induced by 5-FU, and that ABCC11 is directly involved in 5-FU resistance by the efflux transport of the active metabolite FdUMP. Fluorouracil 115-119 ATP binding cassette subfamily C member 11 Homo sapiens 43-49 17237272-7 2007 These data indicate that expression of the ABCC11 gene is induced by 5-FU, and that ABCC11 is directly involved in 5-FU resistance by the efflux transport of the active metabolite FdUMP. Fluorouracil 115-119 ATP binding cassette subfamily C member 11 Homo sapiens 84-90 17397246-0 2007 Rapid detection of the DPYD IVS14+1G>A mutation for screening patients to prevent fluorouracil-related toxicity. Fluorouracil 85-97 dihydropyrimidine dehydrogenase Homo sapiens 23-27 17397246-1 2007 BACKGROUND: Deficiency of dihydropyrimidine dehydrogenase (DPD) has been linked to severe or lethal fluorouracil (FU)-related toxicity. Fluorouracil 100-112 dihydropyrimidine dehydrogenase Homo sapiens 59-62 17963423-0 2007 Rapid detection of the DPYD IVS14+1G>A mutation for screening patients to prevent fluorouracil-related toxicity. Fluorouracil 85-97 dihydropyrimidine dehydrogenase Homo sapiens 23-27 17143493-9 2007 The DPD activity increased by UFT can be inhibited by CPA, and this may represent one of the possible mechanisms responsible for the anti-tumor activity of 5-FU or its derivatives as enhanced by CPA. Fluorouracil 156-160 dihydropyrimidine dehydrogenase Homo sapiens 4-7 17089033-2 2006 Dihydropyrimidine dehydrogenase (DPD) is known to catabolize 5-FU, which is widely used in chemotherapeutic treatments for patients with a variety of malignant tumors including gastric and colorectal cancer. Fluorouracil 61-65 dihydropyrimidine dehydrogenase Homo sapiens 0-31 17089033-2 2006 Dihydropyrimidine dehydrogenase (DPD) is known to catabolize 5-FU, which is widely used in chemotherapeutic treatments for patients with a variety of malignant tumors including gastric and colorectal cancer. Fluorouracil 61-65 dihydropyrimidine dehydrogenase Homo sapiens 33-36 17089033-10 2006 However, among the patients who had received such treatment with 5-FU or its derivatives, the prognosis in cases with low DPD levels was better than that in cases with high DPD expression by immunohistochemical analysis. Fluorouracil 65-69 dihydropyrimidine dehydrogenase Homo sapiens 122-125 17089033-10 2006 However, among the patients who had received such treatment with 5-FU or its derivatives, the prognosis in cases with low DPD levels was better than that in cases with high DPD expression by immunohistochemical analysis. Fluorouracil 65-69 dihydropyrimidine dehydrogenase Homo sapiens 173-176 17015056-1 2006 BACKGROUND AND OBJECTIVES: Dihydropyrimidine dehydrogenase (DPD) plays a key role in the catabolism of 5-fluorouracil (5-FU) to 5-fluoro-5,6-dihydrouracil (5-FDHU), and as such, an impairment of DPD has been recognized as an important factor for altered 5-FU and 5-FDHU pharmacokinetics, predisposing patients to the development of severe 5-FU-associated toxicity. Fluorouracil 254-258 dihydropyrimidine dehydrogenase Homo sapiens 27-58 17015056-1 2006 BACKGROUND AND OBJECTIVES: Dihydropyrimidine dehydrogenase (DPD) plays a key role in the catabolism of 5-fluorouracil (5-FU) to 5-fluoro-5,6-dihydrouracil (5-FDHU), and as such, an impairment of DPD has been recognized as an important factor for altered 5-FU and 5-FDHU pharmacokinetics, predisposing patients to the development of severe 5-FU-associated toxicity. Fluorouracil 254-258 dihydropyrimidine dehydrogenase Homo sapiens 60-63 17015056-1 2006 BACKGROUND AND OBJECTIVES: Dihydropyrimidine dehydrogenase (DPD) plays a key role in the catabolism of 5-fluorouracil (5-FU) to 5-fluoro-5,6-dihydrouracil (5-FDHU), and as such, an impairment of DPD has been recognized as an important factor for altered 5-FU and 5-FDHU pharmacokinetics, predisposing patients to the development of severe 5-FU-associated toxicity. Fluorouracil 254-258 dihydropyrimidine dehydrogenase Homo sapiens 195-198 17015056-1 2006 BACKGROUND AND OBJECTIVES: Dihydropyrimidine dehydrogenase (DPD) plays a key role in the catabolism of 5-fluorouracil (5-FU) to 5-fluoro-5,6-dihydrouracil (5-FDHU), and as such, an impairment of DPD has been recognized as an important factor for altered 5-FU and 5-FDHU pharmacokinetics, predisposing patients to the development of severe 5-FU-associated toxicity. Fluorouracil 254-258 dihydropyrimidine dehydrogenase Homo sapiens 27-58 17015056-1 2006 BACKGROUND AND OBJECTIVES: Dihydropyrimidine dehydrogenase (DPD) plays a key role in the catabolism of 5-fluorouracil (5-FU) to 5-fluoro-5,6-dihydrouracil (5-FDHU), and as such, an impairment of DPD has been recognized as an important factor for altered 5-FU and 5-FDHU pharmacokinetics, predisposing patients to the development of severe 5-FU-associated toxicity. Fluorouracil 254-258 dihydropyrimidine dehydrogenase Homo sapiens 60-63 17015056-1 2006 BACKGROUND AND OBJECTIVES: Dihydropyrimidine dehydrogenase (DPD) plays a key role in the catabolism of 5-fluorouracil (5-FU) to 5-fluoro-5,6-dihydrouracil (5-FDHU), and as such, an impairment of DPD has been recognized as an important factor for altered 5-FU and 5-FDHU pharmacokinetics, predisposing patients to the development of severe 5-FU-associated toxicity. Fluorouracil 254-258 dihydropyrimidine dehydrogenase Homo sapiens 195-198 17038885-2 2006 The aim of this study was to validate, in a routine clinical setting, a simple and rapid method to determine the DPD status in a subset of cancer patients, all presenting with life-threatening toxicities following 5-FU or capecitabine intake. Fluorouracil 214-218 dihydropyrimidine dehydrogenase Homo sapiens 113-116 16421754-2 2006 PATIENTS AND METHODS: We describe an Indian patient who presented to clinic for the treatment of gastric adenocarcinoma with 5-flurouracil (5-FU) therapy who subsequently was diagnosed with DPD deficiency by using the peripheral blood mononuclear cell (PBMC) DPD radioassay. Fluorouracil 140-144 dihydropyrimidine dehydrogenase Homo sapiens 190-193 16865249-8 2006 Our data suggest that GSTT1-null is associated with a greater probability of developing toxicity to 5-Fu/CPT-11/Lv treatments, indicating a potential application of this genetic analysis in predicting adverse effects of this regimen. Fluorouracil 100-104 glutathione S-transferase theta 1 Homo sapiens 22-27 16965690-2 2006 Dihydropyrimidine dehydrogenase (DPD) is the key rate-limiting enzymes which is closely related to toxicities of 5-FU in chemotherapy. Fluorouracil 113-117 dihydropyrimidine dehydrogenase Homo sapiens 0-31 16965690-2 2006 Dihydropyrimidine dehydrogenase (DPD) is the key rate-limiting enzymes which is closely related to toxicities of 5-FU in chemotherapy. Fluorouracil 113-117 dihydropyrimidine dehydrogenase Homo sapiens 33-36 16965690-3 2006 This study was to explore the relationship between activity of DPD and concentration of 5-FU, and their correlation to adverse events among advanced gastric cancer patients treated with the same regimen containing 5-FU continuous infusion. Fluorouracil 88-92 dihydropyrimidine dehydrogenase Homo sapiens 63-66 16965690-3 2006 This study was to explore the relationship between activity of DPD and concentration of 5-FU, and their correlation to adverse events among advanced gastric cancer patients treated with the same regimen containing 5-FU continuous infusion. Fluorouracil 214-218 dihydropyrimidine dehydrogenase Homo sapiens 63-66 16965690-11 2006 The DPD activity was inversely correlated with 5-FU concentration (r=-0.376, P=0.024). Fluorouracil 47-51 dihydropyrimidine dehydrogenase Homo sapiens 4-7 16855390-1 2006 5-fluorouracil forms classic (covalent, ternary) complexes consisting of thymidylate synthase, fluoro-deoxyuridine monophosphate, and 5,10-methylene tetrahydrofolate. Fluorouracil 0-14 thymidylate synthase Mus musculus 73-93 16855390-3 2006 We visualized classic complexes unaccompanied by unbound thymidylate synthase, inferring complete enzymatic inhibition, in 5-fluorouracil-treated S. cerevisiae and cancer cells in vitro and in murine tumors in vivo treated with 5-fluorouracil. Fluorouracil 123-137 thymidylate synthase Saccharomyces cerevisiae S288C 57-77 16572420-1 2006 Gene expression levels of thymidylate synthase (TS), dihydropyrimidine dehydrogenase (DPD), thymidine phosphorylase (TP) and orotate phosphoribosyl transferase (OPRT) have been shown to be associated with response to 5-fluorouracil-based therapies. Fluorouracil 217-231 dihydropyrimidine dehydrogenase Homo sapiens 53-84 16820916-6 2006 There was a strong correlation between 5-FU and CDHP concentrations in peritoneal tissues. Fluorouracil 39-43 cadherin 3 Homo sapiens 48-52 16477629-3 2006 In this study, the mRNA expression levels of these 81 selected genes and the genes of 5-FU-related enzymes, including thymidylate synthase (TS), dihydropyrimidine dehydrogenase (DPD) and orotate phosphoribosyltransferase (OPRT), were measured using real-time quantitative RT-PCR assays of surgically resected materials from primary colorectal tumors in 22 patients. Fluorouracil 86-90 dihydropyrimidine dehydrogenase Homo sapiens 145-176 16477629-3 2006 In this study, the mRNA expression levels of these 81 selected genes and the genes of 5-FU-related enzymes, including thymidylate synthase (TS), dihydropyrimidine dehydrogenase (DPD) and orotate phosphoribosyltransferase (OPRT), were measured using real-time quantitative RT-PCR assays of surgically resected materials from primary colorectal tumors in 22 patients. Fluorouracil 86-90 dihydropyrimidine dehydrogenase Homo sapiens 178-181 16477629-5 2006 Four genes (TNFRSF1B, SLC35F5, NAG-1 and OPRT) had significantly different expression profiles in 5-FU-nonresponding and responding tumors (p < 0.05). Fluorouracil 98-102 TNF receptor superfamily member 1B Homo sapiens 12-20 16477629-5 2006 Four genes (TNFRSF1B, SLC35F5, NAG-1 and OPRT) had significantly different expression profiles in 5-FU-nonresponding and responding tumors (p < 0.05). Fluorouracil 98-102 solute carrier family 35 member F5 Homo sapiens 22-29 16477629-5 2006 Four genes (TNFRSF1B, SLC35F5, NAG-1 and OPRT) had significantly different expression profiles in 5-FU-nonresponding and responding tumors (p < 0.05). Fluorouracil 98-102 growth differentiation factor 15 Homo sapiens 31-36 16477629-8 2006 Our "Response Index" system, consisting of TNFRSF1B, SLC35F5 and OPRT, has great potential for predicting the efficacy of 5-FU-based chemotherapy against liver metastases from colorectal cancer. Fluorouracil 122-126 solute carrier family 35 member F5 Homo sapiens 53-60 16187112-2 2006 Methylenetetrahydrofolate reductase (MTHFR) may play a central role in the action of 5-FU, an inhibitor of thymidylate synthase, by converting 5,10-methylenetetrahydrofolate to 5-methyltetrahydrofolate. Fluorouracil 85-89 methylenetetrahydrofolate reductase Homo sapiens 0-35 16187112-2 2006 Methylenetetrahydrofolate reductase (MTHFR) may play a central role in the action of 5-FU, an inhibitor of thymidylate synthase, by converting 5,10-methylenetetrahydrofolate to 5-methyltetrahydrofolate. Fluorouracil 85-89 methylenetetrahydrofolate reductase Homo sapiens 37-42 16897970-10 2006 The AUC0-10h of FBAL was markedly lower and plasma uracil concentrations were significantly higher for S-1 than for PVI of 5-FU, clearly demonstrating the effect of DPD inhibition. Fluorouracil 123-127 dihydropyrimidine dehydrogenase Homo sapiens 165-168 16897985-8 2006 It has a component that enhances the cytotoxic activity of tegafur by inhibiting dihydropyrimidine dehydrogenase (DPD) and also has a component that reduces phosphorylation of 5-fluorouracil in the gastrointestinal tract to potentially reduce toxicity. Fluorouracil 176-190 dihydropyrimidine dehydrogenase Homo sapiens 114-117 16897985-11 2006 The varying efficiency is thought to be due to the presence of certain polymorphisms in the CYP2A6 gene responsible for metabolizing tegafur to 5-fluorouracil. Fluorouracil 144-158 cytochrome P450 family 2 subfamily A member 6 Homo sapiens 92-98 16716109-4 2006 Sensitivity of cells to 5-FU can be further increased by expression of uracil phosphoribosyltransferase (UPRT), which catalyzes the conversion of 5-FU to 5-fluorouridine monophosphate. Fluorouracil 24-28 uracil phosphoribosyltransferase homolog Homo sapiens 71-103 16716109-4 2006 Sensitivity of cells to 5-FU can be further increased by expression of uracil phosphoribosyltransferase (UPRT), which catalyzes the conversion of 5-FU to 5-fluorouridine monophosphate. Fluorouracil 24-28 uracil phosphoribosyltransferase homolog Homo sapiens 105-109 16716109-4 2006 Sensitivity of cells to 5-FU can be further increased by expression of uracil phosphoribosyltransferase (UPRT), which catalyzes the conversion of 5-FU to 5-fluorouridine monophosphate. Fluorouracil 146-150 uracil phosphoribosyltransferase homolog Homo sapiens 71-103 16716109-4 2006 Sensitivity of cells to 5-FU can be further increased by expression of uracil phosphoribosyltransferase (UPRT), which catalyzes the conversion of 5-FU to 5-fluorouridine monophosphate. Fluorouracil 146-150 uracil phosphoribosyltransferase homolog Homo sapiens 105-109 16595493-12 2006 CONCLUSION: After DOX or 5FU therapy, the relationship between (3)H-FDG uptake and viable cell number can become disjointed, with transient declines in (3)H-FDG uptake in excess of the decline in cell number despite increased Glut-1 mRNA levels. Fluorouracil 25-28 solute carrier family 2 member 1 Homo sapiens 226-232 16397116-1 2006 Uridine phosphorylase (UPase) has been shown to play an important role in the antineoplastic activity of 5-fluorouracil (5-FU) and in the anabolism of its oral prodrug, capecitabine, through the conversion of 5"-deoxy-5-fluorouridine (5"-DFUR) into 5-FU. Fluorouracil 105-119 uridine phosphorylase 1 Mus musculus 23-28 16397116-1 2006 Uridine phosphorylase (UPase) has been shown to play an important role in the antineoplastic activity of 5-fluorouracil (5-FU) and in the anabolism of its oral prodrug, capecitabine, through the conversion of 5"-deoxy-5-fluorouridine (5"-DFUR) into 5-FU. Fluorouracil 121-125 uridine phosphorylase 1 Mus musculus 23-28 16397116-1 2006 Uridine phosphorylase (UPase) has been shown to play an important role in the antineoplastic activity of 5-fluorouracil (5-FU) and in the anabolism of its oral prodrug, capecitabine, through the conversion of 5"-deoxy-5-fluorouridine (5"-DFUR) into 5-FU. Fluorouracil 249-253 uridine phosphorylase 1 Mus musculus 23-28 16555161-10 2006 Expression of VEGF in liver metastases was clearly inhibited by YH-16 in combination with 5-FU or 5-FU alone compared to the control group, and MVD in middle-dose and high-dose YH-16 group, 5-FU group and combination group was lower than that in control group (P< 0.05). Fluorouracil 90-94 vascular endothelial growth factor A Mus musculus 14-18 16555161-10 2006 Expression of VEGF in liver metastases was clearly inhibited by YH-16 in combination with 5-FU or 5-FU alone compared to the control group, and MVD in middle-dose and high-dose YH-16 group, 5-FU group and combination group was lower than that in control group (P< 0.05). Fluorouracil 98-102 vascular endothelial growth factor A Mus musculus 14-18 16075279-9 2006 Western blotting showed that PXL exposure followed by 5-FU up-regulated Chk1 and Wee1 protein expressions until PXL removal and 5-FU exposure, when these expressions gradually decreased to their basal levels. Fluorouracil 54-58 WEE1 G2 checkpoint kinase Homo sapiens 81-85 16407331-3 2006 A yeast strain lacking the enzyme uracil DNA glycosylase (Ung1), which excises uracil from the DNA backbone leaving an abasic site, showed significant protection against the toxic effects of 5-FU, a G1/S cell cycle arrest phenotype, and accumulated massive amounts of U/A base pairs in its genome (approximately 4% of T/A pairs were now U/A). Fluorouracil 191-195 uracil-DNA glycosylase Saccharomyces cerevisiae S288C 34-56 16407331-3 2006 A yeast strain lacking the enzyme uracil DNA glycosylase (Ung1), which excises uracil from the DNA backbone leaving an abasic site, showed significant protection against the toxic effects of 5-FU, a G1/S cell cycle arrest phenotype, and accumulated massive amounts of U/A base pairs in its genome (approximately 4% of T/A pairs were now U/A). Fluorouracil 191-195 uracil-DNA glycosylase Saccharomyces cerevisiae S288C 58-62 17690560-1 2006 PURPOSE: We investigated whether a 5-fluorouracil (5-FU)-resistant tumor could regain chemosensitivity after the administration of 5-aza-2"-deoxycytidine (DAC) as a demethylating agent. Fluorouracil 35-49 dachshund family transcription factor 1 Mus musculus 155-158 17690560-1 2006 PURPOSE: We investigated whether a 5-fluorouracil (5-FU)-resistant tumor could regain chemosensitivity after the administration of 5-aza-2"-deoxycytidine (DAC) as a demethylating agent. Fluorouracil 51-55 dachshund family transcription factor 1 Mus musculus 155-158 17690560-10 2006 By pretreating with DAC at a nontoxic level, we confirmed the restoration of 5-FU chemosensitivity and apoptosis induction. Fluorouracil 77-81 dachshund family transcription factor 1 Mus musculus 20-23 16399440-4 2005 The preliminary finding that methylenetetrahydrofolate reductase polymorphisms modify 5-fluorouracil response supports the hypothesis that response or resistance to therapy in esophageal cancer patients may be modulated by genetic variants involved in the metabolism or mechanism of chemotherapy drug action. Fluorouracil 86-100 methylenetetrahydrofolate reductase Homo sapiens 29-64 16370225-3 2005 An emerging body of in vitro and clinical evidence suggests that these MTHFR SNPs may be an important pharmacogenetic determinant of predicting response to and toxicity of methotrexate and 5-fluorouracil-based cancer and anti-inflammatory treatments because of their well-defined and highly relevant biochemical effects on intracellular folate composition and one-carbon transfer reactions. Fluorouracil 189-203 methylenetetrahydrofolate reductase Homo sapiens 71-76 16160472-2 2005 Thymidylate synthase (TS), thymidine phosphorylase (TP), and dihydropyrimidine dehydrogenase (DPD) are known to be important biomarkers to predict tumor response to 5-FU-based therapy. Fluorouracil 165-169 dihydropyrimidine dehydrogenase Homo sapiens 61-92 16160472-2 2005 Thymidylate synthase (TS), thymidine phosphorylase (TP), and dihydropyrimidine dehydrogenase (DPD) are known to be important biomarkers to predict tumor response to 5-FU-based therapy. Fluorouracil 165-169 dihydropyrimidine dehydrogenase Homo sapiens 94-97 16162975-0 2005 SMS 201-995 enhances S-phase block induced by 5-fluorouracil in a human colorectal cancer cell line. Fluorouracil 46-60 spermine synthase Homo sapiens 0-3 16162975-5 2005 The most evident finding after the combination of SMS (0.2 microg/ml) and 5-FU (0.1 microg/ml) was a potentiation of 5-FU-induced S-phase block by a further 7.9, 12.9 and 42.1% at 24, 36 and 72 h, respectively. Fluorouracil 117-121 spermine synthase Homo sapiens 50-53 16162975-8 2005 The data emphasize that SMS exhibits pro-apoptotic and anti-proliferative effects, which in proper dose combinations might enhance the effects of 5-FU on human colorectal cancer cells expressing mp53. Fluorouracil 146-150 spermine synthase Homo sapiens 24-27 16315867-0 2005 [Radiation, 5-FU and OK-432: inhibitory effect of IL-10 and TGF-beta]. Fluorouracil 12-16 interleukin 10 Homo sapiens 50-55 16315867-3 2005 When the PBMCs were stimulated by 5-FU (5 microg/ml) or X-ray (2 Gy) simultaneously with OK-432, production of IL-10 and TGF-beta was significantly inhibited, while no significant change in Th1 cytokine production was observed. Fluorouracil 34-38 interleukin 10 Homo sapiens 111-116 16315867-3 2005 When the PBMCs were stimulated by 5-FU (5 microg/ml) or X-ray (2 Gy) simultaneously with OK-432, production of IL-10 and TGF-beta was significantly inhibited, while no significant change in Th1 cytokine production was observed. Fluorouracil 34-38 negative elongation factor complex member C/D Homo sapiens 190-193 16145066-1 2005 PURPOSE: The conversion rate of tegafur (a component of S-1) to fluorouracil (FU) differs in Asians and whites because of polymorphic differences in the CYP2A6 gene. Fluorouracil 64-76 cytochrome P450 family 2 subfamily A member 6 Homo sapiens 153-159 16101140-2 2005 PATIENTS AND METHODS: The impact of gemcitabine, irinotecan and oxaliplatin + 5-FU upon the serum markers vascular endothelial growth factor (VEGF) (pro-angiogenic) and IFN-gamma-inducible protein (IP)-10 (anti-angiogenic) was evaluated by ELISA in locally advanced and/or metastatic cancer versus clinical efficacy and survival. Fluorouracil 78-82 C-X-C motif chemokine ligand 10 Homo sapiens 169-204 16270533-2 2005 Metabolizing enzymes such as thymidylate synthase (TS) and dihydropyrimidine dehydrogenase (DPD) have long been known to be useful for predicting response and outcome in patients receiving 5-fluorouracil (5-FU). Fluorouracil 189-203 dihydropyrimidine dehydrogenase Homo sapiens 59-90 16270533-2 2005 Metabolizing enzymes such as thymidylate synthase (TS) and dihydropyrimidine dehydrogenase (DPD) have long been known to be useful for predicting response and outcome in patients receiving 5-fluorouracil (5-FU). Fluorouracil 189-203 dihydropyrimidine dehydrogenase Homo sapiens 92-95 16270533-2 2005 Metabolizing enzymes such as thymidylate synthase (TS) and dihydropyrimidine dehydrogenase (DPD) have long been known to be useful for predicting response and outcome in patients receiving 5-fluorouracil (5-FU). Fluorouracil 205-209 dihydropyrimidine dehydrogenase Homo sapiens 59-90 16270533-2 2005 Metabolizing enzymes such as thymidylate synthase (TS) and dihydropyrimidine dehydrogenase (DPD) have long been known to be useful for predicting response and outcome in patients receiving 5-fluorouracil (5-FU). Fluorouracil 205-209 dihydropyrimidine dehydrogenase Homo sapiens 92-95 15993511-0 2005 The role of thymidylate synthase and dihydropyrimidine dehydrogenase in resistance to 5-fluorouracil in human lung cancer cells. Fluorouracil 86-100 dihydropyrimidine dehydrogenase Homo sapiens 37-68 15993511-3 2005 The expression of DPD was significantly correlated with the concentration of 5-FU for 50% cell survival in 15 non-small-cell lung cancer (NSCLC) cell lines (p<0.05), but the expressions of TS, TP, and OPRT were not. Fluorouracil 77-81 dihydropyrimidine dehydrogenase Homo sapiens 18-21 15993511-4 2005 Treatment with 5-chloro-2,4-dihydroxypyridine, an inhibitor of DPD, altered the sensitivity to 5-FU in DPD-expressing RERF-LC-MT cells, indicating that modulation of DPD activity could increase the 5-FU sensitivity in lung cancer. Fluorouracil 95-99 dihydropyrimidine dehydrogenase Homo sapiens 63-66 15993511-4 2005 Treatment with 5-chloro-2,4-dihydroxypyridine, an inhibitor of DPD, altered the sensitivity to 5-FU in DPD-expressing RERF-LC-MT cells, indicating that modulation of DPD activity could increase the 5-FU sensitivity in lung cancer. Fluorouracil 95-99 dihydropyrimidine dehydrogenase Homo sapiens 103-106 15993511-4 2005 Treatment with 5-chloro-2,4-dihydroxypyridine, an inhibitor of DPD, altered the sensitivity to 5-FU in DPD-expressing RERF-LC-MT cells, indicating that modulation of DPD activity could increase the 5-FU sensitivity in lung cancer. Fluorouracil 95-99 dihydropyrimidine dehydrogenase Homo sapiens 103-106 15993511-4 2005 Treatment with 5-chloro-2,4-dihydroxypyridine, an inhibitor of DPD, altered the sensitivity to 5-FU in DPD-expressing RERF-LC-MT cells, indicating that modulation of DPD activity could increase the 5-FU sensitivity in lung cancer. Fluorouracil 198-202 dihydropyrimidine dehydrogenase Homo sapiens 103-106 15993511-4 2005 Treatment with 5-chloro-2,4-dihydroxypyridine, an inhibitor of DPD, altered the sensitivity to 5-FU in DPD-expressing RERF-LC-MT cells, indicating that modulation of DPD activity could increase the 5-FU sensitivity in lung cancer. Fluorouracil 198-202 dihydropyrimidine dehydrogenase Homo sapiens 103-106 15993511-7 2005 Our results indicate that degradation of 5-FU due to DPD is an important determinant in 5-FU sensitivity, while induction of TS contributes to acquired resistance against 5-FU in lung cancer. Fluorouracil 41-45 dihydropyrimidine dehydrogenase Homo sapiens 53-56 15996645-7 2005 Although the amount of Na(+)-dependent glucose co-transporter (SGLT1) in 5-FU-treated rats decreased, the overshoot magnitude of d-glucose uptake in BBMV was not altered. Fluorouracil 73-77 solute carrier family 5 member 1 Rattus norvegicus 63-68 15996645-11 2005 Because the amounts of SGLT1 in 5-FU-treated rats decreased, the increase of turnover rate of SGLT1 and/or an expression of unknown Na(+)-dependent glucose co-transporter with high affinity for d-glucose and phlorizin sensitivity would contribute to the enhancement of d-glucose transport in 5-FU-treated rats. Fluorouracil 32-36 solute carrier family 5 member 1 Rattus norvegicus 23-28 15996645-11 2005 Because the amounts of SGLT1 in 5-FU-treated rats decreased, the increase of turnover rate of SGLT1 and/or an expression of unknown Na(+)-dependent glucose co-transporter with high affinity for d-glucose and phlorizin sensitivity would contribute to the enhancement of d-glucose transport in 5-FU-treated rats. Fluorouracil 292-296 solute carrier family 5 member 1 Rattus norvegicus 23-28 16115930-0 2005 Analysis of the DPYD gene implicated in 5-fluorouracil catabolism in a cohort of Caucasian individuals. Fluorouracil 40-54 dihydropyrimidine dehydrogenase Homo sapiens 16-20 16080558-4 2005 RESULTS: The response rate was significantly higher in patients with DPD-positive tumors than in those with DPD-negative tumors in the S-1 group (45.5%, 10.0%: p < 0.05), as compared to the 5-FU group (0%, 5.6%: p = 0.398). Fluorouracil 193-197 dihydropyrimidine dehydrogenase Homo sapiens 69-72 15896711-8 2005 Under same conditions, the induction of Glut-1 by 5-FU was diminished by the combination treatment with 5-FU and genistein. Fluorouracil 50-54 solute carrier family 2 member 1 Homo sapiens 40-46 15896711-8 2005 Under same conditions, the induction of Glut-1 by 5-FU was diminished by the combination treatment with 5-FU and genistein. Fluorouracil 104-108 solute carrier family 2 member 1 Homo sapiens 40-46 15944938-1 2005 Thymidylate synthase (TS) is a major target of 5-fluorouracil (5-FU) and dihydropyrimidine dehydrogenase (DPD) is a rate-limiting enzyme in the degradation of 5-FU. Fluorouracil 47-61 dihydropyrimidine dehydrogenase Homo sapiens 106-109 15944938-1 2005 Thymidylate synthase (TS) is a major target of 5-fluorouracil (5-FU) and dihydropyrimidine dehydrogenase (DPD) is a rate-limiting enzyme in the degradation of 5-FU. Fluorouracil 159-163 dihydropyrimidine dehydrogenase Homo sapiens 73-104 15944938-1 2005 Thymidylate synthase (TS) is a major target of 5-fluorouracil (5-FU) and dihydropyrimidine dehydrogenase (DPD) is a rate-limiting enzyme in the degradation of 5-FU. Fluorouracil 159-163 dihydropyrimidine dehydrogenase Homo sapiens 106-109 15949589-3 2005 However, the significance of DPD expression in 5-FU based chemotherapy has not been well investigated in non-small cell lung cancer (NSCLC). Fluorouracil 47-51 dihydropyrimidine dehydrogenase Homo sapiens 29-32 15949589-7 2005 There was a reversal correlation between protein expression of DPD and sensitivity to 5-FU (r = -0.65; p < 0.001). Fluorouracil 86-90 dihydropyrimidine dehydrogenase Homo sapiens 63-66 15949589-8 2005 Six (33.3%) of 18 cases with strong expression of DPD showed 10% or more increment of the anti-tumor effect by adding CDHP to 5-FU. Fluorouracil 126-130 dihydropyrimidine dehydrogenase Homo sapiens 50-53 15772079-12 2005 These data indicate that UPase is a critical enzyme in the regulation of uridine homeostasis and pyrimidine nucleotide metabolism, and 5-fluorouracil activity. Fluorouracil 135-149 uridine phosphorylase 1 Mus musculus 25-30 15890242-0 2005 Thymidylate synthase and dihydropyrimidine dehydrogenase gene expression in breast cancer predicts 5-FU sensitivity by a histocultural drug sensitivity test. Fluorouracil 99-103 dihydropyrimidine dehydrogenase Homo sapiens 25-56 15890242-1 2005 Thymidylate synthase (TS), Dihydropyrimidine dehydrogenase (DPD) and Thymidine Phosphorylase (TP) gene expressions are reported to be predictive markers for 5-fluorouracil (5-FU) sensitivity in gastrointestinal cancer. Fluorouracil 157-171 dihydropyrimidine dehydrogenase Homo sapiens 27-58 15890242-1 2005 Thymidylate synthase (TS), Dihydropyrimidine dehydrogenase (DPD) and Thymidine Phosphorylase (TP) gene expressions are reported to be predictive markers for 5-fluorouracil (5-FU) sensitivity in gastrointestinal cancer. Fluorouracil 157-171 dihydropyrimidine dehydrogenase Homo sapiens 60-63 15890242-1 2005 Thymidylate synthase (TS), Dihydropyrimidine dehydrogenase (DPD) and Thymidine Phosphorylase (TP) gene expressions are reported to be predictive markers for 5-fluorouracil (5-FU) sensitivity in gastrointestinal cancer. Fluorouracil 173-177 dihydropyrimidine dehydrogenase Homo sapiens 27-58 15890242-1 2005 Thymidylate synthase (TS), Dihydropyrimidine dehydrogenase (DPD) and Thymidine Phosphorylase (TP) gene expressions are reported to be predictive markers for 5-fluorouracil (5-FU) sensitivity in gastrointestinal cancer. Fluorouracil 173-177 dihydropyrimidine dehydrogenase Homo sapiens 60-63 15890242-7 2005 The group of high TS and high DPD gene expression in Ca was resistant to 5-FU, and the group of low TS and low DPD gene expression in Ca was sensitive to 5-FU (P=0.048 chi-square test). Fluorouracil 73-77 dihydropyrimidine dehydrogenase Homo sapiens 30-33 15890242-7 2005 The group of high TS and high DPD gene expression in Ca was resistant to 5-FU, and the group of low TS and low DPD gene expression in Ca was sensitive to 5-FU (P=0.048 chi-square test). Fluorouracil 154-158 dihydropyrimidine dehydrogenase Homo sapiens 111-114 15890242-8 2005 TS and DPD mRNA expressions measured using LCM+RT-PCR might be useful predictive markers for 5-FU sensitivity in human breast cancer. Fluorouracil 93-97 dihydropyrimidine dehydrogenase Homo sapiens 7-10 15958060-6 2005 The protein expressions of TS, FPGS, and RFC1 were significantly associated with IC50 for 5-fluorouracil, but no such association was found for pemetrexed chemosensitivity. Fluorouracil 90-104 replication factor C subunit 1 Homo sapiens 41-45 15905808-0 2005 Improved analysis of 5-Fluorouracil and 5,6-dihydro-5-Fluorouracil by HPLC with diode array detection for determination of cellular dihydropyrimidine dehydrogenase activity and pharmacokinetic profiling. Fluorouracil 21-35 dihydropyrimidine dehydrogenase Homo sapiens 132-163 15905808-1 2005 Administration of 5-fluorouracil (5-FU) may be associated with severe toxicities in patients who are deficient of dihydropyrimidine dehydrogenase (DPD) activity. Fluorouracil 18-32 dihydropyrimidine dehydrogenase Homo sapiens 114-145 15905808-1 2005 Administration of 5-fluorouracil (5-FU) may be associated with severe toxicities in patients who are deficient of dihydropyrimidine dehydrogenase (DPD) activity. Fluorouracil 18-32 dihydropyrimidine dehydrogenase Homo sapiens 147-150 15905808-1 2005 Administration of 5-fluorouracil (5-FU) may be associated with severe toxicities in patients who are deficient of dihydropyrimidine dehydrogenase (DPD) activity. Fluorouracil 34-38 dihydropyrimidine dehydrogenase Homo sapiens 114-145 15905808-1 2005 Administration of 5-fluorouracil (5-FU) may be associated with severe toxicities in patients who are deficient of dihydropyrimidine dehydrogenase (DPD) activity. Fluorouracil 34-38 dihydropyrimidine dehydrogenase Homo sapiens 147-150 15905808-2 2005 For this reason, a sensitive HPLC method for the analysis of 5-FU and 5-fluoro-5,6-dihydrouracil (5-FDHU) was developed in the present study for the determination of DPD activity in nucleated cells of peripheral blood and pharmacokinetic analysis of 5-FU and 5-FDHU in humans. Fluorouracil 61-65 dihydropyrimidine dehydrogenase Homo sapiens 166-169 15905808-2 2005 For this reason, a sensitive HPLC method for the analysis of 5-FU and 5-fluoro-5,6-dihydrouracil (5-FDHU) was developed in the present study for the determination of DPD activity in nucleated cells of peripheral blood and pharmacokinetic analysis of 5-FU and 5-FDHU in humans. Fluorouracil 250-254 dihydropyrimidine dehydrogenase Homo sapiens 166-169 15905808-8 2005 The present assay proved to be sufficiently sensitive and specific to evaluate cellular DPD activity and measure 5-FU and 5-FDHU plasma concentrations in cancer patients, thus allowing therapeutic 5-FU monitoring in patients and identification of DPD-deficient subjects at major risk of severe toxicities. Fluorouracil 197-201 dihydropyrimidine dehydrogenase Homo sapiens 88-91 15694393-2 2005 The SNU-601/Cis2 showed cross-resistance to carboplatin, heptaplatin, doxorubicin, mitomycin C, and 5-fluorouracil compared with the SNU-601/WT whereas the SNU-601/Cis10 displayed collateral sensitivity to these drugs with the exception of cisplatin compared with the SNU-601/Cis2, suggesting that the cross-resistance and collateral sensitivity of cisplatin-resistant gastric cancer cells are dependent upon cisplatin concentrations. Fluorouracil 100-114 suppressor of cytokine signaling 2 Homo sapiens 12-16 15608676-7 2005 5-FU confers S-phase arrest through Chk1-mediated Cdc25A proteolysis leading to inhibition of Cdk2. Fluorouracil 0-4 cell division cycle 25A Homo sapiens 50-56 15684607-3 2005 This analysis included the study of effects of chemotherapeutic drugs (5-fluorouracil [5-FU], gemcitabine, cisplatin) commonly used in the treatment of pancreatic cancer patients on IL-18 production and processing. Fluorouracil 71-85 interleukin 18 Homo sapiens 182-187 15684607-7 2005 However, the chemotherapeutic agent 5-FU, by inducing Caspase-1 and Caspase-3 activation, induced secretion of proteolytically processed mature and degraded IL-18 species, respectively, in Capan-2 cells. Fluorouracil 36-40 interleukin 18 Homo sapiens 157-162 15684607-8 2005 Conditioned medium from 5-FU-treated but not control Capan-2 cells induced IFN-gamma production by activated T cells in an IL-18-dependent manner. Fluorouracil 24-28 interleukin 18 Homo sapiens 123-128 15684607-9 2005 Furthermore, adjuvant polychemotherapy including 5-FU significantly increased serum levels of mature, bioactive IL-18 in pancreatic carcinoma patients. Fluorouracil 49-53 interleukin 18 Homo sapiens 112-117 15684607-10 2005 Treatment of pancreatic cancer cells with 5-FU induced Caspase-dependent processing of pro-IL18 leading to the secretion of biologically active IL-18. Fluorouracil 42-46 interleukin 18 Homo sapiens 144-149 15709199-11 2005 Furthermore, IFN-alpha/type 2 IFN receptor long form-transfected HuH7 cells treated with combination therapy showed strong DNA fragmentation compared with nontransfected or transfected with IFN-alpha- and 5-FU-treated HuH7. Fluorouracil 205-209 MIR7-3 host gene Homo sapiens 65-69 15709199-11 2005 Furthermore, IFN-alpha/type 2 IFN receptor long form-transfected HuH7 cells treated with combination therapy showed strong DNA fragmentation compared with nontransfected or transfected with IFN-alpha- and 5-FU-treated HuH7. Fluorouracil 205-209 MIR7-3 host gene Homo sapiens 218-222 15607317-4 2005 The method was applied to study the alteration of BRCA1 gene expression after exposure to taxol, doxorubicin, 5-fluorouracil, etoposide or gamma irradiation in human MCF-7 breast cancer cells. Fluorouracil 110-124 BRCA1 DNA repair associated Homo sapiens 50-55 16147904-1 2005 Dihydropyrimidine dehydrogenase (DPD) is a rate-limiting enzyme of 5-fluorouracil (5-FU) catabolism. Fluorouracil 67-81 dihydropyrimidine dehydrogenase Homo sapiens 0-31 16147904-1 2005 Dihydropyrimidine dehydrogenase (DPD) is a rate-limiting enzyme of 5-fluorouracil (5-FU) catabolism. Fluorouracil 67-81 dihydropyrimidine dehydrogenase Homo sapiens 33-36 16151913-2 2005 DPD is the enzyme that catalyses the first and the rate-limiting step in the catabolism of uracil, thymine and the analogue 5-fluorouracil. Fluorouracil 124-138 dihydropyrimidine dehydrogenase Homo sapiens 0-3 15720820-6 2005 Downregulation of PKB/Akt, NF-kappaB, and cyclin D1, and upregulation of caspase-3 protein expression level were observed in cells and tumor lesions on treatment with a combination of CF101 and 5-FU. Fluorouracil 194-198 cyclin D1 Mus musculus 42-51 15720820-6 2005 Downregulation of PKB/Akt, NF-kappaB, and cyclin D1, and upregulation of caspase-3 protein expression level were observed in cells and tumor lesions on treatment with a combination of CF101 and 5-FU. Fluorouracil 194-198 caspase 3 Mus musculus 73-82 15598584-0 2005 Dihydropyrimidine dehydrogenase expression predicts survival outcome and chemosensitivity to 5-fluorouracil in patients with oral squamous cell carcinoma. Fluorouracil 93-107 dihydropyrimidine dehydrogenase Homo sapiens 0-31 15598584-1 2005 Dihydropyrimidine dehydrogenase (DPD) is the rate-limiting enzyme of 5-fluorouracil (5-Fu) catabolism. Fluorouracil 69-83 dihydropyrimidine dehydrogenase Homo sapiens 0-31 15598584-1 2005 Dihydropyrimidine dehydrogenase (DPD) is the rate-limiting enzyme of 5-fluorouracil (5-Fu) catabolism. Fluorouracil 69-83 dihydropyrimidine dehydrogenase Homo sapiens 33-36 15598584-1 2005 Dihydropyrimidine dehydrogenase (DPD) is the rate-limiting enzyme of 5-fluorouracil (5-Fu) catabolism. Fluorouracil 85-89 dihydropyrimidine dehydrogenase Homo sapiens 0-31 15598584-1 2005 Dihydropyrimidine dehydrogenase (DPD) is the rate-limiting enzyme of 5-fluorouracil (5-Fu) catabolism. Fluorouracil 85-89 dihydropyrimidine dehydrogenase Homo sapiens 33-36 15598584-2 2005 The aim of this study was to evaluate the prognostic value of DPD expression and the correlation between DPD expression and efficacy of 5-Fu. Fluorouracil 136-140 dihydropyrimidine dehydrogenase Homo sapiens 105-108 15598584-8 2005 Furthermore, heterogeneity of DPD expression may be a clue for predicting sensitivity to 5-Fu in patients with OSCC. Fluorouracil 89-93 dihydropyrimidine dehydrogenase Homo sapiens 30-33 15591715-0 2004 Multiple organ failure due to 5-fluorouracil chemotherapy in a patient with a rare dihydropyrimidine dehydrogenase gene variant. Fluorouracil 30-44 dihydropyrimidine dehydrogenase Homo sapiens 83-114 15566669-0 2004 [Relationship between dihydropyrimidine dehydrogenase(DPD) activity and toxicity of 5-FU-based adjuvant chemotherapy in colorectal cancer patients]. Fluorouracil 84-88 dihydropyrimidine dehydrogenase Homo sapiens 22-53 15566669-0 2004 [Relationship between dihydropyrimidine dehydrogenase(DPD) activity and toxicity of 5-FU-based adjuvant chemotherapy in colorectal cancer patients]. Fluorouracil 84-88 dihydropyrimidine dehydrogenase Homo sapiens 54-57 15566669-3 2004 This study is to measure DPD activity in blood and to analyze the relationship among DPD activity, the toxicity of 5-FU based adjuvant chemotherapy and the 5-FU plasma concentration in colorectal cancer patients. Fluorouracil 115-119 dihydropyrimidine dehydrogenase Homo sapiens 85-88 15566669-9 2004 The relationship among the DPD activity in blood, the toxicity of chemotherapy and the plasma concentration of 5-FU in all patients were analyzed. Fluorouracil 111-115 dihydropyrimidine dehydrogenase Homo sapiens 27-30 15566669-13 2004 There was a negative relationship between the DPD activity in blood and the 5-FU plasma concentration at day 1 (r=-0.773, P=0.00), and day 5 after 5-FU infusion(r = -0.833, P = 0.00). Fluorouracil 76-80 dihydropyrimidine dehydrogenase Homo sapiens 46-49 15566669-13 2004 There was a negative relationship between the DPD activity in blood and the 5-FU plasma concentration at day 1 (r=-0.773, P=0.00), and day 5 after 5-FU infusion(r = -0.833, P = 0.00). Fluorouracil 147-151 dihydropyrimidine dehydrogenase Homo sapiens 46-49 15566669-15 2004 The 5-Fu associated toxicities had a negative relationship with DPD activity in blood, and had a positive relationship with 5-FU plasma concentration (P< 0.05). Fluorouracil 4-8 dihydropyrimidine dehydrogenase Homo sapiens 64-67 15566669-16 2004 CONCLUSION: The results indicated that the DPD activity in blood can be used to predict the toxicity and the 5-FU plasma concentration in patients with 5-FU based chemotherapy. Fluorouracil 109-113 dihydropyrimidine dehydrogenase Homo sapiens 43-46 15566669-16 2004 CONCLUSION: The results indicated that the DPD activity in blood can be used to predict the toxicity and the 5-FU plasma concentration in patients with 5-FU based chemotherapy. Fluorouracil 152-156 dihydropyrimidine dehydrogenase Homo sapiens 43-46 15539941-1 2004 The thymidylate synthase (TS) inhibitors raltitrexed (RTX) and 5-fluorouracil (FUra) have shown promising anti-tumor activity in preclinical and clinical settings for the treatment of colorectal cancer. Fluorouracil 63-77 thymidylate synthase Mus musculus 4-24 15539941-1 2004 The thymidylate synthase (TS) inhibitors raltitrexed (RTX) and 5-fluorouracil (FUra) have shown promising anti-tumor activity in preclinical and clinical settings for the treatment of colorectal cancer. Fluorouracil 79-83 thymidylate synthase Mus musculus 4-24 15452397-0 2004 Recurrent thrombophlebitis in a colon cancer patient with C677T heterozygous genotype for MTHFR treated with 5-fluorouracil-based adjuvant chemotherapy. Fluorouracil 109-123 methylenetetrahydrofolate reductase Homo sapiens 90-95 15446569-7 2004 Since the cancer appeared to be resistant to 5-fluorouracil (5-FU), the patient was treated by weekly TXL therapy. Fluorouracil 61-65 thioredoxin like 1 Homo sapiens 102-105 15271097-0 2004 A simple and rapid high-performance liquid chromatographic (HPLC) method for 5-fluorouracil (5-FU) assay in plasma and possible detection of patients with impaired dihydropyrimidine dehydrogenase (DPD) activity. Fluorouracil 77-91 dihydropyrimidine dehydrogenase Homo sapiens 197-200 15271097-1 2004 BACKGROUND: Dihydropyrimidine dehydrogenase (DPD) gene polymorphism may lead to severe toxicity with 5-fluorouracil (5-FU), a major anticancer drug extensively used in clinical oncology. Fluorouracil 101-115 dihydropyrimidine dehydrogenase Homo sapiens 12-43 15271097-1 2004 BACKGROUND: Dihydropyrimidine dehydrogenase (DPD) gene polymorphism may lead to severe toxicity with 5-fluorouracil (5-FU), a major anticancer drug extensively used in clinical oncology. Fluorouracil 101-115 dihydropyrimidine dehydrogenase Homo sapiens 45-48 15271097-1 2004 BACKGROUND: Dihydropyrimidine dehydrogenase (DPD) gene polymorphism may lead to severe toxicity with 5-fluorouracil (5-FU), a major anticancer drug extensively used in clinical oncology. Fluorouracil 117-121 dihydropyrimidine dehydrogenase Homo sapiens 12-43 15271097-1 2004 BACKGROUND: Dihydropyrimidine dehydrogenase (DPD) gene polymorphism may lead to severe toxicity with 5-fluorouracil (5-FU), a major anticancer drug extensively used in clinical oncology. Fluorouracil 117-121 dihydropyrimidine dehydrogenase Homo sapiens 45-48 15271097-11 2004 Data from a patient with 5-FU toxicity suggest that the method was capable of identifying DPD metabolic phenotype in cancer patients, based on measurement of plasma U/UH2 ratio. Fluorouracil 25-29 dihydropyrimidine dehydrogenase Homo sapiens 90-93 15246190-5 2004 Based on these results, the quantitation of TS and DPD mRNA levels may predict the efficacy of 5-FU after surgery for patient with NSCLC. Fluorouracil 95-99 dihydropyrimidine dehydrogenase Homo sapiens 51-54 15213713-2 2004 Functional polymorphisms in DNA-repair genes XPD, ERCC1, XRCC1, XPA, and metabolising genes glutathione S-transferase GSTP1, GSTT1, GSTM1, and thymidylate synthase (TS) were assessed retrospectively in 106 patients with refractory stage IV disease who received 5-FU/oxaliplatin combination chemotherapy, using a polymerase chain reaction-based RFLP technique. Fluorouracil 261-265 glutathione S-transferase theta 1 Homo sapiens 125-130 14729579-8 2004 HIP expression in HCT-116 cells was also significantly decreased in parallel with apoptosis after treatment with 50 micro M camptothecin and 20 micro M 5-fluorouracil. Fluorouracil 152-166 ribosomal protein L29 Homo sapiens 0-3 15222105-0 2004 [Tumoral dihydropyrimidine dehydrogenase expression and efficacy of 5-fluorouracil plus leucovorin plus UFT therapy in patients with colorectal cancer]. Fluorouracil 68-82 dihydropyrimidine dehydrogenase Homo sapiens 9-40 15222105-1 2004 The purpose of