PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 23822592-9 2013 EGFR mAbs combined with oxaliplatin and an infusional 5-FU regimen was associated with significantly improved RR, PFS and OS as first-line treatment in KRAS wild-type mCRC. Fluorouracil 54-58 KRAS proto-oncogene, GTPase Homo sapiens 152-156 24211581-10 2013 Moreover, we found that 5-aza-2"-deoxycytidine-mediated or enforced up-regulation of BNIP3 in DLD-1 cells results in KRas-dependent resistance to 5-Fluorouracil. Fluorouracil 146-160 KRAS proto-oncogene, GTPase Homo sapiens 117-121 23730514-9 2013 For two patients, KRAS mutation status changed after application of neoadjuvant 5-FU radiochemotherapy. Fluorouracil 80-84 KRAS proto-oncogene, GTPase Homo sapiens 18-22 23689915-3 2013 METHODS: Newly diagnosed K-RAS wild-type colorectal cancer patients with unresectable liver-only metastases were treated with 5-fluorouracil, leucovorin, and oxaliplatin (FOLFOX6) plus cetuximab every 2 weeks for a maximum of 12 cycles. Fluorouracil 126-140 KRAS proto-oncogene, GTPase Homo sapiens 25-30 23730514-12 2013 CONCLUSIONS: So one can conclude that (I) KRAS mutations status may change after neoadjuvant 5-FU radiochemotherapy relevant for further therapeutic decisions; (II) MSI-H patients do not respond to neoadjuvant 5-FU radiochemotherapy. Fluorouracil 93-97 KRAS proto-oncogene, GTPase Homo sapiens 42-46 23555026-9 2013 These results suggest that combining ISC-4 and cetuximab should be explored in patients with 5-FU-resistant colon cancer harboring wild-type KRAS. Fluorouracil 93-97 KRAS proto-oncogene, GTPase Homo sapiens 141-145 22740893-0 2012 Good response to leucovorin and fluorouracil plus oxaliplatin and cetuximab therapy in a patient with metastatic ascending colon cancer harboring a KRAS p.G13D mutation. Fluorouracil 32-44 KRAS proto-oncogene, GTPase Homo sapiens 148-152 21855038-1 2011 BACKGROUND: This prospective analysis evaluated the effect of tumor KRAS status on efficacy of second-line panitumumab plus folinic acid/5-fluorouracil/irinotecan (FOLFIRI). Fluorouracil 137-151 KRAS proto-oncogene, GTPase Homo sapiens 68-72 20972872-3 2011 The aim of this study was to evaluate the association between k-ras status and addition of oxaliplatin to fluorouracil plus leucovorin (FOLFOX) chemotherapy in CRC patients with curative surgical resection. Fluorouracil 106-118 KRAS proto-oncogene, GTPase Homo sapiens 62-67 21228335-1 2011 BACKGROUND: The randomized phase II OPUS (Oxaliplatin and Cetuximab in First-Line Treatment of Metastatic Colorectal Cancer) study showed that tumor KRAS mutation status was predictive for outcome in patients receiving cetuximab plus FOLFOX-4 (oxaliplatin/5-fluorouracil/folinic acid) as first-line therapy for metastatic colorectal cancer (mCRC). Fluorouracil 256-270 KRAS proto-oncogene, GTPase Homo sapiens 149-153 9816002-3 1995 We studied 37 patients who received chemotherapy with 5-fluorouracil and leucovorin, Exon 1 of the c-K-ras gene was PCR amplified from DNA extracted from paraffin-embedded tumor blocks. Fluorouracil 54-68 KRAS proto-oncogene, GTPase Homo sapiens 99-106 21635994-6 2011 RESULTS: For the metastatic colorectal cancer LLD population with K-ras wild-type genotype, mean overall survival estimates were 37.7 months for first-line treatment with cetuximab plus FOLFIRI (irinotecan, leucovorin, fluorouracil) and 30.4 months for bevacizumab plus FOLFOX (oxaliplatin, leucovorin, fluorouracil). Fluorouracil 