PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 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 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 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 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 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 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 33613715-11 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 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 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 33389946-6 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 33389946-7 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 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 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 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 125-129 tumor protein p53 Homo sapiens 57-60 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 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 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 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 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 32457882-12 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 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 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 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 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 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 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 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 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 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 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 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 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 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 31544060-10 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 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 31592435-11 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 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 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 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 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 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 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 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 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 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 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 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 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 30059758-10 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 28928082-1 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 28928082-8 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 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 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 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 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 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 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 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 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 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 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 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 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 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 28178647-6 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 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 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 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 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 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 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 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 tumor protein p53 Homo sapiens 31-34 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 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 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 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 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 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 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 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 27621580-8 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 27621580-1 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 79-82 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 27621580-1 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 27621580-6 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 27621580-6 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 27621580-8 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 27621580-9 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 27621580-9 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 27621580-10 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 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 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 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 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 29-43 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 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 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 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 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 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 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 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 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 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 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 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 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 26774139-8 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 24634414-6 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 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 24733045-7 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 24733045-8 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 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 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 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 24587255-5 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 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 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 tumor protein p53 Homo sapiens 158-161 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 tumor protein p53 Homo sapiens 37-40 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 tumor protein p53 Homo sapiens 124-127 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 22192357-5 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 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 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 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 21674128-4 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 21674128-9 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 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 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 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 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 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 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 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 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 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 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 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 21036698-8 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 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 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 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 20704765-12 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 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 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 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 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 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 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 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 tumor protein p53 Homo sapiens 62-65 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 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 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 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 19810096-8 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 18497992-9 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 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 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 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 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 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 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 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 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 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 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 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 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 17982676-1 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 47-51 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 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 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 298-302 tumor protein p53 Homo sapiens 47-51 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 17982676-8 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 17982676-1 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 17982676-8 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 17982676-2 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 17982676-6 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 17982676-6 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 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 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 17275163-8 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 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 17634554-0 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 17634554-13 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 17634554-1 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 17634554-3 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 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 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 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 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 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 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 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 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 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 17056233-13 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 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 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 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 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 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 75-79 tumor protein p53 Homo sapiens 20-23 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 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 tumor protein p53 Homo sapiens 95-98 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 17207318-0 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 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 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 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 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 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 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 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 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 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 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 tumor protein p53 Homo sapiens 58-61 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 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 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 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 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 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 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 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 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 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 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 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 15886465-11 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 15124184-8 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 122-126 tumor protein p53 Homo sapiens 180-183 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 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 15041737-9 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 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 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 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 15041737-8 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 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 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 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 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 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 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 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 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 15520875-11 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 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 tumor protein p53 Homo sapiens 246-249 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 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 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 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 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 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 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 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 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 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 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 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 12776195-7 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 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 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 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 12530065-7 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 12530065-8 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 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 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 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 12115540-2 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 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 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 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 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 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 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 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 11920608-6 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 11044365-2 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 11044365-2 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 11044365-2 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 11044365-5 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 11044365-5 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 99-103 tumor protein p53 Homo sapiens 47-50 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 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 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 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 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 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 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 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 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 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 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 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 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 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 14646558-8 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 tumor protein p53 Homo sapiens 324-327 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 45-49 tumor protein p53 Homo sapiens 120-123 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 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 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 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 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 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 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 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 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 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 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 35071232-14 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 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