this study was to examine the relation between tumoral expression of dihydropyrimidine dehydrogenase (DPD), the rate limiting enzyme of the degradation pathway 5-fluorouracil (5-FU), and the efficacy of 5-FU based chemotherapy for colorectal cancer. Fluorouracil 175-189 dihydropyrimidine dehydrogenase Homo sapiens 84-115 15222105-1 2004 The purpose of this study was to examine the relation between tumoral expression of dihydropyrimidine dehydrogenase (DPD), the rate limiting enzyme of the degradation pathway 5-fluorouracil (5-FU), and the efficacy of 5-FU based chemotherapy for colorectal cancer. Fluorouracil 175-189 dihydropyrimidine dehydrogenase Homo sapiens 117-120 15222105-1 2004 The purpose of this study was to examine the relation between tumoral expression of dihydropyrimidine dehydrogenase (DPD), the rate limiting enzyme of the degradation pathway 5-fluorouracil (5-FU), and the efficacy of 5-FU based chemotherapy for colorectal cancer. Fluorouracil 191-195 dihydropyrimidine dehydrogenase Homo sapiens 84-115 15222105-1 2004 The purpose of this study was to examine the relation between tumoral expression of dihydropyrimidine dehydrogenase (DPD), the rate limiting enzyme of the degradation pathway 5-fluorouracil (5-FU), and the efficacy of 5-FU based chemotherapy for colorectal cancer. Fluorouracil 191-195 dihydropyrimidine dehydrogenase Homo sapiens 117-120 15222105-1 2004 The purpose of this study was to examine the relation between tumoral expression of dihydropyrimidine dehydrogenase (DPD), the rate limiting enzyme of the degradation pathway 5-fluorouracil (5-FU), and the efficacy of 5-FU based chemotherapy for colorectal cancer. Fluorouracil 218-222 dihydropyrimidine dehydrogenase Homo sapiens 84-115 15222105-1 2004 The purpose of this study was to examine the relation between tumoral expression of dihydropyrimidine dehydrogenase (DPD), the rate limiting enzyme of the degradation pathway 5-fluorouracil (5-FU), and the efficacy of 5-FU based chemotherapy for colorectal cancer. Fluorouracil 218-222 dihydropyrimidine dehydrogenase Homo sapiens 117-120 15222106-1 2004 Thymidylate synthase (TS) and dihydropyrimidine dehydrogenase (DPD) have been identified as a predictor of response to 5-fluorouracil (5-FU). Fluorouracil 119-133 dihydropyrimidine dehydrogenase Homo sapiens 30-61 15222106-1 2004 Thymidylate synthase (TS) and dihydropyrimidine dehydrogenase (DPD) have been identified as a predictor of response to 5-fluorouracil (5-FU). Fluorouracil 119-133 dihydropyrimidine dehydrogenase Homo sapiens 63-66 15222106-1 2004 Thymidylate synthase (TS) and dihydropyrimidine dehydrogenase (DPD) have been identified as a predictor of response to 5-fluorouracil (5-FU). Fluorouracil 135-139 dihydropyrimidine dehydrogenase Homo sapiens 30-61 15222106-1 2004 Thymidylate synthase (TS) and dihydropyrimidine dehydrogenase (DPD) have been identified as a predictor of response to 5-fluorouracil (5-FU). Fluorouracil 135-139 dihydropyrimidine dehydrogenase Homo sapiens 63-66 15132128-2 2004 5-FU interferes with DNA synthesis by blocking thymidylate synthase (TS) but is inactivated by dihydropyrimidine dehydrogenase (DPD). Fluorouracil 0-4 dihydropyrimidine dehydrogenase Homo sapiens 95-126 15132128-2 2004 5-FU interferes with DNA synthesis by blocking thymidylate synthase (TS) but is inactivated by dihydropyrimidine dehydrogenase (DPD). Fluorouracil 0-4 dihydropyrimidine dehydrogenase Homo sapiens 128-131 15132128-3 2004 Favorable enzyme profiles (high TP and low DPD) generate high intratumor levels of 5-FU that are effective against many tumors, especially those with low TS. Fluorouracil 83-87 dihydropyrimidine dehydrogenase Homo sapiens 43-46 15132136-2 2004 Over 80% of the 5-FU administered is metabolized by dihydropyrimidine dehydrogenase (DPD) in the liver. Fluorouracil 16-20 dihydropyrimidine dehydrogenase Homo sapiens 52-83 15124184-8 2004 Our results showed that combined treatment with 5-FU and anti-CD8 antibody could enhance the rate of apoptosis induced by 5-FU or anti-CD8 antibody through increased expression of p53 and by promoting activation of caspase-3 and Bid. Fluorouracil 48-52 CD8a molecule Homo sapiens 135-138 15124184-8 2004 Our results showed that combined treatment with 5-FU and anti-CD8 antibody could enhance the rate of apoptosis induced by 5-FU or anti-CD8 antibody through increased expression of p53 and by promoting activation of caspase-3 and Bid. Fluorouracil 122-126 CD8a molecule Homo sapiens 62-65 15093568-2 2004 Dihydropyrimidine dehydrogenase (DPD) is the initial and rate-limiting enzyme in the catabolism of 5-fluorouracil (5-FU). Fluorouracil 99-113 dihydropyrimidine dehydrogenase Homo sapiens 0-31 15093568-2 2004 Dihydropyrimidine dehydrogenase (DPD) is the initial and rate-limiting enzyme in the catabolism of 5-fluorouracil (5-FU). Fluorouracil 99-113 dihydropyrimidine dehydrogenase Homo sapiens 33-36 15093568-2 2004 Dihydropyrimidine dehydrogenase (DPD) is the initial and rate-limiting enzyme in the catabolism of 5-fluorouracil (5-FU). Fluorouracil 115-119 dihydropyrimidine dehydrogenase Homo sapiens 0-31 15093568-2 2004 Dihydropyrimidine dehydrogenase (DPD) is the initial and rate-limiting enzyme in the catabolism of 5-fluorouracil (5-FU). Fluorouracil 115-119 dihydropyrimidine dehydrogenase Homo sapiens 33-36 14689231-2 2004 Thymidylate synthase (TS), the target enzyme of FUra, and dihydropyrimidine dehydrogenase (DPD), the rate-limiting catabolic enzyme of pyrimidines, have both been reported to be predictors of the response to FUra-based chemotherapies. Fluorouracil 208-212 dihydropyrimidine dehydrogenase Homo sapiens 58-89 14689231-2 2004 Thymidylate synthase (TS), the target enzyme of FUra, and dihydropyrimidine dehydrogenase (DPD), the rate-limiting catabolic enzyme of pyrimidines, have both been reported to be predictors of the response to FUra-based chemotherapies. Fluorouracil 208-212 dihydropyrimidine dehydrogenase Homo sapiens 91-94 14689231-13 2004 A strong correlation was found between the IC(50) of FUra and the mRNA level of DPD (r=0.912, P=0.0295). Fluorouracil 53-57 dihydropyrimidine dehydrogenase Homo sapiens 80-83 14689231-15 2004 DPD plays an important role in the sensitivity to FUra, and the DPD mRNA expression level may be used to predict the response to FUra-based chemotherapy for HCC. Fluorouracil 50-54 dihydropyrimidine dehydrogenase Homo sapiens 0-3 14689231-15 2004 DPD plays an important role in the sensitivity to FUra, and the DPD mRNA expression level may be used to predict the response to FUra-based chemotherapy for HCC. Fluorouracil 129-133 dihydropyrimidine dehydrogenase Homo sapiens 64-67 15025949-1 2004 BACKGROUND & OBJECTIVE: Anti-cancer effect of 5-Fluorouracil (5-FU) is mediated mainly by inhibition of the thymidylate synthase (TS), while dihydropyrimidine dehydrogenase (DPD) is an initial and a rate-limiting catabolic enzyme of 5-FU. Fluorouracil 50-64 thymidylate synthase Mus musculus 112-132 15025949-1 2004 BACKGROUND & OBJECTIVE: Anti-cancer effect of 5-Fluorouracil (5-FU) is mediated mainly by inhibition of the thymidylate synthase (TS), while dihydropyrimidine dehydrogenase (DPD) is an initial and a rate-limiting catabolic enzyme of 5-FU. Fluorouracil 50-64 thymidylate synthase Mus musculus 134-136 15025949-1 2004 BACKGROUND & OBJECTIVE: Anti-cancer effect of 5-Fluorouracil (5-FU) is mediated mainly by inhibition of the thymidylate synthase (TS), while dihydropyrimidine dehydrogenase (DPD) is an initial and a rate-limiting catabolic enzyme of 5-FU. Fluorouracil 66-70 thymidylate synthase Mus musculus 112-132 15025949-1 2004 BACKGROUND & OBJECTIVE: Anti-cancer effect of 5-Fluorouracil (5-FU) is mediated mainly by inhibition of the thymidylate synthase (TS), while dihydropyrimidine dehydrogenase (DPD) is an initial and a rate-limiting catabolic enzyme of 5-FU. Fluorouracil 66-70 thymidylate synthase Mus musculus 134-136 15025949-1 2004 BACKGROUND & OBJECTIVE: Anti-cancer effect of 5-Fluorouracil (5-FU) is mediated mainly by inhibition of the thymidylate synthase (TS), while dihydropyrimidine dehydrogenase (DPD) is an initial and a rate-limiting catabolic enzyme of 5-FU. Fluorouracil 237-241 thymidylate synthase Mus musculus 112-132 15025949-1 2004 BACKGROUND & OBJECTIVE: Anti-cancer effect of 5-Fluorouracil (5-FU) is mediated mainly by inhibition of the thymidylate synthase (TS), while dihydropyrimidine dehydrogenase (DPD) is an initial and a rate-limiting catabolic enzyme of 5-FU. Fluorouracil 237-241 thymidylate synthase Mus musculus 134-136 15006714-3 2004 Dihydropyrimidine dehydrogenase (DPD) is the rate-limiting enzyme in the catabolism of 5-FU and its deficiency is responsible for the severe toxicities encountered in cancer patients receiving 5-FU. Fluorouracil 87-91 dihydropyrimidine dehydrogenase Homo sapiens 0-31 15006714-3 2004 Dihydropyrimidine dehydrogenase (DPD) is the rate-limiting enzyme in the catabolism of 5-FU and its deficiency is responsible for the severe toxicities encountered in cancer patients receiving 5-FU. Fluorouracil 87-91 dihydropyrimidine dehydrogenase Homo sapiens 33-36 15006714-3 2004 Dihydropyrimidine dehydrogenase (DPD) is the rate-limiting enzyme in the catabolism of 5-FU and its deficiency is responsible for the severe toxicities encountered in cancer patients receiving 5-FU. Fluorouracil 193-197 dihydropyrimidine dehydrogenase Homo sapiens 0-31 15006714-3 2004 Dihydropyrimidine dehydrogenase (DPD) is the rate-limiting enzyme in the catabolism of 5-FU and its deficiency is responsible for the severe toxicities encountered in cancer patients receiving 5-FU. Fluorouracil 193-197 dihydropyrimidine dehydrogenase Homo sapiens 33-36 14744810-4 2004 In this study, we identified the dihydrouracil/uracil (UH2/Ura) ratio in plasma or urine as a potential biomarker reflecting the activity of dihydropyrimidine dehydrogenase (DPD), the rate-limiting enzyme in 5-FUra metabolism. Fluorouracil 208-214 dihydropyrimidine dehydrogenase Homo sapiens 141-172 15025795-2 2004 This study was undertaken to examine the contribution of commonly occurring polymorphisms in the dihydropyrimidine dehydrogenase (DPYD) gene to interpatient variability in 5-FU pharmacokinetics and toxicity. Fluorouracil 172-176 dihydropyrimidine dehydrogenase Homo sapiens 97-128 15025795-2 2004 This study was undertaken to examine the contribution of commonly occurring polymorphisms in the dihydropyrimidine dehydrogenase (DPYD) gene to interpatient variability in 5-FU pharmacokinetics and toxicity. Fluorouracil 172-176 dihydropyrimidine dehydrogenase Homo sapiens 130-134 14726200-1 2004 Thymidylate synthase (TS) is the target in colon cancer therapeutic protocols utilizing such drugs as 5-fluorouracil and raltitrexed. Fluorouracil 102-116 APC down-regulated 1 Homo sapiens 22-24 15015608-1 2004 BACKGROUND: Dihydropyrimidine dehydrogenase (DPD) is an enzyme that catabolizes 5-fluorouracil (5-FU), which is widely used for chemotherapy in patients with advanced colorectal cancer (CRC). Fluorouracil 80-94 dihydropyrimidine dehydrogenase Homo sapiens 12-43 15015608-1 2004 BACKGROUND: Dihydropyrimidine dehydrogenase (DPD) is an enzyme that catabolizes 5-fluorouracil (5-FU), which is widely used for chemotherapy in patients with advanced colorectal cancer (CRC). Fluorouracil 80-94 dihydropyrimidine dehydrogenase Homo sapiens 45-48 15015608-1 2004 BACKGROUND: Dihydropyrimidine dehydrogenase (DPD) is an enzyme that catabolizes 5-fluorouracil (5-FU), which is widely used for chemotherapy in patients with advanced colorectal cancer (CRC). Fluorouracil 96-100 dihydropyrimidine dehydrogenase Homo sapiens 12-43 15015608-1 2004 BACKGROUND: Dihydropyrimidine dehydrogenase (DPD) is an enzyme that catabolizes 5-fluorouracil (5-FU), which is widely used for chemotherapy in patients with advanced colorectal cancer (CRC). Fluorouracil 96-100 dihydropyrimidine dehydrogenase Homo sapiens 45-48 15015608-2 2004 However, the clinical importance of tumor dihydropyrimidine dehydrogenase (DPD) expression in patients with CRC treated with 5-FU remains unclear. Fluorouracil 125-129 dihydropyrimidine dehydrogenase Homo sapiens 42-73 15015608-2 2004 However, the clinical importance of tumor dihydropyrimidine dehydrogenase (DPD) expression in patients with CRC treated with 5-FU remains unclear. Fluorouracil 125-129 dihydropyrimidine dehydrogenase Homo sapiens 75-78 15224198-1 2004 BACKGROUND: Although 5-fluorouracil (5-FU) and cis-diamminedichloroplatinum (cisplatin) in combination have synergistic cytotoxicity against both murine and human neoplasms, the precise mechanism of the synergism, and the effects on thymidylate synthase and its percent inhibition, and the effects on dihydropyrimidine dehydrogenase (DPD) remained to be elucidated. Fluorouracil 21-35 dihydropyrimidine dehydrogenase Homo sapiens 301-332 15224198-1 2004 BACKGROUND: Although 5-fluorouracil (5-FU) and cis-diamminedichloroplatinum (cisplatin) in combination have synergistic cytotoxicity against both murine and human neoplasms, the precise mechanism of the synergism, and the effects on thymidylate synthase and its percent inhibition, and the effects on dihydropyrimidine dehydrogenase (DPD) remained to be elucidated. Fluorouracil 21-35 dihydropyrimidine dehydrogenase Homo sapiens 334-337 15224198-1 2004 BACKGROUND: Although 5-fluorouracil (5-FU) and cis-diamminedichloroplatinum (cisplatin) in combination have synergistic cytotoxicity against both murine and human neoplasms, the precise mechanism of the synergism, and the effects on thymidylate synthase and its percent inhibition, and the effects on dihydropyrimidine dehydrogenase (DPD) remained to be elucidated. Fluorouracil 37-41 dihydropyrimidine dehydrogenase Homo sapiens 301-332 15224198-1 2004 BACKGROUND: Although 5-fluorouracil (5-FU) and cis-diamminedichloroplatinum (cisplatin) in combination have synergistic cytotoxicity against both murine and human neoplasms, the precise mechanism of the synergism, and the effects on thymidylate synthase and its percent inhibition, and the effects on dihydropyrimidine dehydrogenase (DPD) remained to be elucidated. Fluorouracil 37-41 dihydropyrimidine dehydrogenase Homo sapiens 334-337 15224198-7 2004 The long-term administration of 5-FU significantly increased both total thymidylate synthase and the percent thymidylate synthase inhibition rate. Fluorouracil 32-36 thymidylate synthase Mus musculus 72-92 15224198-7 2004 The long-term administration of 5-FU significantly increased both total thymidylate synthase and the percent thymidylate synthase inhibition rate. Fluorouracil 32-36 thymidylate synthase Mus musculus 109-129 14654904-9 2004 When evaluated in patients treated with 5-FU or 5-FU derivatives, DPD expression was a significantly (p<0.05) poorer prognostic factor in disease-free and overall survival. Fluorouracil 40-44 dihydropyrimidine dehydrogenase Homo sapiens 66-69 14654904-9 2004 When evaluated in patients treated with 5-FU or 5-FU derivatives, DPD expression was a significantly (p<0.05) poorer prognostic factor in disease-free and overall survival. Fluorouracil 48-52 dihydropyrimidine dehydrogenase Homo sapiens 66-69 15452381-0 2004 5-Fluorouracil-induced coronary spasm: may inhibition of hyperpolarization factors produced by CYP2C enzymes be the cause? Fluorouracil 0-14 cytochrome P450 family 2 subfamily C member 19 Homo sapiens 95-100 14635116-0 2003 Detailed analysis of five mutations in dihydropyrimidine dehydrogenase detected in cancer patients with 5-fluorouracil-related side effects. Fluorouracil 104-118 dihydropyrimidine dehydrogenase Homo sapiens 39-70 14635116-1 2003 Complete or partial loss of dihydropyrimidine dehydrogenase (DPD or DYPD) function has been described in cancer patients experiencing severe side effects upon administration of the fluoropyrimidine anticancer drug 5-fluorouracil (5-FU). Fluorouracil 214-228 dihydropyrimidine dehydrogenase Homo sapiens 28-59 14635116-1 2003 Complete or partial loss of dihydropyrimidine dehydrogenase (DPD or DYPD) function has been described in cancer patients experiencing severe side effects upon administration of the fluoropyrimidine anticancer drug 5-fluorouracil (5-FU). Fluorouracil 214-228 dihydropyrimidine dehydrogenase Homo sapiens 61-64 14635116-1 2003 Complete or partial loss of dihydropyrimidine dehydrogenase (DPD or DYPD) function has been described in cancer patients experiencing severe side effects upon administration of the fluoropyrimidine anticancer drug 5-fluorouracil (5-FU). Fluorouracil 230-234 dihydropyrimidine dehydrogenase Homo sapiens 28-59 14635116-1 2003 Complete or partial loss of dihydropyrimidine dehydrogenase (DPD or DYPD) function has been described in cancer patients experiencing severe side effects upon administration of the fluoropyrimidine anticancer drug 5-fluorouracil (5-FU). Fluorouracil 230-234 dihydropyrimidine dehydrogenase Homo sapiens 61-64 14612954-1 2003 Thymidylate synthase (TS) and dihydropyrimidine dehydrogenase (DPD) has been suggested to be sensitivity-limiting factors of 5-fluorouracil therapy in cancer patients. Fluorouracil 125-139 dihydropyrimidine dehydrogenase Homo sapiens 63-66 14612954-10 2003 Moreover, breast cancer was characterized by high TS activity and lung cancer by high DPD activity as compared with gastric and colon cancers, and their high activity levels may influence to the effectiveness of 5-fluorouracil against cancers of these organs. Fluorouracil 212-226 dihydropyrimidine dehydrogenase Homo sapiens 86-89 14612954-11 2003 The results for expression of TS and DPD in clinically dissected tumors would be useful to estimate the efficacy of 5-fluorouracil in the treatment of cancer patients. Fluorouracil 116-130 dihydropyrimidine dehydrogenase Homo sapiens 37-40 14562041-6 2003 We next analysed the apoptotic response to 5-FU and temozolomide in doubly mutant Mbd4(-/-), Mlh1(-/-) mice but observed no additive decrease. Fluorouracil 43-47 mutL homolog 1 Mus musculus 93-97 14551502-0 2003 Dihydropyrimidine dehydrogenase inhibition as a strategy for the oral administration of 5-fluorouracil: utility in the treatment of advanced colorectal cancer. Fluorouracil 88-102 dihydropyrimidine dehydrogenase Homo sapiens 0-31 14551502-1 2003 Dihydropyrimidine dehydrogenase (DPD), the rate-limiting enzyme in 5-fluorouracil (5-FU) catabolism, has been a key target for the development of novel oral fluoropyrimidines. Fluorouracil 67-81 dihydropyrimidine dehydrogenase Homo sapiens 0-31 14551502-1 2003 Dihydropyrimidine dehydrogenase (DPD), the rate-limiting enzyme in 5-fluorouracil (5-FU) catabolism, has been a key target for the development of novel oral fluoropyrimidines. Fluorouracil 67-81 dihydropyrimidine dehydrogenase Homo sapiens 33-36 14551502-1 2003 Dihydropyrimidine dehydrogenase (DPD), the rate-limiting enzyme in 5-fluorouracil (5-FU) catabolism, has been a key target for the development of novel oral fluoropyrimidines. Fluorouracil 83-87 dihydropyrimidine dehydrogenase Homo sapiens 0-31 14551502-1 2003 Dihydropyrimidine dehydrogenase (DPD), the rate-limiting enzyme in 5-fluorouracil (5-FU) catabolism, has been a key target for the development of novel oral fluoropyrimidines. Fluorouracil 83-87 dihydropyrimidine dehydrogenase Homo sapiens 33-36 14551502-2 2003 DPD-inhibiting oral fluoropyrimidines showing promise in early clinical studies included UFT (the 5-FU prodrug, tegafur, plus the DPD substrate, uracil), eniluracil (an irreversible DPD inhibitor that improves the oral bioavailability of 5-FU) and S-1 (tegafur plus a reversible DPD inhibitor, 5-chloro-2,4-dihydroxypyridine, and oxonic acid). Fluorouracil 98-102 dihydropyrimidine dehydrogenase Homo sapiens 0-3 12942110-11 2003 The AUC(0-10 h) of FBAL was markedly lower and plasma uracil concentrations were significantly higher for S-1 than for PVI of 5-FU, clearly demonstrating the effect of DPD inhibition. Fluorouracil 126-130 dihydropyrimidine dehydrogenase Homo sapiens 168-171 12920208-0 2003 5-fluorouracil blocks transforming growth factor-beta-induced alpha 2 type I collagen gene (COL1A2) expression in human fibroblasts via c-Jun NH2-terminal kinase/activator protein-1 activation. Fluorouracil 0-14 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 136-141 12920208-5 2003 5-FU induces c-Jun phosphorylation and activates both AP-1-specific transcription and DNA binding. Fluorouracil 0-4 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 13-18 12920208-6 2003 Overexpression of an antisense c-jun expression vector, or that of a dominant-negative form of MKK4 that interferes with c-Jun N-terminal kinase (JNK) activation, blocks the inhibitory activity of 5-FU on TGF-beta-induced COL1A2 transcription. Fluorouracil 197-201 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 31-36 14650374-9 2003 The influence of CDHP on the elimination of 5-FU was well described by an enzymatic inhibition model. Fluorouracil 44-48 cadherin 3 Homo sapiens 17-21 12851835-1 2003 Dihydropyrimidine dehydrogenase (DPD) is a rate-limiting enzyme of (fluorinated) pyrimidine degradation that plays a significant role in the pharmacokinetics of 5-fluorouracil (5-FU). Fluorouracil 161-175 dihydropyrimidine dehydrogenase Homo sapiens 0-31 12851835-1 2003 Dihydropyrimidine dehydrogenase (DPD) is a rate-limiting enzyme of (fluorinated) pyrimidine degradation that plays a significant role in the pharmacokinetics of 5-fluorouracil (5-FU). Fluorouracil 161-175 dihydropyrimidine dehydrogenase Homo sapiens 33-36 12851835-1 2003 Dihydropyrimidine dehydrogenase (DPD) is a rate-limiting enzyme of (fluorinated) pyrimidine degradation that plays a significant role in the pharmacokinetics of 5-fluorouracil (5-FU). Fluorouracil 177-181 dihydropyrimidine dehydrogenase Homo sapiens 0-31 12851835-1 2003 Dihydropyrimidine dehydrogenase (DPD) is a rate-limiting enzyme of (fluorinated) pyrimidine degradation that plays a significant role in the pharmacokinetics of 5-fluorouracil (5-FU). Fluorouracil 177-181 dihydropyrimidine dehydrogenase Homo sapiens 33-36 12851835-2 2003 In addition, a catabolite of 5-FU induces a certain toxicity, and the sensitivity of 5-FU is determined by DPD activity in tumors. Fluorouracil 85-89 dihydropyrimidine dehydrogenase Homo sapiens 107-110 12851835-4 2003 Drugs have been developed that control variations of the pharmacokinetics of 5-FU by controlling or inhibiting DPD, thereby reducing toxicity and improving sensitivity. Fluorouracil 77-81 dihydropyrimidine dehydrogenase Homo sapiens 111-114 12851835-5 2003 These fluorinated pyrimidines with DPD-inhibiting activity, called DPD-inhibitory fluoropyrimidines, contribute to oral therapy with 5-FU for cancer. Fluorouracil 133-137 dihydropyrimidine dehydrogenase Homo sapiens 35-38 12851835-5 2003 These fluorinated pyrimidines with DPD-inhibiting activity, called DPD-inhibitory fluoropyrimidines, contribute to oral therapy with 5-FU for cancer. Fluorouracil 133-137 dihydropyrimidine dehydrogenase Homo sapiens 67-70 12851835-6 2003 This paper summarizes the important role of DPD in cancer chemotherapy with 5-FU. Fluorouracil 76-80 dihydropyrimidine dehydrogenase Homo sapiens 44-47 12851836-0 2003 Clinical implications of dihydropyrimidine dehydrogenase (DPD) activity in 5-FU-based chemotherapy: mutations in the DPD gene, and DPD inhibitory fluoropyrimidines. Fluorouracil 75-79 dihydropyrimidine dehydrogenase Homo sapiens 25-56 12851836-0 2003 Clinical implications of dihydropyrimidine dehydrogenase (DPD) activity in 5-FU-based chemotherapy: mutations in the DPD gene, and DPD inhibitory fluoropyrimidines. Fluorouracil 75-79 dihydropyrimidine dehydrogenase Homo sapiens 58-61 12851836-0 2003 Clinical implications of dihydropyrimidine dehydrogenase (DPD) activity in 5-FU-based chemotherapy: mutations in the DPD gene, and DPD inhibitory fluoropyrimidines. Fluorouracil 75-79 dihydropyrimidine dehydrogenase Homo sapiens 117-120 12851836-0 2003 Clinical implications of dihydropyrimidine dehydrogenase (DPD) activity in 5-FU-based chemotherapy: mutations in the DPD gene, and DPD inhibitory fluoropyrimidines. Fluorouracil 75-79 dihydropyrimidine dehydrogenase Homo sapiens 117-120 12851836-2 2003 DPD is also responsible for the degradation of 5-fluorouracil (5-FU), which is the most frequently prescribed anticancer drug for the treatment of malignancies of the gastrointestinal tract. Fluorouracil 47-61 dihydropyrimidine dehydrogenase Homo sapiens 0-3 12738713-2 2003 Methylenetetrahydrofolate reductase (MTHFR) could play an important role in the action of 5-FU, an inhibitor of thymidylate synthetase, by converting 5,10-methylenetetrahydrofolate, a substrate of thymidylate synthetase, to 5-methyltetrahydrofolate. Fluorouracil 90-94 methylenetetrahydrofolate reductase Homo sapiens 0-35 12738713-2 2003 Methylenetetrahydrofolate reductase (MTHFR) could play an important role in the action of 5-FU, an inhibitor of thymidylate synthetase, by converting 5,10-methylenetetrahydrofolate, a substrate of thymidylate synthetase, to 5-methyltetrahydrofolate. Fluorouracil 90-94 methylenetetrahydrofolate reductase Homo sapiens 37-42 12738713-5 2003 The aim of the present study was to investigate the association between the MTHFR polymorphism and response to 5-FU and other fluoropyrimidines in patients with metastatic colorectal cancer. Fluorouracil 111-115 methylenetetrahydrofolate reductase Homo sapiens 76-81 12870370-0 2003 Intratumoural thymidylate synthase and dihydropyrimidine dehydrogenase activities are good predictors of 5-fluorouracil sensitivity in colorectal cancer. Fluorouracil 105-119 dihydropyrimidine dehydrogenase Homo sapiens 39-70 12870370-3 2003 The activities of TS and DPD were significantly lower in the tumours sensitive to 5-FU compared with those that were not sensitive to 5-FU. Fluorouracil 82-86 dihydropyrimidine dehydrogenase Homo sapiens 25-28 12870370-3 2003 The activities of TS and DPD were significantly lower in the tumours sensitive to 5-FU compared with those that were not sensitive to 5-FU. Fluorouracil 134-138 dihydropyrimidine dehydrogenase Homo sapiens 25-28 12870370-6 2003 Tumour sensitivity to 5-FU can be more precisely predicted by taking the activities of both TS and DPD into consideration than by using either alone. Fluorouracil 22-26 dihydropyrimidine dehydrogenase Homo sapiens 99-102 12684419-5 2003 We investigated the activity of TS in 68 RCCs and the association with dihydropyrimidine dehydrogenase (DPD) activities, which is a principal enzyme in the degradation of 5-FU and pyrimidine nucleotides. Fluorouracil 171-175 dihydropyrimidine dehydrogenase Homo sapiens 71-102 12684419-5 2003 We investigated the activity of TS in 68 RCCs and the association with dihydropyrimidine dehydrogenase (DPD) activities, which is a principal enzyme in the degradation of 5-FU and pyrimidine nucleotides. Fluorouracil 171-175 dihydropyrimidine dehydrogenase Homo sapiens 104-107 12684419-6 2003 The relationship between TS/DPD activities in primary cultured RCC cell lines and their sensitivity to 5-FU was also examined. Fluorouracil 103-107 dihydropyrimidine dehydrogenase Homo sapiens 28-31 12684419-18 2003 Furthermore, RCC cells with both high TS activity and low DPD activity were more sensitive to 5-FU, compared with those with either low TS activity or high DPD activity. Fluorouracil 94-98 dihydropyrimidine dehydrogenase Homo sapiens 58-61 12617910-1 2003 A series of tumor-activated prodrugs of the inhibitors of dihydropyrimidine dehydrogenase (DPD), an enzyme catabolizing 5-fluorouracil (5-FU: 4g), has been designed and synthesized. Fluorouracil 120-134 dihydropyrimidine dehydrogenase Homo sapiens 91-94 12617910-1 2003 A series of tumor-activated prodrugs of the inhibitors of dihydropyrimidine dehydrogenase (DPD), an enzyme catabolizing 5-fluorouracil (5-FU: 4g), has been designed and synthesized. Fluorouracil 136-140 dihydropyrimidine dehydrogenase Homo sapiens 91-94 12751387-4 2003 We investigated the activity of DPD in 68 RCC and the relationship between DPD activity and the sensitivity to 5-FU. Fluorouracil 111-115 dihydropyrimidine dehydrogenase Homo sapiens 75-78 12751387-5 2003 The levels of DPD activity in RCC and normal kidney samples were determined by the 5-FU degradation assay. Fluorouracil 83-87 dihydropyrimidine dehydrogenase Homo sapiens 14-17 12751387-10 2003 There was an inverse correlation between DPD activity in RCC cells and their sensitivity to 5-FU. Fluorouracil 92-96 dihydropyrimidine dehydrogenase Homo sapiens 41-44 12751387-11 2003 Furthermore, 5-chloro-2,4-dihydroxypyridine (CDHP), a potent DPD inhibitor, enhanced the sensitivity to 5-FU. Fluorouracil 104-108 dihydropyrimidine dehydrogenase Homo sapiens 61-64 12751387-12 2003 The current study is the first to demonstrate that the level of DPD activity was inversel correlated with both the progression of the disease and increased grade of RCC, and that DPD activity was inversely associated with the sensitivity of RCC to 5-FU, which was enhanced by a DPD inhibitor. Fluorouracil 248-252 dihydropyrimidine dehydrogenase Homo sapiens 179-182 12751387-12 2003 The current study is the first to demonstrate that the level of DPD activity was inversel correlated with both the progression of the disease and increased grade of RCC, and that DPD activity was inversely associated with the sensitivity of RCC to 5-FU, which was enhanced by a DPD inhibitor. Fluorouracil 248-252 dihydropyrimidine dehydrogenase Homo sapiens 179-182 12751387-14 2003 In addition, it may be possible to overcome 5-FU resistance by using DPD inhibitors in the treatment protocols of 5-FU-based chemotherapy for RCC. Fluorouracil 44-48 dihydropyrimidine dehydrogenase Homo sapiens 69-72 12751387-14 2003 In addition, it may be possible to overcome 5-FU resistance by using DPD inhibitors in the treatment protocols of 5-FU-based chemotherapy for RCC. Fluorouracil 114-118 dihydropyrimidine dehydrogenase Homo sapiens 69-72 12619061-1 2003 BACKGROUND AND OBJECTIVES: Although studies have focused on modulating the bioavailability of 5-FU through inhibition of dihydropyrimidine dehydrogenase (DPD) to improve efficacy of the drug, activity of this enzyme in breast cancer has not been thoroughly examined. Fluorouracil 94-98 dihydropyrimidine dehydrogenase Homo sapiens 121-152 12619061-1 2003 BACKGROUND AND OBJECTIVES: Although studies have focused on modulating the bioavailability of 5-FU through inhibition of dihydropyrimidine dehydrogenase (DPD) to improve efficacy of the drug, activity of this enzyme in breast cancer has not been thoroughly examined. Fluorouracil 94-98 dihydropyrimidine dehydrogenase Homo sapiens 154-157 12562666-0 2003 Lethal 5-fluorouracil toxicity associated with a novel mutation in the dihydropyrimidine dehydrogenase gene. Fluorouracil 7-21 dihydropyrimidine dehydrogenase Homo sapiens 71-102 12647010-6 2003 In initial studies, subcutaneous administration of 10 or 100 microg/kg per day of AII starting either 2 days before or 2 days after intravenous administration of 5-fluorouracil (5FU) accelerated WBC recovery (return to baseline between 7 and 14 days). Fluorouracil 162-176 arginase type II Mus musculus 82-85 12647010-6 2003 In initial studies, subcutaneous administration of 10 or 100 microg/kg per day of AII starting either 2 days before or 2 days after intravenous administration of 5-fluorouracil (5FU) accelerated WBC recovery (return to baseline between 7 and 14 days). Fluorouracil 178-181 arginase type II Mus musculus 82-85 12527930-1 2003 Dihydropyrimidine dehydrogenase (DPD) is the first and rate-limiting enzyme in the degradation of pyrimidines and pyrimidine base analogs including the anticancer drugs 5-fluorouracil (5-FU) and Xeloda. Fluorouracil 169-183 dihydropyrimidine dehydrogenase Homo sapiens 0-31 12527930-1 2003 Dihydropyrimidine dehydrogenase (DPD) is the first and rate-limiting enzyme in the degradation of pyrimidines and pyrimidine base analogs including the anticancer drugs 5-fluorouracil (5-FU) and Xeloda. Fluorouracil 169-183 dihydropyrimidine dehydrogenase Homo sapiens 33-36 12527930-1 2003 Dihydropyrimidine dehydrogenase (DPD) is the first and rate-limiting enzyme in the degradation of pyrimidines and pyrimidine base analogs including the anticancer drugs 5-fluorouracil (5-FU) and Xeloda. Fluorouracil 185-189 dihydropyrimidine dehydrogenase Homo sapiens 0-31 12527930-1 2003 Dihydropyrimidine dehydrogenase (DPD) is the first and rate-limiting enzyme in the degradation of pyrimidines and pyrimidine base analogs including the anticancer drugs 5-fluorouracil (5-FU) and Xeloda. Fluorouracil 185-189 dihydropyrimidine dehydrogenase Homo sapiens 33-36 12527930-2 2003 A decreased DPD enzyme activity has been described in cancer patients experiencing severe and life-threatening toxicity after 5-FU treatment and distinct sequence variants in the DPD gene (DPYD) have been associated with impaired enzyme function. Fluorouracil 126-130 dihydropyrimidine dehydrogenase Homo sapiens 12-15 12527930-2 2003 A decreased DPD enzyme activity has been described in cancer patients experiencing severe and life-threatening toxicity after 5-FU treatment and distinct sequence variants in the DPD gene (DPYD) have been associated with impaired enzyme function. Fluorouracil 126-130 dihydropyrimidine dehydrogenase Homo sapiens 179-182 12527930-2 2003 A decreased DPD enzyme activity has been described in cancer patients experiencing severe and life-threatening toxicity after 5-FU treatment and distinct sequence variants in the DPD gene (DPYD) have been associated with impaired enzyme function. Fluorouracil 126-130 dihydropyrimidine dehydrogenase Homo sapiens 189-193 12527930-4 2003 This underlines the need for a test system for DPYD mutations in patients undergoing chemotherapy with 5-FU or with Xeloda. Fluorouracil 103-107 dihydropyrimidine dehydrogenase Homo sapiens 47-51 12662441-2 2003 Present studies evaluated the myeloprotective capabilities of Lkn-1 in vivo against Ara-C and 5-fluorouracil (5-FU). Fluorouracil 94-108 C-C motif chemokine ligand 15 Homo sapiens 62-67 12662441-2 2003 Present studies evaluated the myeloprotective capabilities of Lkn-1 in vivo against Ara-C and 5-fluorouracil (5-FU). Fluorouracil 110-114 C-C motif chemokine ligand 15 Homo sapiens 62-67 12542909-1 2003 Dihydropyrimidine dehydrogenase (DPD) is the initial and rate-limiting enzyme in the catabolism of 5-fluorouracil (5FU). Fluorouracil 99-113 dihydropyrimidine dehydrogenase Homo sapiens 0-31 12542909-1 2003 Dihydropyrimidine dehydrogenase (DPD) is the initial and rate-limiting enzyme in the catabolism of 5-fluorouracil (5FU). Fluorouracil 99-113 dihydropyrimidine dehydrogenase Homo sapiens 33-36 12542909-1 2003 Dihydropyrimidine dehydrogenase (DPD) is the initial and rate-limiting enzyme in the catabolism of 5-fluorouracil (5FU). Fluorouracil 115-118 dihydropyrimidine dehydrogenase Homo sapiens 0-31 12542909-1 2003 Dihydropyrimidine dehydrogenase (DPD) is the initial and rate-limiting enzyme in the catabolism of 5-fluorouracil (5FU). Fluorouracil 115-118 dihydropyrimidine dehydrogenase Homo sapiens 33-36 12497203-1 2003 PURPOSE: Thymidine phosphorylase (TdR-Pase) and dihydropyrimidine dehydrogenase (DPD) are thought to be key enzymes in the metabolic pathways of 5-fluorouracil (5-FU). Fluorouracil 145-159 dihydropyrimidine dehydrogenase Homo sapiens 48-79 12497203-1 2003 PURPOSE: Thymidine phosphorylase (TdR-Pase) and dihydropyrimidine dehydrogenase (DPD) are thought to be key enzymes in the metabolic pathways of 5-fluorouracil (5-FU). Fluorouracil 145-159 dihydropyrimidine dehydrogenase Homo sapiens 81-84 12497203-1 2003 PURPOSE: Thymidine phosphorylase (TdR-Pase) and dihydropyrimidine dehydrogenase (DPD) are thought to be key enzymes in the metabolic pathways of 5-fluorouracil (5-FU). Fluorouracil 161-165 dihydropyrimidine dehydrogenase Homo sapiens 48-79 12497203-1 2003 PURPOSE: Thymidine phosphorylase (TdR-Pase) and dihydropyrimidine dehydrogenase (DPD) are thought to be key enzymes in the metabolic pathways of 5-fluorouracil (5-FU). Fluorouracil 161-165 dihydropyrimidine dehydrogenase Homo sapiens 81-84 12497203-2 2003 Theoretically, tumors which have low DPD and/or high TdR-Pase expression should be 5-FU-sensitive. Fluorouracil 83-87 dihydropyrimidine dehydrogenase Homo sapiens 37-40 12497203-11 2003 There was a significant inverse correlation between DPD expression and 5-FU sensitivity. Fluorouracil 71-75 dihydropyrimidine dehydrogenase Homo sapiens 52-55 12708484-1 2003 The chemosensitivity of micrometastases in the peritoneal cavity to a 5-fluorouracil derivative (TS-1) was examined with a micrometastasis model featuring a human gastric cancer cell line tagged with the green fluorescence protein (GFP) gene in nude mice. Fluorouracil 70-84 Trichinella spiralis resistance 1 Mus musculus 97-101 15618749-2 2003 It has been reported that CYP2A6 and thymidine phosphorylase (TP) are involved in the formation of 5-FU from FT. Fluorouracil 99-103 cytochrome P450 family 2 subfamily A member 6 Homo sapiens 26-32 15618749-5 2003 The formation of 5-FU from FT in human liver S9 was inhibited over 82% by 8-methoxypsoralen, a CYP2A6-selective inhibitor. Fluorouracil 17-21 cytochrome P450 family 2 subfamily A member 6 Homo sapiens 95-101 15618749-7 2003 The results indicated that CYP2A6 played a major role in 5-FU formation, which was consistent with the results using human liver S9. Fluorouracil 57-61 cytochrome P450 family 2 subfamily A member 6 Homo sapiens 27-33 12557710-1 2003 Individual differences exist in the pharmacodynamics of fluorouracil-derived anticancer agents, with circadian variability even in the same patient probably due to individual differences in the distribution of dihydrophrimidine dehydrogenase (DPD), a decomposing enzyme. Fluorouracil 56-68 dihydropyrimidine dehydrogenase Homo sapiens 210-241 12557710-1 2003 Individual differences exist in the pharmacodynamics of fluorouracil-derived anticancer agents, with circadian variability even in the same patient probably due to individual differences in the distribution of dihydrophrimidine dehydrogenase (DPD), a decomposing enzyme. Fluorouracil 56-68 dihydropyrimidine dehydrogenase Homo sapiens 243-246 12743424-2 2003 This report addressed the time-dependent dynamic alterations in the expression of three tumor-associated antigens: carcinoembryonic antigen (CEA), colon-specific antigen (CSAp) and mucin-1 (MUC-1) following chemotherapy with 5-fluorouracil (5-FU) or radioimmunotherapy (RAIT; (131)I-labeled anti-CEA IgG) in human colonic tumor xenografts. Fluorouracil 225-239 centriole, cilia and spindle associated protein Homo sapiens 147-176 12451471-4 2002 RESULTS: Liver microsomes catalyzed 5-FU formation from 5"-DFUR at rates of 10.0-160.1 pmol/min per mg protein and correlated well with CYP2A6-dependent coumarin 7-hydroxylase activity. Fluorouracil 36-40 cytochrome P450 family 2 subfamily A member 6 Homo sapiens 136-142 12451471-4 2002 RESULTS: Liver microsomes catalyzed 5-FU formation from 5"-DFUR at rates of 10.0-160.1 pmol/min per mg protein and correlated well with CYP2A6-dependent coumarin 7-hydroxylase activity. Fluorouracil 36-40 cytochrome P450 family 2 subfamily A member 6 Homo sapiens 153-175 12451471-5 2002 The rates of microsomal 5-FU formation from FT ranged from 44.9 to 808.3 pmol/min per mg protein and also correlated with coumarin 7-hydroxylase activity. Fluorouracil 24-28 cytochrome P450 family 2 subfamily A member 6 Homo sapiens 122-144 12359059-4 2002 We estimated the nuclear transfer of GSTpi induced by the anti-cancer drugs cisplatin (CDDP), irinotecan hydrochloride (CPT-11), etoposide (VP-16) and 5-fluorouracil (5-FU). Fluorouracil 167-171 host cell factor C1 Homo sapiens 140-145 12214467-1 2002 We analyzed the interim results of prognostic significance of pyrimidine nucleoside phosphorylase (PyNPase), thymidylate synthase (TS), and dihydropyrimidine dehydrogenase (DPD) in 5-FU-based chemotherapy for breast cancer. Fluorouracil 181-185 dihydropyrimidine dehydrogenase Homo sapiens 140-171 12084458-9 2002 The enzyme uridine-cytidine monophosphate kinase (UMPK) is an essential and rate-limiting enzyme in 5-FU activation while dihydropyrimidine dehydrogenase (DPD) is a catabolic enzyme that inactivates 5-FU. Fluorouracil 100-104 dihydropyrimidine dehydrogenase Homo sapiens 122-153 12084458-9 2002 The enzyme uridine-cytidine monophosphate kinase (UMPK) is an essential and rate-limiting enzyme in 5-FU activation while dihydropyrimidine dehydrogenase (DPD) is a catabolic enzyme that inactivates 5-FU. Fluorouracil 100-104 dihydropyrimidine dehydrogenase Homo sapiens 155-158 12084458-9 2002 The enzyme uridine-cytidine monophosphate kinase (UMPK) is an essential and rate-limiting enzyme in 5-FU activation while dihydropyrimidine dehydrogenase (DPD) is a catabolic enzyme that inactivates 5-FU. Fluorouracil 199-203 dihydropyrimidine dehydrogenase Homo sapiens 122-153 12084458-9 2002 The enzyme uridine-cytidine monophosphate kinase (UMPK) is an essential and rate-limiting enzyme in 5-FU activation while dihydropyrimidine dehydrogenase (DPD) is a catabolic enzyme that inactivates 5-FU. Fluorouracil 199-203 dihydropyrimidine dehydrogenase Homo sapiens 155-158 12084458-10 2002 Alterations in UMPK and DPD may therefore explain failure of 5-FU response in the absence of alterations in TS or p53. Fluorouracil 61-65 dihydropyrimidine dehydrogenase Homo sapiens 24-27 12095978-1 2002 BACKGROUND: Determination of intratumoral dihydropyrimidine dehydrogenase (DPD) is of clinical interest because increased DPD levels can influence the tumor response to 5-fluorouracil-based chemotherapy through increased inactivation of the agent in tumor cells. Fluorouracil 169-183 dihydropyrimidine dehydrogenase Homo sapiens 42-73 12095978-1 2002 BACKGROUND: Determination of intratumoral dihydropyrimidine dehydrogenase (DPD) is of clinical interest because increased DPD levels can influence the tumor response to 5-fluorouracil-based chemotherapy through increased inactivation of the agent in tumor cells. Fluorouracil 169-183 dihydropyrimidine dehydrogenase Homo sapiens 75-78 12095978-1 2002 BACKGROUND: Determination of intratumoral dihydropyrimidine dehydrogenase (DPD) is of clinical interest because increased DPD levels can influence the tumor response to 5-fluorouracil-based chemotherapy through increased inactivation of the agent in tumor cells. Fluorouracil 169-183 dihydropyrimidine dehydrogenase Homo sapiens 122-125 12095978-9 2002 High DPD mRNA levels in liver metastasis and advanced colorectal cancer may have clinical importance for 5-fluorouracil-based chemosensitivity. Fluorouracil 105-119 dihydropyrimidine dehydrogenase Homo sapiens 5-8 12111108-14 2002 CONCLUSIONS: CDHP clearance was prolonged in the presence of renal impairment, leading to a delayed T(1/2), and high AUC of 5-FU. Fluorouracil 124-128 cadherin 3 Homo sapiens 13-17 12141533-1 2002 Dehydropyrimidine dehydrogenase (DPD) is the initial key enzyme in the regulation of 5-fluorouracil catabolism and thus controls availability of 5-fluorouracil for anabolism. Fluorouracil 85-99 dihydropyrimidine dehydrogenase Homo sapiens 0-31 12141533-1 2002 Dehydropyrimidine dehydrogenase (DPD) is the initial key enzyme in the regulation of 5-fluorouracil catabolism and thus controls availability of 5-fluorouracil for anabolism. Fluorouracil 85-99 dihydropyrimidine dehydrogenase Homo sapiens 33-36 12141533-1 2002 Dehydropyrimidine dehydrogenase (DPD) is the initial key enzyme in the regulation of 5-fluorouracil catabolism and thus controls availability of 5-fluorouracil for anabolism. Fluorouracil 145-159 dihydropyrimidine dehydrogenase Homo sapiens 0-31 12141533-1 2002 Dehydropyrimidine dehydrogenase (DPD) is the initial key enzyme in the regulation of 5-fluorouracil catabolism and thus controls availability of 5-fluorouracil for anabolism. Fluorouracil 145-159 dihydropyrimidine dehydrogenase Homo sapiens 33-36 12141533-2 2002 Modulation of DPD activity may increase the antitumor effect and avoid toxic side effects in 5-fluo-rouracil-based chemotherapy. Fluorouracil 93-108 dihydropyrimidine dehydrogenase Homo sapiens 14-17 12164772-1 2002 A prominent example of the potential application of pharmacogenomics and pharmacogenetics to oncology is the study of dihydropyrimidine dehydrogenase (DPD) in 5-fluorouracil (5-FU) metabolism. Fluorouracil 159-173 dihydropyrimidine dehydrogenase Homo sapiens 151-154 12164772-1 2002 A prominent example of the potential application of pharmacogenomics and pharmacogenetics to oncology is the study of dihydropyrimidine dehydrogenase (DPD) in 5-fluorouracil (5-FU) metabolism. Fluorouracil 175-179 dihydropyrimidine dehydrogenase Homo sapiens 151-154 12164772-3 2002 DPD is the rate-limiting enzyme in the catabolism and clearance of 5-FU. Fluorouracil 67-71 dihydropyrimidine dehydrogenase Homo sapiens 0-3 12164772-5 2002 Molecular studies have suggested there is a relationship between allelic variants in the DPYD gene (the gene that encodes DPD) and a deficiency in DPD activity, providing a potential pharmacogenetic basis for 5-FU toxicity. Fluorouracil 209-213 dihydropyrimidine dehydrogenase Homo sapiens 89-93 12164772-5 2002 Molecular studies have suggested there is a relationship between allelic variants in the DPYD gene (the gene that encodes DPD) and a deficiency in DPD activity, providing a potential pharmacogenetic basis for 5-FU toxicity. Fluorouracil 209-213 dihydropyrimidine dehydrogenase Homo sapiens 122-125 12164772-7 2002 This article reviews the basis and discusses the challenges of pharmacogenetic and pharmacogenomic testing of DPD for the determination of 5-FU efficacy and toxicity. Fluorouracil 139-143 dihydropyrimidine dehydrogenase Homo sapiens 110-113 12044515-10 2002 These findings suggest that the combination of fluoropyrimidine and CDHP for the treatment of tumours with a high basal DPD elicits a greater antitumour effect than treatment with fluoropyrimidines alone and we suggest that CDHP inhibits the degradation of 5-FU in the tumour. Fluorouracil 257-261 dihydropyrimidine dehydrogenase Homo sapiens 120-123 12627817-2 2002 We investigated the therapeutic and adverse drug reaction of intensive chemotherapy using cisplatin (CDDP), 5-FU and dl-leucovorin (LV) (PFL-therapy), which may be producing dual biochemical modulation effect of 5-FU for advanced colorectal carcinoma. Fluorouracil 108-112 profilin 2 Homo sapiens 137-140 12627817-2 2002 We investigated the therapeutic and adverse drug reaction of intensive chemotherapy using cisplatin (CDDP), 5-FU and dl-leucovorin (LV) (PFL-therapy), which may be producing dual biochemical modulation effect of 5-FU for advanced colorectal carcinoma. Fluorouracil 212-216 profilin 2 Homo sapiens 137-140 12006517-1 2002 PURPOSE: This study determined the effect of different weekly dosing schedules of 5-fluorouracil (5-FU)/leucovorin (LV)/eniluracil on dihydropyrimidine dehydrogenase (DPD) activity and plasma uracil levels. Fluorouracil 82-96 dihydropyrimidine dehydrogenase Homo sapiens 134-165 12006517-1 2002 PURPOSE: This study determined the effect of different weekly dosing schedules of 5-fluorouracil (5-FU)/leucovorin (LV)/eniluracil on dihydropyrimidine dehydrogenase (DPD) activity and plasma uracil levels. Fluorouracil 82-96 dihydropyrimidine dehydrogenase Homo sapiens 167-170 12006517-1 2002 PURPOSE: This study determined the effect of different weekly dosing schedules of 5-fluorouracil (5-FU)/leucovorin (LV)/eniluracil on dihydropyrimidine dehydrogenase (DPD) activity and plasma uracil levels. Fluorouracil 98-102 dihydropyrimidine dehydrogenase Homo sapiens 134-165 12074825-1 2002 OBJECTIVE: Dihydropyrimidine dehydrogenase (DPD) catalyzes the degradation of thymine, uracil, and the chemotherapeutic drug 5-Fluorouracil. Fluorouracil 125-139 dihydropyrimidine dehydrogenase Homo sapiens 44-47 12022983-2 2002 High levels of thymidylate synthase (TS) and dihydropyrimidine dehydrogenase (DPD) have been associated with resistance to 5-FU in advanced colorectal cancer. Fluorouracil 123-127 dihydropyrimidine dehydrogenase Homo sapiens 45-76 12022983-2 2002 High levels of thymidylate synthase (TS) and dihydropyrimidine dehydrogenase (DPD) have been associated with resistance to 5-FU in advanced colorectal cancer. Fluorouracil 123-127 dihydropyrimidine dehydrogenase Homo sapiens 78-81 12022983-3 2002 The aim of this study was to investigate the association of TS and DPD mRNA levels with recurrence-free survival in patients with colorectal cancer who are receiving adjuvant 5-FU-based chemotherapy. Fluorouracil 175-179 dihydropyrimidine dehydrogenase Homo sapiens 67-70 11956089-3 2002 In this cellular model, we establish the critical role of UPase as an important anabolic enzyme in 5-fluorouracil (5-FU) activation and pyrimidine salvage pathway regulation. Fluorouracil 99-113 uridine phosphorylase 1 Mus musculus 58-63 11956089-3 2002 In this cellular model, we establish the critical role of UPase as an important anabolic enzyme in 5-fluorouracil (5-FU) activation and pyrimidine salvage pathway regulation. Fluorouracil 115-119 uridine phosphorylase 1 Mus musculus 58-63 11956089-4 2002 It has long been known that UPase regulates the plasma concentration of uridine; however, little is known of the role of UPase in the activation and metabolism of 5-FU and its derivatives, mainly because of the lack of an appropriate model system. Fluorouracil 163-167 uridine phosphorylase 1 Mus musculus 121-126 11956089-5 2002 The experimental data indicate that the disruption of UPase activity in murine ES cells leads to a 10-fold increase in 5-FU IC(50) and a 2-3-fold reduction in its incorporation into nucleic acids, whereas no differences in toxicity is seen with other pyrimidine nucleoside analogues such as 5-fluorouridine, 2"-deoxy-5-fluorouridine, and 1-beta-D-arabinofuranosylcytosine compared with WT (wild-type) ES cells. Fluorouracil 119-123 uridine phosphorylase 1 Mus musculus 54-59 11956089-7 2002 Our data also shows the effect of UPase on the cytotoxicity of 5"-deoxy-5-fluorouridine (5"DFUR), a 5-FU prodrug. Fluorouracil 100-104 uridine phosphorylase 1 Mus musculus 34-39 11956089-13 2002 Considering the role of UPase in 5-FU metabolism and the elevated expression of this protein in cancer cells compared with paired normal tissues, additional investigation should be warranted to firmly establish the clinical role of UPase in the tumor selective activation of 5-FU and capecitabine. Fluorouracil 275-279 uridine phosphorylase 1 Mus musculus 232-237 11894136-1 2002 Topoisomerase I inhibitors of the camptothecin (CPT) family have emerged as potent clinical chemotherapeutic agents in first-line treatment of solid colorectal cancer and in second-line for 5-fluorouracil resistant patients. Fluorouracil 190-204 choline phosphotransferase 1 Homo sapiens 48-51 11901535-5 2002 In this study, cisplatin and UFT, a form of uracil and tegafur which is a prodrug of 5-FU, were administered with immunomodulator Polysaccharide K (PSK) to ten patients with colorectal cancer, who showed distant metastasis in the liver or lung, and the serum levels of sIL-2R and sTNF-R1 and the production of gamma-interferon (gamma-INF) and interleukin-10 by peripheral blood mononuclear cells were measured. Fluorouracil 85-89 TAO kinase 2 Homo sapiens 148-151 11936589-0 2002 Influence of 5-fluorouracil and folinic acid on interleukin-18 production in colorectal cancer patients. Fluorouracil 13-27 interleukin 18 Homo sapiens 48-62 11936589-1 2002 AIMS AND BACKGROUND: This study was carried out to evaluate the IL-18 blood concentrations of operated colorectal cancer patients and their possible variation in response to combination chemotherapy with 5-fluorouracil (5-FU) and folinic acid. Fluorouracil 204-218 interleukin 18 Homo sapiens 64-69 11936589-1 2002 AIMS AND BACKGROUND: This study was carried out to evaluate the IL-18 blood concentrations of operated colorectal cancer patients and their possible variation in response to combination chemotherapy with 5-fluorouracil (5-FU) and folinic acid. Fluorouracil 220-224 interleukin 18 Homo sapiens 64-69 11936589-2 2002 METHODS: IL-18 levels were assayed in sera of 18 healthy donors and 18 surgical colorectal cancer patients before and after adjuvant chemotherapy with 5-fluorouracil and folinic acid. Fluorouracil 151-165 interleukin 18 Homo sapiens 9-14 11936589-6 2002 CONCLUSIONS: This study suggests that treatment with 5-fluorouracil and folinic acid may provoke an increase in IL-18 serum levels in colorectal cancer patients. Fluorouracil 53-67 interleukin 18 Homo sapiens 112-117 12065876-2 2002 METHODS: The expression of p53 and mdm2 was analyzed by an immunohistochemical assay in 80 formalin-fixed paraffin embedded primary tumour samples and related to the clinical response to 5-fluorouracil therapy and to the prognosis of the patients. Fluorouracil 187-201 MDM2 proto-oncogene Homo sapiens 35-39 12138245-0 2002 High-dose 5-Fluorouracil with uridine-diphosphoglucose rescue increases thymidylate synthase inhibition but not 5-Fluorouracil incorporation into RNA in murine tumors. Fluorouracil 10-24 thymidylate synthase Mus musculus 72-92 11679189-2 2001 Moreover, the recent availability of oral formulations of 5-FU together with the ability to modulate the anabolic and catabolic metabolism of 5-FU with leucovorin and dihydropyrimidine dehydrogenase (DPD) inhibitors, respectively, may provide a substantial improvement in the ease of administration and the efficacy of fluoropyrimidine therapy. Fluorouracil 58-62 dihydropyrimidine dehydrogenase Homo sapiens 152-198 11679189-2 2001 Moreover, the recent availability of oral formulations of 5-FU together with the ability to modulate the anabolic and catabolic metabolism of 5-FU with leucovorin and dihydropyrimidine dehydrogenase (DPD) inhibitors, respectively, may provide a substantial improvement in the ease of administration and the efficacy of fluoropyrimidine therapy. Fluorouracil 58-62 dihydropyrimidine dehydrogenase Homo sapiens 200-203 11679189-2 2001 Moreover, the recent availability of oral formulations of 5-FU together with the ability to modulate the anabolic and catabolic metabolism of 5-FU with leucovorin and dihydropyrimidine dehydrogenase (DPD) inhibitors, respectively, may provide a substantial improvement in the ease of administration and the efficacy of fluoropyrimidine therapy. Fluorouracil 142-146 dihydropyrimidine dehydrogenase Homo sapiens 152-198 11679189-2 2001 Moreover, the recent availability of oral formulations of 5-FU together with the ability to modulate the anabolic and catabolic metabolism of 5-FU with leucovorin and dihydropyrimidine dehydrogenase (DPD) inhibitors, respectively, may provide a substantial improvement in the ease of administration and the efficacy of fluoropyrimidine therapy. Fluorouracil 142-146 dihydropyrimidine dehydrogenase Homo sapiens 200-203 11681250-1 2001 TS-1, a novel oral formation of 5-fluorouracil, consists of tegafur (5-FU), CDHP and Oxo. Fluorouracil 32-46 cadherin 3 Homo sapiens 76-80 11604622-10 2001 The wounds treated with 5-fluorouracil produced scars that had a significant (p < 0.01) reduction in all the markers assayed, apart from CD-68. Fluorouracil 24-38 CD68 molecule Homo sapiens 140-145 11505394-5 2001 The authors investigated the activity of TS in 82 bladder cancers and prognostic significance of the levels of TS and/or activities of dihydropyrimidine dehydrogenase (DPD), an important enzyme in the degradation of 5-FU. Fluorouracil 216-220 dihydropyrimidine dehydrogenase Homo sapiens 135-166 11505394-5 2001 The authors investigated the activity of TS in 82 bladder cancers and prognostic significance of the levels of TS and/or activities of dihydropyrimidine dehydrogenase (DPD), an important enzyme in the degradation of 5-FU. Fluorouracil 216-220 dihydropyrimidine dehydrogenase Homo sapiens 168-171 11712813-8 2001 The data suggest that the polymorphism in exon 10 of the XRCC1 gene may be associated with resistance to oxaliplatin/5-FU chemotherapy in advanced colorectal cancer. Fluorouracil 117-121 X-ray repair cross complementing 1 Homo sapiens 57-62 11353746-3 2001 Of 12 cDNA-expressed rat P450 enzymes tested, CYP1A2, CYP3A1, and CYP2C11 had high 5-FU formation rates from 100 microM and 1.0 mM tegafur concentrations. Fluorouracil 83-87 cytochrome P450, family 1, subfamily a, polypeptide 2 Rattus norvegicus 46-52 11350878-1 2001 Dihydropyrimidine dehydrogenase (DPD) is the initial and rate-limiting enzyme in the catabolism of 5-fluorouracil (5FU), and it is suggested that patients with a partial deficiency of this enzyme are at risk from developing a severe 5FU-associated toxicity. Fluorouracil 99-113 dihydropyrimidine dehydrogenase Homo sapiens 0-31 11350878-1 2001 Dihydropyrimidine dehydrogenase (DPD) is the initial and rate-limiting enzyme in the catabolism of 5-fluorouracil (5FU), and it is suggested that patients with a partial deficiency of this enzyme are at risk from developing a severe 5FU-associated toxicity. Fluorouracil 99-113 dihydropyrimidine dehydrogenase Homo sapiens 33-36 11350878-1 2001 Dihydropyrimidine dehydrogenase (DPD) is the initial and rate-limiting enzyme in the catabolism of 5-fluorouracil (5FU), and it is suggested that patients with a partial deficiency of this enzyme are at risk from developing a severe 5FU-associated toxicity. Fluorouracil 115-118 dihydropyrimidine dehydrogenase Homo sapiens 0-31 11350878-1 2001 Dihydropyrimidine dehydrogenase (DPD) is the initial and rate-limiting enzyme in the catabolism of 5-fluorouracil (5FU), and it is suggested that patients with a partial deficiency of this enzyme are at risk from developing a severe 5FU-associated toxicity. Fluorouracil 115-118 dihydropyrimidine dehydrogenase Homo sapiens 33-36 11350878-1 2001 Dihydropyrimidine dehydrogenase (DPD) is the initial and rate-limiting enzyme in the catabolism of 5-fluorouracil (5FU), and it is suggested that patients with a partial deficiency of this enzyme are at risk from developing a severe 5FU-associated toxicity. Fluorouracil 233-236 dihydropyrimidine dehydrogenase Homo sapiens 0-31 11350878-1 2001 Dihydropyrimidine dehydrogenase (DPD) is the initial and rate-limiting enzyme in the catabolism of 5-fluorouracil (5FU), and it is suggested that patients with a partial deficiency of this enzyme are at risk from developing a severe 5FU-associated toxicity. Fluorouracil 233-236 dihydropyrimidine dehydrogenase Homo sapiens 33-36 11383215-0 2001 [Correlation between 5-fluorouracil (5-FU) sensitivity as measured by collagen gel droplet embedded culture drug sensitivity test (CD-DST) and expression of orotate phosphoribosyl transferase (OPRT), thymidylate synthase (TS), and dihydropyrimidine dehydrogenase (DPD) in colorectal cancer]. Fluorouracil 37-41 dihydropyrimidine dehydrogenase Homo sapiens 231-262 11383215-0 2001 [Correlation between 5-fluorouracil (5-FU) sensitivity as measured by collagen gel droplet embedded culture drug sensitivity test (CD-DST) and expression of orotate phosphoribosyl transferase (OPRT), thymidylate synthase (TS), and dihydropyrimidine dehydrogenase (DPD) in colorectal cancer]. Fluorouracil 37-41 dihydropyrimidine dehydrogenase Homo sapiens 264-267 11295091-4 2001 5-FU is catabolized to 2-fluoro-beta-alanine by dihydropyrimidine dehydrogenase (DPD) in liver and tumors. Fluorouracil 0-4 dihydropyrimidine dehydrogenase Homo sapiens 48-79 11295091-4 2001 5-FU is catabolized to 2-fluoro-beta-alanine by dihydropyrimidine dehydrogenase (DPD) in liver and tumors. Fluorouracil 0-4 dihydropyrimidine dehydrogenase Homo sapiens 81-84 11283924-1 2001 BACKGROUND: The oral administration of 5-fluorouracil (5-FU) is hindered by erratic bioavailability due to catabolism of 5-FU by the enzyme dihydropyrimidine dehydrogenase (DPD) in the gastrointestinal tract. Fluorouracil 39-53 dihydropyrimidine dehydrogenase Homo sapiens 140-171 11283924-1 2001 BACKGROUND: The oral administration of 5-fluorouracil (5-FU) is hindered by erratic bioavailability due to catabolism of 5-FU by the enzyme dihydropyrimidine dehydrogenase (DPD) in the gastrointestinal tract. Fluorouracil 39-53 dihydropyrimidine dehydrogenase Homo sapiens 173-176 11283924-1 2001 BACKGROUND: The oral administration of 5-fluorouracil (5-FU) is hindered by erratic bioavailability due to catabolism of 5-FU by the enzyme dihydropyrimidine dehydrogenase (DPD) in the gastrointestinal tract. Fluorouracil 55-59 dihydropyrimidine dehydrogenase Homo sapiens 140-171 11283924-1 2001 BACKGROUND: The oral administration of 5-fluorouracil (5-FU) is hindered by erratic bioavailability due to catabolism of 5-FU by the enzyme dihydropyrimidine dehydrogenase (DPD) in the gastrointestinal tract. Fluorouracil 55-59 dihydropyrimidine dehydrogenase Homo sapiens 173-176 11283924-1 2001 BACKGROUND: The oral administration of 5-fluorouracil (5-FU) is hindered by erratic bioavailability due to catabolism of 5-FU by the enzyme dihydropyrimidine dehydrogenase (DPD) in the gastrointestinal tract. Fluorouracil 121-125 dihydropyrimidine dehydrogenase Homo sapiens 140-171 11283924-1 2001 BACKGROUND: The oral administration of 5-fluorouracil (5-FU) is hindered by erratic bioavailability due to catabolism of 5-FU by the enzyme dihydropyrimidine dehydrogenase (DPD) in the gastrointestinal tract. Fluorouracil 121-125 dihydropyrimidine dehydrogenase Homo sapiens 173-176 11283924-2 2001 Eniluracil is a potent inactivator of DPD which results in 100% oral bioavailability of 5-FU. Fluorouracil 88-92 dihydropyrimidine dehydrogenase Homo sapiens 38-41 11329775-3 2001 By controlling DPD activity, a new class of fluorinated pyrimidines have been developed to minimize the variability of 5-FU pharmacodynamics, to decrease 5-FU toxicity, and improve its efficacy. Fluorouracil 119-123 dihydropyrimidine dehydrogenase Homo sapiens 15-18 11329775-3 2001 By controlling DPD activity, a new class of fluorinated pyrimidines have been developed to minimize the variability of 5-FU pharmacodynamics, to decrease 5-FU toxicity, and improve its efficacy. Fluorouracil 154-158 dihydropyrimidine dehydrogenase Homo sapiens 15-18 11329775-4 2001 Recently, these drugs, referred to as DIFs (DPD inhibitory fluoropyrimidines), have brought us to a new era of oral 5-FU therapy. Fluorouracil 116-120 dihydropyrimidine dehydrogenase Homo sapiens 44-47 11241325-2 2001 The recent availability of oral formulations of 5-FU in conjunction with the ability to modulate the anabolic and catabolic metabolism of 5-FU with leucovorin and dihydropyrimidine dehydrogenase (DPD) inhibitors, respectively, may provide a substantial improvement in the ease of administration and the efficacy of fluoropyrimidine therapy. Fluorouracil 48-52 dihydropyrimidine dehydrogenase Homo sapiens 148-194 11241325-2 2001 The recent availability of oral formulations of 5-FU in conjunction with the ability to modulate the anabolic and catabolic metabolism of 5-FU with leucovorin and dihydropyrimidine dehydrogenase (DPD) inhibitors, respectively, may provide a substantial improvement in the ease of administration and the efficacy of fluoropyrimidine therapy. Fluorouracil 48-52 dihydropyrimidine dehydrogenase Homo sapiens 196-199 11299748-16 2001 These results suggest a link between MTHFR genotype and the folate pool in gastrointestinal cancer, leading to the association of MTHFR genotype with TS inhibition rate upon 5-FU exposure. Fluorouracil 174-178 methylenetetrahydrofolate reductase Homo sapiens 37-42 11299748-16 2001 These results suggest a link between MTHFR genotype and the folate pool in gastrointestinal cancer, leading to the association of MTHFR genotype with TS inhibition rate upon 5-FU exposure. Fluorouracil 174-178 methylenetetrahydrofolate reductase Homo sapiens 130-135 11299748-17 2001 The MTHFR genotype might be considered in the design of 5-FU-based chemotherapy, especially in patient-specific strategies with leucovorin supplementation. Fluorouracil 56-60 methylenetetrahydrofolate reductase Homo sapiens 4-9 11291832-12 2001 2) The administration of 5FU with an inhibitor of dihydropyrimidine dehydrogenase (DPD) to minimise the erratic absorption and variable clearance of 5FU: the preparations UFT, S1, and ethinyluracil/5FU contain an oral fluoropyrimidine co-administered orally with inhibitors of this enzyme. Fluorouracil 25-28 dihydropyrimidine dehydrogenase Homo sapiens 50-81 11291832-12 2001 2) The administration of 5FU with an inhibitor of dihydropyrimidine dehydrogenase (DPD) to minimise the erratic absorption and variable clearance of 5FU: the preparations UFT, S1, and ethinyluracil/5FU contain an oral fluoropyrimidine co-administered orally with inhibitors of this enzyme. Fluorouracil 25-28 dihydropyrimidine dehydrogenase Homo sapiens 83-86 11291832-12 2001 2) The administration of 5FU with an inhibitor of dihydropyrimidine dehydrogenase (DPD) to minimise the erratic absorption and variable clearance of 5FU: the preparations UFT, S1, and ethinyluracil/5FU contain an oral fluoropyrimidine co-administered orally with inhibitors of this enzyme. Fluorouracil 149-152 dihydropyrimidine dehydrogenase Homo sapiens 50-81 11291832-12 2001 2) The administration of 5FU with an inhibitor of dihydropyrimidine dehydrogenase (DPD) to minimise the erratic absorption and variable clearance of 5FU: the preparations UFT, S1, and ethinyluracil/5FU contain an oral fluoropyrimidine co-administered orally with inhibitors of this enzyme. Fluorouracil 149-152 dihydropyrimidine dehydrogenase Homo sapiens 83-86 11291832-12 2001 2) The administration of 5FU with an inhibitor of dihydropyrimidine dehydrogenase (DPD) to minimise the erratic absorption and variable clearance of 5FU: the preparations UFT, S1, and ethinyluracil/5FU contain an oral fluoropyrimidine co-administered orally with inhibitors of this enzyme. Fluorouracil 149-152 dihydropyrimidine dehydrogenase Homo sapiens 50-81 11291832-12 2001 2) The administration of 5FU with an inhibitor of dihydropyrimidine dehydrogenase (DPD) to minimise the erratic absorption and variable clearance of 5FU: the preparations UFT, S1, and ethinyluracil/5FU contain an oral fluoropyrimidine co-administered orally with inhibitors of this enzyme. Fluorouracil 149-152 dihydropyrimidine dehydrogenase Homo sapiens 83-86 11334264-3 2001 Interactions between bropirimine and 5-fluorouracil (5-FU) were investigated on dihydropyrimidine dehydrogenase (DPD) activity, the rate-limiting enzyme of 5-FU metabolism, in human liver cytosol. Fluorouracil 53-57 dihydropyrimidine dehydrogenase Homo sapiens 80-111 11334264-3 2001 Interactions between bropirimine and 5-fluorouracil (5-FU) were investigated on dihydropyrimidine dehydrogenase (DPD) activity, the rate-limiting enzyme of 5-FU metabolism, in human liver cytosol. Fluorouracil 53-57 dihydropyrimidine dehydrogenase Homo sapiens 113-116 11334264-8 2001 Apparent DPD activity for 5-FU (25 microM) in the cytosol from 12 individual donors ranged from 0.017 to 0.39 (0.16 +/- 0.12) nmol min(-1) mg(-1) protein, indicating a large intersubject variance. Fluorouracil 26-30 dihydropyrimidine dehydrogenase Homo sapiens 9-12 11175343-8 2000 In vitro, Bcr-Abl/p210 induced more growth of myeloid colonies from 5-fluorouracil treated bone marrow than v-Abl/p160. Fluorouracil 68-82 c-abl oncogene 1, non-receptor tyrosine kinase Mus musculus 14-17 11175343-8 2000 In vitro, Bcr-Abl/p210 induced more growth of myeloid colonies from 5-fluorouracil treated bone marrow than v-Abl/p160. Fluorouracil 68-82 envoplakin Mus musculus 18-22 11081569-3 2000 Approximately 85% of 5-FU is degraded by dihydropyrimidine dehydrogenase (DPD); inhibition of this enzyme pathway can increase the amount of circulating 5-FU. Fluorouracil 21-25 dihydropyrimidine dehydrogenase Homo sapiens 41-72 11081569-3 2000 Approximately 85% of 5-FU is degraded by dihydropyrimidine dehydrogenase (DPD); inhibition of this enzyme pathway can increase the amount of circulating 5-FU. Fluorouracil 21-25 dihydropyrimidine dehydrogenase Homo sapiens 74-77 11081569-3 2000 Approximately 85% of 5-FU is degraded by dihydropyrimidine dehydrogenase (DPD); inhibition of this enzyme pathway can increase the amount of circulating 5-FU. Fluorouracil 153-157 dihydropyrimidine dehydrogenase Homo sapiens 41-72 11081569-3 2000 Approximately 85% of 5-FU is degraded by dihydropyrimidine dehydrogenase (DPD); inhibition of this enzyme pathway can increase the amount of circulating 5-FU. Fluorouracil 153-157 dihydropyrimidine dehydrogenase Homo sapiens 74-77 11081572-2 2000 Eniluracil is an effective mechanism-based inactivator of dihydropyrimidine dehydrogenase (DPD), the first enzyme in the catabolic pathway of 5-FU. Fluorouracil 142-146 dihydropyrimidine dehydrogenase Homo sapiens 58-89 11081572-2 2000 Eniluracil is an effective mechanism-based inactivator of dihydropyrimidine dehydrogenase (DPD), the first enzyme in the catabolic pathway of 5-FU. Fluorouracil 142-146 dihydropyrimidine dehydrogenase Homo sapiens 91-94 11081573-1 2000 The pharmacological inactivation of dihydropyrimidine dehydrogenase (DPD) represents one strategy to improve 5-FU therapy, which historically has been associated with unpredictable pharmacological behavior and toxicity. Fluorouracil 109-113 dihydropyrimidine dehydrogenase Homo sapiens 36-67 11081573-1 2000 The pharmacological inactivation of dihydropyrimidine dehydrogenase (DPD) represents one strategy to improve 5-FU therapy, which historically has been associated with unpredictable pharmacological behavior and toxicity. Fluorouracil 109-113 dihydropyrimidine dehydrogenase Homo sapiens 69-72 11081573-2 2000 This is principally due to high interpatient differences in the activity of DPD, the enzyme that mediates the initial and rate-limiting step in 5-FU catabolism. Fluorouracil 144-148 dihydropyrimidine dehydrogenase Homo sapiens 76-79 11081573-3 2000 By inactivating DPD and suppressing the catabolism of 5-FU, eniluracil has dramatically altered the pharmacological profile of 5-FU. Fluorouracil 127-131 dihydropyrimidine dehydrogenase Homo sapiens 16-19 11092985-0 2000 Regulation of dihydropyrimidine dehydrogenase and pyrimidine nucleoside phosphorylase activities by growth factors and subsequent effects on 5-fluorouracil sensitivity in tumor cells. Fluorouracil 141-155 dihydropyrimidine dehydrogenase Homo sapiens 14-45 11092985-1 2000 Dihydropyrimidine dehydrogenase (DPD) and pyrimidine nucleoside phosphorylase (PyNPase) are the first and rate-limiting enzymes that regulate 5-fluorouracil (5-FU) metabolism, and tumoral DPD activity appears to be a promising predictor of 5-FU sensitivity. Fluorouracil 142-156 dihydropyrimidine dehydrogenase Homo sapiens 0-31 11092985-1 2000 Dihydropyrimidine dehydrogenase (DPD) and pyrimidine nucleoside phosphorylase (PyNPase) are the first and rate-limiting enzymes that regulate 5-fluorouracil (5-FU) metabolism, and tumoral DPD activity appears to be a promising predictor of 5-FU sensitivity. Fluorouracil 142-156 dihydropyrimidine dehydrogenase Homo sapiens 33-36 11092985-1 2000 Dihydropyrimidine dehydrogenase (DPD) and pyrimidine nucleoside phosphorylase (PyNPase) are the first and rate-limiting enzymes that regulate 5-fluorouracil (5-FU) metabolism, and tumoral DPD activity appears to be a promising predictor of 5-FU sensitivity. Fluorouracil 158-162 dihydropyrimidine dehydrogenase Homo sapiens 0-31 11092985-1 2000 Dihydropyrimidine dehydrogenase (DPD) and pyrimidine nucleoside phosphorylase (PyNPase) are the first and rate-limiting enzymes that regulate 5-fluorouracil (5-FU) metabolism, and tumoral DPD activity appears to be a promising predictor of 5-FU sensitivity. Fluorouracil 158-162 dihydropyrimidine dehydrogenase Homo sapiens 33-36 11092985-1 2000 Dihydropyrimidine dehydrogenase (DPD) and pyrimidine nucleoside phosphorylase (PyNPase) are the first and rate-limiting enzymes that regulate 5-fluorouracil (5-FU) metabolism, and tumoral DPD activity appears to be a promising predictor of 5-FU sensitivity. Fluorouracil 240-244 dihydropyrimidine dehydrogenase Homo sapiens 0-31 11092985-1 2000 Dihydropyrimidine dehydrogenase (DPD) and pyrimidine nucleoside phosphorylase (PyNPase) are the first and rate-limiting enzymes that regulate 5-fluorouracil (5-FU) metabolism, and tumoral DPD activity appears to be a promising predictor of 5-FU sensitivity. Fluorouracil 240-244 dihydropyrimidine dehydrogenase Homo sapiens 33-36 11092985-8 2000 The tumor environmental factors, EGF and TGF-alpha, may act as intrinsic regulators of DPD and PyNPase activities that affect the 5-FU sensitivity of individual tumors. Fluorouracil 130-134 dihydropyrimidine dehydrogenase Homo sapiens 87-90 11057323-1 2000 We studied dihydropyrimidine dehydrogenase (DPD) and thymidylate synthase (TS), key enzymes in regulating the pharmacokinetics and chemosensitivity to 5-FU, in 36 breast cancer patients as a control group and 18 patients as a 5-FU group, in which 5-FU was given orally for 2 weeks before surgery at a dose of 200 mg/day. Fluorouracil 151-155 dihydropyrimidine dehydrogenase Homo sapiens 11-42 11057323-1 2000 We studied dihydropyrimidine dehydrogenase (DPD) and thymidylate synthase (TS), key enzymes in regulating the pharmacokinetics and chemosensitivity to 5-FU, in 36 breast cancer patients as a control group and 18 patients as a 5-FU group, in which 5-FU was given orally for 2 weeks before surgery at a dose of 200 mg/day. Fluorouracil 151-155 dihydropyrimidine dehydrogenase Homo sapiens 44-47 10995874-2 2000 Many reports have demonstrated that thymidylate synthase (TS) and dihydropyrimidine dehydrogenase (DPD) are biomarkers for the response and prognosis of patients treated with 5-fluorouracil (5-FU)-based chemotherapy. Fluorouracil 175-189 dihydropyrimidine dehydrogenase Homo sapiens 66-97 10995874-2 2000 Many reports have demonstrated that thymidylate synthase (TS) and dihydropyrimidine dehydrogenase (DPD) are biomarkers for the response and prognosis of patients treated with 5-fluorouracil (5-FU)-based chemotherapy. Fluorouracil 175-189 dihydropyrimidine dehydrogenase Homo sapiens 99-102 10995874-2 2000 Many reports have demonstrated that thymidylate synthase (TS) and dihydropyrimidine dehydrogenase (DPD) are biomarkers for the response and prognosis of patients treated with 5-fluorouracil (5-FU)-based chemotherapy. Fluorouracil 191-195 dihydropyrimidine dehydrogenase Homo sapiens 66-97 10995874-2 2000 Many reports have demonstrated that thymidylate synthase (TS) and dihydropyrimidine dehydrogenase (DPD) are biomarkers for the response and prognosis of patients treated with 5-fluorouracil (5-FU)-based chemotherapy. Fluorouracil 191-195 dihydropyrimidine dehydrogenase Homo sapiens 99-102 11192824-0 2000 Early 5-fluorouracil-induced changes of poly(A) polymerase in HeLa and WISH cells. Fluorouracil 6-20 poly(A) polymerase alpha Homo sapiens 40-58 11192824-1 2000 5-Fluorouracil (5-FU), a drug with numerous mechanisms of action which has a long-term suppressive effect on human cancer cell proliferation, mediates both partial dephosphorylation and inactivation of poly(A) polymerase (PAP) [EC. Fluorouracil 0-14 poly(A) polymerase alpha Homo sapiens 202-220 11192824-1 2000 5-Fluorouracil (5-FU), a drug with numerous mechanisms of action which has a long-term suppressive effect on human cancer cell proliferation, mediates both partial dephosphorylation and inactivation of poly(A) polymerase (PAP) [EC. Fluorouracil 0-14 poly(A) polymerase alpha Homo sapiens 222-225 11192824-1 2000 5-Fluorouracil (5-FU), a drug with numerous mechanisms of action which has a long-term suppressive effect on human cancer cell proliferation, mediates both partial dephosphorylation and inactivation of poly(A) polymerase (PAP) [EC. Fluorouracil 16-20 poly(A) polymerase alpha Homo sapiens 202-220 11192824-1 2000 5-Fluorouracil (5-FU), a drug with numerous mechanisms of action which has a long-term suppressive effect on human cancer cell proliferation, mediates both partial dephosphorylation and inactivation of poly(A) polymerase (PAP) [EC. Fluorouracil 16-20 poly(A) polymerase alpha Homo sapiens 222-225 11192824-3 2000 When the same experiment is done in the presence of phosphatase inhibitors, 5-FU-induced partial PAP dephosphorylation is abolished. Fluorouracil 76-80 poly(A) polymerase alpha Homo sapiens 97-100 11192824-5 2000 These results suggest that 5-FU induces early direct or indirect changes in the structure and function of PAP and may regulate pre-mRNA cleavage-polyadenylation. Fluorouracil 27-31 poly(A) polymerase alpha Homo sapiens 106-109 11098485-1 2000 Over the past decade, increasing data have emphasized both the importance of dihydropyrimidine dehydrogenase (DPD), the initial, rate-limiting enzyme in the catabolism of fluorouracil (5-FU), and its role as a control step in 5-FU metabolism, regulating the availability of 5-FU for anabolism. Fluorouracil 171-183 dihydropyrimidine dehydrogenase Homo sapiens 77-108 11098485-1 2000 Over the past decade, increasing data have emphasized both the importance of dihydropyrimidine dehydrogenase (DPD), the initial, rate-limiting enzyme in the catabolism of fluorouracil (5-FU), and its role as a control step in 5-FU metabolism, regulating the availability of 5-FU for anabolism. Fluorouracil 171-183 dihydropyrimidine dehydrogenase Homo sapiens 110-113 11098485-1 2000 Over the past decade, increasing data have emphasized both the importance of dihydropyrimidine dehydrogenase (DPD), the initial, rate-limiting enzyme in the catabolism of fluorouracil (5-FU), and its role as a control step in 5-FU metabolism, regulating the availability of 5-FU for anabolism. Fluorouracil 185-189 dihydropyrimidine dehydrogenase Homo sapiens 77-108 11098485-1 2000 Over the past decade, increasing data have emphasized both the importance of dihydropyrimidine dehydrogenase (DPD), the initial, rate-limiting enzyme in the catabolism of fluorouracil (5-FU), and its role as a control step in 5-FU metabolism, regulating the availability of 5-FU for anabolism. Fluorouracil 185-189 dihydropyrimidine dehydrogenase Homo sapiens 110-113 11098485-1 2000 Over the past decade, increasing data have emphasized both the importance of dihydropyrimidine dehydrogenase (DPD), the initial, rate-limiting enzyme in the catabolism of fluorouracil (5-FU), and its role as a control step in 5-FU metabolism, regulating the availability of 5-FU for anabolism. Fluorouracil 226-230 dihydropyrimidine dehydrogenase Homo sapiens 77-108 11098485-1 2000 Over the past decade, increasing data have emphasized both the importance of dihydropyrimidine dehydrogenase (DPD), the initial, rate-limiting enzyme in the catabolism of fluorouracil (5-FU), and its role as a control step in 5-FU metabolism, regulating the availability of 5-FU for anabolism. Fluorouracil 226-230 dihydropyrimidine dehydrogenase Homo sapiens 110-113 10891390-5 2000 In addition, the expression of TRAF-2 and cIAP-1, which are transcriptionally regulated by NF-kappaB and function as anti-apoptotic molecules through the interruption of caspase pathway, was also inhibited by 5-FU. Fluorouracil 209-213 TNF receptor associated factor 2 Homo sapiens 31-37 11060767-5 2000 However, oral administration of 5-FU has been hampered by incomplete and erratic bioavailability due to substantial variability in the activity of dihydropyrimidine dehydrogenase (DPD), the rate-limiting enzyme in 5-FU catabolism. Fluorouracil 32-36 dihydropyrimidine dehydrogenase Homo sapiens 147-178 11060767-5 2000 However, oral administration of 5-FU has been hampered by incomplete and erratic bioavailability due to substantial variability in the activity of dihydropyrimidine dehydrogenase (DPD), the rate-limiting enzyme in 5-FU catabolism. Fluorouracil 32-36 dihydropyrimidine dehydrogenase Homo sapiens 180-183 11060767-5 2000 However, oral administration of 5-FU has been hampered by incomplete and erratic bioavailability due to substantial variability in the activity of dihydropyrimidine dehydrogenase (DPD), the rate-limiting enzyme in 5-FU catabolism. Fluorouracil 214-218 dihydropyrimidine dehydrogenase Homo sapiens 147-178 11060767-5 2000 However, oral administration of 5-FU has been hampered by incomplete and erratic bioavailability due to substantial variability in the activity of dihydropyrimidine dehydrogenase (DPD), the rate-limiting enzyme in 5-FU catabolism. Fluorouracil 214-218 dihydropyrimidine dehydrogenase Homo sapiens 180-183 11060767-6 2000 Eniluracil (ethynyluracil, GlaxoWellcome, USA), a uracil analogue, which irreversibly inhibits DPD, increases the oral bioavailability of 5-FU to 100%, facilitating uniform absorption and predictable toxicity. Fluorouracil 138-142 dihydropyrimidine dehydrogenase Homo sapiens 95-98 11060767-15 2000 Eniluracil is a promising drug, which permits reliable and safe administration of oral 5-FU and has the potential to overcome 5-FU resistance mediated by overexpression of DPD. Fluorouracil 126-130 dihydropyrimidine dehydrogenase Homo sapiens 172-175 10853017-1 2000 5-fluorouracil (5-FU) has been used widely, including in gastrointestinal cancer, breast cancer, and non-small cell lung cancer (NSCLC), and its efficacy has been reported to be associated with intratumoral expression of thymidylate synthase (TS) and dihydropyrimidine dehydrogenase (DPD). Fluorouracil 0-14 dihydropyrimidine dehydrogenase Homo sapiens 251-282 10853017-1 2000 5-fluorouracil (5-FU) has been used widely, including in gastrointestinal cancer, breast cancer, and non-small cell lung cancer (NSCLC), and its efficacy has been reported to be associated with intratumoral expression of thymidylate synthase (TS) and dihydropyrimidine dehydrogenase (DPD). Fluorouracil 0-14 dihydropyrimidine dehydrogenase Homo sapiens 284-287 10853017-1 2000 5-fluorouracil (5-FU) has been used widely, including in gastrointestinal cancer, breast cancer, and non-small cell lung cancer (NSCLC), and its efficacy has been reported to be associated with intratumoral expression of thymidylate synthase (TS) and dihydropyrimidine dehydrogenase (DPD). Fluorouracil 16-20 dihydropyrimidine dehydrogenase Homo sapiens 251-282 10853017-1 2000 5-fluorouracil (5-FU) has been used widely, including in gastrointestinal cancer, breast cancer, and non-small cell lung cancer (NSCLC), and its efficacy has been reported to be associated with intratumoral expression of thymidylate synthase (TS) and dihydropyrimidine dehydrogenase (DPD). Fluorouracil 16-20 dihydropyrimidine dehydrogenase Homo sapiens 284-287 10853017-6 2000 The Cox regression analysis of prognostic variables for NSCLC patients treated with 5-FU demonstrated that the simultaneous evaluation for both TS and DPD expression was found to be a significant indicator of a poor prognosis (P=0.0043). Fluorouracil 84-88 dihydropyrimidine dehydrogenase Homo sapiens 151-154 10853017-7 2000 Our results demonstrated that the evaluation of intratumoral TS and DPD activity can be used to accurately predict responsiveness to 5-FU-based chemotherapy in NSCLC patients. Fluorouracil 133-137 dihydropyrimidine dehydrogenase Homo sapiens 68-71 10873092-9 2000 Of the anticancer agents prescribed for patients with colorectal cancers, including doxorubicin, mitomycin C, cisplatin, 5-fluorouracil, etoposide, and a camptothecin derivative, mRNA expression of MRP2 was significantly associated with resistance to cisplatin. Fluorouracil 121-135 ATP binding cassette subfamily C member 2 Homo sapiens 198-202 10778957-0 2000 Colorectal tumors responding to 5-fluorouracil have low gene expression levels of dihydropyrimidine dehydrogenase, thymidylate synthase, and thymidine phosphorylase. Fluorouracil 32-46 dihydropyrimidine dehydrogenase Homo sapiens 82-113 10778957-4 2000 In this study, we investigated the association between intratumoral gene expression of the pyrimidine catabolism enzyme dihydropyrimidine dehydrogenase (DPD) and the response of colorectal tumors to the same 5-FU-based protocol. Fluorouracil 208-212 dihydropyrimidine dehydrogenase Homo sapiens 120-151 10778957-4 2000 In this study, we investigated the association between intratumoral gene expression of the pyrimidine catabolism enzyme dihydropyrimidine dehydrogenase (DPD) and the response of colorectal tumors to the same 5-FU-based protocol. Fluorouracil 208-212 dihydropyrimidine dehydrogenase Homo sapiens 153-156 10778957-5 2000 DPD expressions were measured by quantitative reverse transcription-PCR in 33 pretreatment biopsies of colorectal tumors from patients who went on to receive treatment with 5-FU and leucovorin (LV). Fluorouracil 173-177 dihydropyrimidine dehydrogenase Homo sapiens 0-3 10778957-6 2000 The range of DPD gene expression in those tumors that were nonresponsive to 5-FU was much broader than that of the responding tumors. Fluorouracil 76-80 dihydropyrimidine dehydrogenase Homo sapiens 13-16 10778957-9 2000 All of the tumors that responded to 5-FU therapy (11 of 33) had expression values of all three of the genes, TS, TP, and DPD, below their respective nonresponse cutoff values, whereas, in each of the nonresponding tumors, at least one of these gene expressions was high. Fluorouracil 36-40 dihydropyrimidine dehydrogenase Homo sapiens 121-124 10778957-11 2000 The results of this study show that intratumoral gene expression level of DPD is associated with tumor response to 5-FU and that the use of more than one independent determinant of response permits the identification of a high percentage of responding patients. Fluorouracil 115-119 dihydropyrimidine dehydrogenase Homo sapiens 74-77 10803677-1 2000 Dihydropyrimidine dehydrogenase (DPD) degrades over 80% of administered 5-fluorouracil (5FU), thereby regulating the efficacy of this commonly used anticancer agent. Fluorouracil 72-86 dihydropyrimidine dehydrogenase Homo sapiens 0-31 10803677-1 2000 Dihydropyrimidine dehydrogenase (DPD) degrades over 80% of administered 5-fluorouracil (5FU), thereby regulating the efficacy of this commonly used anticancer agent. Fluorouracil 72-86 dihydropyrimidine dehydrogenase Homo sapiens 33-36 10803677-1 2000 Dihydropyrimidine dehydrogenase (DPD) degrades over 80% of administered 5-fluorouracil (5FU), thereby regulating the efficacy of this commonly used anticancer agent. Fluorouracil 88-91 dihydropyrimidine dehydrogenase Homo sapiens 0-31 10803677-1 2000 Dihydropyrimidine dehydrogenase (DPD) degrades over 80% of administered 5-fluorouracil (5FU), thereby regulating the efficacy of this commonly used anticancer agent. Fluorouracil 88-91 dihydropyrimidine dehydrogenase Homo sapiens 33-36 10811492-1 2000 BACKGROUND: Dihydropyrimidine dehydrogenase (DPD) is the first enzyme that metabolizes 5-fluorouracil (5-FU). Fluorouracil 87-101 dihydropyrimidine dehydrogenase Homo sapiens 12-43 10811492-1 2000 BACKGROUND: Dihydropyrimidine dehydrogenase (DPD) is the first enzyme that metabolizes 5-fluorouracil (5-FU). Fluorouracil 87-101 dihydropyrimidine dehydrogenase Homo sapiens 45-48 10811492-1 2000 BACKGROUND: Dihydropyrimidine dehydrogenase (DPD) is the first enzyme that metabolizes 5-fluorouracil (5-FU). Fluorouracil 103-107 dihydropyrimidine dehydrogenase Homo sapiens 12-43 10811492-1 2000 BACKGROUND: Dihydropyrimidine dehydrogenase (DPD) is the first enzyme that metabolizes 5-fluorouracil (5-FU). Fluorouracil 103-107 dihydropyrimidine dehydrogenase Homo sapiens 45-48 10811492-11 2000 CONCLUSIONS: We investigated the characterization of DPD immunohistochemically, and showed that immunohistochemical expression of DPD can be used to predict the sensitivity of colorectal carcinomas to 5-FU. Fluorouracil 201-205 dihydropyrimidine dehydrogenase Homo sapiens 130-133 10811509-0 2000 MTHFR gene polymorphism and severe toxicity during adjuvant treatment of early breast cancer with cyclophosphamide, methotrexate, and fluorouracil (CMF) Fluorouracil 134-146 methylenetetrahydrofolate reductase Homo sapiens 0-5 10738119-3 2000 Dihydropyrimidine dehydrogenase (DPD) activity may be a potential factor controlling fluorouracil (FU) responsiveness at the tumoral level and its importance is stressed. Fluorouracil 85-97 dihydropyrimidine dehydrogenase Homo sapiens 0-31 10738119-3 2000 Dihydropyrimidine dehydrogenase (DPD) activity may be a potential factor controlling fluorouracil (FU) responsiveness at the tumoral level and its importance is stressed. Fluorouracil 85-97 dihydropyrimidine dehydrogenase Homo sapiens 33-36 10679758-9 2000 In a chemosensitivity test, PSK-1 cells were found to be sensitive in vitro to cisplatin, etoposide, and doxorubicin, but resistant to dacarbazine and 5-fluorouracil. Fluorouracil 151-165 TAO kinase 2 Homo sapiens 28-33 10854135-1 2000 BACKGROUND/PURPOSE: Dihydropyridmidine dehydrogenase (DPD) is the initial and rate-limiting enzyme in the catabolism of 5-fluorouracil (5FU). Fluorouracil 120-134 dihydropyrimidine dehydrogenase Homo sapiens 20-52 10854135-1 2000 BACKGROUND/PURPOSE: Dihydropyridmidine dehydrogenase (DPD) is the initial and rate-limiting enzyme in the catabolism of 5-fluorouracil (5FU). Fluorouracil 120-134 dihydropyrimidine dehydrogenase Homo sapiens 54-57 10854135-1 2000 BACKGROUND/PURPOSE: Dihydropyridmidine dehydrogenase (DPD) is the initial and rate-limiting enzyme in the catabolism