219-231 KRAS proto-oncogene, GTPase Homo sapiens 66-71 21635994-6 2011 RESULTS: For the metastatic colorectal cancer LLD population with K-ras wild-type genotype, mean overall survival estimates were 37.7 months for first-line treatment with cetuximab plus FOLFIRI (irinotecan, leucovorin, fluorouracil) and 30.4 months for bevacizumab plus FOLFOX (oxaliplatin, leucovorin, fluorouracil). Fluorouracil 303-315 KRAS proto-oncogene, GTPase Homo sapiens 66-71 22811812-3 2010 In this study, we aimed to address the impact of KRAS on the pattern of metastatic disease at presentation and on RR and PFS with first-line 5-fluorouracil, leucovorin, and oxaliplatin (FOLFOX) chemotherapy. Fluorouracil 141-155 KRAS proto-oncogene, GTPase Homo sapiens 49-53 20740189-4 2010 Case Reports: Here we describe the cases of 2 patients with metastatic KRAS wild-type colorectal cancer who received a fourth-line monotherapy with panitumumab after failure of 5-fluorouracil, irinotecan, oxaliplatin, and bevacizumab. Fluorouracil 177-191 KRAS proto-oncogene, GTPase Homo sapiens 71-75 20354524-5 2010 A multiplexed RT-PCR assay was used to identify KRAS-controlled apoptosis regulators after exposure to 5-FU or oxaliplatin. Fluorouracil 103-107 KRAS proto-oncogene, GTPase Homo sapiens 48-52 20354524-7 2010 RESULTS: Oncogenic KRAS sensitised colorectal tumour cells to oxaliplatin and 5-FU in a p53-dependent manner and promoted p53 phosphorylation at Ser37 and Ser392, without affecting p53 stabilisation, p21 induction, or cell-cycle arrest. Fluorouracil 78-82 KRAS proto-oncogene, GTPase Homo sapiens 19-23 20354524-11 2010 CONCLUSION: Oncogenic KRAS determines the cellular response to p53 activation by oxaliplatin or 5-FU, by facilitating apoptosis induction through Noxa. Fluorouracil 96-100 KRAS proto-oncogene, GTPase Homo sapiens 22-26 12827409-8 2004 CONCLUSION: Considering also our own findings, this review presents the latest developments in the scientific discussion of the tumor suppressor/oncogenes p53, k-ras, and DCC, biochemical determinants of the 5-fluorouracil metabolism, and defects of the DNA repair system. Fluorouracil 208-222 KRAS proto-oncogene, GTPase Homo sapiens 160-165 11745689-8 2001 These results suggest that the type of Ki-ras mutation could be a clinically useful molecular marker for the identification of CRC subgroups that are likely to benefit from 5-fluorouracil-based adjuvant chemotherapy. Fluorouracil 173-187 KRAS proto-oncogene, GTPase Homo sapiens 39-45 9515799-12 1998 In stage III, adjuvant therapy with 5FU plus levamisole improved 7-year survival in patients with wild-type Ki-ras (76 versus 44%; HR, 0.4; 95% CI, 0.2-0.8) and in those without p53 overexpression (64 versus 26%; HR, 0.3; 95% CI, 0.1-0.7). Fluorouracil 36-39 KRAS proto-oncogene, GTPase Homo sapiens 108-114 9515799-16 1998 Exploratory analyses suggest that patients with stage III colon cancer with wild-type Ki-ras or no p53 expression benefit from adjuvant 5FU plus levamisole, whereas those with Ki-ras mutations or p53 overexpression do not. Fluorouracil 136-139 KRAS proto-oncogene, GTPase Homo sapiens 86-92 9345343-0 1997 Irinotecan hydrochloride (CPT-11) resistance identified by K-ras mutation in patients with progressive colon cancer after treatment with 5-fluorouracil (5-FU). Fluorouracil 137-151 KRAS proto-oncogene, GTPase Homo sapiens 59-64 9345343-0 1997 Irinotecan hydrochloride (CPT-11) resistance identified by K-ras mutation