of 5-fluorouracil (5FU). Fluorouracil 136-139 dihydropyrimidine dehydrogenase Homo sapiens 20-52 10854135-1 2000 BACKGROUND/PURPOSE: Dihydropyridmidine dehydrogenase (DPD) is the initial and rate-limiting enzyme in the catabolism of 5-fluorouracil (5FU). Fluorouracil 136-139 dihydropyrimidine dehydrogenase Homo sapiens 54-57 10741292-0 2000 Can dihydropyrimidine dehydrogenase impact 5-fluorouracil-based treatment? Fluorouracil 43-57 dihydropyrimidine dehydrogenase Homo sapiens 4-35 10741292-1 2000 More than 80% of an administered 5-fluorouracil (5-FU) dose is degraded by dihydropyrimidine dehydrogenase (DPD), making it an important regulator of this commonly used anticancer agent. Fluorouracil 33-47 dihydropyrimidine dehydrogenase Homo sapiens 75-106 10741292-1 2000 More than 80% of an administered 5-fluorouracil (5-FU) dose is degraded by dihydropyrimidine dehydrogenase (DPD), making it an important regulator of this commonly used anticancer agent. Fluorouracil 33-47 dihydropyrimidine dehydrogenase Homo sapiens 108-111 10741292-1 2000 More than 80% of an administered 5-fluorouracil (5-FU) dose is degraded by dihydropyrimidine dehydrogenase (DPD), making it an important regulator of this commonly used anticancer agent. Fluorouracil 49-53 dihydropyrimidine dehydrogenase Homo sapiens 75-106 10741292-1 2000 More than 80% of an administered 5-fluorouracil (5-FU) dose is degraded by dihydropyrimidine dehydrogenase (DPD), making it an important regulator of this commonly used anticancer agent. Fluorouracil 49-53 dihydropyrimidine dehydrogenase Homo sapiens 108-111 10646641-2 2000 The uracil phosphoribosyltransferase (UPRT) gene, which is absent from mammalian cells, directly converts 5-fluorouracil (5-FU) to 5-fluorouridine 5"-monophosphate. Fluorouracil 106-120 uracil phosphoribosyltransferase homolog Homo sapiens 38-42 10646641-2 2000 The uracil phosphoribosyltransferase (UPRT) gene, which is absent from mammalian cells, directly converts 5-fluorouracil (5-FU) to 5-fluorouridine 5"-monophosphate. Fluorouracil 122-126 uracil phosphoribosyltransferase homolog Homo sapiens 4-36 10646641-2 2000 The uracil phosphoribosyltransferase (UPRT) gene, which is absent from mammalian cells, directly converts 5-fluorouracil (5-FU) to 5-fluorouridine 5"-monophosphate. Fluorouracil 122-126 uracil phosphoribosyltransferase homolog Homo sapiens 38-42 10646641-4 2000 In vitro study showed that 9L cells, transduced with the UPRT gene by an adenovirus, were 16 times more sensitive to 5-FU, and CD + UPRT-transduced cells were 6,000 times more sensitive to 5-FC than parent cells, indicating that the acquisition of CD and UPRT further increased the 5-FC sensitivity of 9L cells compared with cells transduced with CD alone. Fluorouracil 117-121 uracil phosphoribosyltransferase homolog Homo sapiens 57-61 10606257-5 1999 The inconsistent absorption of oral 5-FU may be attributed to varying levels of dihydropyrimidine dehydrogenase (DPD) in the gastrointestinal tract. Fluorouracil 36-40 dihydropyrimidine dehydrogenase Homo sapiens 80-111 10606257-5 1999 The inconsistent absorption of oral 5-FU may be attributed to varying levels of dihydropyrimidine dehydrogenase (DPD) in the gastrointestinal tract. Fluorouracil 36-40 dihydropyrimidine dehydrogenase Homo sapiens 113-116 10606257-6 1999 Two methods have been used to circumvent 5-FU"s metabolism by DPD in the gastrointestinal tract. Fluorouracil 41-45 dihydropyrimidine dehydrogenase Homo sapiens 62-65 10606257-7 1999 First, DPD may be inactivated, allowing for reliable, consistent absorption of 5-FU. Fluorouracil 79-83 dihydropyrimidine dehydrogenase Homo sapiens 7-10 10584579-6 1999 Thymidylate synthase (TS) and dihydropyrimidine dehydrogenase (DPD), which are enzymes in 5-FU metabolism, and the labeling index (ID) of DNA fragmentation in the tumor were estimated before and after UFT. Fluorouracil 90-94 dihydropyrimidine dehydrogenase Homo sapiens 63-66 10519414-1 1999 Uridine phosphorylase (UPase) plays an important role in the activation of 5-fluorouracil and in the regulation of tissue and plasma concentration of uridine, a potential biochemical modulator of 5-fluorouracil therapy. Fluorouracil 75-89 uridine phosphorylase 1 Mus musculus 23-28 10519414-1 1999 Uridine phosphorylase (UPase) plays an important role in the activation of 5-fluorouracil and in the regulation of tissue and plasma concentration of uridine, a potential biochemical modulator of 5-fluorouracil therapy. Fluorouracil 196-210 uridine phosphorylase 1 Mus musculus 23-28 10537327-0 1999 Dihydropyrimidine dehydrogenase: its role in 5-fluorouracil clinical toxicity and tumor resistance. Fluorouracil 45-59 dihydropyrimidine dehydrogenase Homo sapiens 0-31 10537350-1 1999 Dihydropyrimidine dehydrogenase (DPD) is the rate-limiting enzyme for 5-fluorouracil catabolism. Fluorouracil 70-84 dihydropyrimidine dehydrogenase Homo sapiens 0-31 10537350-1 1999 Dihydropyrimidine dehydrogenase (DPD) is the rate-limiting enzyme for 5-fluorouracil catabolism. Fluorouracil 70-84 dihydropyrimidine dehydrogenase Homo sapiens 33-36 10560382-6 1999 Our results suggested that the efficacy of intra-arterial infusion for metastatic liver tumor is mainly due to the fact that the high concentration of 5-FU is enough to overcome the high clearance of 5-FU, which is caused by DPD. Fluorouracil 200-204 dihydropyrimidine dehydrogenase Homo sapiens 225-228 10499633-8 1999 In addition, biochemical examination revealed that 5-FU and HU blocked the antimitotic agent-induced increase of p21WAF1/CIP1 protein levels, as well as prevented the hyperphosphorylation of the bcl-2 and c-raf-1 proteins. Fluorouracil 51-55 TNF receptor associated factor 3 Homo sapiens 205-212 10499634-1 1999 Dihydropyrimidine dehydrogenase (DPD) is responsible for degradation of the pyrimidines uracil and thymine and the inactivation of the chemotherapeutic agent 5-fluorouracil. Fluorouracil 158-172 dihydropyrimidine dehydrogenase Homo sapiens 0-31 10499634-1 1999 Dihydropyrimidine dehydrogenase (DPD) is responsible for degradation of the pyrimidines uracil and thymine and the inactivation of the chemotherapeutic agent 5-fluorouracil. Fluorouracil 158-172 dihydropyrimidine dehydrogenase Homo sapiens 33-36 10499634-2 1999 DPD activity is highly variable in cancer populations, and this variation may influence the antitumor efficacy of 5-fluorouracil. Fluorouracil 114-128 dihydropyrimidine dehydrogenase Homo sapiens 0-3 10499641-3 1999 At the basal gene expression level, glutathione S-transferase pi (GSTpi) expression correlated with the observed resistance to CDDP, whereas dihydropyrimidine dehydrogenase (DPD) and multidrug resistance-associated protein (MRP) expression was related to 5-FU resistance. Fluorouracil 255-259 dihydropyrimidine dehydrogenase Homo sapiens 141-172 10473079-0 1999 Life-threatening toxicity in a dihydropyrimidine dehydrogenase-deficient patient after treatment with topical 5-fluorouracil. Fluorouracil 110-124 dihydropyrimidine dehydrogenase Homo sapiens 31-62 10473079-1 1999 In humans, 80-90% of an administered dose of 5-fluorouracil (5-FU) is degraded by dihydropyrimidine dehydrogenase (DPD; EC 1.3.1.2), the initial rate-limiting enzyme in pyrimidine catabolism. Fluorouracil 45-59 dihydropyrimidine dehydrogenase Homo sapiens 82-113 10473079-1 1999 In humans, 80-90% of an administered dose of 5-fluorouracil (5-FU) is degraded by dihydropyrimidine dehydrogenase (DPD; EC 1.3.1.2), the initial rate-limiting enzyme in pyrimidine catabolism. Fluorouracil 45-59 dihydropyrimidine dehydrogenase Homo sapiens 115-118 10473079-1 1999 In humans, 80-90% of an administered dose of 5-fluorouracil (5-FU) is degraded by dihydropyrimidine dehydrogenase (DPD; EC 1.3.1.2), the initial rate-limiting enzyme in pyrimidine catabolism. Fluorouracil 61-65 dihydropyrimidine dehydrogenase Homo sapiens 82-113 10473079-1 1999 In humans, 80-90% of an administered dose of 5-fluorouracil (5-FU) is degraded by dihydropyrimidine dehydrogenase (DPD; EC 1.3.1.2), the initial rate-limiting enzyme in pyrimidine catabolism. Fluorouracil 61-65 dihydropyrimidine dehydrogenase Homo sapiens 115-118 10489900-2 1999 This in vivo study investigated the ability of hypoxia to regulate the gene expression of thymidylate synthase (TS), the target enzyme of 5-FU. Fluorouracil 138-142 thymidylate synthase Mus musculus 90-110 10489900-2 1999 This in vivo study investigated the ability of hypoxia to regulate the gene expression of thymidylate synthase (TS), the target enzyme of 5-FU. Fluorouracil 138-142 thymidylate synthase Mus musculus 112-114 10436410-3 1999 The use of oral 5-FU was abandoned because of erratic absorption caused by varying levels of dihydropyrimidine dehydrogenase (DPD) found in the gastrointestinal tract. Fluorouracil 16-20 dihydropyrimidine dehydrogenase Homo sapiens 93-124 10436410-3 1999 The use of oral 5-FU was abandoned because of erratic absorption caused by varying levels of dihydropyrimidine dehydrogenase (DPD) found in the gastrointestinal tract. Fluorouracil 16-20 dihydropyrimidine dehydrogenase Homo sapiens 126-129 10442353-1 1999 Dihydropyrimidine dehydrogenase (DPD) is the initial, rate-limiting enzyme in the catabolism of 5-fluorouracil (5-FU). Fluorouracil 96-110 dihydropyrimidine dehydrogenase Homo sapiens 0-31 10442353-1 1999 Dihydropyrimidine dehydrogenase (DPD) is the initial, rate-limiting enzyme in the catabolism of 5-fluorouracil (5-FU). Fluorouracil 96-110 dihydropyrimidine dehydrogenase Homo sapiens 33-36 10442353-1 1999 Dihydropyrimidine dehydrogenase (DPD) is the initial, rate-limiting enzyme in the catabolism of 5-fluorouracil (5-FU). Fluorouracil 112-116 dihydropyrimidine dehydrogenase Homo sapiens 0-31 10442353-1 1999 Dihydropyrimidine dehydrogenase (DPD) is the initial, rate-limiting enzyme in the catabolism of 5-fluorouracil (5-FU). Fluorouracil 112-116 dihydropyrimidine dehydrogenase Homo sapiens 33-36 10442353-2 1999 DPD has an important role in regulating the availability of 5-FU for anabolism. Fluorouracil 60-64 dihydropyrimidine dehydrogenase Homo sapiens 0-3 10442353-3 1999 It is now clear that DPD also accounts for much of the variability observed with the therapeutic use of 5-FU, including variable drug levels during 24-hour infusion, erratic pharmacokinetics, variable bioavaialability, inconsistent toxicity, and variability in drug response (resistance). Fluorouracil 104-108 dihydropyrimidine dehydrogenase Homo sapiens 21-24 10224280-5 1999 In a murine bone marrow transduction/transplantation model, the three forms of BCR/ABL were equally potent in the induction of a chronic myeloid leukemia (CML)-like myeloproliferative syndrome in recipient mice when 5-fluorouracil (5-FU)-treated donors were used. Fluorouracil 216-230 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 79-86 10224280-5 1999 In a murine bone marrow transduction/transplantation model, the three forms of BCR/ABL were equally potent in the induction of a chronic myeloid leukemia (CML)-like myeloproliferative syndrome in recipient mice when 5-fluorouracil (5-FU)-treated donors were used. Fluorouracil 232-236 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 79-86 10097742-5 1999 In combination with CDHP, 5-FU gradually released from FT remained longer in plasma, and consequently had high anti-tumor activity, while the combined Oxo significantly suppressed GI toxicity due to 5-FU. Fluorouracil 26-30 cadherin 3 Homo sapiens 20-24 10086734-11 1999 125I-BMP-9 bound specifically to a high percentage of blast cells in lineage-depleted post-fluorouracil bone marrow cells and to megakaryocytes in normal and post-fluorouracil bone marrow, indicating that BMP-9R are expressed on these cells. Fluorouracil 91-103 growth differentiation factor 2 Mus musculus 5-10 10086734-11 1999 125I-BMP-9 bound specifically to a high percentage of blast cells in lineage-depleted post-fluorouracil bone marrow cells and to megakaryocytes in normal and post-fluorouracil bone marrow, indicating that BMP-9R are expressed on these cells. Fluorouracil 163-175 growth differentiation factor 2 Mus musculus 5-10 10359051-0 1999 Circumvention of 5-fluorouracil resistance in human stomach cancer cells by uracil phosphoribosyltransferase gene transduction. Fluorouracil 17-31 uracil phosphoribosyltransferase homolog Homo sapiens 76-108 10359051-7 1999 NUGC-3/ SFU/L transfected with the UPRT gene showed very high sensitivity to 5-FU with an IC50 of 3.2 micromol/liter. Fluorouracil 77-81 uracil phosphoribosyltransferase homolog Homo sapiens 35-39 11263191-7 1999 CDDP and 5-FU increased ICAM-1 expression significantly and the sensitivity of SKOV3 cell to LAK cell lysis was well related to the ICAM-1 expression. Fluorouracil 9-13 intercellular adhesion molecule 1 Homo sapiens 24-30 11263191-7 1999 CDDP and 5-FU increased ICAM-1 expression significantly and the sensitivity of SKOV3 cell to LAK cell lysis was well related to the ICAM-1 expression. Fluorouracil 9-13 intercellular adhesion molecule 1 Homo sapiens 132-138 10027339-1 1999 Dihydropyrimidine dehydrogenase (DPD) is responsible for the breakdown of the widely used antineoplastic agent 5-fluorouracil (5FU), thereby limiting the efficacy of the therapy. Fluorouracil 111-125 dihydropyrimidine dehydrogenase Homo sapiens 0-31 10027339-1 1999 Dihydropyrimidine dehydrogenase (DPD) is responsible for the breakdown of the widely used antineoplastic agent 5-fluorouracil (5FU), thereby limiting the efficacy of the therapy. Fluorouracil 111-125 dihydropyrimidine dehydrogenase Homo sapiens 33-36 10027339-1 1999 Dihydropyrimidine dehydrogenase (DPD) is responsible for the breakdown of the widely used antineoplastic agent 5-fluorouracil (5FU), thereby limiting the efficacy of the therapy. Fluorouracil 127-130 dihydropyrimidine dehydrogenase Homo sapiens 0-31 10027339-1 1999 Dihydropyrimidine dehydrogenase (DPD) is responsible for the breakdown of the widely used antineoplastic agent 5-fluorouracil (5FU), thereby limiting the efficacy of the therapy. Fluorouracil 127-130 dihydropyrimidine dehydrogenase Homo sapiens 33-36 10027340-1 1999 Dihydropyrimidine dehydrogenase (DPD) is the initial and rate-limiting enzyme of 5-fluorouracil (5-FU) catabolism. Fluorouracil 81-95 dihydropyrimidine dehydrogenase Homo sapiens 0-31 10027340-1 1999 Dihydropyrimidine dehydrogenase (DPD) is the initial and rate-limiting enzyme of 5-fluorouracil (5-FU) catabolism. Fluorouracil 81-95 dihydropyrimidine dehydrogenase Homo sapiens 33-36 10027340-1 1999 Dihydropyrimidine dehydrogenase (DPD) is the initial and rate-limiting enzyme of 5-fluorouracil (5-FU) catabolism. Fluorouracil 97-101 dihydropyrimidine dehydrogenase Homo sapiens 0-31 10027340-1 1999 Dihydropyrimidine dehydrogenase (DPD) is the initial and rate-limiting enzyme of 5-fluorouracil (5-FU) catabolism. Fluorouracil 97-101 dihydropyrimidine dehydrogenase Homo sapiens 33-36 10037177-2 1999 Due to rapid, predominantly hepatic metabolism by dihydropyrimidine dehydrogenase (DPD) and suggested clinical benefit from prolonged drug exposure, 5-FU is commonly given by continuous infusion. Fluorouracil 149-153 dihydropyrimidine dehydrogenase Homo sapiens 83-86 10037177-3 1999 Eniluracil is a novel DPD-inactivator designed to prolong the half-life of 5-FU and provide sustained plasma concentrations of 5-FU with oral dosing. Fluorouracil 75-79 dihydropyrimidine dehydrogenase Homo sapiens 22-25 10037177-3 1999 Eniluracil is a novel DPD-inactivator designed to prolong the half-life of 5-FU and provide sustained plasma concentrations of 5-FU with oral dosing. Fluorouracil 127-131 dihydropyrimidine dehydrogenase Homo sapiens 22-25 10037177-22 1999 Cumulative myelosupression was the significant dose-limiting toxicity of oral 5-FU given with the DPD-inactivator eniluracil on an every-other-week schedule. Fluorouracil 78-82 dihydropyrimidine dehydrogenase Homo sapiens 98-101 9893658-2 1998 CDHP inhibits dihydropyrimidine dehydrogenase (DPD), an enzyme which degrades 5-FU, and maintains prolonged 5-FU concentrations in the blood and tumours. Fluorouracil 78-82 cadherin 3 Homo sapiens 0-4 9893658-2 1998 CDHP inhibits dihydropyrimidine dehydrogenase (DPD), an enzyme which degrades 5-FU, and maintains prolonged 5-FU concentrations in the blood and tumours. Fluorouracil 78-82 dihydropyrimidine dehydrogenase Homo sapiens 14-45 9893658-2 1998 CDHP inhibits dihydropyrimidine dehydrogenase (DPD), an enzyme which degrades 5-FU, and maintains prolonged 5-FU concentrations in the blood and tumours. Fluorouracil 78-82 dihydropyrimidine dehydrogenase Homo sapiens 47-50 9893658-2 1998 CDHP inhibits dihydropyrimidine dehydrogenase (DPD), an enzyme which degrades 5-FU, and maintains prolonged 5-FU concentrations in the blood and tumours. Fluorouracil 108-112 cadherin 3 Homo sapiens 0-4 9893658-4 1998 S-1 improves the tumour-selective toxicity of 5-FU by the actions of two modulators, CDHP and Oxo. Fluorouracil 46-50 cadherin 3 Homo sapiens 85-89 9789291-7 1998 TPase activity which results in conversion to 5-FU was much lower in malignant glioma and metastatic brain tumors compared with tumors in other extracranial organs. Fluorouracil 46-50 thymidine phosphorylase Mus musculus 0-5 9726090-3 1998 This trial demonstrated that intratumoral TS/beta-actin messenger RNA (mRNA) ratio can accurately predict which metastatic colorectal tumors will be resistant to a leucovorin-modulated 5-FU infusion and which have a high likelihood of responding to such a regimen. Fluorouracil 185-189 POTE ankyrin domain family member F Homo sapiens 45-55 9485021-2 1998 5"-dFUrd is metabolized to 5-FUra by thymidine phosphorylase (dThdPase) located in high levels in various types of solid tumors from patients, whereas 5-FUra generated is catabolized to dihydrofluorouracil by dihydropyrimidine dehydrogenase (DPD). Fluorouracil 27-33 dihydropyrimidine dehydrogenase Homo sapiens 209-240 9485021-2 1998 5"-dFUrd is metabolized to 5-FUra by thymidine phosphorylase (dThdPase) located in high levels in various types of solid tumors from patients, whereas 5-FUra generated is catabolized to dihydrofluorouracil by dihydropyrimidine dehydrogenase (DPD). Fluorouracil 27-33 dihydropyrimidine dehydrogenase Homo sapiens 242-245 9485021-2 1998 5"-dFUrd is metabolized to 5-FUra by thymidine phosphorylase (dThdPase) located in high levels in various types of solid tumors from patients, whereas 5-FUra generated is catabolized to dihydrofluorouracil by dihydropyrimidine dehydrogenase (DPD). Fluorouracil 151-157 dihydropyrimidine dehydrogenase Homo sapiens 209-240 9485021-2 1998 5"-dFUrd is metabolized to 5-FUra by thymidine phosphorylase (dThdPase) located in high levels in various types of solid tumors from patients, whereas 5-FUra generated is catabolized to dihydrofluorouracil by dihydropyrimidine dehydrogenase (DPD). Fluorouracil 151-157 dihydropyrimidine dehydrogenase Homo sapiens 242-245 9472644-1 1998 Dihydropyrimidine dehydrogenase (DPD) is the rate-limiting enzyme for degradation of 5-fluorouracil (5-FU). Fluorouracil 85-99 dihydropyrimidine dehydrogenase Homo sapiens 0-31 9472644-1 1998 Dihydropyrimidine dehydrogenase (DPD) is the rate-limiting enzyme for degradation of 5-fluorouracil (5-FU). Fluorouracil 85-99 dihydropyrimidine dehydrogenase Homo sapiens 33-36 9472644-1 1998 Dihydropyrimidine dehydrogenase (DPD) is the rate-limiting enzyme for degradation of 5-fluorouracil (5-FU). Fluorouracil 101-105 dihydropyrimidine dehydrogenase Homo sapiens 0-31 9472644-1 1998 Dihydropyrimidine dehydrogenase (DPD) is the rate-limiting enzyme for degradation of 5-fluorouracil (5-FU). Fluorouracil 101-105 dihydropyrimidine dehydrogenase Homo sapiens 33-36 9472644-3 1998 Characterization of DPD in colorectal cancer is of clinical interest through its role in the regulation of 5-FU, the main chemotherapeutic agent used in this disease. Fluorouracil 107-111 dihydropyrimidine dehydrogenase Homo sapiens 20-23 9472650-1 1998 Individuals with a deficiency in the enzyme dihydropyrimidine dehydrogenase (DPD) may experience severe life-threatening toxicity when treated with 5-fluorouracil (5-FU). Fluorouracil 148-162 dihydropyrimidine dehydrogenase Homo sapiens 44-75 9472650-1 1998 Individuals with a deficiency in the enzyme dihydropyrimidine dehydrogenase (DPD) may experience severe life-threatening toxicity when treated with 5-fluorouracil (5-FU). Fluorouracil 148-162 dihydropyrimidine dehydrogenase Homo sapiens 77-80 9472650-1 1998 Individuals with a deficiency in the enzyme dihydropyrimidine dehydrogenase (DPD) may experience severe life-threatening toxicity when treated with 5-fluorouracil (5-FU). Fluorouracil 164-168 dihydropyrimidine dehydrogenase Homo sapiens 44-75 9472650-1 1998 Individuals with a deficiency in the enzyme dihydropyrimidine dehydrogenase (DPD) may experience severe life-threatening toxicity when treated with 5-fluorouracil (5-FU). Fluorouracil 164-168 dihydropyrimidine dehydrogenase Homo sapiens 77-80 9323539-2 1997 Dihydropyrimidine dehydrogenase (DPD) catalyzes the reduction of the naturally occurring pyrimidines, uracil and thymine, and the fluoropyrimidine anticancer drug, 5-fluorouracil (FUra) to 5,6-dihydropyrimidines. Fluorouracil 164-178 dihydropyrimidine dehydrogenase Homo sapiens 0-31 9323539-2 1997 Dihydropyrimidine dehydrogenase (DPD) catalyzes the reduction of the naturally occurring pyrimidines, uracil and thymine, and the fluoropyrimidine anticancer drug, 5-fluorouracil (FUra) to 5,6-dihydropyrimidines. Fluorouracil 164-178 dihydropyrimidine dehydrogenase Homo sapiens 33-36 9323539-2 1997 Dihydropyrimidine dehydrogenase (DPD) catalyzes the reduction of the naturally occurring pyrimidines, uracil and thymine, and the fluoropyrimidine anticancer drug, 5-fluorouracil (FUra) to 5,6-dihydropyrimidines. Fluorouracil 180-184 dihydropyrimidine dehydrogenase Homo sapiens 0-31 9280881-7 1997 Authors intended to collect data about the dihydropyrimidine dehydrogenase activity of colorectal cancer patients, in order to screen enzyme deficiency or very low enzyme activity, which might be in connection with the appearance of severe side effects, moreover to determine the optimal dose of 5-fluorouracil before the treatment. Fluorouracil 296-310 dihydropyrimidine dehydrogenase Homo sapiens 43-74 9280881-8 1997 Dihydropyrimidine dehydrogenase activity was determined in the lymphocytes of 48 colorectal cancer patients, treated by 5-fluorouracil, at the beginning of each cytostatic cycle. Fluorouracil 120-134 dihydropyrimidine dehydrogenase Homo sapiens 0-31 9280881-12 1997 Authors conclude that the determination of the dihydropyrimidine dehydrogenase activity in the lymphocytes is a valuable method in the prediction of the toxic side effects of 5-fluorouracil, in the screening of the congenital enzyme deficiency and in the individualization of the 5-fluorouracil dosage. Fluorouracil 175-189 dihydropyrimidine dehydrogenase Homo sapiens 47-78 9280881-12 1997 Authors conclude that the determination of the dihydropyrimidine dehydrogenase activity in the lymphocytes is a valuable method in the prediction of the toxic side effects of 5-fluorouracil, in the screening of the congenital enzyme deficiency and in the individualization of the 5-fluorouracil dosage. Fluorouracil 280-294 dihydropyrimidine dehydrogenase Homo sapiens 47-78 9264323-0 1997 Dual modulation of 5-fluorouracil cytotoxicity using folinic acid with a dihydropyrimidine dehydrogenase inhibitor. Fluorouracil 19-33 dihydropyrimidine dehydrogenase Homo sapiens 73-104 9264323-1 1997 Dihydropyrimidine dehydrogenase (DPD) is the key enzyme of the fluorouracil (FU) catabolic pathway. Fluorouracil 63-75 dihydropyrimidine dehydrogenase Homo sapiens 0-31 9264323-1 1997 Dihydropyrimidine dehydrogenase (DPD) is the key enzyme of the fluorouracil (FU) catabolic pathway. Fluorouracil 63-75 dihydropyrimidine dehydrogenase Homo sapiens 33-36 9155534-6 1997 A 1.5-fold increase in 5-FU sensitivity was observed in C26-10 and C26-10/F (by murine IFN-alpha, beta); in SW948, WiDr and WiDr/F (by human IFN-gamma) and in SW948 and WiDr/ F (by human IFN-alpha). Fluorouracil 23-27 interferon alpha Mus musculus 87-96 9155534-7 1997 In none of the cell lines did human IFN-alpha, IFN-gamma or murine IFN-alpha, beta increase FdUMP levels after exposure to 5-FU. Fluorouracil 123-127 interferon alpha Mus musculus 67-76 9010022-1 1997 A mutation at codon 974 of the dihydropyrimidine dehydrogenase (DPD) gene was previously described in a cancer patient with undetectable DPD enzyme activity who experienced severe toxicity when treated with 5-fluorouracil. Fluorouracil 207-221 dihydropyrimidine dehydrogenase Homo sapiens 31-62 9010022-1 1997 A mutation at codon 974 of the dihydropyrimidine dehydrogenase (DPD) gene was previously described in a cancer patient with undetectable DPD enzyme activity who experienced severe toxicity when treated with 5-fluorouracil. Fluorouracil 207-221 dihydropyrimidine dehydrogenase Homo sapiens 64-67 9010022-1 1997 A mutation at codon 974 of the dihydropyrimidine dehydrogenase (DPD) gene was previously described in a cancer patient with undetectable DPD enzyme activity who experienced severe toxicity when treated with 5-fluorouracil. Fluorouracil 207-221 dihydropyrimidine dehydrogenase Homo sapiens 137-140 8996526-0 1997 Dihydropyrimidine dehydrogenase inactivation and 5-fluorouracil pharmacokinetics: allometric scaling of animal data, pharmacokinetics and toxicodynamics of 5-fluorouracil in humans. Fluorouracil 156-170 dihydropyrimidine dehydrogenase Homo sapiens 0-31 8996526-1 1997 UNLABELLED: The pharmacokinetics of 5-fluorouracil (5-FU) in different animal species treated with the dihydropyrimidine dehydrogenase (DPD) inactivator, 5-ethynyluracil (776C85) were related through allometric scaling. Fluorouracil 36-50 dihydropyrimidine dehydrogenase Homo sapiens 136-139 8996166-8 1997 RESULTS: Recognition that greater than 95% of the injected dose of 5-FU is rapidly inactivated by dihydropyrimidine dehydrogenase (DPD) to therapeutically inactive products, but with toxicity to normal tissues, led to the development of inhibitors of this enzyme with the aim to modify the therapeutic index of 5-FU. Fluorouracil 67-71 dihydropyrimidine dehydrogenase Homo sapiens 98-129 8996166-8 1997 RESULTS: Recognition that greater than 95% of the injected dose of 5-FU is rapidly inactivated by dihydropyrimidine dehydrogenase (DPD) to therapeutically inactive products, but with toxicity to normal tissues, led to the development of inhibitors of this enzyme with the aim to modify the therapeutic index of 5-FU. Fluorouracil 67-71 dihydropyrimidine dehydrogenase Homo sapiens 131-134 8996166-8 1997 RESULTS: Recognition that greater than 95% of the injected dose of 5-FU is rapidly inactivated by dihydropyrimidine dehydrogenase (DPD) to therapeutically inactive products, but with toxicity to normal tissues, led to the development of inhibitors of this enzyme with the aim to modify the therapeutic index of 5-FU. Fluorouracil 311-315 dihydropyrimidine dehydrogenase Homo sapiens 98-129 8996166-8 1997 RESULTS: Recognition that greater than 95% of the injected dose of 5-FU is rapidly inactivated by dihydropyrimidine dehydrogenase (DPD) to therapeutically inactive products, but with toxicity to normal tissues, led to the development of inhibitors of this enzyme with the aim to modify the therapeutic index of 5-FU. Fluorouracil 311-315 dihydropyrimidine dehydrogenase Homo sapiens 131-134 8957081-4 1996 Recipient mice were able to survive more than one treatment of 5-fluorouracil (5-FU) at a dose that normally eliminates cycling hemopoietic progenitor cells; subsequently, transduced HSCs could become activated and undergo clonal expansion, resulting in abl-induced leukemic development. Fluorouracil 63-77 c-abl oncogene 1, non-receptor tyrosine kinase Mus musculus 20-23 8957081-4 1996 Recipient mice were able to survive more than one treatment of 5-fluorouracil (5-FU) at a dose that normally eliminates cycling hemopoietic progenitor cells; subsequently, transduced HSCs could become activated and undergo clonal expansion, resulting in abl-induced leukemic development. Fluorouracil 79-83 c-abl oncogene 1, non-receptor tyrosine kinase Mus musculus 20-23 8781516-4 1996 In this study, we investigated the biorecognizability of specific oligopeptide sequences linking 5-fluorouracil to a water-soluble copolymer carrier based on N-(2-hydroxypropyl) methacrylamide by human cathepsin B (EC 3.4.22.1), cathepsin H(EC 3.4.22.6), and a homogenate of the human colon adenocarcinoma cell line SW 480. Fluorouracil 97-111 cathepsin B Homo sapiens 202-213 8911125-7 1996 Inhibition of thymidylate synthase, the enzyme involved in IdU dehalogenation, by 5-fluorouracil plus folic acid, or by novel inhibitors AG337 and ZD1694 led to a 3- to 5-fold increase in the 125IdU incorporation. Fluorouracil 82-96 thymidylate synthase Mus musculus 14-34 8857547-0 1996 Individualizing therapy with 5-fluorouracil related to dihydropyrimidine dehydrogenase: theory and limits. Fluorouracil 29-43 dihydropyrimidine dehydrogenase Homo sapiens 55-86 8857547-1 1996 5-Fluorouracil (FU) is metabolized by dihydropyrimidine dehydrogenase (DPD). Fluorouracil 0-14 dihydropyrimidine dehydrogenase Homo sapiens 38-69 8857547-1 1996 5-Fluorouracil (FU) is metabolized by dihydropyrimidine dehydrogenase (DPD). Fluorouracil 0-14 dihydropyrimidine dehydrogenase Homo sapiens 71-74 21594447-2 1996 In a prospective study we evaluated the efficacy of 5-FU plus levamisole as an aduvant therapy for 153 patients with Dukes" B-2 or C colon or rectal cancer following a curative-intended surgery. Fluorouracil 52-56 immunoglobulin kappa variable 5-2 Homo sapiens 124-127 8639826-12 1996 In contrast, 40% and 100% of mice that received SCF + IL-11 before the first dose of 5-FU, survived a second dose of 5-FU given respectively after 7 or 10 days. Fluorouracil 117-121 interleukin 11 Mus musculus 54-59 8666781-10 1996 As expected, EL4 cells treated with 5-FUra were prevented from forming multinucleate cells upon infection with dsSIN:C3. Fluorouracil 36-42 epilepsy 4 Mus musculus 13-16 8622093-9 1996 The average CRA rate reported in regimens based on cyclophosphamide, methotrexate, and fluorouracil (CMF) is 68% (95% confidence interval [CI], 66% to 70%), with a range of 20% to 100%. Fluorouracil 87-99 myotubularin related protein 11 Homo sapiens 12-15 8610637-8 1996 PFL is an active, toxic induction regimen for far-advanced HN cancer, yielding a response rate in the range of the widely used cisplatin and 5-FU (PF) schedule; a comparative trial is warranted before concluding that PFL is superior to the latter combination. Fluorouracil 141-145 profilin 2 Homo sapiens 0-3 8680084-1 1996 Dihydropyrimidine dehydrogenase (DPD) is the principal enzyme involved in the catabolism of 5 fluorouracil (5 FU). Fluorouracil 92-106 dihydropyrimidine dehydrogenase Homo sapiens 0-31 8680084-1 1996 Dihydropyrimidine dehydrogenase (DPD) is the principal enzyme involved in the catabolism of 5 fluorouracil (5 FU). Fluorouracil 92-106 dihydropyrimidine dehydrogenase Homo sapiens 33-36 8630403-6 1996 When the CD44neg/dim subset was sorted from BM of mice treated with 5-fluorouracil (5-FU) day before (-1FUBM), there were about 30% T cells, but no NK-1.1+ cells. Fluorouracil 68-82 CD44 antigen Mus musculus 9-13 8630403-6 1996 When the CD44neg/dim subset was sorted from BM of mice treated with 5-fluorouracil (5-FU) day before (-1FUBM), there were about 30% T cells, but no NK-1.1+ cells. Fluorouracil 84-88 CD44 antigen Mus musculus 9-13 8687107-3 1996 In this study we evaluated the efficacy of mitomycin C (MMC) and 5-FU against the human pancreatic adenocarcinoma cell line PAN-12 in an orthotopic human metastatic pancreatic cancer nude mice model. Fluorouracil 65-69 NLR family pyrin domain containing 9 Homo sapiens 124-130 8542939-8 1995 5-FU pretreatment of CML CD34+ cells markedly reduced their clonogenic potential and growth factor-mediated cell proliferation but favored higher frequency of BCR-ABL-free colonies. Fluorouracil 0-4 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 159-166 7493914-4 1995 In contrast, a biphasic change of p210bcr/abl and the abl-associated kinase activities was observed upon treatment with 5-FU. Fluorouracil 120-124 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 42-45 7493914-4 1995 In contrast, a biphasic change of p210bcr/abl and the abl-associated kinase activities was observed upon treatment with 5-FU. Fluorouracil 120-124 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 54-57 8535028-1 1995 Dihydropyrimidine dehydrogenase (DPD) is the initial enzyme of 5-fluorouracil (5-FU) catabolism. Fluorouracil 79-83 dihydropyrimidine dehydrogenase Homo sapiens 0-31 8535028-1 1995 Dihydropyrimidine dehydrogenase (DPD) is the initial enzyme of 5-fluorouracil (5-FU) catabolism. Fluorouracil 79-83 dihydropyrimidine dehydrogenase Homo sapiens 33-36 8535028-2 1995 The clinical importance of DPD has recently been demonstrated with the identification of severe and/or lethal 5-FU-related toxicity in patients with suspected or proven DPD deficiency revealed in lymphocytes. Fluorouracil 110-114 dihydropyrimidine dehydrogenase Homo sapiens 27-30 8680797-1 1995 Interferon-alpha (IFN-alpha) exhibits synergistic antitumor activity when combined with tumor necrosis factor-alpha (TNF-alpha) in vitro and in vivo and increases the cytotoxicity of 5-fluorouracil (5-FU) in vitro. Fluorouracil 183-197 interferon alpha Mus musculus 0-16 8680797-1 1995 Interferon-alpha (IFN-alpha) exhibits synergistic antitumor activity when combined with tumor necrosis factor-alpha (TNF-alpha) in vitro and in vivo and increases the cytotoxicity of 5-fluorouracil (5-FU) in vitro. Fluorouracil 183-197 interferon alpha Mus musculus 18-27 8680797-1 1995 Interferon-alpha (IFN-alpha) exhibits synergistic antitumor activity when combined with tumor necrosis factor-alpha (TNF-alpha) in vitro and in vivo and increases the cytotoxicity of 5-fluorouracil (5-FU) in vitro. Fluorouracil 199-203 interferon alpha Mus musculus 0-16 8680797-1 1995 Interferon-alpha (IFN-alpha) exhibits synergistic antitumor activity when combined with tumor necrosis factor-alpha (TNF-alpha) in vitro and in vivo and increases the cytotoxicity of 5-fluorouracil (5-FU) in vitro. Fluorouracil 199-203 interferon alpha Mus musculus 18-27 7749156-0 1995 A phase III randomized trial of cyclophosphamide, mitoxantrone, and 5-fluorouracil (CNF) versus cyclophosphamide, adriamycin, and 5-fluorouracil (CAF) in patients with metastatic breast cancer. Fluorouracil 68-82 NPHS1 adhesion molecule, nephrin Homo sapiens 84-87 7534710-3 1995 We also showed that 5-FU-resistant PBSC have a greater capacity for expansion of IL-1/IL-3/SCF-responsive immature progenitors (p = 0.05), amplification of IL-3 plus GM-CSF responsive progenitors (p = 0.01), and production of committed single growth factor-responsive (granulocyte-macrophage colony-stimulating factor [GM-CSF]) precursors (p = 0.01) than the untreated PBSC. Fluorouracil 20-24 KIT ligand Homo sapiens 91-94 7828673-0 1995 Modified thrombopoietic response to 5-FU in mice following transplantation of Lin-Sca-1+ bone marrow cells. Fluorouracil 36-40 ataxin 1 Mus musculus 82-87 7874692-2 1995 Modifications of spleen and thymus PAF contents after a single dose of the chemotherapeutic drug 5-fluorouracil in mice. Fluorouracil 97-111 patchy fur Mus musculus 35-38 7874692-4 1995 A significant increase of the spleen (P = 0.005) and thymus (P < 0.05) PAF concentrations was noted 48 h after 5-FU infusion. Fluorouracil 114-118 patchy fur Mus musculus 74-77 7874692-8 1995 Thus, the chemotherapeutic drug 5-FU modulates in vivo PAF production in haematopoietic organs of mice. Fluorouracil 32-36 patchy fur Mus musculus 55-58 7577082-0 1995 Antitumour activity, toxicity and inhibition of thymidylate synthase of prolonged administration of 5-fluorouracil in mice. Fluorouracil 100-114 thymidylate synthase Mus musculus 48-68 7825962-1 1994 Fluorouracil (FU) is essentially eliminated in the liver through the rate limiting enzyme dihydropyrimidine dehydrogenase (DPD). Fluorouracil 0-12 dihydropyrimidine dehydrogenase Homo sapiens 90-121 7825962-1 1994 Fluorouracil (FU) is essentially eliminated in the liver through the rate limiting enzyme dihydropyrimidine dehydrogenase (DPD). Fluorouracil 0-12 dihydropyrimidine dehydrogenase Homo sapiens 123-126 7973772-1 1994 In a randomized phase II study by the Cancer and Leukemia Group B, the cisplatin/5-fluorouracil/leucovorin (PFL) combination produced a 29% response rate in advanced, unresectable non-small cell lung cancer. Fluorouracil 81-95 profilin 2 Homo sapiens 108-111 8083224-0 1994 cDNA cloning and chromosome mapping of human dihydropyrimidine dehydrogenase, an enzyme associated with 5-fluorouracil toxicity and congenital thymine uraciluria. Fluorouracil 104-118 dihydropyrimidine dehydrogenase Homo sapiens 45-76 7522897-2 1994 The resulting 5-FU-resistant cells were evaluated for (1) the production of GM-CSF-responsive clonogenic elements (CE), (2) the production of IL-3+GM-CSF-responsive CE, and (3) their self-renewal capacity (production of IL-1+IL-3+SCF-responsive CE). Fluorouracil 14-18 KIT ligand Homo sapiens 230-233 7910230-9 1994 Addition of PSK to adjuvant chemotherapy with mitomycin and fluorouracil is beneficial as treatment after curative gastrectomy. Fluorouracil 60-72 TAO kinase 2 Homo sapiens 12-15 8017848-6 1994 On the other hand, the sequence of 5-FU before JM-8 showed the lowest toxicity in all the treated groups, in terms of death rate, body weight loss and spleen weight loss. Fluorouracil 35-39 calcium voltage-gated channel subunit alpha1 F Homo sapiens 47-51 8017850-5 1994 This was also confirmed in THP or ADM combination chemotherapy with mitomycin C and 5-fluorouracil on St-15 and MKN-45. Fluorouracil 84-98 uromodulin Homo sapiens 27-30 7880618-1 1994 Interferon-alpha (IFN-alpha) enhances the activity of the 5-fluorouracil (5-FU) prodrug 5"-deoxy-5-fluorouridine (5"-dFUrd) in colorectal cancer cells in vitro by upregulating the enzyme pyrimidine nucleoside phosphorylase (PNPase), which is responsible for converting 5"-dFUrd to 5-FU. Fluorouracil 281-285 interferon alpha Mus musculus 0-16 7880618-1 1994 Interferon-alpha (IFN-alpha) enhances the activity of the 5-fluorouracil (5-FU) prodrug 5"-deoxy-5-fluorouridine (5"-dFUrd) in colorectal cancer cells in vitro by upregulating the enzyme pyrimidine nucleoside phosphorylase (PNPase), which is responsible for converting 5"-dFUrd to 5-FU. Fluorouracil 281-285 interferon alpha Mus musculus 18-27 8054813-6 1994 The simultaneous treatment with EGF and 5-fluorouracil (5-FU) produced a nearly 2.4-fold enhancement of 5-FU cytotoxicity against TSG6 cells. Fluorouracil 40-54 TNF alpha induced protein 6 Homo sapiens 130-134 8054813-6 1994 The simultaneous treatment with EGF and 5-fluorouracil (5-FU) produced a nearly 2.4-fold enhancement of 5-FU cytotoxicity against TSG6 cells. Fluorouracil 56-60 TNF alpha induced protein 6 Homo sapiens 130-134 8054813-6 1994 The simultaneous treatment with EGF and 5-fluorouracil (5-FU) produced a nearly 2.4-fold enhancement of 5-FU cytotoxicity against TSG6 cells. Fluorouracil 104-108 TNF alpha induced protein 6 Homo sapiens 130-134 8054813-8 1994 Moreover, we found that the incorporation of 5-FU into the TSG6 cells was increased with the addition of EGF. Fluorouracil 45-49 TNF alpha induced protein 6 Homo sapiens 59-63 8221682-0 1993 Dihydropyrimidine dehydrogenase activity in human peripheral blood mononuclear cells and liver: population characteristics, newly identified deficient patients, and clinical implication in 5-fluorouracil chemotherapy. Fluorouracil 189-203 dihydropyrimidine dehydrogenase Homo sapiens 0-31 8221682-1 1993 Dihydropyrimidine dehydrogenase (DPD) is the initial and rate-limiting enzyme in the catabolism of 5-fluorouracil (FUra), one of the most widely used anticancer drugs. Fluorouracil 99-113 dihydropyrimidine dehydrogenase Homo sapiens 0-31 8221682-1 1993 Dihydropyrimidine dehydrogenase (DPD) is the initial and rate-limiting enzyme in the catabolism of 5-fluorouracil (FUra), one of the most widely used anticancer drugs. Fluorouracil 99-113 dihydropyrimidine dehydrogenase Homo sapiens 33-36 8221682-1 1993 Dihydropyrimidine dehydrogenase (DPD) is the initial and rate-limiting enzyme in the catabolism of 5-fluorouracil (FUra), one of the most widely used anticancer drugs. Fluorouracil 115-119 dihydropyrimidine dehydrogenase Homo sapiens 0-31 8221682-1 1993 Dihydropyrimidine dehydrogenase (DPD) is the initial and rate-limiting enzyme in the catabolism of 5-fluorouracil (FUra), one of the most widely used anticancer drugs. Fluorouracil 115-119 dihydropyrimidine dehydrogenase Homo sapiens 33-36 8221682-10 1993 We now suggest that measurement of DPD activity may be useful in routine screening of cancer patients prior to FUra treatment. Fluorouracil 111-115 dihydropyrimidine dehydrogenase Homo sapiens 35-38 8330647-8 1993 Furthermore, colony formation by 5-fluorouracil (5-FU)-treated marrow cells could be induced by granulocyte-macrophage (GM)-CSF plus CPA but not by GM-CSF alone. Fluorouracil 33-47 colony stimulating factor 2 (granulocyte-macrophage) Mus musculus 96-127 8330647-8 1993 Furthermore, colony formation by 5-fluorouracil (5-FU)-treated marrow cells could be induced by granulocyte-macrophage (GM)-CSF plus CPA but not by GM-CSF alone. Fluorouracil 33-47 colony stimulating factor 2 (granulocyte-macrophage) Mus musculus 148-154 8330647-8 1993 Furthermore, colony formation by 5-fluorouracil (5-FU)-treated marrow cells could be induced by granulocyte-macrophage (GM)-CSF plus CPA but not by GM-CSF alone. Fluorouracil 49-53 colony stimulating factor 2 (granulocyte-macrophage) Mus musculus 96-127 8330647-8 1993 Furthermore, colony formation by 5-fluorouracil (5-FU)-treated marrow cells could be induced by granulocyte-macrophage (GM)-CSF plus CPA but not by GM-CSF alone. Fluorouracil 49-53 colony stimulating factor 2 (granulocyte-macrophage) Mus musculus 148-154 8479746-0 1993 ABL oncogenes directly stimulate two distinct target cells in bone marrow from 5-fluorouracil-treated mice. Fluorouracil 79-93 c-abl oncogene 1, non-receptor tyrosine kinase Mus musculus 0-3 8479746-1 1993 Mice reconstituted with BCR/ABL-infected 5-fluorouracil-treated bone marrow are considered a model system for human chronic myelogenous leukemia, a malignancy that arises in hematopoietic stem cells. Fluorouracil 41-55 BCR activator of RhoGEF and GTPase Homo sapiens 24-27 8479746-3 1993 To examine the BCR/ABL-sensitive target cells present in the marrow of mice treated with 5-fluorouracil, we used a single-step in vitro assay. Fluorouracil 89-103 c-abl oncogene 1, non-receptor tyrosine kinase Mus musculus 19-22 8426214-1 1993 PURPOSE: To increase the activity of cisplatin, fluorouracil (5-FU), and leucovorin (PFL) through further biochemical modulation and study the pharmacologic interaction of 5-FU and interferon alfa-2b (IFN). Fluorouracil 172-176 profilin 2 Homo sapiens 85-88 8426214-12 1993 CONCLUSION: The recommended doses for PFL-IFN are 640 mg/m2/d for 5-FU and 2.0 x 10(6) U/m2/d for IFN. Fluorouracil 66-70 profilin 2 Homo sapiens 38-41 8468977-4 1993 When mitomycin C, doxorubicin, cisplatin, and 5-fluorouracil were assessed by the SRB assay, the concentration-effect curves revealed a sharp slope between plateaux at low and high concentrations, suggesting that this assay has an excellent sensitivity which can assess the effect of drugs as "all or none." Fluorouracil 46-60 chaperonin containing TCP1 subunit 4 Homo sapiens 82-85 1469133-7 1992 Treatment with topical 5-fluorouracil cream led to the disappearance of the HLP lesions, whereas topical tretinoin was ineffective. Fluorouracil 23-37 HLP Homo sapiens 76-79 1333263-5 1992 19F MRS examines pharmacokinetics of 5-fluorouracil and by demonstrating its retention predicts response of a cancer to treatment. Fluorouracil 37-51 MROS Homo sapiens 4-7 1449968-3 1992 Results from preclinical models have demonstrated that biochemical modulation of 5-fluorouracil metabolism can be demonstrated by MRS. Fluorouracil 81-95 MROS Homo sapiens 130-133 1379119-4 1992 6-Aminonicotinamide produced a severe block of the pentose shunt, and 5-fluorouracil severely inhibited both thymidylate synthase and thymidine kinase in the treated tumors. Fluorouracil 70-84 thymidylate synthase Mus musculus 109-129 2087010-3 1990 NSP also enhanced the DTH suppressed with 5-fluorouracil (5-FU). Fluorouracil 42-56 sperm antigen with calponin homology and coiled-coil domains 1 Homo sapiens 0-3 2087010-3 1990 NSP also enhanced the DTH suppressed with 5-fluorouracil (5-FU). Fluorouracil 58-62 sperm antigen with calponin homology and coiled-coil domains 1 Homo sapiens 0-3 2087010-4 1990 Moreover, NSP inhibited the fatal effect of 5-FU and restored the decrease of body weight caused by 5-FU. Fluorouracil 44-48 sperm antigen with calponin homology and coiled-coil domains 1 Homo sapiens 10-13 2087010-4 1990 Moreover, NSP inhibited the fatal effect of 5-FU and restored the decrease of body weight caused by 5-FU. Fluorouracil 100-104 sperm antigen with calponin homology and coiled-coil domains 1 Homo sapiens 10-13 2087010-5 1990 However, NSP reduced partially but significantly the suppression of the tumor growth by 5-FU. Fluorouracil 88-92 sperm antigen with calponin homology and coiled-coil domains 1 Homo sapiens 9-12 2204540-0 1990 Indomethacin augments granulocyte-macrophage colony-stimulating factor-induced hematopoiesis following 5-FU treatment. Fluorouracil 103-107 colony stimulating factor 2 (granulocyte-macrophage) Mus musculus 22-70 2204540-1 1990 We have previously reported that granulocyte-macrophage colony-stimulating factor (GM-CSF) given after the administration of 5-fluorouracil (5-FU) results in augmented hematopoietic recovery as evidenced by increased white blood cell and neutrophil counts. Fluorouracil 125-139 colony stimulating factor 2 (granulocyte-macrophage) Mus musculus 33-81 2204540-1 1990 We have previously reported that granulocyte-macrophage colony-stimulating factor (GM-CSF) given after the administration of 5-fluorouracil (5-FU) results in augmented hematopoietic recovery as evidenced by increased white blood cell and neutrophil counts. Fluorouracil 125-139 colony stimulating factor 2 (granulocyte-macrophage) Mus musculus 83-89 2204540-1 1990 We have previously reported that granulocyte-macrophage colony-stimulating factor (GM-CSF) given after the administration of 5-fluorouracil (5-FU) results in augmented hematopoietic recovery as evidenced by increased white blood cell and neutrophil counts. Fluorouracil 141-145 colony stimulating factor 2 (granulocyte-macrophage) Mus musculus 33-81 2204540-1 1990 We have previously reported that granulocyte-macrophage colony-stimulating factor (GM-CSF) given after the administration of 5-fluorouracil (5-FU) results in augmented hematopoietic recovery as evidenced by increased white blood cell and neutrophil counts. Fluorouracil 141-145 colony stimulating factor 2 (granulocyte-macrophage) Mus musculus 83-89 2204540-2 1990 Mice receiving GM-CSF following 5-FU administration were observed to have a marked elevation in splenic granulocyte-macrophage colony-forming cells (GM-CFC) and a decrease in the femoral bone marrow GM-CFC. Fluorouracil 32-36 colony stimulating factor 2 (granulocyte-macrophage) Mus musculus 15-21 2344373-3 1990 The uptake of FUra during a 1-hr drug exposure, its metabolism to ribo- and deoxyribonucleotides, incorporation into RNA, and inhibition of thymidylate synthase were similar in GC3C1 and GC3TK- cells as were the IC50 values for FUra (26 and 23 microM respectively). Fluorouracil 14-18 thymidylate synthase Mus musculus 140-160 2189013-2 1990 The HPP-CFC have been characterized by: 1) a relative resistance to treatment in vivo with the cytotoxic drug 5-fluorouracil, 2) a high correlation with cells capable of repopulating the bone marrow of lethally irradiated mice, 3) their multipotential ability to generate cells of the macrophage, granulocyte, megakaryocyte and erythroid lineages, and 4) their multifactor responsiveness. Fluorouracil 110-124 tubulin-specific chaperone C Mus musculus 8-11 2189783-4 1990 The FUR1 genes for three recessive fur1 alleles, having different sensibilities to 5-fluorouridine (5-FUR) but identical levels of resistance to 5-fluorouracil (5-FU), were cloned and sequenced. Fluorouracil 145-159 uracil phosphoribosyltransferase Saccharomyces cerevisiae S288C 4-8 2189783-4 1990 The FUR1 genes for three recessive fur1 alleles, having different sensibilities to 5-fluorouridine (5-FUR) but identical levels of resistance to 5-fluorouracil (5-FU), were cloned and sequenced. Fluorouracil 145-159 uracil phosphoribosyltransferase Saccharomyces cerevisiae S288C 35-39 2189783-4 1990 The FUR1 genes for three recessive fur1 alleles, having different sensibilities to 5-fluorouridine (5-FUR) but identical levels of resistance to 5-fluorouracil (5-FU), were cloned and sequenced. Fluorouracil 100-104 uracil phosphoribosyltransferase Saccharomyces cerevisiae S288C 4-8 2189783-4 1990 The FUR1 genes for three recessive fur1 alleles, having different sensibilities to 5-fluorouridine (5-FUR) but identical levels of resistance to 5-fluorouracil (5-FU), were cloned and sequenced. Fluorouracil 100-104 uracil phosphoribosyltransferase Saccharomyces cerevisiae S288C 35-39 2141051-4 1990 In the present study the therapeutic effect and metabolism of 5-FU and its masked compounds: FT, UFT (uracil + FT), HCFU (Carmofur), 5"-DFUR (Doxifluridine) were assessed by using MOPC-104E plasmacytoma transplanted subcutaneously in BALB/c mice with CCl4-induced chronic liver dysfunction. Fluorouracil 62-66 chemokine (C-C motif) ligand 4 Mus musculus 251-255 2293556-0 1990 Relationship between dihydropyrimidine dehydrogenase activity and plasma 5-fluorouracil levels with evidence for circadian variation of enzyme activity and plasma drug levels in cancer patients receiving 5-fluorouracil by protracted continuous infusion. Fluorouracil 73-87 dihydropyrimidine dehydrogenase Homo sapiens 21-52 2293556-0 1990 Relationship between dihydropyrimidine dehydrogenase activity and plasma 5-fluorouracil levels with evidence for circadian variation of enzyme activity and plasma drug levels in cancer patients receiving 5-fluorouracil by protracted continuous infusion. Fluorouracil 204-218 dihydropyrimidine dehydrogenase Homo sapiens 21-52 2293556-1 1990 The activity of dihydropyrimidine dehydrogenase (DPD) in peripheral blood mononuclear cells and plasma concentration of 5-fluorouracil (FUra) were simultaneously determined in cancer patients receiving FUra by protracted continuous infusion (300 mg/m2/day). Fluorouracil 202-206 dihydropyrimidine dehydrogenase Homo sapiens 49-52 2293556-7 1990 An inverse relationship between the circadian patterns of DPD activity and FUra plasma levels was also noted, suggesting that an association may exist between DPD activity and FUra plasma concentration. Fluorouracil 75-79 dihydropyrimidine dehydrogenase Homo sapiens 58-61 2293556-7 1990 An inverse relationship between the circadian patterns of DPD activity and FUra plasma levels was also noted, suggesting that an association may exist between DPD activity and FUra plasma concentration. Fluorouracil 75-79 dihydropyrimidine dehydrogenase Homo sapiens 159-162 2293556-7 1990 An inverse relationship between the circadian patterns of DPD activity and FUra plasma levels was also noted, suggesting that an association may exist between DPD activity and FUra plasma concentration. Fluorouracil 176-180 dihydropyrimidine dehydrogenase Homo sapiens 58-61 2293556-7 1990 An inverse relationship between the circadian patterns of DPD activity and FUra plasma levels was also noted, suggesting that an association may exist between DPD activity and FUra plasma concentration. Fluorouracil 176-180 dihydropyrimidine dehydrogenase Homo sapiens 159-162 2293556-8 1990 Further evidence of an association between DPD activity in peripheral blood mononuclear cells and plasma FUra concentration was demonstrated by a linear relationship between the two parameters in all patients (r = -0.627) and within individual patients (-0.978 less than r less than -0.742). Fluorouracil 105-109 dihydropyrimidine dehydrogenase Homo sapiens 43-46 2293556-9 1990 With the recent advent of programmable pumps, information on the circadian pattern of FUra and/or DPD may be useful in planning continuous infusion schedules in order that optimal plasma drug concentration may be maintained over a 24-h cycle, thereby enhancing the therapeutic efficacy of FUra administered by continuous infusion. Fluorouracil 289-293 dihydropyrimidine dehydrogenase Homo sapiens 98-101 2145240-3 1990 The pretreatment with 5-FU, but not CY, abrogated the suppressor activity of Con A-induced T-cells followed by restoration of the LMT/HMT ratio of Con A-induced T-cells to that of normal T-cells. Fluorouracil 22-26 histamine N-methyltransferase Homo sapiens 134-137 33794252-11 2021 The propolis combined with 5FU reduced the expression of Cox-2, iNOS, and beta-catenin proteins. Fluorouracil 27-30 catenin (cadherin associated protein), beta 1 Mus musculus 74-86 33816780-0 2021 The lncRNA DLGAP1-AS1/miR-149-5p/TGFB2 axis contributes to colorectal cancer progression and 5-FU resistance by regulating smad2 pathway. Fluorouracil 93-97 DLG associated protein 1 Mus musculus 11-17 33816780-0 2021 The lncRNA DLGAP1-AS1/miR-149-5p/TGFB2 axis contributes to colorectal cancer progression and 5-FU resistance by regulating smad2 pathway. Fluorouracil 93-97 microRNA 149 Mus musculus 22-29 33816780-3 2021 This work aims to analyze the functions and molecular basis of DLGAP1-AS1 in CRC progression and 5-fluorouracil resistance. Fluorouracil 97-111 DLG associated protein 1 Mus musculus 63-69 33816780-7 2021 Functional assays showed that silencing DLGAP1-AS1 expression remarkably inhibited cell proliferation and aggressiveness ability and enhanced apoptosis rate and cell chemosensitivity to 5-FU. Fluorouracil 186-190 DLG associated protein 1 Mus musculus 40-50 33816780-10 2021 These new findings indicate that DLGAP1-AS1 knockdown inhibited the progression of CRC and enhanced the 5-FU sensitivity of CRC cells through miR-149-5p/TGFB2 regulatory axis, suggesting that DLGAP1-AS1 may be a promising therapeutic target for CRC. Fluorouracil 104-108 DLG associated protein 1 Mus musculus 33-39 33816780-10 2021 These new findings indicate that DLGAP1-AS1 knockdown inhibited the progression of CRC and enhanced the 5-FU sensitivity of CRC cells through miR-149-5p/TGFB2 regulatory axis, suggesting that DLGAP1-AS1 may be a promising therapeutic target for CRC. Fluorouracil 104-108 microRNA 149 Mus musculus 142-149 33816780-10 2021 These new findings indicate that DLGAP1-AS1 knockdown inhibited the progression of CRC and enhanced the 5-FU sensitivity of CRC cells through miR-149-5p/TGFB2 regulatory axis, suggesting that DLGAP1-AS1 may be a promising therapeutic target for CRC. Fluorouracil 104-108 DLG associated protein 1 Mus musculus 192-198 34725458-7 2022 RESULTS: Tumour-infiltrating TIM3+ cells" high subgroups experienced poorer overall survival and disease-free survival and predicted inferior therapeutic responsiveness to fluorouracil-based adjuvant chemotherapy. Fluorouracil 172-184 hepatitis A virus cellular receptor 2 Homo sapiens 29-33 34665902-0 2022 Thymol ameliorates 5-fluorouracil-induced intestinal mucositis: Evidence of down-regulatory effect on TGF-beta/MAPK pathways through NF-kappaB. Fluorouracil 19-33 transforming growth factor alpha Rattus norvegicus 102-110 34927777-10 2022 Functionally, SOX4 triggered drug resistance of CRC cells to 5-FU through the miR-17/CYLD axis. Fluorouracil 61-65 SRY-box transcription factor 4 Homo sapiens 14-18 34927777-10 2022 Functionally, SOX4 triggered drug resistance of CRC cells to 5-FU through the miR-17/CYLD axis. Fluorouracil 61-65 CYLD lysine 63 deubiquitinase Homo sapiens 85-89 34951582-7 2022 EGFR and KRAS gene expression analysis under the influence of PFNPs, FGNPs, PFGNPs, and 5-FU was studied and observed maximum potency for PFNPs. Fluorouracil 88-92 KRAS proto-oncogene, GTPase Homo sapiens 9-13 34863048-1 2022 Five-fluorouracil (5-FU) is a chemotherapeutic agent that is mainly metabolized by the rate-limiting enzyme dihydropyrimidine dehydrogenase (DPD). Fluorouracil 19-23 dihydropyrimidine dehydrogenase Homo sapiens 108-139 34645611-4 2021 In the present study, we report that macrophages specifically overexpress dihydropyrimidine dehydrogenase (DPD) in hypoxia, leading to macrophage-induced chemoresistance to 5-FU via inactivation of the drug. Fluorouracil 173-177 dihydropyrimidine dehydrogenase Homo sapiens 74-105 34645611-4 2021 In the present study, we report that macrophages specifically overexpress dihydropyrimidine dehydrogenase (DPD) in hypoxia, leading to macrophage-induced chemoresistance to 5-FU via inactivation of the drug. Fluorouracil 173-177 dihydropyrimidine dehydrogenase Homo sapiens 107-110 34245831-10 2021 When OP9 cells were treated with both SIP (10 g L-1) and 5-FU (2.5 x 10-2 g L-1) for 24 h, compared with the model group, the early apoptosis rates significantly decreased, and the activity of caspase 3 was significantly reduced. Fluorouracil 57-61 caspase 3 Mus musculus 193-202 34747284-3 2021 The aim of the current study was to screen the effect of a new selective histamine receptor 1 blocker and platelet-activating factor (PAF) blocker on 5-FU induced intestinal toxicity. Fluorouracil 150-154 PCNA clamp associated factor Rattus norvegicus 106-132 34747284-3 2021 The aim of the current study was to screen the effect of a new selective histamine receptor 1 blocker and platelet-activating factor (PAF) blocker on 5-FU induced intestinal toxicity. Fluorouracil 150-154 PCNA clamp associated factor Rattus norvegicus 134-137 34747284-6 2021 5-FU injection caused marked elevation of MDA, NO, TNF-alpha, IL-1beta, IL-6, PAF, histamine, myeloperoxidase, caspase-3, and NF-kappaB expressions. Fluorouracil 0-4 PCNA clamp associated factor Rattus norvegicus 78-81 34747284-9 2021 In conclusion, rupatadine is a dual histamine receptor 1, and a PAF blocker could reduce 5-FU-induced oxidative damage, inflammation, apoptosis, and ulceration of the intestinal epithelium. Fluorouracil 89-93 PCNA clamp associated factor Rattus norvegicus 64-67 34790580-10 2021 Restoration of the expression of HOXD10 in 5-fluorouracil (5-FU)-resistant cells significantly upregulates the expressions of miR-7 and IGFBP3 and enhances chemosensitivity to 5-FU. Fluorouracil 43-57 leukocyte immunoglobulin like receptor B1 Homo sapiens 126-131 34790580-10 2021 Restoration of the expression of HOXD10 in 5-fluorouracil (5-FU)-resistant cells significantly upregulates the expressions of miR-7 and IGFBP3 and enhances chemosensitivity to 5-FU. Fluorouracil 59-63 leukocyte immunoglobulin like receptor B1 Homo sapiens 126-131 34588619-0 2021 Epigenetic induction of lipocalin 2 expression drives acquired resistance to 5-fluorouracil in colorectal cancer through integrin beta3/SRC pathway. Fluorouracil 77-91 lipocalin 2 Homo sapiens 24-35 34588619-2 2021 We observed significant upregulation of lipocalin 2 (LCN2) expression in a newly established 5-FU-resistant colorectal cancer (CRC) cell line. Fluorouracil 93-97 lipocalin 2 Homo sapiens 40-51 34588619-2 2021 We observed significant upregulation of lipocalin 2 (LCN2) expression in a newly established 5-FU-resistant colorectal cancer (CRC) cell line. Fluorouracil 93-97 lipocalin 2 Homo sapiens 53-57 34588619-3 2021 In this study, we demonstrated that 5-FU-treated CRC cells developed resistance through LCN2 upregulation caused by LCN2 promoter demethylation and that feedback between LCN2 and NF-kappaB further amplified LCN2 expression. Fluorouracil 36-40 lipocalin 2 Homo sapiens 88-92 34588619-3 2021 In this study, we demonstrated that 5-FU-treated CRC cells developed resistance through LCN2 upregulation caused by LCN2 promoter demethylation and that feedback between LCN2 and NF-kappaB further amplified LCN2 expression. Fluorouracil 36-40 lipocalin 2 Homo sapiens 116-120 34588619-3 2021 In this study, we demonstrated that 5-FU-treated CRC cells developed resistance through LCN2 upregulation caused by LCN2 promoter demethylation and that feedback between LCN2 and NF-kappaB further amplified LCN2 expression. Fluorouracil 36-40 lipocalin 2 Homo sapiens 170-174 34588619-3 2021 In this study, we demonstrated that 5-FU-treated CRC cells developed resistance through LCN2 upregulation caused by LCN2 promoter demethylation and that feedback between LCN2 and NF-kappaB further amplified LCN2 expression. Fluorouracil 36-40 lipocalin 2 Homo sapiens 207-211 34588619-5 2021 LCN2 attenuated the cytotoxicity of 5-FU by activating the SRC/AKT/ERK-mediated antiapoptotic program. Fluorouracil 36-40 lipocalin 2 Homo sapiens 0-4 34778377-2 2021 5-Fu/LV prevents cell proliferation by inhibiting thymidylate synthase, which catalyzes the conversion of deoxyuridine monophosphate to deoxythymidine monophosphate. Fluorouracil 0-4 thymidylate synthase Mus musculus 50-70 34146401-3 2021 When Lipocalin 2 is over-expressed it leads to resistance to 5-fluorouracil in colon cancer cell lines in vitro and in vivo by inhibiting ferroptosis. Fluorouracil 61-75 lipocalin 2 Homo sapiens 5-16 34391754-5 2021 In tumor tissues of groups that received 5-FU and andrographolide sulfonate, CD4+ and CD8+ T cell infiltration was increased, and the expression of IFN-gamma and Granzyme B detected by immunohistochemistry and qPCR was upregulated, reflecting improved antitumor immunity. Fluorouracil 41-45 CD4 antigen Mus musculus 77-80 34659563-12 2021 More importantly, advanced GAC patients with low dysbindin expression were likely to benefit from fluorouracil-based PACT. Fluorouracil 98-110 RB binding protein 6, ubiquitin ligase Homo sapiens 117-121 34510641-1 2021 OBJECTIVES: To investigate the potential effect of fatty acid synthase (FASN) inhibitor orlistat to enhance the effectiveness of chemotherapy drugs widely used to treat oral squamous cell carcinomas (OSCC), such as 5-fluorouracil, cisplatin, and paclitaxel. Fluorouracil 215-229 fatty acid synthase Homo sapiens 51-70 34510641-1 2021 OBJECTIVES: To investigate the potential effect of fatty acid synthase (FASN) inhibitor orlistat to enhance the effectiveness of chemotherapy drugs widely used to treat oral squamous cell carcinomas (OSCC), such as 5-fluorouracil, cisplatin, and paclitaxel. Fluorouracil 215-229 fatty acid synthase Homo sapiens 72-76 34507320-11 2021 CONCLUSION: 5-FU possesses a pro-pigmentary activity through activation of the CXCL12/CXCR4 axis to drive the chemotactic migration of melanocytes. Fluorouracil 12-16 chemokine (C-X-C motif) receptor 4 Mus musculus 86-91 34548224-8 2021 The overexpression of CK2alpha promoted tumor sphere formation, increased the percentage of CD133(+) and side population cells, caused the resistance of liver cancer cells to 5-FU treatment, increased the expression levels of NANOG, OCT4, SOX2, Gli1 and Ptch1, and enhanced the ability of CD133(+) cell clone formation and invasion. Fluorouracil 175-179 casein kinase 2 alpha 2 Homo sapiens 22-30 34552494-0 2021 Albuca Bracteate Polysaccharides Synergistically Enhance the Anti-Tumor Efficacy of 5-Fluorouracil Against Colorectal Cancer by Modulating beta-Catenin Signaling and Intestinal Flora. Fluorouracil 84-98 catenin (cadherin associated protein), beta 1 Mus musculus 139-151 34373709-0 2021 mRNA expression level of CDH2, LEP, POSTN, TIMP1 and VEGFC modulates 5-fluorouracil resistance in colon cancer cells. Fluorouracil 69-83 cadherin 2 Homo sapiens 25-29 34373709-13 2021 Taken together, the results suggested that CDH2, LEP, POSTN, TIMP1 and VEGFC might play a role in chemotherapeutic resistance in colon cancer and represent potential targets for overcoming 5-FU resistance in colon cancer. Fluorouracil 189-193 cadherin 2 Homo sapiens 43-47 34157171-0 2021 Decreased Annexin A1 expression enhances sensitivity to docetaxel, cisplatin and 5-fluorouracil combination induction chemotherapy in oral squamous cell carcinoma. Fluorouracil 81-95 annexin A1 Homo sapiens 10-20 34571731-5 2021 Certain resistance mechanisms that are 5-FU-specific have also been ascertained to include the upregulation of thymidylate synthase, dihydropyrimidine dehydrogenase, methylenetetrahydrofolate reductase, and the downregulation of thymidine phosphorylase. Fluorouracil 39-43 dihydropyrimidine dehydrogenase Homo sapiens 133-164 34571731-5 2021 Certain resistance mechanisms that are 5-FU-specific have also been ascertained to include the upregulation of thymidylate synthase, dihydropyrimidine dehydrogenase, methylenetetrahydrofolate reductase, and the downregulation of thymidine phosphorylase. Fluorouracil 39-43 methylenetetrahydrofolate reductase Homo sapiens 166-201 34463253-6 2021 We assessed the functional sources of THPO following two common myeloablative perturbations: 5-fluorouracil (5-FU) administration and irradiation. Fluorouracil 93-107 thrombopoietin Mus musculus 38-42 34463253-6 2021 We assessed the functional sources of THPO following two common myeloablative perturbations: 5-fluorouracil (5-FU) administration and irradiation. Fluorouracil 109-113 thrombopoietin Mus musculus 38-42 34489705-14 2021 Compared with untreated group and 5-FU group, CHB-II-F also enhanced the expression of OX1R, GHSR, NPY, and AgRP protein and gene and decreased the expression of Ob-R, POMC, and CART protein and gene in hypothalamus of mice, and the gene expression was consistent with the protein expression. Fluorouracil 34-38 hypocretin (orexin) receptor 1 Mus musculus 87-91 34489705-14 2021 Compared with untreated group and 5-FU group, CHB-II-F also enhanced the expression of OX1R, GHSR, NPY, and AgRP protein and gene and decreased the expression of Ob-R, POMC, and CART protein and gene in hypothalamus of mice, and the gene expression was consistent with the protein expression. Fluorouracil 34-38 CART prepropeptide Mus musculus 178-182 34386857-11 2022 TRAP expression was significantly higher in NIC-5FU as compared with NIC-CIS at 50 and 95 days. Fluorouracil 48-51 acid phosphatase 5, tartrate resistant Rattus norvegicus 0-4 34522210-8 2021 High CD45 expression promotes CRC cell survival upon 5-fluorouracil or radiation treatment, while CD45 depletion sensitizes CRC cells to CRT. Fluorouracil 53-67 protein tyrosine phosphatase receptor type C Homo sapiens 5-9 34498246-5 2021 We report experience from DPYD testing in 368 patients planned for 5-FU treatment. Fluorouracil 67-71 dihydropyrimidine dehydrogenase Homo sapiens 26-30 34214844-14 2021 Autophagy activator, SDF-1 treatment and CXCR4 activation reversed the promoted effects of RB1 on 5-FU sensitivity in GC cells. Fluorouracil 98-102 C-X-C motif chemokine receptor 4 Homo sapiens 41-46 34308783-4 2021 To assess the cytotoxic effect, immuno-magnetically sorted circulatory CD44+ cells were subjected to increasing concentrations of 5FU, Cisplatin and Salinomycin. Fluorouracil 130-133 CD44 molecule (Indian blood group) Homo sapiens 71-75 34299245-5 2021 Initial experimental validation of selected pseudogene-derived lncRNA (PLEKHA8P1) and its parental gene (PLEKHA8), a well-studied transport protein in Golgi complex recently implicated as an oncogene in both colorectal and liver cancer, indicates that the pseudogene/parental gene pair promotes tumor progression and that their dysregulated expression levels affect 5-FU-induced chemoresistance in human HCC cell line FT3-7. Fluorouracil 366-370 pleckstrin homology domain containing A8 pseudogene 1 Homo sapiens 71-80 34299245-5 2021 Initial experimental validation of selected pseudogene-derived lncRNA (PLEKHA8P1) and its parental gene (PLEKHA8), a well-studied transport protein in Golgi complex recently implicated as an oncogene in both colorectal and liver cancer, indicates that the pseudogene/parental gene pair promotes tumor progression and that their dysregulated expression levels affect 5-FU-induced chemoresistance in human HCC cell line FT3-7. Fluorouracil 366-370 pleckstrin homology domain containing A8 Homo sapiens 105-112 34299245-6 2021 Our study has thus confirmed cancer-related functions of PLEKHA8, and laid the groundwork for identification and validation of oncogenic pseudogene-derived lncRNA that shows potential as a novel therapeutic target in circumventing chemoresistance induced by 5-FU. Fluorouracil 258-262 pleckstrin homology domain containing A8 Homo sapiens 57-64 34238199-9 2022 We provided evidence that the upregulation of SHP2 expression by transfection significantly inhibited the cytotoxicity of 5-FU and DTA3. Fluorouracil 122-126 protein tyrosine phosphatase non-receptor type 11 Homo sapiens 46-50 34238199-10 2022 SHP2 knockdown enhanced the antiproliferation activity of 5-FU, indicating targeting SHP2 sensitized cervical cancer cells to 5-FU. Fluorouracil 58-62 protein tyrosine phosphatase non-receptor type 11 Homo sapiens 0-4 34238199-10 2022 SHP2 knockdown enhanced the antiproliferation activity of 5-FU, indicating targeting SHP2 sensitized cervical cancer cells to 5-FU. Fluorouracil 58-62 protein tyrosine phosphatase non-receptor type 11 Homo sapiens 85-89 34238199-10 2022 SHP2 knockdown enhanced the antiproliferation activity of 5-FU, indicating targeting SHP2 sensitized cervical cancer cells to 5-FU. Fluorouracil 126-130 protein tyrosine phosphatase non-receptor type 11 Homo sapiens 85-89 34238199-11 2022 CONCLUSION: Our study demonstrates that SHP2 inhibitor DTA3 and 5-FU have a synergistic cytotoxic effect on cervical cancer cells. Fluorouracil 64-68 protein tyrosine phosphatase non-receptor type 11 Homo sapiens 40-44 34238199-12 2022 The synergistic combination of SHP2 inhibitor and 5-FU may present a promising strategy for the treatment of cervical cancer. Fluorouracil 50-54 protein tyrosine phosphatase non-receptor type 11 Homo sapiens 31-35 34185243-7 2021 RESULTS: The current study showed that 5FU succeeded in inducing cardiotoxicity, manifested by significantly elevated levels of cardiac enzymes, tissue malondialdehyde (MDA), interleukin 6 (IL-6), signal transducer and activator of transcription 4 (STAT4), and caspase-3. Fluorouracil 39-42 signal transducer and activator of transcription 4 Homo sapiens 197-247 34185243-7 2021 RESULTS: The current study showed that 5FU succeeded in inducing cardiotoxicity, manifested by significantly elevated levels of cardiac enzymes, tissue malondialdehyde (MDA), interleukin 6 (IL-6), signal transducer and activator of transcription 4 (STAT4), and caspase-3. Fluorouracil 39-42 signal transducer and activator of transcription 4 Homo sapiens 249-254 34155879-0 2021 MicroRNA-29b-3p promotes 5-fluorouracil resistance via suppressing TRAF5-mediated necroptosis in human colorectal cancer. Fluorouracil 25-39 TNF receptor associated factor 5 Homo sapiens 76-81 34155879-5 2021 Rescue of TRAF5 could reverse the effect of miR-29b-3p on 5-FU-induced necroptosis, which was consistent with the role ofnecrostatin-1 (a specific necroptosis inhibitor). Fluorouracil 58-62 TNF receptor associated factor 5 Homo sapiens 10-15 34168463-3 2021 The expressions of OCT3/4 and Nanog in cells treated with 5-Fu or CDDP were measured by immunofluorescence, Western blot and qPCR. Fluorouracil 58-62 Nanog homeobox Homo sapiens 30-35 34605693-6 2021 Pretreatment of cells with the anticancer agent 5-fluorouracil (5-FU) significantly increased ROS production, which potentiated TRPM2-mediated calcium signaling, decreased cell proliferation, and increased apoptosis in TE-1 cells, suggesting that the therapeutic effect of 5-FU in ESCC cells may be mediated by the TRPM2 channel-mediated calcium influx. Fluorouracil 48-62 transient receptor potential cation channel subfamily M member 2 Homo sapiens 128-133 34605693-6 2021 Pretreatment of cells with the anticancer agent 5-fluorouracil (5-FU) significantly increased ROS production, which potentiated TRPM2-mediated calcium signaling, decreased cell proliferation, and increased apoptosis in TE-1 cells, suggesting that the therapeutic effect of 5-FU in ESCC cells may be mediated by the TRPM2 channel-mediated calcium influx. Fluorouracil 48-62 transient receptor potential cation channel subfamily M member 2 Homo sapiens 315-320 34605693-6 2021 Pretreatment of cells with the anticancer agent 5-fluorouracil (5-FU) significantly increased ROS production, which potentiated TRPM2-mediated calcium signaling, decreased cell proliferation, and increased apoptosis in TE-1 cells, suggesting that the therapeutic effect of 5-FU in ESCC cells may be mediated by the TRPM2 channel-mediated calcium influx. Fluorouracil 64-68 transient receptor potential cation channel subfamily M member 2 Homo sapiens 128-133 34605693-6 2021 Pretreatment of cells with the anticancer agent 5-fluorouracil (5-FU) significantly increased ROS production, which potentiated TRPM2-mediated calcium signaling, decreased cell proliferation, and increased apoptosis in TE-1 cells, suggesting that the therapeutic effect of 5-FU in ESCC cells may be mediated by the TRPM2 channel-mediated calcium influx. Fluorouracil 64-68 transient receptor potential cation channel subfamily M member 2 Homo sapiens 315-320 34605693-6 2021 Pretreatment of cells with the anticancer agent 5-fluorouracil (5-FU) significantly increased ROS production, which potentiated TRPM2-mediated calcium signaling, decreased cell proliferation, and increased apoptosis in TE-1 cells, suggesting that the therapeutic effect of 5-FU in ESCC cells may be mediated by the TRPM2 channel-mediated calcium influx. Fluorouracil 273-277 transient receptor potential cation channel subfamily M member 2 Homo sapiens 128-133 34605693-6 2021 Pretreatment of cells with the anticancer agent 5-fluorouracil (5-FU) significantly increased ROS production, which potentiated TRPM2-mediated calcium signaling, decreased cell proliferation, and increased apoptosis in TE-1 cells, suggesting that the therapeutic effect of 5-FU in ESCC cells may be mediated by the TRPM2 channel-mediated calcium influx. Fluorouracil 273-277 transient receptor potential cation channel subfamily M member 2 Homo sapiens 315-320 35506454-0 2022 Visfatin inhibits colon cancer cell apoptosis and decreases chemosensitivity to 5-FU by promoting the SDF-1/CXCR4/Akt axis. Fluorouracil 80-84 C-X-C motif chemokine receptor 4 Homo sapiens 108-113 35506454-10 2022 A positive correlation between visfatin and SDF-1 was observed, with the knockdown of visfatin enhancing cell sensitivity to 5-FU chemotherapy by targeting the SDF-1/C-X-C chemokine receptor type 4 (CXCR4) axis. Fluorouracil 125-129 C-X-C motif chemokine receptor 4 Homo sapiens 166-197 35506454-10 2022 A positive correlation between visfatin and SDF-1 was observed, with the knockdown of visfatin enhancing cell sensitivity to 5-FU chemotherapy by targeting the SDF-1/C-X-C chemokine receptor type 4 (CXCR4) axis. Fluorouracil 125-129 C-X-C motif chemokine receptor 4 Homo sapiens 199-204 35506454-11 2022 Furthermore, the Akt signalling pathway downstream of SDF-1/CXCR4 proved to be critical in the decreased sensitisation of colon cancer cells to 5-FU induced by visfatin. Fluorouracil 144-148 C-X-C motif chemokine receptor 4 Homo sapiens 60-65 35462225-0 2022 SPOCK1 silencing decreases 5-FU resistance through PRRX1 in colorectal cancer. Fluorouracil 27-31 SPARC (osteonectin), cwcv and kazal like domains proteoglycan 1 Homo sapiens 0-6 35462225-3 2022 However, the relationship between development of resistance to 5-FU and SPOCK1 remain unclear. Fluorouracil 63-67 SPARC (osteonectin), cwcv and kazal like domains proteoglycan 1 Homo sapiens 72-78 35462225-4 2022 In this study, we established two 5-fluorouracil (5-FU)-resistant CRC cell lines, HCT116/FU and LOVO/FU, and found that SPOCK1 is upregulated in 5-FU-resistance CRC cells compared with its parental cell line. Fluorouracil 34-48 SPARC (osteonectin), cwcv and kazal like domains proteoglycan 1 Homo sapiens 120-126 35462225-4 2022 In this study, we established two 5-fluorouracil (5-FU)-resistant CRC cell lines, HCT116/FU and LOVO/FU, and found that SPOCK1 is upregulated in 5-FU-resistance CRC cells compared with its parental cell line. Fluorouracil 50-54 SPARC (osteonectin), cwcv and kazal like domains proteoglycan 1 Homo sapiens 120-126 35462225-4 2022 In this study, we established two 5-fluorouracil (5-FU)-resistant CRC cell lines, HCT116/FU and LOVO/FU, and found that SPOCK1 is upregulated in 5-FU-resistance CRC cells compared with its parental cell line. Fluorouracil 145-149 SPARC (osteonectin), cwcv and kazal like domains proteoglycan 1 Homo sapiens 120-126 35462225-5 2022 knockdown of SPOCK1 in 5-FU-resistant CRC cells increases their sensitivity to 5-FU. Fluorouracil 23-27 SPARC (osteonectin), cwcv and kazal like domains proteoglycan 1 Homo sapiens 13-19 35462225-5 2022 knockdown of SPOCK1 in 5-FU-resistant CRC cells increases their sensitivity to 5-FU. Fluorouracil 79-83 SPARC (osteonectin), cwcv and kazal like domains proteoglycan 1 Homo sapiens 13-19 35462225-6 2022 In contrast, transient transfection of SPOCK1 enhanced HCT116 and LOVO cell resistance to 5-FU and reduced cell apoptosis. Fluorouracil 90-94 SPARC (osteonectin), cwcv and kazal like domains proteoglycan 1 Homo sapiens 39-45 35462225-7 2022 Mechanistically, SPOCK1 promoted 5-FU resistance by regulating PRRX1 expression and the downstream apoptosis signaling pathway. Fluorouracil 33-37 SPARC (osteonectin), cwcv and kazal like domains proteoglycan 1 Homo sapiens 17-23 35462225-8 2022 Taken together, our results revealed for the first time that SPOCK1 plays a crucial role in the resistance of CRC cells to 5-FU and indicated that targeting SPOCK1 may be a promising therapeutic strategy to overcome 5-FU resistance in CRC. Fluorouracil 123-127 SPARC (osteonectin), cwcv and kazal like domains proteoglycan 1 Homo sapiens 61-67 35462225-8 2022 Taken together, our results revealed for the first time that SPOCK1 plays a crucial role in the resistance of CRC cells to 5-FU and indicated that targeting SPOCK1 may be a promising therapeutic strategy to overcome 5-FU resistance in CRC. Fluorouracil 123-127 SPARC (osteonectin), cwcv and kazal like domains proteoglycan 1 Homo sapiens 157-163 35462225-8 2022 Taken together, our results revealed for the first time that SPOCK1 plays a crucial role in the resistance of CRC cells to 5-FU and indicated that targeting SPOCK1 may be a promising therapeutic strategy to overcome 5-FU resistance in CRC. Fluorouracil 216-220 SPARC (osteonectin), cwcv and kazal like domains proteoglycan 1 Homo sapiens 157-163 35600882-8 2022 High-throughput miRNA and mRNA sequencing analyses identified a subset of miRNAs and mRNAs under regulation of both 5-Fu and GM-CSF in gastric cancer cells, including upregulation of miR-877-3p and downregulation of SOCS2. Fluorouracil 116-120 suppressor of cytokine signaling 2 Homo sapiens 216-221 35367196-5 2022 Moreover, 5-Fu induced GATA3 in MSS CRC cells and tumors, which were eradicated by atosiban. Fluorouracil 10-14 GATA binding protein 3 Homo sapiens 23-28 35367196-6 2022 Further investigation showed that atosiban strengthened the antitumor activity of 5-Fu through eradiation of 5-Fu-induced GATA3 in MSS-type CRC cells. Fluorouracil 82-86 GATA binding protein 3 Homo sapiens 122-127 35367196-6 2022 Further investigation showed that atosiban strengthened the antitumor activity of 5-Fu through eradiation of 5-Fu-induced GATA3 in MSS-type CRC cells. Fluorouracil 109-113 GATA binding protein 3 Homo sapiens 122-127 35367196-7 2022 Taken together, our findings suggest that atosiban potentiates the antitumor effect of 5-Fu by abolishing 5-Fu-induced GATA3, which provides a novel therapeutic strategy for MSS-type CRC via the combination of atosiban and 5-Fu. Fluorouracil 87-91 GATA binding protein 3 Homo sapiens 119-124 35367196-7 2022 Taken together, our findings suggest that atosiban potentiates the antitumor effect of 5-Fu by abolishing 5-Fu-induced GATA3, which provides a novel therapeutic strategy for MSS-type CRC via the combination of atosiban and 5-Fu. Fluorouracil 106-110 GATA binding protein 3 Homo sapiens 119-124 35522902-0 2022 Targeting DCLK1 overcomes 5-fluorouracil resistance in colorectal cancer through inhibiting CCAR1/beta-catenin pathway-mediated cancer stemness. Fluorouracil 26-40 doublecortin like kinase 1 Homo sapiens 10-15 35522902-4 2022 Moreover, we perform clinical specimen research, in vitro and in vivo experiments and molecular mechanism research, to reveal the biological effects and the mechanism of DCLK1 promoting 5-fluorouracil resistance, and to clarify the potential clinical value of DCLK1 as a target of 5-fluorouracil resistance in CRC. Fluorouracil 186-200 doublecortin like kinase 1 Homo sapiens 170-175 35522902-5 2022 RESULTS: We discover that doublecortin-like kinase 1 (DCLK1), a cancer stem cell maker, is correlated with 5-fluorouracil resistance, and functionally promotes cancer stemness and 5-fluorouracil resistance in CRC. Fluorouracil 107-121 doublecortin like kinase 1 Homo sapiens 26-52 35522902-5 2022 RESULTS: We discover that doublecortin-like kinase 1 (DCLK1), a cancer stem cell maker, is correlated with 5-fluorouracil resistance, and functionally promotes cancer stemness and 5-fluorouracil resistance in CRC. Fluorouracil 107-121 doublecortin like kinase 1 Homo sapiens 54-59 35522902-5 2022 RESULTS: We discover that doublecortin-like kinase 1 (DCLK1), a cancer stem cell maker, is correlated with 5-fluorouracil resistance, and functionally promotes cancer stemness and 5-fluorouracil resistance in CRC. Fluorouracil 180-194 doublecortin like kinase 1 Homo sapiens 26-52 35522902-5 2022 RESULTS: We discover that doublecortin-like kinase 1 (DCLK1), a cancer stem cell maker, is correlated with 5-fluorouracil resistance, and functionally promotes cancer stemness and 5-fluorouracil resistance in CRC. Fluorouracil 180-194 doublecortin like kinase 1 Homo sapiens 54-59 35522902-8 2022 Subsequently, we prove that blocking beta-catenin inhibits DCLK1-mediated 5-fluorouracil resistance in CRC cells. Fluorouracil 74-88 doublecortin like kinase 1 Homo sapiens 59-64 35522902-9 2022 Importantly, we demonstrate that DCLK1 inhibitor could block CCAR1/beta-catenin pathway-mediated cancer stemness and consequently suppresses 5-fluorouracil resistant CRC cells in vitro and in vivo. Fluorouracil 141-155 doublecortin like kinase 1 Homo sapiens 33-38 35522902-10 2022 CONCLUSIONS: Collectively, our findings reveal that DCLK1 promotes 5-fluorouracil resistance in CRC by CCAR1/beta-catenin pathway-mediated cancer stemness, and suggest that targeting DCLK1 might be a promising method to eliminate cancer stem cells for overcoming 5-fluorouracil resistance in CRC. Fluorouracil 67-81 doublecortin like kinase 1 Homo sapiens 52-57 35522902-10 2022 CONCLUSIONS: Collectively, our findings reveal that DCLK1 promotes 5-fluorouracil resistance in CRC by CCAR1/beta-catenin pathway-mediated cancer stemness, and suggest that targeting DCLK1 might be a promising method to eliminate cancer stem cells for overcoming 5-fluorouracil resistance in CRC. Fluorouracil 67-81 doublecortin like kinase 1 Homo sapiens 183-188 35522902-10 2022 CONCLUSIONS: Collectively, our findings reveal that DCLK1 promotes 5-fluorouracil resistance in CRC by CCAR1/beta-catenin pathway-mediated cancer stemness, and suggest that targeting DCLK1 might be a promising method to eliminate cancer stem cells for overcoming 5-fluorouracil resistance in CRC. Fluorouracil 263-277 doublecortin like kinase 1 Homo sapiens 52-57 35288979-11 2022 Similarly, overexpression of PFKFB3 can regulate CRC cell behavior and 5-FU resistance caused by miR-197-3p. Fluorouracil 71-75 microRNA 1973 Homo sapiens 97-107 35288979-13 2022 Circ_0014130 modulates 5-FU resistance in colorectal cancer by modulating the miR-197-3p/PFKFB3 axis, which is helpful for drug chemotherapy in colorectal cancer. Fluorouracil 23-27 microRNA 1973 Homo sapiens 78-88 35461243-0 2022 Macrophage-targeted anti-CCL2 immunotherapy enhances tumor sensitivity to 5-fluorouracil in a Balb/c-CT26 murine colon carcinoma model measured using diffuse reflectance spectroscopy. Fluorouracil 74-88 chemokine (C-C motif) ligand 2 Mus musculus 25-29 35461243-4 2022 In this study, we examine whether blockade of monocyte recruitment via CCL2 (macrophage chemoattractant protein-1) leads to enhanced sensitivity of 5-fluorouracil (5-FU) in a CT26-Balb/c mouse model of CRC. Fluorouracil 164-168 chemokine (C-C motif) ligand 2 Mus musculus 71-75 35461243-8 2022 This shows that the addition of anti-CCL2 to 5-FU slowed the fold-change (change from the original measurement to the final measurement) in tumor volume from Day 0 to Day 12 (~ 5 fold). Fluorouracil 45-49 chemokine (C-C motif) ligand 2 Mus musculus 37-41 35448938-6 2022 In our results, the three SCFAs could inhibit ROS expressions, NLRP3, Caspase-1, IL-1beta, IL-6, IL-18, Beclin-1 and LC3-II, when induced by 5-FU. Fluorouracil 141-145 interleukin 18 Homo sapiens 97-102 35448938-6 2022 In our results, the three SCFAs could inhibit ROS expressions, NLRP3, Caspase-1, IL-1beta, IL-6, IL-18, Beclin-1 and LC3-II, when induced by 5-FU. Fluorouracil 141-145 beclin 1 Homo sapiens 104-112 35448938-6 2022 In our results, the three SCFAs could inhibit ROS expressions, NLRP3, Caspase-1, IL-1beta, IL-6, IL-18, Beclin-1 and LC3-II, when induced by 5-FU. Fluorouracil 141-145 microtubule associated protein 1 light chain 3 alpha Homo sapiens 117-120 35235860-8 2022 RESULTS: Valsartan suppressed CRC cell-growth and synergistically enhanced the anti-tumor-activities of 5-FU by induction of apoptosis, BAX, BCL2, P53 and modulation of the cell cycle. Fluorouracil 104-108 BCL2-associated X protein Mus musculus 136-139 35408480-5 2022 In this work, a formulation containing 5-FU and siRNA against the VEGF/VEGFR signaling pathway into N-acetyl-galactosamine (GalNAc)-modified nanocarriers is established. Fluorouracil 39-43 vascular endothelial growth factor A Mus musculus 66-70 35309455-8 2022 The release rate of 5-FU from MCM-41 and aminopropyl-substituted MCM-41 (MCM-NH2) was studied using molecular dynamics simulations which revealed that the release rate of 5-FU from the MCM-NH2 surface was slower compared to that of plain MCM-41. Fluorouracil 20-24 methylmalonyl-CoA mutase Homo sapiens 185-188 35309455-8 2022 The release rate of 5-FU from MCM-41 and aminopropyl-substituted MCM-41 (MCM-NH2) was studied using molecular dynamics simulations which revealed that the release rate of 5-FU from the MCM-NH2 surface was slower compared to that of plain MCM-41. Fluorouracil 171-175 methylmalonyl-CoA mutase Homo sapiens 73-76 35309455-8 2022 The release rate of 5-FU from MCM-41 and aminopropyl-substituted MCM-41 (MCM-NH2) was studied using molecular dynamics simulations which revealed that the release rate of 5-FU from the MCM-NH2 surface was slower compared to that of plain MCM-41. Fluorouracil 171-175 methylmalonyl-CoA mutase Homo sapiens 185-188 35051860-0 2022 CDX2 controls genes involved in the metabolism of 5-fluorouracil and is associated with reduced efficacy of chemotherapy in colorectal cancer. Fluorouracil 50-64 caudal type homeobox 2 Homo sapiens 0-4 35051860-5 2022 Unexpectedly, we discovered that the prognosis value of CDX2 for disease-free survival of patients affected with CRC is lost upon chemotherapy and that CDX2 expression enhances resistance of colon cancer cells towards 5-FU. Fluorouracil 218-222 caudal type homeobox 2 Homo sapiens 152-156 35051860-6 2022 At the molecular level, we found that CDX2 expression correlates with higher levels of genes regulating the bioavailability of 5-FU through efflux (ABCC11) and catabolism (DPYD) in patients affected with CRC and CRC cell lines. Fluorouracil 127-131 caudal type homeobox 2 Homo sapiens 38-42 35051860-6 2022 At the molecular level, we found that CDX2 expression correlates with higher levels of genes regulating the bioavailability of 5-FU through efflux (ABCC11) and catabolism (DPYD) in patients affected with CRC and CRC cell lines. Fluorouracil 127-131 ATP binding cassette subfamily C member 11 Homo sapiens 148-154 35051860-6 2022 At the molecular level, we found that CDX2 expression correlates with higher levels of genes regulating the bioavailability of 5-FU through efflux (ABCC11) and catabolism (DPYD) in patients affected with CRC and CRC cell lines. Fluorouracil 127-131 dihydropyrimidine dehydrogenase Homo sapiens 172-176 35051860-7 2022 We further showed that CDX2 directly regulates the expression of ABCC11 and that the inhibition of ABCC11 improves 5-FU-sensitivity of CDX2-expressing colon cancer cells. Fluorouracil 115-119 caudal type homeobox 2 Homo sapiens 23-27 35051860-7 2022 We further showed that CDX2 directly regulates the expression of ABCC11 and that the inhibition of ABCC11 improves 5-FU-sensitivity of CDX2-expressing colon cancer cells. Fluorouracil 115-119 ATP binding cassette subfamily C member 11 Homo sapiens 99-105 35051860-7 