in patients with progressive colon cancer after treatment with 5-fluorouracil (5-FU). Fluorouracil 153-157 KRAS proto-oncogene, GTPase Homo sapiens 59-64 9345343-9 1997 CONCLUSION: Determination of the presence of a K-ras mutation may predict survival in patients with progressive colon cancer after treatment with 5-fluorouracil who receive CPT-11. Fluorouracil 146-160 KRAS proto-oncogene, GTPase Homo sapiens 47-52 9327152-0 1997 Prognostic implications of c-Ki-ras2 mutations in patients with advanced colorectal cancer treated with 5-fluorouracil and interferon: a study of the eastern cooperative oncology group (EST 2292) PURPOSE: Mutations in c-Ki-ras2 (ras) occur in about 40% of patients with colorectal cancers and occur early in the pathogenesis of this disease. Fluorouracil 104-118 KRAS proto-oncogene, GTPase Homo sapiens 27-36 9327152-0 1997 Prognostic implications of c-Ki-ras2 mutations in patients with advanced colorectal cancer treated with 5-fluorouracil and interferon: a study of the eastern cooperative oncology group (EST 2292) PURPOSE: Mutations in c-Ki-ras2 (ras) occur in about 40% of patients with colorectal cancers and occur early in the pathogenesis of this disease. Fluorouracil 104-118 KRAS proto-oncogene, GTPase Homo sapiens 218-227 9816002-10 1995 Patients with colon cancers bearing either wild-type or mutant c-K-ras alleles are indistinguishable in overall survival and are equally likely to respond to 5-fluorouracil-based chemotherapy. Fluorouracil 158-172 KRAS proto-oncogene, GTPase Homo sapiens 63-70 32062671-1 2020 BACKGROUND The aim of this study was to perform an accurate exploration on the efficacy of oxaliplatin/5-fluorouracil/capecitabine-cetuximab combination therapy and its effects on K-Ras mutations in advanced colorectal cancer. Fluorouracil 103-117 KRAS proto-oncogene, GTPase Homo sapiens 180-185 35445157-0 2022 Synergistic combination of PMBA and 5-fluorouracil (5-FU) in targeting mutant KRAS in 2D and 3D colorectal cancer cells. Fluorouracil 36-50 KRAS proto-oncogene, GTPase Homo sapiens 78-82 35445157-0 2022 Synergistic combination of PMBA and 5-fluorouracil (5-FU) in targeting mutant KRAS in 2D and 3D colorectal cancer cells. Fluorouracil 52-56 KRAS proto-oncogene, GTPase Homo sapiens 78-82 35445157-2 2022 The study has been conducted to investigate the effect and efficacy of 2-pyridin-4-yl methylene beta-boswellic acid (PMBA) and 5-Flourouracil (5-FU) in combination therapy for the treatment of KRAS mutant colon cancer. Fluorouracil 143-147 KRAS proto-oncogene, GTPase Homo sapiens 193-197 35445157-6 2022 When examined for plasma level of PMBA (20 mg) and PMBA+5-FU (20 + 40 mg), a time-dependent increase in the level of the drug (5-FU) was detected, indicating its absorption and bioavailability with excellent half-life of the PMBA for both routes of administration (IV and Oral), thereby indicating a new adjuvant therapy for KRAS mutant colon cancer. Fluorouracil 56-60 KRAS proto-oncogene, GTPase Homo sapiens 325-329 35445157-6 2022 When examined for plasma level of PMBA (20 mg) and PMBA+5-FU (20 + 40 mg), a time-dependent increase in the level of the drug (5-FU) was detected, indicating its absorption and bioavailability with excellent half-life of the PMBA for both routes of administration (IV and Oral), thereby indicating a new adjuvant therapy for KRAS mutant colon cancer. Fluorouracil 127-131 KRAS proto-oncogene, GTPase Homo sapiens 325-329 32814111-20 