2022 We further showed that CDX2 directly regulates the expression of ABCC11 and that the inhibition of ABCC11 improves 5-FU-sensitivity of CDX2-expressing colon cancer cells. Fluorouracil 115-119 caudal type homeobox 2 Homo sapiens 135-139 35252173-8 2022 Furthermore, Cd treatment attenuated the efficacy of 5-fluorouracil, cisplatin and irradiation treatment in CCT-ESCC cells both in vitro and in vivo. Fluorouracil 53-67 CCT Homo sapiens 108-111 35252200-4 2022 Results: A total of 3,175 differentially expressed mRNAs (DEGs), lncRNAs (DELs), and miRNAs (DEMs) related to 5-FU resistance were identified, including significantly upregulated IL33, H19, and miR-17-5p; the downregulated AKR1B10, LINC01012, and miR-125b-5p; and chromatin modifiers such as INO80C, HDAC6, and KDM5A. Fluorouracil 110-114 lysine demethylase 5A Homo sapiens 311-316 35252200-5 2022 The construction of the ceRNA regulatory network revealed that H19, HOXA11-AS, and NEAT1 might function as ceRNAs associated with 5-FU resistance in HCT15 cells. Fluorouracil 130-134 nuclear paraspeckle assembly transcript 1 Homo sapiens 83-88 35252200-9 2022 Finally, we obtained several critical TFs and their potential targets associated with DARs and 5-FU resistance, including FOXA1 and KLF3. Fluorouracil 95-99 Kruppel like factor 3 Homo sapiens 132-136 35093082-13 2022 TYMS knockdown reversed the 5-FU resistance caused by FOXM1 overexpression and re-sensitized HCC cells to 5-FU treatment. Fluorouracil 28-32 forkhead box M1 Homo sapiens 54-59 35022331-0 2022 TIMP-2 regulates 5-Fu resistance via the ERK/MAPK signaling pathway in colorectal cancer. Fluorouracil 17-21 TIMP metallopeptidase inhibitor 2 Homo sapiens 0-6 35022331-4 2022 Using a cytokine array, we established that tissue inhibitor metalloproteinase 2 (TIMP-2) is highly expressed in 5-Fu resistant colorectal cancer patients. Fluorouracil 113-117 TIMP metallopeptidase inhibitor 2 Homo sapiens 44-80 35022331-4 2022 Using a cytokine array, we established that tissue inhibitor metalloproteinase 2 (TIMP-2) is highly expressed in 5-Fu resistant colorectal cancer patients. Fluorouracil 113-117 TIMP metallopeptidase inhibitor 2 Homo sapiens 82-88 35022331-6 2022 In a 5-Fu-resistant patient-derived xenograft (PDX) model, TIMP-2 was also found to be highly expressed. Fluorouracil 5-9 TIMP metallopeptidase inhibitor 2 Homo sapiens 59-65 35022331-7 2022 We established an autocrine mechanism through which elevated TIMP-2 protein levels sustained colorectal cancer cell resistance to 5-Fu by constitutively activating the ERK/MAPK signaling pathway. Fluorouracil 130-134 TIMP metallopeptidase inhibitor 2 Homo sapiens 61-67 35022331-8 2022 Inhibition of TIMP-2 using an anti-TIMP-2 antibody or ERK/MAPK inhibition by U0126 suppressed TIMP-2 mediated 5-Fu-resistance in CRC patients. Fluorouracil 110-114 TIMP metallopeptidase inhibitor 2 Homo sapiens 35-41 35022331-8 2022 Inhibition of TIMP-2 using an anti-TIMP-2 antibody or ERK/MAPK inhibition by U0126 suppressed TIMP-2 mediated 5-Fu-resistance in CRC patients. Fluorouracil 110-114 TIMP metallopeptidase inhibitor 2 Homo sapiens 94-100 35022331-9 2022 In conclusion, a novel TIMP-2-ERK/MAPK mediated 5-Fu resistance mechanism is involved in colorectal cancer. Fluorouracil 48-52 TIMP metallopeptidase inhibitor 2 Homo sapiens 23-29 35022331-10 2022 Therefore, targeting TIMP-2 or ERK/MAPK may provide a new strategy to overcome 5-Fu resistance in colorectal cancer chemotherapy. Fluorouracil 79-83 TIMP metallopeptidase inhibitor 2 Homo sapiens 21-27 35071232-0 2021 Deficient or R273H and R248W Mutations of p53 Promote Chemoresistance to 5-FU via TCF21/CD44 Axis-Mediated Enhanced Stemness in Colorectal Carcinoma. Fluorouracil 73-77 CD44 molecule (Indian blood group) Homo sapiens 88-92 35071232-16 2021 Overexpression of TCF21 or knockdown of CD44 could rescue the sensitivity to 5-FU in deficient and mutant p53 HCT116 cell lines. Fluorouracil 77-81 CD44 molecule (Indian blood group) Homo sapiens 40-44 35019820-9 2022 In conclusion, combination therapy of Nab-paclitaxel and IL-15 fusion protein can effectively stimulate the antitumor activity of immune effector cells, thereby inhibiting immunosuppressive cells within the TME of colorectal cancer, and the overall therapeutic effect has a significant advantage over monotherapy.AbbreviationsInterleukin 15, IL-15; Human serum albumin, HSA; Myeloid-derived suppressor cells, MDSC; Albumin binding domain, ABD; Tumor drainage lymph node, TDLN; Natural killer (NK); Tumor-draining lymph node (TDLN); Tumor infiltrating lymphocyte, TIL; Immunogenic cell death, ICD; Enhanced permeability retention, EPR; Liposomal doxorubicin, Doxil; 5-fluorouracil, 5-FU. Fluorouracil 665-679 interleukin 15 Mus musculus 57-62 35019820-9 2022 In conclusion, combination therapy of Nab-paclitaxel and IL-15 fusion protein can effectively stimulate the antitumor activity of immune effector cells, thereby inhibiting immunosuppressive cells within the TME of colorectal cancer, and the overall therapeutic effect has a significant advantage over monotherapy.AbbreviationsInterleukin 15, IL-15; Human serum albumin, HSA; Myeloid-derived suppressor cells, MDSC; Albumin binding domain, ABD; Tumor drainage lymph node, TDLN; Natural killer (NK); Tumor-draining lymph node (TDLN); Tumor infiltrating lymphocyte, TIL; Immunogenic cell death, ICD; Enhanced permeability retention, EPR; Liposomal doxorubicin, Doxil; 5-fluorouracil, 5-FU. Fluorouracil 681-685 interleukin 15 Mus musculus 57-62 34976591-15 2022 CD44-Apt1 when conjugated with inhibitor 5-FU showed efficient guidance of 5-FU into HCC cells that significantly enhanced drug toxicity by more than thousands-fold. Fluorouracil 41-45 CD44 molecule (Indian blood group) Homo sapiens 0-4 34976591-15 2022 CD44-Apt1 when conjugated with inhibitor 5-FU showed efficient guidance of 5-FU into HCC cells that significantly enhanced drug toxicity by more than thousands-fold. Fluorouracil 75-79 CD44 molecule (Indian blood group) Homo sapiens 0-4 2573433-3 1989 Bone marrow from mice treated with 5-fluorouracil was depleted of cells expressing Mac-1, CD4, and CD8 and incubated on lymphocyte-free monolayer cultures of adherent thymic stromal cells. Fluorouracil 35-49 CD4 antigen Mus musculus 90-93 2971656-2 1988 Exposure of L1210 cells to folinic acid resulted in expansion of intracellular pools of 5,10-CH2-H4PteGlun, delayed the reappearance of catalytically active thymidylate synthase (TS) following 5-fluoro-2"-deoxyuridine exposure, and stabilized inhibited TS complexes over the same concentration range that augmented the cytotoxic effects of fluorodeoxyuridine and 5-fluorouracil. Fluorouracil 363-377 thymidylate synthase Mus musculus 179-181 3107475-8 1987 rhG-CSF was demonstrated to accelerate the recovery from neutropenia induced in mice and monkeys by 5-fluorouracil or cyclophosphamide. Fluorouracil 100-114 colony stimulating factor 2 (granulocyte-macrophage) Mus musculus 4-7 3789759-5 1986 When Sarcoma 180-bearing mice were injected with CCl4 to induce liver dysfunction and subsequently administered 5-FU, the AUCs of 5-FU in the plasma and tumor tissue were increased by 2 and 1.3 times, respectively, as compared with non-treated mice. Fluorouracil 112-116 chemokine (C-C motif) ligand 4 Mus musculus 49-53 3789759-5 1986 When Sarcoma 180-bearing mice were injected with CCl4 to induce liver dysfunction and subsequently administered 5-FU, the AUCs of 5-FU in the plasma and tumor tissue were increased by 2 and 1.3 times, respectively, as compared with non-treated mice. Fluorouracil 130-134 chemokine (C-C motif) ligand 4 Mus musculus 49-53 3525762-7 1986 Like LAK, both HAK and D-LAK were able to compensate for the immunosuppressive effect of the cytotoxic drugs dianhydrogalactitol, vincristine, and 5-fluorouracil, which all have different mechanisms of action, provided that combined treatment by polypeptide and drug was applied repeatedly before the SRBC immunization. Fluorouracil 147-161 alpha-kinase 2 Mus musculus 15-18 4044100-2 1985 Furthermore, thymosin alpha 1 increased the levels of colony stimulating factor (CSF) in sera or in culture media of spleen cells derived from 5-FU-treated mice. Fluorouracil 143-147 colony stimulating factor 2 (granulocyte-macrophage) Mus musculus 54-79 4044100-2 1985 Furthermore, thymosin alpha 1 increased the levels of colony stimulating factor (CSF) in sera or in culture media of spleen cells derived from 5-FU-treated mice. Fluorouracil 143-147 colony stimulating factor 2 (granulocyte-macrophage) Mus musculus 81-84 4044100-6 1985 The present study indicates that thymosin alpha 1 exerts its protective effect against the 5-FU-induced bone marrow toxicity, at least partially, through its effect on the maturation of immature T cells to functional T cells which produce various kinds of lymphokines including CSF. Fluorouracil 91-95 colony stimulating factor 2 (granulocyte-macrophage) Mus musculus 278-281 7074558-2 1982 In patients with advanced uterine corpus carcinoma treated with the combination chemotherapy of megestrol, cyclophosphamide, and doxorubicin (MCA) or with this combination and 5-fluorouracil (MCAF), the overall response rate was 22%. Fluorouracil 176-190 activating transcription factor 7 interacting protein Homo sapiens 192-196 6213271-1 1982 The uncoupling of 2-oxoglutarate decarboxylation from hydroxylation in the reaction catalyzed by thymine 7-hydroxylase (thymine, 2-oxoglutarate:oxygen oxidoreductase (7-hydroxylating), EC 1.14.11.6) in the presence of 5-fluorouracil has been studied. Fluorouracil 218-232 thioredoxin reductase 1 Homo sapiens 151-165 7040822-10 1982 The reasons why the GM-CFC-1 should be more sensitive to 5-FU than other low density progenitors are discussed and the relation of these low density precursors to one another in terms of their position within the haemopoietic developmental lineage is elucidated. Fluorouracil 57-61 cripto, FRL-1, cryptic family 1 Mus musculus 23-28 1003701-4 1976 High doses of 5-fluorouracil (5-FU) and cyclophosphamide (CP) given parenterally for 6 days caused a partial decrease in whole body weight and the microsomal enzyme content such as cytochrome P-450 and cytochrome b5. Fluorouracil 14-28 cytochrome b5 type A Rattus norvegicus 202-215 1003701-4 1976 High doses of 5-fluorouracil (5-FU) and cyclophosphamide (CP) given parenterally for 6 days caused a partial decrease in whole body weight and the microsomal enzyme content such as cytochrome P-450 and cytochrome b5. Fluorouracil 30-34 cytochrome b5 type A Rattus norvegicus 202-215 33838133-11 2021 Collectively, we proposed such a combination treatment to overcome 5-FU resistance in HCC from the perspective of epigenetically restoring OAT2. Fluorouracil 67-71 solute carrier family 22 member 7 Homo sapiens 139-143 33741693-7 2021 Engineered mouse models treated with the therapeutic agent 5-fluorouracil showed that upon increased MSI1 levels, Lgr5high-SCs remain sensitive while Lgr5low-progenitors reprogram to a drug-resistant phenotype. Fluorouracil 59-73 musashi RNA-binding protein 1 Mus musculus 101-105 33741693-7 2021 Engineered mouse models treated with the therapeutic agent 5-fluorouracil showed that upon increased MSI1 levels, Lgr5high-SCs remain sensitive while Lgr5low-progenitors reprogram to a drug-resistant phenotype. Fluorouracil 59-73 leucine rich repeat containing G protein coupled receptor 5 Mus musculus 114-118 33741693-7 2021 Engineered mouse models treated with the therapeutic agent 5-fluorouracil showed that upon increased MSI1 levels, Lgr5high-SCs remain sensitive while Lgr5low-progenitors reprogram to a drug-resistant phenotype. Fluorouracil 59-73 leucine rich repeat containing G protein coupled receptor 5 Mus musculus 150-154 33978826-14 2022 These findings allow a more precise stratification upon the co-evaluation with CD8+ T cells to better clinical management for patients who would benefit from 5-fluorouracil. Fluorouracil 158-172 CD8a molecule Homo sapiens 79-82 33927358-8 2021 Co-administration of GA also retarded the 5-FU-induced central fatigue-like behavior accompanied by down-regulating the expression of IL-6, iNOS and COX2 in the hippocampus through inhibiting TLR4/Myd88/NF-kappaB pathway. Fluorouracil 42-46 myeloid differentiation primary response gene 88 Mus musculus 197-202 33755421-2 2021 5-Fluorouracil (5FU) is also a substrate for DPD and a common chemotherapeutic agent used to treat numerous cancers. Fluorouracil 16-19 dihydropyrimidine dehydrogenase Homo sapiens 45-48 33755421-4 2021 Patients with high DPD activity levels typically have poor outcomes when treated with 5FU. Fluorouracil 86-89 dihydropyrimidine dehydrogenase Homo sapiens 19-22 33648930-9 2021 This novel approach using TUG1-DDS in combination with 5-FU may serve as an effective therapeutic option to attenuate DPD activity and meet appropriate 5-FU dosage requirements in targeted PDAC cells, which can reduce the systemic adverse effects of chemotherapy. Fluorouracil 55-59 dihydropyrimidine dehydrogenase Homo sapiens 118-121 33472949-0 2021 Crosstalk between YAP and RAR-RXR drives expression of stemness genes to promote 5-FU resistance and self-renewal in colorectal cancer cells. Fluorouracil 81-85 retinoid X receptor alpha Homo sapiens 30-33 33735188-5 2021 We assessed the response to conventional chemotherapy drugs, including fluorouracil, a compound of fluoropyrimidine S-1, oxaliplatin, and all-trans-retinoic acid (ATRA), in gastric cancer cell lines with high SLC2A1 expression. Fluorouracil 71-83 solute carrier family 2 member 1 Homo sapiens 209-215 33674443-10 2021 Human peripheral blood monocytes co-cultured with ESCC cells treated with 5-FU/CDDP increased the expression of CD163, which was attenuated by the treatment with CSF-1R inhibitors. Fluorouracil 74-78 CD163 molecule Homo sapiens 112-117 33838628-12 2021 The treatment with HDC and ML-385 (specific inhibitor of Nrf-2) augmented the 5-FU-mediated apoptotic cell death of HCT-116/R cells, which suggests that NOX-2 and Nrf-2 are involved in the development of the chemoresistant phenotype of these cells. Fluorouracil 78-82 cytochrome b-245 beta chain Homo sapiens 153-158 33476960-0 2021 5-Fluorouracil enhances the chemosensitivity of gastric cancer to TRAIL via inhibition of the MAPK pathway. Fluorouracil 0-14 tumor necrosis factor (ligand) superfamily, member 10 Mus musculus 66-71 33491253-0 2021 Haplotype structure defines effects of common DPYD variants c.85T>C (rs1801265) and c.496A>G (rs2297595) on DPD activity: implication for 5-fluorouracil toxicity. Fluorouracil 138-152 dihydropyrimidine dehydrogenase Homo sapiens 46-50 33491253-0 2021 Haplotype structure defines effects of common DPYD variants c.85T>C (rs1801265) and c.496A>G (rs2297595) on DPD activity: implication for 5-fluorouracil toxicity. Fluorouracil 138-152 dihydropyrimidine dehydrogenase Homo sapiens 108-111 33491253-1 2021 AIM: The aim of this study was to identify risk variants and haplotypes that impair dihydropyrimidine dehydrogenase (DPD) activity and are, therefore, candidate risk variants for severe toxicity to 5-fluorouracil (5-FU) chemotherapy. Fluorouracil 198-212 dihydropyrimidine dehydrogenase Homo sapiens 84-115 33491253-1 2021 AIM: The aim of this study was to identify risk variants and haplotypes that impair dihydropyrimidine dehydrogenase (DPD) activity and are, therefore, candidate risk variants for severe toxicity to 5-fluorouracil (5-FU) chemotherapy. Fluorouracil 198-212 dihydropyrimidine dehydrogenase Homo sapiens 117-120 33491253-1 2021 AIM: The aim of this study was to identify risk variants and haplotypes that impair dihydropyrimidine dehydrogenase (DPD) activity and are, therefore, candidate risk variants for severe toxicity to 5-fluorouracil (5-FU) chemotherapy. Fluorouracil 214-218 dihydropyrimidine dehydrogenase Homo sapiens 84-115 33491253-1 2021 AIM: The aim of this study was to identify risk variants and haplotypes that impair dihydropyrimidine dehydrogenase (DPD) activity and are, therefore, candidate risk variants for severe toxicity to 5-fluorouracil (5-FU) chemotherapy. Fluorouracil 214-218 dihydropyrimidine dehydrogenase Homo sapiens 117-120 33491253-9 2021 CONCLUSION: Based on our data, DPYD-c.496A>G is a strong candidate risk allele for 5-FU toxicity. Fluorouracil 83-87 dihydropyrimidine dehydrogenase Homo sapiens 31-35 33467560-12 2021 Treatment with 5FU-PLNs induced a higher cytoprotective effect compared to free 5FU as indicated by lower mucosal histopathologic score and reduction in number of Ki-67 immunpositive proliferating nuclei. Fluorouracil 15-18 antigen identified by monoclonal antibody Ki 67 Mus musculus 163-168 33131720-8 2021 In the CFU-GM colony assay, the 5-FU-induced reduction of colony number was alleviated by Trpm2 deficiency. Fluorouracil 32-36 transient receptor potential cation channel, subfamily M, member 2 Mus musculus 90-95 33131720-9 2021 Moreover, the reduction of leukocytes in blood by administration with 5-FU in WT mice was also alleviated in Trpm2 KO mice. Fluorouracil 70-74 transient receptor potential cation channel, subfamily M, member 2 Mus musculus 109-114 33131720-10 2021 The activation of TRPM2 in bone marrow cells seems to be involved in 5-FU-induced myelosuppression. Fluorouracil 69-73 transient receptor potential cation channel, subfamily M, member 2 Mus musculus 18-23 33201175-3 2021 Here, we showed that T cells including CD4+ T cells and CD8+ T cells of the patients with advanced gastric cancer after platinum and fluorouracil chemotherapy exhibited enhanced ex vivo proliferation ability as compared to that before chemotherapy. Fluorouracil 133-145 CD8a molecule Homo sapiens 56-59 33423619-2 2022 The enzyme dihydropyrimidine dehydrogenase (DPD) is the first and rate limiting enzyme of 5-FU catabolism. Fluorouracil 90-94 dihydropyrimidine dehydrogenase Homo sapiens 11-42 33423619-2 2022 The enzyme dihydropyrimidine dehydrogenase (DPD) is the first and rate limiting enzyme of 5-FU catabolism. Fluorouracil 90-94 dihydropyrimidine dehydrogenase Homo sapiens 44-47 33140501-7 2021 Base excision repair (BER) and homologous recombination (HR) were found to be involved in the DNA repair of 5-FU and uracil misincorporation caused by dUTPase inhibition in genetically modified chicken DT40 cell lines and siRNA-treated HeLa cells. Fluorouracil 108-112 Deoxyuridine triphosphatase Drosophila melanogaster 151-158 33220257-7 2021 Finally, NMIIA protects CRC cells from 5-FU-induced apoptosis and proliferation inhibition through the AMPK/mTOR pathway. Fluorouracil 39-43 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 103-107 32621791-2 2021 The yCD::UPRT-MSC exosomes are internalized by tumor cells and intracellularly convert prodrug 5-fluorocytosine (5-FC) to cytotoxic drug 5-fluorouracil (5-FU). Fluorouracil 137-151 uracil phosphoribosyltransferase homolog Homo sapiens 9-13 32621791-2 2021 The yCD::UPRT-MSC exosomes are internalized by tumor cells and intracellularly convert prodrug 5-fluorocytosine (5-FC) to cytotoxic drug 5-fluorouracil (5-FU). Fluorouracil 153-157 uracil phosphoribosyltransferase homolog Homo sapiens 9-13 32990355-7 2021 Besides, CRC cell lines transfected by miR-488 mimic demonstrated decreases in glucose uptake and lactate secretion, increases in oxaliplatin/5-Fu-sensistivity, as well as diminished capability of proliferating, invading, and migratory (P < .05), which were reversible by extra transfection of pcDNA3.1-PFKFB3 (ie, miR-488 mimic + pcDNA3.1-PFKFB3 group). Fluorouracil 142-146 microRNA 488 Homo sapiens 39-46 33325631-6 2021 A significantly higher expression of sortilin was observed in vivo, in 5-FU-treated tumours engrafted in Nude mice, as compared with non-treated tumour. Fluorouracil 71-75 sortilin 1 Mus musculus 37-45 33325631-7 2021 A study of transcriptional regulation allowed identifying a decrease in ATF3 expression, as an explanation of sortilin overexpression following 5-FU treatment. Fluorouracil 144-148 sortilin 1 Mus musculus 110-118 33325631-10 2021 Collectively, our findings identify sortilin as a potential biomarker of 5-FU resistance associated with poor clinical outcomes and aggressiveness in CRC. Fluorouracil 73-77 sortilin 1 Mus musculus 36-44 33292253-0 2020 Targeting REV7 effectively reverses 5-FU and oxaliplatin resistance in colorectal cancer. Fluorouracil 36-40 MAD2 mitotic arrest deficient-like 2 Mus musculus 10-14 33292253-9 2020 RESULTS: In this study, we found that expression of REV7, which is a key component of translesion synthesis (TLS) polymerase zeta (POL zeta), is significantly increased in both 5-FU and oxaliplatin resistant CRC cells. Fluorouracil 177-181 MAD2 mitotic arrest deficient-like 2 Mus musculus 52-56 33292253-10 2020 TLS efficiency analysis revealed that upregulated REV7 protein level results in enhanced TLS in response to 5-FU and oxaliplatin. Fluorouracil 108-112 MAD2 mitotic arrest deficient-like 2 Mus musculus 50-54 33292253-11 2020 Importantly, inhibition of REV7 by CRISPR/Cas9 knockout exhibited significant synergy with 5-FU and oxaliplatin in cell culture and murine xenograft model. Fluorouracil 91-95 MAD2 mitotic arrest deficient-like 2 Mus musculus 27-31 33238487-0 2020 Association of 5-FU Therapeutic Drug Monitoring to DPD Phenotype Assessment May Reduce 5-FU Under-Exposure. Fluorouracil 15-19 dihydropyrimidine dehydrogenase Homo sapiens 51-54 33238487-0 2020 Association of 5-FU Therapeutic Drug Monitoring to DPD Phenotype Assessment May Reduce 5-FU Under-Exposure. Fluorouracil 87-91 dihydropyrimidine dehydrogenase Homo sapiens 51-54 32561283-6 2020 Further mechanistic studies indicated that the 5-Fu + SATP group showed a decrease in hepatotoxicity caused by 5-Fu via a reduction in the levels of interleukin-1beta (IL-1beta), an increase in the expression of Bcl-2 and decreases in the expression of p-p38, p-JNK and Bax. Fluorouracil 47-51 mitogen-activated protein kinase 8 Mus musculus 262-265 32561283-6 2020 Further mechanistic studies indicated that the 5-Fu + SATP group showed a decrease in hepatotoxicity caused by 5-Fu via a reduction in the levels of interleukin-1beta (IL-1beta), an increase in the expression of Bcl-2 and decreases in the expression of p-p38, p-JNK and Bax. Fluorouracil 47-51 BCL2-associated X protein Mus musculus 270-273 28520372-3 2012 The DPYD gene encodes dihydropyrimidine dehydrogenase (DPD), an enzyme that catalyzes the rate-limiting step in fluorouracil metabolism. Fluorouracil 112-124 dihydropyrimidine dehydrogenase Homo sapiens 4-8 28520372-3 2012 The DPYD gene encodes dihydropyrimidine dehydrogenase (DPD), an enzyme that catalyzes the rate-limiting step in fluorouracil metabolism. Fluorouracil 112-124 dihydropyrimidine dehydrogenase Homo sapiens 22-53 28520372-3 2012 The DPYD gene encodes dihydropyrimidine dehydrogenase (DPD), an enzyme that catalyzes the rate-limiting step in fluorouracil metabolism. Fluorouracil 112-124 dihydropyrimidine dehydrogenase Homo sapiens 55-58 32935949-7 2020 Compared with siRNA/PEI/5-FU/CNT group, ki-67 proliferation index, and matrix metallopeptidase 9 (MMP9) expression are significantly decreased in the Chim/PEI/5-FU/CNT group, while the proportion of apoptotic cells is markly increased. Fluorouracil 159-163 matrix metallopeptidase 9 Homo sapiens 71-96 32935949-7 2020 Compared with siRNA/PEI/5-FU/CNT group, ki-67 proliferation index, and matrix metallopeptidase 9 (MMP9) expression are significantly decreased in the Chim/PEI/5-FU/CNT group, while the proportion of apoptotic cells is markly increased. Fluorouracil 159-163 matrix metallopeptidase 9 Homo sapiens 98-102 33275228-13 2020 Further rescue experiments showed that HOXD13overexpression can synergistically reverse the inhibitory effect of GALNT10 knockdown on GC cell proliferative and migration ability, which further demonstrated that GALNT10 could promote GC cell metastasis ability and reduce the sensitivity to 5-Fu by regulating HOXD13. Fluorouracil 290-294 homeobox D13 Homo sapiens 39-45 33275228-13 2020 Further rescue experiments showed that HOXD13overexpression can synergistically reverse the inhibitory effect of GALNT10 knockdown on GC cell proliferative and migration ability, which further demonstrated that GALNT10 could promote GC cell metastasis ability and reduce the sensitivity to 5-Fu by regulating HOXD13. Fluorouracil 290-294 polypeptide N-acetylgalactosaminyltransferase 10 Homo sapiens 113-120 33275228-13 2020 Further rescue experiments showed that HOXD13overexpression can synergistically reverse the inhibitory effect of GALNT10 knockdown on GC cell proliferative and migration ability, which further demonstrated that GALNT10 could promote GC cell metastasis ability and reduce the sensitivity to 5-Fu by regulating HOXD13. Fluorouracil 290-294 polypeptide N-acetylgalactosaminyltransferase 10 Homo sapiens 211-218 33275228-14 2020 CONCLUSIONS: GALNT10 could regulate the proliferative and migration ability of GC cells and reduce the sensitivity to 5-Fu by enhancing the expression of HOXD13. Fluorouracil 118-122 polypeptide N-acetylgalactosaminyltransferase 10 Homo sapiens 13-20 33275228-14 2020 CONCLUSIONS: GALNT10 could regulate the proliferative and migration ability of GC cells and reduce the sensitivity to 5-Fu by enhancing the expression of HOXD13. Fluorouracil 118-122 homeobox D13 Homo sapiens 154-160 33275228-15 2020 Therefore, GALNT10 was expected to be a new therapeutic target for diagnosis of 5-fluorouracil resistance in GC. Fluorouracil 80-94 polypeptide N-acetylgalactosaminyltransferase 10 Homo sapiens 11-18 33209492-5 2020 Finally, overexpression of CBX1 mRNA was significantly related to the poor prognosis of gastric cancer patients treated with adjuvant 5-fluorouracil-based chemotherapy. Fluorouracil 134-148 chromobox 1 Homo sapiens 27-31 33042471-10 2020 CONCLUSIONS: CD44 enhances chemoresistance in response to anti-cancer drugs (fluorouracil and oxaliplatin) in colon cancer cells. Fluorouracil 77-89 CD44 molecule (Indian blood group) Homo sapiens 13-17 32782608-9 2020 RBX1 gene silencing inhibited the proliferation of human EC cells and enhanced the antitumor effect of 5-FU. Fluorouracil 103-107 ring-box 1 Homo sapiens 0-4 32729895-7 2020 Additionally, CD133+CD44+ cells presented significant chemoresistance compared with corresponding nontumorigenic CD133-CD44- cells following exposure to oxaliplatin or 5-FU. Fluorouracil 168-172 CD44 molecule (Indian blood group) Homo sapiens 20-24 32748110-0 2020 ABCB1 and ABCC2 genetic polymorphism as risk factors for neutropenia in esophageal cancer patients treated with docetaxel, cisplatin, and 5-fluorouracil chemotherapy. Fluorouracil 138-152 ATP binding cassette subfamily C member 2 Homo sapiens 10-15 32626967-6 2020 The effect of Siva-1 overexpression on anticancer drug resistance was assessed by measuring the 50% inhibitory concentration of KATO III/VCR cells to VCR, 5-fluorouracil and doxorubicin. Fluorouracil 155-169 SIVA1 apoptosis inducing factor Homo sapiens 14-20 32626967-9 2020 The results of the current study revealed that the Siva-1-overexpressed KATO III/VCR gastric cancer cells exhibited a significantly decreased sensitivity to VCR, 5-fluorouracil and doxorubicin. Fluorouracil 162-176 SIVA1 apoptosis inducing factor Homo sapiens 51-57 32801865-7 2020 Moreover, an in vivo tumor xenotransplantation of nude mice was conducted to determine the effect of miR-145 on 5-FU-resistant HCC cells. Fluorouracil 112-116 microRNA 145a Mus musculus 101-108 32764967-9 2020 MORC4 overexpression significantly elevated BCL-2 expression in MCF-7 cells and increased their resistance to adriamycin (ADM), 5-fluorouracil (5-FU), and cisplatin (DDP). Fluorouracil 128-142 MORC family CW-type zinc finger 4 Homo sapiens 0-5 32764967-9 2020 MORC4 overexpression significantly elevated BCL-2 expression in MCF-7 cells and increased their resistance to adriamycin (ADM), 5-fluorouracil (5-FU), and cisplatin (DDP). Fluorouracil 144-148 MORC family CW-type zinc finger 4 Homo sapiens 0-5 32627138-7 2020 Expressions of tested ABC transporters (ABCA5, ABCB1, ABCB6, ABCC1, ABCC2, ABCC3, ABCC5, ABCC10 and ABCF2, and ABCG2) were also deregulated in 5-FU resistant Hep-2 cells. Fluorouracil 143-147 ATP binding cassette subfamily C member 2 Homo sapiens 68-73 32347269-7 2020 With 5-Fu loading, AMD-ZIF-7(Mn)/5-Fu showed a synergistic therapeutic effect in DNA damage and CXCR4 inhibition of esophageal squamous cell cancer. Fluorouracil 33-37 C-X-C motif chemokine receptor 4 Homo sapiens 96-101 32586901-4 2021 After 5-FU treatment, CAR cKO HSCs had lower levels of Notch1 expression and elevated protein level of Numb, a Notch antagonist. Fluorouracil 6-10 NUMB endocytic adaptor protein Homo sapiens 103-107 32585842-2 2020 Preclinical and clinical studies have demonstrated a strong association between development of Pt-drug resistance and increased thymidylate synthase (hTS) expression, and the consequent cross-resistance to the hTS inhibitors 5-fluorouracil (5-FU) and raltitrexed (RTX). Fluorouracil 225-239 APC down-regulated 1 Homo sapiens 150-153 32585842-2 2020 Preclinical and clinical studies have demonstrated a strong association between development of Pt-drug resistance and increased thymidylate synthase (hTS) expression, and the consequent cross-resistance to the hTS inhibitors 5-fluorouracil (5-FU) and raltitrexed (RTX). Fluorouracil 225-239 APC down-regulated 1 Homo sapiens 210-213 32585842-2 2020 Preclinical and clinical studies have demonstrated a strong association between development of Pt-drug resistance and increased thymidylate synthase (hTS) expression, and the consequent cross-resistance to the hTS inhibitors 5-fluorouracil (5-FU) and raltitrexed (RTX). Fluorouracil 241-245 APC down-regulated 1 Homo sapiens 150-153 32585842-2 2020 Preclinical and clinical studies have demonstrated a strong association between development of Pt-drug resistance and increased thymidylate synthase (hTS) expression, and the consequent cross-resistance to the hTS inhibitors 5-fluorouracil (5-FU) and raltitrexed (RTX). Fluorouracil 241-245 APC down-regulated 1 Homo sapiens 210-213 32585842-11 2020 Overall, the results suggest that the association of standard drugs, such as cDDP and/or 5-FU and/or RTX, with the novel peptidic TS inhibitor encapsulated into PEGylated pH-sensitive liposomes can represent a promising strategy for fighting resistance to cDDP and anti-hTS drugs. Fluorouracil 89-93 APC down-regulated 1 Homo sapiens 130-132 32606803-0 2020 Circ-PRKDC Contributes to 5-Fluorouracil Resistance of Colorectal Cancer Cells by Regulating miR-375/FOXM1 Axis and Wnt/beta-Catenin Pathway. Fluorouracil 26-40 forkhead box M1 Homo sapiens 101-106 32606803-13 2020 MiR-375 suppressed 5-FU resistance by targeting FOXM1. Fluorouracil 19-23 forkhead box M1 Homo sapiens 48-53 32606803-16 2020 Conclusion: Circ-PRKDC enhanced 5-FU resistance in CRC by regulating FOXM1/miR-375 axis and wnt/beta-catenin pathway. Fluorouracil 32-36 forkhead box M1 Homo sapiens 69-74 32592951-2 2020 We recently found that whole body deletion of Gpr68 (Gpr68-/- mice) reduced the number of B lymphocytes with age and during hematopoietic regeneration, such as in response to fluorouracil (5-FU) administration. Fluorouracil 175-187 G protein-coupled receptor 68 Mus musculus 46-51 32592951-2 2020 We recently found that whole body deletion of Gpr68 (Gpr68-/- mice) reduced the number of B lymphocytes with age and during hematopoietic regeneration, such as in response to fluorouracil (5-FU) administration. Fluorouracil 175-187 G protein-coupled receptor 68 Mus musculus 53-58 32592951-2 2020 We recently found that whole body deletion of Gpr68 (Gpr68-/- mice) reduced the number of B lymphocytes with age and during hematopoietic regeneration, such as in response to fluorouracil (5-FU) administration. Fluorouracil 189-193 G protein-coupled receptor 68 Mus musculus 46-51 32592951-2 2020 We recently found that whole body deletion of Gpr68 (Gpr68-/- mice) reduced the number of B lymphocytes with age and during hematopoietic regeneration, such as in response to fluorouracil (5-FU) administration. Fluorouracil 189-193 G protein-coupled receptor 68 Mus musculus 53-58 31675755-12 2020 FTL expression upregulated in CRC via Linc00467/ miR-133b axis, and leads to CRC cell resistance against 5-FU treatment and promotes CRC metastasis. Fluorouracil 105-109 ferritin light chain Homo sapiens 0-3 32546132-1 2020 BACKGROUND: 5-Fluorouracil (5-FU) and capecitabine are fluoropyrimidine derivatives that mainly metabolized with dihydropyrimidine dehydrogenase enzyme (DPD). Fluorouracil 12-26 dihydropyrimidine dehydrogenase Homo sapiens 153-156 32546132-1 2020 BACKGROUND: 5-Fluorouracil (5-FU) and capecitabine are fluoropyrimidine derivatives that mainly metabolized with dihydropyrimidine dehydrogenase enzyme (DPD). Fluorouracil 28-32 dihydropyrimidine dehydrogenase Homo sapiens 153-156 32415349-10 2020 5-Fu decreased the levels of total protein and albumin in serum, and significantly increased the levels of IL-6 and TNF-alpha in muscle tissue. Fluorouracil 0-4 albumin Rattus norvegicus 47-54 32460371-6 2020 In a xenografted mouse model of cancer, HEP with 5-Fu significantly suppressed tumor growth, inhibited inflammatory markers such as interferon (IFN)-gamma, interleukin (IL)-1beta, IL-2, IL-6, tumor necrosis factor (TNF)-alpha, and lipopolysaccharide (LPS), and regulated the expression of Akt, CCDN1, CKD4, FOXM1, MMP7, MYC, PPAR-alpha, and PPAR-gamma. Fluorouracil 49-53 forkhead box M1 Mus musculus 307-312 32460371-6 2020 In a xenografted mouse model of cancer, HEP with 5-Fu significantly suppressed tumor growth, inhibited inflammatory markers such as interferon (IFN)-gamma, interleukin (IL)-1beta, IL-2, IL-6, tumor necrosis factor (TNF)-alpha, and lipopolysaccharide (LPS), and regulated the expression of Akt, CCDN1, CKD4, FOXM1, MMP7, MYC, PPAR-alpha, and PPAR-gamma. Fluorouracil 49-53 matrix metallopeptidase 7 Mus musculus 314-318 32142918-11 2020 Drosha wild type GCSCs with SHMT2 are sensitive to 5-fluorouracil; however, Drosha low-expressing GCSCs with SHMT1 are 5-FU-resistant. Fluorouracil 51-65 drosha ribonuclease III Homo sapiens 0-6 32478266-1 2020 The effect of the integration between MCM-48 and some biopolymers (starch, chitosan, and beta-cyclodextrin) on enhancing the pharmaceutical properties of MCM-48 as advanced carriers for the 5-fluorouracil drug was studied considering the loading capacities and the release profiles. Fluorouracil 190-204 methylmalonyl-CoA mutase Homo sapiens 38-41 31677131-8 2020 RESULTS: Among the 12 candidate genes, down-regulation of JMJD2A showed the maximum effect on GC susceptibility to anti-cancer drugs and increased the IC50 values for 5-FU, cisplatin, and docetaxel 15.3-, 2.7-, and 4.0-fold, respectively. Fluorouracil 167-171 lysine demethylase 4A Homo sapiens 58-64 32269616-5 2020 Moreover, GAS5 knockdown sensitized CSCs to the chemotherapeutic agents 5-fluorouracil and doxorubicin by inducing apoptosis detected by Annexin V-FITC/PI double staining. Fluorouracil 72-86 growth arrest specific 5 Homo sapiens 10-14 31124054-0 2020 Reduced expression of annexin A1 promotes gemcitabine and 5-fluorouracil drug resistance of human pancreatic cancer. Fluorouracil 58-72 annexin A1 Homo sapiens 22-32 32098204-9 2020 Further, combination therapy of anti-SMC2 micelles with paclitaxel (PTX) and 5-Fluorouracil (5-FU) was also explored. Fluorouracil 77-91 structural maintenance of chromosomes 2 Homo sapiens 37-41 32098204-10 2020 For this, PTX and 5-FU were respectively loaded into an anti-SMC2 decorated PM. Fluorouracil 18-22 structural maintenance of chromosomes 2 Homo sapiens 61-65 32062671-1 2020 BACKGROUND The aim of this study was to perform an accurate exploration on the efficacy of oxaliplatin/5-fluorouracil/capecitabine-cetuximab combination therapy and its effects on K-Ras mutations in advanced colorectal cancer. Fluorouracil 103-117 KRAS proto-oncogene, GTPase Homo sapiens 180-185 32127943-6 2020 We found that B7-H3 could effectively enhance the resistance to a chemotherapeutic drug (oxaliplatin or 5-fluorouracil) via CDC25A. Fluorouracil 104-118 cell division cycle 25A Homo sapiens 124-130 31843717-8 2020 The 5Fu in CS-GCNCs retained high cancer cell killing bioactivity by enhancing the caspase-3 expression level. Fluorouracil 4-7 caspase 3 Mus musculus 83-92 31778273-1 2020 The high expression of human equilibrative nucleoside transporter-1 (hENT1) and the low expression of dihydropyrimidine dehydrogenase (DPD) are reported to predict a favorable prognosis in patients treated with gemcitabine (GEM) and 5-fluorouracil (5FU) as the adjuvant setting, respectively. Fluorouracil 233-247 dihydropyrimidine dehydrogenase Homo sapiens 102-133 31778273-1 2020 The high expression of human equilibrative nucleoside transporter-1 (hENT1) and the low expression of dihydropyrimidine dehydrogenase (DPD) are reported to predict a favorable prognosis in patients treated with gemcitabine (GEM) and 5-fluorouracil (5FU) as the adjuvant setting, respectively. Fluorouracil 233-247 dihydropyrimidine dehydrogenase Homo sapiens 135-138 31778273-1 2020 The high expression of human equilibrative nucleoside transporter-1 (hENT1) and the low expression of dihydropyrimidine dehydrogenase (DPD) are reported to predict a favorable prognosis in patients treated with gemcitabine (GEM) and 5-fluorouracil (5FU) as the adjuvant setting, respectively. Fluorouracil 249-252 dihydropyrimidine dehydrogenase Homo sapiens 102-133 31778273-1 2020 The high expression of human equilibrative nucleoside transporter-1 (hENT1) and the low expression of dihydropyrimidine dehydrogenase (DPD) are reported to predict a favorable prognosis in patients treated with gemcitabine (GEM) and 5-fluorouracil (5FU) as the adjuvant setting, respectively. Fluorouracil 249-252 dihydropyrimidine dehydrogenase Homo sapiens 135-138 31811910-8 2020 Taken together, our results suggest that FoxO3 could reverse 5-FU resistance in CRC via inhibiting the Nrf2/TR1 signaling pathway, and increasing the level of intracellular reactive oxygen species. Fluorouracil 61-65 thioredoxin reductase 1 Homo sapiens 108-111 31811910-9 2020 Chemotherapeutic agents targeting FoxO3 and/or TR1, including AUR, might be promising adjuvant sensitizers to reverse chemoresistance in 5-FU-resistant CRC. Fluorouracil 137-141 thioredoxin reductase 1 Homo sapiens 47-50 31760170-0 2020 LncRNA HAND2-AS1 inhibits 5-fluorouracil resistance by modulating miR-20a/PDCD4 axis in colorectal cancer. Fluorouracil 26-40 heart and neural crest derivatives expressed 2 Homo sapiens 7-12 31711924-8 2020 MIA PaCa-2 cells that overexpressed ZIP4 had increased resistance to gemcitabine, 5-fluorouracil, and cisplatin, whereas AsPC-1 cells with ZIP4 knockdown had increased sensitivity to these drugs. Fluorouracil 82-96 solute carrier family 39 member 4 Homo sapiens 36-40 31870774-9 2020 What"s more, BCLAF1 promoted 5-Fu resistance and the expression of P-gp and MRP1 in hepatocellular carcinoma cells by targeting NEAT1. Fluorouracil 29-33 BCL2 associated transcription factor 1 Homo sapiens 13-19 31898732-7 2020 Additionally, SRPK2 had no association with mutant p53 (mtp53) in SW480 and SW620 cells, but negatively regulated Numb and wild-type p53 (wtp53) in response to 5-fluorouracil or cisplatin treatment in HCT116 cells. Fluorouracil 160-174 NUMB endocytic adaptor protein Homo sapiens 114-118 31898732-8 2020 Moreover, SRPK2, Numb and p53 coimmunoprecipitated into a triple complex without or with the treatment of 5-fluorouracil in HCT116 cells, and p53 knockdown reversed the upregulation of wtp53 induced by SRPK2 silencing with chemical agent treatment. Fluorouracil 106-120 NUMB endocytic adaptor protein Homo sapiens 17-21 32426701-1 2020 Objective: To investigate the expressions of MAPK10, c-Jun and Itga6 in laryngeal carcinoma and its influence on the sensitivity to docetaxel, cisplatin and 5-fluorouracil (TPF) chemotherapy. Fluorouracil 157-171 integrin subunit alpha 6 Homo sapiens 63-68 33463228-6 2020 The Sr/Fe co-substituted samples demonstrated extended drug (5-fluorouracil and amoxicillin) release profiles at the pH of physiological medium. Fluorouracil 61-75 general transcription factor IIE subunit 1 Homo sapiens 7-9 31371781-9 2020 In a tail vein injection pulmonary metastasis mouse model, intraperitoneal administration of garcinol (20 mg/kg) or 5-FU (20 mg/kg) significantly decreased the number of lung tumor nodules and the expression levels of Ki-67, p300, and p-Smad2/3 in lung tissues. Fluorouracil 116-120 antigen identified by monoclonal antibody Ki 67 Mus musculus 218-223 31371781-9 2020 In a tail vein injection pulmonary metastasis mouse model, intraperitoneal administration of garcinol (20 mg/kg) or 5-FU (20 mg/kg) significantly decreased the number of lung tumor nodules and the expression levels of Ki-67, p300, and p-Smad2/3 in lung tissues. Fluorouracil 116-120 E1A binding protein p300 Mus musculus 225-229 33097678-2 2020 DNA repair mechanisms, such as O6-alkylguanine DNA alkyltransferase (MGMT) and mismatch repair (MMR) systems, have also been correlated to 5-FU resistance in CRC. Fluorouracil 139-143 O-6-methylguanine-DNA methyltransferase Homo sapiens 69-73 31897166-6 2020 The combination of oxymatrine and 5-FU reduced the protein expression of snail family transcriptional repressor 2 and vimentin, phosphorylated p65 and induced the expression of E-cadherin, by inhibiting the nuclear factor kappaB (NF-kappaB) signaling pathway. Fluorouracil 34-38 snail family transcriptional repressor 2 Homo sapiens 73-113 31742586-1 2019 The cytotoxic effect of 5-fluorouracil (5-FU) on yeast cells is thought to be mainly via a misincorporation of fluoropyrimidines into both RNA and DNA, not only DNA damage via inhibition of thymidylate synthase (TYMS) by fluorodeoxyuridine monophosphate (FdUMP). Fluorouracil 24-38 thymidylate synthase Saccharomyces cerevisiae S288C 190-210 31742586-1 2019 The cytotoxic effect of 5-fluorouracil (5-FU) on yeast cells is thought to be mainly via a misincorporation of fluoropyrimidines into both RNA and DNA, not only DNA damage via inhibition of thymidylate synthase (TYMS) by fluorodeoxyuridine monophosphate (FdUMP). Fluorouracil 24-38 thymidylate synthase Saccharomyces cerevisiae S288C 212-216 31742586-1 2019 The cytotoxic effect of 5-fluorouracil (5-FU) on yeast cells is thought to be mainly via a misincorporation of fluoropyrimidines into both RNA and DNA, not only DNA damage via inhibition of thymidylate synthase (TYMS) by fluorodeoxyuridine monophosphate (FdUMP). Fluorouracil 40-44 thymidylate synthase Saccharomyces cerevisiae S288C 190-210 31742586-1 2019 The cytotoxic effect of 5-fluorouracil (5-FU) on yeast cells is thought to be mainly via a misincorporation of fluoropyrimidines into both RNA and DNA, not only DNA damage via inhibition of thymidylate synthase (TYMS) by fluorodeoxyuridine monophosphate (FdUMP). Fluorouracil 40-44 thymidylate synthase Saccharomyces cerevisiae S288C 212-216 31482228-6 2019 Dihydropyrimidine dehydrogenase (DPD) is an enzyme majorly involved in the metabolism of pyrimidines in the human body and has the same metabolising effect on 5-FU, a pyrimidine analogue. Fluorouracil 159-163 dihydropyrimidine dehydrogenase Homo sapiens 0-31 31482228-6 2019 Dihydropyrimidine dehydrogenase (DPD) is an enzyme majorly involved in the metabolism of pyrimidines in the human body and has the same metabolising effect on 5-FU, a pyrimidine analogue. Fluorouracil 159-163 dihydropyrimidine dehydrogenase Homo sapiens 33-36 31482228-7 2019 Multiple mutations in the DPD gene have been linked to 5-FU toxicity and inadequate dosages. Fluorouracil 55-59 dihydropyrimidine dehydrogenase Homo sapiens 26-29 31482228-8 2019 DPD inhibitors have also been used to inhibit excessive degradation of 5-FU for meeting appropriate dosage requirements. Fluorouracil 71-75 dihydropyrimidine dehydrogenase Homo sapiens 0-3 31482228-9 2019 This article focusses on the role of dihydropyrimidine dehydrogenase in the metabolism of the anticancer drug 5-FU and other associated drugs. Fluorouracil 110-114 dihydropyrimidine dehydrogenase Homo sapiens 37-68 31641844-1 2019 PURPOSE: The presence of deleterious variants of dihydropyrimidine-dehydrogenase gene (DPYD) is associated with 5-Fluorouracil toxicity. Fluorouracil 112-126 dihydropyrimidine dehydrogenase Homo sapiens 87-91 31638260-10 2019 Furthermore, the silencing of Tex10 enhanced the sensitivity of the ESCC cells to 5-fluorouracil. Fluorouracil 82-96 testis expressed 10 Homo sapiens 30-35 31704100-0 2019 CO ameliorates endothelial senescence induced by 5-fluorouracil through SIRT1 activation. Fluorouracil 49-63 sirtuin 1 Homo sapiens 72-77 31704100-8 2019 The SIRT1 inhibitor EX527 reversed the inhibitory effect of CO on the 5FU-induced endothelial senescence. Fluorouracil 70-73 sirtuin 1 Homo sapiens 4-9 31704100-9 2019 Furthermore, SIRT1 deficiency abolished the stress granule formation by CO. Our results suggest that CO alleviates the endothelial senescence induced by 5FU through SIRT1 activation and may hence have therapeutic potential for the treatment of vascular diseases. Fluorouracil 153-156 sirtuin 1 Homo sapiens 13-18 31704100-9 2019 Furthermore, SIRT1 deficiency abolished the stress granule formation by CO. Our results suggest that CO alleviates the endothelial senescence induced by 5FU through SIRT1 activation and may hence have therapeutic potential for the treatment of vascular diseases. Fluorouracil 153-156 sirtuin 1 Homo sapiens 165-170 31474334-6 2019 Moreover, in vitro experiments showed that RAB13 deletion enhanced the sensitization of AGS and NCI-N87 cells toward cisplatin (CDDP) and 5-fluorouracil (5-FU) treatment respectively. Fluorouracil 138-152 RAB13, member RAS oncogene family Homo sapiens 43-48 31474334-6 2019 Moreover, in vitro experiments showed that RAB13 deletion enhanced the sensitization of AGS and NCI-N87 cells toward cisplatin (CDDP) and 5-fluorouracil (5-FU) treatment respectively. Fluorouracil 154-158 RAB13, member RAS oncogene family Homo sapiens 43-48 31474334-7 2019 Together, these data demonstrate that RAB13 promotes the proliferation and confers CDDP and 5-FU resistance to GC cells, which provides experimental support to target this protein in future clinical practice. Fluorouracil 92-96 RAB13, member RAS oncogene family Homo sapiens 38-43 31356847-9 2019 Drug sensitivity experiments showed TMC5 knockdown significantly enhanced cells sensitivity to 5-Fluorouracil. Fluorouracil 95-109 transmembrane channel like 5 Homo sapiens 36-40 31579069-0 2019 miR-361 enhances sensitivity to 5-fluorouracil by targeting the FOXM1-ABCC5/10 signaling pathway in colorectal cancer. Fluorouracil 32-46 forkhead box M1 Homo sapiens 64-69 30734664-17 2019 Using this reporter system, we demonstrated pharmacological actions of anticancer medications such as antimetabolite 5-fluorouracil (5-FU) and antimalaria medication artesunate (ART), which inhibited both tumorigenesis and beta-catenin/MMP regulatory signaling. Fluorouracil 117-131 catenin (cadherin associated protein), beta 1 Mus musculus 223-235 30734664-17 2019 Using this reporter system, we demonstrated pharmacological actions of anticancer medications such as antimetabolite 5-fluorouracil (5-FU) and antimalaria medication artesunate (ART), which inhibited both tumorigenesis and beta-catenin/MMP regulatory signaling. Fluorouracil 133-137 catenin (cadherin associated protein), beta 1 Mus musculus 223-235 31491980-8 2019 QC increases the susceptibility of CRC cells to 5-FU under hypoxic conditions by enhancing JNK1-dependent Nrf2 degradation. Fluorouracil 48-52 mitogen-activated protein kinase 8 Mus musculus 91-95 31471337-14 2019 However, with 5-FU treatment, the relative expression level of BECN1 in HT29-KD cells was much lower than that in HT29-NC cells. Fluorouracil 14-18 beclin 1 Homo sapiens 63-68 31152734-6 2019 Furthermore, HCRP1 increased the sensitivity of ESCC cells towards cisplatin/fluorouracil. Fluorouracil 77-89 VPS37A subunit of ESCRT-I Homo sapiens 13-18 31341363-9 2019 Also, RA decreased protein expression of Wee1, while the combinational effect of RA and 5-Fu decreased protein expressions of cyclooxygenase-2, B cell lymphoma 2, and Wee1 but increased protein levels of Bax, cyclin D1, and cyclin E. CONCLUSION: Taken together, the results suggest that RA acts as an anti-cancer agent and enhancer of 5-Fu in bile duct cancer cells via regulating multiple cell cycle and apoptosis-related proteins. Fluorouracil 88-92 WEE1 G2 checkpoint kinase Homo sapiens 167-171 31217433-9 2019 The repression of 5-FU-induced caspase-1 activity by DHA supplementation is partially due to beta-arrestin-2-dependent inhibition of NLRP3 inflammasome activity but was independent of JNK pathway. Fluorouracil 18-22 mitogen-activated protein kinase 8 Mus musculus 184-187 31217433-10 2019 Interestingly, we showed that DHA, through beta-arrestin-2-mediated inhibition of JNK pathway, reduces V5-tagged mature IL-1beta release induced by 5-FU, in MDSC stably overexpressing a V5-tagged mature IL-1beta form. Fluorouracil 148-152 mitogen-activated protein kinase 8 Mus musculus 82-85 31033216-5 2019 Inhibition of RAD18 expression in rectal cancer cells pronouncedly attenuated the proliferation and promoted apoptosis after exposing to irradiation or/and 5-fluorouracil (5-Fu). Fluorouracil 156-170 RAD18 E3 ubiquitin protein ligase Homo sapiens 14-19 31033216-5 2019 Inhibition of RAD18 expression in rectal cancer cells pronouncedly attenuated the proliferation and promoted apoptosis after exposing to irradiation or/and 5-fluorouracil (5-Fu). Fluorouracil 172-176 RAD18 E3 ubiquitin protein ligase Homo sapiens 14-19 30923017-6 2019 Additionally, we indicated that the VDR also participates in 5-FU mechanism of action. Fluorouracil 61-65 vitamin D receptor Homo sapiens 36-39 30923017-7 2019 5-FU significantly increased TYMS (gene encoding thymidylate synthase (TS)) and BIRC5 (gene encoding survivin) level in HT-29 cells with silenced VDR. Fluorouracil 0-4 baculoviral IAP repeat containing 5 Homo sapiens 80-85 30923017-7 2019 5-FU significantly increased TYMS (gene encoding thymidylate synthase (TS)) and BIRC5 (gene encoding survivin) level in HT-29 cells with silenced VDR. Fluorouracil 0-4 vitamin D receptor Homo sapiens 146-149 30923017-11 2019 In conclusion, we suggest that both VDR and CaSR might be useful as molecular markers for predicting treatment outcomes and identifying the CRC patient subgroups who might benefit from 5-FU-based chemotherapy combined with vitamin D analog. Fluorouracil 185-189 vitamin D receptor Homo sapiens 36-39 30706227-10 2019 ASCL2 knockdown also played a critical role in sensitivity to treatment by 5-fluorouracil and radiotherapy in addition to PB. Fluorouracil 75-89 achaete-scute family bHLH transcription factor 2 Homo sapiens 0-5 30884120-1 2019 This study aims to explore the mechanism of Circular RNA CDR1as implicating in regulating 5-fluorouracil (5-FU) chemosensitivity in breast cancer (BC) by competitively inhibiting miR-7 to regulate CCNE1. Fluorouracil 90-104 cyclin E1 Mus musculus 197-202 30884120-1 2019 This study aims to explore the mechanism of Circular RNA CDR1as implicating in regulating 5-fluorouracil (5-FU) chemosensitivity in breast cancer (BC) by competitively inhibiting miR-7 to regulate CCNE1. Fluorouracil 106-110 cyclin E1 Mus musculus 197-202 30884120-13 2019 CDR1as may regulate chemosensitivity of 5-FU-resistant BC cells by inhibiting miR-7 to regulate CCNE1. Fluorouracil 40-44 cyclin E1 Mus musculus 96-101 30651398-1 2019 LESSONS LEARNED: The upregulation of dihydropyrimidine dehydrogenase (DPD) and thymidylate synthase (TS) are important mechanisms of resistance to 5-fluorouracil (5-FU) in metastatic colorectal cancer (mCRC) after long exposure to 5-FU.S-1 (containing a DPD inhibitor) combined with raltitrexed (a TS inhibitor) showed a moderate effect, which needs further study as a third- or later-line therapy in mCRC. Fluorouracil 147-161 dihydropyrimidine dehydrogenase Homo sapiens 70-73 30651398-1 2019 LESSONS LEARNED: The upregulation of dihydropyrimidine dehydrogenase (DPD) and thymidylate synthase (TS) are important mechanisms of resistance to 5-fluorouracil (5-FU) in metastatic colorectal cancer (mCRC) after long exposure to 5-FU.S-1 (containing a DPD inhibitor) combined with raltitrexed (a TS inhibitor) showed a moderate effect, which needs further study as a third- or later-line therapy in mCRC. Fluorouracil 147-161 dihydropyrimidine dehydrogenase Homo sapiens 254-257 30651398-1 2019 LESSONS LEARNED: The upregulation of dihydropyrimidine dehydrogenase (DPD) and thymidylate synthase (TS) are important mechanisms of resistance to 5-fluorouracil (5-FU) in metastatic colorectal cancer (mCRC) after long exposure to 5-FU.S-1 (containing a DPD inhibitor) combined with raltitrexed (a TS inhibitor) showed a moderate effect, which needs further study as a third- or later-line therapy in mCRC. Fluorouracil 163-167 dihydropyrimidine dehydrogenase Homo sapiens 70-73 30651398-1 2019 LESSONS LEARNED: The upregulation of dihydropyrimidine dehydrogenase (DPD) and thymidylate synthase (TS) are important mechanisms of resistance to 5-fluorouracil (5-FU) in metastatic colorectal cancer (mCRC) after long exposure to 5-FU.S-1 (containing a DPD inhibitor) combined with raltitrexed (a TS inhibitor) showed a moderate effect, which needs further study as a third- or later-line therapy in mCRC. Fluorouracil 163-167 dihydropyrimidine dehydrogenase Homo sapiens 254-257 30651398-1 2019 LESSONS LEARNED: The upregulation of dihydropyrimidine dehydrogenase (DPD) and thymidylate synthase (TS) are important mechanisms of resistance to 5-fluorouracil (5-FU) in metastatic colorectal cancer (mCRC) after long exposure to 5-FU.S-1 (containing a DPD inhibitor) combined with raltitrexed (a TS inhibitor) showed a moderate effect, which needs further study as a third- or later-line therapy in mCRC. Fluorouracil 231-235 dihydropyrimidine dehydrogenase Homo sapiens 70-73 30651398-1 2019 LESSONS LEARNED: The upregulation of dihydropyrimidine dehydrogenase (DPD) and thymidylate synthase (TS) are important mechanisms of resistance to 5-fluorouracil (5-FU) in metastatic colorectal cancer (mCRC) after long exposure to 5-FU.S-1 (containing a DPD inhibitor) combined with raltitrexed (a TS inhibitor) showed a moderate effect, which needs further study as a third- or later-line therapy in mCRC. Fluorouracil 231-235 dihydropyrimidine dehydrogenase Homo sapiens 254-257 30651398-4 2019 The upregulation of dihydropyrimidine dehydrogenase (DPD) and/or thymidylate synthase (TS) are important mechanisms of resistance of 5-FU. Fluorouracil 133-137 dihydropyrimidine dehydrogenase Homo sapiens 53-56 31052357-4 2019 A single enzyme, dihydropyrimidine dehydrogenase (DPD), mediates 80% of 5-fluorouracil elimination, through hepatic metabolism. Fluorouracil 72-86 dihydropyrimidine dehydrogenase Homo sapiens 17-48 31052357-4 2019 A single enzyme, dihydropyrimidine dehydrogenase (DPD), mediates 80% of 5-fluorouracil elimination, through hepatic metabolism. Fluorouracil 72-86 dihydropyrimidine dehydrogenase Homo sapiens 50-53 30944308-0 2019 VPS33B interacts with NESG1 to modulate EGFR/PI3K/AKT/c-Myc/P53/miR-133a-3p signaling and induce 5-fluorouracil sensitivity in nasopharyngeal carcinoma. Fluorouracil 97-111 cilia and flagella associated protein 45 Homo sapiens 22-27 30213181-8 2019 5-Fluorouracil treatment also accelerated the expression of the pro-apoptotic protein BAX and decelerated the expression of the anti-apoptotic protein Bcl-xL on melanoma cell line. Fluorouracil 0-14 BCL2-associated X protein Mus musculus 86-89 30894562-8 2019 Differential expression of DPYD, an enzyme involved in 5-fluorouracil (5-FU) catabolism, was associated with variable LCL growth inhibition mediated by 5-FU. Fluorouracil 55-69 dihydropyrimidine dehydrogenase Homo sapiens 27-31 30894562-8 2019 Differential expression of DPYD, an enzyme involved in 5-fluorouracil (5-FU) catabolism, was associated with variable LCL growth inhibition mediated by 5-FU. Fluorouracil 71-75 dihydropyrimidine dehydrogenase Homo sapiens 27-31 30894562-8 2019 Differential expression of DPYD, an enzyme involved in 5-fluorouracil (5-FU) catabolism, was associated with variable LCL growth inhibition mediated by 5-FU. Fluorouracil 152-156 dihydropyrimidine dehydrogenase Homo sapiens 27-31 30832616-2 2019 Recently, by the screening of the environmental metagenomic libraries we identified a novel isocytosine deaminase (ICD), termed Vcz, which is able of specifically converting a prodrug 5-fluoroisocytosine (5-FIC) into toxic drug 5-fluorouracil (5-FU). Fluorouracil 228-242 C-C motif chemokine ligand 7 Homo sapiens 207-210 30832616-2 2019 Recently, by the screening of the environmental metagenomic libraries we identified a novel isocytosine deaminase (ICD), termed Vcz, which is able of specifically converting a prodrug 5-fluoroisocytosine (5-FIC) into toxic drug 5-fluorouracil (5-FU). Fluorouracil 244-248 C-C motif chemokine ligand 7 Homo sapiens 207-210 30369513-0 2019 Design, Synthesis, and Biological Evaluation of a Conjugate of 5-Fluorouracil and an LSD1 Inhibitor. Fluorouracil 63-77 lysine demethylase 1A Homo sapiens 85-89 30369513-4 2019 In vitro assays showed that the PCPA-5-FU conjugate (1) released 5-FU upon the inhibition of LSD1. Fluorouracil 37-41 lysine demethylase 1A Homo sapiens 93-97 30369513-4 2019 In vitro assays showed that the PCPA-5-FU conjugate (1) released 5-FU upon the inhibition of LSD1. Fluorouracil 65-69 lysine demethylase 1A Homo sapiens 93-97 30369513-6 2019 Thus, the PCPA-5-FU conjugate (1) was able to function as a prodrug of 5-FU, activated by LSD1 inhibition, and provided a useful new lead structure for further development. Fluorouracil 15-19 lysine demethylase 1A Homo sapiens 90-94 30369513-6 2019 Thus, the PCPA-5-FU conjugate (1) was able to function as a prodrug of 5-FU, activated by LSD1 inhibition, and provided a useful new lead structure for further development. Fluorouracil 71-75 lysine demethylase 1A Homo sapiens 90-94 30824833-6 2019 Most importantly, in vivo use of PERK inhibitor synergizes with 5-FU in suppressing the growth of colon cancer cells in mouse models. Fluorouracil 64-68 eukaryotic translation initiation factor 2 alpha kinase 3 Mus musculus 33-37 30703870-0 2019 The MicroRNA-551a/MEF2C Axis Regulates the Survival and Sphere Formation of Cancer Cells in Response to 5-Fluorouracil. Fluorouracil 104-118 microRNA 551a Homo sapiens 4-17 30703870-3 2019 Here, we demonstrate miR-551a as a novel factor regulating cell survival after 5-FU treatment. Fluorouracil 79-83 microRNA 551a Homo sapiens 21-29 30703870-4 2019 miR-551a-expressing cells (Hep3B-lenti-miR-551a) were resistant to 5-FU-induced cell death, and after 5-FU treatment, and showed significant increases in cell viability, cell survival, and sphere formation. Fluorouracil 67-71 microRNA 551a Homo sapiens 0-8 30703870-4 2019 miR-551a-expressing cells (Hep3B-lenti-miR-551a) were resistant to 5-FU-induced cell death, and after 5-FU treatment, and showed significant increases in cell viability, cell survival, and sphere formation. Fluorouracil 67-71 microRNA 551a Homo sapiens 39-47 30703870-4 2019 miR-551a-expressing cells (Hep3B-lenti-miR-551a) were resistant to 5-FU-induced cell death, and after 5-FU treatment, and showed significant increases in cell viability, cell survival, and sphere formation. Fluorouracil 102-106 microRNA 551a Homo sapiens 0-8 30703870-4 2019 miR-551a-expressing cells (Hep3B-lenti-miR-551a) were resistant to 5-FU-induced cell death, and after 5-FU treatment, and showed significant increases in cell viability, cell survival, and sphere formation. Fluorouracil 102-106 microRNA 551a Homo sapiens 39-47 30703870-6 2019 Our results suggest that miR-551a plays a novel function in regulating 5-FU-induced cell death, and targeting miR-551a might be helpful to sensitize cells to anti-cancer drugs. Fluorouracil 71-75 microRNA 551a Homo sapiens 25-33 30703870-6 2019 Our results suggest that miR-551a plays a novel function in regulating 5-FU-induced cell death, and targeting miR-551a might be helpful to sensitize cells to anti-cancer drugs. Fluorouracil 71-75 microRNA 551a Homo sapiens 110-118 30770552-4 2019 It was found that LEP-2a notably enhanced 5-FU sensitivity in HepG2 cells in a synergistic manner. Fluorouracil 42-46 late cornified envelope 1B Homo sapiens 18-23 30770552-9 2019 These findings demonstrate that LEP-2a enhanced 5-FU sensitivity and combination of 5-FU and LEP-2a exerts synergistic antitumor efficiency through multiple approaches. Fluorouracil 48-52 late cornified envelope 1B Homo sapiens 32-37 30226808-0 2019 Long noncoding RNA LINC00261 induces chemosensitization to 5-fluorouracil by mediating methylation-dependent repression of DPYD in human esophageal cancer. Fluorouracil 59-73 dihydropyrimidine dehydrogenase Homo sapiens 123-127 30226808-1 2019 Approximately 85% of a single administered dose of 5-fluorouracil (5-FU) will be degraded by dihydropyrimidine dehydrogenase (DYPD). Fluorouracil 51-65 dihydropyrimidine dehydrogenase Homo sapiens 93-124 30226808-1 2019 Approximately 85% of a single administered dose of 5-fluorouracil (5-FU) will be degraded by dihydropyrimidine dehydrogenase (DYPD). Fluorouracil 67-71 dihydropyrimidine dehydrogenase Homo sapiens 93-124 30226808-3 2019 Hence, the aim of the present study was to evaluate the prevailing hypothesis which suggests that overexpression of LINC00261 possesses the ability to modulate the methylation-dependent repression of DPYD, ultimately resulting in an elevation of the sensitivity of human esophageal cancer cells to 5-FU. Fluorouracil 298-302 dihydropyrimidine dehydrogenase Homo sapiens 200-204 30487159-8 2019 It was also revealed that high expression of SIKE had favorable OS when treated with other adjuvant therapies, while worse OS when treated only with 5FU therapy. Fluorouracil 149-152 suppressor of IKBKE 1 Homo sapiens 45-49 31582661-7 2019 In contrast, 5-fluorouracil significantly inhibited proglucagon, GLP-2 receptor, IGF-1, and TGF-beta2 mRNA expression as well as the number of anti-GLP-2 antibody-positive cells. Fluorouracil 13-27 glucagon-like peptide 2 receptor Rattus norvegicus 65-79 30307354-2 2019 CASE PRESENTATION: Here we present a KRAS/NRAS/BRAF wild-type mCRC patient who has been previously treated with FOLFIRI (fluorouracil, leucovorin, and irinotecan), XELOX (capecitabine and oxaliplatin), cetuximab and bevacizumab, and then received the next generation sequencing (NGS) and whose metastatic subcutaneous nodule was resected to generate patient-derived xenograft (PDX) models. Fluorouracil 121-133 KRAS proto-oncogene, GTPase Homo sapiens 37-41 30307354-2 2019 CASE PRESENTATION: Here we present a KRAS/NRAS/BRAF wild-type mCRC patient who has been previously treated with FOLFIRI (fluorouracil, leucovorin, and irinotecan), XELOX (capecitabine and oxaliplatin), cetuximab and bevacizumab, and then received the next generation sequencing (NGS) and whose metastatic subcutaneous nodule was resected to generate patient-derived xenograft (PDX) models. Fluorouracil 121-133 NRAS proto-oncogene, GTPase Homo sapiens 42-46 30320939-0 2019 Nuclear factor I/B promotes colorectal cancer cell proliferation, epithelial-mesenchymal transition and 5-fluorouracil resistance. Fluorouracil 104-118 nuclear factor I B Homo sapiens 0-18 30320939-6 2019 In addition, NFIB weakened the sensitivity of CRC cells to 5-fluorouracil (5-FU). Fluorouracil 59-73 nuclear factor I B Homo sapiens 13-17 30320939-6 2019 In addition, NFIB weakened the sensitivity of CRC cells to 5-fluorouracil (5-FU). Fluorouracil 75-79 nuclear factor I B Homo sapiens 13-17 30320939-9 2019 Our results showed that NFIB promoted cell proliferation and increased 5-FU resistance by activating the Akt pathway. Fluorouracil 71-75 nuclear factor I B Homo sapiens 24-28 30320939-10 2019 In summary, our findings suggested that NFIB induced EMT of CRC cells via upregulating snail expression and promoted cell proliferation and 5-FU resistance by activating the Akt pathway. Fluorouracil 140-144 nuclear factor I B Homo sapiens 40-44 31372308-8 2019 DCLK1+ and WT cells were treated with 5-Fluorouracil (5-Fu) at different doses for 24 or 48 hours. Fluorouracil 38-52 doublecortin like kinase 1 Homo sapiens 0-5 31372308-12 2019 Results: Our results demonstrated that IC50 of 5-Fu for the DCLK1+ cells was significantly higher than that of the WT cells for both 24 and 48-hour treatment (p=0.002 and 0.048 respectively), indicating increased chemoresistance of the DCLK1+ cells. Fluorouracil 47-51 doublecortin like kinase 1 Homo sapiens 60-65 31372308-12 2019 Results: Our results demonstrated that IC50 of 5-Fu for the DCLK1+ cells was significantly higher than that of the WT cells for both 24 and 48-hour treatment (p=0.002 and 0.048 respectively), indicating increased chemoresistance of the DCLK1+ cells. Fluorouracil 47-51 doublecortin like kinase 1 Homo sapiens 236-241 31372308-13 2019 Gene expression of casp-3, casp-4, and casp-10 were significantly inhibited in the DCLK1+ cells after 5-Fu treatment compared to the WT cells (p=7.616e-08, 1.575e-05 and 5.307e-08, respectively). Fluorouracil 102-106 doublecortin like kinase 1 Homo sapiens 83-88 31372308-14 2019 Cleaved casp-3 amount and casp-3 positive cells were significantly decreased in the DCLK1+ cells after 5-Fu treatment compared to the WT cells (p=0.015). Fluorouracil 103-107 doublecortin like kinase 1 Homo sapiens 84-89 31372308-15 2019 Conclusions: In conclusion, our results demonstrated that DCLK1 overexpression enhanced the chemoresistance of CRC cells to 5-Fu treatment by suppressing gene expression of key caspases in the apoptosis pathway and activation of the apoptosis pathway. Fluorouracil 124-128 doublecortin like kinase 1 Homo sapiens 58-63 30485509-4 2018 In our study, we found that DEC2 can obviously increase the sensibility of GC cells to 5-Fu by promoting 5-Fu-induced apoptosis. Fluorouracil 87-91 basic helix-loop-helix family member e41 Homo sapiens 28-32 30485509-4 2018 In our study, we found that DEC2 can obviously increase the sensibility of GC cells to 5-Fu by promoting 5-Fu-induced apoptosis. Fluorouracil 105-109 basic helix-loop-helix family member e41 Homo sapiens 28-32 30485509-8 2018 Furthermore, enhanced chemosensitivity mediated by DEC2 can be reversed by STAT5A which confer GC cells resistance to apoptosis induced by 5-Fu. Fluorouracil 139-143 basic helix-loop-helix family member e41 Homo sapiens 51-55 30485509-9 2018 Together, our results suggest that through inhibiting activation of STAT5A, DEC2 enhances 5-Fu-induced apoptosis and suppression of proliferation in GC cells. Fluorouracil 90-94 basic helix-loop-helix family member e41 Homo sapiens 76-80 30451820-0 2018 Long non-coding RNA H19 confers 5-Fu resistance in colorectal cancer by promoting SIRT1-mediated autophagy. Fluorouracil 32-36 sirtuin 1 Homo sapiens 82-87 30333885-0 2018 Histone deacetylase inhibitors sensitize 5-fluorouracil-resistant MDA-MB-468 breast cancer cells to 5-fluorouracil. Fluorouracil 41-55 histone deacetylase 9 Homo sapiens 0-19 30333885-0 2018 Histone deacetylase inhibitors sensitize 5-fluorouracil-resistant MDA-MB-468 breast cancer cells to 5-fluorouracil. Fluorouracil 100-114 histone deacetylase 9 Homo sapiens 0-19 30333885-3 2018 In the present study, a 5-FU-resistant breast cancer cell line was established, and the effects of HDAC inhibitors in these cells were examined. Fluorouracil 24-28 histone deacetylase 9 Homo sapiens 99-103 30333885-8 2018 The HDAC inhibitors, valproic acid and suberanilohydroxamic acid sensitized the two cell lines to 5-FU in a concentration-dependent manner. Fluorouracil 98-102 histone deacetylase 9 Homo sapiens 4-8 30333885-9 2018 In conclusion, the results of the present study revealed that HDAC inhibitors increase the sensitivity to 5-FU in 5-FU-sensitive and -resistant cells. Fluorouracil 106-110 histone deacetylase 9 Homo sapiens 62-66 30333885-9 2018 In conclusion, the results of the present study revealed that HDAC inhibitors increase the sensitivity to 5-FU in 5-FU-sensitive and -resistant cells. Fluorouracil 114-118 histone deacetylase 9 Homo sapiens 62-66 30356105-9 2018 SNPs in MTHFR affect metabolism of statins, 5-fluorouracil and methotrexate-based cancer drugs. Fluorouracil 44-58 methylenetetrahydrofolate reductase Homo sapiens 8-13 30069943-0 2018 A novel inhibitor of ADAM17 sensitizes colorectal cancer cells to 5-Fluorouracil by reversing Notch and epithelial-mesenchymal transition in vitro and in vivo. Fluorouracil 66-80 ADAM metallopeptidase domain 17 Homo sapiens 21-27 30069943-13 2018 CONCLUSIONS: A novel ADAM17 inhibitor ZLDI-8 may be a potential chemosensitizer which sensitized CRC cells to 5-fluorouracil or irinotecan by reversing Notch and EMT pathways. Fluorouracil 110-124 ADAM metallopeptidase domain 17 Homo sapiens 21-27 30151975-0 2018 Bevacizumab-enhanced antitumor effect of 5-fluorouracil via upregulation of thymidine phosphorylase through vascular endothelial growth factor A/vascular endothelial growth factor receptor 2-specificity protein 1 pathway. Fluorouracil 41-55 kinase insert domain receptor Homo sapiens 145-190 29327356-1 2018 Deleterious variants in dihydropyrimidine dehydrogenase (DPD, DPYD gene) can be highly predictive of clinical toxicity to the widely prescribed chemotherapeutic 5-fluorouracil (5-FU). Fluorouracil 161-175 dihydropyrimidine dehydrogenase Homo sapiens 24-55 29327356-1 2018 Deleterious variants in dihydropyrimidine dehydrogenase (DPD, DPYD gene) can be highly predictive of clinical toxicity to the widely prescribed chemotherapeutic 5-fluorouracil (5-FU). Fluorouracil 161-175 dihydropyrimidine dehydrogenase Homo sapiens 57-60 29327356-1 2018 Deleterious variants in dihydropyrimidine dehydrogenase (DPD, DPYD gene) can be highly predictive of clinical toxicity to the widely prescribed chemotherapeutic 5-fluorouracil (5-FU). Fluorouracil 161-175 dihydropyrimidine dehydrogenase Homo sapiens 62-66 29327356-1 2018 Deleterious variants in dihydropyrimidine dehydrogenase (DPD, DPYD gene) can be highly predictive of clinical toxicity to the widely prescribed chemotherapeutic 5-fluorouracil (5-FU). Fluorouracil 177-181 dihydropyrimidine dehydrogenase Homo sapiens 24-55 29327356-1 2018 Deleterious variants in dihydropyrimidine dehydrogenase (DPD, DPYD gene) can be highly predictive of clinical toxicity to the widely prescribed chemotherapeutic 5-fluorouracil (5-FU). Fluorouracil 177-181 dihydropyrimidine dehydrogenase Homo sapiens 57-60 29327356-1 2018 Deleterious variants in dihydropyrimidine dehydrogenase (DPD, DPYD gene) can be highly predictive of clinical toxicity to the widely prescribed chemotherapeutic 5-fluorouracil (5-FU). Fluorouracil 177-181 dihydropyrimidine dehydrogenase Homo sapiens 62-66 29327356-5 2018 An examination of feature importance within the model provided additional insight into functional aspects of the DPD protein relevant to 5-FU toxicity. Fluorouracil 137-141 dihydropyrimidine dehydrogenase Homo sapiens 113-116 30188916-7 2018 Treatment with 5-FU-based regimens improved prognosis in patients with the combination of MSS tumours, KRAS mutation and CIMP negative (log rank P = 0.003) as well as in patients with MSS tumours plus BRAF and KRAS wild-type and CIMP negative (log-rank P<0.001). Fluorouracil 15-19 KRAS proto-oncogene, GTPase Homo sapiens 103-107 30188916-7 2018 Treatment with 5-FU-based regimens improved prognosis in patients with the combination of MSS tumours, KRAS mutation and CIMP negative (log rank P = 0.003) as well as in patients with MSS tumours plus BRAF and KRAS wild-type and CIMP negative (log-rank P<0.001). Fluorouracil 15-19 KRAS proto-oncogene, GTPase Homo sapiens 210-214 30103904-5 2018 Indeed, 80% of the 5-FU dose is catabolized in the liver by dihydropyrimidine dehydrogenase (DPD) into inactive compounds. Fluorouracil 19-23 dihydropyrimidine dehydrogenase Homo sapiens 93-96 29423671-12 2018 Compared to ST6Gal-I- CRC cells, ST6Gal-I+ CRC cells generated significantly more tumor spheres in culture, were more resistant to fluorouracil-induced apoptosis likely through upregulating cell autophagy, and generated tumor more frequently after serial adoptive transplantation. Fluorouracil 131-143 ST6 beta-galactoside alpha-2,6-sialyltransferase 1 Homo sapiens 33-41 31949859-0 2018 c-Jun and Camk2a contribute to the drug resistance of induction docetaxel/cisplatin/5-fluorouracil in hypopharyngeal carcinoma. Fluorouracil 84-98 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 0-5 30214243-0 2018 STARD13 is positively correlated with good prognosis and enhances 5-FU sensitivity via suppressing cancer stemness in hepatocellular carcinoma cells. Fluorouracil 66-70 StAR related lipid transfer domain containing 13 Homo sapiens 0-7 30214243-8 2018 Functionally, overexpression of STARD13 inhibited cells stemness and enhanced 5-FU sensitivity in HCC cells. Fluorouracil 78-82 StAR related lipid transfer domain containing 13 Homo sapiens 32-39 30214243-10 2018 Notably, the inhibitory effects of STARD13 on HCC cells stemness and 5-FU sensitivity were rescued by RhoA or YAP-5SA overexpression. Fluorouracil 69-73 StAR related lipid transfer domain containing 13 Homo sapiens 35-42 30214243-11 2018 Conclusion: Our results indicate that STARD13 could enhances 5-FU sensitivity by suppressing cancer stemness in hepatocellular carcinoma cells via attenuating YAP transcriptional activity. Fluorouracil 61-65 StAR related lipid transfer domain containing 13 Homo sapiens 38-45 30096914-9 2018 Treatment with 5-FU caused significant reductions in Notch1, sex determining region Y-box 2 (SOX2), nestin, doublecortin (DCX), and nuclear factor erythroid 2-related factor 2 (Nrf2) levels within the hippocampus. Fluorouracil 15-19 doublecortin Rattus norvegicus 108-120 30096914-9 2018 Treatment with 5-FU caused significant reductions in Notch1, sex determining region Y-box 2 (SOX2), nestin, doublecortin (DCX), and nuclear factor erythroid 2-related factor 2 (Nrf2) levels within the hippocampus. Fluorouracil 15-19 doublecortin Rattus norvegicus 122-125 30096914-10 2018 In addition, 5-FU significantly increased p21 positive cell number in the subgranular zone (SGZ) and malondialdehyde (MDA) levels in the hippocampus. Fluorouracil 13-17 KRAS proto-oncogene, GTPase Rattus norvegicus 42-45 30096914-11 2018 Administration with both AA and 5-FU in prevention and throughout was able to prevent decreases in Notch1 SOX2, nestin, DCX, and Nrf2 caused by 5-FU. Fluorouracil 32-36 doublecortin Rattus norvegicus 120-123 29845393-10 2018 CONCLUSION: Genetic polymorphism in DPYD seems to be associated with DFS in CRC patients receiving an adjuvant regimen of 5-FU/capecitabine-based chemotherapy. Fluorouracil 122-126 dihydropyrimidine dehydrogenase Homo sapiens 36-40 30002278-0 2018 Resveratrol Chemosensitizes TNF-beta-Induced Survival of 5-FU-Treated Colorectal Cancer Cells. Fluorouracil 57-61 lymphotoxin alpha Homo sapiens 28-36 30002278-5 2018 We found that TNF-beta promoted chemoresistance in CRC cells to 5-FU compared to control cultures and resveratrol chemosensitizes TNF-beta-induced increased capacity for survival and invasion of HCT116 and HCT116R cells to 5-FU. Fluorouracil 64-68 lymphotoxin alpha Homo sapiens 14-22 30002278-5 2018 We found that TNF-beta promoted chemoresistance in CRC cells to 5-FU compared to control cultures and resveratrol chemosensitizes TNF-beta-induced increased capacity for survival and invasion of HCT116 and HCT116R cells to 5-FU. Fluorouracil 223-227 lymphotoxin alpha Homo sapiens 130-138 28934847-0 2018 Participation of CCL1 in Snail-Positive Fibroblasts in Colorectal Cancer Contribute to 5-Fluorouracil/Paclitaxel Chemoresistance. Fluorouracil 87-101 snail family zinc finger 1 Mus musculus 25-30 28934847-9 2018 CT26 co-cultured with 3T3-Snail resisted the impairment from 5-fluorouracil and paclitaxel in vitro. Fluorouracil 61-75 snail family zinc finger 1 Mus musculus 26-31 28934847-12 2018 Conclusion: Taken together, Snail-expressing 3T3 fibroblasts display CAFs properties that support 5-fluorouracil and paclitaxel chemoresistance in CRC via participation of CCL1 and suggest that inhibition of the Snail-expression fibroblasts in tumor may be a useful strategy to limit chemoresistance. Fluorouracil 98-112 snail family zinc finger 1 Mus musculus 28-33 30042281-4 2018 NAC with 5-fluorouracil, epirubicin, and cyclophosphamide(FEC)followed by docetaxel(DTX)was administered. Fluorouracil 9-23 X-linked Kx blood group Homo sapiens 0-3 29715584-5 2018 First, we showed that 5-FU-resistant SNUC5 colon cancer cells (SNUC5/FUR cells) undergo EMT by analyzing the expression of EMT markers such as N-cadherin, vimentin and E-cadherin. Fluorouracil 22-26 cadherin 2 Homo sapiens 143-153 29625079-0 2018 DPD functional tests in plasma, fresh saliva and dried saliva samples as predictors of 5-fluorouracil exposure and occurrence of drug-related severe toxicity. Fluorouracil 87-101 dihydropyrimidine dehydrogenase Homo sapiens 0-3 29532356-3 2018 Herein, we hypothesized that the maleimide group-containing 5-FU prodrug (EMC-5-FU) could improve the intestinal mucoadhesion because the maleimide end group can covalently target thiol residues of mucin glycoprotein covering the intestinal enterocytes. Fluorouracil 60-64 solute carrier family 13 member 2 Rattus norvegicus 198-203 29532356-3 2018 Herein, we hypothesized that the maleimide group-containing 5-FU prodrug (EMC-5-FU) could improve the intestinal mucoadhesion because the maleimide end group can covalently target thiol residues of mucin glycoprotein covering the intestinal enterocytes. Fluorouracil 78-82 solute carrier family 13 member 2 Rattus norvegicus 198-203 29756138-8 2018 Our results showed that CMP in combination with 5-FU reversed intestinal shortening (p < 0.01) and alleviated 5-FU-induced colon injury (p < 0.001) via suppression of ROS production; increasing the levels of CAT, GSH-Px and GSH; decreasing expression of NF-kappaB, p-p38 and Bax; and elevating the levels of Nrf2 and Bcl-2. Fluorouracil 48-52 BCL2-associated X protein Mus musculus 281-284 29740490-0 2018 Silencing Livin improved the sensitivity of colon cancer cells to 5-fluorouracil by regulating crosstalk between apoptosis and autophagy. Fluorouracil 66-80 baculoviral IAP repeat containing 7 Homo sapiens 10-15 29740490-8 2018 The results of the present study confirmed that silencing Livin significantly enhanced colon cancer cell death in the presence of 5-FU, increased expression levels of various apoptosis- and autophagy-associated proteins and augmented chemotherapeutic sensitivity to 5-FU. Fluorouracil 130-134 baculoviral IAP repeat containing 7 Homo sapiens 58-63 29740490-8 2018 The results of the present study confirmed that silencing Livin significantly enhanced colon cancer cell death in the presence of 5-FU, increased expression levels of various apoptosis- and autophagy-associated proteins and augmented chemotherapeutic sensitivity to 5-FU. Fluorouracil 266-270 baculoviral IAP repeat containing 7 Homo sapiens 58-63 29755597-6 2018 The results indicated that, compared with parental cells, proteins associated with the Wnt/beta-catenin signaling pathway and aldehyde dehydrogenase 1 were overexpressed, the number and size of spheres in the 5-FU-resistant cells were increased, the ratio of CD44+/CD24-/low cells was increased and the migratory ability was improved in vitro compared with the 5-FU-susceptible cells. Fluorouracil 209-213 catenin beta 1 Canis lupus familiaris 91-103 29747253-5 2018 The results showed that the IC(50) values of 5-FU for the NC group and c-fos shRNA group were (306.2+-6.3)mumol/L and (81.3+-3.9)mumol/L, respectively, which was decreased by 73% in the c-fos shRNA group compared to that in the NC group (P<0.05). Fluorouracil 45-49 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 71-76 29747253-5 2018 The results showed that the IC(50) values of 5-FU for the NC group and c-fos shRNA group were (306.2+-6.3)mumol/L and (81.3+-3.9)mumol/L, respectively, which was decreased by 73% in the c-fos shRNA group compared to that in the NC group (P<0.05). Fluorouracil 45-49 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 186-191 29747253-6 2018 Similarly, the results showed that the IC(50) values for 5-FU were (55.3+-9.4) mumol/L in NC group and (288.1+-7.3)mumol/L in c-fos WT group, which was increased 5.21-fold in c-fos WT cells. Fluorouracil 57-61 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 126-131 29747253-6 2018 Similarly, the results showed that the IC(50) values for 5-FU were (55.3+-9.4) mumol/L in NC group and (288.1+-7.3)mumol/L in c-fos WT group, which was increased 5.21-fold in c-fos WT cells. Fluorouracil 57-61 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 175-180 29560281-9 2018 Accordingly, the protein levels of E-cadherin and claudin-1 were reduced in 5-FU-treated cells. Fluorouracil 76-80 claudin 1 Homo sapiens 50-59 29370570-6 2018 For further, we showed that PIK3R3 could enhance 5-FU induced apoptosis by regulating the expression of thymmidine phosphorylase (TP). Fluorouracil 49-53 phosphoinositide-3-kinase regulatory subunit 3 Homo sapiens 28-34 29370570-7 2018 In conclusion, PIK3R3 could be considered as a predictor of 5-FU sensitivity for personalized treatment, and a therapeutic target for colorectal cancer. Fluorouracil 60-64 phosphoinositide-3-kinase regulatory subunit 3 Homo sapiens 15-21 29061341-6 2018 There was a significant increase in the expression of the drug-metabolizing cytochrome P450 enzymes CYP1A2 and CYP2A6 in 5-FU-resistant cells. Fluorouracil 121-125 cytochrome P450 family 2 subfamily A member 6 Homo sapiens 111-117 29203613-7 2018 Furthermore, Nfe2l1-KD cells were resistant to damage by the chemotherapeutic drugs STZ and 5-fluorouracil, which was linked to binding of hexokinase 1 with mitochondria, enhanced mitochondrial membrane potential and closed mitochondrial potential transition pore. Fluorouracil 92-106 hexokinase 1 Mus musculus 139-151 29258758-2 2018 Our aim was to investigate the role of dTMP dysmetabolism via inhibition of TYMS by an inhibitor, 5-fluorouracil (5-FU) in the occurrence of neural tube defects (NTDs). Fluorouracil 98-112 thymidylate synthase Mus musculus 76-80 29258758-2 2018 Our aim was to investigate the role of dTMP dysmetabolism via inhibition of TYMS by an inhibitor, 5-fluorouracil (5-FU) in the occurrence of neural tube defects (NTDs). Fluorouracil 114-118 thymidylate synthase Mus musculus 76-80 29258758-4 2018 TYMS activity was significantly inhibited with decreased dTMP and accumulation of dUMP after 5-FU injection. Fluorouracil 93-97 thymidylate synthase Mus musculus 0-4 29483928-11 2018 C-fos overexpression in HEp-2 cells (c-fos WT) resulted in increased P-gp expression and increased the IC50 for 5-FU. Fluorouracil 112-116 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 0-5 29483928-11 2018 C-fos overexpression in HEp-2 cells (c-fos WT) resulted in increased P-gp expression and increased the IC50 for 5-FU. Fluorouracil 112-116 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 37-42 29512369-9 2018 Our results revealed that combination of DC vaccine and 5-FU reduced number of MDSCs (3%) and also tumor growth rate(10%)(p<0.05) and increased mice survival (70%) and increased CD8+ /CD107a+ T cells (25%). Fluorouracil 56-60 lysosomal-associated membrane protein 1 Mus musculus 187-193 29343747-4 2018 The present computational approach made the methylomic data more accessible to each transcriptional unit and allowed to identify candidate genes, including the tumour necrosis factor receptor-associated factor 4 (TRAF4), as novel therapeutic targets with a strong response to anti-tumour agents, such as 5-FU and CDDP, and whose significance has been confirmed in a mouse model in vivo. Fluorouracil 304-308 TNF receptor associated factor 4 Mus musculus 160-211 29343747-4 2018 The present computational approach made the methylomic data more accessible to each transcriptional unit and allowed to identify candidate genes, including the tumour necrosis factor receptor-associated factor 4 (TRAF4), as novel therapeutic targets with a strong response to anti-tumour agents, such as 5-FU and CDDP, and whose significance has been confirmed in a mouse model in vivo. Fluorouracil 304-308 TNF receptor associated factor 4 Mus musculus 213-218 29371831-7 2018 Results: In cervical cancer, we found that SHP-2 suppressed apoptosis induced by Oxaliplatin and 5-FU. Fluorouracil 97-101 protein tyrosine phosphatase non-receptor type 11 Homo sapiens 43-48 32039342-0 2018 Dose modification for safe treatment of a compound complex heterozygous DPYD variant carrier with 5-fluorouracil. Fluorouracil 98-112 dihydropyrimidine dehydrogenase Homo sapiens 72-76 28956217-0 2018 Chemoresistance to 5-FU inhibited by 635 nm LED irradiation in CD133+ KB cell line. Fluorouracil 19-23 prominin 1 Mus musculus 63-68 30321081-5 2018 We found that the downregulation or complete depletion of SND1 enhanced the apoptosis levels of HepG2 and SMMC-7721 cells upon stimulation with 5-Fu (5-fluorouracil), a chemotherapeutic drug for HCC (hepatocellular carcinoma). Fluorouracil 144-148 staphylococcal nuclease and tudor domain containing 1 Homo sapiens 58-62 30321081-5 2018 We found that the downregulation or complete depletion of SND1 enhanced the apoptosis levels of HepG2 and SMMC-7721 cells upon stimulation with 5-Fu (5-fluorouracil), a chemotherapeutic drug for HCC (hepatocellular carcinoma). Fluorouracil 150-164 staphylococcal nuclease and tudor domain containing 1 Homo sapiens 58-62 30321081-6 2018 SND1 affected the 5-Fu-induced apoptosis levels of HCC cells by modulating the expression of UCA1 (urothelial cancer associated 1), which is a lncRNA (long non-coding RNA). Fluorouracil 18-22 staphylococcal nuclease and tudor domain containing 1 Homo sapiens 0-4 28051340-8 2018 The expression level of mRNAs for hepatic CYP2C6 and CYP2C11 was significantly lower than in the control group when the rats were pretreated with 5-FU. Fluorouracil 146-150 cytochrome P450, family 2, subfamily C, polypeptide 6, variant 1 Rattus norvegicus 42-48 28051340-10 2018 These results demonstrated that the pharmacokinetic profile of TB was altered by the treatment with 5-FU through a metabolic process, which may be responsible for the decreased CYP2C6/11 expression at mRNA levels. Fluorouracil 100-104 cytochrome P450, family 2, subfamily C, polypeptide 6, variant 1 Rattus norvegicus 177-183 29237416-13 2017 From the signature, we found that PTGES gene was up-regulated in CRC cells which were more resistant to 5-Fu. Fluorouracil 104-108 prostaglandin E synthase Homo sapiens 34-39 29237416-14 2017 Knock-down of PTGES indicated a growth inhibition and up-regulation of apoptotic markers induced by 5-Fu in CRC cells. Fluorouracil 100-104 prostaglandin E synthase Homo sapiens 14-19 28849584-2 2017 This study aimed to investigate quantitatively the effect of 5-FU-induced intestinal damage on the expression of intestinal transporters: P-glycoprotein (P-gp), breast cancer resistance protein (BCRP) and peptide transporter 1 (PEPT1) in rats. Fluorouracil 61-65 ATP-binding cassette, subfamily B (MDR/TAP), member 1B Rattus norvegicus 138-152 28849584-2 2017 This study aimed to investigate quantitatively the effect of 5-FU-induced intestinal damage on the expression of intestinal transporters: P-glycoprotein (P-gp), breast cancer resistance protein (BCRP) and peptide transporter 1 (PEPT1) in rats. Fluorouracil 61-65 ATP-binding cassette, subfamily B (MDR/TAP), member 1B Rattus norvegicus 154-158 28849584-6 2017 In the 5-FU-treated rats, the protein levels of P-gp and Bcrp in the upper segment were significantly increased to 15- and 2.6-fold of the control, respectively, while those in other segments were unaffected. Fluorouracil 7-11 ATP-binding cassette, subfamily B (MDR/TAP), member 1B Rattus norvegicus 48-52 28720546-5 2017 NEAT1 promoted invasion through inducing Epithelial-mesenchymal transition (EMT) and NEAT1 played a role in 5-fluorouracil (5-FU) resistance. Fluorouracil 108-122 nuclear paraspeckle assembly transcript 1 Homo sapiens 0-5 28720546-5 2017 NEAT1 promoted invasion through inducing Epithelial-mesenchymal transition (EMT) and NEAT1 played a role in 5-fluorouracil (5-FU) resistance. Fluorouracil 108-122 nuclear paraspeckle assembly transcript 1 Homo sapiens 85-90 28720546-5 2017 NEAT1 promoted invasion through inducing Epithelial-mesenchymal transition (EMT) and NEAT1 played a role in 5-fluorouracil (5-FU) resistance. Fluorouracil 124-128 nuclear paraspeckle assembly transcript 1 Homo sapiens 0-5 28720546-5 2017 NEAT1 promoted invasion through inducing Epithelial-mesenchymal transition (EMT) and NEAT1 played a role in 5-fluorouracil (5-FU) resistance. Fluorouracil 124-128 nuclear paraspeckle assembly transcript 1 Homo sapiens 85-90 28720546-8 2017 LncRNA NEAT1 induced EMT and 5-FU resistance through the miR-211/HMGA2 axis. Fluorouracil 29-33 nuclear paraspeckle