2020 Knockout of SLC25A22 in CRC cells that express mutant KRAS increased their sensitivity to 5-fluorouacil. Fluorouracil 90-103 KRAS proto-oncogene, GTPase Homo sapiens 54-58 32814111-22 2020 CONCLUSIONS: In CRC cells that express activated KRAS, SLC25A22 promotes accumulation of succinate, resulting in increased DNA methylation, activation of WNT signaling to beta-catenin, increased expression of LGR5, proliferation, stem cell features, and resistance to 5-fluorouacil. Fluorouracil 268-281 KRAS proto-oncogene, GTPase Homo sapiens 49-53 32879665-0 2020 Interleukin-1 receptor antagonist enhances chemosensitivity to fluorouracil in treatment of Kras mutant colon cancer. Fluorouracil 63-75 KRAS proto-oncogene, GTPase Homo sapiens 92-96 34951582-7 2022 EGFR and KRAS gene expression analysis under the influence of PFNPs, FGNPs, PFGNPs, and 5-FU was studied and observed maximum potency for PFNPs. Fluorouracil 88-92 KRAS proto-oncogene, GTPase Homo sapiens 9-13 34360807-7 2021 In Caco-2 cells, LMWF enhanced the suppressive effects of 5-FU on cell viability through both the c-mesenchymal-epithelial transition (MET)/Kirsten rat sarcoma virus (KRAS)/extracellular signal-regulated kinase (ERK) and the c-MET/phosphatidyl-inositol 3-kinases (PI3K)/protein kinase B (AKT) signaling pathways. Fluorouracil 58-62 KRAS proto-oncogene, GTPase Homo sapiens 167-171 33120790-4 2020 PATIENT CONCERNS: A 72-year-old man diagnosed with stage IV rectal adenocarcinoma (KRAS mutation) with peritoneal carcinomatosis and liver metastases developed resistance to 2 lines of treatment (bevacizumab/irinotecan/S-1 and bevacizumab/oxaliplatin/HDFL [high-dose 24-hour infusion of 5-fluorouracil and leucovorin regimen]) within 5 months. Fluorouracil 287-301 KRAS proto-oncogene, GTPase Homo sapiens 83-87 32990544-13 2021 CONCLUSION: We suggest that inhibition of autophagy along with Pd(II) and 5-FU treatment has a synergistic effect in KRAS-mutant colorectal cancer cells. Fluorouracil 74-78 KRAS proto-oncogene, GTPase Homo sapiens 117-121 30579838-0 2019 Schedule-dependent synergistic effects of 5-fluorouracil and selumetinib in KRAS or BRAF mutant colon cancer models. Fluorouracil 42-56 KRAS proto-oncogene, GTPase Homo sapiens 76-80 31126331-1 2019 BACKGROUND: The 5-fluorouracil/leucovorin plus oxaliplatin (FOLFOX) regimen is the standard first-line treatment for metastatic colorectal cancer (mCRC), however, the optimal second-line regimen for KRAS wild-type mCRC patients is still investigational. Fluorouracil 16-30 KRAS proto-oncogene, GTPase Homo sapiens 199-203 31010234-10 2019 Treatment with 5-fluorouracil (5-FU) significantly enhanced YB-1 phosphorylation in KRAS(G13D)-mutated HCT116 cells but not in KRAS wild-type SW48 cells. Fluorouracil 15-29 KRAS proto-oncogene, GTPase Homo sapiens 84-88 31010234-10 2019 Treatment with 5-fluorouracil (5-FU) significantly enhanced YB-1 phosphorylation in KRAS(G13D)-mutated HCT116 cells but not in KRAS wild-type SW48 cells. Fluorouracil 31-35 KRAS proto-oncogene, GTPase Homo sapiens 84-88 30579838-12 2019 Our results suggest that sequential administration of 5-FU plus selumetinib would be a promising strategy for patients having KRAS or BRAF mutant colon cancers. Fluorouracil 54-58 KRAS proto-oncogene, GTPase Homo sapiens 126-130 30307354-2 2019 CASE PRESENTATION: Here we present a KRAS/NRAS/BRAF wild-type mCRC patient who has been previously treated with FOLFIRI (fluorouracil, leucovorin, and