assembly transcript 1 Homo sapiens 7-12 28720546-8 2017 LncRNA NEAT1 induced EMT and 5-FU resistance through the miR-211/HMGA2 axis. Fluorouracil 29-33 microRNA 211 Homo sapiens 57-64 28767179-7 2017 Interestingly, up-regulation of miR-135b or miR-182 increased drug resistance and proliferation, but decreased apoptosis in 5-FU resistant CRC cell lines. Fluorouracil 124-128 microRNA 135b Homo sapiens 32-40 28767179-7 2017 Interestingly, up-regulation of miR-135b or miR-182 increased drug resistance and proliferation, but decreased apoptosis in 5-FU resistant CRC cell lines. Fluorouracil 124-128 microRNA 182 Homo sapiens 44-51 28767179-11 2017 Taken together, miR-135b and miR-182 may reverse the resistance to 5-FU in CRC cells by targeting ST6GALNAC2 via PI3K/AKT pathway, which render potential chemotherapy targets for the treatment of CRC. Fluorouracil 67-71 microRNA 135b Homo sapiens 16-24 28767179-11 2017 Taken together, miR-135b and miR-182 may reverse the resistance to 5-FU in CRC cells by targeting ST6GALNAC2 via PI3K/AKT pathway, which render potential chemotherapy targets for the treatment of CRC. Fluorouracil 67-71 microRNA 182 Homo sapiens 29-36 28767179-11 2017 Taken together, miR-135b and miR-182 may reverse the resistance to 5-FU in CRC cells by targeting ST6GALNAC2 via PI3K/AKT pathway, which render potential chemotherapy targets for the treatment of CRC. Fluorouracil 67-71 ST6 N-acetylgalactosaminide alpha-2,6-sialyltransferase 2 Homo sapiens 98-108 28714026-3 2017 Overexpressing EHF downregulated the antitumor effect of 5-fluorouracil (5-FU) in NCI-N87 cells. Fluorouracil 57-71 ETS homologous factor Homo sapiens 15-18 28714026-3 2017 Overexpressing EHF downregulated the antitumor effect of 5-fluorouracil (5-FU) in NCI-N87 cells. Fluorouracil 73-77 ETS homologous factor Homo sapiens 15-18 28815216-5 2017 We find that PB1 T123A has higher replicative fitness than the wild type, PR8, and maintains its level of genome production during 5-fluorouracil (2,4-dihydroxy-5-fluoropyrimidine) treatment. Fluorouracil 131-145 polybromo 1 Homo sapiens 13-16 28815216-5 2017 We find that PB1 T123A has higher replicative fitness than the wild type, PR8, and maintains its level of genome production during 5-fluorouracil (2,4-dihydroxy-5-fluoropyrimidine) treatment. Fluorouracil 147-179 polybromo 1 Homo sapiens 13-16 29416616-0 2018 MicroRNA-761 promotes the sensitivity of colorectal cancer cells to 5-Fluorouracil through targeting FOXM1. Fluorouracil 68-82 forkhead box M1 Homo sapiens 101-106 29416616-10 2018 Elevated expression of FOXM1 suppressed the sensitivity of miR-761-overexpressing HT29 cells to 5-FU. Fluorouracil 96-100 forkhead box M1 Homo sapiens 23-28 28501750-1 2017 The plasma 5,6-dihydrouracil/uracil (UH2/U) ratio is a possible phenotypic marker of dihydropyrimidine dehydrogenase (DPD) activity, hence an index of 5-fluorouracil (5-FU) response and toxicity. Fluorouracil 151-165 dihydropyrimidine dehydrogenase Homo sapiens 85-116 28501750-1 2017 The plasma 5,6-dihydrouracil/uracil (UH2/U) ratio is a possible phenotypic marker of dihydropyrimidine dehydrogenase (DPD) activity, hence an index of 5-fluorouracil (5-FU) response and toxicity. Fluorouracil 151-165 dihydropyrimidine dehydrogenase Homo sapiens 118-121 28501750-1 2017 The plasma 5,6-dihydrouracil/uracil (UH2/U) ratio is a possible phenotypic marker of dihydropyrimidine dehydrogenase (DPD) activity, hence an index of 5-fluorouracil (5-FU) response and toxicity. Fluorouracil 167-171 dihydropyrimidine dehydrogenase Homo sapiens 118-121 28498554-0 2017 Differential resistance to platinum-based drugs and 5-fluorouracil in p22phox-overexpressing oral squamous cell carcinoma: Implications of alternative treatment strategies. Fluorouracil 52-66 cytochrome b-245, alpha polypeptide Mus musculus 70-77 28781687-0 2017 Role of depth of response and MTHFR genotype as predictors of fluorouracil rechallenge therapy for refractory metastatic colorectal cancer. Fluorouracil 62-74 methylenetetrahydrofolate reductase Homo sapiens 30-35 28781687-10 2017 In patients receiving third-line chemotherapy with 5-FU rechallenge therapy, the methylenetretrahydrofolate reductase (MTHFR) (C677T) CC genotype and a DoR >60% were significantly associated with a good prognosis in multivariate analysis. Fluorouracil 51-55 methylenetetrahydrofolate reductase Homo sapiens 81-117 28781687-12 2017 Patients with a DoR >60% following first-line chemotherapy and a MTHFR (C677T) CC genotype exhibited a survival benefit from 5-FU retreatment. Fluorouracil 128-132 methylenetetrahydrofolate reductase Homo sapiens 68-73 28781687-13 2017 Therefore, the DoR and MTHFR genotype are potential markers for selecting patients with refractory mCRC that would benefit from 5-FU rechallenge therapy. Fluorouracil 128-132 methylenetetrahydrofolate reductase Homo sapiens 23-28 28765596-0 2017 A polymorphism in ABCC4 is related to efficacy of 5-FU/capecitabine-based chemotherapy in colorectal cancer patients. Fluorouracil 50-54 ATP binding cassette subfamily C member 4 Homo sapiens 18-23 28765596-4 2017 Statistical analysis showed that a polymorphism rs3742106 in the 3"-UTR of ATP-binding cassette subfamily C member 4 (ABCC4) gene was significantly associated with the efficacy of 5-FU/capecitabine-based chemotherapy in CRC. Fluorouracil 180-184 ATP binding cassette subfamily C member 4 Homo sapiens 75-116 28765596-4 2017 Statistical analysis showed that a polymorphism rs3742106 in the 3"-UTR of ATP-binding cassette subfamily C member 4 (ABCC4) gene was significantly associated with the efficacy of 5-FU/capecitabine-based chemotherapy in CRC. Fluorouracil 180-184 ATP binding cassette subfamily C member 4 Homo sapiens 118-123 28765596-8 2017 Furthermore, we found that the intracellular concentration of 5-FU was elevated by miR-3190-5p, and consequently the sensitivity of CRC cells to 5-FU was also enhanced. Fluorouracil 62-66 membrane associated ring-CH-type finger 8 Homo sapiens 83-86 28835573-2 2017 Dihydropyrimidine dehydrogenase (DPD) is a rate-limiting enzyme in pyrimidine catabolism and is important in catabolism of 5-fluorouracil (5-FU). Fluorouracil 123-137 dihydropyrimidine dehydrogenase Homo sapiens 0-31 28835573-2 2017 Dihydropyrimidine dehydrogenase (DPD) is a rate-limiting enzyme in pyrimidine catabolism and is important in catabolism of 5-fluorouracil (5-FU). Fluorouracil 123-137 dihydropyrimidine dehydrogenase Homo sapiens 33-36 28835573-2 2017 Dihydropyrimidine dehydrogenase (DPD) is a rate-limiting enzyme in pyrimidine catabolism and is important in catabolism of 5-fluorouracil (5-FU). Fluorouracil 139-143 dihydropyrimidine dehydrogenase Homo sapiens 0-31 28835573-2 2017 Dihydropyrimidine dehydrogenase (DPD) is a rate-limiting enzyme in pyrimidine catabolism and is important in catabolism of 5-fluorouracil (5-FU). Fluorouracil 139-143 dihydropyrimidine dehydrogenase Homo sapiens 33-36 28487386-7 2017 Cell biology investigations showed that miR-23b regulated CSC phenotypes globally at the level of proliferation, cell cycle, self-renewal, epithelial-mesenchymal transition, invasion, and resistance to the colorectal cancer chemotherapeutic agent 5-fluorouracil. Fluorouracil 247-261 microRNA 23b Homo sapiens 40-47 28515355-8 2017 Among these genes, we showed that 5-FU increases the mRNA translation of HIVEP2, which encodes a transcription factor whose translation in normal condition is known to be inhibited by mir-155. Fluorouracil 34-38 microRNA 155 Homo sapiens 184-191 28515355-9 2017 In response to 5-FU, the expression of mir-155 decreases thus stimulating the translation of HIVEP2 mRNA. Fluorouracil 15-19 microRNA 155 Homo sapiens 39-46 28646148-0 2017 miR-15b-5p resensitizes colon cancer cells to 5-fluorouracil by promoting apoptosis via the NF-kappaB/XIAP axis. Fluorouracil 46-60 microRNA 15b Homo sapiens 0-7 28646148-0 2017 miR-15b-5p resensitizes colon cancer cells to 5-fluorouracil by promoting apoptosis via the NF-kappaB/XIAP axis. Fluorouracil 46-60 X-linked inhibitor of apoptosis Homo sapiens 102-106 28646148-3 2017 Over-expression of miR-15b-5p not only promoted 5-fluorouracil (5-FU)-induced cellular apoptosis but also reversed the chemoresistance of 5-FU in vitro and in vivo. Fluorouracil 48-62 microRNA 15b Homo sapiens 19-26 28646148-3 2017 Over-expression of miR-15b-5p not only promoted 5-fluorouracil (5-FU)-induced cellular apoptosis but also reversed the chemoresistance of 5-FU in vitro and in vivo. Fluorouracil 64-68 microRNA 15b Homo sapiens 19-26 28646148-3 2017 Over-expression of miR-15b-5p not only promoted 5-fluorouracil (5-FU)-induced cellular apoptosis but also reversed the chemoresistance of 5-FU in vitro and in vivo. Fluorouracil 138-142 microRNA 15b Homo sapiens 19-26 28646148-7 2017 These findings suggest that miR-15b-5p may be a potential agent for CRC treatment, particularly for 5-FU-resistant CRC. Fluorouracil 100-104 microRNA 15b Homo sapiens 28-35 27836590-0 2017 Aptamer and 5-fluorouracil dual-loading Ag2S quantum dots used as a sensitive label-free probe for near-infrared photoluminescence turn-on detection of CA125 antigen. Fluorouracil 12-26 mucin 16, cell surface associated Homo sapiens 152-157 27836590-2 2017 Based on electrostatic interactions, 5-fluorouracil (5-Fu) was combined with the aptamer of CA125 antigen to fabricate aptamer/5-Fu complex. Fluorouracil 37-51 mucin 16, cell surface associated Homo sapiens 92-97 27836590-2 2017 Based on electrostatic interactions, 5-fluorouracil (5-Fu) was combined with the aptamer of CA125 antigen to fabricate aptamer/5-Fu complex. Fluorouracil 53-57 mucin 16, cell surface associated Homo sapiens 92-97 27836590-2 2017 Based on electrostatic interactions, 5-fluorouracil (5-Fu) was combined with the aptamer of CA125 antigen to fabricate aptamer/5-Fu complex. Fluorouracil 127-131 mucin 16, cell surface associated Homo sapiens 92-97 28433634-6 2017 Additional Western blot analyses have shown that possible mechanisms underlying enhanced sensitivity to 5-FU induced by dual Sphk 1/2 inhibition could include abrogation of FAK-regulated IGF-1R activity and down-regulation of osteopontin expression culminating in the inhibition of NF-kappaB activity and its downstream signalling mediated by sirtuin 1 and p38 MAPK. Fluorouracil 104-108 insulin like growth factor 1 receptor Homo sapiens 187-193 28433634-6 2017 Additional Western blot analyses have shown that possible mechanisms underlying enhanced sensitivity to 5-FU induced by dual Sphk 1/2 inhibition could include abrogation of FAK-regulated IGF-1R activity and down-regulation of osteopontin expression culminating in the inhibition of NF-kappaB activity and its downstream signalling mediated by sirtuin 1 and p38 MAPK. Fluorouracil 104-108 sirtuin 1 Homo sapiens 343-352 28670496-6 2017 For example, resistance to 5-fluorouracil is mediated by alterations in miR-21, miR-27a/b, and miR-155; the sensitivity to Docetaxel is influenced by miR-98, miR-192, miR-194, miR-200b, miR-212, and miR-424; and the resistance to Cisplatin is mediated by miR-let-7, miR-15, miR-16 miR-21 and miR-214. Fluorouracil 27-41 microRNA 155 Homo sapiens 95-102 28670496-6 2017 For example, resistance to 5-fluorouracil is mediated by alterations in miR-21, miR-27a/b, and miR-155; the sensitivity to Docetaxel is influenced by miR-98, miR-192, miR-194, miR-200b, miR-212, and miR-424; and the resistance to Cisplatin is mediated by miR-let-7, miR-15, miR-16 miR-21 and miR-214. Fluorouracil 27-41 membrane associated ring-CH-type finger 8 Homo sapiens 72-75 28670496-6 2017 For example, resistance to 5-fluorouracil is mediated by alterations in miR-21, miR-27a/b, and miR-155; the sensitivity to Docetaxel is influenced by miR-98, miR-192, miR-194, miR-200b, miR-212, and miR-424; and the resistance to Cisplatin is mediated by miR-let-7, miR-15, miR-16 miR-21 and miR-214. Fluorouracil 27-41 membrane associated ring-CH-type finger 8 Homo sapiens 80-83 28670496-6 2017 For example, resistance to 5-fluorouracil is mediated by alterations in miR-21, miR-27a/b, and miR-155; the sensitivity to Docetaxel is influenced by miR-98, miR-192, miR-194, miR-200b, miR-212, and miR-424; and the resistance to Cisplatin is mediated by miR-let-7, miR-15, miR-16 miR-21 and miR-214. Fluorouracil 27-41 membrane associated ring-CH-type finger 8 Homo sapiens 80-83 28266023-5 2017 KEY FINDINGS: Astragaloside II was able to significantly decrease the expression of LC3-II and Beclin-1 in a dose-dependent manner, Astragaloside II (80 mum) further decreased LC3-II formation, Beclin-1 and GFP-LC3 puncta dots stimulated with 5-fluorouracil (0.2 mm) in Bel-7402/FU cells (P < 0.05). Fluorouracil 243-257 microtubule associated protein 1 light chain 3 alpha Homo sapiens 84-87 28588704-4 2017 By comparing the gene expression profiles of Ell3 OE cells with control cells, the present data revealed that Lipocalin2 (LCN2) and Wnt signaling activity are associated with 5-FU resistance of Ell3 OE. Fluorouracil 175-179 lipocalin 2 Homo sapiens 110-120 28588704-4 2017 By comparing the gene expression profiles of Ell3 OE cells with control cells, the present data revealed that Lipocalin2 (LCN2) and Wnt signaling activity are associated with 5-FU resistance of Ell3 OE. Fluorouracil 175-179 lipocalin 2 Homo sapiens 122-126 28588704-5 2017 siRNA-mediated suppression of LCN2 reversed 5-FU resistance in Ell3 OE cells. Fluorouracil 44-48 lipocalin 2 Homo sapiens 30-34 28588704-8 2017 These findings suggest that enhanced expression of LCN2 and activation of the Wnt signaling pathway may induce 5-FU resistance in Ell3 OE cells as a means of evading apoptosis. Fluorouracil 111-115 lipocalin 2 Homo sapiens 51-55 28881782-0 2017 miR-106b regulates the 5-fluorouracil resistance by targeting Zbtb7a in cholangiocarcinoma. Fluorouracil 23-37 microRNA 106b Homo sapiens 0-8 28881782-8 2017 RESULTS: The microRNA-106b (miR-106b) was significantly down-regulated in 5-FU resistant CCA cells. Fluorouracil 74-78 microRNA 106b Homo sapiens 13-26 28881782-8 2017 RESULTS: The microRNA-106b (miR-106b) was significantly down-regulated in 5-FU resistant CCA cells. Fluorouracil 74-78 microRNA 106b Homo sapiens 28-36 28881782-9 2017 Instead, over-expression of miR-106b could re-sensitize resistant CCA cells to 5-FU through down-regulation of Zbtb7a. Fluorouracil 79-83 microRNA 106b Homo sapiens 28-36 28881782-11 2017 CONCLUSION: Our study demonstrates that miR-106b can reverse 5-FU resistance via Zbtb7a suppression, thus offer a novel and powerful strategy for CCA chemotherapy. Fluorouracil 61-65 microRNA 106b Homo sapiens 40-48 28062363-6 2017 Erythrocytes from 5-fluorouracil-treated Trib3-/- mice additionally were more prone to lysis and exhibited elevated peroxide-induced reactive oxygen species. Fluorouracil 18-32 tribbles pseudokinase 3 Mus musculus 41-46 27878958-0 2017 Inhibition of Orai1-mediated Ca2+ entry enhances chemosensitivity of HepG2 hepatocarcinoma cells to 5-fluorouracil. Fluorouracil 100-114 ORAI calcium release-activated calcium modulator 1 Homo sapiens 14-19 27878958-8 2017 5-FU treatment decreased SOCE and Orai1 expressions, but had no effects on Stim1 and TRPC1 expressions. Fluorouracil 0-4 ORAI calcium release-activated calcium modulator 1 Homo sapiens 34-39 28529594-7 2017 Using annexin V and terminal deoxynucleotidyl transferase 2"-deoxyuridine 5"-triphosphate nick end labeling assays, it was demonstrated that levels of apoptosis induction in HT-29 cells treated with PsA or 5-FU were significantly increased compared with the untreated control cells (P<0.05). Fluorouracil 206-210 DNA nucleotidylexotransferase Homo sapiens 20-57 28413604-0 2017 The role of GLI1 for 5-Fu resistance in colorectal cancer. Fluorouracil 21-25 GLI family zinc finger 1 Homo sapiens 12-16 28413604-5 2017 Through exome sequencing, we discovered that elevated GLI1 signaling axis is a major genetic alteration in the 5-FU resistant cells. Fluorouracil 111-115 GLI family zinc finger 1 Homo sapiens 54-58 28413604-7 2017 We demonstrated that knockdown of GLI1 or GLI2 sensitized LoVo-R cells to 5-FU treatment, reduced cell invasiveness. Fluorouracil 74-78 GLI family zinc finger 1 Homo sapiens 34-38 28413604-8 2017 The relevance of our studies to colorectal cancer patients is reflected by our discovery that high expression of GLI1 signaling molecules was associated with a high incidence of cancer relapse and a shorter survival in a larger cohort of colorectal cancer patients who underwent chemotherapy (containing 5-FU). Fluorouracil 304-308 GLI family zinc finger 1 Homo sapiens 113-117 28160563-8 2017 MiR-3622b-5p turned ERBB2-positive cancer cells more vulnerable to the apoptosis induced by cisplatin and 5-fluorouracil. Fluorouracil 106-120 membrane associated ring-CH-type finger 8 Homo sapiens 0-3 27641154-7 2017 Polymorphisms in DPYD, TPMT, and UGT1A1 have been described that have a major impact on the pharmacokinetics of 5-fluorouracil, mercaptopurine, and irinotecan, respectively. Fluorouracil 112-126 dihydropyrimidine dehydrogenase Homo sapiens 17-21 27641154-7 2017 Polymorphisms in DPYD, TPMT, and UGT1A1 have been described that have a major impact on the pharmacokinetics of 5-fluorouracil, mercaptopurine, and irinotecan, respectively. Fluorouracil 112-126 UDP glucuronosyltransferase family 1 member A1 Homo sapiens 33-39 28454373-0 2017 Inhibition of CYFIP2 promotes gastric cancer cell proliferation and chemoresistance to 5-fluorouracil through activation of the Akt signaling pathway. Fluorouracil 87-101 cytoplasmic FMR1 interacting protein 2 Homo sapiens 14-20 28454373-7 2017 Furthermore, 5-fluorouracil (5-FU)-induced apoptosis was decreased following inhibition of CYFIP2 expression. Fluorouracil 13-27 cytoplasmic FMR1 interacting protein 2 Homo sapiens 91-97 28454373-7 2017 Furthermore, 5-fluorouracil (5-FU)-induced apoptosis was decreased following inhibition of CYFIP2 expression. Fluorouracil 29-33 cytoplasmic FMR1 interacting protein 2 Homo sapiens 91-97 28454373-9 2017 These 5-FU-induced effects were reduced following CYFIP2 knockdown. Fluorouracil 6-10 cytoplasmic FMR1 interacting protein 2 Homo sapiens 50-56 28454373-10 2017 In addition, inhibition of the Akt signaling pathway using the Akt inhibitor LY294002 restored CYFIP2-knockdown SGC7901 cell chemosensitivity to 5-FU. Fluorouracil 145-149 cytoplasmic FMR1 interacting protein 2 Homo sapiens 95-101 28454373-11 2017 The results of the present study demonstrate that decreased CYFIP2 expression is associated with increased gastric tumor growth in vitro and that CYFIP2 knockdown-induced activation of the Akt pro-survival signaling pathway confers resistance to 5-FU-based chemotherapy in gastric cancer cells. Fluorouracil 246-250 cytoplasmic FMR1 interacting protein 2 Homo sapiens 146-152 28182993-3 2017 METHODS: The EpCAM+ cell lines HuH1 and HuH7 were treated with 5-fluorouracil (5-FU) or epirubicin in vitro. Fluorouracil 63-77 MIR7-3 host gene Homo sapiens 40-44 28182993-7 2017 RESULTS: 5-FU or epirubicin treatment resulted in the generation of CD90+ and CD105+ cells in vitro in HuH1 and HuH7 cells, which originally contain no CD90+ or CD105+ cells. Fluorouracil 9-13 MIR7-3 host gene Homo sapiens 112-116 28314255-11 2017 Expression of VEGF-D and VEGFR-3 in the 5-FU-treated group was not significantly increased (p>0.05). Fluorouracil 40-44 vascular endothelial growth factor D Mus musculus 14-20 28351329-9 2017 Together, these data suggest that Crocetin may shift autophagic cell survival to autophagic cell death in fluorouracil-treated breast cancer cells, possibly through modulation of the expression of ATG1 and Beclin-1. Fluorouracil 106-118 beclin 1 Homo sapiens 206-214 28055957-6 2017 Furthermore, 5-FU significantly induced c-Jun N-terminal kinase (JNK) activation and the expression of pro-inflammatory genes IL-8 and ICAM-1. Fluorouracil 13-17 intercellular adhesion molecule 1 Homo sapiens 135-141 28055957-7 2017 Also in vivo, 5-FU significantly induced hepatic ACOX1 and HMOX1 expression as well as JNK-activation, pro-inflammatory gene expression and immune cell infiltration. Fluorouracil 14-18 acyl-CoA oxidase 1 Homo sapiens 49-54 27757686-0 2017 TAX1BP1 downregulation by EBV-miR-BART15-3p enhances chemosensitivity of gastric cancer cells to 5-FU. Fluorouracil 97-101 Tax1 binding protein 1 Homo sapiens 0-7 27757686-0 2017 TAX1BP1 downregulation by EBV-miR-BART15-3p enhances chemosensitivity of gastric cancer cells to 5-FU. Fluorouracil 97-101 membrane associated ring-CH-type finger 8 Homo sapiens 30-33 27757686-9 2017 Moreover, miR-BART15-3p strongly promoted chemosensitivity to 5-fluorouracil (5-FU). Fluorouracil 62-76 membrane associated ring-CH-type finger 8 Homo sapiens 10-13 27757686-9 2017 Moreover, miR-BART15-3p strongly promoted chemosensitivity to 5-fluorouracil (5-FU). Fluorouracil 78-82 membrane associated ring-CH-type finger 8 Homo sapiens 10-13 27757686-10 2017 Our results suggest that miR-BART15-3p targets the anti-apoptotic TAX1BP1 gene in cancer cells, causing increased apoptosis and chemosensitivity to 5-FU. Fluorouracil 148-152 membrane associated ring-CH-type finger 8 Homo sapiens 25-28 27757686-10 2017 Our results suggest that miR-BART15-3p targets the anti-apoptotic TAX1BP1 gene in cancer cells, causing increased apoptosis and chemosensitivity to 5-FU. Fluorouracil 148-152 Tax1 binding protein 1 Homo sapiens 66-73 28456772-9 2017 Lafutidine significantly suppressed 5-FU-increased MPO activity and inflammatory cytokine expression on day 6, but not apoptosis induction in intestinal crypts on day 1. Fluorouracil 36-40 myeloperoxidase Mus musculus 51-54 28903334-11 2017 Imbalancing BER by overexpression of MPG, but not XRCC1, sensitises MMR-deficient colon cancer cells to 5-FU and TMZ and leads to ATP depletion and lactate accumulation. Fluorouracil 104-108 N-methylpurine DNA glycosylase Homo sapiens 37-40 28127258-14 2017 Moreover, the up-regulation of RIP3 (a necroptosis marker) by 5-FU, and the activation of RIP3 by TNF-alpha, synergistically triggered necroptosis (programmed necrosis). Fluorouracil 62-66 receptor-interacting serine-threonine kinase 3 Mus musculus 31-35 28127258-15 2017 Knockdown of RIP3 attenuated the synergetic effect of TNF-alpha and 5-FU. Fluorouracil 68-72 receptor-interacting serine-threonine kinase 3 Mus musculus 13-17 28068992-3 2017 METHODS: We reported that hyaluronic acid (HA)-coated chitosan NPs promoted the drug delivery of 5-fluorouracil (5-Fu) into tumor cells that highly expressed CD44. Fluorouracil 97-111 CD44 molecule (Indian blood group) Homo sapiens 158-162 28068992-3 2017 METHODS: We reported that hyaluronic acid (HA)-coated chitosan NPs promoted the drug delivery of 5-fluorouracil (5-Fu) into tumor cells that highly expressed CD44. Fluorouracil 113-117 CD44 molecule (Indian blood group) Homo sapiens 158-162 28068992-6 2017 CONCLUSIONS: Biocompatible and biodegradable HA-coated chitosan NPs were developed to encapsulate a chemotherapeutic drug (5-Fu) to enhance drug accumulation in tumor cells and to improve the agent"s antitumor efficiency by offering targeted drug delivery via CD44. Fluorouracil 123-127 CD44 molecule (Indian blood group) Homo sapiens 260-264 29199237-14 2017 Under such experimental condition, CXCL1 gene, protein levels of neutrophil elastase and myeloperoxidase upregulation induced by 5-FU in the colon was attenuated by HST. Fluorouracil 129-133 myeloperoxidase Mus musculus 89-104 28128059-4 2017 Enzymes involved in this pathway include dihydropyrimidine dehydrogenase (DPD), which breaks down 5-FU and its prodrugs. Fluorouracil 98-102 dihydropyrimidine dehydrogenase Homo sapiens 41-72 28128059-4 2017 Enzymes involved in this pathway include dihydropyrimidine dehydrogenase (DPD), which breaks down 5-FU and its prodrugs. Fluorouracil 98-102 dihydropyrimidine dehydrogenase Homo sapiens 74-77 28128059-5 2017 Candidate gene approaches have demonstrated associations between 5-FU treatment outcomes and germline polymorphisms in DPD. Fluorouracil 65-69 dihydropyrimidine dehydrogenase Homo sapiens 119-122 28255193-8 2017 In conclusion, high levels of intratumoral DPD expression have a negative impact on sensitivity to 5-FU in GC patients, but no prognostic value for long-term survival was uncovered. Fluorouracil 99-103 dihydropyrimidine dehydrogenase Homo sapiens 43-46 28027897-0 2017 Relevance of dihydropyrimidine-dehydrogenase and thymidylate-synthase in patients with pancreatic neuroendocrine neoplasms treated with 5-FU-based chemotherapy. Fluorouracil 136-140 dihydropyrimidine dehydrogenase Homo sapiens 13-44 28027897-9 2017 Biochemical response (p = 0.005) and high DPD expression (p = 0.018) were predictive markers of response to 5-FU-based chemotherapy. Fluorouracil 108-112 dihydropyrimidine dehydrogenase Homo sapiens 42-45 28027897-12 2017 CONCLUSIONS: DPD expression and biochemical response represent promising predictive biomarkers for response to 5-FU based chemotherapy. Fluorouracil 111-115 dihydropyrimidine dehydrogenase Homo sapiens 13-16 27904848-9 2016 CONCLUSION: siRNA-mediated down-regulation of livin gene expression could significantly suppress colon cancer growth and enhance the cytotoxic effects of anticancer drugs such as 5-FU and L-OHP. Fluorouracil 179-183 baculoviral IAP repeat containing 7 Homo sapiens 46-51 28051262-8 2016 Knockdown of IGF1R significantly decreased IC50 of 5-FU, paclitaxel (PTX) and Doxorubicin (DOX) in Huh7 and HepG2 cells. Fluorouracil 51-55 insulin like growth factor 1 receptor Homo sapiens 13-18 28105142-8 2016 In the rAd/p53 + 5-Fu group, the tumor necrosis ratio, and Smad4 and Brca1 expression levels also significantly increased at various time points (P<0.05). Fluorouracil 17-21 BRCA1 DNA repair associated Homo sapiens 69-74 27942212-10 2016 The oral absorption of OXA/DCK and 5-FU from the nanoemulsion also increased significantly, and the resulting oral bioavailability values of OXA/DCK and 5-FU in the nanoemulsive system were 9.19- and 1.39-fold higher than those of free OXA and 5-FU, respectively. Fluorouracil 35-39 deoxycytidine kinase Mus musculus 145-148 27942212-10 2016 The oral absorption of OXA/DCK and 5-FU from the nanoemulsion also increased significantly, and the resulting oral bioavailability values of OXA/DCK and 5-FU in the nanoemulsive system were 9.19- and 1.39-fold higher than those of free OXA and 5-FU, respectively. Fluorouracil 153-157 deoxycytidine kinase Mus musculus 27-30 27942212-10 2016 The oral absorption of OXA/DCK and 5-FU from the nanoemulsion also increased significantly, and the resulting oral bioavailability values of OXA/DCK and 5-FU in the nanoemulsive system were 9.19- and 1.39-fold higher than those of free OXA and 5-FU, respectively. Fluorouracil 153-157 deoxycytidine kinase Mus musculus 27-30 27500968-6 2016 In addition, the clinical chemotherapeutic drug 5-fluorouracil was used to investigate the impact of GGCT silencing on drug sensitivity by an Annexin V/7-AAD double-staining assay. Fluorouracil 48-62 gamma-glutamylcyclotransferase Homo sapiens 101-105 27578004-0 2016 Histone H3K27 Trimethylation Modulates 5-Fluorouracil Resistance by Inhibiting PU.1 Binding to the DPYD Promoter. Fluorouracil 39-53 dihydropyrimidine dehydrogenase Homo sapiens 99-103 27578004-2 2016 Dihydropyrimidine dehydrogenase (DPD) is a major determinant of 5-FU response and toxicity. Fluorouracil 64-68 dihydropyrimidine dehydrogenase Homo sapiens 0-31 27578004-2 2016 Dihydropyrimidine dehydrogenase (DPD) is a major determinant of 5-FU response and toxicity. Fluorouracil 64-68 dihydropyrimidine dehydrogenase Homo sapiens 33-36 27578004-3 2016 Although DPYD variants may affect 5-FU metabolism, they do not completely explain the reported variability in DPD function or the resultant differences in treatment response. Fluorouracil 34-38 dihydropyrimidine dehydrogenase Homo sapiens 9-13 27578004-4 2016 Here, we report that H3K27 trimethylation (H3K27me3) at the DPYD promoter regulated by Ezh2 and UTX suppresses DPYD expression by inhibiting transcription factor PU.1 binding, leading to increased resistance to 5-FU. Fluorouracil 211-215 dihydropyrimidine dehydrogenase Homo sapiens 60-64 27578004-4 2016 Here, we report that H3K27 trimethylation (H3K27me3) at the DPYD promoter regulated by Ezh2 and UTX suppresses DPYD expression by inhibiting transcription factor PU.1 binding, leading to increased resistance to 5-FU. Fluorouracil 211-215 dihydropyrimidine dehydrogenase Homo sapiens 111-115 27578004-6 2016 Lastly, tumor expression data suggest that DPYD repression by Ezh2 predicts poor survival in 5-FU-treated cancers. Fluorouracil 93-97 dihydropyrimidine dehydrogenase Homo sapiens 43-47 27578004-7 2016 Collectively, the findings of the present article suggest that a previously uncharacterized mechanism regulates DPD expression and may contribute to tumor resistance to 5-FU. Fluorouracil 169-173 dihydropyrimidine dehydrogenase Homo sapiens 112-115 27899780-4 2016 Two cycles of TACE with 5-FU, DOC, MMC, and superabsorbent polymer microspheres(SAP-MS)with BV resulted in considerable reduction of the tumor thrombus. Fluorouracil 24-28 ADAM metallopeptidase domain 17 Homo sapiens 14-18 27899782-7 2016 Consequently, it was decided to treat the patient with trans-arterial chemoembolization(TACE)by selectingintra -arterial infusion of 5-FU, epirubicin(EPI), and mitomycin C prior to EPI-loaded HepaSphere(super-absorbent polymer microsphere)embolization, combined with concurrent systemic gemcitabine chemotherapy. Fluorouracil 133-137 ADAM metallopeptidase domain 17 Homo sapiens 88-92 27245475-10 2016 CONCLUSIONS: Because hENT1 and OAT2 are crucial for the uptake of gemcitabine and 5-fluorouracil, respectively, our results suggest that patients with AFP-producing GC could potentially benefit from gemcitabine/fluoropyrimidine combination chemotherapy. Fluorouracil 82-96 solute carrier family 22 member 7 Homo sapiens 31-35 27716991-0 2016 Early-Onset 5-Fluorouracil Toxicity in a Patient Negative for Dihydropyrimidine Dehydrogenase Mutations: The Clinical Course of Reversal with Uridine Triacetate. Fluorouracil 12-26 dihydropyrimidine dehydrogenase Homo sapiens 62-93 27509880-2 2016 In the present study, we found that a very low concentration of depsipeptide, an HDAC inhibitor, potentiated the antitumor activity of 5-fluorouracil (5-FU) in a human colon cancer cell model using HCT-116, HT29, and SW48 cells via the inhibition of colony formation ability or cellular viability. Fluorouracil 135-149 histone deacetylase 9 Homo sapiens 81-85 27509880-2 2016 In the present study, we found that a very low concentration of depsipeptide, an HDAC inhibitor, potentiated the antitumor activity of 5-fluorouracil (5-FU) in a human colon cancer cell model using HCT-116, HT29, and SW48 cells via the inhibition of colony formation ability or cellular viability. Fluorouracil 151-155 histone deacetylase 9 Homo sapiens 81-85 27468921-2 2016 METHODS: Protein content of ABCC10 and ABCC11 was assessed in tumor tissue blocks of 140 colorectal cancer patients and associated with survival of patients with regard to 5-fluorouracil-based therapy. Fluorouracil 172-186 ATP binding cassette subfamily C member 11 Homo sapiens 39-45 27468921-5 2016 Analysis of patients treated with regimens based on 5-fluorouracil revealed that patients with low ABCC11 content in their tumors had shorter disease-free interval than those with higher content (P = 0.024). Fluorouracil 52-66 ATP binding cassette subfamily C member 11 Homo sapiens 99-105 27602108-7 2016 In addition, MTS assays demonstrated that SYK(L) and SYK(S) increased the cellular sensitivity to 5-fluorouracil (5-FU), suggesting that SYK(L) and 5-FU produce a significant synergistic effect on CRC cell proliferation, while SYK(S) has an effect on modulating CRC 5-FU sensitivity. Fluorouracil 148-152 spleen associated tyrosine kinase Homo sapiens 53-59 27602108-7 2016 In addition, MTS assays demonstrated that SYK(L) and SYK(S) increased the cellular sensitivity to 5-fluorouracil (5-FU), suggesting that SYK(L) and 5-FU produce a significant synergistic effect on CRC cell proliferation, while SYK(S) has an effect on modulating CRC 5-FU sensitivity. Fluorouracil 148-152 spleen associated tyrosine kinase Homo sapiens 53-56 27602108-7 2016 In addition, MTS assays demonstrated that SYK(L) and SYK(S) increased the cellular sensitivity to 5-fluorouracil (5-FU), suggesting that SYK(L) and 5-FU produce a significant synergistic effect on CRC cell proliferation, while SYK(S) has an effect on modulating CRC 5-FU sensitivity. Fluorouracil 148-152 spleen associated tyrosine kinase Homo sapiens 227-233 27299503-8 2016 Similar to the in vitro coculture stress, in vivo genotoxic stress in 5-FU-treated Sfrp2(-) (/) (-) mice increased cell cycle activity of LSK cells with higher levels of BrdU incorporation, increased expression of Ki-67, and canonical Wnt signaling. Fluorouracil 70-74 secreted frizzled-related protein 2 Mus musculus 83-88 27299503-8 2016 Similar to the in vitro coculture stress, in vivo genotoxic stress in 5-FU-treated Sfrp2(-) (/) (-) mice increased cell cycle activity of LSK cells with higher levels of BrdU incorporation, increased expression of Ki-67, and canonical Wnt signaling. Fluorouracil 70-74 antigen identified by monoclonal antibody Ki 67 Mus musculus 214-219 27527606-7 2016 RESULTS: Upon treatment with 5-fluorouracil (5-FU), apoptosis was increased in latently infected ACH2 cells encoding competent p53 compared with uninfected parent A3.01 cells, while the apoptosis of latently infected p53 null J1.1 cells was less than that of uninfected cells. Fluorouracil 45-49 acyl-CoA thioesterase 1 Homo sapiens 97-101 27527606-8 2016 Treatment with 5-FU increased the levels of cleaved caspase-3 and PARP in ACH2 cells compared with uninfected and latently infected p53 null J1.1 cells. Fluorouracil 15-19 acyl-CoA thioesterase 1 Homo sapiens 74-78 27648358-5 2016 Knockdown of PCDH20 expression increases Akt phosphorylation, which leads to elevated mTOR activity and enhanced 5-fluorouracil resistance; whereas rescue of PCDH20 expression in miR-122-expressing cells decreases Akt and mTOR phosphorylation, re-sensitizing hepatocellular carcinoma cell to 5-fluorouracil induced apoptosis. Fluorouracil 292-306 microRNA 122 Homo sapiens 179-186 27648358-6 2016 Moreover, a specific and potent Akt inhibitor reverses miR-122-conferred 5-fluorouracil resistance. Fluorouracil 73-87 microRNA 122 Homo sapiens 55-62 27648358-8 2016 A major implication of our study is that inhibition of miR-122 or restoration of PCDH20 expression may have significant therapeutic potential to overcome drug resistance in hepatocellular carcinoma and that the combined use of an Akt inhibitor with 5-fluorouracil may increase efficacy in liver cancer treatment. Fluorouracil 249-263 microRNA 122 Homo sapiens 55-62 26216193-0 2016 Genotype-phenotype correlations in 5-fluorouracil metabolism: a candidate DPYD haplotype to improve toxicity prediction. Fluorouracil 35-49 dihydropyrimidine dehydrogenase Homo sapiens 74-78 26216193-3 2016 This study aimed to correlate a phenotypic marker of 5-fluorouracil metabolism (the individual degradation rate of 5-fluorouracil-5-FUDR) with 15 functional polymorphisms in the dihydropyrimidine dehydrogenase gene (DPYD). Fluorouracil 53-67 dihydropyrimidine dehydrogenase Homo sapiens 178-209 26216193-3 2016 This study aimed to correlate a phenotypic marker of 5-fluorouracil metabolism (the individual degradation rate of 5-fluorouracil-5-FUDR) with 15 functional polymorphisms in the dihydropyrimidine dehydrogenase gene (DPYD). Fluorouracil 53-67 dihydropyrimidine dehydrogenase Homo sapiens 216-220 26216193-7 2016 Haplotype assessment could improve the predictive value of DPYD genetic markers aimed at the pre-emptive identification of patients at risk of severe 5-fluorouracil toxicity.The Pharmacogenomics Journal advance online publication, 28 July 2015; doi:10.1038/tpj.2015.56. Fluorouracil 150-164 dihydropyrimidine dehydrogenase Homo sapiens 59-63 26886287-9 2016 LY294002 inhibits the proliferation and invasion of MHCC97H-derived CD90+ LCCs and sensitized CD90+ LCCs-derived tumors to 5-FU in the current study which may provide insight into the association between the LY294002 combined 5-FU and liver cancer stem cell (LCSCs). Fluorouracil 123-127 GLE1 RNA export mediator Homo sapiens 100-104 27323852-6 2016 In vivo, NNMT attenuates 5-FU-induced inhibition of CRC tumor growth in nude mice. Fluorouracil 25-29 nicotinamide N-methyltransferase Mus musculus 9-13 27175567-0 2016 B7-H3 upregulates BRCC3 expression, antagonizing DNA damage caused by 5-Fu. Fluorouracil 70-74 BRCA1/BRCA2-containing complex subunit 3 Homo sapiens 18-23 27175567-5 2016 In SW480 cells that overexpress B7-H3, knockdown of BRCC3 similarly permitted greater 5-Fu-induced DNA damage. Fluorouracil 86-90 BRCA1/BRCA2-containing complex subunit 3 Homo sapiens 52-57 27175567-6 2016 Altogether, results suggest that BRCC3 may play a role in B7-H3-induced 5-Fu resistance, such that B7-H3 upregulates BRCC3 expression, enhancing DNA repair in colorectal cancer cells. Fluorouracil 72-76 BRCA1/BRCA2-containing complex subunit 3 Homo sapiens 33-38 27175567-6 2016 Altogether, results suggest that BRCC3 may play a role in B7-H3-induced 5-Fu resistance, such that B7-H3 upregulates BRCC3 expression, enhancing DNA repair in colorectal cancer cells. Fluorouracil 72-76 BRCA1/BRCA2-containing complex subunit 3 Homo sapiens 117-122 26787540-2 2016 In this study, we found that overexpression of B7-H3 protected SW80 and HCT8 cells from 5-fluorouracil (5-FU) using CCK-8 assays by inducing resistance to 5-FU chemotherapy. Fluorouracil 88-102 CD276 antigen Mus musculus 47-52 26787540-2 2016 In this study, we found that overexpression of B7-H3 protected SW80 and HCT8 cells from 5-fluorouracil (5-FU) using CCK-8 assays by inducing resistance to 5-FU chemotherapy. Fluorouracil 104-108 CD276 antigen Mus musculus 47-52 26787540-2 2016 In this study, we found that overexpression of B7-H3 protected SW80 and HCT8 cells from 5-fluorouracil (5-FU) using CCK-8 assays by inducing resistance to 5-FU chemotherapy. Fluorouracil 155-159 CD276 antigen Mus musculus 47-52 26787540-5 2016 These results implied that B7-H3 can induce colorectal cancer cell resistance to 5-FU by increasing TS expression and PI3K/Akt/TS signaling and plays an important role during these processes. Fluorouracil 81-85 CD276 antigen Mus musculus 27-32 26787540-5 2016 These results implied that B7-H3 can induce colorectal cancer cell resistance to 5-FU by increasing TS expression and PI3K/Akt/TS signaling and plays an important role during these processes. Fluorouracil 81-85 thymidylate synthase Mus musculus 100-102 27446484-6 2016 Because dihydropyrimidine dehydrogenase (DPD) was reported to be involved in 5-FU metabolism to block DNA damage, we compared the survival rate with 5-FU treatment and the level of DPD expression in 15 different glioma cell lines. Fluorouracil 77-81 dihydropyrimidine dehydrogenase Homo sapiens 8-39 27446484-6 2016 Because dihydropyrimidine dehydrogenase (DPD) was reported to be involved in 5-FU metabolism to block DNA damage, we compared the survival rate with 5-FU treatment and the level of DPD expression in 15 different glioma cell lines. Fluorouracil 77-81 dihydropyrimidine dehydrogenase Homo sapiens 41-44 27446484-6 2016 Because dihydropyrimidine dehydrogenase (DPD) was reported to be involved in 5-FU metabolism to block DNA damage, we compared the survival rate with 5-FU treatment and the level of DPD expression in 15 different glioma cell lines. Fluorouracil 149-153 dihydropyrimidine dehydrogenase Homo sapiens 41-44 27446484-7 2016 DPD-deficient cells showed higher sensitivity to 5-FU, and the regulation of DPD level by either siRNA or overexpression was directly related to the 5-FU sensitivity. Fluorouracil 49-53 dihydropyrimidine dehydrogenase Homo sapiens 0-3 27446484-7 2016 DPD-deficient cells showed higher sensitivity to 5-FU, and the regulation of DPD level by either siRNA or overexpression was directly related to the 5-FU sensitivity. Fluorouracil 149-153 dihydropyrimidine dehydrogenase Homo sapiens 0-3 27868409-7 2016 After treatment with different concentrations of cisplatin or 5-FU, the survival rate of the two cell groups was reduced (all P<0.05), and the IC50 of RAD18-siRNA group was significantly lower than that of non-transfected group (P<0.05). Fluorouracil 62-66 RAD18 E3 ubiquitin protein ligase Homo sapiens 154-159 26794347-0 2016 DPYD Genotyping to Predict Adverse Events Following Treatment With Fluorouracil-Based Adjuvant Chemotherapy in Patients With Stage III Colon Cancer: A Secondary Analysis of the PETACC-8 Randomized Clinical Trial. Fluorouracil 67-79 dihydropyrimidine dehydrogenase Homo sapiens 0-4 26794347-1 2016 Importance: Previous pharmacogenetic studies have shown the prognostic impact of several rare dihydropyrimidine dehydrogenase gene (DPYD) variants on fluorouracil-related adverse events (fluorouracil AEs). Fluorouracil 150-162 dihydropyrimidine dehydrogenase Homo sapiens 132-136 26794347-3 2016 Objective: To determine the impact of DPYD variants on fluorouracil AEs in patients with stage III CC treated with a fluorouracil, leucovorin, and oxaliplatin (FOLFOX4) regimen. Fluorouracil 55-67 dihydropyrimidine dehydrogenase Homo sapiens 38-42 26794347-3 2016 Objective: To determine the impact of DPYD variants on fluorouracil AEs in patients with stage III CC treated with a fluorouracil, leucovorin, and oxaliplatin (FOLFOX4) regimen. Fluorouracil 117-129 dihydropyrimidine dehydrogenase Homo sapiens 38-42 26794347-9 2016 The incidence of grade 3 or greater fluorouracil AEs in D949V and V732I (DPYD*6) carriers was 18 in 21 (85.7%) and 121 in 199 (60.8%), respectively. Fluorouracil 36-48 dihydropyrimidine dehydrogenase Homo sapiens 73-77 26794347-13 2016 Conclusions and Relevance: In this large phase 3 study, statistically significant associations were found between DPYD variants (D949V and V732I) and increased incidence of grade 3 or greater fluorouracil AEs in patients treated with adjuvant fluorouracil-based combination chemotherapy. Fluorouracil 192-204 dihydropyrimidine dehydrogenase Homo sapiens 114-118 26794347-13 2016 Conclusions and Relevance: In this large phase 3 study, statistically significant associations were found between DPYD variants (D949V and V732I) and increased incidence of grade 3 or greater fluorouracil AEs in patients treated with adjuvant fluorouracil-based combination chemotherapy. Fluorouracil 243-255 dihydropyrimidine dehydrogenase Homo sapiens 114-118 27009861-7 2016 Bisulfite sequencing polymerase chain reaction showed that demethylation of the Sox2 promoter by 5-FU resulted in Sox2 expression in the dormant stem cells. Fluorouracil 97-101 SRY-box transcription factor 2 Homo sapiens 80-84 27009861-7 2016 Bisulfite sequencing polymerase chain reaction showed that demethylation of the Sox2 promoter by 5-FU resulted in Sox2 expression in the dormant stem cells. Fluorouracil 97-101 SRY-box transcription factor 2 Homo sapiens 114-118 27027355-2 2016 We found that low dose 5-FU selectively suppresses TH17 and TH1 cell differentiation without apparent effect on Treg, TH2, and significantly suppresses thymidylate synthase (TS) expression in TH17 and TH1 cells but has a lesser effect in tumor cells and macrophages. Fluorouracil 23-27 negative elongation factor complex member C/D Homo sapiens 51-54 27027355-2 2016 We found that low dose 5-FU selectively suppresses TH17 and TH1 cell differentiation without apparent effect on Treg, TH2, and significantly suppresses thymidylate synthase (TS) expression in TH17 and TH1 cells but has a lesser effect in tumor cells and macrophages. Fluorouracil 23-27 negative elongation factor complex member C/D Homo sapiens 60-63 27027355-4 2016 Finally, low dose 5-FU is effective in ameliorating colitis development by suppressing TH17 and TH1 cell development in a T cell transfer colitis model. Fluorouracil 18-22 negative elongation factor complex member C/D Homo sapiens 87-90 27027355-5 2016 Taken together, the results highlight the importance of the anti-inflammatory functions of low dose 5-FU by selectively suppressing TH17 and TH1 immune responses. Fluorouracil 100-104 negative elongation factor complex member C/D Homo sapiens 132-135 26804652-1 2016 Dihydropyrimidine dehydrogenase (DPD) is the initial and rate-limiting enzyme in the catabolism of the pyrimidine bases uracil, thymine and the antineoplastic agent 5-fluorouracil. Fluorouracil 165-179 dihydropyrimidine dehydrogenase Homo sapiens 33-36