irinotecan), XELOX (capecitabine and oxaliplatin), cetuximab and bevacizumab, and then received the next generation sequencing (NGS) and whose metastatic subcutaneous nodule was resected to generate patient-derived xenograft (PDX) models. Fluorouracil 121-133 KRAS proto-oncogene, GTPase Homo sapiens 37-41 30188916-7 2018 Treatment with 5-FU-based regimens improved prognosis in patients with the combination of MSS tumours, KRAS mutation and CIMP negative (log rank P = 0.003) as well as in patients with MSS tumours plus BRAF and KRAS wild-type and CIMP negative (log-rank P<0.001). Fluorouracil 15-19 KRAS proto-oncogene, GTPase Homo sapiens 103-107 30188916-7 2018 Treatment with 5-FU-based regimens improved prognosis in patients with the combination of MSS tumours, KRAS mutation and CIMP negative (log rank P = 0.003) as well as in patients with MSS tumours plus BRAF and KRAS wild-type and CIMP negative (log-rank P<0.001). Fluorouracil 15-19 KRAS proto-oncogene, GTPase Homo sapiens 210-214 26130327-0 2015 5-Fluorouracil preferentially sensitizes mutant KRAS non-small cell lung carcinoma cells to TRAIL-induced apoptosis. Fluorouracil 0-14 KRAS proto-oncogene, GTPase Homo sapiens 48-52 29508026-14 2018 CONCLUSIONS: Fluorouracil monotherapy combined with panitumumab was safely administered to patients with KRAS WT mCRC intolerant to oxaliplatin and irinotecan. Fluorouracil 13-25 KRAS proto-oncogene, GTPase Homo sapiens 105-109 27144434-4 2016 In colon cancer cells, 5-FU exposure impaired endogenous KRAS/MEK5/ERK5 expression and/or activation. Fluorouracil 23-27 KRAS proto-oncogene, GTPase Homo sapiens 57-61 28551618-0 2017 MEK162 Enhances Antitumor Activity of 5-Fluorouracil and Trifluridine in KRAS-mutated Human Colorectal Cancer Cell Lines. Fluorouracil 38-52 KRAS proto-oncogene, GTPase Homo sapiens 73-77 28101205-8 2016 Cytoplasmic KRAS levels decreased whereas nuclear MutS protein homolog 2 (MSH2) levels increased slightly in CRC HCT116 cells that were microsatellite instable, following treatment with 76.9 microM 5-FU for 2 days. Fluorouracil 198-202 KRAS proto-oncogene, GTPase Homo sapiens 12-16 26130327-5 2015 In the current study, we found that NSCLC cells with a KRAS mutation were highly sensitive to treatment with TRAIL and 5-fluorouracil (5FU). Fluorouracil 119-133 KRAS proto-oncogene, GTPase Homo sapiens 55-59 26130327-5 2015 In the current study, we found that NSCLC cells with a KRAS mutation were highly sensitive to treatment with TRAIL and 5-fluorouracil (5FU). Fluorouracil 135-138 KRAS proto-oncogene, GTPase Homo sapiens 55-59 25870609-5 2015 In this study, we propose to analyze the different clinical outcomes and disease prognosis of patients with stage IV CRC treated with FOLFOX chemotherapy (fluorouracil, leucovorin, oxaliplatin) based on different Kirsten ras (KRAS) mutation patterns. Fluorouracil 155-167 KRAS proto-oncogene, GTPase Homo sapiens 213-224 25937522-1 2015 BACKGROUND: The OPUS study demonstrated that addition of cetuximab to 5-fluorouracil, folinic acid and oxaliplatin (FOLFOX4) significantly improved objective response and progression-free survival (PFS) in the first-line treatment of patients with KRAS exon 2 wild-type metastatic colorectal cancer (mCRC). Fluorouracil 70-84 KRAS proto-oncogene, GTPase Homo sapiens 248-252 25919696-0 2015 MicroRNA-224 is associated with colorectal cancer progression and response to 5-fluorouracil-based chemotherapy by KRAS-dependent and -independent mechanisms. Fluorouracil 78-92 KRAS proto-oncogene, GTPase Homo sapiens 115-119 25605843-1 2015 PURPOSE: The phase III CRYSTAL study demonstrated that addition of cetuximab to fluorouracil, leucovorin, and irinotecan (FOLFIRI) significantly improved overall survival, progression-free survival, and objective response in the first-line treatment of patients with KRAS codon 12/13 (exon 2) wild-type metastatic colorectal cancer (mCRC). Fluorouracil 80-92 KRAS proto-oncogene, GTPase Homo sapiens 267-271 25325304-3 2015 We aimed to investigate the effect of silencing both mutant and wild-type Kristen Rous sarcoma (k-ras) on the response of human colorectal tumor 116 (HCT-116) as a colon cancer cell line to the cytotoxic effect of 5-flurouracil (5-FU). Fluorouracil 229-233 KRAS proto-oncogene, GTPase Homo sapiens 96-101 25325304-12 2015 In conclusion, silencing mutant and wild-type k-ras would increase the resistance of HCT-116 cell line as a model of colorectal cancer to 5-FU. Fluorouracil 138-142 KRAS proto-oncogene, GTPase Homo sapiens 46-51 25325304-14 2015 Therefore, both mutant and wild-type k-ras may play a role in sensitizing colorectal cancer cells to 5-FU as a common chemotherapeutic drug. Fluorouracil 101-105 KRAS proto-oncogene, GTPase Homo sapiens 37-42 24889488-2 2015 The purpose of this study was to assess the prognostic impact of KRAS and BRAF mutation in patients treated with adjuvant 5-fluorouracil/leucovorin/oxaliplatin (FOLFOX). Fluorouracil 122-136 KRAS proto-oncogene, GTPase Homo sapiens 65-69 25216706-6 2014 The expression of some K-ras mutations resulted in a reduced sensitivity to gefitinib, 5-FU, docetaxel and gemcitabine, while showed no effects on erlotinib or cisplatin. Fluorouracil 87-91 KRAS proto-oncogene, GTPase Homo sapiens 23-28 24764659-5 2014 The CRYSTAL study showed that adding cetuximab to FOLFIRI (regimen of irinotecan, infusional fluorouracil and leucovorin) significantly improved results in the first-line treatment of KRAS wild-type mCRC. Fluorouracil 93-105 KRAS proto-oncogene, GTPase Homo sapiens 184-188 24692733-0 2014 Multicenter phase II study of second-line cetuximab plus folinic acid/5-fluorouracil/irinotecan (FOLFIRI) in KRAS wild-type metastatic colorectal cancer: the FLIER study. Fluorouracil 70-84 KRAS proto-oncogene, GTPase Homo sapiens 109-113 24692733-1 2014 BACKGROUND: This study was the first multicenter phase II study of cetuximab plus folinic acid/5-fluorouracil/irinotecan (FOLFIRI) in KRAS wild-type mCRC as a second-line treatment in Japan including BRAF and PIK3CA genotyping. Fluorouracil 95-109 KRAS proto-oncogene, GTPase Homo sapiens 134-138 25209093-5 2014 In general, participants agreed that 5-fluorouracil (5-FU) infusion regimens in doublets can be substituted with UFT (capecitabine, tegafur-uracil) and S1 (tegafur, 5-chloro-2,4-dihydroxypyridine and oxonic acid), and that the monoclonal antibodies cetuximab and panitumumab are recommended for KRAS wild type tumors. Fluorouracil 37-51 KRAS proto-oncogene, GTPase Homo sapiens 295-299 25209093-5 2014 In general, participants agreed that 5-fluorouracil (5-FU) infusion regimens in doublets can be substituted with UFT (capecitabine, tegafur-uracil) and S1 (tegafur, 5-chloro-2,4-dihydroxypyridine and oxonic acid), and that the monoclonal antibodies cetuximab and panitumumab are recommended for KRAS wild type tumors. Fluorouracil 53-57 KRAS proto-oncogene, GTPase Homo sapiens 295-299